2007
DOI: 10.1159/000109573
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Pathological Laughter as an Unusual Manifestation of Acute Stroke

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Cited by 14 publications
(7 citation statements)
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“…[ 5 ] Interruption of cortico-pontine-cerebellar pathways including the ventral pontomedullary laughing center has been implicated for pathological laughter in PCA stroke. [ 8 12 13 ] Memory impairment in our case might be due to involvement of lateral posterior choroidal arteries (branch of PCA), feeding inferomedial portion of temporal lobe, hippocampal gyrus, and hippocampus. Pain in the left half of body at earliest which improved later indicates thalamic involvement by thalamogniculate branches.…”
Section: Discussionmentioning
confidence: 85%
“…[ 5 ] Interruption of cortico-pontine-cerebellar pathways including the ventral pontomedullary laughing center has been implicated for pathological laughter in PCA stroke. [ 8 12 13 ] Memory impairment in our case might be due to involvement of lateral posterior choroidal arteries (branch of PCA), feeding inferomedial portion of temporal lobe, hippocampal gyrus, and hippocampus. Pain in the left half of body at earliest which improved later indicates thalamic involvement by thalamogniculate branches.…”
Section: Discussionmentioning
confidence: 85%
“…Although some reports show relationship of the left cerebral hemisphere to the production of laughter, 14 , 15) this case illustrates non-dominant hemisphere also have at least some influence. Although precise mechanism of pathological laughing is still unclear, extensive research to locate a precise area responsible for pathogenesis of pathological laughing has been done, but the following brain regions, namely basis pontis, 12 , 13 , 16 , 17) cerebellar white matter and gray matter, 18) basal ganglia, frontoparietal area, middle cerebral artery territory, 11 , 14 , 19 , 20) and frontal lobe 21) are advocated. In addition, by the study with ALS patients, McCullagh and Feinstein insisted the importance of the prefrontal cortex.…”
Section: Discussionmentioning
confidence: 99%
“…Lesions confined to the cerebellum [37][38][39], to the basis pontis, a relay center to the cerebellum [40][41][42], or to the thalamus, an output node from the cerebellum [43], have been sufficient to produce PBA symptoms without any other known brain pathology. Indeed, in a recent detailed review of the available neuroanatomical evidence for localization of PBA [30], the basis pontis, a convergence point for descending pathways carrying cerebellar input, "stands out as the only identified site where a discrete lesion can cause [PBA]."…”
Section: Cerebellar Mechanismsmentioning
confidence: 99%
“…Dextromethorphan binding is most prominent in the brainstem and cerebellum [66], brain areas known to be rich in s-1 receptors [67] and key sites implicated in the pathophysiology of PBA [37][38][39][40][41][42]. Evidence from an ERP study also suggests glutamatergic modulation at the cortical level [36].…”
Section: Dextromethorphan/quinidinementioning
confidence: 99%