The prevalence of crying in acute stroke patients has been estimated at between 12% and 27%, but disorders of emotional expression control are more frequent (11-40%) and often appear delayed after stroke onset . This disorder consists of uncontrollable outbursts of laughing, crying or both, with paroxysmal onset, transient duration of seconds or minutes, stereotyped, precipitated by nonspecific or inappropriate stimuli but also by appropriate stimuli in an inappropriate context. Patients cannot control the extent or duration of the episode. The outbursts are incongruent or exaggerated in comparison with the emotional feelings. There is no mood change during the episode and no sense of relief when it ends. There are many crying situations and many content areas of crying situations. The crying frequency is very high. It is more frequent in men and in the presence of others.
Disorders of emotional expression control are sometimes associated with depression but more often they can be dissociated. Other behavioral and cognitive correlates include irritability and ideas of reference, decreased sexual activity and lower MMSE
scores. Disorders of emotional expression control have an adverse impact on the quality of life of stroke survivors. They can disrupt communication, cause embarrassment and therefore curtail social activities.
Disorders of emotional expression control have been classically associated with bilateral subcortical strokes. More recent systematic studies have shown that they can follow not only bilateral subcortical strokes, but also bilateral pontine and unilateral strokes, including large anterior, cortico-subcortical lesions, lenticulocapsular or thalamocapsular lesions, and also basal pontine strokes.
The pathophysiology of the uncontrolled outbursts of laughing and crying is poorly understood. Wilson  proposed a patho-anatomical model consisting of a putative fasciorespiratory control center for emotional expression located in the brainstem with a dual route of control from the motor cortex: a voluntary pathway through the pyramidal and gen-iculate tracts, which initiates voluntary laughter and crying and inhibits involuntary initiated laughter or crying, and an involuntary pathway consisting of a frontal/temporal-basal ganglia-ventral brainstem circuitry, which initiates and also terminates involuntary laughter or crying. Uncontrolled laughing and crying could result from release of the fasciorespiratory control center from the motor cortex or from disruption of the involuntary pathway. Parvizi and the Damasios  proposed a modified version of Wilson's model, in which the cerebellar structures play a role in adjusting the execution of laughter and crying to the cognitive and situational context. There is recent evidence of disruption of ascending serotoninergic pathways in disorders of emotional expression control.
An uncontrollable prolonged burst of laughing, called after Fere fou rire prodromique, can exceptionally anticipate by seconds to days the onset of the focal deficit in acute stroke .
Disorders of emotional expression control (outbursts of laughing, crying or both) are frequent and are often associated with bilateral subcortical strokes.
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