Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank

Lacunar stroke was diagnosed in 337 (26%) of the 1,273 patients with cerebral infarction among the 1,805 total in the Stroke Data Bank. We analyzed the 316 patients with classic lacunar syndromes. Among these, 181 (57%) had pure motor hemiparesis, 63 (20%) sensorimotor syndrome, 33 (10%) ataxic hemiparesis, 21 (7%) pure sensory syndrome, and 18 (6%) dysarthria-clumsy hand syndrome. No striking differences were found among the risk factors for the lacunar subtypes, but differences were found between lacunar stroke as a group and other types of infarcts. Compared to 113 patients with large-vessel atherosclerotic infarction, those with lacunar stroke had fewer previous transient ischemic attacks and strokes. Compared to 246 with cardioembolic infarction, patients with lacunar stroke more frequently had hypertension and diabetes and less frequently had cardiac disease. We found a lesion in 35% of the lacunar stroke patients' computed tomograms, with most lesions located in the internal capsule and corona radiata. The mean infarct volume was greater in patients with pure motor hemiparesis or sensorimotor syndrome than in those with the other lacunar stroke subtypes. In patients with pure motor hemiparesis and infarcts in the posterior limb of the internal capsule, there was a correlation between lesion volume and hemiparesis severity except for the few whose infarct involved the lowest portion of the internal capsule; in these patients severe deficits occurred regardless of lesion volume. Taken together, the computed tomographic correlations with the syndromes of hemiparesis showed only slight support for the classical view of a homunculus in the internal capsule.     

Should computed tomography appearance of lacunar stroke influence patient management?

Patients with a lacunar stroke syndrome may have cortical infarcts on brain imaging rather than lacunar infarcts, and patients with the clinical features of a small cortical stroke (partial anterior circulation syndrome, PACS) may have lacunar infarcts on imaging. The aim was to compare risk factors and outcome in lacunar syndrome (LACS) with cortical infarct, LACS with lacunar infarct, PACS with cortical infarct, and PACS with lacunar infarct to determine whether the clinical syndrome should be modified according to brain imaging. As part of a hospital stroke registry, patients with first ever stroke from 1990 to 1998 were assessed by a stroke physician who assigned a clinical classification using clinical features only. A neuroradiologist classified recent clinically relevant infarcts on brain imaging as cortical, posterior cerebral artery territory or lacunar. Of 1772 first ever strokes, there were 637 patients with PACS and 377 patients with LACS who had CT or MRI. Recent infarcts were seen in 395 PACS and 180 LACS. Atrial fibrillation was more common in PACS with cortical than lacunar infarcts (OR 2.3, 95% confidence interval (95% CI) 0.9-5.5), and in LACS with cortical than lacunar infarcts (OR 3.9, 1.2-12). Severe ipsilateral carotid stenosis or occlusion was more common in PACS with cortical than lacunar infarcts (OR 3.5, 1.3-9.5); and in LACS with cortical than lacunar infarcts (OR 3.7, 1.1-12). In conclusion, patients with cortical infarcts are more likely to have severe ipsilateral carotid stenosis or atrial fibrillation than those with lacunar infarcts irrespective of the presenting clinical syndrome. Brain imaging should modify the clinical classification and influence patient investigation.     

Capsular hypesthetic ataxic hemiparesis

Twenty-three patients with hypesthetic ataxic hemiparesis underwent computed tomography or magnetic resonance imaging. Twenty-two patients had infarcts of lacunar or slightly larger size in the contralateral posterior limb of the internal capsule. In 15 patients the infarct extended superiorly into the adjacent paraventricular region, and in seven it extended into the lateral thalmus. In eight patients the infarct was limited to the posterior limb of the internal capsule, and in only two patients was an ipsilateral to capsular pontine lacune found. Despite a location similar to that of pure motor and pure sensory lacunar stroke, hypesthetic ataxic hemiparesis correlates with larger infarcts, most often located in the posterior medial superior territory of the anterior choroidal artery. Some infarcts appeared to be localized immediately posterolateral to this region, in the posterior cerebral artery territory. The presence and extent of infarction is better detected by the addition of magnetic resonance imaging to computed tomography.     

