Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relation between cerebrospinal fluid (CSF) and serum osmolality was studied in 16 patients with hyperosmolar hypernatraemic dehydration before treatment. After correcting shock and acidosis, 0-45% saline in 2-5 or 5% dextrose was infused in each patient over a 48- to 72-hour period. During rehydration, serum osmolality, electrolyte concentrations, urea nitrogen, and blood pH were measured sequentially. Five patients developed severe neurological abnormalities within 48 hours of addmission (convulsions 2, convulsions with hemiplegia 2, hemiplegia 1). Of these, 3 had residual defects on follow-up at least one year later. This group was indistinguishable from the 11 without significant neurological abnormality, both on clinical grounds before rehydration, and after analysis of admission and subsequent serum biochemical variables. A significant osmolar gap (greater than 4 mmol/kg H2O) between serum and CSF was found in 13 patients. Severe neurological disturbance only occurred when CSF osmolality exceeded that of serum by 7 or more mmol/kg H2O. Discriminant analysis of the paired osmolar data showed that D = -117+1-74 X(CSF osmolality) -1-41 X (serum osmolality), and that severe neurological abnormality was predicted when D was positive.
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PMID:Osmolar relation between cerebrospinal fluid and serum in hyperosmolar hypernatraemic dehydration. 1 53

Twenty-three children with 4 clinical subtypes of cerebral palsy were studied using 2-deoxy-2(18F)fluoro-D-glucose (FDG) and positron emission tomography (PET). Subtypes included spastic quadriparesis (N = 6), spastic diplegia (N = 4), infantile hemiplegia (N = 8), and choreoathetosis (N = 5). FDG-PET images were correlated with magnetic resonance imaging or computed tomography. Although the location of glucose metabolic abnormalities corresponded, in general, to abnormalities of brain structure demonstrated by structural imaging studies, the distribution of metabolic impairment almost invariably extended beyond the region of anatomic involvement. The following observations in specific subtypes of cerebral palsy were determined with FDG-PET: (1) In spastic diplegic patients, PET revealed focal areas of cortical hypometabolism in the absence of apparent structural abnormality; (2) A relatively normal pattern of cortical metabolism was observed in most patients with choreoathetoid cerebral palsy, despite marked hypometabolism in the thalamus and lenticular nuclei; and (3) In patients with infantile hemiplegia, FDG-PET disclosed symmetric cerebellar glucose metabolism with absence of crossed cerebellar hypometabolism (diaschisis). This finding is contrary to the typical persistence of crossed cerebellar diaschisis in adult patients with acquired cerebral lesions and suggests metabolic recovery due to developmental plasticity. The possibility that FDG-PET may be clinically useful in identifying the cerebral palsy patient with potential learning handicap and in the study of functional recovery or sparing following brain injury should be explored further.
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PMID:Regional cerebral glucose metabolism in clinical subtypes of cerebral palsy. 179 7

A 10-year-old boy known to have type 1 diabetes presented to the emergency department with history of sudden onset of right-sided hemiplegia after exercise. He did not respond to oral glucose administration, but had an almost immediate resolution of symptoms with intravenous bolus of dextrose. Hemiplegic hypoglycemia is a rare complication in diabetic children, mostly affects the right side of the body, and is rarely recurrent. Children have normal brain imaging and angiography testing, and electroencephalogram may show slow-wave activity. The recovery takes place within 24 hours, and the prognosis is excellent with no focal neurological deficits noted. Our patient responded within minutes to intravenous dextrose, which is unusual and has not been reported previously. The mechanisms leading to development of hypoglycemic hemiplegia are unclear, but may involve effects of hypoglycemia on intracellular signaling pathways or molecules on motor neurons, as recent studies have shown normal brain cell glucose uptake and metabolism in hypoglycemia. While hypoglycemic hemiplegia is rare, it is a frightening experience to caregivers, and efforts should concentrate on its prevention by preventing hypoglycemia.
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PMID:Exercise-induced hypoglycemic hemiplegia in a child with type 1 diabetes: a rare find with multiple potential causative mechanisms. 2216

Alternating hemiplegia of childhood is a rare, predominantly sporadic disorder. Diagnosis is clinical, and little is known about genetics. Glucose transporter 1 deficiency syndrome shares with alternating hemiplegia of childhood paroxysmal and nonparoxysmal symptoms. The aim of the study was to investigate glucose transporter 1 mutations in 30 Italian patients. Genetic material was analyzed by DNA amplification and glucose transporter 1 region sequencing. Mutational analysis findings of the SLC2A1 gene were negative in all patients. The pattern of movement disorders was reviewed. Interictal dystonia and multiple paroxysmal events were typical of alternating hemiplegia of childhood. In conclusion, alternating hemiplegia of childhood is a heterogeneous clinical condition, and although glucose transporter 1 deficiency can represent an undiagnosed cause of this disorder, mutational analysis is not routinely recommended. Alternatively, a careful clinical analysis and the 3-O-methyl-D-glucose uptake test can allow prompt identification of a subgroup of patients with alternating hemiplegia of childhood treatable with a ketogenic diet.
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PMID:Lack of SLC2A1 (glucose transporter 1) mutations in 30 Italian patients with alternating hemiplegia of childhood. 2289 93

Hypoglycemia is a common presenting feature of diabetes in the emergency department. Cardiovascular and neuroglycopenia features are well documented in the literature. We here report a case of 55-year-old female who came to our emergency with clinical features suggestive of cerebellar stroke. Laboratory investigations revealed severe hypoglycemia. The cerebellar signs and symptoms improved completely with intravenous dextrose infusion. Her MR imaging and Doppler of carotid and vertebrobasilar arteries were noncontributory. Hypoglycemia causes behavioral changes, confusion, loss of consciousness, and seizures. It is also well known to cause hemiplegia and aphasia. Hypoglycemia presenting as cerebellar stroke is rarely reported in the literature. This case highlights an uncommon manifestation of a common clinical condition. Physician must rule out hypoglycemia in every stroke patients.
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PMID:Severe hypoglycemia masquerading as cerebellar stroke. 2565 61