The term "stroke" or "paralytic stroke" is commonly used to describe a sudden neurological affliction that is usually related to cerebral blood supply. A "stroke," therefore, can be due to cerebral ischemia, infarction, or hemorrhage, and usually implies permanent neurological deficits. (1) All three of these causes, cerebral ischemia, infarction, or hemorrhage, would be characterized as manifestations of cerebrovascular disease.

Cerebrovascular disease can be further defined as any type of pathophysiologic vascular disease of the brain. This vascular pathology can include any abnormality of the vessel, blood flow, or quality of the blood. (2) Other terms for this abrupt onset neurologic deficit include apoplexy, or cerebrovascular accident (CVA). In the United States, the term stroke is most often used to describe cerebral infarction. It is preferable to use the more precise terms, cerebral ischemia, cerebral infarction, or intracranial hemorrhage. Cerebral ischemia is caused by a reduction in blood flow that lasts for several seconds or a few minutes. If the cessation of flow lasts for more than a few minutes, infarction of brain tissue results.

Ischemia and infarction constitute 85-90 percent of strokes in western countries, with 10-15 percent being caused by intracranial hemorrhages. The morbidity and mortality from cerebrovascular diseases has actually decreased in recent years, due mostly to better recognition and treatment of underlying factors such as hypertension and cardiac diseases that increase the risk of stroke.

General population studies show atherothrombotic infarction is the most common type of stroke, representing almost 65 percent of the reported cases of the 85 percent caused by ischemia. Therefore, the majority of strokes are caused by ischemia and infarction secondary to disease of the large, small, and medium-sized arteries supplying the brain. Cerebral embolism causes stroke about 20 percent of the time. Hemorrhage into the brain tissue (cerebral or intraparenchymal hemorrhage) and subarachnoid hemorrhages account for about 15 percent of all strokes.

Ischemic cerebrovascular disease is divided into two broad categories: thrombotic and embolic. When it occurs in elderly patients, particularly those with manifestations of atherosclerosis, the term atherothrombotic, or atherothromboembolic may be used. Although the precise reason for ischemia may not be determined, the term is used when it seems likely that atherosclerosis-induced thrombosis occurred and the thrombus then lysed, or embolized, distally and fragmented. Thrombotic strokes occur without warning symptoms in 80-90 percent of patients. Between 10 and 20 percent are heralded by one or more transient ischemic attacks. Thrombotic strokes often present with stuttering, fluctuating symptoms that worsen over several minutes or hours. Embolic strokes usually present with a neurologic deficit that is maximum at onset. (3)

Cerebral ischemia is further divided into focal and general, or global, ischemia. Global ischemia refers to a situation where little or no collateral circulation exists and irreversible brain damage occurs in a short period of time. In focal ischemia, however, there is some degree of collateral circulation, which may allow for survival of brain cells and reversal of neuronal damage after periods of ischemia.

Normal cerebral blood flow in humans is about 53ml/100g of brain tissue per minute. Reductions in the cerebral blood flow to the range of 15-18ml/100g/min result in abnormal brain electrical activity. At a flow of 10ml/g/min, alterations in intracellular calcium and extracellular potassium homeostasis occur. Also, free fatty acids are released, and adenosine triphosphate (ATP) is depleted. A severe intracellular acidosis ensues in cells in the ischemic area. (4)

Within 10 seconds after cerebral blood flow ceases, metabolic failure of brain tissue occurs. The encephalogram shows slowing electrical activity, and brain dysfunction becomes clinically manifest. If the circulation is immediately restored, there is abrupt and complete recovery of function. If the perfusion abnormality persists for a few minutes, neuronal injury results. With restoration of flow, the recovery of function takes several minutes or hours and may be incomplete. (5) Additionally, during the period of circulatory failure, blood elements may sludge, the capillary endothelium may swell, and blood flow may not reestablish itself, even when the initial cause of blood flow failure has been corrected. This is known as the "no re-flow" phenomenon. Longer periods of ischemia will result in frank tissue necrosis.

Atherosclerosis of the brain arteries occurs in a similar fashion to atherosclerosis found anywhere else in the body. It is generally felt that the atherosclerotic process occurs in a parallel fashion throughout the body, although the arteries of the brain might be affected slightly less than the aorta, coronary arteries, and arteries of the extremities. Atherosclerosis is usually maximal at arterial bifurcations, and in the brain, seems to most commonly affect the origin of the internal carotid artery in the neck, and the origin of the major and minor arterial branches inside the head. The atherosclerotic process includes plaque formation and subsequent narrowing or occlusion of arteries and constitutes the most common cause of aortocranial stenosis. Plaque formation also stimulates platelet aggregation, which further increases the risk of thrombosis.

Occlusion of the small arterial branches of the circle of Willis and of the cerebral and basilar arteries can result in infarcts deep within the cerebral hemispheres and brainstem. These are termed lacunar infarcts. They are generally anywhere from 2-15mm in diameter. The terms "lacunar" or "lacune" are derived from the term used to describe the small cavity left after necrotic tissue has been removed. The pathophysiology of these infarcts is somewhat different from those occurring closer to the surface of the brain. About 25 percent of all strokes are a result of lacunar infarcts. Arterial hypertension is closely related to the occurrence of these infarcts and is the major risk factor for lacunar disease.

The pathophysiology of the small arteries has been described as being a degenerative process in the media of the artery (lipohyalinosis), leading to vessel occlusion. The degenerative occlusive process may be, on occasion, histologically different in appearance compared with the atherosclerotic process affecting extracranial and other large intracranial arteries, and may in fact, circumscribe portions of the involved artery. (6) The patient’s clinical presentation will reflect which small branches are involved in the occlusive process.

As stated earlier, there are two broad categories of ischemic cerebrovascular disease. Thus far, thrombotic causes of stroke have been discussed. The other broad category of cerebrovascular ischemia is cerebral embolism. Approximately 20 percent of strokes are caused by emboli. While any region of the brain may be affected by embolism, the middle cerebral artery is commonly involved. The most common types of embolism result from pieces or fragments of an arterial thrombus that have broken off, or from a heart valve vegetation. The embolus usually circulates until it is too large to traverse the arterial lumen. The point of occlusion is often a bifurcation or other narrowed area, and both hemispheres of the brain appear to be equally affected. Hemorrhage often occurs in the embolic process, due to reperfusion of blood into ischemic tissues. The size of the embolus may vary greatly; from large to so small that the infarct is virtually undetectable. Emboli may result from other sources, such as an ulcerated atheromatous plaque, air, fat or tumor cells, but these occur infrequently.

Cerebral embolism from bacterial sepsis occurs frequently, but bacterial emboli large enough to produce a stroke are infrequent. Cerebral embolism secondary to thrombotic disease usually has a rapid onset and is not preceded by TIA. This rapid onset is problematic because there is less time for collateral circulation to develop, as in cerebral thrombosis. As a result, embolic strokes are often functionally devastating. (7) Embolism has been associated with many types of heart disease, but by far, the most common cause is atrial fibrillation. Thromboembolism is also found frequently in patients with valvular heart disease, and those with prosthetic heart valves, as well as patients with mitral stenosis.

