RESUMEN
Background: Opsoclonus is a rare disorder characterized by conjugate multidirectional, horizontal, vertical, and torsional saccadic oscillations, without intersaccadic interval, resulting from dysfunction within complex neuronal pathways in the brainstem and cerebellum. While most cases of opsoclonus are associated with autoimmune or paraneoplastic disorders, infectious agents, trauma, or remain idiopathic, opsoclonus can also be caused by medications affecting neurotransmission. This review was prompted by a case of opsoclonus occurring in a patient with Multiple System Atrophy, where amantadine, an NMDA-receptor antagonist, appeared to induce opsoclonus. Methods: Case report of a single patient and systematized review of toxic/drug-induced opsoclonus, selecting articles based on predefined criteria and assessing the quality of included studies. Results: The review included 30 articles encompassing 158 cases of toxic/drug-induced opsoclonus. 74% of cases were attributed to bark scorpion poisoning, followed by 9% of cases associated with chlordecone intoxication. The remaining cases were due to various toxics/drugs, highlighting the involvement of various neurotransmitters, including acetylcholine, glutamate, GABA, dopamine, glycine, and sodium channels, in the development of opsoclonus. Conclusion: Toxic/drug-induced opsoclonus is very rare. The diversity of toxics/drugs impacting different neurotransmitter systems makes it challenging to define a unifying mechanism, given the intricate neuronal pathways underlying eye movement physiology and opsoclonus pathophysiology.
Asunto(s)
Amantadina , Atrofia de Múltiples Sistemas , Trastornos de la Motilidad Ocular , Humanos , Masculino , Amantadina/efectos adversos , Atrofia de Múltiples Sistemas/tratamiento farmacológico , Atrofia de Múltiples Sistemas/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Trastornos de la Motilidad Ocular/fisiopatología , AncianoRESUMEN
BACKGROUND: The benefits of intraarterial thrombolytic treatment (IATT) in reversing hyaluronic acid (HA)-related visual deficits remain unclear. This study aimed to report a 5-year experience in the treatment of visual deficits resulting from HA embolization by IATT in a tertiary medical center. METHODS: From December of 2015 to June of 2021, the medical records of consecutive patients with HA-related visual deficits who underwent IATT were reviewed retrospectively. The demographics, clinical features, imaging data, treatment details, and follow-up results of the patients were analyzed. RESULTS: A total of 72 consecutive patients were analyzed, including five men (6.9%) men and 67 women (3.1%), aged 29.3 ± 7.6 years (range, 17 to 50 years). Thirty-two patients (44.4%) showed preserved visual acuity, and 40 (55.6%) exhibited no light perception on admission. Ocular motility disorders were detected in 63 patients (87.5%), ptosis was detected in 61 patients (84.7%), and facial skin changes were detected in 54 patients (75%). The technical success rate of IATT was 100%, with successful recanalization of the occlusive artery. No procedure-related complications were detected, and all skin injuries, ptosis, and ocular motility disorders were healed. Improved visual acuity was detected in 26 cases (36.1%). In the binary logistic regression model, only preoperative preserved visual acuity was independently associated with a good outcome. CONCLUSIONS: IATT for selective patients with HA-related visual deficits is efficient and safe. Preoperative preserved visual acuity was independently associated with a good outcome after IATT. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.
Asunto(s)
Ácido Hialurónico , Trastornos de la Motilidad Ocular , Masculino , Humanos , Femenino , Ácido Hialurónico/efectos adversos , Estudios Retrospectivos , Pronóstico , Fibrinolíticos/uso terapéutico , Trastornos de la Motilidad Ocular/inducido químicamente , Trastornos de la Motilidad Ocular/tratamiento farmacológico , Resultado del TratamientoRESUMEN
OBJECTIVES: Oculogyric crisis is a dystonic movement disorder characterized by continuous contraction of the ocular muscles and spasmodic movements of the pupils in a fixed position, usually upward. METHODS: In this case report, an early-stage acute oculogyric crisis due to low-dose olanzapine in a 15-year-old adolescent boy is presented. RESULTS: To the best of our knowledge, this is the first report showing that acute oculogyric crisis can develop with low-dose olanzapine administration. CONCLUSIONS: Even though second-generation antipsychotics are safer than conventional antipsychotics in terms of extrapyramidal adverse effects, this possibility should always be taken into consideration through this case report.
