Midbrain Infarction Causing Diplopia and Atypical Neurological Symptoms: An Abducens Palsy Review

A 68 year old white male reports distance horizontal diplopia immediately following a cerebrovascular accident.

Neuroimaging shows acute right midbrain infarction. While rarely associated with , neurologic sixth nerve palsies occur and entail further workup.

i. CASE HISTORY

a. PT DEMOGRAPHICS: 68 year old white male

b. CHIEF COMPLAINT: On 8/12/16 patient reports recent onset of horizontal diplopia in the distance

for two weeks and reduction of right gaze. Noted diplopia, dizziness, and trace left sided

extremity/facial weakness after recent stroke on 07/28/16, but reported no pain, visual field loss,

or ataxia.

c. OCULAR HISTORY:

i. Mild Non-Proliferative Diabetic Retinopathy OS (10-2015)

d. MEDICAL HISTORY

i. 1999: Diabetes Mellitus

ii. 1999: Hypertension

iii. 1999: Hyperlipidemia

iv. 2009: Cerebrovascular accident

v. 2009: Right vertebral artery stent

vi. 2014: Transient ischemic attack

vii. 2014: Severe posterior circulation disease

e. MEDICATIONS

i. Metformin

ii. Amlodipine

iii. Hydrochlorothiazide

iv. Lisinopril

v. Tamsulosin

vi. Clopidogrel bisulfate

f. OTHER SALIENT INFORMATION

i. MRI 06-26-09; Subacute infarction in left ventral pons ii. MRI 04-20-16; Subacute infarction of left caudate

iii. CT Brain without contrast 06-25-09; Subacute infarction in left ventral pons

iv. CT Brain without contrast 01-02-16; unremarkable

ii. PERTINENT FINDINGS

a. CLINICAL

i. Vision

1. OD: 20/20-1 cc

2. OS: 20/20 cc

ii. Pupils: equal, round and reactive to light with no afferent defect

iii. Cover Test (thru habitual Rx)

1. Distance: 10^ Right Esotropia

2. Near: ~4^ Right Esotropia

iv. Maddox Rod: 15^ Base Out OD at distance

v. Subjective Prism: 12^ base out OD eliminated diplopia

vi. Extraocular Motility: Limited right abduction by approximately 30% (IMAGE OF PATIENT)

1. (+) right gaze diplopia, (-) pain

vii. Confrontations: Full to finger count

viii. Anterior Segment: Unremarkable with (-) ptosis, iris neovascularization

ix. Posterior Segment: Unremarkable with (-) optic nerve pallor, neovascularization, hemes,

cotton wool spots, exudates

b. PHYSICAL

i. Results from neurology examination 07-29-16 (Summarized)

c. SELECTED LABORATORY STUDIES

i. Vitals- 08/04/16

1. Blood Pressure: 148/72

2. Pulse: 58

ii. Labs

1. Glucose -08/03/16

a. 113

2. HbA1C- 07/30/16

a. 6.1% d. RADIOLOGY STUDIES

i. CT Brain with contrast 07-29-16

1. No pertinent findings

ii. MRI Brain without contrast 07-29-16 (IMAGE OF PATIENT’S MRI)

1. Radiology Impression

“Acute infarct right paramedian pontomedullary junction with multiple remote

infarcts and chronic microangiopathy” iii. DIFFERENTIAL DIAGNOSIS

a. PRIMARY/LEADING

i. Gaze paresis secondary to vascular disease

1. Most common cause of CN 6 palsy

b. OTHERS

i.

ii. Tumor

iii. Muscle entrapment

iv. Giant cell arteritis

v.

vi. Raymonds Syndrome

vii. Millard Gubler Syndrome

viii. Foville’s Syndrome

ix. Internuclear ophthalmoplegia iv. DIAGNOSIS AND DISCUSSION

a. FINAL DIAGNOSIS: Cranial nerve 6 palsy with neurological findings secondary to midbrain

infarction

i. MRI confirms acute right infarct, at the right paramedian pontomedullary junction

b. ELABORATE ON CONDITION—Cranial Nerve 6 Palsy

i.

1. Horizontal diplopia greater in distance

2. Abduction defect

3. Esotropia at distance

a. Ipsilateral to abduction defect

ii. Epidemiology 1. 11.3 in 100,0004

a. Most common of all Cranial Nerve Palsies

2. 15% of all CN 6 palsies caused by Stroke5

3. Literature reveals 5.8% of stroke cohort had a CN 6 palsy8

4. 47% of all stroke causing CN palsies occur in cerebellum8

c. EXPOUND ON UNIQUE FEATURES—Cranial Nerve 6 Palsy due to midbrain infarction

i. Nuclear 6th Cranial Nerve Palsy

1. Ipsilateral gaze palsy that cannot be overcome by vestibular testing

a. Contralateral abduction weakness

b. Ipsilateral peripheral facial nerve palsy

i. One and a half syndrome

ii. Foville’s syndrome

iii. Gaze palsy

ii. Fascicular 6th Cranial Nerve Palsy

1. Results from location of surrounding structures in the Pons

a. Contralateral hemiplegia

i. Raymond’s syndrome

b. Ipsilateral facial weakness with contralateral hemiplegia

i. Millard Gubler Syndrome

2. **UNIQUE FEATURES OF THIS PATIENT**

a. trace contralateral limb weakness

b. trace contralateral facial weakness

iii. Recommended Neuro-Ophthalmic Evaluation

1. Cranial nerve testing

2. Vestibular system and cerebellum testing

3. Evaluation of deep tendon reflexes and peripheral motor system

4. Optic nerve head evaluation v. TREATMENT AND RESPONSE TO TREATMENT

a. TREATMENT OPTIONS

i. Patching paretic eye or frosting spectacle lens

ii. Temporary Fresnel Prism

iii. Injection of Botulinum Toxin in ipsilateral medial rectus muscle iv. Surgical intervention

1. Indicated after 6 months of stable deviation

b. PROGNOSIS

i. Approximately 50% of all CN6 palsies resolve spontaneously after onset (within 3

months) 4

1. Vasculopathic etiologies resolve more rapidly (4-6 weeks) 4

ii. 31-35% recurrence rate for vasculopathic patients 4

c. MANAGEMENT OF CASE

i. 12^ BO Fresnel Prism placed on right lens

ii. Patient to Return to Clinic on 9/12/16 for follow up

vi. CONCLUSION

a. Sixth cranial nerve palsies are the most common oculomotor cranial nerve palsies

i. Most often caused by vasculopathic disorders in at risk patients over 50 years old.

1. Current treatment protocol does not indicate neuroimaging for these patients.

b. When neurological findings are present with cranial nerve palsy, more severe diagnoses should

be considered such as cerebrovascular accident, neoplasm or aneurysm.

c. Midbrain infarctions causing a sixth cranial nerve palsy are rare and are often associated with

additional gaze deficits, facial paresis, or hemiplegia.

d. Any patient diagnosed with CN6 palsy and presenting with additional neurological symptoms

should be sent for neuroimaging and a further neurological workup regardless of age or presence

of vascular risk factors.

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