The third most frequent cause, accounting for approximately 15 percent of strokes, is intracranial hemorrhage. Some frequent causes of intracranial hemorrhage include hypertensive intracerebral hemorrhage, ruptured saccular aneurisms, hemorrhage associated with bleeding disorders, anticoagulation, and arteriovenous malformations. Hypertensive intracerebral hemorrhage occurs as a result of significantly elevated blood pressure and rupture of an artery. This allows for extravasation of blood into the brain tissue, which forms a mass. As bleeding continues, the mass enlarges, pushing aside other tissue. As tissue is pushed, displaced, and compressed, brain function may be impaired.

While many risk factors have been identified that predispose patients to stroke, hypertension, is by far, the greatest. Hypertension is strongly related to atherothrombotic infarction as well as hemorrhage, and has been identified as a factor in 70 percent of all strokes. The Framingham study indicated that there is a direct relationship between elevation of blood pressure and stroke risk. (8)

Impaired cardiac function is the next most important single treatable risk factor for stroke. Individuals with cardiac diseases such as coronary heart disease, congestive heart failure, left ventricular hypertrophy, and arrhythmias (specifically atrial fibrillation) have more than twice the stroke risk compared to those with normal cardiac function. (9) Atrial fibrillation is strongly correlated with embolic stroke, and those patients with nonrheumatic atrial fibrillation have a six fold increase in stroke frequency over those without fibrillation. (10) , (11) , (12)

Transient ischemic attacks (TIAs) are defined as episodes of focal ischemic neurologic deficit lasting less than 24 hours. (13) The most common duration is a few seconds up to five to 10 minutes, depending upon the territory of the brain where the event occurs. Complaints and symptoms depend upon the part of the cerebrovascular tree (e.g., carotid artery, vertebrobasilar artery, or both) that has been affected by diminished or absent blood flow. Often, TIAs occur as a result of emboli, which break away from distant blood clots. These emboli are then dissolved by the fibrinolytic system, allowing return of normal blood flow and neurologic function. The more frequently TIAs occur, the higher the probability of stroke, and a previous stroke is a greater risk factor for subsequent stroke than a TIA alone. (14) The term reversible ischemic neurologic defect (RIND) has also been used when describing ischemic events the last greater than 24 hours, but completely resolves within three weeks.

Other patient populations considered at higher risk for the development of stroke include those with sickle cell disease, and middle-aged male patients with a maternal history of stroke. Patients with an elevated hematocrit are also considered at higher risk for stroke due to increased blood viscosity.

Hyperlipidemia and hypercholesterolemia are risk factors for the development of atherosclerosis, which increases the risks of both coronary heart disease and stroke. Another major risk factor for both ischemic and hemorrhagic stroke is cigarette smoking. Postulated causes include increased blood concentration of fibrinogen, increased platelet aggregability, decreased HDL-C, damage to the vascular endothelium, and increased hematocrit. Smokers had two to three times the risk of stroke compared with non-smokers, and a four fold to six fold increase in stroke risk compared with those who had never smoked. (15)


World Health Organization, 2002.

  • Annually, 15 million people worldwide suffer a stroke.
  • Of these, 5 million die and another 5 million are left permanently disabled, placing a burden on family and community.
  • Stroke is uncommon in people under 40 years; when it does occur, the main cause is high blood pressure.
  • Stroke also occurs in about 8% of children with sickle cell disease.
  • Treating hypertension can reduce the risk of a stroke by up to 40%.

American Heart Association Statistical Update, 2005.

    Each year 700,000 people experience a stroke. On average, someone in the United States has a stroke every 45 seconds, and every 3 minutes, someone dies from a stroke. 40,000 more women than men experience strokes. Strokes accounted for more than 1 in 15 deaths in the US in 2002. From 1992 to 2002, the rate of deaths actually dropped, but the number of strokes increased.
  • African Americans have about twice the risk of a first stroke incident than Caucasians.

Not available

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Thrombosis of cerebral vessels produces different clinical signs and symptoms when compared to embolic disease or intracranial hemorrhage.

Thromboses involving the middle cerebral arteries:

  • Mono- or hemiplegia
  • Mono- or hemiparesthia
  • Blindness in one eye
  • Speech disturbance
  • Short lived and resolve in less than 10 minutes
  • Most often develops as a single attack or may present as an intermittent progression over hours to days
  • Signs and symptoms vary based upon the area of the brain affected: Progressing stroke – patient suffers partial stroke, improves for several hours, then develops full paralysis of one or more parts of the body with other parts become paralyzed in a stepwise manner until the stroke is completed
If the vertebrobasilar system is involved, symptoms may include:
  • Dizziness
  • Diplopia Numbness Impaired vision Dysarthria
Lacunar infarcts:
    Depends upon the perforating cerebral arteries involved
  • Most frequent symptom is pure motor hemiparesis manifesting as hemiparesis or hemiplegia of the arm, face, leg, and trunk
  • Mild dysarthria may occur without sensory or consciousness alterations or visual field defects
  • Produces same degree of weakness in all affected body parts unlike strokes that take place in the anterior or middle cerebral artery which cause varying degrees of weakness in affected parts of the body
    Difficult diagnosis as episode is usually over before the patient can be examined
  • Diagnosis made usually based upon the patient’s recollection of symptoms
  • Last only five to 10 minutes
  • TIAs lasting one or more hours may be the result of an embolism
  • Signs and symptoms vary based upon the area of the brain affected
  • Carotid system lesion and anterior cerebral artery - weakness in opposite leg and shoulder
  • Anterior cortical branches of the middle cerebral artery - sensory and motor loss in contralateral face, arm, and hand
  • If ischemia is in the dominant hemisphere, often a nonfluent (Broca’s) aphasia is present
Posterior portion of middle cerebral artery:
    Contralateral sensory loss
  • Homonymous hemianopia (defective vision or blindness that affects the right halves or left halves of the visual fields of the two eyes)
  • If the ischemia is in the dominant hemisphere, fluent aphasia is likely
  • Lenticulostriate arteries (generally lacunar infarcts)
  • Motor hemiparesis of the arm, face, leg, and trunk
Cerebral embolism - Clinical features suggestive of cardiogenic brain embolism include as primary features:
    Abrupt onset of maximal deficit
  • Presence of potential embolic source (atrial fibrillation, valvular heart disease, prior stroke)
  • Infarct involving the cerebral cortex or cerebellum
  • Previous ischemic events in other vascular territories
  • Secondary features include:
    • Hemorrhagic infarct by CT
    • Absence of occlusive cerebrovascular disease by cerebral angiography or reliable noninvasive imaging
    • Angiographic evidence of vanishing occlusions
    • Evidence of embolism to other organs
    • Cardiac thrombi demonstrated by echocardiography, catheterization, cardiac CT, or MRI
Intracranial hemorrhage:
    Abrupt onset of signs/symptoms
  • Changes occur over minutes to hours
  • Gradual evolution may depend upon bleeding rate and accounts for the time range for deficit to become maximal
  • Neurologic findings vary with the location of bleeding, and the size of the bleed;
  • Loss of consciousness is usual
  • Head pain and dizziness prior to losing consciousness
Hypertension-related external capsule (putaminal) hemorrhage:
    Hemiplegia quickly develops with loss of consciousness
  • Most often associated with prolonged hypertension and usually occurs when awake
  • Conjugate deviation of the eyes to the side opposite the affected limbs is commonly seen
  • Headache (approx 50 percent of patients)
  • Neck rigidity is common
  • Vomiting may occur
  • Convulsions may occur
Internal capsule (thalamic) hemorrhage:
    Similar onset as hypertension-related external capsule
  • If the patient is still alert, a homonymous hemianopia may be observed due to optic nerve involvement

Treatment Options


Treatments for cerebrovascular disease are generally divided into categories of prevention and acute management. Many risk factors for stroke have been clearly identified. Family history of thrombotic stroke, diabetes mellitus, hypertension, tobacco smoking, and elevated cholesterol are among those proven or are at least probable to increase risk of stroke, largely by their link to atherosclerosis. Of the atherosclerosis factors, hypertension is of the greatest importance. Generally speaking, all hypertension should be treated, as all stages of hypertension are linked with increased risk of cardiovascular disease events and renal disease. The first line of treatment should be through life-style modification and diet.

