Intracranial Atherosclerosis

What is intracranial artery atherosclerosis?

Intracranial atherosclerosis is deposition of cholesterol and lipids in the wall of the arteries inside the brain. Similar to carotid stenosis in the neck, it is caused by a buildup of plaque in the inner wall of the blood vessels. This narrowing of the blood vessels causes decreased blood flow to the area of the brain that the affected vessels supply. 

There are three ways in which intracranial artery atherosclerosis can result in a stroke:

•       Plaque can grow larger and larger, severely narrowing the artery and reducing blood flow to the brain. Plaque can eventually completely block (occlude) the artery.

•       Plaque can roughen and deform the artery wall, causing blood clots to form and blocking blood flow to the brain.

•       Plaque can rupture and break away, traveling downstream to lodge in a smaller artery and blocking blood flow to the brain.

What are the symptoms?

The symptoms of intracranial artery atherosclerosis are a transient ischemic attack (TIA) or stroke, which can be described with the mnemonic FAST:

F: for facial weakness or droop, especially on one side

A: for arm or leg weakness, tingling, or numbness, especially on one side

S: for slurred speech

T: for time. It is essential to seek immediate medical attention if the above symptoms occur.

Symptoms of a TIA and stroke are similar. TIAs result when blood flow to the brain is temporarily interrupted and then restored. The symptoms typically last a couple of minutes and then resolve completely, and the person returns to normal. However, TIAs should not be ignored; they are a warning that an ischemic stroke and permanent brain injury may be impending.

What are the causes?

Atherosclerosis is a major cause of intracranial artery stenosis. It can begin in early adulthood, but symptoms may not appear for several decades. Some people have rapidly progressing atherosclerosis during their thirties, others during their fifties or sixties. Atherosclerosis begins with damage to the inner wall of the artery caused by high blood pressure, diabetes, smoking, and elevated LDL cholesterol. Other risk factors include obesity, heart disease, family history, and advanced age.

How is a diagnosis made?

Computed Tomography Angiography, or CT angiogram, is a noninvasive X-ray that provides detailed images of anatomical structures within the brain. It involves injecting a contrast agent into the blood stream so that arteries of the brain can be seen. This type of test provides the best pictures of both blood vessels (through angiography) and soft tissues (through CT). It enables doctors to see the narrowed artery and to determine how much it has narrowed.

Magnetic Resonance Angiography (MRA) is similar to the CT angiogram. Contrast dye is injected through an IV to visualize blood vessels in the neck.

Angiogram is a minimally invasive test that uses X-rays and a contrast agent injected into the arteries through a catheter in the groin. It enables doctors to visualize all arteries and veins in the brain. It carries a low risk of permanent neurologic complications. Beyond identifying the area of disease, angiography provides valuable information about the degree of stenosis and shape of the plaque.

Transcranial Doppler Ultrasound is a quick, inexpensive test used to measure the velocity of blood flow through blood vessels in the brain. This technique measures blood flow velocity by emitting a high-pitched sound wave from an ultrasound probe. Different speeds of blood flow appear in different colors on a computer screen. The more sluggish the blood flow, the greater the risk of stroke.

CT or MR Perfusion imaging is a noninvasive test that detects blood flow in the brain and is used in planning surgery. It involves injecting a contrast agent into the bloodstream so that doctors 1) can study how much blood flow is reaching the brain and 2) can determine which areas of the brain are most at risk of stroke.

What treatments are available?

The goal of treatment is to reduce the risk of stroke. Treatment options for intracranial atherosclerosis vary according to the severity of the narrowing and whether you are experiencing stroke-like symptoms or not. Patients are first treated with medication and are encouraged to make lifestyle changes to reduce their risk of stroke. Surgery is limited to patients whose symptoms do not respond to medication.

