eMedicine Specialties > Physical Medicine and Rehabilitation > Stroke

Lacunar Stroke

Adam B Agranoff, MD, Physiatrist and Partner, Chelsea Back Care, Chelsea Community Hospital
Edward H Wong, MB, BCh, Stroke Fellow, Department of Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario

Updated: Jul 16, 2008

Introduction

Background

The lacunar hypothesis proposes that (1) symptomatic lacunes present with distinctive lacunar syndromes and (2) a lacune is due to occlusion of a single deep penetrating artery generated by a specific vascular pathology. This concept is controversial because different definitions of lacunes have been used. Lacunes may be confused with other empty spaces, such as enlarged perivascular (Virchow-Robbins) spaces, in which the specific small-vessel pathology occasionally is absent. Originally, lacunes were defined pathologically, but lacunes now are diagnosed on clinical and radiological grounds. This problem is compounded by the present inability to image a single penetrating artery.¹

Lacunes may be defined as small subcortical infarcts (<15 mm in diameter) in the territory of the deep penetrating arteries; lacunes may present with specific lacunar syndromes or may be asymptomatic. Unfortunately, the 5 classical lacunar syndromes and the radiologic appearances are not specific for lacunes (see History). Lacunes occur most frequently in the basal ganglia and in the internal capsule, thalamus, corona radiata, and pons.

Much of our current knowledge of lacunar strokes is due to Fisher's prior cadaveric dissection of post-mortem stroke patients. He found that most symptomatic lacunar strokes are due to the occlusion of penetrating arteries of 200-800 μ m in diameter, whereas those with smaller-diameter penetrating artery infarcts tended to be asymptomatic.

Related eMedicine topic:
Lacunar Syndromes

Related Medscape topic:
Resource Center Stroke/Cerebrovascular Disease

Pathophysiology

Lacunes are caused by occlusion of a single penetrating artery. The deep penetrating arteries are small, nonbranching end arteries (usually smaller than 500 μ m in diameter), which arise directly from much larger arteries (eg, the middle cerebral artery, anterior choroidal artery, anterior cerebral artery, posterior cerebral artery, posterior communicating artery, cerebellar arteries, basilar artery). Their small size and proximal position predispose them to the development of microatheroma and lipohyalinosis.²

Initially, lipohyalinosis was thought to be the predominant small-vessel pathology of lacunes; however, microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma).

A hemodynamic (hypoperfusion) mechanism is suggested when there is a stenosis (and not occlusion) of the penetrating artery. When no evidence of small-vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism or cardioembolism. In one series, 25% of patients with clinical, radiologically defined lacunes had a potential cardiac cause for their strokes.

Frequency

United States

In the United States and other Western nations, lacunes account for 15-25% of all ischemic strokes. In 2 community - based studies in the United States, the annual incidence rates of lacunar strokes were 13.4 and 19.5 cases per 100,000 population.

International

Two European community-based studies found higher annual incidence rates (31.7 and 53 cases per 100,000 population). This difference in incidence rates between the US and European studies may be due in part to different definitions used in the studies.

Mortality/Morbidity

• The early (<30 d) survival rate for patients who have had a lacunar stroke is approximately 96-97%. This compares to an early survival rate of 85% for patients who have suffered a nonlacunar stroke.
• The late (1 yr) survival rates are 87% and 65-70% following lacunar and nonlacunar strokes, respectively.
• Between 70% and 80% of patients who have suffered a lacunar stroke are functionally independent at 1 year, compared with fewer than 50% of patients who have had a nonlacunar stroke.

Race

Some studies have found higher frequencies of lacunar strokes in African Americans, Mexican Americans, and Hong Kong Chinese.⁶

Sex

Some studies have indicated that there is a higher incidence of lacunar strokes in men.

Age

The incidence of lacunar strokes increases with age. The mean age of first lacunar stroke is approximately 65 years.

Clinical

History

Lacune-related symptoms may occur suddenly or may evolve in either a fluctuating (eg, the capsular warning syndrome) or a progressive manner.Each of the 5 classical lacunar syndromes has a symptom complex that is relatively specific to it. Occasionally, cortical infarcts and intracranial hemorrhages can mimic a lacunar syndrome.⁷ Cortical symptoms (eg, aphasia, neglect) and visual field defects are absent.