Clinical trials have shown the beneficial effects of aspirin in men in prevention of secondary TIAs as well as in producing a decrease in major vascular events. A dose of 325mg to 1,300mg/day can be recommended in preventing strokes and TIAs. (16) The effectiveness of doses less than 300mg/d for TIA or minor strokes of arterial origin is still unresolved and further study needs to be conducted.

Other general recommendations are as follows:

    Aspirin 325mg/day for secondary stroke prevention, if the stroke is not due to atrial fibrillation. The use of enteric-coated aspirin may be beneficial and better tolerated in some individuals. Ticlopidine 250mg twice a day or clopidogrel 75mg daily orally are currently recommended alternatives to aspirin in cases of patient intolerance to aspirin, or if failure to eliminate or decrease TIAs occurs. For patients with nonvalvular atrial fibrillation who are at low risk for stroke, aspirin 325mg/day is recommended. For patients with nonvalvular atrial fibrillation who are at high risk for stroke, warfarin is recommended. Dosing must be done very carefully, with particular attention being paid to the patient’s INR. Patients must be monitored closely for bleeding. Alteplase 0.9mg/kg infused over one hour after a bolus of 10% total dose is recommended as emergency therapy in acute ischemic stoke if CT scan is negative for intracranial hemorrhage and if therapy can be initiated within three hours of the acute event. Patient selection is critical and strict adherence to AHA guidelines is mandatory in order to avoid bleeding complications. Monitor patient closely for bleeding. (17)

Surgery is done when the goal is removal of the source of occlusion and/or embolus, and increase in cerebral blood flow to an ischemic area. Carotid endarterectomy is the most common surgical procedure used for occlusive cerebrovascular disease. The procedure involves exposing the carotid artery in the neck and removing the occlusive atheromatous plaque usually at the carotid bifurcation. The indications for such procedure are generally TIAs and mild completed stroke in the presence of ulcerated or highly stenotic (>75%) plaque.

Nutritional Supplementation


Policosanol is a natural mixture of higher aliphatic primary alcohols isolated from sugar cane wax with cholesterol-lowering effects demonstrated in experimental models and in patients with type II hyperlipoproteinemia. (18) , (19) , (20) , (21) The lowering of blood cholesterol can be directly correlated to a decrease in stroke and/or CVA. (22) , (23)

In a laboratory animal study, oral administration of policosanol in rats provided a partial inhibition of lipid peroxidation, protecting against membrane lipid peroxidation and to some extent against free radical-associated diseases. (24) Policosanol has also been reported to protect against the development of atherosclerotic lesions in laboratory animal studies. (25) Another laboratory study reported that policosanol has an anti-ischemic effect in animals with cerebral ischemia, suggesting a possible therapeutic effect in cerebral vascular disorders. (26)

Folic Acid, Vitamin B6

Elevated plasma homocysteine levels are now recognized as an important independent risk factor to stroke and other forms of cardiovascular disease. (27) It is now well accepted that three B-vitamins, folic acid, vitamin B6, and vitamin B12 are methyl donors that are required for the metabolism of homocysteine. Inadequate levels of any of these B-vitamins can result in hyperhomocysteinemia, which represents an increased risk to stroke as well as a host of other cerebral and cardiovascular problems. (28) , (29)

Docosahexaenoic Acid (DHA)

Animal studies with stroke-prone spontaneously hypertensive rats indicate that administration of DHA for 5 weeks resulted in a significant reduction of blood viscosity, hematocrit, and fibrinogen when compared with the placebo controls. These improvements reduce the risk of thrombosis. (30)

Dietary fish oils are becoming increasingly recognized for their ability to protect against cardiovascular disease. (31) This prompted the design of a study that examined the relative effect of eicosapentaenoic acid and docosahexaenoic acid on cardiovascular risks. Docosahexaenoic acid proved to be significantly more effective at reducing stroke-related risk factors such as hypertension and inhibition of thromboxane-like vasoconstriction. (32) These results indicate that docosahexaenoic acid may be the primary agent in fish oils that is responsible for providing cardiovascular protection.

A Japanese study reported levels of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were significantly higher in individuals who lived in fishing villages where deaths from strokes were relatively low compared to people who lived in farming villages where the incidence and death rate from strokes was much higher. (33)


Results from the Nurses Health Study reported that the dietary intake of potassium was inversely associated with the incidence of ischemic stroke in women (34) and potassium has also been identified as a significant modulator of stoke risk in men. (35) , (36) In an 8-year study, men with the highest dietary potassium intake were 38% less likely to incur a stroke compared to men with the lowest potassium intakes. (37)

The results from a 12-year prospective study support the hypothesis that a high intake of potassium from food sources provides a substantial level of protection against stroke-related deaths. (38) It was also determined from this study that a 10-mmol increase in daily potassium intake was resulted in a 40 percent decline in the risk of stroke-associated mortality.


Data from the Nurses Health Study revealed the dietary intake of magnesium was inversely associated with the incidence of ischemic stroke in women. (39) Studies also report that magnesium is a significant modulator of stoke risk in men (40) and that men have a higher dietary intake of magnesium have a substantially lower risk of stroke compared to men consuming lower amounts of magnesium. (41) It has also been reported that patients with ischemic stroke have significantly lower magnesium concentrations in blood serum and cerebrospinal fluid compared with control patients. (42)

Antioxidant Nutrients

Oxidative free radical damage probably plays a role in the neuronal damage induced by the ischemia-reperfusion process that accompanies strokes. The levels of several antioxidant nutrients, including ascorbic acid, are associated with the degree of post-stroke neurological impairment. These results indicate that plasma antioxidant activity may be an important factor providing neurological protection from stroke-associated oxidative stress. (43)

Data from the Second National Health and Nutrition Examination Survey (NHANES-II) revealed that serum ascorbic acid levels were closely associated with the prevalence of coronary heart disease and stroke. An increase in serum ascorbic acid levels of 0.5 mg/dL resulted in an 11% reduction in the occurrence of coronary heart disease and strokes. (44)

Outcome data from the 30-year prospective Chicago Western Electric Study evaluated the effect of various antioxidants on the risk of strokes. Individuals in the upper quartile of dietary vitamin C consumption had a 29% reduction in the incidence and mortality from strokes compared to individuals in the lower quartile of dietary vitamin C consumption. (45)

In a larger review of studies from 1966 to 1996, researchers found that vitamin C provided significant protective effects against strokes in two of two ecological studies, none of one case-control study, and two of seven cohort studies. These results, although limited, suggest that vitamin C provides some level of protection against strokes. (46)