Medications

Blood thinner medications, also called anticoagulants (aspirin, Clopidogrel, Coumadin), allow the blood to pass through the narrowed arteries more easily and prevent clotting. Studies show that aspirin and Coumadin provide similar benefits. Because blood-thinners are associated with an increased risk of bleeding, patients may be monitored for abnormal bleeding. Aspirin has fewer side effects than Coumadin and is associated with a lower risk of bleeding or hemorrhage. Patients taking Coumadin must have their blood monitored periodically; patients taking aspirin and/or Plavix do not require monitoring.

Cholesterol-lowering medications help reduce additional plaque formation in atherosclerosis. These medications can reduce LDL (low-density lipoprotein) cholesterol by an average of 25 to 30% when combined with a low-fat, low-cholesterol diet.

Blood pressure medications (diuretics, ACE inhibitors, angiotensin blockers, beta blockers, calcium channel blockers, etc.) help control and regulate blood pressure. Because high blood pressure is a major risk factor of stroke, regular blood pressure screenings are recommended, along with taking your medication regularly.

Surgery / Endovascular Therapy

The aim of surgery is to prevent stroke by removing or reducing the plaque buildup and enlarging the artery to allow more blood flow to the brain. Surgical treatment is considered for patients whose symptoms do not respond to medication. For example, those who continue to have TIAs or strokes, those with a high grade of stenosis, and those with insufficient blood supply to an area of the brain.

Balloon angioplasty / stenting is a minimally invasive endovascular procedure that compresses the plaque and widens the diameter of the artery. Endovascular means that the procedure is performed inside the artery, from within the bloodstream, with a small flexible catheter. The catheter is inserted into the femoral artery in the groin during an angiogram. The catheter is then advanced through the bloodstream to where the plaque-narrowed artery is located. A small balloon is then slowly inflated within the narrowed artery to dilate it and compress the plaque against the artery wall.

The aim is to reduce stenosis by less than 50%, as a small increase of the vessel diameter results in large increases in blood flow to the brain. The balloon is then deflated and removed. In some cases, a self-expanding mesh-like tube called a stent is placed over the plaque, holding open the artery. Complications from angioplasty can include stroke, tearing of the vessel wall from the catheter or balloon, and vasospasm.

Angioplasty is typically recommended for patients who have high-grade artery stenosis (greater than 70%) and recurrent TIA or stroke symptoms despite medication treatment. Angioplasty / stenting can successful reduce the stenosis to less than 30% without complications in 60 to 80% of patients.

Cerebral artery bypass is a surgical procedure that reroutes the blood supply around the plaque-blocked area. This procedure requires making an opening in the skull, called a craniotomy. A donor artery from the scalp is detached from its normal position on one end, redirected to the inside of the skull, and connected to an artery on the surface of the brain. The scalp artery now supplies blood to the brain and bypasses the blocked vessel (see Cerebral Bypass Surgery). Complications from bypass can include stroke, vasospasm, and clotting in the donor vessel.

Bypass is typically recommended when the artery is 100% blocked and angioplasty is not possible. Results of artery bypass vary widely depending on the location and type of bypass. 

Despite treatment with medications, patients who have had a stroke or TIA due to intracranial artery stenosis face a 12 to 14% risk of recurrent stroke during the 2-year period after the initial stroke. In some high-risk groups, the annual risk of recurrent stroke may exceed 20%.

After angioplasty, restenosis can occur in 7.5 to 32.4% of patients and is usually not symptomatic. The long-term outcome of stroke prevention after angioplasty is not yet known, but short-term results are promising and is currently being studied in clinical trials.

It’s important to understand that atherosclerosis is a progressive disease. 

Lifestyle changes, medications help to prevent progression of the disease and occurrence of stroke. Surgery and Endovascular therapy are required in selected cases to prevent stroke.

Queries

In case of queries, please write to mumbaistrokecare@gmail.com

Management of Asymptomatic Carotid Artery Stenosis

Introduction

Asymptomatic stenosis of the carotid artery is not an uncommon finding encountered by many doctors in clinical practice.

