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PubMed1984

Laughter.

Knowledge of laughter, other than of its clinical manifestations, is tenuous. A unique, ubiquitous human phenomenon, laughter has largely been neglected by medical investigators and relegated to philosophers and naturalists, particularly Darwin. Clinical manifestations are well described, but the many physiological changes accompanying laughter are not. Neurological pathways remain speculative, and those described are based on pathological evidence. Laughter, as a behavior, has many causes, including humor, incongruity, relief, and a sense of well-being. Laughter may have developed for its cathartic effects and adaptive value. As an evolutionary device, laughter may have served to thwart aggression, spread information, and preserve social unity. Laughter's potential for a variety of clinical uses awaits future investigation.

Adolescent↗
PubMed2006

Pathological laughter in trigeminal schwannoma: case report and review of the literature.

Pathological laughter is an uncommon manifestation of neurosurgical diseases. Very few cases of trigeminal schwannoma have been reported in the literature presenting with pathological laughter as a predominant symptom. We are reporting on a case of multi-compartmental trigeminal schwannoma presenting as pathological laughter and discuss a review of the literature. A 23-year-old lady presented with pathological laughter, along with symptoms pertaining to other cranial nerves and cerebellar dysfunction. Magnetic resonance imaging (MRI) of the brain was suggestive of a dumbbell-shaped mass in the middle and posterior cranial fossa on the left side, causing significant compression of the pons. She was investigated and operated for multi-compartmental trigeminal schwannoma. Following surgery, abnormal laughter disappeared immediately and no recurrence of symptoms was -present for a follow-up of 16 months. This case supports the role of the brainstem, especially the pons, in the control of laughter and, perhaps, of the medial temporal lobe too.

Adult↗
PubMed1997

Pathologic laughter after unilateral stroke.

Pathologic laughter which usually occurs after bilateral or diffuse cerebral lesions was rarely reported in patients with unilateral stroke. I describe clinical and radiological findings of 13 patients presenting pathologic laughter due to unilateral stroke. Their laughter was excessive, unmotivated, uncontrollable and most often occurred during conversation especially at the initiation of speaking. There usually was a latent period between the onset of stroke and occurrence of the pathologic laughter. The degree and duration of the pathologic laughter varied, but its severity tended to diminish during the follow up. Some of them also had emotional instability evidenced by easy weeping. Imaging studies showed that 12 patients had infarcts and one had a haemorrhage. The lesions were located in the lenticulocapsular area in 8, pontine base in 3, thalamocapsular area in 1, and cerebral cortical-subcortical area in one. The lenticulocapsular stroke usually involved the upper part of the basal ganglia and a genu or an anterior portion of the posterior limb of the internal capsule/corona radiata. In conclusion, unilateral, usually subcortical, strokes can produce pathologic laughter. Although the neuroradiological data presented here generally support the motor release hypothesis, the delayed onset symptoms suggest that more complex mechanisms may be involved.

Adult↗
PubMed2001

Pathological laughter and crying: a link to the cerebellum.

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.

Cerebellum↗
PubMed1993

Vocal affect in three-year-olds: a quantitative acoustic analysis of child laughter.

Recordings were obtained of the laughter vocalizations of four 3-year-old children during three sessions of spontaneous free-play between mother and child in a laboratory playroom. Acoustic analysis was used to determine laughter durations, laughter events, F0, and harmonic characteristics, and to suggest a taxonomy of laughter types. Melodic contours were assessed from patterns of F0 change during laughter. Mean duration of laughs ranged from 200 ms to 2.0 s, but events within a laugh were usually about 200-ms duration. Laughs were intuitively classified into four major types, and, following the acoustic analyses, were further defined and classified into types and subtypes of exclamatory and dull comment; chuckle; basic, variable, and classical rhythmical; and squeal. Melodic contours included more rising contours than previously reported for cry, but there was great variability in the types of contours produced especially for rhythmical laughs. The results of the acoustic analyses are discussed in relation to (a) the development of a taxonomy of laughter and (b) different features of the vocal affect characteristics of high-intensity emotion.

Child Behavior↗
PubMed1999

Involuntary laughter and inappropriate hilarity.

Laughter is a particularly human behavior. Neuropsychiatrists are faced with disorders of laughter, yet the nature of this behavior and its disturbances remains obscure. The authors report an unusual patient with involuntary and unremitting laughter for 20 years and review the literature. The nature of laughter suggests that it has a unique role in human communication, particularly in the social exploration of incongruous information. The disorders of laughter suggest a neuroanatomical circuitry that includes the anterior cingulate gyrus, caudal hypothalamus, temporal-amygdala structures, and a pontomedullary center. Treatment includes the use of antidepressant and antimanic agents for disorders of laughter.

