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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical observations suggest that overt rhabdomyolysis may occur if severe hypophosphatemia is superimposed upon a pre-existing subclinical myopathy. To examine this possibility, a subclinical muscle cell injury was induced in 23 dogs by feeding them a phosphorus- and calorie-deficient diet until they lost 30% of their original weight. To induce acute, severe hypophosphatemia in the animals after partial starvation, 17 of the dogs were given large quantities of the same phosphorus-deficient diet in conjunction with an oral carbohydrate supplement, which together provided 140 kcal/kg per day. After phosphorus and caloric deprivation, serum phosphorus and creatine phosphokinase (CPK) activity were normal. Total muscle phosphorus content fell from 28.0+/-1.3 to 26.1+/-2.5 mmol/dg fat-free dry solids. Sodium, chloride, and water contents rose. These changes resembled those observed in patients with subclinical alcoholic myopathy. When studied after 3 days of hyperalimentation, the animals not receiving phosphorus showed weakness, tremulousness, and in some cases, seizures. Serum phosphorus fell, the average lowest value was 0.8 mg/dl (P <0.001). CPK activity rose from 66+/-357 to 695+/-1,288 IU/liter (P <0.001). Muscle phosphorus content fell further to 21.1+/-7.7 mmol/dg fat-free dry solids (P <0.001). Muscle Na and Cl contents became higher (P <0.01). Sections of gracilis muscle showed frank rhabdomyolysis.6 of the 23 phosphorus- and calorie-deprived dogs were also given 140 kal/kg per day but in addition, each received 147 mmol of elemental phosphorus. These dogs consumed their diet avidly and displayed no symptoms. They did not become hypophosphatemic, their CPK remained normal, and derangements of cellular Na, Cl, and H(2)O were rapidly corrected. The gracilis muscle appeared normal histologically in these animals. These data suggest that a subclinical myopathy may set the stage for rhabdomyolysis if acute, severe hypophosphatemia is superimposed. Neither acute hypophosphatemia nor rhabdomyolysis occur if abundant phosphorus is provided during hyperalimentation.
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PMID:Hypophosphatemia and rhabdomyolysis. 74 77

A five-year-old boy is presented with an undifferentiated myopathy, retinitis pigmentosa, incomplete cleft lip, short stature (less than third percentile), mild delay in development, and seizures. To date, no etiology or pathogenetic mechanism has been discovered to account for these, and no similar cases have been encountered in the literature.
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PMID:Syndrome of myopathy, short stature, seizures, retinitis pigmentosa, and cleft lip. 89 94

HIV-1-related neurological diseases, excluding opportunistic infections and HIV encephalitis, are considered here. Most occur in severely immunosuppressed patients, with CD4 counts of under 200 x 10(6) l-1. Primary brain lymphoma and metastases from systemic non-Hodgkin's lymphoma, the second commonest cause of cerebral mass lesions in AIDS, are usually aggressive B cell tumours. Their poor median survival after treatment, compared with that of lymphomas in non-AIDS patients, seems related to systemic complications, particularly opportunistic infections. Kaposi's sarcoma produces neurological symptoms exceptionally. Cerebral infarction is often unrecognized clinically but large vessel arteritic occlusions may occur. Intracranial haemorrhages occur mostly in thrombocytopenic patients. Seizures are frequently referred to the neurologist; investigation may lead to a diagnosis of AIDS. Nearly 50% of patients with seizures have cerebral toxoplasmosis or cryptococcal meningitis; HIV-1 encephalitis is presumed to be the cause in 30%. A subacute or chronic vacuolar myelopathy with pyramidal and posterior column signs is the commonest form of spinal cord involvement in AIDS; its cause remains unknown. Peripheral nerve syndromes occur at all stages of HIV-1 infection. Distal symmetrical peripheral neuropathies are the most frequent, particularly a painful form with axonal atrophy, associated with CMV infection, and seen during ARC or AIDS. Mononeuritis multiplex due to vasculitis, CMV, or lymphoma and a serious lumbosacral polyradiculopathy due to CMV are infrequent. The commonest myopathy is due to zidovudine (AZT); it usually responds to drug withdrawal. The nature, prognosis and optimal management of most other myopathies is yet to be determined.
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PMID:Other neurological diseases in HIV-1 infection: clinical aspects. 134 49

In recent years there are a considerable increase in alcohol consumption in Taiwan, which may have been accompanied by increased incidence of alcohol-related physical disease. This study was designed for an understanding of neurological problems in chronic alcoholic patients. One hundred and five cases of chronic alcoholics with neurological problems were collected. All had taken more than 100 g alcohol daily for more than 8 years. They were all males, with a mean age of 47.0 +/- 1.3 years, mean daily alcohol consumption of 185.1 +/- 9.0 g (mean +/- S.E.). These chronic alcoholic patients showed various neurological problems. Patients showing typical clinical features of alcoholic neurological disease are now rather rare. Most of the patients had manifestations of more than one problems: polyneuropathy (74.3%), alcoholic tremor (37.1%), hallucinosis (30.5%), myopathy (26.7%), head injury (24.8%), withdrawal seizures (18.1%), Wernicke encephalopathy (15.2%), paranoia (13.3%), and stroke (15.2%). Furthermore, we divided all the patients into 5 categories, they were: encephalopathy, 59 cases (56.2%); stroke, 16 cases (15.2%); cerebellar degeneration, 12 cases (11.4%); neuropathy, 78 case (74.3%); and myopathy, 28 cases (16.7%). The daily alcohol consumption and duration of daily drinking were different significantly (p less than 0.05) among five different syndrome categories.
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PMID:Neurological problems in chronic alcoholics. 165 33

