Pathologic Laughing Research Articles

Emotional Incontinence in a Patient with Neuromyelitis Optica Spectrum Disorder

The pathologic laughing is involuntary and associated with brain damage seen in a variety of disorders, which occurs as a result of lesions in various locations and is often seen associated with prefrontal or brainstem lesions. Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system characterized by severe attacks of optic neuritis and myelitis, and also develops brain lesions involving the bilateral diencephalic regions adjacent to the third ventricles, the brainstem and cerebellum surrounding the fourth ventricles, and the periventricular white matter adjacent to the lateral ventricles. Emotional incontinence refers to episodic laughing or crying, and occurs as a result of brain damage in various locations and is often seen associated with prefrontal or brainstem lesions. Emotional incontinence has been well described in multiple sclerosis, however the emotional incontinence in NMO has not been systemically documented. My report a characteristic patient with NMO showing the pathologic laughing as an initial manifestation, and the plasmapheresis therapy showed remarkable improvement in severity and occurrence of the pathologic laughing.

Emotional Incontinence in a Patient with Neuromyelitis Optica Spectrum Disorder

The pathologic laughing is involuntary and associated with brain damage seen in a variety of disorders, which occurs as a result of lesions in various locations and is often seen associated with prefrontal or brainstem lesions. Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system characterized by severe attacks of optic neuritis and myelitis, and also develops brain lesions involving the bilateral diencephalic regions adjacent to the third ventricles, the brainstem and cerebellum surrounding the fourth ventricles, and the periventricular white matter adjacent to the lateral ventricles. Emotional incontinence refers to episodic laughing or crying, and occurs as a result of brain damage in various locations and is often seen associated with prefrontal or brainstem lesions. Emotional incontinence has been well described in multiple sclerosis, however the emotional incontinence in NMO has not been systemically documented. My report a characteristic patient with NMO showing the pathologic laughing as an initial manifestation, and the plasmapheresis therapy showed remarkable improvement in severity and occurrence of the pathologic laughing.

Pathologic tearfulness after limbic encephalitis: A novel disorder and its neural basis.

ObjectiveWe investigated the nature and neural foundations of pathologic tearfulness in a uniquely large cohort of patients who had presented with autoimmune limbic encephalitis (aLE).MethodsWe recruited 38 patients (26 men, 12 women; median age 63.06 years; interquartile range [IQR] 16.06 years) in the postacute phase of aLE who completed questionnaires probing emotion regulation. All patients underwent structural/functional MRI postacutely, along with 67 age- and sex-matched healthy controls (40 men, 27 women; median age 64.70 years; IQR 19.87 years). We investigated correlations of questionnaire scores with demographic, clinical, neuropsychological, and brain imaging data across patients. We also compared patients diagnosed with pathologic tearfulness and those without, along with healthy controls, on gray matter volume, resting-state functional connectivity, and activity.ResultsPathologic tearfulness was reported by 50% of the patients, while no patient reported pathologic laughing. It was not associated with depression, impulsiveness, memory impairment, executive dysfunction in the postacute phase, or amygdalar abnormalities in the acute phase. It correlated with changes in specific emotional brain networks: volume reduction in the right anterior hippocampus, left fusiform gyrus, and cerebellum, abnormal hippocampal resting-state functional connectivity with the posteromedial cortex and right middle frontal gyrus, and abnormal hemodynamic activity in the left fusiform gyrus, right inferior parietal lobule, and ventral pons.ConclusionsPathologic tearfulness is common following aLE, is not a manifestation of other neuropsychiatric features, and reflects abnormalities in networks of emotion regulation beyond the acute hippocampal focus. The condition, which may also be present in other neurologic disorders, provides novel insights into the neural basis of affective control and its dysfunction in disease.

Treatment of Poststroke Pathologic Laughing With Duloxetine: A Case Series.

