Focal Myoclonus Research Articles

Paraneoplastic opsoclonus-myoclonus syndrome as a rare presentation of parotid adenocarcinoma

Paraneoplastic Opsoclonus-Myoclonus Ataxia Syndrome (POMA) is a rare neurological condition that affects approximately 1 in 10,000,000 people annually. This syndrome is poorly understood and can lead to long-term cognitive, behavioral, and motor complications. Opsoclonus is characterized by involuntary, rapid, repetitive, multi-vectorial oscillations of the eyes occurring in all directions of gaze. It is accompanied by diffuse or focal body myoclonus and may or may not include ataxia and other cerebellar signs. POMA is typically a paraneoplastic syndrome associated with neuroblastoma in childhood and breast carcinoma or small-cell lung carcinoma in adults. Additionally, viral or toxic agents are known to play a role in its etiology, and the immune system is involved in the pathogenesis. We report a case of a 41-year-old man with anti-Ri antibody opsoclonus-myoclonus syndrome and parotid adenocarcinoma involvement. After diagnosing opsoclonus-myoclonus syndrome, the patient underwent multimodal immunotherapy treatment, resulting in partial remission of the neurological symptoms.

Tacrolimus-Induced Focal Myoclonus of Unilateral Hand in a Kidney Transplant Recipient.

Tacrolimus-Induced Focal Myoclonus of Unilateral Hand in a Kidney Transplant Recipient.

Opsoclonus Myoclonus Syndrome Associated With a New Diagnosis of HIV

Abstract Opsoclonus myoclonus syndrome (OMS) is a rare neurological disorder characterized by rapid saccadic eye movements, focal myoclonus, and gait disturbances. Both neoplastic and infectious processes have been found to be associated with OMS. In this report, we present a case of OMS in the setting of a new diagnosis of HIV. After diagnosis, the patient was initiated on antiretroviral therapy in addition to clonazepam with some improvement in her neurological symptoms. It was not until she was started on prednisone as an outpatient that her symptoms completely resolved and she returned to her functional baseline.

A Case of Dancing Eyes and Feet (P4-5.006)

<h3>Objective:</h3> To present a case of opsoclonus-myoclonus-ataxia syndrome in an adult patient following Epstein Barr Virus infection. <h3>Background:</h3> Opsoclonus-myoclonus-ataxia syndrome (OMAS), also called disorder of dancing eyes and feet, is a condition that causes opsoclonus along with diffuse or focal body myoclonus and truncal titubation with or without ataxia and other cerebellar signs. It is commonly seen as a paraneoplastic syndrome in children with neuroblastoma; however, there are several associated post-infectious and paraneoplastic etiologies in children and adults. <h3>Design/Methods:</h3> NA <h3>Results:</h3> A 26-year-old woman developed generalized malaise, abdominal discomfort, and right upper quadrant abdominal swelling. One week later, she developed blurred vision and gait impairment, for which she presented to the emergency room. On physical exam, she had opsoclonus, left appendicular ataxia, and left hemi-ataxic gait. Brain magnetic resonance imaging was normal. Serologic studies revealed elevated liver function tests and positive Epstein Barr Virus (EBV) IgM and IgG. Evaluation of cerebrospinal fluid revealed normal cells, glucose, and protein, negative oligoclonal bands as well as negative meningitis/encephalitis polymerase chain reaction panel and negative autoimmune encephalopathy panel. Workup for occult neoplasms was unrevealing. She was diagnosed with post-infectious OMAS due to EBV. She was treated with high-dose steroids with taper and intravenous immunoglobulin, which led to further improvement. Gabapentin, clonazepam, and topiramate were used for symptomatic treatment of opsoclonus. <h3>Conclusions:</h3> We describe clinical features, diagnostic workup, and treatment of a case of Epstein Barr Virus-associated post-infectious opsoclonus-myoclonus-ataxia syndrome in an adult. Despite recovery from the viral illness, the patient continued to have symptoms for several weeks which were ultimately improved with steroids and IVIG. <b>Disclosure:</b> Dr. Ahden has nothing to disclose. Dr. George has nothing to disclose. Dr. Samkoff has nothing to disclose.

