PRINCIPLES OF NEUROLOGY - PART 2 ppsx

Cerebellar disorders of equilibrium and gait are described in Chap. 7. Table 5-1 summarizes the main disorders that are characterized by generalized cerebellar ataxia, according to their mode of onset (rate of development) and the degree of permanence of the ataxia. For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 84–93. ADDITIONAL READING Brooks VB: The Neural Basis of Motor Control. New York, Oxford University, 1986. Ghez C: The cerebellum, in Kandel ER, Schwartz JH, Jessel TM (eds): Principles of Neural Science, 3rd ed. New York, Elsevier, 1991, pp 626–646. Holmes G: The cerebellum of man. Hughings Jackson Lecture. Brain 62:1, 1939. Thach WT Jr: The cerebellum, in Mountcastle VB (ed): Medical Physiology, 14th ed. St. Louis, Mosby, 1980, vol 1, pp 837–858. Watts RL, Koller WC (eds): Movement Disorders. Neurologic Principles and Practice. New York, McGraw-Hill, 1997, pp 365–417. CHAPTER 5 / THE CEREBELLUM 45 4777 Victor Ch 5 pp41-45 6/11/01 1:53 PM Page 45 6 Tremor, Myoclonus, Focal Dystonias, and Tics These disorders of movement are commonly observed in the course of medical practice. Although all of them are manifestations of disease, their clinical significance is quite variable. Moreover, their physiology is not fully understood, and only infrequently is their pathologic basis established. From the clinician’s viewpoint, once each of these phe- nomena has been seen, there is little difficulty in recognizing it on sub- sequent occasions and assessing its medical implications. TREMOR This is defined as a more or less rhythmic oscillation of a part of the body around a fixed point. It is customary to categorize tremor as being of two general types: (1) normal or physiologic and (2) pathologic. Physiologic tremor is clinically imperceptible but present in everyone and involves all muscle groups. One element is a fine reverberation from cardiac systole (seen by ballistocardiography), but the more important component is a reflection of incomplete fusion of the twitches of large motor units, which contract at a rate too slow to pro- duce a fused tetanus. It is irregular in both frequency and amplitude; the rate is 8 to 12 Hz or higher and amplitude less than 0.1° at fingers and wrist (Young). Enhancement of physiologic tremor occurs during hyperadrenergic states (fright, injection of norepinephrine, thyrotoxicosis, use of caf- feine, nicotine, and corticosteroids), whereupon it becomes visible when the fingers and hands are outstretched. It is quieted by anxiolytic drugs or when the patient is calm and relaxed. There are several identifiable types of pathologic tremor (Table 6-1), the common ones being essential-familial “action” tremor, parkinsonian tremor, and cerebellar tremors, both the “intention” and coarse, flapping (“rubral”) types, and rhythmic myoclonus (Table 6-1). The essential or familial action tremor is the most frequent. Most often it involves the upper extremities, but it may affect the head, jaw and laryngeal muscles (quavering voice), all or in part, and rarely the lower extremities. Its frequency is 5 to 7 Hz and its range may be several millimeters, enough to interfere with writing, eating, etc. A unique characteristic is its appearance only during movement and its immedi- ate arrest upon relaxation, and the tremor increases when the target is 46 4777 Victor Ch 6 6/11/01 1:53 PM Page 46 Copyright 1998 The McGraw-Hill Companies, Inc. Click Here for Terms of Use. 47 TABLE 6-1 MAJOR TYPES OF TREMOR Frequency, Predominant Enhancing Attenuating Type of tremor Hz location(s) agents agents Physiologic 8–13 Hands Epinephrine, ␤-adrenergics Alcohol, ␤-adrenergic (enhances) antagonists Parkinson (rest) 3–5 Hands and forearms, Emotional stress L -Dopa, anticholinergics fingers, feet, lips, tongue Cerebellar (intention 2–4 Limbs, trunk, head Emotional stress Alcohol or ataxic) Postural, or action 5–8 Hands Anxiety, fright, ␤-adrenergics, alcohol withdrawal, xanthines, lithium, exercise Essential (familial, 4–8 Hands, head, vocal cords Anxiety, fright, ␤-adrenergics, Alcohol, propranolol, senile) alcohol withdrawal, xanthines, primidone lithium, exercise Essential-kinetic- 3.5–6 Hands, head Anxiety, fright, ␤-adrenergics, Clonazepam, alcohol, predominant alcohol withdrawal, xanthines, ␤-adrenergic antagonists lithium, exercise Orthostatic 4–8, irregular Legs Quiet standing Repose, walking clonazepam, valproate Tremor of neuropathy 4–7 Hands Palatal myoclonus 60–100/min Palate, sometimes