13 results on '"Ocular Motility Disorders drug therapy"'
Search Results
2. Oculomotor effects of medical and surgical treatments of Parkinson's disease.
- Author
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Patel S, Fitzgerald JJ, and Antoniades CA
- Subjects
- Humans, Models, Neurological, Neuronavigation, Antiparkinson Agents pharmacology, Basal Ganglia drug effects, Basal Ganglia physiopathology, Basal Ganglia surgery, Deep Brain Stimulation, Ocular Motility Disorders drug therapy, Ocular Motility Disorders etiology, Ocular Motility Disorders physiopathology, Ocular Motility Disorders surgery, Parkinson Disease complications, Parkinson Disease drug therapy, Parkinson Disease physiopathology, Parkinson Disease surgery, Saccades drug effects, Saccades physiology
- Abstract
Oculomotor abnormalities are fast becoming a proxy for disease diagnosis and progression. Saccades-ballistic eye movements-are known to be affected by dopaminergic cell loss in the basal ganglia, caused by Parkinson's disease. Pharmaceutical and neurosurgical interventions such as deep brain stimulation and functional neurosurgery have both been noted to have an effect on saccades. Comparing and contrasting these effects may yield insights into Parkinson's disease pathophysiology, and the mechanisms of pharmacological and neurosurgical treatments. Computational models of saccadic control, such as the LATER model, can help to interpret the distribution of saccadic latencies, providing a framework for objectively comparing the effects of pharmaceutical interventions and deep brain stimulation., (© 2019 Elsevier B.V. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
3. Granulomatosis with polyangiitis provoked by trauma.
- Author
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Carter S, Ramjiani V, Dunkley L, and Salvi S
- Subjects
- Adult, Biomarkers metabolism, Cyclophosphamide therapeutic use, Drug Therapy, Combination, Glucocorticoids therapeutic use, Granulomatosis with Polyangiitis diagnostic imaging, Granulomatosis with Polyangiitis drug therapy, Humans, Immunologic Factors therapeutic use, Immunosuppressive Agents therapeutic use, Male, Methylprednisolone therapeutic use, Ocular Motility Disorders diagnostic imaging, Ocular Motility Disorders drug therapy, Orbital Fractures diagnostic imaging, Orbital Fractures drug therapy, Rituximab therapeutic use, Tomography, X-Ray Computed, Eye Injuries etiology, Granulomatosis with Polyangiitis etiology, Ocular Motility Disorders etiology, Oculomotor Muscles pathology, Orbital Fractures etiology
- Published
- 2016
- Full Text
- View/download PDF
4. Bilateral septic cavernous sinus thrombosis, congestive orbitopathy, and ischemic optic neuropathy.
- Author
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Shams PN, Policeni B, Carter KD, Shriver E, and Thurtell MJ
- Subjects
- Aged, Anti-Infective Agents therapeutic use, Anticoagulants therapeutic use, Bacteremia diagnosis, Bacteremia drug therapy, Cavernous Sinus Thrombosis diagnosis, Cavernous Sinus Thrombosis drug therapy, Drug Therapy, Combination, Eye Infections, Bacterial diagnosis, Eye Infections, Bacterial drug therapy, Female, Glucocorticoids therapeutic use, Heparin, Low-Molecular-Weight therapeutic use, Humans, Magnetic Resonance Imaging, Methylprednisolone therapeutic use, Metronidazole therapeutic use, Ocular Motility Disorders diagnosis, Ocular Motility Disorders drug therapy, Optic Neuropathy, Ischemic diagnosis, Optic Neuropathy, Ischemic drug therapy, Streptococcal Infections diagnosis, Streptococcal Infections drug therapy, Tomography, X-Ray Computed, Bacteremia microbiology, Cavernous Sinus Thrombosis microbiology, Eye Infections, Bacterial microbiology, Ocular Motility Disorders microbiology, Optic Neuropathy, Ischemic microbiology, Streptococcal Infections microbiology, Streptococcus anginosus isolation & purification
- Published
- 2016
- Full Text
- View/download PDF
5. Neurocysticercosis presenting as a vertical one-and-a-half syndrome with associated contralesional horizontal gaze paresis.