Pathologic laughing is characterized by episodes of uncontrollable laughter caused by underlying neurologic disturbances, such as stroke. Several types of medication, including selective serotonin reuptake inhibitors, have demonstrated only limited success at treating the condition. Duloxetine, a dual serotonin-norepinephrine reuptake inhibitor, is reportedly effective in treating the symptoms of mood disorders. We herein introduce a prospective consecutive sample of stroke patients with pathologic laughing treated with duloxetine. We enrolled patients without a history of psychological illness who exhibited poststroke pathologic laughter. Duloxetine administration was commenced at an initial dose of 30 mg once daily. The dose was increased to 60 mg once daily within 2 weeks for all patients except 2. The effect of the treatment was assessed by means of the Pathological Laughter and Crying Scale. A total of 7 patients were included in the study. Improvements were observed within an average of 10 days after duloxetine administration. Pathological Laughter and Crying Scale score decreased after duloxetine administration in all patients, and 4 patients demonstrated a decrease in score of more than 50%. All patients reported subjective improvement of symptoms, and no adverse effects were observed. This case series demonstrates that duloxetine could attenuate pathologic laughing exhibited by stroke patients; however, further randomized controlled studies are necessary to validate our findings.

The Diagnosis and Natural History of Multiple System Atrophy, Cerebellar Type.

The objective of this study was to identify key features differentiating multiple system atrophy cerebellar type (MSA-C) from idiopathic late-onset cerebellar ataxia (ILOCA). We reviewed records of patients seen in the Massachusetts General Hospital Ataxia Unit between 1992 and 2013 with consensus criteria diagnoses of MSA-C or ILOCA. Twelve patients had definite MSA-C, 53 had possible/probable MSA-C, and 12 had ILOCA. Autonomic features, specifically urinary urgency, frequency, and incontinence with erectile dysfunction in males, differentiated MSA-C from ILOCA throughout the disease course (p = 0.005). Orthostatic hypotension developed later and differentiated MSA-C from ILOCA (p < 0.01). REM sleep behavior disorder (RBD) occurred early in possible/probable MSA-C (p < 0.01). Late MSA-C included pathologic laughing and crying (PLC, p < 0.01), bradykinesia (p = 0.01), and corticospinal findings (p = 0.01). MRI distinguished MSA-C from ILOCA by atrophy of the brainstem (p < 0.01) and middle cerebellar peduncles (MCP, p = 0.02). MSA-C progressed faster than ILOCA: by 6years, MSA-C walker dependency was 100% and ILOCA 33%. MSA-C survival was 8.4 ± 2.5years. Mean length of ILOCA illness to date is 15.9 ± 6.4years. A sporadic onset, insidiously developing cerebellar syndrome in midlife, with autonomic features of otherwise unexplained bladder dysfunction with or without erectile dysfunction in males, and atrophy of the cerebellum, brainstem, and MCP points strongly to MSA-C. RBD and postural hypotension confirm the diagnosis. Extrapyramidal findings, corticospinal tract signs, and PLC are helpful but not necessary for diagnosis. Clarity in early MSA-C diagnosis can prevent unnecessary investigations and facilitate therapeutic trials.

Paroxetine-Induced Dysarthria in a 42-Year-Old Man with Pathologic Laughing

A 42-year-old man was referred to the psychiatric department on the eighth day after cranioplasty in November 2008 due to his involuntary and uncontrollable outbursts of laughter. About two months ...

Treatment of pathologic laughing and crying

Pathologic laughing and crying (PLC) denotes paroxysms of involuntary and uncontrollable crying and/or laughing resulting from neurologic illnesses. These paroxysms of affect are often provoked by nonsentimental stimuli; even when the inciting stimulus is sentimentally meaningful, the intensity of the affective response is excessive. The crying and/or laughing of PLC are variably accompanied by episode-congruent subjective emotional feelings. In unusual cases, episode-related feelings are of a valence contradictory to the expressed affect (ie, feeling happy while crying, or vice versa). PLC does not bear a predictable relationship to the prevailing mood of the patient, and the occurrence of such episodes does not produce a sustained mood disturbance. Therefore, patients with PLC must not be misunderstood as "depressed" or "manic" solely on the basis of their frequent episodic crying or laughing. In rare circumstances, PLC or PLC-like symptoms may be the presenting symptom of a neurologic illness. In such circumstances, a prompt and thorough diagnostic evaluation for that neurologic illness should be undertaken before initiating treatment for PLC. Selective serotonin reuptake inhibitors (SSRIs) are efficacious, safe, and well-tolerated treatments for PLC and are recommended as first-line treatments for this condition. Tricyclic antidepressants, dextromethorphan/quinidine, or dopaminergic agents may be useful alternative treatments in patients in whom SSRIs are ineffective or poorly tolerated. Education and supportive therapy may help patients and families mitigate the social isolation and embarrassment that PLC episodes frequently produce.

