Lacunar Syndrome
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The term lacune has been in the medical literature for more than 150 years and was first used to describe the small cavity that remains after a small stroke has healed. [1] After a period of relative obscurity, the term was revived in the English-language medical literature in the 1960s. The association of characteristic neurologic syndromes with lacunar strokes in specific brain regions has occasionally sparked heated debate, as the different lacunar syndromes are good but not infallible predictors of an appropriately situated ischemic lesion.
The introduction of new brain imaging techniques—initially computed tomography (CT) scanning and, since the 1980s, magnetic resonance imaging (MRI)—has enabled the detection of most lacunae in vivo. The use of other improved diagnostic techniques has shown that etiologies other than hypertension can cause lacunar infarcts. [2]
This brief review focuses on lacunar strokes and tries to demonstrate that the concept of the lacuna is still a useful one. In this article, the term lacuna is used to describe a small infarct or a small cavity in the brain tissue that develops after the necrotic tissue of a deep infarct is resorbed. A lacuna is attributed to arterial insufficiency in the distribution of a penetrating branch of a large cerebral artery.
For patient education information, see eMedicineHealth’s Brain and Nervous System Center, as well as Stroke.
Go to Medscape Reference articles Ischemic Stroke in Emergency Medicine, Lacunar Stroke, and Acute Management of Stroke for more information on these topics.
Dechambre, a French physician, used the term lacune to describe a small cavity formed in the core of cerebral infarcts in the course of liquefaction and resorption of the infarct. Lacune derives from the Latin lacuna and in French refers to an “empty space.” Max Durand-Fardel provided a more detailed description, identifying lacunae as healed, small infarcts. [3] He also coined the term ” état criblé,” which can be translated as “tissue riddled with holes” and “sievelike state,” and indicated “dilatations of perivascular space.” [4]
Pierre Marie published his famous paper ” Des foyers lacunaires de disintegration et le differents autres états cavitaires du cerveau ” (“On lacunar foci of disintegration and other cavities of the brain”) in 1901, and he concluded that lacunae are small softenings caused by atherosclerosis, distinguishing them from état criblé. He also suggested that the lesions could be hemorrhagic.
The modern period in the history of lacunar infarcts started with Charles Miller Fisher, who, in the 1960s, redefined lacunae as “small, deep cerebral infarcts,” essentially returning to Durand-Fardel’s definition. [5, 6, 7, 8, 9, 10] Based on meticulous pathologic studies, Fisher also described the arterial lesions that caused lacunar infarcts, which, according to his first descriptions, were due almost exclusively to arteriolopathy of the perforators caused by hypertension. He described the disorganization of the vessel wall as “lipohyalinosis.” Fisher and a few of his younger colleagues correlated well-defined clinical syndromes with the discrete areas of infarction seen in lacunae; thus, the so-called “classic lacunar syndromes,” as well as variants and rarer syndromes, were variously revived or delineated for the first time.
Aging, hypertension, diabetes mellitus, hyperlipidemia, and smoking are the most significant risk factors for the development of lacunar infarcts. [5, 6, 9, 10, 11, 12, 13, 14, 110, 113] Although intrinsic penetrator disease is the most common etiologic mechanism, lacunar infarcts can occur secondary to cardioembolism or large artery atherosclerosis (see Pathophysiology and Neuropathology). A detailed evaluation for cardiac and large artery sources in patients with lacunar infarcts should be performed, especially if these risk factors are not present. [15]
Fisher and his coworkers, in their classic papers from the 1960s and 1970s, described local arteriopathy as the most common etiology of lacunar infarcts. [8, 11, 16]
Lipohyalinosis, which appears as an eosinophilic deposit in the connective tissue of the vessel wall, was considered the most common cause of pathologic lacunae. Other terms used to describe this condition are segmental arterial disorganization and angionecrosis. A similar condition is fibrinoid necrosis, which is found in the capillaries of the brain, retina, and kidneys in patients with malignant hypertension. These lesions are postulated to occur secondary to damaged cerebrovascular autoregulation, which occurs with aging and higher blood pressure levels. [11]
As Fisher described in a subsequent series of pathologic studies, however, microatheroma stenosing or occluding a penetrating artery was found in 6 of 11 capsular infarcts. This type of intracranial branch atheromatous disease is believed at present to be the most common etiology underlying lacunae that cause symptoms. [11] The microatheroma is essentially a tiny focus of atheromatous deposit, similar to the one seen in larger arteries. In hypertensive patients, atheromatous lesions are widespread in both large and smaller arteries and may eventually cause penetrating vessel stenosis or occlusion, resulting in a lacuna.
