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6
Posterior inferior cerebellar artery
Quadrigeminal artery
Closed medulla Pons
travel in the oculomotor nerve to the ciliary ganglion.
Dilation of the pupils occurs more indirectly via sympathetic stimulation of the pupillary dilator muscle by
postganglionic fibres from the superior cervical ganglion.
Damage to the sympathetic nervous system fibres results
in Horner’s syndrome, characterized by pupil constriction
(miosis), decreased facial sweating (anhydrosis) and ptosis (drooping of the eyelid). As the sympathetic pathway
has a complex course from the hypothalamus through
the brainstem to the T1 thoracic cord, and then on to the
superior cervical ganglion before returning to the head,
Paramedian artery
Posterior spinal artery
Vertebral artery
Anterior spinal artery
Open medulla
Anterior spinal artery
Vertebral artery
Fig. 6.7 Arterial blood supply to different regions of the
brainstem. Only one side is shown for clarity.
Short circumferential artery
Anterior inferior cerebellar artery
Superior cerebellar artery
Midbrain
Thalamoperforate artery
Medial posterior choroidal artery
damage anywhere along this pathway can cause this syndrome. Parasympathetic fibre damage results in dilated
pupils (mydriasis), as the fibres are located superficially
within the nerve. Ophthalmologists use short- acting
parasympathetic- blocking drugs that are derivatives of
atropine to dilate the pupil to examine the interior of
the eye.
If only the illuminated pupil constricts, then there
is damage to the crossing fibres, that is, damage in the
Box
Brainstem death
6.5
Brain cells require an adequate oxygen supply to function
normally. Prolonged hypoxia or ischemia may be fatal to
brain cells. Inadequate or incomplete resuscitation may
fail to revive brain functions and thus lead to brain death,
whereby all cortical function is lost, but brainstem reflexes
and spontaneous breathing are still present. This is termed
a persistent vegetative state.
In brainstem death, spontaneous breathing ceases and
there is a loss of reflexes. Cardiovascular function can be
artificially maintained for a short while but will eventually
deteriorate due to loss of function of the brainstem regulatory centres in the medulla. RF cell death leads to the loss
of cortical arousal, and thus the lack of brain activity and
hence brain death.
Several criteria must be met in order to diagnose brainstem death. There must be no pupillary, corneal, gag,
cough, caloric or doll’s eye reflex responses or response to
painful stimuli applied to cranial nerve territories. Absence
of spontaneous breaths can only be confirmed after hypercapnia tests, where the pCO2 is above 45 mmHg.
Brainstem death tests are performed by two doctors
either independently or together, and are then repeated,
prior to declaration of brain death. Before testing, any
analgesic medications, drugs, neuromuscular blockers, metabolic imbalances or lowered body temperature should be
allowed to clear or reverse, as these may account for brainstem inactivity. An EEG is not necessary.
CRANIAL NERVES AND THE BRAINSTEM
Table 6.5 Location and pathways of brainstem reflexes
Reflex Afferent arc Efferent arc Brainstem area
Pupillary light reflex CN II CN III (E- W) Midbrain
Accommodation reflex CN II CN III (E- W) Midbrain
Vestibulo- ocular reflex CN VIII CN III, IV, VI Pons- midbrain
Blinking—sound (startle), light
(e.g. flashing lights),
corneal touch
Jaw jerk CN V
Gag reflex CN IX CN X Medulla
CN, Cranial nerve; E-W, Edinger -Westphal nucleus; V1, ophthalmic and V3, mandibular branches of nerve V.
CN VIII
CN II
CN V
CN VII (eyelid close)
CNIII (eyelid open)
1
3
CN V
3
Pons
Midbrain
Pons
129THE NERVOUS SYSTEM
6
midbrain. If the optic nerve (afferent input) is damaged
on one side, both the direct and consensual reflexes will
be lost from the blind eye. The unaffected eye will show
both reflexes in response to light. If cranial nerve III (efferent output from the Edinger–Westphal nucleus) is damaged, both reflexes will be lost in the ipsilateral eye and
pupillary dilation will be observed in that eye. A unilateral fixed and dilated pupil is suggestive of increased
intracranial pressure, pressing on cranial nerve III.
