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

While post-vaccinal encephalitis in children is unfortunately well known, its occurrence in adults is rather exceptional. The calendar of a poly vaccination situated so close to each other, most probably account for such an evolution. The case reported concerns a man of 27 years who presented 10 days after a polyvaccination (7 vaccines in 2 months) altered consciousness, epileptic fits, right hemiplegia, vegetative dysfunctions and meningeal status. Evolutionary clinical course led to death in 21 days. Neuropathological findings showed lymphocytic infiltrates in the cortex and basal ganglia, congestive aspect with petechial areas in the white matter and inflammatory meningeal infiltrates. All viral investigations both in the blood, brain and cerebrospinal fluid remained negative. Post-vaccinal encephalitis is reviewed. Vaccination cannot be condemned, but in case of polyvaccination lapse of time in between vaccines should be longer so as to prevent such exceptional evolution and fatal course.
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PMID:[Postvaccinal encephalitis in adult. A case with anatomo-clinical report (author's transl)]. 4 21

The factors underlying acute infantile hemiplegia are seldom identified. Coxsackie A9 focal encephalitis was documented for the first time in a 3-month-old infant with fever, hemiconvulsions, and hemiplegia followed by a static motor deficit and epilepsy. It has been suggested that the acute infantile hemiplegia associated with encephalitis results from an arteritis or venous sinus thrombosis with subsequent cerebral infarction. However, this was not observed in our patient. Rather, a series of brain scans, computerized tomograms, and a cerebral angiogram clearly documented the evolution of a focal necrotizing encephaloclastic process resulting in a porencephalic cyst. Serial cerebrospinal fluid viral cultures were necessary to isolate the etiologic agent (tcoxsackie A9). The infant did not have a neutralizing antibody response to the infecting viral agent despite an apparently intact immune system, which possibly may be explained by the developed of immune tolerance or an insufficient amount of infecting viral antigen. This emphasizes that serologic studies alone may not be adequate to document an acute central nervous system viral infection. This patient also typifies the poor prognosis in infants presenting with acute hemiplegia, fever, and convulsions in the absence of cerebrovascular occlusion.
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PMID:Coxsackie A9 focal encephalitis associated with acute infantile hemiplegia and porencephaly. 19 71

The case histories of 125 children with hypertension and no apparent primary CNS disease were analyzed for neurological symptoms or complications. Eleven children had neurological symptoms of high blood pressure. In only one of these patients was the diagnosis of arterial hypertension made before the observation of the neurological findings. The symptoms were severe headache in eight children, convulsions and coma in four, hemiplegia in two, and impaired vision and apraxia in one child. Symptomatology was rapidly reversed by antihypertensive treatment in four children, while six had long-term stigmata and one child died in hypertensive crisis. Because elevated arterial pressure can cause severe neurological disease, routine blood pressure measurement in children--especially those with neurological symptomatology--is stressed.
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PMID:Central nervous system involvement in severe arterial hypertension of childhood. 51 Mar 17

The record of 67 cases under 15 years of age who were hospitalized during status convulsivus from 1975 to 1978, the 348 cases who visited the hospital for the first time with epilepsy (Oct. 1977 to Sept. 1978) and the 32 cases who were hospitalized during status epilepticus from 1969 to 1974 and who are being followed up as outpatients were studied. The frequency of status epilepticus was 8% among epileptic children. There was no difference in the frequency of incidence between male and female. Patients with mental retardation, however, were revealed to have status epilepticus twice to three times more frequently as compared to cases without mental retardation. The major seizure types of status epilepticus in childhood were generalized tonic clonic convulsion and unilateral clonic convulsion. In 25% of the cases, status epilepticus was the first ictal manifestation. The major cause of status convulsivus was epilepsy, followed by encephalitis and encephalopathy, but cases due to brain tumor were rare. The drug of first choice for status convulsivus is diazepam. If there is any difficulty in controlling status convulsivus with diazepam, it may be worthwhile to consider what the problem is, causes of status convulsivus, seizure type, or basic disease of the patient. The effective dose of diazepam was within the range of 0.3--0.5 mg/kg. When the effect is not sufficient, the dose of diazepam should be increased to 1 mg/kg while watching the general condition of the patient. Factors affecting the prognosis of status convulsivus were its cause, duration, onset age and effectiveness of therapy during the acute stage. The frequency of cases who suffered disability after status epilepticus was 56%. (transient disability 43%, permanent disability 13%) The most frequent type of transient disability was hemiplegia. Most epileptic children who had repetitive status convulsivus revealed psychomotor retardation before first status. Factors which cause repetitive status seem to be hemispheric brain damage or diffuse corticocentrencephalic damage.
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PMID:Therapy and prognosis of status convulsivus in childhood. 52 Sep 66

