Journal of Athletic Training 2010;45(4):407–410

g by the National Athletic Trainers’ Association, Inc

www.nata.org/jat
case report

Fourth Cranial Nerve Palsy in a Collegiate Lacrosse

Player: A Case Report
Jennifer L. Stiller-Ostrowski, PhD, ATC
Lasell College, Newton, MA
Objective: To present the case of a National Collegiate to a neurologist, ophthalmologist, and finally a neuro-ophthal-
Athletic Association Division I men’s lacrosse athlete with fourth mologist before a definitive diagnosis was made. The palsy did
cranial nerve injury as the result of a minor traumatic blow. not necessitate surgical intervention, resolving with conserva-
Background: The athlete was struck on the right side of his tive treatment. The athlete was able to return to full athletic
head during a lacrosse game. On-field evaluation revealed no ability at his preinjury level by 8 months postinjury.
cervical spine involvement or loss of consciousness. He Uniqueness: Superior oblique palsy as the result of fourth
complained of headache and dizziness, with delayed reports cranial nerve injury is the most frequent isolated cranial nerve
of visual disturbance. Sideline visual acuity and cranial nerve palsy; however, these palsies are often underdiagnosed by
screenings appeared within normal limits. Consultation with the health professionals. Such palsies are uncommon within the
team physician indicated that immediate referral to the athletic realm, making timely diagnosis even less likely.
emergency department was unnecessary. Conclusions: Cranial nerve palsy may present very subtly in
Differential Diagnosis: Concussion, third cranial nerve patients. Therefore, on-field health care providers should be
palsy, fourth cranial nerve palsy. aware of the descriptions and types of compensations that
Treatment: The certified athletic trainer safely removed the signal nerve injury.
athlete from the playing field and monitored him on the sideline. Key Words: trochlear nerve, neurologic injuries, visual
After being seen by the team physician, the patient was referred disturbances

C
ranial nerve (CN) examination is a routine compo- questioning, and I eliminated the possibility of neck injury
nent of the evaluation for any head injury. Three through palpation and demonstration of full sensory and
cranial nerves control eye motion: CN III (oculo- motor ability of all extremities. I helped the athlete into a
motor), CN IV (trochlear), and CN VI (abducens). Injury sitting position and then a standing position in increments
to any of these nerves is rare in sport-related head injury; and walked off the field with him. Sideline evaluation
however, the location of the fourth cranial nerve makes it methods included a clinical examination, symptoms
especially susceptible to injury with severe head trauma.1 checklist, and standard assessment of concussion.
Unfortunately, CN IV palsies are underdiagnosed by The athlete initially complained of headache and dizziness
hospital services.2 The purposes of this report are to but denied nausea or tinnitus. His pupils were equal and
present the unique case of a CN IV injury in a collegiate reactive to light and accommodation. His pulse rate was
lacrosse athlete and to review relevant clinical evaluation normal (56 beats/min). Cranial nerve screening revealed no
components that may assist certified athletic trainers in obvious deficit. Initially, the athlete was not oriented to
timely diagnosis of this injury. place or time of game and could not answer basic questions
about events that happened in weeks before that day, earlier
that day, or immediately after the concussive event. After
CASE REPORT approximately 20 minutes of sideline monitoring, he became
A 19-year-old collegiate male lacrosse player (National oriented to his surroundings and began to slowly regain his
Collegiate Athletic Association Division I) with no history memory of the events leading up to the injury. At this time,
of concussion was struck on the head just above his right he was able to repeat strings of numbers in reverse order,
ear by an opponent’s elbow during a game. The athlete was recite the months of the year in reverse order, and recall 5 of
wearing a helmet at the time of the blow, but his 5 words 5 minutes after hearing them and 4 of 5 words after
mouthguard appeared to have been knocked out by the 10 minutes. He was able to recall events from several weeks
blow. When I arrived on the field, the athlete was not ago and all events before the hit but was unable to recall the
moving but was fully conscious. Teammates who arrived at hit, how he was taken off of the field, or what occurred
his side seconds after the blow stated that he never lost during the first 20 minutes postinjury. The athlete was now
consciousness. The athlete was lying supine, with his following the game and was reacting appropriately to events
mouthguard hanging out of the side of the mouth and on the field. At this time, he complained of blurry vision and
the helmet chin strap pushed up on his chin. The athlete thought he had lost a contact lens. Inspection of his eyes
was not coherent upon initial questioning and could not revealed that both contact lenses were in place; however, the
say what had happened to him. He also could not say athlete continued to complain of blurry vision. He was able
whether he initially had any neck pain. After approximate- to see clearly through each individual eye with the other eye
ly 30 seconds, he began responding coherently to my closed but experienced a type of double vision with both eyes

