If Hillary was in EXCELLENT HEALTH she would not be on Lovenox.

 Hillary's excellent health on Lovenox and Diazepam.. 

Hillary Clinton's doctor states she is in Good Health... Good health could mean she is in Good Health for one who had blood disorders and is having blood clots leading to the brain. Once you destroy a portion of the brain as in MS or other debilitating causes  that area of the Brain is not in "Good Health" Maybe she is in Good Health  for her condition she has.

Lets look at the Good Health of Hillary. She is taking Coumadin, That is a blood thinner.

• Reduce your risk of forming blood clots if you have had a heart-valve replacement or if you have an irregular, rapid heartbeat, called atrial fibrillation.
• Lower the risk of death if you've had a heart attack, as well as lowering your risk of having another heart attack, stroke, and having blood clots move to another part of your body.

People in "Good Health" don't take Coumadin.

COUMADIN can cause bleeding which can be serious and sometimes lead to death. This is because COUMADIN is a blood thinner medicine that lowers the chance of blood clots forming in your body.

• You may have a higher risk of bleeding if you take COUMADIN and:
• are 65 years of age or older
• have a history of stomach or intestinal bleeding
• have high blood pressure (hypertension)
• have a history of stroke, or “mini-stroke” (transient ischemic attack or TIA)
• have serious heart disease
• have a low blood count or cancer
• have had trauma, such as an accident or surgery
• have kidney problems
• take other medicines that increase your risk of bleeding, including:
  • a medicine that contains heparin
  • other medicines to prevent or treat blood clots
  • nonsteroidal anti-inflammatory drugs (NSAIDs)
• take warfarin sodium for a long time. Warfarin sodium is the active ingredient in COUMADIN

According to this Good Doctors notes she is had a  transverse sinus venous thrombosis

Thrombosis of the dural sinus and/or cerebral veins (CVT) is an uncommon form of stroke, usually affecting young individuals.Despite advances in the recognition of CVT in recent years, diagnosis and management can be difficult because of the diversity of underlying risk factors and the absence of a uniform treatment approach. CVT represents ≈0.5% to 1% of all strokes. Multiple factors have been associated with CVT, but only some of them are reversible. Prior medical conditions (eg, thrombophilias, inflammatory bowel disease), transient situations (eg, pregnancy, dehydration, infection), selected medications (eg, oral contraceptives, substance abuse), and unpredictable events (eg, head trauma) are some predisposing conditions.
Given the diversity of causes and presenting scenarios, CVT may commonly be encountered not only by neurologists and neurosurgeons but also by emergency physicians, internists, oncologists, hematologists, obstetricians, pediatricians, and family practitioners. Our purpose in the present scientific statement is to review the literature on CVT and to provide recommendations for its diagnosis and management. Writing group members were appointed by the American Heart Association (AHA) Stroke Council's Scientific Statement Oversight Committee and the Council on Epidemiology and Prevention. The panel included members with several different areas of expertise. The panel reviewed relevant articles on CVT in adults and children using computerized searches of the medical literature through July 2010. These articles were supplemented by other articles known to the authors. The evidence is organized within the context of the AHA framework and is classified according to the joint AHA/American College of Cardiology Foundation and supplementary AHA Stroke Council methods of classifying the level of certainty and the class and level of evidence (Tables 1 and 2).⁵ After review by the panel members, the manuscript was reviewed by expert peer reviewers and members of the Stroke Council Leadership Committee and was subsequently approved by the AHA's Science Advisory and Coordinating Committee.

Diagnosis and Management of Cerebral Venous Thrombosis Table 1.

• AHA/ASA Scientific Statement

Diagnosis and Management of Cerebral Venous Thrombosis

Table 2.

