Occipital Lobe Stroke: An Optometrist’s Role Disclosures...Occipital Lobe Stroke: An...
Transcript of Occipital Lobe Stroke: An Optometrist’s Role Disclosures...Occipital Lobe Stroke: An...
Occipital Lobe Stroke: An Optometrist’s Role
Virginia Bice, ODDisclosures
None
Course Objectives:
Identify neurologic visual field patterns
through confrontation testing
01Recognize uncommon symptoms of stroke, specific to occipital
lobe infarct
02Understand the
subsequent ocular testing needed to identify location of
stroke
03 71‐year‐old Caucasian
male
• Provider reason for visit:
• Primary open angle glaucoma f/u and DFE
• Patient reason for visit:
• Blue and red spots on left side of vision 2 weeks prior, episode lasted 2 days
• Unable to discern left field OU or OS only
• Blue/red spots intermittent, unable to remember duration
• Headache, band pattern around head, dull pain, moderate, constant
• No trauma or fall
Patient History
Medical
• Type 2 Diabetes Mellitus
• Abdominal aortic aneurysm
• Chronic Obstructive Pulmonary Disease
• Benign prostatic hyperplasia• Morbid obesity
• Essential hypertension• Hyperlipidemia
Ocular
• Primary open angle glaucoma OU, mild stage OU
• Mild nuclear senile cataract OU
• No h/o diabetic retinopathy OU
Differentials?Headache• Migraine with aura
• Giant cell arteritis
• Ocular ischemic syndrome
• Malignant hypertension
• Acute angle closure
• Intracranial lesion/mass/stroke
Flashes of lights• Retinal break/detachment
• Posterior vitreous detachment
• Retinitis
• Uveitis
• Retinal Migraine
Upon further questioning
Pt denies changes in vision, double vision, flashes, floaters, or pain currently
Pt denies fever, malaise, loss of appetite, fatigue, jaw claudication
Pt denies numbness/tingling/weakness to face or extremities
Pt denies mobility difficulties
Pt denies confusion/memory loss
Pt denies difficulty speaking/slurred speech
Exam Findings
• VA: distance cc
• OD: 20/25+2 PH 20/20‐2
• OS: 20/25‐2 PHNI
• Pupils: PERRL(‐)APD
• EOMs: Full
• Confrontation: inferior left constriction to fixation OD and OS
• Possible inferior left quadranopsia
• Habitual Rx:
• OD: ‐0.75 sph
• OS: ‐0.75 ‐1.75 x 120
• Refraction
• OD: ‐1.00 ‐0.25 x 047 20/20
• OS: ‐0.75 ‐3.50 x 118 20/25
Anterior Segment Findings
• Adnexa: Unremarkable
• Lids: Clear
• Conj: Clear
• Cornea: Clear, no Krukenberg spindle
• Anterior Chamber: Deep and Quiet
• Iris: Flat, no TID’s, no PXF Material, no NVI
• Lens: 1+ NS
• Ant Vitreous: Quiet, no Shafer sign
Posterior Segment Findings
• Nerve: No Drance hemes, no NVD, margins distinct
• C/D:
• OD: 0.55h/0.60v
• OS: 0.50h/0.55v
• Macula: Flat
• Posterior Pole: No NVE
• A/V: 2/3, mild tortuosity
• Periphery: Flat 360, no breaks
• Vitreous: Clear
Looking Back At Our Differentials:
No signs of venous stasis, retinal
hemorrhages, AC reaction
No signs of retinal break or PVD/Weiss
ring
No signs of shallow AC, pupil block, elevated IOP
No signs of elevated optic nerve margins, hemorrhages, or
CWSs
No signs of inflammation within vitreous, retina, or
choroid
Intracranial lesion, mass, or stroke…
Prior Visual Field
Visual Field Day of Exam The Visual Pathway
Assessment and Plan:
1. Other localized visual field defect, bilateral
• Ed pt on findings, visual field defects neurological, not corresponding to glaucomatous damage. Spoke on the phone with urgent care chief regarding case and suspected stroke 2 weeks prior, warm hand‐off of patient to urgent care clinic for further work up. PCP notified.