Clonazepam, valproic acid (1–2/s) facial, pharyngeal, proximal limb muscles 4777 Victor Ch 6 6/11/01 1:53 PM Page 47 approached. For this reason, it is sometimes mistakenly called an intention tremor. A slower type of essential tremor that is most apparent in the act of movement has been termed kinetic-predominant tremor. Essential tremor is the most frequent movement abnormality seen (400 to 2000 per 100,000 persons), and approximately 50 percent are familial. The inheritance pattern is autosomal dominant. The tremor usually appears during adult years, sometimes first in old age, when it is called senile tremor. Seldom is it manifest in a child. In a rare form of essential tremor, the lower limbs are involved disproportionately, most prominently during quiet standing (orthostatic tremor). There is controversy about the mechanism of essential tremor. One view is that it is merely an enhanced physiologic tremor. One type has been observed with a polyneuropathy (Adams et al). Young has ad- duced evidence in favor of a central origin, probably in the brainstem and cerebellum, but no pathologic change has been found in these parts. Brooks and Thach produced a similar tremor with lesions in the in- terpositus nucleus of the cerebellum, and it can be abolished ipsi- laterally by an infarct in the cerebellum and contralaterally by a ventrolateral thalamic lesion. More puzzling is its enhancement by adrenergic stimulation. The finer, more rapid varieties, disclosed by EMG recording, are due to simultaneous activation of agonist-antagonist muscles. It responds well to propranolol 40 to 80 mg tid and to other beta-adrenergic blocking agents, alcohol, and primidone 25 to 50 mg tid (see Fig. 6-1). The coarser essential-familial tremors correspond to alternating activation of agonist-antagonist muscles in a limb; in our experience, they are not reliably responsive to these medications. Diazepam sometimes proves to be helpful. The parkinsonian (rest) tremor has been mentioned in Chap. 4. It is a coarser 3- to 5-Hz tremor that involves the fingers, hands and arms, jaw, lips and tongue, and rarely the feet. It is present when the limb is in an attitude of repose and disappears momentarily upon voluntary movement. For this reason, it is seldom as disabling as the essential- familial type. It fluctuates in severity, being enhanced by excitement and reduced by relaxation. When studied physiologically, the tremor is seen to correspond with alternating bursts of activity in opposing muscle groups (Fig. 6-1). Often there is superimposed a faster-frequency action tremor. Most often it is a manifestation of Parkinson disease, but it may occur as an isolated phenomenon in an elderly person without akinesia, rigidity, or mask-like facies. Some of the antiparkinson drugs may alleviate the tremor, but often it does not respond to any known medication (see Chap. 38). So-called intention tremor, in contrast to the parkinsonian tremor, is absent when the limbs are inactive and even during the first part of a voluntary movement. The latter feature distinguished it from essential- 48 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE 4777 Victor Ch 6 6/11/01 1:53 PM Page 48 familial tremor, as does its conjunction with ataxia. However, as movement continues, and particularly if precision or fine control of the movement is required (e.g., touching the examiner’s finger) a slow (2- to 3-Hz), slightly irregular oscillation of the arm occurs. With bilateral cerebellar lesions, a rhythmic oscillation of the head (titubation), trunk, or outstretched arms may appear. The presence of these types of tremors always points to involvement of the cerebellum or its connections. CHAPTER 6 / TREMOR, MYOCLONUS, FOCAL DYSTONIAS, AND TICS 49 FIG. 6-1 Types of tremor. In each, the lowest trace is an acceleromet- ric recording from the outstretched hand; the upper two traces are surface electromyographs from the wrist extensor (upper) and flexor (middle) muscle groups. A. A physiologic tremor; there is no evidence of synchronization of electromyographic (EMG) activity. B. Essential-familial tremor; the movements are very regular, and EMG bursts occur simulta- neously in antagonistic muscle groups. C. Neuropathic tremor (Adams et al, 1972); movements are irregular and EMG bursts vary in timing between the two groups. D. Parkinsonian (“rest”) tremor; EMG bursts alternate between antagonistic muscle groups. Calibration is 1 s. (Cour- tesy of Dr. Robert R. Young.) 