Does the Cerebellum Have a Sense of Humor?
Abstract & Commentary
Source: Parvizi J, et al. Pathological laughter and crying. A link to the cerebellum. Brain. 2001;124:1708-1719.
The term pathological laughter and crying (PLC) refers to uncontrollable episodes of laughter or crying that occur without apparent reason or with insufficient cause. PLC, therefore, is a disorder of emotional expression rather than a primary disturbance of mood. The most common cause of PLC is pseudobulbar palsy but it also has been reported in multiple sclerosis, gelastic epilepsy, and in association with infarcts and tumors of posterior fossa structures.
Parvizi and associates studied a 51-year-old righthanded man with PLC following a right cerebellar stroke. Pathological crying was noted by his family immediately after the stroke and pathological laughter soon afterwards. Acutely, the neurological evaluation was remarkable for gait ataxia and dysmetria of the right limbs. Cranial nerve examination was normal except for gaze-evoked nystagmus on rightward gaze.
Fourteen months later, ambulation and coordination had improved but PLC persisted unchanged. On cognitive testing, attention and recent memory were mildly impaired, executive function was more impaired. There were no depressive or anxiety-related symptoms.
On MRI there were 3 small infarcts in the right and left middle cerebellar peduncles and mid basis pontis, and 2 larger infarcts in the superior and inferior semilunar lobules of the right cerebellar hemisphere. No lesions were detected elsewhere in the brain.
Based on their evaluations, Parvizi and colleagues concluded that there was a partial deafferentation of the cerebellum from descending inputs of left telencephalic structures. Therefore, they postulate that PLC in this case was due to disruption of pathways between forebrain structures that process emotionally competent stimuli and their relevant context, and then signal this information to the cerebellum. The cerebellum in turn computes a certain profile and level of emotional response which it then communicates to cortical and subcortical motor areas involved in generating emotional responses.
The patient’s PLC improved following administration of a selective serotonin reputake inhibitor (SSRI), in accord with previous reports that the condition is responsive to treatment with either SSRI or tricyclic antidepressants.
In times past, philosophers and psychologists pondered over the mechanism of laughter. Ever since the discovery of "laughing gas," or nitrous oxide anesthesia, in the last century, scientists have examined laughter as a chemical and physical phenomenon that is distinct from an emotional state of amusement.
PLC is an example of laughter divorced from emotion and context. The patient with PLC not only laughs or cries for no apparent reason, but also may both laugh and cry in response to the same stimulus. In other situations, a patient may laugh inappropriately in response to sad news. In patients with pseudo bulbar palsy, PLC has been explained as a result of disinhibition of subcortical "centers for laughing and crying," presumably located in the brainstem adjacent to the facial nerve nuclei and respiratory control nuclei. Disinhibition or mere loss of cortical control cannot explain the phenomena observed in patients with PLC.
Parvizi et al’s alternative view of PLC helps to explain some of the clinical phenomenology in affected patients but it also raises questions that only further neuroanatomical and neurophysiological studies can answer. —John J. Caronna
Dr. Caronna, Vice-Chairman, Department of Neurology, Cornell University Medical Center; Professor of Clinical Neurology, New York Hospital, is Associate Editor of Neurology Alert.