The common question that comes up is

What is the management of these patients?

Should they undergo carotid revascularization surgery?

Current guidelines recommend revascularization in most patients with severe asymptomatic carotid artery stenosis. However, these guidelines are based on older studies that do not reflect the changing natural history of asymptomatic carotid artery stenosis with current optimal medical management.

Conventional treatment

Current recommendations for revascularization for asymptomatic carotid artery stenosis are predominantly based on two landmark studies performed in the 1990s.

The Asymptomatic Carotid Artery Study (ACAS) was a well-conducted study that assessed carotid endarterectomy (CEA) in asymptomatic carotid artery stenosis (>60%) for stroke prevention. The study was halted because of a projected safety favoring carotid endarterectomy (CEA). The perioperative stroke rate was 2.3%. The five-year projected rate of ipsilateral stroke was 11% for the medical group versus 5.1% for the surgical group.

In the Asymptomatic Carotid Surgery Trial (ACST), the 30-day risk of stroke or death was 3.1%. The five-year rates were 6.4% for CEA and 11.7% for medical therapy arm.

However, medical therapy in these trials was not up to current standards, with only a minority of patients receiving lipid-lowering therapy (Statins) and blood pressure (BP) was also significantly higher than today's standards.

Evolving Natural History of Asymptomatic Carotid Artery Stenosis

Recent evidence suggests that the natural history of asymptomatic carotid artery stenosis has improved remarkably, and the risk-benefit analysis of revascularization will need to be re-evaluated. Current optimal medical management consists of high-dose statin drugs, optimal BP control, smoking cessation, antiplatelet therapy (generally aspirin alone), optimal diabetes control and other lifestyle changes. Hence, the annual risk of stroke with current OMT is likely <1%.

Who is a "High-Risk" Patient?

The reality is that the majority of patients with asymptomatic carotid artery stenosis will never become symptomatic and may undergo unnecessary procedures if these studies do show benefit of endarterectomy or stenting

Clinical Features

There are few clinical predictors of increased stroke risk in asymptomatic carotid artery stenosis. Certain clinical characteristics, such as male sex, current smoking, poorly controlled hypertension, and history of contralateral transient ischemic attack (TIA)/stroke impart a higher risk of future stroke. However these are too non-specific to serve as useful guides for deciding about revascularization.

Stenosis Severity

Patients with 50-69% stenosis had a lower risk compared to those with 70-89% and 90-99% stenosis. However, stenosis severity alone is not a strong enough predictor to be used alone in decision making.

Progression of Stenosis

Progression of stenosis on periodic examination has been shown to impart at least twice the risk of stroke in patients.

Plaque Characteristics

Using ultrasound, atherosclerotic plaques can be characterized based on their surface irregularity, ulcerations, echolucency and gray-scale values. Studies show that patients with predominantly echolucent, lipid-rich plaque have significantly higher stroke risk (3%) than those with mostly echodense, fibrotic plaque (0.8-0.4%). Ulceration on plaque surface detected by three-dimensional ultrasound has also been shown to identify high-risk subjects. Magnetic resonance imaging (MRI) has also been used to detect the presence of intraplaque hemorrhage as indicative of a high-risk plaque. Intraplaque hemorrhage detected by MRI is associated with an increased risk of cerebrovascular events

Silent Emboli Detection

Since both progressive stenosis and high-risk imaging features identify unstable plaque more prone to atheroembolic events, another way to identify patients at risk is to assess for active silent emboli or evidence of prior asymptomatic cerebral emboli using transcranial doppler study. However, most patients with these signals did remain stroke free at three years, and thus, this test lacks the specificity for stand-alone clinical use.

Silent Embolic Infarcts on Computed Tomography (CT) or MRI

Presence of ipsilateral silent embolic infarcts on neuroimaging may be predictive of increased risk of ipsilateral stroke.