- Author
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Mesraoua B, Deleu D, D'souza A, Imam YZ, and Melikyan G
- Subjects
- Abducens Nerve Diseases diagnosis, Adult, Albendazole therapeutic use, Anthelmintics therapeutic use, Blepharoptosis etiology, Dexamethasone therapeutic use, Diagnosis, Differential, Diplopia drug therapy, Drug Therapy, Combination, Headache etiology, Humans, Male, Mesencephalon parasitology, Mesencephalon physiopathology, Neurocysticercosis diagnosis, Neurocysticercosis drug therapy, Neurocysticercosis physiopathology, Nystagmus, Pathologic drug therapy, Ocular Motility Disorders drug therapy, Oculomotor Nerve Diseases diagnosis, Oculomotor Nerve Diseases drug therapy, Oculomotor Nerve Diseases parasitology, Reflex, Abnormal, Thalamus parasitology, Thalamus physiopathology, Diplopia etiology, Neurocysticercosis complications, Nystagmus, Pathologic etiology, Ocular Motility Disorders etiology, Oculomotor Nerve Diseases etiology
- Abstract
We describe a patient presenting with vertical one-and-a-half syndrome and concomitant contralesional horizontal gaze paresis as the result of a solitary neurocysticercosis (NCC) lesion in the right midbrain extending into the thalamomesencephalic junction. The patient received an albendazole-dexamethasone course which resulted in resolution of his symptoms. The neuro-ophthalmological complications of NCC are reviewed and the clinical topography of the neuro-ophthalmological findings of this unusual observation are discussed., (Copyright © 2012 Elsevier B.V. All rights reserved.)
- Published
- 2012
- Full Text
- View/download PDF
6. Paroxysmal alternating nystagmus.
- Author
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Lee SJ, Sohn SY, Kim JS, and Moon SY
- Subjects
- Humans, Male, Nystagmus, Pathologic diagnosis, Nystagmus, Pathologic drug therapy, Ocular Motility Disorders diagnosis, Ocular Motility Disorders drug therapy, Vertigo diagnosis, Vertigo drug therapy, Vestibular Diseases complications, Young Adult, Nystagmus, Pathologic physiopathology, Ocular Motility Disorders physiopathology, Vertigo physiopathology, Vestibular Diseases physiopathology
- Abstract
Paroxysmal reversal of spontaneous nystagmus has rarely been described. Herein, we report recurrent bouts of vertigo and oscillopsia in association with reversed spontaneous nystagmus in a patient with prior surgical resection of the cerebellar vermis due to medulloblastoma and subsequent labyrinthine damage. The symptoms almost completely resolved with carbamazepine. The episodes may be ascribed to paroxysmal reversal of the vestibular asymmetry due to intermittent decompensation by the deficient cerebellum., (Copyright © 2012 Elsevier B.V. All rights reserved.)
- Published
- 2012
- Full Text
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7. Ophthalmic manifestations of central nervous system tuberculosis--two case reports.
- Author
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Lolly P, Rachita S, and Satyasundar M
- Subjects
- Adolescent, Child, Female, Humans, Magnetic Resonance Imaging, Male, Tomography, X-Ray Computed, Treatment Outcome, Tuberculoma, Intracranial complications, Tuberculoma, Intracranial diagnosis, Tuberculoma, Intracranial drug therapy, Tuberculoma, Intracranial pathology, Tuberculoma, Intracranial physiopathology, Antitubercular Agents therapeutic use, Brain Stem pathology, Eye Movement Measurements, Ocular Motility Disorders drug therapy, Ocular Motility Disorders etiology, Ocular Motility Disorders physiopathology, Temporal Lobe pathology, Visual Acuity drug effects
- Abstract
In this report, we present two unusual ocular manifestations due to CNS tuberculosis. One of the cases is a 7 years' old boy with brain stem tuberculoma who presented with horizontal gaze palsy. The other is a 14 years' old girl with temporal lobe tuberculoma who presented with unilateral sixth nerve paresis and papilledema. Both responded well to treatment with antitubercular drugs. It highlights the importance of gaze palsy as a rare manifestation of CNS tuberculosis.
