Showing papers by "Michael P. Alexander published in 1989"
TL;DR: This paper presents a general theory of frontal functions, a brief summary of experimental and anatomical literatures in support of defined frontal functional systems, and clinical observations that delineate these functional systems for the specific modalities of language and communication.
312 citations
TL;DR: Analysis of the language function of patients with transcortical sensory aphasia, of the influence of sensory modalities on language function, and of the interaction between semantic memory and semantic lexical functions suggests the existence of a specific brain system for semantic functions.
Abstract: • We examined four patients with transcortical sensory aphasia and eight with milder language disturbances but with similar thalamic and/or temporo-occipital lesions. Specific attention was paid to differentiation of the computed tomographic lesion site of the milder cases from the transcortical sensory aphasia cases. The critical lesion for transcortical sensory aphasia in these patients involved pathways in the posterior periventricular white matter adjacent to the posterior temporal isthmus, pathways that are probably converging on the inferolateral temporo-occipital cortex. Analysis of the language function of these patients, of the influence of sensory modalities on language function, and of the interaction between semantic memory and semantic lexical functions suggests the existence of a specific brain system for semantic functions. This semantic system has a particular distributed anatomy. We propose that damage to this system may have a variety of clinical manifestations in language and in memory, depending on the exact lesion configuration.
139 citations
TL;DR: A 61-year-old man with autopsy-proven Creutzfeldt-Jakob disease (CJD) whose major initial manifestation was a progressive, fluent aphasia is reported, believing that this case of CJD is unique in its presentation of profound and isolated aphasIA.
Abstract: Progressive aphasia without dementia (primary progressive aphasia) is increasingly recognized as an important neurobehavioral syndrome. Clinical diagnosis of progressive aphasia is difficult early in its course, and the differential diagnosis is usually said to include Alzheimer's and Pick's diseases. We report a 61-year-old man with autopsy-proven Creutzfeldt-Jakob disease (CJD) whose major initial manifestation was a progressive, fluent aphasia. Myoclonus was absent, and characteristic EEG abnormalities appeared relatively late. We believe that this case of CJD is unique in its presentation of profound and isolated aphasia. CJD should be considered in the differential diagnosis of the progressive aphasia syndrome.
130 citations
TL;DR: Analysis of 34 cases from the literature with anatomical documentation of lesion site suggests that they represent at least two populations, and there may be general conclusions concerning mechanisms of cerebral lateralization to be learned from the investigation of anomalous groups such as crossed aphasics.
Abstract: Individual cases of crossed aphasia (aphasia after a right hemisphere lesion in a right-hander) have often been reported. A number of theories have been proposed as to the neuropsychological and/or nerobiological mechanisms that might underlie this phenomenon, but there is still disagreement about its language phenomenology and possible significance. We report 2 cases of crossed aphasia after stroke and review 34 cases from the literature with anatomical documentation of lesion site. Analysis of this material suggests that they represent at least two populations. There may be general conclusions concerning mechanisms of cerebral lateralization to be learned from the investigation of anomalous groups such as crossed aphasics.
108 citations
TL;DR: Traumatic basal ganglia hemorrhage (TBGH) is a rare entity compatible with a favorable recovery, especially when occurring in isolation, and cognitive impairment and speed and quality of recovery are more related to associated cerebral damage.
Abstract: Traumatic basal ganglia hemorrhage (TBGH) is probably secondary to rupture of lenticulostriate or anterior choroidal arteries. We evaluated 6 consecutive cases of this entity to define its clinical and pathologic dimensions. Relative frequency of TBGH was 3% (3 left, 3 right) in this acute rehabilitation population. Lesion size and associated pathology varied. Contralateral hemiparesis, present in all, recovered to varying extents, apparently related to lesion location (posterior limb, internal capsule, or midperiventricular white matter), not size. Prolonged muteness occurred in 4 of 6; these 4 patients also had severe diffuse axonal injury. Clinical findings corresponded with previously recognized subcortical hemisphere profiles. All achieved a moderate disability or good recovery rating on the Glasgow Outcome Scale. Rather than any features of the TBGH itself, duration of coma and/or associated temporal herniation predicted slower recovery and worse outcome. In conclusion, TBGH is a rare entity compatible with a favorable recovery, especially when occurring in isolation. The hemorrhage itself determines clinical signs related to particular subcortical structures involved and the side of the lesion. Overall cognitive impairment and speed and quality of recovery are more related to associated cerebral damage.
65 citations
TL;DR: It is suggested that the written spelling agraphia seen in these two patients arises from different underlying deficits, which were markedly different at the patients' CT scan lesion sites.
38 citations