PRINCIPLES OF NEUROLOGY - PART 9 docx

444 TABLE 46-2 Intrinsic Brainstem Syndromes Involving Cranial Nerves Eopnymic Cranial nerves Tracts and nuclei syndrome Site involved involved Signs Usual causes Weber Base of III Corticospinal tract Oculomotor palsy with Infarction, midbrain crossed hemiplegia tumor Claude Tegmentum of III Red nucleus and Oculomotor palsy with Infarction, midbrain brachium conjunctivum contralateral cerebellar tumor ataxia and tremor Benedikt Tegmentum of III Red nucleus, Oculomotor palsy with Infarction, midbrain corticospinal tract, and contralateral cerebellar hemorrhage, tumor brachium conjunctivum ataxia, tremor, and corticospinal signs Nothnagel Tectum of Unilateral or Superior cerebellar Ocular palsies, Tumor, infarction midbrain bilateral III peduncles paralysis of gaze, and cerebellar ataxia Parinaud Dorsal midbrain Supranuclear mecha- Paralysis of upward Pinealoma, nism for upward gaze gaze and accommo- hydrocephalus and other structures dation; fixed pupils and other lesions in periaqueductal gray of dorsal midbrain matter 4777 Victor Ch 46 p440-448 6/11/01 2:22 PM Page 444 445 Millard-Gubler Tegmentum and VII and often VI Corticospinal tract Facial and abducens Infarction or tumor and base of pons palsy and contralateral Raymond-Foville hemiplegia; sometimes gaze palsy to side of lesion Avellis Tegmentum of X Spinothalamic tract; Paralysis of soft palate Infarction or tumor medulla sometimes descending and vocal cord and sympathetic fibers, with contralateral Horner syndrome hemianesthesia Jackson Tegmentum of X, XII Corticospinal tract Avellis syndrome plus Infarction or tumor medulla ipsilateral tongue paralysis Wallenberg Lateral Spinal V, IX, X Vestibular nuclei, lateral Nystagmus, ipsilateral Occlusion of tegmentum spinothalamic tract, V, IX, X, XI palsy, vertebral or of medulla descending Horner syndrome and posteroinferior pupillodilator fibers cerebellar ataxia; cerebellar artery Spinocerebellar and contralateral loss of olivocerebellar tracts, pain and temperature medial longitudinal sense, ipsilateral central fasciculus facial analgesia, INO 4777 Victor Ch 46 p440-448 6/11/01 2:22 PM Page 445 or radiate from throat to ear, implicating the auricular branch of the vagus (hence, vagoglossopharyngeal neuralgia). Occasionally the pain activates afferent fibers in the ninth nerve, which in turn stimulate brainstem vasomotor mechanisms and induce bradycardia and vasode- pressor syncope. This condition should be treated like trigeminal neuralgia—i.e., with carbamazepine or other antiepileptic drugs. If this is unsuccessful, the glossopharyngeal nerve and upper rootlets of the vagus can be interrupted surgically. More often, cranial nerve IX is compressed together with nerves X and XI by a tumor (neurofibroma, meningioma, plasmacytoma, metastatic Ca) at the jugular foramen. Then there is hoarseness, difficulty in swallowing, deviation of the soft palate to the sound side (weakness of stylopharyngeus muscle), anesthesia of the posterior wall of the pharynx, and weakness of the upper trapezius and sternomastoid muscles (see Table 46-1). The lesion is often visible with MRI. The Tenth, or Vagus, Nerve Complete interruption of one vagus nerve intracranially results in ipsilateral weakness of the soft palate, deviation of the uvula to the normal side, unilateral loss of the gag reflex, hoarse voice and immobile vocal cord on one side, and loss of sensation in the pharynx, external auditory meatus, and back of the pinna. The vagus nerve on one side may be implicated at the meningeal level by tumors, granulomatous disease, and infective processes and within the medulla by vascular lesions (Wallenberg syndrome), by motor system disease, and occasionally by herpes zoster. It may be injured with the other lower cranial nerve by a number of processes including carotid artery dissection. The left recurrent laryngeal nerve, which has a longer course in the mediastinum than the right, may be compressed by an aneurysm of the aorta or a mediastinal or lung tumor. There is no dysphagia with such lesions because the branches to the pharynx leave the vagus nerve more proximally; only the vocal cord is paralyzed. Bilateral vagal lesions occur in some cases of Chiari malformation (defects on phonation and laryngeal stridor) and Shy-Drager syndrome (multiple system atrophy) and in rare instances of familial hypertrophic and alcoholic-nutritional polyneuropathy. Bilateral destruction of the nucleus ambiguus (motor system disease, poliomyelitis) is probably fatal. The Eleventh, or Accessory, Nerve This nerve has two parts: a major spinal one, derived from the anterior horn cells of the upper cervical cord, and a minor medullary one, which issues with the lower bundles of the vagus (vagal-accessory nerve). A complete lesion paralyzes the sternocleidomastoid and upper part of the trapezius muscles. Motor system disease, poliomyelitis, syringobulbia, 446 PART V / DISEASES OF PERIPHERAL NERVE AND MUSCLE 4777 Victor Ch 46 p440-448 6/11/01 2:22 PM Page 446 and Chiari malformation are well-documented causes. Intracranially or extracranially, where it leaves the skull, the eleventh nerve may be affected with cranial nerves IX and X and sometimes with XII (see Table 46-1). An idiopathic accessory nerve palsy akin to Bell’s palsy is also a known entity. Polymyositis may affect the trapezius and sternomastoid muscles bilaterally as well as the muscles of the pharynx and larynx and needs to be distinguished from bilateral eleventh-nerve lesions. Hypoglossal Nerve Lesions involving only the twelfth nerve are rare. It may be compressed by metastatic or meningeal tumor at or near the hypoglossal foramen, by the bony overgrowth of Paget disease of the clivus, or by a dissection of the carotid artery or in the course of carotid endarterectomy. Complete interruption causes unilateral weakness and atrophy of the tongue, with fasciculations. On protrusion, the tongue deviates to the affected side. Intramedullary lesions—those due to vertebral and anterior spinal artery thrombosis—simultaneously affect the pyramid, medial lemniscus, and hypoglossal nerve; the result is paralysis and atrophy of one side of the tongue together with spastic weakness and loss of deep sensation in the opposite arm and leg. Multiple Cranial Nerve Palsies Involvement of multiple cranial nerves may be due to intracranial extramedullary leptomeningeal carcinomatosis, tumors and granulomas, or lesions of the brainstem (infarcts, tumors, hemorrhages), in which case cranial nerve and long tract signs are conjoined. The extramedullary cranial nerve syndromes are listed in Table 46-1, and the intrinsic brainstem syndromes in Table 46-2. For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1370–1385. ADDITIONAL READING Devinsky O, Feldmann E: Examination of the Cranial and Peripheral Nerves. New York, Churchill Livingstone, 1988. Jannetta PJ: Posterior fossa neurovascular compression syndrome other than neu- ralgias, in Wilkins RH, Rengachary SS (eds): Neurosurgery. New York, McGraw-Hill, 1985, pp 1901–1906. Jannetta PJ: Structural mechanisms of trigeminal neuralgia: Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. J Neu- rosurg 26:159, 1967. CHAPTER 46 / DISEASES OF THE CRANIAL NERVES 447 4777 Victor Ch 46 p440-448 6/11/01 2:22 PM Page 447 Karnes WE: Diseases of the seventh cranial nerve, in Dyck PJ, Thomas PK, et al (eds): Peripheral Neuropathy, 3rd ed. Philadelphia, Saunders, 1993, pp 818–836. Lecky BRF, Hughes RAC, Murray NMF: Trigeminal sensory neuropathy. Brain 110:1463, 1987. Mayo Clinic and Mayo Foundation: Clinical Examinations in Neurology, 6th ed. St. Louis, Mosby–Year Book, 1991. Murakami S, Mizobuchi M, Nakashiro Y, et al: Bell palsy and herpes simplex virus: Identification of viral DNA in endoneurial fluid and muscle. Ann Intern Med 124:27, 1996. Silverman JE, Liu GT, Volpe NJ, Galetta SL: The crossed paralyses. Arch Neu- rol 52:635, 1995. Sweet WH: The treatment of trigeminal neuralgia (tic douloureux). New Engl J Med 315:174, 1986. Wilson-Panels L, Akesson EJ, Stewart PA: Cranial Nerves: Anatomy and Clini- cal Comments. St. Louis, Mosby–Year Book, 1988. 