Cases reported "Movement Disorders"

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11/18. Nonhaemorrhagic thalamic infarction. Clinical, neuropsychological and electrophysiological findings in four anatomical groups defined by computerized tomography.

    Twenty-five patients with nonhaemorrhagic infarcts of the thalamus were studied clinically and by neuropsychological testing, computerized tomography and somatosensory evoked response (SER) recordings. Our aim was to determine whether the findings in these different tests would form distinct symptom clusters associated with different anatomical territories of the thalamus. infarction conforming to the tuberothalamic arterial territory caused a facial paresis for emotional movements, severe neuropsychological deficits and a delay of the SER after P14. infarction conforming to the interpeduncular profundus arterial territory caused a supranuclear vertical gaze paresis, severe neuropsychological deficits and a delay in the P60 component of the SER. infarction conforming to the anterior choroidal territory caused a hemiparesis, moderate neuropsychological deficits and varied sensory evoked responses. patients with infarctions conforming to the entire geniculothalamic territory had sensory loss in multiple modalities, minimal neuropsychological deficits and absence of sensory evoked responses after P14. A lacune in this territory caused pure hemisensory loss involving part of the body for the modalities of pain and light touch but not proprioception or vibration. Neuropsychological deficits were uncommon and N32 and N60 were delayed in the SER.
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12/18. Involuntary motor phenomena in the locked-in syndrome.

    Several involuntary movements were observed in patients who were totally immobile except for vertical gaze due to bilateral pyramidal transverse lesion at the pontine or midbrain level. In those conscious locked-in patients extensor spasms and flexor spasms could be elicited by nonspecific stimulation. Mimic pain reactions, pathological crying, and primordial screaming ("cat crying') were also noted. Other motor patterns were whining, moaning, groaning, sighing, and yawning. The pathophysiological implications of these observations are discussed.
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13/18. Periodic alternating skew deviation.

    A 78-year-old hypertensive woman suddenly developed blurred vision, followed shortly by dizziness, difficulty walking with a tendency to veer to the left, and vertical diplopia. Examination 3 weeks later revealed a unique neuro-ophthalmologic motility pattern, which may be described as periodic alternating skew deviation. This previously unreported motility disturbance was associated with downbeat nystagmus in our patient, and a focal lesion at the level of the interstitial nucleus of Cajal was demonstrated on computed tomography. The spectrum of physiologically related motility patterns--including periodic alternating nystagmus, cyclic oculomotor paralysis, see-saw nystagmus, periodic alternating gaze deviation, "ping-pong" gaze, and intermittent aperiodic alternating skew deviation--has been considered and is helpful in topical neuro-ophthalmologic diagnosis.
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14/18. Inverse ocular bobbing.

    A new form of abnormal spontaneous eye movement termed inverse ocular bobbing is described. It consists of a slow downward eye movement followed by delayed quick return upward to midposition. It is contrasted with other types of abnormal vertical eye movements.
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15/18. The syndrome of 'pure akinesia' and its relationship to progressive supranuclear palsy.

    Five patients developed a stereotyped syndrome of progressive akinesia of gait, speech, and hand-writing without rigidity, tremor, or dementia. The symptoms did not improve with levodopa. These clinical findings conform to a syndrome described repeatedly in japan since 1974 as "pure akinesia." Evidence has indicated that pure akinesia often represents a pre-ocular motor, and in some cases an ocular motor-sparing, form of progressive supranuclear palsy (PSP). Although we found disorders of eyelid movements, none of the patients demonstrated a gaze palsy on clinical examination. Four patients underwent eye movement recordings. The two patients with the longest disease duration had slow or small vertical saccades. These findings support the notion that patients with pure akinesia may develop a vertical gaze palsy, similar to that in PSP, late in their course. Our patients show that pure akinesia occurs in north america as well as in japan. Recognition of the syndrome of pure akinesia may suggest the diagnosis of PSP before the development of abnormalities of ocular movement.
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16/18. Cortical cerebellar degeneration associated with a specific disorder of standing and locomotion.

    The three patients presented showed a rhythmic bobbing of the body when standing with flexed legs. It was produced by slow, coarse, synchronous extensions-flexions in the legs. Platform and accelerometer records demonstrated an almost clockwork regularity of rate in the 2.5--3.5 c/sec range. In Romberg's test there occurred slow rhythmic extensions-flexions of the feet. The patients walked with a peculiar stiff "heel-gait", which was not conspicously broad-based, unsteady or trembling. On ascending a platform they displayed a slow leg tremor and a marked disorder of forward-vertical movement. This very uniform motor syndrome retained its specific features over the years. An upper limb involvement was observed in one of the patients. Post-mortem examination in one patient, a chronic alcoholic, showed a pronounced atrophy of the superior cerebellar vermis. Tomographic pneumoencephabgrams demonstrated the superior vermis atrophy in the two other patients.
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17/18. The ocular tilt reaction. A paroxysmal dyskinesia associated with elliptical nystagmus.

    The ocular tilt reaction, a synkinesis of ocular torsion, skew deviation, and head tilting, was a paroxysmal disorder in a patient with multiple sclerosis. In this distinctive pattern of eye and head motion, the 12 o'clock corneal meridians of both eyes are rotated conjugately in the direction of the lower skewed eye and the head is inclined laterally in the same direction. Paroxysmal activation of brain stem otolithic vestibular projections is proposed responsible for the dyskinesia. Coincident attacks of vertical and horizontal low amplitude pendular oscillation of the eyes produced elliptical nystagmus. This ocular motor disorder was treated effectively with carbamazepine.
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18/18. Bobble-head doll syndrome associated with subduroperitoneal shunt malfunction.

    Bobble-head doll syndrome is known to be associated with aqueductal stenosis or cystic lesions of the III ventricle. The direction of movement is usually vertical. In the literature, only five cases of purely horizontal movement have been reported. Bobble-head doll syndrome manifested as a sign of shunt malfunction has been described in one case with a ventriculoperitoneal shunt. The authors report on a 10-year-old boy who showed subduroperitoneal shunt malfunction associated with horizontal bobble-head doll syndrome. The head bobbing disappeared immediately after shunt revision. Unlike the previously reported cases, in the present case the lesion was asymmetric, though the significance of this for the lateral movement is not clear. This case also showed more marked ventricular dilatation on subduroperitoneal shunt malfunction than in the pre-shunt state. The underlying mechanism of the ventricular dilatation is unknown.
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