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.     

Clinical study of 222 patients with pure motor stroke

The objective was to assess the frequency of pure motor stroke caused by different stroke subtypes and to compare demographic, clinical, neuroimaging, and outcome data of pure motor stroke with those of patients with other lacunar stroke as well as with those of patients with non-lacunar stroke. Data from 2000 patients with acute stroke (n=1761) or transient ischaemic attack (n=239) admitted consecutively to the department of neurology of an acute care 350 bed teaching hospital were prospectively collected in the Sagrat Cor Hospital of Barcelona stroke registry over a 10 year period. For the purpose of the study 222 (12.7%) patients with pure motor stroke were selected. The other study groups included 218 (12.3%) patients with other lacunar strokes and 1321 (75%) patients with non-lacunar stroke. In relation to stroke subtype, lacunar infarcts were found in 189 (85%) patients, whereas ischaemic lacunar syndromes not due to lacunar infarcts occurred in 23 (10.4%) patients (atherothrombotic stroke in 12, cardioembolic stroke in seven, infarction of undetermined origin in three, and infarction of unusual aetiology in one) and haemorrhagic lacunar syndromes in 10 (4.5%). Patients with pure motor stroke showed a better outcome than patients with non-lacunar stroke with a significantly lower number of complications and in hospital mortality rate, shorter duration of hospital stay, and a higher number of symptom free patients at hospital discharge. After multivariate analysis, hypertension, diabetes, obesity, hyperlipidaemia, non-sudden stroke onset, internal capsule involvement, and pons topography seemed to be independent factors of pure motor stroke in patients with acute stroke. In conclusion, about one of every 10 patients with acute stroke had a pure motor stroke. Pure motor stroke was caused by a lacunar infarct in 85% of patients and by other stroke subtypes in 15%. Several clinical features are more frequent in patients with pure motor stroke than in patients with non-lacunar stroke.     

Acute isolated capsular stroke. A clinical study of 148 cases

The objectives of the study were to assess differential features between capsular stroke of ischemic and hemorrhagic origin, and to compare capsular strokes with all other (non-capsular) strokes. Data of 148 patients with isolated capsular stroke were collected from a prospective hospital-based stroke registry in which 2000 consecutive acute stroke patients were included. Isolated capsular stroke accounted for 8.4% of strokes included in the registry (8.4% of ischemic strokes and 10.5% of intracerebral hemorrhages). Capsular stroke of hemorrhagic origin (n = 24) was more severe than ischemic capsular stroke (n = 124) as determined by a significantly higher in-hospital mortality, length of stay, and lower number of patients free of functional deficit at discharge. After multivariate analysis, limb weakness, sudden onset, and sensory symptoms were independently associated with capsular hemorrhage, whereas pure motor hemiparesis appeared to be associated with capsular infarction. In summary, one of each 12 patients with acute ischemic stroke and one of each 10 patients with acute intracerebral hemorrhage had an isolated capsular stroke. Lacunar syndrome was the most frequent clinical presentation being more common (particularly pure motor hemiparesis) in ischemic than in hemorrhagic capsular stroke. Capsular hemorrhage and capsular infarction showed identical risk factor profiles suggesting the same underlying vascular pathology for both conditions.     

One-year follow-up in a child with McArdle disease: exercise is medicine

A hemorrhagic stroke in children is rarely secondary to cerebral paragonimiasis. We describe a 9-year-old boy in whom an intracerebral hemorrhage was the leading clinical indication of acute cerebral paragonimiasis. He was hospitalized because of a sudden onset of headache, right hemiparesis, and dysarthria. A computed tomography scan revealed an intracerebral hemorrhage in the left parietal lobe. Magnetic resonance angiography did not confirm any vascular abnormalities at the location of the hematoma. Four weeks later, he presented with right hemiparesis again, and fever. A diagnosis of cerebral paragonimiasis was based on repeated magnetic resonance imaging of the brain and an enzyme-linked immunosorbent assay for paragonimiasis. The patient gradually recovered with praziquantel treatment. Cerebral paragonimiasis should be considered in the differential diagnosis of hemorrhagic strokes in children in areas where paragonimiasis is epidemic.     