Asunto(s)
Antipsicóticos , Distonía , Trastornos de la Motilidad Ocular , Adolescente , Antipsicóticos/efectos adversos , Distonía/inducido químicamente , Humanos , Masculino , Trastornos de la Motilidad Ocular/inducido químicamente , Olanzapina/efectos adversosRESUMEN
The caudal fastigial nuclei (cFN) are the output nuclei by which the medio-posterior cerebellum influences the production of saccades toward a visual target. On the basis of the organization of their efferences to the premotor burst neurons and the bilateral control of saccades, the hypothesis was proposed that the same unbalanced activity accounts for the dysmetria of all saccades during cFN unilateral inactivation, regardless of whether the saccade is horizontal, oblique, or vertical. We further tested this hypothesis by studying, in two head-restrained macaques, the effects of unilaterally inactivating the caudal fastigial nucleus on saccades toward a target moving vertically with a constant, increasing or decreasing speed. After local muscimol injection, vertical saccades were deviated horizontally toward the injected side with a magnitude that increased with saccade size. The ipsipulsion indeed depended on the tested target speed but not its instantaneous value because it did not increase (decrease) when the target accelerated (decelerated). By subtracting the effect on contralesional horizontal saccades from the effect on ipsilesional ones, we found that the net bilateral effect on horizontal saccades was strongly correlated with the effect on vertical saccades. We explain how this correlation corroborates the bilateral hypothesis and provide arguments against the suggestion that the instantaneous saccade velocity would somehow be "encoded" by the discharge of Purkinje cells in the oculomotor vermis.NEW & NOTEWORTHY Besides causing dysmetric horizontal saccades, unilateral inactivation of caudal fastigial nucleus causes an ipsipulsion of vertical saccades. This study is the first to quantitatively describe this ipsipulsion during saccades toward a moving target. By subtracting the effects on contralesional (hypometric) and ipsilesional (hypermetric) horizontal saccades, we find that this net bilateral effect is strongly correlated with the ipsipulsion of vertical saccades, corroborating the suggestion that a common disorder affects all saccades.
Asunto(s)
Núcleos Cerebelosos/fisiología , Agonistas de Receptores de GABA-A/farmacología , Percepción de Movimiento/fisiología , Muscimol/farmacología , Trastornos de la Motilidad Ocular/fisiopatología , Movimientos Sacádicos/fisiología , Animales , Conducta Animal/efectos de los fármacos , Conducta Animal/fisiología , Núcleos Cerebelosos/efectos de los fármacos , Modelos Animales de Enfermedad , Tecnología de Seguimiento Ocular , Agonistas de Receptores de GABA-A/administración & dosificación , Macaca mulatta , Masculino , Percepción de Movimiento/efectos de los fármacos , Muscimol/administración & dosificación , Trastornos de la Motilidad Ocular/inducido químicamente , Movimientos Sacádicos/efectos de los fármacosRESUMEN
An oculogyric crisis is a tonic conjugated deviation of the eyes, usually upward. We present two cases with a drug induced oculogyric crisis. The differential diagnoses should include epilepsy, a functional neurological movement disorder, ocular tics, ocular dyskinesia or ocular bobbing. Typically, in an oculogyric crisis the patient's awareness is intact; accompanied signs can be blepharospasm, neck flexion, jaw opening with or without tongue protrusion and autonomic symptoms. The underlying pathophysiology seems an imbalance between cholinergic and dopaminergic pathways. Most frequently an oculogyric crisis is caused by antidopaminergic medications, for example neuroleptics and metoclopramide. Treatment of medication-induced oculogyric crisis with parenteral anticholinergics typically leads to a fast remission of symptoms. Consider tocontinue anticholinergic therapy orally for a few days.
Asunto(s)
Antipsicóticos , Distonía , Oftalmopatías , Trastornos de la Motilidad Ocular , Antipsicóticos/efectos adversos , Antagonistas Colinérgicos/efectos adversos , Distonía/inducido químicamente , Distonía/diagnóstico , Humanos , Trastornos de la Motilidad Ocular/inducido químicamente , Trastornos de la Motilidad Ocular/diagnósticoAsunto(s)
Trastornos de Alimentación y de la Ingestión de Alimentos/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Fenciclidina/toxicidad , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Adulto , Femenino , Humanos , Recién Nacido , Masculino , EmbarazoRESUMEN
BACKGROUND: Lithium salts have been commonly used for prophylaxis and treatment of bipolar disorder and have numerous side effects. However, there has been no report of skew deviation and downbeat nystagmus associated with lithium. Herein, we report the first case of lithium-induced skew deviation and downbeat nystagmus. CASE PRESENTATION: A 39 years-old woman presented with intermittent vertical diplopia and dizziness within 1-2 months. Ophthalmologic examination revealed downbeat nystagmus and 6 prism diopters of right hypertropia. Funduscopic examination showed mild incyclotorsion on right eye. However, ductions and versions were within normal range. Other neurological examinations were also normal. She had a history of bipolar disorder treated with daily 600-900 mg of lithium for past 6 years, and 2 months before the first visit, daily dose of lithium was increased to 1200 mg. We referred the patients to psychiatrist. Although the serum level of lithium was within the normal therapeutic range, her daily dose of lithium was reduced to 600 mg and then stopped. 6 days after cessation of lithium, down beat nystagmus and right hypertropia were completely resolved and symptoms did not recur over a year. CONCLUSION: Even within a normal therapeutic range, downbeat nystagmus and skew deviation can occur as side effect of lithium. Dehydration may contribute to the neurotoxicity of lithium.
