A sixth cranial nerve palsy refers to dysfunction of the abducens nerve that causes a lateral rectus palsy.
The abducens nerve is the sixth (VI) cranial nerve, which provides innervation to the lateral rectus muscle. This is one of the extra-ocular muscles that causes eye abduction, which is needed for horizontal gaze.
A VI nerve palsy is the most common cranial nerve palsy in isolation. A palsy can develop due to a lesion anywhere along the path of the nerve from pons to lateral rectus muscle.
The abducens nerve innervates the lateral rectus muscle.
The sixth nerve nucleus is located in the dorsal (posterior) pons of the brainstem. The nerve then begins on a long intracranial route.
It exits the brainstem at the pontomedullary junction and enters the subarachnoid space. It subsequently travels over the petrous apex (pyramid-shaped anteromedial part) of the temporal bone and passes through Dorello’s canal. It then passes through the cavernous sinus lateral to the internal carotid artery before entering the orbit via the superior orbital fissure.
The VI nerve has predominantly motor function and provides innervation to the ipsilateral (same-side) lateral rectus muscle that is needed for eye abduction involved in horizontal gaze. In addition, several interneurons travel to the contralateral third nerve nucleus via the medial longitudinal fasciculus (MLF).
Communication between the third and sixth cranial nerves is needed for coordinated conjugate lateral gaze. This means when we look laterally to the left or the right, both eyes move together in a symmetrical manner and prevent diplopia (double vision). Damage to the MLF can result in a conjugate lateral gaze palsy known as intranuclear ophthalmoplegia (INO). For more information see Multiple sclerosis notes.
A lesion at any point during the course of the sixth nerve can cause palsy.
A variety of pathologies can lead to a VI nerve palsy. These are generally divided according to location. Each location has several possible causes and associated clinical manifestations.
Increases in intracranial pressure may result in unilateral or bilateral abducens nerve palsies. This is because of the long intracranial course of the VI nerve, which is particularly prone to compression along the skull base.
Particularly among older adults, an isolated abducens nerve palsy is commonly due to ischaemic mononeuropathy, which occurs in relation to diabetes mellitus and/or hypertension. In children, an abducens nerve palsy is more commonly related to tumours, trauma, an increase in ICP or a congenital lesion.
A sixth nerve palsy may affect one or both of the paired cranial nerves. Bilateral sixth nerve palsies are more likely to occur in global pathologies such as raised ICP or trauma.
An isolated sixth nerve palsy refers to the absence of additional neurological deficits. On the contrary, a nonisolated sixth nerve palsy refers to the presence of additional neurological deficits. Characteristic neurological features in a nonisolated sixth nerve palsy are often specific to a region such as the cavernous sinus (e.g. cavernous sinus thrombosis) or orbit (e.g. orbital apex syndrome).
A sixth nerve palsy is characterised by failure in eye abduction leading to horizontal diplopia.
These may be seen in patients with a nonisolated sixth nerve palsy.
Identification of a sixth nerve palsy is a clinical diagnosis.
A sixth nerve palsy is usually easily recognised at the bedside based on the presence of diplopia and failed eye abduction. Further investigations are warranted to determine the underlying cause.
This is the investigation of choice for a sixth nerve palsy. Magnetic resonance imaging (MRI) is the modality of choice, but a computed tomography (CT) of the head may be completed initially to exclude major differentials (e.g. tumour, intracerebral haemorrhage) whilst awaiting an MRI.
Neuroimaging is needed to exclude the majority of causes of a sixth nerve palsy. The urgency of imaging depends on the cause. In adults, a sixth nerve palsy is commonly isolated due to microvascular damage to the nerve (i.e. ischaemic mononeuropathy). In these cases, the need for urgent imaging of the head is less pressing.
Additional investigations may be required depending on the suspected cause. Examples include ESR/CRP in suspected giant cel arteritis or lumbar puncture in suspected idiopathic intracranial hypertension.
The treatment of a sixth nerve palsy is directed towards the underlying cause.
There are numerous causes of a sixth nerve palsy and treatment should be directed towards the underlying cause. This is particularly relevant for infectious, inflammatory of neoplastic lesions, whereby treatment may alleviate diplopia.
In patients with an isolated, unilateral, nontraumatic sixth nerve palsy (usually due to microvascular disease), spontaneous recovery is common. This is also true for traumatic sixth nerve palsies.
In patients with persistent symptoms, or those unlikely to recover (e.g. bilateral at presentation or complete palsy), treatments can include patching (covering one eye to prevent binocular diplopia), use of prisms, strabismus surgery or even botox injections. Patients should be referred to an ophthalmologist.
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