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Atul Goel - One of the best experts on this subject based on the ideXlab platform.

  • Trigeminal neuroma: analysis of surgical experience with 73 cases.
    Neurosurgery, 2003
    Co-Authors: Atul Goel, Dattatraya Muzumdar, Chandrashekhar Raman
    Abstract:

    Objective We reviewed the clinical and radiological features of 73 cases of trigeminal neuromas treated with radical surgery. Methods The records for 73 patients with trigeminal neuromas who were surgically treated in the neurosurgery department of King Edward VII Memorial Hospital and Seth Gordhandas Sunderdas Medical College (Mumbai, India), between 1989 and 2001, were retrospectively analyzed. The appropriateness of the selected surgical route was studied. The postoperative and follow-up data for the patients were analyzed, to determine the outcomes of radical surgery. Results In addition to the other presenting features of trigeminal neuromas, nine patients presented with the rarely reported symptom of Pathological Laughter. Three approaches were observed to be appropriate for treatment of these tumors, i.e., the infratemporal fossa interdural approach, the lateral basal subtemporal approach, and the retrosigmoid approach. In 51 cases (70%), total tumor excision was achieved. Two patients died during the postoperative period. With an average follow-up period of 38 months, there has been a recurrence in 1 case and 71 patients are leading independent and active lives. Conclusion Radical surgery is associated with excellent clinical outcomes and long-term tumor control. A majority of tumors, even those that are large and multicompartmental, can be removed in a single surgical stage and exposure.

  • Pathological Laughter as a presenting symptom of acoustic schwannoma: report of two cases.
    Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia, 2003
    Co-Authors: Dattatraya Muzumdar, Atul Goel
    Abstract:

    Two cases of acoustic schwannoma in a 48-year-old woman and 18-year-old male are reported. Both patients presented with an extremely unusual symptom of Pathological Laughter as a principal presenting symptom. Complete resection of the tumour via a retrosigmoid route resulted in an immediate resolution of Pathological Laughter.

  • Pathological Laughter as a presenting symptom of petroclival meningioma--case report.
    Neurologia medico-chirurgica, 2001
    Co-Authors: Dattatraya Muzumdar, Prasanna Agrahar, Ketan I. Desai, Atul Goel
    Abstract:

    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.

  • Pathological Laughter as a presenting symptom of massive trigeminal neuromas: report of four cases.
    Neurosurgery, 2000
    Co-Authors: Mohinish Bhatjiwale, Ketan I. Desai, Trimurti D. Nadkarni, Atul Goel
    Abstract:

    OBJECTIVE AND IMPORTANCE: This is a report of four cases of huge trigeminal neuromas that presented with the principle symptom of Pathological Laughter (PL). CLINICAL PRESENTATION: All four patients were male and were in either the third or fourth decade of life. In addition to PL, there were neurological deficits related to trigeminal nerve, brainstem, and cerebellar dysfunctions. INTERVENTION: All tumors were radically excised via a lateral basal temporal approach. The PL was cured immediately after surgery. CONCLUSION: PL sometimes precedes other neurological manifestations and may be a useful localizing sign. The clinical and radiological features in our cases suggest that PL is a result of extra-axial compression of the pons and adjoining neural structures.

  • Pathological Laughter as a presenting symptom of trigeminal neurinoma--case report.
    Neurologia medico-chirurgica, 1996
    Co-Authors: Mohinish Bhatjiwale, Atul Goel, Ketan I. Desai
    Abstract:

    A 26-year-old male presented with a trigeminal neurinoma manifesting as Pathological Laughter. After resection of the large tumor, the symptom disappeared completely. Pathological Laughter sometimes precedes other manifestations of tumors around the brainstem and may be a useful localizing sign.

Virgil Ionescu - One of the best experts on this subject based on the ideXlab platform.