Definition of Classes and Levels of Evidence Used in AHA Stroke Council Recommendations

Class I	Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective.
Class II	Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.
Class IIa	The weight of evidence or opinion is in favor of the procedure or treatment.
Class IIb	Usefulness/efficacy is less well established by evidence or opinion.
Class III	Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful.
Therapeutic recommendations
Level of Evidence A	Data derived from multiple randomized clinical trials or meta-analyses
Level of Evidence B	Data derived from a single randomized trial or nonrandomized studies
Level of Evidence C	Consensus opinion of experts, case studies, or standard of care
Diagnostic recommendations
Level of Evidence A	Data derived from multiple prospective cohort studies using a reference standard applied by a masked evaluator
Level of Evidence B	Data derived from a single grade A study, or ≥1 case-control studies, or studies using a reference standard applied by an unmasked evaluator
Level of Evidence C	Consensus opinion of experts

 

Although information about the cause and clinical manifestations of CVT is included for the convenience of readers who may be unfamiliar with these topics, the group's recommendations emphasize issues regarding diagnosis, management, and treatment. The recommendations are based on the current available evidence and were approved by all members of the writing group. Despite major progress in the evaluation and management of this rare condition in recent years, much of the literature remains descriptive. In some areas, evidence is lacking to guide decision making; however, the writing group made an effort to highlight those areas and provide suggestions, with the understanding that some physicians may need more guidance, particularly in making decisions when extensive evidence is not available. Continued research is essential to better understand issues related to the diagnosis and treatment of CVT. Identification of subgroups at higher risk would allow a more careful selection of patients who may benefit from selective interventions or therapies.

Epidemiology and Risk Factors for CVT

CVT is an uncommon and frequently unrecognized type of stroke that affects approximately 5 people per million annually and accounts for 0.5% to 1% of all strokes.¹ CVT is more commonly seen in young individuals. According to the largest cohort study (the International Study on Cerebral Venous and Dural Sinuses Thrombosis [ISCVT]), 487 (78%) of 624 cases occurred in patients <50 years of age (Figure 1).^1,6 Clinical features are diverse, and for this reason, cases should be sought among diverse clinical index conditions. A prior pathological study found a prevalence of CVT of 9.3% among 182 consecutive autopsies.⁷ No population studies have reported the incidence of CVT. Very few stroke registries included cases with CVT. This may result in an overestimation of risk associated with the various conditions owing to referral and ascertainment biases. In the Registro Nacional Mexicano de Enfermedad Vascular Cerebral (RENAMEVASC), a multihospital prospective Mexican stroke registry, 3% of all stroke cases were CVT.⁸A clinic-based registry in Iran reported an annual CVT incidence of 12.3 per million.⁹ In a series of intracerebral hemorrhage (ICH) cases in young people, CVT explained 5% of all cases.⁹

Cause and Pathogenesis: Underlying Risk Factors for CVT

Predisposing causes of CVT are multiple. The risk factors for venous thrombosis in general are linked classically to the Virchow triad of stasis of the blood, changes in the vessel wall, and changes in the composition of the blood. Risk factors are usually divided into acquired risks (eg, surgery, trauma, pregnancy, puerperium, antiphospholipid syndrome, cancer, exogenous hormones) and genetic risks (inherited thrombophilia).

Table 3 summarizes the evidence for a cause-and-effect relationship^10,11 between prothrombotic factors and CVT.^12,–,55 Evidence for the strength and consistency of association, biological plausibility, and temporality is summarized. These criteria are most closely met for deficiency of antithrombin III, protein C, and protein S; factor V Leiden positivity; use of oral contraceptives; and hyperhomocysteinemia, among others.

• AHA/ASA Scientific Statement

Diagnosis and Management of Cerebral Venous Thrombosis

Table 3.

Predisposing Conditions for CVT and Principles in Favor of a Cause-and-Effect Relationship

