The pupils Medical Assignment Help

Sympathetic impulses from fibres in the nasociliary nerve stimulate the dilator muscle of the pupil (dilator pupillae).
Preganglionic sympathetic fibres to the eye (and face) {yiginate in the hypothalamus, pass uncrossed through re midbrain and lateral medulla and emerge finally from the spinal cord at Tl (close to the lung apex). Postganglionic fibres begin in the superior cervical ganglion. These pass to the pupil in the nasociliary nerve from a plexus surrounding the internal carotid artery. Those fibres to the face (sweating and pilo-erection) form a plexus surrounding the external carotid artery. This arrangement is of clinical importance in Horner’s syndrome. Parasympathetic impulses from the ciliary ganglion in the short ciliary nerves to the sphincter muscle of the pupil (sphincter pupillae) cause the pupil to constrict. An outline of the arrangement of parasympathetic fibres to the pupils and the mechanism of the light reflex is shown.

The light reflex

Afferent fibres in each optic nerve (some crossing in the chiasm, see Fig. 18.5) pass to both lateral geniculate bodies and relay to the Edinger-Westphal nuclei via the pretectal nucleus. Efferent (parasympathetic) fibres from each Edinger- Westphal nucleus pass via the third nerve to the ciliary ganglion and thence to the pupil.
Light constricts the pupil of the eye being tested (direct reflex) and the contralateral pupil (consensual reflex).

The convergence reflex

Fixation on a near object requires convergence of the ocular axes and is accompanied by pupillary constriction. The afferent fibres in each optic nerve, which pass through both lateral geniculate bodies, also relay to the convergence centre. This centre receives la spindle afferent fibres from the extraocular muscles-principally the medial recti, which are innervated by the third nerve. The efferent route is from the convergence centre to the Edinger-Westphal nucleus, ciliary ganglion and pupils. Voluntary or reflex fixation on a near object is thus accompanied by appropriate convergence and pupillary constriction.

Clinical abnormalities of the pupils

DEGENERATIVE CHANGES.IN OLD AGE. The pupil tends to become small (3-3.5 mrn) in old age (senile miosis) and may be irregular; a bright light is necessary to demonstrate constriction and the convergence reflex is sluggish. A slight difference between the size of the pupils is common (physiological anisocoria) but the changes may cause confusion with the Argyll Robertson pupil.
THE ARGYLL ROBERTSON PUPIL. This is a small, irregular (3 mm or less) pupil that is fixed to light, but constricts on convergence. The lesion is believed to be in the area surrounding the aqueduct. The Argyll Robertson pupil is (almost) diagnostic of neurosyphilis. Similar changes are occasionally seen in diabetes mellitus.
THE MYOTONIC PUPIL (HOLMEs-ADIE PUPIL). This is a dilated pupil seen most commonly in young women. It is usually unilateral. There is no reaction (or a very slow reaction) to a bright light and also an incomplete constriction to convergence. The condition is due to denervation in the ciliary ganglion. The myotonic pupil is of no pathological significance but is often associated with diminished or absent tendon reflexes.
HORNER’S SYNDROME. This syndrome is due to interruption of sympathetic fibres to one eye. It presents as unilateral pupillary constriction with slight relative ptosis and enophthalmos. The conjunctival vessels may be injected. There is loss of sweating of the same side of the face or body; the extent depends upon the level of the lesion. The syndrome indicates a lesion of the sympathetic pathway on the same side. Causes of Horner’s syndrome.
The level of the lesion is indicated by the distribution of the loss of sweating:
CENTRAL LESIONS affect sweating over the entire half of the head, arm and upper trunk.
LESIONS OF THE NECK PROXIMAL TO THE SUPERIOR CERVICAL GANGLION cause diminished sweating on
the face.
LESIONS DISTAL TO THE SUPERIOR CERVICAL GANGLION do not affect sweating at all. Pharmacological tests may indicate the level of the lesion. For example, a lesion distal to the superior cervical ganglion causes denervation hypersensitivity of the pupil, which dilates when 1 : 1000 adrenaline is instilled. This dose has little effect on the normal pupil or a proximal lesion. In clinical practice the test is of limited value. Other abnormalities of the pupils seen in coma are discussed.

