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ADAMS RD: Thayer lectures: I Principles of myopathology: II Principles of clinical myology Johns Hopkins Med J 131:24, 1972 ALEKSIC S, BUDZILOVICH C, CHOY A: Congenital ophthalmoplegia in oculoauriculovertebral dysplasia hemifacial microsomia (GoldenharGorlin syndrome) Neurology 26:638, 1976 ANDRE-THOMAS, CHESNI Y, SAINT-ANNE DARGASSIES S: The neurological examination of the infant, in MacKeith RC, Polani PE, ClaytonJones E (eds): Little Club Clinics in Developmental Medicine, No 1 London, National Spastics Society, 1960 ANDREU AL, HANNA MG, REICHMAN H, et al: Exercise intolerance due to mutations in the cytochrome b gene of mitochondrial DNA N Engl J Med 341:1037, 1999 ARMSTRONG RB: Mechanisms of exercise-induced, delayed onset muscular soreness: A brief review Med Sci Sports Exerc 16:529, 1984 BLEXRUD MD, WINDEBANK AJ, DAUBE JR: Long-term follow-up of 121 patients with benign fasciculations Ann Neurol 34:622, 1993 BRODY I: Muscle contracture induced by exercise: A syndrome attributable to decreased relaxing factor N Engl J Med 281:187, 1969 EDWARDS RHT: New techniques for studying human muscle function, metabolism and fatigue Muscle Nerve 7:599, 1984 ENGEL AG, FRANZINI-ARMSTRONG C (eds): Myology, 3rd ed New York, McGraw-Hill, 2004 FENICHEL GM, COOPER DO, BROOKE MH (eds): Evaluating muscle strength and function: Proceedings of a workshop Muscle Nerve 13(suppl):S1 57, 1990 FRANZINI-ARMSTRONG C: The membrane systems of muscle cells, in Engel AG, Franzini-Armstrong C (eds): Myology, 3rd ed New York, McGraw-Hill, 2004, pp 232 256 GOSPE SM, LAZARO RP, LAVA NS, et al: Familial X-linked myalgia and cramps: A nonprogressive myopathy associated with a deletion in the dystrophin gene Neurology 39:1277, 1989 GOWERS WR: A lecture on myopathy, a distal form BMJ 2:89, 1902 HOWELL DA, LEES AJ, TOGHILL PJ: Spinal internuncial neurons in progressive encephalomyelitis with rigidity J Neurol Neurosurg Psychiatry 42:773, 1979 KANDEL ER, SCHWARTZ JH, JESSELL TM (eds): Transmitter release, in Principles of Neural Science, 4th ed New York, McGraw-Hill, 2000, pp 253 279 KARPATI G, CHARUK J, CARPENTER S, et al: Myopathy caused by a de ciency of Ca-adenosine triphosphatase in sarcoplasmic reticulum (Brody s disease) Ann Neurol 20:38, 1986 KATZ JS, WOLFE GI, BURNS DK, et al: Isolated neck extensor myopathy: A common cause of dropped head syndrome Neurology 46:917, 1996 KUGELBERG E, WELANDER L: Heredofamilial juvenile muscular atrophy simulating muscular dystrophy Arch Neurol Psychiatry 75:500, 1956 MASTAGLIA FL, LAING NG: Investigation of muscle disease J Neurol Neurosurg Psychiatry 60:256, 1996 MIELKE U, RICKER K, EMSER W, BOXLER K: Unilateral calf enlargement following S1 radiculopathy Muscle Nerve 5:434, 1982 UMAPATHI T, CHAUDRY V, CORNBLATH D, et al: Head drop and camptocornia J Neurol Neurosurg Psychiatry 73:1, 2002 WALTON JN, KARPATI G, HILTON-JONES D (eds): Disorders of Voluntary Muscle, 6th ed Edinburgh, Churchill Livingstone, 1994 WELANDER L: Myopathia distalis tarda hereditaria Acta Med Scand 141(suppl 265):1, 1951 WOHLFART G, FEX J, ELIASSON S: Hereditary proximal spinal muscle atrophy simulating progressive muscular dystrophy Acta Psychiatr Neurol 30:395, 1955.

The discovery that striated skeletal muscle and cardiac muscle could be the sole targets of a number of infectious diseases came about during the era of the development of microbiology and occupied the attention of many prominent clinicians, including Osler As these diseases were being characterized, however, a number of other in ammatory states affecting muscle were found for which there was no infectious cause Later, an autoimmune mechanism was postulated, but even today this is not securely established This group of idiopathic in ammatory myopathies gures so prominently in clinical myology that the authors feel justi ed in devoting a chapter to the subject But rst, the infections of muscle are described

The commercial success of any product often results in products claiming to mimic its bene t The neurotransmitter-blocking peptides currently incorporated into cosmeceutical products were developed as topical mimics of the

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34-7 Two types of clinometer At A, the output voltage is a simple function of slope At B, upslope causes positive output voltage; downslope causes negative output voltage

cranial subarachnoid hemorrhage from a ruptured saccular aneurysm Treatment The rate of progression of the myelopathy from these various lesions varies greatly In some cases, as already noted, it may become a matter of some urgency to reverse the venous congestion and avoid infarction of the cord Other lesions require a more measured approach By occluding the feeding artery of a spinal AVM or stula, which is often single, and eliminating the pressure in veins, the course of disease can be arrested and pain reduced (Symon et al) In most of our cases, there has been postoperative improvement in the neurologic de cit over a few weeks or months In cases of the larger racemose AVMs, stripping the enlarged veins along the dorsal cord is no longer considered necessary and may be dangerous Increasingly, one resorts to obliteration of a stula or a reduction of the AVM by the use of endovascular techniques, using special catheters and varioius types of embolic particles The procedure is long and painstaking, for the radiologist must identify and embolize all the feeding vessels of the malformation; general anesthesia is required in most cases This approach has certain drawbacks; recanalization occurs in many instances, as does distal occlusion of the venous drainage system For these reasons, surgical ligation of the arterial supply is still preferred as the initial procedure for larger AVMs Some surgeons advise a staged approach in which the size of the malformation is rst reduced by endovascular techniques thereby making the surgery less complicated Intradural stulas are usually treated solely by endovascular methods Interventional radiologic techniques have also been used to advantage in the intramedullary malformations, either as the sole treatment or in combination with surgery Focused radiation has bee tried but the results are dif cult to evaluate since most series are small.

the vertebral body adjacent to a collapsed disc and herniation of disc tissue into a vertebral body (Tosi et al) The explanation suggested by Yogananden and colleagues is that the high intravertebral pressure forces nucleus pulposus material into venules and arteries of the marrow of the vertebral body, and thence into the adjacent radicular vessels This mechanism has probably been overlooked in many cases of acute ischemic myelopathy

Caisson Disease (Decompression Sickness, the Bends )

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