Acute Vertical Ophthalmoplegia Secondary to Unilateral Thalamic Stroke

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1 Acute Vertical Ophthalmoplegia Secondary to Unilateral Thalamic Stroke Shane Stevens, OD Richard Frick OD, FAAO, ABCMO Andrea Murphy, OD, FAAO White River Junction, VT VAMC

2 Patient & Chief Complaint 64 year old Caucasian male Presents to ER with sudden onset double vision, mild nausea, and a gait disturbance The double vision is described as constant, but resolves if either eye is closed The two images were described as separated diagonally

3 Physical Report from ER The patient exhibited disequilibrium while standing and displayed mild left sided gait disturbance while walking Otherwise, he was alert and had no other signs or symptoms of neurological deficits Blood pressure: 169/102 Pulse: 108

4 Initial Studies CT Scan (Head & Neck): Unremarkable Labs: Glucose: 125 mg/dl (high) Triglycerides: 159 mg/dl (high) All other lab work was unremarkable

5 Medical History Hypertension white coat syndrome (untreated) Impaired fasting glucose Obesity Possible TIA with left lower arm weakness in A full stroke work-up was performed at the time and all testing came back normal

6 Medications Aspirin, 325 mg QD Ibuprofen BID PO PRN Tadalafil 10mg PO PRN Multivitamin PO QD

7 Ocular History H/O retinal tear OS, s/p laser repair Nuclear Sclerotic Cataracts OU Refractive Error with presbyopia OU

8 Exam 1 Day 1 VA (cc): 20/20 OD and OS Pupils: PERRLA (-) APD EOMS: Complete conjugate restriction of elevation and depression of both eyes in primary, right and left gazes Horizontal gazes were intact No gaze evoked nystagmus

9 Exam 1 (cont.) Day 1 CT (cc): 4^Right Hypertropia with a 5^ D & N Park s 3 Step/Red Lens Testing: unable to isolate single cranial nerve palsy All other cranial nerve testing was normal Ocular health via slit lamp examination and undilated funduscopy was unremarkable

10 Primary/leading: Differential Diagnosis Vascular: stroke or hemorrhage, midbrain or thalamus [1] Other differentials: Compressive Mass eg. tumor Progressive Supranuclear Palsy (PSP) Hydrocephalus eg. cerebral aqueduct stenosis Parinaud s Dorsal Midbrain Syndrome

11 Treatment Plan Exam 1 Eye patch (Via the ER physician) patient was started on Clopidogrel Bisulfate and Atorvastatin The 325mg daily Aspirin was discontinued

12 Radiology Studies Day 3 MRI (Orbits): Unremarkable MRI/MRA (Brain): No mass, mass effect, or acute hemorrhage 3-mm of increased signal in the inferomedial right thalamus, suggesting a subacute right thalamic lacunar infarct The brainstem and cerebellum sections showed no signs of infarct

13 MRI

14 Incidence Acute ischemic strokes of the posterior circulation 11-14% = thalamic infarction 16% = paramedian infarcts 89% = inferomedial leading neurological findings: 87% = drowsiness 39% = vertical gaze palsy [11,12]

15 Exam 2 Day 5 CC: constant double vision, but improving, especially superior gaze EOMS: Improved upgaze with greater elevation OD than OS, with upgaze evoked cyclonystagmus OU Downgaze still partially restricted Horizontal gaze remained intact

16 Exam 2 (cont.) Day 5 Doll s Head (oculocephalic maneuver): Vertical & Horizontal Vestibulo-ocular reflex (VOR) intact Optokinetic Drum: Horizontal saccades and smooth pursuits preserved Vertical saccades and smooth pursuit response absent Visual Field 30-2: reliable w/o defects OU

improve [2] Referral to neurology for consultation Referred to internal medicine to control

17 Treatment Plan Exam 2 Dispensed 4^BD Fresnel prism OD after the patient reported subjective improvement At this exam, the patient was educated that his double vision may continue to improve [2] Referral to neurology for consultation Referred to internal medicine to control vascular risk factors Return to clinic 4-6 weeks to reassess binocular vision posture & cranial nerve testing

18 Exam 3 7 weeks CC: Complete resolution of diplopia EOMS w/ Red Lens: SAFE Cyclonystagmus resolved No detectable restriction of vertical gazes Treatment Plan: Ground in prism not indicated Continue as scheduled with neurology and primary care

19 Neurology of Vertical Gaze Pursuits= EOMS & VOR Saccades= Saccade Testing & OKN Drum

20 Control of Saccades Frontal Eye Fields Superior Colliculus Rostral Interstitial Nucleus of MLF Interstital Nucleus of Cajal (INC) CN III & CN IV nucleus [1]

21 Control of Pursuits not well understood Visual Cortex/Parieto-Occipital Junction Pontine Nuclei/Cerebellum MLF Rostral Interstitial Nucleus of MLF Interstital Nucleus of Cajal (INC) CN III & CN IV nucleus [1]