The pupillary light reflex is a very important reflex
and occurs even when someone is unconscious. The circuitry involved in these reflexes is detailed in Chapter 7
(see Fig. 7.6B).
Accommodation reflex
The accommodation reflex is associated with cranial
CRANIAL NERVES AND THE BRAINSTEM
nerve III. At rest, the lens is thin to allow the eye to focus
on far objects. To focus on near objects, the lens must
thicken by a process called accommodation, as described
in Chapter 7. Accommodation and convergence of the
eyes are mediated by increased tone of the medial rectus
muscle and pupil constriction (contraction of the pupillae constrictor muscle), which occur together when a person views a close object. The pathway is as follows: optic
nerve afferents travel to the lateral geniculate nucleus
and then to the primary visual cortex in the occipital
lobe. For the efferent pathway, occipital lobe fibres project to cells of the accommodation centre in the midbrain.
From here, they travel to the Edinger–Westphal nucleus.
Parasympathetic fibre activation results in ciliary muscle
contraction, which shortens the suspensory ligament,
allowing relaxation of the lens and causing passive thickening. The accommodation centre also stimulates the
somatic motoneurons of the medial rectus muscles, producing convergence of the eyes to a near object, so that
focus is maintained (see Chapter 7 and Fig. 7.7C for further details).
Doll’s eye (vestibulo- ocular) reflex
This involves conjugate eye movements in response to
head movement. The normal response is for the patient’s
eyes to deviate in the opposite direction to head turning,
that is, if the head is briskly extended, the eyes go downwards and if the move is to the right, the eyes move to
the left. Normally the cortex inhibits these reflexes, but in
a comatose patient, they are disinhibited (see Chapter 8).
If present, they show that the pathway (medial longitudinal fasciculus) between the relevant nuclei in the pons
and midbrain is intact.
Gag reflex
Stimulation of the uvula (soft palate) or the lateral
walls of the oropharynx triggers closing of the trachea.
However, under general anaesthesia, this reflex does
not work and unconscious patients may vomit. Thus it
is important that no food or drink be consumed for 8–12
hours before an operation, otherwise vomit could enter
the trachea, which can be very dangerous.
Jaw jerk reflex
This monosynaptic reflex is the head equivalent of the
patella reflex in the spinal cord. It is mediated by the trigeminal nerve, and in normal people, the reflex is weak
or absent. It only becomes prominent if there is damage
to the descending corticobulbar fibres.
Blink reflexes
There are several blink reflexes (Table 6.5). Unilateral
touching of the cornea induces a bilateral blink
response. A novel (loud) sound induces a bilateral
blink (startle) response. Flashing lights induce a bilateral blink response. Stimulation of sensory afferents
from cranial nerves II or VIII activates RF interneurons
that project bilaterally to the facial and oculomotor
motor nucleus to innervate the eyelid muscles orbicularis oculi (closes eyelid) and evator palpebrae superioris (opens eyelid), respectively. However, corneal
sensory afferents activate spinal trigeminal neurons
that project to the facial and oculomotor nuclei bilaterally. In contrast, unconscious blinking functions to
maintain normal hydration of the eye, and this process
is likely mediated by the RF.
Brainstem lesions
Brainstem damage can be caused by vascular accidents, tumours or raised intracranial pressure that,
if not treated, ultimately leads to brain tissue herniation. Vascular lesions are the most common cause
and produce characteristic clinical syndromes (Table
6.6). Brainstem lesions are unique in that unilateral
lesions produce ipsilateral cranial nerve dysfunction
and contralateral dysfunction of the ascending tracts
(i.e. ipsilateral facial deficits and contralateral body
deficits). Certain common symptoms are associated
with brainstem lesions depending on their mediolateral location. Unilateral medial lesions in general
damage the corticospinal tract, producing contralateral spastic hemiplegia (partial paralysis of muscles,
increased muscle tone) and a Babinski sign. Damage
to the medial lemniscal pathway results in contralateral loss of light touch, position and vibration senses.
