Visual symptoms are very common following both ischemic and hemorrhagic stroke. These complaints have a tendency to receive the label “blurred” or “blurry” by both patients and healthcare providers, but an important part of accurate diagnosis and increasing the chance of improving these symptoms for the patient involves understanding what the problem is. Not all “blurry” vision after a stroke is actually “blurry”! Over time, I have found that visual deficits following a substantial brain injury tend to fall into one of the following categories. While scores of neurological conditions can result in these visual syndromes, for our purposes we will keep the focus on stroke.

Diplopia, or double vision, occurs when more than one image of an object is being visualized by the patient. This occurs most commonly because the eyes are not aligning properly to fixate on a visual target, and as a result of failing to converge at a specific point, mixed visual information is presented to the brain. When a patient has experienced a stroke, most often I find that the injury was in the brainstem, as there are centers controlling eye movements in this location. Double vision can also occur if there is an injury to one of the cranial nerves controlling eye movement closer to the eye itself, even if the brainstem is not injured.

Visual aura often is described as “blurry vision” by patients, but is much more complex than this description would suggest. Stroke patients may experience temporary visual illusions, such as the visualization of distorted surroundings, blurring of a crescent-shaped area or a larger section in a person’s visual world, flashing lights, wavy lines, development of “tunnel vision,” or any other number of transient visual symptoms. Fortunately, visual aura is very benign and treatable in most cases. Patients may be concerned that episodes of visual aura are TIAs, or transient ischemic attacks, that may represent the start of another stroke. I have seen people who have been taking warfarin or other big-gun anticlotting therapy for years because of “TIAs,” but when we get down to it turns out to be visual aura.

This MRI was obtained from a young postpartum woman after she noticed that she was unable to see objects in the right half of her vision. MRI confirmed the presence of a left occipital and temporal lobe injury due to stroke.

• Homonymous Hemianopia occurs when a visual field is distorted or absent, meaning that one half of someone’s visual world is impacted. Often patients will think they have lost vision in the right eye or in the left eye, when in reality upon testing, the eyes are fine, but the right half of the person’s visual world is absent. This typically occurs with an injury to the occipital lobe, the brain’s visual processing center. Put simply, the right occipital lobe processes visual information in the left field of vision, and the left occipital lobe processes the right field. A stroke impacting the right occipital lobe may result in loss of vision in the left visual field. The MRI brain (figure 1) was obtained from a young postpartum woman with a left occipital infarction with hemorrhagic conversion, which resulted in loss of vision in her right visual field.

Visual Hallucinations occur when a patient detects objects or movement that is not actually present. This can occur for a variety of reasons, involving either the brain or the eye. Charles Bonnet Syndrome is the name given to visual loss followed by the brain “filling in” missing visual information in the form of hallucinations. I have seen cases where the hallucinations are pleasant (a cuddly appearing kitten), and cases where they are disturbing (large insects). If visual hallucinations are present after a stroke, I always think it is worth performing an electroencephalogram (EEG) during the hallucination to better exclude seizure activity in the area of injury.

Oscillopsia is present when a patient perceives that objects at rest are “swaying” back and forth when movement is not actually present. This can occur with brainstem or cerebellar stroke, but I have seen it in other locations as well. Patients without stroke may experience this visual phenomenon with benign paroxysmal position vertigo (“inner ear” vertigo, as a lot of patients describe it) or with migraine as well.

Cortical Blindness typically involves injury to both occipital lobes. Patients lack vision, even though the eyes may be healthy. This can be devastating for patients, as these are typically patients who have always relied on vision who abruptly become blind without warning since stroke is usually of sudden onset. I attended an event in 2013 (Dining in the Dark) in which a nice dinner was served to us as we wore blindfolds. Have you ever considered how heavily you might depend on your vision to get through simple tasks, such as a meal? It gave me tremendous appreciation for what patients with cortical blindness after stroke must experience – to have vision one day, and for it to be gone the next is difficult to imagine. To make things even more challenging, some patients with cortical blindness develop Anton Syndrome, which involves blindness without the recognition that blindness exists. Now can you imagine everything around you seeming real, but none of what you are visualizing is actually there?

Finally, there is vision that is truly blurry. Regardless of the stroke’s location, patients often complain that their glasses prescription does not seem correct any longer. They may obtain a new prescription after the stroke, only to find that it is no longer accurate six weeks later. A neuroophthalmologist (this is a neurologist or an ophthalmologist who specializes in visual problems after a brain injury) can be helpful here, but it takes patience from both patient and physician as symptoms tend to fluctuate.

Just after New Year’s Day in 2013, I was asked by a local news station about a story in the mainstream media involving a “blood clot in the brain.” At-the-time Secretary of State Hillary Clinton had fallen and hit her head, and this was followed soon afterwards by a diagnosis of a blood clot “in the vein between the brain and…skull,” according to this news article. I recognized over the following week while the story played out in the news that, while Clinton’s clot was not the same thing as one might think of an ischemic stroke, there was little understanding outside of the medical community of how her neurological issue differed from the large majority of blood clots in the brain. I even received several questions about it from patients, the most common one being – did Hillary Clinton have a stroke? And my answer was – not exactly.

