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At least 991 records · Page 55Linked to original sources
PubMed2002

Why not laugh?

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Adaptation, Psychological↗
PubMed2002

[A case of multiple sclerosis with pathological laughing caused by pontine base lesions].

We report a case of multiple sclerosis (MS) with pathological laughing for which lesions in pontine bases are considered to be responsible. A 30-year-old man was diagnosed as having MS based on left hemiparesis, and pathological laughing, and MRI findings showing a plaque in the right pontine base as well as several plaques in the bilateral periventricular deep white matter. After remission for 6 years, his pathological laughing exacerbated in association with development of right hemiparesis. A new lesion in the left pontine base was demonstrated by MRI studies in addition to a few supratentorial lesions. Steroid pulse therapy was effective for both pathological laughing and right hemiparesis. We speculate that the anatomical lesion responsible for the pathological laughing is located in the pontine base.

Adult↗
PubMed2003

[Gelastic seizures: etiology, semiology, therapeutic perspectives].

Gelastic seizures (laughing seizures) are a rare type of epileptic seizure in which laugh in a main and dominating manifestation of the seizure. As a rule, the seizures are caused by organic cerebral pathology and are often reported as a specific epilepsy marker related to hypothalamic hamartoma. The interictal EEG frequently shows a focal activity. Based on examination of 2 patients with gelastic seizures and hypothalamic hamartoma, clinical features, EEG characteristics and therapeutic perspectives for the disorder are discussed.

Adolescent↗
PubMedDate not supplied

[Leonardo's laugh].

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Famous Persons↗
PubMed2003

[A case of intractable epilepsy showing frequent gelastic seizures by administration of clobazam].

A 13-year-old boy patient had severe mental retardation and spastic quadriplegia due to fetal distress and hypoxic-ischemic brain damage in the perinatal period. He suffered from West syndrome at the age of 7 months, and subsequently was diagnosed as having symptomatic localization-related epilepsy. His intractable epileptic seizures were not controlled by combination of various antiepileptic drugs. After prescribing nitrazepam and zonisamide for more than 1 year, we added clobazam (CLB), which has been marketed in Japan since 2000, to this combination therapy. After the introduction of CLB, tonic seizures disappeared. However, gelastic seizures laughing with a stiff face and a wry mouth appeared frequently before falling asleep, and sleep disturbance worsened subsequently. It has not been reported previously that gelastic seizures are a side effect of CLB, although irritability and sleep disturbance have been described.

Adolescent↗
PubMed1976

The relationship between affective and cognitive development in Down's Syndrome infants.

A close association between affective expression and cognitive development was demonstrated in a longitudinal study of 14 Down's syndrome infants. It was found that the Down's syndrome infants laughed to groups of stimulus items in the same order as did previous samples of normal infants. Although the process was delayed by several months, the retarded babies too laughed first at physically intrusive items and only later to items calling for greater cognitive sophistication. In addition, cognitive developmental status, assessed by the Bayley and Uzgiris-Hunt scales, paralleled and was predicted by the level of affective development. Predictive and concurrent correlations between Bayley mental scores and various indices of affectivity ranged from .68 to .92. There was striking individual consistency across affective, mental, and motor measures, suggesting the organized nature of retarded development. Finally, since Down's syndrome infants frequently smiled under conditions when normal babies would laugh, a role for tension production, in addition to cognitive factors, was suggested in accounting for the behavior of these infants.

Affect↗
PubMed1977

Suppression of lymphoproliferation by high concentrations of normal human mononuclear leukocytes.

Mononuclear leukocytes (MNL) include cells that suppress lymphoproliferation in unstimulated and antigen-stimulated cultures. Suppression is demonstrated by increasing the concentration of cells added to cultures and does not require preactivation of suppressor cells. Suprression of 3H-thymidine incorporation occurred if the high concentrations of MNL were added to cultures before the proliferative responses commenced. This suppressive effect of high cell concentration upon 3H-thymidine incorporation is removed by depleting MNL present in high numbers of cells that adhere to foreign surfaces or by preincubating these cells with cycloheximide, puromycin, or pactamycin. The suppressor cell, which only functions when present in a viable state, is radioresistant, adheres to foreign surfaces, remains active through 5 days in culture, and equates with the presence of a cell that is rich in cytoplasmic esterase. The suppressor cell may be of the monocyte series and did not appear to belong to either the T or the B lymphocyte series. This study provides additional evidence that normal immune reactivity in man is under regulatory control. The suppressor mechanism identified herein with normal human MNL is probably related to a similar type of suppression (but at a much lower cell concentration) that has been described with Hodgkin's disease and solid tumors.

Aging↗