Condition	Prevalence, %*	Consistency1†	Strength of Association2†OR (95% CI)	Biological Plausibility3†	Temporality4†	Biological Gradient5†
Prothrombotic conditions	34.1
Antithrombin III deficiency		Yes12,13	NA	Yes	Yes	Yes‡
Protein C deficiency		Yes12,13	11.1 (1.9–66.0)	Yes	Yes	Yes‡
Protein S deficiency		Yes12,13	12.5 (1.5 to 107.3)	Yes	Yes	Yes‡
Antiphospholipid and anticardiolipin antibodies	5.9	Yes12,14,15*	8.8 (1.3–57.4)*	Yes	Yes	Yes‡
Resistance to activated protein C and factor V Leiden		Yes16–27	3.4 (2.3 to 5.1)	Yes	Yes	Yes‡
Mutation G20210A of factor II		Yes28	9.3 (5.9 to 14.7)	Yes	Yes	Yes55‡
Hyperhomocysteinemia	4.5	Yes13,16,17,29,30	4.6 (1.6–12.0)	Yes	Yes	Yes13
Pregnancy and puerperium	21	Yes31–35	NA	Yes	Yes	NA
Oral contraceptives	54.3	Yes13,17,18,23,27,32,36–38	5.6 (4.0−7.9)*	Yes	Yes	Yes
Drugs
Androgen, danazol, lithium, vitamin A, IV immunoglobulin, ecstasy	7.5		NA	Yes	Yes	NA
Cancer related	7.4	Yes39–41	NA	Yes	Yes	NA
Local compression
Hypercoagulable
Antineoplastic drugs (tamoxifen, L-asparaginase)
Infection	12.3		NA	Yes	Yes	NA
Parameningeal infections (ear, sinus, mouth, face, and neck)		Yes2,42–44
Mechanical precipitants	4.5	Yes45–47	NA	Yes	Yes	NA
Complication of epidural blood patch
Spontaneous intracranial hypotension
Lumbar puncture	1.9
Other hematologic disorders	12	Yes48–51	NA	Yes	Yes	NA
Paroxysmal nocturnal hemoglobinuria
Iron deficiency anemia		Yes	NA	Yes	Yes	NA
Nephrotic syndrome	0.6
Polycythemia, thrombocythemia	2.8
Systemic diseases	7.2	Yes52,53	NA	Yes	Yes	NA
Systemic lupus erythematosus	1
Behçet disease	1
Inflammatory bowel disease	1.6
Thyroid disease	1.7
Sarcoidosis	0.2
Other	1.7
None identified	12.5		NA	NA	NA	NA

• CVT indicates cerebral venous thrombosis; OR, odds ratio; CI, confidence interval; NA, nonapplicable/nonavailable; and IV, intravenous.
• ↵* Prevalence as per Ferro et al.¹⁰ Percentages for CVT associated with oral contraceptives or pregnancy/puerperium are reported among 381 women ≤50 years of age.
• ↵† Cause-and-effect relationship determined as follows: (1) Consistency of association: Has the association been repeatedly observed by different investigators (yes/no)? (2) Strength of association: How strong is the effect (relative risk or OR)? (3) Biological plausibility: Does the association make sense, and can it be explained pathophysiologically (yes/no)? (4) Temporality: Does exposure precede adverse outcome (yes/no)? (5) Biological gradient: Does a dose-response relationship exist (yes/no)? Evidence of a strong and consistent association, evidence of biological plausibility, a notable risk of recurrent events, and detection of a biological gradient are suggestive of causation rather than association by chance alone. Modified from Grimes and Schulz⁵⁴ with permission of the publisher. Copyright © 2002, Elsevier.
• ↵‡ Evidence for the biological gradient is not specific for CVT but for VTE: Anticardiolipins and CVT—based on a case-matched control study (Christopher et al)¹⁵; oral contraceptives—from Dentali et al²⁸; cancer—results among 7029 patients with cancer, 20 of whom (0.3%) developed CVT, combined with results from Ferro et al (OR 27.9, 95% CI 16.5 to 47.2)¹⁰; hyperhomocysteinemia and CVT—Martinelli et al.¹³For patients with the prothrombin 20210 mutation, having a heterozygous mutation increases the risk of developing a first venous thrombotic event by approximately 2 to 3 times the background risk (or 2 to 3 in 1000 people each year). Having homozygous prothrombin mutations increases the risk further, but it is not yet well established how much the risk is increased (Varga et al).⁵⁵

Prothrombotic Conditions

The most widely studied risk factors for CVT include prothrombotic conditions. The largest study, the ISCVT, is a multinational, multicenter, prospective observational study with 624 patients. Thirty-four percent of these patients had an inherited or acquired prothrombotic condition.¹⁰ The prevalence of different prothrombotic conditions is summarized in Table 3. Recently, another group in the United States reported that 21% of 182 CVT case subjects in 10 hospitals had a prothrombotic condition.

Antithrombin III, Protein C, and Protein S Deficiency

Two studies have analyzed the role of natural anticoagulant protein deficiencies (antithrombin III, protein C, and protein S) as risk factors for CVT. One study compared 121 patients with a first CVT with 242 healthy control subjects.³⁶ The other study compared 51 patients with CVT with 120 healthy control subjects.¹²Only 1 patient (2%) had antithrombin III deficiency. The combined odds ratio (OR) of CVT when these 2 studies were combined was 11.1 for protein C deficiency (95% confidence interval [CI] 1.87 to 66.05; P=0.009) and 12.5 for protein S deficiency (95% CI 1.45 to 107.29; P=0.03).

