[PDF] Cerebellar Ischemia Manifesting As Vertical Diplopia: A Case Study

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MILITARY MEDICINE,180, 1:e168, 2015

Cerebellar Ischemia Manifesting As Vertical Diplopia: A Case

Study on Skew Deviation

Jennifer A. Bateman, OD, FAAO; Amy Chang, OD, FAAO; LTC Jose Capo-Aponte, MS, USA

ABSTRACTPurpose: Skew deviation mimics superior oblique palsy. Associated findings can include ocular torsion,

head tilt, headache, and neurologic symptoms that may help localize the responsible intracranial lesion. Accurate

diagnosis is essential in determining and treating the underlying cause. Imaging options will be reviewed. Case Report:

A 29-year-old white male presented to the emergency room with sudden onset vertical diplopia after self-neck

manipulation. An ophthalmic evaluation led to the diagnosis of skew deviation. Diagnostic imaging revealed an infarct

of the cerebellum likely secondary to a vertebral artery dissection. Besides neck manipulation, other possible contribut-

ing factors include smoking, elevated cholesterol, and elevated testosterone. Symptoms resolved within 24 hours and the

patient was treated with aspirin and atorvastatin calcium. Conclusions: Skew deviation must be a consideration in

patients with vertical diplopia, and ruled out before a superior oblique palsy diagnosis. Vertebral artery dissections are

uncommon in the general population but can account for up to 25% of ischemic strokes in the young and middle-aged.

Smoking, high cholesterol, and high testosterone are known risk factors of stroke. Research is inconclusive on spinal

manipulation's relation to stroke. This report presents an example of neck manipulation directly preceding skew

deviation secondary to stroke.INTRODUCTION Skew deviation is a vertical misalignment of the eyes usually caused by a supranuclear lesion in the posterior fossa1 that affects the prenuclear vestibular input to oculomotor nuclei. 2 Unlike in fourth cranial nerve (CN) palsy, it cannot be local- ized to one muscle. The definition and understanding of skew deviation is still developing. Although it used to be considered a diagnosis of exclusion, now thereis a better understanding of its connection to the otolithic pathways. Until the last 2 decades, skew deviation was considered uncommon and thought to occur primarily in neurologically debilitated patients. Recent studies show skew deviation is not uncommon and is caused by a focal lesion. It can occur in ambulatory patients and often presents as a component of the ocular tilt reaction (OTR).2 The OTR is comprised of skew deviation, ocular torsion, and head tilt. Skew deviation is usually seen with injury to the posterior fossa (to include the brainstem and cerebellum), but can also result from injury to the peripheral vestibular system. 1,3 Most commonly caused by stroke, it may present secondary to trauma, multiple sclerosis, tumor, abscess, hemorrhage, or surgery. 1,2

It can be classified as comitant (the most common

type), laterally comitant (incomitant deviation where hyper- deviation increases in one lateral field of gaze), or laterally alternating (hyperdeviation of the abducting eye in lateral field of gaze).

2Associated neurologic findings in skew deviation may

include gaze-evoked nystagmus, internuclear ophthalmoplegia, dysarthia, ataxia, and hemiplegia. 1

Accompanying symptoms

help localize the lesion; that is, presentation of an internuclear ophthalmoplegia localizes to the medial longitudinal fascicu- lus and concurrent ataxia localizes to the cerebellum.

4Since skew deviation presents with vertical diplopia, its

appearance is similar to superior oblique or trochlear nerve palsy. 1,5 Both present with vertical misalignment in primary gaze. Trochlear nerve palsy is incomitant and can be isolated using the Park's 3-Step method, whereas skew deviation may be comitant, noncomitant, or alternating. Some cases of skew deviation closely mimic a trochlear palsy and isolate to the fourth nerve on Park's 3-Step testing. In trochlear nerve palsy, the hypertropia will worsen on ipsilateral head tilt whereas skew deviation may or may not vary with head tilt. Patients with a CN IV palsy will have a compensatory head tilt contralateral to the hypertropic eye that minimizes the diplopia, whereas those with skew devia- tion may present with a similar head tilt that is pathologic. This head tilt results from an adjustment made to fix a per- ceived deviation from true vertical because of damage to the utriculo-ocular pathway. The vertical axis calculation is inac- curate. This accounts for all three components of the OTR. Trochlear palsy will manifest with excyclotortion of the hypertropic eye, whereas skew deviation may have incyclo- torsion of the hypertropic eye if present, and excyclotortion of the hypotropic eye. Commonly, the trochlear palsy will not present with other neurologic signs unless caused by a brainstem lesionortrauma.1 This case examines the clinical findings and diagnosis of skew deviation to include a discussion of imaging and the upright-supine test. Vertebral artery dissection (VAD), and

the patient's risk factors are reviewed. An accurate diagnosisOptometry Department, Womack Army Medical Center, 2817 Reilly

Road, Fort Bragg, NC 28310.