The level of a medial brainstem lesion is determined
by the involvement of the cranial motor nerves XII, VI
and III.
Unilateral lateral lesions, in general, produce five
common symptoms that are distinct from medial
symptoms:
1. Contralateral loss of pain/thermal sensation
(spinothalamic tract damage)
130 SYSTEMS OF THE BODY
Table 6.6 Unilateral vascular lesions of the medial brainstem
Brainstem area Possible vascular cause Specific symptoms (in addition to common symptoms)
6
CRANIAL NERVES AND THE BRAINSTEM
Medulla (Déjerine’s
syndrome)
Pons Basilar artery branches—paramedian
Midbrain (Weber’s
syndrome, Benedict’s
syndrome)
Table 6.7 Unilateral vascular lesions of the lateral brainstem
Brainstem area Possible vascular cause Specific symptoms (in addition to common symptoms)
Medulla (Wallenberg’s syndrome) Posterior inferior cerebellar artery CN IX–X
Pons Anterior inferior cerebellar artery CN V, VII, VIII
Midbrain Superior cerebellar artery, branches of
Anterior spinal/vertebral artery CN XII: ipsilateral weakness and wasting of the tongue muscles
CN VI: medial deviation of the eye (adduction paralysis)
pontine
Posterior cerebral artery CN III: ophthalmoplegia (eye deviates down and out)
posterior cerebral artery
Pontine RF (gaze centre): ipsilateral gaze paralysis
Cerebellar systems (pons): ipsilateral limb ataxia (loss of muscle co-
ordination) and nystagmus (rapid oscillation of the eyeballs)
Red nucleus: contralateral cerebellar ataxia
Dysarthria, dysphagia (difficulty in talking and swallowing),
hoarseness (ipsilateral vocal cord paralysis)
Loss of gag reflex
Partial loss of taste sensation
Deafness or tinnitus
Partial loss of taste sensation
Ipsilateral facial muscle paralysis, inability to shut eyes
Impaired salivation/lacrimation
Hyperacusis (abnormally loud sounds)
Jaw deviation during opening
Contralateral hemi- anaesthesia (ascending tracts’ damage)
Intentional tremor (damage to superior cerebellar peduncle)
2. Ipsilateral loss of facial skin sensation
(trigeminothalamic tract damage)
3. Horner’s syndrome: miosis, ptosis and impaired
sweating (descending autonomic fibres injured)
4. Nystagmus, nausea and vomiting (vestibular and
dorsal motor vagal nuclei injury)
5. Ipsilateral limb ataxia (cerebellar peduncle
damage)
As with medial lesions, the level is determined by the
involvement of cranial nerves V–X (see Table 6.7).
Bilateral motor and sensory signs are almost certainly
an indication of a brainstem lesion. Vascular occlusion
of the basilar artery, which supplies the majority of the
ventral part of the brainstem, can be catastrophic, resulting in quadriplegia and often death, due to respiratory
failure. It may result in ‘locked- in syndrome’, where the
patient presents with quadriplegia, muteness and facial
paralysis. The symptoms resemble coma, but the patient
can communicate through eye/eyelid movement (EEG
activity is normal). Damage to the basilar artery in the
midbrain region produces complex syndromes that
include visual hallucinations, gaze palsies and oculomotor dysfunction.
Damage to the MLF results in a (horizontal) gaze disorder called internuclear ophthalmoplegia. It disconnects
the abducens nucleus from the contralateral oculomotor nucleus and is characterized by disconjugate gaze
with nystagmus and impaired adduction of the abducting eye (Fig. 6.8). The most common cause in the young,
or if damage is bilateral, is multiple sclerosis; in older
patients, vascular disease is more likely.