Haemorrhagic pure motor stroke

To describe the clinical characteristics of haemorrhagic pure motor stroke (PMS). Twelve patients with haemorrhagic PMS were identified. Haemorrhagic PMS accounted for 3.2% of all cases of pure motor hemiparesis ( n  = 380) and 3.3% of intracerebral haemorrhage ( n  = 364) entered in the database. When compared with PMS of ischaemic origin, patients with haemorrhagic PMS were more likely to be younger (62.2 vs. 75.2 years, P  = 0.003) and to have headache (33% vs. 6.3%, P  =0.007) and thalamus involvement (25% vs. 2.4%, P  = 0.005). Limb weakness (100% vs. 74.1%; P  = 0.03), involvement of the internal capsule (50% vs. 17.3%, P  = 0.012) and symptom free at discharge (25% vs. 3.7%, P  = 0.012) were significantly more frequent in patients with haemorrhagic PMS than in the remaining cases of haemorrhagic stroke, whereas nausea and vomiting (0% vs. 25.9%, P  = 0.03), altered consciousness (0% vs. 42.9%, P  = 0.001), sensory symptoms (8.3% vs. 46.9%, P  =0.007) and ventricular haemorrhage (0% vs. 26.1%, P  = 0.028) were significantly less frequent. Haemorrhagic PMS is a very infrequent stroke subtype. Headache at stroke onset may be useful sign for distinguishing haemorrhagic PMS from other causes of lacunar stroke. There are important differences between haemorrhagic PMS and the remaining intracerebral haemorrhages.     

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.     

Admission markers predict lacunar and non-lacunar stroke in young patients

Stroke in young adults is an important cause of lifelong morbidity. The aim of this study was to explore some possible admission indicator of subsequent lacunar or non-lacunar strokes. We enrolled 626 patients with the first young cerebral strokes and divided them into lacunar and non-lacunar stroke based on clinical presentation and neuroradiological findings; and the analyses were adjusted for the effects of potential confounders. Hypertension, hyperlipidemia, atrial fibrillation, cerebral vascular moyamoya malformation were significantly more frequent in non-lacunar patients than lacunar patients (respectively P = 0.005, 0.048, 0.000, 0.015, 0.030). Serum BUN, Triglyceride, Cholesterol, HDL, UA, White cell count, Fibrinogen, INR and bilirubin (including Total bilirubin, Direct bilirubin, Indirect bilirubin) levels on admission were higher in non-lacunar strokes than in lacunar strokes. Serum white blood cell count (Odds Ratio 1.097; 95% Confidence Interval 1.006-1.195, P = 0.035), lower high-density lipoprotein levels (defined as HDL < 0.9 mmol/L)(Odds Ratio 1.884; 95% Confidence Interval 1.035-3.285, P = 0.038) and serum total bilirubin (Odds Ratio 1.054; 95% Confidence Interval 1.019-1.091, P = 0.003) were associated with increased risk for non-lacunar stroke, whereas lacunar stroke was related to age at onset (Odds Ratio 0.929; 95% Confidence Interval 0.888-0.972, P = 0.001) and SUA (Odds Ratio 0.997; 95% Confidence Interval 0.995-0.999, P = 0.015). The excess risks were blood WBC, lower HDL and total bilirubin levels for non-lacunar strokes, and serum UA and age at onset for lacunar strokes in young Chinese patients.     

Are sensorimotor strokes lacunar strokes? A case-control study of lacunar and non-lacunar infarcts.

To determine whether sensorimotor strokes should be considered as lacunar syndromes 34 consecutive patients with first-ever ischaemic sensorimotor stroke were evaluated and compared with 103 patients with non-lacunar infarcts and another 88 patients with lacunar infarcts. Potential thromboembolic sources were more frequent in patients with non-lacunar infarcts (p = 0.003, versus sensorimotor strokes). Although the overall prevalence of hypodense lesions at CT scan was not significantly different among the three groups, lacunar lesions were found in 47.1% of sensorimotor strokes, compared with 6.8% of non-lacunar infarcts (p less than 0.0001). In a mean follow up period of 28.7 months, the incidence of stroke and myocardial infarction among sensorimotor strokes was similar to that of patients with lacunar infarct, but significantly lower than in non-lacunar infarcts (p less than 0.05). These results demonstrate important differences between sensorimotor and non-lacunar infarcts, but quite similar findings in sensorimotor and lacunar strokes, and thus support the theory that sensorimotor strokes are commonly due to lacunar lesions.     

Lacunar versus non-lacunar infarcts: pathogenetic and prognostic differences.

