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Biomedical subjects

J F Butzer

Publications and source records attributed to J F Butzer.

7 recordsLinked to original sources

Computerized axial tomography of intracerebral hematoma. A clinical and neuropathological study.

Excellent correlation between computerized axial tomographic (CT) scans and the location and extent of pathologically verified intracerebral hematomas was demonstrated in eight patients. Superficial and intraventricular extension, hydrocephalus, and mass effect were easily identified; CT scanning was superior to angiography and radionuclide brain scanning in diagnosing hematoma and in determining its extent and associated ventricular size. Angiography was superior to CT scanning in demonstrating aneurysms and arteriovenous malformations as a cause of intracerebral hematoma. Computerized axial tomographic scanning is also useful in following the resolution of hematomas and in guiding surgical intervention.

Adult

F-wave conduction velocity in Guillain-Barré syndrome. Assessment of nerve segment between axilla and spinal cord.

The F-wave conduction velocity (FWCV) in the central segment (axilla to spinal cord) of the median and ulnar nerves was compared to the motor nerve conduction velocity (MNCV) in the more distal segments in nine patients with mild cases of the Guillain-Barré syndrome. In four patients, FWCV was slow despite normal or borderline MNCV. In four others, both FWCV and MNCV were abnormal. One patient showed slow MNCV with normal FWCV. The average FWCV was significantly decreased (40.9 +/- 12.0 meters/sec for median and 42.9 +/- 8.3 meters/sec for ulnar nerves) when compared to the corresponding normal values (64.3 +/- 6.4 meters/sec and 63.1 +/- 5.9 meters/sec). These data support the hypothesis that the central segment of a nerve is predominantly involved in some patients with Guillain-Barré syndrome.

Adult

Infantile neuroaxonal dystrophy. An electron microscopic study of a case clinically resembling neuronal ceroid-lipofuscinosis.

An unusual case of infantile neuroaxonal dystrophy (INAD) in which seizures were the presenting and predominant clinical feature is described. Although the clinical manifestations were indistinguishable from neuronal ceroid-lipofuscinosis, the diagnosis was readily established by electron microscopic examination of the brain biopsy specimen. Even after the ultrastructural features were known, the dystrophic axons were not evident by light microscopy. This case broadens the clinical picture of INAD to include seizures as the presenting complaint and suggests that some patients with childhood epilepsy who "deteriorate" may have this genetically determined disease.

Axons

Amantadine in Parkinson's disease. A double-blind, placebo-controlled, crossover study with long-term follow-up.

A double-blind, placebo-controlled, crossover study with long-term follow-up of amantadien i- Parkinson's disease was performed on 26 patients. Other antiparkinsonian medications were discontinued in all but three patients. Amantadine resulted in a statistically significant 12 percent overall improvement over placebo. Twenty of 26 patients, without breaking the code, selected amantadine for long-term usage. Ten patients continued treatment for 10 to 12 months, and an overall statistically significant improvement was noted at 2 weeks and at 1, 2, 3, and 10 to 12 months. Improvements in tremor and rigidity remained relatively constant, while there was some apparent loss of efficacy in timed tests and quality of timed tests. Amantadine appears effective in the long-term treatment of some patients with Parkinson's disease.

Activities of Daily Living

Transient ischemic attacks.

The treatment of TIA must be individualized. TIA is one of several manifestations of generalized atherosclerosis. While one-third of patients with TIA will suffer a stroke in five years, one-half of the same group will die of myocardial infarction. The risk of stroke is greater in carotid rather than vertebral-basilar TIA, in older patients, and in those with a cluster of TIAS, an is highest in the first month after the TIA. Treatment should reflect this knowledge.

Anticoagulants