OCULOMOTOR RESPONSES
The brainstem nuclei and pathways that con-
trol eye movements lie in close association with
the ascending arousal system. Hence, it is un-
usual for a patient with a structural cause of
coma to have entirely normal eye movements,
and the type of oculomotor abnormality often
identifies the site of the lesion that causes
coma. A key clinical tenet of the coma exami-
nation is that, with rare exception (e.g., a co-
matose patient with a congenital strabismus),
asymmetric oculomotor function typically iden-
tifies a patient with a structural rather than
metabolic cause of coma.
Functional Anatomy of the
Peripheral Oculomotor System
Eye movements are due to the complex and
simultaneous contractions of six extraocular
muscles controlling each globe. In addition, the
muscles of the iris (see above), the lens accom-
modation system, and the eyelid receive input
from some of the same central cell groups and
cranial nerves. Each of these can be used to
identify the cause of an ocular motor distur-
bance, and may shed light on the origin of coma
(Figure 2–8).
93
Lateral movement of the globes is caused by
the lateral rectus muscle, which in turn is un-
Vestibular Cortex
Dorsolateral
Prefrontal Cortex
MT (V5)
Striate Cortex (VI)
MST
Angular gyrus
Supramarginal gyrus
SUPERIOR PARIETAL LOBULE
INFERIOR
PARIETAL
LOBULE
Parietal Eye Field
Frontal Eye Field
Supplementary Eye Field
Middle
Frontal
Gyrus
Inferior
Frontal Gyrus
MLF Vln
PPRF
PPRF
MVn
SVn
SCol
RIC
RIMLF
MLF
Illn
MLF
IVn
MLF
IVn
SCol
RIC
RIMLF
MLF
Illn
Superior Frontal
Gyrus
Figure 2–8. A summary diagram showing the major pathways responsible for eye movements. The frontal eye fields (A)
provide input to the superior colliculus (SCol) to program saccadic eye movements. The superior colliculus then provides
input to a premotor area for causing horizontal saccades (the paramedian pontine reticular formation [PPRF]), which in
turn contacts neurons in the abducens nucleus. Abducens neurons (VIn) send axons across to the opposite medial longi-
tudinal fasciculus (MLF) and to the opposite oculomotor nucleus (IIIn) to activate medial rectus motor neurons for the
opposite eye. Vertical saccades are controlled by inputs from the superior colliculus to the rostral interstitial nucleus of
the MLF (RIMLF) and rostral interstitial nucleus of Cajal (RIC), which act as a premotor area to instruct the neurons in
the oculomotor and trochlear (IVn) nuclei to perform a vertical saccade. Vestibular and gaze-holding inputs come to the
same ocular motor nuclei from the medial (MVN) and superior (SVN) vestibular nucleus. Note the intimate relationship
of these cell groups and pathways with the ascending arousal system.
60
Plum and Posner’s Diagnosis of Stupor and Coma
der the control of the abducens or sixth cranial
nerve. The superior oblique muscle and troch-
lear or fourth cranial nerve have more complex
actions. Because the trochlear muscle loops
through a pulley, or trochleus, it attaches be-
hind the equator of the globe and pulls it for-
ward rather than back. When the eye turns
medially, the action of this muscle is to pull the
eye down and in. When the eye is turned lat-
erally, however, the action of the muscle is to
intort the eye (rotate it on its axis with the top
of the iris moving medially). All of the other
extraocular muscles receive their innervation
through the oculomotor or third cranial nerve.
These include the medial rectus, whose action
is to turn the eye inward; the superior rectus,
which pulls the eye up and out; and the infe-
rior rectus and oblique, which turn the eye down
and out and up and in, respectively. It should
be clear from the above that, whereas impair-
ment of mediolateral movements of the eyes
mainly indicates imbalance of the two cog-
nate rectus muscles, disturbances of upward or
downward movement are far more complex to
work out, as they result from dysfunction of
the complex set of balanced contractions of the
other four muscles. This situation is reflected
in the central control of these movements, as
will be reviewed below.
The oculomotor nerve exits the brainstem
through the medial part of the cerebral pedun-
cle, then travels anteriorly between the supe-
rior cerebellar and posterior cerebral arteries.
It passes through the tentorial opening and
runs adjacent to the posterior communicating
artery, where it is subject to injury by posterior
communicating artery aneurysms. The nerve
then runs through the cavernous sinus and su-
perior orbital fissure to the orbit, where it di-
vides into superior and inferior branches. The
superior branch innervates the superior rectus
muscle and the levator palpebrae superioris,
which raises the eyelid, and the inferior branch
supplies the medial and inferior rectus and
inferior oblique muscles as well as the ciliary
ganglion. The abducens nerve exits from the
base of the pons, near the midline. This slender
nerve, which is often avulsed when the brain is
removed at autopsy, runs along the clivus,
through the tentorial opening, into the cavern-
ous sinus and superior orbital fissure, on its
way to the lateral rectus muscle. The trochlear
nerve is a crossed nerve (i.e., it consists of ax-
ons whose cell bodies are on the other side of
the brainstem) and it is the only cranial nerve
that exits from the dorsal side of the brainstem.
The axons emerge from the anterior medullary
vellum just behind the inferior colliculi, then
wrap around the brainstem, pass through the
tentorial opening, enter the cavernous sinus,
and travel through the superior orbital fissure
to innervate the superior oblique muscle.
Unilateral or even bilateral abducens palsy
is commonly seen as a false localizing sign in
patients with increased intracranial pressure.
Although the long intracranial course of the
nerve is often cited as the cause of its predis-
position to injury, the trochlear nerve (which
is rarely injured by diffusely increased intra-
cranial pressure) is actually longer,
94
and the
sharp bend of the abducens nerve as it enters
the cavernous sinus may play a more decisive
role. From a clinical point of view, however, it
is important to remember that isolated unilat-
eral or bilateral abducens palsy does not nec-
essarily indicate a site of injury. The emergence
of the trochlear nerve from the dorsal mid-
brain just behind the inferior colliculus makes
it prone to injury by the tentorial edge (which
runs along the adjacent superior surface of the
cerebellum) in cases of severe head trauma.
Thus, trochlear nerve palsy after head trauma
does not necessarily represent a focal brain-
stem injury (although the dorsal brainstem
at this level may be damaged by the same
process).
The course of all three ocular motor nerves
through the cavernous sinus and superior or-
bital fissure means that they are often damaged
in combination by lesions at these sites. Thus, a
lesion of all three of these nerves unilaterally
indicates injury in the cavernous sinus or supe-
rior orbital fissure rather than the brainstem.
Head trauma causing a blowout fracture of
the orbit may trap the eye muscles, resulting
in abnormalities of ocular motility unrelated to
any underlying brain injury. The entrapment
of the eye muscles is determined by forced
duction (i.e., resistance to physically moving
the globe) as described below in the exami-
nation.
Functional Anatomy of the Central
Oculomotor System
The oculomotor nuclei receive and integrate
a large number of inputs that control their
Examination of the Comatose Patient
61