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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Delayed neurological deterioration following anoxia is known to result from carbon monoxide exposure. However, it may also occur with anoxia of other types as well. The present report describes a case of delayed postanoxic encephalopathy with bilateral striatal lesions demonstrated by magnetic resonance imaging. A 27-year-old man exhibited anoxic anoxia caused by upper airway obstruction following general anesthesia for shoulder fracture surgery. Initially he was delirious and markedly excited for one day and became apparently normal for the following three days. Then he relapsed into delayed neurological deterioration with speech and gait disturbance, clumsiness of hand, pyramidal signs and metamorphopsia. Thereafter, he became bed-ridden and fell into semicomatose state with marked motor restlessness, involuntary movement of the tongue and decorticate posture. Twenty-five days later he had a second recovery period after hyperbaric oxygenation that lead to the sequelae with speech and motor disturbances and mild mental changes. I examined the present case as an expert witness in a civil suit eleven years after initial anoxia. The patient showed slight intellectual impairment and personality change. Impairment in figure-ground differentiation and disorders of spatial thought were also observed. Neurological examination revealed anisocoria, dysarthria with acquired stuttering, disturbances of fractionated movement of fingers, writer's cramp and Babinski's sign bilaterally. Postural dystonia of both hands and fingers, rigidity and spasticity of all extremities were also present. Magnetic resonance imaging (MRI) showed bilateral lesions of the corpus striatum, especially of the putamen. Some portion of the caudate nucleus was also involved. Cerebral cortices and white matter were slightly atrophic. From the above clinical course and neurological findings, we diagnosed the present case as delayed postanoxic encephalopathy. Ginsberg (1979) noted that in cases of anoxia not related to carbon monoxide, diffuse demyelinative changes of cerebral hemispheral white matter tended to be associated with relapsing clinical course, and gray matter injury was only seen in a few cases. MRI findings in the present case suggest that main site of the lesion to be in gray matter of the corpus striatum. In this respect, the present case is considered to be noteworthy.
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PMID:[A case of delayed postanoxic encephalopathy with bilateral lesions of the corpus striatum]. 281 6

Although organic solvents are essential components of an industrial economy, they are not used without risk. The relationship between excessive exposure to organic solvents and subsequent development of chronic encephalopathy has been recognized for nearly 100 years. Fifteen industrial painters who underwent evaluation in an occupational health clinic for symptoms that they related to their work were found to have a high prevalence of neurasthenic symptoms, most frequently, memory loss and personality change. Although neurologic and screening laboratory examinations showed no consistent abnormalities, psychological tests documented poor short-term memory and an array of neuropsychologic deficits. Personality profiles revealed depression, anxiety, and preoccupation with somatic concerns. These findings agree well with previous reports of "chronic painter's syndrome." Heightened awareness among industrial physicians and prospective studies to evaluate existing threshold limit values and personal protective equipment requirements are indicated.
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PMID:Organic solvent-induced encephalopathy in industrial painters. 395 Jul 85

Nineteen children aged 8-14 years were admitted over a six-year period with an acute encephalopathy due to toluene intoxication. Seven had a history of euphoria and hallucinations. The remainder presented with coma (4), ataxia (3), convulsions (3), and behaviour disturbance with diplopia (2), A history of glue sniffing was elicited in 14, but in the remainder toluene assay confirmed the diagnosis. Thirteen children recovered completely; five still had psychological impairment and personality change on discharge from hospital but were lost to follow-up, and one has a persistent cerebellar ataxia one year after the acute episode, despite absence of further exposure. Toluene inhalation is an important cause of encephalopathy in children and may lead to permanent neurological damage. Diagnosis is most important if further damage due to continued abuse is to be prevented, and toluene assay is a valuable aid to diagnosis.
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PMID:Solvent encephalopathy. 679 Jan 21

A 49-year-old normotensive man died after a series of strokes, slowly evolving dementia and personality change occurring over a period of 23 years. CT scan showed large infarcts involving the cortex and white matter of the temporo-occipital areas, small subcortical infarcts and low attenuation in the white matter of the frontal and parietal lobes. Neuropathological examination revealed large cortical and small subcortical infarcts corresponding to the radiological findings as well as degeneration/demyelination of central white matter corresponding to the areas of low attenuation seen on CT. The basic underlying pathological process was hyaline arteriosclerosis and atheroma which diffusely affected the small intracerebral arteries and to a lesser extent the arteries of the circle of Willis. Though usual because of the absence of hypertension, the very early age at onset of the syndrome and the presence of large cortical infarcts this case illustrates the clinical, radiological and neuropathological features of subcortical arteriosclerotic encephalopathy (Binswanger's type).
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's type) and cortical infarcts in a young normotensive patient. 708 53

We report a 21-year-old man with agammaglobulinemia and chronic progressive encephalopathy. The patient was diagnosed as having X-linked agammaglobulinemia at 6 months of age, and gamma globulin supplementation was initiated. He exhibited normal development until he was 11 years old, when he showed a decline in school performance and a personality change. Computed tomography images at that time disclosed diffuse cerebral atrophy. Several generalized tonic-clonic convulsions, myoclonus and spasticity appeared at the age of 13 years. He lost his ability to walk and speak at the age of 17 years old. He is currently 21 years old and displays severe mental deterioration and spastic tetraplegia. Magnetic resonance imaging showed progressive diffuse cerebral atrophy with no change in intensity. The cerebellum and the brain stem were relatively well maintained. Viral isolations were negative and serum antibody titers for rubella, measles, and human immune deficiency virus were not elevated. Our patient's symptoms resemble those previously reported as chronic progressive encephalopathy without viral isolation. This condition may be a complication of agammaglobulinemia. It is possible that the encephalopathy of our patient has the same etiology as that described in the other reports. Further attempts to identify the etiology of the encephalopathy using molecular techniques are necessary.
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PMID:[A case of agammaglobulinemia with chronic progressive encephalopathy]. 795 27