The pupils: afferent and parasympathetic efferent pathways.

The pupils: afferent and
parasympathetic efferent pathways.

Hemisphere and brain stem lesions
Massive cerebral infarction
Pontine glioma
Lateral medullary syndrome
‘Coning’ of the temporal lobe
Cervical cord lesions
Syringomyelia
Cord tumours
T1 root lesions
Bronchial neoplasm (apical)
Apical tuberculosis
Cervical rib
Brachial plexus trauma
Sympathetic chain in the neck
Following thyroid/laryngeal surgery
Carotid artery occlusion
Neoplastic infiltration
Cervical sympathectomy
Miscellaneous
Congenital
Migrainous neuralgia (usually transient)

THE OCULAR MOVEMENTS AND, THIRD, FOURTH AND SIXTH CRANIAL NERVES

The control of eye movement can be divided into:
1 The central upper motor neurone mechanisms, which drive the normal yoked parallel movements of the eyes (conjugate gaze)
2 The oculomotor, abducens and trochlear nerves and the muscles they supply

Conjugate gaze

Fast voluntary and reflex eye movements originate in each. frontal lobe. Fibres pass in the anterior limb of the internal capsule and cross in the pons to end in the centre for lateral gaze (paramedian pontine reticular formation (PPRF)) (Fig. 18.6a), which is close to each sixth nerve nucleus. It also receives fibres from:
THE IPSILATERAL OCCIPITAL CORTEX. These pathways are concerned with movements to track or pursueobjects within the visual fields.
BOTH VESTIBULAR NUCLEI. These pathways are concerned with the relationship between eye movements and the position of the head and neck.
Lateral eye movements are coordinated from the centre of lateral gaze through the medial longitudinal fasciculus (MLF) (Fig. 18.6b). Fibres from the centre pass to both the ipsilateral sixth nerve nucleus and, having crossed the midline, the opposite third nerve nucleus via the MLF. Each sixth nerve nucleus (supplying the lateral rectus) and the opposite third nerve nucleus (supplying the medial rectus and others) are thus linked. The eyes move with parallel axes and at the same velocity.

Abnormalities of conjugate lateral gaze

A destructive lesion of one side of the brain allows the eyes to be driven laterally by the intact opposite pathway. A destructive frontal-lobe lesion (e.g. an infarct) causes failure of conjugate lateral gaze to the side opposite to the lesion. In an acute lesion the eyes are often deviated past the midline to the side of the lesion and therefore look towards the normal limbs. There is usually a contralateral hemiparesis.
An irritative frontal-lobe lesion (e.g. an epileptic focus), by stimulating the opposite lateral gaze centre, drives the eyes away from the side of the lesion. A unilateral destructive brain stem lesion involving the centre causes failure of horizontal conjugate gaze towards  the side of the lesion. There is usually a hemiparesis and the eyes are deviated towards the paralysed limbs.

(a) Conjugate lateral gaze: principal input to paramedian pontine reticular formation, or 'centre for lateral gaze'.

(a) Conjugate lateral gaze: principal input to
paramedian pontine reticular formation, or ‘centre for lateral gaze’.

Doll’s head reflexes and skew deviation

These are of diagnostic value in coma. Internuclear ophthalmoplegia Internuclear ophthalmoplegia (INO) is one of the commoner complex brain stem signs that involve the oculomotor system. It is due to a lesion within the MLF. It is a common sign in MS. When present bilaterally it is almost pathognomonic of MS. Unilateral lesions are also caused by small brain stem infarcts. In a right INO there is a lesion of the right MLF. On attempted left lateral gaze the right eye fails to adduct. The left eye develops coarse nystagmus in abduction.

The side of the lesion is on the side of impaired adduction, not on the side of the nystagmus.

