Difficulties in the clinical diagnosis of lithium toxicity.
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Biomedical subjects
Publications and source records attributed to H H Funkenstein.
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The speech disturbance resulting from infarction limited to the Broca area has been delineated; it differs from the speech disorder called Broca aphasia, which results from damage extending far outside the Broca area. Nor does Broca area infarction cause Broca aphasia. The lesions in 20 cases observed since 1972 were documented by autopsy, computerized tomography, or arteriogram; the autopsy records from the Massachusetts General hospital for the past 20 years and the published cases since 1820 were also reviewed. The findings suggest that infarction affecting the Broca area and its immediate environs, even deep into the brain, causes a mutism that is replaced by rapidly improving dyspraxic and effortful articulation, but that no significant distrubance in language function persists. The more complex syndrome traditionally referred to as Broca aphasia, including Broca's original case, is characterized by protracted mutism, verbal stereotypes, and agrammatism. It is associated with a considerably larger infarct which encompasses the operculum, including the Broca area, insula, and adjacent cerebrum, in the territory supplied by the upper division of the left middle cerebral artery.
A cisternogram characteristic of normal-pressure hydrocephalus was obtained from a patient on Diamox who was being evaluated for rapid mental deterioration. A repeat cisternogram after Diamox was discontinued was nearly normal. We hypothesize that the initial abnormality resulted from reduced cerebrospinal fluid production caused by carbonic anhydrase inhibition; this defect (reduced flow) led to a net reflux of tracer into the ventricles. The reflux is believed to be due to the reduction of bulk cerebrospinal fluid from the ventricles.
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The hospital records and head CT scans of 44 patients with hemorrhagic infarction were retrospectively analyzed. The majority of cases (73%) were embolic or possibly embolic in etiology, and 55% were not associated with anticoagulant therapy. Adverse prognosis was most clearly related to infarct size, underlying systemic illness, and symptomatic hemorrhage. Of the nineteen patients in whom serial CT scans documented conversion from bland to hemorrhagic infarction, 12 exhibited no clinical worsening at the time that hemorrhagic infarction was observed; the remaining seven, all of whom worsened, were receiving anticoagulant therapy at the time of documented conversion. Fourteen patients in whom anticoagulant therapy was used despite the findings of hemorrhagic infarction remained stable or improved during hospitalization.