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)

4 cases of nonketotic hyperglycinemia (glycine encephalopathy), one with autopsy, are presented and the literature on 61 cases is reviewed. Major clinical signs include early hypotonia, lethargy and erratic and massive myoclonias with respiratory distrubances, starting during the first days of life after a symptom-free interval. Early death is common. Survivors are severely retarded and exhibit various types of seizures including infantile spasms. The EEG pattern consists initially of periodical paroxysmal bursts on an almost flat tracing, evolving later into a hypsarrhythmic pattern. Spongiosis of the myelinated pathways is the main pathological finding. Elevated CSF glycine seems to be the essential determinant of the neurological disturbances and it is, therefore, suggested that the term glycine encephalopathy be used instead of non-ketotic hyperglycinemia. A classification of disorders associated with hyperglycinemia is proposed.
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PMID:Glycine encephalopathy. 58 64

Severe conjugate downward eye deviation of several days' duration in a lethargic patient with subarachnoid hemorrhage and of several weeks' duration in a comatose patient with hypoxic encephalopathy occurred in the absence of structural pretectal lesions. Persisting downgaze in a stuporous or comatose patient does not necessarily indicate anatomic pretectal damage.
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PMID:Sustained downgaze deviation. Two cases without structural pretectal lesions. 94 4

Twenty-one neonates of over 36 weeks' gestation suffered perinatal asphyxia but not chronic hypoxia. Three clinical stages of postanoxic encephalopathy were distinguished. Stage 1 lasted less than 24 hours and was characterized by hyperalertness, uninhibited Moro and stretch reflexes, sympathetic effects, and a normal electroencephalogram. Stage 2 was marked by obtundation, hypotonia, strong distal flexion, and multifocal seizures. The EEG showed a periodic pattern sometimes preceded by continuous delta activity. Infants in stage 3 were stuporous, flaccid, and brain stem and autonomic functions were suppressed. The EEG was isopotential or had infrequent periodic discharges. Infants who did not enter stage 3 and who had signs of stage 2 for less than five days appeared normal in later infancy. Persistence of stage 2 for more than seven days or failure of the EEG to revert to normal was associated with later neurologic impairment or death.
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PMID:Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. 98 69

Scrapie and transmissible mink encephalopathy were studied in hamsters; clinical signs, pathology, and the replication of the agents of each disease in brain and spleen were compared. The most noticeable clinical sign in scrapie-affected hamsters was a distinct cerebellar ataxia beginning 16 weeks after inoculation. Ataxia was not prominent in animals affected with transmissible mink encephalopathy; these animals gradually became more and more lethargic. The pathology in the central nervous system in both diseases consisted of astrocytic hypertrophy, microvacuolation of the neuropil, and neuronal degeneration. The scrapie agent appeared to have a greater effect on nuclear masses, especially those present in brain stem and the central white matter of the cerebellum. The earliest lesions in both diseases were detected near pia arachnoid surfaces and adjacent to the ventricular system. These initial sites of involvement suggest that the cerebrospinal fluid may be an important route by which inocula are disseminated to susceptible cells after intracerebral inoculation. Both agents multiplied rapidly in brain, reaching titers greater than 10-8 ld-50/0.05 ml before the onset of clinical signs. Titers in spleen were 4-6 logs lower than titers in brain at every point measured during the asymptomatic or clinical course of disease.
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PMID:Comparison of scrapie and transmissible mink encephalopathy in hamsters. II. Clinical signs, pathology, and pathogenesis. 116 84

Reye's syndrome (fatty infiltration of the liver with encephalopathy) is an uncommon disease of children and has not previously been noted in adult patients. We present a 25-year-old male who survived this syndrome after presenting a stuporous state. Etiologic and pathophysiologic mechanisms are considered.
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PMID:Reye's syndrome in an adult. 120 12

This peculiar 11-14 Hz spindle activity appears predominantly in the frontal area, and was observed in eight patients with impaired consciousness caused by nontraumatic diffuse encephalopathy. Characteristic of this frontal spindle activity is its transience and accordance with changes in the arousal level of the patient. When the degree of impaired consciousness in the patient was minimal and clinically not very apparent, this spindle activity appeared during light drowsiness. In lethargic patients, it was observed when the patient's level of consciousness rose (e.g. immediately after opening and closing the eyes). These frontal spindles disappeared at the onset of Stage 2 sleep, when normal physiologic spindle waves that are dominant in the vertex area appeared. A paroxysmal discharge was sometimes recorded in association with the frontal spindle activity and it disappeared at about the same time as these spindles. The prognosis was satisfactory for all patients in whom frontal spindle activity was observed; its correlation to spindle coma is also studied.
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PMID:Frontal spindle activity that appears in conjunction with nontraumatic diffuse encephalopathy. 139 58