448 PART V / DISEASES OF PERIPHERAL NERVE AND MUSCLE 4777 Victor Ch 46 p440-448 6/11/01 2:22 PM Page 448 47 Principles of Clinical Myology: Diagnosis and Classification of Muscle Diseases The symptoms and signs of diseases of muscle, the diagnostic methods utilized in their detection, and the various means of treating them constitute a relatively new branch of medicine known as clinical myology. As one would expect from a tissue of uniform structure and function, the symptoms and signs by which diseases of striated muscle express themselves are also relatively uniform and few in number. Weakness, fatigue, limpness or stiffness, spasm, pain, a muscle mass, or change in muscle volume constitute the clinical manifestations. This explains the fact that many different muscle diseases share certain symptoms and syndromes. It is expedient, therefore, first to discuss the symptoms and signs common to all the diseases of striated muscle and in later chapters to specify those peculiar to certain diseases. Myopathic Weakness and Fatigue These two symptoms are often confused. While fatigue is a prominent feature of a few muscle diseases, the complaint of fatigue, without demonstrable weakness, is far more often indicative of anxiety, depres- sion, or an endocrine or other systemic disease (see Chap. 24). To dis- tinguish between weakness and fatigue, it is necessary to assess the patient’s capacity to walk and climb stairs and to arise from a sitting, kneeling, squatting, or reclining position. Difficulty in performing these tasks, either as a single test of peak power or repeatedly in tests of endurance, signifies weakness rather than fatigue. The same applies to difficulty in working with the arms above shoulder level. More localized muscle weakness is manifested by drooping of the eyelids; diplopia and strabismus; changes in facial expression and voice; difficulty in chewing and swallowing, closing the mouth, and pursing the lips; and failure of contraction of single muscles or groups of muscles of the limbs. Of course, impairment of muscle function may be due to a neuropathic or CNS disorder rather than a myopathic one, but usually these conditions can be separated by the methods described further on in this chapter and in Chap. 3. Ascertaining the pattern of muscle weakness, whether restricted or generalized, and its degree requires the systematic testing of the major muscle groups. The actions of the various muscle groups and their 449 4777 Victor Ch 47 p449-454 6/11/01 2:22 PM Page 449 Copyright 1998 The McGraw-Hill Companies, Inc. Click Here for Terms of Use. innervation have already been considered in relation to the peripheral nerve diseases (Table 45-3). Grading of Muscle Weakness Grading of muscle weakness by using a standard scale permits the accu- rate recording of the severity of weakness and comparison from one examination to another. The most widely used rating scale recognizes the following grades of muscle strength: 0 ϭ complete paralysis 1 ϭ minimal contraction 2 ϭ active movement, with gravity eliminated 3 ϭ weak contraction, against gravity 4 ϭ active movement against gravity and resistance 5 ϭ normal strength Finer degrees of weakness can be denoted by a plus or minus sign; e.g., 4ϩ would represent barely detectable weakness and 4Ϫ, easily detectable weakness. This permits the denomination of 10 gradations of muscle power. Such tests of peak power require the full cooperation of the patient, and the examiner must watch for signs of lack of effort or a “giving way” quality, which has the same significance. Pain during contraction may also hamper tests of strength (antalgic pseudoparesis). Topography or Patterns of Muscle Weakness Seldom is a primary disease of muscle the cause of an acute widespread paralysis; the usual cause of such a syndrome is acute polyneuropathy or some spinal cord disease. Nevertheless, in exceptional circumstances certain myopathic disorders can give rise to a rapidly evolving diffuse weakness: botulinus poisoning and rare instances of myasthenia gravis, hypo- or hyperkalemia, and the acute myopathy of critically ill patients that is associated with the combined use of high-dose steroids and neuromuscular blocking agents. Paresis of widespread distribution and subacute evolution (over a period of weeks) is attributable to a much wider spectrum of diseases, including some that are clearly myopathic, such as the infective and idiopathic polymyositides, dermatomyositis, and several of the metabolic myopathies. Each of the primary muscle diseases exhibits a par- ticular pattern of involvement. That is to say, a given pattern of muscle involvement tends to be similar in all patients with the same disease. Thus, topography or pattern of muscle affection becomes an important diagnostic attribute of myopathic disease, as indicated in Table 47-1. 