A small hemorrhage due to the rupture of a Charcot-Bouchard miliary aneurysm, which is a common arteriopathy in patients who are hypertensive, is another event considered an occasional cause of a lacuna. However, controversy exists regarding whether this arteriopathy is a true aneurysm or a dissection into the wall of a microatheroma or if it is merely a variant in the spectrum of the vascular effects of hypertension.
Fisher and others suggested that embolisms (microembolisms or macroembolisms) were etiologies for lacunar infarcts, because a patent feeding penetrating artery was found in pathologic studies of some lacunar infarcts. [8, 17, 18] In other pathologic studies, large-vessel occlusions were found in patients with small deep infarcts. [19, 20] Cardioembolism has also been associated with lacunar infarcts. [21, 22] Studies using diffusion-weighted imaging (DWI) have shown that, in some patients presenting with classic lacunar infarcts, multiple infarcts can be demonstrated, suggesting an embolic mechanism. [23, 24]
Unusual etiologies of lacunar infarcts include polycythemia [25] , cholesterol emboli [26] , vasculitis [27] , chronic neurosyphilis and other forms of chronic meningitis [11] , granulomatous angiitis, autoimmune disorders including systemic lupus erythematosus [28] , neurocysticercosis [29] , central nervous system (CNS) Lyme disease [30] , and drug abuse. [31]
Lacunar infarcts are small deep infarcts with a maximum diameter of 1.5 cm and a volume of 0.2-3.4 cm3. [6, 32] The penetrating vessels that feed lacunar infarcts have a diameter of 100-400 µm. Some deep infarcts whose diameters exceed 1.5 cm have been called “giant lacunae” or “super lacunae.” However, these are generally distinct in etiology and presentation from typical lacunae. An embolus in the trunk of the middle cerebral artery often causes these larger lacunar infarcts, simultaneously occluding several of the lenticulostriate perforating vessels.
Lacunar infarcts mainly occur in the basal ganglia, lenticular nucleus, and especially the putamen, thalamus, and white matter of the internal capsule, pons, and centrum semiovale. Lacunar infarcts occasionally occur in the cerebellum, cerebral gyri, and spinal cord, [33, 34] but they are rare in the gray matter of the cerebral surface, corpus callosum, and visual radiations.
Most lacunar infarcts occur in the territory of the deep penetrating arteries, mainly the lenticulostriate branches of the middle cerebral artery, but also in the anterior striate and Heubner arteries (ie, branches of anterior cerebral artery), anterior choroidal artery, paramedian branches of the basilar artery, and thalamoperforator branches of the posterior cerebral artery. The lenticulostriates and thalamoperforators have lumen diameters of 100-400 µm, whereas the diameter of the paramedian branches of the basilar artery ranges from 40-500 µm. These vessels directly arise from the larger vessels, without the gradual stepdown in size that occurs in the distal cortical vessels. [11, 35]
In the largest autopsy-based study, lacunar infarctions were found during postmortem examinations in 6% of 2859 consecutive individuals, who were chosen without taking into account stroke history. [12] In the Stroke Data Bank, 27% of patients (337 of 1273) with stroke had typical lacunar syndromes. [32] In several series and registries, the frequency of lacunar strokes was found to be approximately 15-20%. [36, 37, 38, 39] In another study in which clinical criteria, imaging, and other testing were used to identify lacunar infarcts, 28% of patients had lacunar strokes. [40]
Fisher, who compared series from the 1950s to the 1970s, reported a decrease in the frequency of lacunae in autopsy studies (11% vs 8%); this decrease was possibly due to a more widespread use of antihypertensive agents. [5, 6, 10]
The prevalence of lacunar infarcts appears to be higher in black and Hispanic people (31% of total strokes) than in white people (17%), as found in the Northern Manhattan Stroke Study. [40] In addition, the frequency of lacunar infarcts increases with age. According to a population-based study in Dijon, France, the prevalence was 2.8 per 100,000 women aged 30 years and 186 per 100,000 women aged 85 years. [41] The prevalence was 12.3 per 100,000 men aged 40 years and 398 per 100,000 men aged 85 years. [41]
No significant sex difference in the prevalence of lacunar infarcts has been reported in the different series and databases.