Journal of Athletic Training 407

Table. Results of Tests of Planes of Vision
Findings in Gaze Positions, Diopters
Time Postinjury, wk Primarya Left Right Down Right Head Tilt
5 10 (hypertropiab) 8 (exotropia); 20 (hypertropia) WNL NA 25 (hypertropia)
15 6 (exotropiac); 4 (hypertropia) 4 (exotropia); 15 (hypertropia) WNL 15 (hypertropia) NA
22 2 (hyperphoriad) 18 (hypertropia) WNL 4 (hyperphoria) NA
Abbreviations: WNL, within normal limits; NA, not available.
a
Some measurements were taken more than once.
b
Hypertropia is a misalignment of the eyes in which the visual axis of one eye is higher than that of the other. In this case, hypertropia was on the
right.
c
Exotropia is a misalignment of the eyes in which the eyes are deviated outward.
d
Hyperphoria is the tendency of the eye to deviate vertically.

open. The athlete continued to complain of headache and not when the right lower field was examined). He had mild
dizziness. No immediate concussion grading scale was used nystagmus on extreme lateral gaze in either direction but no
in this case, as both the team physician and I use the Vienna evidence of abducens muscle weakness in either eye. The
concussion definitions.3 I spoke with 2 team general patient was diagnosed with a contusion or stretch injury to
medicine physicians on the phone to determine if the athlete CN III (oculomotor nerve) as the result of the blow to the
should be referred to the emergency department that night, head. The neurologist’s impression was that the injury was
but neither physician felt that this case warranted immediate so microscopic that it would not have appeared on MRI. At
referral. However, recommendations were made for contin- this time, the patient was given a prognosis of full resolution
ued observation overnight by a roommate. At 10:00 PM on of symptoms within 3 to 4 weeks and was advised to
the day of the injury, the athlete checked in with me over the continue to use the eye normally. The neurologist stated that
phone: he reported no increase in symptoms, but headache the concussion was resolved, and the patient was cleared to
and visual disturbance continued. bike and resume noncontact lacrosse activities. The patient
was also referred to a neuro-ophthalmologist to see if there
COURSE OF TREATMENT were any exercises to retrain and reeducate deficient eye
muscles to facilitate nerve healing. Unfortunately, the
The patient was seen in the athletic training facility the
patient could not be seen by the neuro-ophthalmologist in
following day by the team general medicine physician. He
continued to complain of headache and blurry vision as well our area until 5 weeks postinjury.
as some dizziness while walking that he attributed to the Beginning about day 7 postinjury, the patient developed
visual disturbance. He reported that walking down stairs and a head posture that involved tucking the chin and tilting
watching television were particularly difficult. The patient the head to the right. He felt this position helped him to
had no problems falling asleep or staying asleep and had focus on only one of the 2 planes of vision that he
been awakened twice during the night by his roommates continued to see. Over the next 3 weeks, the patient
without problems. He had also been able to eat 2 meals reported subtle improvements in vision, but ptosis of the
without difficulty. Single-eye visual acuity remained unaf- right eye continued, as did his report of seeing 2 distinct
fected, but vision remained abnormal when the patient was visual planes that remained tilted with respect to one
looking straight ahead with both eyes open. The patient another. Despite the neurologist’s prognosis regarding
stated that tilting his head down, tucking his chin, and symptom resolution, visual disturbances were not resolved
looking upward seemed to help. Upon reevaluation, the by the 4-week mark. At this time, and when adopting the
pupils initially dilated in response to light and then chin-tucked, head-tilted posture, he could focus when
constricted. Cranial nerves and upper and lower dermatome, looking ahead and to the left for extended periods, but
myotome, and reflex screening all appeared within normal quick head motions or panning caused him to lose focus.
limits. Because of the pupil abnormality and continued vision Based on a battery of functional tests performed during the
disturbances, a brain magnetic resonance imaging (MRI) neuro-ophthalmologist appointment in week 5, the original
scan was ordered. The test was interpreted as normal. diagnosis of CN III injury was rejected. The patient was
By day 2 postconcussion, the patient’s headache had now diagnosed with palsy of the right superior oblique
resolved completely, but his vision had not improved. He muscle secondary to right CN IV palsy. This diagnosis was
reported double vision, with one image slanted relative to based on a positive Bielschowsky head-tilt test (a test to
the other. He had also developed ptosis of the right eyelid. detect superior oblique muscle palsy), the double Maddox
Single-eye vision remained unaffected. At this point, the rod test (a test to detect and measure ocular torsion), and a
decision was made to refer the patient to both a neurologist test of planes of vision (using prisms). Cover testing was
and an ophthalmologist. The ophthalmology examination performed in various gaze positions (Table). The patient
on day 5 postinjury revealed no problems with single-eye was given a prognosis of full resolution of symptoms within
visual acuity. An MRI of the orbits was ordered at this time 3 to 4 months postinjury. The patient continued to be
and was read as normal (ie, globes were within normal disqualified from contact lacrosse activities until his vision
limits). Upon examination by the neurologist on day 6, mild returned to normal. At this point, with vision still altered
ptosis and decreased adduction of the right eye were noted. and only 4 games left in the lacrosse season, the patient
Diplopia was confirmed by the red glass test (the patient was chose to apply for a medical hardship waiver.
able to see the red light in the lower and more lateral After returning to his home state for the summer, the
positions when the left lower visual field was examined but patient had a follow-up appointment with a different

