Anatomy

• The oculomotor (III) nerve nucleus lies in the ventral midbrain just anterior to the periaqueductal grey matter. The nerve passes between the cerebral peduncles into the interpeduncular CSF cistem. It passes just below the free edge of the tentorium in relation to the posterior com municating artery and enters the dura surrounding the cavernous sinus. It then enters the orbital fossa through the superior oblique fissure, where it subdivides into its terminal branches. The nerve innervates the superior (SR), medial (MR) and inferior (IR) recti, the inferior oblique (IO) and levator palpebrae superioris (LPS) muscles. These muscles open the upper lid (LPS) and move the globe upwards (SR. 10), downwards (IR) and medially (MR). Through the parasympathetic fibres arising from the Edinger-Westphal nerves, the nerve also indirectly supplies the sphincter muscles of the iris, which cause constriction of the pupil, and the ciliary muscle, which is responsible for focusing the lens for near vision.

• The trochlear (IV) nerve arises from a nucleus in the caudal midbrain. The fibres decussate before leaving the midbrain just below the inferior colliculus. The nerve then passes forward and laterally in relation to the rostral pons and the free edge of the tentorium. It pierces the dura of the tentorial edge and passes through the cavernous sinus and superior orbital fissure. In the orbit it innervates the superior oblique (SO) muscle, contraction of which causes downward movement of the globe when the eye is adducted.

• The abducent (VI) nerve originates from a nucleus located near the midline of the caudal pons, where it forms part of the facial colliculus. The nerve emerges from the ventral pontomedullary junction just lateral to the pyramid, passes through the prcpontine CSP cistern and pierces the basal dura to enter Dorello's canal and then traverse the cavernous sinus. Here the nerve is in direct relation to the internal carotid artery before it passes through the superior orbital fissure to the lateral rectus (LR) muscle. Contraction of the LR causes abduction of the eye.

Ocular motility is dependent not only on the integrity of the III. IV and VI nerves but also on a central brain stem tract, the medial longitudinal fasciculus (MLF), which interconnects the nuclei. The MLF also receives direct and indirect input from the vestibular nuclei, cerebellar flocculus and the para-abducens nucleus, also called the nucleus of the paramedian pontine reticular formation (PPRF). This is important for lateral gaze. The MLF provides a mechanism by which the optical axes remain parallel or conjugate when the eyes are turned to one side or when there is movemeni of the head. There are also supranuclear connections. There is also a centre for vertical gaze at the mesod¡encephalic junction with medial and lateral neuronal pools subserving downgaze and upgaze respectively. Sympathetic fibres dilate the pupil and also innervate pan of the LPS. The preganglionic sympathetic fibres arise in the posterior hypothalamus to emerge through the ventral roots of the first two or three segments of the thoracic spinal cord and ascend through the sympathetic chain to the superior cervical ganglion. Postganglionic fibres ascend in the carotid neural plexus and into the orbit with the ophthalmic artery to terminate in the radial muscle of the iris (dilator of the pupil). In area S of the frontal lobe there is the frontal eye field (FEF). When this area is slimulated the eyes turn conjugalely away from the side of stimulation.

Eye movements

The six external ocular muscles move the eyeball in the directions shown in Figure 6.14.

While the MR and LR subserve horizontal eye movements, vertical eye movement is more complex and mediated both by the 10 and SR (upgaze) and the SO and IR (downgaze). Because of the different long axes of the various ocular muscles, the superior oblique is mainly responsible for downgaze and the inferior oblique mainly responsible for upgaze in the adducted eye. The appropriate recti are responsible for vertical gaze in the abducted eye (see Fig. 6.14 and Fig. 7.9, p. 250).

The assessment of eye movements is conveniently combined with looking for nystagmus. Minor degrees ot nystagmus occur in normal subjects at extremes of lateral gaze, particularly if maintained for more than 10 seconds.

Examination sequence

□ Inspect the eyes for any abnormality.

□ With both eyes open, test for ocular movements with the patient's head in the neutral position and, if necessary, held there by one of the examiner's hands on the crown of the head.

□ Examine carefully for any squint (strabismus) or other abnormality, including nystagmus.

□ First ask the patient to look up and down, and to the right and the left.

□ Then ask (he patient to fix the gaze on the examiner's finger and to report if double vision occurs while following the movement of the finger held about 60 cm away. "s----

Superior rectus

Superior rectus

External Ocular Muscle Images

Inferior rectus

Fig. 6.14 External ocular muscle function,

Inferior rectus

Fig. 6.14 External ocular muscle function,

□ Move ihe finger up and down, (hen lo the right and up and down, and then to the left and up and down. If necessary, repeal the examination, one eye at a time, lo distinguish muscle and gaze palsies.

C Record the direction in which double vision is present and where maximal separation of the images occurs.

□ If diplopia is reported ask the patient to close one eye at a lime to identify which eye is producing Ihc false image.

□ To test convergence, ask the patient to focus on the linger as il is brought from a distance towards the tip of the nose.

□ Look for nystagmus while examining eye movements.

□ Record the presence of vertical, horizontal or rotatory nystagmus and the direction of gaze in which it is most marked.

□ Note the direction of the fast component of nystagmus, whether il changes direction with the direction of gaze and whether the degree of nystagmus is different in each eye.

Common abnormalities

The palpebral fissures are normally symmetrical. Abnormalities that may be present on inspection include ptosis (drooping of an eyelid), widening of the palpebral fissures, inequality in pupillary size (anisocoria), abnormal eye movements at rest (nystagmus, opsoclonus and square wave jerks), asymmetrical blinking, conjunctival injection and orbital pulsation. A lesion of the sympathetic pathway gives rise to Horner's syndrome (Fig. 6.9).