 Reduced Cerebrovascular Reserve

In patients with severe ipsilateral carotid stenosis, the presence of an incomplete circle of Willis or presence of intracranial or contralateral occlusive disease can reduce cerebral perfusion pressure. Cerebrovascular reserve in such patients can be assessed using TCD velocity measurements in response to acetazolamide or breathing 5% CO2.

Elderly

The elderly (especially those over 80 years of age) is a group in which the benefit of revascularization for asymptomatic carotid artery stenosis is most controversial because However, age cannot be an absolute contraindication with increasing life expectancy of the overall population; certainly in carefully selected patients, excellent outcomes after both CEA (Carotid Endarterectomy) and CAS (Carotid Artery Stenting) have been demonstrated. Overall CEA has more favorable outcomes for those over 70 years of age and CAS for those under 70 years of age.

Conclusions and Recommendations for Clinical Practice

Both medical and surgical management arms of asymptomatic carotid artery stenosis are rapidly evolving and will continue to result in decreased stroke risk.

• We recommend that for asymptomatic carotid artery stenosis patients (even those with >80%) stenosis there is enough evidence for a more conservative approach and decisions regarding revascularization should be made after discussing the stroke risk with the patients.
• Serial ultrasounds should be performed and revascularization offered to those with >70% stenosis with evidence of progression of stenosis severity.
• All patients with asymptomatic carotid artery stenosis should be on Optimal Medical Management.
• For the very elderly (>80 years) and life expectancy less than five years, a conservative approach is most reasonable in most situations.
• Carotid Endarterectomy remains the gold-standard for revascularization of carotid stenosis. Carotid Artery Stenting should be considered in patients with high risk of surgery from associated cardiac co-morbidity.
• Individual patient and anatomic risks for CEA and CAS are different and should be considered and a multi-specialty approach should be followed.

How are incidental Brain Aneurysms managed?

Brain aneurysms are sometimes found incidentally in patients who have imaging scans for another reason. The questions that come immediately to the patient's and doctor's mind are

Are these patients at high risk of subarachnoid hemorrhage? 

When should they see a stroke specialist, and should incidental aneurysms always be treated? 

What is the risk of an unruptured brain aneurysm?

Rupture risk assessment is complex and depends on many factors. When an aneurysm is found incidentally, it is recommended that the patient consult a Vascular Neurosurgeon for evaluation and discussion of risk and treatment options.

While there is no concrete data from literature, 7 mm is generally considered the outer limit of a “small” aneurysm.Lesions smaller than 7 mm carry between 0.5 to 5 percent risk of rupture in the next five years, while a 12-mm aneurysm has a risk as high as 12 percent and a 25-mm lesion, 50 percent.

Aneurysms located on certain arteries carry more risk of rupture than others. Those located on the anterior communicating artery, posterior communicating artery and the posterior circulation i.e., vertebro-basilar system have a higher risk of rupture than those located elsewhere. Aneurysms with certain morphologic features, such as those containing “daughter sac" may have higher risk over time. Finally, 20 to 30 percent of patients with aneurysms have more than one lesion. This increases rupture risk, especially if one has ruptured previously.

How common are unruptured Brain Aneurysms?

Approximately 3 percent of the population has unruptured intracranial aneurysms. Most are asymptomatic. Patients with severe, sudden, acute-onset headache, often described as “the worst headache of my life,” may have a ruptured aneurysm, especially if they also have stiff neck, nausea, vomiting and syncope. These patients should go to the emergency department immediately.

Patients who recently had severe headache and stiff neck but did not seek treatment may have had a sentinel subarachnoid hemorrhage.These patients have 50 percent risk of a second, potentially fatal hemorrhage in the next 30 days. These patients should also go to the emergency department immediately.

Unruptured aneurysms should also be suspected in patients with:

• Unusually severe headache with acute onset, including associated with sexual activity
• Drooping of one eyelid
• Blurred or double vision

Should patients be screened?

