Reference Work Entry

Atlas of Epilepsies

pp 471-473

Aphasic Seizures

  • John M. SternAffiliated withGeffen School of Medicine at UCLA

Definition

Aphasic seizures are epileptic impairments of language that are not due to motor or sensory dysfunction and have aphasia as the predominant manifestation.

Classification

Ictal aphasia without additional cognitive dysfunction (aphasic seizure) is a simple partial seizure, but aphasia may also occur during complex partial seizures, which are distinguished from simple partial seizures by the additional cognitive dysfunction of amnesia. The individual having a complex partial seizure is amnestic for events during the seizure. Aphasic seizures are more specifically categorized by the International League Against Epilepsy as motor seizures without elementary motor phenomena.

Clinical Manifestation

Both aphasic and dysphasic seizures are manifested by primary language dysfunction and differ only in the degree of impairment, with aphasia indicating greater dysfunction. The abnormality may be evident in the impairment of comprehension or output, and output may be abnormal in fluency, content, or both. Paraphasic errors, such as semantic or phonemic substitutions, are an example of abnormal content. The dysfunction is due to the seizure localization, so aphasic seizures have similar language manifestations to other causes of aphasia. However, the aphasia of aphasic seizures most commonly lasts seconds to minutes and is not the fixed deficit that occurs when aphasia is caused by stroke or neurodegenerative disease.

Particularly, detailed testing of memory during and after the seizure is needed when the only apparent deficit during the seizure is language function because the apparent aphasia may actually reflect a complex partial seizure’s more global cognitive impairment. As a pearl of wisdom, a patient’s production of paraphasic errors while attempting to communicate during a seizure is especially supportive of the aphasic seizure diagnosis. The more challenging situation is when a patient is attentive and poorly cooperative because the condition may be either a complex partial seizure with partially retained interaction or a simple partial seizure with aphasia. Postictal testing of the patient for recall of details during the seizure is the best means to establish whether impairment in addition to aphasia occurred during the seizure.

Localization

Aphasic seizures most commonly have a dominant hemispheric frontal or neocortical temporal lobe source, but localization to central and temporo-occipital regions has been reported. Temporal lobe localization may be the most common, but this is confounded by frontal lobe seizures manifesting aphasia as speech arrest, which may be under-recognized as aphasia during the brief occurrence of a seizure. Nevertheless, the classical categorization of aphasias according to fluency, comprehension, and repetition is not as predictive of the seizure’s localization as it is for structural disorders of the brain. Nonfluent aphasia commonly occurs with temporal lobe seizures (Figs. 70-1 and 70-2 ).
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Figure 70-1

MRI identifies abnormally increased T2 signal in the left amygdala and the surrounding left anterior mesial temporal lobe, including the evidence of hippocampal sclerosis. The patient is an 18-year-old woman with a 12-year history of partial-onset seizures. The seizures follow an indescribable olfactory hallucination aura and are manifested by speech arrest that sometimes is accompanied by amnesia. Postictally, speech returns quickly but may be slowed and slurred

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Figure 70-2

EEG recorded from patient with MRI in Fig. 70-1 . Intermittent, pathologic slowing occurs across the left anterior temporal region

Etiology

The manifestation as aphasia is dependent on localization, and numerous possible etiologies are possible for frontal and neocortical temporal lobe epilepsy. Among these, congenital abnormalities, such as cortical dysplasia, and acquired structural abnormalities, such as postinfarction, are common.

Pathophysiology

Aphasia is a negative (deficit) phenomenon. This contrasts with many other seizure phenomena, which are positive phenomena defined as manifestation of an abnormal sensation or movement. The basis for this difference in manifestation is not evident in the electrophysiologic pattern, which is the same for both negative and positive epileptic phenomena. Memory dysfunction is another negative phenomenon and it is also localized to the temporal lobes.

Associated Epileptic Syndromes

Focal epilepsies may produce aphasic seizures and do so when the seizure includes dominant hemisphere temporal or inferior frontal neocortex before more global cognitive impairment occurs. Lateral temporal lobe epilepsy is the most likely syndrome to produce aphasic seizures but other focal epilepsies, including mesial temporal lobe epilepsy, orbito-frontal lobe epilepsy, and parietal and occipital lobe epilepsies are other possible causes.

Diagnostic Procedures

Detailed verbal interaction during Electroencephalography (EEG) monitoring is necessary to accurately diagnose aphasic seizures. The interaction must include specific and complex commands to assess comprehension and detailed questioning to assess spoken language production. Simultaneous EEG allows distinction from postictal aphasia, which may also result from a dominant hemisphere focal seizure. Functional and structural imaging provides supportive evidence for the localization, but does not address whether the seizure was manifested by aphasia.

Differential Diagnosis

Complex partial seizures with some retention of ictal interaction may appear similar to an aphasic seizure. In such seizures, the individual may follow simple commands, answer simple yes/no questions, or verbalize short phrases, but more sophisticated testing during the seizure indicates that the impairment is more global and includes attention and memory dysfunction. If true aphasia is present intermittently, the differential diagnosis includes focal hypoperfusion (transient ischemic attack), but this is an unlikely diagnosis for a long-standing episodic aphasia without the development of a fixed deficit from a stroke. Landau–Kleffner syndrome manifests as a fixed aphasia related to focal seizures, but the aphasia is not ictal in the same sense as is used for more common temporal lobe epilepsy. The deficit is due to electrical status epilepticus of sleep with associated and fixed language dysfunction during wakefulness.

Management

The treatment of aphasic seizures is the same as with other focal seizures. If the seizures are only simple partial, the decision to treat depends upon the degree of disability they produce. Very brief and infrequent simple partial aphasic seizures may not be sufficiently disabling to warrant medical treatment if the treatment produces unacceptable adverse effects. If treated, first-line intervention should be any of the antiepileptic medications efficacious for focal seizures. Additional testing with video-EEG monitoring is indicated when antiepileptic medications fail to provide seizure control.

Related Topics

Cognition and Epilepsy

Epileptic Encephalopathy with Continuous Spike- and- Wave During Sleep

Familial Lateral Temporal Lobe Epilepsy

Frontal Lobe Epilepsies

Landau–Kleffner Syndrome

Lateral Temporal Lobe Epilepsies

Pathophysiology of Neocortical Epileptic Seizures

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© Springer-Verlag London Limited 2010
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