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1.
Clin Neurophysiol ; 132(8): 1830-1844, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34130251

RESUMO

Possessing a discrete functional repertoire, the anterior horn cell can be in one of two electrophysiological states: on or off. Usually under tight regulatory control by the central nervous system, a hierarchical network of these specialist neurons ensures muscular strength is coordinated, gradated and adaptable. However, spontaneous activation of these cells and their axons can result in abnormal muscular twitching. The muscular twitch is the common building block of several distinct clinical patterns, namely fasciculation, myokymia and neuromyotonia. When attempting to distinguish these entities electromyographically, their unique temporal and morphological profiles must be appreciated. Detection and quantification of burst duration, firing frequency, multiplet patterns and amplitude are informative. A common feature is their persistence during sleep. In this review, we explain the accepted terminology used to describe the spontaneous phenomena of motor hyperexcitability, highlighting potential pitfalls amidst a bemusing and complex collection of overlapping terms. We outline the relevance of these findings within the context of disease, principally amyotrophic lateral sclerosis, Isaacs syndrome and Morvan syndrome. In addition, we highlight the use of high-density surface electromyography, suggesting that more widespread use of this non-invasive technique is likely to provide an enhanced understanding of these motor hyperexcitability syndromes.


Assuntos
Esclerose Amiotrófica Lateral/fisiopatologia , Eletromiografia/métodos , Fasciculação/fisiopatologia , Síndrome de Isaacs/fisiopatologia , Neurônios Motores/fisiologia , Mioquimia/fisiopatologia , Esclerose Amiotrófica Lateral/diagnóstico , Fasciculação/diagnóstico , Humanos , Síndrome de Isaacs/diagnóstico , Mioquimia/diagnóstico , Doenças do Sistema Nervoso Periférico/diagnóstico , Doenças do Sistema Nervoso Periférico/fisiopatologia
2.
Intern Med ; 60(16): 2687-2691, 2021 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-33678744

RESUMO

We herein report a 48-year-old woman receiving eribulin mesylate for breast cancer who presented with gait disorder, distal limb paresthesia, and weakness progressing monthly. A nerve conduction study indicated demyelination with multifocal conduction block. Considering the immune-mediated pathology of her condition, she was administered intravenous immunoglobulin. Her neurological symptoms improved promptly after intravenous immunoglobulin therapy and eribulin withdrawal. Furthermore, the limb myokymia seen at the time of admission disappeared. Her symptoms continued to improve without additional treatment. We conclude that eribulin was a rare cause of demyelinating neuropathy with multifocal conduction block derived from immune-mediated pathology.


Assuntos
Neoplasias da Mama , Mioquimia , Neoplasias da Mama/complicações , Neoplasias da Mama/tratamento farmacológico , Feminino , Furanos/efeitos adversos , Humanos , Cetonas/efeitos adversos , Pessoa de Meia-Idade , Condução Nervosa
3.
Muscle Nerve ; 63(6): 861-867, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33675544

RESUMO

INTRODUCTION: Myokymic discharges are classically associated with nerve injury from prior radiation but may occur in other neuromuscular disorders. Using quantitative analysis we aimed to identify the spectrum of conditions in which myokymic discharges are present and determine if there are electrophysiological features that distinguish postradiation from nonradiation causes of myokymia. METHODS: We reviewed the clinical history of all patients examined in our electromyography labs with myokymic discharges recorded from June 2017 to February 2020. Quantitative analysis of each myokymic discharge was performed using a custom MATLAB script, assessing features such as burst frequency, spikes per burst, and burst regularity. RESULTS: Eighty-eight distinct myokymic discharges (70 patients) were analyzed: 51 postradiation recordings from 35 patients and 37 recordings from 35 nonradiation patients. The diagnostic spectrum of nonradiation cases was diverse, with common causes being median neuropathy (n = 8), cervical (n = 7), and lumbar (n = 5) radiculopathy, and motor neuron disease (n = 5). On quantitative analysis, postradiation myokymia had an increased burst-to-silence ratio (median, 0.29; nonradiation, 0.08) and greater peak number (median, 15; nonradiation, 7). Except for one patient with hereditary peripheral nerve hyperexcitability, all patients who had two or more muscles demonstrating myokymic discharges belonged to postradiation group. CONCLUSIONS: Myokymic discharges can be seen in diverse neuromuscular conditions; most common in our cohort was chronic median neuropathy. Postradiation myokymia appears to have distinguishing morphological features when quantitatively analyzed compared with nonradiation cases.


