Clinical Neuroanatomy (LANGE) [29th Edition] 9781260452365

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Clinical Neuroanatomy (LANGE) [29th Edition]

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Table of contents :
Clinical Neuroanatomy, 29th Edition [Stephen G. Waxman]......Page 1
Title Page......Page 3
Copyright......Page 4
Key Features of this Edition......Page 6
Contents......Page 9
Preface......Page 13
Chapter 1 Fundatnentals of the Nervous Systetn......Page 17
Chapter 2 Developlllent and Cellular Constituents of the Nervous Systelll......Page 23
Chapter 3 Signaling in the Nervous Systeni......Page 35
Chapter 4 The Relationship Between Neuroanatomy and Neurology......Page 49
Chapter 5 The Spinal Cord......Page 59
Chapter 6 The Vertebral Colutnn and Meninges Surrounding the Spinal Cord......Page 81
Chapter 7 The Brain Stem and Cerebellunt......Page 93
Chapter 8 Cranial Nerves and Associated Pathways......Page 115
Chapter 9 Diencephalon: Thalamus and Hypothalatnus......Page 135
Chapter 10 Cerebral Hentispheres/ Telencephalon......Page 147
Chapter 11 Ventricles and Coverings of the Brain......Page 165
Chapter 12 Vascular Supply of the Brain......Page 179
Chapter 13 Control of Moventent......Page 195
Chapter 14 Sotnatosensory Systetns......Page 207
Chapter 15 The Visual Systelll......Page 213
Chapter 16 The Auditory Systelll......Page 227
Chapter 17 The Vestibular System......Page 233
Chapter 18 Reticular Fortnation......Page 237
Chapter 19 The Liinbic Systein......Page 241
Chapter 20 The Autononiic Nervous Systeni......Page 253
Chapter 21 Higher Cortical Functions......Page 267
Chapter 22 Iinaging of the Brain......Page 277
Chapter 23 Electrodiagnostic Tests......Page 287
Chapter 24 Cerebrospinal Fluid Exainination......Page 295
Chapter 25 Discussion of Cases......Page 297
Appendix B Testing Muscle Function......Page 321
Appendix A The N eurologic Exaniination......Page 313
Appendix C Spinal Nerves and Plexuses......Page 337
Appendix D Questions and Answers......Page 355
Index......Page 363

Citation preview

a LANGE medical book

Clinical N euroanatoiny Twenty-Ninth Edition

Stephen G. Waxman, MD, PhD Bridget Marie Flaherty Professor ofNeurology, Neurobiology, & Pharmacology Director, Center for Neuroscience & Regeneration Research Yale University School of Medicine New Haven, Connecticut

New York Chicago San Francisco Athens London Madrid Mexico City Milan New Delhl Singapore Sydney Toronto

Copyright © 2020 by McGraw-Hill Education. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-1-26045236-5 1-26-045236-0 MHID: The material in this eBook also appears in the print version of this title: ISBN: 978-1-26-045235-8, MHID: 1-26-045235-2. eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in corporate training programs. To contact a representative, please visit the Contact Us page at

Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The author and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time ofpublication. However, in view of the possibility of human error or changes in medical sciences, neither the author nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. TERMS OF USE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education's prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK. IS PROVIDED "AS IS." McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK. INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill Education has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation ofliability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

For Chl.oe... "No laughing!"

Key Features of this Editio,n ! • A comprehensive, full-co lor gui de to n ew oan atc·rn:,1 Qnd ils func11orial and d lr11ca l aoplicat16nS- the r'rH:>S1 trus1ed ·e$ol.l t ce fO( 1s ~nd praic;lll•oners

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FIGURE 2-2 ScMmatic illustration of MrYe cell tJpes. A: Central nervous system cells: {1) motor neuron projecting to striated muscle, (2) special sensory neuron, and (3) general sensory neuron from skin, B: Autonomic cells to smooth muscle, Notice how the position of the cell body with respect to the axon varies.

along the mkrotubules. Tue amn conducts electrical signals (action potentials) from the initial segment (the proximal part of the axon, near the cell body) to the synaptic terminals. 1he initial aegment has distinctive morphological features; it differs from both cell body and mm. The axoienuna of the initial segment contains a high density of sodium channels, which permit the initial segment to act as a trigger zone. In this zone, action potentials are generated so that they can travel along the axon, finally invading the terminal axonal branches and triggering synaptic activity, which impinges on other neurons. The initial segment does not contain Nissl substance (see Fig 2-3). In large neurons, the initial segment arises conspicuously from the uon hillock. a cone-shaped portion of the cell body. Axons range in length from a rew microns (in interneurons) to well over a meter (ie, in a lumbar motor neuron that projects from the spinal cord to the muscles of the foot) and in diameter from 0.1 µm to more than 20 µ.m.

CHAPTER 2 Development and Cellular Constituents of the Nervous System


FIGURE 2-4 Elactron mlaograph of• narve all bodr (CB) .urrounclacl by n•rv• proc:e.uas. The neuronal surface Is completely «ivered by either synaptic endings of other neurons (S) or processes of gllal cells. Many other precesses around this ceU are myeUnated axons (M}. CB, neuronal cell body, N, nudeus, xS,000. (Used whh permission from Dr. DM Md>oriald.J

A.Myelin Many axons are covered by myelin. 'Ihe myelin consists of multiple concentric layers of lipid-rich membrane produced by Schwann cells in the peripheral nervous system (PNS) and by oligodendrocytes (a type of glial cell) in the central nervous system (CNS) (Figs 2-6 to 2-10). 'Ihe myelin sheath is divided into segments about 1 mm long separated by small gaps (1 µm long) where myelin is absent; these are the nodes ofRanvier. lhe smallest axons are unmyelinated. As noted in Chapter 3, myelin functions as an insulator. In general, myelination serves to increase the speed of impulse conduction along the axon.

8. Axonal Transport In addition to conducting action potentials, axons transport materials from the cell body to the synaptic terminals (anterograde transport) and from the synaptic terminals to the

cell body (retlograde transport). It is generally thought that ribosomes are not present in the axon, and this new protein must be synthesized and moved to the axon. 'Ihis occurs via several types of axonal transport, which differ in terms of the rate and the material transported. Anterograde transport may be fast (up to 4(10 mm/d) or slow (about 1 mm/d).Retrograde transport is similar to rapid anterograde transport. Fast transport involves microtubules extending through the cytoplasm of the neuron. An axon can be injured by being cut or severed, crushed, or compressed. After injury to the axon, the neuronal cell body responds by entering a phase called the uon reaction, or chromatolysil. In general, axons within peripheral nerves can regenerate quickly after they are severed, whereas those within the CNS do not tend to regenerate. lhe axon reaction and axonal regeneration are further discussed in Chapter 22.


SECTION I Basic Principles

FIGURE 2-5 Dendrite from pyrarnldll nauron In the motor cortex. Note the spines on the main dendrite and on Its smallet' branches. Scale= 10 µ.m. (Used with pennlsslon from Dr. Andrew T;m, Yale University.)

Synapses Transmission of information between neurons occurs at synapses. Communication betwun neurons usually occurs from the axon terminal of the transmitting neuron (presynaptic side) to the receptive region of the receiving neuron (postsynaptic side) (Figs 2-6 and 2-11). 'Ibis specialized interneuronal complex is a synapse, or synaptic junction. & outlined in Table 2-1, some synapses are located between an axon and a dendrite (a:mdendritic synapses, which tend to be excitatory), or small dendritic spine which protrudes from the dendrite (Fig 2-12). Other synapses are located between an

FIGURE 2-6 Dilg,.mrmrtlc view, lnthr" dimensions, of • prototypic n1M1ron. Dendrites {1) radiate from the neuronal cell body, which contains the nudeus (3). The axon arises from the cell body at the initial segment (2). Axodendritic (4) and axosomatic (S) synapses Impinge en the dendrites and cell body. Myelln sheaths (6) are present around some axons.

axon and a nerve cell body (uosomatic synapses, which tend to be inhibitory). Still other synapses are located between an u:on terminal and another axon; these u::ouonic synapses modulate transmitter release by the postsynaptic axon. Synaptic transmission pennits information from many presy.naptic neurons to converge on a single postsynaptic neuron. Some neuronal large cell bodies receive several thousand synapses (see Fig 2-4). Impulse transmission at most synaptic sites involves the release of a chemical transmitter substance (see Chapter 3); at other sites, current passes directly from cell to cell through specialized junctions called electrical synapses,

TABLE 2-1 Types of Synapses In the CNS. Funclian


PNsymiptlc Ellim11nt


Axon terminal


Usually excltatoiy


Axon terminill

Cell body

Usually inhibitory


Axon terminal

Axon tennlnal

Pn!synaptlc Inhibition (modulates transmitter

release in postsynaptic axon) Dendrodendrttlc



Local Interactions (may be excitatory or Inhibitory) in axonless neurons, eg, in retinil

CHAPTER 2 Development and Cellular Constituents of the Nervous System

Sdlwann cell nucleus


Synapses are very diverse in their shapes and other properties. Some are inhibitory and some e:xci.tatory; in some, the transmitter is acetylcholine; in others, it is a catecholamine, amino acid, or other substance (see Chapter 3). Some synaptic vesicles are large, some small; some have a dense core, whereas others do not. Flat synaptic vesicles appear to contain an inhibitory mediator; dense-core vesicles contain catecholamines. In addition to calcium-dependent, vesicular neurotransmitter release, there is also a second, nonvesicular mode of neurotransmitter release that is not calcium-dependent. 1his mode of release depends on transporter molecules, which W1ually serve to take up transmitter from the synaptic cleft.

Sdtwann cell nucleus A



Inner mesaxon

FIGURE 2-7 Schwann cells and their relatronshlps with axons. A: In the peripheral nervous system (PNS), unmyellnated axons are located within grooves on the surface of Schwann cells. These axons are not, however, Insulated by a myelln sheath. B: Myellnated PNS fibers are surrounded by a myelln sheath that Is furmed by a spiral wrapping of the axon by a Schwann cell. Panels 1-4 show fuur consecutive phases of myelin fonnation in peripheral nerve fibers. (Reproduced with permission from Junquelra LC. CarnefroJ, Kelley RO: Basic

Nerve cell bodies are grouped characteristically in many parts of the nervoWI system. In the cerebral and cerebellar cortices, cell bodiet aggregate to form layen called laminas. Nerve cell bodies in the spinal cord, brain stem, and cerebrum form compact groups, or nuclei. Each nucleus contains projection neurons, whose axons carry impulses to other parts of the nervous system. and intemeoron1, which act as short relays within the nucleus. In the peripheral nervous system. these compact groups of nerve cell bodies are called ganglia. Groups of nerve cells are connected by pathways formed by bundles of axons. In some pathways. the axon bundles are sufficiently defined to be identified as trada, or faaclc:oli; in others, there are no discrete bundles of axons. Aggregates of tracts in the spinal cord are referred to as a>lumm, or funiculi (see Chapter 5). Within the brain, certain axon tracts are referred to as lemnlsd. In some regions ofthe brain, axons are intermingled with dendrites and do not run in bundles so that pathways are difficult to identify. These web-like networks are called the neuropll (Fig 2-13).

Histology. Teirt &Atlas, 11th ed. New Yorlr, NY: McGraw-Hiii Education; 2005.)

GLIA or gap junctions. Electrical synapses are most common in invertebrate nervous sy1tems, although they are found in a small number of sites in the mammalian CNS. Chemical synapses have several distinctive characteristics: synaptic vesicles on the presynaptic side, a synaptic cleft, and a dense thickening of the cell membrane on both the receiving cell and the presynaptic side (see Fig 2-11). Synaptic vesicles contain neurotransmitters, and each vesicle contains a small packet, or quanta, of transmitter. When the synaptic terminal is depolarized (by an action potential in its parent axon), there is an influx of calcium. This calcium influx leads to phosphorylation of a class of proteins called synapsins. After phosphorylation of synapsins, synaptic vesicles dock at the presynaptic membrane facing the synaptic cleft, fuse with it, and release their transmitter (see Chapter 3).

Neuroglial cells. commonly called glial cells. outnumber neurons in the brain and spinal cord 10:1. They do not form synapses. 1hese cells appear to play a number of important roles, including myelin formation, guidance of developing neurons. maintenance of extracellular K+ levels. and reuptake of transmitters after synaptic activity. 1here are two broad classes of glial cells, macroglia and microglia (Table 2-2).

Macroglia 1he term maaoglia refers to astrocytes and oligodendrocytes, both of which are derived from ectoderm. In contrast to neurons, these cells may have the capability, under some circumstances, to regenerate.



Basic Principles

FIGURE 2-8 Electron mlcrogr•ph of my· alinatlld (M) and unm,.elinat:ecll (U) axoll.I of• pariph•ral nM"V8. Sc:hwann cells (S) may surround one myefinated or several unmyellnated axons. x 16,000. (Used with permission tiom Dr. OM McDon;;ildJ

Astrocytes 1here are two broad classes of astrocytes: protoplasmic and fibrom. Protoplasmic astrocytes are more delicate, and their many processes are branched. '!hey occur in gray matter. Fibrous astrocytes are more fibrous, and their processes (containing glial fibrils) are seldom branched. Astrocytic processes radiate in all directions from a small cell body. 1hey surround blood vessels in the nervous system, and

they cover the exterior surface of the brain and spinal cord below the pia. Astrocytes provide structural support to nervous tissue and act during development as guidewires that direct neuronal migration. They also maintain appropriate concentrations of ions such as K+ within the extracellular space of the brain and spinal cord. Astrocytes may also play a role in synaptic transmission. Many synapses are closely invested by astrocytic processes, which appear to participate in the reuptake

TABLE 2-2 Nomendature 11nd Principal Functions of Gli11I Cells.

Gllal cells

r Macroglla





Prtndpml Functions


Myelln fonnation In CNS


Regulate Ionic environment; reuptake of neurotransmitters; guidance of growing axons

Mlcrogllal cells

Immune surveillance of the CNS

CHAPTER 2 Development and Cellular Constituents of the Nervous System


inhibits regeneration of injured neurons, is currently being studied.


Ollgodendrocytes Oligodendrocytes predominate in white matter; they extend arm-lilc.e processes which wrap tightly around axons, extruding the oligodendroglial cytoplasm to form a compact sheath of myelin which acts as an insulator around axons in the CNS. Oligodendrocytes may also provide some nutritive support to the neurons they envelop. A single oligodendrocyte may wrap myelin sheaths around many (up to 30-40) axons (see Figs 2-9 and 2-10). In peripheral nerves, by contrast, each myelin sheath is formed by Schwann cella. Each Schwann cell myelinates a single axon, and remyelination can occur at a brisk pace after injury to the myelin in the peripheral nerves.


FIGURE 2-9 Oligodandroqtes fonn myalin in the cantral narvous system (CNS). A single ollgodendrocyte myellnates an entire family of axons (2-50). There ls little ollgodendrocyte cytoplasm (Cyt) In the ollgodendrocyte processes that spiral around the axon to form myelln, and the myelln sheaths are connected to their parent ollgcdendrocyte cell body by only thin tongues of cytoplasm. This may account, at least In part, for the paucity of remyellnatlon after damage to the myelln In the CNS. The myelln Is perlodlcally Interrupted at nodes of Ranvler, where the axon (A) Is exposed to the extracellular space (ES). (Reproduced with pemiission from Bunge M. BI.Inge R, Pappas G: Ultrastl\ldur•I study of remyelrnatlon In an expertrnental lesion In a.dult at spinal cord,JBJophysBlodletn()ttol. 1961 May.10:67-94.)

of neurotransmitters. Astrocytes also surround endothelial cells within the CNS, which are joined by tight junctions that impede the transport of molecules across the capillary epithelium, and contribute to the formation of the blood-brain barrier (see Chapter 11). Although astrocytic processes around capillaries do not form a functional barrier, they can selectively take up materials to provide an environment optimal for neuronal function. Astrocytes form a covering on the entire CNS surface and proliferate within damaged neural tissue (Fig 2-14). These reactive astrocytes are larger, are more easily stained, and can be definitively identified in histological sections because they contain a characteristic, astrocyte-specific protein: glial fibrillary addle protein (GFAP). Chronic astrocytic proliferation leads to glfoafs, sometimes called glial •earring. Whether glial scarring is beneficial, or

Microglial cells are macrophage-like c:ells, or scavengers of the CNS. lhey constantly survey the brain and spinal cord, acting as sentries to detect, and destroy, invaders (such as bacteria). When an area of the brain or spinal cord is damaged or infected, microglia activate and migrate to the site of injury to remove cellular debris. Some microglia are always present in the brain, but when injury or infection occurs, others enter the brain from blood vessels. Microglia play an important role in protecting the nervous system from outside invaders such as bacteria. '!heir role after endogenous insults, including stroke or neurodegenerative diseases such as Alzheimer disease, is under investigation.

Extracellular Space lhe fluid-filled space between the various cellular components ofthe CNS accounts for, under most circumstances, about 20% of the total volume of the brain and spinal cord. Because transmembrane gradients ofions, such as K+ and Na+, are important in electrical signaling in the nervous system (see Chapter 3), regulation of the levels of these ions in the extracellular compartment (ionic homeostasls) is an important function, which is, at least in part. performed by astrocytes. 'Ihe capillaries within the CNS are completely invested by glial or neural processes. Moreover, capillary endothelial cells in the brain (in contrast to capillary endothelial cells in other organs) form tight junctlona, which are impermeable to diffilsion, thus creating a blood-brain barrier. lhis barrier isolates the brain extracellular space from the intravascular compartment.

Clinical Correlation In cerebral edema, there is an increase in the bulk of the brain. Cerebral edema can be either vasogenic (primarily extracellular) or cytotoxic (primarily intracellular). Because of the limited size of the cranial vault within the skull, cerebral edema must be treated emergently.


SECTION I Basic Principles

FIGURE 2-10 Electron mkrogr•ph showing ollgodendrocyte (01) In the spin.I cord, wfllch has myellrmed two axons (A,, A:rJ. x6,600. The Inset shows axon A1 and Its myelln sheath at higher magnification. The myelln Is a spiral of ollgodendrocyte membrane that sur· rounds the axon. Most of the ollgoclendrocyte cytoplasm Is extruded from the myelln. Because the myelln Is compact, It has a high electrical resistance and low capacitance so that It can function as an Insulator around the axon. x 16,000.

DEGENERATION AND REGENERATION The neuronal cell body maintains the functional and anatomic integrity of the axon (Fig 2-14). If the axon is cut, the part distal to the cut degenerates (wallerian degeneration), because materials fo.r maintaining the axon (mostly proteins) are formed in the cell body and can no longer be transported down the axon (axoplumlc transport). Distal to the level of axonal transeG . .~~~~-

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motor neuron

FIGURE 5-23 Testing fur extensor plantar reflexes also called Babinski reflexes.


Spinal cord - \ \

\\ •,


syphilis (see later discussion), which is rare at present because of the availability of antibiotics (Fig 5-24C). (4) An irregular peripheral lesion (eg, stab wound or compression of the cord) involves long pathways and gray matter; functions below the level of the lesion are abolished. In practice, many penetrating wounds of the spinal cord (stab wounds, gunshot wounds) cause in'egular lesions (Fig 5-240). (S) Complete hemiaection of the cord produces a Brownsequard ayndrome (see later discussion; Figs 5-24E and 5-25). Lesions outside the cord (extramedullary lesions) may affect the function of the cord itself as a result of direct mechanical injury or secondary isc.hemic injury resulting from the compromise of the vascular structures or vasospasm.

Lower motor neuron

nerve Motor - -



Motor pathways dMded Into upper- and lowermotor-neuron regions.

(3) A clonal column lesion affects the dorsal columns, leaving other parts of the spinal cord intact 1hus, proprioceptive and vibratory sensation are involved, but other functions are nonnal. Isolated involvement of the dorsal columns occurs in tabes dorsalis, a form of tertiary

(6) A tumor of the dorsal root (such as a neurofi.broma or schwannoma) involves the first-order sensory neurons of a segment and can produce pain u well as sensory loss. Deep tendon reflexes at the appropriate level may be lost because of damage to la :fibers (Fig 5-24F). (7) A tumor of the meninges or the bone (extramedullary masses) may compress the spinal cord against a vertebra, causing dysfunction of ascending and descending fiber s}'5tems (Fig 5-24G). Tum.ors can metastasize to the epidural space, causing spinal cord compression. Herniated intervertebral disks can also compress the spinal cord. Spinal cord compression may be treatable if diagnosed early. Suspected spinal cord compression thus requires aggressive diagnostic workup on an urgent basis.

TABLE 5-6 Lower- Versus Upper-Motor-Neuron Lesions. UpJMr-Motor-Neuron l.ellon

V•rillble Weakness

Flaccld paralysis

Spastic paralysis

Deep tendon reflexes

Decreased or absent


Bablnskl's reflex




May be marted

Absent or resulting from disuse

Fasciculations and librlllatlons

May be present



SECTION III Spinal Cord and Spine

EXAMPLES OF SPECIFIC SPINAL CORD DISORDERS Spinal Cord Compression Spinal cord compresaion-due, for example, to an extramedullary tumor such as meningioma, neurofibroma, or metastatic cancer, an epidural abscess, or a ruptured intervertebral disc-can injure the spinal cord and can rapidly progress to irreversible paraplegia or quadriplegia if not promptly diagnosed and treated. Spinal cord compression should be suspected in any patient with weakness, numbness or sensory loss in the legs. A "sensory level." that is, impaired sensation below a specific dermatomal level, or the presence ofBabinski reflexes and hyperreftexia in the lower extremities supports the diagnosis (although in the acute phase of spinal cord compression, spinal shock can produce transient hyporeflexia below the lesion). Bowel or bladder dysfunction may be present Pain over the spinal column, or tenderness on mild percussion, provides further support for the diagnosis. If the lesion compresses the conw medullaris or cauda equina, there may be sensory loss in a "saddle· distribution and hyporeftexia. Spinal cord compression is surgically treatable but can rapidly progress to irreversible paraplegia if not treated. Imaging of the spine is required on an urgent basis in any patient in whom spinal

A. Small oentral lesion

B. Large central leslon

C. Dorsal column lesion

D. Irregular lesion

cord compression is suspected.

Syringomyelia Syringomyelia presents a classical clinical picture, characterized by loss of pain and temperature sensation at several segmental levels, although the patient usually retains touch and pressure sense as well as vibration and position sense (dissociated anelthesla) (Fig 5-26). Because the lesion usually involves the central part of the spinal cord and is confined to a limited number of segments, it affects decussating spinothalamic tracts only in these segments and results in a pattern of segmental loss of pain and temperature sense. When this type of injury occurs in the cervical region, there is a cape-like pattern of sensory loss. If the lesion also involves the ventral gray matter, there may be LMN lesions and atrophy of the denervated muscles.

