Cases reported "Epilepsy, Temporal Lobe"

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1/20. Comparison of auras and triggering factors in epilepsy.

    case reports of five patients are presented, each with a specific aura at the onset of the seizures. All of these patients' had seizures during the waking state. Their auras were carefully replicated and presented to the patients under various conditions. The presentation of the auras evoked neither clinical nor EEG evidence of seizures. A sixth patient had seizures only when asleep which were preceded by vivid nightmares. Since the seizures occurred only when the patient was asleep, we considered that the seizures could be reflex in nature and evoked by a dream. Replication of the dream, however, did not evoke clinical or EEG evidence of epilepsy. The dreams, therefore, were auras or a part of the seizure complex.
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2/20. Pharyngeal dysesthesias as an aura in temporal lobe epilepsy associated with amygdalar pathology.

    PURPOSE: Pharyngeal dysesthetic auras are typically described with centrotemporal and opercular seizure-onset localizations. In this report we describe the fourth case in literature with temporal lobe seizures, apparently secondary to an amygdalar lesion on magnetic resonance imaging (MRI), presenting with prominent pharyngeal dysesthesias as the initial, or only, seizure manifestation. methods: Because of diagnostic uncertainty regarding the nature of the pharyngeal sensations, our case underwent prolonged extracranial video-EEG monitoring. RESULTS: Video-EEG information documented the epileptic origin of the dysesthesias and was concordant with the side and location of the amygdalar lesion. CONCLUSIONS: Pharyngeal dysesthetic auras may be produced by epileptic activity originating from the amygdala, and perhaps other mediotemporal structures. The underlying topography of this aura is not known with certainty, and it may reflect seizure spread from the amygdala and adjacent areas to the closely interconnected insular and opercular cortex, whose secondary activation could elicit similar sensations.
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3/20. Management of the difficult patient with complex partial seizures.

    Successful treatment of partial complex seizures (and the epilepsies in general) is a process of management over time and involves several factors. It starts with accurate and adequate diagnostic formulations. To this end the physician must be thoroughly familiar with the ictal manifestations of partial complex and other epilepsies as well as the clinical features of other transient but reversible episodes that might present difficulties in differential diagnosis. The diagnosis is based upon the history of a patient experiencing partial complex seizures, and the most important resource is a careful and detailed history of the ictal events and the circumstances under which they occur. Clinical observation and electrophysiologic monitoring of the patient during attacks, either spontaneous or induced, is the most powerful technique available in cases which present difficult diagnostic problems. In addition to recognition and proper classification of the seizures themselves, diagnosis and treatment of the cause of the seizures, particularly when it is an active disease, is of prime importance. Even after accurate diagnosis, the heterogenous nature of the population of patients with partial complex seizures is such that marked variation in response to treatment with antiepileptic drugs is to be anticipated. The use of these drugs must be individualized and based upon a thorough and working knowledge of their clinical pharmacology. The most frequent mistakes in our experience have been prescribing the drugs in too little doses or for too short a time. Less often the problem is overmedication. The best indicator of the effectiveness of the drugs is the clinical response of the individual patient, and in general each drug should be prescribed in increasing doses until either the seizures are controlled or unacceptable degrees of toxicity develop. The use of serum level determinations can be very helpful if not invaluable, particularly in identifying and understanding potential adverse effects of the drugs. Patient noncompliance in adhering to drug schedules is widespread, but usually can be detected by measuring serum levels. Even with the most efficient use of the drugs, however, some patients will be intractable, and elective surgical treatment should be considered. Finally, control of seizure occurrence alone is not necessarily adequate treatment, as many patients will have difficult psychosocial problems associated with their epilepsy. Treatment of such associated problems is necessary on its own merits, but occasionally can result in significant improvement in seizure control.
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4/20. Encephalofacial angiomatosis sparing the occipital lobe and without facial nevus: on the spectrum of sturge-weber syndrome variants?

    We report two cases of leptomeningeal angiomatosis in atypical frontoparietotemporal locations without an associated facial port-wine stain. Evidence of a leptomeningeal angioma was found in each when they were evaluated for headaches and seizures. The diagnosis of a leptomeningeal angioma was suggested by calcifications noted on computed tomographic scan of the head and confirmed with contrast-enhanced magnetic resonance images of the brain. We hypothesize that given the lack of occipital involvement with the angioma, and therefore the noncontiguous nature of this lesion with the developing upper facial ectoderm, the failure to develop a facial angioma would be expected. We found that the useof an anticonvulsant along with a migraine prophylactic medication appeared to have the greatest efficacy in these two cases, whereas anticonvulsants alone were less helpful. This diagnosis should be considered in any child presenting with seizures or complicated migraines and intracranial calcifications.
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5/20. Transient postoperative prosopagnosia.