Unusual Presentations Accentuating the Diagnostic Confusion of CJD (P2-6.010)

<h3>Objective:</h3> To report an unusual case of Creutzfeldt-Jakob Disease (CJD) presenting with worsening extrapyramidal symptoms preceding the onset of cognitive dysfunction. <h3>Background:</h3> CJD is a fatal progressive neurodegenerative disease mediated by misfolded proteins or prions. While definitive diagnosis requires histopathological confirmation, diagnostic criteria exist to predict the disease antemortem. However, only a few patients with CJD meet all components of this criteria. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> A 71-year-old healthy female presented with 2-months of recurrent falls and intermittent jerking of left arm and leg that started 5 days after her COVID-19 vaccine booster. At baseline she lives by herself and can manage her 10-acre property. On exam, she has appropriate mood, intact cognition, and orientation. Speech was dysarthric and was rigid in all muscle groups associated with hyperreflexia. The intermittent left hemibody jerking was consistent with focal myoclonus associated with spike and wave discharges on EEG. Brain magnetic resonance imaging (MRI) showed increased signal in the bilateral caudate, putamen, medial thalami, and right cerebral cortex on diffusion-weighted imaging. Cerebrospinal fluid (CSF) analysis showed normal cell count, protein and negative for autoimmune/paraneoplastic antibodies. While in the hospital over a few weeks her symptoms progressed to akinetic mutism, and she developed cognitive dysfunction. Real-time Quaking Induced Conversion (RT-QuIC), T-tau protein, and 14-3-3 protein ultimately resulted positive on CSF confirming diagnosis of CJD. She was discharged home with palliative care. <h3>Conclusions:</h3> Unusual presentations in a rare fatal condition like CJD can mimic many other neurological conditions at presentation. This can pose challenges in diagnosis and providing the prognosis to the caregivers. <b>Disclosure:</b> Mrs. Weeks has nothing to disclose. Dr. Mannyam has nothing to disclose. Dr. Bhatti has nothing to disclose. Dr. Gunturu has nothing to disclose.

Erratum: Case Report: Focal Myoclonus with a Striatal Lesion as a Presentation of Subacute Sclerosing Panencephalitis

Erratum: Case Report: Focal Myoclonus with a Striatal Lesion as a Presentation of Subacute Sclerosing Panencephalitis

A case of Dravet syndrome with focal cortical myoclonus

BackgroundDravet syndrome (DS) is a severe epileptic encephalopathy in children dominated by polymorphic seizures. Focal cortical myoclonus indicated on conventional electroencephalogram (EEG) was rarely observed in DS.Case presentationThe child, boy, thirteen months old, suffered from clonic seizures during bathing at two months old. Later he suffered from recurrent afebrile or febrile generalized tonic–clonic seizures often developing into status epilepticus. A genetic analysis of the SCN1A gene revealed a de novo heterozygous frame shift mutation in exon 21(c.3836_c.3837del AT).His myoclonic jerks of unilateral arm occurred spontaneously in response to movement. A spike wave from right central-parietal cortex immediately preceded a left myoclonic muscle activity, while a spike wave from left immediately preceded a right myoclonic muscle activity. The onset of the detected spike preceded the onset of myoclonic muscle activity by 42 ms using jerk-locked back-averaging of electroencephalogram data. The focal cortical myoclonus was not noted when one year old.ConclusionsFocal cortical myoclonus could be a form of seizures during the first year of life in DS, which may broaden the types of seizures of DS and may provide some diagnostic clues for DS.

Development of a nonhuman primate model for mammalian bornavirus infection.

Until recently, it was assumed that members of the family Bornaviridae could not induce severe disease in humans. Today, however, Borna disease virus 1 (BoDV-1), as well as the more recently emerged variegated squirrel bornavirus 1 (VSBV-1), are known as causative agents of lethal encephalitis in humans. In order to establish animal models reflecting the pathogenesis in humans and for countermeasure efficacy testing, we infected twelve rhesus macaques (Macaca mulatta) either with VSBV-1 or with BoDV-1. For each virus, three monkeys each were inoculated with 2 × 104 focus forming units by the intracerebral route or by multiple peripheral routes (intranasal, conjunctival, intramuscular, and subcutaneous; same dose in total). All BoDV-1 and VSBV-1 intracerebrally infected monkeys developed severe neurological signs around 5 to 6 or 8 to 12 weeks postinfection, respectively. Focal myoclonus and tremors were the most prominent observations in BoDV-1 and VSBV-1-infected animals. VSBV-1-infected animals also showed behavioral changes. Only one BoDV-1 peripherally infected animal developed similar disease manifestations. All animals with severe clinical disease showed high viral loads in brain tissues and displayed perivascular mononuclear cuffs with a predominance of lymphocytes and similar meningeal inflammatory infiltrates. In summary, rhesus macaques intracerebrally infected with mammalian bornaviruses develop a human-like disease and may serve as surrogate models for human bornavirus infection.