Some brainstem syndromes are more common than
others. Wallenberg’s syndrome (Fig. 6.9) is the most common brainstem stroke, and many patients show gradual
recovery of function after this stroke. Anterior inferior
cerebellar artery infarcts are only a tenth of the prevalence of posterior inferior cerebellar artery strokes, and
Déjerine’s syndrome is rare, accounting for only 0.5% of
all brain strokes. Bilateral occlusions are rarer than unilateral occlusions and generally have a poorer prognosis.
Compression injuries of the brainstem by cerebellar or
cortical herniation are often fatal (see Chapter 9). In addition, hydrocephalus or a pineal gland tumour (pinealoma)
may cause Parinaud’s syndrome, which is characterized
131THE NERVOUS SYSTEM
6
Right eye Left eye
Convergence
Right eye Left eye
Midline
Abducens nuclei
Left lateral
gaze
MLF
Right lateral
gaze
CRANIAL NERVES AND THE BRAINSTEM
Fig. 6.8 Internuclear ophthalmoplegia results from a lesion in the medial longitudinal fasciculus (MLF) pathway, which connects the abducens
nucleus to the contralateral oculomotor nucleus. On the side of the lesion (left MLF, indicated by the ‘X’), the person is unable to adduct the
eye during contralateral gaze but is able to adduct the eye on convergence, thus distinguishing it from oculomotor nerve palsy. (Adapted from
Kingsley RE (2000). Concise Text of Neuroscience, 2nd ed. LWW.)
Fig. 6.9 Brainstem lesions resulting from vascular damage. Left
side: arrows demarcate damage to the medulla area supplied by the
posterior inferior cerebellar artery leading to symptoms associated
with Wallenberg’s syndrome. Right side: arrows demarcate damage in
the territory supplied by the anterior spinal artery.
by compression of the dorsal (tectum) midbrain region,
encompassing the superior colliculi and midbrain tegmentum. Symptoms include paralysis of upward gaze
and accommodation, fixed pupils and nystagmus.
Comments on the case history
This case (see Box 6.1) is an example of Weber’s syndrome caused by damage to the posterior cerebral artery
that supplies the ventral midbrain. This affects the corticospinal and corticobulbar tracts, red nucleus and fibres
of the oculomotor nerve.
The oculomotor nerve has somatic fibres that innervate all the extrinsic eye muscles that adduct and elevate
the eyeball and upper eyelid, and parasympathetic fibres
of the Edinger–Westphal nucleus that innervate the ciliary and pupillary muscles regulating the processes of
accommodation and pupil constriction. Damage to this
nerve causes the eye to deviate down and out, due to
the unopposed action of lateral rectus (abductor) and
superior oblique (depressor) muscles innervated by the
abducens and trochlear nerves, respectively. Paralysis of
the superior levator muscle causes severe ptosis due to
the unopposed action of the orbicularis oculi (innervated
by the facial nerve). In this case, the left and right optic
nerves and right oculomotor nerve are intact, but the left
oculomotor nerve (including its parasympathetic component) is not. A fully dilated, non- reactive pupil is due
to the unopposed action of the dilator pupillae muscle
(supplied by the sympathetic nervous system). Pupils
are always monitored during head injury cases because
rapidly increasing intracranial pressure (often resulting
from an acute cranial bleed) compresses the oculomotor
nerve against the temporal bone. Autonomic nervous
system fibres reside superficially in this nerve, and these
are affected first so that the pupil dilates progressively on
the affected side. Pupillary dilation is an urgent indication of surgical decompression of the brain.