Assuntos
Mioquimia/etiologia , Doenças do Sistema Nervoso Periférico/complicações , Lesões por Radiação/complicações , Adulto , Idoso , Idoso de 80 Anos ou mais , Eletromiografia , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Mioquimia/fisiopatologia , Doenças do Sistema Nervoso Periférico/fisiopatologia , Lesões por Radiação/fisiopatologia , Adulto Jovem
4.
Clin Neuropharmacol ; 44(2): 75-76, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33480615

RESUMO

BACKGROUND: Gabapentin is a commonly used medication for neuropathic pain and epilepsy that is prescribed by a wide range of medical specialties. Adverse effects including asterixis and myoclonus have been described in patients with chronic kidney disease, but myokymia has not been previously reported. CASE PRESENTATION: A 69-year-old man with a history of traumatic brain injury, peripheral neuropathy, amnesia, and posttraumatic stress disorder presented to the hospital after multiple falls attributed to acute onset muscle spasms. He reported taking a total daily dose of 9600 mg of gabapentin, as prescribed. Physical examination demonstrated stimulus-sensitive myoclonus, painful muscle spasms in all extremities, and myokymia in his bilateral calves. Diffuse action tremors, as well as tongue tremors, were also observed.Initial workup, including basic laboratory investigations, brain imaging, and electroencephalogram, was unrevealing. Gabapentin toxicity was suspected, and a gabapentin holiday was initiated with the improvement of myokymia by hospital day 3. The patient was found to have a high gabapentin level (25.8 µg/mL; reference range, 2.0-20.0 µg/mL) measured the morning after hospital presentation. After restarting on a lower dose of gabapentin with multimodal pain control, the patient continued to improve with diminution of his myoclonus, tremor, and gait instability. CONCLUSIONS: Myokymia is a newly described motor symptom associated with gabapentin toxicity. The mechanism of gabapentin-associated myokymia is currently unknown. A brief medication holiday resulted in the resolution of motor symptoms without significant withdrawal symptoms. Knowledge of this newly reported adverse manifestation can aid physicians in the diagnosis of gabapentin toxicity and prompt treatment, as gabapentin levels are not widely or immediately available.


Assuntos
Ácidos Cicloexanocarboxílicos , Mioquimia , Idoso , Aminas/efeitos adversos , Animais , Bovinos , Ácidos Cicloexanocarboxílicos/efeitos adversos , Gabapentina , Humanos , Masculino , Ácido gama-Aminobutírico/efeitos adversos
5.
J Peripher Nerv Syst ; 26(1): 90-98, 2021 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-33179828

RESUMO

Limited literature is available on stimulus induced after discharges (SIAD) in patients with peripheral nerve hyperexcitability (PNH). The aim of the study was to examine the diagnostic utility of SIAD in the diagnosis and monitoring of primary PNH disorders. In this retrospective study, we studied 26 patients who were admitted with a diagnosis of primary PNH to the department of Neurology from January 2013 to April 2019. Their clinical profile, immunological characteristics were extracted from the database and nerve conduction studies were relooked for the presence of SIAD. 76% of patients in the primary PNH cohort had SIAD with 90% of them being voltage-gated potassium channel complex antibody positive; predominantly against contactin-associated protein-2 antigen and rest being paraneoplastic. There was also resolution of SIAD following treatment indicating reversible hyperexcitability. SIAD is a sensitive marker for Primary PNH syndrome with monitoring and diagnostic implications.


Assuntos
Potenciais de Ação/fisiologia , Eletrodiagnóstico/normas , Doenças Musculares/diagnóstico , Doenças Musculares/fisiopatologia , Condução Nervosa/fisiologia , Doenças do Sistema Nervoso Periférico/diagnóstico , Doenças do Sistema Nervoso Periférico/fisiopatologia , Nervo Tibial/fisiologia , Adulto , Eletrodiagnóstico/métodos , Eletromiografia , Feminino , Seguimentos , Humanos , Síndrome de Isaacs/diagnóstico , Síndrome de Isaacs/fisiopatologia , Masculino , Pessoa de Meia-Idade , Mioquimia/diagnóstico , Mioquimia/fisiopatologia , Estudos Retrospectivos
6.
Int J Mol Sci ; 21(20)2020 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-33066705

