eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke
Lacunar Stroke: Treatment & Medication
Updated: Jul 16, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Rehabilitation Program
Physical Therapy
After the initial assessment of a patient who has suffered a lacunar stroke, a physical therapy program should provide passive exercises, with the major joints of the paretic limb being put through a full range of motion (ROM). As soon as patients are stable and can tolerate more active therapy, encourage them to sit up (initially in bed and later in a chair), to stand, and to transfer safely; then, they can commence ambulating with assistance and aids, as required. The physical therapist can provide splints and braces to support joints and limbs, to treat and prevent complications (eg, shoulder-hand syndrome, spasticity), and to assist the patient in walking.
Occupational Therapy
When the patient who has had a lacunar stroke becomes stable, assess his/her ability to perform activities of daily living (ADLs), such as dressing and undressing, bathing, personal grooming, toileting, preparing meals, and eating. The occupational therapist can advise on equipment that may allow the patient to be more independent. If the patient is returning home, an assessment of the residence identifies potential problems and necessary modifications (eg, handrails, moving a bed to a ground level room), thereby providing confidence to the patient and family.
Speech Therapy
A speech-language therapist can assist with speech-language problems and swallowing disorders in patients who have had a lacunar stroke. Early assessment of a patient with swallowing problems may prevent dehydration and malnutrition from inadequate intake, as well as prevent aspiration and pneumonia. In addition to the bedside assessment, cinefluoroscopy with barium swallow may be required. Treatment may require a change in food consistency, a change in positioning or compensatory swallowing technique, or placement of a feeding tube. Patients with lacunes may be dysarthric (but not dysphasic), requiring treatment to improve functional communication.
Recreational Therapy
Following stroke, recreational therapy improves a patient's independence, self-confidence, and ability to function, through participation in individual and group recreational activities that the patient previously enjoyed, as well as through participation in new ones. The recreational therapist must assess the medical condition and physical capabilities of the patient, in addition to that individual's interests and hobbies. Then, the therapist must help the patient to set realistic goals and to make any modifications needed to achieve them. Recreational therapy not only allows the stroke patient to practice motor skills but also allows him/her to remain socially active. Recreational therapy includes leisure activities, such as going for a walk, fishing, and gardening, as well as involvement in family and community activities, such as playing cards or going to a restaurant or to church.
Medical Issues/Complications
The prevention of deep venous thrombosis (DVT), aspiration pneumonia, urinary tract infection, and decubitus ulcers are important considerations for any patient following stroke.
Surgical Intervention
Surgery (eg, gastrostomy/jejunostomy) rarely is required as a result of a lacunar stroke, but patients with severe dysphagia may require long-term tube feeding.
Consultations
A social worker should be consulted to assess personal and family resources, to inform the patient and family of available government resources, to facilitate discharge planning, and to coordinate community services.
Other Treatment
Some patients with spasticity or joint contractures following a lacunar stroke may benefit from the injection of botulinum toxin or neurolytic agents.
Medication
The medications used in the management of lacunes are not specific to this stroke subtype.
Fibrinolytics
These agents are used to improve stroke outcome. The National Institute of Neurological Disorders and Stroke (NINDS) study on recombinant tissue-type plasminogen activator (rt-PA) showed an 11-13% absolute increase in the number of ischemic stroke patients with a favorable outcome at 3 months with tissue plasminogen activator (t-PA).13,14
Alteplase (Activase)
T-PA used in management of acute myocardial infarction (AMI), acute ischemic stroke, and pulmonary embolism (PE). No other IV-administered fibrinolytic has been shown to have clinical efficacy. A post hoc analysis showed that all stroke subtypes benefit from t-PA treatment.
