PHT 404

Clinical Posting III

Cranial Nerve
 Olfactory (I) nerve
• Anatomy. Olfactory cells are a series of bipolar
neurones which pass through the cribriform
plate to the olfactory bulb.

• Signs. Reduced taste and smell, but not to

ammonia which stimulates the pain fibres
carried in the trigeminal nerve.

• Causes. Trauma, frontal lobe tumour,

meningitis.
 Optic (II) nerve - 1
• Anatomy.
– The optic nerve fibres are the axons of the retinal
ganglion cells.
– At the optic chiasm, only the fibres derived from
the nasal parts of the retina decussate, join with
the non-decussating fibres and pass backwards in
their respective optic tracts to the visual cortex.
 Optic (II) nerve - 2
• Signs and causes:
– Visual field defects - see the separate article on
Visual Field Defects:
• Field defects start as small areas of visual loss (scotomas).
• Monocular blindness: lesions of one eye or optic nerve - eg, MS, giant
cell arteritis.
• Bilateral blindness: methyl alcohol, tobacco amblyopia; neurosyphilis.
• Bitemporal hemianopia: optic chiasm compression - eg, internal
carotid artery aneurysm, pituitary adenoma or craniopharyngioma.
• Homonymous hemianopia: loss of the same half (left or right) of the
visual field of both eyes, on the opposite side to the lesion (eg, a right
side lesion causes loss of the left side of the visual field of both eyes).
Lesions lie behind the optic chiasm in the optic tract, lateral
geniculate nucleus, optic radiations or the occipital cortex - eg, stroke,
abscess, tumour.
 Optic (II) nerve - 3
– Pupillary abnormalities - see the separate article on
Pupillary Abnormalities:
– Optic neuritis (pain on moving the eye, loss of central vision,
afferent pupillary defect, papilloedema). Causes: demyelination;
rarely, sinusitis, syphilis, collagen vascular disorders.
– Optic atrophy (pale optic discs and reduced acuity): MS, frontal
tumours, Friedreich's ataxia, retinitis pigmentosa, syphilis,
glaucoma, Leber's optic atrophy, optic nerve compression.
– Papilloedema (swollen discs):
• Raised intracranial pressure (ICP) (tumour, abscess, encephalitis,
hydrocephalus, benign intracranial hypertension).
• Retro-orbital lesion (eg, cavernous sinus thrombosis).
• Inflammation (eg, optic neuritis).
• Ischaemia (eg, accelerated hypertension).
 Oculomotor (III) nerve - 1
• Anatomy.
– This nerve emerges from the brainstem on the medial aspect of the crus
cerebri and then passes forwards between the posterior cerebral and
superior cerebellar arteries, very close to the posterior communicating
artery. It pierces the dura near the edge of the tentorium cerebelli, and
passes through the lateral part of the cavernous sinus with the IV and VI
nerves to enter the orbit.

• Signs.
– The initial sign is often a fixed dilated pupil which doesn't accommodate;
then ptosis develops and then a complete internal ophthalmoplegia
(masked by ptosis).
– Unopposed lateral rectus causes outward deviation of the eye.
– If the ocular sympathetic fibres are also affected behind the orbit, the
pupil will be fixed but not dilated.
 Oculomotor (III) nerve - 2
• Causes of a single III lesion.
– Diabetes mellitus, giant cell arteritis, syphilis, posterior
communicating artery aneurysm, idiopathic;
– raised ICP - it causes uncal herniation through the
tentorium - this compresses the nerve.
– Third nerve palsies without a dilated pupil are due to
diabetes mellitus or another vascular cause.
– Early dilatation of a pupil implies a compressive lesion.
– Diplopia from a third nerve lesion may cause nystagmus.
 Trochlear (IV) nerve
• Anatomy. Passes backwards in the brainstem, decussates in the
anterior medullary velum and emerges to pass round the
cerebral peduncle between it and the temporal lobe, passing
over the tentorium to enter the cavernous sinus with II and VI,
and enters the orbit to supply the superior oblique muscle.