RESUMO

(1) Background: Episodic ataxia type 1 is caused by mutations in the KCNA1 gene encoding for the voltage-gated potassium channel Kv1.1. There have been many mutations in Kv1.1 linked to episodic ataxia reported and typically investigated by themselves or in small groups. The aim of this article is to determine whether we can define a functional parameter common to all Kv1.1 mutants that have been linked to episodic ataxia. (2) Methods: We introduced the disease mutations linked to episodic ataxia in the drosophila analog of Kv1.1, the Shaker Kv channel, and expressed the channels in Xenopus oocytes. Using the cut-open oocyte technique, we characterized the gating and ionic currents. (3) Results: We found that the episodic ataxia mutations variably altered the different gating mechanisms described for Kv channels. The common characteristic was a conductance voltage relationship and inactivation shifted to less polarized potentials. (4) Conclusions: We suggest that a combination of a prolonged action potential and slowed and incomplete inactivation leads to development of ataxia when Kv channels cannot follow or adapt to high firing rates.


Assuntos
Ataxia/genética , Ativação do Canal Iônico , Canal de Potássio Kv1.1/genética , Mutação , Mioquimia/genética , Animais , Humanos , Canal de Potássio Kv1.1/química , Canal de Potássio Kv1.1/metabolismo , Xenopus
7.
Ophthalmic Plast Reconstr Surg ; 36(6): 566-568, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32810032

RESUMO

PURPOSE: To describe a novel observation of ipsilateral eyelid myokymia in the context of Marcus Gunn jaw-winking synkinesis (MGJWS). METHODS: A retrospective case series of 5 patients observed to have myokymia in the context of MGJWS in 2 tertiary hospitals in Riyadh, Saudi Arabia was conducted. Demographic profile including age and gender, and clinical features were analyzed. RESULTS: Five patients (3 males and 2 females) with MGJWS were noted to demonstrate the phenomenon of ipsilateral eyelid myokymia. All but 1 had right-sided MGJWS. The myokymia was seen as upper eyelid twitching in a vertical fashion along the levator palpebrae superioris muscle field of action. All subjects also had ipsilateral Monocular elevation deficiency. CONCLUSION: Ipsilateral upper eyelid myokymia is a potential feature of MGJWS. Monocular elevation seems to be a constant feature among MGJWS patients with levator muscle myokymia.Marcus Gunn jaw-winking synkinesis (MGJWS) is not well understood. Ipsilateral eyelid myokymia is a potential feature of MGJWS. This finding suggests that peripheral dysinnervation is likely to be a part of MGJWS.Supplemental Digital Content is available in the text.


Assuntos
Blefaroptose , Mioquimia , Sincinesia , Pálpebras , Feminino , Cardiopatias Congênitas , Humanos , Anormalidades Maxilomandibulares , Masculino , Doenças do Sistema Nervoso , Músculos Oculomotores , Reflexo Anormal , Estudos Retrospectivos , Sincinesia/diagnóstico
8.
Wilderness Environ Med ; 31(3): 354-357, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32826164

RESUMO

A number of crotaline species have been associated with neurotoxic envenomation in North America. One clinical sign that can occur is myokymia: fine, involuntary, wave-like muscle movements occurring at regular intervals. We report an unusual scenario in which a single snakebite resulted in simultaneous envenomation of 2 patients. Both developed myokymia, with 1 having respiratory compromise. One patient also developed a hypersensitivity reaction to antivenom. Envenomation by the Grand Canyon rattlesnake, Crotalus oreganus abyssus, can produce significant neurotoxicity and resultant respiratory compromise. Antivenom may be helpful but can produce hypersensitivity reactions.


