Cases reported "Movement Disorders"

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1/20. Hypotonia, congenital nystagmus, ataxia, and abnormal auditory brainstem responses: a report on the first white patient.

    A white Italian boy, aged 5 years and 8 months, is reported with failure to thrive, hypotonia, truncal ataxia, psychomotor retardation, and congenital horizontal pendular nystagmus with only waves I and II on auditory brainstem responses. Our patient's clinical picture resembles that previously reported in 10 male Oriental patients. He did not manifest spastic diplegia by the age of 2 years, as did the subjects reported in the literature, but knee-jerk hyperreflexia was evident at the most recent clinical reevaluation. Serial brain MRI studies revealed a cystic brain lesion and peritrigonal hyperintensities with no brainstem abnormalities. To date, no other child with a similar syndrome has been described either in europe or in America. The clinical features of this condition are consistent and characteristic. A definitive diagnosis is achieved by demonstrating the absence of all waves following wave I or wave II on auditory brainstem responses as early as 3 months of age. Due to the predominance of males, the occurrence in siblings, the early age at onset, the non-progressive course, and the characteristic auditory brainstem response findings, the syndrome may have a genetic origin and be attributable to a dysgenetic brainstem lesion.
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2/20. Neurotological evaluation of vertical semicircular canal function in inner ear malformation. A case report.

    A 9-year-old boy with inner ear malformation complained of slight deafness and unsteadiness. CT revealed a normal cochlea despite enlargement of the lateral semicircular canals. The vertical semicircular canals developed more or less normally. The caloric test showed complete canal paresis bilaterally; however, a horizontal rotational stimulus elicited a vestibulo-ocular response, which showed only rightward and downward nystagmus, and their maximal slow-phase velocities were low. In addition, the examination of the vertical semicircular canal function using the head-tilted rotation test revealed a more active response, and the maximal slow-phase velocities were higher than those of a standard horizontal rotational test. These results suggest that the function of the vertical semicircular canal was well preserved and that it may have perceived the horizontal acceleration instead of the lateral semicircular canal.
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3/20. Tullio phenomenon with dehiscence of the superior semicircular canal.

    HYPOTHESIS: The goal of the investigation was to determine if vector analysis of nystagmus in a patient with the Tullio phenomenon could determine the source of the nystagmus. BACKGROUND: The Tullio phenomenon consists of the combination of vertigo and abnormal eye and/or head movements provoked by sound. Dehiscence of the superior semicircular canal can be found in certain patients with the Tullio phenomenon. methods: The patient was tested with pure tones ranging from 250 to 3,000 Hz at 95dB HL. The time course of the three-dimensional vector of eye movement, including torsion and vertical and horizontal displacement angles was determined by individual stop-frame analysis of digitized video. RESULTS: Torsion amplitude varied from 1 to 7 degrees; vertical amplitude varied from 1 to 5 degrees; and horizontal amplitude varied less than 1.5 degrees. The maximal response occurred on stimulation of the right ear with a 1,250-Hz 95-dB HL tone. This elicited a reliable counterclockwise torsional and down-beating fast phase nystagmus as seen from the examiner's point of view. Comparison of the nystagmus with known canal vectors identified the right superior semicircular canal as the source of stimulation. High-resolution computed tomography scan of the temporal bone showed a definite right superior canal dehiscence. CONCLUSION: The origin of nystagmus from the Tullio phenomenon can be identified by calculating the three-dimensional vector of the observed nystagmus. We show that vector analysis of the observed eye movement can be used to infer the source of nystagmus in these patients. The development of real-time, three-dimensional vector analysis of nystagmus is desirable.
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ranking = 1.6
keywords = nystagmus
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4/20. Acquired anomalous head posture following loss of vision in one eye.

