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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.
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You will often see application and Activity used interchangeably. The difference between the two is that an application can be composed of multiple Activities, but one application must have at least one Activity. Each window or screen of your application is a separate Activity. Therefore, if you create a fairly simple application with only one screen of data (like the Hello World! application in this chapter), that will be one Activity. In future chapters you will create applications with multiple Activities.
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al) rather than solely in the cortex; this holds for postanoxic as well as traumatic cases. A review by H Adams and colleagues found these thalamic changes but attributed them to secondary degeneration from white matter and cortical lesions. However, in several of our cases the thalamic damage stood almost alone as the cause of persistent awake coma. In traumatic cases, the pathologic ndings are of diffuse subcortical white matter degeneration (described as diffuse axonal injury), prominent thalamic degeneration, and ischemic damage in the cortex. These anatomic ndings suggest the concept that PVS is a state in which the cortex is either diffusely injured or effectively disconnected and isolated from the thalamus. In either the traumatic or anoxic types of PVS, atrophy of the white matter may lead to ventricular enlargement and thinning of the corpus callosum. It is also noteworthy that a PVS may be the terminal phase of progressive cortical degenerative processes such as Alzheimer and Creutzfeldt-Jakob disease (where the pathologic changes may include the thalamus). In all these clinical states, the profound and widespread dysfunction of the cerebrum is re ected by extreme reductions in cerebral blood ow and metabolism, measured with positron emission tomography (PET) and other techniques. On the basis of PET studies in a patient with carbon monoxide poisoning, Laureys and colleagues observed that the main difference between the PVS and the recovered state was the degree of hypometabolism in the parietal lobe association areas. The nding in this PET study that noxious somatosensory stimulation fails to activate the association cortices is consistent with the concept that large regions of cortex are isolated from thalamic input. This view notwithstanding, there is little doubt that the neuroanatomic and neurophysiologic basis of the vegetative state will prove to be complex. Additional terms that have been used to describe this syndrome of preserved autonomic and respiratory function without cognition include apallic syndrome and neocortical death. A position paper has codi ed the features of the PVS and suggests dropping a number of related ambiguous terms, although some, such as akinetic mutism, discussed further on, have a more speci c neurologic meaning and still nd use (see Multi-Society Task Force on PVS). The condition of PVS blends into a state of profound dementia that has been recently termed the minimally conscious state, wherein the patient is capable of some rudimentary behavior such as following a simple command, gesturing, or producing single words or brief phrases, always in an inconsistent way from one examination to another (see Giacino and colleagues). Here there is preservation of the ability to carry out basic motor behaviors that demonstrate a degree of alertness at least at some times. The minimally conscious state is found as either a transitional or permanent condition and is dif cult to separate from akinetic mutism discussed further on. Any notion of such a patient s self-awareness is purely conjectural. The causes and pathologic changes underlying the minimally conscious state are identical to those of the vegetative state, including the frequent nding of thalamic and multiple cerebral lesions, and the distinction between them is one of degree. It is dif cult to predict which patients will fall permanently into the PVS category (see page 961). Plum and Posner have reported that of 45 patients with signs of the vegetative state at 1 week after onset, 13 had awakened and 5 of these had satisfactory outcomes; after being vegetative for close to 2 weeks, only 1 recovered to a level of moderate disability. After 2 weeks, the prognosis was uniformly poor. Larger studies by Higashi and colleagues
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