Ocular Motor (ocular + motor)

Distribution by Scientific Domains

Selected Abstracts

Anomalous development of brain structure and function in spina bifida myelomeningocele

Jenifer Juranek
Abstract Spina bifida myelomeningocele (SBM) is a specific type of neural tube defect whereby the open neural tube at the level of the spinal cord alters brain development during early stages of gestation. Some structural anomalies are virtually unique to individuals with SBM, including a complex pattern of cerebellar dysplasia known as the Chiari II malformation. Other structural anomalies are not necessarily unique to SBM, including altered development of the corpus callosum and posterior fossa. Within SBM, tremendous heterogeneity is reflected in the degree to which brain structures are atypical in qualitative appearance and quantitative measures of morphometry. Hallmark structural features of SBM include overall reductions in posterior fossa and cerebellum size and volume. Studies of the corpus callosum have shown complex patterns of agenesis or hypoplasia along its rostral-caudal axis, with rostrum and splenium regions particularly susceptible to agenesis. Studies of cortical regions have demonstrated complex patterns of thickening, thinning, and gyrification. Diffusion tensor imaging studies have reported compromised integrity of some specific white matter pathways. Given equally complex ocular motor, motor, and cognitive phenotypes consisting of relative strengths and weaknesses that seem to align with altered structural development, studies of SBM provide new insights to our current understanding of brain structure,function associations. © 2010 Wiley-Liss, Inc. Dev Disabil Res Rev 2010;16:23,30. [source]

The contribution of the intrinsic excitability of vestibular nucleus neurons to recovery from vestibular damage

Cynthia L. Darlington
Abstract Damage to the peripheral vestibular system results in a syndrome of ocular motor and postural abnormalities that partially and gradually abate over time in a process known as ,vestibular compensation'. The first, rapid, phase of compensation has been associated with a recovery of spontaneous resting activity in the ipsilateral vestibular nucleus complex (VNC), as a consequence of neuronal and synaptic plasticity. Increasing evidence suggests that normal VNC neurons in labyrinthine-intact animals, as well as ipsilateral VNC neurons following unilateral vestibular deafferentation (UVD), rely to some extent on intrinsic pacemaker activity provided by voltage-dependent conductances for their resting activity. Modification of this intrinsic pacemaker activity may underlie the recovery of resting activity that occurs in ipsilateral VNC neurons following UVD. This review summarizes and critically evaluates the ,intrinsic mechanism hypothesis', identifying discrepancies amongst the current evidence and suggesting experiments that may test it further. [source]

The relation between accommodative facility and general binocular dysfunction

Ángel Garc
Summary This study was designed to evaluate the relation between accommodative facility and accommodative and binocular dysfunctions. We determined whether failure to achieve 8 cycles per minute of binocular accommodative facility or 11 cycles per minute of monocular accommodative facility tends to be associated with these dysfunctions. Forty eight subjects, ages 10,30 years were examined and classified into four groups: 13 subjects with accommodative dysfunctions, 11 patients with binocular dysfunctions, 12 subjects with accommodative and binocular dysfunctions and 12 control subjects with refractive errors but no accommodative or binocular anomalies. Monocular and binocular accommodative facility was conducted using ±2.00 D flip lenses. In general, statistical analysis indicates that subjects with binocular and accommodative (ocular motor) anomalies performed significantly poorer than subjects of normal group on monocular and binocular facility tests. Monocular accommodative facility results showed more information about the dysfunction of the patient compared with the results of the binocular accommodative facility. In general data supported a relation between reduced accommodative facility and a general binocular dysfunction (accommodative or binocular) which demonstrates the importance of the accommodative facility test in diagnosing an accommodative or binocular anomaly. [source]

Ocular motor delayed-response task performance among patients with schizophrenia and their biological relatives

Jennifer E. McDowell
Schizophrenia patients and their relatives have saccadic abnormalities characterized by problems inhibiting a response. The dorsolateral prefrontal cortex and its associated circuitry ostensibly mediate inhibition and support correct delayed response performance. In this context, two components of delayed response task performance are of interest: memory saccade metrics and error saccades made during the delay. To evaluate these variables, an ocular motor delayed response task was presented to 23 schizophrenia patients, 25 of their first-degree biological relatives, and 19 normal subjects. The measure that best differentiated groups was an increased frequency of error saccades generated during the delay by schizophrenia subjects and relatives. Decreased memory saccade gain also characterized patients and relatives. The similar pattern of results demonstrated by the patients with schizophrenia and their relatives suggests that performance on ocular motor delayed response tasks, either alone or in combination with other saccadic variables, may provide useful information about neural substrates associated with a liability for developing schizophrenia. [source]

4345: Confusion and controversies in diagnosis and treatment of myasthenia

Myasthenia gravis is an afferent ocular motor mimic. The disease may appear with any pattern of pupil-sparing, painless ocular misalignment with or without ptosis; accordingly, common mistaken diagnoses included CN3 palsy or internuclear ophthalmoplegia. Variability adds to diagnostic confusion, as patients may be asymptomatic and have a normal exam at certain stages in the disease. Clinical context remains the first diagnostic key, however, lab and electrophysiology are very helpful. Acetylcholine receptor antibodies are present in approximately 50% of ocular MG, but are highly specific. Single fiber EMG is perhaps the most sensitive test, being abnormal in approximately 90% of cases. Treatment is symptom dependent; pyridostigmine is often used as initial therapy and quite effective for ptosis and dysphagia, while additional immunosuppressives are often required for diplopia. We often initiate therapy with low dose every other day prednisone, and have a low threshold to add mycophenolate mofetil. [source]