Focal Myoclonus Research Articles

An Unusual Case of Spinal Myoclonus

Study design: A case report of Spinal myoclonus. Objectives: To illustrate an unusual case of spinal myoclonus and its management. Setting: Changi General Hospital, Singapore. Case report: A 48 year old male was admitted with minor trauma to his lower back for which he needed epidural analgesia. He later developed focal myoclonus of the left lower limb. He was subsequently investigated and treated with a combination of valproate and clonazepam and responded well. Conclusion: There are various known predisposing factors for the development of spinal myoclonus, which can be challenging to diagnose and treat. Clonazepam with or without sodium valproate can be used as first line agents. Some patients may require more than 2 agents for controlling the movements.

Corticobasal Syndrome Presenting With Partial Gerstmann’s Syndrome and Digit Agnosia

Back to table of contents Previous article Next article LettersFull AccessCorticobasal Syndrome Presenting With Partial Gerstmann’s Syndrome and Digit AgnosiaMichele Poletti, Claudio Lucetti, Andrea Vergallo, and Ubaldo BonuccelliMichele PolettiSearch for more papers by this author, Claudio LucettiSearch for more papers by this author, Andrea VergalloSearch for more papers by this author, and Ubaldo BonuccelliSearch for more papers by this authorPublished Online:1 Apr 2013https://doi.org/10.1176/appi.neuropsych.12060155AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Gerstmann’s syndrome (GS) is a clinical picture characterized by finger agnosia, left–right confusion, agraphia, and acalculia, associated with focal left posterior-inferior parietal lesions.1 Partial presentations of GS have been reported in neurodegenerative diseases,2,3 as we describe in a patient presenting with GS and digit agnosia as early symptoms.A 62-year-old, right-handed woman, with 8 years of formal education, came to our attention because of mild cognitive difficulties involving limb praxis. The neurological examination detected upper limb tremor, more left-lateralized; global bradykinesia; rigidity of left limbs; bilateral focal myoclonus, stimulus-sensitive, more evident on the left limbs; and gait apraxia; the alien limb phenomenon was not present. Instrumental examinations detected bilateral temporo-parietal alterations (EEG), cortical atrophy (RMI), bilateral hypometabolism in the frontal-temporal-parietal cortices, and bilateral striatal degeneration (DAT-SCAN).The neuropsychological assessment detected executive difficulties, impaired visuospatial functions, and bilateral ideomotor limb apraxia, and therefore focused on GS. The patient showed finger agnosia (Two-Point Finger test,1 Finger Agnosia test,1 In-Between test)1 and toe agnosia;4 that is, digit agnosia. She also presented acalculia (being unable to count backward from 10 to 0 and perform multiplication tables), Left–Right Confusion (3/5 in the two-stage command1 and 2/5 in relation to experimenter body) and agraphia (5/20 correct words in dictation; no signs of alexia), although limb motor difficulties hampered its examination.Although only a pathological examination could confirm the clinical diagnosis, her clinical picture was suggestive of a parkinsonism, probably a corticobasal syndrome (CBS); a progressive neurodegenerative disease with atrophy, gliosis, and tau-immunoreactive pathology of both gray and white matter of neocortex, basal ganglia, and substantia nigra, and clinically characterized by asymmetric akinesis and rigidity; dystonia of the upper limb; apraxia, myoclonus, and dementia.5The neuropsychological assessment evidenced digit agnosia and at least a partial GS; indeed, although her limb motor difficulties hampered the examination of agraphia, it appeared likely. Interestingly, the neuropsychological pattern of CBS partially overlaps the clinical presentation of GS as regards acalculia, number processing, and agraphia, and both CBS and GS are associated with parietal lesions.1,5 Despite their possible phenotypic overlapping, only two cases of pathologically-confirmed corticobasal degeneration and partial presentation of GS have been described.2 The current study confirmed that GS, including digit agnosia, may characterize the early clinical stages of a neurodegenerative disease affecting parietal lobes, as CBS.Dept. of Neuroscience, University of Pisa, Via Rome, Pisa, ItalyNeurology Unit, Versilia Hospital, Via Aurelia, Lido di Camaiore (LU), ItalyCorrespondence: Prof. Ubaldo Bonuccelli, Department of Neuroscience, University of Pisa, Italy; e-mail: u.[email protected]unipi.itReferences1 Rusconi E, Pinel P, Dehaene S, et al.: The enigma of Gerstmann’s syndrome revisited: a telling tale of the vicissitudes of neuropsychology. Brain 2010; 133:320–332Crossref, Medline, Google Scholar2 Wingard EM, Barrett AM, Crucian GP, et al.: The Gerstmann syndrome in Alzheimer’s disease. J Neurol Neurosurg Psychiatry 2002; 72:403–405Crossref, Medline, Google Scholar3 Tang-Wai DF, Josephs KA, Boeve BF, et al.: Pathologically confirmed corticobasal degeneration presenting with visuospatial dysfunction. Neurology 2003; 61:1134–1135Crossref, Medline, Google Scholar4 Tucha O, Steup A, Smely C, et al.: Toe agnosia in Gerstmann syndrome. J Neurol Neurosurg Psychiatry 1997; 63:399–403Crossref, Medline, Google Scholar5 Mahapatra RK, Edwards MJ, Schott JM, et al.: Corticobasal degeneration. Lancet Neurol 2004; 3:736–743Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited BySome evidence on Gerstmann’s syndrome: A case study on a variant of the clinical disorderBrain and Cognition, Vol. 148 Volume 25Issue 2 Spring 2013Pages E70-E70 Metrics PDF download History Published online 1 April 2013 Published in print 1 April 2013