Antiphospholipid and Anticardiolipin Antibodies

The first study mentioned above found a higher prevalence of antiphospholipid antibodies in patients with CVT (9 of 121) than in control subjects (0 of 242).³⁶ In another study from India with 31 CVT patients, anticardiolipin antibodies were detected in 22.6% of CVT patients compared with 3.2% of normal control subjects.¹² Similar findings (5.9%) were observed in the ISCVT study.¹⁰

Factor V Leiden Gene Mutation and Resistance to Activated Protein C

Resistance to activated protein C is mainly caused by the presence of the factor V Leiden gene mutation, which is a common inherited thrombophilic disorder. A recent meta-analysis of 13 studies, including 469 CVT cases and 3023 control subjects,²⁸ reported a pooled OR of CVT of 3.38 (95% CI 2.27 to 5.05) for factor V Leiden, which is similar to its association with venous thromboembolism (VTE) in general.

Prothrombin G20210A Mutation

The prothrombin G20210A mutation is present in ≈2% of whites and causes a slight elevation of prothrombin level.^55,56A meta-analysis of 9 studies,³⁸ including 360 CVT patients and 2688 control subjects, reported a pooled OR of CVT of 9.27 (95% CI 5.85 to 14.67) for this mutation,²⁸ which is stronger than its association with VTE in general.

Hyperhomocysteinemia

Hyperhomocysteinemia is a risk factor for deep vein thrombosis (DVT) and stroke but has not been clearly associated with an increased risk of CVT. Five case-control studies evaluated hyperhomocysteinemia in patients with CVT.^{13,16,17,29,30}Researchers from Milan¹³ reported on 121 patients with a first CVT and 242 control subjects, finding hyperhomocysteinemia in 33 patients (27%) and 20 control subjects (8%; OR 4.2, 95% CI 2.3 to 7.6). Low levels of serum folate and the 677TT methylenetetrahydrofolate reductase genotype were not associated with CVT risk, independent of homocysteine level.¹³

A study of 45 patients with CVT and 90 control subjects in Mexico reported an adjusted OR of CVT of 4.6 (95% CI 1.6 to 12.8) associated with high fasting homocysteine and an OR of 3.5 (95% CI 1.2 to 10.0) associated with low folate.²⁹ A small Italian study of 26 consecutive patients with CVT and 100 healthy control subjects reported that 38.5% of case subjects and 13% of control subjects had hyperhomocysteinemia (OR 4.2, 95% CI 1.6 to 11.2).¹⁶ No significant differences were found in the prevalence of prothrombin or methylenetetrahydrofolate reductase mutation. No factor V Leiden mutation was found. Another Italian group¹⁷ found a strong and significant association of the prothrombin G20210A mutation (30% versus 2.5% in patients versus control subjects, respectively,P=0.001; OR 16.2, P=0.002) and hyperhomocysteinemia (43.3% versus 10%,P=0.002; OR 6.9, P=0.002).

Pregnancy and Puerperium

Pregnancy and the puerperium are common causes of transient prothrombotic states.⁵⁷ Approximately 2% of pregnancy-associated strokes are attributable to CVT.³¹ The frequency of CVT in the puerperium is estimated at 12 cases per 100 000 deliveries, only slightly lower than puerperal arterial stroke.⁵⁸

In a study from Mexico, ≈50% of CVT occurred during pregnancy or puerperium.³²Most pregnancy-related CVT occurs in the third trimester or puerperium. Seven of 8 CVTs among 50 700 admissions for delivery in Canada occurred postpartum.³³During pregnancy and for 6 to 8 weeks after birth, women are at increased risk of venous thromboembolic events.³⁴ Pregnancy induces several prothrombotic changes in the coagulation system that persist at least during early puerperium. Hypercoagulability worsens after delivery as a result of volume depletion and trauma. During the puerperium, additional risk factors include infection and instrumental delivery or cesarean section. One study reported that the risk of peripartum CVT increased with increasing maternal age, increasing hospital size, and cesarean delivery, as well as in the presence of hypertension, infections, and excessive vomiting in pregnancy.³⁵ Recently, it was reported that in pregnant women, hyperhomocysteinemia was associated with increased risk of puerperal CVT (OR 10.8, 95% CI 4.0 to 29.4) in a study of 60 case subjects and 64 control subjects.³⁰