The incidence of harboring a brain aneurysm is about 9% in patients who have two or more one first-degree relative with an aneurysm, and these patients should be screened for aneurysms with magnetic resonance angiography or CT angiography. Patients with certain genetic diseases such as autosomal dominant polycystic kidney disease should also be screened.

Should unruptured Brain Aneurysms be treated?

The question of whether and when to treat an unruptured brain aneurysm is highly individualized and depends on a number of patient and aneurysm factors.

Observation or Watchful Waiting

Patients whose aneurysms are not treated but observed, should have good blood pressure control and stop smoking, if they smoke. Excessive alcohol consumption should also be avoided, although there is no evidence in this regard. These lifestyle changes decrease the risk of developing an aneurysm, rupture and treatment complications.

Patients with small, asymptomatic aneurysms should be screened with magnetic resonance angiography, with repeat screening in a year. If the aneurysm is stable, they can be followed up with serial MRAs at two and three years. If an aneurysm grows or changes shape or the patient exhibits mass effects or cranial nerve symptoms, the risk goes up and such an aneurysm should be considered for treatment.

Endovascular coiling and Surgery

The main interventions for an unruptured aneurysm are surgical clipping and endovascular coiling or flow diversion. Risk of treatment depends on aneurysm complexity, patient health and other factors. The decision for surgical clipping or endovascular therapy should be discussed with the patient by an experienced vascular neurosurgery team. Depending upon the nature of the aneurysm and experience of the treating vascular neurosurgeon, surgical clipping and endovascular therapy should be chosen.

The usual duration of stay for a patient with unruptured brain aneurysm undergoing surgery at our center is 8 days whereas that for a patient undergoing endovascular therapy is about 3-4 days.

Subarachnoid Hemorrhage

What is Subarachnoid Hemorrhage (SAH)?

The brain is surrounded by three layers of coverings. All the important arteries supplying blood to the brain and veins draining impure blood from the brain run between these three layers. Bleeding into the subarachnoid space is known as Subarachnoid Hemorrhage (SAH).

What causes SAH?

The most common cause of SAH is head injury. However, the most devastating cause of SAH is due to rupture of a brain aneurysm. Often the bleeding stops, and the person survives. In more serious cases, the bleeding may cause brain damage with paralysis or coma. In the most severe cases, the bleeding leads to death. Bleeding into the cerebrospinal fluid may lead to acute increase in the intracranial pressure. Other conditions that can cause SAH are vascular malformation of the brain and venous stroke

What are the symptoms of SAH?

The main symptom is a sudden severe headache and neck pain. Other symptoms include

• Seizures
• Confusion
• Irritability
• Sensitivity to light
• Decreased vision
• Nausea
• Vomiting
• Loss of consciousness

What to do when someone is diagnosed with SAH?

Immediate referral to a center with neurosurgery and neurointerventional facilities is paramount to appropriate diagnosis and management of the patient with SAH and prevent brain damage. If your aneurysm is being clipped, a craniotomy is performed and the aneurysm is closed. A craniotomy involves opening the skull to expose the area of involvement. Alternatively, endovascular coiling involves introducing a long catheter through one of the arteries in the groin, navigating it all the way into the aneurysm in the brain and closing the aneurysm using coils (thin threads made of platinum alloy).

If SAH causes a coma, treatment will include appropriate life support with artificial ventilation, protection of the airways, and placement of a draining tube in the brain to relieve pressure.

What are the complications of SAH?

