We evaluated reproductive endocrine function in women with unilateral temporolimbic epilepsy and normal control subjects to assess the effects of epilepsy, epilepsy laterality, and antiepileptic drug use on the cerebral regulation of hormonal secretion. The findings indicate that reproductive endocrine function differs between women with epilepsy and normal control subjects. Significant differences exist at all levels of the reproductive neuroendocrine axis, that is, hypothalamus, pituitary, and peripheral gland. Differences show significant relationships to the epilepsy itself as well as to medication use. Reproductive neuroendocrine changes occur in a stochastic manner such that the laterality of unilateral temporolimbic discharges is associated with predictable directional changes in hormonal secretion at all levels of the reproductive neuroendocrine axis. These directional changes are consistent with the finding that different reproductive disorders may develop in relation to left- and right-sided temporolimbic epilepsy. Hormonal changes can show close temporal relationship to the occurrence of interictal epileptiform discharges and may vary in relation to the laterality of the discharges. Antiepileptic drugs differ in their effects on reproductive hormone levels. There are notable differences between enzyme-inducing and noninducing drugs. Menstrual disorders are more common among women with interictal discharges as well as women with abnormal hormonal findings.

Menstrual disorders and infertility are common among women with epilepsy of temporal lobe origin (TLE). Reproductive endocrine disorders may be the cause. Polycystic ovarian syndrome (PCO) and hypothalamic amenorrhea (hypogonadotropic hypogonadism, HH), in particular, are significantly overrepresented and attributable to hypothalamic dysfunction. We therefore compared the hypothalamic function of 14 women with clinically and electrographically documented TLE with that of eight age-matched normal controls by determining the interictal pulse frequency and amplitude of luteinizing hormone (LH) secretion. Serum for LH measurement was drawn every 15 minutes from 8 AM to 4 PM in both groups. LH pulse frequency values were significantly more variable (p < 0.05) and lower (p < 0.05) among women with TLE than among controls. Women with left temporal EEG foci showed a trend toward higher pulse frequencies compared to women with right foci (p = 0.05 to 0.10). Among five women with reproductive endocrine disorders, the three with PCO had left-sided foci and average LH pulse frequency two times higher than that of the two women with HH, who had right-sided foci. Eight reproductively normal, medically treated women with TLE had significantly lower LH pulse frequencies than did the one reproductively normal, untreated woman with TLE (p < 0.05) and the eight normal controls (p < 0.001). These findings suggest that LH pulse frequencies in women with TLE may be influenced by the laterality of the epileptic focus, the reproductive endocrine status, and the use of antiseizure medications.

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The authors present two patients with dementia who displayed recurrent transient episodes of amnestic wandering and disorientation characterized by getting lost in familiar environments. At other times these patients did not wander or become disoriented. The inability to recall any information during these episodes, and the marked difference of the episodic amnesia exacerbations from the progressive amnesia characteristic of Alzheimer disease seen in these patients led to their evaluation. These clinical episodes and the bilateral interictal epileptiform electroencephalographic changes found in both patients led to the diagnosis of transient epileptic amnesia, a syndrome that can be diagnostically elusive. These transient amnestic wandering events subsided after treatment with antiepileptic drugs in both patients. The authors suggest that transient wandering of this type may be caused by ictal events or postictal confusional states. This report emphasizes the importance of recognizing transient epileptic amnesia as an easily treatable cause of episodic behavioral abnormalities responsive to antiepileptic therapy, especially in those patients who have a markedly inconsistent pattern of wandering, disorientation in familiar settings, and amnesia exacerbation manifested by no recall of the emotional stress of getting lost or of any information during these episodes. Recognition of this type of behavioral disruption and its proper treatment can lead to improved quality of life for these patients, maintain these patients in their homes and out of chronic care institutions longer, and facilitate the community's and caretaker's interactive roles with the patient.

L-Carnitine (16 mmoles per kg, injected intraperitoneally) is reported to protect mice against subsequent injection of ammonium acetate given at the unprotected LD100. The present studies in rats show a variable protective effect of L-carnitine (16 mmoles per kg) administered 1 hr prior to an LD100 dose of ammonium acetate. Survival ranged from 100% to 35%. In two experiments, protection was highly significant; in a third experiment, L-carnitine did not protect against death but did significantly prolong time to death. Although the cause of this variability is not known, the data establish the protective effect in rats of L-carnitine given 1 hr before ammonium acetate. D-Carnitine and deoxycarnitine, chemically related analogs unable to substitute for L-carnitine metabolically, are without protective effect. The protective effect of L-carnitine is short-lived and is, for example, completely lost if ammonium acetate is given 24 hr after L-carnitine administration. In contrast, the free carnitine content of brain rises slowly but continuously for at least 24 hr following a single dose of L-carnitine. The observation that protection from ammonia toxicity is not correlated with brain carnitine levels strongly suggests a major peripheral component to the protective effect. Chronically hyperammonemic (portacaval-shunted) rats were found to have significantly depressed total and free carnitine levels in blood compared to normal and sham-operated controls. The hypocarnitinemia, but not the hyperammonemia, was completely reversed in portacaval-shunted rats given drinking water containing 10 mM L-carnitine.(ABSTRACT TRUNCATED AT 250 WORDS)