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)

One hundred and twenty-nine aortic aneurysm patients (true 68 and dissection 61) underwent aortic arch repair from January 1987 to December 1995. Postoperative brain damage was evaluated regarding both preoperative brain lesions and techniques of selective cerebral perfusion (SCP) in that one pump for SCP until April 1992, then two pumps were employed, one for right and the other for left hemisphere of the brain. Overall hospital mortalities were 21% in true and 13% in dissecting aneurysms. Ten patients were complicated with postoperative brain damages (coma 8 and hemiplegia 2), registering 7.8% of total patients. Both history of stroke and silent cerebral infarction (SCI) detected by CT and/or MRI were considered to be positive in the mean of having preoperative brain lesions. Although there was no significant difference between incidences of postoperative brain damage in true and dissecting aneurysms, registering 11% and 4% respectively, preoperative brain lesions in true aneurysm (68%) was significantly greater than dissecting aneurysm (32%). Furthermore, the incidence of postoperative brain damage was 22% in one-pump SCP which was significantly greater than 3% in two-pumps SCP in the patients with a true aneurysm. But there was no postoperative brain complication in patients with SCI even using either one two pumps for SCP. The present data suggest two-pumps SCP is better technique for cerebral protection compared to one-pump SCP for aortic arch repair.
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PMID:[Brain damage following aortic arch repair with regard to techniques of selective cerebral perfusion and preoperative cerebral lesions]. 952 20

A ten month old unconscious boy with hemiplegia (Hunt and Hess IV) was first admitted to a district hospital without a CT scanner or a neurosurgical service (Glasgow-Coma-Score 4, no pathological pupillary signs). Therefore, he was transferred to the Pediatric Department of the University Hospital the same night. An emergency CT scan that night showed intracerebral and subarachnoid hemorrhage with enlarged ventricle (Fisher grade 5). Angiography was not available within reasonable time. Thus in the stage of progressively increasing clinical deterioration, still without pupillary signs, an external ventricular drain-age was placed. Immediately after reduction of the cerebrospinal fluid volume, arterial hypertension was noticed--the right pupil was mydriatic and fixed. Without further apparative diagnosis an emergency craniotomy was performed for decompression under the suspicion of a secondary hemorrhage due to a rerupture of a middle cerebral artery aneurysm. A bleeding aneurysm of the right middle cerebral artery was found and clipped. A mass transfusion was necessary and a pulmonary air embolism occurred. The infant died in tabula. The histological specimens revealed disruption of the internal elastic membrane of both MCA. This emphasizes a congenital nature of the aneurysm. We conclude that cerebral arterial aneurysms have to be considered in the differential diagnosis of stroke-like symptoms in infancy and early childhood, although the incidence of reported cases is less than one case per year. Since no valid screening parameter is available, diagnosis is often made only after rupture of the aneurysm. This causes problems for emergency management. Infants and children with stroke or stroke-like symptoms should immediately be transferred to a hospital with a neurosurgical unit.
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PMID:Management of a ruptured cerebral aneurysm in infancy. Report of a case of a ten-month-old boy. 979 53

Carbohydrate-deficient glycoprotein syndrome type 1 (CDGS-1) is an autosomal recessive hereditary metabolic disorder, the gene locus of which is chromosome 16p13. The disorder is characterised by genetic heterogeneity, and by decrease in the gene product, phosphomannomutase 2, though the heterogeneity is far less manifest in affected Swedish families. Its incidence is 1/80,000 live births, and the under-5 mortality rate over 30 per cent. The causes of death are liver failure, cardiac tamponade, haemorrhaging, and severe infection. The characteristic biochemical aberration is the occurrence of deficient carbohydrate chains in many but not all circulating glycoproteins, and the serum and blood concentrations of some glycoproteins may be above or below normal. These changes may improve over time, but never normalise. The clinical picture is generally more problematic during the first years of life when psychomotor retardation is complicated by failure to thrive, liver dysfunction, pericardial effusions, and stroke-like episodes. In addition, strabismus, lipocutaneous anomalies, and gluteal fat pads are always present, and muscular hypotonia and restricted joint mobility are common. Failure to thrive is common, with vomiting and diarrhoea and subsequent slow growth. Inflammation is a constant finding in the liver, and very common in the small bowel. Pancreatic function is also affected. Pericardial effusion has been reported in 50 per cent of the youngest children, requiring pericardectomy in 30 per cent of cases. Haemorrhaging and thromboembolic complications may occur, and the serum concentrations of several factors and inhibitors are low, particularly those of factors V and XI, protein C and antithrombin. Stroke-like episodes occur in about 30 per cent of cases, often following an infection, with coma lasting for hours to several days. Such sequelae as hemiplegia, blindness, and other focal neurological pathology have been observed transiently. Diagnosis is based on the serum carbohydrate-deficient transferrin level, verified by isoelectric focusing. Molecular genetic procedures enable point mutations to be identified and prenatal diagnosis to be performed in many families.
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PMID:[CDGS-1--a recently discovered hereditary metabolic disease. Multiple organ manifestations, incidence 1/80,000, difficult to treat]. 988 93

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
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PMID:[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset]. 1006 67

We report a young patient who was operated on for a penetrating slow impact craniocerebral injury in the left frontal region caused by an axe. The patient was admitted comatose, with right hemiplegia. The blade of the axe was embedded deeply into his head. A craniectomy was carried out around the axe blade and it was removed easily. The cerebral wound was 6 cm long in horizontal plane and about 7 cm deep. Significant amount of contused and necrotic brain tissue was aspirated. The patient showed an uneventful recovery.
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PMID:Severe craniocerebral injury by an axe with good outcome: case report. 1021 80