Acetyl-L-Carnitine (ALC)

Results from animal studies indicate that acetyl-L-carnitine promotes neurological recovery from experimentally induced stroke in rats. In this study, treatment with acetyl-L-carnitine improved early clinical recovery and reduced the level of weight loss in the animals that experienced strokes. (47) A group of human patients with chronic cerebrovascular disease, who suffered an ischaemic stroke at least 6 months before the study, received intravenous acetyl-L-carnitine. Administration of IV acetyl-L-carnitine resulted in a significant increase in cerebral flood flow. (48)


In a study of 1,110 men in Finland between the ages of 55 to 74 who were initially free of cardiovascular disease, there was a strong correlation between low serum selenium levels and subsequent strokes. (49)


Outcome data from the 30-year prospective Chicago Western Electric Study involving 1,843 middle-aged men evaluated the effect of various antioxidants on the risk of strokes. Individuals in the upper quartile of dietary beta-carotene consumption had a 16% reduction in the incidence and mortality from strokes compared to individuals in the lower quartile of dietary beta-carotene consumption. (50)

Herbal Supplementation


Ginkgo is among the oldest living species on earth and has been used extensively as a medicinal agent worldwide for centuries, and is the most frequently prescribed medicinal herb in Europe. The most dramatic benefits are reported in improving circulation in the elderly. (51) , (52) This can lead to enhanced memory, delaying the onset of Alzheimer's (53) and reducing senile dementia, (54) tinnitus, (55) and vertigo. (56) Ginkgo’s memory-enhancing effects are reported in younger populations as well. The main active components of ginkgo are the flavoglycosides. These compounds act as strong free radical scavengers or antioxidants. (57) Ginkgo is also reported to inhibit platelet activating factor (PAF) which could reduce the adhesive nature of platelets possibly through competitive binding, thereby decreasing the risk of stroke and/or cardiovascular accident. Ginkgo may foster vasodilation by stimulating endothelium releasing factor and prostacyclin. (58) It may also stimulate venous tone and improves the clearance of homotoxins during ischemic episodes. (59) Gingko reportedly acts as a tonic for the circulatory system. It may increase cerebral brain flow and, therefore, improve delivery of nutrients to the brain, enhancing elimination of the by-products of cell metabolism and oxygenating the tissues. (60) Ginkgo may normalize acetylcholine receptors and, therefore, improve cholinergic function. (61)


Hawthorn is used as a vasodilator and circulatory stimulant. (62) It has been used extensively by doctors in Europe in its standardized form in various cardiovascular and peripheral circulatory conditions. Studies have reported a reduction in blood pressure due to arteriosclerosis and chronic nephritis with the use of hawthorn. (63) It is also used for peripheral vascular diseases, such as Raynaud’s disease. Hawthorn is used in Europe by physicians to help maintain digoxin levels while decreasing the need for the pharmaceutical medication. Hawthorn is reported to have the ability to regulate both low and high blood pressure. Its bioflavonoids reportedly dilate both peripheral and coronary blood vessels. (64) This leads to its use in decreasing angina attacks. The proanthocyanidin (PCO) content is claimed to support the spasmolytic effects. (65) The PCO content also is thought to be responsible for the coronary circulatory effects, increasing the amplitude of the heartbeat. (66) Hawthorn’s glycoside component reportedly increases the vagal tone of the heartbeat. (67) It is also thought that hawthorn inhibits angiotensin-converting enzyme. (68) It has a slight diuretic effect which may help lower high blood pressure. Laboratory studies have reported that proanthocyanidins may actually aid in reversing atherosclerotic plaque. (69)


Cordyceps provides potential value in stroke cases because of its ability to improve VO2max by approximately 10%. This could result in improved perfusion of oxygen to ischemic areas. Cordyceps may modulate immune function and optimize endocrine systems, increasing physical strength and endurance. (70) , (71) Cordyceps has traditionally been used for its improvement in respiration and in individuals with decreased lung function, such as asthma and bronchitis, by increasing oxygenation (improving VO2 max by 9-15%). (72) Cordyceps has been reported to have anticancer effects by decreasing proliferation and differentiation of cancerous cells and has immunomodulatory effects. (73) , (74) , (75) Cordyceps has been used for decreasing the renal toxicity of aminoglycosides and cyclosporine (76) , (77) and in individuals with chronic renal failure. (78) Kidney protection is claimed to be due to: protecting tubular cell sodium pump activity; attenuating tubular cell lysosome overfunction stimulated by phagocytosis of aminoglycoside; and decreasing tubular cell lipoperoxidation in response to toxic injury. (79) Cordyceps was also reported to protect stem cells and red blood cells during chemotherapy and radiation. (80)

Acupuncture & Acupressure

It was reported that in the treatment of 40 cases of apoplectic sequelae with scalp-acupuncture, bilateral Ding Nie Qian Xie Xian (MS 6, Qian Shen Chong EX-HN 1 to Xuan Li – Gb 6) were punctured with the needle tip downward about 1.5 cun deep; or bilateral Ding Pang Xian I (MS 8, Cheng Guang – BL 6 to Tong Tian – BL 7) punctured with the needle tip backward about 1.5 cun deep. The needles were manipulated for 1 minute with the uniform reinforcing - reducing method about 150 times per minute and then retained for 10 minutes. After the treatment, 13 cases were resolved, 11 cases showed marked improvement, 13 improved slightly, and 3 cases did not show any noticeable changes. The effectiveness rate was 92.5%. (81)

In the treatment of 35 cases of cerebral apoplectic sequelae with epilepsy, at the stage of an attack, Bai Hui (GV 20), Ren Zhong (GV 26), Ju Que (RN 14), Jian Shi (PC 5), and Xing Jian (LR 2) were punctured and stimulated with the strong reducing method. The needles were retained for 30-60 minutes. In the stage of intermittence, Tai Chong (LR 3), Tai Xi (KI 3), Feng Long (ST 40), Zu San Li (ST 36), Shen Men (HT 7), Dian Xian-point, Qu Chi (LI 11), and Bai Hui (GV 20) were punctured and stimulated with the uniform reinforcing-reducing method. The needles were retained for 30 minutes and manipulated once again every 10 minutes. After 5 courses of treatment, 12 cases had remarkable improvement, 20 improved slightly, and 3 had no apparent effect. (82)

280 cases of sequelae of cerebrovascular accident were treated. Nei Guan (PC 6) and Ren Ying (ST 9) were used as the main acupoints. The following points were also used at the affected lower-limb, combined with Jian Yu (SJ 14), Qu Chi (LI 11), Wai Guan (TE 5), and He Gu (LI 4) at the affected upper-limb; with Huan Tiao (GB 30), Fu Tu (ST 32), Yang Ling Quan (GB 34), Zu San Li (ST 36), Feng Long (ST 40), Xuan Zhong (GB 39), and Tai Chong (LR 3), etc. The needles were retained for 20 minutes and connected to an electroacupuncture therapeutic apparatus for stimulation for 30 minutes. The treatment was given once a day. 12 sessions constituted one therapeutic course. The results showed that 78 cases had significant improvement, 148 showed some improvement, and 54 had no significant changes. The total effectiveness rate was 80.71%. (83)