TABLE 5-7 Common Symptoms and Signs 1n Spinal Cord Compression. Weakness or sensory lms In the legs Babinski reflexes

Hyper reflexla ln the lower extremities (although, ln the acute phase of compression or ln lesions of the con us medullarls or cauda equine,

there c;m be hyporeflexia) A •sensory level•

Pain or tenderness on percussion ever the vertebral column

E. Complete hemiseclion

~f?~ --~~/-'

F. Dorsal root tumor

G. Compression of cord within lhe wrtebra by axtramedullary mass

FIGURE 5-24 Schematic Illustrations (A-G) of various types of spinal cord lesions.

CHAPTER. S The Spinal Cord


Tabes Dorsalis Tabes dorsalis, a form of tertiary neurosyphilis, is now rare, but was common in the pre-antibiotic era. and is characterized by damage to the dorsal roots and dorsal columns. As a result of this damage, there is impairment of proprioception and vibratory sensation, together with loss of deep tendon reflexes, which cannot be elicited because the la afferent pathway has been damaged. Patients exhibit "sensory ataxia." Romberg's sign (inability to maintain a steady posture with the feet close together, after the eyes are closed, because ofloss of proprioceptive input) is usually present Charc:ot's joint.a (destruction of articular surfaces as a result of repeated injury ofinsensitive joints) are sometimes present. Subjective sensory disturbances known as tabetic c:riles consist ofsevere cramping pains in the stomach, larynx. or other viscera.

}. y .J



}ll [

This syndrome is caused by hemisection of the spinal cord as a result of, for example, bullet or stab wounds, syringomyelia. spinal cord tum.or, or hematomyelia. Signs and symptoms include ipsilateral LMN paralysis in the segment of the lesion (resulting from damage to LMNs) (see Fig 5-25); ipsilateral upper-motor-neuron paralysis below the level of the lesion (resulting from damage to the lateral corticospinal tract); an ipsilateral zone of cutaneous anesthesia in the segment of the lesion (resulting from damage to afferent fibers that have entered the cord and have not yet crossed); and

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ipsilateral loss of proprioceptive, vibratory, and two-point discrimination sense below the level of the lesion (resulting from damage to the dorsal columns). There is also a contralateral loss of pain and temperature sense below the lesion (resulting from damage to the spinothalamic tracts, which have already de FIGURE 1-16 Diagram of taste pathways.


SECTION IV Anatomy of the Brain

Sensation to lower pharynx Trapezius muscle


:; ·-

{ r.

Epiglotlic and lingual rami


Arytenold, thyroarytenold, and crlcoarytenold muscles



Esophagus - - ~~ ~=

Right subdavlan artery - -


lnfartor pharyngeal constrictor


Cricothyroid muscle

---~-;:, Right recurrent laryngeal nerve _;.: Left recurrent laryngeal nerve .c~~!,_




\ Primary visual


FIGURE 10-13 Lateral view of the left hemisphere showing the functions of the cortical areas.



SECTION IV Anatomy of the Brain

TABLE 10-1 SpeclaHzedConlcalAreas. Funclian

Frontal lobe:

Prtmary motor cortex Premotor cortex Frontal eye fleld

Voluntary muscle activation

Contributes to cortlcosplnal tract

6 8

Eye movements



Motor aspects af speech

Sends projections to lateral gaze center (paramedlum pontlne retlcular formation) Projects to Wernlcke's area via arcuate fasclculus

Parletal lobe:

3, 1,2

Primary sensory cortex


Input from VPL, VPM

Occlpltal lobe:


Striate cortex=

18, 19

prlmaryvtsual cortex Extrastrtate = vtsual association cortax

Processing af vlsual stimuli Processing af vlsual stimuli

Input from lateral genlculate only Projects to areas 18, 19 lnputfromarea 17

Processing af auditory stlmull

Input from medlal genlculate

Temporal lobe:



Prtmary auditory cortex


Associative auditory cortex


Wernlcke's area

Language comprehension

Inputs from auditory association cortex, vlsual association cortex,, Broca's

area (via arcuate fascia.1lus)

CLINICAL ILLUSTRATION 10-1 A 47-year-old male, previously healthy, began to suffer from focal seizures. The seizures began with twitching of the left hand and face, and 1hen extended to Involve the enttre left ann, then the entire left side of 1he body tncludlng the leg. Sometimes 1he seizures generallzed, Involving both sides of 1he body. Neurologlcal examination revealed mlld weakness, Increased tendon reflexes, and an extensor plantar response, all on the left Imaging demonstrated a small tumor, thought to be a low-grade astrocytoma, In 1he white matter lmmed~ ately below 1he face and hand area of the precentral gyrus on the right As Illustrated by this case, focal onset ofaseizure can have locallztng value. Probably reftectfng 1he amount of brain d~ voted to control of these body parts, the face (partlcularly 1he llps) and hand are relatively large compared with other parts of the body within the homunculus (Fig 10-14). Thus, It Is not unusual for focal seizures to begin wtth twitching of 1he face or hand. In this case, the seizures •marched• from Its site of onset In the face and hand, to Involve more and more ofthe body. This has been termed 1he "Jacksonlan march,• and this type of seizure has been termed •Jacksonlan epllepsy" In honor of the nlneteen1h-century British neurol~ gist John Hughllngs Jackson who, from cllnlcal observations on the march of focal seizures, predicted the presence of a homunculus within the cortex.

control and buccolingual movements. 'Ihe arm. trunk. and hip are then represented in order higher on the convexity; and the foot. lower leg, and genitals are draped into the interhemispheric fissure (Fig 10-14). Area 6 (the premotor area) contains a second motor map. Several other motor zones, including the supplementary motor area (located on the medial aspect of the hemisphere), are clustered nearby.

FIGURE 10-14 Motor homunculus drawn on acoronal section through the precentral gyrus. The location ofcortical con1rol of various body parts Is shown.

CHAPTER 10 Cerebral Hemispberestrelencephal.on

Area 8 (the &ontal eye field) is concerned with eye movements. Within the inferior frontal gyrus, areas 44 and 45 (Broca>s area) are located anterior to the motor cortex controlling the lips and tongue. Broca's area is an important area for speech. Anterior to these areas, the pre&ontal c:orta: has extensive reciprocal connections with the dorsomedial and ventral anterior thalamus and with the limbic system. This asoc:iation area receives inputs from multiple sensory modalities and integrates them. The pre:frontal cortex serves "executive"' functions, planning and initiating adaptive actions and inhibiting maladaptive ones; prioritizing and sequencing actions; and weaving elementary motor and sensory functions into a coherent. goal-directed stream of behavior. The prefrontal cortex, like the motor and sensory cortices, is compartmentalized into areas that perform specific functions. When prefrontal areas are injured (eg, as a result of tumors or head trauma). patients become either apathetic (lacking initiative or, in some cases, motionless and mute) or uninhibited and distractible, with loss of social graces and impaired judgment. 2. Potletal lobe-Area 3, 1, and 2 are the primary sensory areu, which are somatotypically represented (again in the form of a homunculus) in the postcentral gyrus (Fig 10-15). This area receives somatosensory input from the ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei in the thalamus. The remaining areas are sensory or multimodal association areas.

3. Ocdpitcrl lobe-Area 17 is the striate-the primary -.isaal-corte:i:. The geniculocalcarine radiation relays visual


input from the lateral geniculate to the striate cortex. Upper parts of the retina (lower parts of the visual field) are represented in upper parts of area 17, and lower parts of the retina (upper parts of the visual field) are represented in lower parts of area 17. Areu 18and19 are visual usoclation areas within the occipital lobe. 1here are also visual maps within the temporal and parietal lobes. Each of these maps represents the entire visual world, but extracts information about a particular aspect of it (forms, colors, movements) from the incoming visual signals. (This is further described in Chapter 15.)

4. Tempotal lobe-Area 41 is the primary auditory cortex; area 42 is the asaociative (secondary) auditory cortex. Together, these areas are referred to as Hescbl~s gyrus. Immediately adjacent to Heschl's gyrus lies the planum temporale, which is located on the superior surface of the tempura! lobe (Fig 10-16). which is larger on the left in right-handed individuals, and is involved in language and music. 1hese regions receive input (via the auditory radiations) from the medial geniculate. The surrounding temporal cortex (area 22) is the auditory association cortex. In the posterior part of area 22 (in the posterior third of the superior temporal gyrus) is Wemicke's area, which plays an important role in the comprehension of language. The remaining temporal areas are multimodal association areas.

5. Multlmodal association areas-As noted earlier, for each sensory modality, there is a primary sensory cortex as well as modality-specific association areas. A number of multimodal association areas also receive converging projections from different modality-specific association areas. Within these multimodal association areas, information about different attributes of a stimulus (eg, the visual image ofa dog, the sound of its bark. and the feel of its fur) all appear

FIGURE 10-15 Sensory homunculus drawn overlying a coro-

FIGURE 10-16 Magnetic resonance Image showing Heschl's gyrus (HG, red} and planum temporal (PT, blue) within the upper part of the temporal lcbe. (Reproduced with permission from Oertel·

nal section through the postcentral gyrus. The location of the cortical representation of various body parts is shown.

Knochel v. Linden DEJ: Cerebl'lll asymmetry in schizophreni1. ~st. 2011 Oct;17(5):456--467J


SECTION IV Anatomy of the Brain

to converge, so that higher order information processing can take place. A multi.modal association area has been found in the temporoparietal area within the inferior parietal lobule and the area around the superior temporal sukus. Another multimodal association area is located in the prefrontal region. These multimodal association regions project, in turn, to the limbic cortex.

PHYSIOLOGY OF SPECIALIZED CORTICAL REGIONS .Reflecting its parcellated organization, dllferent parts of the cortex subserve different functions. Focal injury of various parts of the cortex can produce di.strict clinical syndromes. Thus, in many cues it is possible to predict, from the history and neurological examination, which parts of the cortex are damaged.

FIGURE 10-17 Motor activity in the cerebral cortex, visualized with functional magnetic resonance Imaging. Changes In signal Intensity result ftom changes In the flow, volume, and oxygenation of the blood. This study was performed on a 7-year-old boy. The stimulus was repetitive squeezing of a foam-rubber ball at the rate of two to four squeezes per second. Changes In cortical activity associated with squeezing the ball with the right hand are shown In black. Changes In cortical activity associated with squeezing the ball with the left hand are shown In white. (Reproduced with permission from Novobly EJ: Functlonal ~netle reson•nce l~tng (IMRO '" pedtrtrtc epilepsy.

Primary Motor Cortex A. Location and Function The primary motor projection cortex (area 4; see Chapter 13) is located on the anterior wall of the central suku.s and the adjacent portion of the precentral gyrus, corresponding generally to the distribution of the giant pyramidal (Betz"s) cells. These cells control voluntary movements ofskeletal muscle on the opposite side of the body, with the impulses traveling over their axons in the cortic:obulbar and corticospinal tracts to the branchial and somatic efferent nuclei in the brain stem and to the ventral horn in the spinal cord. A somatotopic representation within the motor areas, mapped by electrical stimulation during brain surgery, appears in Figure 10-14. Secondary and tertiary areas of motor function can be mapped around the primary motor cortex. Contralateral conjugate deviation of the head and eyes occurs on stimulation of the posterior part of the middle frontal gyrus (area 8), tenned the frontal eye fields. Functional magnetic resonance imaging, which is described in Chapter 22, shows activation of motor cortex associated with squeezing a foam-rubber ball with the contralateral hand (Fig 10-17).

B. Clinical Correlations Irritative lesions of the motor centers may cause seizures that begin as focal twitching and spread (in a somatotopic manner, reflecting the organization ofthe homunculus) to involve large muscle groups. As noted in Clinical nlustration 10-1, as abnormal electrical disclaarge spreads across the motor cortex, the seizure "marches"' along the body in a "Jacksonian march.• There may also be modification of consciousness and postc:onvulsive weakness or paralysis. Destructive lesions of the motor cortex (area 4) produce contralateral flaccid paresis, or paralysis, of affected muscle groups. Spasticity is more apt to occur if area 6 is also ablated.

Epi"psia 1994; Dec;35(5'upp 8):36J

Primary Sensory Cortex A. Location and Fundlon The primary sensory projection cortex for sensory information received from the skin, mucosa, and other tissues of the body and face is located in the postcentral gyrus and is called the tomatesthetic area (areas 3, 1, and 2; see Fig 1015). From the thalamic ndiations, this area receives :fibers that convey touch and proprioceptive (muscle, joint, and tendon) sensations from the opposite side of the body (see Chapter 14). A relatively wide portion of the adjacent frontal and parietal lobes can be considered a secondary sensory cortex because this area also receives sensory stimuli The primary sensorimotor area is, therefore, considered capable of functioning as both a motor and a sensory cortex. with the portion ofthe cortex anterior to the centl'al sulcus predominantly motor and that behind it predominantly sensory. The cortical taste area is located close to the facial sensory area and extends onto the opercular surface of the lateral cerebral :fissure (see Fig 8-19). This cortical area receives gustatory information, which is relayed from the solitary nucleus in the medulla via the ventral posteromedial nucleus of the thalamus.

8. Clinical Correlations Irritative lesions of this area produce pareathesias (eg, numb-

ness, abnormal sensations of tingling, electric shock, or pins and needles) on the opposite side of the body. Destructive lesions produce subjective and objedive impairments in sensibility, such as an impaired ability to localize or measure the intensity ofpainful stimuli and impaired perception of various forms of cutaneous sensation. Complete anesthesia on a cortical basis is rare.

CHAPTER 10 Cerebral Hemispberestrelencephal.on

Primary Visual Cortex and Visual Association Cortex A. Location and Function 1he primary visual receptive (striate) cortex (area 17) is located in the occipital lobe. It lies in the cortex of the calcarine fissure and adjacent portions of the cuneus and the lingual gyrus. In primates, an extensive posterior portion of the occipital pole is concerned primarily with high-resolution macular vision; more anterior parts ofthe calcarine cortex are concerned with peripheral vision. 1he visual cortex in the right occipital lobe receives impulses from the right half of each retina, whereas the left visual cortex (area 17) receives impulses from the left half of each retina. The upper portion of area 17 represents the upper half of each retina, and the lower portion represents the lower half. Visual association is a function of areas 18 and 19. Area 19 can receive stimuli from the entire cerebral cortex; area 18 receives stimuli mainly from area 17 (see Chapter 15).

B. Cllnlcal Correlatlons Irritative lesions of area 17 can produce such visual hallucinations as flashes oflight, rainbows, brilliant stars, or bright lines. Destructive lesions can cause contralateral homonymous defeasy) llbers

Perforant pa:thway

This circuit, called the Papez circuit, ties together the cer-

ebral cortex and the hypothalamus. It provides an anatomic substrate for the convergence of cognitive (cortical) activities, emotional experience, and expression. A number of cortical structures feed into, or are part of, the Papez circuit. The subcallosal gyrus is the portion of

gray matter that covers the inferior aspect of the rostrum of the corpus callosum. It continues posteriorly as dngulate gyms and parahlppoaunpalgyros (see Figs 19-2and19-11). In the area of the genu of the corpus callosum, the subcallosal gyrus also contains fibers coursing into the supracallosal gyms. The supracalloaal gyrm (iD.dusium griseum) is a

FIGURE 11-11

Schematic illustration of pathways between the hippocampal formation and the dlencephalon. Notice the presence of a loop (Papez circuit), Including the parahlppocampal gyrus, hippocampus, mamillary bodies, anterior thalamus, and cingulate gyrus. Notice also that the neocortex feeds into this loop.






SECTION V Functional Systems

thin layer of gray matter that extends from the subcallosal gyrus and covers the upper surface of the corpus callosum (see Fig 19-11). The medial and lateral longitudinal striae are delicate longitudinal strands that extend along the upper surface of the corpus callosum to and from the hippocampal formation.

The corticomedial nuclear group of the amygdala, located close to the olfactory cortex, is interconnected with it as well as the olfactory bulb. Connections also run, via the stria terminalis and amygdalofugal pathway, to and from the brain stem and hypothalamus.

Fundions of the Amygdala Anterior Commissure The anterior commissure is a band-like tract of white fibers that crosses the midline to join both cerebral hemispheres (see Fig 19-11). It contains two fiber systems: an interbulbar system, which joins both anterior olfactory nuclei near the olfactory bulbs, and an intertemporal system, which connects the temporal lobe areas of both cerebral hemispheres.

Septal Area The septal area, also called the septal nuclei or septal complex, is an area of gray matter lying above the lamina terminalis and below the rostrum of the corpus callosum, near and around the anterior commissure (Fig 19-12). The septal area is a focal point within the limbic system, and is connected with the olfactory lobe, amygdala, hippocampus, and hypothalamus. The septal area is a "pleasure center" in the brain. Rats with electrodes implanted in the septal area will press a bar repeatedly to receive stimuli in this part of the brain. A portion of the septal area, the septum lucidum, is a double sheet of gray matter below the genu of the corpus callosum. In humans, the septum separates the anterior portions of the lateral ventricles.

Amygdala and Hypothalamus The amygdala (amygdaloid nuclear complex) is a gray matter mass that lies in the medial temporal pole between the uncus and the parahippocampal gyrus (Figs 19-12 to 19-14). It is situated just anterior to the tip of the anterior horn of the lateral ventricle. Its fiber connections include the semicircular stria tenninalis to the septal area and anterior hypothalamus and a direct amygdalofugal pathway to the middle portion of the hypothalamus (see Fig 19-12). Some fibers of the stria pass across the anterior commissure to the opposite amygdala. The stria terminalis courses along the inferior horn and body of the lateral ventricle to the septal and preoptic areas and the hypothalamus. Two distinct groups of neurons, the large basolateral nuclear group and the smaller corticomedial nuclear group, can be differentiated. The basolateral nuclear group receives higher order sensory information from association areas in the frontal, temporal, and insular cortex. Axons run back from the amygdala to the association regions ofthe cortex, suggesting that activity in the amygdala may modulate sensory information processing in the association cortex. The basolateral amygdala is also connected, via the stria terminalis and the amygdalofugal pathway, to the ventral striatum and the thalamus.

Because of its interconnections with the sensory association cortex and hypothalamus, it has been suggested that the amygdala plays an important role in establishing associations between sensory inputs and various affective states. Activity of neurons within the amygdala is increased during states of apprehension, for example, in response to frightening stimuli. The amygdala also appears to participate in regulating endocrine activity, sexual behavior, and food and water intake, possibly by modulating hypothalamic activity. As described later in this chapter, bilateral damage to the amygdala and neighboring temporal cortex produces the KliiverBucy syndrome. The fomix and medial forebrain bundle, coursing within the hypothalamus, are also considered part of the limbic system.

FUNCTIONS AND DISORDERS The limbic system plays a central role in behavior. Experimental studies in both animals and humans indicate that stimulating or damaging some components of the limbic system causes profound changes. Stimulation alters somatic motor responses, leading to bizarre eating and drinking habits, changes in sexual and grooming behavior, and defensive postures of attack and rage. There can be changes in autonomic responses, altering cardiovascular or gastrointestinal function, and in personality, with shifts from passive to aggressive behavior. Damage to some areas of the limbic system may also profoundly affect memory.

Autonomic Nervous System The hierarchical organization of the autonomic nervous system (see Chapter 20) includes the limbic system; most of the limbic system output connects to the hypothalamus in part via the medial forebrain bundle. The specific sympathetic or parasympathetic aspects of autonomic control are not well localized in the limbic system, however.

SEPTALAREA The septal area, or complex, is relatively large in such animals as the cat and rat. Because it is a pivotal region with afferent fibers from the olfactory and limbic systems and efferent fibers to the hypothalamus, epithalamus, and midbrain, no single function can be ascribed to the area. Experimental studies have shown the septal area to be a substrate mediating the sensations of pleasure upon self-stimulation or

CHAPTER.19 The Limbic System


Corpus callosum Lcnghudlnal striae

Great limbic lobe

_,..,...- Septum lucidum


Corpus callosum - -

Sepia) area ------.__

Olfactory bulb

-/ __, Medial fotebrain bundle


Arnygdalold ' nuclear complex (amygdala)

Arnygdalohypothalamlc ftbers (direct)

FIGURE 19--12 Diagram of the principal connections of the limbic system. A: Hlppocampal system and great limbic lobe. B: Olfactory and amygdalold connections.

self-reward. Test animals will press a bar repeatedly to receive a (presumed) pleasurable stimulus in the septal area. Additional areas of pleasure have been found in the hypothalamus and midbrain; the stimulation of yet other areas reportedly evokes the opposite response. Antipsychotic drugs may act in part by modifying dopaminergic inputs from the midbrain to the septal area. An ascending pathway to the

septal area may be involved in the euphoric feelings described by narcotic addicts.

Behavior Hypothalamic regions associated with typical patterns of behavior such as eating, drinking, sexual behavior, and


SECTION V Functional Systems

converting short-term memory (up to 60 minutes) to longterm memory (several days or more). 1he anatomic substrate for long-term memory probably includes the temporal lobes. Patients with bilateral damage to the hippocampus can demonstrate a profound anterograde amnesia, in which no new long-term memories can be established. 1his lack of memory storage is also present in patients with bilateral interruption of the fomices (eg. by removal of a colloid cyst at the interventricular foramen). Memory processes also involve other structures, including the dorsomedial nuclei of the thalamus and the mamillary bodies of the hypothalamus, as discussed in Chapter 21. Long-term potentiation, a process whereby synaptic strength is increased when specific efferent inputs to the hippocampus are excited in a paired manner, provides a cellular-molecular basis for understanding the role of the hippocampus in memory and learning.

FIGURE 19-13

Location oftheamygdale(red)within a coro-

nal slice of the brain. (Reproduced with pennfssfon from Koenigs M, Grafman J: PosttTaumallc stress disorder. the role of media! prefrontaf cot'tl!K and amygdala, Nl!urosclentlst. 20090ct;15(S):S~548.)

aggyession receive input from the limbic system, especially the amygdaloid and septal complexes. Lesions in these areas can modify, inhibit, or unleash these behaviors. For example, lesions in the lateral amygdala induce unrestrained eating (bulimia), whereas those in the medial amygdala induce anorexia, accompanied by hypersexuality. Electrical stimulation of the amygdala in humans may produce fear, anxiety, or rage and aggyession.