Specific symptoms and signs occur in the different lacunar syndromes. The 5 classic lacunar syndromes, established by Fisher in the 1960s and 1970s, are pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, and clumsy-hand dysarthria. Several other syndromes have been described, and Fisher listed more than 70 in a review paper in 1991. [10] However, the 5 syndromes named are the ones encountered most frequently in daily clinical practice and are described in more detail separately.
Pure motor hemiparesis was the first clinically recognized lacunar syndrome, [8, 33, 42] and it is also the most common of the lacunar syndromes, accounting for approximately one half to two thirds of the cases in several series. [32, 12, 38, 40, 43, 44, 45, 46]
In the classic paper by Fisher and Curry, pure motor hemiparesis was described as “a paralysis of face, arm and leg on one side, unaccompanied by sensory signs, visual field defect, dysphasia or apractagnosia.” [8] Subsequently, this definition was expanded to include patients without involvement of the face and with transient numbness or subjective heaviness of the affected limbs at the onset of the motor deficit. [43]
In autopsy studies, pure motor hemiparesis has been reported in patients with infarction in the corona radiata, internal capsule (especially the genu and posterior limb), pons, or medullary pyramid. [8, 47, 48] Differentiating hemiparesis secondary to a capsular lesion from hemiparesis secondary to a pontine lesion is difficult or impossible, because the motor involvement and symptoms may be identical. Cortical infarction rarely causes pure motor hemiparesis, usually nonproportional. [49] Because of the variability of the patterns of motor weakness and the intensity of the deficit, a reliable localization based on clinical findings cannot be made.
Several reports of partial motor syndromes associated with capsular infarcts have been published, suggesting an anteroposterior face-arm-leg somatotopic organization of the corticospinal/bulbar tract in the internal capsule. [50, 51] In other patients, however, no reproducible fractional hemiparesis pattern was found, confounding the hypothesis of a homunculus organization of fibers in the internal capsule. [11, 43, 52] Monoparesis almost never occurs secondary to a lacunar infarct, [10] although some cases, without sufficient clinical details or pathologic verification, have been described. [53, 54]
The clinical syndrome of pure motor hemiparesis has been reported to be secondary to several causes, including hemorrhaging in the internal capsule [48, 49] , caudate [55] , putamen [56] , and pons. Other reported causes include complications, ischemia, or both after a neurosurgical procedure [57] ; nocardial abscess [58] ; cerebral metastases; subdural hematoma; and demyelinating disease. [49]
The clinical course is often stuttering, with the symptoms developing in a stepwise fashion over several hours. [8, 48] Transient ischemic attacks (TIAs), the so-called “capsular warning syndrome,” precede (within 48 h) the lacunar syndrome of pure motor hemiparesis in 30% of patients. [43] In general, the clinical course is more benign than that of other types of hemiplegia, particularly larger cortical infarctions. [27] When the hemiparesis is incomplete, the recovery is more extensive. [11, 48]
Pure sensory stroke is less common than pure motor hemiparesis, occurring in approximately 6-7% of patients in an examined series of lacunar infarctions. [38, 40]
In the few autopsied cases of patients with pure sensory stroke, the most common lesion location has been the thalamus, particularly the posteroventral region. [5, 6, 59, 60] The underlying arterial disease was found to be microatheroma and lipohyalinosis. [59, 60] The lesions have been very small, and computed tomography (CT) scan findings can be negative for lesions in patients with this lacunar syndrome. Brain imaging studies, including head CT scanning and magnetic resonance imaging (MRI), have shown other anatomic areas associated with this syndrome, including a cortical infarct in the middle cerebral artery territory [61] and in the centrum semiovale/thalamocortical pathway. [62]
The clinical syndrome of pure sensory stroke has occasionally been associated with a small hemorrhage involving the corona radiata and the posterior limb of the internal capsule [63] and in the thalamus in a CT scan study. [62]
The symptoms in the pure sensory type of lacunar syndrome are limited to “a persistent or transient numbness and mild sensory loss over one side of the body, including face, arm, and leg,” without associated hemiparesis, visual field defect, brainstem dysfunction, memory loss, dyslexia, or other deficits. [10]
The symptoms are mainly paresthetic, with patients experiencing affected parts that are numb, hot, asleep, heavy, tight, itching, or “dead.” Sensory loss extends over the entire side of the body, splitting it almost exactly in the midline, which appears to be a characteristic of thalamic and thalamocortical pathway lesions. [5, 6, 36]
Dysesthetic symptoms, as in the classic thalamic pain syndrome of Dejerine-Roussy, have also been reported. [64] The dysesthesias or even hyperpathic pain may start at the onset of the symptoms or appear hours to months later. This is a bothersome symptom, and treatment is frequently initiated with tricyclic antidepressants (eg, amitriptyline) and other neuropathic pain agents, although not always successfully.