The oculomotor nerve forms the efferent arc of two
important visual reflexes. The first is the pupillary light
reflex that results in constriction of the iris muscle of
the pupil to bright light. This reflex involves four sets of
Oculomotor
nuclei
Convergence
centre
132 SYSTEMS OF THE BODY
6
neurons. Light activates retinal afferents (CN II) that terminate in the midbrain pretectal nuclei. Axons from this
area innervate both Edinger- Westphal nuclei; preganglionic parasympathetic fibres from the Edinger- Westphal
nucleus travel in the oculomotor nerve and synapse in
the ciliary ganglion, whose postganglionic fibres innervate the constrictor muscle of iris (sphincter pupillae).
The second reflex affected in this case is the accommodation reflex. As the pupil is fixed, it fails to respond
to changes in depth of the visual field; thus vision is
blurred in the affected eye.
The vascular lesion has also damaged the left
descending upper motoneuron fibres of the corticobulbar and corticospinal tracts, resulting in muscle paralysis/paresis and abnormal reflexes. This is manifest
in the inability to smile voluntarily on the right (contralateral) side. There is no direct damage to the facial
nerve because paralysis would affect all the muscles
of facial expression, and the other facial nerve motor
tests (Chapter 3) would reveal abnormal responses.
An upper motoneuron lesion affecting the corticobulbar tract results in contralateral lower facial muscle
paralysis/paresis, since the upper facial muscles are
innervated by both the contralateral and ipsilateral
corticobulbar tracts, and thus remain innervated by
the contralateral side. Similarly, impairment of the left
corticospinal tract results in right- sided hyperreflexia
(due to disinhibition of lower motoneurons), a Babinski
sign and increased muscle tone. The prognosis for this
patient is poor, and any improvement in functional
recovery is unlikely.
Self- assessment case study
A 46- year- old woman, a mother of four who has been
taking oral contraceptives for the past 15 years, arrived
at Accident and Emergency presenting with nausea and
vomiting that had been ongoing for the past few days.
Neurologic testing further revealed an absence of a left
side gag reflex, dysphagia and Horner’s syndrome.
Sensory testing showed a loss of pinprick sensation on
the left side of her face and the right side of her neck,
limbs and trunk. Reflexes were normal, as was muscle
strength and tone, but left- sided ataxia was noted in
the arm and leg. She was admitted to hospital and discharged a week later. At an outpatient appointment 9
months later, she was asymptomatic.
• Accountforthesymptomsdescribedinthispatient
This patient presents with symptoms that are consistent with lateral brainstem injury, specifically
Wallenberg’s syndrome. Several cranial nerve nuclei are
affected and a dissociated sensory deficit involving the
face and body is present. Damage to the spinal trigeminal nucleus/tract results in ipsilateral loss of pain and
temperature sensation to the face, and contralateral loss
of pain and temperature sensation from the body is due
to damage of the spinothalamic tract. Dysphagia and
loss of the gag reflex indicate involvement of the glossopharyngeal and vagus nerve nuclei (nucleus ambiguus),
while damage to the inferior vestibular nucleus and dorsal motor vagal nucleus produces nausea and vomiting,
respectively. Ataxia (loss of coordination) occurs because
of injury to the inferior cerebellar peduncle. Horner’s
symptoms are ptosis (droopy eyelid), miosis (small
pupils) and anhydrosis (warm dry facial skin), and are
due to damage of the descending sympathetic fibres
that run in the lateral part of the medullary tegmentum.
Reflexes and motor strength were normal as the pyramidal tract is unaffected.
• Whatisthemostlikelycauseofthelesion?
The most likely cause is a vascular lesion affecting the
posterior inferior cerebellar artery. A tumour is unlikely,
as the symptoms are sudden in onset and tumour
symptoms present as progressive worsening of affected
structures.
• Whyistheuseoforalcontraceptivesrelevant?
In some patients who suffer brainstem strokes, there
are predisposing factors such as hypertension, diabetes
and transient ischaemic attacks. In women the use of
the pill has been associated with cerebrovascular occlusive disease, especially in women who smoke or have
hypertension.
