Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 5-year-old girl developed a progressive febrile neurological illness consisting of right focal seizures, right hemiparesis, and stupor evolving over a period of six weeks. During the month preceding the onset of her illness she had received two apparently unsuccessful smallpox vaccinations without a skin lesion. Elevation of cerebrospinal fluid gamma globulin and findings on brain biopsy were consistent with postinfectious encephalitis, and a simultaneous increase in serum vaccinia antibody titer suggested that the illness was postvaccinial encephalitis. Clinically, the child developed a severe extrapyramidal movement disorder during the acute phase followed by nine months of stuporous unresponsiveness, yet subsequently made a substantial recovery.
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PMID:Postvaccinal encephalomyelitis without cutaneous vaccination reaction. 3 58

Seven patients with cancer complicated by nonmetastatic sagittal sinus thrombosis were encountered in a 7-year period. Five had hematologic malignancies and two had solid tumors. There were two different presentations. In the first, neurologic signs and symptoms (e.g., headaches, seizures, hemiparesis, lethargy) occurred suddenly in five patients shortly after initiation of cancer therapy. Four of these five patients recovered with minimal residua; the fifth died as a direct result of the sinus thrombosis. The second presentation occurred in the two patients with terminal cancer who declined gradually without focal signs; both patients died. Only arteriography can reliably establish the diagnosis of sagittal sinus occlusion. In patients with cancer, sagittal sinus occlusion probably results from a "hypercoagulable state" associated with the systemic neoplasm.
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PMID:Nonmetastatic superior sagittal sinus thrombosis complicating systemic cancer. 28 38

A 40-year-old hypertensive black female, who suddenly developed aphasia, lethargy, and a right hemiparesis, and a 42-year-old non-hypertensive black male, who suddenly developed intractable headache, drowsiness, and vomiting, were found by angiography to have moyamoya disease. This condition is characterized by a decreased caliber of the internal carotid arteries and bilateral occlusion of the anterior and middle cerebral arteries with visualization of an extensive collateral network of tortuous blood vessels of the rete mirabile type at the base of the brain.
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PMID:Moyamoya disease in black adults. 44 57

A 41-year-old man is described in whom after a febrile disease with disturbances of sleep rhytm and exessive somnolence, extrapyramidal signs appeared increasing progressively in intensity, with a hypertonic-hypokinetic syndrome with evidence of right-sided spastic hemiparesis and hypaesthesia. After treatment with Viregyt and low doses of L-Dopa a striking improvement was obtained. Parkinsonism following lethargic encephalitis was diagnosed.
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PMID:[Parkinsonism following lethargic encephalitis]. 59 10

A simple implanted device was used to occlude acutely the left middle cerebral artery (MCA) of 16 conscious cats. Eight received no treatment and 8 were given intravenous mannitol (1.2 gm/kg) at the time of occlusion. The initial neurological findings in both groups were similar, that is, agitation, forced circling, and right hemiparesis. The treated cats remained alert but the untreated cats became lethargic and drowsy. Perfusion with a mixture of colloidal carbon and buffered paraformaldehyde was carried out from 30 minutes to 6 hours following MCA occlusion. Results of morphological examination of brains from the treated and untreated groups suggested that mannitol had a protective effect upon cerebral tissue during the primary phase of acute focal ischemia. Light microscopic analysis of neuronal alterations demonstrated considerable preservation of neurons in brains of treated cats. Beneficial effect of mannitol was attributed partly to prevention of capillary narrowing and suppression of ischemic cerebral edema.
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PMID:Modification of acute focal ischemia by treatment with mannitol. 62 43

A case report was presented in which a 15-year-old boy was beaten about the head with a baseball bat. Intraoral trauma and facial lacerations were repaired. Since results of the neurological examination were within normal limits, the patient was discharged. The next day, the patient became lethargic; however, the patient's mother did not bring the patient back to the hospital until the routine postoperative visit. At that time, the patient had right hemiparesis, was unable to speak, and was clearly obtunded. A carotid angiogram disclosed a left venous epidural hematoma in the parietal area. A craniotomy was performed with good results. The importance of follow-up neurologic examinations in cases of trauma to the face and head is stressed.
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PMID:Epidural hematoma after minor oral trauma. 106 13