- Published
- 2011
8. Sensorimotor transformation deficits for smooth pursuit in first-episode affective psychoses and schizophrenia.
- Author
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Lencer R, Reilly JL, Harris MS, Sprenger A, Keshavan MS, and Sweeney JA
- Subjects
- Adolescent, Adult, Affective Disorders, Psychotic drug therapy, Antipsychotic Agents pharmacology, Antipsychotic Agents therapeutic use, Case-Control Studies, Female, Follow-Up Studies, Humans, Male, Motion Perception physiology, Neuropsychological Tests, Ocular Motility Disorders drug therapy, Photic Stimulation methods, Psychiatric Status Rating Scales, Psychomotor Performance drug effects, Pursuit, Smooth drug effects, Reaction Time, Schizophrenia drug therapy, Visual Fields, Young Adult, Affective Disorders, Psychotic complications, Ocular Motility Disorders etiology, Psychomotor Performance physiology, Pursuit, Smooth physiology, Schizophrenia complications
- Abstract
Background: Smooth pursuit deficits are an intermediate phenotype for schizophrenia that may result from disturbances in visual motion perception, sensorimotor transformation, predictive mechanisms, or alterations in basic oculomotor control. Which of these components are the primary causes of smooth pursuit impairments and whether they are impaired similarly across psychotic disorders remain to be established., Methods: First-episode psychotic patients with bipolar disorder (n = 34), unipolar depression (n = 24), or schizophrenia (n = 77) and matched healthy participants (n = 130) performed three smooth pursuit tasks designed to evaluate different components of pursuit tracking., Results: On ramp tasks, maintenance pursuit velocity was reduced in all three patients groups with psychotic bipolar patients exhibiting the most severe impairments. Open loop pursuit velocity was reduced in psychotic bipolar and schizophrenia patients. Motion perception during pursuit initiation, as indicated by the accuracy of saccades to moving targets, was not impaired in any patient group. Analyses in 138 participants followed for 6 weeks, during which patients were treated and psychotic symptom severity decreased, and no significant change in performance in any group was revealed., Conclusions: Sensorimotor transformation deficits in all patient groups suggest a common alteration in frontostriatal networks that dynamically regulate gain control of pursuit responses using sensory input and feedback about performance. Predictive mechanisms appear to be sufficiently intact to compensate for this deficit across psychotic disorders. The absence of significant changes after acute treatment and symptom reduction suggests that these deficits appear to be stable over time., (Copyright 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)
- Published
- 2010
- Full Text
- View/download PDF
9. Opsoclonus-myoclonus-ataxia syndrome with autoantibodies to glutamic acid decarboxylase.
- Author
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Markakis I, Alexiou E, Xifaras M, Gekas G, and Rombos A
- Subjects
- Adult, Anti-Inflammatory Agents therapeutic use, Anticonvulsants therapeutic use, Autoantibodies blood, Autoantibodies cerebrospinal fluid, Female, Gait Ataxia drug therapy, Humans, Methylprednisolone therapeutic use, Myoclonus drug therapy, Ocular Motility Disorders drug therapy, Radioimmunoassay, Syndrome, Valproic Acid therapeutic use, Autoantibodies analysis, Autoimmune Diseases complications, Autoimmune Diseases immunology, Gait Ataxia etiology, Gait Ataxia immunology, Glutamate Decarboxylase immunology, Myoclonus etiology, Myoclonus immunology, Ocular Motility Disorders etiology, Ocular Motility Disorders immunology
- Abstract
Opsoclonus-myoclonus-ataxia syndrome (OMS) is a rare neurological disorder of probably autoimmune origin. Most cases are associated with a remote neoplasm or a viral infection; however in some instances no underlying aetiology can be demonstrated. We report the presence of anti-glutamic acid decarboxylase antibodies (anti-GAD Abs) in the serum and CSF of a patient with idiopathic OMS. Treatment with intravenous immunoglobulin led to a remarkable clinical improvement with parallel reduction of anti-GAD titers. Anti-GAD Abs have been associated with several neurological syndromes. They could also be responsible for the clinical triad of OMS, by impairing GABAergic transmission in specific brainstem and cerebellar circuits. We propose that testing for anti-GAD Abs should be performed in OMS, especially when no other aetiological association can be demonstrated.
- Published
- 2008
- Full Text
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10. Aminopyridines for the treatment of cerebellar and ocular motor disorders.
