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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

We present a patient who presented with cortical blindness (CB) 1 week after repeated cardiac arrest while undergoing treatment for an acute myocardial infarction. He had been revived within 5 min in each instance and was apparently neurologically normal until presentation. Magnetic resonance imaging showed subtle hyperintensities on fluid-attenuated inversion recovery and diffusion-weighted imaging in both temporooccipital cortices. A rapid recovery over the next 2 weeks was remarkable for the appearance of metamorphopsia. CB may present even days to weeks after hypoxic-ischemic encephalopathy following cardiac arrest, even in patients apparently without immediate neurological sequelae. The pathogenesis of this phenomenon remains to be fully elucidated, but is likely to be due to delayed effects of anoxia on the occipital cortex and may be analogous to the previously described syndrome of delayed posthypoxic leukoencephalopathy. Prognosis for visual recovery appears to be good.
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PMID:Delayed-onset Reversible Cortical Blindness after Resuscitation from Cardiac Arrest. 2893 91

BACKGROUND Posterior reversible encephalopathy syndrome (PRES) is a poorly characterized and enigmatic syndrome. Despite consistently presenting with nervous system vasogenic edema, this malady has been associated with variable triggers, neurological symptoms, and natural history. CASE REPORT The report presents a 25-year old African American female who presented with altered mental status and bilateral cortical blindness. Neuroimaging identified vasogenic edema in the cerebellum, parietal lobe, and occipital lobe. Her PRES was associated with a hypertensive emergency, renal failure, and an atrial septum vegetation (culture-negative endocarditis). All 3 contributing etiologies were addressed, upon which the patient began to recover. During recovery, the patient experienced cerebral metamorphopsia, visualizing her entire environment in the form of a cartoon. After 2 weeks of treatment she recovered to baseline state of heath, with vasogenic edema resolved on follow-up neuroimaging. CONCLUSIONS This case presents a rarely catalogued phenomena during PRES recovery, cerebral metamorphopsia, along with a new potential association (culture negative atrial septum endocarditis). The report also highlights how PRES recovery patients (with cortical blindness) should be explicitly assessed for cerebral metamorphopsia and Charles Bonnet syndrome - which may distress patients. Lastly, the atypical presentation of cerebellar vasogenic edema in our patient validates existing literature that PRES does not have a uniform picture and is not well served by its current name or proposed diagnostic criteria. Therefore, renaming the disorder to reversible vasogenic edema syndrome and derestricting the diagnostic criteria, may prevent clinicians from being discouraged when faced with diagnosing PRES in the face of atypical findings.
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PMID:Cerebellar Parieto-occipital Posterior Reversible Encephalopathy Syndrome and Cerebral Metamorphopsia Associated with Asymptomatic Atrial Septum Vegetation and Renal Disease: Case Report. 3251 3