Asunto(s)
Trastorno Bipolar/tratamiento farmacológico , Compuestos de Litio/efectos adversos , Nistagmo Patológico/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Adulto , Encéfalo/diagnóstico por imagen , Diplopía/fisiopatología , Femenino , Humanos , Compuestos de Litio/administración & dosificación , Imagen por Resonancia Magnética , Nistagmo Patológico/fisiopatología , Trastornos de la Motilidad Ocular/fisiopatología , Visión Binocular/fisiologíaRESUMEN
A 19-year-old female was seen at the emergency department following an auto-intoxication. An oculogyric crisis (ogc) was observed, in the absence of other extrapyramidal symptoms (eps). In a second anamnesis, patient indicated that she had taken risperidone 3 mg (an atypical antipsychotic). This particular case description of an isolated ogc shows that care providers should be attentive to the occurrence of ogc, even if the most frequent eps are absent. This case also emphasizes the importance of a complete history in order to efficiently and timely guide the care provider to the correct diagnosis.
Asunto(s)
Antipsicóticos/efectos adversos , Distonía/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Risperidona/efectos adversos , Diagnóstico Diferencial , Distonía/diagnóstico , Femenino , Humanos , Trastornos de la Motilidad Ocular/diagnóstico , Trastornos Psicóticos/tratamiento farmacológico , Adulto JovenRESUMEN
PURPOSE OF REVIEW: To summarize the visual and oculomotor outcomes in children with prenatal opioid exposure and review the effects of opioids on the developing central nervous system. RECENT FINDINGS: Animal models and imaging studies in children suggest that prenatal opioid exposure may affect neuronal survival and result in delayed maturation of white matter tracts and decreased volumes in certain brain areas. Visual evoked potential testing in children demonstrates delayed maturation of the afferent visual system in opioid-exposed groups compared with controls, though 'catch-up' development is seen with longitudinal follow-up. Strabismus and nystagmus are also more common in exposed children, and these findings appear to persist. SUMMARY: As rates of opioid dependence and prenatal opioid exposure continue to increase, it is important to evaluate the short-term and long-term effects of opioids on the developing visual system. An understanding of these risks is important when counseling the parents or guardians of opioid-exposed children, though larger studies with more long-term follow-up will improve our prognostic abilities.
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Analgésicos Opioides/efectos adversos , Nistagmo Patológico/inducido químicamente , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Estrabismo/inducido químicamente , Animales , Encéfalo/efectos de los fármacos , Potenciales Evocados Visuales/efectos de los fármacos , Femenino , Humanos , Trastornos de la Motilidad Ocular/inducido químicamente , EmbarazoAsunto(s)
Antipsicóticos/efectos adversos , Trastorno de la Conducta/tratamiento farmacológico , Trastornos de la Motilidad Ocular/inducido químicamente , Risperidona/efectos adversos , Discinesia Tardía/inducido químicamente , Adolescente , Antipsicóticos/administración & dosificación , Trastorno por Déficit de Atención con Hiperactividad/tratamiento farmacológico , Estimulantes del Sistema Nervioso Central/administración & dosificación , Humanos , Masculino , Metilfenidato/administración & dosificación , Risperidona/administración & dosificaciónRESUMEN
Ictal gaze deviation and oculogyric crisis (OGC) can show identical clinical manifestations. We report a case of repeated drug induced OGCs in a 38â¯year old patient with secondary progressive multiple sclerosis. He was referred to our center for treatment of "intractable" epilepsy manifesting as episodic eye and head deviations with apparent unresponsiveness. In the epilepsy monitoring unit, ten typical spells were captured without epileptiform electroencephalographic correlates, but we discovered chronic exposure to metoclopramide. A diagnosis of OGC was suspected and Metoclopramide was stopped. This robustly improved the frequency of his spells. In a setting of usage of antidopaminergic medications and/or pontomesencephalic lesions, a low threshold should be kept for the diagnosis of oculogyric crisis, thus avoiding seizure diagnoses and inappropriate treatment of the phenomenon. Video-EEG monitoring is essential for teasing apart epilepsy and OGC.