Abnormalities of vertical gaze

A failure of up-gaze is caused by an upper brain stem lesion, such as a supratentorial mass pressing from above, or a tumour of the brain stem (e.g. a pinealoma). When the pupillary convergence reflex fails, this combination is called Parinaud’s syndrome. Defective up-gaze also occurs in certain degenerative disorders (e.g. progressive supranuclear palsy). Impairment of up-gaze also occurs as part of normal ageing.

Weakness of the extraocular muscles (diplopia)

Diplopia (double vision) implies that there is weakness of one or more of the extraocular muscles. The cause is usually a lesion of the third, fourth or sixth cranial nerves (or a combination of these) or their nuclei, or disease of the neuromuscular junction (myasthenia gravis) or the ocular muscles.

Squint (strabismus)

This is the appearance of the eyes when the visual axes fail to meet at the fixation point.
PARALYTIC SQUINT. Paralytic or ‘incornitant’ squint occurs when there is an acquired defect of the movement of an eye. There is a squint (and hence diplopia) maximal in the direction of action of the weak muscle.

NON-PARALYTIC SQUINT. Non-paralytic or ‘concomitant’ squint describes a squint beginning in childhood in which the angle between the visual axes does not vary when the eyes are moved, i.e. the squint remains the same in all directions of gaze. Diplopia is almost never a symptom. The deviating eye (the one that does not fixate) usually has defective vision; this is called ‘amblyopia ex anopsia’.
Non-paralytic squint may be latent, i.e. only visible at certain times, such as when the patient is tired. The cover test is used to assess squint and to recognize latent squint. The patient is asked to fix on an object. The eye that is apparently fixing the object centrally is covered. If the uncovered eye makes any movement to take up fixation, then a squint must have been present. The test is repeated with the opposite eye-the fixing eye will not move when the other, squinting, eye is covered or uncovered.

The oculomotor nerve (third cranial nerve)

The nucleus of the third nerve lies ventral to the aqueduct in the midbrain. Efferent fibres to four external ocular muscles (the superior, inferior and medial recti, and the inferior oblique), the levator palpebrae superioris and the sphincter pupillae (parasympathetic) enter the orbit through the superior orbital fissure.
The common causes of an oculomotor nerve lesion are given. Signs of such a lesion are:
• Unilateral complete ptosis
• The eye facing ‘down and out’
• Fixed and dilated pupil
‘Sparing of the pupil’ means that the parasympathetic fibres which run in a discrete bundle on the superior surface of the nerve are undamaged by the lesion and the pupil reacts normally.
In diabetes, infarction of the nerve usually spares the pupil. In a third nerve palsy the eye can still abduct (sixth nerve) and ‘intort’ (fourth nerve). When a patient with a right third nerve lesion attempts to converge and look downwards, the conjunctival vessels of the right eye can be seen to twist clockwise; this is ‘intortion’ and indicates that the trochlear nerve is intact.

Aneurysm of the posterior communicating artery ‘Coning’ of the temporal lobe.
Infarction of the nerve
In diabetes mellitus
Atheroma
Midbrain infarction
Midbrain tumour

The trochlear nerve (fourth cranial nerve)

The trochlear nerve supplies the superior oblique muscle. An isolated fourth nerve lesion is a rarity. The head is tilted away from the side of the lesion. The patient complains of diplopia when attempting to look down and away from the affected side. The abducens nerve (sixth cranial nerve).
The abducens nerve supplies the lateral rectus muscle. In a sixth nerve lesion there is a convergent squint with diplopia maximal on looking to the side of the lesion. The eye cannot be abducted beyond the midline. There are many causes of a sixth nerve lesion. The nerve may be involved in the brain stem, e.g. MS. In raised intracranial pressure it is compressed against the tip of the petrous temporal bone. The nerve sheath may be infiltrated by tumours, particularly nasopharyngeal carcinoma. An isolated sixth nerve palsy due to infarction may occur in diabetes mellitus. A sixth nerve lesion is a common sequel of head injury.

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