• RTC in 2 months for repeat 30‐2 HVF and DFE
2. Nuclear senile cataracts, bilateral
• Monitor.
3. Primary open angle glaucoma, mild stage, bilateral
• Stable ONH appearance, IOP well controlled, c/w Latanoprost 1 gtt QHS OU
Impression:1. There is a small area of
encephalomalacia involving the medial right occipital lobe within the right posterior cerebral artery distribution. This exhibits small areas of laminar necrosis. There is also involvement of small areas within the right hippocampus which would also be within the right posterior cerebral artery distribution. There is a third separate focus of encephalomalacia present in the left parietal lobe. This would be in the left middle cerebral artery distribution. Given the multiplicity of the vascular distributions, further evaluation with a CT angiogram of the head and neck may be useful as well as to evaluate for potential embolic source below the level of the aortic arch. 2. There is a mild to moderate degree of chronic small vessel ischemia.
6 Weeks Later
CT Scan report: “The diffusion‐weighted images are normal. There is no evidence of acute or subacute cerebral infarction.”
Same Day Urgent Care Clinic Testing:
2 Weeks Later Cardiologist Testing:
Echocardiogram Interpretation: There is mild concentric left ventricular hypertrophy. Left ventricular systolic function is low normal. Estimated left ventricular ejection fraction is 50‐55%.There is mild aortic valve sclerosis.The ascending aorta is mildly dilated at 4.2 cm.*No clots
Stroke Symptoms. Remember to act FAST!
• Facial drooping, where one side of the face sags downward
• Arm weakness, one arm cannot be lifted as high as the other
• Slurred speech, where the person cannot talk like normal
• Time – where time is of the essence for treatment!
Stroke Evaluation and Treatment
• Neuroimaging: CT then MRI
• Lab work: CBC, Glucose, PT/PTT/INR, Total Cholesterol/HDL/LDL, troponin, electrolytes, A1C
• If ischemic: tissue plasminogen activator, thrombolytic to break blood clots • ***must be within 3 hours of symptoms***
• If over 3‐6 hours, endovascular treatment• Angioplasty, stenting, mechanical embolectomy, intra‐arterial thrombolysis
• Prognosis: 5th leading cause of death, leading cause of disability, however low mortality rate from occipital lobe/PCA stroke
Occipital Lobe Stroke
Symptoms: visual field deficits, unilateral headaches, mild motor or sensory deficits, vertigo, memory impairment
Other areas affected by PCA stroke: inferomedial temporal lobe, thalamus, upper brainstem and midbrain
Etiology: embolism from large and small arteries, aortic and cardiac artery.
Less frequent: embolism from proximal vertebrobasilar artery
Uncommon: localized atherothrombotic stenosis of PCA
Other less common symptoms:
• Cortical blindness/visual anosognosia• Bilateral infarction of occipital lobes
• Visual agnosia/apperceptive or associative inability to describe/understand objects seen• Large left PCA stroke
• Prosopagnosia/difficulty recognizing faces• Inferior occipital area/right PCA
• Alexia/difficulty reading• Dominant occipital lobe often with right homonymous hemianopsia
• Achromatopsia• Ventral occipital cortex. Will be hemi!
Are we leaving out an important symptom?