Oral Contraceptives

A 1998 study compared the prevalence of several risk factors, including use of oral contraceptives, among 40 female patients with CVT, 80 female patients with DVT of the lower extremities, and 120 female control subjects.³⁶ Nearly all CVT case subjects were using oral contraceptives (96%), which conferred 22.1-fold increased odds of CVT (95% CI 5.9 to 84.2). The OR for women with the prothrombin G20210A mutation who used oral contraceptives was 149.3 (95% CI 31.0 to 711.0) compared with those with neither characteristic. Stratification for the presence of factor V Leiden or prothrombin mutation and the use of oral contraceptives showed similar point estimates for the coagulation abnormalities alone and the use of oral contraceptives alone, whereas the presence of both risk factors gave an OR of 30.0 (95% CI 3.4 to 263.0) for factor V Leiden and 79.3 (95% CI 10.0 to 629.4) for the prothrombin mutation. A study in the Netherlands³⁷ found that of 40 female CVT patients, 85% used oral contraceptives, with an adjusted OR of 13 (95% CI 5 to 37). The combination of oral contraceptives with a prothrombotic condition also dramatically increased the risk of CVT. A study from Brazil showed similar results.¹⁸ In a meta-analysis that included 16 studies, the authors reported an increased risk of CVT in oral contraceptive users (relative risk 15.9, 95% CI 6.98 to 36.2).⁵⁹ In another meta-analysis of 17 studies,²⁸ an increased risk of CVT was found in patients who used oral contraceptives (OR 5.59, 95% CI 3.95 to 7.91;P<0.001). It is clear that the use of oral contraceptives is associated with an increased risk of CVT, that the great majority of younger nonpregnant women with CVT are oral contraceptive users, and that the risk of CVT with oral contraceptive use in women is greater among those with a hereditary prothrombotic factor.

Other Uncommon Causes

New neuroimaging procedures have increased the ability to detect CVT in recent years and have also helped to identify other potential causes, including infections, mainly in parameningeal locations (ear, sinus, mouth, face, and neck). These causes only explained 8.2% of all cases in the ISCVT series.² In contrast, CVT caused by infection is more common in children. In a recent series of 70 children with CVT in the United States, 40% had infection-related CVT.¹⁶ Conversely, a French study of 62 adults with isolated lateral sinus thrombosis found that only 3 cases were related to parameningeal infections.⁴²

Other conditions have been associated with CVT in case reports or small series, including paroxysmal nocturnal hemoglobinuria,⁴⁸ iron deficiency anemia,⁴⁹thrombocythemia,⁵⁰ heparin-induced thrombocytopenia,⁶¹ thrombotic thrombocytopenic purpura,¹⁴ nephrotic syndrome,⁵¹ inflammatory bowel disease,^10,62 systemic lupus erythematosus,⁵² Behçcet disease,⁵³ mechanical precipitants, epidural blood patch,⁴⁵ spontaneous intracranial hypotension,⁴⁶ and lumbar puncture.⁴⁷

Clinical Diagnosis of CVT

Principal Clinical Findings

The diagnosis of CVT is typically based on clinical suspicion and imaging confirmation. Clinical findings in CVT usually fall into 2 major categories, depending on the mechanism of neurological dysfunction: (1) Those that are related to increased intracranial pressure attributable to impaired venous drainage and (2) those related to focal brain injury from venous ischemia/infarction or hemorrhage. In practice, many patients have clinical findings due to both mechanisms, either at presentation or with progression of the underlying disease. Headache, generally indicative of an increase in intracranial pressure, is the most common symptom in CVT and was present in nearly 90% of patients in the ISCVT.¹⁰Similar headache frequency has been reported in other populations studied.⁶³ The headache of CVT is typically described as diffuse and often progresses in severity over days to weeks. A minority of patients may present with thunderclap headache, suggestive of subarachnoid hemorrhage, and a migrainous type of headache has been described.⁶⁴ Isolated headache without focal neurological findings or papilledema occurs in up to 25% of patients with CVT and presents a significant diagnostic challenge.⁶⁵ CVT is an important diagnostic consideration in patients with headache and papilledema or diplopia (caused by sixth nerve palsy) even without other neurological focal signs suggestive of idiopathic intracranial hypertension. When focal brain injury occurs because of venous ischemia or hemorrhage, neurological signs and symptoms referable to the affected region are often present; most common are hemiparesis and aphasia, but other cortical signs and sensory symptoms may occur. Psychosis, in conjunction with focal neurological signs, has also been reported.⁶⁶