To characterise the pathogenetic and prognostic features of lacunar infarcts, 88 patients with these infarcts were compared with 103 patients with non-lacunar infarcts. Potential cardioembolic sources were significantly more frequent among patients with non-lacunar infarcts (p = 0.0025). Although the prevalence of hypertension was higher among lacunar infarcts, this difference was not statistically significant. However, the distribution of hypertensive patients in the two groups of lacunar and non-lacunar infarcts was influenced by the presence or absence of cardioembolic sources: hypertension was significantly associated with the presence of cardioembolic sources among non-lacunar infarcts, whereas among lacunar infarcts it was significantly more frequent in patients without a cardioembolic source. This indicates that cardioembolism may exert a confounding effect by suppressing the relation between hypertension and lacunar infarcts. In a mean follow up period of 28.1 months, lacunar infarcts had a significantly lower incidence of stroke recurrence and of myocardial infarction (age-adjusted survival analysis: p = 0.0008); mortality from all causes was also lower in patients with lacunar infarct (age-adjusted survival analysis: 0.04 less than p less than 0.05). In a multivariate regression analysis, stroke subtype was an independent predictor of new major vascular events. These findings support the lacunar hypothesis and should be considered in the planning of epidemiological and therapeutic studies in patients with cerebral infarction.     

脑微出血与脑卒中

目的探讨脑微出血与脑卒中发生、发展的联系。方法卒中患者83例，分为脑缺血组（43例）和脑出血组（40例），以同期住院的50岁以上非脑卒中患者设立对照组（32例）。采用T2加权梯度回波MRI观察各病例脑微出血、卒中病灶、腔隙性梗塞以及白质疏松情况，同时记录卒中患者的高血压、糖尿病、高脂血症、卒中病史以及阿司匹林使用史。结果微出血在缺血组和出血组的发生率分别为34．9％、75．0％，对照组9．4％。各组微出血均最常见于基底节区。微出血与高血压、卒中病史相关（P〈0．01），与高脂血症、糖尿病病史及使用阿司匹林无关（P〉0．05）。微出血的严重程度与腔隙性梗塞、白质疏松的严重程度相关（P〈0．01）．．微出血在卒中病灶区域同侧或对侧分布无显著性差异（P〉0．05）。出血组微出血在卒中病灶区域的分布率明显高于缺血组。结论微出血与脑卒中．特别是与出血性脑卒中有密切关系，对卒中患者出血性转化具有预测意义。     

Association of Left Ventricular Hypertrophy and Atrial Fibrillation with Hemorrhagic Evolution of Small Vessel Disease

ObjectivesCerebral small vessel disease (SVD) is often associated with hypertension and may evolve towards intracerebral hemorrhage (ICH) or lacunar ischemic stroke. However, the factors favoring the evolution towards ICH or lacunar stroke are not well understood.Materials and MethodsThis retrospective study included 326 consecutive patients (71.1±13.2 years, 38% women): 143 with deep ICH and 183 with lacunar lesions (LL) <2 cm, which were visible in a deep location on brain CT scan. Among LL patients, 143 had a small-artery occlusion (SAO) stroke according to the TOAST classification. Clinical characteristics plus laboratory and neuroradiological variables of these patients had been prospectively collected and a subgroup underwent echocardiography.ResultsIn multivariate analysis, ICH patients (97% hypertensive), compared to SAO patients (89% hypertensive), had greater left ventricular wall thickness (LVWT; OR 4.15, 95%CI 1.64-10.53, for those with LVWT ≥ 1.4 cm, 70% of whom were hemorrhagic) and lower prevalence of white matter lesions (OR 0.30, 95%CI 0.13-0.70), ever smokers (OR 0.39, 95%CI 0.18–0.82) and diabetics (OR 0.29, 95% CI 0.10-0.84). Moreover, ICH patients had a greater prevalence of atrial fibrillation than LL patients (OR 3.14, 95%CI 1.11-8.93), and so they were more often anticoagulated.ConclusionsMost SVD patients were hypertensive, but those evolving towards ICH were characterized by organ damage at the cardiac level (increase in LVWT and atrial fibrillation), while those evolving towards lacunar stroke were characterized by a higher prevalence of smokers and diabetics, and by organ damage at the cerebral level (white matter lesions).     

Lacunar syndromes due to intracerebral hemorrhage]

Nine cases (seven men and two women, mean age 64.5 years) of classical lacunar syndromes due to intracerebral hemorrhage are reported. Three patients presented with pure motor hemiparesis (two putaminal hematomas with proportional weakness and one cortical hemorrhage with brachio-crural hemiparesis). Four patients presented with sensorimotor stroke due to thalamo-capsular hemorrhage. The last two patients had thalamic hemorrhage causing ataxic hemiparesis or dysarthria-clumsy hand syndrome. Four subjects had arterial hypertension, one was diabetic, and two were treated with anti-vitamin K. Abrupt onset was noted in all instances. Only one patient experienced moderate inaugural headaches. Good recovery occurred in all cases. Lacunar syndromes are a very uncommon presentation of intracerebral bleeding. Hemorrhages are yet the second etiology of such syndromes. Distinguishing hemorrhage from infarction is not clinically possible and needs early unenhanced CT scan.     

