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Disorders of gaze-holding-organized by a neural network located in the brainstem or the cerebellum-may lead to nystagmus. Based on previous animal studies it was concluded that one key player of the cerebellar part of this gaze-holding neural network is the flocculus. Up to now, in humans there are no systematic studies in patients with cerebellar lesions examining one of the most common forms of nystagmus: gaze-evoked nystagmus (GEN). The aim of our present study was to clarify which cerebellar structures are involved in the generation of GEN.
Twenty-one patients with acute unilateral cerebellar stroke were analyzed by means of modern MRI-based voxel-wise lesion-behavior mapping.
Our data indicate that cerebellar structures such as the vermal pyramid, the uvula, and the tonsil, but also parts of the biventer lobule and the inferior semilunar lobule, were affected in horizontal GEN.
It seems that these structures are part of a gaze-holding neural integrator control system. Furthermore, GEN might present a diagnostic sign pointing toward ipsilesionally located lesions of midline and lower cerebellar structures.
Department of Neurology, University of Mainz, Langenbeckstr. 1, 55131 Mainz, Germany firstname.lastname@example.org.
This article was published in the following journal.
Cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS) is a newly described condition with onset in adulthood, characterized by progressive balance impairment and sensory disturbance...
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Pharmacological treatment of cerebellar ataxias and cerebellar nystagmus still remains difficult. The efficacy of most of the agents recommended in the past for symptomatic or even causative therapy c...
We report here a case with unidirectional abnormalities of smooth eye movements without gaze nystagmus. Abnormalities of eye movements were confined to unidirectional (leftward) horizontal pursuit and...
Involuntary oscillations of the eyes (nystagmus) impairs vision so that affected patients, who have neurological disorders such as Multiple Sclerosis (MS) , cannot read or watch TV. Two me...
The purpose of this study is to investigate the long-term safety, tolerability and efficacy of neramexane mesylate in the treatment of congenital idiopathic nystagmus (CIN). In addition, a...
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Cerebellar degeneration associated with a remote neoplasm. Clinical manifestations include progressive limb and GAIT ATAXIA; DYSARTHRIA; and NYSTAGMUS, PATHOLOGIC. The histologic type of the associated neoplasm is usually carcinoma or lymphoma. Pathologically the cerebellar cortex and subcortical nuclei demonstrate diffuse degenerative changes. Anti-Purkinje cell antibodies (anti-Yo) are found in the serum of approximately 50% of affected individuals. (Adams et al., Principles of Neurology, 6th ed, p686)
The recorded electrical responses from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported. Often used synonymously to event-related potentials which are associated with higher level cognitive processes.
Involuntary rhythmical movements of the eyes in the normal person. These can be naturally occurring as in end-position (end-point, end-stage, or deviational) nystagmus or induced by the optokinetic drum (NYSTAGMUS, OPTOKINETIC), caloric test, or a rotating chair.
The electric response evoked in the CEREBRAL CORTEX by stimulation along AFFERENT PATHWAYS from PERIPHERAL NERVES to CEREBRUM.
Elicitation of a rotatory nystagmus by stimulating the semicircular canals with water or air which is above or below body temperature. In warm caloric stimulation a rotatory nystagmus is developed toward the side of the stimulated ear; in cold, away from the stimulated side. Absence of nystagmus indicates the labyrinth is not functioning.
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