Brachial plexus injury presenting as focal myoclonus

Myoclonus is characterised by quick, involuntary muscle jerks. It can be focal or generalized. It arises most commonly from the sensorimotor cortex, brainstem or the spinal cord. Rarely focal lesions of the peripheral nerves, plexus, or nerve roots may produce peripheral myoclonus.1 Here we report a case of 32 years old female who presented with focal myoclonus of the left upper limb secondary to brachial plexus injury and got treated successfully with botulinum toxin injection. Keywords: Myoclonus, Focal Myoclonus, Brachial Plexus, Botulinum Toxin Injection

The presenting symptoms of Lafora Disease: An electroclinical and genetic study in five Apulian (Southern Italy) families

PurposeTo elucidate the presenting symptoms of Lafora Disease (LD) to differentiate it from Juvenile Myoclonic Epilepsy (JME). MethodsWe collected and evaluated the early electroclinical data of 5 unrelated Apulian (Southern Italy) LD families, 30 LD patients selected from the literature, and 30 Apulian JME patients. ResultsThe Apulian LD patients presented with generalised tonic-clonic and focal visual seizures, followed by myoclonic seizures and action-postural myoclonus. In these patients, EEG background slowing and occipital epileptiform abnormalities were significantly more evident than in the other groups. Genetic analysis revealed the presence of mutations in the EPM2A gene in 4 families, and in the NHLRC1 gene in the remaining family. In detail, we identified 2 different point mutations in EPM2A and only 1 in NHLRC1, and expanded the molecular spectrum of the EPM2A gene mutations reporting for the first time a patient carrier of the c.243_246del genetic variant. In the previously reported LD cases, generalised tonic-clonic and focal visual seizures and myoclonus were the most frequent symptoms, as confirmed by the first EEGs showing occipital or diffuse epileptiform abnormalities with photosensitivity in the background activity slowing. In the Apulian JME patients, myoclonus appeared earlier, usually at awakening, with diffuse epileptiform abnormalities during sleep and photosensitivity in the normal background activity. The diagnosis of JME was established much earlier than the LD one. During evolution, unlike JME patients, LD patients showed a significant resistance to drugs. ConclusionsTonic-clonic and focal visual seizures followed by myoclonic seizures and action-postural myoclonus together with EEG background slowing with diffuse and occipital epileptiform abnormalities suggest a diagnosis of LD. An early molecular confirmation allows a better diagnosis, counselling and management of affected patients and their families, and it may be useful to improve the patients’ quality of life using, when possible, emerging personalized treatments that may slow the evolution of the disease.

Neuronal Ceroid Lipofuscinosis in a Domestic Cat Associated with a DNA Sequence Variant That Creates a Premature Stop Codon in CLN6.

A neutered male domestic medium-haired cat presented at a veterinary neurology clinic at 20 months of age due to progressive neurological signs that included visual impairment, focal myoclonus, and frequent severe generalized seizures that were refractory to treatment with phenobarbital. Magnetic resonance imaging revealed diffuse global brain atrophy. Due to the severity and frequency of its seizures, the cat was euthanized at 22 months of age. Microscopic examination of the cerebellum, cerebral cortex and brainstem revealed pronounced intracellular accumulations of autofluorescent storage material and inflammation in all 3 brain regions. Ultrastructural examination of the storage material indicated that it consisted almost completely of tightly-packed membrane-like material. The clinical signs and neuropathology strongly suggested that the cat suffered from a form of neuronal ceroid lipofuscinosis (NCL). Whole exome sequence analysis was performed on genomic DNA from the affected cat. Comparison of the sequence data to whole exome sequence data from 39 unaffected cats and whole genome sequence data from an additional 195 unaffected cats revealed a homozygous variant in CLN6 that was unique to the affected cat. This variant was predicted to cause a stop gain in the transcript due to a guanine to adenine transition (ENSFCAT00000025909:c.668G > A; XM_003987007.5:c.668G > A) and was the sole loss of function variant detected. CLN6 variants in other species, including humans, dogs, and sheep, are associated with the CLN6 form of NCL. Based on the affected cat’s clinical signs, neuropathology and molecular genetic analysis, we conclude that the cat’s disorder resulted from the loss of function of CLN6. This study is only the second to identify the molecular genetic basis of a feline NCL. Other cats exhibiting similar signs can now be screened for the CLN6 variant. This could lead to establishment of a feline model of CLN6 disease that could be used in therapeutic intervention studies.

