Discussion
Pathological laughing has been reported across literature in cases of tumor1,2, infarction and abscess3. The exact mechanism is still poorly understood, with various pathological proposals. Oppenheim, Siemerling, and Wilson suggested that modulation is facilitated by direct corticobulbar pathways and in a liner top-down model.4,5 They posited that PLC occurs when the voluntary control of the emotional expression fails due to bilateral lesions of the descending corticobulbar tracts. Parvizi et al, suggested that an intact relationship between the cerebral cortex and cerebellum is important for a normal regulation of emotional expression.6 They propose therefore that problems with an exaggerated or contextually inappropriate emotional response result when the cerebellar modulation of these behaviors is impaired by a lowered emotional threshold, or by a incorrect, contextually inappropriate response. Wilson et al, suggested that a brainstem faciorespiratory center could act as a mechanism of this phenomenon.5 This center was presumed to be under the control of higher centers, and pathological laughter was thought to ensue when they were incapable of exerting their inhibitory influence on the faciorespiratory center.
Structures such as the pre frontal cortex, anterior cingulated cortex, internal capsule, thalamus, subthalamic nucleus, basis pontis, and cerebellar white and gray matter have been implicated in PLC, as revealed by many studies. The basis pontis stands out as the only identified site where a discrete lesion can cause PLC.7
Functional imaging studies have proved helpful in discovering the neural correlates for both pathological and normal regulation of emotional expression.8 They used three types of fMRI experiment tasks, including facial recognition,semantic decision, and motor function to establish the response to non-specific stimuli. The patient showed consistently abnormal pontine activation while performing all tasks before treatment, which was not present for any of the controls. However, the exaggerated pontine activation was normalized after patients were treated with paroxetine, terminating the laughing episodes. Thus, their study suggested that serotonergic replacement decreases the aberrant activity in a circuit that involves the pons.
Various reports suggested that tricyclic antidepressants such as amitriptyline and nortriptyline and selective serotonin reuptake inhibitors (SSRIs) are effective in treating PLC.9,10Abnormal fMRI results disappearing with clinical improvement after treatment with paroxetine also suggested some SSRI efficacy in PLC.8
Pathological laughing was the only feature shown by the case reported. The patient’s postoperative recovery was uneventful with mild hemiparesis and facial palsy. He had no purposeless laughing after the surgery. The patient was discharged with satisfactory outcome with a KPS of 50%. Postoperatively, the patient was scheduled for referral to a cancer center for further treatment. However, he suffered from pneumonia and passed away in another local hospital during the pneumonia treatment process.