Asunto(s)
Antieméticos/efectos adversos , Epilepsia Refractaria/diagnóstico , Metoclopramida/efectos adversos , Esclerosis Múltiple Crónica Progresiva/complicaciones , Trastornos de la Motilidad Ocular/inducido químicamente , Adulto , Diagnóstico Diferencial , Distonía/inducido químicamente , Electroencefalografía , Humanos , MasculinoRESUMEN
Upgaze or sustained elevation of the eyes, is an alteration of ocular motility initially described in hypoxic coma. We report a 65-year-old woman admitted with hypotension and alteration of sensorium due to the ingestion of 9.5 g of Bupropion. She presented two seizures of short duration, without epileptic activity on the EEG. She had a persistent asynchronous myoclonus in extremities, tachycardia and prolonged Q-t. She suffered a cardiac arrest caused by asystole, which recovered quickly in five minutes. At that moment, upgaze appeared, associated with a persistent ocular opening, which persisted for days, but finally disappeared, without remission of coma. A magnetic resonance imaging done at the eighth day, showed hyperintensity of the oval center and corpus callosum which disappeared in a new imaging study done 30 days later, where images of hypoxia in the basal nuclei and cortex appeared. The patient died forty seven days after admission. Up-gaze is an ominous oculomotor alteration linked to an important but incomplete damage in the cerebral cortex, a condition that perverts some sequences of the ocular opening, reversing the Bell phenomenon and producing eyelid retraction.
Asunto(s)
Antidepresivos de Segunda Generación/efectos adversos , Bupropión/efectos adversos , Coma/inducido químicamente , Sobredosis de Droga/complicaciones , Hipoxia Encefálica/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Anciano , Resultado Fatal , Femenino , Humanos , Imagen por Resonancia Magnética , Trastornos de la Personalidad/tratamiento farmacológico , SuicidioAsunto(s)
Materiales Biocompatibles/efectos adversos , Técnicas Cosméticas/efectos adversos , Rellenos Dérmicos/efectos adversos , Diplopía/inducido químicamente , Durapatita/efectos adversos , Dolor Ocular/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Conjuntiva/irrigación sanguínea , Diplopía/diagnóstico , Dolor Ocular/diagnóstico , Femenino , Cefalea/inducido químicamente , Cefalea/diagnóstico , Humanos , Trastornos de la Motilidad Ocular/diagnóstico , Rinoplastia , Enfermedades Vasculares/inducido químicamente , Enfermedades Vasculares/diagnóstico , Vómitos/inducido químicamente , Vómitos/diagnóstico , Adulto JovenRESUMEN
Upgaze or sustained elevation of the eyes, is an alteration of ocular motility initially described in hypoxic coma. We report a 65-year-old woman admitted with hypotension and alteration of sensorium due to the ingestion of 9.5 g of Bupropion. She presented two seizures of short duration, without epileptic activity on the EEG. She had a persistent asynchronous myoclonus in extremities, tachycardia and prolonged Q-t. She suffered a cardiac arrest caused by asystole, which recovered quickly in five minutes. At that moment, upgaze appeared, associated with a persistent ocular opening, which persisted for days, but finally disappeared, without remission of coma. A magnetic resonance imaging done at the eighth day, showed hyperintensity of the oval center and corpus callosum which disappeared in a new imaging study done 30 days later, where images of hypoxia in the basal nuclei and cortex appeared. The patient died forty seven days after admission. Up-gaze is an ominous oculomotor alteration linked to an important but incomplete damage in the cerebral cortex, a condition that perverts some sequences of the ocular opening, reversing the Bell phenomenon and producing eyelid retraction.
Asunto(s)
Humanos , Femenino , Anciano , Trastornos de la Motilidad Ocular/inducido químicamente , Hipoxia Encefálica/inducido químicamente , Bupropión/efectos adversos , Coma/inducido químicamente , Antidepresivos de Segunda Generación/efectos adversos , Sobredosis de Droga/complicaciones , Trastornos de la Personalidad/tratamiento farmacológico , Suicidio , Imagen por Resonancia Magnética , Resultado FatalRESUMEN
FK506 (tacrolimus) is an immunosuppressive drug and more potent than cyclosporine. FK506 is widely used for immunosuppression in the prevention and treatment of graft-versus-host disease after allogeneic bone marrow transplantation and solid organ transplantation. Neurotoxicity is a recognized complication of FK506 therapy, but ptosis and weakness of eye abduction unilaterally has not been reported in association with FK506 administration to date. We discuss a 13-year-old male patient who developed ptosis and weakness of eye abduction unilaterally 90 days after transplantation with bone marrow from an unrelated donor, for acute lymphoblastic leukemia in this case report. FK506 therapy was administered for graft-versus-host disease prophylaxis and CMV infection was treated with ganciclovir. The physical examination findings completely resolved 72 to 96 hours after concomitant FK506 and ganciclovir treatment were terminated.
