Medication Summary
While only 1 drug, recombinant tissue-type plasminogen activator (alteplase or generically referred to as rt-PA), has demonstrated efficacy and effectiveness in treating acute ischemic stroke and is approved by the FDA, other medications are equally important. National consensus panels have included the use of antihypertensives, anticonvulsants, and osmotic agents in their recommendations. Additional agents may be required for comorbid illnesses in many patients with stroke.
Medications for the management of ischemic stroke can be distributed into the following categories:
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Anticoagulation
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Reperfusion
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Antiplatelet
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Neuroprotective
Thrombolytics
Class Summary
Thrombolytic—more accurately, fibrinolytic—agents convert entrapped plasminogen to plasmin and initiate local fibrinolysis by binding to fibrin in a clot.
Alteplase (Activase)
Alteplase is a t-PA used in management of acute myocardial infarction (MI), acute ischemic stroke, and pulmonary embolism. Safety and efficacy with concomitant administration of heparin or aspirin during the first 24 hours after symptom onset have not been investigated.
Anticonvulsants, Other
Class Summary
While seizures associated with stroke are relatively uncommon, recurrent seizures may be life threatening. Generally, agents used for treating recurrent convulsive seizures are also used in patients with seizures after stroke. Benzodiazepines, typically diazepam and lorazepam, are the first-line drugs for ongoing seizures.
Diazepam (Valium)
Diazepam acts on the gamma-aminobutyric acid (GABA) receptor complex in the limbic system and thalamus, producing a calming effect. The drug is useful in controlling active seizures and should be augmented by longer-acting anticonvulsants, such as phenytoin or phenobarbital.
Lorazepam (Ativan)
Lorazepam is a short-acting benzodiazepine with a moderately long half-life. It has become the drug of choice in many centers for treating active seizures.
Antiplatelet Agents
Class Summary
Although antiplatelet agents have proved useful for preventing recurrent stroke or stroke after transient ischemic attacks (TIAs), efficacy in the treatment of acute ischemic stroke has not been demonstrated. Early aspirin therapy is recommended within 48 hours of the onset of symptoms but should be delayed for at least 24 hours after rt-PA administration. Aspirin should not be considered as an alternative to intravenous fibrinolysis or other therapies aimed at improving outcomes after stroke.
Aspirin (ASA)
Aspirin blocks prostaglandin synthetase action, which in turn inhibits prostaglandin synthesis and prevents the formation of platelet-aggregating thromboxane A2. It also acts on the hypothalamic heat-regulating center to reduce fever.
Dipyridamole and aspirin (Aggrenox)
The combination of extended-release dipyridamole and aspirin reduces the relative risk of stroke, death, and myocardial infarction (MI). It is used for the secondary prevention of ischemic stroke and TIAs.
Clopidogrel (Plavix)
Clopidogrel inhibits platelet aggregation and is used for secondary stroke prevention. It is indicated for the reduction of atherothrombotic events following a recent stroke.
Anticoagulants, Hematologic
Class Summary
Anticoagulants such as warfarin are used for secondary stroke prevention.
Warfarin (Coumadin, Jantoven)
Warfarin is an anticoagulant used to reduce the risk of death, recurrent MI, and thromboembolic events such as stroke or systemic embolization after MI.
Dabigatran (Pradaxa)
Dabigatran is a competitive, direct inhibitor of thrombin that can prevent thrombus development. This agent inhibits free and clot-bound thrombin and thrombin-induced platelet aggregation. It may be used as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with paroxysmal to permanent atrial fibrillation and risk factors for stroke or systemic embolization.
Rivaroxaban (Xarelto)
Rivaroxaban is a Factor Xa inhibitor indicated to reduce the risk of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The dose is adjusted according to estimated creatinine clearance.
Apixaban (Eliquis)
Apixaban is a factor Xa inhibitor that inhibits platelet activation by selectively and reversibly blocking the active site of factor Xa without requiring a cofactor (eg, antithrombin III) for activity. It inhibits free and clot-bound factor Xa and prothrombinase activity. Although this agent has no direct effect on platelet aggregation, it does indirectly inhibit platelet aggregation induced by thrombin. Apixaban is indicated to reduce risk of stroke and systemic embolism associated with nonvalvular atrial fibrillation.
Edoxaban (Savaysa)
Edoxaban is a Factor Xa inhibitor indicated to reduce the risk of stroke and systemic embolism in patients with nonvalvular atrial fibrillation. A lower dose is needed with CrCl < 50 mL/min. Do not use with CrCL >95 mL/min. In the ENGAGE AF-TIMI 48 study, patients with NVAF with CrCL >95 mL/min had an increased rate of ischemic stroke with edoxaban 60 mg/day compared with patients treated with warfarin.
Analgesics, Other
Class Summary
Hyperthermia in acute stroke is potentially harmful and should be treated. Agents with potential bleeding risk should be avoided, if possible.
Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)
Acetaminophen reduces fever by acting directly on hypothalamic heat-regulating centers, which increases the dissipation of body heat via vasodilation and sweating.