Acute posthypoxic myoclonus after cardiopulmonary resuscitation

BackgroundAcute posthypoxic myoclonus (PHM) can occur in patients admitted after cardiopulmonary resuscitation (CPR) and is considered to have a poor prognosis. The origin can be cortical and/or subcortical and this might be an important determinant for treatment options and prognosis. The aim of the study was to investigate whether acute PHM originates from cortical or subcortical structures, using somatosensory evoked potential (SEP) and electroencephalogram (EEG).MethodsPatients with acute PHM (focal myoclonus or status myoclonus) within 72 hours after CPR were retrospectively selected from a multicenter cohort study. All patients were treated with hypothermia. Criteria for cortical origin of the myoclonus were: giant SEP potentials; or epileptic activity, status epilepticus, or generalized periodic discharges on the EEG (no back-averaging was used). Good outcome was defined as good recovery or moderate disability after 6 months.ResultsAcute PHM was reported in 79/391 patients (20%). SEPs were available in 51/79 patients and in 27 of them (53%) N20 potentials were present. Giant potentials were seen in 3 patients. EEGs were available in 36/79 patients with 23/36 (64%) patients fulfilling criteria for a cortical origin. Nine patients (12%) had a good outcome. A broad variety of drugs was used for treatment.ConclusionsThe results of this study show that acute PHM originates from subcortical, as well as cortical structures. Outcome of patients admitted after CPR who develop acute PHM in this cohort was better than previously reported in literature. The broad variety of drugs used for treatment shows the existing uncertainty about optimal treatment.

Focal cortical myoclonus in rolandic cortical dysplasia presenting as hemifacial twitching

A 2-year-old girl presented with brief episodes of left hemifacial twitching. On ictal electroencephalography, repetitive focal spike discharges appeared at the right fronto-centro-temporal regions; these discharges preceded the onset of each twitch by 12ms. Magnetic resonance imaging showed a linear abnormal signal intensity in the subcortical white matter at the right postcentral gyrus, where a cluster of dipole sources was detected by magnetoencephalography. These findings suggested that the patient had focal cortical myoclonus due to rolandic focal cortical dysplasia.

Involuntary Craniofacial Lingual Movements in Intensive Care-Acquired Quadriplegia

The syndrome of involuntary craniofacial lingual movements in the setting of acute intensive care-acquired quadriplegia (critical illness neuromyopathy) following sepsis-associated encephalopathy has not been previously described. We suggest a localization and treatment for this disabling condition. Three patients (2 female) from our center were quadriplegic from critical illness neuromyopathy when they developed involuntary craniofacial lingual movements following sepsis-associated encephalopathy. Extensive investigations failed to identify an etiology for the abnormal movements. Movements were of large amplitude, of moderate speed, and semi-rhythmic in the jaw, tongue, and palate, persistent and extremely bothersome to all patients. Injection with Botulinum toxin type A was very beneficial. Involuntary craniofacial lingual movements in the setting of flaccid quadriplegia following sepsis-associated encephalopathy are consistent with focal craniofacial brainstem myoclonus and constitutes a new syndrome. Botulinum toxin type A treatment maybe helpful in treatment.

