Biomedical subjects
Publications and source records attributed to A Kertesz.
A young woman developed Wernicke's encephalopathy after gastroplasty for morbid obesity. Her clinical presentation of nystagmus and ocular gaze palsies, ataxia, and a sensorimotor neuropathy is described. A small number of previously described patients are compared with respect to clinical features, response to treatment, and investigative procedures.
We studied motor impersistence with a standardized clinical test of sustained actions, both in patients with acute focal stroke lesions, who were matched for age and size of lesion, and normal controls. Patients with right-sided lesions had significantly more impersistence than did those with left-sided lesions. The most discriminating tests were eye-closure, mouth-opening, tongue-protrusion, and gaze to the left. Right central and frontal lesions seemed to be more responsible for motor impersistence than were posterior or left-sided lesions. Although motor impersistence is sometimes seen with diffuse cerebral disease, it is also a sign of right-hemisphere lesions; the phenomenon is probably related to mechanisms of directed attention that are necessary to sustain motor activity.
A persistent hemispatial neglect developed in a patient following a small infarction of the posterior limb of the right internal capsule. This defect was restricted to tasks requiring spontaneous motor performance on the contralateral hemispace, especially when carried out under visual control. It was not associated with an extinction phenomenon. Verbal cues improved exploratory behavior, suggesting that hemispatial akinesia in this case was due to an intentional disorder. A pulvinar-parietal disconnection, depriving the right parietal cortex from relevant visuospatial information from the contralateral hemispace, was probably the anatomic basis of hemispatial neglect in this case.
Language recovery in aphasic patients who received one of three types of speech and language treatment was compared with that in aphasic patients who received no treatment. One hundred aphasic patients were followed from 2 to 4 weeks postonset for 1 year or until recovery, using a standardized test battery administered at systematic intervals. Both treatment methods provided by trained speech-language pathologists were efficacious, while the method provided by trained nonprofessionals approached statistical significance. Small group size prevented resolution of the question of whether one type of treatment was superior to another.
Lesion size correlated positively with the severity of apraxia in the acute (one month) and chronic (one year) stage in 177 stroke patients, but accounted for only 25 per cent of the variance of the apraxia scores. Apraxia was measured on a standardized battery and defined in relation to normal controls. Lesions visualized by CT were traced objectively and measured on standard templates. Small lesions (less than one-tenth of the hemispheric volume) producing moderate or severe apraxia were mostly frontal and close to the body of the lateral ventricle. The lesions of the deep parieto- and occipitofrontal and anterior callosal fibres seem to be crucial in apraxia, rather than the parietal cortex as traditionally claimed. Large lesions (more than three-tenths of the hemisphere) without apraxia were associated with atypical asymmetries in half of the cases, as measured by the torque and the width of the frontal and occipital lobes on CT scan, suggesting a right hemisphere role in sparing and recovery of praxis.
We studied the functional and anatomical relationship between aphasia and apraxia in 177 patients with CT evidence of left hemisphere stroke. In six severe aphasics, praxis was spared; these cases were analyzed in detail. One patient had a small temporal lesion with severe Wernicke's aphasia. Large frontoparietal lesions were found in the others. The sparing of praxis suggested bilateral representation of visuokinesthetic motor patterns, and functionally active right parietofrontal connections. Some of these patients had uncommon patterns of skull asymmetries that may have been related to bilateral distribution of function.
The rate, duration and the predictability of natural recovery, the effect of therapy, and major contributory factors are reviewed, with special emphasis on aphasia. The most likely mechanism of second-stage recovery is physiological and functional substitution by connected areas in the brain. Recovery from aphasia shows a predictable time course. Aphasia type overlaps severity to a great extent and language components depend on the test method and patient selection. Comprehension probably recovers better than other modalities. The pattern of evolution of aphasic syndromes and an overall prognostic guide are presented.
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Transcortical sensory aphasia is a syndrome characterized by poor comprehension but excellent repetition. The lesions shown on computed tomography and isotope scans of 15 patients who satisfied the objective criteria based on test scores were studied. The overlap technique showed a unique posterior parieto-occipital location of lesions. The lesions seem to separate into two groups: one is more medial, inferior, and posterior and is clearly in the posterior cerebral artery territory, and the other is relatively more lateral, superior, and anterior and seems to be in a watershed area between middle cerebral and posterior cerebral arteries. The lesion sizes correlated with severity. Frequent recovery and good prognosis are associated with this entity. Association with transient visual agnosia and hemianopsia confirmed the anatomical correlation.
This quantitative study of apraxia in aphasics establishes the extent and characteristics of apraxia in various aphasic groups, the differences between various categories of praxis, and the correlation between praxis and language parameters. Broca's aphasics have more severe apraxia than Wernicke's aphasics even though their comprehension is significantly better. Apraxia, however, correlates best with comprehension deficit and secondly with the severity of aphasia. Among the nonverbal parameters, drawing shows the highest correlations. Our study confirms the prominence of facial apraxia in Broca's aphasia. Praxis and language are closely related and appear to share the same neural structures.
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A number of studies have shown superior written over oral performance in fluent aphasia. One reasonable explanation for this result is that writing in these cases takes place through a different set of output mechanisms than oral naming. Specifically, conversion of lexical information directly into graphemic code can occur for writing whereas output requires access to underlying phonology. If phonological processing is impaired, it is possible that written performance can still be sustained via lexicographic retrieval of information. A case study is described supporting this account of incongruous written over oral naming. Written naming for single words was markedly superior to spoken naming. Performance in rhyme matching tasks disclosed impaired retrieval of the underlying sound component of words and nonlexical phonological processing was severely impaired in writing to dictation. This suggests that written naming was mediated entirely by nonphological processes. In addition, recovery of function indicated considerable independence of phonological processing between reading and writing. While grapheme-phoneme conversion improved substantially six months post-onset, phoneme-grapheme transcoding remained severely impaired. This suggests that different neural mechanisms mediate access to phonology for reading and writing systems.
Sex differences and age distribution are examined in various types of aphasia and in right hemisphere-damaged patients due to acute infarct. The language and performance deficits were measured by a standardized test allowing us to group patients meaningfully. The higher male to female ratio of aphasia is shown to relate to a similar sex distribution in infarcts rather than to sex differences in cerebral organization. Broca's aphasics were somewhat younger than the other groups and the slight difference may be related to pathophysiological factors favouring embolic strokes in the anterior territory of the middle cerebral artery. Sex and aphasia types were not significantly different in various age groups except about 50 years of age where the female aphasics reversed the ratio.
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Seven members of a family succumbed to prolonged dementing illnesses. In two, those dementia lasted 10 years, spongiform encephalopathy was found at autopsy. This duration of illness has not been a feature in other instances of familial Creutzfeldt-Jakob disease.