We report an 85-year-old man with Hashimoto's encephalopathy (HE) who showed spontaneous complete remission. The autoantibody against the amino (NH2) terminal region of alpha-enolase was positive in our patient. Neuropsychological manifestations, such as personality change and progressive cognitive impairment, gradually improved over approximately 6 weeks after onset of disease without corticosteroid treatment in parallel with a decrease in the anti-thyroglobulin antibody in the cerebrospinal fluid. HE should be considered as a possible diagnosis even in elderly patients with neuropsychiatric symptoms, particularly when a previous history of thyroid disease is present.
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PMID:An 85-year-old case with Hashimoto's encephalopathy, showing spontaneous complete remission. 1787 54

Mefloquine is a 4-methanolquinoline anti-malarial that in recent years has fallen out of favor for use as chemoprophylaxis against infection with chloroquine-resistant Plasmodium falciparum malaria owing in part to growing concerns of side effects and potential neurotoxicity. Despite over 20 years of licensed use, the pathophysiological mechanisms underlying mefloquine's neuropsychiatric and physical side effects and the clinical significance of the drug's neurotoxicity have remained poorly understood. In this report, an adverse reaction to mefloquine chemoprophylaxis is described characterized by prodromal symptoms of anxiety with subsequent development of psychosis, short-term memory impairment, confusion and personality change accompanied by complaints of disequilibrium and vertigo, with objective findings of central vestibulopathy. It is posited that these effects represent an idiosyncratic neurotoxic syndrome of progressive limbic encephalopathy and multifocal brainstem injury caused by the drug. This case provides insights into the clinical significance of mefloquine neuronal gap junction blockade and neurotoxicity demonstrated in animal models, points to recommendations for the management of affected patients including diagnostic considerations and appropriate referrals, and highlights critical implications for the continued safe use of the medication.
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PMID:Limbic encephalopathy and central vestibulopathy caused by mefloquine: a case report. 2249 97

A 51-year-old man presented with a focal epileptic, fluctuating encephalopathy. Antibodies to voltage-gated potassium channels (VGKC-Abs) were detected in his serum. Several features of this case were different from those previously reported in VGKC-Ab-associated encephalitis, illustrating that it may have a broader phenotype than previously documented. These features were: excess hepatic iron deposits without cirrhosis, reduced consciousness and fluctuating neurological signs. Previous history included personality change, depression, type 2 diabetes mellitus, pupil sparing third nerve palsy and epilepsy secondary to a head injury. He had never drunk alcohol and had recovered from a similar episode 4 years previously. Both episodes resolved after approximately 2 months. The cerebrospinal fluid had a raised protein content but no organisms. The patient was heterozygous for C282Y and negative for H63D mutations excluding classical idiopathic haemochromatosis. He recovered with supportive care to his premorbid level of health.
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PMID:Voltage-gated potassium channel antibody-related encephalopathy: a case which may extend the documented phenotype of this condition. 2269 27

Here, we report a case of Hashimoto's encephalopathy (HE) mimicking Creutzfeldt-Jakob disease (CJD). A 57-year-old man was admitted to our hospital for status epilepticus. He had gradually presented personality change over the last two years. On admission, he was in state of akinetic mutism. He exhibited seizures on the left side of his body, including the face, and intermittent myoclonic movement. Routine laboratory tests showed no abnormalities, including thyroid functions. An EEG study showed typical periodic synchronous discharge (PSD). Brain MRI showed high-intensity areas in the bilateral frontal cortex, thalamus, and right insula on diffusion-weighted imaging (DWI). So, initially, sporadic CJD was suspected. However, there were no abnormalities in the caudate or putamen on MRI. Anti-TG and anti-TPO antibodies, as well as anti-NAE antibody were all positive. He was administered methylpredonisolone pulse therapy. Subsequently, his consciousness levels and EEG and MRI findings markedly improved. So, he was finally diagnosed with HE. HE should be considered in patients with PSD on EEG, even if the patients have typical MRI abnormalities of CJD. Anti-thyroid antibodies should be examined in such patients.
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PMID:[Hashimoto's encephalopathy presenting periodic synchronous discharge, as a differential diagnosis for Creutzfeldt-Jakob disease]. 2409 20

A 46-year-old man had a smoke inhalation injury. Within 1 month, he developed neuropsychiatric problems including toxic encephalopathy, cognitive disorder, depression symptoms and personality change. From 3 to 14 years after the toxic inhalation injury, the patient received treatment with sertraline and methylphenidate. The (18)F-fluorodeoxyglucose positron emission tomography scan at 3 years after injury showed deterioration of glucose metabolism in the hippocampus and orbital frontal region; at 14 years after injury, the hippocampus had no significant change but the orbital frontal region had deterioration of glucose metabolism. It was hypothesised that sertraline may have provided selective hippocampal neuroprotection. Further study is justified to evaluate sertraline as a possible neuroprotective agent after smoke inhalation injury.
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PMID:Limiting progressive hippocampal metabolic abnormalities after smoke inhalation injury. 2457 74


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