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Stroke Diagnosis and Treatment

Ischemic stroke damage is time-dependent. Following initial arterial occlusion, cell death cascades to greater areas of the brain until blood flow is reestablished (van der Worp 2007). Hemorrhagic stroke damage is also time-dependent. As blood continues to leak from the original rupture site, the area of the brain damaged by the hematoma increases (Qureshi 2001). It is therefore critical to treat stroke victims as fast as possible to avoid widespread brain damage.

Once a stroke victim has arrived at the hospital, physicians use imaging tests to determine what kind of stroke (ischemic or hemorrhagic) occurred (PubMed Health 2011). Determining the type of stroke is critical because the medications used to treat ischemic stroke will not work for hemorrhagic stroke, and vice versa (Lansberg 2012).

Brain imaging can help detect strokes and determine their nature.

  • Computerized tomography angiography (CTA). Computerized tomography angiography is utilized to look for aneurysms, arterial and venous malformations, as well as narrowing of arteries in the neck and brain.
  • Computerized tomography (CT). Computerized tomography is a medical imaging tool that can be used to identify cerebral hemorrhaging.
  • Magnetic resonance imaging (MRI). Magnetic resonance imaging techniques can aid in the diagnosis of stroke (Schellinger 1999).
  • Magnetic resonance angiography (MRA). Magnetic resonance angiography uses a magnetic field, radio waves, and a dye injected into the veins to evaluate arteries in the neck and brain.

Emergency treatment of ischemic stroke. Treatment of ischemic stroke within 4.5 hours of symptom onset is critical. Studies show that rapid dissolution of the blood clot within 4.5 hours of symptom onset can dramatically reduce brain damage (Lansberg 2012). Unfortunately, many ischemic stroke patients do not get to the hospital and receive the appropriate thrombolytic agent until significant brain damage has already occurred (Zerwic 2007).

  • Intravenous injection of tissue plasminogen activator (tPA). tPA is FDA-approved to treat acute ischemic stroke (Roth 2011). tPA is an enzyme that converts plasminogen to plasmin - the major enzyme that stimulates clot breakdown. It helps decrease ischemic injury and salvage brain tissue. tPA administration within 4.5 hours of symptom onset is a first choice therapy among patients with no contraindications (Miller 2012; Del Zoppo 2009).Unfortunately, studies indicate that only 2 - 8% of ischemic stroke patients receive this potentially life-saving treatment (Alberts 2012). One study found that 18% of these treatment omissions are avoidable (Cocho 2005). In fact, in many instances, even eligible patients may be denied tPA treatment (Alberts 2012). Sadly, bureaucratic barriers, such as legal liability concerns and insufficient insurance reimbursement, contribute to these deadly denials (Bambauer 2006).Another oft-cited reason for tPA avoidance during acute ischemic stroke treatment is bleeding risk. Physicians often hesitate to treat ischemic stroke victims with tPA if the patient has been taking warfarin for fear of brain hemorrhage. However, evidence suggests that warfarin-treated stroke victims whose INR is less than or equal to 1.7 can be treated with tPA without excess risk of intracranial hemorrhage (Xian 2012).Part of the burden of ensuring timely treatment lies with the patient and/or their caregivers as well. Doctors cannot deliver tPA within the critical 4.5 hour window if a stroke victim arrives at the hospital long after this period has expired. Unfortunately, one study showed that the median time to emergency department admission was 16 hours after onset of stroke symptoms (Zerwic 2007). Calling 911 immediately upon experiencing stroke symptoms is the patient’s and his/her caregivers’ role in ensuring optimal stroke treatment.
  • Aspirin & antiplatelet agents. Aspirin is established as an important treatment for ischemic stroke. Studies have shown that 160 or 300 mg doses of aspirin given within 48 hours of ischemic stroke onset can reduce the death rate over time (at hospital discharge or at 6 months ) (van der Worp 2007).
  • Surgical procedures. If necessary, emergency procedures must be performed as soon as possible. For example, if a burst aneurysm (a weakness in a blood vessel) causes associated subarachnoid hemorrhage in the brain, a surgeon can clip the aneurysm and stop the bleeding. Another procedure, called balloon angioplasty, can be used to improve blood flow in occluded arteries (Mayo Clinic 2012b).

Secondary ischemic stroke prevention. After stroke, there is a significant risk of a repeat stroke or secondary stroke (Geeganage 2012). To help prevent secondary stroke, patients may be prescribed anti-platelet therapy, including low-dose aspirin or Plavix®, or anticoagulant therapy such as long-term warfarin (Coumadin®) (Alberts 2011; Awada 2011; Bousser 2012).

Emergency treatment of hemorrhagic stroke. Emergency treatment of hemorrhagic stroke focuses on controlling bleeding and reducing pressure in the brain. Surgical procedures are often used to drain the blood that collects outside the blood vessels during a hemorrhage (hematoma) (Dey 2012). If older types of anticoagulant medication (eg, Coumadin®, also known as warfarin) had been taken to prevent blood clots, intervention with vitamin K may be used to counteract the effects of warfarin. Anti-clotting agents (eg, aspirin and tPA) may increase bleeding and cannot be used (Mayo Clinic 2012b).

The medication nimodipine, a calcium channel blocker, is often used to help control vasospasm and may improve outcome among patients with subarachnoid hemorrhage. Nimodipine lowers central blood pressure, and its ability to control vasospasm is thought to be due to inhibition of vasoconstriction (Choi 2012; NSA 2009a; BAF 2011; Kim 2009). An experimental drug called clazosentan, an endothelin receptor antagonist, has been reported in some human and animal studies to reduce the risk of blood vessel spasm and constriction after hemorrhagic stroke and greatly improve chances of survival (Schubert 2008; Sabri 2011; Macdonald 2012). However, other studies have failed to corroborate these findings, so more investigation is needed (Macdonald 2011).

Secondary hemorrhagic stroke prevention. After the acute treatment, medications may be prescribed to control blood pressure, which is a major risk factor for a second stroke (Rashid 2003). Prescription medications for lowering blood pressure include diuretics, calcium channel blockers, beta blockers, ACE inhibitors, and others (AHA 2012a).​