Other auditory stimuli could also elicit seizures. She had an 11-year history of recurrent partial complex and secondarily generalized seizures evoked almost exclusively by answering the telephone. (2007) reported a 36-year-old woman with lateral temporal lobe epilepsy manifest as telephone-induced seizures. Five individuals had visual symptoms and 7 had secondarily generalized seizures. Age at onset ranged from 8 to 50 years (mean, 19.2 years), and auditory auras occurred in 10 of 14 affected individuals. (1996), was Australian of British descent. One of the families was of Ashkenazi Jewish descent and the other, previously reported by Berkovic et al. (2004) identified heterozygous mutations in the LGI1 gene. In affected members of 2 of 4 families with ADPEAF, Berkovic et al. A subset of patients with mutations also had idiopathic generalized epilepsy. The most common auditory symptoms were simple, unformed sounds, such as buzzing and ringing. There were no specific clinical features unique to those patients with LGI1 mutations, but autonomic symptoms were less common and auditory symptoms more common in those with LGI1 mutations. (2004) estimated a disease penetrance of 54% (35 to 73%) and noted that LGI1 mutations had been identified in approximately 50% of families tested, suggesting genetic heterogeneity. Including data from an earlier report ( Kalachikov et al., 2002), Ottman et al. (2004) identified different mutations in the LGI1 gene that cosegregated with the disease phenotype. In 3 of 10 families with autosomal dominant partial epilepsy with auditory features, Ottman et al. Two patients died unexpectedly in their twenties. EEG recordings in 4 patients showed temporal lobe activity and the symptoms suggested localization to the lateral neocortical temporal lobe. Twelve affected members were studied: mean age of onset was 18 years (range 4-42) 11 had simple partial seizures, 8 of which were characterized by aphasic features, and many experienced auditory hallucinations all had secondary generalized tonic-clonic seizures that improved with age. (2002) reported a large Norwegian family in which 20 members over 5 generations had seizures in an autosomal dominant pattern. (2000) emphasized that the features suggested a lateral temporal lobe onset zone.īrodtkorb et al. Some reported formed sounds, singing and voices, and one subject's description suggested seizures provoked by auditory stimuli. The auditory symptoms ranged from unformed sounds, such as humming and ringing, to distortions and volume changes. Occasional psychic/emotional symptoms were reported (e.g., fear, deja vu, panic, depersonalization). Autonomic symptoms (visceral/epigastric and cardiac palpitations) occurred in 45% of patients. Partial seizures were characterized most frequently by sensory symptoms (73% of subjects), including a high frequency of auditory symptoms (55% of subjects), followed in frequency by cephalic, visual, olfactory, and vertiginous symptoms. (2000) described the family reported by Ottman et al. (1995) noted that the auditory features suggested a neocortical (or lateral) temporal lobe origin. Phenytoin was the primary antiseizure medication prescribed in 10 of the 11 subjects the remaining subject received carbamazapine. Seizures occurred infrequently 7 of the 11 had been free of seizures for 3 years or more before interview. All family members had normal intelligence. The age at onset of epilepsy ranged from 8 to 19 years. None of the interictal EEGs showed an epileptiform abnormality. In 6 of those with idiopathic/cryptogenic epilepsy and in 1 with remote symptomatic epilepsy, nonspecific auditory disturbances (such as a ringing noise that grew louder or a humming like a machine) were reported as a simple partial component of their seizures. Epilepsy was clearly localization-related in all but 1 of the individuals the remaining person had only nocturnal seizures and thus could not be classified. (1995) studied a family in which 11 individuals in 3 generations had partial epilepsy classified as idiopathic/cryptogenic. However, relatives of probands with partial epilepsy have an increased risk of epilepsy compared with the general population, suggesting a genetic influence on at least some partial epilepsies ( Ottman et al., 1995). Most partial or focal epilepsies in which seizures begin in a specific brain region are assumed to be nongenetic.
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