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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of hypertensive intracerebellar hematoma surgically treated and cured was reported. The 41-year-old male had two cerebrovascular attacks with headache and vomiting followed by left hemiparesis. Drowsiness and dysarthria appeared the next day. The patient was admitted to a hospital, where right facial palsy, loss of right gag reflex and paralytic hemiplegia on the left side were noted. On the 7th day, the patient's consciousness became clear byt the other neurological evidences did not change. On the 14th day, bradycardia and central hyperventilation appeared and he became drowsy again. The patient was transferred to the authors' clinic. When the patient was admitted, he showed typical cerebellar signs such as nystagmus, ataxia, and slurring speech with pyramidal sign on left side and cranial nerves paralysis on right side, and also showed the changes of vital signs as a medullary syndrome in the late stage of the course. The vertebral angiogram revealed a space taking process in the right cerebellar hemisphere. The old blood (30g) was removed by suboccipital craniectomy. The hematoma cavity had a communication with the IVth ventricle through a small perforation in the medial wall of the hematoma. Spontaneour intracerebellar hematoma including of hypertensive origin is not rare in the reports of autopsy but surgically treated case has only rarely been reported. The main reason of few survivals should be in its fulminate course.
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PMID:[A cured case of hypertensive intracerebellar hematoma (author's transl)]. 94 80

A 70 years-old man was admitted at our hospital because of unstable angina pectoris. He had essential hypertension and right hemiplegia from a ischemic stroke two years before admission. On neurologic examination, it was found mental disorientation, unstable emotionality, right spastic hemiparesis with right Babinski sign, and segmental myoclonus affecting the superior lip and the palate (palatal nystagmus) on the right side. On the CT scan, a giant aneurysm of the basilar artery was detected. We conclude that the segmental myoclonus could be explained by ischemic lesions in the Guillain-Mollaret triangle.
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PMID:Segmental myoclonus and basilar artery. Giant aneurysm. Case report. 130 61

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

Inverse ocular bobbing (IOB) is an uncommon abnormal eye movement. Its characteristics are slow downward eye movement with rapid upward return, a nadir at the extreme of downgaze position and horizontal roving eye movement. We present a case of IOB associated with cerebral embolism and diabetes insipidus. A 69 year-old right-handed woman was admitted because of a consciousness disturbance. She had been well until November 10, 1983, when she was found dysarthric and left hemiplegic. On admission, she was stuporous. There were conjugate deviation to the right, central left facial and hypoglossal palsy, left hemiplegia with spasticity, left hyperreflexia with positive pathologic reflex and anosognosia. A CT scan performed on November 11 showed extensive hypodense area in the region supplied by the right middle cerebral artery. A right carotid angiography revealed multiple occlusions in the top of the right internal carotid artery with poor collateral circulation. After admission, the level of consciousness gradually deteriorated and became comatose on November 18, when the following abnormal eye movements were observed. Following spontaneous horizontal roving eye movement, both eyes deviated downward slowly from midposition, taking 1 to 2 seconds to reach the nadir. The eyes then remained in the position for 1 to 15 seconds, followed by a rapid return to the midposition. These abnormal eye movements are compatible with inverse ocular bobbing (IOB) described by Knobler. Electronystagmography detected typical IOB and spontaneous upward nystagmus. There was no evidence of hypoxia when these abnormal eye movements were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inverse ocular bobbing associated with cerebral embolism and diabetes insipidus--a case report]. 274 84

From 6 months of age on this girl experienced frequent episodes of hemiplegia involving both sides of the body and lasting up to 8 days. The attacks were often precipitated by tonic deviation of the head and/or the eyes to one side and nystagmus. At this stage the girl used to cry. Squinting, tonic stiffening of body and extremities, and dystonic posturing also occurred. Autonomic dysfunctions such as paleness of the skin, sweating, respiratory embarrassment, tachycardia, and mydriasis were associated features of the attacks. Motor and mental development of the girl is delayed. Improvement concerning severity, duration and frequency of the attacks has been achieved by permanent treatment with flunarizine in combination with acetazolamide and acetylsalicylic acid. If the child falls asleep immediately after rectal application of chloral hydrate at the onset of an attack there is no hemiplegia after awakening.
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PMID:[Alternating hemiplegia in childhood. Clinical report and single photon emission computed tomography study]. 326 84

