Behavioral change in temporal lobe epilepsy.
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Biomedical subjects
Publications and source records attributed to N Geschwind.
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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.
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This paper presents a set of probabilistic models which reproduce the proximodistal gradient of sensory deficit in peripheral neuropathies, on the basis of the occurrence of axonal dysfunction as a result of randomly distributed abnormalities. The models, which are based on conduction block, loss of temporal coherence, and weak interactions between nerve fibers, demonstrate that randomly distributed axonal dysfunction provides a sufficient condition for distal sensory deficit. The models predict a marked reduction in the length for normal sensory conduction with small increases in the probability of axomal dysfunction, providing a possible correlate for the rapid clinical progression of some neuropathies. The hypothesis that weak interactions between fibers result in paresthesiae in peripheral neuropathies is also discussed.
Three patients presenting predominantly with acute confusional states (ACS) are shown to have infarctions in the distribution of the right middle cerebral artery. It is suggested that the main deficit in ACS is in the function of selective attention. On the basis of cortical connections of homologous areas in the monkey brain, it is argued that this deficit arises from lesions in convergence areas for association cortex.
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Formed auditory hallucinations associated with acquired deafness have seldom been reported in the English literature. In the past year we have had the unusual opportunity of examining two deaf patients whose complaint when first seen was that of hearing music.
A distinct syndrome of interictal behavior changes occurs in many patients with temporal lobe epilepsy. These changes include alterations in sexual behavior, religiosity, and a tendency toward extensive, and in some cases compulsive, writing and drawing. The concomitants of abnormal limbic acitivity therefore include behavior alterations as well as manifest seizures. The demonstration of interictal spike activity in temporal structures provides a pathophysiologic basis for this syndrome. The constellation of behavioral changes may be of great diagnostic value. In addition, it provides an example of a human behavioral syndrome assocaited with dysfunction at specific anatomic loci. The behavior syndrome of temporal lobe epilepsy may prove to be a useful model in studies on the neural substrates for behavior.
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Asymmetries are found in the cerebral hemispheres of some great apes, particularly in the orangutan, that are similar to those seen in man. Studies in the orangutan might be more likely to help in understanding the evolution of handedness or language than studies in chimpanzees.
Liepmann suggested that the left hemisphere contained the engrams for motor sequences. Other investigators have suggested that ideomotor apraxia may be caused by either a destruction of these engrams or a disconnection of these engrams from motor systems in the nondominant hemisphere. If these hypotheses are correct, then ideomotor apraxics should not only show a defect on previously learned motor tasks but also a defect in new motor learning. Nine right-handed, hemiparetic, aphasic apraxics were given six trials on a rotary pursuit meter. Eight right-handed hemiparetic, aphasic, nonaprixic patients served as controls. All subjects were instructed to use their left (nonparetic) hand. The performance of the control group on the sixth trial was significantly better than that on the first trial, showing a distinct learning effect. In the apraxic group, however, there was no significant difference between the first and sixth trial, suggesting a defect in motor learning. This defect appeared to be caused by a combined defect of both acquisition and retention.
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