Memory Memory involves Immediate recall. short-term memory, and long-term memory. The hippocampus is involved in

Place Cells, Grid Cells, and Spatial Problem Solving The hippocampus and entorhinal cortex play important roles in spatial navigation. In 2014, John O'Keefe received the Nobel Prize for discovering that the hippocampus contains "place cells• that encode spatial memory. ("Where have I been?•) Recalling of places, and of the routes required to navigate to them, requires hippocampal activation. Place cells within the hippocampus build, within the brain, an inner map of the environment. and are thus involved in navigation and spatial problem solving. May-Britt and Edvard Moser extended this work, and shared the 2014 Nobel Prize by showing that the entorhinal cortex. which is the largest input to the hippocampus, contains "grid cells." The grid cells are arranged in a hexagonal pattern and fire when an animal is in a particular location. Together, the place cells and grid cells provide a GPS system within the brain.

Neurogenesis and Depression Neurogenesis (the production of new neurosis) continues to OCQlr throughout adulthood in the dentate gyrus. Recent studies have shown a reduced rate of neurogenesis in the dentate gyrus in association with depression. Conversely, antidepressant medications have been reported to increase neurogenesis in the dentate gyrus. and this may contribute to their mechanism of action.

Other Disorders of the Limbic System '· Straight sinus

FIGURE 19-14 Horizontal section ttuough the head at the level of the mtdbraln and amygdala. (Reproduced with permfnfon from deGroot J: CDm!latfve Nf!uroanatomyofCompured Tomognzphy andMagnetic #lf!sonana Imaging, 215t ed. New York, NY: Appleton &Lange; 1991.)

A. Kiiver-Bucy Syndrome This disturbance of limbic system activities occurs in patients with bilateral temporal lobe lesions. The major characteristics of this syndrome are hyperorality (a tendency to explore objects by placing them in the mouth together with the indiscriminate eating or chewing of objects and

CHAPTER.19 The Limbic System




A 59-year-old man was brought to the hospital because of bizarre behavior for nearly a week. During the prior 2 days he had been confused and had had two shaking "fits." His wife said that he did not seem to be able to remember things. Twenty-four hours before admission. he had a severe headache. generalized malaise, and a temperature of 101 ~ (38.8 •q; he refused to eat. On examination, the patient was lethargic and confused, and had dysphasia. He could only remember one of

three objects after 3 minutes. There was no stiffness of the neck. The serum glucose level was 165 mg/dL. Lumbar puncture findings were as follows: pressure, 220 mm H20; white blood count, 153/µL, mostly lymphocytes; red blood cells, 1450/µL, with xanthochromia; protein, 71 mg/dL; and glucose, 101 mg/di... An electroencephalogram showed focal slowing over the temporal region on both sides, with sharp periodic bursts. Brain biopsy revealed the features of an active granuloma, without pus formation. A computed tomography scan is shown in Figure 19-15. What is the differential diagnosis? Over the next 8 days, the patient became increasingly drowsy and dysphasic. A repeated scan showed extensive defects of both temporal lobes. The patient died on the lOth day after admission despite appropriate drug treatment.

Cases are discussed further in Chapter 25.

all kinds of food); hyperse:mality, sometimes described as a lack of sexual inhibition; plfdW: blindness, or visual agnosia, in which objects are no longer visually recognized; and personality changet, usually with. abnormal passivity or docility. Psychic blindness in th.e Kluver-Bucy syndrome presumably results from damage to the amydala, which normally functions as a site of transfer of information between sensory association cortex and the hypothalamus. After damage to the amygdala, visual stimuli can no longer be paired with. affective (pleasurable or unpleasant) responses. B. Temporal Lobe Epilepsy The temporal lobe (especially the hippocampus and amygdala) has a lower threshold for epileptic seizure activity than the other cortical areas. Seizures that originate in these regions, called psydtomoto.r (complex partial) seizures, differ from the jacksonian seizures that originate in or near the motor cortex (see Chapter 21). Temporal lobe epilepsy may include abnormal sensations, especially bizarre olfactory sensations, sometimes called uncinate fits; repeated involuntary

FIGURE 19-15 Magnetic resonance image of horizontal section through the head at the level of the temporal lobe. The large leslon In the left temporal lobe and a smaller one en the right side are Indicated by •rrowheads. Computed tomography scans confinned the presence of muhlple small hemorrhaglc leslcns In both temporal lobes.

movements such as chewing, swallowing, and lip smacking; disorders of consciousness; memory loss; hallucinations; and disorders of recall and recognition. 'Ihe underlying cause of th.e seizures may sometimes be difficult to determine. A l\lmor (eg. astrocytoma or oligodendroglioma) may be responsible. or glial scar formation after trauma to th.e temporal poles may trigger seizures. Small hamartomas or areas of temporal sclerosis have been found in patients with temporal lobe epilepsy. Although anticonvulsant drugs are often given to control th.e seizures, they may be ineffective. In these cases, neurosurgical removal of the seizure focus in th.e temporal lobe may provide excellent seizure con-


REFERENCES Adolphs R: 1h.e human am.ygdala and emotion. Neurosdenttst. 1999;6:125.

Anderson P, Morris R. Amaral D, Bliss T, O'Keefe J (editors): ~ Hippocampus Book. Oxford University Press, 2007. Banasr M, Duman RS. Cell atrophy and loss in depression: Reversal by antidepressant treatment Cu" Opin Cell Biol 2011;23: 730-738. Damasio AR.: Toward a neurobiology of emotion and feeling. Neuroscientist. 1995;1:19. Dityatev A, Bolshakov V: Amygd.ala, long·term potentiation, and fear c;onditioning. Neuroscientist. 2005;11:75-88.


SECTION V Functional Systems

Hartley T, Lever C, Burgess N, O'Keefe J: Space In the brain: How the hippocampal formation supports spatial cognition. Phil Trans Roy Soc B. 2014; 369:20120510. Koenigs M, Grafrnan J: Posttrawnatic: stress disorder: Role of the medial prefrontal cortex: and amygdala. Neuroscumtist. 2009;15:54-0-548. Levin GR: The amygdala, the hippocampus, and emotional modulation of memory. Neuroscientist. 2004;10:31-39. Macguire EA. Frackowiak SJ, Frith CD: Recalling routes around London: Activation of the right hippocampus In taxi drivers. I Neurosd. 1997;17:7103. McCarthy G: Functional neurolm.aging of memory. Neuroscientist. 1995;1:155. Moter EL Roudl Y, Witter MP, Kentros C. Bonhoeffer T, Moser MB: Grid cells and c:orti.c::al representation. Nat Rev Neurosci. 2014; 15:466-481. Moulton DG, Beidler LM: Struc:ture and function in the peripheral olfactory syltem. Physiol Rev. 1987;47:1. O'Keefe J. Nadel L: The Hippocampus as a Cognitive Ma.p. Oxford University Press, 1978. Reed RR: How does the nose know? Cell. 1990;60:1. Warren-Schmidt JL, Duman RS. Hippocampal Neurogene.sis: Opposing effects of stress and antidepre11ant treatment. Hippocampus. 2006;16:239-249. Zola-Morgan S, Squire LR: Neuroanatomy of memory. Ann Rev Neurosci. 1993;16:547.

BOX 19-1 Essentials for the Clinical Neuroanatomlst After reading and digesting this chapter, you should know and understand: • The llmblclobeand llmblcsystem {Tables 19-1and19-2) • Role In aggression, expression of emotion, autonomic. sexual and appetitive behavlor • Olfactlon: perlpheral olfactory receptors and central p~ jectlons • Htppocampal foimatlon (Figs 19-3, 19-9, 19-10, and 19-11) • Htppocampus: roles In memory and leamtng • The Papez: circuit • Septa! area and Its role as a •pleasure center"' • Amydala • Place cells and grid cells and their roles In navigation Cllnlcal correlations: KIOver-Bucy syndrome and tem~ ral lobe epllepsy

• L


The Autononiic Nervous Systeni The autonomic (visceral) nervous system (ANS) is concerned with control of target tissues: the cardiac muscle, the smooth muscle in blood vessels and viscera, and the glands. It helps maintain a constant internal body environment (homeostasis). The ANS consists of efferent pathways, afferent pathways, and groups of neurons in the brain and spinal cord that regulate the system's functions. It is modulated by supraspinal centers such as brain stem nuclei and the hypothalamus. The ANS is divided into two major anatomically distinct divisions with opposing actions: the sympathetic (thoracolumbar) and parasympathetic (craniosac.ral) divisions (Fig 20-1). The sympathetic and parasympathetic divisions of the ANS are anatomically distinct. and are different in terms of their pharmacological properties, that is, their response to medications. They are sometimes referred to as the sympathetic nervous system and the parasympathetic nervous system. The autonomic nervous system is of critical importance in clinical medicine. Abnormalities associated with autonomic dysfunction, such as cardiac arrythmias, high or low blood pressure, or disturbances of gastrointestinal function are common in the clinic. Many commonly used medications (eg, medications for treating high blood pressure, for regulating gastrointestinal function, or for maintaining a regular heart beat) have their major actions on neurons within these systems. Some authorities consider the intrinsic neurons of the gut as forming a separate enteric nervous system.

AUTONOMIC OUTFLOW The efferent components of the autonomic system are organized into sympathetic and parasympathetic divisions, which arise from preganglionic cell bodies in different locations. The autonomic outflow system is organized more diffusely than the somatic motor system. In the somatic motor system, lower motor neurons project directly from the spinal cord or brain, without an interposed synapse, to innervate a relatively small group of target cells (somatic muscle cells). This permits individual muscles to be activated separately so that motor action is finely tuned. In contrast, a more slowly conducting two-neuron chain characterizes the autonomic outflow. The cell body of the primary neuron (the presynaptic, or preganglionic, neuron) within the central nervous system is located in the intermediolateral gray column of the spinal

cord or in the brain stem nuclei. It sends its axon, which is usually a small-diameter, myelinated B fiber (see Chapter 3), out to synapse with the secondary neuron (the postsynaptic, or postganglionic, neuron) located in one of the autonomic ganglia. From there, the postganglionic axon passes to its terminal distribution in a target organ. Most postganglionic autonomic axons are unmyelinated C fibers. The autonomic outflow system projects widely to most target tissues and is not as highly focused as the somatic motor system. Because the postganglionic fibers outnumber the preganglionic neurons by a ratio of about 32:1, a single preganglionic neuron may control the autonomic functions of an extensive terminal area.

Sympathetic Division The sympathetic nervous system, or sympathetic (thoracolumbar) division of the ANS arises from preganglionic cell bodies located in the intermediolateral cell columns of the 12 thoracic segments and the upper two lumbar segments of the spinal cord (Fig 20-2).

A. Preganglionic Sympathetic Efferent Fiber System Preganglionic sympathetic fibers are mostly myelinated. Coursing with the ventral roots, they form the white communicating rami of the thoracic and lumbar nerves, through which they reach the ganglia of the sympathetic chains or trunks (Fig 20-3). These trunk ganglia lie on the lateral sides of the bodies of the thoracic and lumbar vertebrae. On entering the ganglia, the fibers may synapse with ganglion cells, pass up or down the sympathetic trunk to synapse with ganglion cells at a higher or lower level, or pass through the trunk ganglia and out to one of the collateral (intermediary) sympathetic ganglia (eg, the celiac and mesenteric ganglia). The splanchnic nerves arising from the lower seven thoracic segments pass through the trunk ganglia to the celiac and superior mesenteric ganglia. There, synaptic connections occur with ganglion cells whose postganglionic axons then pass to the abdominal viscera via the celiac plexus. The splanchnic nerves arising from spinal cord segments in the lowest thoracic and upper lumbar region convey fibers to synaptic stations in the inferior mesenteric ganglion and to small ganglia associated with the hypogastric plexus, through which postsynaptic fibers are distributed to the lower abdominal and pelvic viscera. 237


SECTION V Functional Systems


Puplllary dllator )--· -•• -••• Lacrimal gland )·... ... \ and nasal glands " •.. •




Submax1llaryand )-··· ··subllngual glands ··., : Parotld gland )· • • • • ••


Otlc ganglion


• < Parotid gland

I 'I



:. Superior sympathetic ganglion '


•· .. · ··• >--+--+-4 T1

;. ....... . . . . ---- T2 Heart ) ··· ••• : :- • • • • • •: • • • • • ·•

Lungs >- ····


. ~ ---·-•



Stomach )-· - -~ Cellac ganglion /_"_..--;-.,....-----,..-. T6 Llwr )-- · ··: Pancl'88S ) · • • • ~.. • • T7 Spleen >···,;





r---~-------t-e T11


Colon )· " " Kidney )· - •

T.>""""-+ . L1

+[ ..

Bladder > ····


>···· ·········-..)





Sympathetic trunk




T7 T8 T9

TIO T11 T12 L1

Small intestine

Spinal cord



Pregangllonlc flbers Postgangllonlc flbers -·--·--·--

,Sax organs Bladder


Sympathetic division of the autonomic nervous system {left half). CG, ceflac ganglion; IMG, Inferior mesenterlc ganglion; SMG, superior mesenterlc gangllon.


SECTION V Functional Systems

Cranial nerve&_ "'·VII, IX, X

From spinal cord, medulla, hypothalamus Brain stem

o ,h

l .( Pre


To blood vessels,

._-( sweat glands _____ Sympathetic ganglion -~~

-- Gray ramus communicans Sacral outflow




Sympethdc dlvlelon

Paruympathetlc dlvlelon


Types of outflow In autonomic nervous system. Pre, pregangllon!c neuron; Post, postgangllonlc neuron; CR, communicating ram us. (Reproduced with pennrssron from Ganong WF: Revl'ewofMedl'cal Physrotogy, 22.nd ed. New York. NY: Mdil'IW-+!111 Education; lOOS.)

B. The Adrenal Gland

Parasympathetic Division

Preganglionic sympathetic axons in the splanchnic nerves also project to the adrenal gland, where they synapse on chromatlin cells in the adrenal medulla. The adrenal chromaffin cells. which receive direct synaptic input from preganglionic sympathetic axons, are derived from neural crest and can be considered to be modified postganglionic cells that have lost their axons.

1he parasympathetic nervous system or parasympathetic (craniosacral) division of the ANS arises from preganglionic cell bodies in the gray matter ofthe brain stem (medial part of the oc:ulomotor nucleus, Edinger-Westphalnucleus, superior and inferior salivatory nuclei) and the middle three segments of the sacral cord (S2-4) (Pigs 20-3 and 20-5). Most preganglionic nbers from S2, S3, and S4 run without interruption from their central origin within the spinal cord to either the wall of the viscus they supply or the site where they synapse with terminal ganglion cells associated with the plexuses of Meissner and Auerbach in the wall of the intestinal tract (see Enteric Nervous System section). Because the parasympathetic postganglionic neurons are located close to the tissues they supply, they have relatively short axons. 1he parasympathetic distribution is confined entirely to visceral structures. Four cranial nerves convey preganglionic parasympathetic (visceral efferent) fibers. 1he oculomotor, faclal, and glo11opharyngeal. nervea (cranial nerves lII, VII, and IX) distribute parasympathetic or visceral efferent fibers to the head (see Fig 20-4 and Chapters 7 and 8). Parasympathetic amns in these nerves synapse with postganglionic neurons in the ciliary, sphenopalatine, submu:illary, and otic ganglia, respectively (see Autonomic Innervation of the Head section). 1he ngaa nerve (cranial nerve X) distributes its autonomic fibers to the thoracic and abdominal viscera via the preverteb.ral pla:utea. 1he pelvic: nerve (nemis erigentes) distributes parasympathetic fibers to most ofthe large intestine and to the pelvic viscera and genitals via the hypotpstric plems.

C. Postganglionic Efferent Fiber System 1he mostly unmyelinated postganglionic sympathetic 6.bers form the gray communicating rami. The 6bers may course with the spinal nerve for some distance or go directly to their target tissues. 1he gray communicating rami join each of the spinal nerves and distribute the vasomotor, pilomotor, and sweat gland innervation throughout the somatic areas. Branches of the superior cerri.caJ. sympathetic: ganglion enter into the formation of the sympathetic carotid plexuses around the internal and external carotid arteries for distribution of sympathetic fibers to the head (Fig 20-4). After exiting from the carotid plexus, these postganglionic sympathetic axons project to the salivary and lacrimal glands, the muscles that dilate the pupil and raise the eyelid, and sweat glands and blood vessels of the face and head. 1he superior cardiac nervea from the three pairs of cervical sympathetic ganglia pass to the cardiac pi.ems at the base of the heart and distnbute cardioaccelerator fibers to the myocardium. Vasomotor branches from the upper five thoracic ganglia pass to the thoracic aorta and to the posterior pulmonary plexus. through which dilator fibers reach the bronchi.

CHAPTER. 20 The Autonomic Nervous System

Centnll origin

Cranial autonomic ganglia


Suoir/al oortion of oculomolor nucioue



Sup sail\ nucl



_,, Trad and1









: ·"-. ,.-.



. ---

,!...·~- ;--(~ .. .--···: .;_c0r digilorum superficialis

Flexor digitorum


profundu1 (radial pordon)

Flexer pollicis longus --....._


Abductor pollicis brevis ---

Pronator quadratua

Opponens pollicis -

Flamr polllcls bnMs (su perllcial head)

•- - Anastomosis with ulnar nerve

Flrl!lt and second lumbrtcalee


The median nerve (C6-8;T1).

Unopposed thumb

Spinal Nerves and Plemaes

Lateral cord Medial cord

Humeral portion (no branches)

Area of isolated supply


I \

Sen110ry dlltrtbutlon


,..___ Ulnar nerve

Flexor digitorum profundus (median half)



Palmaris brevis


Abductor digit! qulntl

Rexor polllcls breWI - -+-.f-"'1.--...._. (deep head)

Opponens dlgHI quint! - Flexer digiti quin1i

See median nerve

Clawhand deformity in ulnar lesions

FIGURE C-9 The ulnar nerve (C8, Tl).

• • •

Dorsal intel'O$$ei (4) Palmar lnterossel (3) Ulnar lumbrlcales (2)



Appendix C

Branchee Tennlnal branchee

Plexu• roota


From anterior primary dMslons

(Posterior shaded) lllohypogutrlc nerve (T12, L1)


Iliac branch


Hypogastric branch lllolngulnal narve (L1)

Oenltofemoral nerve (L1, 2)

L.umbolngulnal branch Extemal spermatic branch L3

Lateral femoral cuWt90U9 ntll'¥9 (L2.

3) L4

* L5

Femoral nerve (L2, 3, 4)

*To lntertransversarll and quadratus muscles


The lumbar plexus.

Obturator nerve (L2, 3, 4)

Lumboucral trunk (to sacral plexus)

Spinal Nervea and Plexwies


·-... Obblrator n•l'V8

Femoral artery _ _ __,..._ _-t-- .·


Anterior branch Poeterlor branch

.- Peclineus muscle

Middle cutaneous netVe -·--.....Medial or internal - -cutaneous nerve

Anterior femoral cutaneous

-- Adductor ~ magnua

! l

I - Adductor I longus


\ 't


Vastus laterali&

~!a._ J\




Subaartorial or cutaneous branch of obturator



' lI I

,q~'---MM ~~ I




Sen11ary dlmlbullon

FIGURE C-11 The femoral (l2-4) and obturator(ll-4) nerves.




Appendix C

Plnusrvot Division• Termlnal and collateral branch•

(From anterior primary divisions)

(Posterior (black] and anterior} (To lumber plexus)


B1'1111chee tram paelllrlar division• (Lumboeacral trunk)

L5 Inferior gluteal nerve (LS; S1, 2) __.

S1 Branch tram bath •nterlor ud posterior divisions

Posterior femoral


cutaneous nerve (81, 2, 3)


Tlblal nerve

(To namatrlng muacle8)

a,.nch•trom anterior dlvlalana To quadratus femorta and1J L4 5 . 51 gemellus lnfertor muectes ' '

To obturator intemus and } gemellua supertor muecles

FIGURE C-12 The sacral plexus.


LS· 1 2 ' '

Spinal Nerves and Plemaes


FIGURE C-13 Segmental innervation of the right lower extremity, anterior view. Note the similarity between dermatomes (on Id) and myotomes (on right).

L1 l2



:~ \ L4





L5 S1

FIGURE C-14 Segmental innervation of the right lower extremity, posterior view.


Appendix C

Hamlltrfng mu8Claa

Semitendinosus - - -

Adductor magnus


-- -- Common peroneal nerve

Tiblal nerve -----

FIGURE C-15 The sciatic nerve (L4, 5; S1-3).

Spinal Nerves and Plemaes

Common . . . . _ pilronMI



- Recul'l1)nt articular nerve


!.. . .- peroneal Common

SUP1rflclal ~



Peroneus longus '-.... muscle ·""


Peroneus brevis -...,_ muade •

Sural nerve

-- Extensor dlgltorum longus / /"'

Superficial peroneal

"- Extensor hallucis longus

Peroneus tertius muscle

---... Extensor digitonJm brevis muscle

-.. Terminal cutaneous rami to the foot

FIGURE C-16 The common peroneal nerve(L4,S;S1,2).

_,,. Deep peroneal

Sensory distribution



Appendix C








_,..., t

\ / ,Ii



\, I'


llblal nerve C.lfmueci.. ·

Gastrocnemius ---~ Medial aural Popllteus - - - -

' - Lateral aural


___ Lateral


Medial ·plantar nerve

cutaneous nel'Y8

Sural nerw


cutaneous nel'Y8 s.risory dlstrlbuUon --- --- Sural nerve Soleus -----

r=7~-~ llblalls posterior



Flaxor digitorum longus

Medlal plantar ..,.,,.

_ - - Lalll!ral plantar nerve



Fl.,.. dlglloium """"' __


Abductor nallucis ----





Medial plantar ·nerw Lateral pl111tar "'


Plantar vl• of the foot Superftclal branc:h af latarsl plantar nerva t Deep brand1 af la111.ral plantar nerva ~ Adductor ltallucis (transverse and oblique) • Plantar lntel'088al (3)


• Dorsal intarossei (4) • Lateral lumbricales (3)

FIGURE C-17 The tiblal nerve (L.4, S; 51-3).

Spinal Nerves and Plemaes

* S2


* S5


To levator anl, coceygeus, and { sphincter anl externus muscles


Anoccccygeal nerves *Viscera! branches

FIGURE C-18 The pudenda! and coccygeal plexuses.