Assuntos
Antivenenos/efeitos adversos , Venenos de Crotalídeos/toxicidade , Crotalus , Hipersensibilidade/terapia , Mioquimia/terapia , Mordeduras de Serpentes/patologia , Mordeduras de Serpentes/terapia , Adulto , Animais , Arizona , Humanos , Hipersensibilidade/etiologia , Masculino , Pessoa de Meia-Idade , Mioquimia/etiologia , Mioquimia/patologia , Mioquimia/fisiopatologia , Mordeduras de Serpentes/complicações , Mordeduras de Serpentes/fisiopatologia
9.
Acta Myol ; 39(1): 36-39, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32607479

RESUMO

Mutations of the main voltage-gated K channel members Kv1.1 are linked to several clinical conditions, such as periodic ataxia type 1, myokymia and seizure disorders. Due to their role in active magnesium reabsorption through the renal distal convoluted tubule segment, mutations in the KCNA1 gene encoding for Kv1.1 has been associated with hypomagnesemia with myokymia and tetanic crises. Here we describe a case of a young female patient who came to our attention for a history of muscular spasms, tetanic episodes and muscle weakness, initially misdiagnosed for fibromyalgia. After a genetic screening she was found to be carrier of the c.736A > G (p.Asn255Asp) mutation in KCNA1, previously described in a family with autosomal dominant hypomagnesemia with muscular spasms, myokymia and tetanic episodes. However, our patient has always presented normal serum and urinary magnesium values, whereas she was affected by hypocalcemia. Calcium supplementation gave only partial clinical benefit, with an improvement on tetanic episodes yet without a clinical remission of her spasms, whereas magnesium supplementation worsened her muscular symptomatology.


Assuntos
Cálcio/administração & dosagem , Hipocalcemia , Canal de Potássio Kv1.1/genética , Magnésio/sangue , Mioquimia , Tetania , Adulto , Encéfalo/diagnóstico por imagem , Hormônios e Agentes Reguladores de Cálcio/administração & dosagem , Diagnóstico Diferencial , Feminino , Humanos , Hipocalcemia/diagnóstico , Hipocalcemia/etiologia , Hipocalcemia/terapia , Imageamento por Ressonância Magnética/métodos , Mutação , Mioquimia/diagnóstico , Mioquimia/tratamento farmacológico , Mioquimia/genética , Mioquimia/fisiopatologia , Exame Neurológico/métodos , Tetania/diagnóstico , Tetania/tratamento farmacológico , Tetania/genética , Tetania/fisiopatologia
10.
Mol Genet Genomic Med ; 8(10): e1434, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32705822

RESUMO

BACKGROUND: Pathogenic KCNA1 variants have been linked to episodic ataxia type 1 (EA1), a rare neurological syndrome characterized by continuous myokymia and attacks of generalized ataxia that can be triggered by fever, abrupt movements, emotional stress, and fatigue. Currently, over 40 KCNA1 variants have been identified in individuals with EA1. METHODS: A male patient displayed partial seizures in addition to EA1 symptoms, often triggered by fever. A sibling presented with typical EA1 symptoms, seizures, and learning difficulties. In addition, the older brother displayed cognitive impairment, developmental delay, and slurred speech, which were absent in his younger sister. Whole-exome sequencing was performed for the patients. RESULTS: A novel de novo missense variant in KCNA1 (p.Ala261Thr) was identified in the male patient, which is located in a base of the 3rd transmembrane domain (S3). The other novel KCNA1 variant (p.Gly376Ser) was identified in the sibling and was inherited from an unaffected father with low-level mosaicism. The variant was located in the S5-S6 extracellular linker of the voltage sensor domain of the Kv channel. Next, we systematically reviewed the available clinical phenotypes of individuals with EA1 and observed that individuals with KCNA1 variants at the C-terminus were more likely to suffer from seizures and neurodevelopmental disorders than those with variants at the N-terminus. CONCLUSION: Our study expands the mutation spectrum of KCNA1 and improves our understanding of the genotype-phenotype correlations of KCNA1. Definitive genetic diagnosis is beneficial for the genetic counseling and clinical management of individuals with EA1.