4777 Victor Ch 6 6/11/01 1:53 PM Page 49 Another group of coarse rhythmic tremors are more difficult to classify. One type is the wide-ranging tremor of the arms and trunk that occurs whenever these parts are activated. These oscillations may be of several inches in range; they are present from the instant of voluntary contraction and continue until the part is fully relaxed. The limbs are useless; the patient may need to sit or lie on the arms to stop the tremor. There may also be ataxia, but movements are so ineffectual that it is difficult to detect. Such coarse action or kinetic tremors occur in Wilson disease, in multiple sclerosis, and with vascular and other lesions that involve the dentatorubrothalamic pathway, usually at a mesencephalic level. It has been incorrectly called rubral tremor. Like the parkinsonian and coarse essential-familial tremors, it can be relieved by stereo- tactically placed lesions in the contralateral ventrolateral nucleus of the thalamus. Rhythmic contractions of the uvula and palate (1 or 2 per second), referred to as palatal myoclonus, are sometimes associated with coarse rhythmic nystagmus, and sometimes with contractions of ocular, facial, or shoulder muscles. We prefer to classify this as a tremor. But here the lesion (vascular, traumatic, neoplastic, degenerative) always involves the larger neurons of the lower part of the red nucleus or the central tegmental tract or an inferior olivary or ambiguous nucleus on one or both sides. An idiopathic variety has been identified. Clonazepam and valproic acid suppress the disorder. These several types of tremor must not be confused with myoclonus, asterixis (negative tremor), coarse fasciculations, or clonus, which are described below. ASTERIXIS This movement disorder consists of brief (35 to 200 ms), coarse arrhythmic lapses of sustained posture. Asterixis can be elicited in any muscle group that is under sustained contraction but most easily by hav- ing the patient hold the arms outstretched and the hands and fingers dorsiflexed; the latter then undergo abrupt flexion movements at irregular intervals. A fine asterixis of the fingers may simulate an irregular high-frequency tremor, and only EMG can separate them. In most instances, asterixis is a manifestation of a metabolic disorder, such as impending liver coma, uremia, hypercapnia, or drug intoxication (e.g., phenytoin). Fluctuations are to be expected as the metabolic disorder waxes and waves. Rarely, asterixis is unilateral, the result of a lesion in the contralateral ventrolateral nucleus of the thalamus or cerebrum. CLONUS, MYOCLONUS, AND POLYMYOCLONUS Clonus, myoclonus, and polymyoclonus are symptomatic of a large number of diverse neurologic disorders. Precise usage of these terms is 50 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE 4777 Victor Ch 6 6/11/01 1:53 PM Page 50 essential if they are to be neurologically meaningful. The following def- initions are in common use. Clonus refers to a series of rhythmic, uniphasic (undirectional) contractions and relaxations of a group of muscles. These movements involve only an agonist group of muscles and thus differ from tremors, which are diphasic (bidirectional) and involve both agonist muscles and their antagonists. Myoclonus specifies the arrhythmic, shock-like contractions of a muscle or group of muscles, almost always asynchronous and asym- metric on the two sides of the body. The contractions are extremely brief in duration (36 to 300 ms or less), much briefer than choreic movements. A single contraction or a few repeated contractions of this type are designated as segmental myoclonus or myoclonus sim- plex. Polymyoclonus refers to widespread lightning-like, arrhythmic contractions of muscles in many parts of the body. This is seen most often after a severe anoxic episode. It can be mistaken for tremor. The most common type of clonus occurs in relation to corticospinal tract lesions, when the spastic muscles are subjected to sustained stretch. A rhythmic type of palatal movement, incorrectly called palatal nystagmus or palatal myoclonus, has already been described. Epilepsia partialis continua is a special variety of clonus due to an ongoing seizure discharge, in which one group of muscles is involved in a series of rhythmic monophasic contractions, continuing sometimes for months or even years on end without spreading or becoming generalized. A special form of myoclonus may appear as a single massive flexor spasm of the neck, shoulders, arms, and trunk in West