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Questions and Answers Section I: Chapters 1through3 In the following questions, select the single best answer. 1. The basic neuronal signaling unit is A. the equilibrium potential B. the action potential C. the resting potential D. the supernormal period 2. In a motor neuron at rest, an excitatory synapse produces an EPSP of 15 m V, and an inhibitory synapse produces an IPSP of 5 m V. If both the EPSP and IPSP occur simultaneously, then the motor neuron would A. depolarize by about 10 mV B. depolarize by 20 m V C. depolarize by more than 20 mV D. change its potential by less than 1 m V

3. The equilibrium potential for K+ in neurons is ordinarily nearest A. the equilibrium potential for Na+ B. resting potential C. reversal potential for the EPSP D. the peak of the action potential 4. Generation of the action potential A. depends on depolarization caused by the opening of K+ channels B. depends on hyperpolarization caused by the opening ofK+ channels C. depends on depolarization caused by the opening of Na+ channels D. depends on hyperpolarization caused by the opening of Na+ channels E. depends on second messengers 5. The cerebrum consists of the A. thalamus and basal ganglia B. telencephalon and midbrain C. telencephalon and diencephalon D. brain stem and prosencephalon E. cerebellum and prosencephalon

6. The somatic nervous system innervates the A. blood vessels of the skin B. blood vessels of the brain C. muscles of the heart D. muscles of the body wall E. muscles of the viscera 7. The peripheral nervous system A. includes the spinal cord B. is sheathed in fluid-filled spaces enclosed by membranes C. includes cranial nerves D. does not include spinal nerves E. is surrounded by bone 8. ATP provides an essential energy source in the CNS for A. division of neurons B. maintenance of ionic gradients via ATPase C. generation of action potentials D. EPSPs and IPSPs 9. Myelin is produced by A. oligodendrocytes in the CNS and Schwann cells in thePNS B. Schwann cells in the CNS and oligodendrocytes in thePNS C. oligodendrocytes in both CNS and PNS D. Schwann cells in both CNS and PNS In the following questions, one or more answers may be correct. Select A if 1, 2, and 3 are correct B if 1 and 3 are correct C if 2 and 4 are correct D if only 4 is correct E if all are correct 10. A spinal motor neuron in an adult I. maintains its membrane potential via the active transport of sodium and potassium ions 2. synthesizes protein only in the cell body and not in the axon 3. does not synthesize DNA for mitosis 4. does not regenerate its axon following section of its peripheral portion



Appendix D

11. The myelin sheath is 1. produced within the CNS by oligodendrocytes 2. produced within the peripheral nervous system by Schwann cells 3. interrupted periodically by the nodes of Ranvier 4. composed of spirally wrapped plasma membrane

20. The cell layer around the central canal of the spinal cord 1. is called the ventricular zone 2. is the same as the pia 3. encloses cerebrospinal fluid 4. is called the marginal zone

12. Astrocytes 1. may function to buffer extracellular K+ 2. are interconnected by gap junctions 3. can proliferate to form a scar after an injury 4. migrate to the CNS from bone marrow

21. Norepinephrine is found in the 1. sympathetic nervous trunk 2. locus ceruleus 3. lateral tegmentum of the midbrain 4. neuromuscular junction

13. The cell body of most neurons 1. cannot divide in the adult 2. is the main site of protein synthesis in the neuron 3. is the site of the cell nucleus 4. contains synaptic vesicles

22. Glutamate 1. is the transmitter at the neuromuscular junction 2. may be involved in excitotoxicity 3. is a major inhibitory transmitter in the CNS 4. is a major excitatory transmitter in the CNS

14. Most synaptic terminals of axons that form chemical synapses in the CNS contain 1. synaptic vesicles 2. presynaptic densities 3. neurotransmitter(s) 4. rough endoplasmic reticulum

23. Decussations are 1. aggregates of tracts 2. fiber bundles in a spinal nerve 3. horizontal connections crossing within the CNS from the dominant to nondominant side 4. vertical connections crossing within the CNS from left to right or vice versa

15. Na, K-ATPase 1. utilizes ATP 2. acts as an ion pump 3. maintains the gradients of Na+ and K+ ions across neuronal membranes 4. consumes more than 25% of cerebral energy production 16. In axoplasmic transport 1. some macromolecules move away from the cell body at rates of several centimeters per day 2. mitochondria move along the axon 3. microtubules seem to be involved 4. some types of molecules move toward the cell body at rates of up to 300 mm per day 17. The brain stem includes 1. the midbrain (mesencephalon) 2. pons 3. medulla oblongata 4. telencephalon 18. A ganglion is defined as a 1. part of the basal ganglia 2. group of nerve cell bodies within the hypothalamus 3. layer of similar cells in the cerebral cortex 4. group of nerve cell bodies outside the neuraxis 19. Neurotransmitters found in the brain stem include 1. acetylcholine 2. norepinephrine 3. dopamine 4. serotonin

24. Inhibitory transmitters in the CNS include 1. glutamate (presynaptic inhibition) 2. GABA (presynaptic inhibition) 3. glutamate (postsynaptic inhibition) 4. GABA (postsynaptic inhibition) 25. The neurotransmitter dopamine 1. is produced by neurons that project from the substantia nigra to the caudate and putamen 2. mediates transmission at the neuromuscular junction 3. is depleted in Parkinson's disease 4. is the major excitatory transmitter in the CNS

Sedion Ill: Chapters S and 6 In the following questions, select the single best answer. 1. The lateral column of the spinal cord contains the A. lateral corticospinal tract B. direct corticospinal tract C. Lissauer's tract D. gracile tract 2. A sign ofan upper-motor-neuron lesion in the spinal cord is

A. B. C. D. E.

severe muscle atrophy hyperactive deep tendon reflexes flaccid paralysis absence of pathologic reflexes absence of withdrawal responses

Questions and Answers

3. The following fiber systems in the spinal cord are ascending tracts except for the A. cuneate tract B. ventral spinocerebellar tract C. spinothalamic tract D. spinoreticular tract E. reticulospinal tract 4. Axons in the spinothalamic tracts decussate A. in the medullary decussation B. in the medullary lemniscus C. within the spinal cord, five to six segments above the level where they enter D. within the spinal cord, within one to two segments of the level where they enter E. in the medial lemniscus 5. The spinal subarachnoid space normally

A. B. C. D. E.

lies between the pachymeninx and the arachnoid lies between the pia and the arachnoid ends at the cauda equina communicates with the peritoneal space is adjacent to the vertebrae

6. The subclavian artery gives rise directly to the A. lumbar radicular artery B. great ventral radicular artery C. anterior spinal artery D. vertebral artery 7. The dorsal nucleus (of Clarke) in the spinal cord A. receives contralateral input from dorsal root ganglia B. terminates at the L2 segment C. terminates in the midbrain D. terminates in the ipsilateral cerebellum E. receives fibers from the external cuneate nucleus 8. A patient complains of unsteadiness. Examination shows a marked diminution of position sense, vibration sense, and stereognosis of all extremities. He is unable to stand without wavering for more than a few seconds when his eyes are closed. There are no other abnormal findings. The lesion most likely involves the A. lateral columns of the spinal cord, bilaterally B. inferior cerebellar peduncles, bilaterally C. dorsal columns of the spinal cord, bilaterally D. spinothalamic tracts, bilaterally E. corticospinal tracts In the following questions, one or more answers may be correct Select A if I, 2, and 3 are correct B if 1 and 3 are correct C if 2 and 4 are correct D if only 4 is correct E if all are correct


9. Fine-diameter dorsal root axons of LS on one side terminate in the I. marginal layer of the ipsilateral dorsal horn 2. ipsilateral substantia gelatinosa 3. ipsilateral lamina V of the dorsal horn 4. ipsilateral dorsal nucleus (of Clarke) 10. Axons in the spinothalamic tract I. carry information about pain and temperature (lateral spinothalamic tract) and light touch (anterior spinothalamic tract) 2. carry information about pain (lateral spinothalamic tract) and temperature (anterior spinothalamic tract) 3. decussate within the spinal cord, within one or two segments of their origin 4. synapse in the gracile and cuneate nuclei 11. The dorsal spinocerebellar tract I. arises in the dorsal nucleus of Clarke and, above CS, in the accessory cuneate nucleus 2. carries information arising in the muscle spindles, Golgi tendon organs, touch and pressure receptors 3. ascends to terminate in the cerebellar cortex 4. projects without synapses to the basal ganglia and cerebellum 12. Second-order neurons in the dorsal column system I. convey information about pain and temperature 2. cross within the lemniscal decussation 3. cross within the pyramidal decussation 4. convey well-localized sensations of fine touch, vibration, two-point discrimination, and proprioception 13. The following rules about dermatomes are correct I. the C4 and T2 dermatomes are contiguous over the anterior trunk 2. the nipple is at the level of CS 3. the thumb, middle finger, and Sth digit are within the C6, C7, and C8 dermatomes, respectively 4. the umbilicus is at the level of L2 14. Signs of upper-motor-neuron lesions include I. Babinski's sign 2. hypoactive deep tendon reflexes and hyporeflexia 3. spastic paralysis 4. severe muscle atrophy 15. A-delta and C peripheral afferent fibers I. terminate in laminas I and II of the dorsal horn 2. convey the sensation of pain 3. terminate in lamina V of the dorsal horn 4. convey the sensation oflight touch


Appendix D

16. The following are correct 1. the diaphragm is innervated via the C3 and C4 roots 2. the deltoid and triceps are innervated via the CS root 3. the biceps are innervated via the CS root 4. the gastrocnemius is innervated via the 14 root

17. The long-term consequences of a left hemisection of the spinal cord at midthoracic level would include 1. loss of voluntary movement of the left leg 2. loss of pain and temperature sensation in the right leg 3. diminished position and vibration sense in the left leg 4. diminished deep tendon reflexes in the left leg

18. The spinal nerve roots 1. exit below the corresponding vertebral bodies in the cervical spine exit above the corresponding vertebral bodies in the cervical spine 3. exit above the corresponding vertebral bodies in the lower spine 4. exit below the corresponding vertebral bodies in the lower spine 2.

19. Gamma-efferent motor neurons 1. are located in the intermedial lateral cell column of the spinal cord 2. cause contraction of intrafusal muscle fibers 3. provide vasomotor control to blood vessels in muscles 4. are modulated by axons in the vestibulospinal tract 20. The dorsal column system of one side of the spinal cord 1. is essential for normal two-point discrimination on that side 2. arises from both dorsal root ganglion cells and dorsal horn neurons 3. synapses on neurons of the ipsilateral gracile and cuneate nuclei 4. consists primarily of large, myelinated, rapidly conducting axons

21. Large-diameter dorsal root axons of one side of LS terminate in the 1. marginal layer of the ipsilateral dorsal horn 2. ipsilateral gracile nucleus 3. ipsilateral cuneate nucleus 4. ipsilateral dorsal nucleus (of Clarke)

22. The fibers carrying information from the spinal cord to the cerebellum 1. can arise from Clarke's column cells (dorsal nucleus) 2. represent the contralateral body half in the dorsal spinocerebellar tract

3. can arise from cells of the external cuneate nucleus 4. are important elements in the conscious sensation of joint position

23. The intermediolateral gray column 1. contains preganglionic neurons for the autonomic nervous system 2. is prominent in the thoracic region 3. is prominent in upper lumbar regions 4. is prominent in cervical regions 24. In adults 1. there is very little myelin in the spinal cord 2. the dorsal columns and lateral columns are heavily myelinated 3. the spinal cord terminates at the level of the SS vertebrae 4. the spinal cord terminates at the level ofthe 11 or 12 vertebra 25. In humans, the spinothalamic tract 1. carries information from the ipsilateral side of the body 2. exhibits topographic organization 3. arises principally from neurons of the same side of the cord 4. mediates information about pain and temperature

Sedion IV: Chapters 7 through 12 In the following questions, select the single best answer. I. Examination of a patient revealed a drooping left eyelid, together with weakness of adduction and elevation of the left eye, loss of the pupillary light reflex in the left eye, and weakness of the limbs and lower facial muscles on the right side. A single lesion most likely to produce all these signs would be located in the A. medial region of the left pontomedullary junction B. basomedial region of the left cerebral peduncle C. superior region of the left mesencephalon D. dorsolateral region of the medulla on the left side E. periaqueductal gray matter on the left side

2. A neurologic syndrome is characterized by loss of pain and thermosensitivity on the left side of the face and on the right side of the body from the neck down; partial paralysis of the soft palate, larynx. and pharynx on the left side; ataxia on the left side; and hiccuping. This syndrome could be expected from infarction in the territory of the A. basilar artery B. right posterior inferior cerebellar artery C. left posterior inferior cerebellar artery D. right superior cerebellar artery E. left superior cerebellar artery

Questions and Answers

3. Hemiplegia and sensory deficit on the right side of the body may be caused by infarction in the territory of the A. left middle cerebral artery B. right anterior cerebral artery c. left posterior cerebral artery D. left superior cerebellar artery E. anterior communicating artery

4. If the oculomotor nerve (III) is sectioned, each of the following may result except for

A. partial ptosis B. abduction of the eyeball


D. E.

dilation of the pupil impairment of lacrimal secretion paralysis of the ciliary muscle

5. Structures in the ventromedial regions of the medulla receive their blood supply from the

A. posterior spinal and superior cerebellar arteries B. vertebral and anterior spinal arteries


posterior spinal and posterior cerebral arteries

D. posterior spinal and posterior inferior cerebellar arteries

E. posterior and anterior inferior cerebellar arteries 6. The efferent axons of the cerebellar cortex arise from A. Golgi cells B. vestigial nucleus cells c. granule cells D. Purkinje cells E. pyramidal cells

7. A lesion in the nucleus of cranial nerve IV would produce a deficit in the

A. upward gaze of the ipsilateral eye B. upward gaze of the contralateral eye


downward gaze of the contralateral eye

D. downward gaze of the ipsilateral eye 8. Sensory input for taste is carried by A. the vestibulocochlear (VIII) nerve B. the facial (VII) nerve for the entire tongue C. the facial (VII) and glossopharyngeal (IX) nerves for the anterior two-thirds and posterior one-third of the tongue, respectively D. the glossopharyngeal (IX) and vagus (X) nerves for the anterior two-thirds and posterior one-third of the tongue, respectively 9. In central facial paralysis resulting from damage of the facial (VII) nucleus there is A. paralysis of all ipsilateral facial muscles B. paralysis of all contralateral facial muscles C. paralysis of ipsilateral facial muscles except the buccinator D. paralysis of all contralateral muscles except the buccinator E. paralysis of contralateral facial muscles except the frontalis and orbicularis oculi


10. Within the internal capsule, descending motor fibers for the face A. are located in front of fibers for the arm, in the anterior part of the anterior limb B. are located posterior to the fibers for the leg, in the posterior half of the posterior limb C. are located in front of the fibers for the arm, in the anterior part of the posterior limb D. travel within the corticovestibular tract E. synapse in the capsular nucleus 11. Brodmann's area 4 corresponds to the A. primary motor cortex B. premotor cortex C. Broca's area D. primary sensory cortex E. striate cortex 12. In a stroke affecting the territory of the middle cerebral artery A. weakness and sensory loss are most severe in the contralateral leg B. weakness and sensory loss are most severe in the contralateral face and arm C. weakness and sensory loss are most severe in the ipsilateral leg D. weakness and sensory loss are most severe in the ipsilateral face and arm E. akinetic mutism is often seen In the following questions, one or more answers may be correct. Select A if I, l, and 3 are correct B if I and 3 are correct C if 2 and 4 are correct D if only 4 is correct E if ail are correct 13. Cortical area 17 1. is also termed the striate cortex 2. is involved in the processing of auditory stimuli 3. receives input from the lateral geniculate body 4. receives input from the medial geniculate body 14. Within the cerebellum 1. climbing fibers and mossy fibers carry afferent information 2. Purkinje cells provide the primary output from the cerebellar cortex 3. Purkinje cells project to the ipsilateral deep cerebellar nuclei 4. efferents from the deep cerebellar nuclei project to the contralateral red nucleus and thalamic nuclei 15. In a patient with a missile wound involving the left cerebral hemisphere, the following might be expected 1. dense neglect of stimuli on the left side 2. hemiplegia involving the right arm and leg 3. hemiplegia involving the left arm and leg 4. aphasia


Appendix D

16. The striatum includes 1. the caudate nucleus 2. the globus pallidus 3. the putamen 4. the substantia nigra 17. The ventroposterior medial nucleus of the thalamus 1. receives axons from neurons located in the contralateral cuneate nucleus in the medulla 2. receives axons from neurons located in area 4 on the medial surface of the ipsilateral cerebral hemisphere 3. contains neurons that respond to olfactory stimuli applied ipsilaterally 4. contains neurons whose axons project to the somatosensory cortex of the ipsilateral cerebral hemisphere 18. A healthy 25-year-old man had an episode of blurred vision in the left eye that lasted 2 weeks and then resolved. Six months later he developed difficulty walking. Examination showed decreased visual acuity in the left eye, nystagmus, loss of vibratory sensation and position sense at the toes and knees bilaterally, and hyperactive deep tendon reflexes with a Babinski reflex on the right Three years later, the man was admitted to the hospital with dysarthria, intention tremor of the left arm, and urinary incontinence. The clinical features are consistent with 1. myasthenia gravis 2. a series of strokes 3. a cerebellar tumor 4. multiple sclerosis 19. The vagus (X) nerve contains 1. visceral afferent fibers 2. visceral efferent fibers 3. branchial efferent fibers 4. somatic efferent fibers 20. Lesions of the cerebral cortex on one side can result in a deficit in muscles innervated by the 1. contralateral spinal motor neurons 2. ipsilateral spinal motor neurons 3. contralateral facial (VII) nerve 4. ipsilateral facial (VII) nerve 21. The trigeminal nuclear complex 1. has somatic afferent components 2. participates in certain reflex responses of cranial muscles 3. has a branchial efferent component 4. receives projections of axons coursing with nerve X 22. The solitary nucleus 1. serves visceral functions, none of which are consciously perceived 2. gives rise to preganglionic parasympathetic axons

3. mediates pain arising from the heart during myocardial ischemia 4. receives axons running with nerve VII

23. Sensory nuclei of the thalamus include 1. lateral geniculate 2. superior geniculate 3. ventral posterior, lateral 4. ventral anterior

24. Axon pathways that decussate before they terminate include the 1. optic nerve (II) fibers from the temporal halves of the two retinas 2. gracile fasciculus 3. cuneate fasciculus 4. olivocerebellar fibers

25. A 55-year-old patient presented with an 8-month history of gradually progressive incoordination in the right arm and leg. Examination revealed hypotonia and ataxia in the limbs on the right side. The most likely diagnosis is 1. a stroke 2. a tumor 3. in the left cerebellar hemisphere 4. in the right cerebellar hemisphere

Sedion V: Chapters 13 through 21 In the following questions, select the single best answer. 1. A lesion of the right frontal cortex (area 8) produces A. double vision (diplopia) B. impaired gaze to the right C. impaired gaze to the left D. dilated pupils E. no disturbances of the ocular motor system 2. Axons in the optic nerve originate from A. rods and cones B. retinal ganglion cells C. amacrine cells D. all of the above 3. Meyer's loop carries optic radiation fibers representing A. the upper part of the contralateral visual field B. the lower part of the contralateral visual field C. the upper part of the ipsilateral visual field D. the lower part of the ipsilateral visual field 4. Which ofthe following statements about the auditory system is not true? A. the lateral lemniscus carries information from both ears B. it has a major synaptic delay in the midbrain C. it has a major synaptic delay in the thalamus D. it has a major synaptic delay in the inferior olivary nucleus E. crossing fibers pass through the trapezoid body

Questions and Answers

5. The hippocampal formation consists of the A. dentate gyrus B. hippocampus c. subiculwn D. all of the above

6. Which of the following is not part of the Papez circuit? A. hippocampus

B. mamillary bodies


posterior thalamic nuclei

D. cingulate gyrus E. parahippocampal gyrus 7. Wernicke's aphasia is usually caused by A. a lesion in the superior temporal gyrus B. a lesion in the inferior temporal gyrus c. a lesion in the inferior frontal gyrus of the dominant hemisphere

D. lesions in the midbrain E. alcohol abuse 8. Which of the following statements about the globus pallidus is not true? A. it is located adjacent to the internal capsule B. it receives excitatory axons from the caudate and putamen C. it is the major outflow nucleus of the corpus striatwn D. it sends inhibitory axons to the thalamus 9. In a patient with hemiparkinsonism (unilateral Parkinson's disease) affecting the right arm, a lesion is most likely in the A. right subthalamic nucleus B. left subthalamic nucleus C. right substantia nigra D. left substantia nigra E. right globus pallidus F. left globus pallidus 10. Complex cells in the visual cortex have receptive fields that A. are smaller than the receptive fields of simple cells B. respond to lines or edges with a specific orientation, only when presented at one location in the visual field C. respond to lines or edges with a specific orientation, presented anywhere within the visual field D. contain "on" or "off' centers In the following questions, one or more answers may be correct. Select A if I, 2, and 3 are correct B if I and 3 are correct C if 2 and 4 are correct D if only 4 is correct E if all are correct


11. Auditory stimuli normally cause impulses to pass through the I. trapezoid body 2. inferior olivary nucleus 3. medial geniculate nucleus 4. medial lemniscus 12. The principal neurotransmitter(s) released by synaptic terminals of sympathetic axons is/are I. epinephrine 2. norepinephrine 3. acetylcholine 4. gamma-arninobutyric acid 13. Alzheimer's disease is characterized by I. neurofibrillary tangles 2. loss of neurons in the basal forebrain (Meynert) nucleus 3. senile plaques 4. severe pathology in CA 1

14. Destruction of the lower cervical and upper thoracic ventral roots on the left side leads to I. dilated right pupil 2. constricted right pupil 3. dilated left pupil 4. constricted left pupil 15. After transection of the peripheral nerve, the I. axons and Schwann cells distal to the cut undergo degeneration and disappear 2. sensory axons distal to the cut survive, but motor axons degenerate 3. motor neurons whose axons were cut degenerate and disappear 4. surviving axons of the proximal stump will send out new growth cones to attempt regeneration 16. The Kluver-Bucy syndrome I. is characterized by hyperorality and hypersexuality 2. is characterized by psychic blindness and personality changes 3. is seen in patients with bilateral temporal lobe lesions 4. is seen in patients with lesions of the anterior thalamus 17. Pain sensation I. is carried in large myelinated (A-alpha) axons 2. is carried by small myelinated and unmyelinated (A-delta and C) axons 3. is carried upward in the dorsal columns of the spinal cord 4. is carried upward in the spinothalamic tract and spinoreticulothalamic system 18. Parasympathetic fibers are carried in I. cranial nerves III and VII 2. cranial nerves IX and X 3. sacral roots S2-4 4. thoracic roots TS-12



19. A 68-year-old teacher with hypertension complained of a severe headache and was taken to the hospital. Examination revealed that he could write normally but could not read. His speech was normal. The lesion(s) most likely involved the I. corpus callosum 2. Broca's area 3. left visual cortex 4. left angular gyrus 20. In the patient described in Question No. 19 I. the left anterior cerebral artery was probably involved 2. there was probably a right homonymous hemianopia 3. the left middle cerebral artery was probably involved 4. the left posterior cerebral artery was probably involved 21. The extrastriate cortex I. is Brodmann's areas 18 and 19 2. receives input from area 17 3. is the visual association cortex 4. is the primary auditory cortex 22. The corticospinal tract passes through I. the internal capsule 2. the crus cerebri 3. the pyramids of the medulla 4. the lateral and anterior columns of the spinal cord 23. The homunculus in the motor cortex I. contains magnified representations of the face and hand 2. represents the face highest on the convexity of the hemisphere 3. is located largely within the territory of the middle cerebral artery 4. gives rise to all of the axons that descend as the corticospinal tract 24. The optic chiasm I. is located close to the pineal and is often compressed by pineal tumors 2. is located close to the pituitary and is often cornpressed by pituitary tumors 3. contains decussating axons that arise in the temporal halves of the retinas 4. contains decussating axons that arise in the nasal halves of the retinas

In the following question, select the single best answer. 25. A 54-year-old accountant, who worked until the day of his illness, was found on the floor, with a right hemiparesis (arm and face more severely affected than the leg) and severe aphasia. The diagnosis is most likely A. a tumor involving the thalamus on the left B. a large tumor of the left cerebral hemisphere a stroke involving the right middle cerebral territory D. a stroke involving the right anterior cerebral territory E. a stroke involving the left middle cerebral territory F. a stroke involving the left anterior cerebral territory



Sedion I 1. B 2. A 3. B 4. c 5. c

6. D 7. c 8. B 9. A 10. A

11. 12. 13. 14. 15.