The views, opinions, and/or Þndings expressed in this report are those of the author(s) and should not be construed as an ofÞcial Department of the Army position, policy or decision, unless so designated by other ofÞcial documentation. doi: 10.7205/MILMED-D-14-00292

MILITARY MEDICINE,Vol. 180, January 2015e168Downloaded from https://academic.oup.com/milmed/article/180/1/e168/4159974 by guest on 06 July 2023

is beneficial in the discovery of the underlying cause and ensuring speedy treatment. Although several case reports exist documenting VAD as sequelae of chiropractic neck manipulation, 6-9 this is the third case report describing VAD secondary to self-neck manipulation in the literature. 10,11 To our knowledge, this is the first reported case of skew devia- tion occurred after self-neck manipulation.

CASE REPORT

A 29-year-old white male was referred to the Optometry Clinic at Womack Army Medical Center, Fort Bragg, North Carolina, by his emergency room (ER) physician. The patient reported experiencing sudden onset binocular vertical diplo- pia after "cracking his neck" from side to side (which he reported doing daily) while driving to work. The physician had completed a head computerized tomography (CT) with- out contrast, which showed no acute intracranial abnormality and referenced the orbits as normal (Fig. 1). The diplopia was accompanied by vertigo, gait ataxia, and occipital neuralgia, but no anesthesia or paresthesia in the limbs. The patient had no complaint of pain or blurred vision and was taking no medication. He reported taking workout supplements and exercising for at least 90 min/day. No other systemic complaints were elicited. The patient reported a history of tobacco use, but no alcohol. Uncorrected vision was 20/30 at distance and near in the right eye and 20/25 at distance and near in the left. Noncontact left eye. Pupil evaluation revealed equally round and reactive to light with no afferent pupillary defect. Extraocular muscle movements were smooth and full with no pain and no appre- ciation of under-action, despite the patient complaint of con- stant diplopia.Diplopia was neutralized using a prism bar and alternating cover test. In primary gaze, the diplopia was 4 prism diopters (PD) of constant left hypertropia. It lessened on right gaze to 3 PD and increased to 7 PD on left gaze. The diplopia did not change significantly on head tilt right and left, each measuring as 5 PD of left hypertropia. Gross evaluation revealed a mild ptosis of the right lid. This was reported as longstanding and confirmed so on photo comparison of his driver's license from years earlier. The anterior segment of each eye and undilated posterior segments were unremark- able. The optic nerves were pink, flat, and distinct. The neuro-optometrist was consulted. No deficiency, beyond the vertical tropia, was elicited on CN testing. Arm and leg strength was within normal limits. The final diagnosis was skew deviation. The ER physician was contacted, informed of the diagno- sis, and a CT angiography (CTA) and magnetic resonance angiography (MRA) of the head and neck with contrast were recommended to rule out an aneurysm. The patient was dispensed plano glasses with a 3 PD base down Fresnel prism over the left lens, which neutralized diplopia on pri- mary gaze. He was educated to avoid driving and to follow up with the optometry clinic in 3 weeks. The CTA indicated no aneurysm. The following day diffusion-weighted imaging (DWI), magnetic resonance imaging (MRI), and T2 fluid attenuated inversion recovery (FLAIR) MRI with and without contrast of the head identified a subacute (1

1cm) left cerebellar infarct

(Figs. 2 and 3). Time-of-flight (TOF) 2D and 3D MRA images and a maximum intensity projection (MIP) image of the neck showed likely dissection of the left vertebral artery at the level of the C1 transverse foramen (Figs. 4-6). FIGURE 1.Axial CT without contrast of the head, cross section through the cerebellum.FIGURE 2.Axial DWI MRI cross section through the cerebellum. Infarct evident within the left cerebellar hemisphere.

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Laboratory results ordered during the initial presentation included elevated cholesterol, triglycerides, low-density lipo- proteins (LDL), and testosterone (932 ng/dL). The complete blood count with differential, coagulation panel, basic meta- bolic panel, cortisol, a-1-Fetoprotein Tumor Marker, Beta- human chorionic gonadotropin (Beta-hCG) tumor marker, protein S panel, factor II Gene Mutation G20210A and Factor V Gene Mutation Analysis, cardiolipin Ab IgA, IgG, IgM and protein C Ag, hCG were all within normal limits. The hepatic panel showed mildly elevated alanine aminotrasferase and aspartate aminotransferase, and the protein C and antithrombin III levels were mildly elevated.Before discharge, the patient was evaluated by neurology The occipital neuralgia was persistent and successfully treated with an occipital nerve block. Aspirin 81 mg was prescribed for the treatment of the dissection and secondary stroke pre- vention, and atorvastatin calcium to treat the elevated choles- terol. An echocardiogram revealed a small patent foramen ovale with low embolic risk. The patient was assessed to be doing well at the second Neurology appointment, despite consistently elevated testos- terone levels at 1218 ng/dL (age normal: 280-800 ng/dL). Follow-up was recommended for 3 months. Unfortunately, the patient was lost to optometry follow-up.

