Eye Movements
The accurate control
of eye movements involves a number of different structures, from the
extraocular muscles to the frontal cortex, and failure to achieve this control
results symptomatically in either double vision (diplopia), blurred vision or
oscillopsia (perception of an oscillating image or environmental movement). In
clinical practice, disruption of the final pathway from the oculomotor nuclei
(third, fourth and sixth cranial nerves) to the extraocular muscle represents
one of the major causes of diplopia (e.g. myasthenia gravis; see
Chapter 16), as does inflammation (e.g. multiple sclerosis) in
the medial longitudinal fasciculus (MLF) pathway linking the oculomotor nuclei.
Types of eye movement
There are three major
types of eye movement.
· Smooth pursuit or the following of a target
accurately – which is controlled primarily by posterior parts of the cortex in
conjunction with the cerebellum.
· Saccadic eye movements – where there is a sudden shift of
the eyes to a new target and which are controlled by more anterior cortical
areas, the basal ganglia and superior colliculi in the midbrain.
· Sustained gaze – where the eyes are fixed in one
direction and which is primarily a function of the brainstem (especially the paramedian
pontine reticular formation [PPRF] and rostral interstitial nucleus of the
MLF).
Eye movements, like the
motor system in general, can be either voluntary (when the command comes
from the frontal eye field) or reflex (when the command originates from
subcortical structures and posterior parietal cortex).
Manifestations of
disordered eye movement include a loss of conjugate movements; broken pursuit
movements; inaccurate saccades; gaze palsies; and nystagmus. Nystagmus is
defined as a biphasic ocular oscillation containing an abnormal slow and
corrective fast phase, the latter defining the direction of the nystagmus.
Anatomy and
physiology of central nervous system control of eye movements
· The frontal eye fields (FEF;
predominantly Brodmann’s area 8) are found anterior to the premotor cortex
(PMC; see Chapter 38). Stimulation of this structure produces eye movements,
typically saccades, to the contralateral side, and may be seen clinically in
some epileptic patients.
Damage to this area
reduces the ability to look to the contralateral side so the patient tends to
look towards the side of the lesion. The FEF primarily receives from the
posterior parietal cortex and projects to the superior colliculus, other
brainstem centres and the basal ganglia.
· The posterior parietal cortex (corresponds
to Brodmann’s area 7 in monkeys) contains a large number of neurones responsive
to complex visual stimuli, as well as coding for some visually guided eye
movements (see Chapter 34). It is especially important in the generation of
saccades to objects of visual significance via its connections with the FEF and
superior colliculus.
Damage to this area, in
addition to causing deficiencies in visual attention and saccades to objects in
the contralateral hemifield, can impair smooth pursuit eye movements as
evidenced by loss of the optokinetic reflex. This is a reflex in which
the eyes fixate by a series of rapid movements on a moving target,
such as a rotating drum, with vertical lines as fixation targets.
• The
primary visual cortex and its associated extrastriate areas are involved
in both saccadic and smooth pursuit eye movements (see Chapters 25 and 26).
Their role in saccadic movements is primarily through the projection of V1 to
the superior colliculus, while the role in smooth pursuit is via extrastriate
area V5 (see Chapter 26), and projections to the FEF, posterior parietal cortex
and pons.
Damage to the striate
and extrastriate areas, in addition to producing field defects and specific
deficiencies of visual function (see Chapters 25 and 26), can also cause major
abnormalities in smooth pursuit eye movements.
• The
basal ganglia have a major role in the control of saccadic eye movements
(see Chapters 41 and 42). The caudate nucleus receives from the FEF and
projects via the SNr to the superior colliculus.
Abnormalities in
saccadic eye movements are seen clinically in a number of basal ganglia
disorders. For example, in Parkinson’s disease the saccadic eye
movements tend to be slightly inaccurate with undershooting to the target
(hypometric saccades).
• The
superior colliculus in the midbrain is important in the accurate
execution of saccades (see Chapter 25). The cerebellum and vestibular nuclei
have important complex inputs into the brainstem oculomotor system and are
especially important in the control of pursuit movements, as well as mediating
the vestibuloocular reflex (see Chapters 29, 40 and 49).
Damage to the cerebellum
and vestibular system causes broken pursuit eye movements, inaccurate saccades
and nystagmus.
• The
rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF)
is important in the control of vertical saccades and vertical gaze (both up-
and downgaze) and receives important inputs from the FEF and superior
colliculus while projecting to all the oculomotor nuclei.
Damage to this structure
or disruption of its afferent inputs therefore produces deficiencies in both
these eye movements, and this can occur in a number of conditions including
some neurodegenerative diseases.
• The
PPRF receives from the FEF, superior colliculus and cerebellum and is
responsible for horizontal saccades and gaze. It is thought that this structure
may work in conjunction with another pontine nucleus, the nucleus raphé
interpositus. This latter nucleus contains omnipause neurones, which
normally exert tonic inhibition on the burst neurones of the PPRF (and riMLF)
mediating the saccadic impulse.
Damage to nucleus raphé
interpositus results in random chaotic eye movements or opsoclonus.
In contrast, damage to the PPRF causes deficiencies in saccadic eye movements
as well as ipsilateral gaze paresis.
• The
MLF mediates conjugate eye movements through interconnections between
all the oculomotor nuclei and is commonly affected in some diseases of the
central nervous system (CNS) such as multiple sclerosis (see
Chapter 62).
A lesion in this
structure causes an internuclear ophthalmoplegia, with nystagmus
in the abducting eye and slowed or absent adduction in the other eye.
