2A

Acute Painless Homonymous

Hemianopsia

CASE NO. 2A

A 67-year-old woman presented in the emergency room complaining of grayish cloud over her right side vision which started in the morning. She also related some imbalance of walking that she felt was due to her visual field defect. When the symptoms did not resolve after about an hour, she decided to seek medical attention. Past medical history was significant for hypertension and diabetes. She was on oral antihypertensive and diabetic treatments. She did not smoke or drink. She had no prior ocular history. She denied any other neurologic signs or symptoms. There was no headadche, jaw claudication, or temporal artery tenderness.

On examination, the patient’s visual acuity was 20/25 in each eye. External examination was unremarkable and the temporal arteries were normal. Ocular motility was full in both eyes. The Goldmann visual field (Fig. 2A.1) revealed a dense right homonymous hemianopia. Slit lamp examination was normal. Ophthalmoscopy was unremarkable in both eyes.

Discussion

Dr. Brazis. A complete right homonymous hemianopia in this case indicates damage to retrochiasmal pathways on the left side. Because the hemianopia is complete, localization to specific structures (e.g. optic tract, occipital lobe, etc.,) cannot be determined without

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Emergencies in Neuro-Ophthalmology: A Case Based Approach

Fig. 2A.1. Goldman visual field showing the complete right homonymous hemianopia.

neuroimaging. However, an acute homonymous hemianopia without other neurologic impairments suggests an occipital lesion. As the onset of the visual field loss was acute, a vascular event, e.g. an ischemic infarct or cerebral hemorrhage, is the most likely etiology for the visual field defect.

The patient needs urgent neuroimaging. If an intracerebral hemorrhage is discovered, there may be little else to offer except supportive care and possible admission to the hospital. However, if the deficit is due to an acute ischemic infarction and the patient otherwise satisfies the criteria for treatment with tissue plasminogen activator (tPA), a tPA injection would be a consideration as long as the patient and/or her family fully understand and are willing to accept the potential risk of intracerebral hemorrhage (approximately 6.4% of patients injected) with this treatment.

Inclusion criteria for tPA treatment include:

•A clear time of onset of symptoms

•Injection within 3 hours onset of symptoms (defined as last time patient was symptom-free) – remember “Time is Brain”

•Measurable deficit on the NIH stroke scale (NIHSS)

•Patient’s age >18 years

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Acute Painless Homonymous Hemianopsia

Exclusion criteria for tPA treatment include:

•Intracranial hemorrhage or early changes of major infarction on CT scan

•History of stroke or head trauma in last 3 months

•Major surgery within last 14 days

•History of intracranial hemorrhage

•Severe hypertension (BP >185/110 mm Hg)

•Rapidly improving or minor symptoms

•Symptoms suggestive of subarachnoid hemorrhage

•Gastrointestinal or urinary tract hemorrhage within last 21 days

•Arterial puncture at non-compressible site within last 7 days

•Seizure at onset of stroke

•Use of oral anticoagulants or heparin

•Recent myocardial infarction

•Protime (PT) >15 seconds

•Platelet count <100,000/mm

•Glucose <50 or >400 mg/dl

The patient needs to have urgent neuroimaging in order to consider tPA treatment. We perform CT imaging including dynamic CT scanning with CT angiography and CT perfusion studies that rely on rapid rate scanning to follow the passage of an intravenously injected iodinated contrast agent through the cerebral circulation. Reduced cerebral perfusion in the absence of a cerebral blood volume abnormality is indicative of ischemic, yet potentially salvageable, brain tissue. Mismatch can thus be obtained by comparing the size of the cerebral blood volume abnormality with that of the perfusion disturbance. A mismatch implies tissue is at risk.

In this patient, a CT scan revealed no cerebral hemorrhage but the CT perfusion study (Fig. 2A.2) revealed an area of left occipital ischemia. Therefore, intravenous infusion of tPA would be warranted to attempt to improve her visual field deficit. Patients with cerebral infarct who received tPA are at least 30% more likely to have

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Emergencies in Neuro-Ophthalmology: A Case Based Approach

Fig. 2A.2. CT perfusion of the brain demonstrates increased mean transient time in the left PCA distribution consistent with ischemic change (circle).

minimal neurologic or no disability at 3 months as compared with patient’s who do not receive this drug. Thirty-one to fifty percent have complete or near-complete recovery at one year versus 20%–38% of a placebo group.

Treating physician should document in the medical record the reasons for the use or non-use of thrombolytic drugs. If the patient meets the treatment guidelines, and the ophthalmologist and the patient/family choose not to use thrombolysis, then we strongly recommend that the rationale and the clear discussion of the benefits and risks be documented. Likewise, if the patient does not meet the treatment guidelines, these should be documented as well.

Some facilities have experienced stroke teams available on a 24-hour basis that can perform urgent angiography on ischemic

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Acute Painless Homonymous Hemianopsia

stroke patients. In these centers, intra-arterial tPA or angioplasty/ stenting of the specifically occluded vessel causing the stroke is possible.

If the emergency department concerned does not have adequate coverage by physicians experienced in stroke care and modern technology, there are several options:

•Choose not to accept patients suspected of having stroke and divert them to a nearby stroke center if one is available.

•Upgrade the facility to meet the standards and then accept patients. This requires improving technology, adding experienced stroke clinicians, and facilitating throughput.

•If it is not feasible to divert to a nearby facility, consider connecting with such a facility by telemedicine or consultative arrangements to facilitate care.

Whether or not tPA is given for the acute infarction, the patient should be admitted to the hospital to further investigate the etiology of the infarction (e.g. a cardiac embolic source, atrial fibrillation, vertebral-basilar atherosclerotic disease, etc.) and to aggressively treat ischemic risk factor.

Dr. Lee. Like Dr. Brazis, the stroke treatment protocols for reperfusion in acute ischemic stroke (including those producing a homonymous hemianopsia) are at the discretion of the stroke team. Typically the ophthalmologist is making the diagnosis, ordering the imaging study urgently, and then referring the patient to the stroke service. The primary acute imaging of choice remains the non-contrast head CT scan to exclude acute hemorrhage or a large volume infarction. Although cranial CT is superior to MRI for acute bleed, a CT scan is not as sensitive as MRI with specialized sequences (e.g. diffusion or perfusion imaging) for acute cerebral ischemia. Unfortunately, reperfusion therapy may be inadvertently given to patients with a “stroke mimic” (e.g. migraine or seizure related Todd’s paralysis) and this decision is best left to the experts. Special MRI sequences based upon the restriction of the diffusion of water called diffusion-weighted

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Emergencies in Neuro-Ophthalmology: A Case Based Approach

imaging (DWI) can detect hyperacute ischemic stroke before structural change on CT or traditional MRI. In many of my patients who present with an acute, subacute or unknown duration for a homonymous hemianopsia, the CT scan is negative. If the initial CT is negative, then I typically recommend a cranial MRI with DWI sequences and contrast. If there is evidence for a prior old infarct but no acute infarct (negative DWI), then typically I will contact the stroke service by phone and let them proceed with an outpatient stroke evaluation at their individual discretion and timing rather than admit the patient.

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