Treatment of pathologic laughing and crying

Treatment of pathologic laughing and crying

Pathologic laughing and intractable hiccups can occur early in multiple sclerosis

Pathologic laughing occurs in approximately 10% of patients with multiple sclerosis (MS), especially when patients have entered the chronic stage. We describe four patients with MS who, at an early stage, developed pathologic laughing associated, in two cases, with intractable hiccups. In two patients, MRI showed an enhanced lesion in the medulla oblongata and the mesencephalon, two regions suspected of being involved in pathologic laughing and intractable hiccups.

Treatment of neuropsychiatric syndromes in multiple sclerosis

The treatment of multiple sclerosis has been revolutionized during the past 10 years by the introduction of disease-modifying therapies. However, day-to-day management of the symptoms and complications of this condition will, for the foreseeable future, continue to be important management concerns. Among the most problematic and troublesome manifestations of multiple sclerosis are its neuropsychiatric manifestations. Most prominent among these are depression, pathologic laughing and crying, fatigue, cognitive problems, sleep disorders and disorders of sexual function. There have been relatively few randomized controlled trials of pharmacologic treatments for these conditions. Available treatments for the management of fatigue and cognitive deficits remain inadequate and patients must often accommodate these symptoms in their lifestyle.

Cognitive impairments in the locked-in syndrome: A case report

New PW, Thomas SJ. Cognitive impairments in the locked-in syndrome: a case report. No neuropsychologic studies have been reported that assess cognitive functioning in survivors of locked-in syndrome (LIS) due to purely pontine lesions and then document the process of recovery by serial testing over a lengthy period. A previously well man in his early thirties was admitted to the hospital with progressive stroke symptoms and signs. Investigations showed occlusion of the basilar artery and acute infarction of the pons, including basis and tegmentum. Despite thrombolysis, he had persisting clinical features of the LIS. He had minimal change during the first month but then slowly improved. Recovery continued gradually, and he was discharged home 7 months after stroke; at this time he was ambulating with a cane, was mildly dysarthric, was able to swallow foods of modified consistency, and was independent in all self-care activities. Neuropsychologic testing, done 6 months after stroke, showed noteable cognitive impairments. These included mild difficulties with attention and concentration, significant reduction in speed of processing, moderate impairment of perceptual organization skills, mild inefficiencies in new learning of verbal information, and a moderate reduction in executive skills. Pathologic laughing and crying were also noted. There was progressive improvement in most areas of physical and cognitive functioning until at least 2 years after stroke. Neuropsychologic testing in this patient suggests that the LIS may be associated with impairments of higher-level cognitive functioning.

October 26 Highlight and Commentary

The Brooks et al. controlled clinical trial found that dextromethorphan and quinidine, compared with either drug alone, safely reduced the severity and frequency of pseudobulbar affect (pathologic laughing and crying) episodes in amyotrophic lateral sclerosis (ALS) patients. They also demonstrated an improvement in quality of life related to treatment. see page 1364 Commentary by Jonathan Katz, MD Pseudobulbar affect is a term used to describe uncontrolled episodes of laughter or crying. These emotional outbursts occur in a large number of patients with ALS and can be a major problem in their interpersonal interactions.1 …

Psychiatric Symptoms in Progressive Supranuclear Palsy

Progressive supranuclear palsy (PSP) is an unusual neurodegenerative disorder that superficially resembles Parkinson's disease (PD). It is characterized by gaze palsy, bulbar signs, parkinsonian signs, and mental changes. While mental changes are a frequent finding, they have, with the exception of dementia, been poorly defined. In this study, 19 patients with PSP were evaluated psychiatrically and compared with 42 patients with PD. Fifty-two percent of the patients had some degree of dementia, as measured by the Mini-Mental State Exam. Eight (42%) of the PSP patients had other psychiatric diagnoses, mostly relatively mild depression or anxiety, though two patients had more severe depression. Six (32%) patients had pathologic laughing or crying, and four of these had a psychiatric diagnosis other than dementia. The PSP patients did not differ from the PD patients on measures of depression or anxiety and did not have a greater rate of formal psychiatric diagnoses. This study confirms previous reports of dementia as a common feature of PSP. It further suggests that psychiatric disturbances, while common, are generally relatively mild, though more serious psychiatric illness may be seen.