Beta Blockers, Alpha Activity
Class Summary
Optimal blood pressure management in acute stroke remains subject to some debate. Treatment parameters depend largely on whether the patient is a candidate for fibrinolytic therapy. While the target blood pressures may differ, the therapeutic agents are primarily the same.
Labetalol (Normodyne, Trandate)
Labetalol is an adrenergic receptor-blocking agent with nonselective beta-adrenergic and selective alpha1 competitive receptor-blocking actions. It produces dose-related decreases in blood pressure without inducing reflex tachycardia.
ACE Inhibitors
Class Summary
Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Enalapril (Vasotec)
An ACE inhibitor, enalapril decreases circulating angiotensin II levels and suppresses the renin-angiotensin-aldosterone system, lowering overall blood pressure.
Calcium Channel Blockers
Class Summary
Optimal blood pressure management in acute stroke remains subject to some debate. Treatment parameters depend largely on whether the patient is a candidate for fibrinolytic therapy. While the target blood pressures may differ, the therapeutic agents are largely the same.
Nicardipine (Cardene)
A calcium channel blocker, nicardipine inhibits calcium ion influx into vascular smooth muscle and myocardium. [92]
Vasodilators
Class Summary
Vasodilators lower blood pressure through direct vasodilation and relaxation of the vascular smooth muscle. They are used more for blood pressure lowering in severe or refractory situations and should be used with caution.
Nitroprusside sodium (Nipride, Nitropress, Sodium Nitroprusside)
Nitroprusside sodium is a vasodilator that decreases peripheral vascular resistance by relaxing arteriolar smooth muscle. It also decreases venous return through venous dilation.
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Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.
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Axial noncontrast computed tomography (NCCT) scan demonstrates diffuse hypodensity in the right lentiform nucleus with mass effect upon the frontal horn of the right lateral ventricle in a 70-year-old woman with a history of left-sided weakness for several hours.
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Magnetic resonance imaging (MRI) scan in a 70-year-old woman with a history of left-sided weakness for several hours. An axial T2 fluid-attenuated inversion recovery (FLAIR) image (left) demonstrates high signal in the lentiform nucleus with mass effect. The axial diffusion-weighted image (middle) demonstrates high signal in the same area, with corresponding low signal on the apparent diffusion coefficient (ADC) maps, consistent with true restricted diffusion and an acute infarction. Maximum intensity projection from a 3-dimensional (3-D) time-of-flight magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
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Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon.
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Axial noncontrast computed tomography (CT) scan demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in a 60-year-old man with acute onset of right-sided weakness. The lesion demonstrates high signal on the fluid-attenuated inversion recovery (FLAIR) sequence (middle image) and diffusion-weighted magnetic resonance imaging (MRI) scan (right image), with low signal on the apparent diffusion coefficient (ADC) maps indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem, and cerebellum.
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Magnetic resonance imaging (MRI) scan was obtained in a 62-year-old man with hypertension and diabetes and a history of transient episodes of right-sided weakness and aphasia. The fluid-attenuated inversion recovery (FLAIR) image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep border-zone, or watershed, infarction, in this case the anterior and posterior middle cerebral artery (MCA) watershed areas. The left-sided infarcts have corresponding low signal on the apparent diffusion coefficient (ADC) map (right), signifying acuity. An old left posterior parietal infarct is noted as well.
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A 48-year-old man presented with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference. Angiogram with selective injection of the right internal carotid artery demonstrates occlusion of the M1 segment of the right middle cerebral artery (MCA) and A2 segment of the right anterior cerebral artery (ACA; images courtesy of Concentric Medical).
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Follow-up imaging after mechanical embolectomy in 48-year-old man with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference demonstrates complete recanalization of the right middle cerebral artery (MCA) and partial recanalization of the right A2 segment (images courtesy of Concentric Medical).
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Cerebral angiogram performed approximately 4.5 hours after symptom onset in a 31-year-old man demonstrates an occlusion of the distal basilar artery (images courtesy of Concentric Medical).
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Image on the left demonstrates deployment of a clot retrieval device (older generation device) in a 31-year-old man. Followup angiogram after embolectomy demonstrates recanalization of the distal basilar artery with filling of the superior cerebellar arteries and posterior cerebral arteries. The patient had complete resolution of symptoms following embolectomy (images courtesy of Concentric Medical).
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Noncontrast computed tomography (CT) scan in a 52-year-old man with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement with mass effect involving the left anterior and middle cerebral artery territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity noted suggestive of developing petechial hemorrhage in this large area of infarction.
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Magnetic resonance angiogram (MRA) in a 52-year-old man demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal middle cerebral artery (MCA) trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the apparent diffusion coefficient (ADC) map consistent with acute infarction.
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Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery (MCA), with the apex representing the Sylvian point.
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Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICAs) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICAs) arise from the proximal basilar artery. The superior cerebellar arteries (SCAs) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries (PCAs).
