Alterations in grip strength during male sexual arousal.

Although it is known that alterations in grip strength occur under a number of conditions, little is known about relationships between grip strength and sexual arousal. This relationship was investigated in 30 healthy heterosexual males, who viewed both erotic and nonerotic videos. A questionnaire was used to assess the extent of sexual arousal. The grip strengths of both hands were measured with a five-position (P1-P5) dynamometer, before and after watching the videos. After watching the erotic video, there was a statistically significant reduction in grip strength for the P2 position, with nonsignificant overall reductions in grip strength for all other positions tested. No such effect was observed in control tests. The results indicate that during sexual arousal, the neural system is likely to reduce the output to muscles not directly related to sexual function, presumably to enhance the physiological responses of sexual arousal.

Dysphagia in lateral medullary infarction (Wallenberg's syndrome): an acute disconnection syndrome in premotor neurons related to swallowing activity?

BACKGROUND AND PURPOSE: We have investigated the pathophysiological mechanisms of dysphagia in Wallenberg's syndrome (WS) that are due to lateral medullary infarction (LMI). METHODS: Twenty patients with WS were evaluated by means of clinical and electrophysiological methods that measured the oropharyngeal phase of voluntarily initiated swallowing. For comparison, 22 patients with unilateral hemispheric infarction were investigated during the acute stage of stroke, and 4 patients with unilateral peripheral 9th and 10th cranial nerve palsies were studied. Age-matched 30 healthy control subjects were also included in the study. RESULTS: It was found that dysphagia was clinically more severe in WS patients than in the patients in the other groups. The pharyngeal phase of swallowing was predominantly impaired, whereas in patients with hemispheric stroke, dysphagia was related only to the delay of triggering of the voluntarily induced swallowing. In WS patients, the swallowing reflex was extremely slow in spite of the unilateral involvement due to LMI, whereas the pharyngeal phase of reflex swallowing remained within normal limits in patients with unilateral hemispheric stroke and patients with unilateral peripheral 9th and 10th cranial nerve palsies. CONCLUSIONS: Although in WS the lesion due to LMI is unilateral, its effect on oropharyngeal swallowing is bilateral. In LMI, primarily the premotor neurons in the nucleus ambiguous and their connections seem to be affected. Consequently, a disruption and/or disconnection of their linkage to swallowing-related cranial motor neuron pools bilaterally and to the contralateral nucleus ambiguous could produce the swallowing disorders in WS. However, the remaining intact ipsilateral premotor neurons and the contralateral center in the medulla oblongata may eventually begin to operate and overcome the severity and long-term persistence of dysphagia.

Cricopharyngeal sphincter muscle responses to transcranial magnetic stimulation in normal subjects and in patients with dysphagia.

OBJECTIVE: Cricopharyngeal (CP) muscle of the upper oesophageal sphincter (UES) has a significant role in the pharyngo-esophageal phase of deglutition. The linkage between the CP muscle of UES and the motor cortex has not been previously studied electrophysiologically in healthy humans and in patients with neurogenic dysphagia. METHODS: Needle recordings of EMG responses were carried out from the CP sphincter muscle following transcranial magnetic stimulation (TMS) over the vertex around the Cz electrode position (cortical MEP), and on the parieto-occipital skull and the occiput ipsilaterally (peripheral MEP) in 14 healthy control subjects and in 26 patients with and without neurogenic dysphagia. Needle recordings obtained from the cricothyroid muscle of the larynx were also evaluated in six healthy subjects. RESULTS: The cortical motor latency of CP sphincter muscle was 10.7+/-0.5 ms with an amplitude of 0.8+/-0.2 mV in healthy subjects. Both the latency and amplitude of CP-MEP were facilitated during swallowing. The peripheral MEP of the CP muscle was very stable in all normal subjects (5.1+/-0.3 ms; 1.3+/-0.3 mV) and swallowing did not influence these parameters. The cortically elicited CP-MEP was significantly longer than the cortical MEPs obtained from the cricothyroid muscle of the larynx. In 10 dysphagic patients with corticobulbar tract involvement (6 ALS and 4 pseudobulbar palsy) and with pathologic and hyperreflexic EMG of the CP-sphincter muscle, the cortical MEP of CP muscle of the upper esophageal sphincter could not be elicited, although the peripheral CP-MEPs were obtained. TMS never produced a swallowing movement in neither healthy subjects nor patients. CONCLUSION: The CP muscle of the upper esophageal sphincter can produce MEPs by cortical TMS and by stimulation at the root/nerve levels of vagus nerve. The MEP latency values and central motor delay suggest that there is an oligosynaptic corticobulbar pathway to the motoneurons of CP muscles. When the pathway is affected by a pathology (i.e. ALS or pseudobulbar palsy) the CP sphincter becomes hyperreflexic due to disinhibition and the cortical MEP of the CP muscle disappears due to degeneration of the corticobulbar pathway. These mechanisms appear to be responsible for the pathogenesis of dysphagia.