• Twenty consecutive men with partial seizures of temporal lobe origin were evaluated for sexual or reproductive dysfunction. Eleven (55%) had diminished sexual interest or reduced potency. Nine of them had reproductive endocrine disorders, with features of hypogonadotropic hypogonadism in five, hyperprolactinemia in two, and hypergonadotropic hypogonadism in two. Among these nine were cases in which the reproductive endocrine abnormalities could not readily be attributed to antiseizure medication use. Other possible interpretations are as follows: (1) epileptic discharges in medial temporal lobe structures may disrupt hypothalamic regulation of pituitary secretion, (2) hypogonadism may promote the development of epileptic discharges, and (3) temporal lobe epilepsy and associated reproductive endocrine disorders may represent the parallel effects of prenatal factors common to the development of both the brain and the reproductive system.

Reproductive endocrine disorders in women with partial seizures of temporal lobe origin.

The consequences of refractory epilepsy and its treatment

Kindling: basic mechanisms and clinical validity.

Summary: Purpose: Previous studies of patients with epilepsy and animal models of epilepsy suggest that sleep increases the frequency, duration, and secondary generalization of seizures. This information is, however, incomplete.



Methods: We retrospectively examined video-EEG monitoring reports from our comprehensive epilepsy center. We recorded seizure type, site of onset (for partial seizures), sleep state at onset, and whether partial seizures secondarily generalized. Seizures arising from sleep were then reviewed to determine sleep state.



Results: We analyzed 1,116 seizures in 188 patients. Thirty-five percent of complex partial seizures (CPSs) starting during sleep underwent secondary generalization compared with 18% in wakefulness (p < 0.0001). Frontal lobe CPSs secondarily generalized at equal rates during sleep (22%) and wakefulness (20%), but temporal lobe CPSs generalized much more frequently during sleep (45%) than in wakefulness (19%; p < 0,0001). Frontal lobe seizures were more likely to occur during sleep (37%) than were temporal lobe seizures (26%; p = 0.0068). CPSs were more frequent in stages 1 and 2 and occurred rarely during REM. Seizures starting during slow-wave sleep were significantly longer than seizures starting during wakefulness or stage 2 sleep. Psychogenic nonepileptic seizures (PNESs) were rare between midnight and 6 a.m. and never occurred during sleep.



Conclusions: Sleep has a pronounced effect on secondary generalization of partial seizures, especially those of temporal lobe origin. Frontal lobe seizures occur more often during sleep than do temporal lobe seizures, and occurrence during sleep helps to distinguish PNESs from CPSs.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1528-1157.1997.tb01077.x

Effects of sleep and sleep stage on epileptic and nonepileptic seizures

Role of forebrain catecholamines in amygdaloid kindling.

Seizure development and transference phenomenon were investigated in hippocampal and amygdaloid kindled cats. The behavioral and electrographic findings during the kindling procedures showed that motor seizure development in hippocampal seizures occurred with the emergence of independent discharging in the amygdala, globus pallidus and contralateral hippocampus. Furthermore, secondary site convulsions developed upon the first stimulation of these structures in the hippocampal group but only after over a month of hippocampal stimulation in the amygdaloid group. It was, therefore, concluded that role of the amygdala and globus pallidus in hippocampal seizure development was more essential than that of hippocampal stimulation in amygdaloid seiqure development. The common findings between the hippocampal and amygdaloid kindled animals were the systematic progression to seizures, the all-or-nothing nature of the electrical response and the relative permanency of the seizure susceptibility. Seizure susceptibility increased during slow wave sleep and decreased during REM sleep. These latter findings were examined with preliminary data of brain bioassays of catecholamines.

/pdf/kindling-secondary-epileptogenesis-sleep-and-catecholamines-1nxodh261u.pdf

Mitsumoto Sato

Papers

Kindling: secondary epileptogenesis, sleep and catecholamines.