• Remleiding from the aneurysm is a serious concern in a patient with aneurysm rupture. Hence, the aneurysm needs to be closed as soon as possible by either open surgery or endovascular therapy
• Bleeding into the CSF (cerebrospinal fluid) and in the space around the brain (subarachnoid space). The pool of blood forms a clot. Blood can irritate, damage, or destroy nearby brain cells. This may cause problems with body functions or mental skills.
• Blood from an aneurysm rupture can block CSF circulation. This can lead to fluid buildup and increased pressure on the brain. Because blood is spread around the base of the brain, the possibility of fluid buildup exists, causing hydrocephalus. The CSF containing spaces in the brain, called ventricles, may enlarge. It can make a patient lethargic, confused, or comatose. To stop fluid buildup, a drain may be placed in the ventricles. The tube is called a ventriculostomy, and often drains into a bag at the patient's bedside. This removes leaked blood and trapped CSF. If the hydrocephalus persists, the patient may require a ventriculoperitoneal shunt surgery to drain the CSF permanently.
• The blood around the base of the brain can also produce a problem called vasospasm. Vasospasm typically develops 5-8 days after the initial hemorrhage. Narrowing of the blood vessels can occur and at times not enough blood is supplied to the brain and a stroke may result. To treat vasospasm, blood pressure is often elevated with medicines. Certain medications are also given to try to reduce vasospasm. Finally, catheters can be introduced inside the artery in an attempt to use balloons or medications delivered to the vessel directly to open up these narrowed vessels. Vasospasm does subside over several days.

What is the outcome of SAH?

SAH survivors usually have a much longer recovery time than unruptured aneurysm patients, as well as more serious deficits. Symptoms are proportional to the degree of hemorrhage and the initial clinical condition. Patients who are comatose or semi-comatose after a hemorrhage have longer recoveries and have more significant neurocognitive problems as compared to patients with smaller hemorrhages or unruptured aneurysms.

Reversing Paralysis from Stroke

http://strokesupport.in/reversing-paralysis-from-stroke/

Physical activity and Exercise tips for stroke survivors

Stroke is one of the leading causes of long term disability in India. It has emotional, psychological, physical and financial effects on the stroke survivor as well as his/her family. Stroke survivors are predisposed to a sedentary lifestyle that limits performance of activities of daily living, increased risk of falls and heightened risk for recurrent stroke and cardiovascular disease. Activity limitations (also referred to as “disabilities”) are manifested by reduced ability to perform daily functions, such as dressing, bathing, or walking. The magnitude of activity limitation is generally related to but not completely dependent on the level of body impairment (ie, severity of stroke). Other factors that influence level of activity limitation include intrinsic motivation and mood, adaptability and coping skill, cognition and learning ability, severity and type of preexisting and acquired medical comorbidity, medical stability, physical endurance levels, effects of acute treatments, and the amount and type of rehabilitation training. All the above effects create a vicious circle of further decreased activity and greater exercise intolerance, leading to secondary complications such as reduced cardiorespiratory fitness, muscle atrophy, osteoporosis, and impaired circulation to the lower extremities in stroke survivors. In addition, a diminished self-efficacy, greater dependence on others for activities of daily living, and reduced ability for normal societal interactions can have a profound negative psychological impact

Goals of Physical activity / Exercise

Traditionally, the physical rehabilitation of individuals typically ended within several months after stroke because it was believed that most if not all recovery of motor function occurred during this interval. Nevertheless, recent research studies have shown that aggressive rehabilitation beyond this time period, including treadmill exercise with or without body weight support, increases aerobic capacity and sensorimotor function. The three major rehabilitation goals for stroke patients are preventing complications of prolonged inactivity, decreasing recurrent stroke and cardiovascular events, and increasing aerobic fitness.

 Preventing complications of prolonged physical inactivity

The stroke patient needs to initiate a physical conditioning regimen designed to regain prestroke levels of activity as soon as possible. For inpatients, simple exposure to orthostatic or gravitational stress (ie, intermittent sitting or standing) during hospital convalescence has been shown to prevent much of the deterioration in exercise tolerance that normally follows a cardiovascular event or intervention. Shortly after hospital discharge, the continuum of exercise therapy may range from remedial gait retraining in hemiparetic stroke patients to supervised or home-based walking or treadmill training programs. 

