stroke

Stroke causes sudden loss of neurological function by disrupting
the blood supply to the brain. It is the biggest cause
of physical disability in developed countries, and a leading
cause of death. It is also common in many developing countries.
The great majority of strokes come on without warning. This
means that for most patients the aims of management are to
limit the damage to the brain, optimize recovery and prevent recurrence.
Strategies to prevent strokes are clearly important.
They concentrate on treating the vascular risk factors that
predispose to stroke, such as hypertension, hyperlipidaemia,
diabetes and smoking.
The two principal pathological processes that give rise to
stroke are occlusion of arteries, causing cerebral ischaemia or
infarction, and rupture of arteries, causing intracranial
haemorrhage (Fig. 2.1). Haemorrhage tends to be much more
destructive and dangerous than ischaemic stroke, with higher
mortality rates and a higher incidence of severe neurological
disability in survivors. Ischaemic stroke is much more common,
and has a much wider range of outcomes.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD13

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

PROGNOSIS

· Variable depending on severity of stroke

· Posterior circulation strokes have a higher acute mortality rate, but generally make a better functional recovery than do hemispheric strokes.

COMPLICATIONS

· Shoulder subluxation

· Hyperextension knee injury

· Depression

· Sympathetic dystrophy

PATIENT MONITORING

Follow the patient every 3 months for the 1st year, then yearly.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD12

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

MEDICATION (DRUGS)

First Line

· IV tissue plasminogen activator (tPA) 0.9 mg/kg in highly selected cases within 3 hours of ischemic stroke symptom onset

· Enteric-coated aspirin 50-325 mg/d or

· Dipyridamole-aspirin (Aggrenox): Extended release, 200 mg/25 mg capsule PO b.i.d.; more efficacious than aspirin or dipyridamole alone. (3)[A]

· Clopidogrel (Plavix): 75 mg/d; fewer side effects, but shows only slight advantage over aspirin

· Warfarin: INR adjusted dose 2-4 for patients with atrial fibrillation and cardioembolic stroke has shown decreased risk of recurrent stroke compared to ASA 300 mg/d at 2.3 years. (1)[A]

· Contraindications

  - Enteric-coated aspirin: Active peptic ulcer disease, hypersensitivity to aspirin, patients who had bronchospastic reaction to aspirin or other NSAIDs

  - Warfarin: Intolerance or allergy, dementia, liver disease, active bleeding, pregnancy, recent head injury

· Precautions

  - Enteric-coated aspirin: May aggravate pre-existing peptic ulcer disease, may worsen symptoms in some patients with asthma

  - Clopidogrel and ticlopidine: Thrombotic thrombocytopenic purpura can occur.

  - Warfarin: Poor balance, alcohol/drug abuse, age >80

· Significant possible interactions

  - Enteric-coated aspirin: May potentiate effects of anticoagulants and sulfonylurea, hypoglycemic agents

  - Ticlopidine: Digoxin plasma levels decreased 15%, theophylline half-life increased from 8.6-12.2 hours

  - Warfarin: Aspirin, NSAIDs, antibiotics, tranquilizers

Second Line

Ticlopidine (Ticlid): The treatment of 250 mg PO b.i.d. has fallen out of favor, because of an unfavorable side-effect profile, risk of neutropenia, and need for CBC monitoring.

· Caution: 2.4% of patients develop neutropenia (0.8% severe neutropenia) that is reversible with cessation of drug; monitor blood counts every 2 weeks for the 1st 3 months

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD11

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

TREATMENT

· Acute phase: Inpatient care

· Surgical therapy

  - In medically fit patients with nondisabling stroke, carotid endarterectomy is indicated for stenosis of >70% on side ipsilateral to stroke.

  - Medical therapy for <50% stenosis, 50-69% depends on risk factors

GENERAL MEASURES

· Maintain oxygenation.

· Monitor cardiac rhythm for 48 hours.

· Control hyperglycemia (keep glucose <220 mg/dL [12.1 mmol/L]).

· Treat blood pressure >185/110 if patient will be or has been treated with IV tissue plasminogen activator.

· Do not treat elevated BP unless acute end-organ dysfunction (encephalopathy, myocardial ischemia, aortic dissection, acute renal failure) is suspected.

· Prevent hyperthermia.

· Introduce physiotherapy and ambulation early.

· Subcutaneous heparin 5,000 units SC q12h

Diet

· Alert with no dysphagia: Diet as tolerated (no added salt if hypertensive)

· Alert with dysphagia: Pureed dysphagia diet or nasogastric feeding tube if indicated

Activity

Ambulate as soon as possible.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD10

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

DIFFERENTIAL DIAGNOSIS

· Migraine

· Focal seizure

· Tumor

· Subdural hematoma

· Hypoglycemia; hyperglycemia; hypercalcemia

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD9

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

TESTS

· Duplex carotid ultrasonography

· Cerebral angiography

· ECG

· Transthoracic ECG; if normal and a cardiac source is suspected, follow-up with transesophageal ECG.

· Holter monitoring

· EEG for suspected seizure

· Prothrombin time (PT) and partial thromboplastin time (PTT)

  - Coumadin prolongs PT.

· Antiphospholipid antibodies

· Cardiac enzymes

Imaging

Acute phase

· Multimodal CT of head

· MRI scan of brain with diffusion weighted imaging (DWI) remains the most powerful and accurate method for stroke identification.

