Cases reported "Movement Disorders"

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1/18. 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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2/18. 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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3/18. Discrepancy between dysmetric centrifugal movements and normometric centripetal movements in psychogenic ataxia.

    A method to unravel an aberrant motor behaviour in psychogenic ataxia is reported. The kinematic features of fast reaching movements in the vertical plane are described in a patient presenting a psychogenic ataxia. The procedure compared centrifugal and centripetal movements. Path ratios were computed for each phase, as well as the ratios of the paths for centrifugal and centripetal directions. Trajectories of centrifugal phases were erratic but centripetal movements were very regular, whereas both centripetal and centrifugal movements were irregular in patients presenting an organic cerebellar syndrome. A similar incongruity between movements in opposite directions is also shown for a second patient exhibiting psychogenic ataxia. Discrepancies between the centrifugal phase and the centripetal phase of multi-joint reaching movements support the diagnosis of a psychogenic movement disorder.
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4/18. 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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5/18. 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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6/18. Dystonic rabbit syndrome from citalopram.

    OBJECTIVE: Two cases are described of dystonic rabbit syndrome induced by citalopram. This syndrome is a movement disorder with a 5-Hz rhythmic vertical motion of the mouth and lips without involvement of the tongue. METHOD: The patients were interviewed and examined, and additional history was taken from the medical records. The Naranjo adverse drug reaction rating scale was applied. Relevant literature was reviewed. RESULTS: Two patients developed dystonic rabbit syndrome soon after starting escitalopram 10 mg/day or citalopram 5 mg/day. Neither patient had any past or current exposure to a dopamine-blocking drug or any history of movement disorder. [Es]citalopram discontinuation led to disappearance of the movement disorder. The Naranjo scale indicates high probability of dystonic rabbit syndrome from citalopram. CONCLUSION: citalopram can rapidly induce dystonic rabbit syndrome. This effect suggests that for some patients citalopram has neuropsychiatric effects similar to those of a dopamine-blocking antipsychotic drug. This might be of concern with patients who cannot communicate well (eg, young children; patients with dementia, developmental disabilities, or aphasia).
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7/18. The adult form of Niemann-Pick disease type C.

    Niemann-Pick disease type C (NPC) is a fatal neurovisceral lipid storage disease of autosomal inheritance resulting from mutations in either the NPC1 (95% of families) or NPC2 gene. The encoded proteins appear to be involved in lysosomal/late endosomal transport of cholesterol, glycolipids and other molecules but their exact function is still unknown. The clinical spectrum of the disease ranges from a neonatal rapidly fatal disorder to an adult-onset chronic neurodegenerative disease. Based upon a comprehensive study of 13 unrelated adult patients diagnosed in france over the past 20 years as well as the analysis of the 55 other cases published since 1969, we have attempted to delineate the major clinical, radiological, biochemical and genotypic characteristics of adult NPC. overall, mean age at onset ( /-SD) of neuropsychiatric symptoms was 25 /- 9.7 years. The diagnosis of NPC was established after a mean delay of 6.2 /- 6.4 years and the mean age at death (calculated from 20 cases) was 38 /- 10.2 years. Major clinical features included cerebellar ataxia (76%), vertical supranuclear ophthalmoplegia (VSO, 75%), dysarthria, (63%), cognitive troubles (61%), movement disorders (58%), splenomegaly (54%), psychiatric disorders (45%) and dysphagia (37%). Less frequent signs were epilepsy and cataplexy. During the course of the disease, clinical features could be subdivided into (i) visceral signs (hepatomegaly or splenomegaly), (ii) cortical signs (psychiatric cognitive disorders and epilepsy); and (iii) deep brain signs (VSO, ataxia, movement disorders, dysarthria, dysphagia, cataplexy) which exhibited different evolution patterns. Asymptomatic and non-evolutive visceral signs were often noticed since early childhood (38.5% of our patients), followed by mild cortical signs in childhood (learning difficulties) and early adulthood (62% of cases among which 38% were psychiatric disorders). Deep brain signs were observed in 96% of patients and were usually responsible for death. In general, there was a good correlation between clinical signs and the localization of brain atrophy on MRI. The 'variant' biochemical phenotype characterized by mild abnormalities of the cellular trafficking of endocytosed cholesterol was over-represented in the adult form of NPC and seemed associated with less frequent splenomegaly in childhood and lesser psychiatric signs. Involvement of the NPC1 gene was shown in 33 families and of the NPC2 gene in one. Improving the knowledge of the disease among psychiatrists and neurologists appears essential since emerging treatments should be more efficient at the visceral or cognitive/psychiatric stages of the disease, before the occurrence of widespread deep brain neurological lesions.
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8/18. Oculomasticatory myorhythmia: a unique movement disorder occurring in Whipple's disease.

    We describe two patients and a previously reported patient who acquired unique pendular vergence oscillations of the eyes and concurrent contractions of the masticatory muscles, i.e., oculomasticatory myorhythmia (OMM). The smooth disjunctive eye movements cycled with a frequency of 0.8 to 1.2 Hz. An analysis of peak velocities (15 to 200 degrees/sec) with respect to peak amplitudes (5 to 25 degrees) revealed dynamics characteristic of normal vergence movements. The pathological alterations resulting in pendular vergence oscillations implicate a separately functioning, physiologically normal vergence system within the brainstem. In addition to paralysis of vertical gaze, each patient also experienced progressive somnolence and intellectual deterioration. An intestinal biopsy in 1 patient established a diagnosis of Whipple's disease, which led to appropriate treatment and amelioration of the OMM. A pathological diagnosis of Whipple's disease of the central nervous system was made in the other 2 patients; results of an intestinal biopsy in one of these patients were normal. No patient had palatal myoclonus, and olivary pseudohypertrophy was not found in two autopsy examinations. Thus, OMM is a distinct movement disorder and has been recognized only in Whipple's disease. We conclude that patients with OMM should be treated presumptively for Whipple's disease of the central nervous system, even if a jejunal biopsy is normal.
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9/18. Presentation of pinealoblastoma with ocular dipping and deafness.

    Ocular dipping and deafness as presenting manifestations in a patient with pinealoblastoma are highly unusual. Presence of a discrete lesion allows us to postulate a mechanism to explain ocular dipping in light of the present understanding of vertical eye movement control. A mechanism for deafness, probably a false localizing sign of raised intracranial pressure, is proposed also.
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10/18. eye movements in patients with absent voluntary horizontal gaze.

    Despite the complete absence of horizontal saccades, two patients with pontine gliomas had horizontal reflex eye movements within a range of /- 20 degrees. The gain (peak eye velocity/peak stimulus velocity) and phase of the vestibulo-ocular reflex were normal, but the optokinetic gain was decreased. The latency, accuracy, and peak velocity of vertical saccades were normal. Apparently the voluntary gaze centers in the pontine reticular formation are not crucial for generating horizontal vestibular or vertical saccadic eye movements.
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