How cerebrovascular disease has affected American history

ine American presidents are known to have suffered from strokes. In the case of John Quincy Adams and Chester Arthur, there were multiple strokes. In the case of Woodrow Wilson and FDR, crippling strokes occurred while they were in office, leaving the country without an effective leader.

The information in the table above is from the article “Stroke and the American presidency” by Meschia et al.^[1]

In both cases, the government and news media covered it up. Woodrow Wilson had a transient ischemic attack while giving a speech advocating for the League of Nations. As he began to say “Germany must never be allowed ...” he lost the ability to speak (aphasia) and shortly thereafter lost the ability to move his left arm and leg. Woodrow Wilson's stroke severely reduced his mental capacity, and was said to have saluted empty sidewalks. While bedridden in the White House, his wife Edith effectively ran the country as an unelected president.

Before he died of a stroke while still in office in 1945, FDR, who had been partially paralyzed from polio since 1932, became increasingly incapacitated. Some historians say this played a role in allowing Stalin to dominate eastern Europe in the Cold War. FDR's successor, Harry Truman, was unprepared for office, and the decisions he made still affect us today. If Truman had known about the atomic bomb earlier, would it have affected his decision? FDR's medical records mysteriously disappeared after his death, so the full impact of cerebrovascular disease on world history may never be known.

Years later, Lomazow and Fettman wrote a book^[2] claiming that FDR's stroke actually resulted from metastatic melanoma which spread from his forehead to his brain. Evidence for this comes from photos from that period, which the authors say showed a gradually increasing spot over his left eyebrow.

Eisenhower had a heart attack in 1955, and was being treated with coumadin (warfarin), and had a mild stroke two years later while still in office, leaving him with a speech impediment.

What is cerebral venous sinus thrombosis?

In 2012 Hillary Clinton, now a candidate for president, had a concussion. Two weeks later she was given an MRI scan and found to have a blood clot in the right transverse venous sinus, a large blood vessel in the back of the head near the occipital lobe. Because the Clinton campaign has not been forthcoming about her medical condition, there has been considerable speculation about her health. Is she having seizures? Is the party planning to replace her at the last minute? Does she have early Parkinson's disease, as one doctor claimed? We know very little.

Here is some basic information on cerebral venous sinus thrombosis, or CVST, taken from a variety of neurology textbooks and from the scientific literature.

The terminology means:

• Concussion = a head injury leading to unconsciousness. Head injury is regarded as synonymous with brain injury. Concussion is a vague term and usually means a head injury that causes an immediate but transient loss of consciousness followed by a short period of amnesia. About 10–15% of those with concussion have persistent post-concussion syndrome (PPCS), which is defined as cognitive symptoms (memory loss, depression, mood swings, and lack of concentration) lasting for one year or more.
• Cerebral = in the brain
• Venous sinus = A large vein that collects blood from other veins and sinuses on its way back to the heart. Brain sinuses are drained mostly by the internal jugular veins.
• Thrombosis = a blood clot

A CVST is a clot blocking the brain's venous sinuses. A CVST reduces the flow of blood leaving the brain. If the blood backs up it can compress brain tissue, or it can lead to hemorrhage and permanent loss of brain function. The clot can also get bigger and extend to the other sinuses that drain into it.

Removal may be attempted by injecting tPA, an enzyme that ‘dissolves’ blood clots. This is considered more aggressive treatment. Anticoagulants have no effect on the clot but reduce the risk that the clot will get bigger and completely occlude the vein. Although there is risk of hemorrhage with anticoagulant therapy it is considered lower than the danger of an untreated clot.

In 50% of cases CVST progresses to venous infarction. Infarction or stroke is death of the surrounding tissue, in this case the brain areas around the clot.

Here is what the medical literature says about the risk factors, symptoms and treatment.

Risk factors^[10]

• Head trauma with or without skull fracture (14% of patients)
• Prothrombic polymorphisms, commonly called thrombophilia (25.4%). A history of deep-vein thrombosis in the lower limb is a sign that genetic factors such as factor V Leiden or prothrombin mutations (e.g. G20201A) might be present.^[11]
• Hormonal stress in women, esp. oral contraceptive use or hormone replacement therapy (46%). Women are more likely to get CVST than men.
• Infections of head and neck (7%)
• Brain tumor (8%)

Symptoms

• Headache resembling migraine, sometimes severe or ‘explosive’ and long-lasting
• Sometimes pulsatile tinnitus
• Double vision or blurry vision
• Papilloedema (swelling of the optic disk in retina due to increased pressure in the brain)
• Altered conscious state or coma
• Focal deficits such as hemiparesis, seizures, impairment of consciousness in 1/3 to 3/4 of cases. Seizures may appear within the first year after CVT
• Nausea and vomiting
• Death occurs in 5.5 to 30% of cases.

