RAMB - Julho 2016

morim

RLO

380

ssoc

ras

2016; 62(4):377-384

parasympathetic pathways, the effect on pupil size, mio-

sis or mydriasis, will depend on the action of the system

affected the least or still intact. The pupillary reflex con-

sists of the pupillary contraction after light stimulation

via the parasympathetic pathway.

As the areas related to consciousness control are ad-

jacent to these pathways, pupil changes can help us in

the differentiation and location of possible causes of coma.

Hypothalamic lesions, especially in the posterior and

ventrolateral region, can produce ipsilateral pupillary

constriction, usually associated with ptosis and anhidro-

sis (Horner syndrome). Thalamus lesions can lead to small,

reactive pupils, known as diencephalic pupils.

Mesencephalic lesions can produce three types of pu-

pil changes depending on the location of the damage:

dorsal tectal region lesions, lesions that disrupt pupillary

reaction to light, pupils with medium or little dilation (5

to 6 mm), and fixed pupils with preservation of the ac-

commodation reflex. Pupillary size oscillations may oc-

cur (hippus) alongside maintenance of the ciliospinal re-

flex; mesencephalic nuclear lesions, usually affect both

the sympathetic and parasympathetic pathways, leading

to medium-fixed pupils (4 to 5 mm), generally a little ir-

regular, and generally related to transtentorial hernia-

tion; lesions of bilateral cranial nerve III lead to paralyt-

ic mydriasis, usually associated with uncal herniation.

Pontine lesions lead to extreme bilateral miosis (<1 mm),

with preservation of the pupillary light reflex, which is

very hard to perceive. Pinpoint pupils due to pontine hem-

orrhages may result from sympathetic pathway lesions

and irritation of parasympathetic pathways.

In patients in a coma related to toxic-metabolic chang-

es, in general the pupils are isochoric and reactive to light,

except in the terminal stage. The actions of drugs wheth-

er local or systemic can lead to pupil changes due to their

effect on the sympathetic or parasympathetic pathways.

Anticholinergic drugs such as atropine or scopolamine,

can lead to pupillary dilation. Opiates (heroin and mor-

phine) can lead to miosis, similar to pontine hemorrhage.

Barbiturates may lead to fixed pupils. Data from the clin-

ical history and other data from the neurological exam

can help us in the differentiation of these cases. Post-ic-

tal patients usually present mydriatic but reactive pupils.

Ocular motility

Ocular motility depends on the integrity of structures lo-

cated in the brain, cerebellum and brainstem. Since we

cannot evaluate voluntary ocular motility in unrespon-

sive patients, we must evaluate the integrity of reflex path-

ways located in the brainstem. The absence of changes in

ocular motility means that the region located between the

vestibular nuclei, in the medulla oblongata-pons junction,

up to the oculomotor nuclei in the midbrain are intact.

In coma patients, we must evaluate three aspects with

respect to ocular motility: (1) primary gaze at rest, to as-

sess the presence of deviations; (2) observe the presence

of spontaneous eye movements and (3) test eye movements.

The presence of deviations in the rest position can

provide us with evidence of cranial nerve palsies. Conju-

gate deviations of the lateral gaze may be the result of le-

sions from the cortex to the contralateral pontine retic-

ular formation, which is common in strokes. Disconjugate

deviations of the lateral gaze may reflect abducens and

oculomotor nerve paralysis, or internuclear ophthalmo-

plegia. The presence of downward eye deviations can mean

brainstem lesions, compression of the mesencephalic tec-

tum, which may be present in hydrocephalus. Thalamic

and subthalamic lesions can lead to conjugate deviation

both upward and downward. Other conditions that can

lead to upward deviation of the eyes are sleep, epileptic

seizure, syncope, apnea in Cheyne-Stokes respiration,

bleeding in the cerebellar vermis, ischemia or brainstem

encephalitis. Skew deviation is a vertical misalignment of

the eyes, usually corresponding to brainstem or cerebel-

lar lesions.

The observation of spontaneous eye movements can

offer important information. The presence of roving

movements, consisting of slow and spontaneous conju-

gate movements of the lateral gaze, can indicate the in-

tegrity of the oculomotor pathways and their connec-

tions. The presence of nystagmus in comatose patients

can be indicative of an irritative supratentorial focus. Oc-

ular bobbing is characterized by fast conjugate move-

ments downwards followed by a slow return to the pri-

mary position, occurring generally in brainstem lesions,

especially in the pons.

The evaluation of reflex eye movements can be done

through the oculo-cephalic maneuver or the caloric test

(vestibular-ocular). The oculo-cephalic maneuver is car-

ried out by vertical or lateral rotation of the head and ob-

servation of the eye movement. This test is not conduct-

ed in patients with suspicion of trauma, due to the

possibility of cervical lesion. In patients where this reflex

is preserved, the eyes move in unison and in the opposite

direction to the movement of the head.

The caloric test consists of stimulation of the vestib-

ular-ocular pathways using cold water (50 to 100 mL) ap-

plied to the auditory canal. The ears are irrigated sepa-

rately in an interval lasting a few minutes. The normal

response consists of a deviation of the slow phase conju-