The clinical course of the pure sensory stroke is usually benign, and the symptoms subside within a few days or weeks, although, in cases of central poststroke pain, the symptoms may persist. [53]
A small, deep infarct causes this lacunar syndrome’s symptoms, which include a motor and a sensory deficit, as the name implies. A few pathologically confirmed cases have been described.
In one study, a lacuna in the posteroventral thalamus was found with an additional zone of pallor in the posterior limb of the adjacent internal capsule. [65] This is considered an unusual topography for an infarct, given the established knowledge that the vascular supply of the thalamus is separate from the one for the internal capsule. [66, 67, 68] However, similar cases support the view of some authors that the boundaries between the middle and posterior artery territories are not as strict as previously thought. [11]
Several cases have been demonstrated based on brain imaging studies, mainly computed tomography (CT) scans. Lesions in the thalamus, internal capsule, [64] caudate and putamen, [69] and lateral pons have been reported. On magnetic resonance imaging (MRI) studies, the lesion that causes a sensorimotor lacunar stroke is larger than lesions that cause other lacunar syndromes. [44]
The frequency of sensorimotor stroke in case series studies of lacunar strokes varies and has been reported to be as high as 38%, but it appears to be less than the frequency of pure motor hemiparesis. In a well-designed study using clinical and radiologic criteria to define the different lacunar syndromes, the prevalence of sensorimotor stroke was found to be 20%. [40]
Fisher initially described and named this syndrome, which consists of a combination of homolateral ataxia and crural paresis. [7, 59] Ataxic hemiparesis occurs in as many as 18% of case series of lacunar infarctions. [38, 40, 43]
The usual clinical features as described by Fisher and Cole include “weakness of the lower limb, especially the ankle and toes, and a Babinski sign, associated with striking dysmetria of the arm and leg on the same side.” [7] Some of the patients also had transient paresthesias, with a stuttering course of symptoms noted. Fisher later renamed the syndrome “ataxic hemiparesis,” meaning any combination of weakness and incoordination, out of proportion to weakness, on the same side of the body.
Lesions that simultaneously interrupt pyramidal systems (weakness) and adjoining frontopontocerebellar systems (ataxia) produce ataxic hemiparesis. The corona radiata and the anterior limb of the internal capsule are common sites of injury. Fisher reported 3 autopsied cases that showed contralateral lacunar infarcts in the upper basis pontis. [59, 60] A computed tomography (CT)-based series of patients with ataxic hemiparesis has also shown lesions in the internal capsule (posterior limb), corona radiata, lentiform nucleus, and thalamus. [43, 70, 71] Overall, no distinct clinical features differentiate lacunar infarctions originating in the capsule from those in the pons. [72]
In addition to small, deep infarcts, larger anterior cerebral artery infarcts have been recognized as a cause of ataxic hemiparesis with leg-predominant weakness. Ataxic hemiparesis also has been described in several nonischemic lesions, particularly hemorrhages [73, 74] and tumors [75, 76] .
