DISORDERS OF MOTILITY - PRINCIPLES OF NEUROLOGY

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 23

bers are mixed with sensory and autonomic ones. Each large muscle is supplied by several adjacent roots but usually by only a single nerve.

Therefore, the pattern of paralysis following disease of anterior horn cells and roots differs from that following interruption of individual nerves.

Any given movement requires the activity of many muscles, some acting as prime movers or agonists, others as antagonists, fixators, or synergists. These relationships are integrated in the spinal cord or brainstem, an arrangement known as reciprocal innervation. Complex motor activities such as flexor withdrawal responses, support reactions, crossed extensor and tonic neck reflexes, the maintenance of tone, pos-ture, stance and gait, and the performance of voluntary and habitual actions depend on intersegmental spinal mechanisms and their integra-tion with corticospinal and other suprasegmental systems.

The myotatic or tendon reflex depends on the sudden stretch ex-citation of the muscle spindles, which lie parallel to muscle fibers (Fig. 3-1). The afferent impulses from the spindles are conducted to the corresponding spinal segments and are transmitted by direct (monosyn-aptic) connections to the alpha motor neurons where they have an inhibitory influence. The small gamma motor neurons keep the muscle fibers of the spindle in a proper state of tension. There are also sensory nerve endings in muscle such as Golgi tendon organs, which are sensi-tive to tension and may induce inhibition. In the spinal cord, inhibition is mediated by Renshaw cells (1A inhibitory interneurons). Although the muscle spindle and the Golgi tendon organ have opposite effects on the pool of motor neurons, they are complementary in calibrating the range and force of movements.

The nociceptive or flexor withdrawal reflex is activated by the exci-tation of A- and small caliber afferent C fibers; this is a polysynaptic reflex in which the afferent volleys excite many anterior horn cells (which flex the limb) and other motor neurons, which inhibit extensor antigravity muscles.

When all or practically all the anterior horn cells or their peripheral motor fibers to a group of muscles are interrupted, all voluntary, pos-tural, and reflex movements are lost. The paralyzed muscles become lax and soft and offer little or no resistance to passive stretching. This state is referred to as flaccidity and is due to a loss of normal muscle tone (atonia or hypotonia). Also, the denervated muscles slowly undergo extreme atrophy, losing 70 to 80 percent of their normal bulk over a period of 3 to 4 months. By contrast, in disuse atrophy (e.g., limb in a plaster cast), the loss of bulk usually does not exceed 25 to 30 per-cent. In lower motor neuron paralysis, tendon reflexes are abolished and electrodiagnostic studies demonstrate a reduced amplitude of the muscle action potential obtained by stimulating the nerve and the pres-ence of fibrillation potentials in the affected muscles. By contrast, nonreflexive contractility to a tap on the muscle may be preserved (idiomuscular response.)

24 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 24

25 FIG. 3-1 Patellar tendon reflex. The principal receptors are the muscle spindles, which respond to a brisk stretching of the muscle effected by tapping the patellar tendon. Afferent fibers from muscle spindles are shown entering the L3 segment, while afferent fibers from the Golgi ten-don organ are shown entering the L2 spinal segment. In this monosyn-aptic reflex, afferent fibers entering segments L2 and L3 and efferent fibers issuing from the anterior horn cells of these and contiguous lower levels complete the reflex arc. Motor fibers, which are shown leaving the S2 spinal segment and passing to the hamstring muscles, illustrate the disynaptic pathway by which inhibitory influences are exerted upon an antagonistic muscle group.

The small diagram illustrates the gamma loop. Gamma efferent fibers pass to the muscle spindle. Contraction of the intrafusal fibers in the polar parts of the spindle stretch the nuclear bag region and cause an afferent impulse to be conducted centrally. The afferent fibers from the spindle synapse with many alpha motor neurons, whose peripheral processes pass to extrafusal muscle fibers, thus completing the loop. Both alpha and gamma motoneurons are influenced by descending fiber systems from supraspinal levels. (Redrawn, with permission, from Carpenter and Sutin.)