A case of delayed subrachnoid hemorrhage from vertebrobasilar artery dissecting aneurysm]

We report a case of delayed subarachnoid hemorrhage (SAH) from a vertebrobasilar artery dissecting aneurysm (VBA-DA). The patient was a healthy 32-year-old woman with a sudden onset of severe occipitalgia. Next day, her headache improved gradually, and she consulted with our department. Although we initially suspected that she was suffering from SAH, neurological findings, CT, and cerebrospinal fluid examination did not reveal any abnormal conditions, including SAH. Therefore, she was treated conservatively with analgesics. Twelve days after the initial onset of the headache, she was admitted because of severe re-attack of headache, rt. hemiparesis with rt. oculomotor nerve palsy and loss of consciousness. CT revealed moderate SAH and cerebral angiograms showed VBA-DA. After the cerebral angiography, bleeding reoccurred two times and she lost her life. We present the case, review the literature and discuss the relationship between presenting symptom of headache and non-hemorrhagic VBA-DA. A few cases of non-hemorrhagic VBA-DA have been reported in the literature in which the only presenting symptom was headache, followed by delayed SAH from non-hemorrhagic dissecting aneurysm. Consequently, we concluded that her initial symptom of headache was due to dissection of vertebrobasilar artery, and that SAH was due to delayed hemorrhage of non-hemorrhagic VBA-DA. Even when neurological findings, CT and cerebrospinal fluid examination reveal no abnormalities in the early stage after the sudden onset of headache, especially in the occiptal or nuchal regions, non-hemorrhagic VBA-DA, which has a risk of fatal hemorrhage, cannot be ruled out with certainty. Therefore, MRI, MRA, three-dimensional CT, or cerebral angiography should be performed in such cases.     

Dysarthria in acute ischemic stroke: lesion topography, clinicoradiologic correlation, and etiology

BACKGROUND AND PURPOSE: Although dysarthria is a frequent symptom in cerebral ischemia, there is little information on its anatomic specificity, spectrum of associated clinical characteristics, and etiologic mechanisms. METHODS: An investigation of 68 consecutive patients with sudden onset of dysarthria due to a single infarction confirmed by MRI or CT was conducted. RESULTS: Dysarthria was associated with a classic lacunar stroke syndrome in 52.9% of patients. Isolated dysarthria and dysarthria-central facial and lingual paresis occurred in 2.9% (n = 2) and 10.3% (n = 7), respectively. Dysarthria-clumsy hand syndrome was observed in 11.7% (n = 8) of patients and associated with pure motor hemiparesis and/or ataxic hemiparesis in 27.9% (n = 19). The lesions were due to small-vessel disease in 52.9% (n = 36), to cardioembolism in 11.8% (n = 8), and to large-vessel disease in only 4.4% (n = 3) of cases. Infarctions were located in the lower part of the primary motor cortex (5.9%; n = 4), middle part of the centrum semiovale (23.5%; n = 16), genu and ventral part of the dorsal segment of the internal capsule (8.8%; n = 6), cerebral peduncle (1.5%; n = 1), base of the pons (30.9%; n = 21), and ventral pontomedullary junction (1.5%; n = 1). Isolated cerebellar infarctions affected the rostral paravermal region in the superior cerebellar artery territory. CONCLUSIONS: Extracerebellar infarcts causing dysarthria were located in all patients along the course of the pyramidal tract. This finding correlates with the frequent occurrence of associated pyramidal tract signs in 90.7% (n = 62) of patients. Isolated cerebellar infarcts leading to dysarthria were in all cases located in the territory of the superior cerebellar artery.     

Isolated dysarthria due to extracerebellar lacunar stroke: a central monoparesis of the tongue

OBJECTIVES: The pathophysiology of dysarthria can preferentially be studied in patients with the rare lacunar stroke syndrome of "isolated dysarthria". METHODS: A single study was carried out on seven consecutive patients with sudden onset of isolated dysarthria due to single ischaemic lesion. The localisation of the lesion was identified using MRI. The corticolingual, cortico-orofacial, and corticospinal tract functions were investigated using transcranial magnetic stimulation. Corticopontocerebellar tract function was assessed using 99mTc hexamethylpropylene amine oxime-single photon emission computerised tomography (HMPAO-SPECT) in six patients. Sensory functions were evaluated clinically and by somatosensory evoked potentials. RESULTS: Brain MRI showed the lesions to be located in the corona radiata (n=4) and the internal capsule (n=2). No morphological lesion was identified in one patient. Corticolingual tract function was impaired in all patients. In four patients with additional cortico-orofacial tract dysfunction, dysarthria did not differ from that in patients with isolated corticolingual tract dysfunction. Corticospinal tract functions were normal in all patients. HMPAO-SPECT showed no cerebellar diaschisis, suggesting unimpaired corticopontocerebellar tract function. Sensory functions were not affected. CONCLUSION: Interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of isolated dysarthria after extracerebellar lacunar stroke.     