CRANIAL NERVES AND THE BRAINSTEM
133THE NERVOUS SYSTEM
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THE VISUAL SYSTEM
Chapter summary
1. The eye is a sensory organ divided into two segments. The anterior
segment refracts light rays through the cornea and lens into the
posterior segment to converge onto the retina, which contains the
photoreceptors. The captured image is back- to- front and inverted.
2. The retina comprises of photoreceptors (rods and cones) and bipolar,
amacrine and retinal ganglion cells. Rods are sensitive to dim light
levels and are monochromatic, while cones use daylight to create
colour vision. Cones are concentrated in the centre of the retina
(fovea), while rods are more prevalent around the periphery.
3. Visual processing of motion, colour and shape begins in the retina.
Processes related to each of these characteristics are relayed as
parallel streams to the visual cortex. Information from the nasal
side of the retina crosses at the optic chiasm to project onto the
contralateral side, while the temporal retina field remains ipsilateral.
Retinal ganglion cell axons synapse in the lateral geniculate nuclei
(thalamus). From here, information is relayed to the primary
visual cortex, so these cells receive information from both eyes.
Information is distributed to the visual association cortices to build
a picture of the image and to other cortical regions for object
identification and location.
7
4. Damage to the optic nerve produces unilateral, ipsilateral loss of
vision; damage at the optic chiasm results in bitemporal hemianopsia
(tunnel vision), and after the chiasm causes contralateral
homonymous hemianopsia.
7
Introduction
‘Beauty is in the eye of the beholder.’ Most of our ideas
about our surroundings and our memory of them are
based on sight. But how do we see and assign emotional
meaning to what we see? Vision is the process by which
the brain receives light from the outside world and
converts it into a recognizable percept. This is a com-
THE VISUAL SYSTEM
plex process that starts with the focusing of light rays
onto the retina—the specialised sensory component of
the eye. This two- dimensional image is then conveyed
to regions of the brain that take different properties of
the image, such as colour, form, movement and depth,
and seamlessly convert them into a three- dimensional
percept. Furthermore, objects are recognized in many
different orientations, under a wide range of lighting
conditions, and, when they are at different distances
from the observer, at a variety of sizes. Nearly half of the
cerebral cortex is involved in visual processing, suggesting that vision is the most complex task that the brain
performs.
As humans are very visually oriented, visual deficits
have profound effects on daily life. Depending on the
cause, the deficit can be monocular (restricted to one eye)
or binocular (affecting both eyes) (Table 7.1). The World
Health Organization estimates that 2.2 billion people
worldwide have some form of visual impairment. Nearly
60% of these are elderly (>60 years old) and 5% are
under the age of 14 years. It is estimated that almost 50%
of visual deficits could be remedied with a simple visit to
the optician or appropriate drugs.
The three main causes of visual loss in the developed
world are uncorrected refractive errors, cataracts and
glaucoma; in the less developed world, cataracts and
infections such as trachoma and river blindness (onchocerciasis) account for 75% of blindness cases. The latter
Table 7.1 Some causes of blindness
Monocular causes Binocular causes
Vascular
• Transientischaemicattack
• Amaurosisfugax
Inflammation
• Temporalarteritis
• Opticneuritis
Trauma
• Opticnervedamage
• Retinadetachment
Disease
• Cataracts
• Multiplesclerosis
Trauma to visual pathway
(post- chiasm)
• Stroke
• Tumour(e.g.pituitary
adenoma)
• Raisedintracranialpressure
(papilloedema)
Disease
• Diabetes
• Trachoma
• Glaucoma
• Riverblindness
• Maculardegeneration(oldage)
• Cataracts
Genetics
• Retinitispigmentosa(X-linked)
two diseases cause inflammation of the conjunctiva and
scarring of the cornea, which eventually leads to blindness. River blindness affects over 20 million people
worldwide, and in parts of Africa produces blindness
rates of up to 35%. It can be treated (and prevented for 9
months) with a single dose of ivermectin, a drug which
kills the larvae of the Oncocherca volvulus filarial worm
that causes the disease. Trachoma is easily treated with
antibiotics such as tetracycline. Uncorrected refractive
errors (e.g. myopia and presbyopia) are common to both
adults (see Box 7.1) and children, and the annual global
costs of productivity losses associated with uncorrected
myopia and presbyopia are estimated to be US$244 billion and US$25.4 billion, respectively.