A 20-year-old farmer who had headache and fever for 1 month, suddenly developed left hemiplegia, tremor in left arm and titubation followed by deep coma. Cranial CT scan revealed an infarction in right crus of midbrain. His CSF revealed 66 mg/dl protein, 10 lymphocytes/mm3, and 70 mg/dl glucose. CSF was positive for cryptococcal antigen. He improved following i.v. amphotericin 0.5 mg/kg and fluconazole 200 mg daily, continued for 6 and 12 weeks respectively. Infarctions though rare in cryptococcal meningitis should be considered in patients with chronic meningitis with vasculitis.
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PMID:Midbrain infarction: a rare presentation of cryptococcal meningitis. 1035 Jan 99

Massive cerebral infarction is often accompanied by early death secondary to transtentorial herniation. Decompressive hemicraniectomy has been suggested as a lifesaving procedure. We report the case of a 61 year old man who had an acute infarction in the distribution area of the right middle cerebral artery. Initially, he was awake and suffered from total left-sided hemiparalysis. Over the next two days, his level of consciousness deteriorated to a Glasgow Coma Scale score of 5. Intracranial pressure (ICP) monitoring was then established. Three days later, the ICP increased from 20 to 40 mm Hg. We performed a right-sided decompressive hemicraniectomy, and the ICP was normalized immediately. Ten months after surgery the patient was at home and functioning with minimal assistance. He had moderate paresis of the left leg and was able to walk, but his left arm was paralytic. The presented case confirms that decompressive hemicraniectomy may prevent death and allow survival without severe disability in patients with massive cerebral infarction.
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PMID:[Decompression craniectomy--life-saving treatment in acute cerebral infarction]. 1066 83

We conducted a retrospective review to specify the frequency, identify the aetiological factors of bacterial meningitis in adults (BMA) and to evaluate the therapeutic protocol used. This study was conducted on 85 (BMA) cases of hospitalised patients between January 1991 and December 1995 (5 years) on our service. The BMA represented 3% of all admissions for infectious diseases at the Foundation Jeanne Ebori in Libreville. It occurred in an endemosporadic fashion. All patients were Black Africans with an average age of 33 years (range: 16-60 years). Males predominated by a ratio of 2.4. Tha patients were seen late in the evolution of the disease, as shown by the folloxing clinical signs: neuropsychic problems (100%), 25 patients (29%) were in a profound coma, 5 (6%) had a hemiplegia, 2 (2%) an hypoacousie and 1 (1%) seizure. Aetiological factors were found in 17 cases (20%) to be in the ORL sphere (sinusitis: n = 8, ear infection: n = 4), pneumopathies (n = 4) and one case of breach dure-mere. The predominant germ was pneumocoque, isolated in 55 cases (65%), 15 cases had a LCR clear (18%). Bacteria gram negative (6%) were identified in the immunocompromised HIV. Third generation cephems had an efficiency higher than beta lactamines: 83% against 73%. The mortality was 18%; 3% of the remaining patients had neurological deafness. The seriousness of the results of this survey calls for the urgent implementation of a surveillance programme.
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PMID:[Bacterial meningitis in the adult. Study of 85 cases observed in the infectious disease unit of the Fondation Jeanne Ebori (F.J.E.), Libreville, Gabon]. 1069 Apr 60

Familial hemiplegic migraine is caused by CACNA1A missense mutations in 50% of families, including all families with cerebellar ataxia. A patient with healthy parents, who experienced prolonged attacks of migraine with hemiplegia, coma, and seizures, is reported. The patient also had mental retardation, permanent cerebellar ataxia with cerebellar atrophy, and right-sided brain atrophy. This patient carried a de novo Tyr 1385 Cys mutation in the CACNA1A gene and illustrates a novel phenotype associated with CACNA1A mutations.
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PMID:CACNA1A gene de novo mutation causing hemiplegic migraine, coma, and cerebellar atrophy. 1106 Dec 67

Patients surviving severe traumatic brain injury (TBI) often suffer from residual impairments in motor control, communication skills, cognition and social behaviour. These distinctly hamper their capability to return to their 'pre-trauma' activity. Comprehensive and integrated rehabilitation programmes initiate, during the acute phase, a prolonged treatment process which starts at the most sophisticated medical systems. There is no clear end point for the treatment of these patients, since the recovery process and the rehabilitation activity may continue for years, even after patients return home to live with their families. The inherent inability to make a firm early prediction regarding outcome of patients and the late appearance of additional symptoms stress the need for a comprehensive close long-term follow-up. The following presentation concerns the description of the treatment strategy and long-term improvement of a 22-year-old male who suffered from very severe TBI. On admission to the emergency room, he was in the decerebrated position and his Glasgow Coma Scale (GCS) was at the lowest (3). The focus of this presentation is on the recovery of motor function. The initial motor disabilities included weakness in all four limbs, in particular left hemiplegia, and right hemiparesis with severe bilateral ataxic elements and a marked tremor of the right arm. Range of motion was limited in hips, and he suffered from stiff trunk and neck. Goals of physiotherapy were directed towards improving range of motion (ROM) and active movement. Casting, use of orthoses, biofeedback, hydrotherapy, hippotherapy, medication and nerve blocks for reducing spasticity were timely applied during the process. The motor improvement in this very severe TBI patient who is now over 3 years post-injury still continues and has a functional meaning. He has succeeded in being able to stand up by himself from a chair and is able to walk unaided and without orthoses for very short distances--up to five steps. He is able to drink soup without assistance and play a few notes on the piano. Marked cognitive improvement occurred as well. It is concluded that motor improvement may be evident over long periods of time and various timely interventions may assist in the process.
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PMID:Combined motor disturbances following severe traumatic brain injury: an integrative long-term treatment approach. 1142 91


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