Neuropsychological abnormalities associated with lacunar infarction

The objective of this study was to assess neuropsychological abnormalities in 40 patients with lacunar infarction. Topography of infarction, presence of isolated or multiple silent infarcts and white matter hyperintensities were correlated with results of neuropsychological tests and subtypes of lacunar infarction. Patients were studied within 1 month after stroke. A total of 21 patients were males and the mean age was 70.7 years; 30% had a single infarction (mean number of infarctions was 3.4). Twelve patients had pure motor hemiparesis, 9 pure sensory stroke, 8 dysarthria-clumsy hand/ataxic hemiparesis, 8 atypical lacunar syndrome, and 3 sensorimotor stroke. The mean score of the Mini-Mental State Examination was 28.4. Mild cognitive impairment of subcortical vascular features occurred in 23 patients and isolated executive disturbances in 4. Neuropsychological results showed that patients with atypical lacunar syndrome followed by pure motor hemiparesis showed significantly more cognitive executive disturbances. Patients with dysarthria-clumsy hand/ataxic hemiparesis accounted for the best scores in some tests of visuoconstructive function and visual memory. In summary, mild neuropsychological disturbances (57.5%) are not infrequent in acute lacunar infarcts especially in patients with atypical lacunar syndrome and pure motor hemiparesis. Neuropsychological impairment should be considered as common clinical feature in acute lacunar infarction.     

Lacunar syndromes due to brainstem infarct and haemorrhage.

Nine patients with brainstem infarct and two with brainstem haemorrhage presented with pure motor stroke, pure supranuclear facial palsy, sensorimotor stroke or ataxic hemiparesis. Despite the clinical similarity with hemispheric lacunes, brainstem infarcts causing lacunar syndromes probably have a greater tendency to progress. Small brainstem haemorrhages should also be considered as a cause of lacunar syndromes and the difficulty in differentiating them from small infarcts without CT is emphasised.     

Lacunar syndrome due to neurocysticercosis

Seven patients with neurocysticercosis presented with a lacunar syndrome. Four patients had sensorimotor stroke, two had pure motor hemiparesis, and one had ataxic hemiparesis. In every patient, computed tomography or magnetic resonance imaging or both showed a lacunar infarct that was secondary to the occlusion of a terminal vessel affected by endarteritis and was most commonly associated with cysticerci in the suprasellar cistern. Diagnosis of neurocysticercosis was difficult on clinical grounds, but proper integration of data from computed tomography and cerebrospinal fluid analysis provided an accurate diagnosis in every case. Neurocysticercosis should be considered in the differential diagnosis of young adults with a lacunar syndrome who come from areas of the world where this disease is endemic.     

Predictive value of clinical lacunar syndromes for lacunar infarcts on magnetic resonance brain imaging

OBJECTIVE: We prospectively investigated the predictive value of clinical and CT-supported lacunar syndromes for lacunar infarcts on magnetic resonance (MR) brain imaging. PATIENTS AND METHODS: The 54 prospective, consecutive patients had clinical lacunar syndromes of acute onset and early computed tomography (CT; on admission day, i.e. < or =48 h after onset of symptoms) showing either a small deep infarct or no corresponding lesion. Taking MR (at day 2 to 4 after admission) as the gold standard, the positive predictive value of the CT-supported clinical syndrome for corresponding lacunar lesions was calculated. RESULTS: In 27 (50%) patients, early CT showed a lacunar infarct corresponding to the clinical syndrome, a further 27 (50%) patients had no fresh ischemic lesion. In 51 patients (94%), MR showed a recent lacunar infarct (hyperintense lacune in T2-weighted scans, no demarcation on T1-weighted scans and/or positive gadolinium-enhancement) corresponding to the clinical syndrome (positive predictive value 0.94, 95%, CI: 0.88 to 0.98). In 3 (6%) patients MR was normal. Aside from old unrelated ischemic (macro- and/or microangiopathic) lesions, MR revealed no acute non-lacunar infarct. CT and MR sites of lacunar lesions were matching. Compared to gold standard MR, the sensitivity of early CT for suspected lacunar lesions was 0.53 (95% CI: 0.38 to 0.67). CONCLUSION: Lacunar syndromes were highly predictive for small deep infarcts on MR. Magnetic resonance brain imaging may be redundant in the setting of a lacunar syndrome supported by a CT that excludes non-ischemic causes of stroke; it may therefore be abandoned in order to reduce costs in the health care system.     

