Faculty Bibliography

Behavioral changes are common in epilepsy patients, with the overall spectrum of behavior in this population skewed toward cognitive impairment and psychopathology. Unfortunately, in many cases, the diagnosis is overlooked and therapeutic opportunities are missed. The pathogenesis of these disorders may include central nervous system pathology, ictal and interictal epileptiform activity, antiepileptic drugs, psychologic and environmental factors, and genetic predisposition. Although therapy for behavioral disorders is often deferred for fear of exacerbating epilepsy, treatment with psychopharmacologic agents is unlikely to increase seizure severity or frequency. Indeed, treating depression, anxiety, psychosis, and other disorders can improve sleep, reduce stress, and may even reduce seizure activity. Antiepileptic drugs have psychotropic properties that can be positive or negative and their effects may differ in epilepsy and purely psychiatric populations

PURPOSE: Nonepileptic seizures (NES) are expressions of a psychiatric disease state, usually conversion disorder, that mimic epileptic seizures (ES) but are not associated with the neurophysiologic changes of epilepsy. Conversion has not been demonstrated to emerge from the sleeping state. Emergence out of sleep is usually considered a virtual exclusion criterion for NES, signifying the presence instead of ES. We sought to test this hypothesis. METHODS: We retrospectively reviewed the video-EEG of all patients admitted to our epilepsy unit over a 3-year period, who were suspected of manifesting NES. We examined the relation between NES and the patients' sleep/wake state in this cohort. Two epileptologists blindly reviewed an intermixture of cases suspected to represent NES emerging out of sleep, together with control cases. Classification of each case was made independently. RESULTS: We found that in a small minority of patients (<1%), NES began either while the patient was sleeping, or within several seconds of arousal, well before a plan to simulate a seizure could likely have been formulated in the wakeful state. CONCLUSIONS: In some cases, NES are not the product of the awake mind, but rather represent a psychiatric condition that can be manifest in sleep

A 38-year-old woman with a right posterior temporo-occipital brain tumor developed partial seizures with illusory motion perception of environmental objects going from the center to the periphery within her left visual field. Subdural EEG recordings during visual seizures revealed onsets in the right temporo-parieto-occipital junction. Her ictal visual distortion was probably caused by activation of V5, an area involved in motion perception. Given that the tumor location corresponds with the ictal onset in the V5 area, and the semiology of her seizures, this case supports that epileptic dysfunction in V5 can cause illusions of visual motion

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

We report two patients whose eating disorder resolved after right temporal lobe lesions. The first case report involves a woman with a history of bulimia nervosa and partial seizures arising from the occipital and right temporal regions. The second case is a woman with a history of anorexia nervosa that resolved after a head injury that resulted in right-sided inferofrontal and temporal encephalomalacia. Not only did both patients' eating disorders resolve, but their moods and libidos improved

Acute pathologic neurologic laughter has been described as an ictal phenomenon in epilepsy, as a result of electrical brain stimulation to the cortex and to deep brain structures, in brain tumors, and in stroke. We report what is, to our knowledge, the first report of a case of postictal pathologic laughter. Previously diagnosed with medically refractory complex partial seizures, our patient was admitted to the hospital with phenytoin toxicity. During video-EEG monitoring she experienced multiple brief absence seizures as well as a prolonged episode of absence status epilepticus. Immediately following cessation of the seizure she began to laugh. Her laughter was mirthful and infectious. This lasted several minutes and was followed immediately by several minutes of crying and then a return to normal. We propose that diffuse cortical inhibition led to release of subcortical structures involved in emotional expression. Possible neural substrates of laughter are discussed

Callosotomy has played a unique role in the treatment of epilepsy and in the understanding of human brain function. The pioneering work of Dejerine and Liepmann presenting the first findings of callosal lesion pathology at the turn of the 20th century was accepted but then quickly forgotten. Two schools resurrected the phoenix of callosal syndromes: Roger Sperry and Michael Gazzaniga leading in experimental neuroscience, and Norman Geschwind leading in clinical neurology. Callosotomy remains an effective technique to treat atonic, tonic, and tonic-clonic seizures, especially in patients with symptomatic generalized epilepsies such as Lennox-Gastaut syndrome. Neurologic, cognitive, and behavioral complications limit its use given that precise characterization of these complications as well as their frequency is difficult. The high frequencies of developmental delays, severe seizures, head injuries, antiepileptic drug burden, and other factors limit the ability to attribute a specific change to surgical intervention, since surgery can change multiple factors. For example, subtle behavioral changes in executive function and personality are difficult to delineate in a population with preexisting neurologic and psychiatric disorders. Despite this, a clearer picture of the effects of callosotomy, as defined by clinical neurology and neuropsychology as well as cognitive neuroscience, is emerging

PURPOSE: Women in the United States who have epilepsy give birth to about 20000 newborns every year. Because seizures during late gestation and delivery may seriously affect the fetus, and because primary generalized tonic-clonic (GTC) seizures may occur during labor and delivery in 1-2% of women with epilepsy, we attempted to define the rate, risks, and causes of seizures during labor and delivery. METHODS: To characterize seizures during labor and delivery, we retrospectively analyzed 89 consecutive pregnancies of women with epilepsy on antiepileptic drugs (AEDs). Six epileptologists in our group had treated these patients. We confirmed data and acquired new information by telephone for 83.1% of the pregnancies, and categorized the women as having primary generalized or partial epilepsy. Most of the patients (78%) were on monotherapy during pregnancy; 20% took two AEDs, and 3% took three AEDs during that period. RESULTS: Seizures during labor and delivery occurred in 4/32 (12.5%) patients with primary generalized epilepsy, but in none of the 57 women with partial epilepsy (P<0.05). None of the 38 patients with therapeutic AED levels before labor and delivery had seizures, compared to 3/37 (8.1%) of the subtherapeutic group. However, drug levels were taken at variable times in relation to delivery, limiting their value. Also, the levels sampled were both total and free levels; the latter would be more helpful to determine the adequacy of AED drug coverage. CONCLUSIONS: Maintaining therapeutic AED levels during the last trimester may help prevent seizures during labor and delivery, especially in women with generalized epilepsy. Women with epilepsy who had subtherapeutic AED levels and had been seizure-free may be at-risk for seizures during labor and delivery. Our sample was small, and a random sampling bias may have affected the results