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 25

26 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE

The atrophic, areflexive paralysis of lower motor neuron disease varies with the location of the lesion. If combined with loss of sensory and autonomic function, it indicates disease of the peripheral nerve. If sensory changes are absent, the affliction is usually one of anterior horn cells (spinal ), of anterior roots (radicular), or of motor nerve fibers (neuropathy). The spinal form is exemplified by progressive muscular atrophy, amyotrophic lateral sclerosis, and poliomyelitis (now rare).

The common acute radicular-nerve disease, usually with less sensory than motor loss, is the Guillain-Barré syndrome.

Spinal motor neuron activity may under certain circumstances be enhanced, giving rise to muscle cramps, fasciculations, myokymia (continuous rippling activity of muscle), and spasms of diverse type.

These phenomena are discussed in Chap. 54.

DISORDERS OF THE CORTICOSPINAL AND OTHER UPPER MOTOR NEURONS

The motor cortex is defined physiologically as the electrically excitable region from which isolated movements can be evoked by stimuli of minimal intensity. Anatomically, this cortical region lies in the poste-rior part of the frontal lobes and comprises three areas: the precental (area 4), the premotor (area 6), and the supplementary motor, on the medial surface of the superior frontal and cingulate convolutions.

The descending motor pathways that originate in the motor cortex are designated as pyramidal, corticospinal, and upper motor neuron; the terms are often used interchangeably, but such usage is not completely accurate. Strictly speaking, the pyramidal tract is only the portion of the corticospinal system that passes through the pyramid of the medulla. A destructive lesion confined to the medulla does not fully reproduce the permanent hemiplegic paralysis that follows corticospinal lesions at higher levels. The direct corticospinal tract has its origin in the Betz cells of the motor cortex (numbering 25,000 to 30,000); in other neu-rons of the motor, premotor, and supplementary motor cortices; and in cells of several somatosensory regions of the parietal lobe (Brodmann’s areas 1,3,5, and 7; see Fig. 22-2). The axons of these cells descend in the corona radiata, posterior limb of the internal capsule, cerebral peduncle, basis pontis, and medullary pyramid (Fig. 3-2). The pyramid contains approximately 1 million fibers, only 60 percent of which orig-inate in the motor cortices. At the junction of the medulla and spinal cord, the majority (70 to 90 percent) of these fibers decussate and descend as the crossed lateral corticospinal pathway, synapsing at var-ious segmental levels of the spinal cord—most with internuncial pro-prioceptive intra- and intersegmental neurons (which, in turn, project to anterior horn cells) and the remainder (20 to 25 percent) directly with anterior horn cells. A smaller contingent of direct corticospinal tract fibers do not decussate and descend as the uncrossed anterior and lat-eral corticospinal tracts.

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 26

In the brainstem, the corticospinal tracts are accompanied by the cor-ticobulbar tracts, which are distributed to the motor nuclei of the cranial nerves. The corticospinal tract is the only direct long-fiber connection between the cerebral cortex and the spinal cord. Offshoots of the corti-cospinal tracts are to the red nuclei, forming the corticorubrospinal tract, the reticular formations of the brainstem (corticoreticulospinal), the mesencephalic tectum (corticotectospinal), the vestibular nuclei

CHAPTER 3 / MOTOR PARALYSIS 27

FIG. 3-2 The corticospinal and corticobulbar pathways, from their ori-gin in the cerebral cortex to their nuclei of termination. Variable lines indi-cate the trajectories from particular parts of the cortex.

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 27

(corticovestibulospinal), and the pontine nuclei and cerebellum (cor-ticopontocerebellar). These indirect corticobrainstem-spinal fibers, which do not run in the pyramid, are also involved in volitional as well as reflex and postural movement, supplementing the direct corti-cospinal system. Ascending sensory systems influence the motor ones at all levels (see Principles of Neurology for details). At the cortical level, motor activity is guided both by the prefrontal cortex (planning and programming of movement) and by sensory projections from the parietal cortex.

In all voluntary movements, the entire motor cortex is activated, but large numbers of neurons can be destroyed without causing weakness or causing only a loss of fine finger control.