Prospective study of lacunar infarction using magnetic resonance imaging

Using computed tomography and magnetic resonance imaging, we prospectively studied 100 patients hospitalized with a lacunar infarct. Our aim was to evaluate the capabilities of magnetic resonance imaging in the detection and delineation of lacunes in a project of clinicotopographic correlations. Seventy-nine patients had a classic lacunar syndrome; 35 had pure motor stroke, 26 had ataxic hemiparesis, seven had sensorimotor stroke, and 11 had pure sensory stroke. A miscellaneous group of 21 patients had less typical lacunar syndromes, primarily with brainstem signs and symptoms. Among a total of 153 lacunes, magnetic resonance imaging detected at least one lacune appropriate to the symptoms in 89 patients. In 16 patients at least two lesions correlated with the clinical features, and precise clinicotopographic correlations were possible in 68 patients. Magnetic resonance imaging was more effective when it was performed a few days after the stroke. Lesions causing different types of lacunar syndromes had significantly different volumes, suggesting that the size of the lesion may influence clinical features. Magnetic resonance imaging may be the imaging technique of choice in the study of lacunar syndromes.     

Epidemiological characteristics of lacunar infarcts in a population

BACKGROUND AND PURPOSE: This study evaluated the characteristics and natural history of patients with lacunar (small, deep) cerebral infarcts in a defined population for comparison of these characteristics to those in patients with nonlacunar infarcts. METHODS: This is a population-based study in Rochester, Minnesota, from 1960 to 1984, that used the medical record-linkage system to identify and characterize patients with cerebral infarction. RESULTS: The age- and sex-adjusted average annual incidence rate of lacunar cerebral infarction was 13.4/100,000 persons, accounting for 12% of all first cerebral infarcts. Temporal trends in incidence rates, stroke recurrence rates, prevalence of diabetes mellitus, and causes of death (given survival for 30 days) for cases of lacunar infarction were not significantly different from those for cases of nonlacunar infarction. Hypertension was found in 81% of patients who had a lacunar infarct and in 70% of patients who had a nonlacunar infarct (p = 0.05). A potential cardiac source of embolism was found in 12% of patients who had a lacunar infarct and in 28% of patients who had a nonlacunar infarct (p = 0.002). Survival was significantly better after a lacunar infarct than after a nonlacunar infarct. CONCLUSIONS: Small, deep cerebral infarcts had many of the epidemiological characteristics of other cerebral infarcts but there was a slightly higher frequency of hypertension, significantly lower frequency of a cardiac embolic source, and significantly better survival in patients with lacunar infarction than in those with nonlacunar infarction.     

Identification of lacunar infarcts before thrombolysis in the ECASS I study

BACKGROUND: The identification of lacunar infarcts before thrombolysis would make it possible either to exclude them from treatment or to show that they also may benefit from it. OBJECTIVE: To determine whether clinical presentation or early CT findings of patients enrolled in the first European Cooperative Acute Stroke Study (ECASS I) trial would identify lacunar infarcts before treatment. METHODS: Predictive values, sensitivity, specificity, and accuracy of clinical presentation as pure motor hemiparesis (PMH) or sensorimotor stroke (SMS) syndromes and of baseline CT findings in predicting lacunar infarcts were calculated in the ECASS I patients. RESULTS: Of 514 patients, 44 placebo (17%) and 44 recombinant tissue plasminogen activator (rt-PA) (18%) patients had PMH/SMS involving at least two of three areas. Thirty-one placebo (12%) and 32 rt-PA (13%) patients had PMH/SMS involving three areas. The 7-day CT was compatible with a lacunar infarct in 32 placebo (12%) and 44 rt-PA (18%) patients. PMH/SMS involving at least two areas had a positive predictive value of 30% both in placebo and rt-PA patients, whereas positive predictive values of the involvement of three areas were 23% and 31%. Those of absence of early CT signs were 21% and 30%, and those of leukoaraiosis or previous lacunar infarcts were 21% and 23%. Positive predictive values of PMH/SMS involving at least two areas combined with absence of early CT signs were 36% in placebo and 33% in t-PA patients, and those of PMH/SMS plus leukoaraiosis or previous lacunes were 28% and 7%, respectively. CONCLUSIONS: In the ECASS I trial, lacunar infarcts were not recognizable on clinical grounds, and early CT findings, alone or in combination with the clinical picture, added poorly to the differential diagnosis.     