    BACKGROUND: We studied the anomalous head postures (AHPs) of five monocular viewing patients and investigated the possible causes and the appropriate surgical strategies to correct each condition. methods: Five patients with acquired visual loss in one eye and associated head tilt and/or turn were examined and treated for correcting the head posture according to the etiology of their respective AHPs. RESULTS: Three types of anomalous head position have been detected: head tilt related to cyclotropia, face turn associated with adduction blocked monocular nystagmus, and face turn to centre the visual field. Surgical plans were prepared according to the mechanism of the AHP in question. After surgery, all patients showed a marked reduction of the head tilt, except one who had a recurrence of the face turn 1 week postoperatively. Mean follow-up time was 19 months. Horizontal transposition of the vertical muscles for correcting cyclotropia offered stable normalization of the AHP in three monocular viewing patients with head tilt, and represents a safe, viable and easy alternative to the Harada Ito procedure. Horizontal recession of the medial rectus of the fixing eye minimized the abduction nystagmus and relieved the need to adduct the fixing eye and subsequently rotate the head toward the fixing eye in one patient. recurrence of the AHP occurred in one patient. CONCLUSION: Different mechanisms may account for AHP in monocular viewing patients. Different surgical procedures may be used to correct the anomalous position. Careful patient selection and etiological diagnosis of AHP is required prior to developing a surgical strategy.
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keywords = nystagmus
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5/20. lightning eye movements.

    Physiologic studies were performed on a patient who demonstrated lightning eye movements, palatal myoclonus and myoclonic jerks of the left platysma and sternocleidomastoid muscles. The myoclonus and lightning eye movements were separate phenomena with no defined relationship to each other. Analysis of this ocular dyskinesia identified strictly horizontal saccadic oscillations, 2 to 5 Hz in frequency, with amplitudes varying greatly but often reaching 25 degrees. A brief stationary period between each saccadic oscillation was frequently observed. They were particularly induced by vertical or horizontal ocular pursuit as well as sustained upward or downward ocular deviation. Caloric nystagmus abolished the oscillations but they persisted, irregularly, during optokinetic nystagmus. Thus a faulty visual fixation mechanism is postulated to precipitate lightning eye movements. Constrast studies revealed a mass lesion arising from the right dorsolateral portion of the medulla. These results indicate that lightning eye movements occur with caudal as well as rostral brain-stem lesions. From the clinical findings cerebellar pathway involvement is likely.
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ranking = 0.4
keywords = nystagmus
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6/20. Leaky neural integration observed in square-wave jerks.

    PURPOSE: To clarify the neuronal mechanism for the square-wave jerks (SWJs). methods: A 66-year-old man presented with oscillatory eye movements. He showed horizontal nystagmus in rightward gaze and SWJs during fixation at straight ahead. We recorded his eye movements with search coil methods and quantitatively analyzed them. RESULTS: Visually guided rightward saccades were followed by exponential drifts with average time constants of 0.3-1.0 second, indicating a leaky rightward velocity-to-position integrator. Amplitude of SWJs ranged from 0.5 to 2.5 degrees and average intersaccadic interval was 0.2 seconds. In addition, exponential drifts similar to those observed after visually guided saccades were observed in the SWJs. Rightward fast eye movements of SWJs were followed by exponential drifts lasting for 0.2 seconds with average time constant ( /-SD) of 0.7 /-0.3 seconds. CONCLUSIONS: Position signals after visually guided saccades and SWJs were outputs of the identical velocity-to-position integrator. SWJs are generated by the neural circuits involving a pulse generator and a velocity-to-position integrator.
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ranking = 0.2
keywords = nystagmus
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7/20. Neuroepithelial cysts presenting with movement disorders: two cases.