Assuntos
Ataxia/genética , Deficiências do Desenvolvimento/genética , Canal de Potássio Kv1.1/genética , Mutação de Sentido Incorreto , Mioquimia/genética , Ataxia/patologia , Pré-Escolar , Deficiências do Desenvolvimento/patologia , Feminino , Humanos , Lactente , Canal de Potássio Kv1.1/química , Masculino , Mosaicismo , Mioquimia/patologia , Fenótipo , Domínios Proteicos
11.
J Neurol Neurosurg Psychiatry ; 91(10): 1076-1084, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32651251

RESUMO

OBJECTIVE: Antibodies against contactin-associated protein-like 2 (CASPR2-Abs) have been described in acquired neuromyotonia, limbic encephalitis (LE) and Morvan syndrome (MoS). However, it is unknown whether these constitute one sole spectrum of diseases with the same immunopathogenesis or three distinct entities with different mechanisms. METHODS: A cluster analysis of neurological symptoms was performed in a retrospective cohort of 56 CASPR2-Abs patients. In parallel, immunological features and human leucocyte antigen (HLA) were studied. RESULTS: Cluster analysis distinguished patients with predominant limbic symptoms (n=29/56) from those with peripheral nerve hyperexcitability (PNH; n=27/56). In the limbic-prominent group, limbic features were either isolated (LE/-; 18/56, 32.1%), or combined with extralimbic symptoms (LE/+; 11/56, 19.6%). Those with PNH were separated in one group with severe PNH and extralimbic involvement (PNH/+; 16/56, 28.6%), resembling historical MoS descriptions; and one group with milder and usually isolated PNH (PNH/-; 11/56, 19.6%). LE/- and LE/+ patients shared immunogenetic characteristics demonstrating a homogeneous entity. HLA-DRB1*11:01 was carried more frequently than in healthy controls only by patients with LE (94.1% vs 18.3%; p=1.3×10-10). Patients with LE also had serum titres (median 1:40 960) and rates of cerebrospinal fluid positivity (93.1%) higher than the other groups (p<0.05). Conversely, DRB1*11:01 association was absent in PNH/+ patients, but only they had malignant thymoma (87.5%), serum antibodies against leucine-rich glioma-inactivated 1 protein (66.7%) and against netrin-1 receptor deleted in colorectal carcinoma (53.8%), and myasthenia gravis (50.0%). INTERPRETATION: Symptoms' distribution supports specific clinical phenotypes without overlap between LE and MoS. The distinct immunogenetic characteristics shared by all patients with LE and the particular oncological and autoimmune associations of MoS suggest two very different aetiopathogenesis.


Assuntos
Autoanticorpos/imunologia , Síndrome de Isaacs/fisiopatologia , Encefalite Límbica/fisiopatologia , Proteínas de Membrana/imunologia , Mioquimia/fisiopatologia , Proteínas do Tecido Nervoso/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Ataxia/fisiopatologia , Análise por Conglomerados , Receptor DCC/imunologia , Epilepsia do Lobo Temporal/fisiopatologia , Função Executiva/fisiologia , Feminino , Antígenos HLA/genética , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/imunologia , Síndrome de Isaacs/genética , Síndrome de Isaacs/imunologia , Encefalite Límbica/genética , Encefalite Límbica/imunologia , Masculino , Transtornos da Memória/fisiopatologia , Pessoa de Meia-Idade , Mioquimia/genética , Mioquimia/imunologia , Fenótipo
13.
J Pharmacol Exp Ther ; 373(3): 391-401, 2020 06.
Artigo em Inglês | MEDLINE | ID: mdl-32217768

RESUMO

Loss of function of voltage-gated potassium (Kv) channels is linked to a range of lethal or debilitating channelopathies. New pharmacological approaches are warranted to isoform-selectively activate specific Kv channels. One example is KCNA1 Potassium Voltage-Gated Channel Subfamily A Member 1 (KCNA1) (Kv1.1), an archetypal Shaker-type Kv channel, in which loss-of-function mutations cause episodic ataxia type 1 (EA1). EA1 causes constant myokomia and episodic bouts of ataxia and may associate with epilepsy and other disorders. We previously found that the inhibitory neurotransmitter γ-aminobutyric acid and modified versions of glycine directly activate Kv channels within the KCNQ subfamily, a characteristic favored by strong negative electrostatic surface potential near the neurotransmitter carbonyl group. Here, we report that adjusting the number and positioning of fluorine atoms within the fluorophenyl ring of glycine derivatives produces isoform-selective KCNA1 channel openers that are inactive against KCNQ2/3 channels, or even KCNA2, the closest relative of KCNA1. The findings refine our understanding of the molecular basis for KCNQ versus KCNA1 activation and isoform selectivity and constitute, to our knowledge, the first reported isoform-selective KCNA1 opener. SIGNIFICANCE STATEMENT: Inherited loss-of-function gene sequence variants in KCNA1, which encodes the KCNA1 (Kv1.1) voltage-gated potassium channel, cause episodic ataxia type 1 (EA1), a movement disorder also linked to epilepsy and developmental delay. We have discovered several isoform-specific KCNA1-activating small molecules, addressing a notable gap in the field and providing possible lead compounds and a novel chemical space for the development of potential future therapeutic drugs for EA1.