Structure of the eye
Fig. 7.1 details the structure of the eye. It consists of three
layers and two regions: (1) the anterior segment (comprising the cornea, anterior chamber, posterior chamber,
and lens) is concerned with light refraction and focusing
and (2) the posterior segment, consisting of the choroid
and, most importantly, the retina, where light waves are
converted into electrical impulses that are transmitted
via the optic nerve to the brain.
The eyeball has three layers. The outermost layer is
the sclera. This white, opaque, fibrous layer protects the
eye and allows attachment of the muscles controlling
Box
Case history
7.1
Fifty- five- year- old Mr Magoo visits his optician for a sight
test, as he is finding it difficult to read with his old pair of
glasses and thinks that he may need a new pair. When he
was younger, his eyesight was good, except that he was
colour- blind and could not distinguish red from green. His
optician measures his visual acuity and examines his eye
with an ophthalmoscope. He also measures the intraocular
pressure. He finds that there are no signs of raised intraocular pressure or visual field defects, but that Mr Magoo’s
myopia has got significantly worse. He prescribes a new
pair of glasses.
This case gives rise to the following questions:
1. What is the structure of the eye, and what are the
pathways that convey visual information?
2. Can defects in vision indicate specific defects in the
visual pathways?
3. How does the eye respond to light?
4. What is visual acuity, why does it decline with age and
how can it be remedied?
5. How is colour perceived and processed by the visual
system, and what are the causes of colour- blindness?
6. Which areas of the brain are involved in processing
visual information, and how is this information coded?
136
SYSTEMS OF THE BODY
7
Suspensory ligaments
Optic nerve
the movement of the eye—the extraocular muscles.
The movement of these muscles is controlled by cranial
nerves III, IV and VI. At the anterior pole of the eye, the
sclera becomes the conjunctiva (white of the eye), and
this merges with the transparent cornea that allows light
into the eye. The cornea is the eye’s primary refractive
surface. It is richly innervated with nociceptive fibres,
which, in response to irritation, trigger blinking and the
secretion of tears from the lacrimal gland, keeping the
cornea free of dust.
The middle layer consists of the choroid, the ciliary body and the iris; together they form the uvea. The
choroid lines the whole of the posterior segment, except
where the optic nerve leaves the eye. It is a highly vascularized brown membrane. The colour pigment is produced by the melanocytes of the retinal epithelium; these
absorb light that has not been detected by the retina and
prevents it from being scattered back onto the retina and
confusing the image.
At the junction of the anterior and posterior segments
of the eye, and continuous with the choroid, is the ciliary
body. This consists of radial and circular smooth muscle
fibres—the ciliary muscles—which are under autonomic
nervous system control and involved in changing the
shape of the lens during the process of focusing. The epithelial cells of the ciliary body continually produce and
secrete a clear fluid—the aqueous humour—into the small
posterior chamber. The fluid then flows through the pupil
into the anterior chamber, providing nutrients to the lens
and cornea. It eventually drains into the venous blood
through the canal of Schlemm, which is a lymphatic- like
vessel. Production and reabsorption of this fluid produce the intraocular pressure in the anterior compartment, which is normally 13–29 mm Hg. Blockage of this
reabsorption leads to glaucoma by causing ocular hypertension. This reduces blood flow in the retinal capillaries
(Fig. 7.2C), and the subsequent ischemia causes damage to
the retina and may lead to blindness. The suspensory ligaments extend from the ciliary body to attach to the lens.
