Porth's Essentials of Pathophysiology, 4e

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Disorders of Brain Function

C h a p t e r 3 7

TABLE 37-5 Signs and Symptoms of Stroke by Involved Cerebral Artery Cerebral Artery Brain Area Involved Signs and Symptoms*

Anterior cerebral

Infarction of the medial aspect of one frontal lobe if lesion is distal to communicating artery; bilateral frontal infarction if flow in other anterior cerebral artery is inadequate

angiography. CT angiography is exquisitely detailed for a noninvasive technique, but is limited in availability and requires iodinated contrast, which is nephrotoxic. Catheter angiography remains the gold standard in sen- sitivity and allows visualization of dynamic patterns of collateral flow, but is invasive and requires significant contrast doses. CT angiography and magnetic reso- nance angiography have largely replaced angiography as a screening tool for vascular lesions. Ultrasonographic techniques allow quick bedside assessment of the carotid bifurcation (duplex ultrasonography) or of flow velocities in the cerebral circulation (transcranial Doppler). Treatment. Treatment of acute ischemic stroke has changed markedly since the early 1990s, with an empha- sis on salvaging brain tissue, preventing secondary stroke, and minimizing long-term disability. The care of patients with stroke has shifted away from the “near- est hospital” to stroke centers that have been certified by some external agency, most commonly the state or Joint Commission. 33 Certification establishes that a hos- pital can manage stroke patients with appropriate care throughout the continuum—from emergency treat- ments, through the inpatient stay, and into the rehabili- tation phase. With this advancement, the medical and lay communities acknowledge that care of the patient with stroke requires specialized personnel and resources to minimize stroke’s devastating effects, as stroke is the leading cause of adult disability in the United States. Stroke care begins with emergency treatments aimed at reversing the evolving ischemic brain injury. The real- ization that there is a window of opportunity during Paralysis of contralateral foot or leg; impaired gait; paresis of contralateral arm; contralateral sensory loss over toes, foot, and leg; problems making decisions or performing acts voluntarily; lack of spontaneity, easily distracted; slowness of thought; aphasia depends on the hemisphere involved; urinary incontinence; cognitive and affective disorders Contralateral hemiplegia (face and arm); contralateral sensory impairment; aphasia; homonymous hemianopia; altered consciousness (confusion to coma); inability to turn eyes toward paralyzed side; denial of paralyzed side or limb (hemiattention); possible acalculia, alexia, finger agnosia, and left–right confusion; vasomotor paresis and instability Homonymous hemianopia and other visual defects such as color blindness, loss of central vision, and visual hallucinations; memory deficits, perseveration (repeated performance of same verbal or motor response) Loss of all sensory modalities; spontaneous pain; intentional tremor; mild hemiparesis; aphasia Oculomotor nerve palsy with contralateral hemiplegia Visual disturbance such as diplopia, dystaxia, vertigo, dysphagia, dysphonia

Middle cerebral

Massive infarction of most of lateral hemisphere and deeper structures of the frontal, parietal, and temporal lobes; internal capsule; basal ganglia

Posterior cerebral

Occipital lobe; anterior and medial portion of temporal lobe

Thalamus involvement

Basilar and vertebral

Cerebral peduncle involvement Cerebellum and brain stem

*Depend on hemisphere involved and adequacy of collaterals.

hemorrhage or ischemia, identify the stroke or TIA mech- anism (i.e., large-vessel or small-vessel, atherothrombotic, cardioembolic, hemorrhagic, cryptogenic, or other), char- acterize the severity of clinical deficits, and unmask the presence of risk factors. 31–34 A careful history, including documentation of previous TIAs, the time of onset and pattern and rapidity of system progression, the specific focal symptoms (to determine the likely vascular terri- tory), and any coexisting diseases, can help to determine the type of stroke that is involved. Computed tomographic scans and magnetic resonance imaging have become essential brain imaging tools in diagnosing stroke, differentiating cerebral hemorrhage from ischemia, and excluding intracranial lesions that mimic stroke clinically. CT scans are a necessary screening tool in the acute setting for rapid identification of hemor- rhage, but are insensitive to ischemia within 24 hours and to any brain stem or small infarcts. MRI is superior for imaging ischemic lesions in all territories and differentiat- ing other nonstroke pathologic processes (e.g., tumors, contusion, infection). Newer MRI techniques such as per- fusion- and diffusion-weighted imaging (DWI) can reveal cerebral ischemia immediately after onset and identify areas of potentially reversible damage (i.e., penumbra). Vascular imaging is accomplished with CT angiog- raphy (CTA), magnetic resonance angiography (MRA), catheter-based “conventional” arteriography, and ultra- sonography. All except ultrasonography can demonstrate the site of vascular abnormality (intracranial and extracra- nial) and afford visualization of most intracranial vascu- lar areas. MRA is noninvasive and most widely available, but less sensitive and specific than CTA or catheter