CHAPTER 79 Stroke
An understanding of stroke is important for psychiatrists for several reasons: it is common, effective treatment is predicated on early recognition, and significant neuropsychiatric sequelae often result from injury to brain parenchyma. Stroke is defined as the acute onset of a neurological deficit due to a cerebrovascular cause. Strokes may be categorized as ischemic (in which the deficit is caused by blockage of an arterial feeding vessel, which results in a lack of oxygen and metabolic nutrients to the affected territory [Figure 79-1]) or hemorrhagic (in which the deficit is caused by vessel rupture). Ischemic strokes occur roughly four times as often as hemorrhagic strokes. Ischemic strokes usually produce focal neurological deficits due to the cessation of blood flow to a specific territory of the brain. In contrast, hemorrhagic strokes, in addition to causing focal deficits, can cause more diffuse symptoms as a result of cerebral edema and an increase in intracranial pressure.
By convention, a stroke has occurred if the clinical deficit persists for longer than 24 hours or if a permanent deficit is seen on neuroimaging that directly correlates with the patient’s syndrome. A transient ischemic attack (TIA), in contrast, involves no permanent tissue damage. Classically, it has been described as a focal deficit that lasts less than 24 hours. However, most patients with a TIA have symptoms for a shorter duration, typically less than 45 minutes. Recognition of TIAs is essential, as they may be a harbinger of stroke. In one study, 10.5% of patients sustained a stroke in the 3 months following the diagnosis of a TIA.1
For suspected acute stroke, the time of onset and the duration of symptoms should be documented as accurately and as rapidly as possible. It is also crucial to confirm the history with a detailed neurological examination and a neuroimaging study. Time is of the essence with the diagnosis and acute management of acute stroke, as rapid treatment may reduce morbidity and mortality rates. Thus, stroke and TIA are medical emergencies that require prompt attention.
Strokes involve specific vessels of the cerebral circulation and result in focal neurological signs referable to the territory supplied by the affected vessels. Stroke syndromes can broadly be categorized into anterior (carotid) or posterior (vertebro-basilar) circulation phenomena (Figure 79-2). The anterior circulation includes branches of the internal carotid artery and the lenticulostriate arteries, which penetrate deep into the cerebral cortex. These vessels supply much of the cerebral cortex, the subcortical white matter, the basal ganglia, and the internal capsule. Symptoms of anterior circulation strokes depend on the hemisphere involved and the handedness of the patient. Manifestations include aphasia, apraxia, hemi-neglect, hemiparesis, sensory disturbances, and visual field defects. Specific deficits associated with the branches of the anterior circulation are listed in Table 79-1.
|Anterior||Anterior cerebral||Contralateral lower extremity paresis, mutism, apathy, pseudobulbar affect|
|Anterior||Middle cerebral||Contralateral hemiparesis, hemi-sensory loss, hemianopsia/quadrantanopsia, aphasia (dominant hemisphere), hemi-inattention (nondominant hemisphere)|
|Posterior||Posterior cerebral||Contralateral homonymous hemianopsia, alexia without agraphia (dominant hemisphere)|
|Posterior||Basilar||Coma, “locked in” syndrome, cranial nerve palsies, hemiparesis/quadriparesis, ataxia|
|Posterior||Vertebral||Lateral medullary (Wallenburg) syndrome, appendicular or truncal ataxia|
Data from Kaufman DM: Clinical neurology for psychiatrists, Philadelphia, 2001, Saunders/Elsevier, p 275.
The posterior circulation consists of a pair of vertebral arteries and a single basilar artery with their branches, including the posterior cerebral arteries (PCAs). These vessels supply the brainstem, the cerebellum, the thalamus, and parts of the occipital and temporal lobes. Symptoms may localize to the brainstem (including coma, vertigo, nausea, cranial nerve palsies, or ataxia). Specific syndromes associated with the branches of the posterior circulation are also listed in Table 79-1.
Stroke is the third most common cause of death in the United States, following only heart disease and cancer.2 It is the most common disabling neurological disorder. Each year in the United States, over 700,000 new or recurrent strokes and over 160,000 deaths from stroke occur.3 Furthermore, stroke is a major cause of functional impairment: 15% to 30% of stroke survivors are considered permanently disabled.3
Several major risk factors for stroke exist. Of these, age is the most important nonmodifiable risk factor; the risk of stroke more than doubles for each decade beyond age 55 years.4 Other nonmodifiable factors include gender (male > female), race (African Americans and Hispanics > European Americans), and genetic contributions.5–10 A number of modifiable stroke risk factors have also been identified. Hypertension is one of the most important, and it is an excellent target for both primary and secondary prevention. Other risk factors include prior stroke or TIA, atrial fibrillation (AF), diabetes mellitus (DM), excessive alcohol use, tobacco use, and hypercholesterolemia.11 In addition, newly identified risk factors for stroke include the metabolic syndrome and obstructive sleep apnea.11
Patients at risk for stroke may be stratified according to a variety of risk factors, including advanced age, hypertension, smoking status, DM, hypercholesterolemia, history of cardiovascular disease, and electrocardiographic evidence of left ventricular hypertrophy or AF. One risk-profile model, the Framingham Stroke Profile, uses the Cox proportional-hazards method to generate an individual’s 10-year, gender-specific prediction of stroke risk.12 These and other models are important, as primary prevention efforts often focus on high-risk patients.
