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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Diagnosis of respiratory chain defects in cultured skin fibroblasts is a difficult diagnostic procedure. We investigated the feasibility of using survival of skin fibroblasts in culture medium with galactose as the major carbon source as a method of quickly diagnosing cell lines that were compromised in oxidative metabolism. We found that cells from patients with most forms of cytochrome oxidase deficiency, cells with complex I deficiency, cells with multiple respiratory chain defects and cells with severe pyruvate dehydrogenase (PDH) complex deficiency failed to survive when subcultured into galactose (5 mM) medium. Cells from patients with Lebers hereditary optic neuropathy (LHON), Kearns-Sayre syndrome (KSS), myoclonus-epilepsy-lactic acidosis-stroke (MELAS), the hepatic form of cytochrome oxidase deficiency, and mild PDH complex deficiency survived well in galactose (5 mM)-containing medium. This could be used as a rapid screening test for skin fibroblasts with major oxidative defects.
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PMID:Nonviability of cells with oxidative defects in galactose medium: a screening test for affected patient fibroblasts. 132 73

Drugs, either self-administered or prescribed by physicians, can result in substantial neurologic disability in psychiatric patients. It is clear that the use of neuroleptic agents to treat psychiatric illness may result in a variety of tardive movement disorders. Most commonly, these take the form of orobuccal dyskinesias, but choreic movements of the trunk and extremities, dystonic postures, myoclonus, tics, parkinsonism, and akathisic syndromes also may occur. The choreic tardive syndromes are thought to occur more commonly in the elderly female population, but tardive variants may affect a different population. The neuroleptic malignant syndrome carries a significant mortality and remains a diagnostic and therapeutic challenge. Early detection and vigorous treatment reduces the morbidity and mortality from this condition. Stroke, seizures, and various movement disorders may complicate the illicit use of cocaine and complicate the rehabilitation of those patients dependent on its use. The unsatisfactory treatment of tardive syndromes, neuroleptic malignant syndrome, and cocaine-induced neurologic disease underscores our incomplete understanding of the neurochemistry of dopamine, the function of newly discovered dopamine receptors, and the role they play in maintaining normal emotional and motoric function. For now, awareness of the varied neurologic syndromes related to neurotransmitter-modulating agents should provide the impetus for careful use of these agents and for the continued development of improved drugs for the treatment of psychiatric disease.
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PMID:Neurologic complications of drugs. Tardive dyskinesias, neuroleptic malignant syndrome, and cocaine-related syndromes. 135 Dec 85

A 9-year-old female MELAS patient with myoclonus is reported, with emphasis on the results of electrophysiological studies of the myoclonus. At age 5 years she experienced a stroke-like episode, and a diagnosis of MELAS was made at age 6 years on the basis of muscle biopsy findings. At age 9 years spontaneous and segmental myoclonus, predominantly affecting the upper extremities, developed because of complications. Electrophysiological examination, including of somatosensory-evoked potentials (SEPs) and averaged EMG for long loop reflexes, revealed so-called "giant SEP" and enhanced long loop reflexes reflecting cortical hyperexicitability. Jerk-locked averaging yielded no myoclonus related spikes, but myoclonus-contingent 4-5 Hz theta bursts appeared. These findings suggest that some types of MELAS may be associated with cortical types of myoclonus.
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PMID:Cortical reflex myoclonus associated with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS): a case report. 144 10

Point mutations of mitochondrial DNA have been described in the muscle of patients with syndromes of myoclonic epilepsy and ragged red fibres (MERRF) and of mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). We have found the MERRF mutation in members of 6 British kindreds; 2 of these had unusual phenotypes but all index patients had myoclonus. The MELAS mutation was detected in 17 patients from 16 families, who had a wide range of clinical features that particularly affected the central nervous system; stroke-like episodes were observed in 10.3 patients with mitochondrial DNA mutations did not have ragged red fibres on muscle biopsy, generally considered to be the morphological hallmark of mitochondrial diseases. In all 6 patients with the MERRF mutation, and 10 of 11 with the MELAS mutation, the genetic defect was easily detected in blood cells as well as muscle (blood samples were not available in 6 patients with MELAS mutations in muscle). Molecular genetic analysis of blood samples represents an inexpensive and reliable screening test for mitochondrial encephalopathies, and use of such techniques could influence diagnosis and genetic counselling in patients with seizure disorders and young-onset stroke.
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PMID:Mitochondrial encephalopathies: molecular genetic diagnosis from blood samples. 167 25