Aged↗
PubMed1989

Conspecific screams and laughter: cardiac and behavioral reactions of infant chimpanzees.

The present study examined cardiac and behavioral reactions of infant chimpanzees to white noise and to conspecific screams and laughter. Chimpanzee screams evoked typical deceleratory cardiac orienting responses. Analysis of stimulus-evoked changes in respiratory sinus arrhythmia suggested that this cardiac deceleration arose from an increase in parasympathetic activity. In contrast, chimpanzee laughter evoked notable cardiac acceleration. Laughter also evoked vocalizations from the infant subjects, which were reminiscent of adult threat-barks. Analysis of respiratory sinus arrhythmia suggested that the cardioacceleratory response likely resulted from sympathetic activation, and was not associated with an inhibition of parasympathetic activity. The autonomic and vocal responses to laughter emerged early in development, were minimally dependent on social contact with adults, and declined in magnitude with increasing age. A consideration of the phylogeny of laughter raised the possibility that the functional reaction to this vocalization may be related to its origin in more primitive agonistic facio-vocal signals.

Animals↗
PubMedDate not supplied

Patients' perception of laughter in a rehabilitation hospital.

This article describes a study of patients in a rehabilitation hospital regarding their perception of laughter and its effect on their mood, their opinion of nurses who laugh with patients, and the appropriateness of laughter in this setting. Results from 35 surveys indicated that patients welcome laughter and perceive nurses who laugh with their patients to be therapeutic. Coupled with information from the literature, which described the positive physical, psychological, and social benefits of laughter, the results of this survey support laughter as a therapeutic intervention that nurses can use in helping patients and families through the process of rehabilitation.

Adult↗
PubMed1992

The dynamics of laughter.

The benefits of humor have been accepted throughout human history. Humor is widely accepted for its positive physiological and psychological effects in a variety of situations. The psychiatric literature purports humor as an effective tool in psychiatric illness and psychotherapy. The benefits of humor in business, management, and education are also being described because the right perspective facilitates problem solving both interpersonally and in a group setting, and humor puts people at ease, promoting expression and the exchange of ideas. In the nursing literature, humor and laughter are increasingly presented as an approach that can assist the nurse in meeting health-related goals and objectives. Not only can humor benefit the patient, but the use of humor can facilitate effective management of staff and others encountered in the health care setting. Humor also has negative functions. Although the nursing literature on humor identifies that there are some situations in which humor is contraindicated, little attention is given to the problem created for the nurse when others, i.e., patients or family members, fellow staff members, or physicians, laugh inappropriately. This article discusses the assessment of laughter. Benefits of laughter and humor are described. The causes of inappropriate laughter are outlined, and the dynamics of inappropriate laughter are considered. Finally, implications for nursing practice are discussed.

Adaptation, Psychological↗
PubMed2004

Fou rire prodromique and history of pathological laughter in the XIXth and XXth centuries.

Fou rire prodromique (prodrome of crazy laughter) is a rarely described nosological entity. In 1903, Charles Féré, a French neurologist, introduced the term fou rire prodromique to describe pathological laughter heralding an apoplectic event. He was also among the first to describe gelastic epilepsy. His description was influenced by Edouard Brissaud, who supported the existence of a thalamic center for laughter regulation and suggested that spasmodic laughter and crying were due to lesions of the faisceau psychique (anterior internal capsule) or to irritation of the faisceau géniculé (corticobulbar tract). One hundred Years later, we review the evolution of the theories about pathological laughter and crying from Charles Bell in the early XIXth Century, up to the seminal works of Kinnier Wilson and James Papez and the era of modern neuroscience.

Crying↗
PubMed1975

Humorous laughter in children.

This experiment examines the notion that the sharing of humor enhances overt expressive responses (laughter and smiling) and humor ratings. Independent groups of seven- to eight-year-old children listened on headphones to amusing material. They were tested alone or in dyads or triads with confederates of the same sex. In triads, duration of laughter and smiling was inversely related to the amount that confederates looked at one another; this was the case whether confederates were thought to be listening to the same or different recordings. Laughter and smiling scores support the notion that sharing the social situation is crucial in the facilitation of "humorous laughter." A theory of socially facilitated laughter is proposed which draws upon social-facilitation drive theory and the tension-reduction aspects of humor theory.