• >75% sensitivity when used by ambulance staff• In this study, patients have already been admitted, unable to determine how many patients do not seek medical treatment with only visual symptoms
• 5‐10% of ischemic strokes include the occipital lobe
• Replacement: Act Very FAST, “VFAST”• V: visual field loss
• Delay in hospital admission means ineligibility for thrombolytic agents or endovascular treatment
We haven’t discussed the blue and red lights yet…
• Case Report: 64‐year‐old female with sudden right field loss and right field hallucinations including “colored pinwheels and lines at right angles…light exacerbated the positive phenomenon”
• MRI revealed signs of left occipital infarct
• Positive symptoms decreased over 1 week
• “The hallucinations may have resulted from infarction, with disinhibition of higher visual centers, or from simple partial seizures not detected by surface EEG”
• Reply: “Visual information reaches intact extrastriatevisual areas via pathways that bypass the main geniculostriate route” or “neural plasticity causes surviving areas of primary visual cortex to stimulate regions of higher visual areas that are not usually excited by this activity”
• Case Report: 56‐year‐old male with uncontrolled HTN and DM initially saw “a beautiful array of colorful waves lasting for 2 days over his right visual field”• Visual field revealed right homonymous hemianopia• MRI revealed subacute left posterior cerebral artery infarct • “Release hallucinations have been described as flashes of white or colored lights that originate from the retina or the primary receptive area for vision in the occipital cortex…corresponding to the visual field opposite to the lesion”• “Positive symptoms (hallucinations) to negative symptoms (hemianopsia) can be explained by ischemia that was followed by disinhibition of higher visual centers”
• 2 cases of visual hallucination in the visual field opposite location of subacute posterior cerebral artery occlusion
• Patient 1: right field, formed and prolonged hallucinations followed by paracentral scotoma
• Patient 2: left field, unformed, paroxysmal then prolonged hallucinations followed by paracentral scotoma
• In both cases, release hallucinations in opposite field of infarct
And the optometrist’s role?
Patient Outcomes, Possible Rehabilitation?
• Mortality low for occipital lobe stroke, morbidity high for field loss
• Inability to drive, loss of independence
• Inability to read comfortably left to right, loss of hobbies
• Patients with greater visual field defects report lower quality of life
• However, “About 10% of patients with VFD reported driving one‐month post‐stroke and 38% after 6 months.”
• Also, “Evaluation of VFD after 6 months revealed improvement in 52%.”
https://www.nei.nih.gov/sites/default/files/2019‐06/vfq_sa.pdf
Can we predict visual field recovery vs permanent
loss?• “Residual visual cortex activity for stimuli presented in the blind field soon after the stroke predicted the degree of retinal GCC thinning six months later”
• “Lesions of the occipital pole and convexity were not significantly associated with visual‐field recovery”
• “Homonymous visual‐field defects in our patients improved within 6 months. Restoration of the lower quadrants and especially the peripheral zones was noted. Incomplete damage to the striate cortex, which has a varying pattern of vascular supply, could explain this finding. Magnification factor theory, which is the increment of the receptive‐field size of striate cortex cells with visual‐field eccentricity, may explain the more significant improvement in the peripheral zones.”
Can we do therapy or
rehabilitation?
• “the early post‐stroke period appears characterized by gradual‐rather than sudden‐loss of visual processing”
• “subacute recovery was attained six times faster; it also generalized to deeper, untrained regions of the blind field, and to other (untrained) aspects of motion perception, preventing their degradation upon reaching the chronic period”
• “Our findings suggest that after V1 damage, rather than waiting for vision to stabilize, early training interventions may be key to maximize the system's potential for recovery.”
Glaucoma vs Neuro visual field defects and RNFL/GCL+IPL
changes!
The importance of optometric follow up!
A reduction of the cpRNFL thickness corresponding to the hemianopic visual field loss due to acquired post‐geniculate visual pathway lesions was detected using SD‐OCT, and the change was more evident at 24 months than at the initial visit. The latter finding suggests that this change is, at least partially, caused by transsynaptic retrograde degeneration.
And now back to our patient!
Visual Field 4 Month F/U
Exam DetailsDistance Visual Acuity: trifocalsOD: 20/25OS: 20/30‐2
Pinhole:OD: 20/NIOS: 20/NI
Pupils: PERRL, (‐) APDEOMs: Full, no restrictionsCover Test: ortho at distanceConfrontation: full to finger count OD and OS
Habitual:OD: ‐0.75 sphOS: ‐0.75 ‐1.50 x 114Add: +2.50
Refraction: Final: yesOD: ‐0.75 sph 20/25OS: ‐0.25 ‐1.50 x 110 20/25+2Add: +2.50
IOP: Goldmann @ 14:31OD: 14OS: 14
Anterior and Posterior Segments Stable
Vision Recovery
Reduction in the size of the visual field defect
Stable RNFL and GCL+IPL
Improvement in mobility and comfort ‘getting around’ independently
Still not driving, doesn’t feel comfortable yet
• Pt will return for a binocular visual field
References1. https://www.cdc.gov/stroke/treatments.htm
2. Brandt T, Steinke W, Thie A, PessinMS, Caplan LR. Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature. Cerebrovasc Dis. 2000 May‐Jun;10(3):170‐82. doi: 10.1159/000016053. PMID: 10773642.
