Describe the functional neuro-anatomy underlying eye movement defects; oculomotor, trochlear and abducens palsies and internuclear ophthalmoplegiaEdit
Before attempting to understand the problems that nerve palsies cause, it is important to understand how each eye muscle contributes to eye movement, and the innervation of each muscle.
OCULOMOTOR (CN III) NERVE PALSYEdit
Oculomotor nerve supplies medial rectus, superior and inferior rectus, the inferior oblique, and the levator palpebrae muscles. CNIII also has a parasympathetic component, responsible for iris sphincter contraction.
Thus, a palsy of the oculomotor nerve causes a classic 'down and out' disturbance of the affected eye, along with a fixed pupil dilatation and ptosis.
TROCHLEAR (CN IV) NERVE PALSYEdit
The trochlear nerve inervates the superior oblique muscle of the eye.
A palsy of the trochlear nerve will be most noticeable when the affected eye is adducted. In this position, the affected eye will be 'upward looking', and cannot move down and in.
The video below shows a woman with left CN IV palsy.
ABDUCENS (CN VI) NERVE PALSYEdit
The abducens nerve innervates the lateral rectus muscles of the eye. Thus, a CN VI nerve palsy would cause a loss of abduction.
Patients may complain of double vision of horizontal gaze.
Internuclear ophthalmoplegia is an eye movement disorder of central origin. It is caused by a lesion in an area of the brain called the medial longitudinal fasiculus (MLF). It may be unilateral or bilateral.
Internuclear ophthalmoplegia is clinically characterized by total or partial failure to adduct one eye in lateral gaze and a monocular nystagmus of the abducting eye.
It is commonly observed in patients with multiple sclerosis (MS).