Reduced emotionality in humans, albeit one that is very restricted in scope, is associated with acute lesions in the right, or nondominant, parietal lobe. The patient may not only be indifferent to the accompanying paralysis but, as Bear points out, also appear unconcerned about other diseases as well as personal and family problems, be less able to interpret the emotional facial expressions of others, and be inattentive in general. There may be a lack of emotional inflection to speech (aprosodia) and an inability to interpret the emotional state of other individuals, as discussed in Chap. 22. Dimond and coworkers interpret this to mean that the right hemisphere is more involved in affective-emotional experience than the left, which is committed to language. Observations derived from the study of split-brain patients and from selective anesthetization of the cerebral hemispheres by intracarotid injection of amobarbital (Wada test) lend some support to this probably oversimplified view. Rarely, lesions of the left (dominant) hemisphere appear to induce the opposite effect, a frenzied excitement lasting for days or weeks.
The normal pattern of sexual behavior in both males and females may be altered by cerebral disease quite apart from impairment due to physical disability or to diseases that affect segmental reflex mechanisms (see Chap. 26).
Hypersexuality in men or women is a rare but well-documented complication of neurologic disease. It has long been believed that lesions of the orbital frontal lobes may remove moral-ethical restraints and lead to indiscriminate sexual behavior, and that superior frontal lesions may be associated with a general loss of initiative that reduces all, including sexual, impulsivity. In rare cases, extreme hypersexuality marks the onset of encephalitis or develops gradually with tumors of the temporal region. Possibly the limbic parts of the brain are disinhibited, the ones from which MacLean and Ploog could evoke penile erection and orgasm by electrical stimulation (medial dorsal thalamus, medial forebrain bundle, and septal preoptic region).
In humans, Heath has observed that stimulation of the ventroseptal area (through depth electrodes) evokes feelings of pleasure and lust. Also, Gorman and Cummings have described two patients who became sexually disinhibited after a shunt catheter had perforated the dorsal septal region. This is in keeping with the experience of Heath and Fitzjarrell, who found that infusion of acetylcholine into the septal region (as an experimental treatment for Parkinson disease) produced euphoria and orgasm, and with Heath’s recordings from the septum of patients during sexual intercourse, showing greatly increased activity with spikes and slow waves. Although it remains unproven, perhaps these are examples of a true overdrive of libido, as contrasted with simple disinhibition of sexual behavior.
In clinical practice, the most common cause of disinhibited sexual behavior, next to the aftermaths of head injury and cerebral hemorrhage, is the use of dopaminergic drugs in Parkinson disease. An intriguing effect of the administration of l-dopa in a few patients has been excessive or perverse sexual behavior, as in the cases described by Quinn and colleagues. Usually there are other manifestations of manic behavior. Primary mania may do the same.
Hyposexuality, meaning loss of libido, is a typical accompaniment of depressive illness. However, certain medications, notably antihypertensive, antiepileptic, serotonergic antidepressant, and neuroleptic drugs may be responsible in individual patients. A variety of cerebral diseases may also have this effect, in parallel with a loss of interest and drive in a number of spheres.