Epilepsy & Behavior 23 (2012) 500–502
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Case Report
Ictal aphasia: An unusual presentation of temporal lobe seizures Syed B. Sadiq a,⁎, Syed A. Hussain a, John W. Norton a, b a b
Department of Neurology, University of Mississippi Medical Center, Jackson, MS, USA Department of Psychiatry, University of Mississippi Medical Center, Jackson, MS, USA
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Article history: Received 13 January 2012 Revised 25 January 2012 Accepted 29 January 2012 Available online 8 March 2012 Keywords: Aphasia Seizures Epilepsy Language disturbances
a b s t r a c t Language disturbances during epileptic seizures are not uncommon, but isolated speech impairment is rare. We report a 67-year-old male with sudden onset of aphasia initially thought to be the result of an infarction of left middle cerebral artery territory. He had recurrent episodes of non-fluent, severely aphasic speech with intact comprehension as the primary manifestation, without other clinical seizure activity. After the administration of antiepileptic medication, his language returned to the baseline level. This case suggests that paroxysmal non-fluent aphasia can result from a seizure focus in the dominant temporal lobe. This is an important differential to be considered in patients with aphasia, which will assist in early diagnosis and treatment. © 2012 Elsevier Inc. All rights reserved.
1. Introduction Aphasia occurs in a variety of cerebrovascular, traumatic, and degenerative conditions. It is often caused by a stroke and is estimated to occur in one-third of stroke cases [1]. The association of a language disorder with epilepsy is frequent in children, especially with Landau–Kleffner syndrome. This entity exemplifies the concept of the language dysfunction caused directly by epileptic discharges in critical language areas of brain [2]. The nature of speech and language disturbances that result from seizure activity is complex [3]. 2. Case A 67-year-old, right-handed white male presented with sudden onset of difficulty with speech. His initial symptom was numbness in the right elbow which resolved in a few minutes. Later that afternoon, he experienced brief intermittent episodes of trouble speaking with normal speech pattern in between the episodes. He denied weakness, headache, fever or visual complaints. There was no history of witnessed seizure, loss of consciousness or confusion. His past medical history indicated diabetes and hypertension, with no past history of epilepsy or head trauma. Upon neurological examination, his spontaneous speech was labored, halting and non-fluent. He could not repeat simple words or sentences and his words were marked by paraphasic errors. He was unable to name a few objects although he recognized others through signs. He was unable to read or write a sentence although ⁎ Corresponding author at: Department of Neurology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA. Fax: + 1 601 984 5503. E-mail address:
[email protected] (S.B. Sadiq). 1525-5050/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2012.01.024
comprehension was intact. The remainder of his neurological examination and general physical examination was normal. A non-contrast computed tomography (CT) of the head illustrated focal hypodensity in the left temporal region with subtle changes. An MRI of the brain did not reveal restricted diffusion in diffusion weighted images (DWI) and corresponding apparent diffusion coefficient (ADC map) (Fig. 1). The FLAIR/T2 sequence failed to demonstrate any temporal pathology. An electroencephalogram (EEG) demonstrated independent focal epileptiform discharges in the left temporal lobe (Fig. 2). He was started on a 1000-mg loading dose of levetiracetam and then maintained on 500 mg twice a day. The following day, the aphasia had improved markedly, and his speech was fluent. He was discharged on antiepileptic medication, and follow-up EEG was normal. 3. Discussion In patients who present with sudden onset of aphasia in association with right facial and arm weakness, the index of suspicion is high for left middle cerebral artery (MCA) stroke. For the clinician, it becomes challenging if aphasia is the primary presenting symptom, and the neurological examination and imaging findings are inconclusive for stroke. In this clinical scenario, a re-evaluation of differential diagnosis should include the possibility of migraine, transient ischemic attacks (TIA) and seizure. Aphasia is associated with aura in cases of familial hemiplegic migraine, sporadic hemiplegic migraine and non-hemiplegic migraine with aura. The presence of aphasia during a TIA is one risk factor that identifies an individual at relatively high risk of stroke in the next few days and weeks. In relation to seizures, aphasia may be either an ictal phenomenon (e.g., brief speech arrest at onset of a simple and complex partial seizure or secondary generalized seizure) or a postictal manifestation [4].
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Fig. 1. Diffusion-weighted magnetic resonance (MR) imaging (A) and the corresponding apparent diffusion- coefficient (ADC) map (B) confirming no restricted diffusion.
The occurrence of prolonged, relatively isolated language deficits with seizures was reported in cases of aphasic status epilepticus [5–7]. The unique presentation of our case is the occurrence of ictal aphasia in the absence of other clinical seizure activity. In our patient, there were paroxysmal episodes of non-fluent aphasia associated with paraphasic errors. The patient's consciousness was intact during the episodes. The diagnostic criteria for epileptic aphasia were first defined by Rosenbaum [8] and modified further by Grimes [9]. Our patient's aphasic symptoms fulfilled the above criteria of ictal aphasia. Thus, we hypothesize that a simple partial seizure in the dominant temporal lobe caused the ictal aphasia, as supported by electroencephalogram (EEG) findings (Fig. 2). Ictal aphasia can present with receptive, expressive, transcortical or global aphasia [10]. Several mechanisms could account for the clinical manifestations in the present case. Ictal speech arrest, without alteration of consciousness, may be due to negative or positive motor responses [11]. Positive motor responses, by definition, would be accompanied by discernible involvement of buccofacial musculature, which was not present in this case. The absence of motor accompaniments to
the seizure indicates that the epileptogenic discharges did not extend far enough posteriorly to involve the motor strip. When an adult presents with aphasia, stroke being high in the differential, often a standardized evaluation and management, plan are pursued for cerebrovascular accident (CVA). This can sometimes result in administration of anti-thrombotic therapy, which is a relative contraindication in seizures. EEG and brain imaging (including functional brain imaging) could help differentiate an aphasic seizure from aphasia from other causes such as a stroke or migraine. CT perfusion measuring cerebral perfusion has become a widely acceptable method for localizing the epileptogenic zone [12]. CT perfusion when available can be an added tool in the differential of aphasia. It is supposed that aphasia occurs when the ictal discharge involves any part of the speech network [13]. The relation between clinical manifestations and the precise site of seizure origin is generally not straight forward. While there is a tendency for temporal lobe seizures to cause Wernicke aphasia, as demonstrated in our case the language impairment was suggestive of expressive aphasia. This could be explained in part by the rapid propagation of electrical activity into the
Fig. 2. Electroencephalogram (EEG) shows spikes over the region of the dominant temporal lobe (shown by red arrow).
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adjacent or distant cortex or even to the contralateral side [14]. Consequently, every type of aphasia may occur as an ictal manifestation. 4. Conclusion The relevance of this case is that it demonstrates brief intermittent episodes of expressive aphasia as one of the clinical presentations of temporal lobe seizures without other clinical seizure activity. The evaluation and management of seizures should be pursued when a patient presents with aphasia as the primary symptom, especially when brain imaging findings are inconclusive. References [1] Pedersen PM, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS. Aphasia in acute stroke: incidence, determinants, and recovery. Ann Neurol 1995;38:659–66. [2] J Clin Neurophysiol Jul 1991;8(3):288–98. Acquired epileptiform aphasia in children (Landau-Kleffner syndrome). Deonna TW. Brain Lang 1992 May;42(4):419–30
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