Adult
0.9 mg/kg (not to exceed 90 mg), 10% given as bolus IV and remainder infused over 1 h IV
Pediatric
Not established
Drugs that alter platelet function (aspirin, ticlopidine, and clopidogrel) and anticoagulants may increase risk of bleeding with alteplase therapy; AHA guidelines recommend withholding antiplatelet agents and anticoagulants for 24 h after alteplase administration because of risk of intracerebral hemorrhage (ICH)
American Heart Association (AHA) guidelines:
1) Beyond 3 h of stroke onset (or when last well)
2) CT scan evidence of recent major infarction
3) Concomitant anticoagulation (with prolonged aPTT or PT greater than 15 s or INR greater than 1.7)
4) Platelet count <100,000/μ L
Documented hypersensitivity; another stroke or major head injury in last 3 mo; major surgery in last 14 d; pretreatment systolic BP >185 mm Hg or diastolic BP >110 mm Hg; rapidly improving signs; mild deficit; prior intracerebral hemorrhage; blood glucose <50 mg/dL or >400 mg/dL; seizure at onset of stroke; gastrointestinal or urinary bleeding in last 21 d; recent myocardial infarction
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following alteplase administration (when managing acute ischemic stroke); do not use >0.9 mg/kg to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH
Antiplatelet agents
These agents for secondary stroke prevention, if commenced within 48 hours of stroke onset, confer a small survival benefit.
Aspirin (Anacin, Ascriptin, Bayer Aspirin)
Alternatives to aspirin include ticlopidine and clopidogrel. These drugs and a combination of aspirin and dipyridamole may be marginally superior to aspirin alone.
Adult
30-1300 mg/d PO; in US, usual dose is 325 mg PO qd
Pediatric
Not established
Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses greater than 2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Documented hypersensitivity; liver damage, hypoprothrombinemia, vitamin K deficiency, bleeding disorders, asthma; due to association of aspirin with Reye syndrome, do not use in children (age <16 y) with flu
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in past history of peptic ulcer disease; bleeding disorder, thrombocytopenia, renal disease, severe hepatic disease, asthmatic patient with nasal polyps; may cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia or with a history of blood coagulation defects or in patients who are taking anticoagulants
Clopidogrel (Plavix)
Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein (GP) IIb/IIIa complex, thereby inhibiting platelet aggregation. Indicated for reduction of atherothrombotic events following recent stroke.
Adult
75 mg PO qd
Pediatric
Not established
Coadministration with naproxen associated with increased occult GI blood loss; clopidogrel prolongs bleeding time; safety of coadministration with warfarin not established
Documented hypersensitivity; active pathological bleeding, such as peptic ulcer, or intracranial hemorrhage
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (such as ulcers)
Anticoagulants
These agents are employed for prophylaxis of DVT and pulmonary embolism.
Heparin
Can be used in conjunction with compression stockings or pneumatic stockings. Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not lyse actively but can inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.
Adult
5000 U SC bid
Pediatric
Not established
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity
Documented hypersensitivity, subacute bacterial endocarditis, active bleeding, and history of heparin-induced thrombocytopenia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
In neonates, preservative-free heparin is recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock
Angiotensin-converting enzyme inhibitors
These agents are used for secondary stroke prevention.15
Ramipril (Altace)
The Heart Outcomes Prevention Evaluation (HOPE) study showed the benefit of ramipril in patients with vascular disease and in patients with diabetes who have vascular risk factors. It is not known whether this is a class effect.
Adult
Initial dose: 2.5 mg PO qd; titrate up to 10 mg PO qd
Pediatric
Not established
Ramipril may increase digoxin, lithium, and allopurinol levels; probenecid may increase ramipril levels; coadministration with diuretics or NSAIDs increase hypotensive effects
Documented hypersensitivity; history of angioedema
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Renal impairment, severe congestive heart failure, hypertensive patient with renal artery stenosis, and aortic stenosis
More on Lacunar Stroke |
| Overview: Lacunar Stroke |
| Differential Diagnoses & Workup: Lacunar Stroke |
 Treatment & Medication: Lacunar Stroke |
| Follow-up: Lacunar Stroke |
| References |
| « Previous Page | Next Page » |
References
Bamford JM, Warlow CP. Evolution and testing of the lacunar hypothesis. Stroke. Sep 1988;19(9):1074-82. [Medline].
