Search PubMed⌕ Search

Biomedical subjects

A B Rubens

Publications and source records attributed to A B Rubens.

42 records · Page 3Linked to original sources
PubMed1977

Posttraumatic cerebral hemispheric disconnection syndrome.

Gross and microscopic lesions of the corpus callosum and neighboring structures are common in severe closed head injury. This report is the first, to our knowledge, to confirm neuropathologically the occurrence of extensive traumatic destruction of the corpus callosum in a patient with left-sided apraxia and agraphia. It also demonstrates that large traumatic lesions of the corpus callosum may occur without prolonged posttraumatic coma, vegetative state, or death. In our patient, coexisting extracallosal hemispheric lesions may have modified the effects of callosal pathology. Cases of this type may be more common than generally appreciated, but since symptoms of hemispheric disconnection are not apparent in ordinary behavior, specific tests of callosal function must be employed if disconnection phenomena are to be detected in the posttraumatic period.

Aged↗
PubMed1976

Asymmetry of the lateral (sylvian) fissures in man.

We compared the courses of right and left lateral (sylvian) fissures by superimposing left lateral and reversed right lateral photographic slide projections and tracing the sulci and fissures of each hemisphere in different colors. A characteristic pattern of divergence of posterior regions of the lateral fissures was noted in 25 of 36 adult brains. After pursuing similar courses, the right lateral fissure angulates sharply upward into the inferior parietal area while the left one continues posteriorly. As a consequence, on the right, there is a smaller parietal operculum, a shorter planum temporale, a higher sylvian point, and compensatory expansion of the inferior parietal region posterior to the lateral fissure.

Adolescent↗
PubMed1975

Aphasia with infarction in the territory of the anterior cerebral artery.

Two right-handed patients with clinical evidence of major infarction in the territory of the left anterior cerebral artery developed a profound but transient aphasia characterized by (1) a striking dissociation between intact repetition and grossly disturbed spontaneous conversational speech, (2) an absence of phonemic paraphasia, (3) a lack of speech inhibition and (4) relative preservation of conformation naming and comprehension. Despite the initially profound motor aphasia, servicable spontaneous conversational speech returned in two to three months. However, more subtle changes in the form of lack of speech initiative and difficulties in narrating stories and describing complex pictures, remained many months after the onset. In these patients the major features of the disturbance could not be explained only on the basis of an interruption of the downgoing pathway from the dominant motor speech area, and in fact, may have been due to damage to the superior and mesial pre-motor area (particularly the supplementary motor region), an area that has been shown to play a role in processes which govern the initiation, continuation and inhibition of speech.

Aged↗