450 PART V / DISEASES OF PERIPHERAL NERVE AND MUSCLE 4777 Victor Ch 47 p449-454 6/11/01 2:22 PM Page 450 451 TABLE 47-1 Patterns of Weakness in Myopathic and Neuropathic Diseases Pattern of weakness Causative diseases 1. Bilateral ocular palsies, strabismus, ptosis, Myasthenia gravis; oculopharyngeal dystrophy; exophthalmic ophthalmoplegia and impaired closure of eyelids—diplopia of thyroid disease; myotonic dystrophy; progressive external ophthalmoplegia; prominent, pupils spared botulism (autonomic symptoms are added) 2. Bifacial weakness—inability to smile, Myasthenia gravis; myotonic dystrophy; sarcoid; facioscapulohumeral dystrophy; expose teeth, and close eyelids centronuclear, nemaline, and carnitine myopathies; Guillain-Barré syndrome; Lyme disease, Möbius syndrome 3. Bulbar palsy—dysphonia, dysarthria, Myasthenia gravis; progressive bulbar palsy (ALS); myotonic dystrophy; botulism; dysphagia, amyotrophy of tongue; rarely polymyositis, Chiari malformation, and basilar invagination weak masseter and facial muscles in some 4. Cervical muscle palsies—inability to lift Polymyositis; inclusion body myositis; muscular dystrophy; rarely progressive head or extend neck spinal muscular atrophy (motor system disease) 5. Weakness of respiratory and trunk muscles Motor system disease; acid maltase deficiency; muscular dystrophy; GBS; myasthenia gravis 6. Bibrachial palsy—dangling arms Motor system disease (ALS); GBS or porphyria not usually a manifestation of muscle disease except scapulohumeral dystrophy 7. Bicrural palsy Usually a polyneuropathy or motor system disease 8. Limb-girdle palsies Polymyositis; congenital myopathies; progressive muscular dystrophy 9. Distal limb palsies—foot drop, steppage Distal muscular dystrophies; scapuloperoneal syndromes; Welander-Kugelberg gait, wrist drop, weak hands amyotrophy Familial polyneuropathies; chronic nonfamilial polyneuropathies 10. Generalized or universal paralysis Episodic: Hypo- or hyperkalemic paralysis Persistent: Werdnig-Hoffmann disease (infants); progressive spinal muscular atrophy (children); rarely advanced dystrophy; Guillain-Barré syndrome (acute) 11. Paralysis of single muscles or groups of muscles Almost always neuropathic or spinal; sometimes inclusion body myositis 4777 Victor Ch 47 p449-454 6/11/01 2:22 PM Page 451 Qualitative Changes in Muscle Contractility Apart from simple weakness and proportionate diminution in tendon reflexes, affected muscles undergo a number of special (qualitative) changes in function, mostly in relation to sustained activity. In myasthenia gravis, sustained or repeated muscle contraction rapidly induces increasing weakness and resting restores power. Thus, upward gaze that is held for 2 to 3 min causes progressive ptosis, which is quickly relieved by closing and resting the eyes; diplopia and strabismus increase with persistent horizontal or upward gaze; talking for a few minutes causes progressive dysarthria and nasality of the voice. These phenomena, by themselves, establish the diagnosis of myasthenia gravis. A state of weakness in which a series of successive contractions actu- ally increase the power of a group of muscles (e.g., abduction of the arm) is diagnostic of the myasthenic syndrome of Eaton-Lambert. Slowness and stiffness of contraction of the handgrip, which lessen with each contraction, are typical of myotonia; the opposite—increasing slowness and stiffness with each contraction (paradoxical myotonia)—occurs in some cases of Eulenburg paramyotonia. The fixed shortening of muscle that follows a series of strong contractions, especially under ischemic conditions (BP cuff on arm), is characteristic of McArdle disease (phosphorylase deficiency). This state, referred to as true contracture, needs to be distinguished from cramp and from pseudocontracture (myostatic contracture), which occurs whenever muscle is immobilized for a long period in a shortened position (spastic states, polyneuropathy, casting). Myotonia, a persistence of contraction for several seconds during attempted relaxation, is characteristic of myotonic dystrophy, paramyotonia congenita, hyperkalemic periodic paralysis, and congenital myotonia. This phenomenon may also be elicited by a sharp tap on the muscle belly (percussion myotonia). By contrast, the myoedema