Brenner D, Labreuche J, Pico F, et al. The renin-angiotensin-aldosterone system in cerebral small vessel disease. J Neurol. May 2 2008;[Medline].
Sacco S, Marini C, Totaro R, et al. A population-based study of the incidence and prognosis of lacunar stroke. Neurology. May 9 2006;66(9):1335-8. [Medline].
Bamford J, Sandercock P, Jones L, et al. The natural history of lacunar infarction: the Oxfordshire Community Stroke Project. Stroke. May-Jun 1987;18(3):545-51. [Medline].
Bejot Y, Catteau A, Caillier M, et al. Trends in incidence, risk factors, and survival in symptomatic lacunar stroke in Dijon, France, from 1989 to 2006. A population-based study. Stroke. Apr 24 2008;[Medline].
Mok VC, Wong A, Lam WW, et al. A case-controlled study of cognitive progression in Chinese lacunar stroke patients. Clin Neurol Neurosurg. May 2 2008;[Medline].
Bang OY, Joo SY, Lee PH, et al. The course of patients with lacunar infarcts and a parent arterial lesion: similarities to large artery vs small artery disease. Arch Neurol. Apr 2004;61(4):514-9. [Medline]. [Full Text].
Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke. Jan 1993;24(1):35-41. [Medline].
Jackson C, Sudlow C. Are lacunar strokes really different? A systematic review of differences in risk factor profiles between lacunar and nonlacunar infarcts. Stroke. Apr 2005;36(4):891-901. [Medline]. [Full Text].
Inzitari D, Eliasziw M, Sharpe BL, et al. Risk factors and outcome of patients with carotid artery stenosis presenting with lacunar stroke. North American Symptomatic Carotid Endarterectomy Trial Group. Neurology. Feb 8 2000;54(3):660-6. [Medline].
Nitkunan A, Barrick TR, Charlton RA, et al. Multimodal MRI in cerebral small vessel disease. Its relationship with cognition and sensitivity to change over time. Stroke. Apr 24 2008;[Medline].
Rojas JI, Zurru MC, Romano M, et al. Transesophageal echocardiography findings in lacunar stroke. J Stroke Cerebrovasc Dis. May-Jun 2008;17(3):116-20. [Medline].
The National Institute of Neurological Disorders and Stroke. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med. Dec 14 1995;333(24):1581-7. [Medline]. [Full Text].
Adams HP Jr, Brott TG, Furlan AJ, et al. Guidelines for thrombolytic therapy for acute stroke: a supplement to the guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation. Sep 1 1996;94(5):1167-74. [Medline]. [Full Text].
Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. Jan 20 2000;342(3):145-53. [Medline]. [Full Text].
Pullicino PM, Caplan LR, Hommel M, eds. Cerebral Small Artery Disease. Advances in Neurology, vol 62. New York, NY: Raven Press; 1993.
Fisher CM. Capsular infarcts: the underlying vascular lesions. Arch Neurol. Feb 1979;36(2):65-73. [Medline].
Fisher CM. The arterial lesions underlying lacunes. Acta Neuropathol. Dec 18 1968;12(1):1-15. [Medline].
Gan R, Sacco RL, Kargman DE, et al. Testing the validity of the lacunar hypothesis: the Northern Manhattan Stroke Study experience. Neurology. May 1997;48(5):1204-11. [Medline].
Post-stroke Rehabilitation Guideline Panel. Post-stroke Rehabilitation. Gaithersburg, Md: Aspen Pub; 1996.
Rabinstein AA. Case 5-2004: a man with slurred speech and left hemiparesis. N Engl J Med. May 20 2004;350(21):2213-4; author reply 2213-4. [Medline].
Zweifler RM. Management of acute stroke. South Med J. Apr 2003;96:380-5. [Medline].
Further Reading
Keywords
lacunar stroke, lacunar infarct, lacunar infarction, lacune, ischemic stroke, small-vessel disease, hemiparesis, ataxic hemiparesis, dysarthria, clumsy hand, motor stroke, sensory stroke, sensorimotor stroke, hypertension, diabetes mellitus, embolism, cardioembolism, artery-to-artery embolism