Clinical phenotypes of TBC1D24 gene related epilepsy

Objective: To summarize the clinical features of TBC1D24 gene mutations associated with epilepsy. Methods: All the patients with TBC1D24 gene compound heterozygous mutations were retrospectively collected at the Pediatric Department of Peking University First Hospital from March 2015 to July 2017, and the features of clinical manifestations, electroencephalogram, and neuroimaging were analyzed. Results: Eighteen cases with TBC1D24 gene compound heterozygous mutations were included. The age of seizure onset was 1 day to 8 months, and the median age was 90 days. Seizure types included generalized tonic-clonic seizures (GTCS) in 3 cases, focal seizures in 18 cases, myoclonus in 18 cases, and 17 cases had focal myoclonus and myoclonus status. The focal myoclonus involving one or multiple muscle groups, sometimes migrating and alternating, lasting up to minutes to several days, and could be terminated by sleep or sedation drugs. In 11 cases, myoclonus was exacerbated by fever or infections, and 2 cases developed into myoclonic status during infection, in a severe case with the loss of consciousness. The magnetic resonance imaging (MRI) of seven patients was abnormal, including cerebral atrophy or cerebellar atrophy with abnormal signals. Segment myoclonus was captured in 10 patients, but without correlated epileptiform discharges. There were ten cases had varying degrees of developmental delay, 7 were normal, and one patient died of status epilepticus at the age of 4 months. Three cases had hearing disorders. In the 18 patients, the clinical phenotype of 4 cases consisted of epilepsy of infancy with migrating focal seizures, 2 with progressive myoclonus epilepsies, 1 with Dravet syndrome, 1 with DOORS syndrome, and 3 with unclassified epileptic encephalopathy. Conclusions: The clinical feature of TBC1D24 gene mutation related epilepsy was focal myoclonus, and tended to develop into myoclonic status epilepticus, and could be aggravated by infections, and terminated by sleep or sedation drugs. Mental retardation involved or not, neuroimaging could present with cerebral atrophy or cerebellar atrophy with abnormal signals.

Clinical features and gene analysis of TBC1D24 gene mutation related early-onset focal myoclonic epilepsy

Objective: To investigate the clinical features and genetic characteristics of patients with TBC1D24 gene mutation related early-onset focal myoclonic epilepsy. Methods: Clinical data of 3 patients with TBC1D24 gene mutation related early-onset focal myoclonic epilepsy of Xuanwu Hospital from November 2016 to June 2017 was collected and analyzed.Candidate gene mutations were screened by second generation sequencing. Results: Among the 3 patients, 1 was male and 2 were females.Seizure onset age was 4 months, 3 years and 5 years after birth respectively. Two patients had family history of epilepsy.They all had prolonged episodes of focal myoclonus. Two patients had mental retardation.Scalp electroencephalograms (EEG) was recorded in all 3 cases and myoclonic seizures were captured.The ictal EEGs were normal in all cases. In one patient, the ictal EEG of generalized seizure showed alpha rhythm originating from left fronto-central region. Brain magnetic resonance imaging (MRI) was normal in 2 patients. Abnormal signal was found bilaterally in cerebellum in 1 patient. The gene screening showed that two patients carried compound heterozygous mutation of TBC1D24 gene and one carried homozygous mutation, all of which were de novo mutations.All the patients were treated with multiple antiepileptic drugs (AEDs) and seizures were uncontrolled in 2 patients. One patient was followed up for 10 months without recurrence. Conclusions: TBC1D24 gene related early-onset focal myoclonic epilepsy is clinically characterized by early onset, prolonged focal myoclonus which relieved with sleep, mental retardation and poor response to AEDs.The interictal and ictal EEG usually show normal. Genetic analysis can assist in diagnosis and genetic counseling.