Myoclonic disorders: a practical approach for diagnosis and treatment

Myoclonus is a sudden, brief, involuntary muscle jerk. It is caused by abrupt muscle contraction, in the case of positive myoclonus, or by sudden cessation of ongoing muscular activity, in the case of negative myoclonus (NM). Myoclonus may be classified in a number of ways, although classification based on the underlying physiology is the most useful from the therapeutic viewpoint. Given the large number of possible causes of myoclonus, it is essential to take a good history, to clinically characterize myoclonus and to look for additional findings on examination in order to limit the list of possible investigations. With regards to the history, the age of onset, the character of myoclonus, precipitating or alleviating factors, family history and associated symptoms and signs are important. On examination, it is important to see whether the myoclonus appears at rest, on keeping posture or during action, to note the distribution of jerks and to look for the stimulus sensitivity. Electrophysiological tests are very helpful in determining whether myoclonus is cortical, subcortical or spinal. A single pharmacological agent rarely control myoclonus and therefore polytherapy with a combination of drugs, often in large dosages, is usually needed. Generally, antiepileptic drugs such as valproate, levetiracetam and piracetam are effective in cortical myoclonus, but less effective in other forms of myoclonus. Clonazepam may be helpful with all types of myoclonus. Focal and segmental myoclonus, irrespective of its origin, may be treated with botulinum toxin injections, with variable success.

Asymmetric Involvement in Sporadic Creutzfeldt-Jakob Disease: Clinical, Brain Imaging, and Electroencephalographic Studies

Objective: To ascertain the characteristics of patients with sporadic Creutzfeldt-Jakob disease (CJD) and to determine the findings of electroencephalography (EEG) and brain magnetic resonance imaging (MRI). Methods: We pooled patients at a hospital from 2000 to 2008, and classified them according to WHO diagnostic criteria as having probable or possible CJD. We retrospectively analyzed their clinical manifestations, brain MRI, and EEG findings to evaluate correlations among them. Results: In this study, 12 probable and 4 possible CJD patients were identified. Ten patients with probable CJD had asymmetric manifestations with hemiparesis, focal myoclonus, dystonia or apraxia; 9 had clinical manifestations mimicking the corticobasal syndrome. In contrast, neurological examinations did not show asymmetric signs in 4 patients with possible CJD. EEG showed a typical periodic sharp wave complex (PSWC) in 12 patients with probable CJD; most of them had bright signal intensity on diffusion-weighted imaging of the cortex and/or basal ganglia. There was a high tendency for asymmetric clinical manifestations that correlated with the presentation of PSWC and cortical lesions observed on the brain MRI scan. Conclusions: Our study indicates that asymmetric extrapyramidal symptoms/signs, in clinical features with characteristic abnormalities on MRI and EEG findings, might contribute to early diagnosis of sporadic CJD.

Clonazepam (Ro 5-4023) in the treatment of myoclonus epilepsy. Four case reports.

Progressive hereditary myoclonus epilepsy is a relentless disease which responds poorly to conventional drug therapy. Clonazepam (Ro 5-4023) a new benzodiazepine derivative, was given to 3 patients with progressive myoclonus epilepsy (Unverricht-Lundborg), and to 1 with focal myoclonus epilepsy (Kojewnikow). All 4 were females. Their ages ranged from 19 to 21 years. The duration of symptoms varied from 5 to 12 years. The duration of the trial was 30, 19, 3, and 4 months, respectively. With a daily dose of 6–8 mg, clonazepam effectively reduced the number of jerks in all patients; this effect appeared after 1 month of treatment. The duration of the effect looks promising. Intratrial EEG showed a clear decrease in spike-and-wave paroxysms. Photic stimulation provoked less jerks than before the trial; the amplitude of evoked activity was also reduced. There was some drowsiness when clonazepam was first given, but it disappeared after some weeks of treatment.