16. 17. 18. 19. 20.


21. A 22. c 23. D 24. c 25. B

11. 12. 13. 14. 15.


16. B 17. A 18. c 19. c 20. E

21. c 22. B 23. A 24. c 25. c

11. 12. 13. 14. 15.


11. 12. 13. 14. 15.

Sedion Ill 1. 2. 3. 4. 5.


6. 7. 8. 9. 10.


c A B

Sedion IV 1. 2. 3. 4. 5.


c A D B

6. D 7. D 8. c 9. E 10. c


16. 17. 18. 19. 20.


21. 22. 23. 24. 25.


16. A 17. c 18. A 19. B 20. c

21. 22. 23. 24. 25.



SedionV 1. 2. 3. 4. 5.

c B A D D

6. c 7. A 8. B 9. D 10.



c E

Index Page numben followed by f and t indie&te figures and tables, rupectlvdy.

A Abduceiu nel'ft (cranial nel'ft VI). 10-4-108, 104f: 167

paralysis, 108 Absence sei%ure$, 272 Acceuory nerve (cranial nerve XI), llS-116, llSf Accoltllllodation, 106,200,200!

Acetylcholine (ACh), 29, 247 actioru, 27t a.teas of concentration, 26t Action potcntlala, 19-21, 2lf

conduction o£ 23-25 types of nerve fiben, 23, 25t Adamlciewkz, artery o£ 66 Adaptation, 191 Additive, 20

Adenobypophysis, 123 Adenosine, 247 Adenoaine tripho1phate (ATP), 247 Adiadochokineail (dy.diadochokineail), 94.188 Adrenal chromaffin cell1, 240 Adrenetgic diviaion. 247 Adrenocorticot:roplc hormone, 128t

A1ferent connections cerebellum, 91, 92t. 95f hypothalamus, 122-123, 125t .Afferent fibera, 5 .Afferent neuron, 54 A fibers, 23 Agnosia, 25-4-255, 255f .Alc.inesia, 186 Alar plate, 43, 44f. 77, 78f Alexia, 253, 254f-255/ with agraphia, 253

aphasic aleDa. 253 without agraphla. 253, 254f Allocortex (arc:hicorta:), 137 Allodynia. 194

Alpha block. 272 Alpha motor neurons, 57, 58 Alpha rhythm, 271 Alternating abducens (VI), &cial (V). or trigeminal hemiplegi.a, 88 Alternating hypoglonal hemiplegi.a, 87, 89f Alvear pathwa)'I. 228 Alveus,229 Amacrine cella. 197 Ambiguus nucleua, 82, 111, 112f

Amman's horn (hlppocampua), 225, 228 AMPA type of glutamate receptor, 29 Ampulla, 217 Amygdala, 122, 226, 226t, 232, 233f-234f Amygdalofugal pathway, 232 Amygdaloid nuclear complex, 232 Amyotrophic lateral sclerosis, 34, 186, 284 Analgesia, 192 Anastomotic veim, 166 Anatomic le1ions, 33 Aneurymu. 107 Angiography, 261-262, 262f-265f Angular gyrm. 135

Annuloaplnal endinga, 57 Annulus fibroawi, 69 Anomic aphasia, 253 Anosmia, 227 Anosognosia, 255-256 Ansalenticularis, 126, 144, 180 Anterior, St Anterior cerebral arterie&, 163 Anterior cerebral artery, 164 Anterior choroidal artery, 164 Anterior clinoid process, 158 Anterior commilllll?e, 136, 231£, 232 Anterior communicating artery, 163, 164 Anterior condylar canal. 156, 160 Anterior aanial fona, 157 Anterior born, 149 Anterior limb of internal capsule. 144 Anterior medullary velum, 150 Anterior olfactory nucleus, 102, 226 Anterior perforated substance, 226 Anterior pituitary function, 125 hormonc1, 127f Anterior IJ>inothalam.ic tract, 53 Anterior tbalamic tubercle, 119

Anterior (ventral) corticoapinal tract, 50, 52t Anterior (ventral) white commilaure, 44 Anterograde amnesia, 234, 257 Anterograde transport, 9 Anterolateral 1ulcus, 44 Apex, 150

Aphasia, 251-25.3, 252t, 253f with impaired repetition, 252-25.3, 252t, 253f with intact repetition, 252t, 253




Apnea, 223 Appetitive behavior, 128t Apraxia, 256 Arachnoid, 150, 152, 152f Arachnoid barrier, 155 Arachnoid granulations, 152 Arachnoid mater, 65 Arachnoid trabeculae, 152 Arborization, 7 Archicerebellum, 89, 188 Archicortex, 225 Arcuate fasciculus, 136, 251 Arcuate nuclei, 121 Arousal, 221 Arterial corona, 66 Arterial supply of the brain, 163-164 carotid territory, 163-164 cerebral blood flow and autoregulation, 164 characteristics of cerebral arteries, 163 circle of Willis, 163 cortical supply, 164, 167f-168f principal arteries, 163, 164f vertebrobasilar territory, 163, 164f-166f Arteries of the spinal cord, 66-67, 68f Arteriovenous malformations (AVMs), 170, 175, l 75f Articular processes, 68 Articulation, 68 Ascend, 4 Ascending fiber systems, 51-54, 52t clinical correlations, 54 dorsal column tracts, 52-53, 53f-54f spinocerebellar tracts, 54, 56f spinoreticular pathway, 54 spinothalamic tracts, 53-54, 55f Ascending tracts in the medulla, 82 Association area, 141 Associative (secondary) auditory cortex, 141 Astereognosis, 254 Astigmatism, 202 Astrocytes, 12-13 Astrocytomas, 94, 295, 295f Asynergy, 188 Ataxia, 94 of extremities, 188 Atherosclerosis, 170, 172, 173f Athetosis, 186-187 ATP (adenosine triphosphate), 247 Atrium, 149 Atrophy,60 Auditory (eustachian) tube, 156 Auditory pathways in the pons, 86 Auditory system, 211-215 anatomy and function, 211, 2llf-212f auditory pathways, 211-215, 213f-214f clinical correlations, 213 overview, 211 Auerbach, plexus of, 240 Auerbach's plexus, 247 Autonomic bladder, 245 Autonomic fibers, 47 Autonomic nervous system, 237-250

autonomic innervation of the head, 241f, 243-244 autonomic outflow, 237-243 autonomic plexuses, 238f-239f, 243, 243f parasympathetic division, 240, 240f-242f sympathetic division, 237-240, 238f-239f clinical correlations, 243 hierarchical organization of, 245-247 cerebral cortex, 246-247 enteric nervous system, 247 hypothalamus, 246 limbic system, 246 medulla, 246 midbrain, 246 pons, 246 spinal cord, 245, 245f-246f overview,237,238f transmitter substances, 247-250 functions, 247, 248t-249t, 249f receptors, 247-249, 248t-249t, 249f sensitization, 250 types, 247 visceral afferent pathways, 244-245, 244t pathways to brainstem, 244-245, 245f pathways to spinal cord, 244 to spinal cord, 244 Autonomic plexuses, 238f-239f, 243, 243f AVMs (arteriovenous malformations), 170, 175-177, 175f Axoaxonal synapses, 27 Axoaxonic synapses, 10, lOt Axodendritic synapses, 10, lOt Axolemma, 8 Axonal transport, 9 Axon hillock, 8 Axon reaction, 9, 14 Axons, 2, 7-9, Sf, 10, 10f-14f, 17f Axoplasmic transport, 14 Axosomatic synapses, 10, lOt, 26

B Babinski's sign, 60 Baclofen, 31 BAER (brain stem auditory evoked response), 272, 274, 275f Baroreceptors,245 Barriers in the nervous system, 154-156 blood-brain barrier, 154-155 blood-nerve barrier, 156 ependyma, 156, 156f Basal forebrain nuclei, 136 Basal forebrain nuclei and septal area, 136 Basal forebrain nucleus of Meynert, 29 Basal ganglia, 131, 143-144, 143f-145f, 180-184, 183f, 186-187, 186f caudate nucleus, 143 claustrum and external capsule, 144 fiber connections, 144, l 46f lenticular nucleus, 143-144 Basal plate, 43, 44f, 77, 78f Basal pontine syndromes, 88 Basal veins (of Rosenthal), 165 Basilar artery, 163 Basis, 77, 79f


Basis pontis, 78, 79f, 85 Basket cells, 92, 92t, 93f Basolateral nuclear group, 232 BE (Branchial efferent) components, 80 Behavior, 233-234 Behavioral arousal, 221 Bell's palsy {peripheral facial paralysis), 111, 287 Benedikt's syndrome, 89f, 90 Berry aneurysm, 175 Beta rhythm, 272 Betz's cells, 179 B fibers, 23 Bilateral, St Bilateral symmetry, 3 Bipolar, amacrine, and retinal ganglion cells, 197-200, 200f-20lf Bipolar cells, 197 Blind spot, 198 Blood-brain barrier, 13, 154-155 Blood-CSF barrier, 154 Blood-nerve barrier, 154-156 Body temperature, 124 Border zones {watershed areas), 163 Bradykinesia, 186 Brain, 1, 2f, 3t brain stem. See Brain stem and cerebellum cerebellum. See Brain stem and cerebellum imaging of. See Imaging, brain tumor types according to age and site, 289t vascular supply of. See Vascular supply of the brain ventricles and coverings of. See Ventricles and coverings of the brain Brain stem and cerebellum, 2, 2f, 77-97 brain stem, cranial nerve nuclei in, 80 differences between typical spinal and cranial nerves, 80 motor {efferent) components, 80 sensory {afferent) components, 80, 83f brain stem lesions, 281-282, 295, 295f lesions near the brain stem, 88-89, 89f lesions of the brain stem, 87-88, 89f brain stem organization, 77-80 cerebellar peduncles, 80 cranial nerve nuclei, 78 descending and ascending tracts, 78 descending autonomic system pathways, 80 internal structural components, 78-80, 80t main divisions and external landmarks, 77-78 monoaminergic pathways, 80 reticular formation, 80 cerebellum, 2, 2f, 77, 79f, 89-96, 174, 184, 185f, 187-188 afferents to the cerebellum, 91, 92t, 95f cerebellar cortex, 91-92, 92f-94f deep cerebellar nuclei, 92-93 divisions, 89, 91 efferents from, 93-94 functions, 91, 9lf gross structure, 89, 91f lesions, 282 peduncles, 91 clinical correlations, 94 adiadochokinesis (dysdiadochokinesis), 94 astrocytomas, 94

ataxia, 94 cerebellar infarctions, 94 degenerative diseases, 94 dysmetria, 94 hypertensive hemorrhage, 94 hypotonia, 94 intention tremor, 94 olivopontocerebellar atrophies, 94 tumors, 94 development of brain stem and cranial nerves, 77, 78f-79f medulla, 80-85, 83f-84f ascending tracts, 82 cranial nerve nuclei, 81f, 82, 82t descending tracts, 82 inferior cerebellar peduncle, 85 midbrain, 86-87, 86f basis of, 86 periaqueductal gray matter, 87 superior cerebellar peduncle, 87 tectum, 87 tegmentum, 86-87 overview, 77 pons, 85-86 auditory pathways, 86 basis pontis, 85 middle cerebellar peduncle, 86 pontine tegmentum, 85-86 trigerninal system, 85f, 86 vascularization, 87-89, 87f visceral afferent pathways to, 244-245, 245f whole-head sections, 94-96, 95f-96f Brain stern auditory evoked response (BAER), 272, 274, 275f Brain stem syndromes resulting from vascular occlusion, 174t Branchial efferent (BE) components, 80 Branchial efferent fibers, 99 Broca's aphasia, 252 Broca's area, 141, 251, 252t Brodmann's area, 137 Brown-S~quard syndrome, 55, 61, 63, 63f Burst suppression, 272

c Calcar avis, 149 Calcarine cortex, 205, 205f Calcarine fissure, 131, 135 Calcium hypothesis, 169 Calvaria, 156 sutures of, 156 Carcinomatous meningitis, 279 Cardiac nerves, 240 Cardiac plexus, 240, 243 Carotid artery disease, 173 Carotid body, 111, 112f Carotid canal, 156, 157f, 163 Carotid-cavernous fistula, 177 Carotid groove, 158 Carotid sinus, 111, 112f Carotid sinus reflex, 113 Carotid siphon, 164 Carotid territory, 163-164 Cases, discussion of, 281-296




Cases, discussion of (continued) Case 1 (Chapter 3), 283 Case 2 (Chapter 5), 283-284, 283f-284f Case 3 (Chapter 5), 284, 284f Case 4 (Chapter 6), 284 Case 5 (Chapter 6), 284-285, 285f Case 6 (Chapter 7), 285, 286f Case 7 (Chapter 7), 285-286, 286f-287f, 286t Case 8 (Chapter 8), 286-287 Case 9 (Chapter 8), 287 Case 10 (Chapter 9), 287, 287f Case 11 (Chapter 10), 286t, 287-288, 288f, 289t Case 12 (Chapter 10), 288-289, 289f Case 13 (Chapter 11), 289-290, 290f Case 14 (Chapter 11), 290, 29lf Case 15 (Chapter 12), 290-291 Case 16 (Chapter 12), 291, 29lf Case 17 (Chapter 13), 291 Case 18 (Chapter 13), 291-292, 292f Case 19 (Chapter 14), 292, 292f-293f Case 20 (Chapter 14), 292, 293f Case 21 (Chapter 15), 292-293, 293f-294f Case 22 (Chapter 16), 293-294, 294f Case 23 (Chapter 17), 294 Case 24 (Chapter 19), 294-295 Case 25 (Chapter 20), 295, 295f-296f Case 26 (Chapter 21), 295, 296f Case 27 (Chapter 21), 296 location oflesions, 281-282 nature oflesions, 282-283 overview, 281 Cataract, 200 Catecholamines, 30 Cauda equina (horse's tail), 45f, 46 Caudal, Sf, 5t Caudate nucleus, 143 Cavernous sinuses, 166-167 Celiac ganglia, 237 Celiac plexus, 237, 243 Cell differentiation and migration, 7 Central canal, 43 Central facial lesion, 111 Central nervous system (CNS), 1, 2f Central nervous system nystagmus, 219 Central pattern generators, 179 Central sensitization, 194 Central sulcus, 131 Central tegmental tract, 86 Centromedian nucleus, 119 Centrum semiovale, 136 Cephalic flexure, 77, 78f Cerebellar ataxia, 219, 219f Cerebellar hemorrhage, 266f Cerebellar homunculi, 9lf Cerebellar infarctions, 94 Cerebellar peduncles, 78, 79f, 80 Cerebellopontine angle syndrome, 88 Cerebellopontine angle tumor, 213 Cerebellum, 2, 2f, 77, 79f, 89-96, 174, 184, 185f, 187-188. See also Brain stem and cerebellum afferents to the cerebellum, 91, 92t, 95f cerebellar cortex, 91-92, 92f-94f

deep cerebellar nuclei, 92-93 divisions, 89, 91 efferents from, 93-94 functions, 91, 91f gross structure, 89, 9lf lesions, 282 peduncles, 91 Cerebral abscess, 288, 289f Cerebral angiography, 261-262, 262f-265f Cerebral aqueduct, 77, 78f, 149 Cerebral blood flow and autoregulation, 164 Cerebral cortex, 131, 246-247 lesions of, 282 Cerebral dominance, 256 Cerebral embolism, 170, 172-173 Cerebral hemiatrophy, 266f Cerebral hemispheres/telencephalon, l, 4, 131-147 anatomy of the cerebral hemispheres, 131, 135-136 basal forebrain nuclei and septal area, 136 corpuscallosum, 131, 135 frontal lobe, 135 insula, 134, 135 limbic system components, 135-136 main sulci and fissures, 131, 133f-134f occipital lobe, 135 parietal lobe, 135 temporal lobe, 135 white matter, 136, 136f-137f basal ganglia, 143-144, 143f-145f caudate nucleus, 143 claustrum and external capsule, 144 fiber connections, 144, 146f lenticular nucleus, 143-144 development, 131, 132f-133f internal capsule, 144-145, 146f microscopic structure of the cortex, 136-142 classification of principal areas, 137, 138f-141f, 140-142 cortical columns, 137 layers, 137, 138f types of cortices, 137 overview, 131 physiology of specialized cortical regions, 142-143 primary auditory receptive cortex, 143 primary motor cortex, 142, 142f primary sensory cortex, 142 primary visual cortex and visual association cortex, 143 Cerebral peduncle, 86 Cerebral white matter, 131 Cerebrospinal fluid (CSF), 152-154 circulation,153-154, 154f clinical correlations, 152, 153f composition and volume, 153, 153t examination, 279-280 analysis of the CSF, 279-280, 280t contraindications, 279 indications, 279 overview, 279 function, 152 pressure, 153, 153f Cerebrovascular disease (stroke), 36f, 163, 170, 17lt Cerebrum, 1 Cervical enlargement, 43, 45f


Cervical flexure, 77, 78f Cervical segments, 43 C fibers, 23 Channelopathies, 194 Charcot's joints, 63 Chemical synapse, 24 Chemoreceptors, 245 Chiasmatic cisterna, 152 Chiasmatic groove, 158 Choanae, 156 Cholinergic division, 247 Chorda tympani nerve, 110, 110f Chordoma, 296f Chorea, 187 Choroidal vein, 165 Choroid plexus, 149, 150f-15lf Chromatolysis, 9, 14 Ciliary ganglia, 102, 103t, 203, 204f, 243 Ciliary pupillae, 103 Cingulate gyrus, 135, 231 Cingulum, 136, 230 Circadian rhythm, 125 Circle of Willis, 163, 173f Circular sulcus (circuminsular fissure), 131 Circumferential vessels, 87 Circumventricular organs, 128, 129f Cisterna magna, 152 Cistern of the lateral fissure (cistern ofSylvius), 152 Cisterns, 152 Claustrum and external capsule, 144 Climbing fibers, 91, 94f CNS (central nervous system), 1, 2f Coccygeal segments, 44 Cochlea, 211 Cochlear duct, 211 Cochlear ganglion, 102 Cochlear nuclei, 82, 211 Collateral sprouting, 17 Color vision, 199-200 Columns (cortex), 137 Coma, 221 Commissure of the fornix, 136 Communicating hydrocephalus, 154 Complex cells (visual cortex), 208, 209f Complex partial epilepsy, 257 Complex partial seizures, 272 Compression, 36 Compressive radiculopathy, 285 Computed tomography (CT), 262-264, 266f spine and spinal cord, 72, 73f Conduction aphasia, 252t, 253 Conduction deafness, 213 Cones, retinal, 197 Congenital malformations, 283 Colling, 152 Conjugate gaze, 105 Consciousness, 221-222, 222f, 223t Consensual response, 106 Constriction {miosis), 106 Constrictor pupillae, 103, 104f Contralateral, 5t Control of movement See Movement, control of


Conus medullaris, 43 Convergence theory of referred pain, 194, l 94f Corneal reflex, 109 Coronal sutures, 156 Corpora quadrigemina, 78, 79f, 87 Corpuscallosum,131,135,136 Corpus striatum, 122, 143 Cortex, microscopic structure of, 136-142 classification of principal areas, 137, 138f-14lf, 140-142 cortical columns, 137 layers, 137, 138f types of cortices, 137 Corti, organ of, 211 Cortical areas, specialized, 140t Cortical columns, 137 Cortical functions, higher, 251-260 cerebral dominance, 256 epilepsy, 256-259 complex partial epilepsy, 257 focal (Jacksonian) epilepsy, 257, 258f frontal lobe functions, 251 language and speech, 251-256, 252f agnosia, 254-255, 255f alexia, 253, 254f-255f anosognosia, 255-256 aphasia, 251, 252t aphasias with intact repetition, 2521, 253 aphasia with impaired repetition, 252-253, 2521, 253f apraxia,256 dysarthria, 251 Gerstmann's syndrome, 256 memory and learning, 256, 257f overview, 251 Cortical regions, specialized, physiology of, 142-143 primary auditory receptive cortex, 143 primary motor cortex, 142, 142f primary sensory cortex, 142 primary visual cortex and visual association cortex, 143 Cortical somatosensory areas, 192 Cortical taste area, 142 Corticobulbar {corticonuclear) fibers, 86, 179-180, 180f Corticofugal (efferent) fibers, 136 Corticomedial nuclear group, 232 Corticopetal (afferent) fibers, 136 Corticospinal and corticobulbar tracts, 50, 5lf, 52t, 82, 179-180, 182/ Corticostriate projections, 180 Cranial, St Cranial nerves and associated pathways, 99-117 anatomic relationships, 102-117 cranial nerve I: olfactory nerve, lOOt, 102, 103f cranial nerve II: optic nerve, lOOt, 102-103, 102f cranial nerve III: oculomotor nerve, lOOt, 103, 104f-108f, 104t-105t, 107t cranial nerve IV: trochlear nerve, lOOt, 104, 104f cranial nerve V: trigeminal nerve, lOOt, 108-110, 108f-109f, 1091 cranial nerve VI: abducens nerve, lOOt, 104-108, 104f cranial nerve VII: facial nerve, lOlt, 110-111, llOf cranial nerve VIII: vestibulocochlear nerve, lOOt, 111, 11 lf cranial nerve IX: glossopharyngeal nerve, lOlt, 111, 112f-113f, 113