Lesions that are restricted to the supplementary motor cortex result in a poverty of movement, akinesia, and mutism; this part also seems to be involved more in the planning of voluntary movement than in its execution. Lesions confined to the left premotor cortex result in apraxia and perseveration of movement. With lesions confined to the primary motor area of the cortex there is weakness and hypotonia, without increase in tendon reflexes.

The corticospinal and corticobulbar tracts (referred to collectively as the “upper motor neuron”) may be interrupted at any point in their course, from motor cortex to spinal cord, and the distribution of the paralysis indicates the level of the lesion. Always a group of muscles is involved, never single ones, and always the paralysis is incomplete, in that most of the reflex, postural, and automatic movements are pre-served. A restricted cortical lesion may affect only one limb or even part of a limb. A lesion in the rolandic operculum or genu of the inter-nal capsule may affect the hand and lower face. Lesions of the posterior limb of the capsule paralyze the lower facial and tongue muscles and those of the arm and leg, always on the opposite side. Lesions below the caudal pons spare the face, tongue, and muscles of speech. The hand and arm are usually affected more severely than the foot and leg.

Another general principle is that parts of the body most used for deli-cate fractionated movements—i.e., the fingers and hand—suffer the most from corticospinal lesions. In suprasegmental (hemispheral) hemiplegia, other corticobrainstem connections are interrupted as well.

Muscles that are engaged in bilateral, automatic, and reflexive move-ments, such as respiration, are hardly affected, if at all. Weakness in ipsilateral limb muscles is barely detectable.

With lesions of the cerebrum and upper brainstem, tone of the para-lyzed muscles is not altered in a consistent manner. The tendon reflexes, which at first are slightly reduced or unchanged, later become more active. There are also postural changes. The arm gradually becomes flexed and adducted and the leg extended, and the limbs become spastic. The flexors of hip, leg, and foot and the extensors of arm, hand, and fingers are weaker than their opposing muscles.

28 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 28

Attempts at voluntary movement of a hand or foot may increase the tone or cause involuntary contraction of an entire limb (synkinesia).

With acute lesions of the cervical or thoracic spinal segments, muscle tone and tendon reflexes may be abolished in the legs for days or weeks, a condition known as “spinal shock” (Chap. 43). Spasticity is revealed by the patient’s attempts at active movement and by passive movement. In passive extension of the spastic arm, for example, there is first a brief nonresistant “free interval,” followed by a (velocity-dependent) catch and rapidly increasing resistance, which gradually yields as the passive stretch is continued (clasp-knife phenomenon). In these ways, spasticity differs from the uniform resistance that charac-terizes rigidity (described in the next chapter). The hyperreflexive state often gives rise to clonus, which is a series of rhythmic involuntary muscular contractions in response to an abruptly applied and sustained passive or active stretching of a muscle group. It is most easily evoked at the ankle, knee, and wrist. Its basis is a hyperexcitability of spinal motor neurons, which are released or disinhibited by the corticospinal lesions. The cutaneomuscular (abdominal and cremasteric) reflexes are abolished, and nocifensor spinal reflexes, of which the Babinski sign is a part, are released. The latter sign is most consistently elicited by stroking the lateral side of the sole with a key or similar object, but when the spinal reflexes are greatly enhanced, even pinching or touch-ing any part of the foot or leg may evoke dorsiflexion of the toes and foot and flexion at the knee and hip. Usually, with a corticospinal lesion, both a Babinski sign and heightened tendon reflexes are present;

but since they depend on different mechanisms, they need not appear together or persist together in chronic paralysis. With bilateral cerebral lesions, the cranial muscles may be paralyzed and their stretch reflexes exaggerated; i.e., jaw and buccal jerks are increased (pseudobulbar palsy, see further on).

While it is clinically convenient to think of motility in terms of upper and lower motor neurons, this is a gross simplification. All segments of the spinal cord are integrated in posture and movement, under control of the cerebellar, vestibular, and other brainstem systems, the basal gan-glia, and the motor cortices. Some idea of the complexity of the system is evidenced by the simple act of scratching an insect bite, which involves the action of more than 70 muscles, arranged in many patterns and most of them acting involuntarily.