• Signs.
– Diplopia due to weakness of downward and inward eye movement.
– The most common cause of a pure vertical diplopia.
– The patient tends to compensate by tilting the head away from the
affected side.

• Causes of a single IV lesion.

– Rare and most commonly due to trauma to the orbit.
– It may also occur in diabetes or infarction secondary to hypertension.
 Trigeminal (V) nerve - 1
• Anatomy.
– Forms three trunks: ophthalmic, maxillary and mandibular
divisions.
– The latter contains both sensory and motor fibres.
– There may be considerable individual variation in the exact areas of skin
supplied:

• Ophthalmic division lies with III, IV and VI in the cavernous sinus and
supplies the skin over the medial nose, forehead, and eye (including
corneal reflex).
• Maxillary division passes through the inferior part of the cavernous sinus
and the foramen rotundum and joins with parasympathetic fibres to form
the sphenopalatine ganglion (lacrimation).
– It then enters the orbit as the infraorbital nerve, eventually supplying the skin
of the upper lip, cheek and triangle of skin extending from the angle of eye
and mouth to an apex in the mid-temporal region.
 Trigeminal (V) nerve - 2
– Mandibular division leaves the skull through the foramen ovale carrying
sensory fibres from the skin of the lower lip and chin up to and including
the tragus and upper part of the pinna; mucous membranes of the floor
of the mouth, cheek and anterior two thirds of the tongue (taste fibres
joining it from the chorda tympani branch of the facial nerve). Motor
fibres supply the masseter, temporalis, and pterigoids.
• Signs.
– Reduced sensation or dysasthesia over the affected area. Weakness of
jaw clenching and side-to-side movement.
– If there is a lower motor neurone (LMN) lesion, the jaw deviates to the
weak side when the mouth is opened.
– There may be fasciculation of temporalis and masseter.
• Causes of a single V lesion.
– Sensory: trigeminal neuralgia, herpes zoster, nasopharyngeal carcinoma.
– Motor: bulbar palsy, acoustic neuroma.
 Abducent (VI) nerve
• Anatomy. From the nucleus in the floor of the fourth ventricle,
fibres pass forward in the pons and emerge to follow a long
extracerebral course on the base of the brain, across the apex of
the petrous temporal, through the posterior fossa near the dorsum
sellae to enter the cavernous sinus and thence to the orbit and
lateral rectus muscle.
• Signs.
– Inability to look laterally.
– The eye is deviated medially because of unopposed action of the medial
rectus muscle.
• Note the failure of the lateral rectus to move the left eye is very obvious. Ignore
the eccentric reflection of the light, as the patient is not trying to follow it
• Causes of a single VI lesion. MS, pontine CVA. It is considered a
false localising sign (because of long extracerebral course) in raised
 Facial (VII) nerve - 1
• Anatomy.
• Mainly motor (some sensory fibres from external acoustic
meatus, fibres controlling salivation and taste fibres from the
anterior tongue).
• Fibres loop around the VI nucleus before leaving the pons medial
to VIII and passing through the internal acoustic meatus.
• It passes through the petrous temporal in the facial canal,
widens to form the geniculate ganglion (taste and salivation) on
the medial side of the middle ear, whence it turns sharply (and
the chorda tympani leaves), to emerge through the stylomastoid
foramen to supply the muscles of facial expression.
 Facial (VII) nerve - 2
• Signs.
– Facial weakness. In an LMN lesion the forehead is paralysed - the final
common pathway to the muscles is destroyed; whereas the upper
facial muscles are partially spared in an upper motor neurone (UMN)
lesion because of alternative pathways in the brainstem.
– There appear to be different pathways for voluntary and emotional
movement.
– CVAs usually weaken voluntary movement, often sparing involuntary
movements (eg, spontaneous smiling). The much rarer selective loss of emotional
movement is called mimic paralysis and is usually due to a frontal or thalamic lesion.
• Causes of a single VII lesion:
– LMN: Bell's palsy, polio, otitis media, skull fracture, cerebellopontine
angle tumours, parotid tumours, herpes zoster (Ramsay Hunt
syndrome), Lyme disease.
– UMN: (spares the forehead - bilateral innervation): stroke, tumour.
 Vestibulocochlear (VIII) nerve
• Anatomy.
– Carries two groups of fibres, those to the cochlea (hearing) and to the
semicircular canals, utricle and saccule (balance and posture).
– They pass, together with the facial nerve, from the brainstem across the
posterior fossa to the internal acoustic meatus.