disease, which is one form of infantile or childhood epilepsy (salaam seizures). A less severe form of restricted myoclonus, usually appearing in the morning or with sleep deprivation, is part of juvenile myoclonic epilepsy. The latter is a common form of epilepsy that responds well to valproic acid. Polymyoclonus may occur in pure or “essential” form as a benign, nonprogressive familial disease. It may also be combined with epilepsy and dementia as in the several types of hereditary metabolic “storage” disease (Lafora body disease, cherry-red spot–myoclonus syndrome, lipid storage diseases). A form of polymyoclonus occurring with pro- jected movements follows recovery from hypoxic encephalopathy; it has been called action or intention myoclonus by Lance and Adams. In subacute spongiform encephalopathy (Creutzfeldt-Jakob disease), an abnormal startle response and polymyoclonus are combined with ataxia and dementia. Lithium intoxication has caused widespread myoclonus and confusion, simulating Creutzfeldt-Jakob disease. The pathophysiology of polymyoclonus must be varied. The frequent association with cerebellar ataxia points to a cerebellar, brainstem, or thalamic localization. Specific sensory evocation—by startle, auditory, CHAPTER 6 / TREMOR, MYOCLONUS, FOCAL DYSTONIAS, AND TICS 51 4777 Victor Ch 6 6/11/01 1:53 PM Page 51 visual, and proprioceptive stimuli—suggests a number of different mechanisms centered in the brainstem. Pharmacologic responses are interesting. The massive myoclonic (salaam) seizures of infancy and early childhood respond to adrenocor- ticotropic hormone (ACTH) and anticonvulsants. Epilepsia partialis continua is sometimes relieved by anticonvulsants. Clonazepam and valproic acid are useful in the treatment of action myoclonus. SPASMODIC TORTICOLLIS AND LINGUAL, FACIAL, OROMANDIBULAR, AND MANUAL SPASMS (FOCAL DYSTONIAS) These are involuntary spasms of a particular group of muscles. The spasms may be persistent or intermittent and tonic or irregularly clonic, resulting in a turning and retraction of the head, a forceful grimace, clo- sure of the eyelids, protrusion of the tongue, strained voice, pursing of the lips, or writer’s cramp. Like all involuntary movements, they are worsened by excitement and emotional upset. Some are observed only with a particular volitional and usually automatic movement, such as writing or playing a musical instrument. The patient cannot inhibit the spasms but usually discovers that certain maneuvers modulate or obscure them. As a rule, these movement disorders appear in midlife or later; once started, they seldom recede spontaneously; only rarely do they extend to other parts of the body. The overactive muscles undergo “work hypertrophy.” No pathology has been found in the brain in the few cases coming to postmortem examination. Although these disorders were formerly considered by some to be psychogenic, this hypoth- esis was never substantiated. Current opinion is that they are restricted forms of dystonia, a view supported by the observed cocontraction of agonist and antagonist muscles during the spasm. The following forms of localized spasms or dystonia, which may occur singly or in combi- nation, are recognized: a. Blepharospasm: Involuntary blinking or spasms of orbicularis oculi muscles. b. Spastic (better termed spasmodic) dysphonia: Strained voice due to spasm of laryngeal and respiratory muscles. c. Meige or Brueghel syndrome: Forceful jaw opening associated with spasms of facial and orbicular muscles. d. Spasmodic torticollis: Rotation and retraction of the head due to contraction of sternocleidomastoid, trapezius, and other neck muscles. e. Protrusion of the tongue. f. Writer’s cramp and related occupational spasms: Contraction of hand and forearm muscles during writing or performance of other skilled motor acts such as playing a musical instrument. 