Cranial nerves and associated pathwa}'li (continued) cranial nerve X: vagus nerve, lOlt, 113-115, 114f cranial nerve XI: accessory nerve, lOOt, llS-116, llSf cranial nerve XII: hypoglossal nerve, lOOt, 116-117, 116f development of, 77, 78f-79f functional components, 99, 102 differences between cranial and spinal nerves, 102 ganglia related to cranial nerves, 102, 103t nomenclature, 102 nuclei, 78, 81f, 82, 82t in the brain stem, 80 origin of cranial nerve fibers, 99 overview, 99, 99f, lOOt-lOlt Crescendo pattern, 39 Cribriform plate, 1S7 Crista ampullaris, 217 Crista galli, 157 Crossed representation, 4 Cru cerebri, 86 CSF (cerebrospinal fluid). See Cerebrospinal fluid (CSF) CT (computed tomography), 262-264, 266f spine and spinal cord, 72, 73f Cuneate fasciculus, SO Cuneate nuclei, 53 Cuneocerebellar tract, 54, 82, 92t Cuneus, 135 Cupula, 217 Cytoarchitecture, 137 Cytoskeleton, 8

D DA (dopamine), 30 actions, 27t areas of concentration, 26t DAG (diacylglycerol), 26 Dark adaptation, 198 Deafness, 213 Decerebrate rigidity, 184 Decussation and crossed representation, 4 Deep sensation, 191 Deep tendon reflexes, 57 Defensive reactions regulatory mechanisms, 128t Deficiencies, 282 Degenerative diseases, 283 of the arteries (brain), 170 D~a vu, 2S6 Delta activity, 272 Demyelinating diseases, 283 Demyelination, 24 Dendrites, 7, lOf Dendritic spines, 7 Dendritic zone, 7 Dendrodendritic synapses, lOt Denervation hypersensitivity, 2SO Dentate gyrus, 225, 226t, 227 Dentate ligament, 6S Dentatorubrothalamocortical pathway, 93 Depolarize, 21 Depth electrography, 271 Dermatomes, 47, 48f

Descend, 4 Descending and ascending tracts, 78 Descending autonomic system, Sl, S2t pathways, 80 Descending fiber S}'litems, 50-51, 52t corticospinal tract, 50, Slf, S2t descending autonomic system, S l medial longitudinal fasciculus, S l reticulospinal system, SO-Sl rubrospinal tract, SO tectospinal tract, 51 vestibulospinal tracts, 50 Descending spinal tract ofV, 82, 86 Descending tracts in the medulla, 82 Desynchronization, 271 Diabetes insipidus, 124-126 Diaphragmasellae, 1S2 Diencephalon: Thalamus and hypothalamus, 1, 119-129, 120f circumventricular organs, 128, 129f epithalamus, 127-128 clinical correlations, 129 habenular trigone, 127 pineal body, 127-128 hypothalamus, 121-12S afferentconnections, 122-123,12St clinical correlations, 122, 126 efferent connections, 123-124, 124f, 126f-127f functions, 124-126,128f landmarks, 121, 122f-123f medial hypothalamic nuclei, 121-122 lesions, 282 overview, 119, 120f subthalamus, 126 clinical correlations, 129 fiber connections, 126 landmarks, 126 thalamus, 119-121 functional divisions, 120-121 landmarks, 119, 120f thalamic nuclei, 119-120, 119t, 121f-122f thalamic white matter, 119 Diffusion-weighted imaging, 268, 268f Digital subtraction angiogram, 26Sf Dilation (mydriasis), 106 Diminished or absent deep tendon reflexes, 60 Diplegia, 186 Diploic veins, 16S Diplopia (double vision), 107, 107t Disconnection syndromes, 34 Dissociated anesthesia, 62 Divergence, 59 Dopamine (DA), 30 actions, 27t areas of concentration, 26t Dopaminergic pathway, 80 Dorsal, Sf, St Dorsal column nuclei, 53 Dorsal column tracts, S2-53, 53f-54f Dorsal gray column, 48 Dorsal motor nucleus, 113 Dorsal motor nucleus of X, 82


Dorsal nucleus (Clarke's colwnn), 49 Dorsal pons syndrome, 90 Dorsal roots, 46, 48t Dorsal root (spinal) ganglion, 44 Dorsal {sensory) roots, 5 Dorsal spinocerebellar tract, 82, 92t Dorsolateral fasciculus (Lissauer's tract), 48, 53 Dorsolateral nucleus, 119 Dorsomedial nucleus, 121 Dorswn sellae, 158 Duchenne's muscular dystrophy, 39 Dura, 150-152, 15lf Dura mater, 65 Dynamic response, 57 Dysarthria, 251 Dysdiadochokinesis (adiadochokinesis), 94, 188 Dyskinesia, 186 Dysmetria, 94, 188 Dystrophies, 281

E Eating, 124 Edinger-Westphal nucleus, 106, 203, 204f, 240 Effector, 56 Efferent connections, hypothalamus, 123-124, 124f, 126f-127f Efferent fibers, 5 Efferent neuron, 54 Efferents from the cerebellum, 93-94 Electrical (electronic) synapses, 10-11, 23 Electrodiagnostic tests, 271-278 electroencephalography, 271-272 clinical applications, 271 physiology, 271 technique, 271, 272f types of waveforms, 271-272, 273f electromyography,274,276-277 clinical applications, 274 physiology, 274 repetitive stimulation, 277 single-fiber EMG, 27 technique,274,276f types of activity, 276-277 evoked potentials, 272-274 brain stem auditory evoked response (BAER). 272, 274, 275f somatosensory evoked potentials (SEPs), 274 visual evoked potentials (VEPs), 272 nerve conduction studies, 277-278 H-re:llexes and F-wave, 278 overview, 271 transcranial motor cortical stimulation, 274 Embolic infarction, 296 Embolus, 170 Emissary veins, 167 Emmetropia, 200, 20lf Emotion, expression of, 125 Encephalitis, 294 Endoneurium, 156 Endorphins, 31 Enkephalins, 31 Enteric nervous system, 237, 247 Entorhinal cortex, 102, 226, 228

Ependytna, 7, 156, 156f Ependytnoma,295,295f Epidural hemorrhage, 176, 176f, 290, 291f Epidural space, 65 Epilepsy, 256-259, 272 complex partial epilepsy, 257 focal (Jacksonian) epilepsy, 257, 258f Epinephrine (adrenaline), 30 Epineuriwn, 156 Epithalamus, 127-128 clinical correlations, 129 habenulartrigone,127 pineal body, 127-128 Equilibrium, 218 Equilibrium potential, 19 Evoked potentials, 272-274 brain stem auditory evoked response (BAER), 272, 274, 275f somatosensory evoked potentials (SEPs), 274 visual evoked potentials (VEPs). 272 Excitable, 19 Excitatory and inhibitory synaptic actions, 26-27 Excitatory postsynaptic potentials (EPSPs), 26 Excitatory synapses, 23, 26t Excitotoxic, 30 Excitotoxic hypothesis, 169 Exocytosis, 25 External capsule, 144 External granular layer (isocortex), 137 External medullary lamina, 119 External pyramidal layer (isocortex), 137 Exteroceptors, 191 Extracellular space, 13 Extracranial causes (of coma), 222 Extradural space, 65 Extrafusal fibers, 57 Extrapyramidal motor system, 143, 180 Extrastriate cortex, 205 Eye, 197. See also Visual system anatomy and physiology, 197, 198f-200f clinical correlations, 205 abnormalities of pupillary size, 206 Argyll-Robertson pupils, 206 bitemporal hemianopsia, 205, 207f field defects, 205 homonymous hemianopia, 205, 207f Homer's syndrome, 206 impaired vision in one eye, 205 superior quadrantanopsia, 205 control of ocular movements, 105 gaze and vergence centers, 105-106 pupillary size, 106, 106f reflexes, 106-107, 107f external eye muscles, 104-105, 104t-105t innervation of, 104f, 107f cranial nerve II, lOOt, 102-103, 102f cranial nerve III, lOOt, 103, 104f-108f, 104t-105t, 107t cranial nerve IV, lOOt, 104, 104f cranial nerve VI, lOOt, 104-108, 104f lesions of, 202 local effects of drugs, 206t






Facial nerve {cranial nerve VII), 110-111, llOf, 240 Falx cerebelli, 152 Falx cerebri, 151 Fasciculations (twitches), 276 Fasciculi {tracts), 4, 11 Fasciculus cuneatus, 50, 53 Fasciculus gracilis, 50, 52 Fasciculus lenticularis, 126, 144 Fastigium, 150 Fear regulatory mechanisms, 128t Fibrillations, 276 Fibrous astrocytes, 12 Fields of Forel, 126, 180 Filum terminale, 43 Filum terminale extemum, 65 Filum terminale intemum, 65 Fimbria, 229 First-order neurons, 191 Fissures, 131 Flaccid paralysis, 60 Flocculonodular system, 89 Flower-spray endings, 57 fMRI (functional magnetic resonance imaging), 208f, 268, 269f Focal (Jacksonian) epilepsy, 257, 258f Focal motor seizures, 257 Focal pathology, 36 Focal seizures, 140 Folia, 89 Follicile-stimulating hormone (FSH), 128t Foramen lacerum, 156, 157f, 159 Foramen magnum, 156, 160 Foramen ovale, 156, 157f, 158 Foramen rotundum, 158 Foramens of Monro, 149 Foramen spinosum, 156, 157f, 158 Forebrain, 1 Forel, fields of, 126, 180 Fornix, 122, 225, 228 commissure of, 136 Foster Kennedy's syndrome, 293 Fourth ventricle, 77, 78f, 149-150 Fovea centralis, 198 Frontal area, 179 Frontal eye field, 141 Frontal gyri, 135 Frontal lobe, 135 functions, 251 syndromes, 251 Frontal sulci, 135 FSH {follicle-stimulating hormone), 128t Functional brain imaging, 268 Functional magnetic resonance imaging (fMRI), 208f, 268, 269f Functional recovery, 24 Funiculi (columns), 4, 11 Fusiform gyrus, 135 Fusiform (medial occipitotemporal) gyrus, 135 Fusiform (multiform) layer (isocortex), 137 Fusiform neurons, 136 F-wave,278

Gamma-aminobutyric acid {GABA), 31 actions, 27t areas of concentration, 26t Gamma motor neurons, 57, 58, 59f Ganglia, 2, 11 related to cranial nerves, 102, 103t Ganglion cells, 197 Gap junctions, 11, 23 Gaserian (trigeminal) ganglion, 109 Gate theory, 192 Gene expression, regulation of, 27 Generalized seizures, 257 General somatic afferent components, 80 General somatic efferent (SE or GSE) components, 80 General visceral afferent components, 80 General visceral efferent (VE or GVE), 80 Generator potentials, 20, 20f Geniculate bodies, 119 Geniculate ganglion, 102, 103t, 110, llOf Geniculocalcarine fibers, 203 Genu, 131, 144 George Gershwin syndrome, 228 Gershwin, George, 228 Gerstmann's syndrome, 256 GFAP (glial fibrillary acidic protein), 13 Glasgow Coma Scale, 222, 223t Glia, 11-13, 12t astrocytes, 12-13 clinical correlation, 13 extracellular space, 13 macroglia, 11 microglia, 13 oligodendrocytes, 13, 13f-14f Glial cells, 2 Glial fibrillary acidic protein (GFAP), 13 Glial scarring, 13 Gliosis, 13 Globus pallidus, 143, 180 Glomeruli, 226 Glossopharyngeal nerve (cranial nerve IX), 111, 112f-113f, 113, 240,244 Glutamate, 29-30 actions, 27t Glutamic acid, areas of concentration, 26t Glycine actions, 27t areas of concentration, 26t Golgi cells, 92, 92t, 93f Golgi tendon organs, 58 G-proteins, 26 Gracile fasciculus, 50 Gradle nuclei, 53 Graded, 20 Gradient, 19 Granular layer of cerebellar cortex, 91 Granule cells, 91, 93f Gray communicating rami, 240 Gray matter, 3f, 34 dysfunction can cause neurologic dysfunction, 34-35, 35f spinal cord, 48-49, 49f-50f


Great cerebral vein (of Galen), 165 Great ventral radicular artery, 66 Growth hormone, 128t Guidance molecules, 5 Guillain-Barre syndrome, 24 Gustatory nucleus, 82 Gyri, 131

H H 2 field of Forel, 180 Habenular trigone, 127 Habenulointerpeduncular tract, 127 Hair cells, 211 Hallucinations, visual, 143 Head autonomic innervation of, 24lf, 243-244 trauma, 227 Hemiballismus, 187 Hemiplegia, 186 Hemiplegia alternans, 186 Hemispheres. See Cerebral hemispheres/telencephalon Hemorrhage (brain), 169 Herniation of the nucleus pulposus, 70, 285, 285f Herpes simplex encephalitis, 295 Herring bodies, 123 Heschl's gyrus, 141, 141f Higher cortical functions. See Cortical functions, higher Hippocampal commissure, 136 Hippocampal fissure, 135 Hippocampal formation, 225, 226-232, 230f-23lf amygdala,232,233f-234f anterior commissure, 23 lf, 232 hypothalamus, 232, 234f Papez circuit, 230-232, 23lf septal area, 232, 233f Hippocampus, 225, 226t, 228 input, 228 output, 228 Hirschsprung's disease (megacolon), 243 Holmes-Adie syndrome, 202 Homunculus, 140, 140f Horizontal cells, 197 Homer's syndrome, 243, 243f H-refl.exes and F-wave, 278 Hubel, D., 208 Hunger regulatory mechanisms, 128t Huntington's disease, 187, 187f Hydrocephalus, 266f Hyperalgesia, 192 Hyperopia, 202 Hyperorality, 234 H yperpathia, 194 Hypersexuality, 235 H ypersomnia, 223 Hypertensive hemorrhage, 94, 174, 174f Hypoalgesia, 192 Hypogastric plexus, 237, 240, 243 Hypoglossal canal, 156, 160 Hypoglossal nerve (cranial nerve XII), 116-117, 116f Hypoglossal nucleus, 82, 116, 116f

Hypophyseotropic hormones, 123 Hypothalamohypophyseal tract, 123 Hypothalamus, 121-125, 232, 234f, 246 afferent connections, 122-123,125t clinical correlations, 122, 126 efferent connections, 123-124, 124f, 126f-127f functions, 124-126,128f landmarks, 121, 122f-123f medial hypothalamic nuclei, 121-122 Hypotonia, 94

la fibers, 57 Ideational apraxia, 256 Ideomotor apraxia, 256 II fibers, 57 Imaging, 39 brain, 261-270 cerebral angiography, 261-262, 262f-265f computed tomography (CT), 262-264, 266f diffusion-weighted imaging, 268, 268f functional MRI (fMRI), 268, 269f magnetic resonance imaging (MRI), 264-269, 267f magneticresonancespectroscopy,268 overview,261,26lf positron emission tomograpy (PET), 268, 269f, 270 single photon emission CT (SPECT), 269f, 270 skull x-rays, 261 spine and spinal cord, 71-74 computed tomography (CT), 72, 73f magnetic resonance imaging (MRI), 73, 73f-74f plain x-rays, 71, 72f Immediate recall, 234, 256 Incisura tentoril, 152 Incus, 211 Indusium griseum, 225 Infarction, 169 Infections, 282 Inferior, St Inferior cerebellar arteries, 163 Inferior cerebellar peduncle, 85, 91 Inferior cerebral veins, 166 Inferior colliculi, 78, 79f, 87, 212 Inferior (formerly nodose) ganglion, 114f Inferior (formerly petrosal) ganglia, 111 Inferior glossopharyngeal ganglion, 102 Inferior longitudinal fasciculus, 136 Inferior mesenteric ganglion, 237 Inferior oblique muscle, 103, 104f-105f Inferior olivary nucleus, 77, 78f Inferior parietal lobule, 135 Inferior quadrigeminal brachium, 87 Inferior rectus muscle, 103, 104f-105f Inferior sagittal sinus, 167 Inferior salivatory nuclei, Ill, 112f, 240 Inferior (temporal) horn, 149 Inferior vagal (nodose) ganglion, 102 Inflammations, 282 Inflammatory diseases of the arteries (brain), 170 Inflammatory myopathies, 60 Infratentorial compartment, 159




Infundibular recess, 149 Infundibuluni, 121, l22f Inhibitory hormones, 123 Inhibitory postsynaptic potentials (IPSPs), 26 Inhibitory synapsis, 23, 26t Initial segment, 8 Inner ear, 211 Insula, 134, 135 Integration, 27 Intention tremor, 94, 188 Intercalated neurons (intemeurons), 54 Intermediate zone, 7 Intermediolateral gray column (horn), 48 Intermediolateral nucleus, 49 Internal acoustic meatus, 160 Internal arcuate fibers, 54 Internal arcuate tract, 53 Internal auditory arteries, 163 Internal capsule, 143-145, 146f Internal carotid artery, 163, 167 Internal granular layer {isocortex), 137 Internal jugular vein, 166 Internal pyramidal layer (isocortex), 137 Interneurons, 7, 11, 54 Internuclear ophthalmoplegia, 108, 219 Interpeduncular fossa, 86 Interpenduncular cistern, 152 Interthalamic adhesion (massa intermedia), 119 Interventricular foramens, 149 Intervertebral foramen, 44, 68 Intracerebral hemorrhage, 174, 292, 292f Intrafusal muscle fibers, 57 Intralaminar nuclei, 119, 121 Intramural ganglion, 102, 103t Intraparietal sulcus, 135 Inverse stretch reflex, 58 Investing membranes (meninges), 65, 66f-67f arachnoid mater, 65 clinical correlations, 66 dentate ligament, 65 dura mater, 65 investment of spinal nerves, 65 pia mater, 65 spinal nerves, 65 Ionic homeostasis, 13 Ionotropic, 29 Ion pumps, 19 IP3 (inositol triphosphate), 26 Ipisilateral, St IPSPs (inhibitory postsynaptic potentials), 26 Ischemic cerebrovascular disease, 167, 169 Isocortex, 137, 225, 229f Isolation aphasias, 252t, 253

J Jackson, John Hughlings, 140 Jacksonian epilepsy, 257, 258! Jaw jerk reflex, 109 Jugular foramen, 156, 160 Juxtallocortex, 137,225

K Kainate type of glutamate receptor, 29 Kinesin, 8 Kinetic labyrinth, 217 Kliiver-Bucy syndrome, 234-235

L Laboratory investigations, 39 Labyrinth, 217 Lambdoid sutures, 156 Lambert-Eaton myasthenic syndrome, 29, 277, 281 Lamina, 48-49, 49f, 68 Lamina cribrosa, 202 Languageandspeech,2 51-256,252! agnosia, 254-255, 255! alexia, 253, 254f-255f anosognosia,255-256 aphasia, 251, 252t with impaired repetition, 252-253, 252t, 253f with intact repetition, 252t, 253 apraxia, 256 dysarthria, 251 Gerstmann's syndrome, 256 Lateral, St Lateral aperture (foramen of Luschka), 150 Lateral cerebral fissure (Sylvian fissure), 131 Lateral corticospinal tract, 50, 52t Lateral gaze centers, 105 Lateral geniculate body, 202 Lateral gcniculate nucleus, 120 Lateral hypothalamic area, 121 Lateral lemnisci, 211 Lateral longitudinal striae, 232 Lateral medulla, 35 Lateral medullary syndrome (Wallenberg's syndrome), 87- 88, 89f, 285, 286{ Lateral motor neuron column, 49 Lateral olfactory stria, 226 Lateral recess, 149 Lateral •scout view" (CT), 266 Lateral spinothalarnic tract, 53 Lateral tegmental nuclei, 30 Lateral ventricles, 149, 15lf Lateral vestibulospinal tract, 50 Learning and memory, 234, 256, 257f Lemniscal decussation, 53 Lemniscal system, 191 ventrolatcral system, differences from, l 93t Lemnisci, 11 Lenticular fasciculus, 180 Lenticular nucleus, 143- 144 Lentiform nucleus, 122 Leptomeninges, 65 Lesions identifying, 38-39 time course of the illness, 38f, 39 locating, 36-38, 281-282 localization of the vascular lesion in stroke syndromes, 173, 173f, 174t processes causing neurologic disease, 36-37, 36f


rostrocaudal localization, 37-38, 37f transverse localization, 38 of motor system, clinical signs of, 185t nature of, 282-283 in spinal cord motor pathways, 59-61, 6lt disorders of muscle or neuromuscular endings, 60 localization of spinal cord lesions, 60 lower-motor-neuron lesions, 59-60, 6lf types of spinal cord lesions, 60-61, 6lt. 62f upper-motor-neuron lesions, 60, 6lf Leucine enkephalin (leu-enkephalin), 31 Levator palpebrae superioris muscle, 103, 104f LH (luteinizing hormone), 128t Ligand-gated ion channels, 25-26 Light adaptation, 199 Limbic lobe, 225 Limbic nuclei, 120 Limbic system, 225-236, 246 components, 135-136 disorders, 232, 234-235 Kliiver-Bucy syndrome, 234-235 temporal lobe epilepsy, 235 functions, 232 autonomic nervous system, 232 hippocampal formation, 226-232, 230f-23lf amygdala,232,233f-23 4f anterior commissure, 23lf, 232 hypothalamus, 232, 234f Papez circuit, 230- 232, 23lf septal area, 232, 233f limbic lobe and limbic system, 225, 227f-228f overall structure and histology, 225, 229f olfactory system, 225- 226 olfactory receptors, 225-226, 229f-230f overview,225,226t septal area, 232-235 behavior,233-234 memory,234 neurogenesis and depression, 234 place cells, grid cells, and spatial problem solving, 234 Lingual (lateral occipitotemporal) gyrus, 135 Lissauer's tract (dorsolateral fasciculus), 48, 53 Local,19 Localized function, 34 Locked-in syndrome, 88, 90 Locus ceruleus, 30, 87, 222-223 Longitudinal cerebral fissure, 131 Long-term memory, 234, 256 Long-term potentiation (LTP), 27, 234, 256 Loss of function, 34 Lou Gehrig's disease, 284 Lower motor neurons, 50, 186 Lumbar puncture, 69-71, 279 complications, 70-71 site, 69, 71f technique, 69-70 Lumbar segments, 43-44 Lumbosacral enlargement, 43, 45f Luteinizing hormone (UI), 128t Luys, body of, 126