  • Pathological Laughter as prodromal manifestation of transient ischemic attacks—case report and brief review
    BMC Neurology, 2015
    Co-Authors: Adriana O. Dulamea, Costel Matei, Ioana Mindruta, Virgil Ionescu
    Abstract:

    Background Based on a case report, the authors reviewed the data about involuntary emotional expression disorder (IEED). IEED includes the syndromes of Pathological laughing and crying (PLC) and emotional lability (EL). PLC is a rare disorder of emotional expression characterized by relatively uncontrollable episodes of Laughter and crying or both that do not have an apparent motivating stimulus. Case presentation Authors report the case of a 59-year-old man who presented with recurrent episodes of PLC of approximately 2 min duration, consisting of accelerated breathing, emission of guttural, snoring sounds, frowning of the eyebrows, followed by Laughter accompanied by motor restlessness of all four limbs. PLC episodes preceded left carotid transient ischemic attacks (TIA’s) manifested by reversible aphasia and right hemiparesis. Electroencephalography performed during PLC episodes revealed no spike-wave activity. Brain magnetic resonance imaging showed lacunar infarcts in the left lenticulo-capsulo-thalamic area and multiple round lesions in the cortical-subcortical and in the deep white matter of frontal-parietal-occipital lobes bilaterally, with T2 hyperintensity, T1 isointensity and no diffusion changes. The episodes were interpreted as transient ischemic attacks although gelastic seizures could not be excluded. The etiological investigations revealed unstable plaques on the left carotid artery bulb and the aortic arch and a degenerative mitral valve stenosis. The patient was treated first with antiplatelet therapy and antiepileptic drugs but PLC stopped only after anticoagulation was started. During follow-up the patient continued to have left carotid and vertebrobasilar TIA’s being on oral anticoagulation. The patient became asymptomatic only after mitral valve replacement was performed. Conclusions This case illustrates the difficulty distinguishing between gelastic epilepsy and TIA’s in cases of PLC episodes and discuss the neuroanatomic bases and pathophysiology of this rare condition.

  • Pathological Laughter as prodromal manifestation of transient ischemic attacks—case report and brief review
    BMC neurology, 2015
    Co-Authors: Adriana O. Dulamea, Costel Matei, Ioana Mindruta, Virgil Ionescu
    Abstract:

    Based on a case report, the authors reviewed the data about involuntary emotional expression disorder (IEED). IEED includes the syndromes of Pathological laughing and crying (PLC) and emotional lability (EL). PLC is a rare disorder of emotional expression characterized by relatively uncontrollable episodes of Laughter and crying or both that do not have an apparent motivating stimulus. Authors report the case of a 59-year-old man who presented with recurrent episodes of PLC of approximately 2 min duration, consisting of accelerated breathing, emission of guttural, snoring sounds, frowning of the eyebrows, followed by Laughter accompanied by motor restlessness of all four limbs. PLC episodes preceded left carotid transient ischemic attacks (TIA’s) manifested by reversible aphasia and right hemiparesis. Electroencephalography performed during PLC episodes revealed no spike-wave activity. Brain magnetic resonance imaging showed lacunar infarcts in the left lenticulo-capsulo-thalamic area and multiple round lesions in the cortical-subcortical and in the deep white matter of frontal-parietal-occipital lobes bilaterally, with T2 hyperintensity, T1 isointensity and no diffusion changes. The episodes were interpreted as transient ischemic attacks although gelastic seizures could not be excluded. The etiological investigations revealed unstable plaques on the left carotid artery bulb and the aortic arch and a degenerative mitral valve stenosis. The patient was treated first with antiplatelet therapy and antiepileptic drugs but PLC stopped only after anticoagulation was started. During follow-up the patient continued to have left carotid and vertebrobasilar TIA’s being on oral anticoagulation. The patient became asymptomatic only after mitral valve replacement was performed. This case illustrates the difficulty distinguishing between gelastic epilepsy and TIA’s in cases of PLC episodes and discuss the neuroanatomic bases and pathophysiology of this rare condition.