This article discusses the wide range of neurologic complications of HIV infection according to degree of advancement of systemic HIV disease. The focus is principally on those disorders that appear at least in part to be directly related to HIV: AIDS dementia complex, peripheral neuropathy, and myopathy. Unusual disturbances such as seizures and transient neurologic disorders are also discussed.
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PMID:Medical management of AIDS patients. Central and peripheral nervous system abnormalities. 172 42

A young boy, aged 5 years 7 months, presented with generalized hypotonia and proximal muscle weakness, and had exhibited delayed motor milestones since birth, He showed talipes planovalgus, a myopathic face, nasal tone vocalization, positive Gowers' sign and decreased tendon reflexes, but there was no intellectual impairment or seizure. The serum creatine kinase level and peripheral nerve conduction velocity, as well as the electromyogram and electrocardiogram, were within normal limits. A biopsy specimen from the left biceps brachii muscle revealed minimal nonspecific changes and mild variations in fiber size with an increased number of undifferentiated type 2C fibers, but no subcellular abnormalities were found on either the histochemical or electron microscopic examinations. The patient was diagnosed as having minimal change myopathy and improved clinically in muscle strength after one year of follow-up.
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PMID:Minimal change myopathy: report of a case. 198 82

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

The etiology of dementia can be diagnosed in most patients using a standard clinical approach consisting of physical, neurologic, and mental status examinations, and laboratory testing, lumbar puncture, and neuroimaging. In some cases, however, the clinical presentation or historical data are unusual, or the results of the workup are inconclusive or atypical. A rare cause of dementia may then be present and a complicated evaluation may be necessary to identify the specific disease process. A potentially useful approach to the diagnosis of rare dementing disorders consists of a series of diagnostic algorithms. This approach utilizes results of neuroimaging studies to guide the evaluation through additional diagnostic steps such as specific enzymatic or immunologic assays or biopsy of extraneural tissues. The disorders potentially detected by these algorithms typically have unusual clinical features such as early age of onset, abnormal neurologic signs and symptoms early in the clinical course, early personality and mood changes, extrapyramidal or cerebellar signs and symptoms, seizures, peripheral neuropathy or myopathy, and extraneural abnormalities involving the dermatologic, cardiovascular, musculoskeletal, or ocular systems. Accurate diagnosis of these rare causes of dementia is important for medical and psychiatric management, prognosis, and genetic counseling.
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PMID:Diagnosis of rare dementia syndromes: an algorithmic approach. 220 62

The spectrum of neurological complications associated with heroin addiction has changed in the past six years because of the progressive knowledge of the neurological complications related to HIV infection. We reviewed 48 heroin addicts with neurological complications and 452 heroin overdose who were seen in the Emergency Unit of our hospital during 1988 and the publications since 1967. Regarding the overdose we present the results of a prospective study leading to determine the causes. We emphasize the relationship with the level of total morphine in serum, instead of conjugate morphine, and with the presence of high levels of benzodiazepines found in the plasma rather than an hypothetic hypersensitivity phenomenon. We resume the neurological complications related with heroin addiction: spongiform leukoencephalopathy, epileptic seizures, stroke, transverse myelopathy and neuromuscular complications such mononeuropathy, plexopathy, acute inflammatory demyelinating polyradiculoneuropathy, rhabdomyolysis, fibrosing myopathy, musculoskeletal syndrome and acute bacterial myopathy. Some of such complications (i.e. transverse myelitis, polyradiculoneuropathy, leucoencephalopathy) must rise the suspicion of an HIV infection. Likewise, in patients assisted for overdosage we believe it's necessary rule out myoglobinuria by means of CPK serum levels and detection of urine hematic pigments without red blood cels in the urine sediment, in order to prevent and treat the renal failure. We report the results of muscular biopsy found in the musculoskeletal syndrome, which are similar to those found in alcoholic myopathy. Finally, we describe the clinical and diagnostic aspects in an unusually neuromuscular complication: the acute bacterial myopathy.
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PMID:[Non-infective neurologic complications associated to heroin use]. 256 83

Thirty-four nonambulatory patients with progressive neuromuscular spinal deformity were surgically managed using a 1/4" U-shaped double rod construct with segmental instrumentation from T2 to the pelvis accompanied by posterior spinal fusion. Diagnoses included 17 patients with cerebral palsy, six with spinal bifida, and 11 with other diseases (spinal muscular atrophy, Friedreich's ataxia, polyneuropathy, nemaline myopathy, and polio). Twenty-three patients had single uncompensated thoracolumbar curves, and 11 had a double curve pattern. The mean preoperative major curve was 66 degrees (range, 22-132 degrees), the secondary curve 58 degrees (range, 23-84 degrees). No postoperative spinal support was used. Mean curve correction was 36 degrees or 54.6%. There were four major complications, including two implant failures requiring revision and two patients sustaining excessive intraoperative blood loss necessitating completion of the procedure in a second stage. There were two neurologic complications including one case of postoperative seizures and an L4 monoradicular neuropathy in a spina bifida patient. Four patients had temporary postoperative ileus, one gastroesophageal reflex, and four had urinary tract infections. There were no significant postoperative pulmonary complications. Excluding the patients with rod failure, mean loss of correction at mean follow-up of 21.3 months was 6.5%. The stability and curve correction obtained using this system supports its continued use in patients with progressive neuromuscular scoliosis.
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PMID:Unit rod segmental spinal instrumentation in the management of patients with progressive neuromuscular spinal deformity. 261 59


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