52 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE 4777 Victor Ch 6 6/11/01 1:53 PM Page 52 g. Dystonias provoked by neuroleptic drugs (“tardive dyskinesias,” Chap. 42). The most successful treatment consists of injecting small amounts of botulinum toxin at the innervatory point in the muscle, which often relieves the spasm for several months. The administration of gradually increasing amounts of trihexyphenidyl, until very large dosage is attained, is helpful in some cases (see also Chap. 38). Surgical dener- vation of affected muscles is a last resort. TICS These are quasivoluntary habit spasms; they consist of repeated twitches of a group of muscles, seemingly made to relieve an inner feel- ing of tension. The patient concedes that he makes the movements and that he can suppress them by force of will. The most frequent forms are blinking, sniffing, throat clearing, grimacing, hitching a shoulder, or throwing the head to the side or backward. Children 5 to 10 years old are disposed to the development of tics. Usually, if ignored, they last for only a few weeks. Less pressure, more rest, and a calmer environment are helpful. In others the tics persist into adult life and reappear or worsen whenever the individual is under pressure. If the tics are troublesome and persistent, small doses (10 to 25 mg) of chlorpromazine are helpful. Psychotherapy is of questionable value. A syndrome of multiple tics associated with sniffing, snorting, involuntary vocalization, and the compulsive utterance of obscenities (coprolalia) is the most severe of the tic syndromes (Gilles de la Tourette syndrome). The condition persists for weeks, months, or years. The cause and pathologic basis are not known, but a familial clustering is found in about one-third of the cases. The caudate nuclei have been implicated. There are no consistent psychiatric accompaniments except for a tendency to obsessive-compulsive personality traits. The administration of stimulants to hyperactive boys has preceded the syndrome in some instances. In some series of cases, there has been a higher than expected incidence of “soft neurologic signs” and “organic” impair- ment of intellect. Haloperidol (Haldol) in gradually increasing doses of 2 to 10 mg/day has been the most effective therapy. Pimozide, benz- tropine mesylate, or other antiparkinsonian drug may also be effective. RHYTHMIAS (MOVEMENT STEREOTYPES) In every institution for the mentally retarded, one witnesses a remark- able variety of rhythmic rocking, head-bobbing, hand-waving, eye-rub- bing, or other repetitive movements whenever the patient is idle. These CHAPTER 6 / TREMOR, MYOCLONUS, FOCAL DYSTONIAS, AND TICS 53 4777 Victor Ch 6 6/11/01 1:53 PM Page 53 are reminiscent of the head-banging of babies, but they persist through- out life, seemingly as an outlet for the universal impulse to fidget and squirm during idleness or to derive gratification from rhythmic activity. One of the most striking examples is the incessant hand-wringing seen in Rett syndrome. Their basis is unknown, and the universality of their occurrence in many different types of mental retardation argues against a fixed lesion. STARTLE This is a natural defensive reaction that, for reasons unknown, may in some families be excessive and insuppressible (hyperexplexia). It is also a cardinal feature of the spongiform encephalopathies (Chap. 32). AKATHISIA This term denotes a state of extreme motor restlessness. The patient cannot sit still; he is constantly squirming, shifting his weight, crossing and uncrossing his legs, standing up, walking in place, and pacing the floor. Originally observed in encephalitic illnesses, it is now observed most often as a complication of neuroleptic drugs—i.e., as a symptom of tardive dyskinesia (see Chap. 42). Administration of propranolol and similar drugs may be useful. For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 94–113. ADDITIONAL READING Adams RD, Shahani B, Young RR: Tremor in association with polyneuropathy. Trans Am Neurol Assoc 97:44, 1972. Brooks VB, Thach WT: Cerebellar control of posture and movement, in Brooks VB (ed): Handbook of Physiology, sec 1, The Nervous System, vol II, part 2, Motor Control, American Physiological Society, 1981, pp 877–946. Kennedy RH, Bartley GB, Flanagan JC, Waller RR: Treatment of blepharospasm with botulinum toxin. Mayo Clinic Proc 64:1085, 1989. Lance JW, Adams RD: The syndrome of intention or action myoclonus as a sequel to hypoxic encephalopathy. Brain 87:111, 1963. Lees AS, Robertson M, Trimble MR, Murray HMF: A clinical study of Gilles de la Tourette syndrome in the United Kingdom. J Neurol Neurosurg Psychiatry 47:1, 1984. Narabayashi H: Surgical approach to tremor, in Marsden CD, Fahn S (eds): Move- ment Disorders, London, Butterworth, 1982, pp 292–299. Sheehy MP, Marsden CD: Writer’s cramp—A focal dystonia. Brain 105:461, 1982. 54 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE 4777 Victor Ch 6 6/11/01 1:53 PM Page 54 [...]... of a single body segment, or somite The distribution of the dorsal roots on the surface of the body is illustrated in Figs 9-1 and 9 -2 4777 Victor Ch 9 pp7 5-8 7 6/11/01 1:55 PM Page 77 FIG 9-1 Distribution of the sensory spinal roots on the surface of the body, front and back (From Sinclair, with permission.) 