Clinical anatomic study of pure dysarthria

Nine patients with pure dysarthria underwent computed tomography or magnetic resonance imaging. Eight patients had infarcts of lacunar or larger size in the internal capsule: four in the superior portion of the anterior limb or adjacent corona radiata and four in the superior portion of the genu or the adjacent corona radiata. In one patient, there was a small infarct in the bulbar motor cortex. Dysarthria was transient and characterized by poor articulation in all cases. Five patients also had contralateral facial weakness, and three patients with lesions in the genu had minimal and transient involvement of the contralateral fingers. These three cases appeared to be variants of the dysarthria-clumsy hand syndrome. We submit that this syndrome should sometimes be regarded as a stroke syndrome rather than always as a lacunar syndrome.     

Lacunar syndrome due to intracerebral hemorrhage

It has been recognized that small intracerebral hemorrhage not uncommonly produced lacunar syndromes. In this study, we examined cases of intracerebral hemorrhage presenting as lacunar syndromes. Of 174 cases with recent intracerebral hemorrhage, 19 presented with a lacunar syndrome: 4 presented with pure motor hemiparesis, 5, ataxic hemiparesis, 3, dysarthria-clumsy hand syndrome, 7, sensorimotor stroke, and, none, pure sensory stroke. The sites of hemorrhage were capsular in 11, putamenal in 6, and pontine in 2. In these 19 patients, 17 were hypertensive, and the signs characteristic of parenchymal hemorrhage, e.g., gradual onset, headache, nausea, vomiting and stiff neck, were absent or very rare. Computed tomography revealed that one third of the patients had one or more non-symptomatic lacunae in the basal ganglia, the corona radiata or the anterior limb of the internal capsule. These observations suggests that hypertensive intracerebral hemorrhage causes lacunar syndrome more often than previously considered and is apt to manifest ataxic hemiparesis and sensorimotor stroke. Computed tomography is the only way of differentiating hemorrhagic "lacunar" syndrome from lacunar infarct.     

腔隙性梗死综合征的临床特点

腔隙性梗死临床极为常见,每种腔隙性梗死综合征通常提示为某一特定部位的病变,然而,临床观察发现同一腔隙综合征也可由不同部位的病变所致。同一部位病灶也可导致不同种类的腔隙综合征。腔隙综合征的临床表现复杂多变,远不止Fisher列举的21种腔隙综合征,如手-口综合征、面舌综合征、构音障碍-面轻瘫综合征、单独吞咽困难、单独偏身共济失调及四肢共济失调等多被归入某些综合征的变异型。另外,同时或相继以两组综合征起病的腔隙性梗死极少见,内囊后肢腔隙性梗死更具有其独特的特点。     

Capsular ataxic hemiparesis. Early diagnosis with MRI

The Authors report a case of ataxic hemiparesis caused by a lacunar infarct involving the posterior limb of the right internal capsule, in a 64-year-old hypertensive man who completely recovered in about two weeks. The lesion was detected by MRI four days after the onset of illness, when the CT scan was normal. In patients presenting with ataxic hemiparesis, MRI is the most accurate tool in locating very small causative infarcts of the brainstem or the subcortical white matter.     

How well does the Oxfordshire Community Stroke Project classification predict the site and size of the infarct on brain imaging?

OBJECTIVES: The Oxfordshire Community Stroke Project (OCSP) classification is a simple clinical scheme for subdividing first ever acute stroke. Several small studies have shown that when an infarct is visible on CT or MRI, the classification predicts its site in about three quarters of patients. The aim was to further investigate this relation in a much larger cohort of patients in hospital with ischaemic stroke. METHODS: Between 1994 and 1997, inpatients and outpatients with ischaemic stroke were assessed by one of several stroke physicians who noted the OCSP classification. A neuroradiologist classified the site and extent of recent infarction on CT or MRI. RESULTS: Of 1012 patients with ischaemic stroke, 655 (65%) had recent visible infarcts. These radiological lesions were appropriate to the clinical classification in 69/87 (79%) patients with a total anterior circulation syndrome, 213/298 (71%) with a partial anterior circulation syndrome, 105/144 (73%) with a lacunar syndrome, and 105/126 (83%) with a posterior circulation syndrome. Overall, 75% of patients with visible infarcts were correctly classified clinically. If patients without a visible infarct did have an appropriate lesion in the brain (best case), the classification would have correctly predicted its site and size in 849/1012 (84%) patients, compared with only 492/1012 (49%) in the worst case scenario. CONCLUSION: The OCSP classification predicted the site of infarct in three quarters of patients. When an infarct is visible on brain imaging, the site of the infarct should guide the use of further investigations, but if an infarct is not seen, the OCSP classification could be used to predict its likely size and site.     

Confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome?

We examined six patients with an abrupt change in behavior after infarction involving the inferior genu of the internal capsule. The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation, suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia occurred in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients showed a focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. We infer that the capsular genu infarct interrupted the inferior and anterior thalamic peduncles, resulting in functional deactivation of the ipsilateral frontal cortex. These observations suggest that one mechanism for cognitive deterioration from a lacunar infarct is thalamocortical disconnection of white-matter tracts, in some instances leading to "strategic-infarct dementia."     

Aphasia and agraphia in lesions of the posterior internal capsule and putamen

We studied three right-handed patients with small, lacunar infarcts localized by CT to the posterior and lateral putamen and the posterior limb of the internal capsule. All had moderate or severe right hemiparesis and mild aphasia that was not characteristic of any traditional aphasia syndrome. Two had mild dysarthria. Aphasic abnormalities included mild, nonfluent, telegraphic speech and mild, fluent aphasia with impaired repetition, naming, and comprehension. All three had severely impaired writing. Unlike previously reported patients with subcortical infarcts, these cases indicate that small lesions limited to the posterior capsuloputaminal area can cause aphasia and agraphia as well as dysarthria.     

Clinical study of 39 patients with atypical lacunar syndrome

The aim of this study was to describe the clinical characteristics of atypical lacunar syndrome (ALS) based on data collected from a prospective acute stroke registry. In total, 2500 acute stroke patients were included in a hospital based prospective stroke registry over a 12 year period, of whom 39 were identified as having ALS and radiologically proven (by computed tomography or magnetic resonance imaging) lacunes. ALS accounted for 1.8% of all acute stroke patients, 2.1% of acute ischaemic stroke, and 6.8% of lacunar syndromes. ALS included dysarthria facial paresis (n = 12) or isolate dysarthria (n = 9), isolated hemiataxia (n = 4), pure motor hemiparesis with transient internuclear ophthalmoplegia (n = 4), pure motor hemiparesis with transient subcortical aphasia (n = 3), unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarct syndrome, and hemichorea hemiballismus (n = 2). Atypical lacunar syndromes were due to small vessel disease in 96% of patients. Atherothrombotic infarction occurred in one patient and cardioembolic infarct in another, both presenting pure dysarthria. Outcome was good (in hospital mortality 0%, symptom free at discharge 28.2%). After multivariate analysis, the variables of speech disturbances, nausea/vomiting, ischaemic heart disease, and sensory symptoms were found to be significantly associated with ALS. In conclusion, atypical lacunar syndrome is an infrequent stroke subtype (one of each 14 lacunar strokes). ALS occurred in 6.8% of lacunar strokes. Isolated dysarthria or dysarthria facial paresis were the most frequent presenting forms. The prognosis of this infrequent non-classic lacunar syndrome is good.     

Lacunar infarcts. Pathogenesis and validity of the clinical syndromes.

BACKGROUND AND PURPOSE: In this study, we investigated the lacunar hypothesis to answer three questions: 1) Is the lacunar syndrome valid for diagnosing lacunar infarction? 2) What is the frequency of potential cardiac versus carotid sources of embolism in patients with lacunar versus cortical infarct? 3) What is the frequency of vascular risk factors in these two groups of patients? METHODS: The study was performed in a well-defined prospective series of 103 patients with a first-ever lacunar infarct and 144 other patients with a first-ever infarct involving the cortex. RESULTS: Sensitivity and specificity of the lacunar syndromes in diagnosing lacunar infarction were 95% and 93%, respectively. Positive and negative predictive values of diagnosing lacunar infarction in patients with lacunar syndromes were 90% and 97%, respectively. Risk factor analysis showed no differences for either group of cerebral infarction. A cardiac source of embolism was significantly less frequent in patients with lacunar infarction (odds ratio = 0.32, 95% confidence interval = 0.17-0.61, p less than 0.001). Significant carotid stenosis (diameter reduction greater than or equal to 50%) was also less frequent in patients with lacunar infarction (odds ratio = 0.35, 95% confidence interval = 0.16-0.76, p less than 0.001). CONCLUSIONS: These findings show that the lacunar syndrome is an excellent clinical test for diagnosing lacunar infarction and that cardiac and carotid embolism are unlikely causes of lacunar infarction, supporting the hypothesis that lacunar infarcts are usually caused by small vessel disease.