Child↗
PubMed1996

Pathological laughter and crying in patients with closed traumatic brain injury.

We report on the clinical and radiological features in 16 adult patients who suffered a traumatic brain injury and subsequently developed pathological laughter and crying. Patients with pathological laughter and crying were identified from among 301 consecutive brain-injured admissions to a trauma centre and subsequently to a rehabilitation facility. Patients displaying pathological laughter and crying had a greater severity of injury than patients without the syndrome; they also had other associated neurological features compatible with pseudobulbar palsy. Pathological laughter alone, or combined with crying, was more frequent than crying alone. An attempt to correlate clinical features with focal lesions on neuroimaging studies yielded inconsistent results. The theoretical anatomical substrate for pathological laughter and crying in patients with traumatic brain injury is discussed.

Adolescent↗
PubMed2003

Neural correlates of laughter and humour.

Although laughter and humour have been constituents of humanity for thousands if not millions of years, their systematic study has begun only recently. Investigations into their neurological correlates remain fragmentary and the following review is a first attempt to collate and evaluate these studies, most of which have been published over the last two decades. By employing the classical methods of neurology, brain regions associated with symptomatic (pathological) laughter have been determined and catalogued under other diagnostic signs and symptoms of such conditions as epilepsy, strokes and circumspect brain lesions. These observations have been complemented by newer studies using modern non-invasive imaging methods. To summarize the results of many studies, the expression of laughter seems to depend on two partially independent neuronal pathways. The first of these, an 'involuntary' or 'emotionally driven' system, involves the amygdala, thalamic/hypo- and subthalamic areas and the dorsal/tegmental brainstem. The second, 'voluntary' system originates in the premotor/frontal opercular areas and leads through the motor cortex and pyramidal tract to the ventral brainstem. These systems and the laughter response appear to be coordinated by a laughter-coordinating centre in the dorsal upper pons. Analyses of the cerebral correlates of humour have been impeded by a lack of consensus among psychologists on exactly what humour is, and of what essential components it consists. Within the past two decades, however, sufficient agreement has been reached that theory-based hypotheses could be formulated and tested with various non-invasive methods. For the perception of humour (and depending on the type of humour involved, its mode of transmission, etc.) the right frontal cortex, the medial ventral prefrontal cortex, the right and left posterior (middle and inferior) temporal regions and possibly the cerebellum seem to be involved to varying degrees. An attempt has been made to be as thorough as possible in documenting the foundations upon which these burgeoning areas of research have been based up to the present time.

Brain↗
PubMed2005

Mirthful laughter differentially affects serum pro- and anti-inflammatory cytokine levels depending on the level of disease activity in patients with rheumatoid arthritis.

OBJECTIVES: To examine the effect of mirthful laughter in rheumatoid arthritis (RA), we evaluated the levels of serum cytokines before and after patients experienced mirthful laughter. METHODS: Forty-one patients with RA and 23 healthy subjects were enrolled. They listened to 'Rakugo', a traditional Japanese comic story, to induce mirthful laughter. We measured serum IL-6, IL-1beta, TNF-alpha, IL-4 and IL-1 receptor antagonist (IL-1Ra) concentrations before and after patients listened to the story. The RA subjects were divided into two groups. One was designated the 'difficult-to-control RA' group (CRP > or =1.0 mg/dl); The other group was regarded as the 'easily controlled RA' group (CRP <1.0 mg/dl). RESULTS: The basal levels of serum IL-6 and TNF-alpha in the RA patients were significantly higher than those in the healthy group. After experiencing mirthful laughter, the levels of serum IL-6 decreased significantly in the RA group but not in the healthy subjects. Interestingly, the level of serum TNF-alpha decreased only in the easily controlled RA group. Serum IL-4 concentration in the RA group was significantly higher than that in healthy subjects before the story. After the story, the level of serum IL-4 significantly decreased in the RA group, especially in the difficult-to-control RA group. In contrast, serum IL-1Ra concentration was statistically higher in the RA group than that in healthy subjects before the story, and a further increase was observed after the story, especially in the easily controlled RA group. CONCLUSIONS: Our findings suggest that mirthful laughter affects the levels of serum pro- and anti-inflammatory cytokines differentially, depending on the RA disease activity.

Adult↗
PubMed2005

Striatal reward areas activated by implicit laughter induced by mimic words in humans: a functional magnetic resonance imaging study.