P 122 Stimulus-responsive myoclonic jerks of both levator palpebrae muscles in a comatose survivor of cardiopulmonary resuscitation may pretended awareness

Comatose survivors of cardiopulmonary resuscitation (CPR), who develop myoclonus within 1–2 days after CPR, usually have a poor prognosis. Typically, such myoclonus occurs or increases on sensory stimuli like touching the patient or acoustic stimuli. Myclonic jerks mainly occur in the muscles of the face, shoulder girdle and diaphragm. Sometimes, such jerks may be restricted to one muscle like the diaphragm leading to hiccups. We report one comatose survivor of CPR with stimulus-sensitive myoclonus, which was restricted to both levator palpebrae muscles leading to eye opening on acoustic stimulation and by doing so pretending awareness. A 76-year-old female survivor of CPR opened her eyes on acoustic or sensory stimuli followed by a short period of blinking, which pretended awareness. EEG documented polymorph spike-slow waves after acoustic stimuli and was otherwise flat. Eye opening and blinking were coupled to spike-slow waves discharges and interpreted as restricted myoclonus of the levator palpebare muscles. This was a transient phenomenon for 24 h, and after another day, the patient was brain dead. Early myoclonus in comatose survivors of a CPR usually indicate a poor prognosis, although recent data indicate, that patients with focal myoclonus may have a better prognosis than those with more generalized myoclonus. Bouwes et al. (2012) reported a good outcome in 8 of 48 patients with focal myoclonus compared to 1 of 31 with generalized myoclonus. As shown by our patient, focal or restricted stimulus-sensitive myoclonus may pretend awareness and causes diagnostic problems, which can be solved by EEG.

FOCAL EPILEPTIC MYOCLONUS IN KOZHEVNIKOV–RASMUSSEN SYNDROME

The article presents the clinical, electroencephalographic (EEG) and neuroimaging features, as well as the results of treatment of patients with focal epileptic myoclonus (FEM) with the Kozhevnikov–Rasmussen syndrome (KRS). FEM in KRS-patients was identified in 11 cases, accounting for 0.9 % of all the cases of epilepsy with the onset of seizures up to 18 years (n = 1261). The age at onset of KRS ranged from 3 to 21 years (average – 9.2 ± 5.7 years). In the active period of the disease of all patients in the clinical picture the active FEM appeared and increasing frequency of the secondary generalized seizures (SGS). In addition SGS and FEM, the clinical picture of the disease in most patients (91 %) the focal motor (clonic) and the somatosensory focal seizures were observed. As the disease progressed, the FEM became more pronounced in frequency and intensity, seized more muscle groups, localizing mainly in the muscles of the trunk and limbs. The typical EEG pattern of FEM patients with KRS was regional epileptiform activity that occurs in the structure of the continued regional slowing localizing maximum of the fronto-central-temporal region. During the magnetic resonance tomography of the brain in dynamics all the patients observed the increase in total cortical hemiatrophy. In all the cases, the appointment of antiepileptic therapy resulted in a slowing of the FEM, however, a complete remission was reached at none of the patients. Two patients were made surgical treatment of epilepsy. In one case remission of epileptic seizures was observed after right-side hemispherotomy. Our study showed that FEM is very resistant type of epileptic seizures. This fact calls for the identification of the FEM at the early stages of the disease with the purpose to improve the prognosis, as well as for an earlier surgical treatment.

Spectrum of Abnormal Movement in a Cohort of Neuro-Wilson Patients with Radiological Associations

Background: Disorders of movement are important features of Neuro-Wilson’s disease (NWD) and their recognition helps in early diagnosis. We studied the various types of movement disorders including any novel phenomenology found in our cohort of NWD, along with radiological correlations. Method: A total of 129 consecutive patients of WD (M:F) were examined in Movement Disorders clinic of a tertiary care neurological institute at Kolkata, India. A semi-structured interview and examination determined the various types of movement disorders detected, after proper informed consent. Neuro-imaging (MRI of 1.5 Tesla system) was carried out whenever possible. Results: The common movement disorders were dystonia (91.8%), Parkinsonism (83.72%), and tremor (53.49%). Others were movement induced focal myoclonus (12.4%), ataxia (11.63%), choreo-athetosis (15.5%). The less frequent movement disorders were akathisia (5.2%) and tics disorder (5.42%) and oromandibular dyskinesias (2.33%). MRI lesions were found to be associated with jaw opening dystonia (caudate), neck dystonia (putamen and pons), truncal dystonia (caudate, globus pallidus and cortical atrophy), appendicular dystonia (caudate and putamen), Parkinsonism (mid-brain), postural tremor (caudate and putamen), tics and akathisia (mid-brain and pons in both). Conclusion: WD is associated with a variety of common movement disorders such as dystonia, Parkinsonism and tremor. The less frequent movement disorders were focal myoclonus, stereotypes, tics disorders and orofacial dyskinesia . Radiological lesions can be found in association with majority of the movement disorders except in few cases where functional imaging studies may help.

Elevated antimeasles antibody titre: An association in autoimmune encephalitis.

