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Group atrophy denotes enlarged motor units where all the bers in the group are reduced to the same size; this is typical of progressive denervation Normally, the bers of each motor unit are not clustered, so that when grouping occurs it means that some bers of a denervated unit have been adopted by an adjacent intact motor unit This change typi es axonal neuropathies and many spinal cord diseases that affect the anterior horn cell A related change is particularly well shown in histochemical stains for ATPase, phosphorylase, and oxidases, where the normal mosaic pattern of ber types is altered The use of these stains reveals ber type grouping, the most speci c histologic evidence of denervation and reinnervation Here, muscle bers of similar histochemical type form groups of 15 or more bers as a result of reinnervation by a single motor neuron The diagnosis of denervation atrophy can usually be made from the clinical and EMG examinations; seldom is biopsy necessary for this purpose, but it is still utilized in cases of possible ALS, for example, where the diagnosis remains uncertain after other testing Segmental necrosis of muscle bers with myophagia and various manifestations of regeneration These are the typical changes in idiopathic polymyositis (in combination with in ltrates of in ammatory cells), and infective polymyositis (in the presence of Trichinella, Toxoplasma) These changes may also be observed in more limited form in Duchenne and other rapidly progressive muscular dystrophies In ammation and vasculitis Lymphocytic in ltration of the endomysium is most characteristic of polymyositis and in dermatomyositis it may be predominantly perimysial The lymphocytic in ltrate is often orid in these two processes, whereas it tends to be less intense in inclusion body myositis Lesser degrees of in ammation are common in the myopathies associated with Sjogren syndrome, mixed connec tive tissue disease, and scleroderma Numerous other processes including the infections mentioned earlier and some dystrophies (especially the fascioscapulohumeral type) may be associated with an in ammatory reaction There is usually acute myo brillar destruction in regions of maximal lymphocytic in ltration The muscle is a frequent site of in ammatory vascular destruction (vasculitis) in systemic diseases such as polyarteritis nodosa, and for this reason it is often useful to obtain a small sample of muscle adjacent to a nerve biopsy The nding of a granulomatous myopathy may indicate the presence of systemic sarcoidosis Alterations in the protein and histochemical composition of muscle bers may be shown by special stains for enzymes, glycogen, and structural proteins that are implicated in disease For example, it has become possible to detect the absence or de ciency of speci c structural proteins of the muscle membrane that de ne each of the muscular dystrophies: dystrophin, sarcoglycan, laminin, as discussed in Chap 50 These tests require rapid freezing (in a cryostat) rather than formalin xation Also, a number of enzymatic de ciencies and intra ber glycogen storage that lead to weakness and muscle fatigue may be detected by appropriate histochemical staining (Chap 51) Unusual changes of muscle bers Included here are sarcoplasmic masses and disorganized ring or serpentine collections of myo brils and myo laments (Ringbinden) in myo-.

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after many minutes, seizures and coma The diagnosis depends largely on the history, the documentation of reduced blood glucose during an attack, and reproduction of the patient s spontaneous attacks by an injection of insulin or hypoglycemia-inducing drugs (or ingestion of a high-carbohydrate meal in the case of reactive hypoglycemia) Acute Blood Loss Acute hemorrhage, usually within the gastrointestinal tract, is a cause of weakness, faintness, or even unconsciousness when the patient stands suddenly The cause (gastric or duodenal ulcer is the most common) may remain obscure until the passage of black stools Transient Cerebral Ischemic Attacks The many symptoms comprised by these attacks in the carotid system are fully described in Chap 34, but syncope is not one of the clinical presentations In the case of attacks in the vertebrobasilar territory, an impairment of consciousness is a rare manifestation, but almost always in the context of additional signs of upper brainstem dysfunction The above described syncope of aortic arch occlusive (Takayasu) disease is, however, usually associated with TIAs, some elicited by effort or exercise Drop Attacks This term is generally applied to falling spells that occur without warning and without loss of consciousness or postictal symptoms The patient, usually elderly and more often female, suddenly falls down while walking or standing, rarely while stooping The knees inexplicably buckle There is no dizziness or impairment of consciousness, and the fall is usually forward, with scuf ng of the knees and sometimes the nose The patient, unless obese, is able to right herself and to rise immediately and go her way, quite embarrassed There may be several attacks during a period of a few weeks and none thereafter The interval EEGs and ECGs are normal One potential mechanism is a lapse of tone in leg muscles during the silent phase of an unnoticed myoclonic jerk Drop attacks also occur in hydrocephalics, and these patients, though conscious, may not be able to arise for several hours Drop attacks as de ned above are usually without an identi able mechanism, requiring no treatment if cardiologic studies are normal On uncertain grounds, they are often attributed to brainstem ischemia In only about one-quarter of such cases, according to Meissner and coworkers, can an association be made with cardiovascular or cerebrovascular disease, to which treatment should be directed Rare instances of Meniere disease, in which the patient is suddenly ` thrown to the ground ( otolithic catastrophe of Tumarkin, page 260) may be mistaken for a syncopal or drop attack, but only brie y, until vertigo becomes prominent Seizures and Syncope In the nal analysis, the loss of consciousness in the different types of syncope must be caused by impaired function of the neural elements in those parts of the brain subserving consciousness, ie, in the high brainstem and thalamic reticular activating system In this respect syncope and primary generalized (so-called centrencephalic) epilepsy have a common ground; yet there is, of course, a fundamental difference In epilepsy, whether major or minor, the arrest in consciousness is almost instantaneous, and, as revealed by the EEG, is accompanied by a paroxysm of electrical activity occurring simultaneously in all of the cerebral cortex and thalamus The EEG changes (mainly by way of diffuse slowing delta waves) in syncope appear later in the course of the attack The difference relates to the essential pathophysiology the rapid spread of an electrical discharge in epilepsy and a more gradual failure of cerebral circulation in syncope There are also a number of important clinical distinctions between epileptic and syncopal attacks The epileptic attack may oc-.

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the screen There are six different standard commands that you can use and apply to the Web items, described next