DISCUSSION

On presentation of sudden onset vertical diplopia, thorough history is imperative to evaluate for neurologic symptoms as well as stroke risk factors including hypertension, cardiovas- cular disease, high cholesterol, atrial fibrillation, diabetes, tobacco use, obesity, physical inactivity, atherosclerosis, pre- vious stroke, and family history. 12

If a skew deviation diagno-

sis is confirmed, time becomes a factor and limits extra ophthalmic testing, as emergency conditions including aneu- rysm must be ruled out. Beyond the routine evaluation, an ideal exam would include examination of all CNs, tropia eval- uation in nine positions of gaze, Park's 3-Step the upright- supine test, and double Maddox rod testing or indirect ophthal- moscopy to determine degree of cyclotorsion of each eye. 1,5 CN III palsy was ruled out after lid and pupil evaluation. Vertical diplopia may present with myasthenia gravis or thy- roid eye disease, but no other findings consistent with these were present. Chronic progressive external ophthalmoplegia was excluded as a diagnostic possibility as the patient had full range of motion on extraocular muscle testing. Park's 3-Step testing ruled out superior oblique palsy. The typical findings in this case include concurrent neuro- logical complaints, history of neck pain, the deviation not isolating to one CN, and the VAD associated with a cerebel- lar defect and diplopia. 13

In a review of 51 cases of VAD,

45% experienced diplopia and 33% had misalignment identi-

fied as a CN palsy or skew deviation. 14

A literature review

supports the conclusion that 24-hour resolution of a diplopia complaint (following neck manipulation and VAD) is atypi- cal. There is also the possibility that this finding is not rare, but instead under detected because of misdiagnosis and/or under reported as the symptoms are short lived. As all cases of visual complaints presenting to the ER do not have the benefit of ophthalmologic evaluation, patients may misinter- pret small ocular deviations as blur; there exists the possibil- ity of missed skew or vertical misalignment cases in the literature. Mosby et al 10 documented a case of subjective blur after self-neck manipulation and VAD was found on imaging. The patient was not evaluated by an eye care professional. It is also atypical for skew deviation to present without all com- ponents of the OTR. If the effect of the lesion was longer FIGURE 3.Axial T2 FLAIR cross section through the cerebellum. Infarct evident within the left cerebellar hemisphere. FIGURE 4.Axial 2D TOF MRA cross section through the vertebral arteries. Likely VAD evident within the left vertebral artery.

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standing, head tilt may have developed. Ocular torsion could have been present but was not measured. Assuming the Park's 3-Step test findings were ambiguous, evaluation would have benefited from supine testing to differentiate it from

CN IV palsy.

1 The upright-supine test, proposed by Wong, aids in differ- entiating skew deviation from trochlear nerve palsy. 1 Head position-dependent changes in torsion were evaluated by Wong and the discovery made that torsion and vertical mis- alignment are head position-dependent in skew deviation, "if skew deviation is indeed caused by imbalance of otolithic projections to oculomotor neurons, then the ocular counter roll would be abnormal, the linear vestibular ocular reflex would be abnormal and the abnormal torsion and vertical strabismus might be head position-dependent." 1 Although two separate studies only reviewed small sample sizes, the upright-supine test showed 76% to 80% sensitivity in evaluating skew deviation patients and 100% specificity in ruling out trochlear nerve palsy or other causes. 1,15

A positive

upright-supine test is defined as 50% reduction in the degree of vertical deviation from evaluation of a patient upright to when they are fully reclined. The measurement is taken using prism and the alternating cover test. The authors recommend incorporating this test with the Park's 3-Step when evaluating for skew deviation, and proceeding to brain imaging if a positive result presents. Imaging choices are numerous, and arguably best left to the radiologist to determine based on the suspected diagnosis, Noncontrast CT is widely available in ERs, quick to perform and generally half the cost of MRI. 16

Although good at rec-

ognizing hemorrhage, CT is less sensitive in localizing stroke, and CTA is preferred.quotesdbs_dbs16.pdfusesText_22

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