Hyposexuality produced by temporal lobe epilepsy in the cat.

PURPOSE: The hypothesis tested in this study was that a unilateral irritative focal epileptic lesion in the temporal lobe results in hyposexuality. METHODS: Focal epilepsy was produced in male cats by unilateral injection of aluminum hydroxide into either the basolateral amygdala (temporal lobe group) or anterior sigmoid gyrus (motor cortex group). Weekly sex testing trials with estrous females were conducted prior to and after aluminum hydroxide injection, and mating performance scores were compared with those of normal, unoperated cats (normal control group). RESULTS: All animals receiving aluminum hydroxide developed electroencephalographic and behavioral manifestations of epilepsy; i.e., interictal EEG spiking and partial or generalized seizures. Cats in the temporal lobe group exhibited a dramatic and complete suppression of sexual behavior at periods from 6 to 26 weeks after aluminum hydroxide injection. The duration of the hyposexuality varied between individual animals and returned to normal as suddenly as the onset occurred, despite the use of AEDs to prevent or control generalized seizure activity. Interictal EEG epileptiform spiking in the amygdala preceded the onset of hyposexuality by 1-12 weeks. By contrast, cats in the motor cortex and normal control groups showed no sign of sexual dysfunction throughout the experimental period, independent of seizure activity and/or antiepileptic drug (AED) treatment. CONCLUSIONS: These data support the hypothesis that hyposexuality occurs as a result of epileptiform activity in the temporal lobe, but not in the motor cortex. The precise mechanisms by which this occurs are unknown, but are likely to involve abnormally high-frequency neuronal activity in temporal lobe structures known to connect with and/or to regulate hypothalamic nuclei that organize male sexual behavior toward receptive females.

The relationship between traumatic brain injury-induced changes in brain temperature and behavioral and anatomical outcome.

Alteration of brain temperature, experimentally induced or spontaneous, has been shown to affect the symptoms resulting from a variety of cerebral insults. This study examined the effect of traumatic brain injury (TBI) on brain and body temperature in rats and the relationship between TBI-induced temperature changes, neuropathology, and behavioral recovery. Anesthesia, surgery and TBI all caused changes in brain and body temperatures. The level of brain (but not body) temperature at the time of TBI was positively correlated with the severity of hippocampal and thalamic pathology. In contrast, the measured levels of both brain and body temperatures after TBI were not related to behavioral or neuroanatomical outcome. Interestingly, the increase in brain (but not body) temperature from the time of TBI to 5 to 10 minutes after termination of anesthesia was negatively correlated with behavioral and anatomical outcome. Simply stated, the more rapidly brain temperature returned toward normal, the better the rats' behavioral and anatomical outcome. This rate of return toward normal brain temperature is not interpreted as causally related to outcome but rather as an index of the severity of brain injury.

Chronic dorsal column stimulation: effects on H reflex and symptoms in a patient with multiple sclerosis.

In a case of severe multiple sclerosis primarily affecting the spinal cord, dorsal column stimulation over a 2-year period was followed by some functional improvement in locomotion. Additionally, the H reflex recovery cycle, which was quite abnormal before stimulation, showed a pronounced shift toward a more normal pattern with dorsal column stimulation. These data provide objective support for the apparent symptomatic relief by this procedure in such cases.

Sensory neglect after lesions of substantia nigra or lateral hypothalamus: differential severity and recovery of function.

Sensory neglect was studied in cats after unilateral lesions of: lateral hypothalamus (LH); internal capsule (IC) adjacent to the LH; substantia nigra (SN) or the ventromedial hypothalamus (VMH). Special behavioral tests were employed to yield quantifiable data and also to exclude any confounding due to simple movement deficits. Lesions of SN or IC produced severe and enduring contralateral visual and somesthetic deficits and a facilitation of ipsilateral visual responsiveness. In contrast, LH lesions sparing the adjacent IC produced only weak and transient deficits and VMH lesions had no effects on sensory function. This suggests that lesions of the SN or its forebrain connections are important for producing sensory neglect and that sensory deficits after LH lesions are due to infringement on fibers of passage to or from the SN. Lesions which produced neglect often suppressed the amplitude of flash evoked responses in the ipsilateral caudate nucleus and visual and association cortex. However, these evoked potential effects were transient. There was no effect on the spontaneous EEG and this fails to support the hypothesis of a lack of hemispheric arousal in sensory neglect. The results are discussed in relation to nigrotectal projections and the process of attention. This lesion-behavior model is suggested for studies of recovery of function.

Suppression of cortical epileptiform activity by generalized and localized ECoG desynchronization.

The effects of high frequency electrical stimulation of both diffusely projecting brain regions and regions of more restricted projection were studied on penicillin-induced cortical epileptiform focal activity in the cat. Results obtained were contingent on the level of focal activity present at the time of stimulation. Very active foci (spike rates above 0.5/sec) were uniformly driven by stimulation of all structures under study. Foci exhibiting weak to moderate levels of activity were, on the other hand, inhibited both during and following stimulation. Episodes of spike suppression induced through stimulation of diffusely projecting structures were typically followed by an intensified "rebound" of interictal activity. Episodes of suppression induced through stimulation of regions of limited projection were not followed by such rebounds, an effect most dramatically apparent with caudate stimulation and motor cortex foci. Results are discussed in terms of the interaction between naturally occurring brain rhythms in sleep and arousal with the epileptic process.