Contraction of the ciliary muscles pulls on the suspensory
ligaments and can change the shape of the lens. In the
relaxed eye the suspensory ligaments maintain the lens in
a stretched, flattened shape.
The iris is the coloured part of the eye and extends
from the ciliary body across the front of the lens, leaving
a circular aperture—the pupil—where light passes from
the anterior chamber into the lens. The size of the pupil
controls the amount of light entering the lens and posterior segment, and this is determined by the contraction
of the muscles of the iris.
The lens sits at the junction of the anterior and posterior segments of the eye and is a transparent biconvex
structure. It is a secondary refractor of light waves and
acts as a fine control for focusing light onto the retina,
just like the lens of a camera. As in a camera, the image
on the retina is reversed and upside down. The lens is
surrounded by a flexible capsule and contains concentric
layers of lens fibres, which contain transparent proteins,
called crystallins. Cataracts occur when the lens of the
eye becomes opaque (Fig. 7.2F). The most usual cause
of this is old age, when the crystallin proteins become
oxidized and aggregate. Cataracts are treated by surgical replacement of the affected lens with a synthetic lens.
High levels of ultraviolet light increase the rate at which
the lens becomes opaque; hence the higher prevalence of
cataracts in countries at low latitudes.
The posterior segment of the eye is filled with a transparent, thick gelatinous fluid called vitreous humour,
THE VISUAL SYSTEM
Lateral rectus muscle
Sclera
Canal of Schlemm
Posterior chamber
Anterior chamber
(aqueous humour)
Cornea
Lens
Iris
Ciliary body
Conjunctiva
Medial rectus muscle
Optic disc
Fig. 7.1 Horizontalsectionthroughtherighthumaneye.
Retina
Vitreous humour
Fovea
Macula lutea
Choroid
THE NERVOUS SYSTEM
137
7
composed of fine collagen fibres and large amounts of
water. This maintains the shape of the eyeball and also
contains phagocytic cells, which remove any debris that
might accumulate in the posterior segment and interfere
with light transmission.
The innermost layer of the eye—the retina—covers the
choroid, ciliary body and posterior face of the iris. The
retina can be investigated during examination of the eye
(Box 7.2) and consists of two layers. The outer pigmented
THE VISUAL SYSTEM
layer, like the choroid, prevents light scattering and also
provides a source of vitamin A, which is needed by the
light- gathering cells. Vitamin A deficiency leads to night
blindness (Box 7.3) due to a lack of the protein rhodopsin used by some photoreceptors. The inner neural layer
of the retina consists of the light- gathering cells—photoreceptors and associated neurons—as well as glial cells
and a dense capillary network. Apart from the photoreceptors, there are four other neuronal types—bipolar and
ganglion cells, which are the first- and second- order neurons of the visual pathway, and horizontal and amacrine
cells, which are interneurons (see Table 7.5). The centre of
the retina is called the macula lutea (yellow spot), which
RA
OD
A
B
C
E
Fig. 7.2 Ophthalmoscopeimages. (A)Anormaleye,showingtheopticdisc(OD)andtheretinalarteries(RA);(B)abnormalfundus,showing
papilloedemaduetobulgingoftheopticdisc(arrow);(C)glaucoma,wheretheopticcupislargeranddeeperthannormal(arrow);(D)macular
degeneration,wherethemacularegionisspottyorabsent(arrows);(E)cottonwool-likedepositsareseenintheeyearoundbloodvessels
(arrows)inhypertensivediabeticneuropathy;(F)abnormallensfunction—cataract.(A–E,FromMunroJ,EdwardsC(1995).eds.Macleod’sClinical
Examination.9thed.ChurchillLivingstone.D,Fromwww.eyesearch.com.)
138 SYSTEMS OF THE BODY
D
F