DIAGNOSIS OF PARALYTIC STATES

The term monoplegia designates a paralysis of one limb; hemiplegia, paralysis of an arm and leg on the same side; paraplegia (sometimes referred to as diplegia), paralysis of both legs; and quadriplegia or tetraplegia, paralysis of all four extremities.

CHAPTER 3 / MOTOR PARALYSIS 29 4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 29

30 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE

Bulbar paralysis, or palsy, refers to weakness or paralysis of the muscles innervated by the motor nuclei of the lower brainstem (i.e., muscles of the face, tongue, larynx, and pharynx). The paralysis may be atrophic and flaccid (i.e., lower motor neuron in type), in which case it is most often due to a degeneration of the lower cranial motor nuclei, as occurs in amyotrophic lateral sclerosis. If both right and left cortico-bulbar pathways are interrupted, voluntary movements of the cortico-bulbar musculature are paralyzed, whereas reflexive movements are retained or heightened; this state is referred to as spastic bulbar or “pseudobul-bar” palsy (see also p. 218).

An atrophic monoplegia with loss of tendon reflexes points to a lesion of the anterior horn cells or, if there are also sensory or auto-nomic changes, to a lesion of the peripheral nerves. In the absence of atrophy or reflex loss, monoplegia suggests a unilateral spinal cord or, rarely, a cerebral cortical-subcortical lesion.

Hemiplegia with retained or heightened reflexes is the common man-ifestation of a lesion in the cerebral white matter, internal capsule, cere-bral peduncle, basis pontis, or pyramid. Most often it is due to vascular disease, less often to trauma, tumor, or an infective or demyelinative process. If facial muscles are spared, the lesion is in the lower brainstem or high cervical cord. Since brainstem and cord lesions are often bilat-eral, other motor cranial nerve or nonmotor signs may be added and indicate the level of the corticospinal lesion.

Paraplegia with retained or heightened tendon reflexes (except dur-ing the period of spinal shock, when reflexes are absent) indicates involvement of the motor pathways in the thoracic or upper lumbar cord; quadriplegia, or tetraplegia, points to interruption of motor tracts in the cervical cord, brainstem, or both cerebral hemispheres. Triplegia is usually a transitional state in the development of quadriplegia, due most often to lesions at the cervicomedullary junction. Lesions of the gray matter of the spinal cord may cause an atrophic, areflexive paral-ysis of the legs or arms. Paralparal-ysis of individual muscles points to a lesion of anterior horn cells or a peripheral nerve lesion (see above).

One must always remember that motor paralysis may occur in the absence of any disease in the central or peripheral nervous system.

Conditions such as myasthenia gravis, familial periodic paralysis, severe endocrine and electrolytic disturbances, and botulinus poisoning constitute this category and are considered in the section on diseases of muscle. Also, paralysis is the most common manifestation of hysteria or malingering. Usually such a diagnosis is suggested by inconsisten-cies of voluntary contraction (ability to perform some acts but not oth-ers that utilize the same muscles), an obvious lack of effort, lack of reflex changes, and the presence of other symptoms and signs of hyste-ria (see Chap. 55).

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 30

CHAPTER 3 / MOTOR PARALYSIS 31 APRAXIA

This term, introduced by Liepmann in 1900, refers to a loss of learned patterns of movement in the absence of upper or lower motor neuron signs, ataxia, or extrapyramidal disorder. In Liepmann’s view, apraxia could be subdivided into three types—ideational, ideomotor, and kinetic. In ideational apraxia, there is a failure to conceive or formulate an act, either spontaneously or on command. The anatomic substrate of this activity was thought to be in the dominant parietal lobe. In ideo-motor apraxia, the patient may know and remember the planned action, but cannot execute it with either hand—presumably because of inter-ruption of connections between the dominant parietal lobe and the sup-plementary and premotor cortices of both cerebral hemispheres. Kinetic limb apraxia refers to clumsiness of a limb in the performance of a skilled act that cannot be accounted for by paresis, ataxia, or sensory loss. Frontal lobe lesions account for most cases. One tests for apraxia by observing the patient as he engages in tasks such as washing, shav-ing, and eating. Next the patient is asked to perform a series of symbolic acts—saluting, waving goodbye, blowing a kiss, pretending to comb the hair or brush the teeth. If he fails, he is given the proper utensils with which to perform the act and asked to imitate the examiner. This subject is described further in Chap. 22.