We describe 5 patients with a relapsing encephalopathy in association with Hashimoto's disease and high titers of anti-thyroid antibodies. The presentation is usually with a subacute onset of confusion, alteration in conscious level, and focal or generalized seizures. The relapsing course, association with myoclonus or tremulousness, and episodes of stroke-like deterioration are characteristic features. The long-term prognosis is favorable with steroid therapy, though additional immunosuppressive therapy may be required. Neurologic investigation typically shows a diffusely abnormal EEG, high CSF protein level without pleocytosis, and normal brain CT and cerebral angiogram. Isotope brain scan may show patchy abnormal uptake. Hashimoto's encephalopathy should be recognized as a definite neurologic entity and added to the list of CNS complications of thyroid disease.
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PMID:Hashimoto's encephalopathy: a steroid-responsive disorder associated with high anti-thyroid antibody titers--report of 5 cases. 199 66

Hypertrophic degeneration of the inferior olivary nuclei is the pathologic substrate for palatal myoclonus, but the physiologic correlate of this finding is uncertain. Using the 2-[18F]fluoro-2-deoxy-D-glucose and PET method, we determined the local cerebral metabolic rate of glucose utilization in seven patients with palatal myoclonus (following stroke or infection, or idiopathic), one patient with oculopalatal myoclonus (following a stroke affecting the brainstem), and nine normal subjects. The metabolism of glucose in the medulla of the patients with palatal myoclonus was significantly greater than that of the normal subjects. This may well have been due to increased metabolism of the inferior olivary nuclei. Glucose metabolism in the medulla of the patient with oculopalatal myoclonus was normal. These findings suggest that the inferior olivary nuclei, or a region of the brainstem encompassing the inferior olivary nuclei, are hypermetabolic in palatal myoclonus and may be the generators of the involuntary movements in palatal myoclonus.
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PMID:Increased glucose metabolism in the medulla of patients with palatal myoclonus. 201 Dec 57

We have reported the clinical and autopsy findings in a case with generalized seizures, myoclonus, blindness and deafness which was accompanied by stroke-like episodes. This case was diagnosed as mitochondrial encephalomyopathy, lactic acidosis & stroke-like episodes (MELAS) from these findings. Solitary and continuous lesions of softening were distributed in both hemispheres, more severely in the frontal and occipital poles. These lesions did not correspond to a vascular supply. The pulvinar, lateral and medial geniculate body of the thalamus, cerebellar vermis and dentate nucleus had small lesions of softening. The cortical lesions occurred mainly in layer 4, and the most prominent lesions among them appeared cystic, involving the subcortical white matter, but nerve cells in layer 1 and 2 were preserved. Proliferation of small blood vessels was seen around the softening areas. Electron microscopy revealed increased mitochondria in endothelial cells of these vessels, abnormal dense bodies in skeletal muscle cells and tightly packed mitochondria in choroid plexus epithelial cells. Immunohistochemical study suggested that vimentin positive cells were seen around lesions and proliferated vessels are different from those seen in the intact tissues.
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PMID:[An autopsy case of generalized seizures, myoclonus, blindness and deafness]. 220 39

Palatal myoclonus is a movement disorder consisting of rhythmic myoclonus of the soft palate, pharynx, larynx, and other muscles derived from the embryonal branchial arches. These movements are continuous and involuntary, and the patients are, in general, unaware of them. In the majority of patients, palatal myoclonus persists for life. In oculopalatal myoclonus, the eyes can be involved in the form of a nystagmus. Often a clicking noise in one or both ears is the initial symptom which can be heard by the examiner. A variety of etiologies have been linked to palatal myoclonus. The most common defined cause is a stroke. The variable delay between the proposed cause and the appearance of the disorder causes difficulties in determining the exact etiology. Pathologic findings show a transsynaptic hypertrophic degeneration of the inferior olivary nucleus which is due to a lesion of a specific, inhibitory, anatomic pathway. This somatotopic pathway leaves the contralateral dentate nucleus, passes through the superior cerebellar peduncle, and crosses the posterior commissure before joining the central tegmental tract and descending to the ipsilateral inferior olive. Treatment of palatal myoclonus is only occasionally effective. Some patients have responded to tryptophan, carbamazepine, and trihexyphenidyl. Surgical attempts have not been successful. - In the present paper the authors report on a case of an oculopalatal myoclonus following Leber's optic atrophy which involved the brain stem.
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PMID:[Etiology and clinical aspects of palatal myoclonus]. 224 51

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
Stroke 1990 May
PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51


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