of cachexia and hypothyroidism is a localized bulge in muscle that appears at the point struck, without contraction of the entire muscle. Forceful voluntary contraction is necessary to evoke myotonia; thus, the eyelids open immediately after an ordinary blink but not after forceful closure, and the hand opens slowly and stiffly after being firmly fisted. Certain drugs (aromatic carboxylic acids) that derange Cl con- ductance channels in the sarcolemma may induce myotonia. Myotonia needs to be distinguished from neuromyotonia (see p. 492) and from the spreading tautness and gradual failure of relaxation that occur in mild or localized tetanus and in a number of rare illnesses characterized by excessive activity of spinal motor neurons discussed below. In the tetany of hypocalcemia, the muscle, once excited in any way, may remain in spasm (cramp) for a protracted period. 452 PART V / DISEASES OF PERIPHERAL NERVE AND MUSCLE 4777 Victor Ch 47 p449-454 6/11/01 2:22 PM Page 452 Other Features of Muscle Disease In addition to weakness, denervation of muscle causes a decrease in muscle tone. Infants with hypotonia are said to be “floppy.” This is an especially valuable finding in infants with muscular and neuromuscular disease, in whom graded tests of voluntary contraction cannot be per- formed. Fixed contractures of joints in a neonate, arthrogryposis, is indicative of weakness in utero (see Chap. 51). Diminution or increase in muscle bulk is another useful index of neuromuscular disease. Extreme atrophy (70 to 80 percent loss of bulk) is a mark of muscle dystrophy or of neural denervation. In the former, the atrophy is due to a reduction in the number of muscle fibers and in the latter, to a reduction in their size. Lesser degrees of atrophy (20 to 25 percent reduction in volume) result from disuse of muscle from any cause (disuse atrophy). Enlargement of muscle may be the result of persistent overactivity (work hypertrophy) or an early sign of certain dystrophies. Usually the enlargement in dystrophy is due to infiltration of fat cells, leaving the muscle in a weakened condition; this is called pseudohypertrophy. Twitches, spasms, and cramps are other natural phenomena that may assume prominence in certain muscle diseases. Fibrillations and fasciculations are described in Chaps. 3 and 44. Cramps are considered in Chap. 54. Fibrillations are an EMG change and are due to denervation. Fasciculations and cramps are due to hyperexcitability of motor units and, though ordinarily benign, become pronounced in motor system disease. In the latter condition they are always accompanied by weakness, atrophy, and reflex changes. Disinhibition of the inhibitory motor neurons of the spinal cord gray matter is the basis of the frequent and continuous spasms in tetanus and the “stiff-man” syndrome. Continu- ous muscle activity, wherein parts of many muscles or whole muscles are continually twitching, may be due to excessive irritability of motor units and may also be part of the more generalized twitch-myoclonus- convulsive syndrome of renal failure and hypocalcemia. Pain is a rare complaint in primary muscle disease. Even polymyositis and dermatomyositis are in most cases painless. The pain that follows intense overactivity of unconditioned muscles is probably due to single-fiber necrosis. However, when aching discomfort, especially after every attempt at exercise, is a major complaint, there may be some subtle disorder of muscle contraction, such as one caused by hypothyroidism or by an enzyme deficiency (e.g., a Ca-ATPase deficiency). More often, when pain is associated with evidence of neuromuscular disease, the lesion involves the nerves or blood vessels within muscles or the connective tissue or periarticular structures (e.g., polymyalgia rheumatica, fasciitis, Guillain-Barré syndrome, Lyme disease). Cramps of whatever cause are painful and leave the muscle tender. Most CHAPTER 47 / PRINCIPLES OF CLINICAL MYOLOGY 453 4777 Victor Ch 47 p449-454 6/11/01 2:22 PM Page 453 [...]