  • Pathological Laughter as prodromal manifestation of transient ischemic attacks case report and brief review
    BMC Neurology, 2015
    Co-Authors: Adriana O. Dulamea, Costel Matei, Ioana Mindruta, Virgil Ionescu
    Abstract:

    Based on a case report, the authors reviewed the data about involuntary emotional expression disorder (IEED). IEED includes the syndromes of Pathological laughing and crying (PLC) and emotional lability (EL). PLC is a rare disorder of emotional expression characterized by relatively uncontrollable episodes of Laughter and crying or both that do not have an apparent motivating stimulus. Authors report the case of a 59-year-old man who presented with recurrent episodes of PLC of approximately 2 min duration, consisting of accelerated breathing, emission of guttural, snoring sounds, frowning of the eyebrows, followed by Laughter accompanied by motor restlessness of all four limbs. PLC episodes preceded left carotid transient ischemic attacks (TIA’s) manifested by reversible aphasia and right hemiparesis. Electroencephalography performed during PLC episodes revealed no spike-wave activity. Brain magnetic resonance imaging showed lacunar infarcts in the left lenticulo-capsulo-thalamic area and multiple round lesions in the cortical-subcortical and in the deep white matter of frontal-parietal-occipital lobes bilaterally, with T2 hyperintensity, T1 isointensity and no diffusion changes. The episodes were interpreted as transient ischemic attacks although gelastic seizures could not be excluded. The etiological investigations revealed unstable plaques on the left carotid artery bulb and the aortic arch and a degenerative mitral valve stenosis. The patient was treated first with antiplatelet therapy and antiepileptic drugs but PLC stopped only after anticoagulation was started. During follow-up the patient continued to have left carotid and vertebrobasilar TIA’s being on oral anticoagulation. The patient became asymptomatic only after mitral valve replacement was performed. This case illustrates the difficulty distinguishing between gelastic epilepsy and TIA’s in cases of PLC episodes and discuss the neuroanatomic bases and pathophysiology of this rare condition.

Josef Parvizi - One of the best experts on this subject based on the ideXlab platform.

  • Pathological Laughter and crying in patients with multiple system atrophy cerebellar type
    Movement Disorders, 2007
    Co-Authors: Josef Parvizi, Jeffrey T Joseph, Daniel Z Press, Jeremy D Schmahmann
    Abstract:

    In the cerebellar type of multiple system atrophy (MSA-C), the burden of Pathological changes involves the cerebellum and its associated brainstem structures in the basis pontis and the inferior olivary nucleus, and as a result, the clinical phenotype is dominated early on by the cerebellar dysfunction. We report our clinical and post mortem findings in a patient with MSA-C who exhibited Pathological Laughter in the absence of any congruent changes of mood. A review of the clinical notes of 27 other patients with MSA-C revealed a problem with Pathological Laughter, or crying, or both in 9 more patients. Our finding of about 36% occurrence suggests that the problem of dysregulation of emotional expression is more prevalent in MSA-C than the paucity of reports in the literature suggests. Our findings are consistent with the view that the cerebellum and its interconnected structures may be involved in the regulation of emotional expression. © 2007 Movement Disorder Society

  • Pathological Laughter and crying in patients with multiple system atrophy‐cerebellar type
    Movement disorders : official journal of the Movement Disorder Society, 2007
    Co-Authors: Josef Parvizi, Jeffrey T Joseph, Daniel Z Press, Jeremy D Schmahmann
    Abstract:

    In the cerebellar type of multiple system atrophy (MSA-C), the burden of Pathological changes involves the cerebellum and its associated brainstem structures in the basis pontis and the inferior olivary nucleus, and as a result, the clinical phenotype is dominated early on by the cerebellar dysfunction. We report our clinical and post mortem findings in a patient with MSA-C who exhibited Pathological Laughter in the absence of any congruent changes of mood. A review of the clinical notes of 27 other patients with MSA-C revealed a problem with Pathological Laughter, or crying, or both in 9 more patients. Our finding of about 36% occurrence suggests that the problem of dysregulation of emotional expression is more prevalent in MSA-C than the paucity of reports in the literature suggests. Our findings are consistent with the view that the cerebellum and its interconnected structures may be involved in the regulation of emotional expression.

