The partial adduction defect may be made clinically more apparent by performing horizontal saccades. Ipsilesional adduction deficit (partial or complete) The INO can be unilateral or bilateral and may present with or without (neurologically isolated) other brainstem findings.īinocular INO Copyright: American Academy of Ophthalmology Vertical gaze nystagmus may be noted on upgaze. A skew deviation with the ipsilateral hypertropic eye may be noted. There is a slow adducting saccadic velocity in the affected side. The INO is characterized clinically by an ipsilesional adduction deficit (partial or complete) with a contralateral, dissociated, horizontal abducting saccade/nystagmus on attempted gaze to the contralesional side. The patients may complain of headaches and vertigo.Ī good ocular examination is often all that is required to diagnose INO. The difficulty in looking at the sides may lead to difficulties during driving or walking and may increase the risk of road traffic accidents or falls. Interruption of binocular vision resulting from defective conjugate horizontal movements of eyes may cause reading fatigue, visual confusion, loss of stereopsis, oscillopsia, and diplopia. Vertical oblique diplopia related to associated skew deviation may also be another symptom. The patient may also complain of headaches or other deficits due to the involvement of the brainstem. The diplopia becomes more prominent on looking at objects on the opposite side of the lesion and diplopia is usually not seen in the primary gaze. Horizontal diplopia is caused by the limitation of adduction in the ipsilateral eye. Symptoms range from, horizontal diplopia, difficulty in tracking high-speed objects, or dizziness on lateral gaze.
INO pathway Copyright: American Academy of Ophthalmology Clinical features Symptoms The MLF is also involved in multiple other functions including oculovestibular reflex, vertical pursuit, optokinetic nystagmus, and coordinates the conjugate ocular movements in response to movement of the head and neck. The side of the INO is named by the side of the adduction deficit, which is ipsilateral to the MLF lesion. The activation of the contralateral medial rectus and ipsilateral lateral rectus muscle produces horizontal conjugate eye movement. The signal for contraction of the contralateral medial rectus (for adduction of the contralateral eye) is sent from the CN VI to the contralateral medial rectus subnucleus of CN III via the internuclear pathway called MLF. Some axons from the CN VI innervate the ipsilateral lateral rectus resulting in the abduction of the ipsilateral eye. The frontal eye field controls contralateral saccades and the parietal lobe controls ipsilateral pursuits. Typically, the PPRF receives information from the higher cortical centers such as the frontal eye fields, occipital and parietal lobes, and the superior colliculus. Damage to the PPRF results in impaired horizontal saccade in the same direction. The PPRF or paraabducens nucleus is the key structure in conjugate horizontal gaze and horizontal saccades. CN VI is the final common pathway for lateral horizontal gaze. As both MLFs are close to each other and near to midline, bilateral INO is not rare.įoveation and binocular single vision of the mobile and immobile objects require coordination between the cranial nerves (II, III, IV, and VI), their interneurons, and various supranuclear influences. The MLF is located at the dorsomedial brainstem tegmentum (midbrain and pons) ventral to the aqueduct or the fourth ventricle. Thus, demyelinating lesions in the midbrain or pons often produce a unilateral or bilateral INO in young patients. The MLF is a heavily myelinated nerve tract connecting the oculomotor nucleus (CN III) of the ipsilateral side with the paramedian pontine reticular formation (PPRF) and CN VI of the contralateral pons. The MLF is supplied by branches of the basilar artery and ischemia in the vertebrobasilar system can produce an ischemic INO. The MLF can be damaged by any lesion (e.g., demyelinating, ischemic, neoplastic, inflammatory) in the pons or midbrain. This interneuron is called the medial longitudinal fasciculus (MLF). Internuclear ophthalmoplegia or ophthalmoparesis (INO) is an ocular movement disorder that presents as an inability to perform conjugate lateral gaze and ophthalmoplegia due to damage to the interneuron between two nuclei of cranial nerves (CN) VI and CN III (internuclear).
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