A series of ten cases of infantile hemiplegia with behaviour disorders and with of without fits treated by unilateral stereotactic amygdalotomy is described. Out of the eight cases with fits good releif was seen in six and amelioration of the seizures in two. The behavioural disorders were well controlled in all the patients. When this procedure is compared with hemispherectomy, it is felt that operation of stereotactic amygdalotomy can be done as the procedure of first choice. Some hypotheses have been advanced to explain the modus operandi of the operation.
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PMID:Why hemispherectomy? 78 68

1) Etiology of convulsions starting prior to two years of age was discussed in 418 cases. Neonatal seizures before 30 days old appeared in 86 cases (53 boys and 33 girls). Three hundred and thirty-two patients (172 boys and 160 girls) had convulsions in infancy. Twelve patients (9 boys and 3 girls) suffered from convulsions both in neonatal and infantile period. 2)Etiology of convulsions was prenatal in 67 cases (16%), natal in 49 cases (12%), postnatal in 158 cases (38%) and unknown in 144 cases (34%). Prenatal factors consisted of cerebral malformation (23 cases, 6%), associated physical minor anomaly such as cataracta or finger abomaly (11 cases, 3%), abnormal pernatal history (8 cases, 2%), congenital heart disease 3) cases, 1%), tuberose scleorsis (7 cases, 2%) and positive family history (13 cases, 3%). Postnatal causes included hypocalcemia or hypoglycemia (7 cases, 2%), brain tumors (3 cases, 1%), breath-holding spells (21 cases, 5%), febrile convulsion (44 cases, 11%), bathing (3 cases, 1%), afebrile colds (3 cases, 1%), purulent meningitis (17 cases, 4%), DPT immunization (10 cases 2%), vaccination (7 cases, 2%) and acute hemiplegia (10 cases, 2%). The group of unknown etiology were as fns (38 cases, 9%), epilepsy associated with interictal signs (23 cases, 6%), benign infantile convulsions (57 cases, 14%), neonatal convulsion of unknown etiology (12 cases, 3%) and miscellaneous categories (4%). 3) Pregnancy was abnormal in 53% of cases with cerebral malformation. Asphyxia at birth was noted in 43% of patients with tuberose sclerosis and in 35% of congenital cerebral abomaly. 4) Pneumoencephalographic examinations revealed midline anomaly in 50% of cerebral malformation. It was abnormal in all cases with tuberose sclerosis, head injury and epilepsy with interseizure neurological signs. 5) There were no correlations between the seizure pattern and the etiology in neonatal convulsion. In infancy, focal-unilateral convulsions and infantile spasms were frequently associated with organic damages. Generalized seizures were seen in organic lesions as well as functional ones although approximately half of the cases were febrile convulsion, benign infantile convulsion or breath-holding spell. 6) EEG features of cerebral malformation were asymmetrical or multifocal dischages in neonatal period and hypsarhythmia or focal-unilateral spike discharges in infancy. Tuberose sclerosis showed hypsarhythmia in infancy. In birth injury or cerebral anoxia, EEG mostly revealed focal-unilateral abnormality or suppression-burst activity in newborns and hypsarhythmia or focal features in infants. 7) The occurrence rate of neonatal seizures in autopsy cases with intracranial pathology was demonstrated. EEG with intravenous diazepam was useful to know pathophysiology of infantile spasms.
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PMID:Etiology of convulsions in neonatal and infantile period. 99 19