Mirror movements and involuntary homolateral limb synkinesis in a patient with probable Creutzfeldt–Jakob disease

We report a 63-year-old man, who was diagnosed with probable Creutzfeldt–Jakob disease, manifested by rapid progressive cognitive decline, gait disturbance, right focal hand dystonia, myoclonus, mirror movements, and involuntary homolateral limb synkinesis during alternating limb movements. Although the exact pathophysiology for contralateral and homolateral limb synkinesis is not known, dysfunction of the secondary motor areas and dorsal premotor cortex by spongiform degeneration of gray matter may cause these abnormalities.

Moving ear syndrome: The role of botulinum toxin

We report a 30-year-old man with moving ear syndrome caused by focal myoclonic jerks of the right temporal muscle. This focal myoclonus would disappear while the patient was sleeping, swallowing, or speaking. He was treated with botulinum toxin type A with a favorable outcome. Previous reports of this condition and possible therapeutic approaches are discussed.

Infarctus cérébraux multiples se présentant comme une dégénérescence cortico-basale : pseudo dégénérescence cortico-basale vasculaire ?

We report on five patients with a clinical presentation of corticobasal degeneration (CBD), including gradually progressive, asymmetric, L-DOPA-resistant parkinsonism associated variously with apraxia, focal action myoclonus, focal dystonia, cortical sensory loss and alien limb phenomenon. Some patients also presented an atypical CBD clinical history or signs - notably sudden onset. The disease was however not suggestive of another diagnosis. Magnetic resonance imaging of the brain revealed extensive vascular lesions. Only five similar cases have been published to our knowledge. Although we cannot exclude underlying CBD pathology, our cases illustrate the fact that multi-infarct pathology can masquerade as CBD or alter the clinical phenotype of the disease.

“Alien face” in corticobasal degeneration syndrome: extending clinical features

Corticobasal degeneration syndrome (CBDS) is a neurodegenerative disorder characterized by higher cortical dysfunctions associated with progressive asymmetric akinetic-rigid syndrome, and limb dystonia or focal myoclonus (Lang et al ., 1994). One of the most typical and specific clinical features in CBDS is considered alien limb phenomenon, usually present in advanced disease stage (Doody and Jankovic, 1992).

The contribution of a spinal mechanism in developing peripheral myoclonus: A case report

Focal myoclonus of peripheral origin, i.e., peripheral myoclonus (PM), is a rare disorder. Although PM always accompanies a lesion in the peripheral nerve, supplying the affected muscles, its mechanism remains unclear. Here we present a patient with focal myoclonus of the thigh muscles following a traumatic lesion in the femoral nerve. Lumbar spinal anesthesia, as well as local anesthetic block of the femoral nerve, completely abolished the patient's myoclonus temporarily. This movement was remarkably diminished after a surgical exploration of the wound with the removal of fibrous tissue beneath the scar and liberation of the femoral nerve. This case suggests the contribution of a spinal relay mechanism in the development of PM, in addition to the contribution of a nerve lesion.

Clinical analysis of first-ever acute ischemic stroke involving the territory of paramedian mesencephalic arteries

Abstract To determine one-year clinical outcome of patients with first-ever acute ischemic stroke involving the territory of paramedian mesencephalic arteries (PMAS), we conducted a prospective study evaluating the cognitive functions of 28 patients with PMAS. Neuropsychological tests were performed during the first month of stroke onset and at the 12th month of follow-up. There were 12 women and 16 men. Mean age of onset for women and men was 70 years and 65 years, respectively. Progressing strokes occurred in 62% of patients and 96% developed a full-blown picture of the clinical triad of akinetic mutism, hypersomnolence, and bilateral blepharoptosis and ophthalmoparesis. Involuntary movements occurred in 6, and focal myoclonus in 4 patients. The top four associated risk factors were hypertension (68%), hyperlipidemia (57%), diabetes mellitus (46%), and atrial fibrillation (36%). Unilateral midbrain infarctions occurred in 12 patients and bilateral lesions in 16. Thalamic infarctions were unilateral in 10 and bilateral in 13 cases. Three of the 28 (11%) patients died of recurrent cerebral infarctions within 1 year of the onset of PMAS. The recurrent infarctions involved the basilar artery territory in two cases and the carotid system in another. One patient died of acute myocardial infarction. Of the 24 patients who had survived the stroke by 1 year, 20 (71%) developed dementia. We conclude that first-ever ischemic stroke with PMAS is not a benign syndrome. Most patients developed dementia by 1 year after the stroke.