    BACKGROUND: The authors present two cases of movement disorders caused by neuroepithelial cysts and highlight their management. Neuroepithelial cysts are ependymal or epithelial lined fluid collections of unknown etiology within the central nervous system parenchyma with no obvious ventricular or subarachnoid connection. Most cysts are asymptomatic, however, some present with seizures, mass effect, or rarely with movement disorders. case reports: The first patient, a 27-year-old female, presented with progressive weakness, dystonic posturing, tremor, ballismus and choreoathetotic movements of her right upper extremity. Her symptoms improved after stereotactic drainage of a neuroepithelial cyst in her basal ganglia but recurred within a year. The second case, a 56-year-old female, presented with diplopia, nystagmus, gait imbalance and hemiparesis. Her symptoms improved after stereotactic drainage of a midbrain neuroepithelial cyst. The cyst reaccumulated over the next few years and she became symptomatic with left arm tremor and facial weakness. Aspiration was again performed with symptomatic improvement for nine months. Her tremor recurred and a cyst access device was placed stereotactically. She improved and has remained stable for over a year. CONCLUSION: Simple stereotactic drainage of neuroepithelial cysts has a high recurrence rate. The authors recommend considering placement of a drainage device to facilitate aspiration of the cyst fluid during follow-up, if needed.
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ranking = 0.2
keywords = nystagmus
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8/20. Gaze-evoked involuntary movements.

    Voluntary gaze may evoke a number of neurological phenomena such as vertigo, tinnitus, blepharoclonus, eyelid nystagmus, "facial nystagmus," involuntary laughter, and seizures. We report two patients in whom eccentric gaze evoked facial twitching and arm movement. Electroencephalograms remained unchanged during these movements. The pathogenesis of these movements is unclear but may involve ephaptic transmission.
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ranking = 0.4
keywords = nystagmus
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9/20. Lateropulsion and upbeat nystagmus are manifestations of central vestibular dysfunction.

    An elderly man presented with acute onset of gait instability, characterized by leaning to the left while walking, vertigo, diplopia, and transient facial numbness. The examination was remarkable for ocular lateropulsion and primary position upbeat nystagmus. Computed tomography of the brain revealed a right-hemispheric cerebellar infarction. This report illustrates that lateropulsion can occur in cerebellar lesions, but that it may be contralateral to the cerebellar hemisphere involved. Primary position upbeat nystagmus and lateropulsion may represent forms of central vestibular dysfunction due to interruption of vestibulo-ocular pathways.
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ranking = 1.2
keywords = nystagmus
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10/20. Medical treatment of nystagmus and ocular motor disorders.

    An increased compendium of drugs useful in ocular motor system dysfunction has expanded our capacity to treat selected ocular motility disorders. Adjunctive therapeutic modes (e.g., Fresnel prisms and orthoptic exercises) can also be beneficial. PAN and see-saw nystagmus can be treated with baclofen. Downbeat nystagmus may respond to clonazepam therapy, and prisms may help if the nystagmus can be modified with convergence. Congenital nystagmus may respond minimally to drugs (e.g., baclofen), but prisms or surgical procedures, or both, are still the primary treatment modalities. Innovar may be helpful in patients with severe, incapacitating vestibular disorders, and scopolamine alone or in combination with promethazine may be beneficial in patients with milder ambulatory acute peripheral vestibular disorders. Benign positional vertigo is best treated initially with positional exercises before drug therapy is instituted. Opsoclonus and ocular flutter have been treated successfully with corticosteroids, propranolol, and clonazepam, while microflutter, an extremely rare disorder, can resolve with baclofen. Although therapy with carbamazepine, 5-hydroxtryptophan, and scopolamine has been useful in selected patients with ocular palatal myoclonus, most do not respond to drug treatment. It is not usually necessary to treat voluntary nystagmus, but Fresnel prism lenses should be remembered in refractory patients. Potentially reversible and pseudointernuclear ophthalmoplegias also were discussed. Orthoptic exercises can be beneficial in posttraumatic internuclear ophthalmoplegia. Selected supranuclear palsies can be improved completely with the proper drug regimen. Lastly, superior oblique myokymia can be treated successfully with carbamazepine, with tight surveillance for possible adverse side effects. Descriptive phenomenology and pathophysiological localization must be correlated with brain stem neurochemistry and neuropharmacology to medically treat additional ocular motor system disorders.
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ranking = 1.8
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