Prevent recurrent Stroke and Cardiovascular events

A reduction of risk factors can decrease the incidence of recurrent strokes and cardiac events. An aerobic conditioning program can enhance glucose regulation and promote decreases in body weight and fat stores, blood pressure (particularly in hypertensive patients), and levels of total blood cholesterol, serum triglycerides, and low-density lipoprotein (LDL) cholesterol. Exercise also increases high-density lipoprotein (HDL) cholesterol and improves cardiac function.

Increasing aerobic fitness

Evidence is accumulating that stroke risk can be reduced with regular leisure-time physical activity in men and women of all ages. It has been proven that men in the moderate- and high-fitness groups had a 63% and 68% lower risk of stroke death, respectively, than men who were in the lowest-fitness group at baseline. Moreover, the inverse association between aerobic fitness and stroke mortality remained even in the presence of cigarette smoking, alcohol consumption, obesity, hypertension, diabetes mellitus, and a family history of heart disease. It is essential that the stroke survivor carries out exercise under the close supervision of qualified medical personnel.

Physical Activity and Exercise Recommendations

Stroke survivors:

• Recurrent stroke and cardiovascular disease are the leading causes of mortality in stroke survivors.
• Physical activity remains a cornerstone in the current armamentarium for risk factor management for the prevention and treatment of stroke and cardiovascular disease.
• Activity intolerance is common among stroke survivors, especially the elderly. Their sedentary lifestyle puts them at risk for recurrent stroke and cardiovascular disease.
• Stroke patients achieve significantly lower maximal workloads and heart rate/blood pressure responses than controls during progressive exercise testing.
• Many factors influence activity level after stroke, including physical, mental, and emotional status. Stroke patients may be more disabled by associated cardiac disease than by the stroke itself.
• Energy expenditure during walking in hemiplegic patients varies with degree of altered body structure and function but is generally elevated, often up to 2 times that of able-bodied persons walking at the same submaximal speed.

Benefits of aerobic conditioning:

• Stroke survivors can benefit from counseling on participation in physical activity and exercise training.
• Research studies show that aggressive rehabilitation beyond the usual 6-month period increases aerobic capacity and sensorimotor function.
• An aerobic exercise program can improve multiple cardiovascular risk factors and thereby have important implications for the medical management of stroke survivors.
• Evidence is accumulating that stroke risk can be reduced with regular leisure-time physical activity in multiethnic individuals of all ages and both sexes. Evidence now suggests that the exercise trainability of stroke survivors may be comparable to that of age-matched healthy counterparts.
• Extrapolation of what is known about the training effects of regular exercise by able-bodied individuals suggests that certain levels of exercise that are achieved during many stroke rehabilitation programs may improve aerobic fitness.

Preexercise evaluation:

• It is recommended that all stroke survivors undergo a preexercise evaluation (complete medical history and physical examination, usually including graded exercise testing with ECG monitoring) before they initiate an exercise program.
• When undergoing exercise testing, the testing mode should be selected or adapted to the needs of the stroke survivor (eg, use of handrails, arm cycle ergometry, arm-leg or leg cycle ergometry).

Recommendations for exercise programming:

• Treadmill walking is highly advantageous as the aerobic exercise mode, with inclusion of resistance, flexibility, and neuromuscular training.
• The combination of comorbidities, neurological deficits, and emotional barriers unique to each stroke survivor requires an individual approach to safe exercise programming.
• For patients unable to perform a graded exercise test, light-to-moderate rather than vigorous exercise should be prescribed, with a greater training frequency, duration, or both to compensate for the reduced intensity.
• Subsets of stroke survivors (eg., those with depression, fatigue syndrome, poor family support, or communication, cognitive, and motor deficits) will require further evaluation and subsequent specialization of their rehabilitation program.
• To enhance exercise compliance, the issues of family support and social isolation need to be addressed and resolved.
• Physical activity and exercise training recommendations for stroke survivors should be viewed as one important component of a comprehensive stroke and cardiovascular risk reduction program. 