Treatment

Heparin is given to prevent reoccurrence, followed by warfarin, which interferes with the production of vitamin K-dependent blood clotting factors. This drug is given for 3–6 months but may be needed for the rest of the patient's life if prothrombic conditions are present, that is to say if the patient has a history of blood clots.

Long-term Prognosis

Preter et al. ^[3] followed up 77 patients with CVT, which includes thromboses in smaller veins.

• 66 (85.7%) eventually recovered.
• 11 (14.3%) remained neurologically impaired.
• Of the 11 impaired, 2 were blind and 9 had various other deficits.
• 28 of the 77 had seizures in the acute phase; 4 had recurrent seizures. In all but one patient the seizures began within the first year after CVT. One developed a dural A-V fistula.
• In general CVT survivors had a ‘good’ long-term prognosis, since most of patients do not require long-term anticonvulsive therapy. Only 20% of patients had a second CVT, so only a minority of cases needed long term anticoagulation.
• About 13% of patients with CVST die within the first month after the onset of the disease.^[8]

Additional information: ^[4][5]. A good review of cerebral venous thrombosis and alternatives to warfarin is in ref.^[9]

Parkinson's disease and vascular dementia

There are reports on the Internet that she has Parkinson's disease or subcortical vascular dementia. I could find no reports in the literature linking CVST to Parkinson's disease and only a few linking it to vascular dementia. Repeated brain injury is a risk factor for PD, but a single concussion/stroke is probably unlikely to result in PD or SVD. This, of course, does not mean the claims of PD or SVD are wrong.

Parkinson's disease is not fatal. Patients with vascular dementia typically live about three years.

Memory loss

Subjective complaints including memory loss are common in later life, and their relationship to future risk of dementia is not clear. Studies have found a strong correlation between memory loss and impaired cognitive performance, depression, insomnia, and word-finding difficulties.^[6][7] Many factors besides stroke, including vitamin B12 deficiency and depression, can also cause memory loss.

1. J Meschia, Beth Safirstein, and José Biller “Stroke and the American presidency” J Stroke Cerebrovasc Dis. 1997 Jan–Feb;6(3):141–143 link (paywall)

2. http://www.macleans.ca/culture/books/the-huge-secret-about-fdrs-death/

3. Long-term prognosis in cerebral venous thrombosis. Follow-up of 77 patients. Preter M, Tzourio C, Ameri A, Bousser MG. Stroke. 1996 Feb;27(2):243–246. link

4. http://pmj.bmj.com/content/76/891/12.full

5. http://radiopaedia.org/articles/cerebral-venous-thrombosis

6. Int J Geriatric Psychiatry. 2001 Feb;16(2):168–174. Clinical characteristics of individuals with subjective memory loss in Western Australia: results from a cross-sectional survey. Clarnette RM, Almeida OP, Forstl H, Paton A, Martins RN. link

7. Stroke. 2005 Oct;36(10):2193–2197. Relationship between arterial stiffness and cognitive function in elderly subjects with complaints of memory loss. Hanon O, Haulon S, Lenoir H, Seux ML, Rigaud AS, Safar M, Girerd X, Forette F. link

8. Phlebology. 2015 Feb;30(1):3–10. Cerebral venous sinus thrombosis. Hartel M, Kluczewska E, Gancarczyk-Urlik E, Pierzchała K, Bien K, Zastawnik A. link

9. Neurologist. 2015 Nov;20(5):80–88. Cerebral Venous Thrombosis: Current and Newer Anticoagulant Treatment Options. Patel SI, Obeid H, Matti L, Ramakrishna H, Shamoun FE. link (paywall)

10. Thromb Res. 2016 Jan;137:26–29. Head trauma is the major risk factor for cerebral sinus-vein thrombosis. Giladi O, Steinberg DM, Peleg K, Tanne D, Givon A, Grossman E, Klein Y, Avigdori S, Greenberg G, Katz R, Shalev V, Salomon O. link

11. E.M. Wysokinska, W.E. Wysokinski, R.D. Brown, et al., Thrombophilia differences in cerebral venous sinus and lower extremity deep venous thrombosis, Neurology 70 (2008) 627–633. link

Last updated sep 14, 2016 5:58 am