22 The Underlying Neurology Selective (either upward or downward) vertical ophthalmoplegia is most often the result of bilateral dorsal or tegmental midbrain lesions [6]

23 The Underlying Neurology Although it has been reported in some cases, it is rare to have bilateral ophthalmoplegia from a unilateral thalamic infarct without midbrain involvement, especially involving both upward and downward gaze [3-5]

24 The Thalamus

frontal eye fields, which are responsible for initiating voluntary vertical gazes

26 Theories on Thalamic Involvement Supranuclear afferent oculomotor fibers decussate and/or transverse the mediodorsal nucleus of the thalamus and then project to the frontal eye fields, which are responsible for initiating voluntary vertical gazes [7] Interruption to either of these pathways can lead to vertical gaze palsies [7-9]

27 Oculocephalic (Doll s Head) Maneuver Typically indicated in an awake or comatose patient who has limited or absent voluntary eye movements [1]

28 What makes a VOR intact? Compare the reflex eye movements with VOR head tilt to the voluntary eye movements with EOM testing When the reflex movements are greater, the lesion must lie rostral to the midbrain, and is thus supranuclear [1]

29 Does this correlate with our patient? Vertical ophthalmoplegia Intact vertical VOR = Supranuclear lesion The most common cause of acute supranuclear vertical ophthalmoplegia is a thalamic lesion, most commonly a medial thalamic infarction [1]

initiation of voluntary & involuntary vertical saccades Bilateral (or

30 rostral interstitial MLF (rimlf) Located at the junction of the midbrain and thalamus Functions as the premotor nucleus, and is responsible for initiation of voluntary & involuntary vertical saccades Bilateral (or unilateral) damage typically abolishes all vertical and torsional saccadic movements [10]

patient displayed absent vertical saccades with the OKN drum This finding

31 rimlf & Saccade Testing In an attentive patient with vision 20/200 or better, a robust and symmetric nystagmus should appear in all positions of gaze Our patient displayed absent vertical saccades with the OKN drum This finding suggests either some direct damage to the rimlf or damage to its projections into the thalamus

32 Take Away Points The role of the thalamus in vertical eye movements VOR Testing and the Optokinetic Drum The importance of neuroimaging in ruling out emergent pathology and localizing CNS lesions Fresnel Prism

33 Bibliography 1. Burde RM SP, Trobe JD: Clinical decisions in neuro-ophthalmology, 3 edn. United State of America: Elsevier B.V.; Jones SA, Shinton RA: Improving outcome in stroke patients with visual problems. Age Ageing 2006, 35(6): Bogousslavsky J, Miklossy J, Deruaz JP, Regli F, Assal G: Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study. JNeurol Neurosurg Psychiatry 1986, 49(6): Weidauer S, Nichtweiß M, Zanella FE, Lanfermann H: Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis. European Radiology 2004, 14(9): Blitshteyn S, Hentschel K, Czervionke LF, Eidelman BH: Transient vertical diplopia and nystagmus associated with acute thalamic infarction. Clin Imaging 2006, 30(1): Bender MB: Brain control of conjugate horizontal and vertical eye movements: a survey of the structural and functional correlates. Brain : a journal of neurology 1980, 103(1): Khan M, Sidiropoulos C, Mitsias P: Unilateral thalamic infarction presenting as vertical gaze palsy: a case report. Journal of Medical Case Reports 2011, 5(1): Goerlitz J, Wenz H, Al-Zghloul M, Kerl HU, Groden C, Forster A: Anatomical Variations in the Posterior Circle of Willis and Vascular Pathologies in Isolated Unilateral Thalamic Infarction. J Neuroimaging 2015, 25(6): Clark JM, Albers GW: Vertical gaze palsies from medial thalamic infarctions without midbrain involvement. Stroke 1995, 26(8): Ropper AH, Samuels MA, Klein JP: Chapter 12, 10e. edn. New York, NY: The McGraw-Hill Companies; Forster A, Nolte I, Wenz H, Al-Zghloul M, Kerl HU, Brockmann MA, Groden C: Anatomical variations in the posterior part of the circle of willis and vascular pathology in bilateral thalamic infarction. J Neuroimaging 2014, 24(4): Weidauer S, Nichtweiß M, Zanella FE, Lanfermann H: Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis. European Radiology 2004, 14(9): Goerlitz J, Wenz H, Al-Zghloul M, Kerl HU, Groden C, Forster A: Anatomical Variations in the Posterior Circle of Willis and Vascular Pathologies in Isolated Unilateral Thalamic Infarction. J Neuroimaging 2015, 25(6): IMAGE SOURCES (IN ORDER OF APPEARANCE): Poser JB, et al. Plum and Posner s Diagnosis of Stupor and Coma (4th edition), Oxford university Press,

University Journal of Surgery and Surgical Specialities

University Journal of Surgery and Surgical Specialities Volume 1 Issue 1 2015 PARINAUD'S SYNDROME A CASE REPORT Basker K Shubha Raguram K Stanley Medical College Introduction: Gaze palsies are a group