Overall, improvement occurs within days or weeks. Occasionally, the hemiparesis improves, and the ataxia remains. [77]
Dysarthria-clumsy hand syndrome is characterized by the combination of facial weakness, severe dysarthria, and dysphagia, with mild hand weakness and clumsiness. [10, 78] Occasionally, some weakness of the arm or leg is present. [11, 79] Fisher described dysarthria-clumsy hand syndrome as a variant of ataxic hemiparesis, with the same localizing import. Dysarthria-clumsy hand syndrome is found in 2-16% of all lacunar syndromes. [43]
In Fisher’s initial pathologic description, a lacuna was found in the upper paramedian base of the pons. [78] In computer tomography (CT)-based reports, lesions have been found in the internal capsule and in the junction between the capsule and corona radiata. [43] Other etiologies causing this syndrome include pontine [79] and putaminal hemorrhage. [56] Overall, the prognosis is favorable. [11]
Movement disorders, including hemichorea-hemiballism and dystonia, have been described with deep infarcts in the contralateral subthalamic and putaminal-pallidal regions and the posterolateral thalamus, but these appear to be rare compared with the classic lacunar syndromes already described.
Eye movement disorders with or without hemiparesis, including cranial nerve (CN) III, vertical gaze palsy, and internuclear ophthalmoplegia, as the result of small deep infarcts, have been described. These include the classic brainstem syndromes of Weber (CN III palsy and contralateral hemiparesis) and Millard-Gubler (CN VI palsy and contralateral hemiparesis). [9]
An accumulation of multiple lacunar infarcts causes the so-called état lacunaire, or lacunar state, characterized by a short-step gait, dysarthria, dysphagia, pseudobulbar signs, cognitive impairment, imbalance, and incontinence.
Although the concept of the lacunar syndromes is a useful one, [40] diagnosing a clinical lacunar syndrome does not necessarily mean that the cause must be a small deep stroke. Intracranial hemorrhages (usually small), tumors, infections, neurosyphilis, neuroborreliosis, neurocysticercosis, abscesses, vasculitis, and drug use may cause lacunar syndromes.
Larger strokes or strokes caused by embolism can also manifest clinically as lacunar syndromes, and this is one of the reasons the usefulness of the lacunar hypothesis has been questioned. [80, 81] Therefore, a detailed evaluation for cardiac and large artery sources in patients with lacunar infarcts should be performed, especially if these risk factors are not present. [15]
The use of computerized tomography (CT) scanning in evaluating patients with lacunar infarctions has been reported [82, 83] ; however, the yield of documenting a pertinent lesion has been low. In the Stroke Data Bank, a lesion was found in fewer than 40% of patients with lacunar syndromes imaged with CT. [83] Small lacunar infarctions—and especially brainstem infractions—are difficult to visualize with CT scanning, given also the artifacts from the surrounding bone.
Several series of patients with lacunar syndromes imaged with magnetic resonance imaging (MRI) have also been reported. However, in contrast to computed tomography (CT) scanning, MRI showed a higher sensitivity for imaging of lacunes, approaching 80% in the first study several days after the ictus. [44, 84]
The MRI technique of diffusion-weighted imaging (DWI), which measures the apparent diffusion coefficient (ADC) in acute brain ischemia, has the highest sensitivity and specificity for the imaging of small, subcortical ischemic lesions, with an accuracy of 95%. [85] However, studies have demonstrated that a small percentage of patients with stroke symptoms and deficits imaged with MRI-DWI have normal DWI studies, [86] especially in patients with small brainstem infarctions. [87]
MRI-DWI could also be beneficial in identifying lacunar infarctions that could be associated with an embolic source. In a series of 62 patients with a classic lacunar syndrome, 16% had multiple regions of abnormal signal intensity—of those, one half had a documented cardioembolic source. [23]
Cerebral angiography has been also performed in patients with lacunar syndromes; usually no pertinent vascular abnormalities are demonstrated, [88] an expected finding given the small size of the perforators (< 500 µm) associated with lacunar infarctions.
When evaluating treatment of lacunar syndromes, interventions may include thrombolytic therapy, secondary prevention, and carotid endarterectomy.