408 Volume 45 N Number 4 N August 2010

neuro-ophthalmologist 15 weeks postinjury. Based on 40% of all isolated fourth nerve palsies are traumatic, 30%
prism diopters, the patient’s double vision had resolved are idiopathic, 20% are due to vascular infarct, and 10% are
50% from his previous appointment (Table). He continued due to tumor or aneurysm. Because of the large number of
to have no deviation when using the head-tilted, chin- other neural structures that accompany CN IV as it travels
tucked positioning. It was the opinion of the neuro- through the cavernous sinus and superior orbital fissure,
ophthalmologist that the full amount of vision that will damage to this area rarely results in isolated fourth nerve
return is normally achieved by 6 months postinjury. palsy; more likely, associated palsy of CNs III and VI
Because the patient’s vision was continuing to improve, a occurs.1,4,6–8 In this case, however, superior oblique nerve
decision as to whether surgery was warranted was deferred palsy as the result of CN IV injury occurred without
pending another follow-up visit in 6 weeks. By 5 months additional CN injury. Isolated injury to CN IV can be
postinjury, the patient reported that he had no diplopia caused by any process that stretches or compresses the
about 90% of the time (with most double vision occurring nerve.1,4,6–9 Even relatively minor trauma can transiently
in extreme left gaze). Although he was still symptomatic in stretch CN IV (by displacing the brain stem relative to the
left gaze (Table), this diplopia did not have any functional posterior clinoid process), but generally the trauma must be
implications. The neuro-ophthalmologist informed the severe, with resultant loss of consciousness.4 With trauma,
patient and his family of the risk of returning to high- patients usually report symptoms immediately after regain-
velocity sports with even intermittent diplopia, but the ing consciousness. Patients with minor damage to CN IV
patient received medical clearance to return to competitive complain of blurry vision; patients with more extensive
lacrosse. By 6 months postinjury he reported subjective damage notice frank diplopia and rotational (torsional)
normal vision. At that time, his risk of reinjury was disturbances of the visual fields. Visual acuity is unaffected
equivalent to his preinjury risk. As an extra precaution, the and pain is atypical.2,4,10 In this case, the athlete had severe
patient was referred to a dentist for a custom-molded damage to CN IV (including vertical and torsional diplopia)
mouthguard. He was able to return to full competition as the result of relatively minor head trauma. The patient
during the fall 2008 season and competed fully in both the never lost consciousness and demonstrated no structural
fall 2008 and spring 2009 competitive seasons with no abnormalities on MRI of the brain or orbit.
recurrence of symptoms. At this time, the patient is Cranial nerve screenings by the athletic trainer on the
16 months postinjury and is back to his preinjury level of sideline and by the team general medicine physician the day
competition. after the concussive blow both appeared within normal
limits, although later diagnosis by a neuro-ophthalmologist
DISCUSSION revealed paralysis of the superior oblique muscle, inner-
vated by CN IV. The patient did not report any visual
The fourth CN nucleus is located in the dorsal mesen- disturbances until a full 20 minutes after initial injury,
cephalon. The nerve exits the brain stem dorsally into the which coincided with the time that the athlete began to
subarachnoid space, then courses around the brain to enter regain familiarity with and awareness of his surroundings.
the cavernous sinus, superior orbital fissure, and orbit and This is an important take-home point, as it may imply that
to innervate the superior oblique muscle.4,5 This muscle’s visual acuity and ocular CN testing should be repeated in
actions include rotation in the vertical plane (depression and such athletes, the focus being on subtle noncongruence in
elevation of the eyeball) and rotation in the plane of the face eyes during various gazes. One should note, however, that
(intorsion and extorsion of the eyeball). The force of the paralysis of the superior oblique muscle is often not evident
tendon’s pull, therefore, has 2 components: a forward on screening; torsional deviation and diplopia can often
component that tends to pull the eyeball downward only be measured by the double Maddox rod test.10
(depression) and a medial component that tends to rotate Visual disturbances are the result of paralysis of the
the top of the eyeball toward the nose (intorsion).1,4,6–8 superior oblique muscle, which prevents normal eye
Among the CNs, the trochlear nerve is the smallest nerve movement, and, specifically, weakness of downward eye
in terms of the number of axons it contains, has the greatest movement with consequent vertical diplopia. The affected
intracranial length, is the only CN to decussate before eye drifts upward relative to the normal eye as a result of
innervating its target, and is the only CN to exit from the the unopposed actions of the remaining extraocular
dorsal aspect of the brain stem. The fourth CN enters the muscles. The patient sees 2 visual fields (one from each
cavernous sinus, where it is joined by the other 2 extraocular eye) separated vertically. Diplopia is usually worse on
nerves (CN III and CN VI), the internal carotid artery, and downward gaze and gaze away from the side of the affected
portions of the trigeminal nerve (CN V).1,4,6–8 Contrecoup muscle and is especially problematic as the patient tries to
forces can compress the nerve against the rigid tentorium, read. To compensate for this, patients learn to tilt the head
which lies adjacent to the nerve for much of its course. Injury forward and tuck the chin in order to bring the fields back
to the nerve can occur anywhere along its course from together.4 Less commonly, trochlear nerve palsy also
midbrain to orbit. A peripheral lesion reflects damage to the affects torsion (rotation) of the eyeball in the plane of the
bundle of nerves, whereas a central lesion indicates damage face. When onset is acute, hypertropia is usually most
to the trochlear nucleus or its fascicles within the brain stem. prominent in the field of gaze of the involved superior
Peripheral lesions result in ipsilateral symptoms, and central oblique muscle. In this patient, the right hypertropia that
lesions result in contralateral symptoms.1,4,6–8 Our patient worsened with left gaze and right head tilt is consistent with
had a peripheral lesion, presenting with right-sided symp- right superior oblique palsy. Weakness of intorsion results
toms after right-sided head trauma. in torsional diplopia, in which 2 different visual fields,
The 2 most common causes of CN IV palsy are head tilted with respect to each other, are seen at the same time.
trauma and vascular infarct.2,9,10 In adults, approximately To compensate for this, the patient typically presents with