Assuntos
Glicina/genética , Canal de Potássio Kv1.1/genética , Isoformas de Proteínas/genética , Animais , Ataxia/genética , Epilepsia/genética , Humanos , Mutação/genética , Mioquimia/genética , Xenopus laevis/genética
16.
J Med Genet ; 57(2): 132-137, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31586945

RESUMO

BACKGROUND: Since 1994, over 50 families affected by the episodic ataxia type 1 disease spectrum have been described with mutations in KCNA1, encoding the voltage-gated K+ channel subunit Kv1.1. All of these mutations are either transmitted in an autosomal-dominant mode or found as de novo events. METHODS: A patient presenting with a severe combination of dyskinesia and neonatal epileptic encephalopathy was sequenced by whole-exome sequencing (WES). A candidate variant was tested using cellular assays and patch-clamp recordings. RESULTS: WES revealed a homozygous variant (p.Val368Leu) in KCNA1, involving a conserved residue in the pore domain, close to the selectivity signature sequence for K+ ions (TVGYG). Functional analysis showed that mutant protein alone failed to produce functional channels in homozygous state, while coexpression with wild-type produced no effects on K+ currents, similar to wild-type protein alone. Treatment with oxcarbazepine, a sodium channel blocker, proved effective in controlling seizures. CONCLUSION: This newly identified variant is the first to be reported to act in a recessive mode of inheritance in KCNA1. These findings serve as a cautionary tale for the diagnosis of channelopathies, in which an unreported phenotypic presentation or mode of inheritance for the variant of interest can hinder the identification of causative variants and adequate treatment choice.


Assuntos
Ataxia/genética , Discinesias/genética , Epilepsia/genética , Canal de Potássio Kv1.1/genética , Mioquimia/genética , Ataxia/diagnóstico , Ataxia/tratamento farmacológico , Ataxia/patologia , Canalopatias/diagnóstico , Canalopatias/tratamento farmacológico , Canalopatias/genética , Canalopatias/patologia , Criança , Pré-Escolar , Discinesias/diagnóstico , Discinesias/tratamento farmacológico , Discinesias/patologia , Epilepsia/diagnóstico , Epilepsia/tratamento farmacológico , Epilepsia/patologia , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Homozigoto , Humanos , Lactente , Recém-Nascido , Canal de Potássio Kv1.1/ultraestrutura , Masculino , Mutação/genética , Mioquimia/diagnóstico , Mioquimia/tratamento farmacológico , Mioquimia/patologia , Oxcarbazepina/administração & dosagem , Oxcarbazepina/efeitos adversos , Linhagem , Sequenciamento Completo do Exoma
19.
World Neurosurg ; 131: 197-199, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31299312

RESUMO

BACKGROUND: Superior oblique myokymia (SOM) is a rare disorder characterized by episodic microtremor of the eyeball. in patients with SOM, intermittent contraction of the superior oblique muscle causes irregular and rotatory eye movement, causing oscillopsia and diplopia. Microvascular decompression (MVD) of the trochlear nerve is potentially a definitive treatment method for SOM; however, owing to its rarity, this disorder is not well-known to neurosurgeons, and thus the optimal surgical approach has not yet been determined. CASE DESCRIPTION: A 77-year-old woman with left SOM had experienced oscillopsia for 2 years. MVD was performed via a left lateral superior cerebellar approach with the patient in the park-bench position. Her symptom resolved immediately after the surgery. CONCLUSIONS: We believe that MVD via a left lateral superior cerebellar approach can be safely performed to SOM in elderly patients like our patient. Therefore, MVD should be considered as the definitive treatment method for more patients with SOM.


Assuntos
Mioquimia/cirurgia , Transtornos da Motilidade Ocular/cirurgia , Idoso , Descompressão Cirúrgica/métodos , Feminino , Humanos , Microtecnologia/métodos , Músculos Oculomotores , Procedimentos Cirúrgicos Vasculares/métodos
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