For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 43–63.

ADDITIONAL READING

Alexander GE, DeLong M: Central mechanisms of initiation and control of move-ment, in Asbury AK, McKhann GM, McDonald WI (eds): Diseases of the Ner-vous System, 2nd ed. Philadelphia, Saunders, 1992, pp 285–308.

Asanuma H: The pyramidal tract, in Brooks VB (ed): Handbook of Physiology, sec 1: The Nervous System, vol 2: Motor Control. Bethesda, MD, American Physiological Society, 1981, pp 702–733.

Carpenter MD, Sutin J: Human Neuroanatomy, 8th ed. Baltimore, Williams &

Wilkins, 1983.

Ghez C: The control of movement, in Kandel ER, Schwartz JH, Jessel TM (eds):

Principles of Neural Science, 3rd ed. New York, Elsevier, 1991, pp 533–547.

Lance JW: The control of muscle tone, reflexes and movement: Robert Warten-burg Lecture. Neurology 30:1303, 1980.

Laplane D, Talairach J, Meininger V, et al: Motor consequences of motor area ablations in man. J Neurol Sci 31:29, 1977.

Porter R, Lemon R: Corticospinal Function and Voluntary Movement. Oxford, Oxford University, 1994.

4777 Victor Ch 3 pp21-31 6/11/01 1:51 PM Page 31

4 Abnormalities of Movement and Posture due to Disease of the Basal Ganglia

In this chapter and the next, we shall consider a second group of motor abnormalities, which do not materially reduce muscular power but ren-der it less effective because of rigidity, incoordination, alterations of posture, or the interposition of involuntary movements. These disor-ders, conventionally referred to as extrapyramidal movement disordisor-ders, are conveniently subdivided into two parts: (1) the basal ganglia (cau-date and lenticular nuclei, subthalamic nucleus, substantia nigra, red nucleus, and pontomesencephalic reticular formation) and (2) the cere-bellum. This chapter deals with the basal ganglionic, or striatonigral, system. The cerebellum is considered in the following chapter.

In health, the basal ganglionic functions blend with and modulate the corticospinal and corticobulbar motor systems described in Chap. 3.

Physiologic studies of primates inform us that in the performance of all planned and learned movements, the basal ganglia and cerebellum, which are partly under cerebral-cortical control, are activated before the corticospinal-corticobulbar systems. Also, the effects of lesions in these structures have tended to blur the distinction between the corticospinal and extrapyramidal systems. Nevertheless, such a division remains clinically useful (Table 4-1).

STRIATONIGRAL DISORDERS

As indicated in Figs. 4-1 and 4-2, the prefrontal, premotor, and supple-mentary motor cortices send fibers to the caudate nucleus and putamen (together referred to as the striatum), as do other parts of the cerebral cortex. It is estimated that in each cerebral hemisphere there are 110 million corticostriatal neurons (compared to 1 million corticospinal neurons). The striatal neurons are of many types and sizes and project to the lateral and medial parts of the pallidum; the lateral, or exter-nal, segment, which has to-and-fro connections with the subthalamic nucleus, projects in turn to the internal segment of the pallidum and the pars reticulata (pigmented cells) of the substantia nigra. The putamen and caudate nuclei receive recurrent fibers from the pigmented cells of the substantia nigra. From the pallidum, particularly its medial segment, two bundles of efferent fibers—the ansa and fasciculus lenticularis—

sweep medially and caudally to synapse in the ventrolateral and 4777 Victor Ch 4 pp32-40 6/11/01 1:52 PM Page 32

intralaminar thalamic nuclei. The latter nuclei are also the terminus of a major and distinct pathway of ascending efferent fibers from the den-tate and red nuclei. Here, in the ventral tier of thalamic nuclei, basal ganglionic and cerebellar impulses are integrated and brought to bear on the corticospinal system. The ventrolateral nucleus sends fibers to the precentral and supplementary motor cortices (areas 6 and 8). Yet another loop begins in the frontal association areas of the cerebral cor-tex; it projects to the caudate nucleus and thalamus and then back to the prefontal cortex. In addition, there are several subsidiary loops that involve the centromedian and parafascicular nuclei of the thalamus and the mesencephalic tegmental and subthalamic nuclei. Each structure has to-and-fro modulating connections with all other basal ganglionic structures. The association cortex, via its projecting loops through the basal ganglia, is activated in the initial phases of planned movement.