• Pure motor stroke/hemiparesis
  • This is the most common (33-50%) lacunar syndrome. It consists of hemiparesis or hemiplegia that typically affects the face, arm, and leg equally; however, the face or leg can be involved to a lesser extent than other regions, and occasionally only arm or leg weakness is noted.
  • Transient sensory symptoms (but not signs) may be present.
  • Dysarthria and dysphagia also may be present.
  • The lacune is usually in the posterior limb of the internal capsule, which carries the descending corticospinal and corticobulbar tracts, or the basis pontis.
• Ataxic hemiparesis
  • This is the second most frequent lacunar syndrome and features a combination of cerebellar and motor symptoms, including weakness and clumsiness, on the ipsilateral side of the body.
  • This lacunar syndrome usually affects the leg more than it does the arm; hence, it is known also as homolateral ataxia and crural paresis. The onset of symptoms is often over hours or days.
  • The most frequent sites of infarction are the posterior limb of the internal capsule, basis pontis, and corona radiata.
• Dysarthria/clumsy hand
  • Although now considered to be a variant of ataxic hemiparesis, this disorder usually still is classified as a separate lacunar syndrome. The lesion is in the pons.
  • The main symptoms are dysarthria and clumsiness (ie, weakness) of the hand, which often are most prominent when the patient is writing.
• Pure sensory stroke
  • This lacunar syndrome consists of persistent or transient numbness and/or tingling on one side of the body (eg, face, arm, leg, trunk).
  • Occasionally, patients complain of pain or burning, or of another unpleasant sensation. The infarct is usually in the thalamus.
• Mixed sensorimotor stroke
  • With this lacunar syndrome, hemiparesis or hemiplegia is noted with ipsilateral sensory impairment.
  • The infarct is usually in the thalamus and adjacent posterior internal capsule (seemingly, in the carotid and vertebrobasilar territories).

Physical

Physical examination findings differ in each of the lacunar syndromes, as follows:

• Pure motor stroke/hemiparesis - Hemiparesis or hemiplegia is noted, with hyperreflexia and Babinski sign; no involvement of any other system is observed.
• Ataxic hemiparesis - A combination of pyramidal signs (eg, hemiparesis, hyperreflexia, Babinski sign) and cerebellar ataxia on the same side of the body. Lower extremities are typically more involved than are upper extremities. Nystagmus may be present.
• Dysarthria/clumsy hand - Unilateral lower facial weakness with dysarthric speech is noted. On protrusion, the tongue may deviate to the side of facial weakness. A mild, ipsilateral hemiparesis usually is noted, but the arm is ataxic. Ipsilateral hyperreflexia and Babinski sign may be observed.
• Pure sensory stroke - Unilateral sensory loss is observed. Although the patient may complain of weakness, no weakness is found on examination.
• Mixed sensorimotor stroke - A combination of pyramidal signs (eg, hemiparesis, hyperreflexia, Babinski sign) is noted, as is sensory loss in the absence of any cortical signs.
• A different system for categorization of stroke subtypes also has been developed. The Trial of ORG 10172 in Acute Stroke Treatment (TOAST) developed a classification based on etiology. This system had a high interphysician agreement rate. The 5 subtypes of ischemic stroke in the TOAST study included the following⁸ :
  • Large-artery atherosclerosis
  • Cardioembolism
  • Small-vessel occlusion
  • Stroke of other determined etiology
  • Stroke of undetermined etiology

Causes

The cause of lacunar infarction is occlusion of a single small penetrating artery. This occlusion may be due to microatheroma and lipohyalinosis, which are associated with hypertension, smoking, and diabetes, or may result from microembolism from the heart or carotid arteries.^5,9