  • Pathological Laughter and crying in patients with multiple system atrophy cerebellar type
    Movement Disorders, 2007
    Co-Authors: Josef Parvizi, Jeffrey T Joseph, Daniel Z Press, Jeremy D Schmahmann
    Abstract:

    In the cerebellar type of multiple system atrophy (MSA-C), the burden of Pathological changes involves the cerebellum and its associated brainstem structures in the basis pontis and the inferior olivary nucleus, and as a result, the clinical phenotype is dominated early on by the cerebellar dysfunction. We report our clinical and post mortem findings in a patient with MSA-C who exhibited Pathological Laughter in the absence of any congruent changes of mood. A review of the clinical notes of 27 other patients with MSA-C revealed a problem with Pathological Laughter, or crying, or both in 9 more patients. Our finding of about 36% occurrence suggests that the problem of dysregulation of emotional expression is more prevalent in MSA-C than the paucity of reports in the literature suggests. Our findings are consistent with the view that the cerebellum and its interconnected structures may be involved in the regulation of emotional expression.

  • diagnosis and management of Pathological Laughter and crying
    Mayo Clinic Proceedings, 2006
    Co-Authors: Josef Parvizi, Jeremy D Schmahmann, David B Arciniegas, Gary L Bernardini, Michael Hoffmann, J P Mohr, Mark J Rapoport, Jonathan M Silver, Stanley Tuhrim
    Abstract:

    Patients with various neurologic disorders exhibit exaggerated or inappropriate episodes of Laughter, crying, or both without an apparent motivating stimulus or in response to stimuli that would not have elicited such an emotional response before the onset of the underlying disease. During these episodes, patients have difficulty controlling their emotional expression according to the contextual information. In contrast, patients with mood disorders have a pervasive and sustained change in their emotional experience and thus exhibit spells of Laughter or crying because of an underlying mania or depression. This article focuses on the clinical presentation, diagnosis, prevalence, and proposed pathophysiological mechanisms of and available treatment options for this clinical phenomenon.

  • Pathological Laughter and crying a link to the cerebellum
    Brain, 2001
    Co-Authors: Josef Parvizi, Steven W Anderson, Coleman O Martin, Hanna Damasio, Antonio R Damasio
    Abstract:

    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.

Zeina Chemali - One of the best experts on this subject based on the ideXlab platform.

Salvador Cruz-flores - One of the best experts on this subject based on the ideXlab platform.

  • Fou rire prodromique and history of Pathological Laughter in the XIXth and XXth centuries
    Revue neurologique, 2004
    Co-Authors: Francisco De Assis Aquino Gondim, Florian P Thomas, G.r. Oliveira, Salvador Cruz-flores
    Abstract:

    Fou rire prodromique (prodrome of crazy Laughter) is a rarely described nosological entity. In 1903, Charles Fere, 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 genicule (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.

  • “Fou rire prodromique” as the presentation of pontine ischaemia secondary to vertebrobasilar stenosis
    Journal of neurology neurosurgery and psychiatry, 2001
    Co-Authors: F. De A.a. Gondim, B J Parks, Salvador Cruz-flores
    Abstract:

    “Fou rire prodromique” (prodrome of crazy Laughter) is a rare form of Pathological Laughter of uncertain pathophysiology. A patient is presented with Pathological Laughter as the first manifestation of pontine ischaemia due to vertebrobasilar stenosis. A 65 year old man developed uncontrollable and unemotional Laughter for almost an hour followed by transient right facial-brachial paresis. He had fluctuation of Laughter, right facial brachial paresis, and occasional crying. Magnetic resonance imaging, magnetic resonance angiogram (MRA), and an angiogram showed small left pontine and cerebellar infarcts, left vertebral artery occlusion, and right vertebral and basilar artery stenosis. His condition deteriorated to bilateral brain stem infarction and he died. Necropsy confirmed the extensive brain stem infarction. Pathological Laughter can be the very first presenting manifestation of ischaemia of the ventrotegmental junction of the upper pons. It is hypothesised that the Pathological Laughter in this patient was secondary to ischaemic ephaptic stimulation of the descending corticopontine/ bulbar pathways. (J Neurol Neurosurg Psychiatry 2001;71:802‐804)