3. Kuybu O, Tadi P, Dossani RH. Posterior Cerebral Artery Stroke. [Updated 2021 Jan 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan‐. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532296/
4. Lawlor M, Perry R, Plant GT. Is the 'Act FAST' stroke campaign lobeist? The implications of including symptoms of occipital lobe and eye stroke in public education campaigns. J Neurol Neurosurg Psychiatry. 2015 Jul;86(7):818‐20. doi: 10.1136/jnnp‐2014‐308812. Epub 2014 Nov 10. PMID: 25385853; PMCID: PMC4483785.
5. Gordon C, Bell R, Ranta A. Impact of the national public 'FAST' campaigns. N Z Med J. 2019 Dec 13;132(1507):48‐56. PMID: 31830016.
6. Vivid visual hallucinations from occipital lobe infarction, Alexander C. Flint, John P. Loh, John C.M. Brust; Neurology Sep 2005, 65 (5) 756; DOI: 10.1212/01.wnl.0000180350.58985.5f
7. Release Hallucinations as Harbinger Symptom of Posterior Cerebral Artery Infarction (5043), Carlos Millan, Vasu Saini, Amer Malik; Neurology Apr 2020, 94 (15 Supplement) 5043
8. Brust JC, Behrens MM. "Release hallucinations" as the major symptom of posterior cerebral artery occlusion: a report of 2 cases. Ann Neurol. 1977 Nov;2(5):432‐6. doi: 10.1002/ana.410020516. PMID: 617581.
9. Lawlor M, Perry R, Hunt BJ, Plant GT. Strokes and vision: The management of ischemic arterial disease affecting the retina and occipital lobe. Surv Ophthalmol. 2015 Jul‐Aug;60(4):296‐309. doi: 10.1016/j.survophthal.2014.12.003. Epub 2014 Dec 31. PMID: 25937273.
10. Goto K, Miki A, Yamashita T, Araki S, Takizawa G, Nakagawa M, Ieki Y, Kiryu J. Sectoral analysis of the retinal nerve fiber layer thinning and its association with visual field loss in homonymous hemianopia caused by post‐geniculate lesions using spectral‐domain optical coherence tomography. Graefes Arch Clin Exp Ophthalmol. 2016 Apr;254(4):745‐56. doi: 10.1007/s00417‐015‐3181‐1. Epub 2015 Oct 7. PMID: 26446718; PMCID: PMC4799802.
11. Tharaldsen AR, Sand KM, Dalen I, Wilhelmsen G, Naess H, Midelfart A, Rødahl E, Thomassen L, Hoff JM; NOR‐OCCIP Research Group. Vision‐related quality of life in patients with occipital stroke. Acta Neurol Scand. 2020 Jun;141(6):509‐518. doi: 10.1111/ane.13232. Epub 2020 Mar 18. PMID: 32078166.
12. Schneider CL, Prentiss EK, Busza A, Matmati K, Matmati N, Williams ZR, Sahin B, Mahon BZ. Survival of retinal ganglion cells after damage to the occipital lobe in humans is activity dependent. Proc Biol Sci. 2019 Feb 27;286(1897):20182733. doi: 10.1098/rspb.2018.2733. PMID: 30963844; PMCID: PMC6408898.
13. Çelebisoy M, Çelebisoy N, Bayam E, Köse T. Recovery of visual‐field defects after occipital lobe infarction: a perimetric study. J Neurol Neurosurg Psychiatry. 2011 Jun;82(6):695‐702. doi: 10.1136/jnnp.2010.214387. Epub 2010 Oct 9. PMID: 20935321.
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Questions?