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Internuclear ophthalmoplegia and its components

INO is due to a lesion along the horizontal gaze pathway. This  is one of the most localizing brainstem syndromes, resulting from a lesion in the medial longitudinal fasciculus (MLF) in the dorsomedial brainstem tegmentum of either the pons or the midbrain
Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus. Additionally, the divergence of the eyes leads to horizontal diplopia. So if the right eye is affected the patient will "see double" when looking to the left, seeing two images side-by-side. Converge.
The side of the INO is named by the side of the adduction deficit, which is ipsilateral to the medial longitudinal fasciculus (MLF) lesion.
Types of INO
There are two types of INO that is Cogan's anterior and posterior INO, which refer to an anterior midbrain or posterior pontine localization along the medial longitudinal fasciculus (MLF).
Symptoms and signs  of INO
Diplopia in INO
Patients with internuclear ophthalmoplegia (INO) may complain of horizontal diplopia when there is a significant adduction weakness or limitation on lateral gaze
Diplopia is not usually present in primary gaze.
Diplopia is due to the dysconjugate movement of the two eyes during horizontal gaze results in an interruption in binocular fusion that can lead to visual confusion, oscillopsia, diplopia, reading fatigue, and loss of stereopsis (depth perception) [
Vertigo in INO
Some patients also complain of vertigo
The components of INO are 
  • Impaired horizontal eye movement with weak adduction of the affected eye
  • Abduction nystagmus of the contralateral eye.
  • Convergence is generally preserved in INO
Adduction weakness  in INO
Depending on the severity of the lesion, adduction of the involved eye may be impaired or absent. In milder cases, the deficit may be limited to a decrease in adduction velocity without ocular limitation of ocular movement
Milder forms of INO may be best elicited by asking the patient to perform fast horizontal eye movements (saccades) away from a fixed central point. Due to the Interruption of the ascending axons that arise from the internuclear neurons in the abducens nucleus likely explains the adduction deficit
Abduction nystagmus  in INO
The contralateral abducting eye will usually exhibit a disassociated horizontal nystagmus, although this does not always occur.
The underlying mechanisms causing abducting nystagmus are unknown. There is evidence that more than one mechanism may play a role in different patients and even in the same patient
One theory is that abduction nystagmus is due to an adaptive response to overcome the weakness of the contralateral medial rectus. This is explained by Hering's law of equal innervation, which states that attempts to increase innervation to the weak muscle in one eye are accompanied by a commensurate increase in innervation to the yoke muscle in the other eye.
Alternatively, gaze-evoked nystagmus may occur in patients with INO because of involvement of adjacent structures, such as the vestibular nuclei . The nystagmus is dissociated because adductor weakness limits its manifestation in the affected eye. Subclinical nystagmus in the adducting eye has been demonstrated with electro-ocular techniques
Normal convergence  in INO
 Most lesions of the medial longitudinal fasciculus (MLF) are located in the pons or caudal mesencephalonhence they spare the vergence pathways, including the fibers deriving from the medial rectus subnucleus of cranial nerve III . As a result, convergence is intact in the most of the  affected patients inspite of the adduction weakness on lateral gaze. Thisis an important finding that  finding can be used to  distinguish an INO from a partial third nerve palsy
Abduction slowing
INO may produce slowing of abduction as well as adduction in the affected eye .This small degree of abduction slowing is expected in the context of adduction weakness, due to  the loss of the contribution of the off-pulse of innervation (defective relaxation) when the medial rectus acts as an antagonist .
Abnormal vertical eye movements  in INO
As the  MLF also contains pathways involved in the regulation of vertical pursuit, vertical vestibular signals, and vertical alignment , Patients often exhibit abnormalities with vertical eye movements, including:
  • Diminished vertical gaze holding
  • Abnormal optokinetic and pursuit responses
  • Suppressed vestibular ocular reflex (VOR)
  • Vertical gaze-evoked nystagmus
  • Skew deviation and/or contraversive ocular tilt reaction
These signs are inconsistently present hence not required for the diagnosis of INO
Variants of INO
  • Reverse INO
  • WEBINO syndrome (Wall Eyed Bilateral INO) 
  • One and a half syndrome