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.