Introduction:Autoimmune encephalitis is a group of treatable noninfective encephalitic disorders with great clinical implications. They have a close resemblance to prion disease and some slow virus infections. We report the presence of significant titers of antimeasles antibody in some of our patients with autoimmune encephalitis resulting in diagnostic and therapeutic problems.Patients and Methods:Patients seen by us in the last 4 years with high titers (1:625 dilution) cerebrospinal fiuid (CSF) antimeasles antibody positivity were reviewed retrospectively. The data collected were assessed using SPSS- Statistical Package for Social Sciences Version 15.0 (IBM corporation) software. The groups which showed elevated antimeasles antibody titers but did not have other parameters suggestive of subacute sclerosing panencephalitis (Group 2) were segregated and compared with those who had the typical features (Group 1) using Fisher's Exact Test.Results:There were 33 patients with antimeasles antibody in CSF. Group 1 had 27 and Group 2 had 6 patients. Group 1 had lower age, cognitive dysfunction, slow myoclonus, less generalized tonic-clonic seizures, and focal seizures. Group 2 patients belonged to the higher age, had significant psychosis (P = 0.02), incontinence of bowel and bladder (P = 0.0001). Slow myoclonus was significant in the first group (P = 0.028), and weakness was significant in the second group (P = 0.028) and double incontinence in the second group (P = 0.0001). Magnetic resonance imaging showed significant gray matter and cerebellar involvement in Group 2 P = 0.005 and P = 0.028, respectively.Conclusions:Patients who show significant titers of antimeasles antibodies in the CSF but belonging to older age group with psychosis, generalized tonic-clonic seizures, double incontinence, focal myoclonus, and electroencephalographic and imaging noncorroborative need to be investigated for autoimmune encephalitis in view of the great prognostic and therapeutic relevance.

Super-refractory status epilepticus due to anti-GAD-65 autoimmune encephalitis – biphasic presentations with discognitive crisis with generalization and posterior focal myoclonus

Introduction: Status epilepticus (SE) is a neurologic emergency and many causes should be investigated, such as autoimmune encephalitis. A patient will be described, with high levels of antibodies against 65kDa glutamic acid decarboxylase (GAD), an intracellular enzyme, which developed into super-refractory status. Objective: To emphasize the importance of immunologic mechanisms on the SE. Patient and methods: A 19-year old healthy female suddenly presented behaviour changes and recurrent generalized tonic-clonic crisis. The cerebrospinal fluid investigation was normal, brain MRI showed non-specific image in the white matter right hemisphere. The anti-GAD antibodies, obtained in serum, were with high levels (1960nmol/l). Continuous electroencephalogram (EEG) revealed moderate disorganization, epileptiform paroxysms in the right anterior frontotemporal region and rhythmic delta activity with varied frequencies and amplitudes suggestive of ictal discharges. Different types anticonvulsants drugs were used to control status without success. She recovered 2 months later after methylprednisolone and immunoglobulin. The patient initiated with focal myoclonus in the right upper limb after five months from hospital discharge. We have obtained patient and/or Institutional Review Board (IRB) approval, as necessary. Results: Most described cases of anti-GAD autoimmune encephalitis are presented as limbic encephalitis. Our case report shows a super-refratary status epilepticus and with partial relief of immunotherapy. Conclusion: The use of immunotherapy is essential in this case. Current studies are few to determine the best therapeutic approach.

HEMIBALLISMUS AFTER HEMORRHAGIC STROKE

Ischemic or hemorrhagic stroke may be accompanied by movement disorders (1), either hyperkinetic or hypokinetic. Hyperkinetic movement disorders after stroke comprise dystonia (2-4), chorea with or without hemiballismus (5), tremor (6), parkinsonism (7), segmental or focal myoclonus, athetosis, pseudathetosis, and asterixis (8). Hemiballismus is a movement disorder characterized by involuntary, arrythmic, and large amplitude excursion of a limb, usually from a proximal joint, witn an element of rotation (9). Ballismus is explainable with lesions in the subthalamic nuclei, cerebral cortex, corpus striatum, thalamus and brainstem. (10) The frequency of post-stroke abnormal movements is unclear, the prevalence in a swiss registry being 1% with an incidence of 0.08% per year (8). Of them, hemichorea-hemiballismus is the most common, while dystonia is the next most common disorder (11).

Focal myoclonus following vestibular concussion: A diagnostic and treatment perspective.

Focal myoclonus following vestibular concussion: A diagnostic and treatment perspective.