consecutive patients aged 70 years or older with SE were included. Each patient was matched to three controls without SE seen during the same period. Matching variables were age (±3 years), gender, and comorbidity index (±3). Multivariate logistic regression model were used to compare cases to controls and, among the cases, nonsurvivors to survivors. Key Findings: By multivariate analysis, factors independently associated with SE were acute decompensation (cardiac, respiratory, or hepatic) [adjusted odds ratio (OR a ) 2.57, 95% confidence interval (95% CI) 1.05-6.25] history of epilepsy (OR a 3.93, 95% CI 1.27-12.14), chronic cerebrovascular disease (OR a 7.96, 95% CI 3.31-19.15), nonvascular dementia (OR a 4.16, 95% CI 1.86-9.29), and dysnatremia (OR a 5.08, 95% CI 2.34-11.04). In-hospital 1-month mortality was 2.3 times higher among cases than controls (14/63, 22.0%; 95% CI 12.7-34.5%; vs. 18/189, 9.5%; 95% CI 5.7-14.7%; p = 0.01). Among the cases, factors independently associated with in-hospital death within 1 month were younger age (OR a per 1-year increase 0.87, 95% CI 0.76-0.98), higher comorbidity index (OR a per 1-point increase 1.27, 95% CI 1.07-1.55), and de novo SE (OR a 14.95, 95% CI 2. 24-192.8). Significance: Independent predictors of SE in hospitalized patients aged 70 years or older were acute decompensation (cardiac, respiratory, or hepatic), history of epilepsy, chronic cerebrovascular disease, nonvascular dementia, and dysnatremia. Factors that independently predicted death in patients with SE were younger age, higher comorbidity index, and de novo SE.
We describe the electrophysiological findings in 2 infants with deficient cobalamin intake. After normal development, psychomotor regression appeared after the 6th month, leading to severe hypotonia and apathy before the 12th month. Electrodiagnostic evaluation showed sensory neuropathy in both cases, associated with motor neuropathy in 1 case. Thus, in an acquired floppy infant syndrome, electrophysiological signs of peripheral neuropathy contributed to the diagnosis of a curable metabolic disorder. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 252–254, 1999
Spoken language disorders are rarely mentioned in superficial infarction of the posterior cerebral (PCA) territory. Two clinical types have been reported: transcortical sensory and amnesic aphasia. Between 1979 and 1990, we studied retrospectively 76 patients suffering from an occipitotemporal infarction located in the superficial territory of the posterior cerebral artery, all well documented by CT. Aphasia was one of the first and prominent signs in 18 cases. Middle cerebral artery concomitant infarction could have been the cause of language impairment in 10. In 8 patients aphasia was only explained by a PCA territory infarct. Three patients showed features of transcortical sensory aphasia. CT localization showed internal lobe and thalamic involvement of the dominant hemisphere. Five patients exhibited word finding impairment with various degrees of amnestic syndrome. The dominant internal temporal lobe was always affected. Dominant thalamus involvement was found in one case only. Some correlations between clinical features and anatomical support (vascular supply and anatomical structure) might be suggested in our 8 cases of aphasic disorders due to PCA infarcts. They are discussed and compared with data in the literature.
Although the ability to process numerical symbols may be considered a special case of more general linguistic abilities, deficits affecting numbers and words are usually interpreted within entirely independent frameworks. We report a patient presenting typical deep dyslexia, as confirmed in a series of word and non-word reading tasks. Moreover, the main features of his deficit extended to arabic numerals. The patient was equally unable to read aloud non-words and unfamiliar numerals, whereas he performed significantly better with real words and familiar arabic numerals such as famous dates or brands of cars. Additionally, familiar numerals and words yielded qualitatively similar errors, as did unfamiliar numerals and non-words. This contrasting performance with familiar and unfamiliar numerals seems incompatible with any single-route model of number reading. It is rather consistent with the existence of two routes for number reading: a 'surface' route mapping any digit string into a word sequence according to language-specific rules; and a 'deep' semantic route functioning only with familiar items that possess a specific lexical entry. We therefore suggest that number reading is architecturally similar to word reading, although these two processes probably rest on functionally and anatomically distinct pathways.
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