M Macroglia, 11 Macrophage-like cells (microglial cells), 13 Macula, 198, 200! Macular region, 217 Magnetic resonance angiography (MRA), 267 Magnetic resonance imaging (MRI), 264-269, 267f spine and spinal cord, 73, 73f-74f Magnetic resonance spectroscopy, 268 Magnocellular, 198 Main (principal) trigeminal nucleus, 109 Main sensory nucleus, 86 Malignant glioma, 288, 288f Malleus, 211 Mamillary bodies, 230 Mamillotegmental tract, 123 Mamillothalamic tract. 123, 230 Mammillary bodies, 121, 122f Mammillary nuclei, 122 Mammillary portion, 122 Mandibular division, 109, 109f, 109t Manometric pressure, 279 Maps of the world within the brain, 4-5 Marginal zone, 7 Masticatory nucleus, 86 Matrix, pain, 194, 194f Maxillary division, 109, 109f, 109t May-Britt, 234 Medial, St Medial aperture (foramen ofMagendie), 150 Medial (basal) medullary syndrome, 87 Medial forebrain bundle, 232 Medial geniculate body. 212 Medial geniculate nucleus, 120 Medial hypothalamic area, 121 Medial hypothalamic nuclei, 121-122 Medial lemniscal system, 52 Medial lemniscus, 53, 82 Medial longitudinal fasdculus, 51, 52t, 82, 86, 217 Medial longitudinal striae, 232 Medial motor neuron column, 49 Medial olfactory stria, 226 Medial rectus muscle, 103, 104f-105f Medial vestibulospinal tract. 50, 217 Median, St Median fissure, 44 Median (paramedian) perforators, 87 Medulla, 77, 79f, 80-85, 83f-84f, 246 ascending tracts, 82 cranial nerve nuclei, 8lf, 82, 82t descending tracts, 82 inferior cerebellar peduncle, 85 Medulla oblongata, 2, 2f Medullary pyramid, 50 Medulloblastoma, 88, 95f, 295 Megacolon (Hirschsprung's disease), 243 Meissner, plexus of, 240, 247 Membrane potential, 19-20, 20!, 20t Memory and learning, 234, 256, 257f Memere's disease, 219, 294




Meningeal branches, 47 Meningeal layer, 150 Meningeal veins, 165 Meninges and submeningeal spaces, 150-152, 282. See also Vertebral column and meninges surrounding the spinal cord arachnoid, 152, 152f dura, 150-152, 151f pia, 152 Meningioma, 283 Meningocele, 70 Meningomyelocele, 70 Mesencephalic tract and nucleus, 85f, 86 Mesencephalic trigeminal nucleus (mesencephalic nucleus of V), 109 Mesencephalon, 77, 78f Mesocortex, 225 Mesocortical projection, 30 Mesolimbic projection, 30 Metabolic disorders, 282-283 Metabotropic glutamate receptors, 30 Metencephalon, 77, 78f Methionine enkephalin {met-enkephalin), 31 Meyer's loop, 203 Microaneurysms, 174 Microglia, 13 Microtubles, 8 Midbrain, 2, 2f, 77, 79f, 86-87, 86f, 246 basis of, 86 periaqueductal gray matter, 87 superior cerebellar peduncle, 87 tectum, 87 tegmentum, 86-87 Middle cerebellar peduncle, 86, 91 Middle cerebral artery, 164 Middle cranial fossa, 157-158 Middle meningeal vessels, 158 Middle sacral nerves, 244 Midline raphe system, 222 Mitral cells, 226 Modulatory, 26 Molecular layer, 91, 137 Monoaminergic pathways, 80 Monoplegia, 186 Monosynaptic, 4 Monro, foramens of, 149 Moser, Edvard, 234 Mossy fibers, 91, 94f, 228 Motor disturbances, 184-188, 185t basal ganglia, 186-187, 186f cerebellum, 187-188 lower motor neurons, 186 muscles, 184, 186 upper motor neurons, 186 Motor {efferent) components, 80 Motor end-plates, 28 lesions of, 281 Motor neuron disease, 186, 284 Motor nuclei, 120 motor nucleus ofV, 109 Motor point, 274

Motor systems, 179-184 basal ganglia, 180-184, 183f cerebellum, 184, 185f corticospinal and corticobulbar tracts, 179-180, 182f extrapyramidal motor system, 180 subcortical descending systems, 184 Motor unit potentials {MUPs), 276 Movement, control of, 179-189 major motor systems, 179-184 basal ganglia, 180-184, 183f cerebellum, 184, 18Sf corticospinal and corticobulbar tracts, 179-180, 182/ extrapyramidal motor system, 180 subcortical descending systems, 184 motor disturbances, 184-188, 185t basal ganglia, 186-187, 186f cerebellum, 187-188 lower motor neurons, 186 muscles, 184, 186 upper motor neurons, 186 neural control, 179, 180f-181f MRA {magnetic resonance angiography), 267 MRI {magnetic resonance imaging), 264-269, 267f spine and spinal cord, 73, 73f-74f MR visual area, 208 Muiltimodal association areas, 141 Multifocal pathology, 37 Multimodal nuclei, 121 Multiple sclerosis, 24, 279, 282, 286, 286f-287f MUPs {motor unit potentials), 276 Muscarine, 249 Muscarinic receptors, 26, 249 Muscles, 184, 186 length, 57 lesions, 281 spindles, 57-58, 59f Muscular dystrophies, 60 Myasthenia gravis, 29, 60, 277, 281, 283 Myasthenic syndrome, 283 Myasthenic syndrome {Lambert-Eaton syndrome), 29, 277, 281 Mycotic aneurysm, 175 Myelencephalon, 77, 78f Myelin, 9 Myelinated axons, 22, 22f Myelination, 5 effects of, 21-23, 22f-23f Myenteric plexus, 247 Myopia,202 Myotomes, 47-48, 48f Myotonia, 29

N Na+/K+-ATPase, 19, 20! Narcolepsy, 223 Nasal infections, 227 Nasal rami, 244 Neighborhood signs, 35, 3Sf NE (norepinephrine), 30 areas of concentration, 26t Neocerebellum, 91, 188 Neocortex, 225, 229f


Neologisms, 252 Nernst equation, 19 Nerve conduction studies, 277-27S H-reflexes and F-wave, 27S Nerve fiber layer, 19S Nerve root tumor, 2S3, 2S3f-2S4f Nerve (sensorineural) deafness, 213 Nerve VIII tumor, 294, 294f Nervous system, autonomic. See Autonomic nervous system Nervous system, development and cellular constituents of degeneration and regeneration, 14-17 regeneration, lS-17 glia. 11-13, 12t astrocytes, 12-13 clinical correlation, 13 extracellular space, 13 macroglia, 11 microglia, 13 oligodendrocytes, 13, 13f-14f neural development, 7 cell differentiation and migration, 7 neural tube, 7, Sf neurogenesis, 17 neuronal groupings and connections, 11 neurons, 7-11, Sf axons, S-9, Sf, 10f-14f, 17f dendrites, 7, lOf neuronal cell body (soma), 7, Sf-9f synapses, 10-11, lOf, lOt, lSf Nervous system, fundamentals of, 1-6 crossed representation, 4 development, S functional units, 2 information processing in the nervous system, 2, 4 main divisions, 1 anatomy, 1 function, 1 maps of the world within the brain, 4-5 overview, 1 peripheral nervous system (PNS), 5 planes and neutoanatomic terms, S, Sf, St structural units and overall organization, 1-2, 2f-4f, 3t symmetry, 4 tracts and commissures, 4 Nervous system, signaling in, 19-31 action potentials, 20-21, 2lf clinical correlations, 24, 29 demyelination, 24 myasthenia gravis, 29 myasthenic syndrome (Lambert-Eaton syndrome), 29 myotonia, 29 neuropathies, 24, 2Sf small-fiber neuropathy, 24 conduction of action potentials, 23-2S types of nerve fivers, 23, 2St excitatory and inhibitory synaptic actions, 26-27 generator potentials, 20, 20f membrane potential, 19-20, 20f, 20t myelination, effects of, 21-23, 22f-23f nerve cell membrane contains ion channels, 21 neuromuscular junction and the end-plate potential, 2S-29, 29f


neurotransmitters, 29-31 acetylcholine, 29 catecholamines, 30 endorphins, 31 enkephalins, 31 gamma-aminobutryic acid (GABA), 31 glutamate, 29-30 serotonin, 30-31 overview, 19 presynaptic inhibition, 27-2S, 2Sf synapses, 23-25, 26t, 27 synaptic transmission, 25-26 ligand-gated {fast), 25-26 second-messenger mediated (slow), 26t-2St Nervus intermedius, 110, llOf Netrins, 5 Neural crest, 43, 44f Neural development, 7 cell differentiation and migration, 7 neural plate, 43, 44f neural tube, 7, Sf, 43, 44f, 77 Neural tissue, destruction or compression of, 36, 36t Neuroanatomy and neurology, relationship between, 33-41 imaging and laboratory investigations, 39 overview, 33 symptoms and signs of neurologic diseases, 33-36 compromise of ventricles or vasculature, 36, 36t destruction or compression of neural tissue, 36, 36t lesions of spinal roots and peripheral nerves can cause neurological dysfunction, 34 may be negative or positive, 34 neighborhood signs may help to localize the lesion, 35, 35f neurologic disease can result in syndromes, 35 often reflect focal pathology of nervous system, 34 white and gray matter dysfunction can cause neurologic dysfunction, 34-35, 35f treatment of patients with neurologic disease, 40 what is the lesion?, 3S-39 time course of the illness, 38f, 39 where is the lesion?, 36-3S processes causing neurologic disease, 36-37, 36f rostrocaudal localization, 37-3S, 37f transverse localization, 3S Neurofilaments,8 Neurogenesis, 17 Neurogenic bladder, 245 Neurohypophysis, 123 Neuroimaging, 39 Neuroma, 19S,2S3 Neuromuscular disorders, 2S3 Neuromuscular junction, 28-29, 29f Neuromuscular synapse, 2S Neuronal cell body (soma), 7, 8f-9f Neurons, 2, 7-11, Sf axons, S-9, Sf, 10f-14f, 17f dendrites, 7, lOf destruction of, 36 neuronal cell body (soma), 7, 8f-9f Neuropathic pain, 194 Neuropathy,24,25f Neuropeptides, 28t



Neuropil, 11 Neuroprotective strategies, 169 Neurotransmitters, 24, 29-31 acetylcholine, 29 actions, 27t areas of concentration, 26t catecholamines, 30 endorphins, 31 enkephalins, 31 gamma-aminobutryic acid (GABA), 31 glutamate, 29-30 serotonin, 30-31 Neutoanatomic terms and planes, S, Sf, St New proteins, 27 Nicotine, 249 Nicotinic acetylcholine receptors, 249 Nigrostriatal projection, 181 Nigrostriatal system, 30 Nipple, 47, 48f NMDA receptor, 29 Nociceptive sensation, 191 Nociceptors, 192 Nodes of Ranvier, 9, 22 Nodose ganglia, 247 Nomenclature for cranial nerves, 102 Noncommunicating (obstructive) hydrocephalus, 1S4 Nonmyelinated axons, 21, 22f Noradrenergic pathways, 80 Norepinephrine (NE, noradrenaline), 30 areas of concentration, 26t Normal kyphosis, 68 Normal lordosis, 68 Normal-pressure hydrocephalus, 1S4 Normal scoliosis, 68 Nuclear bag fibers, S7 Nuclear chain fibers, 57 Nuclei, 2, 11 Nuclei of Meynert, 136 Nucleus dorsalis (Clarke's column), 54 Nucleus ofLuys, 182 Nucleus parabrachialis, 246 Nucleus proprius, 49 Nucleus pulposus, 69 Nucleus solitarius, 82 Nystagmus, 188, 219

0 Obex, 149 Obtundation, 222 Occipital condyles, 1S6 Occipital lobe, 13S Occipital sinus, 160 Occipitofrontal fasciculus, 136 Occlusion of the right middle cerebral artery, 29S, 296f Occlusive cerebrovascular disease, 169-170, 172, 172f Ocular dominance columns, 209, 209f Oculomotor nerve (cranial nerve III), 103, 104f-108f, 104t-10St, 107t, 167, 240 paralysis, 107, 108f Oculomotor nuclei, 87, 240 O'Keefe, John, 234 Olfactory bulb, 103f, 226, 229f

Olfactory groove meningiomas, 227, 293, 293f Olfactory mucous membrane, 22S Olfactory nerve (cranial nerve I), 102, 103f, 226, 229f Olfactory projection area, 226 Olfactory stalk, 102 Olfactory sulcus, 102, 13S, 226 Olfactory system, 30, 225-226 olfactory receptors, 22S-226, 229f-230f Olfactory tract (peduncle), 226 Oligodendrocytes, 13, 13f-14f Olivocerebellar tract, 92t Olivocochlear bundle, 212 Olivopontocerebellar atrophies, 94 Opercula, 135 Ophthalmic artery, 164 Ophthalmic division (trigeminal nerve), 109, 109f, 109t, 167 Optic atrophy, 202 Optic canal, 157-158 Optic chiasm, 121, 202 Optic disk, 198 Optic nerve (cranial nerve II), 102-103, 102f, 202 Optic neuritis (papillitis), 202, 203f Optic radiation, 203 Optic recess, 149 Optic tract, 202 Optokinetic (railroad or freeway) nystagmus, 219 Orbital gyri, 135 Orbital rami, 244 Orbital sulci, 13S Organ of Corti, 211 Ossicles, 211 Otic ganglion, 102, 103t, 111, 112f, 244 Otoconia, 217 Otoliths, 2127 Otosclerosis, 213 Outflow, autonomic, 237-243 autonomic plexuses, 238f-239f, 243, 243f parasympathetic division, 240, 240f-242f sympathetic division, 237-240, 239f-240f Oxytocin, 123, 128t

p Pachymeninx, 65 Pacinian corpuscle, 20f Pain, 192-196 descending systems and, 195, 196f innervation of the viscera, 244t pain matrix, 194, 194f pain systems, 192-194 pathways, 192 referred pain, 194-19S, 194f Palatine rami, 244 Paleocerebellwn, 89, 188 Pallidohypothalamic fibers, 122 Panchymenix, lSO Papez circuit, 230-232, 231f Papilledema,202,203f Paracentrallobule, 13S Parahippocampal gyrus, 135, 231 Parallel fibers, 92 Paramedian pontine reticular formation, 105 Paraplegia, 186


Parasympathetic division, 102, 237, 240, 240f-242f Parasympathetic fibers, 47 Paraventricular nuclei, 121 Paresis, 186 Paresthesias, 142 Parietal area, 179 Parietal lobe, 13S Parieto-occipital fissure, 131 Parinaud's syndrome, 88, 89f Parkinson's disease, 30, 187, 187f, 291 Parolfactory area, 122 Parotid gland, 111, 112f, 244 Paroxysmal labryinthine vertigo, 219 Pars caudalis, 82 Pars compacta, 181 Partial (focal, local) seizures, 2S7 Parvocellular, 198 Pathways auditory, 211-215, 213f-214f clinical correlations, 213 cerebellum, 184, 18Sf corticobulbar (corticonuclear) fibers, 179-180, 180f cranial nerves. See Cranial nerves and associated pathways hypothalamus, to and from, 12St pain control pathways, 192, 19S, 196f somatosensory, 191, 193t spinal motor pathways, lesions in. See Lesions, in spinal cord motor pathways subcortical descending systems, 184 vestibular, 217f-218f visceral afferent pathways to brainstem, 244-24S, 24Sf visual, 201-20S, 202f, 204f white matter. See White matter, pathways in Pedicle, 68 Peduncle, 8S, 91 Peduncular syndrome {alternating oculomotor hemiplegia, Weber's syndrome), 89f, 90 Pelvic nerve (nervus erigentes), 240 Pelvic plexuses, 243 Penetrating arteries, 163 Penumbra, 169 Perforantpathways,227-228 Periaqueductal gray matter, 87 Perikaryon,7 Perimetry, 201 Perinatal disorders, 283 Perineurium, 6S, 1S6 Periosteal layer, 150 Peripheral facial paralysis {Bell's palsy), 111, 287 Peripheral nerves, 44 lesions, 281 regeneration, 15-16 Peripheral nervous system (PNS), 1, 2£, 5 Peripheral vestibular nystagmus, 219 Perivascular space, 150 Periventricular system, 123 Personality changes, 235 Petit mal, 272 PET (positron emission tomograpy), 268, 269f, 270 Petrosal sinuses, 167 Petrous pyramid, 159 Pharyngeal (gag) reflex, 111

Pharyngeal rami, 244 Photic stimulation, 271 Physiologic lesions, 33 Physiologic nystagmus, 219 Pia, 150, 152 Pia mater, 6S Pineal body, 127-128 Pineal recess, 149 Pineal region tumors, 88 Pinna, 211 Pituitary adenoma, 287, 287f Place cells, grid cells, and spatial problem solving. 234 Planes and neutoanatomic terms, S, Sf, St Planwn sphenoidal, 157 Planwn temporale, 141 Plasticity in the nervous system, 27 Plexus of Auerbach, 240 Plexus of Meissner, 240, 247 Pneumococcal meningitis, 289, 290f Pneumotaxic center, 246 PNS (peripheral nervous system), 1, 2f, 5 Poliomyelitis, 186 Polymodal nodceptors, 192 Polymyositis, 281 Polyneuropathy,292,293f Polysynaptic, 4 Polysynaptic reflexes, 59, 60f Pons, 2, 2f, 77, 79f, 85-86, 174, 246 auditory pathways, 86 basis pontis, 85 middle cerebellar peduncle, 86 pontine tegmentum, 85-86 trigeminal system, 8Sf, 86 Pontine auditory arteries, 163 Pontine cistern, 1S2 Pontine nuclei, 85 Pontine tegmentum, 78, 79f, 85-86 Pontocerebellar tract, 92t Pore, 21 Portal hypophyseal system, 123 Positive abnormalities, 34 Positron emission tomograpy (PET), 268, 269f, 270 Postcentral sulcus, 135 Posterior, St Posterior cerebral arteries, 163, 164 Posterior clinoid processes, 158 Posterior communicating arteries, 163 Posterior condyloid canal, 156 Posterior cranial fossa, 157, 159-160 Posterior (dorsal) horn, 48 Posterior (dorsal) median sulcus, 44 Posterior limb of interior capsule, 144 Posterior medullary velum, lSO Posterior nucleus, 122 Posterior (occipital) horn, 149 Posterior spinocerebellar tract, 49 Posterolateral sulcus, 44 Postganglionic neuron, 237 Postsynaptic inhibition, 26, 28f Postsynaptic neuron, 237 Potentials,evoked,272-274 brain stem auditory evoked response (BAER), 272, 274, 275f




Potentials, evoked (continuetl) somatosensory evoked potentials (SEPs), 274 visual evoked potentials (VEPs), 272 Precentral gyrus, 135 Precentral sulcus, 135 Precuneus, 135 Preexisting proteins, 27 Prefrontal cortex, 141 Preganglionic neuron, 237 Preganglionic parasympathetic components, 99, 103t Preganglionic sympathetic neurons, 48 Premotor area, 140 Preoptic area, 122 Presbycusis, 213 Presbyopia, 200 Presynaptic inhibition, 27-28, 28f Presynaptic neuron, 237 Presynaptic vesicles, 25 Prevertebral plexuses, 240 Primary auditory cortex, 141, 212 Primary auditory receptive cortex, 143 Primary endings, 57 Primary motor cortex, 142, 142f Primary olfactory cortex (pyriform cortex), 102 Primary sensorimotor area, 142 Primary sensory cortex, 142 Primary somatosensory cortex, 192 Primary visual cortex, 135, 143 Projection neurons, 11 Prolactin, 128t Propagated, 19 Proprioceptors, 191 Propriospinal axons, 59 Prosopagnosia, 254 Protoplasmic astrocytes, 12 Psychic blindness, 235 Psychomotor (complex partial) seizures, 235 Pterygoid plates, 156, 157f Pterygoid plexus, 167 Pterygopalatine ganglion, 102, 110, 1 lOf Ptosis (lid drop), 107 Pulmonary plexus, 240, 243 Pulvinar, 119 Pulvinar nucleus, 120 Pupillary light reflex, 106, 203 Purkinje cells, 91-92, 92f-93f, 92t Putamen, 143, 174 Pyramidal cells, 136 Pyramidal decussation, 50 Pytiform cortex, 226

Q quadrigeminal plate, 78, 79f Quadriplegia. 186 Quanta, 11, 28

R Radiculopathies, 278

Rage regulatory mechanisms, 128t Rami communicantes, 47

Ranvier, nodes of, 9, 22 Raphe nuclei, 31, 85 Rapid eye movement (REM) sleep, 222 Raynaud's disease, 243 Rebound phenomenon, 188 Recent-onset cluster of brief episodes, 39 Receptors, 25, 54, 247-249, 248t-249t, 249f Reciprocal action of antagonists, 59 Reciprocal inhibition, 58 Recurrent laryngeal nerve, 115 Red nucleus, 86-87 Referred pain, 194-195, 194f Reflexes,54-59, 179 simple reflex arc, 54, 56 spinal reflexes, 56-59, 56f alpha motor neurons, 58 clinical correlations, 58-59 gamma motor neurons, 58, 59f Golgi tendon organs, 58 muscle spindles, 57-58, 59f polysynaptic reflexes, 59, 60f Renshaw cells, 58 stretch reflexes and their anatomic substrates, 56f, 57 types of, 56, 57t Refraction, 200 errors of, 202 Regulation of gene expression, 27 Relapsing-remitting course, 39 Relative permeability, 20 Releasing factors, 123 REM (rapid eye movement) sleep, 222 Remyelination, 16 Renshaw cells, 57, 58 Repolarization, 21 Resting potential, 19 Reticular activating system, 221 Reticular formation, 31, 80, 221-223 anatomy,221,22lf functions, 221-223 arousal, 221 consciousness, 221-222, 222f, 223t sleep, 222-223 Reticular nuclei, 119, 121 Reticulospinal system, 50-51, 52t Reticulospinal tract, 184, 221 Retina, 30, 197-201 bipolar, amacrine, and retinal ganglion cells, 197-200, 200f-201f clinical tests of visual function, 201, 20lf neural components of, 199f retinal cones, 197 retinal rods, 197, 200f Retinenel, 197 Retinohypothalamic tract, 122 Retrobulbarneuritis,202 Retrograde amnesia, 257 Retrograde transport, 9 Rexed's laminae, 48-49 Rhodopsin, 197 Rhombencephalon, 77, 78f Rhomboid fossa. 149 Rinne test, 214t