Ischemic strokes, as we think of them, involve an obstruction in an artery that is preventing oxygen-rich blood from reaching its target destination within the brain. Arteries can be blocked by blood clots, plaque accumulation within the wall of the vessel, a torn lining in the wall of the artery (dissection), or even overgrowth of cells within the blood vessel wall (hyperplasia). Veins, on the other hand, drain blood away from the brain and back to the heart once the oxygen has been extracted from it. Veins of significant size in the brain are called venous sinuses, as they are structured more like collecting pools for the drainage of blood that is no longer rich in oxygen. A clot that occurs in one of these venous sinuses are known as a cerebral venous sinus thrombosis (CVST). It is much less common to develop an obstruction blocking blood flow in one of the brain’s veins than it is within an artery. According to the scientific statement published by the American Heart Association/American Stroke Association in 2011, only 0.5 to 1 percent of strokes result from a blood clot in a cerebral vein.

People might be familiar with the concept of a venous clot, such as in a leg if one sits in a car or on an airplane for a prolonged period of time. However, venous clots can occur anywhere in the body, including in the brain.

Various factors may lead to increased risk of clotting in one of the venous sinuses or in a cerebral vein. It is important to understand that in all of us, our blood is in a constant state of flux. Just as the American government is set up with checks and balances such that the branches can more-or-less keep each other in check, our blood has millions of molecules pushing it towards clotting, and millions breaking down clots. We need to clot so we do not hemorrhage. Yet, our blood needs to be able to flow to our organs, and if it can’t because of extensive clotting then heart attacks, strokes, and other catastrophes develop.

There are certain genetic mutations that can cause blood to clot more readily, such as the factor V Leiden mutation or the prothrombin mutation. There are people who lack certain proteins that assist with breaking down clots, and in the absence of these proteins clots are more likely to develop. Deficiencies of protein C and protein S are two of the more common examples of this. Autoimmune disorders can increase the risk for clotting in general, such as can be seen with lupus and antiphospholipid antibody syndrome. The use of certain types of birth control pills can cause elevated risk of CVST, as can pregnancy, because elevated estrogen levels have been associated with thrombosis. Cancers and systemic infections/sepsis can cause massive hemorrhaging or diffuse clotting. Significant concussions or skull fractures can also result in CVST.

The most common initial symptoms of CVST are headache, visual changes, and/or seizure. A headache that continues to escalate for days to weeks, especially in a patient taking birth control pills, who is pregnant, or who has a history of abnormal clotting should undergo MRI of the brain. Standard MRIs are sensitive enough to detect most CVST, but if there is any question an MR-venogram or a CT-venogram of the head should be performed. If CVST is identified, the treatment is an anticlotting medication. Warfarin is the most common medication used for this, although rivaroxaban (Xarelto), apixaban (Eliquis), and dabigatran (Pradaxa) have been used more recently as off-label agents. In pregnant patients, enoxaparin (Lovenox) is typically used because it is thought to be safe (pregnancy Category B). Warfarin is known to cause birth defects (pregnancy Category X), and the effects of the other oral agents on fetal development is unknown at this time. Warfarin can be used safely in breastfeeding mothers once the baby is delivered.

Venous sinuses within the brain drain blood and send it back to the heart. Image source: http://www.dartmouth.edu/~humananatomy/

In my experience, patients with CVST do very well clinically once started on an anticlotting therapy, especially if the clot is identified early. Secretary Clinton’s treating physician claimed in this news article that she had a clot in the transverse sinus. The nice thing about transverse sinuses is that there are two of them, and when one is blocked due to the presence of clot, blood is usually still able to drain from the brain. Her physician also noted that she had a deep venous thrombosis (DVT) in the 1990s, suggesting she might be at risk for clots. If people are at particular risk for clot formation, being dehydrated does not help (Clinton was reported to have influenza during that time), as the blood becomes more concentrated. While he described the condition as “potentially life-threatening,” in the dozens of transverse sinus thromboses I have treated, none of these patients have died, and the recovery is very favorable. Even patients with very large superior sagittal sinus thromboses do very well typically if recognized early and started on therapy.

When making a determination about whether a patient has had a stroke if an artery is blocked, we require that some degree of damage has occurred in the brain before calling it a stroke. If there is no damage and the patient has no lingering symptoms in this scenario, then the diagnosis of a TIA, or transient ischemic attack, is made. In the case of CVST, if diagnosed and treated early and lacking any evidence of damage to the brain, it probably should not be labeled as a stroke either. While it may be convenient to throw all CVST cases in the “stroke” bucket, many of these patients will not sustain permanent brain injury, and will go on to lead productive lives without lingering evidence that such an event ever occurred. So did Secretary Clinton have a stroke? I stand by my answer of – not exactly.

Would I expect something like this in Secretary Clinton’s medical history to prevent her from carrying out the duties of the presidency if she is elected in November? No more than migraines would have stood in Michele Bachmann’s way in 2012, or than atrial fibrillation would have prevented Bill Bradley from performing presidential tasks. By the time adults reach their 50s or 60s, it is almost an inevitability that a health condition of some sort will be present. If we want candidates for president in near-perfect health, we could change our laws and elect a very young person as our commander-in-chief, but then we lose the presence of life experience.