Neurology of laughter and humour: pathological laughing and crying

Introduction. Laughter, which is usually a healthy biological phenomenon, may be also a symptom of several severe brain pathologies. Aim. To review the neurobiological bases of laughter and humour, as well as those of pathological laughing and crying syndrome. Development. At the mesencephalic-pontine junction there is a central coordinator of the nuclei that innervate the muscles involved in laughter (facial expression, respiratory and phonatory). This centre receives connections from three systems: inhibitory (pre-motor and motor cortex), excitatory (temporal cortex, amygdala, hypothalamus) and modulator (cerebellum). Humour is a complex phenomenon with a range of components: the perception of the unexpected incongruence (occipitotemporal area, prefrontal cortex), emotional (reward circuit) and volitional (temporal and frontal cortex). Functional magnetic resonance imaging studies do not reveal a markedly prominent role of the right frontal lobe in processing humour, as had been suggested in the classical studies. The causes of pathological laughing and crying syndrome can be classified in two groups: altered behaviour with unmotivated happiness (Angelman syndrome, schizophrenia, manias, dementia) and interference with the inhibitory/excitatory mechanisms (gelastic epilepsy, fou rire prodromique in strokes, multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease and Parkinson-plus, traumatic injuries, tumours). Serotonin and noradrenalin reuptake inhibitors, levodopa, lamotrigine and the association of dextromethorphan/quinidine can be effective in certain cases of pathological laughing and crying. Conclusions. As human neurobiological phenomena, laughter and humour also belong to the field of clinical neurology; their processing is affected in a number of different diseases and, in certain cases, effective treatment can be established.