In another report, 36 cases of aphasia due to apoplexy were treated with acupuncture therapy by stimulating Ya Men (GV 15), Tong Li (HT 5), Lian Quan (CV 23), and the temple region with the strong needling manipulation. Ya Men (GV 15) and Lian Quan (CV 23) were stimulated with the reducing needling method. The needles were removed immediately. The needles in Ton Li (HT 5) and temple region were retained for 10 minutes and manipulated once again while retained. Ten sessions comprised one therapeutic course of treatment. After treatment, 24 cases were resolved, 8 had improved slightly, and 4 had no noticeable effect. (84)

Li Lan Min, et al. observed the therapeutic effects of acupuncture in treatment of 155 cases of apoplectic aphasia using Jin Jin (EX-HN 12), Yu Ye (EX-HN 13), Shang Lian Quan, Feng Chi (Gb 20), and Tong Li (HT 5). The needles were inserted rapidly and manipulated with the uniform reinforcing-reducing method. After achieving needling sensations, the needles were connected to an electroacupuncture therapeutic apparatus to stimulate the acupoints with continuous waves. The treatment was performed once a day. 15 sessions constituted one course of treatment. The results indicated that 30 cases were resolved, 63 had remarkable improvement, 57 cases had improved, and 5 showed no noticeable effect. The total effectiveness rate was 96%. (85)

Herbal and acupuncture combined treatment
80 cases of apoplectic sequelae were treated with acupuncture of Feng Chi (Gb 20), Feng Fu (GV 16), and other acupoints on the upper and lower limbs. Patients were also given an administration of a modified Bu Yang Huan Wu decoction. The significant effectiveness rate was 75%. (86)

Wang Nai Wen, et al. treated 79 cases of apoplectic sequelae with herbal medicines and acupuncture on the basis of syndrome differentiation. For the type of qi-stagnation and blood stasis, blockage of meridian-collaterals, a modified Bu Tang Huan Wu decoction was given and acupoints of the Three Yang Meridians combined with those of Tai Yang Meridian and Shao Yang Meridian were used; for the type of hyperactivity of the liver-yang and blood stasis in meridian-collaterals, a modified Zhen Gan Xi Feng decoction (a common formula for cerebral apoplexy) was given and acupoints on the hand and foot-yang Ming Meridians with those of the Jue Yin Meridian were employed. For the type of wind-phlegm blocking meridian-collaterals and blood stasis in meridian-collaterals, Tian Ma (Gastrodia), Quan Xie (Scorpio), Dan Nan Xing (Arisaema processed with bile), Yuan Zhi (Polygala Root), Shi Chang Pu (Grassleaved Sweetflag Rhizome), Yu Jin (Curcuma Root), Fu Ling (Poria), etc. were given as a formula and acupuncture of acupoints of Du Mai and Ren Mai were adopted. After these treatments, 3 cases were resolved, 28 had improved significantly, 40 showed some improvement, and 8 did not show any effectiveness. The total effectiveness rate was 89.8%. (87)

Acupoint injection treatment
40 cases of apoplectic sequelae were treated with hydro-acupuncture therapy. The method involved injecting an amino acid (1.5 ml) and ATP (10-20mg) into Feng Chi (GB 20) on the affected side at the early stage of the disease, and injecting vitamin B1 100mg and nicotinamide 50mg into the same acupoint at the advanced stage. In addition, acupoints as Jian Yu (SJ 14), Qu Chi (LI 11), He Gu (LI 4), Shou San Li (LI 10), Wai Guan (TE 5), Jian Zhen (SI 9), etc. were punctured and stimulated with an electroacupuncture therapeutic apparatus. 10 to 14 sessions comprised one course of treatment. The results displayed that 19 cases were resolved, 12 showed significant improvement, 7 showed some improvement, and 2 cases showed no effectiveness. The total effectiveness rate was 95%. (88)

Acupoint plaster treatment
228 cases of apoplectic sequelae were treated with Zhongfeng Plaster. This plaster used the following single herbs: Quan Xie (Scorpion), Dan Shen (Salvia), Yuan Hu (Corydalis), Dan Pi (Moutan Cortex), etc. The herbal plasters were applied to the acupoints Lian Quan (CV 23), Hua Gai (CV 20), Shen Que (CV 8), bilateral Yong Quan (KI 1), etc. They were replaced once a day. 15 days constituted one course of treatment. In the control group, which consisted of 70 cases with same condition, the following acupoints were punctured once a day: Jian Yu (SJ 14), Qu Chi (LI 11), He Gu (LI 4), Wai Guan (TE 5), Zu San Li (ST 36), Yang Ling Quan (GB 34), Xuan Zhong (GB 39), etc. 30 sessions constituted one course of treatment. After 2-4 courses of treatment, the results for the treatment and control groups were, respectively, 44 and 8 cases were resolved, 68 and 15 cases had improved significantly, 98 and 39 had improved slightly, and 18 and 8 had no significant effectiveness. The effectiveness rates were 92.11% and 88.57%, respectively. (89)

Liu Guo Ying, et al. treated 31 cases of apoplectic sequelae by applying Chinese medicinal herbs to the umbilicus. The main ingredients used were Huang Qi (Astragalus), Qiang Huo (Notopterygium Root), Ling Xian (Clematis), Ru Xiang (Mastic), Mo Yao (Myrrha), Hou Po (Succinum), and Rou Gui (Cinnamon Bark). The formula was modified according to individuals' symptoms. For tongue stiffness and slurred speech, Shi Chang Pu (Grassleaved Sweetflag Rhizome) and Ge Gen (Pueraria) were added. For hypertension, Niu Xi (Achyranthes), Di Long (Earthworm), and Xia Ku Cao (Prunella) were added. For severe lower-lim

Traditional Chinese Medicine


Extensive information regarding the treatment of this health condition using Traditional Chinese Medicine is available through the link above.

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for diagnosis and treatment. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Chemistry Profile (Blood)

A multifactorial assessment of chemistry profile values can reveal useful information regarding concurrent disorders and possible nutrient imbalances.

Adrenal Function Profiles

Adrenal insufficiency can contribute to impaired resistance to infection. Stress activates the HPA axis and has impact on the immune system, particularly through the adrenal hormones.

Thyroid Profile

Abnormal thyroid function may result from stroke (90) , (91) and hyperthyroid function has been demonstrated to increase stroke volume. (92)


This screening test offers a general indication of overall health as well as health of the urinary tract. Bacterial counts of >100,000/ml are significant in the evaluation of urinary tract infection and may have an impact on general physiologic response.


A CBC may suggest the involvement of secondary infections, inflammation, and/or nutrient deficiencies. The major mineral consideration in deficiency disorders is iron. Mean corpuscular volume (MCV) may not be sufficient to assess iron and or B12 status. Analysis of serum iron, total iron binding capacity, ferritin, and/or organic acids may be indicated. The CBC includes a platelet count.

C-reactive protein (CRP Thyroid Profile)

An abnormal serum glycoprotein produced by the liver during acute inflammation, CRP has been used to detect or monitor inflammatory processes. CRP disappears rapidly when inflammation subsides; thus it is a reliable measure of current inflammatory process. Recent advances in technology, not yet in common use, provide a very high sensitivity in the measure of this important marker of inflammatory processes.

Cerebrospinal Fluid

Elevations suggest decreased brain oxygenation and/or increased intracranial pressure.


Hypercortisolism is common early after stroke. (93) Hypercortisolism is closely associated with cognitive disturbances and extensive motor impairment.