Physiologically, the basal ganglia have been thought to function as a kind of clearinghouse, in which, during any intended or programmed movement, one set of motor activities is facilitated and other unneces-sary ones are suppressed. Thus they are essential in controlling the direction, speed, and amplitude of movement.

Extensive lesions of the extrapyramidal motor system liberate a num-ber of abnormalities of posture that are normally under brainstem

con-CHAPTER 4 / ABNORMALITIES OF MOVEMENT AND POSTURE 33

33 TABLE 4-1 Clinical Differences between Corticospinal and

Extrapyramidal Syndromes

Corticospinal Extrapyramidal Character of the Clasp-knife effect Plastic rigidity alteration of muscle (spasticity); throughout passive

tone rigidity movement

or intermittent (cogwheel rigidity);

hypotonia in cerebellar disease

Distribution of Flexors of arms, Flexors of limbs and hypertonus extensors of legs trunk (predominantly)

or extensors of all four limbs

Involuntary Absent Presence of tremor,

movements chorea, athetosis,

ballismus, dystonia Tendon reflexes Increased Normal or slightly

increased

Babinski sign Present Absent

Paresis of Present Absent or slight

voluntary movement

4777 Victor Ch 4 pp32-40 6/11/01 1:52 PM Page 33

trol. The ones most clearly exposed by disease are decerebrate rigidity and the antigravity support and righting reflexes. In decerebrate rigid-ity, in which the vestibular nuclei are separated from upper brainstem influences and thereby disinhibited, all four extremities or the arm and leg on one side (ipsilateral to a unilateral lesion) are extended and the cervical and thoracolumbar portions of the spine are dorsiflexed; tonic neck reflexes can often be elicited (passive turning of the head results in ipsilateral extension of the limbs and flexion of the opposite arm).

Disorders of postural fixation and righting are features of several extrapyramidal diseases such as Parkinson disease (see Chap. 38).

Lesions that involve the corticospinal tracts predominantly result not only in paralysis of the contralateral limbs but also in the development of a fixed posture, in which the arm is maintained in flexion and the leg in extension (decorticate posture).

34 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE

FIG. 4-1 Diagram of the striatal afferent pathways, Corticostriate fibers from broad cerebral-cortical areas project to the putamen; from the medial surface of the cortex, fibers project largely to the caudate nucleus.

Nigrostriatal fibers arise from the pars compacta of the substantia nigra.

Thalamostriate fibers arise from the centromedian-parafascicular com-plex of the thalamus. CM, centromedial nucleus; DM, dorsomedial nu-cleus; GP, globus pallidus; IC, internal capsule; PUT, putamen; RN, red nucleus; SN, substantia nigra; VPL, ventral posterolateral nucleus; VPM, ventral posterior medial nucleus.

4777 Victor Ch 4 pp32-40 6/11/01 1:52 PM Page 34

Pharmacologic studies have identified dopamine (synthesized from tyrosine and hydroxyphenylalanine) as the nigrostriatal transmitter.

Dopamine is elaborated by pigmented nigral cells and has an inhibitory effect on receptors of striatal cells. Acetylcholine, which is formed by large striatal cells, has an excitatory effect. Dopamine and acetylcholine are antagonistic. The inhibitory effects of the pallidum are mediated by gamma aminobutyric acid (GABA) and enkephalin. The other impor-tant transmitters and pathways involved in basal ganglionic function are illustrated in Fig. 4-3 and are described in the Principles.

CHAPTER 4 / ABNORMALITIES OF MOVEMENT AND POSTURE 35

FIG. 4-2 Diagram of the basal ganglia, illustrating main striatal effer-ents (see text for details).

4777 Victor Ch 4 pp32-40 6/11/01 1:52 PM Page 35

Dalam dokumen PRINCIPLES OF NEUROLOGY (Halaman 36-200)