• AHA/ASA Scientific Statement

Diagnosis and Management of Cerebral Venous Thrombosis

Figure 2.

Magnetic resonance venogram showing the cerebral venous system and most frequent (%) location of cerebral venous and sinus thrombosis, as reported in the International Study on Cerebral Venous and Dural Sinuses Thrombosis (n=624).⁴⁴

There is more Link and what the Good Doctor is forgetting to tell you Hillary Clinton is in "Good Health" for someone who has Cerebral Venous Sinus Thrombosis which is an added condition from her original diagnosis. But one thing we have to keep reminding ourselves she has not presented the finding of the Neuologist who is treating her for this condition Subcortical Vascular Dementia and Complex Partial Seizures.

I can only tell you what I was told by a Psychologist who was hired by my mother in laws Attorney in order to steal her 2 million dollars he had. This Psychologist said my Mother in Law was Normal for her age even though she scored 13 on the MMSE (Mini Mental State Health exam) which shows "normal" is anyone who sores over the rage of 26. Notice how he got away with the question of Normal. Compared to my mother in laws age which at the time was 95 years old normal was people with Dementia of a score 13 out of 27. My Mother in Law also had a Lacunar Infarct (LACI)  which is a kind of stroke that affects the brain of an individual.

 We need to know all about this condition, its various symptoms and how it is treated. So the incomplete statement is She in good health for someone who has Cerebral Venous Sinus Thrombosis, Subcortical Vascular Dementia and Complex Partial Seizures. But is Hillary's Health good enough to be President?  I persoanlly think not.

All you Democrats scream and yelled Dick Chaney's health was bad after  Bypass surgery fo Vice President  and his health condition was better then Hillary's. 

Mental Health such as Dementia never gets reversed. It gets worse.

Subcortical Vascular Dementia  : Commonly known as Binswanger's disease


Binswanger's disease (BD), also called subcortical vascular dementia, is a type of dementia caused by widespread, microscopic areas of damage to the deep layers of white matter in the brain. The damage is the result of the thickening and narrowing (atherosclerosis) of arteries that feed the subcortical areas of the brain. Atherosclerosis (commonly known as "hardening of the arteries") is a systemic process that affects blood vessels throughout the body. It begins late in the fourth decade of life and increases in severity with age. As the arteries become more and more narrowed, the blood supplied by those arteries decreases and brain tissue dies. A characteristic pattern of BD-damaged brain tissue can be seen with modern brain imaging techniques such as CT scans or magnetic resonance imaging (MRI). The symptoms associated with BD are related to the disruption of subcortical neural circuits that control what neuroscientists callexecutive cognitive functioning: short-term memory, organization, mood, the regulation of attention, the ability to act or make decisions, and appropriate behavior. The most characteristic feature of BD is psychomotor slowness - an increase in the length of time it takes, for example, for the fingers to turn the thought of a letter into the shape of a letter on a piece of paper. Other symptoms include forgetfulness (but not as severe as the forgetfulness of Alzheimer's disease), changes in speech, an unsteady gait, clumsiness or frequent falls, changes in personality or mood (most likely in the form of apathy, irritability, and depression), and urinary symptoms that aren't caused by urological disease. Brain imaging, which reveals the characteristic brain lesions of BD, is essential for a positive diagnosis.

There is no specific course of treatment for BD. Treatment is symptomatic. People with depression or anxiety may require antidepressant medications such as the serotonin-specific reuptake inhibitors (SSRI) sertraline or citalopram. Atypical antipsychotic drugs, such as risperidone and olanzapine, can be useful in individuals with agitation and disruptive behavior. Recent drug trials with the drug memantine have shown improved cognition and stabilization of global functioning and behavior. The successful management of hypertension and diabetes can slow the progression of atherosclerosis, and subsequently slow the progress of BD. Because there is no cure, the best treatment is preventive, early in the adult years, by controlling risk factors such as hypertension, diabetes, and smoking.

