Pathological laughter as a presenting symptom of petroclival meningioma--case report.
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A 35-year-old male presented with symptoms of 'pathological laughter' occurring for 6 months and progressive ataxia and right facial nerve paresis for 2 months. Neuroimaging revealed a large petroclival meningioma. The tumor was well defined and only moderately vascular, and could be relatively easily resected. The symptom of pathological laughter disappeared immediately and his gait improved to normal within a week of surgery. Pathological laughter as a presenting symptom of petroclival meningioma is extremely rare. The symptom of pathological laughter may have localizing value. (+info)
Tentorial meningioma associated with pathological laughter--case report.
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A 33-year-old male presented with involuntary and inappropriate laughter. Neuroimaging revealed a meningioma ventrolateral to the pons and midbrain, attached to the medial middle tentorium on the left side. The pathological laughter ceased immediately after subtotal removal of the tumor. Pathological laughter may be an early focal sign of a mass compressing ventrolateral brainstem. (+info)
Effects of laughing and weeping on mood and heart rate variability.
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We investigated the effects of laughing and weeping induced by watching comedy and tragedy videos on mood and autonomic nervous function. Ten healthy female subjects volunteered for the experiment. Chest electrocardiogram and respiration curve were recorded before, after, and during watching a comedy or a tragedy video. We also asked them to fill out profiles of mood states (POMS) to evaluate their mood states while watching videos. Autonomic nervous function was estimated by spectral analysis of heart rate variability (HRV). All subjects more or less laughed and wept while watching comedy and tragedy videos, respectively. Anger-hostility score of the POMS decreased and vigor score increased significantly after watching comedy videos, while depression-dejection score increased significantly after watching tragedy ones. Although both contents tended to increase a low to high frequency component ratio (LF/HF ratio) of HRV, the time course of responses was different. The LF/HF ratio which reflects cardiac sympathovagal balance increased immediately after they started watching comedy videos, and returned to the basal level right after they stopped watching, whereas the LF/HF ratio increased gradually to a lesser extent while watching tragedy videos. In contrast, the high-frequency component which reflects cardiac parasympathetic nerve activity gradually decreased while watching both videos but did not return to the basal level after watching tragedy ones. These results suggest that laughing has strong but transient effects on the autonomic nervous system, while weeping or feeling sad has moderate but sustained effects on it. (+info)
Pathological laughter in a patient with trigeminal neurinoma.
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We present a 47-year-old woman with a long history of anxiety and a more recent history of shock-like facial pain and episodes of laughter without any motivation. She could not explain the laughing bursts and did not have a sense of mirth preceding it. On neurological examination she presented a VI nerve palsy and trigeminal hypoesthesia (V2 and V3) on the right side. Magnetic resonance imaging exhibited a large cystic lesion on the right middle fossa causing significant compression on the brain stem. A frontoorbitozygomatic and pretemporal combined approach was performed. During intra and extradural exploration a large tumor was found on the trigeminal nerve. The whole lesion was resected, revealing to be a neurinoma on pathological exhamination. She maintained a VI nerve palsy but had complete remission of the unmotivated laughing episodes during the one year follow up. (+info)
Disconnecting surgical treatment of hypothalamic hamartoma in children and adults with refractory epilepsy and proposal of a new classification.
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A series of 17 patients aged from 9 months to 32 years with refractory epilepsy due to hypothalamic hamartoma were treated by total removal (one case) and disconnection (16 cases) between 1997 and 2002. The mean age at seizure onset was 16 months. Sixteen patients had gelastic seizures, 14 had partial seizures and three had generalized tonic-clonic seizures. The mean seizure frequency was 21 per day. Four patients had borderline intelligence quotient and the others were mentally retarded. Five patients presented with precocious puberty, one with acromegaly, and four suffered from obesity. Brain magnetic resonance imaging, performed at least twice in each patient, showed the hamartoma as a stable homogeneous interpeduncular mass implanted either on the mammilary tubercle or on the wall of the third ventricle with variable extension to the bottom. Ictal single photon emission computed tomography, performed in four patients, showed hyperperfusion within the hamartoma in two patients. Twenty-five operations were performed in the 17 patients. The first patient underwent total removal of the hamartoma, whereas the following 16 patients underwent disconnection through open surgery (14 procedures) and/or endoscopy (9 procedures). Eight patients became seizure-free, one patient had only brief gelastic seizures, and eight patients were dramatically improved with a mean follow up of 18.6 months (8 days to 43 months). Surgery was safe in all but two patients: the first patient had transient hemiplegia and the third cranial nerve paresis, and the other developed hemiplegia due to ischemia of the middle cerebral artery territory. The quality of life, and behavior and school performance were greatly improved in most patients. Our series illustrates the feasibility and relative safety of disconnection surgery for hypothalamic hamartomas with seizure relief in 53% of patients and dramatic improvement in the others. Surgical observations led us to propose a new anatomical classification according to the anatomical relationship between the hamartoma and the adjacent hypothalamus and third ventricle. Endoscopic disconnection seems to be a very safe way to treat hamartomas in intraventricular locations. (+info)
Neural correlates of laughter and humour.
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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. (+info)
Corticospinal excitability during laughter: implications for cataplexy and the comparison with REM sleep atonia.
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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. (+info)
Kinematical analysis of emotionally induced facial expressions: a novel tool to investigate hypomimia in patients suffering from depression.
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OBJECTIVE: A novel technique for the kinematic analysis of emotionally induced facial expressions was applied to detect subtle mimic dysfunction in patients with depression. METHODS: Using ultrasound markers at certain points on the face, facial movements were exactly measured while subjects watched a witty sketch ("Mr Bean"). Twenty five medicated patients with depression (11 men, 14 women; mean age, 55.8 years; mean total Hamilton Depression Rating Scale score, 17.1) and 25 healthy controls, matched by sex distribution and handedness, were studied. RESULTS: Depressed patients were characterised by abnormally slow velocity at the beginning of laughing and voluntary facial movements, in addition to reduced laughing frequency. A higher severity of symptoms of depression was significantly associated with slow initial velocity of laughing movements of the left mouth angle (r = -0.45). CONCLUSION: The execution of voluntary and non-voluntary facial movements is abnormally slow in depressed patients, reflecting hypomimia. This mimic slowing is closely associated with the severity of depression. The response of depressed patients to emotional stimuli is also abnormally low, but emotional estimation of the stimuli is similar to normals. This pattern parallels the motor-emotional features known from patients with Parkinson's disease. (+info)