Fatty Acids

Dietary polyunsaturated fatty acids (PUFA) are primarily composed of w-3 and w-6 fatty acids. PUFA are vital in the production of eicosanoids – components involved in regulating inflammatory response, blood vessel leakage, lipid accumulation, immune cell response, and optimal control of virtually every body tissue. (94)


Blood glucose levels vary in response to food intake, stress, physical exertion, and various disorders. Elevations of serum glucose should lead to confirmatory testing such as fasting insulin, serum phosphorus, magnesium, hemoglobin A1c, and/or fructosamine.

Lipid Profile

    Cholesterol, Total Triglycerides HDL LDL

Partial Thromboplastin Time (PTT)

This test may be used to screen for coagulation disorders.

Prothrombin Time (PT)

Prothrombin is a vitamin K dependent glycoprotein necessary for firm fibrin clot formation. It converts to thrombin in the clotting cascade process and should not appear in the serum after clot formation. PT measures the amount of time taken for clot formation after brain tissue extract and calcium are added to citrated plasma. Small PT fluctuations can have dramatic physiologic effects. The INR increases the usability of PT when monitoring anticoagulation therapy response.

Oxidative Stress

Increased oxidation is a documented dynamic of stroke. Oxidant levels increase in relationship to inflammatory processes.

Liver Battery

This profile includes various tests for liver abnormalities that may be useful in monitoring vascular injury.

    Alanine aminotransferase (ALT/SGPT) Alkaline phosphatase (ALP) Aspartate aminotransferase (AST/SGOT) Bilirubin Gamma-glutamyl transferase/transpeptidase (GGT/GGTP) Lactate dehydrogenase (LD/LDH) Leucine aminopeptidase (LAP) 5’ nucleotidase (5’NT/5’N) Protein electrophoresis

Clinical Notes

Coenzyme Q10: Hypertension is a known risk factor for strokes. Individuals with elevated blood pressure have a greater risk of having a stroke, and studies also report that treatment which lowers elevated blood pressure results in a 36% reduction in the incidence of stroke and decreases in cardiovascular events, including myocardial infarctions. (95) No studies have been conducted on the association between coenzyme Q10 levels and the prevention of strokes. However, studies do report that coenzyme Q10 is exceptionally effective at lowering elevated blood pressure, which enables many patients to discontinue the use of from 1 to 3 antihypertensive medications. (96) , (97) The average dose of coenzyme Q10 used in these studies is approximately 225 mg/day. Because coenzyme Q10 is effective at lowering elevated blood pressure, there is a strong theoretical implication that adequate plasma levels of coenzyme Q10 are protective against strokes.

Ribose is a pentose sugar that increases the synthesis of ATP and adenosine monophosphate, which are major energy sources for cardiac function. In one study, 20 patients with severe coronary artery disease underwent treadmill exercise testing, and received ribose orally at 60 gms daily in 4 divided doses for 3 days or a placebo. Upon repeat treadmill testing, the time it took for ischemia to show up in the EKG was significantly longer in the ribose than in the placebo controls. Thus, patients with coronary artery disease who took oral doses of ribose improved their hearts' tolerance to lack of oxygen. (98) These results suggest that ribose might also be beneficial in reducing the damage caused by strokes.