    A 23-year-old right-handed woman developed isolated transient prosopagnosia following surgical resection of a right posterior temporal seizure focus. At 18 years of age she had developed secondarily generalized tonic-clonic seizures. Preoperative neuropsychological evaluation was normal, and neurological examination revealed only a left superior quadrant achromatopsia. MRI revealed a circumscribed lesion in the right inferolateral temporo-occipital junction. Following surgery she was agitated for 36 hours, and afterward, when her attention and orientation improved, she was unable to recognize familiar faces. She could, however, recognize familiar voices. Her prosopagnosia resolved over the next 6-7 days. This case demonstrates that isolated prosopagnosia can occur in patients with lesions restricted to the right inferior posterior temporal-anterior occipital region. The temporary nature of the prosopagnosia may result from postsurgical tissue injury, including focal cerebral edema, with compensation by ipsilateral or contralateral areas.
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6/20. Distal hypoglycemic neuropathy. An insulinoma-associated case, misdiagnosed as temporal lobe epilepsy.

    Peripheral distal neuropathy associated with hypoglycemia secondary to insulinoma is quite rare. So far, less than 40 cases have been reported in literature. In this report, we describe a 50-year-old patient with insulinoma-polineuropathy and neuropsychiatric symptoms, interpreted as temporal lobe epilepsy, over the preceding 7 years. Due to the variability of the clinical presentation, diagnostic mistakes are frequent, and diagnosis of insulinoma is often delayed. Thus, the hypoglycemic nature of neuropathy can be lately recognized.
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7/20. Recurrent fluent aphasia associated with a seizure focus.

    The relationship between dominant hemisphere seizure activity and aphasia is unclear. Although speech arrest, expressive speech problems, and comprehension difficulties have often been associated with temporal lobe seizure activity, neologistic, paraphasic speech is rare. We report a patient with seizures following encephalitis who had recurrent episodes of fluent, severely aphasic speech with impaired comprehension which correlated with continuous, high voltage spike and slow wave activity in the left temporal region. During a several-day period of intermittent electrographic seizure activity, he had fluctuating receptive aphasia, and he developed transient paranoid psychosis following treatment. We discuss the behavioral manifestations of his left temporal seizures and correlate the changing nature of his behavior with therapeutic interventions. This case, as well as a review of others, suggests that paroxysmal fluent aphasia results from a partially treated electrographic seizure focus in the dominant temporal lobe.
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8/20. Specific memory impairment in a multiple disabled male with fragile x syndrome and temporal lobe epilepsy.

    Evaluation of the cognitive repercussions of an epileptic disorder and its treatment are important issues in clinical follow-up. This especially holds true for temporal lobe epilepsy (TLE) where resective surgery can be a valid treatment option. However, in patients where TLE coexists with another neurocognitive disorder, questions can arise about the precise nature of the neuropsychological deficits. The aim of the present study was to evaluate memory impairments, found in a male aged 12 years who had the dual pathology of fragile x syndrome and refractory TLE. memory functions of this child were compared with those of a male aged 11 years 7 months with fragile x syndrome matched for intellectual functioning as indicated by highly comparable verbal (5 y 5 mo vs 5 y 9 mo) and non-verbal (7 y 2 mo vs 6 y 1 mo) cognitive age equivalents. Performance on each neuropsychological measure was evaluated twice, separately with normative data based on chronological age and on verbal or non-verbal cognitive level. A specific, distinguishable profile of task performance could be found only when controlling for general level of cognitive functioning. This made it possible to accurately evaluate neuropsychological abilities before and 6 months after anterior temporal lobe resection even in this male with a complex neurological pathology.
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9/20. Compulsive polydipsia following meningioma resection: an epileptic phenomenon? Case report.

    The authors report the case of an individual who developed compulsive polydipsia following resection of a left sphenoidal ridge meningioma. The episodic, stereotyped nature of his symptoms, response to treatment, and electroencephalographic and magnetic resonance imaging findings are all highly consistent with temporal lobe-onset epilepsy. The pathophysiology of this underrecognized phenomenon is discussed.
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10/20. The nature and management of aggression in epilepsy.

    Minor episodes of aggressive behavior are relatively common in some populations of patients with epilepsy. However, they are probably no more common than in populations who are socially disadvantaged or who have brain damage. The confusion that commonly follows seizures can lead to apparently aggressive behavior. Rarely, the seizure itself may lead to directed aggression; very rarely does it lead to murderous attacks. Although post-ictal psychotic aggression is usually not severe, when it is driven by prominent delusions and hallucinations, it can result in self-destructive acts or serious violence. Clearly, however, it is quite unfair to globally classify epileptics as aggressive, and the time has come to abandon this stereotype.
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