Several pathophysiological mechanisms lead to ischemic stroke: thrombosis, whereby a clot forms within an artery and blocks it; embolism, whereby a clot travels from a remote origin and lodges within an arterial vessel (Figure 79-3); or lipohyalinosis, whereby concentric narrowing of small penetrating arteries results in lacunar infarction. Thrombotic mechanisms cause about 20% of ischemic strokes, embolism causes about 20% of cases, and lacunar infarcts comprise an additional 25%.2 The remainder is caused by more rare conditions or by an undetermined etiology (i.e., “cryptogenic stroke”).
Figure 79-3 Cardioembolism leading to acute ischemic stroke.
(ECG and atrial thrombi images reprinted from Netter Anatomy Illustration Collection, © Elsevier Inc. All rights reserved.)
Given the broad array of etiologies, it is sometimes useful to categorize strokes by their anatomical basis. First, there are cerebrovascular causes of strokes. The most common is atherosclerosis of a large intracranial or extracranial artery, resulting in thrombotic stroke. Lacunar strokes are also vascular in origin, but they only affect the small branch vessels. Arterial dissection is a less common vascular cause of ischemic stroke, but it should be considered in younger patients with stroke, especially in those with a predisposing condition (such as Marfan syndrome or recent trauma to the head or neck). Use of cocaine or methamphetamine may cause stroke, likely secondary to arterial vasospasm or acute atrial dysrhythmias. Other vascular causes of stroke are rare, but include migraine, fibromuscular dysplasia, inflammation (e.g., with cerebral vasculitis), infection, and venous sinus thrombosis. Second, there are strokes related to cardiac causes, which most often result in embolic strokes. The most frequent cause of cardioembolic stroke is embolism of left atrial clot formed as a result of AF. Other, less common, causes include cardiac mural thrombus, a clot formed at the site of a prosthetic heart valve, paradoxical embolus through a patent foramen ovale, and endocarditis. Last, strokes may be caused by blood-related disorders (such as hypercoagulability, sickle cell crisis, or elevations in blood cell counts resulting from polycythemia, leukocytosis, or thrombocytosis).
The hallmark presentation of ischemic stroke is the abrupt onset of a focal neurological deficit. Associated symptoms, such as a seizure or headache, may occur but are less common. Thrombotic and lacunar strokes are more likely to manifest with a stuttering course of waxing and waning neurological symptoms that eventually result in a complete deficit, while embolic strokes are more likely to produce a maximal deficit at the outset.
The classic signs and symptoms of acute ischemic stroke are usually recognizable by physicians. However, a differential diagnosis should always be created, especially in cases with atypical features, such as a nonfocal neurological examina-tion or an impaired level of consciousness. The differential diagnosis includes intracerebral or subarachnoid hemorrhage, epidural or subdural hematoma, TIA, mass lesions (such as a tumor or abscess), seizures, migraine headaches, and metabolic causes, such as hypoglycemia.