BD is a progressive disease; there is no cure. Changes may be sudden or gradual and then progress in a stepwise manner. BD can often coexist with Alzheimer's disease. Behaviors that slow the progression of high blood pressure, diabetes, and atherosclerosis -- such as eating a healthy diet and keeping healthy wake/sleep schedules, exercising, and not smoking or drinking too much alcohol -- can also slow the progression of BD.

The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to BD in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure neurological disorders, such as BD.
http://www.ninds.nih.gov/disorders/binswangers/binswangers.htm

The Good Doctor also notes Hillary is wearing  Fresnel Prisims in her glasses 

Use of fresnel prism glasses to treat stroke patients with hemispatial neglect.

Abstract

OBJECTIVE:

To explore the functional effects of prism adaptation training on patients with hemispatial neglect after stroke.

DESIGN:

Observational study.

SETTING:

Inpatient rehabilitation unit in rural Australia.

PARTICIPANTS:

Four subjects with hemispatial neglect, recruited from consecutive admissions of patients less than 60 days poststroke.

INTERVENTION:

Prism adaptation treatment, consisting of five 10-minute training sessions over 12 to 17 days.

MAIN OUTCOME MEASURES:

The FIM instrument, Catherine Bergego Scale (CBS), subjective straight ahead pointing, Albert's line cancellation, letter cancellation, and line bisection. Ambulatory patients also performed the Timed Up & Go test.

RESULTS:

Immediate effects of prism adaptation training included improvements in both subjective straight ahead pointing and in the Albert's line cancellation task. Letter cancellation, line bisection, FIM, and CBS scores improved in all subjects. Improvements in a functional task were also observed immediately following prism adaptation treatment. Obstacle avoidance while walking improved after prism adaptation training in 2 ambulatory subjects.

CONCLUSIONS:

Prism adaptation training shows promise as a new treatment to supplement current strategies for the clinical management of hemispatial neglect after stroke. This study is limited by small sample size and absence of a control group. Further research will be needed to demonstrate efficacy for this inexpensive and relatively safe device

Now the Good Doctor states Hillary's  Cholesterol 195 we have to understand what Cholesterol means;

• Total cholesterol Hillary's was 195
• LDL (low-density lipoprotein cholesterol, also called "bad"cholesterol) (Hillary's was 118
• HDL (high-density lipoprotein cholesterol, also called "good" cholesterol)  Hillary's was 64
• Triglycerides (fats carried in the blood from the food we eat. Excess calories, alcohol, or sugar in the body are converted intotriglycerides and stored in fat cells throughout the body.) 69

This is what I have been told : If your LDL is 190 or more, it is considered very high. Your doctor will most likely recommend a statin in addition to making healthy lifestyle choices. Statins are medicines that can help lower cholesterol levels.

When it comes to HDL cholesterol -- "good" cholesterol – a higher number means lower risk. This is because HDL cholesterol protects against heart disease by taking the "bad" cholesterol out of your blood and keeping it from building up in your arteries. A statin can slightly increase your HDL, as can exercise

Triglycerides are the form in which most fat exists in food and the body. A high triglyceride level has been linked to higher risk of coronary artery disease. Here's the breakdown.

Triglycerides	Triglyceride Category
Less than 150	Normal
150 - 199	Mildly High
200 - 499	High
500 or higher	Very high

Total Cholesterol

Your total blood cholesterol is a measure of LDL cholesterol, HDL cholesterol, and other lipid components. Your doctor will use your total cholesterol number when determining your risk for heart disease and how best to manage it.

The total cholesterol is 195 and is a risk factor of having another stroke or even mini strokes. Her father died from a stroke but it is not clear if he had Mini strokes in between the Massive one at the end.  Her Mother died of a heart attack but we do not know how many attacks she had of the kind. Congestive Heart Failure is a secondary cause not the primary cause of death. My husband who was a Veternarian got a Zoological virus which infected his heart and he died form that. The Virus caused his Congestive Heart failure. So what this doctor wrote was a smear like a smear of Cream cheese on a bagel  of Hillary's condition labeling it "Excellent" so she won't get sued.