- Author
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Strupp M, Kalla R, Glasauer S, Wagner J, Hüfner K, Jahn K, and Brandt T
- Subjects
- Animals, Ataxia complications, Ataxia drug therapy, Cerebellar Diseases complications, Eye Movements physiology, Humans, Nystagmus, Pathologic etiology, Ocular Motility Disorders etiology, Aminopyridines therapeutic use, Cerebellar Diseases drug therapy, Nystagmus, Pathologic drug therapy, Ocular Motility Disorders drug therapy, Potassium Channel Blockers therapeutic use
- Abstract
Downbeat nystagmus (DBN) is the most frequent form of acquired persisting fixation nystagmus. It is hypothesized to occur when physiological inhibitory cerebellar input, namely of the flocculus, to the vestibular nuclei is inhibited. The second most frequent form of acquired nystagmus is upbeat nystagmus (UBN). UBN is probably caused by an imbalance of vertical vestibulo-ocular reflex tone. GABA-ergic substances like baclofen have been used to treat DBN and UBN, but they have had only moderate success. Animal experiments have shown that aminopyridines [3,4-diaminopyridine (3,4-DAP) and 4-aminopyridine (4-AP)], nonselective blockers of the Kv family of voltage-gated potassium channels, increase Purkinje-cell (PC) excitability. It was assumed that such enhancement of PC activity could restore to normal levels the inhibitory influence of the cerebellar cortex on vertical eye movements. On the basis of these assumptions, we evaluated the efficacy and underlying mechanisms of aminopyridines in DBN and UBN as well as in another cerebellar disorder with an impaired PC function: episodic ataxia type 2 (EA2), which is caused by mutations of the PQ-calcium channel. In a placebo-controlled trial on 17 patients we demonstrated that 3,4-DAP significantly reduces the intensity of DBN. This was confirmed in a recent study with 4-AP, which also showed that 4-AP restores gaze-holding ability independently of fixation in DBN. The efficacy of 4-AP in UBN was demonstrated in single patients. Finally, in an open trial on three patients with EA2 we showed that 4-AP prevents attacks of ataxia. This was also found in an animal model (the tottering mouse) of EA2. The clinical efficacy of 4-AP in EA2 is being further evaluated in an ongoing randomized controlled crossover trial. In conclusion, the use of aminopyridines in DBN, UBN, and EA2 is a new treatment principle for vestibular, cerebellar, and ocular motor disorders.
- Published
- 2008
- Full Text
- View/download PDF
11. Medial longitudinal fascicles.
- Author
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Manfredi M, Bozzao L, and Inghiller M
- Subjects
- Adult, Glucocorticoids therapeutic use, Humans, Male, Methylprednisolone therapeutic use, Ocular Motility Disorders diagnosis, Ocular Motility Disorders drug therapy, Treatment Outcome, Ocular Motility Disorders physiopathology
- Published
- 2003
- Full Text
- View/download PDF
12. Botulinum A exotoxin in clinical ophthalmology.
- Author
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Carruthers JD and Carruthers A
- Subjects
- Animals, Combined Modality Therapy, Drug Evaluation, Electromyography, Facial Muscles drug effects, Facial Muscles innervation, Facial Muscles physiopathology, Humans, Muscle Denervation methods, Ocular Motility Disorders physiopathology, Oculomotor Muscles drug effects, Oculomotor Muscles innervation, Oculomotor Muscles physiopathology, Botulinum Toxins, Type A therapeutic use, Neuromuscular Agents therapeutic use, Ocular Motility Disorders drug therapy
- Published
- 1996
13. Ocular jellyfish stings.
- Author
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Glasser DB, Noell MJ, Burnett JW, Kathuria SS, and Rodrigues MM
- Subjects
- Adult, Animals, Bites and Stings drug therapy, Cnidarian Venoms adverse effects, Corneal Injuries, Eye Injuries drug therapy, Female, Glucocorticoids therapeutic use, Humans, Intraocular Pressure, Iritis drug therapy, Iritis etiology, Male, Middle Aged, Mydriasis drug therapy, Mydriasis etiology, Mydriatics therapeutic use, Ocular Hypertension drug therapy, Ocular Hypertension etiology, Ocular Motility Disorders drug therapy, Ocular Motility Disorders etiology, Visual Acuity, Bites and Stings complications, Eye Injuries etiology, Scyphozoa
- Abstract
Background: Corneal stings from the sea nettle (Chrysaora quinquecirrha) indigenous to the Chesapeake Bay are usually painful but self-limited injuries, with resolution in 24 to 48 hours., Methods: Five patients who developed unusually severe and prolonged iritis and intraocular pressure elevation after receiving corneal sea nettle stings were followed for 2 to 4 years., Results: Decreased visual acuity, iritis, and increased intraocular pressure (32 to 48 mmHg) were noted in all cases. Iritis responded to topical corticosteroids and resolved within 8 weeks. Elevated intraocular pressure responded to topical beta blockers and oral carbonic anhydrase inhibitors. Mydriasis (4 of 5 cases), decreased accommodation (2 of 5 cases), peripheral anterior synechiae (2 of 5 cases), and iris transillumination defects (3 of 5 cases) also were noted. Mydriasis and decreased accommodation persisted for 5 months in 1 case and for more than 2 years in another. One patient has chronic unilateral glaucoma. Visual acuity returned to normal in all cases., Conclusions: The precise relationship between sea nettle venom and the observed clinical responses is not known. Corneal jellyfish stings usually produce a brief and self-limited reaction, but they do have the potential for long-term sequelae.
- Published
- 1992
- Full Text
- View/download PDF
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