Incontinência do choro e infarto protuberancial unilateral

A 64-year-old man presented with pathologic crying and right hemiplegia due to a unilateral pontine infarct from probable branch disease of the basilar artery. The circumscribed nature of the lesion was supported by MRI and short-latency evoked potentials. The weeping spells ceased after a few days of imipramine in low doses. Pathologic laughing and crying can be viewed as a limbic-motor disconnection syndrome, in which the faciovocal motor system is released from forebrain afferents carrying information of emotional content. The inclusion of pathologic laughing and crying in the syndrome pseudobulbar palsy is inaccurate and misleading, since each is related to distinct functional and anatomic systems intrinsic to the human brainstem.

Treatment of pathologic laughing and weeping with amitriptyline

Abstract Patients with bilateral forebrain disease may commonly manifest the syndrome of pathologic laughing and weeping. We investigated the efficacy of low-dose amitriptyline in 12 patients in whom this syndrome was a consequence of multiple sclerosis. In a double-blind crossover study comparing amitriptyline with placebo, eight patients experienced dramatic and significant improvement with amitriptyline (P = 0.02). The mean dose of amitriptyline was 57.8 mg per day and did not exceed 75 mg per day in any patient. Concurrent measurements of depression showed no change during the study. We conclude that amitriptyline is effective in the treatment of this disturbance of affective expression, and that this effect is distinct from the antidepressant effect of the medication. (N Engl J Med 1985; 312:1480–2.)

Treatment of Pathologic Laughing and Weeping with Amitriptyline

Patients with bilateral forebrain disease may commonly manifest the syndrome of pathologic laughing and weeping. We investigated the efficacy of low-dose amitriptyline in 12 patients in whom this syndrome was a consequence of multiple sclerosis. In a double-blind crossover study comparing amitriptyline with placebo, eight patients experienced dramatic and significant improvement with amitriptyline (P = 0.02). The mean dose of amitriptyline was 57.8 mg per day and did not exceed 75 mg per day in any patient. Concurrent measurements of depression showed no change during the study. We conclude that amitriptyline is effective in the treatment of this disturbance of affective expression, and that this effect is distinct from the antidepressant effect of the medication.

Pathologic laughing and crying treated with levodopa.

Levodopa or amantadine hydrochloride was administered to 25 patients with pathologic laughing and/or crying. This symptom was markedly improved in ten cases, most of which were devoid of a cortical atrophy or a periventricular lucency in computed tomographic scan and also devoid of a severe dementia or a disturbance in activity of daily living. The concentration of homovanillic acid in the CSF of the patients was significantly decreased, whereas the concentration of 5-hydroxyindoleacetic acid remained within the normal limit. Because part of pathologic laughing and crying seems to be caused by the decreased function of the dopaminergic neuron, levodopa or amantadine is worth trying.

PATHOLOGIC LAUGHING AND CRYING

The occurrence of affective responses, such as involuntary laughing or crying, associated with lesions of the nervous system has been the topic of several contributions. By pathologic laughing and crying we mean involuntary and uncontrollable attacks of emotional expressions as a result of a cerebral lesion or lesions. The few attempts at correlation of these emotional expressions on a neuroanatomic and physiologic basis in man have led to various interpretations. The problem is beset by many difficulties because in most instances the lesions are neither isolated nor limited to specific areas of the nervous system. This is especially true in the cases of cerebrovascular disease and multiple sclerosis with multiple and bilateral lesions, in which pathologic laughing and crying commonly occur. At times, however, these affective responses appear in case of cerebrovascular disease at the same time as, or soon after, the ictus. In such cases, with utilization of the