The Good Doctor mentions Hillary is on Lovenox LOVENOX® helps reduce the risk of deep vein thrombosis—also known as DVT blood clots—to help avoid a potential pulmonary embolism in patients undergoing abdominal surgery, hip-replacement surgery, knee-replacement surgery, or medical patients with severely restricted mobility during acute illness.

This is a self injected drug. There is a warning on the label

All patients should be carefully monitored by their doctor while taking LOVENOX®. Your doctor is likely to obtain blood tests that measure your blood count and check for signs of hidden bleeding while you are on LOVENOX®.

Lovenox is a very dangerous drug. It's like Coumadin which is commonly used in rat poison. Let's add another reason we need a healthy president  if an aide like Huma Abedin who did not pass the security investigation and is connected to the Muslim Brotherhood could be overdosed Hillary ,she could die and no one would know it since this medication is prescribe by a doctor.

If Hillary was in EXCELLENT HEALTH she would not be on Lovenox... I rest my case in why she is not Mentally or physically fit to be President.

A note to Hillary, The people of the United States are not stupid. We can see through your lies.

And the Good Doctor has left out details . 

From the New York Times  http://www.nytimes.com/politics/first-draft/2015/07/31/doctor-says-hillary-clinton-is-fit-to-serve/?_r=0

Updated, 9:52 p.m. | Hillary Rodham Clinton’s campaign released a letter on Friday from her doctor attesting to Mrs. Clinton’s good health and fitness to serve as president based on a full medical evaluation.

The letter from Dr. Lisa Bardack of Mount Kisco, N.Y., summarized Mrs. Clinton’s history of treatment for a brain concussion, blood clots affecting her legs and brain on separate occasions, an underactive thyroid gland and a family history of heart disease.

Mrs. Clinton, 67, regularly takes thyroid hormone to bring her levels to normal as well as the anticoagulant drug Coumadin to help prevent new blood clots, Dr. Bardack wrote. Mrs. Clinton also takes antihistamine drugs for seasonal pollen allergies and vitamin B-12.

Mrs. Clinton has faced questions about her health since 2012, when, as secretary of state, she suffered a concussion and a blood clot — known as a transverse sinus venous thrombosis — in her brain. Those were a result of a series of events caused by a stomach virus Mrs. Clinton acquired while traveling abroad. While alone in her home after returning, she became dehydrated and then fell from a faint, striking her head. She subsequently experienced double vision and temporarily wore glasses with a Fresnel Prism to ease the difficulty with her eyesight.

Mrs. Clinton was treated at George Washington University Hospital in Washington, and then went to NewYork-Presbyterian/Columbia hospital in Manhattan before returning to her home in Chappaqua, N.Y.

The concussion symptoms and double vision resolved within two months and Mrs. Clinton stopped using the prism, Dr. Bardack wrote.

But former President Bill Clinton told a reporter that his wife’s concussion “required six months of very serious work to get over” and that she had “never lowballed” the severity of her head injury.

Follow-up testing in 2013 showed “complete resolution of the effects of the concussion, as well as total dissolution” of the blood clot, Dr. Bardack wrote. Mrs. Clinton did not release statements from a neurologist, neurosurgeon or other specialist involved in her medical care in Washington or New York.

Mrs. Clinton is the first presidential candidate in this cycle to make public a medical history. But in the past many candidates have released copies of extensive records, agreed to personal interviews or allowed their doctors to be interviewed.

Nick Merrill, a spokesman for Mrs. Clinton, did not reply to an email request to interview Dr. Bardack.

While Mrs. Clinton experienced blood clots in 1998, 2009 and 2012, tests showed that she did not have any underlying disorder that put her at an increased risk of the clots. Tests are performed to monitor the dose of Coumadin she takes and ensure that she has not experienced side effects, Dr. Bardack wrote.

Mrs. Clinton’s electrocardiogram was reported as normal, as were her blood lipids. Cancer screening tests, including mammography, breast ultrasound, colonoscopy and gynecological examination were normal.

Dr. Bardack did not disclose Mrs. Clinton’s height and weight, which are standard items in medical histories.

She said Mrs. Clinton eats a diet rich in lean protein, vegetables and fruits. She exercises regularly, including yoga, swimming, walking and weight training.