Asunto(s)
Trasplante de Médula Ósea/efectos adversos , Quimioterapia Combinada/efectos adversos , Enfermedad Injerto contra Huésped/prevención & control , Trastornos de la Motilidad Ocular/inducido químicamente , Adolescente , Antivirales/uso terapéutico , Blefaroptosis/inducido químicamente , Trasplante de Médula Ósea/métodos , Ganciclovir/uso terapéutico , Enfermedad Injerto contra Huésped/tratamiento farmacológico , Humanos , Inmunosupresores/uso terapéutico , Masculino , Trastornos de la Motilidad Ocular/etiología , Tacrolimus/efectos adversos , Tacrolimus/uso terapéutico , Trasplante Homólogo , Resultado del TratamientoRESUMEN
BACKGROUND: Oculogyric crises are involuntary movements of the eyeballs and can occur due to different etiologies. PHENOMENOLOGY SHOWN: This video abstract shows a man with oculogyric crises due to side effect of neuroleptics. EDUCATIONAL VALUE: Oculogyric crises are easy to recognize if once seen.
Asunto(s)
Antipsicóticos/efectos adversos , Trastornos Distónicos/inducido químicamente , Trastornos de la Motilidad Ocular/inducido químicamente , Antipsicóticos/uso terapéutico , Dibenzocicloheptenos , Compuestos Heterocíclicos de 4 o más Anillos/efectos adversos , Compuestos Heterocíclicos de 4 o más Anillos/uso terapéutico , Humanos , Masculino , Trastornos Mentales/tratamiento farmacológico , Fumarato de Quetiapina/efectos adversos , Fumarato de Quetiapina/uso terapéutico , Adulto JovenAsunto(s)
Tronco Encefálico/fisiopatología , Cerebelo/fisiopatología , Trastornos de la Motilidad Ocular/fisiopatología , Núcleo Olivar/fisiopatología , Sustancias para Mejorar el Rendimiento/efectos adversos , Temblor/fisiopatología , Adulto , Humanos , Masculino , Trastornos de la Motilidad Ocular/inducido químicamente , Temblor/etiologíaRESUMEN
Extrapyramidal symptoms are an uncommon but well-recognized side effect after the administration of general anesthesia in patients without a significant neurologic history. Several case reports implicate propofol as the likely causative agent producing these symptoms, which include ballismus, dystonia, choreoathetosis, and opisthotonus. Currently, there is no clear consensus on first-line treatment of these symptoms. In each of the published cases, anticholinergic medications and benzodiazepines were central to initial management, although the speed and extent of symptom resolution were variable. Here we present a case of a 17-year-old boy with ulcerative colitis who presented with ballismus, torticollis, tongue thrusting, and oculogyric movements after colonoscopy under general anesthesia with propofol. The patient responded promptly to treatment with diphenhydramine. This is the first reported case in which diphenhydramine was successfully used as the primary treatment of severe extrapyramidal symptoms in a pediatric patient after propofol administration.
Asunto(s)
Anestésicos Intravenosos/efectos adversos , Antagonistas Colinérgicos/uso terapéutico , Difenhidramina/uso terapéutico , Propofol/efectos adversos , Adolescente , Colonoscopía , Discinesia Inducida por Medicamentos/tratamiento farmacológico , Discinesia Inducida por Medicamentos/etiología , Humanos , Masculino , Trastornos de la Motilidad Ocular/inducido químicamente , Trastornos de la Motilidad Ocular/tratamiento farmacológico , Tortícolis/inducido químicamente , Tortícolis/tratamiento farmacológicoRESUMEN
Oculogyric crisis (OGC) describes the clinical phenomenon of sustained dystonic, conjugate and typically upward deviation of the eyes lasting from seconds to hours. It was initially observed in patients with postencephalitic parkinsonism, but since then a number of conditions have been associated with OGC. These include drug-induced reactions, hereditary and sporadic movement disorders, and focal brain lesions. Here, we systematically review the literature and discuss the spectrum of disorders associated with OGC in order to aid clinicians place this rare but distinctive clinical sign into the appropriate diagnostic context. We also provide a brief synthesis of putative pathophysiological mechanisms, as well as therapeutic recommendations based on the literature and our own experience.