• Signs. Unilateral sensorineural deafness, tinnitus. Slow-growing

lesions seldom present with vestibular symptoms as
compensation has time to occur.

• Causes of a single VIII lesion. Loud noise; Paget's disease of bone,

Ménière's disease, herpes zoster; neurofibroma, acoustic
neuroma, brainstem CVA, lead, aminoglycosides, furosemide,
aspirin. See also 'Combined cranial nerve lesions', below.
 Glossopharyngeal (IX) nerve
• Anatomy.
– Contains sensory, motor (stylopharyngeus only) and parasympathetic
fibres (salivary glands).
– Passes across the posterior fossa, through the jugular foramen and into
the neck, supplying tonsil, palate and posterior third of tongue.

• Signs.
– Unilateral lesions do not cause any deficit because of bilateral
corticobulbar connections.
– Bilateral lesions result in pseudobulbar palsy. These nerves are closely
interlinked.

• Causes (single nerve lesions exceedingly rare). Trauma,

brainstem lesions, cerebellopontine angle and neck tumours,
polio, Gullain-Barré syndrome (GBS).
 Vagus (X) nerve - 1
• Anatomy.
– The vagus nerve, 'the wanderer', contains motor fibres (to
the palate and vocal cords), sensory components
(posterior and floor of external acoustic meatus) and
visceral afferent and efferent fibres.
– It leaves the skull through the jugular foramen, passes
within the carotid sheath in the neck (giving off cardiac
branches, and the recurrent laryngeal nerves supplying
the vocal cords), through the thorax supplying the lungs,
and continues on via the oesophageal opening to supply
the abdominal organs.
 Vagus (X) nerve - 2
• Signs.
– Palatal weakness can cause 'nasal speech' and nasal
regurgitation of food.
– The palate moves asymmetrically when the patient says
'ahh'. Recurrent nerve palsy results in hoarseness, loss of
volume and 'bovine cough'.

• Causes (single nerve lesions exceedingly rare).

Trauma, brainstem lesions, tumours in the
cerebellopontine angle, jugular foramen and neck;
polio, GBS.
 Spinal accessory (XI) nerve
• Anatomy: motor to sternocleidomastoid and
trapezius.

• Signs: weakness and wasting of these

muscles.

• Causes: as 'Vagus (X) nerve', above.

 Hypoglossal (XII) nerve
• Anatomy. It passes briefly across the posterior fossa, leaves
the skull through the hypoglossal canal and supplies motor
fibres to the tongue and most of the infrahyoid muscles.
• Signs. An LMN lesion produces wasting of the ipsilateral side
of the tongue, with fasciculation; and on attempted
protrusion the tongue deviates towards the affected side, but
the tongue deviates away from the side of a central lesion.
• Note the wasted left side of the tongue and deviation to the
left suggesting a left LMN lesion
• Causes of a single XII lesion: rare. Polio,
syringomyelia tuberculosis, median branch thrombosis of the
vertebral artery.
 Combined cranial nerve lesions
• VII, VIII, then V and sometimes IX: cerebellopontine angle
tumours.

• V, VI (Gradenigo's syndrome): lesions within the petrous

temporal bone.

• Combined III, IV, VI: stroke, tumours, Wernicke's

encephalopathy, aneurysms, MS, myasthenia gravis,
meningitis, muscular dystrophy, myotonic dystrophy,
cavernous sinus thrombosis, GBS, cranial arteritis, trauma
and orbital pathology.