  1. Welty TE. Cerebrovascular Disease, In: Koda-Kimble MA, Young LY, eds. Applied Therapeutics. 5th ed. Vancouver, WA: 1992;14:1-7.
  2. Bradberry JC. Stroke, In: DiPiro et al eds, Pharmacotherapy, A Pathophysiologic Approach. 4th ed. Stamford, CT: Appleton & Lange; 1999:327-347.
  3. Easton JD, Hauser SL, Martin JB. Cerebrovascular diseases. In: Fauci AS, Brunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine 14th edition. McGraw-Hill; 1998:2325-2348.
  4. Bradberry JC. Stroke, In: DiPiro et al eds, Pharmacotherapy, A Pathophysiologic Approach. 4th ed. Stamford, CT: Appleton & Lange; 1999:327-347.
  5. Easton JD, Hauser SL, Martin JB. Cerebrovascular diseases. In: Fauci AS, Brunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine 14th edition. McGraw-Hill; 1998:2325-2348.
  6. Bradberry JC. Stroke, In: DiPiro et al eds, Pharmacotherapy, A Pathophysiologic Approach. 4th ed. Stamford, CT: Appleton & Lange; 1999:327-347.
  7. Bradberry JC. Stroke, In: DiPiro et al eds, Pharmacotherapy, A Pathophysiologic Approach. 4th ed. Stamford, CT: Appleton & Lange; 1999:327-347.
  8. Bronner LL, Kanter DS, Manson JE. Primary Prevention of Stroke. N Engl J Med. 1995;333:1392-1400.
  9. Bradberry JC. Stroke, In: DiPiro et al eds, Pharmacotherapy, A Pathophysiologic Approach. 4th ed. Stamford, CT: Appleton & Lange; 1999:327-347.
  10. View Abstract: Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: The Framingham Study. Stroke. 1991;22:983-988.
  11. Hart RG, Halperin JL. Atrial fibrillation and stroke. Revisiting the dilemmas. Stroke. 1994;25: 1337-1341.
  12. Chesbro JH, Fuster V, Halprin JL. Atrial fibrillation—Risk marker for stroke. N Engl J Med. 1990;323:1556-1558.
  13. Bradberry JC. Stroke, In: DiPiro et al eds, Pharmacotherapy, A Pathophysiologic Approach. 4th ed. Stamford, CT: Appleton & Lange; 1999:327-347.
  14. WHO task force on stroke and other cerebrovascular disorders. Recommendations on stroke prevention, diagnosis, and therapy. Stroke. 1989;20:1407-1431.
  15. View Abstract: Donnan GA, McNeil JJ, Adena MA, et al. Smoking as a risk factor for cerebral ischemia. Lancet. 1989;II:643-647.
  16. Sherman DG, Dyken ML, Gent M, et al. Antithrombotic therapy for cerebrovascular disorders. An Update. Chest. 1995;108(suppl):444S-456S.
  17. Adams HP Jr, Brott TG, Furlan AJ, et al. Guidelines for thrombolytic therapy for acute stroke: A supplement to the guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Circulation. 1996;94:1167-1174.
  18. View Abstract: Menendez R, et al. Oral administration of policosanol inhibits in vitro copper ion-induced rat lipoprotein peroxidation. Physiol Behav. Aug1999;67(1):1-7.
  19. View Abstract: Alcocer L, et al. A comparative study of policosanol Versus acipimox in patients with type II hypercholesterolemia. Int J Tissue React. 1999;21(3):85-92.
  20. View Abstract: Batista J, et al. Effect of policosanol on hyperlipidemia and coronary heart disease in middle-aged patients. A 14-month pilot study. Int J Clin Pharmacol Ther. Mar1996;34(3):134-7.
  21. View Abstract: Canetti M, et al. A two-year study on the efficacy and tolerability of policosanol in patients with type II hyperlipoproteinaemia. Int J Clin Pharmacol Res. 1995;15(4):159-65.
  22. View Abstract: Mormando RM. Lipid Levels. Applying the Second National Cholesterol Education Program Report to Geriatric Medicine. Geriatrics. Aug 2000;55(8):48-53; quiz 54.
  23. View Abstract: Wannamethee SG, Shaper AG, Ebrahim S. HDL-Cholesterol, Total cholesterol, and the Risk of Stroke in Middle-aged British Men. Stroke. Aug 2000;31(8):1882-8.
  24. View Abstract: Fraga V, et al. Effect of policosanol on in vitro and in vivo rat liver microsomal lipid peroxidation. Arch Med Res. 1997;28(3):355-60.
  25. View Abstract: Arruzazabala ML, et al. Protective effect of policosanol on atherosclerotic lesions in rabbits with exogenous hypercholesterolemia. Braz J Med Biol Res. Jul2000;33(7):835-840.
  26. View Abstract: Molina V, et al. Effect of policosanol on cerebral ischemia in Mongolian gerbils. Braz J Med Biol Res. Oct1999;32(10):1269-76.
  27. View Abstract: Boysen G, Truelsen T. Prevention of recurrent stroke. Neurolog Sci. Apr2000;21(2):67-72.
  28. View Abstract: Selhub J, et al. B vitamins, homocysteine, and neurocognitive function in the elderly. Am J Clin Nutr. Feb2000;71(2):614S-620S.
  29. View Abstract: He K. Folate, vitamin B6, and B12 intakes in relation to risk of stroke among men. Stroke. 2004 Jan;35(1):169-74.
  30. View Abstract: Kimura S, et al. Docosahexaenoic acid inhibits blood viscosity in stroke-prone spontaneously hypertensive rats. Res Commun Mol Pathol Pharmacol. Jun1998;100(3):351-61.
  31. View Abstract: Mori TA. Omega-3 fatty acids and inflammation. Curr Atheroscler Rep. 2004 Nov;6(6):461-7.
  32. View Abstract: McLennan P, et al. The cardiovascular protective role of docosahexaenoic acid. Eur J Pharmacol. Apr1996;300(1-2):83-9.
  33. View Abstract: Yamori Y, et al. Comparison of serum phospholipid fatty acids among fishing and farming Japanese populations and American inlanders. J Nutr Sci Vitaminol. Tokyo. Aug1985;31(4):417-22.
  34. View Abstract: Iso H, et al. Prospective study of calcium, potassium, and magnesium intake and risk of stroke in women. Stroke. Sep1999;30(9):1772-9.
  35. View Abstract: Suter PM. The effects of potassium, magnesium, calcium, and fiber on risk of stroke. Nutr Rev. Mar1999;57(3):84-8.
  36. View Abstract: Bazzano LA, He J, Ogden LG, et al. Dietary potassium intake and risk of stroke in US men and women: National Health and Nutrition Examination Survey I epidemiologic follow-up study. Stroke. Jul2001;32(7):1473-80.
  37. View Abstract: Ascherio A, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation. Sep1998;98(12):1198-204.
  38. View Abstract: Khaw KT, Barrett-Connor E. Dietary potassium and stroke-associated mortality. A 12-year prospective population study. N Engl J Med. Jan1987;316(5):235-40.
  39. View Abstract: Iso H, et al. Prospective study of calcium, potassium, and magnesium intake and risk of stroke in women. Stroke. Sep1999;30(9):1772-9.
  40. View Abstract: Suter PM. The effects of potassium, magnesium, calcium, and fiber on risk of stroke. Nutr Rev. Mar1999;57(3):84-8.
  41. View Abstract: Ascherio A, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among US men. Circulation. Sep1998;98(12):1198-204.
  42. View Abstract: Borowik H, Pryszmont M. Concentration of magnesium in serum and cerebrospinal fluid in patients with stroke. Neurol Neurochir Pol. Nov1998;32(6):1377-83.
  43. View Abstract: Leinonen JS, et al. Low plasma antioxidant activity is associated with high lesion volume and neurological impairment in stroke. Stroke. Jan2000;31(1):33-9.
  44. View Abstract: Simon JA, et al. Serum ascorbic acid and cardiovascular disease prevalence in U.S. adults. Epidemiology. May1998;9(3):316-21.
  45. View Abstract: Daviglus ML, et al. Dietary vitamin C, beta-carotene and 30-year risk of stroke: results from the Western Electric Study. Neuroepidemiology. 1997;16(2):69-77.
  46. View Abstract: Ness AR, et al. Vitamin C and cardiovascular disease: a systematic review. J Cardiovasc Risk. Dec1996;3(6):513-21.
  47. View Abstract: Lolic MM, et al. Neuroprotective effects of acetyl-L-carnitine after stroke in rats. Ann Emerg Med. Jun1997;29(6):758-65.
  48. View Abstract: Postiglione A, et al. Effect of acute administration of L-acetyl carnitine on cerebral blood flow in patients with chronic cerebral infarct. Pharmacol Res. Apr1991;23(3):241-6.
  49. View Abstract: Virtamo J, et al. Serum selenium and the risk of coronary heart disease and stroke. Am J Epidemiol. Aug1985;122(2):276-82.
