Third Nerve Palsy Flashcards
The third nerve nucleus originates in the … of the brainstem.
The third nerve nucleus originates in the midbrain of the brainstem.
A third nerve palsy refers to damage to the … cranial nerve.
A third nerve palsy refers to damage to the oculomotor cranial nerve.
Third nerve palsy
The oculomotor nerve is the third cranial nerve that has predominant motor function to the pupil, eyelid and extraocular muscles. Paralysis or ‘palsy’ to the oculomotor nerve can occur anywhere along its course from nucleus in the midbrain to orbital apex.
The third nerve nucleus is comprised of several subnuclei that innervate important visual structures.
Fibres from these nuclei pass from the midbrain into the subarachnoid space and then into the lateral wall of the cavernous sinus. It then enters the superior orbital fissure and divides into superior and inferior branches.
Superior branch: innervates levator palpebrae and superior rectus
Inferior branch: Innervates medial and inferior rectus muscles, inferior oblique, and pupillary sphincter
The third nerve has an important role in the …
The third nerve has an important role in the pupillary light reflex.
Pupillary light reflex - third nerve palsy
The pupillary light reflex controls the diameter of the pupil in response to light. It is mediated by the parasympathetic nervous system and involves the optic and oculomotor cranial nerves.
The basic principle of the parasympathetic pathway is that as light is shone onto one eye there is corresponding equal and symmetrical pupillary constriction. This occurs by contraction of circular fibres of the iris (i.e. pupillary sphincter).
Pupillary light reflex stages
Light source: Light is shone onto the retina and detected by photoreceptors
Transmitted via optic nerve: Retinal fibres transmit this signal via the optic nerve. Nasal retinal fibres cross at the optic chiasm and enter the contralateral pretectal nucleus. Temporal retinal fibres do not cross and enter the ipsilateral pretectal nucleus.
Pre-tectal nucleus to Edinger-Westphal nuclei: Input from the pretectal nucleus is transmitted the Edinger-Westphal (EW) nuclei (a subnuclei of the oculomotor nerve). The ipsilateral pretectal nucleus transmits information to both the ipsilateral and contralateral EW nuclei.
Transmitted to ciliary ganglion: Effector neurons pass from both EW nuclei to the ipsilateral ciliary ganglion. From here, fibres pass via the short ciliary nerve to the ipsilateral pupillary sphincter.
Pupillary constriction: once activated, each pupillary sphincter contracts leading to symmetrical pupillary constriction
A lesion at any point during the course of the third nerve can cause palsy.
A variety of pathologies can lead to a third nerve palsy. These are generally divided according to location. Each location has several possible causes and associated clinical manifestations.
Locations:
Midbrain
Subarachnoid space
Cavernous sinus
Orbital apex
Subarachnoid space
Damage to the oculomotor nerve in the subarachnoid space typically causes an isolated third nerve palsy (absence of other neurological features). A variety of conditions can cause a third nerve palsy in this location:
Inflammation/infection (e.g. meningitis)
Malignancy (e.g. meningeal metastasis, also known as meningeal carcinomatosis)
Ischaemia (e.g. diabetes mellitus, giant cell arteritis): thought to be a microvascular event.
Aneurysm
Trauma
Cavernous sinus - third nerve palsy
The cavernous sinus is one of the dural venous sinuses within the head. It is essentially a cavity bordered by the temporal bone, sphenoid bone and sella turcica, which contains the pituitary gland.
Several important structures run through or adjacent to the cavernous sinus including cranial nerves III, IV, VI, V1, V2 and the carotid artery. Therefore, a third nerve palsy secondary to a cavernous sinus lesion is usually associated with other nerve palsies. Typical causes at this location include thrombosis, tumour or carotid artery aneurysm.
Orbital apex syndrome
Lesions at the orbital apex are associated with other neurological features (e.g. multiple cranial nerve palsies) and ophthalmic signs including chemosis (swelling of the conjunctiva) and proptosis.
Orbital apex syndrome describes the presence of multiple cranial nerve palsies (III, IV, VI, V1) and optic nerve dysfunction due to various pathologies including head and neck tumours, invasive fungal sinusitis, orbital cellulitis or sarcoidosis among many others. Multiple cranial nerve palsies (III, IV, VI, V1) in the absence of optic nerve dysfunction may suggest superior orbital fissure syndrome (these nerves traverse the superior orbital fissure) or cavernous sinus lesions.
A third nerve palsy is characterised by ipsilateral ptosis with a ‘…’ eye appearance.
A third nerve palsy is characterised by ipsilateral ptosis with a ‘down and out’ eye appearance.
Symptoms (third nerve palsy)
Diplopia
Ptosis (drooping eyelid)
Pain
Severe headache (concerning for aneurysmal subarachnoid haemorrhage)
Meningism (headache, neck stiffness, photophobia): suggestive of subarachnoid haemorrhage or meningitis
Signs - third nerve palsy
Ptosis
Eye appearance: ‘down and out’
Pupil dilatation (mydriasis): unless pupillary sparing
Loss of light reflex: unless pupillary sparing
Neck stiffness: suggestive of subarachnoid haemorrhage or meningitis
Focal neurological deficits: particularly if brainstem lesions
Other cranial nerve palsies (IV, VI, V1): particularly if cavernous sinus or orbital apex lesions
A third nerve palsy is a clinical diagnosis.
The diagnosis of a third nerve palsy is made clinically based on characteristic features (e.g. ptosis, ‘down and out’ eye appearance, diplopia). Once identified, it warrants further evaluation for the underlying cause.
Investigations depend in the suspected aetiology with the most concerning being an aneurysmal subarachnoid haemorrhage (or impending haemorrhage). Key investigations including neuroimaging (CT/MRI) and lumbar puncture (if required). Some clinicians and guidelines will recommend neuroimaging for all new third nerve palsies.