Adult‐Onset Rasmussen's Encephalitis: Anatomical‐Electrographic‐Clinical Features of 7 Italian Cases

A limited number of cases of adult-onset Rasmussen's encephalitis (A-RE) have been reported, but the features of the syndrome are still unclear. The aim of this study was to verify the clinical features of A-RE, and outline a noninvasive approach that may allow its early diagnosis and treatment. Retrospective evaluation of extensive noninvasive work-up of seven patients with A-RE, including repeat clinical, neurophysiological, and neuroimaging investigations. The study identified two distinct patterns of disease presentation, one characterized by focal motor epilepsy (the "epileptic" phenotype), and the other by focal cortical myoclonus (the "myoclonic" phenotype). Unilateral neurological deficits and brain atrophy were progressive in both phenotypes, but they were more prominent and were detected earlier in the "epileptic" phenotype. The anatomo-electroclinical features of these patients allowed a noninvasive diagnosis of A-RE and identification of two distinct disease phenotypes. Early noninvasive diagnosis can allow faster initiation of treatment.

Myoclonus and extrapyramidal diseases

Parkinsonism or dystonia are associated with myoclonus in several extrapyramidal diseases. Although the latter symptom is not always prominent, stimulus-sensitive, distal, or focal reflex myoclonus is frequently observed. This review will consider the clinical and electrophysiological features of myoclonus in Parkinson's disease, multiple system atrophy, corticobasal degeneration, progressive supranuclear palsy, Huntington's disease, dentatorubral−pallidoluysian atrophy, Lewy body dementia, and myoclonus with dystonia. The evidence of a long-latency reflex response, the presence of giant somatosensory evoked potentials, and the demonstration of a back-averaged premyoclonus focal cortical EEG activity often lead to classify myoclonus as a cortical phenomenon. However, a subcortical origin cannot always be ruled out.

A case of cerebral Whipple's disease initially presenting with isolated focal myoclonus

Neurological manifestations in Whipple's disease are highly variable and tend to occur at later stages of the disease. However, isolated, focal neurological symptoms are reported to be rare. Here we describe the successful treatment of a case of cerebral Whipple's disease initially presenting solely with isolated myoclonic jerks of the left hand and forearm evolving to a segmental myoclonus at a later stage. Additionally, we present - to our knowledge - a novel treatment by administration of immunomodulatory therapy (IVIg) in addition to established antibiotics.

Language‐induced Epilepsy, Acquired Stuttering, and Idiopathic Generalized Epilepsy: Phenotypic Study of One Family

Language-induced epilepsy involves seizure precipitation by speaking, reading, and writing. Seizures are similar to those of reading epilepsy (RE). The nosologic position of language-induced epilepsy is not clear. We performed a clinical and neurophysiological study in a multigenerational family with the association of idiopathic generalized epilepsy (IGE) with ictal stuttering as a manifestation of reflex language-induced epilepsy. Nine members on three generations were studied. All patients underwent video-polygraphic EEG recordings (awake and during sleep). A standardized protocol was applied to test the effect of language and non-language-related tasks. Six patients presented language-induced jaw jerking that mimicked stuttering and corresponded to focal myoclonus involving facial muscles. This was associated with an IGE phenotype in four of these patients. Focal EEG spikes were found in all six patients by visual analysis and/or back-averaging techniques. The focal spikes were either asymptomatic (when followed by a slow wave) or symptomatic of facial myoclonia (when isolated). Levetiracetam, used as add-on or monotherapy in four patients, suppressed ictal stuttering. One additional case only had a phenotype of IGE without focal features. This family study demonstrates the phenotypic heterogeneity of the association of IGE phenotype with ictal stuttering (language-related reflex seizure). Our data suggest that this particular form of reflex epilepsy related to language has more similarities with generalized epilepsies than with focal ones. Neurophysiological investigations should be performed more systematically in patients with acquired stuttering, especially if there is family history of IGE.