A careful history is a crucial first step in the management of a suspected acute ischemic stroke. The exact time of onset, to the minute if possible, is an essential data point, as some therapies for the management of acute stroke (such as thrombolysis) are only available within strict time frames. If the exact time of onset is not known, or if the patient was not witnessed at the time of symptom development, the time of onset by default becomes the time at which the patient was last seen to be neurologically normal. A history of similar symptoms, which may suggest a recent TIA or even a recent stroke, should also be ascertained. Essential components of the medical history include a history of cardiac problems, hypertension, DM, hypercholesterolemia, and use of tobacco or drugs. The medication list should be reviewed, especially if the patient is taking anticoagulants or antiplatelet agents. A thorough physical examination should follow, which should include the careful assessment of vital signs (including blood pressure [BP] measured in both arms). The examiner should auscultate the carotid arteries to assess for the presence of carotid bruits. Of note, a lack of a bruit may accompany a complete or an impending occlusion. Most important, a focused neurological assessment should be done with the aim of localizing the lesion supplied by the suspected vessel. Most stroke physicians use a standardized scale (such as the National Institutes of Health [NIH] Stroke Scale), which establishes a method of performing a rapid and focused evaluation and establishes standardized values for comparisons among stroke patients for treatment and research purposes.13
Rapid diagnosis is critical to the management of acute ischemic stroke. Use of imaging, including computed tomography (CT) or magnetic resonance imaging (MRI), is essential. CT and MRI imaging help the clinician to distinguish ischemic strokes from intracerebral hemorrhages, to evaluate for other causes of symptoms, and to define the ischemic territory. CT is widely available and is highly accurate in differentiating intracerebral hemorrhage from ischemic stroke. Thus, it is the first choice of imaging in most centers. It must be performed before the administration of a thrombolytic agent in order to rule out an underlying condition (such as a hemorrhage, abscess, or tumor) that would preclude its use. MRI provides superior detection of early ischemic lesions and improved visualization of lesions of the brainstem and the cerebellum. However, in order to identify pathology within the target vessel, imaging with CT angiography (CTA) or MRI angiography (MRA) is required. Laboratory testing should always include a complete blood count (CBC), metabolic panel, serum glucose, liver function tests, and a coagulation profile. These should be obtained before sending the patient for a CT scan. If clinically indicated, such as in younger patients, other laboratory tests, such as a hypercoagulability panel or toxicology screen, should be obtained. An electrocardiogram (ECG) should always be obtained to detect arrhythmias or acute myocardial ischemia. Before any neuroimaging, the patient should be stabilized from a respiratory and hemodynamic standpoint. Consideration should be given to elective intubation if the patient’s airway may be compromised by his or her neurological deficit or by an impaired mental status.
A complete evaluation will include ultrasound of the carotid arteries, 24-hour cardiac monitoring, and echocardiography. In most cases, a transthoracic echocardiogram (TTE) study with an agitated saline bubble contrast study (to look for a patent foramen ovale [PFO]) will suffice. However, a transesophageal echocardiogram (TEE) may be indicated with specific conditions, such as in younger patients with a suspected PFO, valvular disease, or disease of the left atrium or aortic arch. Cerebral angiography is reserved for the investigation of unusual causes of stroke.
In the acute setting, intravenous (IV) thrombolytic therapy with recombinant tissue plasminogen activator (rt-PA) may significantly reduce both the short- and long-term sequelae of stroke. Rt-PA exerts its action by converting plasminogen to plasmin, which helps to dissolve fibrin-containing clots. This therapy, approved in 1996 by the Food and Drug Administration (FDA) after a landmark 1995 trial by the National Institute of Neurologic Disorders and Stroke (NINDS), demonstrated a benefit to patients administered rt-PA with acute stroke less than 3 hours old.14 Overall, patients in the rt-PA group were 30% more likely to show minimal or no disability at 3 months, and the mortality rate was not significantly different between treatment and placebo arms.14 The main adverse event was a significantly higher percentage of symptomatic intracerebral hemorrhage in the treatment arm, and this remains the most important drawback of this treatment.14 Although some trials have indicated a potential benefit for patients who receive rt-PA within 3 to 6 hours, these patients have a higher percentage of symptomatic parenchymal hemorrhages, and thus treatment outside of the 3-hour window is not recommended.15 Some specialized centers may perform intraarterial (IA) thrombolysis as well. However, this is currently of limited availability, and much of the work in this area is considered investigational.16 Another FDA-approved technique for use in acute stroke is the MERCI clot retrieval device, which allows for the mechanical retrieval of an acute thrombus within 8 hours.17 In general, all forms of thrombolytic therapy should be delivered in a dedicated stroke center, where hemodynamic parameters and neurological status may be monitored carefully, and where neurosurgical backup is available in the event that the patient suffers a hemorrhagic event.
Patients who are not considered candidates for thrombolysis should receive multimodal medical management. BP in the acute setting should not be lowered aggressively. Systolic BP in the range of 150 to 160 mm Hg is often tolerated, and it may help to provide additional blood flow to ischemic, but not yet infarcted, tissue (i.e., the “ischemic penumbra”). If a patient has received IV thrombolysis, however, there is a maximum allowable BP of 185/110 mm Hg. Appropriate agents should be used emergently to lower the BP if it exceeds these values. Antiplatelet therapy has also proven beneficial both in the acute setting and for secondary prevention. Anticoagulation, with heparin or Coumadin (or both), may be indicated in conditions that require ongoing anticoagulation (such as AF), but this carries the risk of hemorrhagic conversion of the ischemic infarct. The timing of anticoagulation must take into account the size and location of the stroke, the presence of any hemorrhagic conversion (even if asymptomatic), and the overall risk/benefit profile of the individual patient.
Several primary prevention measures have demonstrated efficacy. Control of hypertension is a crucial factor in the reduction of the incidence of stroke.11 A 1997 meta-analysis determined that the use of beta-blockers and diuretics were both effective in the prevention of stroke.18