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Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery (ICA) illustrates the anterior circulation. The anterior cerebral artery (ACA) consists of the A1 segment proximal to the anterior communicating artery, with the A2 segment distal to it. The middle cerebral artery (MCA) can be divided into 4 segments: the M1 (horizontal segment) extends to the anterior basal portion of the insular cortex (the limen insulae) and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).
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Regions of interest are selected for arterial and venous input (image on left) for dynamic susceptibility-weighted perfusion magnetic resonance imaging (MRI). Signal-time curves (image on right) obtained from these regions of interest demonstrate transient signal drop following the administration of intravenous contrast. The information obtained from the dynamic parenchymal signal changes postcontrast is used to generate maps of different perfusion parameters.
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Vascular distributions: Middle cerebral artery (MCA) infarction. Noncontrast computed tomography (CT) scanning demonstrates a large acute infarction in the MCA territory involving the lateral surfaces of the left frontal, parietal, and temporal lobes, as well as the left insular and subinsular regions, with mass effect and rightward midline shift. There is sparing of the caudate head and at least part of the lentiform nucleus and internal capsule, which receive blood supply from the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (anterior cerebral artery [ACA] territory), thalami, and paramedian occipital lobe (posterior cerebral artery [PCA] territory).
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Vascular distributions: Anterior choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with associated signal dropout on the apparent diffusion coefficient (ADC) map involving the posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal artery, the last branch of the internal carotid artery (ICA) before bifurcating into the anterior and middle cerebral arteries. The anterior choroidal artery may also arise from the middle cerebral artery (MCA).
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Vascular distributions: Anterior cerebral artery (ACA) infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. There is also infarction of the lateral temporoparietal regions bilaterally (both middle cerebral artery [MCA] distributions), greater on the left indicating multivessel involvement and suggesting emboli.
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Vascular distributions: Posterior cerebral artery (PCA) infarction. The noncontrast computed tomography (CT) images demonstrate PCA distribution infarction involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional involvement of the thalamus, also part of the PCA territory.
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The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (MCA; red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes; insula; and basal ganglia. The anterior cerebral artery (ACA; blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (PCA; green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
Tables
VASCULAR TERRITORY |
Structures Supplied |
Anterior Circulation (Carotid) |
|
Anterior Cerebral Artery |
Cortical branches: medial frontal and parietal lobe Medial lenticulostriate branches: caudate head, globus pallidus, anterior limb of internal capsule |
Middle Cerebral Artery |
Cortical branches: lateral frontal and parietal lobes, lateral and anterior temporal lobe Lateral lenticulostriate branches: globus pallidus and putamen, internal capsule |
Anterior Choroidal Artery |
Optic tracts, medial temporal lobe, ventrolateral thalamus, corona radiata, posterior limb of the internal capsule |
Posterior Circulation (Vertebrobasilar) |
|
Posterior Cerebral Artery |
Cortical branches: occipital lobes, medial and posterior temporal and parietal lobes Perforating branches: brainstem, posterior thalamus and midbrain |
Posterior Inferior Cerebellar Artery |
Inferior vermis; posterior and inferior cerebellar hemispheres |
Anterior Inferior Cerebellar Artery |
Anterolateral cerebellum |
Superior Cerebellar Artery |
Superior vermis; superior cerebellum |
|
Category |
Description |
Score |
1a |
level of consciousness (LOC) |
Alert Drowsy Stuporous Coma |
0 1 2 3 |
1b |
LOC questions (month, age) |
Answers both correctly Answers 1 correctly Incorrect on both |
0 1 2 |
1c |
LOC commands (open and close eyes, grip and release nonparetic hand) |
Obeys both correctly Obeys 1 correctly Incorrect on both |
0 1 2 |
2 |
Best gaze (follow finger) |
Normal Partial gaze palsy Forced deviation |
0 1 2 |
3 |
Best visual (visual fields) |
No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia |
0 1 2 3 |
4 |
Facial palsy (show teeth, raise brows, squeeze eyes shut) |
Normal Minor Partial Complete |
0 1 2 3 |
5 |
Motor arm left* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
6 |
Motor arm right* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
7 |
Motor leg left* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
8 |
Motor leg right* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
9 |
Limb ataxia (finger-nose, heel-shin) |
Absent Present in 1 limb Present in 2 limbs |
0 1 2 |
10 |
Sensory (pinprick to face, arm, leg) |
Normal Partial loss Severe loss |
0 1 2 |
11 |
Extinction/neglect (double simultaneous testing) |
No neglect Partial neglect Complete neglect |
0 1 2 |
12 |
Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty") |
Normal articulation Mild to moderate dysarthria Near to unintelligible or worse |
0 1 2 |
13 |
Best language** (name items, describe pictures) |
No aphasia Mild to moderate aphasia Severe aphasia Mute |
0 1 2 3 |
|
Total |
- |
0-42 |
* For limbs with amputation, joint fusion, etc, score 9 and explain ** For intubation or other physical barriers to speech, score 9 and explain. Do not add 9 to the total score. NIH Stroke Scale (PDF) |
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