36 original cases, 24 from the Hopital de Sainte-Anne in Paris and 12 from the surrounding region, of ischemic (30) or hemorrhagic (6) strokes in women taking oral contraceptives are reported. The patients were 20-55 years, half under 30; took various types of pills from 10 weeks to 10 years, mean 28 months; 30 of them for contraception but other for migraine, Reclus disease, amenorrhea, sterility, and endometri osis. 27 women had related history: ischemic vascular accident (5), hyp ertension (5), thromboembolism (4), Basedow disease (3), heavy smoking (3), essential comitiality (2), migraine (1), essential hyperlipidemia (1). The women with ischemic strokes were younger, 61% under 30. A 3rd had premonitory symptoms like headache, progressing rapidly to massive hemiplegia in 17, discrete hemiplegia in 11, loss of consciousness in 6, and convulsions in 3. The cerebrospinal fluid was clear in 11 cases tested. Angiography revealed lesions in the internal carotid in 4, sylvian arteries in 9, posterior cerebral in 1, but no anomaly in 8. Only 5 recovered completely: 3 died and 7 retained major neurologic dysfunction. 6 women had hemorrhagic strokes, 2 intracerebral hematomas, and 4 cerebromeningeal hemorrhages. 5 were operated on, 3 with good results and 2 were left with severe neurologic sequelae. The authors insisted that none of these women had been given any preliminary tests or followed with any attention to their related history while taki ng oral contraceptives.
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PMID:[Cerebrovascular accidents and oral contraceptives (reflections a propos of 36 observations)]. 121 91

We describe 3 children with a progressive encephalopathy that was characterised by irritability, convulsions, cranial nerve palsies, ataxia, nystagmus, walking difficulties, delayed psychomotor development, hemiplegia/tetraplegia, visual disturbance, vomiting, neck stiffness, and non-specific signs of raised intracranial pressure. A final diagnosis was made in all 3 patients from necropsy material. The clinical features were ascribed to multiple inflammatory, predominantly lymphocytic, reactions and raised intracranial pressure. This condition is an atypical form of haemophagocytic lymphohistiocytosis, which normally presents with fever, hepatosplenomegaly, and cytopenias. By contrast, the disease pattern in our 3 children was dominated by cerebromeningeal involvement, which can precede the typical systemic symptoms of haemophagocytic lymphohistiocytosis. An awareness of this condition is important because treatments are available.
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PMID:Cerebromeningeal haemophagocytic lymphohistiocytosis. 134 23

In a retrospective multi-center study, we investigated eighteen infants with unilateral cerebral infarctions confirmed by computed tomography (CT) scans. The initial symptoms were observed in all the patients between 0 and 3 days of age. Convulsions or apneic attacks were the initial symptoms in all but one. Only 4 patients had complicated obstetric histories and none showed polycythemia or electrolyte abnormalities. All of the initial CT scans revealed unilaterally localized hypodense areas. In 10, the initial CT scans were performed within 24 hours after the clinical onset. In 16, the lesions were within the territory of the middle cerebral artery, 9 of which also involved the cortico-spinal tract (CST). In the remaining 2 patients, the lesions were located within the territory of the posterior cerebral artery. None of the 9 patients without CST involvement developed hemiplegia, whereas 5 (56%) of the 9 with CST involvement had hemiplegia, which is a fairly low incidence compared with that in adult cases. This difference was thought to be related to neonatal brain plasticity.
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PMID:Neonatal cerebral infarction: symptoms, CT findings and prognosis. 159 May 27


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