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When experiencing grand mal seizures, individuals may lose consciousness for an extended period and may fall if standing. The seizure begins with a generalized increase in muscle tone (tonic phase) and is followed by a series of jerky movements (clonic phase). During these seizures, the individual may also evacuate their bowels and bladder. The electroencephalogram (EEG) shows widely distributed seizure activity, including EEG spikes that occur between full-blown seizures known as interictal spikes. These spikes arise from abrupt, long-lasting depolarization shifts, triggering repetitive action potentials in cortical neurons. Several changes in epileptic foci contribute to these depolarization shifts, such as regenerative calcium-mediated dendritic action potentials and a reduction in inhibitory interactions in cortical circuits. Increased cortical excitability may also be influenced by electrical field potentials and the release of potassium ions and excitatory amino acids from hyperactive neurons.

The dominance of the left hemisphere in language function has been demonstrated through the effects of left hemisphere lesions resulting in deficits in language function (aphasia). Additionally, transient aphasia, the inability to speak or write, can be induced by introducing a short-acting anesthetic into the left carotid artery. Lesions or anesthetic injection in the nondominant hemisphere typically do not substantially affect language. Various regions in the left hemisphere play a role in language processing. Wernicke's area, located in the posterior part of the superior temporal gyrus extending into the parietal lobe, is a significant language area. Another crucial language area, Broca's area, is found 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, causing difficulty in comprehending spoken and written language while maintaining fluent but meaningless speech production. Conversely, a lesion in Broca's area leads to expressive aphasia, resulting in difficulty generating speech and writing while retaining relatively good language comprehension.

The terms sensory aphasia and motor aphasia are sometimes used interchangeably with receptive aphasia and expressive aphasia, respectively. However, these terms can be misleading as receptive aphasia does not necessarily involve auditory or visual impairment, and expressive aphasia does not indicate a motor control deficit for speech or writing muscles. Aphasia is primarily an inability to decode language-encoded sensory information into concepts or encode concepts into language. Nonetheless, lesions in the dominant hemisphere may be large enough to cause mixed forms of aphasia along with sensory changes or paralysis in certain muscles used for language expression. For example, a lesion in the face representation portion of the motor cortex may result in an inability to manipulate the motor apparatus required for speaking (vocal cords, jaws, tongue, lips) and lead to unclear speech due to dysarthria, a mechanical deficit. However, the affected individual would still be able to write if the motor cortex responsible for upper limb movement remains unaffected.

Interhemispheric communication and information transfer between the cerebral hemispheres is crucial for coordinating activity on both sides of the body. While the hemispheres can function somewhat independently, the corpus callosum plays a significant role in transferring information between them. Some information is also transmitted through other commissures such as the anterior commissure or hippocampal commissure. The importance of the corpus callosum in interhemispheric transfer is illustrated in Figure 10.7A, where an animal with an intact optic chiasm and corpus callosum and the left eye closed learns a visual discrimination task.

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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