Hashimoto Encephalopathy: a do–not–miss in the differential diagnosis of dementia

Sirs: Hashimoto-encephalopathy (HE) is a steroid-sensitive, relapsing or steadily progressive encephalopathy that is far more common than generally thought. It can be treated if recognized in good time and thus ought to be considered in the differentials of dementia. Interestingly, it has been shown to represent an important differential diagnosis of Creutzfeldt-Jakob disease (CJD) [9]. We describe a patient who presented with a rapidly progressive dementia-like syndrome that improved remarkably on steroid treatment. MRI showed diffuse white matter lesions in the parietal and occipital lobes. Antithyroid antibodies were positive, providing the diagnosis of Hashimoto encephalopathy. The pathophysiology of HE is not entirely clear. It is closely associated with Hashimoto thyroiditis (HT) and is similarly thought to be caused by disorders of immune mechanisms. Most recent reports argue in favor of an inflammatory response to antineuronal antibodies [2, 7, 11]. This 79-year-old lady complained of malaise, dizziness and difficulty in concentration progressing over the past 3 weeks. Her past medical history was unremarkable. Examination revealed a friendly elderly lady who was disoriented in time and place and said she felt “funny in my head”. Vital signs were normal (BP 120/75), physical examination showed head tremor, extensor plantar response, and on MMSE she achieved 10/28. The same evening, she had a generalized tonic-clonic seizure. Over the following weeks, her condition slowly deteriorated, she became somnolent, perseverated and hallucinated. Physical examination showed no new focal neurological deficits, myoclonus or oculomotor abnormalities. EEG initially showed continuous focal epileptiform activity over the left temporal lobe. Later EEGs showed an increasingly generalized picture with diffuse background slowing and intermittent periodic sharp-slow waves (Fig. 1a). MRI revealed hyperintense signals on T2-weighted and FLAIR-images over the left temporal and both parieto-occipital lobes in the subcortical white matter (Fig. 2). The CSF showed elevated protein, no pleocytosis and negative oligoclonal bands. In spite of intensive serological screening for infectious, toxic, (para-)neoplastic and metabolic etiologies, none could be determined. PML was excluded by negative PCR for JC-Virus in CSF and negative HIV-Serology. The absence of hypertension, renal insufficiency or immunosuppression ruled out the suspicion of reversible posterior leukencephalopathy [4]. Intriguingly, the CSF was positive for protein 14-3-3 which is considered a relatively sensitive and specific marker for CJD [13]. However, false positives can be obtained after neuronal injury caused by infection, inflammation, ischemia or after an epileptic seizure. The detection of protein 14-3-3 in the CSF has been described in HE [12]. Considering ADEM as a possible diagnosis, we started high-dose corticosteroids. 3 days later, she was walking and responding adequately, she was still disoriented and knew that “something in my head isn’t right”. In parallel to these clinical findings, there was a marked improvement in her EEGfindings (Fig. 1b). Only then, anti-thyroglobulin and anti-microsomal antibodylevels were measured and found to be increased (thyroglobulinautoantibodies 195 kU/l (ref. 85 % of reported cases were female, aged 12–86). Clinically, both focal-neurological and signs of more diffuse brain dysfunction can be found [6]. Characteristic symptoms are dementia, focal or generalized epileptic seizures, psychotic phenomena and impaired level of consciousness [3, 5]. Ataxia and myoclonus have commonly been described, relating to CJD as a possible differential [9]. Physical examination may show pyramidal tract signs. Anti-thyroglobulin and antimicrosomal-antibodies comprise the mainstay of diagnosis. CSF shows elevated protein and in some cases mild pleocytosis, oligoclonal bands may be positive. EEGfindings consist mainly of slowwave abnormalities reflecting the degree of severity of the underlying encephalopathy and often paralleling the course of the disease LETTER TO THE EDITORS

Frequency of obsessive and compulsive symptoms in patients with blepharospasm and hemifacial spasm

Blepharospasm (BS) is a form of central focal dystonia recently associated with psychiatric disorders, particularly obsessive and compulsive symptoms. Hemifacial spasm (HFS) represents a focal myoclonus with peripheral origin in the facial nerve. To determine the frequency of obsessive and compulsive symptoms in patients with BS in comparison with patients with HFS. 30 patients from each group (BS and HFS) followed by the botulinum toxin clinic at the HC-UFPR were evaluated using a structured interview based on the DSM-IV criteria and the Yale-Brown scale. Results were compared by the mean two-tailed t test. We found obsessive or compulsive symptoms in 20 (66.6%) patients with BE and 21 (70%) with HFS. Yale-Brown scale scores for each group were higher among BS patients; however, diferences were not statisticaly significant. Our study did not show a significant diference in the comparison of the prevalence of obsessive and compulsive symptoms among patients with BS and HFS.