Fig.10.6B ).Ingrandmalseizures,consciousnessislostforalongerperiod,andtheaffectedindividualmayfallifstandingwhentheseizurestarts.Theseizurebeginswithageneralizedincreaseinmuscletone(tonic phase), followedbyaseriesofjerkymovements(clonic phase). Thebowelandbladdermaybeevacuated.TheEEGshowswidelydistributedseizureactivity(see
Fig.10.6A
EEGspikesthatoccurbetweenfull-blownseizuresarecalledinterictal spikes. Similareventscanbestudiedexperimentally.Thesespikesarisefromabrupt,long-lastingdepolarizations,calleddepolarization shifts, thattriggerrepetitiveactionpotentialsincorticalneurons.Thesedepolarizationshiftsmayreflectseveralchangesinepilepticfoci.SuchchangesincluderegenerativeCa++-mediateddendriticactionpotentialsincorticalneuronsandareductionininhibitoryinteractionsincorticalcircuits.ElectricalfieldpotentialsandthereleaseofK+ andexcitatoryaminoacidsfromhyperactiveneuronsmayalsocontributetotheincreasedcorticalexcitability.
has been demonstrated (1) by the effects of lesions of the left hemisphere that produce deficits in language function (aphasia) and (2) by the transient aphasia (inability to speak or write) that results when a short-acting anesthetic is introduced into the left carotid artery. Lesions of the nondominant hemisphere and injection of anesthetic into it do not usually affect language substantially.
Several areas in the left hemisphere are involved in language. Wernicke’s area is a large area in the posterior part of the superior temporal gyrus, extending from behind the auditory cortex into the parietal lobe. Another important language area, Broca’s area, is in the posterior part of the inferior frontal gyrus, close to the face representation of the motor cortex. Damage to Wernicke’s area results in receptive aphasia, in which the person has difficulty comprehending spoken and written language; however, speech production remains fluent, if meaningless. Conversely, a lesion in Broca’s area causes expressive aphasia, in which individuals have difficulty in generating speech and writing, although they can understand language relatively well.
The terms sensory aphasia and motor aphasia are often interchanged with receptive aphasia and expressive aphasia, respectively. The former terms, however, are misleading: A person with receptive aphasia may not have auditory or visual impairment, and one with expressive aphasia may have normal motor control of the muscles responsible for speech or writing. Aphasia does not depend on a deficit of sensation or of motor skill; rather, it is an inability to decode language-encoded sensory information into concepts or to encode concepts into language. However, lesions in the dominant hemisphere may be large enough to result in mixed forms of aphasia, as well as sensory changes or paralysis of some of the muscles used to express language. For example, the latter situation could occur with a lesion of the face representation portion of the motor cortex that results in an inability to manipulate the motor apparatus needed for speaking (vocal cords, jaws, tongue, lips) and would be manifest as unclear speech because of dysarthria, a mechanical deficit. An affected individual would, however, be able to write if the motor cortex serving the upper limb were unaffected.
Interhem﻿ispheric Com﻿m﻿unication and the Corpus Callosum﻿
The two cerebral hemispheres can function somewhat independently, as in the control of one hand. However, information must be transferred between the hemispheres to coordinate activity on the two sides of the body. Much of that information is transmitted through the corpus callosum, although some is transmitted through other commissures (e.g., the anterior commissure or the hippocampal commissure).
The importance of the corpus callosum for interhemispheric transfer of information is illustrated in
Figure 10.7A.
An animal with an intact optic chiasm and corpus callosum and with the left eye closed learns a visual discrimination task (see