Four children had progressive degeneration of the cerebral cortex, with hepatic cirrhosis. They and four previously described ones, are representative of a distinct form of hepatocerebral degeneration. Onset of the neurological disorder is between ages 1 and 3 years, at times with mild developmental delay. Explosive onset of intractable convulsions, leaving the child in a stuporous and demented state, is characteristic. Generalized hypotonia or hemiparesis were observed in several affected children. Clinical evidences of hepatic disease, including ascites and jaundice, occurred late, if at all. The illness ended fatally within ten months of onset of convulsions. Pathological findings in the brain are neuronal loss and gliosis, in a pattern that is indistinguishable from that in degeneration of the cerebral gray matter in infancy (Alpers disease). The hepatic lesions consist of cirrhosis or of subacute hepatitis, with superimposed fatty infiltration of hepatocytes. The disorder is genetically determined, with recessive inheritance.
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PMID:Infantile diffuse cerebral degeneration with hepatic cirrhosis. 125 62

Involvement of the central nervous system (CNS) is common in patients with advanced disease due to human immunodeficiency virus (HIV). Symptoms range from lethargy and apathy to coma, incoordination and ataxia to hemiparesis, loss of memory to severe dementia, and focal to major motor seizures. Involvement may be closely associated with HIV infection per se, as in the AIDS dementia complex, but is frequently caused by opportunistic pathogens such as Toxoplasma gondii and Cryptococcus neoformans or malignancies such as primary lymphoma of the CNS. The clinical presentations of attendant and direct CNS involvement are remarkably non-specific and overlapping, yet a correct diagnosis is critical to successful intervention. Toxoplasmic encephalitis is one of the most common and most treatable causes of AIDS-associated pathology of the CNS. A great deal has been learned in the last 10 years about its unique presentation in the HIV-infected patient with advanced disease. Drs. Benjamin J. Luft of the State University of New York at Stony Brook and Jack S. Remington of the Stanford University School of Medicine and Palo Alto Medical Foundation's Research Institute have studied T. gondii for many years and are two of the leading experts in the field. This commentary comprises an update of their initial review (J Infect Dis 1988;157:1-6) and a presentation of the current approaches to diagnosing and managing toxoplasmic encephalitis in HIV-infected patients.
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PMID:Toxoplasmic encephalitis in AIDS. 152 Jul 57

In 1987, a 69-year-old female suffering from epilepsy and right hemiparesis was admitted to the hospital and given conservative therapy. During the next three weeks she became a stuporous state. Steroids were then prescribed, and she made a complete recovery. Following hormonal and immunological investigations, a diagnosis of Hashimoto's disease with hypothyroidism was made. Following her discharge, thyroxin and anticonvulsant treatments continued. On May 30, 1989, at the age of seventy-one, the patient was found lying unconscious at home, and taken to our hospital. She had signs of a confused state, and seizures of her right arm on admission. Cranial computed tomography (CT) revealed a low density area in the left parieto-occipital lobe, which was heterogeneously enhanced by contrast medium. Magnetic resonance imaging (MRI) showed a lesion of low signal intensity in T1-weighted images and high signal intensity in T2-weighted images, which was homogeneously enhanced by Gd DTPA. Cerebral angiography disclosed no abnormality. Two weeks later, follow-up CT showed that the lesion had become larger and markedly enhanced. A brain tumor, probably malignant lymphoma, was suspected. On June 14, stereotaxic biopsy of the enhanced lesion was performed. Histopathological examination disclosed dense infiltration of the entire walls of many small parenchymal vessels, both arterioles and venules, by lymphocytes. Treatment for angiitis (betamethasone 16 mg daily) was started on June 20, then gradually tapered, and the lesion diminished on CT. Our case has some features of both isolated angiitis of the central nervous system and encephalopathy in compensated Hashimoto's disease. It is suggested that some common base of the autoimmune diseases exists in this case.
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PMID:[Isolated angiitis of the CNS associated with Hashimoto's disease]. 161 79

Two patients with posttraumatic dissection of the internal carotid artery were referred to the neurosurgical department with secondary neurological deterioration following a minor head injury with concussion. Both developed aphasia and right hemiparesis during the first few hours after the accident; one patient also had right focal seizures. On admission, both were only mildly lethargic, which contrasted with the severity of the focal neurological signs. Early CT scan was normal in both cases, whereas cerebral blood flow (CBF) studies by single photon emission computerized tomography (SPECT) with Tc-HMPAO (Ceretec) showed perfusion defects in the region supplied by the left middle cerebral artery (MCA), correlating with the clinical picture. Doppler sonography disclosed pathologic flow patterns, and carotid angiography demonstrated dissection of the internal carotid artery, in one patient on the left only and in the other bilaterally, with embolic occlusion of a branch of the left MCA in the latter case. Clinical features, pathogenesis, diagnostic workup and possible treatment (medical, as in our two cases, versus surgical) of this rare pathology are briefly reviewed.
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PMID:[Traumatic dissection of the internal carotid artery]. 218 68


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