Le bâillement, du réflexe à la pathologie

mise à jour du
19 mai 2002
2001, 124; Pt 9; 1708-19
Yawning: an evolutionary perspective
Pathological laughter and crying:
a link to the cerebellum
J. Parvizi, SW. Anderson, et al
Division of cognitive neuroscience, University of Iowa
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Resume : Patients with pathological laughter and crying (PLC) are subject to relatively uncontrollable episodes of laughter, crying or both. The episodes occur either without an apparent triggering stimulus or following a stimulus that would not have led the subject to laugh or cry prior to the onset of the condition. PLC is a disorder of emotional expression rather than a primary disturbance of feelings, and is thus distinct from mood disorders in which laughter and crying are associated with feelings of happiness or sadness. The traditional and currently accepted view is that PLC is due to the damage of pathways that arise in the motor areas of the cerebral cortex and descend to the brainstem to inhibit a putative centre for laughter and crying. In that view, the lesions 'disinhibit' or 'release' the laughter and crying centre.

The neuroanatomical findings in a recently studied patient with PLC, along with new knowledge on the neurobiology of emotion and feeling, gave us an opportunity to revisit the traditional view and propose an alternative.

Here we suggest that the critical PLC lesions occur in the cerebro-ponto-cerebellar pathways and that, as a consequence, the cerebellar structures that automatically adjust the execution of laughter or crying to the cognitive and situational context of a potential stimulus, operate on the basis of incomplete information about that context, resulting in inadequate and even chaotic behaviour.

Sander, K. and H. Scheich (2001). "Auditory perception of laughing and crying activates human amygdala regardless of attentional state." Brain Res Cogn Brain Res 12(2): 181-98.

Adequate behavioral responses to socially relevant stimuli are often impaired after lesions of the amygdala. Such lesions concern especially the recognition of facial and sometimes of vocal expression of emotions. Using low-noise functional magnetic resonance imaging (fMRI), we investigated in which way the amygdala, auditory cortex and insula are involved in the processing of affective nonverbal vocalizations (Laughing and Crying) in healthy humans. The same samples of male and female Laughing and Crying were presented in different experimental conditions: Simply listening to the stimuli, self-induction of the corresponding emotions while listening, and detection of artificial pitch shifts in the same stimuli. All conditions activated the amygdala similarly and bilaterally, whereby the amount of activation was larger in the right amygdala. The auditory cortex was more strongly activated by Laughing than by Crying with a slight right-hemisphere advantage for Laughing, both likely due to acoustic stimulus features. The insula was bilaterally activated in all conditions. The mean signal intensity change with stimulation was much larger in the amygdala than in auditory cortex and insula. The amygdala results seem to be in accordance with the right-hemisphere hypothesis of emotion processing which may not be applicable as strongly to the level of auditory cortex or insula.

Feinstein, A., P. O'Connor, et al. (1999). "Pathological laughing and crying in multiple sclerosis: a preliminary report suggesting a role for the prefrontal cortex." Mult Scler 5(2): 69-73.

As part of a wide ranging study investigating the prevalence, demographic and disease related characteristics of pathological laughing and crying (PLC) in multiple sclerosis (MS), a putative role for the prefrontal cortex was also explored. Eleven multiple sclerosis (MS) patients with carefully defined PLC were compared to a control group of 13 MS patients without PLC on various cognitive indices known to be sensitive to frontal lobe dysfunction. Although the two groups did not differ with respect to age, sex, physical disability, disease course, duration of MS, years of education, premorbid IQ, and depression, the PLC group performed more poorly on the Stroop test and a measure of verbal fluency. They also showed a trend to make more total errors on the Wisconsin Card Sort Test. The relevance of these findings to the pathogenesis of PLC is discussed, in particular whether the syndrome is, in part, mediated by dysfunction of the prefrontal cortex.

Gondim Fde, A., B. J. Parks, et al. (2001). "Fou rire prodromique as the presentation of pontine ischaemia secondary to vertebrobasilar stenosis." J Neurol Neurosurg Psychiatry 71(6): 802-4.

"Fou rire prodromique" (prodrome of crazy laughter) is a rare form of pathological laughter of uncertain pathophysiology. A patient is presented with pathological laughter as the first manifestation of pontine ischaemia due to vertebrobasilar stenosis. A 65 year old man developed uncontrollable and unemotional laughter for almost an hour followed by transient right facial-brachial paresis. He had fluctuation of laughter, right facial brachial paresis, and occasional crying. Magnetic resonance imaging, magnetic resonance angiogram (MRA), and an angiogram showed small left pontine and cerebellar infarcts, left vertebral artery occlusion, and right vertebral and basilar artery stenosis. His condition deteriorated to bilateral brain stem infarction and he died. Necropsy confirmed the extensive brain stem infarction. Pathological laughter can be the very first presenting manifestation of ischaemia of the ventrotegmental junction of the upper pons. It is hypothesised that the pathological laughter in this patient was secondary to ischaemic ephaptic stimulation of the descending corticopontine/ bulbar pathways.

McCullagh, S., M. Moore, et al. (1999). "Pathological laughing and crying in amyotrophic lateral sclerosis: an association with prefrontal cognitive dysfunction." J Neurol Sci 169(1-2): 43-8.

Pathological laughing and crying (PLC) frequently occurs in amyotrophic lateral sclerosis (ALS). The etiology of the syndrome is unclear, but frontal-subcortical circuits are implicated, given their known association with mood and affect regulation. Ten ALS patients with PLC, eight patients without, and ten healthy controls were compared on a number of psychometric measures. Three indices of prefrontal cortical function were given: the Wisconsin Card Sort Test (WCST), the novel 'Gambling task' and a measure of olfactory discrimination. Global cognitive ability, psychiatric symptoms, and illness variables were also examined. No significant between-groups differences emerged with respect to global cognitive ability, mood, olfaction, and performance on the Gambling task. On the WCST, however, patients with PLC made significantly more total errors than the other two groups, and showed a strong trend in a similar direction for perseverative errors. A discriminant function analysis revealed that the WCST variable 'total errors' correctly predicted the presence or absence of pathological affect in 75% of cases. Thus, PLC appears to be associated with impairment in the functional integrity of the prefrontal cortex. Although this was not found for all prefrontal measures, further investigation of this area appears warranted.