77 4777 Victor Ch 9 pp7 5-8 7 78 6/11/01 1:55 PM Page 78 PART II / CARDINAL MANIFESTATIONS OF. .. 1980, vol I, part 5, pp 327 –605 Nathan PW: The gate-control theory of pain: A critical review Brain 99: 123 , 1976 Sato J, Perl ER: Adrenergic excitation of cutaneous pain receptors induced by peripheral nerve injury Science 25 1:1608, 1991 Scadding JW: Neuropathic pain, in Asbury AK, McKhann GM, McDonald WI (eds): Diseases of the Nervous System, 2nd ed Philadelphia, Saunders, 19 92, pp 858–8 72 Sinclair... Gerontol 24 :169, 1969 Nutt JG, Marsden CD, Thompson PD: Human walking and higher-level gait disorders, particularly in the elderly Neurology 43 :26 8, 1993 Sudarsky L: Geriatrics: Gait disorders in the elderly New Engl J Med 322 :1441, 1990 Sudarsky L, Simon S: Gait disorder in late-life hydrocephalus Arch Neurol 44: 26 3, 1987 Yakovlev PI: Paraplegia in flexion of cerebral origin J Neuropathol Exp Neurol 13 :26 7,... groups of motor neurons FIG 8 -2 Spinal cord showing topographic arrangement of nerve fibers within major tracts On the left are indicated the sensory modalities mediated by the spinothalamic tract and posterior funiculi: C, cervical; Th, thoracic; L, lumbar; S, sacral 65 4777 Victor Ch 08 pp6 2- 7 4 66 6/11/01 1:54 PM Page 66 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE FIG 8-3 Diagram of the... floor (astasia-abasia), sometimes despite the capacity to move the legs in bed (see Chap 55) 4777 Victor Ch 7 pp5 6-6 1 6/11/01 1:54 PM Page 61 CHAPTER 7 / DISORDERS OF STANCE AND GAIT 61 For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 114– 124 ADDITIONAL READING Martin JP: The basal ganglia and locomotion Ann R Coll Surg Engl 32: 219, 1963... degrees of this sequence may account for the nondementing gait of the elderly (upper line) Page 59 Fig 7-1 59 4777 Victor Ch 7 pp5 6-6 1 60 6/11/01 1:54 PM Page 60 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE Fig 7 -2 Diagram illustrating the changes in posture and gait that accompany aging (“senile gait”) With aging (figure on left) there occurs a decrease in the length of stride, in excursion of. .. identification and localization of pain sensation), whereas the more slowly conducting polysynaptic medial pathway subserves the affective aspects of pain (i.e., the unpleasant feelings engendered by pain) The segmental arrangement of nerve fibers within major tracts is illustrated in Fig 8 -2 and the main somatosensory and reticulothalamic pathways in Figs 8-3 and 8-4 4777 Victor Ch 08 pp6 2- 7 4 64 6/11/01 1:54... section of spinal cord, illustrating the course of afferent fibers and major ascending pathways Fast-conducting pain fibers are not confined to the spinothalamic tract but are also scattered diffusely in the anterolateral funiculus Several descending tracts are shown as landmarks Page 64 FIG 8-1 4777 Victor Ch 08 pp6 2- 7 4 6/11/01 1:54 PM Page 65 FIG 8-1 (continued) B Subdivision of the gray matter of the... awkwardly, the result of superimposed involuntary movements and postures— plantar flexion, dorsiflexion or inversion of the foot, momentary suspension of the leg in the air, twisting of the trunk or pelvis 4777 Victor Ch 7 pp5 6-6 1 6/11/01 1:54 PM The evolution of erect stance and gait and of paraplegia in flexion of cerebral origin, according to Yakovlev The ripening forebrain of the infant drives... dorsal horn of the spinal cord has been postulated to control or modulate incoming pain impulses Small neurons, believed to be capable of providing an inhibitory gating mechanism, are under the influence of peripheral afferent and descending neuronal systems Details of the gate-control theory and other theories of pain perception are discussed in Principles CLINICAL ASPECTS OF PAIN Activation of the nerve . excessive lateral movements of the trunk, imparting a roll or waddle. Due to impaired fixation of the weight-bearing hip, usually the result of weakness of gluteal muscles, particularly gluteus medius Disorders, London, Butterworth, 19 82, pp 29 2 29 9. Sheehy MP, Marsden CD: Writer’s cramp—A focal dystonia. Brain 105:461, 19 82. 54 PART II / CARDINAL MANIFESTATIONS OF NEUROLOGIC DISEASE 4777 Victor. neuropathy (Charcot-Marie-Tooth), progres- sive spinal muscular atrophy, and certain types of muscular dys- trophy. CHAPTER 7 / DISORDERS OF STANCE AND GAIT 57 4777 Victor Ch 7 pp5 6-6 1 6/11/01 1:54