Source: Circulation 2004;109:2031-2041

Driving after Stroke

Driving after stroke can be a daunting task. It is not only a major concern of individual safety, but, also public safety on the roads. Given the emotional, physical and financial burden of stroke on the stroke survivor's family, it is, but natural for the survivors to want to get back to work as soon as possible. Often survivors don't realize the difficulties that they might have when driving after a stroke. Some may not know all of the effects of their stroke. Driving against doctor's advice is not only dangerous, but also illegal.

How do I know if I can drive?

Many-a-time, the survivors are so keen to get back to normalcy that they ignore some of the signs and symptoms of unsafe driving. After all, they had been doing that for years before the stroke. 

Ask your family if they have noticed changes. Those around you may notice changes in your communication, thinking, judgment or behavior that should be evaluated before you drive again. They often have many more opportunities to observe changes than others do. 

What are the signs and symptoms of unsafe driving?

• Drives too fast or too slow for road conditions
• Needs help or instructions from passengers
• Doesn’t observe signs or signals
• Makes slow or poor distance decisions
• Gets easily frustrated or confused
• Often gets lost, even in familiar areas
• Has accidents or near misses
• Drifts across lane markings into other lanes

Where can I get help?

Talk to your doctor or occupational therapist. He or she can tell you about your stroke and whether it might change if you can drive. Unfortunately, there are no specific regulations for driving for stroke survivors in India. As such, there are no authorized driver rehabilitation specialists to evaluate driving ability. It would be of great help if the survivors enroll in an authorized driving school and receive instructions on how to modify your driving and the car to compensate for the disabilities. As more capable technologies and new advances in mobility equipment are made each day, wheelchair accessible vehicles have become more powerful than ever before. These modified vehicle solutions – such as hand controls, pedal extensions, seat bases, lifts and ramps – have changed the lives of countless stroke survivors and people with disabilities.

Guidelines in the UK
Driver and Vehicle Licensing Agency (DVLA)/Driver and Vehicle Agency (DVA) sets the rules. After a stroke or TIA you must stop driving immediately, but for many people this is temporary. It is possible to return to driving as long as it is safe to do so and the correct procedures are followed. The DVLA produce a factsheet, Car or motorcycle drivers who have had a stroke or transient ischaemic attack (TIA). This outlines when you have to inform them that you have had a stroke. This guide also applies in Northern Ireland and your medical practitioner may refer to these when advising you.

Cars or motorcycles

If you have a licence to drive a car or motorcycle (category B licence) you are not allowed to drive for at least one month after a stroke or TIA. After a month you may start driving again if your doctor is happy with your recovery. If you have had a number of TIAs over a short period of time you will need to wait until you have not had any TIAs for three months before returning to driving. You will also need to notify the DVLA/DVA.
If you have a licence to drive a large goods vehicle (LGV) or a passenger carrying vehicle (PCV) you must tell the DVLA immediately that you have had a stroke. You are not allowed to drive this type of vehicle for one year. After this time you may be able to resume driving, but this will depend on how well you have recovered and also on the results of medical reports and tests.

Specially adapted cars

Even if you have physical disabilities following your stroke, it may still be possible for you to drive. There are various vehicle adaptations and motoring accessories that can make driving possible and more comfortable. Specialist mobility centres can carry out assessments and provide advice about making adaptations to your vehicle which can enable you to return to driving. They can also provide assessments for passengers who have disabilities, and information on how to safely lift wheelchairs in and out of a car.

Pre-driving assessment tools

1. History to determine previous motor vehicle accidents, number of miles driven, psychosocial aspects, medical conditions and current level of psychological functioning
2. Physical examination to identify subtle physical conditions

• Assess joint mobility of neck, shoulders, wrists, hips, knees and ankles
• Assess upper and lower muscle strength manually
• Assess upper and lower coordination through finger-nose, heel to shin and rapid alternating motion
• Current medication
• Visual fitness
• Mental status

3. Neuropsychiatric testing
4. Off-road driving testing (simulator)