... angiopathy) of childhood Medicine 45:261, 196 6 Engel AG, Hohlfeld R, Banker BQ: The polymyositis and dermatomyositis syndromes, in Engel AG, Franzini-Armstrong C (eds): Myology, 2nd ed New York, McGraw-Hill, 199 4, pp 1335–1383 Mikol J, Engel AG: Inclusion body myositis, in Engel AG, Franzini-Armstrong C (eds): Myology, 2nd ed New York, McGraw-Hill, 199 4, pp 1384–1 398 4777 Victor Ch 49 p46 0-4 66 49 6/11/01... Society of Medicine, 199 7 Engel AG, Franzini-Armstrong C (eds): Myology, 2nd ed New York, McGrawHill, 199 4 Harper PS: Myotonic dystrophy Philadelphia, Saunders, 197 9 Hoffman EP, Fischbeck KH, Brown RH, et al: Characterization of dystrophin in muscle-biopsy specimens from patients with Duchenne’s or Becker’s muscular dystrophy New Engl J Med 318:1363, 198 8 Rowland LP: Dystrophin: A triumph of reverse... prior knowledge of a few syndromes A description of these syndromes and the diseases of which they are a manifestation form the content of the chapters that follow (Chaps 48 to 54) For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1386–1401 ADDITIONAL READING Adams RD: Thayer lectures: I Principles of myopathology II Principles of clinical... and the end of the beginning New Engl J Med 318:1 392 , 198 8 Walton JN, Karpati G, Hilton-Jones D (eds): Disorders of Voluntary Muscle, 6th ed Edinburgh, Churchill Livingstone, 199 4 4777 Victor Ch 50 p46 7-4 74 50 6/11/01 2:25 PM Page 467 The Metabolic and Toxic Myopathies There are three classes of metabolic-toxic disease of muscle In one, striated muscle fibers are affected by a disorder of an endocrine... observed in 90 percent of gastrocnemii in people more than 60 years of age In addition, there are increasing accumulations of lipofuscin and signs of degeneration of single muscle cells Some of the remaining ones hypertrophy, so there is greater than normal variation in the fiber size These aging processes, occurring before their expected time (a kind of prese475 Copyright 199 8 The McGraw-Hill Companies,... dominant 4777 Victor Ch 49 p46 0-4 66 462 Table 4 9- 1 The Muscular Dystrophies Disease Duchenne/Becker Emery-Dreifuss Myotonic dystrophy (dystrophia myotonica) Proximal myotonic myopathy (PROMM) Congenital muscular dystrophy (CMD) Classic merosin-positive CMD Classic merosin-negative CMD Fukuyama CMD Walker-Warburg syndrome Muscle-eye-brain disease Facioscapulohumeral Scapuloperoneal Limb-girdle muscular dystrophy... discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1432–1448 ADDITIONAL READING DiMauro S (ed): Symposium: Mitochondrial encephalomyopathies Brain Pathol 2:111, 199 2 DiMauro S, Tonin P, Servidei S: Metabolic myopathies, in Rowland LP, DiMauro S (eds): Handbook of Clinical Neurology, vol 18, rev ed, Myopathies Amsterdam, Elsevier Science, 199 2, pp 4 79 526 Engel... 131:24, 197 2 Brooke MH: A Clinician’s View of Neuromuscular Diseases, 2nd ed Baltimore, Williams & Wilkins, 198 6 Engel AG, Franzini-Armstrong C (eds): Myology, 2nd ed New York, McGrawHill, 199 4 Fenichel GM, Cooper DO, Brooke MH (eds): Evaluating muscle strength and function: Proceedings of a workshop, Muscle Nerve 13(suppl):S1–57, 199 0 Walton JN, Karpati G, Hilton-Jones D (eds): Disorders of Voluntary... Society of Medicine Press, 199 7 Fardeau M, Tomé FMS: Congenital myopathies, in Engel AG, FranziniArmstrong C (eds): Myology, 2nd ed New York, McGraw-Hill, 199 4, pp 1487–1532 Kakulas BA, Adams RD: Diseases of Muscle: The Pathological Foundations of Clinical Myology, 4th ed Philadelphia, Harper & Row, 198 5 Kennedy WR, Alter M, Sung JH: Progressive proximal spinal and bulbar muscular atrophy of late onset Neurology. .. weakness of the paravertebral muscles results in kyphoscoliosis The tendon reflexes diminish in proportion to muscle weakness; Achilles reflexes are usually retained because of the relative escape of calf muscles The weakness of respiratory muscles and the kyphoscoliotic deformity become a 460 Copyright 199 8 The McGraw-Hill Companies, Inc Click Here for Terms of Use 4777 Victor Ch 49 p46 0-4 66 6/11/01 . Franzini-Armstrong C (eds): Myology, 2nd ed. New York, McGraw-Hill, 199 4, pp 1384–1 398 . CHAPTER 48 / THE INFLAMMATORY MYOPATHIES 4 59 4777 Victor Ch 48 p45 5-4 59 6/11/01 2:23 PM Page 4 59 49 The Muscular. discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1386–1401. ADDITIONAL READING Adams RD: Thayer lectures: I. Principles of myopathology. II. Principles of. York, McGraw-Hill, 198 5, pp 190 1– 190 6. Jannetta PJ: Structural mechanisms of trigeminal neuralgia: Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia. J Neu- rosurg

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