Headache at stroke onset: the Lausanne Stroke Registry.

Within 12 hours of stroke onset 2506 patients with first ever stroke admitted to the Lausanne Stroke Registry were questioned about headache. Eighteen per cent of the patients reported headache, 14% with anterior circulation stroke and 29% with posterior circulation stroke (p < 0.001). Headache was reported by 16% of the patients with infarct and 36% of those with haemorrhage (p < 0.001). The prevalence of headache was 9% with lacunar infarct, 15% with middle cerebral artery territory infarct, 37% with infratentorial haemorrhage, and 36% with supratentorial haemorrhage. The most common topography of pain was frontal (41%), followed by diffuse headache (27%; p < 0.001). Diffuse (41%) or occipital (30%) headache was particularly frequent with posterior circulation stroke, whereas frontal headache was associated with anterior circulation stroke (51%; p < 0.001). Headache in stroke may be explained in part by involvement of blood vessels (acute distention or distortion) and mechanical (stretch of haemorrhage) stimulation of intracranial nociceptive afferents. Stroke due to dissection was strongly associated with headache (p < 0.001), whereas embolic (cardiac, artery to artery) stroke was more common without headache (p < 0.001), emphasising the role of extracranial v intracranial arteries in the genesis of headache at stroke onset. Moreover, dual trigeminal-vascular and cervical-vascular system involvement in causing headache may explain the lack of correspondence with the "rules of referral" in up to 38% of the cases.     

Pattern and ethnic variations in stroke in Saudi Arabia.

We report our observations in 427 stroke patients (305 Saudis, 122 non-Saudis with an age range of 14 months to 85 years) seen in a tertiary hospital in the eastern province of Saudi Arabia over an 8-year period. Of these patients, 115 (27%) were between 18 and 45 years old, and constituted the "young stroke patients" for this study. The hospital frequency for the young was 5/10,000 inpatients. In general, there was a male preponderance, with a male:female ratio of 2.2:1 and 7:1 for Saudis and non-Saudis, respectively. Ischemic stroke (55%) was more frequent than hemorrhagic stroke (25%), and the stroke was unspecified in 20%. The main etiologic factors were hypertension, diabetes mellitus and cardiac disorders. In the young population, the frequencies of hemorrhagic and ischemic strokes were similar. In this group, the main causes of intracerebral hemorrhage were aneurysms and arteriovenous malformations, while arteriosclerosis and embolism of cardiac origin were responsible for the ischemic strokes. In Saudis, the stroke types were 59% ischemic, and 17% hemorrhagic, as against 45 and 48% in non-Saudis, respectively. Most ischemic strokes were found in Saudis (78%). Intracerebral hemorrhage accounted for 63% of all hemorrhagic strokes, and was more frequent in Saudis but subarachnoid hemorrhage was three times more common in non-Saudis. In the young stroke patients, interethnic comparison showed that individuals from the Far East were nine times more likely to have hemorrhagic than ischemic stroke compared to the others (odd's ratio = 8.7), and the etiology of ischemic stroke remained undetermined in 67% of those from the Indian subcontinent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Admission glucose level in relation to mortality and morbidity outcome in 252 stroke patients

In a prospective study to correlate admission glucose level with neurologic outcome in stroke, 252 acute stroke patients without prior disability and admitted within 24 hours of onset of ictus were assessed. The stroke was classified into one of three types--cortical infarct, lacunar infarct, or intracerebral hemorrhage--by clinical, computed tomographic, and necropsy findings. Fifty-one diabetic patients were excluded from the entire cohort to form a nondiabetic category for analysis. We found that admission glucose level showed a significantly higher degree of correlation with mortality and morbidity (measured as arm function, leg function, and activities of daily living) when cortical (n = 118) and lacunar (n = 58) infarcts were pooled compared with when they were assessed separately. For intracerebral hemorrhage (n = 76), admission glucose level correlated with mortality but not morbidity. This trend persisted despite exclusion of diabetic patients. These results are consistent with previous observations of a correlation between a high admission glucose level and the severity of stroke. The importance of segregating cortical from lacunar infarcts, two groups with a different natural history and prognosis, in any future analysis is emphasized.