The neurobiological reward components of laughter induced by words were investigated. A functional magnetic resonance imaging-based brain imaging study demonstrated that visualization of mimic words and emotional facial expression words, highly suggestive of laughter, heard by the ear, significantly activate striatal reward centers, including the putamen/caudate/nucleus accumbens, prefrontal cortices, dorsal anterior cingulate cortex and the supplementary motor area, while non-mimic words under the same task that did not imply laughter do not activate these areas in humans. We tested a specific hypothesis that implicit laughter modulates the striatal dopaminergic reward centers by image formation of onomatopoeic words implying laughter and successfully confirmed the hypothesis.

Adult↗
PubMed2004

Corticospinal excitability during laughter: implications for cataplexy and the comparison with REM sleep atonia.

Cataplexy is usually seen as rapid eye movement (REM) sleep atonia occurring at an inopportune moment. REM sleep atonia is the result of postsynaptic inhibition, i.e. inhibition of alpha motor neurones. Although this may explain the suppression of H-reflexes during REM sleep, cataplexy and laughter, it is not the only explanation. Presynaptic inhibition, in which afferent impulses are prevented from reaching motor neurones, is an alternative. Testing H-reflexes and magnetic-evoked potentials (MEPs) helps to tell them apart: in postsynaptic inhibition MEPs and H-reflexes change in tandem, while H-reflexes may decrease independent of MEPs with other inhibition modes. We studied motor inhibition during laughter, the strongest trigger for cataplexy. H-reflexes were evoked every 2 s in the soleus muscle in 10 healthy subjects watching comical video fragments. MEPs were evoked when H-reflexes decreased during laughter, and, as a control, when subjects did not laugh. Pairs of MEPs and the immediately preceding H-reflexes were studied. Compared with the control condition, laughter caused mean MEP area to increase by 60% (P=0.006) and mean H-reflex amplitude to decrease by 33% (P=0.008). This pattern proves that postsynaptic inhibition cannot have been the sole influence. The findings do not prove which mechanisms are involved; one possibility is that the decrease in H-reflex amplitude was the result of presynaptic inhibition, and that cortical and/or spinal facilitation accounted for increased MEPs. Regardless, the pattern differs fundamentally from the reported mechanism of REM sleep atonia. Existing scanty data on cataplexy suggest a pattern of H-reflexes and MEPs similar to that during laughter, but this needs further study.

Arousal↗
PubMed1989

Pathologic laughter and crying in ALS: a search for their origin.

Spells of laughter and crying are well known in patients with amyotrophic lateral sclerosis (ALS). Since ALS occurs mostly in older age groups, this brings up the possibility that aging changes in the brain could play a causative role in the origin of such spells. To rule out or at least reduce the complicating factor of aging, a study was made of the incidence of pathologic laughter and crying in patients whose motor neuron disease had started before the age of 45 years. The data were collected from 73 such individuals, all with confirmed ALS. All told, 36 had experienced episodes of pathologic laughter and/or crying. Of these, 20 had bouts of both laughter and crying. 9 bouts of crying alone and 7 spells of laughter alone. Nearly all with such emotional spells had developed bulbar involvement with the illness. The youngest patient with spells was 31 when his illness began and 35 when he started to have bouts of crying.

Adolescent↗
PubMed2006

Patterns of laryngeal electromyography and the activity of the respiratory system during spontaneous laughter.

Laryngeal muscle electromyography (EMG) and measures of the behavior of the respiratory system have been made during spontaneous laughter in two groups of subjects. The smaller group also had a direct measure of tracheal pressure during this behavior. Laryngeal adductors such as the thyroarytenoid (TA) and lateral cricoarytenoid (LCA) exhibited brief high-amplitude bursts of activity, at a rate of approximately 5 Hz, which were usually associated on a 1 : 1 basis with the sound bursts (ha ha ha) of laughter. The laryngeal abductor, posterior cricoarytenoid (PCA), also showed bursts of activity that were out of phase with TA and LCA. The cricothyroid (CT) was only weakly, if at all, modulated during the bursting activity of the other laryngeal muscles. Tracheal pressure usually exhibited positive pressure pulses during laughter that were often, but not always, temporally correlated to the bursts of laryngeal adductor EMG activity. Such pressure modulations appeared to precisely determine when-and if-phonation was produced during the laugh. During laughter, laryngeal EMG is highly stereotyped both within and between subjects. In most instances, this activity appears to be supported by coordinated pulses of tracheal pressure. The periaqueductal gray (PAG) has been shown in animal studies to produce emotionally indicative vocalizations, in which the laryngeal and respiratory system are coordinated. Therefore, it is suggested that the PAG is involved with the production of laughter.

Action Potentials↗