For the acute treatment of patients with lacunar syndromes due to ischemic infarction, intravenous (IV) tissue plasminogen activator (t-PA) within 3 hours of symptom onset was established based in the National Institute of Neurological Disorders and Stroke (NINDS) trial, in which IV thrombolysis was beneficial regardless of the stroke subtype. [89]
A meta-analysis of the International Stroke Trial (IST) and the Chinese Acute Stroke Trial (CAST) established the benefit of acute treatment with aspirin at a dose of 160-300 mg within 48 hours of symptom onset. [90, 91] Several studies also evaluated unfractionated heparin and low-molecular weight heparin as acute stroke treatments, but no benefit was found compared with placebo. [90, 92] In particular, treatment with danaparoid sodium within 24 hours did not improve the 3-month outcome in patients with acute stroke due to small vessel disease in the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) study. [92]
Carotid endarterectomy in patients with lacunar strokes and ipsilateral significant carotid stenosis (>50%) was shown to be beneficial in the North American Symptomatic Carotid Endarterectomy trial, although to a lesser degree compared with patients with cortical infarctions. [93]
CM Fisher wrote that there should be “zero tolerance” for high blood pressure, and in a provocative statement during a lecture to internists, he mentioned that “if a patient of yours has a stroke, it is your fault.” [94] Although one might disagree with the severity of such a statement, it actually emphasizes that optimal control of the patients’ vascular risk factors, and in particular hypertension, is probably the best approach for minimizing the burden of stroke and especially of lacunar infarctions. [95]
The importance of antihypertensive treatment in stroke prevention, even in normotensive patients, was demonstrated in a large trial of perindopril (angiotensin-converting enzyme inhibitor) and indapamide (diuretic). [96] A large National Institutes of Health (NIH)-sponsored trial (Secondary Prevention of Small Subcortical Strokes [SPS3]) is currently recruiting patients to evaluate the safety and efficacy of antiplatelet and antihypertensive agents in patients with lacunar ischemic infarctions.
For secondary stroke prevention in patients with ischemic noncardioembolic lacunar infarctions, antiplatelets, including aspirin, clopidogrel, and the combination of aspirin and extended release dipyridamole, have shown modest benefit. [97, 98, 99] However, anticoagulation with warfarin did not show benefit over treatment with aspirin in patients with noncardioembolic stroke, [100] even in patients with symptomatic intracranial stenoses. [101]
The combination of clopidogrel and aspirin was not shown to be superior to clopidogrel [99] or to aspirin [102] in 2 large randomized trials. However, treatment with a high-dose atorvastatin showed benefit in secondary stroke prevention in patients with noncardioembolic stroke. [103]
In contrast to patients with other stroke types, patients with lacunar infarcts improve more often and generally have a better prognosis, in particular cortical and hemispheric infarctions. [7, 8, 42, 111] Smaller infarcts, as seen on imaging studies, also indicate a better prognosis.
The prognosis associated with lacunar strokes is generally worse if the deficit is severe, [11] and the presence of a transient ischemic attack before an infarct indicates a worse prognosis.
Acute phase complications, mainly urinary tract infections, occur in 18% of patients. [11] Other studies have addressed the issue of cognitive decline after lacunar infarctions, [104, 105] making the appropriate treatment of patients with lacunar syndromes even more urgent.
The recurrence rate for the first year after a lacunar stroke and for the following years is approximately 10%. [106, 107, 112] Only a minority of recurrent strokes are of lacunar etiology, which emphasizes the need for thorough evaluations of patients with lacunar strokes. In a 10-year follow-up study of patients with pure motor lacunar stroke, the recurrent stroke rate was 23.5%, [108] although an increased risk of death occurred after the first 5 years of follow-up, attributed mainly to cardiovascular causes.
In a community study, the early mortality rate was 1% [38] ; the 30-day mortality rate for patients with lacunar infarcts is approximately 3-5%. [32, 37]
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Nikolaos I H Papamitsakis, MD Assistant Professor of Neurology, Department of Neurosciences, Director of Stroke Service, Department of Adult Neurology, Medical University of South Carolina
Nikolaos I H Papamitsakis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, Stroke Council of the American Heart Association, American Society of Neuroimaging
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center
Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association
Disclosure: Nothing to disclose.
Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center
Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association
Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Executive Committee for the NINDS-funded DEFUSE3 Trial; Physician Advisory Board for Coherex Medical.
Jeffrey L Saver, MD, FAHA, FAAN Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine
Jeffrey L Saver, MD, FAHA, FAAN is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, National Stroke Association
Disclosure: Received the university of california regents receive funds for consulting services on clinical trial design provided to covidien, stryker, and lundbeck. from University of California for consulting.
Lacunar Syndrome
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