Journal of Athletic Training 409

a characteristic head tilt away from the affected side in CONCLUSIONS
order to fuse the 2 images into a single visual plane.4
Persistent double vision in athletes who have suffered a
Interestingly, some patients develop a head tilt toward the
concussion or head injury should be considered a red flag
side of the lesion, called a paradoxic head tilt, to create a
for ocular CN injury. Although CN IV palsy is certainly
wider separation of images, which allows the patient to
not a common occurrence in athletes, it is a potential result
suppress or ignore one image.2,4,10,11 The head tilt occurs in
approximately 70% of all patients, whereas the paradoxic of any head injury or concussion because of the nerve’s
tilt affects only 3% of patients.5 A unique feature of this location in the brain and its susceptibility to trauma. The
case is that the patient developed a same-sided (paradoxic) symptoms are fairly obvious if one is familiar with the
head tilt rather than the more common contralateral head condition, and early diagnosis by a certified athletic trainer
tilt. Certified athletic trainers and other sports medicine or other sports medicine professional can prevent unnec-
professionals should be aware that these types of compen- essary diagnostic testing and psychological stress on the
sations can signal a CN injury. part of the patient and the family. Also, in addition to the
Trochlear nerve palsy is traditionally diagnosed according implications of injury to the nerve itself, an undiagnosed
to cause as acquired, congenital, or idiopathic. Diagnosis is defect in extraocular muscle function may markedly affect
confirmed by evaluating eye movements in all directions. As the individual’s athletic performance. The characteristic
the patient’s gaze is directed to specific areas, one eye appearance of patients with fourth nerve palsies (head
appears slightly higher than the other (evaluation by the titled to one side, chin tucked in) indicates the diagnosis, as
Bielschowsky head-tilt test). This misalignment improves or does the location of the eye during gazes into various
becomes worse with certain head positions.12 The charac- planes of vision. When a CN IV injury is suspected, the
teristic appearance of patients with CN IV palsies (head patient should be immediately referred to a neurologist or
titled to one side, chin tucked in) indicates the diagno- neuro-ophthalmologist, with documentation of pertinent
sis.1,4,10–12 The magnitude of visual disturbance can also be evaluation findings.
evaluated more objectively using prisms. In one study13 the
mean vertical deviation of 20 patients (aged 19–70 years) REFERENCES
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Address correspondence to Jennifer L. Stiller-Ostrowski, PhD, ATC, Lasell College, 1844 Commonwealth Avenue, Wass 8, Newton, MA
02466. Address e-mail to [email protected].

410 Volume 45 N Number 4 N August 2010