Neuroanatomical Hypotheses

Evidence for the neuroanatomy of pathological laughter and crying comes from the following sources: a limited number of autopsy reports; studies of congeni-tally malformed infants; case reports of patients with pathological laughter following neurological disease; EEG activity and electrical stimulation of the cortex; injection of a barbiturate to the right or left cortex, typically done in patients with epilepsy to determine the language-dominant hemisphere; and studies of humor comprehension in patients with left versus right hemisphere damage.

The autopsy data are of limited value in localizing laughter since the patients had suffered diffuse brain pathology. A review of such cases revealed no single cortical lesion as causing PLC. Together with clinical case reports, the autopsy data indicate that both unilateral and bilateral lesions that affect the descending tracts to the bulbar nuclei can cause PLC, as can lesions on either side in the anterior limb and genu of the internal capsule adjacent to the basal ganglia, thalamus, hypothalamus, and pons. Even localized brain stem lesions can cause pathological laughter. Case studies do not explain why some patients develop pathological laughter while others develop pathological crying or both. Studies of congenitally malformed newborns with severe anencephaly but with preserved pons and medulla indicate that newborns do not smile but can cry; those with intact midbrains can both cry and smile.

The predominant neuroanatomical account of pathological laughter and crying, first proposed by Wilson, regards it as arising from a loss of direct motor cortical inhibition of a laughter and crying center located in the upper brain stem. However, this explanation does not fully account for the range of phenomena observed in PLC. A recent alternative account, developed by Parvizi and colleagues, in light of new neuropathological findings, suggests that PLC is caused by dysfunction in circuits that involve the cerebellum (as well as the cortex) and influence brain stem nuclei.

There is evidence that the cerebral hemispheres may play different roles in the control of emotional states. In normal subjects the right hemisphere appears to be specialized for the perception and expression of emotion, particularly negative emotion. Lesions in the right hemisphere have been found to impair prosodic and lexical expression of emotion. Moreover, in epileptic subjects, injection of the right hemisphere with intracarotid sodium amytal has elicited unprovoked laughter, whereas left-sided injection has tended to produce bouts of crying. Patients with crying seizures tend to show right-sided foci, whereas those with gelastic seizures show mainly left-sided foci.

Patients with right hemisphere damage show a preserved sensitivity to the surprise element of humor but a diminished ability to establish narrative coherence. Disorders of humor, such as foolish or silly euphoria (so-called moria), and a tendency toward making inappropriate jokes (so-called witzelsucht), have been reported in patients with frontal lobe disorders including neurosyphilis. In 1999, a functional neuroimaging study by Shammi and Stuss determined that deficits in humor appreciation are restricted to patients with right frontal damage, supporting the view that the right frontal lobe serves an important role in integrating cognitive and affective information.

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