Rods, retinal, 197, 200f Rolando, fissure of, 131 Romberg's sign, 63 Rostral, Sf, St Rostrocaudal localization, 37-38, 37f Rubrospinal tract, 50, 52t, 184 Ruptured (herniated) disk, 70

s Saccades, 105 Saccule, 217 Sacral parasympathetic neurons, 48 Sacral segments, 44 Sagittal sutures, 156 Saltatory nerve impulse conduction, 22, 23f Schaffercollaterals,228 Schwann cells, l lf, 13 Schwannoma, 215f Sciatica, 70, 284 Scotomas, 202 Scotopsin, 197 Seasickness, 219 Secondary endings, 57 Second messengers, 26 Second-order neurons, 191 Segmental lesion, 60 Segmental (radicular) branches, 66 Segment-pointer muscles, 48t Sella turcica, 158 Semaphorins, 5 Semicircular canals, 217 Semi-lunar (gasserian) ganglion, 102, 103t Sensitization, 2SO Sensorimotor cortex, 179 Sensory (afferent) components, 80, 83f Sensory ataxia, 219 Sensory deficits, 192 Sensory ganglia, 244 Sensory level, 60 Sensory nuclei, 120 SEPs (somatosensory evoked potentials), 274 Septal area, 22S, 226t, 232-235, 233f behavior,233-234 memory,234 neurogenesis and depression, 234 place cells, grid cells, and spatial problem solving, 234 Septa! nuclei, 29, 136 Septa! region, 122 Septa! vein, 165 Septum lucidum, 232 Serotonergic pathways, 80 Serotonin (5-HT), 30-31 areas of concentration, 26t Sexual behavior regulatory mechanisms, 128t Sharp waves, 272 Short-term memory, 234, 2S6 Shunts, 177 SIADH (syndrome of inappropriate secretion of antidiuretic hormone), 126 Sigmoid sinuses, 167


Signaling in the nervous system. See Nervous system, signaling in Signs, definition of, 33 Simple reflex arc, 54, 56 Single-fiber EMG, 27 Single photon emission CT (SPECT), 269f, 270 Sinocerebellum, 188 Sinuvertebral nerves, 47 Skin, sensations from afferents in, 194, 194f Skull, 156-161,282 basal view, 1S6 clinical correlations, 159 interior of, 156-161, 157f-160f, 158t trauma, 159 ventricles and coverings of the brain, 1S6-161 basal view, 156 clinical correlations, 159 interior of the skull, 156-161, 1S7f-160f, 158t x-rays, 261 Sleep, 222-223 clinical correlations, 223 hypersomnia and apnea, 223 narcolepsy, 223 periodicity, 222 stages of, 222-223 rapid eye movement (REM) sleep, 222 slow-wave (spindle) sleep, 222 Slowly progressive dysfunction, 39 Small-fi.ber neuropathy, 24 Smooth pursuit, lOS Solitary nucleus, 82 Solitary tract, 82 Soma, 7 Somatesthetic area, 142 Somatic afferent fi.bers, 47, 99 Somatic efferent fibers, 47, 99 Somatic nervous system, 1 autonomic (visceral) nervous system (ANS), 1 Somatosensory cortex, 53 Somatosensory evoked potentials (SEPs), 274 Somatosensory systems, 191-196 connections, 191, 192f-193f clinical correlations, 192 first-order neurons, 191 second-order neurons, 191 third-order neurons, 191 cortical somatosensory areas, 192 overview, 191 pain, 192-196 descending systems and, 195, 196f pain matrix, 194, 194f pain systems, 192-194 pathways, 192 referred pain, 194-195, 194f receptors, 191, 192f somatosensory pathways, 191, 193t Somatostatin, 247 Somatotopic distribution, 53, 191 Spasticity, 59 Spastic paralysis or paresis, 60 Special senses, 191 Special sensory fibers, 102



Special sensory (SS) nuclei, 80 Special visceral efferent fi.bers, 99 Special visceral efferents (SVE), 80 Specific, goal-directed movements, 179 SPECT (single photon emission CT), 269f, 270 Speech and language, 251-256, 252f agnosia, 254-255, 255f alexia, 253, 254f-255f anosognosia, 255-256 aphasia, 251, 252t with impaired repetition, 252-253, 252t, 253f with intact repetition, 252t, 253 apraxi.a, 256 dysarthria, 251 Gerstmann's syndrome, 256 Sphenopalatine (pterygopalatine) ganglion, 243 Sphenoparietal sinuses, 167 Splices, 272 Spina bifida, 70 Spinal cord, 1, 2f, 3t, 43-64, 245, 245f-246f arteries of, 66-67, 68f compression, 62, 62t development, 43, 44f differentiation, 43 disorders, 62-64 Brown-Sequard syndrome, 63, 63f spinal cord compression, 62, 62t spinal shock, 63 subacute combined degeneration (posterolateral sclerosis), 63 syringomyelia, 62, 63f tabes dorsalis, 63 external anatomy, 43-44, 45f enlargements, 43, 45f longitudinal divisions, 44 segments, 43-44, 45f, 46t imaging. 71-74 computed tomography (CT), 72, 73f magnetic resonance imaging (MRI), 73, 73f-74f plain x-rays, 71, 72f internal divisions of, 48-50 gray matter, 48-49, 49f-50f white matter, 49-50 lesions, 281 lesions in the motor pathways, 59-61, 61t disorders of muscle or neuromuscular endings, 60 localization of spinal cord lesions, 60 lower-motor-neuron lesions, 59-60, 61f types of spinal cord lesions, 60-61, 6lt, 62f upper-motor-neuron lesions, 60, 61f overview,43 pathways in white matter. See White matter, pathways in reflexes. See Reflexes spinal roots and nerves, 44-48, 45f-46f branches of typical spinal nerves, 46-47 dermatomes, 47, 48f direction of roots, 46 dorsal roots, 46, 48t myotomes, 47-48, 48f types of nerve fibers, 47 ventral roots, 46, 47f traumatic lesion of, 284

vertebral column and meninges surrounding. See Vertebral column and meninges surrounding the spinal cord visceral afferent pathways to, 244 Spinal muscular atrophy, 186 Spinal nerves and cranial nerves, differences between, 80 Spinal nucleus ofV, 82, 109 Spinal reflexes, 56-59, 56f alpha motor neurons, 58 clinical correlations, 58-59 gamma motor neurons, 58, 59f Golgi tendon organs, 58 muscle spindles, 57-58, 59f polysynaptic reflexes, 59, 60f Renshaw cells, 58 stretch reflexes and their anatomic substrates, 56f, 57 Spinal shock, 63 Spinal tap, 279 Spinal tract ofV, 109 Spine and spinal cord, imaging, 71-74 computed tomography (CT), 72, 73f magnetic resonance imaging (MRI), 73, 73f-74f plain X-rays, 71, 72f Spinocerebellar tracts, 54, 56f Spinoreticular pathway, 54 Spinoreticular tract, 82 Spinoreticulothalamic system, 194 Spinothalamic tracts, 53-54, 55f, 82, 194 Spiral ganglion, 103t, 211 Splanchnic nerves, 237 Splenium, 131 SS (special sensory) nuclei, 80 Stapedius, 211 Stapes, 211 Static labyrinth, 217 Static response, 57 Stellate cells, 92, 92t, 93f Stellate neurons, 136 Stereotypic repetitious movements, 179 Strabismus (squint), 107, 107t Straight gyrus (gyrus rectus), 135 Straight sinus, 165 Stretch reflexes, 56f, 57 Striate cortex, 135, 141, 205 Striaterminalis, 122,232 Striatonigral projection, 181 Striatum, 143, 180 Stroke (cerebrovascular disease), 36f, 163, 170, 171t Stupor, 222 Stylomastoid foramen, 156, 157f Subacute combined degeneration (posterolateral sclerosis), 63 Subacutely progressive dysfunction, 39 Subarachnoid hemorrhage, 175, 175f, 279 Subarachnoid space, 150, 152 Subcallosal gyrus, 231 Subcortical descending systems, 184 Subcortical gray matter (basal ganglia), 282 Subcortical white matter, 282 Subdural hemorrhage, 176, 176f, 291, 291f Subdural space, 65, 150 Subfalcial herniation, 152 Subiculum, 228


Sublingual glands, 244 Submandibular ganglion, 102, 103t Submaxillary ganglion, 244 Submaxillary glands, 244 Submucosa plexus, 247 Substance P, 49, 247 Substantia gelatinosa, 49 Substantia innominata, 136 Substantia nigra, 30, 86, 181, 18lf Subthalamic nucleus, 126, 182 Subthalamus, 126 clinical correlations, 129 fiber connections, 126 landmarks, 126 Sudden onset of a fixed deficit, 39 Sulci, 131 Sulci and fissures, 131, 133f-134f Sulcus limitans, 43, 44f Sulcus tubae auditivae, 156 Summation, 59 Superficial sensation, 191 Superior, Sf, St Superior cerebellar arteries, 163 Superior cerebellar peduncle, 87, 91 Superior cerebral veins, 166 Superior cervical sympathetic ganglion, 240 Superior colliculi, 78, 79f, 87, 202, 203 Superior ganglia, 111, 112f, 114f Superior glossopharyngeal ganglion, 102 Superior longitudinal fasciculus, 136 Superior mesenteric ganglia, 237 Superior olivary nuclei, 86, 211-212 Superior orbital fissure, 158 Superior parietal lobule, 135 Superior quadrigeminal brachium, 87 Superior rectus muscle, 103, 104f-105f Superior sagittal sinus, 167 Superior salivatory nuclei, 82, 240 Superior vasal ganglion, 102 Supplementary motor area, 140 Supracallosal gyrus, 115, 231 Suprachiasmatic nuclei, 121, 125 Supraoptic nuclei, 121 Supraoptic portion, 121 Suprapineal recess, 149 Suprasellar cistern, 152 Supremarginal gyrus, 135 SVE (special visceral efferents), 80 Sylvian fissure, 131 Sylvius, cistern of, 152 Symmetry,4 Sympathetic fibers, 47 Sympathetic ganglia, 30 Sympathetic (thoracolumbar) division, 237-240, 238f-239f adrenal gland, 240 postganglionic efferent fiber system, 240 preganglionic sympathetic efferent fiber system, 237 Symptoms, definition of, 33 Synapses, 2, 4, 10-11, lOf, lOt, 15f, 19, 23-25, 26t Synapsins, 11 Synaptic delay, 25


Synaptic junction, 10 Synaptic plasticity and long-term potentiation, 27 Synaptic terminal, 7 Synaptic transmission, 19, 25-26 ligand-gated (fast), 25-26 second-messenger mediated (slow), 26t-28t Syncope, 221 Syndrome, definition of, 35 Syndrome of inappropriate secretion of antidiuretic hormone (SIADH). 126 Syringomyelia, 62, 63f, 292, 292f

T Tabes dorsalis, 61, 63 Tabetic crises, 63 Taste pathways, 113f Tectobulbar tract, 212 Tectocerebellar tract, 92t Tectospinal tract, 51, 52t, 82, 86, 184, 212 Tectum, 51, 77, 79f, 87 Tegmentum, 77, 79f, 86-87 Tela choroidea, 149, 150 Telencephalon (endbrain), l, 131. See also Cerebral hemispheres/ telencephalon Temperature regulation, 128t Temporal gyri, 135 Temporal lobe, 135 Temporal lobe epilepsy, 235, 257 Temporal sulci, 135 Tendon reflexes, 57 Tensor tympani, 211, 244 Tensor veli palatini, 244 Tentorium cerebelli, 151 Tests, electrodiagnostic, 271-278 electroencephalography, 271-272 clinical applications, 271 physiology, 271 technique, 271, 272f types of waveforms, 271-272, 273f electromyography, 274, 276-277 clinical applications, 274 physiology, 274 repetitive stimulation, 277 single-fiber EMG, 27 technique,274,276f types of activity, 276-277 evoked potentials, 272-274 brain stem auditory evoked response (BAER), 272, 274, 275f somatosensory evoked potentials (SEPs), 274 visual evoked potentials (VEPs), 272 nerve conduction studies, 277-278 H-retlexes and F-wave, 278 overview, 271 transcranial motor cortical stimulation, 274 Tetraplegia, 186 Thalamic fasciculus, 126, 144 Thalamic pain, 122 Thalamic radiations, 119 Thalamic syndrome, 122 Thalamostriate vein, 165 Thalamus, 53, 119-121, 174



Thalamus (continued) functional divisions, 120-121 landmarks, 119, 120f thalamic nuclei, 119-120, 119t, 12lf-122f thalamic white matter, 119 Theta rhythms, 272 Third-order neurons, 191 Third ventricle, 149 Thirst, 128t Thoracic nerves, 244 Thoracic segments, 43 Thoracolumbar division, 237 Threshold, 21 Thrombosis, 170 Thyroid-stimulating hormone, 128t TIAs (transient ischemic attacks), 39 Tic douloureux (trigeminal neuralgia), 110, 287 Tight junctions, 13 Tinnitus, 213 Tongue, sensory innervation of, 113 Tonotopia, 212 Tonotopical organization, 211 Toxic disorders, 282 Toxoplasma gondii, 289 Tracts and commissures, 4, 50 Tractus proprius, 246 Transcranial motor cortical stimulation, 274 Transducin, 197 Transient cerebral ischemia, 169, 173 Transient ischemic attacks (TIAs), 39 Transmitter substances, 247-250 functions,247,248t-249t,249f receptors, 247-249, 248t-249t, 249f sensitization, 250 types, 247 Transporter molecules, 11 Transtentorial herniation, 152 Transverse localization, 38 Transverse processes, 68 Transverse sinuses, 160, 167 Transverse temporal gyrus, 135 Trapezoid body, 211 Trauma,282 Traumatic intracerebral hemorrhage, 266f Trigeminal ganglion, 167 Trigeminal nerve (cranial nerve V), 86, 108-110, 108f-109f, 109t Trigeminal neuralgia (tic douloureux), 110, 287 Trigeminal system, 85f, 86 Trigger zone, 8 Trigone, 149 Trochlear nerve (cranial nerve IV), 104, 104f, 167 paralysis, 107 Trochlear nucleus, 87 Truncal ataxia, 188 Trunk ganglia, 237 Tuberal portion, 121 Tuber cinereum, 121, 122f Tuberculous meningitis, 289-290, 290f Tubercululm sellae, 158 Tuberohypophyseal tract, 123 Tumors, 213, 282-283, 283f-284f, 294, 294f

brain, according to age and site, 289t cerebellum, 94 involving spinal cord, 186 pineal region, 88 Tuning fork tests, 214 Tympanic membrane, 211

u U fibers, 136 Umbilicus, 47 Uncal herniation, 107 Uncinate fasciculus, 136 Uncus, 135 Unilateral neglect, 255 Upper lumbar nerves, 244 Upper motor neurons, 186 Utricle, 217

v Vagus nerve (cranial nerve X), 113-llS, 114f, 240, 244 Vascular disorders, 282 Vascular-endothelial barrier, 154-155 Vascular lesions, 36 Vascular malformations and developmental abnormalities, 170, 17S Vascular supply of the brain, 163-178 arterial supply, 163-164 carotid territory, 163-164 cerebral blood flow and autoregulation, 164 characteristics of cerebral arteries, 163 circle of Willis, 163 cortical supply, 164, 167f-168f principal arteries, 163, 164f vertebrobasilar territory, 163, 164f-166f cerebrovascular disorders, 167-178 atherosclerosis of the brain, 172, 173f AVMs and shunts, 176-177 cerebral embolism, 172-173 classification, 169-170, l 7lt epidural hemorrhage, 176, 176f hemorrhagic cerebrovascular disease: hypertensive hemorrhage, 174, 174f ischemic cerebrovascular disease, 167, 169 localization of the vascular lesion in stroke syndromes, 173, 173f, 174t occlusive cerebrovascular disease, 170, 172, l 72f subarachnoid hemorrhage, 175, 175f subdural hemorrhage, 176, 176f time matters, 178 transient cerebral ischemia, 173 overview, 163 venous drainage, 16S-167 cortical veins, 166, 168f internal drainage, 16S-166 types of channels, 165, 168f-169f venous sinuses, 167, 172f Vasculature, compromise of, 36 Vasoactive intestinal peptide (VIP), 247 Vasopressin, 123, 128t Venous sinuses, 165 Ventral, Sf, St Ventral (anterior) gray column, 48


Ventral (anterior) hom, 48 Ventral anterior nucleus, 119 Ventral lateral nucleus, 119 Ventral (motor) roots, 5 Ventral posterior group, 119 Ventral posterolateral thalamic nuclei, 53 Ventral posterolateral (VPL) nucleus, 119 Ventral posteromedial (VPM) nucleus, 119 Ventral roots, 46, 47f Ventral spinocerebellar pathway, 82 Ventral spinocerebellar tract, 92t Ventral tegmental area, 30 Ventricles and coverings of the brain, 149-161 barriers in the nervous system, 154-156 blood-brain barrier, 154-155 blood-nerve barrier, 156 ependyina, 156, 156f cerebrospinal fluid (CSF), 152-154 circulation, 153-154, 154f clinical correlations, 152, 153f composition and volume, 153, 153t function, 152 pressure, 153, 153f meninges and submeningeal spaces, 150-152 arachnoid, 152, 152f dura, 150-152, 151f pia, 152 skull, 156-161 basal view, 156 clinical correlations, 159 interior of the skull, 156-161, 157f-160f, 158t ventricular system, 149-150, 150f cerebral aqueduct 149 choroid plexus, 149, 150f-151f fourth ventricle, 149-150 lateral ventricles, 149, 151f third ventricle, 149 Ventricular pathways, compromise of, 36 Ventricular zone, 7 Ventrolateral system, 53, 191 and lemniscal system, differences from, 193t Ventromedial nuclei, 121, 122 VEPs (visual evoked potentials), 272 Vergence, 105 Vergence center, 105 Vermis, 89, 91f Vertebral arteries, 163 Vertebral column and meninges surrounding the spinal cord, 65-75 clinical correlations, 70 herniated nucleus pulposus, 70 meningocele, 70 meningomyelocele, 70 ruptured (herniated) disk, 70 sciatica, 70 spina bifida, 70 imaging of spine and spinal cord, 71-74 computed tomography (CT), 72, 73f magnetic resonance imaging (MRI), 73, 73f-74f plain X-rays, 71, 72f investing membranes (meninges), 65, 66f-67f

arachnoid mater, 65 clinical correlations, 66 dentate ligament, 65 dura mater, 65 investment of spinal nerves, 65 pia mater, 65 spinal nerves, 65 lumbar puncture, 69-71 complications, 70-71 site, 69, 71f technique, 69-70 overview, 65 spinal cord circulation, 66-67 arteries, 66-67, 68f veins, 67 vertebral column, 67-69, 69f vertebrae,68-69, 70f Vertebrobasilar artery disease, 173 Vertebrobasilar territory, 163, 164f-166f Vertibular nuclei, 82 Vertical gaze palsy, 88 Vertigo, 219 Vesalius, foramen of, 158 Vestibular ataxia, 219 Vestibular ganglion, 102, 103t, 217 Vestibular nuclei, 217 Vestibular system, 217-220 anatomy,217,217f clinical correlations, 219 functions,217-218,217f-218f overview, 217 vestibular pathways, 217f-218f Vestibulocerebellar tract, 92t Vestibulocerebellum, 188 Vestibulocochlear nerve (cranial nerve VIII), 111, lllf, 213f vestibular component of, 217 Vestibulo-ocular reflex, 105, 218 Vestibulospinal tract, 50, 52t, 184, 217 Vicq d'Azyr, tract of, 123 VIP (vasoactive intestinal peptide), 247 Virchow-Robin's space, 159 Viscera, nociceptors in, 194, 194f Visceral afferent fibers, 47, 99 Visceral afferent pathways, 244-245, 244t pathways to brainstem, 244-245, 245f pathways to spinal cord, 244 Visceral efferent fibers, 47, 99 Visceral sensations, 191 Visual adaptation, 198-199 Visual agnosia, 254 Visual association areas, 141 Visual association cortex, 205-206 Visual evoked potentials (VEPs), 272 Visual pathways, 204f Visual system, 197-210 clinical correlations, 202 eye. See Eye overview, 197 retina, 197-201 bipolar, amacrine, and retinal ganglion cells, 197-200, 200f-201f




Visual system (continued) clinical tests of visual function, 201, 201f retinal cones, 197 retinal rods, 197, 200f visual cortex, 205-210 anatomy, 205 clinical correlations, 205 histology, 206 physiology, 206-209, 207f-209f primary,205,205f visual association (extrastriate) cortex, 205-206 visual pathways, anatomy of, 201-205, 202f, 204f Voltage-sensitive K+ channels, 21 Voltage-sensitive Na+ channels, 21 Voltage-sensitve ion channels, 21 Voltage sensor, 21 VPL (ventral posterolateral) nucleus, 119 VPM (ventral posteromedial) nucleus, 119

w Wallenberg's syndrome, 35, 87-88, 89f, 110, 285, 286f Wallerian degeneration, 14 Water balance, 124 Watershed areas (border zones), 163 Weber's syndrome, 89, 89f, 90 Weber test, 214t W ernicke-Korsakoff syndrome, 257 Wernicke's aphasia, 252 Wernicke's area, 141, 251, 252t White communicating rami, 237 White matter, 1-2, 3f, 34, 136, 136f-137f, 174 association ii.hers, 136, 137f dysfunction can cause neurologic dysfunction, 34-35, 35f projection ii.hers, 136

spinal cord, 49-50 thalamic, 119 transverse (commissural) ii.hers, 136 White matter, pathways in, 50-54 ascending fiber systems, 51-54, 52t clinical correlations, 54 dorsal column tracts, 52-53, 53f-54f spinocerebellar tracts, 54, 56f spinoreticular pathway, 54 spinothalamic tracts, 53-54, 55f descending fiber systems, 50-51, 52t corticospinal tract, 50, 5lf, 52t descending autonomic system, 51 medial longitudinal fasciculus, 51 reticulospinal system, 50-51 rubrospinal tract, 50 tectospinal tract, 51 vestibulospinal tracts, 50 Whole-head sections, 94-96, 95f-96f Wiesel, T., 208 Willis, circle of, 163, 173f

x X-rays

skull, 261 spine and spinal cord, 71, 72f

y Yoke muscle combinations, 105t Young-Helmholtz theory, 199

z Zona incerta, 126