· Arterial occlusions are seen with CTA as well as with MRA.

· Both CTA and MRA are highly reliable, noninvasive methods to verify the results of thrombolytic therapy.

· Quantitative CT perfusion and DWI/PWI (perfusion-weighted imaging) can rapidly provide functional information about brain perfusion and thus guide antithrombotic and neuroprotective strategies.

· Quantitative CTP is limited to a single slab of tissue per bolus, whereas MRI can provide whole-brain cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT).

· The goal of perfusion imaging is to reliably identify and distinguish brain tissue that is ischemic and will develop infarction without a specific intervention from brain tissue that is already damaged and cannot escape infarction.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD8

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

SIGNS AND SYMPTOMS

· Carotid circulation (hemispheric): Hemiplegia, hemianesthesia, neglect, aphasia, visual field defects; less often headaches, seizures, amnesia, confusion

· Vertebrobasilar (brainstem or cerebellar): Diplopia, vertigo, ataxia, facial paresis, Horner syndrome, dysphagia, dysarthria

· Impaired level of consciousness

· Cerebellar lesion in patients with headache, nausea, vomiting, and ataxia

Physical Exam

· Early mortality increases among those with any combination of impaired consciousness, hemiplegia, and conjugate gaze palsy

· Symptoms associated with the diagnosis of stroke or transient ischemic attack (TIA) are a sudden change in speech, visual loss, diplopia, numbness or tingling, paralysis or weakness, and nonorthostatic dizziness

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD7

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

ASSOCIATED CONDITIONS

Cardiac disease is the major cause of death in the 1st 5 years after a stroke.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD6

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

ETIOLOGY

· Ischemic: Carotid atherosclerotic disease with artery-to-artery thromboembolism

· Cardiac

  - Cardioembolism secondary to valvular (mitral valve) pathology

  - Mural hypokinesias or akinesias with thrombosis (acute anterior myocardial infarctions (MIs) or congestive cardiomyopathies)

  - Cardiac arrhythmia (atrial fibrillation)

· Hypercoagulable states

  - Antiphospholipid antibodies, factor V Leiden deficiency, deficiency of protein S, protein C, antithrombin III deficiency

  - Estrogen use (HRT, OCP, etc.)

· Other causes

  - Spontaneous and posttraumatic (i.e., chiropractic manipulation) artery dissection

  - Fibromuscular dysplasia

  - Vasculitis

  - Drugs (cocaine, amphetamines)

· Hemorrhagic

· Hypertension: May cause damage to putamen, internal capsule, cerebellum, brainstem, corona radiata

· Amyloid (congophilic) angiopathy: Lobar (cortical) hemorrhages in the elderly

· Vascular malformations: Arteriovenous malformation, cavernous angioma, venous angioma and capillary angioma

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD5

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

RISK FACTORS

· Uncontrollable

  - Age

  - Sex

  - Race

  - Family history

· Controllable

  - Hypertension

  - Diabetes mellitus

  - Hypercholesterolemia

  - Cardiac disease

  - History of stroke or TIA

  - Atrial fibrillation

  - Valvular heart disease

  - Severe carotid stenosis

  - Intracranial arterial stenosis

  - Hypercoagulable states (antiphospholipid antibodies)

  - Homocystinemia

  - Obesity

  - Smoking

Genetics

Inheritance is polygenic, with a tendency to clustering of risk factors within families.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD4

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

EPIDEMIOLOGY

Incidence

Incidence in the US: 150/100,000

Prevalence

· Prevalence in the US: 550/100,000

· Predominant age: Risk increases >45, and is highest in the 7th and 8th decades.

· Predominant sex: Male > Female (3:1), but equalizes after menopause

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD3

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

GENERAL PREVENTION

· Stop smoking.

· Control BP, diabetes, hyperlipidemia.

· Use alcohol in moderation, if at all.

· Exercise regularly.

· Maintain positive psychologic outlook.

· Seek professional dietary advice on weight control.

· Antiplatelet drugs

· Angiotensin-converting enzyme (ACE) inhibitors

· Statins

· Treat homocystinemia with vitamin B6, vitamin B12, and folic acid.

· Nonvalvular atrial fibrillation should be treated with dose-adjusted heparin to achieve an INR of 2-3 to prevent stroke. (1)[A]

· Women >45 years on ASA 100 mg/d have decreased risk of ischemic stroke and TIA but increased risk of GI bleed needing transfusion. (2)[B]

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD2

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

ALERT

Geriatric Considerations

Amyloid (congophilic) angiopathy is most prevalent in the elderly, especially if the patient also has dementia.

Pediatric Considerations

· Cardiac (especially developmental abnormalities)

· Metabolic: Homocystinuria, Fabry disease

Pregnancy Considerations

· Parturition may increase the risk of rupture for aneurysm; amniotic fluid embolism may cause stroke at the time of delivery.

· The postpartum period is associated with an increased risk for cerebral venous thrombosis.

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD1

STROKE (BRAIN ATTACK) - William A. Tosches, MD; Michael Previti, MD

DESCRIPTION

· The sudden onset of a focal neurologic deficit resulting from either infarction or hemorrhage within the brain.

· Adults <45 years old are most likely to have a cardiac source of embolism.

· 2 broad categories: Hemorrhagic and ischemic

· System(s) Affected: Cardiovascular; Nervous

· Synonym(s): Cerebrovascular accident; Reversible ischemic neurologic accident