• Study results initially indicated that almost all patients with lacunes have hypertension. However, later studies found hypertension in only 44-75% of patients. In the setting of chronic hypertension, the penetrating arteries, which usually are not affected by atherosclerosis, may develop microatheroma and lipohyalinosis.
• Diabetes mellitus is well recognized as a risk factor for development of small-vessel disease throughout the body, including in the penetrating arteries.
• Smoking is an established risk factor for lacunes.
• Embolism (either cardioembolism or artery-to-artery embolism) traditionally was considered a rare mechanism of lacunar stroke, but a potential embolic cause is not uncommon when lacunes are defined clinicoradiologically. A potential embolic cause may be a coincidental finding only. The following treatment modalities are discussed only in passing:
  • The role of anticoagulation or carotid endarterectomy in patients with lacunes has not been fully defined.
  • Although a study showed that the benefit of endarterectomy in patients with lacunes is smaller than it is in patients with nonlacunar strokes, the procedure is superior to medical therapy.
• Atrial fibrillation and ipsilateral carotid stenosis have a stronger association with nonlacunar infarcts.¹⁰
• Data is less clear regarding a strong association between other risk factors and lacunar stroke, including alcohol consumption, elevated cholesterol, and history of prior of stroke.

Related Medscape topic:
CME Surgery Insight: Carotid Endarterectomy -- Which Patients to Treat and When?

Differential Diagnoses

Hypoglycemia
Middle Cerebral Artery Stroke
Migraine Headache

Other Problems to Be Considered

Other stroke subtypes (large artery disease, cardioembolic, hemorrhagic)
Seizure (Todd paresis)
Space-occupying lesion (abscess, tumor)

Workup

Laboratory Studies

• Serum glucose (to rule out hypoglycemia)
• Prothrombin time/international normalized ratio (PT/INR) and activated partial prothrombin time (aPTT)
  • Anticoagulant use with prolonged aPTT or PT (>15 seconds) or INR greater than 1.7 are contraindications to thrombolysis.
• CBC count - Thrombocytopenia is a contraindication for thrombolysis.

Imaging Studies

• Computed tomography (CT) scan of the head - CT scans usually are negative for lacunes in the acute stage; however, CT scanning is the imaging procedure of choice to rule out an intracerebral hemorrhage. It may show a large cortical stroke, an old lacune, or a space-occupying lesion.
• Magnetic resonance imaging (MRI) of the head - MRI is more sensitive than CT scanning for the identification of acute and old lacunes (particularly in the posterior fossa). MRI can help to identify acute hemorrhage, but there is a longer acquisition time than with CT scanning. Magnetic resonance angiography (MRA) also should be performed, because lacunes occasionally result from large-vessel disease. If further anatomical details are needed, the use of diffusion-weighted MRI may be indicated.¹¹

Other Tests

• An electrocardiogram (ECG), a Holter monitor study, a carotid Doppler ultrasonogram, and an echocardiogram may be required to identify a potential embolic cause for the lacune.¹²
• Cerebral angiography is required if a severe (>70% occlusion) carotid stenosis is identified on noninvasive testing (carotid ultrasonography or MRA) and if carotid endarterectomy is contemplated.

Histologic Findings

Lacunes are not examined histologically except at necropsy. Histologically, lacunes are no different from other brain infarcts. Cells undergoing necrosis initially are pyknotic, but their plasma and nuclear membranes then break down. Polymorphonuclear cells appear, followed by macrophages, and the necrotic tissue is removed by phagocytosis. A cavity surrounded by a zone of gliosis is the end result. Careful examination may reveal the underlying small-vessel pathology.

Microatheroma causing occlusion or stenosis of a deep penetrating artery is the most common small-vessel pathology, usually involving the artery in the first half of its course. Histologically, microatheroma is identical to large-vessel atheroma with subintimal deposition of lipids and proliferation of fibroblasts, smooth muscle cells, and lipid-laden macrophages.

Lipohyalinosis is seen in the smaller penetrating arteries (<200 μ m in diameter) and occurs almost exclusively in patients with hypertension. It has features of atheroma formation and fibrinoid necrosis, with lipid and eosinophilic fibrinoid deposition in the media.

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.

Dosing

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

Interactions

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)

Contraindications

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

Precautions

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.

Dosing

Adult

30-1300 mg/d PO; in US, usual dose is 325 mg PO qd

Pediatric

Not established

Interactions

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

Contraindications

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

Precautions

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.

Dosing

Adult

75 mg PO qd

Pediatric

Not established

Interactions

Coadministration with naproxen associated with increased occult GI blood loss; clopidogrel prolongs bleeding time; safety of coadministration with warfarin not established

Contraindications

Documented hypersensitivity; active pathological bleeding, such as peptic ulcer, or intracranial hemorrhage

Precautions

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.