A case of spongy glio-neuronal dystrophy is reported. The clinical features included mental and motor retardation in early infancy after a normal birth, and from the age of 4 years increasingly severe attacks of multifocal epilepsy, with prolonged postictal coma, myoclonic twitching and nystagmus, and at times hemiplegia for one to two weeks. Acidosis was present during the periods of postictal coma. Jaundice occurred several days before death at the age of 5 years. Neuropathological examination revealed severe spongy degeneration in the thalamus and dentate nucleus, and the cerebral cortex to a lesser degree, with sparing of the white matter. There was partial necrosis of liver cells and in some areas regenerative nodules. Possible aetiological factors linking the cerebral and hepatic pathology are discussed.
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PMID:Spongy glio-neuronal dystrophy: a degenerative disease of the nervous system. 469 90

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
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PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78

Five cases of alternating hemiplegia in infancy are reported. Special consideration is given to the associated ictal manifestations (tonic seizures, dystonic posturing and abnormal movements bouts of nystagmus and acute autonomic disturbances), some of which were noted in every case. Previously reported cases are reviewed critically, 14 of whom are considered to belong to the same syndrome as the five presented here. The nosology of the syndrome is discussed, and the differences between alternating hemiplegia and the common types of hemiplegia or basilar migraine are emphasized. Whatever its exact nature, alternating hemiplegia in infancy constitutes a well-defined and recognizable syndrome, with a guarded mental and neurological prognosis.
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PMID:Alternating hemiplegia in infants: report of five cases. 745 Mar 4

By analogy with ophthalmic migraine, hemiplegic migraine is defined by the occurrence during the attacks of unilateral weakness. This simple definition is however far from reflecting the wide range of clinical situations reported under this term. Familial hemiplegic migraine (FHM) is a well individualized autosomal dominant condition. Attacks start in childhood, adolescence, or early adulthood. They invariably include a unilateral weakness lasting 30 to 60 minutes and almost always associated with visual, sensory, or speech disturbances. They are occasionally very severe with a dense hemiplegia, confusion, coma or fever, but they always completely recover. Brain neuroimaging is normal. In 20% of the families, migraine is associated with permanent neurological signs, mainly nystagmus and cerebellar ataxia. FHM is a genetically heterogeneous condition, with half of the families linked to chromosome 19 and the other half in which this link is excluded. By contrast to FHM, which is a well defined entity, other varieties of so called hemiplegic migraine do not deserve to be individualized as such. They include attacks of migraine with typical aura when a unilateral weakness is part of the aura, severe hemiplegic attacks similar to those reported in FHM but sporadic, migrainous infarcts with hemiplegia, and, for some authors, alternating hemiplegia of childhood. The pathogenesis of all these conditions and of migraine itself remaining largely unknown, it is currently impossible to know whether or not they share common pathophysiologic mechanisms. The identification of the gene on chromosome 19 and the discovery of other genes will be major steps to elucidate this question.
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PMID:[Hemiplegic migraine]. 789 22

Alternating hemiplegia of childhood is a rare syndrome characterized by onset before 18 months of age of frequent attacks of alternating paralysis, transient ocular palsies, nystagmus, choreoathetosis, and autonomic dysfunction. We describe features of 10 patients followed for up to 27 years. The mechanism of alternating hemiplegia remains unknown but an association to migraine is suspected because of the strong family history of migraine and aura symptoms in some patients. We treated nine patients with flunarizine, a calcium channel blocker, for up to 5 years; they showed a reduction in duration of the hemiplegic attacks, but the episodes ceased completely in only one patient. With long-term follow-up, the persistent motor, movement, and cognitive deficits are more apparent. It is not certain if the flunarizine alters this course.
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PMID:Alternating hemiplegia of childhood: a study of 10 patients and results of flunarizine treatment. 842 8


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