  50. View Abstract: Daviglus ML, et al. Dietary vitamin C, beta-carotene and 30-year risk of stroke: results from the Western Electric Study. Neuroepidemiology. 1997;16(2):69-77.
  51. View Abstract: Kleijnen J, et al. Ginkgo biloba for Cerebral Insufficiency. Br J Clin Pharm. 1992;34:352-58.
  52. Kleijnen J, et al. Ginkgo biloba. Lancet. 1992;340(8828): 1136-39.
  53. View Abstract: Maurer K, et al. Clinical Efficacy of Ginkgo biloba Special Extract EGb 761 in Dementia of the Alzheimer Type. J Psychiatr Res. 1997;31(6):645-55.
  54. View Abstract: Kanowski S, et al. Proof of Efficacy of the Ginkgo biloba Special Extract EGb 761 in Outpatients Suffering from Mild to Moderate Primary Degenerative Dementia of the Alzheimer Type or Multi-infarct Dementia. Pharmacopsychiatry. 1996;29:47-56.
  55. View Abstract: Meyer B. Multicenter Randomized Double-blind Drug versus Placebo Study of Ginkgo biloba Extract in the Treatment of Tinnitus. Presse Med. 1986;15:1562-64.
  56. Odawara M, et al. Ginkgo biloba. Neurology. 1997;48(3):789-90.
  57. View Abstract: Kose L, et al. Lipoperoxidation Induced by Hydrogen Peroxide in Human Erythrocyte Membranes. 2. Comparison of the Antioxidant Effect of Ginkgo biloba Extract (EGb 761) with Those of Water-soluble and Lipid-soluble Antioxidants. J Intern Med Res. 1995;23:9-18.
  58. View Abstract: Peters H, Kieser M, Holscher U. Demonstration of the efficacy of ginkgo biloba special extract EGb 761 on intermittent claudication--a placebo-controlled, double-blind multicenter trial. Vasa. May1998;27(2):106-10.
  59. View Abstract: Schneider B. Ginkgo biloba extract in peripheral arterial diseases. Meta-analysis of controlled clinical studies. Arzneimittelforschung. Apr1992;42(4):428-36.
  60. Kleijnen J, et al. Ginkgo biloba. Lancet. 1992;340(8828): 1136-39.
  61. View Abstract: Ramassamy C, et al. The Ginkgo biloba Extract, EGb761, Increases Synaptosomal Uptake of 5-hydroxytryptamine: In-vitro and Ex-vivo Studies. J Pharm Pharmacology. 1992;44(11):943-45.
  62. View Abstract: Petkov V. Plants and Hypotensive, Antiatheromatous and Coronarodilatating Action. Am J Chinese Med. 1979;7:197-236.
  63. Racz-Kotilla E, et al. Salidiuretic and Hypotensive Action of Ribes-Leaves. Planta Medica. 1980;29:110-14.
  64. Wagner H, et al. Cardioactive Drugs IV. Cardiotonic Amines from Crataegus oxyacantha. Planta Medica. 1982;45:99-101.
  65. Rewerski W, et al. Some Pharmacological Properties of Flavan Polymers Isolated from Hawthorn. Arzneim-Forsch/Drug Res. 1967;17:490-91.
  66. View Abstract: Taskov M. On the Coronary and Cardiotonic Action of Crataemon. Acta Physiol Pharmacol Bulg. 1977;3(4):53-57.
  67. Petkov E, et al. Inhibitory Effect of Some Flavonoids and Flavonoid Mixtures on Cyclic AMP Phosphodiesterase Activity of Rat Heart. Planta Medica. 1981;43:183-86.
  68. View Abstract: Uchida S, et al. Inhibitory Effects of Condensed Tannins on Angiotensin Converting Enzyme. Jap J Pharmacol. 1987;43(2):242-46.
  69. View Abstract: Wergowski J, et al. The Effect of Procyanidolic Oligomers on the Composition of Normal and Hypercholesterolemic Rabbit Aortas. Biochem Pharm. 1984; 33:3491-97.
  70. Bao TT, et al. Pharmacological actions of Cordyceps sinensis. Chung Hsi I Chieh Ho Tsa Chih. Jun1988;8(6):352-54.
  71. Chen YP. Studies on Immunological Actions of Cordyceps sinensis. I. Effect on Cellular Immunity. Chung Yao Tung Pao. Sep1983;8(5):33-35.
  72. View Abstract: Lei J, et al. Pharmacological Study on Cordyceps sinensis (Berk.) Sacc. and ze-e Cordyceps. Zhongguo Zhong Yao Za Zhi. Jun1992;17(6):364-66.
  73. View Abstract: Zhou DH, et al. Effect of Jinshuibao Capsule on the Immunological Function of 36 Patients with Advanced Cancer. Zhongguo Zhong Xi Yi Jie He Za Zhi. Aug1995;15(8):476-78.
  74. View Abstract: Chen YJ, et al. Effect of Cordyceps sinensis on the Proliferation and Differentiation of Human Leukemic U937 Cells. Life Sci. 1997;60(25):2349-59.
  75. View Abstract: Yoshida J, et al. Antitumor Activity of an Extract of Cordyceps sinensis (Berk.) Sacc. against Murine Tumor Cell Lines. Jpn J Exp Med. Aug1989;59(4):157-61.
  76. View Abstract: Bao ZD, et al. Amelioration of Aminoglycoside Nephrotoxicity by Cordyceps sinensis in Old Patients. Zhongguo Zhong Xi Yi Jie He Za Zhi. May1994;14(5):271-73.
  77. View Abstract: Zhao X, et al. Cordyceps sinensis in Protection of the Kidney from Cyclosporine A Nephrotoxicity. Zhonghua Yi Xue Za Zhi. Jul1993;73(7):410-12.
  78. View Abstract: Guan YJ, et al. Effect of Cordyceps sinesis on T-lymphocyte Subsets in Chronic Renal Failure. Zhongguo Zhong Xi Yi Jie He Za Zhi. Jun1992;12(6):338-39.
  79. View Abstract: Zhen F, et al. Mechanisms and Therapeutic Effect of Cordyceps sinensis (CS) on Aminoglycoside Induced Acute Renal Failure (ARF) in Rats, Zhongguo Zhong Xi Yi Jie He Za Zhi. May1992;12(5):288-91.
  80. Zhu J, et al. CordyMax Cs-4: A Scientific Product Review. Pharmanex Phytoscience Review Series. 1997.
  81. Xu Liu Ying, et al. Therapeutic observations on treating 40 cases of apoplectic sequelae with scalp-acupuncture. Hubei Journal of TCM. 1988;(4):44-45.
  82. Chen Bang Guo. Therapeutic observation on treating apoplectic convulsion with acupuncture. Zhejiang Journal of Traditional Chinese Medicine. 1999;34(3):126.
  83. You Ah Xiang. Treating 280 cases of sequelae of cerebrovascular accident with acupuncture on Nei Guan and Ren Ying points. Fujian Journal of Chinese Medicine. 1998;29(3):26-27.
  84. Li ren Ming, et al. Clinical observation on treating 36 cases of aphasia due to apoplexy with acupuncture. Journal of Acupuncture Clinical Application. 1998;14(5):22.
  85. Li Lan Min, et al. Treating 155 cases of apoplectic aphasia with electro-acupuncture. Journal of Acupuncture Clinical Application. 1998;14(2):25-26.
  86. Zhang Ping, et al. Treating 80 cases of apoplectic sequelae with combination of Chinese herbs and acupuncture. Shaanxi Journal of TCM. 1998;19(5):225.
  87. Wang Nai Wen, et al. Therapeutic observations on treating 79 cases of apoplectic sequelae with combination of Chinese herbs and acpuncture. Journal of Traditional Chinese Medicine Information. 1988;(1):22,10.
  88. Tian Yun Lai, et al. Therapeutic observations on 40 cases of apoplectic sequelae with acupoint injection combined with acpuncture. Journal of Folk Chinese Medical Treatment. 1999;7(5):6-7.
  89. Zhou Bao Ming. Treating 228 cases of apoplectic sequelae by applying Zhongfeng Plaster on acupoints. Shanghai Journal of Acupuncture. 1991;10(2):15.
  90. View Abstract: Hägg E, et al. Serum thyroid-stimulating hormone in cerebrovascular disease. Acta Med Scand. 1986;219(1):53-8.
  91. View Abstract: Olsson T, Asplund K, Hägg E. Pituitary-thyroid axis, prolactin and growth hormone in patients with acute stroke. J Intern Med. Sep1990;228(3):287-90.
  92. View Abstract: Král J, Hradec J, Limanová J. Heart in thyroid diseases. Cor Vasa. 1992;34(2):108-14.
  93. View Abstract: Olsson T, et al. Abnormalities at different levels of the hypothalamic-pituitary-adrenocortical axis early after stroke. Stroke. Nov1992;23(11):1573-6.
  94. Horrobin DF, ed. Clinical Uses of Essential Fatty Acids. Montreal: Eden Press; 1981.
  95. View Abstract: Morgenstern N, Byyny RL. Epidemiology of hypertension in the elderly. Drugs Aging. May1992;2(3):222-42.
  96. View Abstract: Langsjoen P, et al. Treatment of essential hypertension with coenzyme Q10. Mol Aspects Med. 1994;15 Suppl:S265-72.
  97. View Abstract: Langsjoen H, et al. Usefulness of coenzyme Q10 in clinical cardiology: a long-term study. Mol Aspects Med. 1994;15 Suppl:s165-75.
  98. View Abstract: Pliml W, et al. Effects of Ribose on Exercise-Induced Ischemia in Stable Coronary Artery Disease. The Lancet. Aug1992;340:507-510.