Dosing

Adult

5000 U SC bid

Pediatric

Not established

Interactions

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

Contraindications

Documented hypersensitivity, subacute bacterial endocarditis, active bleeding, and history of heparin-induced thrombocytopenia

Precautions

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.

Dosing

Adult

Initial dose: 2.5 mg PO qd; titrate up to 10 mg PO qd

Pediatric

Not established

Interactions

Ramipril may increase digoxin, lithium, and allopurinol levels; probenecid may increase ramipril levels; coadministration with diuretics or NSAIDs increase hypotensive effects

Contraindications

Documented hypersensitivity; history of angioedema

Precautions

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

Follow-up

Further Inpatient Care

• If the patient who has had a lacunar stroke is functionally independent, can return safely home, and would benefit from intensive inpatient rehabilitation, transfer him/her to a rehabilitation facility.

Further Outpatient Care

• Outpatient physical, occupational, and/or speech therapy may be recommended for patients who have had a lacunar stroke.
• Medical follow-up is necessary to assess neurologic and functional improvement, to monitor and treat risk factors, and to monitor drug compliance.

Inpatient & Outpatient Medications

• Discharge on aspirin and ramipril.
• If the patient remains nonambulatory and is at high risk of DVT, continue subcutaneous heparin.

Transfer

• Transfer may be required for further diagnostic evaluation and treatment, including rehabilitation.

Complications

• Stroke progression or recurrent stroke
• Aspiration pneumonia
• DVT and PE
• Urinary tract infection
• Depression
• Shoulder-hand syndrome
• Decubitus ulcers

Prognosis

• Patient survival rates and rates of functional improvement are better for lacunar strokes than they are for other stroke subtypes (see Mortality/Morbidity).^3,4,6
• The risk of recurrent lacunar stroke, no more than 10% at 1 year, is no higher (and possibly is lower) than the recurrent stroke risk noted for other stroke subtypes.^3,4

Patient Education

• The patient and family should know the common stroke symptoms. Inform them early about the importance of presentation, because t-PA (which may be indicated) can be given only within 3 hours of stroke onset.¹⁴
• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

Miscellaneous

Medicolegal Pitfalls

• Most complications of lacunes are preventable with good medical and nursing care.

References

1. Bamford JM, Warlow CP. Evolution and testing of the lacunar hypothesis. Stroke. Sep 1988;19(9):1074-82. [Medline].

2. Brenner D, Labreuche J, Pico F, et al. The renin-angiotensin-aldosterone system in cerebral small vessel disease. J Neurol. May 2 2008;[Medline].

3. 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].

4. 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].

5. 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].

6. 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].

7. 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].

8. 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].

9. 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].

10. 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].

11. 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].

12. 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].

13. 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].

14. 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].

15. 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].

16. Pullicino PM, Caplan LR, Hommel M, eds. Cerebral Small Artery Disease. Advances in Neurology, vol 62. New York, NY: Raven Press; 1993.

17. Fisher CM. Capsular infarcts: the underlying vascular lesions. Arch Neurol. Feb 1979;36(2):65-73. [Medline].

18. Fisher CM. The arterial lesions underlying lacunes. Acta Neuropathol. Dec 18 1968;12(1):1-15. [Medline].

19. 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].

20. Post-stroke Rehabilitation Guideline Panel. Post-stroke Rehabilitation. Gaithersburg, Md: Aspen Pub; 1996.

21. 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].

22. Zweifler RM. Management of acute stroke. South Med J. Apr 2003;96:380-5. [Medline].

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

Contributor Information and Disclosures

Author

Adam B Agranoff, MD, Physiatrist and Partner, Chelsea Back Care, Chelsea Community Hospital
Adam B Agranoff, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and North American Spine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Edward H Wong, MB, BCh, Stroke Fellow, Department of Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario
Edward H Wong, MB, BCh is a member of the following medical societies: American Academy of Neurology and American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Robert J Kaplan, MD, Associate Professor, Department of Physical Medicine and Rehabilitation, University of Kansas School of Medicine and Medical Center
Robert J Kaplan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, International Spine Intervention Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Richard Salcido, MD, Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers, Phoenix
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

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