Symptomatic viral hepatitis A usually only requires supportive therapy and the majority of cases are managed in the community. The prodromal symptoms of nausea, anorexia and lethargy tend to improve with the onset of clinical jaundice. Fulminant hepatic failure is said to be an uncommon complication, occurring in only 0.14-0.35% of hospitalized cases. However, an increasing incidence has been documented in some northern European countries where up to 20% of cases of fulminant viral hepatitis is due to hepatitis A. This trend parallels the increasingly delayed exposure to hepatitis A and the increased severity of the illness when contracted in later life. The risk of developing fulminant hepatic failure is best monitored using coagulation factor assays, with the prothrombin time and factor V levels being the most favoured. The diagnosis is established with the onset of encephalopathy. Patients progressing to grade 4 encephalopathy have a reasonably good prognosis compared to other aetiologies and survival rates of up to 67% have been obtained with medical management, despite the co-existence of such complications as cerebral oedema, renal and respiratory failure and the metabolic sequelae of acute liver failure. Nevertheless, some patients require emergency liver transplantation and 10 such patients have been reported to date. Transplantation is especially required in older patients (> 40 years) and those who are jaundiced for > 7 days before the onset of encephalopathy. The serum bilirubin and the prothrombin time complement these parameters in the decision making process.
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PMID:Management of acute and fulminant hepatitis A. 147

Experimental transmission of the Stetsonville, Wisconsin, U.S.A. source of transmissible mink encephalopathy (TME) to outbred Syrian golden hamsters resulted in two distinct syndromes, termed hyper (HY) and drowsy (DY), that diverge by the third hamster passage. The syndromes differed with respect to clinical signs, incubation period, brain titre, brain lesion profile and pathogenicity in mink. HY hamster TME had an incubation period of 65 +/- 1 days and was characterized by clinical signs of hyperaesthesia and cerebellar ataxia. Lethargy and the absence of hyperexcitability or cerebellar ataxia were representative of DY hamster TME which had an incubation period of 168 +/- 2 days. At endstage, HY and DY infected animals had brain titres of 10(9.5) LD50/g and 10(7.4) LD50/g of tissue, respectively, indicating that the replication kinetics of these two strains is different. Hamster TME passaged back into mink revealed that only DY retained mink pathogenicity. This suggests that the DY agent is the major mink pathogen in the Stetsonville TME source that is also pathogenic in hamsters after a long incubation period. The HY agent is likely to be a minor component of the original TME mink brain that replicates more rapidly than DY agent in hamsters, but alone is non-pathogenic in mink. The presence of the HY and DY strains of agent that retain their biological characteristics on repeated hamster passage in the Stetsonville TME source requires that the informational molecule encoding these transmissible agents has the capacity to account for this biological diversity.
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PMID:Identification of two biologically distinct strains of transmissible mink encephalopathy in hamsters. 153 75

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

Current neurologic assessments consider idling neurons and ischemic penumbras to be metabolically lethargic and electrically nonfunctional or nonviable. Diagnosis, prognosis, and therapeutics of central nervous system dysfunctions require differentiation between viable and nonviable neurons. It is necessary to develop and document efficacious and safe techniques for reactivating idling neurons. The authors present a case study of a near drowning 12 years earlier. Areas of cortical hypometabolism were identified by using SPECT imaging in conjunction with hyperbaric oxygen therapy (HBOT). Delayed imaging after HBOT (1 hour, 1.5 atm abs) suggested viable but metabolically lethargic neurons. After HBOT (80 1-hour treatments, monoplace chamber, 1.5 atm abs), marked improvements in cognitive and motor functioning were demonstrated. The data support the hypothesis that idling neurons and ischemic penumbras, when given sufficient oxygen, are capable of reactivation. Thus, changes in tracer distribution after a single exposure to HBOT may be a good prognostic indicator of viable neurons. HBOT may be valuable not only in recovery from anoxic encephalopathy but also from other traumatic and nontraumatic dysfunctions of the central nervous system, including stroke. HBOT in conjunction with physical and rehabilitative therapy may help reactivated idling neurons to remain permanently active.
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PMID:Identification of hypometabolic areas in the brain using brain imaging and hyperbaric oxygen. 161 42


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