Abducens (or Abducent) nerve Palsy or Cranial nerve six palsy (CN VI) is a common neuro-ophthalmic disorder. Since CN VI has a long intracranial course, it may be affected by multiple aetiologies. It may be unilateral or bilateral condition.
CN VI is a pure motor nerve that innervates ipsilateral (same side) lateral rectus muscle of the eye and controls abduction (outward movement) of the eyeball. This nerve has the longest intracranial course amongst all the cranial nerves. A palsy affecting this nerve alone is less common. Usually, seventh (CN VII or facial) and eighth (CN VIII or vestibulocochlear) cranial nerves are also affected along with it, which signals a central cause.
Children are more likely to be affected by a tumour, and older people are more likely to have vasculopathy producing ischaemia.
CN VI palsy may present with ‘false localising sign’, suggesting impingement, when in fact, the causative reason/tumour may be remotely present, or there may not be any detectable reason/tumour. Similarly, raised intracranial pressure may stretch CN VI, and perhaps compression of its vascular supply.
The sixth cranial nerve is the most commonly affected motor nerve to the eye in adults.
Adams James G, Barton Erik D, Collings Jamie, DeBlieux Peter M C, Gisondi Michael A, Nadel Eric S. Emergency Medicine Clinical Essentials Second Edition. Saunders, an imprint of Elsevier Inc. 2013. P 823- 824.
The causes of Abducens nerve palsy are varied.
Common aetiologies in children are
In addition to the aetiologies seen in children, adults are affected by vasculopathies (most common acquired causes) also, such as
Other conditions include
CN VI nerve palsy is a rare initial presentation in multiple sclerosis.
Recurrence of CN VI may take place more than once, and has been reported in both adults and children.
Inherited autosomal dominant condition may be the reason for familial recurrent CN VI palsy along with involvement of seventh (facial) nerve.
Patients with CN VI paresis present with esotropia (inward deviation) of the affected eye. Outward movement beyond primary position or midline is lost or reduced. Patients presenting with partial or mild palsy adopt posture with head turn toward the affected side to minimise diplopia by keeping the affected eye adducted (inward movement). Severe cases may shut the eye or cover it to avoid diplopia.
Presentation depends upon the aetiology.
Congenital CN VI palsy may present with congenital esotropia reported to occur about six to eight weeks of life. Most cases without peripheral misdirection of nerves are transient and probably are due to perinatal trauma. There are two types of transient CN VI palsy:
Acquired CN VI palsy may be due to varied aetiology:
Benign recurrent CN VI palsy in children may occur after benign acute viral sickness or immunisation. This is an isolated condition with acute onset, and is associated with restriction of abduction.
Patients with vasculopathy present with sudden onset, painless horizontal diplopia. These patients typically show spontaneous and complete resolution within three to six months.
Patients with raised intracranial pressure (ICP) may present with unilateral or bilateral symptoms of headache, visual obscuration, or profound loss of vision.
Intracavernous carotid artery dissection or aneurysm may produce painful CN VI palsy along with ipsilateral Horner syndrome.
Painful CN VI palsy may be present in mastoiditis and petrositis complicating chronic otitis media. A tumour in this region may produce a combined trigeminal-abducens-facial nerve syndrome.
CN VI palsy may be associated with involvement of seventh or eighth cranial nerves.
In unilateral CN VI, four to sixteen prism dioptres of hyperdeviation may be present due to vertical strabismus in children such as dissociated vertical deviation, superior oblique palsy, or physiological hyperphoria.
Like other cranial nerve palsies, root cause of palsy should be treated.
Microvascular ischaemia/vasculopathy secondary to diabetes mellitus and hypertension may lead to Isolated CN VI palsy.
Patient should be observed for three to six months. Most cases resolve on their own within three to six months.
Therapies vary from controlling vasculopathic risk factors to neurosurgical interventions.
Unmanageable cases of complete CN VI palsy may be patched to avoid diplopia. Patching each eye alternately for a few hours each day, may be done to prevent amblyopia in the affected eye.
Prognosis varies with aetiology. Cases due to vasculopathy usually resolve completely. Other CN VI cases have guarded prognosis. Patients are normally observed for six months for spontaneous resolution.