Disorders of ocular movements

There are many non-neurological causes of disordered eye movements. These include disorders of the ocular muscles (myopathies) and the neuromuscular junction (e.g. myasthenia gravis) and metabolic encephalopathy (e.g. toxic levels of phenyloin, carbamazepine).

Cranial neuropathies that involve 111, IV and VI cause characteristic patterns of eye movement disorders with diplopia (double vision).

Oculomotor nerve (III). A complete unilateral lesion of III causes ptosis, weakness of superior, medial and inferior eye movements, pupillary dilatation and an absent direct reflex. Common causes of an isolated III palsy arc diabetic mononcuropathv, carotid-posterior communicating artery aneurysms, pituitary or other tumours, trauma and vascular disease. The III palsy associated with a contralateral hemiplegia (Weber syndrome) is due to a midbrain stroke. Ill nerve lesions may be incomplete depending on the location and type of lesion. Lesions due to diabetes or vascular disease lend not to involve the pupil, in contrast with compressive lesions (e.g. aneurysm).

Trochlear nerve (IV). Isolated lesions are not common. The patient usually complains of diplopia, particularly bad when looking down and reading. The patient will often adopt a compensatory head tilt. Causes of an isolated IV lesion are ischaemic mononeuropathy (diabetes, hypertension) and head trauma, in which the associated intracranial damage to the IV nerve is sometimes bilateral. Damage to the trochlear itself, through which Ihe superior-oblique tendon passes, may be responsible lor (he IV palsy after head injury, ENT surgery and in patients with rheumatoid arthritis.

Abducent nerve (VI). Isolated lesions are common. In many cases, particularly following head injury and in patients with raised intracranial pressure, it is a 'false localising" sign (i.e. the VI nerve is affected by intracranial pathology elsewhere). The patient experiences diplopia worse looking towards the side of the paretic I.R The paralysis may be complete or partial. Abducent paresis may be associated with diabetes and with suppurative otitis media (Gradenigo's syndrome). Lesions of the cavernous sinus (aneurysms, pituitary adenoma, meningioma) quite commonly cause VI nerve paresis. However, cavernous sinus lesions usually produce a constellation of cranial neuropathies. Lesions of the VI nerve are occasionally found in conjunction with ipsilateral V and Vll paresis and contralateral hemiplegia in unilateral pontine stroke.

Other lesions affecting eye movement

Paresis of conjugate upgaze and downgaze may be seen in space-occupying lesions around the pineal gland and lectal region and in patients with aqucductal stenosis and hydrocephalus. Failure of upgaze, together with loss of the pupillary light response but preservation of miosis on accommodation, is termed Parinaud's syndrome or the pretectal syndrome. This is usually due to a lesion of the pineal gland and ventral midbrain.

Lateral gaze paresis may be due lo a lesion in the frontal eye field (FF.F). If (he lesion is destructive (e.g. intra cerebral haemorrhage), the eyes are deviated towards the side of the damaged frontal lobe. In most cases the paresis lasts only a few days and eye movements return to normal. If the FEE lesion is irritative (e.g. epileptic) the eyes and head may be deviated to the side opposite the lesion. If there is a lesion in the paramedian pontine reticular formation (PPRF) ihe eyes arc deviated away from the side of (he lesion. This is most commonly caused by a pontine stroke and therefore associated with a plethora of other brain stem signs. Resolution of the paresis in such cases is much slower than thai following damage to the FEF.

Internuclear ophthalmoplegia (INO) occurs when there is a lesion of the MLF. The ipsilateral eye is unable to adduct and there is nystagmus in the contralateral abducting eye.

INO is most commonly seen in multiple sclerosis but can also occur with vascular disorders and neoplasms of the brain stem. Supranuclear ophthalmoplegia occurs when the corticonuclear fibres are damaged. Spontaneous eye movements and doll's eye elicitation of ocular movements are preserved, but there is paresis of voluntary eye movements (usually downgaze and sometimes upgaze). They may be associated with parkinsonian and dystonic clinical signs in the S tee I e-R ichardson-OIze w sk i syndrome.

Nystagmus. Pendular nystagmus occurs when the amplitude of the two phases of movement are equal and is often due to poor vision. It is thought to be an exaggeration of the normal tiny movements made by the eye to prevent fatigue of the retinal photoreceptors. Congenital blindness and ocular albinism arc often associated with coarse pendular nystagmus.

Horizontal phasic (jerk) nystagmus is usually due to labyrinthine, cerebellar or brain stem dysfunction. The direction of horizontal nystagmus is determined by the direction of the fast phase. The amplitude is usually increased by gaze to that side. It is termed first degree if present only on looking in that direction, second degree if present when looking straight ahead, and third degree if still present on gaze in the opposite direction.

• Nystagmus due to lesions of the brain stem is usually multidirectional. Common causes are Wernicke's encephalopathy, multiple sclerosis, anticonvulsant toxicity and brain stem ischaemia.

• Labyrinthine nystagmus is horizontal or rotary.

• Lesions of the cerebellar hemisphere cause horizontal nystagmus to the side of the diseased hemisphere. Downbeat nystagmus (usually due to a lesion of the cervicomedullary junction). see~m» nystagmus (due to parasellar lesions) and convergence-retraction nystagmus (due to lesions of the tectal and pineal region) are rare forms of disturbance.

Other jerky abnormalities of eye movement which mimic nystagmus arc ocular bobbing (usually due to a pontine haemorrhage), which is characterised by spontaneous downward jerks of both eyes followed by a slow return to rest position, and opsoclonus. The latter is characterised by chaotic rapid eye movements and is seen in children with metastatic neuroblastoma or adults with bronchogenic carcinoma.

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