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.