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Acute isolated capsular stroke
Clinical Neurology and Neurosurgery 107 (2005) 88–94
Acute isolated capsular stroke A clinical study of 148 cases Adrià Arboix a,∗ , Mar´ıa Mart´ınez-Rebollar a , Montserrat Oliveres a , Luis Garc´ıa-Eroles b , Joan Massons a , Cecilia Targa a a
Acute Stroke Unit, Department of Neurology, Hospital del Sagrat Cor, Viladomat 288, E-08029 Barcelona, Spain b Intensive Care Unit, Hospital del Sagrat Cor, Viladomat 288, E-08029 Barcelona, Spain Received in revised form 29 October 2003; accepted 24 November 2003
Abstract 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. © 2003 Elsevier B.V. All rights reserved. Keywords: Capsular stroke; Capsular infarction; Lacunar infarct; Pure motor hemiparesis; Sensorimotor stroke
1. Introduction Isolated internal capsule stroke has been poorly investigated [1] and little is known about its natural history mainly regarding clinical presentation and outcome. Moreover, risk factor profile and prognostic differences between capsular infarcts and capsular hemorrhages are unclear. In case of a similar risk factor profile, then it may be suggested that both disorders may have the same underlying vascular pathology. This is important because although capsular stroke may be seriously disabling, the case fatality rate is low [2] and, therefore, informative autopsy studies are very rare. To contribute to the knowledge of acute isolated capsular stroke, a study based on data collected in a prospective stroke registry was designed with the following purposes: (1) to assess whether there were differences between hemorrhagic and ischemic capsular stroke with regard to risk factor pro∗
Corresponding author. Tel.: +34-93-4948940; fax: +34-93-4948906. E-mail address: [email protected] (A. Arboix).
0303-8467/$ – see front matter © 2003 Elsevier B.V. All rights reserved. doi:10.1016/j.clineuro.2003.11.003
file, clinical features, and outcome data, and (2) to compare capsular strokes with all other (non-capsular) strokes, that is, hemorrhagic capsular stroke versus the remaining intracerebral hemorrhages and capsular infarction versus the remaining ischemic strokes.
2. Patients and methods Between January 1986 and December 1995, data of 2000 acute stroke patients admitted consecutively to the Department of Neurology of Sagrat Cor Hospital of Barcelona, were collected prospectively in a stroke registry [3]. The Department of Neurology has 25 beds and an acute stroke unit. Intensive care unit beds are also available. Our institution is an acute-care 350-bed teaching hospital in the city of Barcelona serving a population of approximately 250 000. Subtypes of stroke were classified according to the Cerebrovascular Study Group of the Spanish Neurological Society [4], which is similar to the National Institute of Neuro-
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logical Disorders and Stroke Classification [5], and are those used by our group in previous studies [6,7]. Subtypes of stroke included transient ischemic attack (TIA) (n = 239), atherothrombotic stroke (n = 452), lacunar stroke (n = 374), cardioembolic infarction (n = 347), infarction of undetermined origin (n = 224), infarction of unusual cause (n = 76), intracerebral hemorrhage (n = 229), subarachnoid hemorrhage (n = 35), spontaneous subdural hematoma (n = 23), and spontaneous epidural hematoma (n = 1). Definitions of cerebrovascular risk factors and lacunar syndromes (pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand, and atypical lacunar syndromes) were those used in previous studies [8–12]. Lacunar syndrome was diagnosed in 440 patients (pure motor stroke 222, pure sensory stroke 72, sensorimotor stroke 59, ataxic hemiparesis 17, dysarthria-clumsy hand 25, and atypical lacunar syndrome 45). Atypical lacunar syndromes included isolated dysarthria in 24 patients, hemichorea/hemiballismus in five, unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarction, pure motor hemiparesis with transient subcortical aphasia in four, pure motor hemiparesis with transient internuclear ophthalmoplegia in four, and isolated hemiataxia in three. For the purpose of this hospital-based prospective study, 148 patients who presented on neuroimaging studies an isolated internal capsule ischemic or hemorrhagic lesion located in the anterior limb and/or genu and/or posterior limb of the internal capsule without extension into the thalamus or the basal ganglia (Figs. 1 and 2) that can be correlated to a focal neurological deficit of more than 24 h duration were included. A total of 124 patients had an acute isolated internal capsule infarct (maximum volume of infarct <15 mm) in the vascular territory of the perforating cerebral arteries, therefore secondary to a presumed small-vessel disease. The remaining 24 patients had capsular hemorrhages (Fig. 2). Isolated capsular topography was defined according to tem-
plates of the vascular territories defined by Ghika et al. [13]. The study was approved by the institutional review committee. All patients were admitted to the hospital within 48 h of the onset of symptoms. On admission, demographic characteristics, salient features of clinical and neurological examination and results of routine laboratory tests (blood cell count, biochemical profile, serum electrolytes, urinalysis), chest radiography, and twelve-lead electrocardiography were recorded. Neurological examination was performed every day after admission to the hospital. In all patients, brain computed tomography (CT) scan was performed within the first week of hospital admission. Overall, 22.1% of patients were studied by MRI and angio-MRI. Other investigations included Doppler ultrasonography of the supra-aortic trunks in 14.5%, arterial digital subtraction angiography in 16.2%, two-dimensional echocardiography in 15.5%, and lumbar puncture in 4.8%. For each patient, demographic data, vascular risk factors, clinical features, neuroimaging findings, and outcome were recorded. Variables were dichotomized as present versus absent and included the following: demographic data (age, sex); anamnestic findings (history of hypertension, diabetes, myocardial infarction or angina, rheumatic heart disease, congestive heart failure, atrial fibrillation, smoking habit (>20 cigarettes per day), alcohol abuse (>80 g per day), intermittent claudication, TIA, previous cerebral infarction, hyperlipidemia, nephropathy, cirrhosis or chronic liver disease, chronic obstructive pulmonary disease (COPD), and age of 85 years or older), clinical variables (sudden onset of symptoms (minute), acute onset (hour), subacute onset (day), headache, dizziness, seizures, nausea or vomiting, altered consciousness (drowsy, stuporous, comatose), limb weakness (hemiparesis or hemiplegia, Babinski’s sign not mandatory), sensory symptoms, hemianopia, aphasia or dysarthria, ataxia, cranial nerve palsy, lacunar syndrome,
Fig. 1. Left: the brain CT scan shows a cerebral infarction in the anterior limb of the left internal capsule in a patient with a dysarthria-clumsy hand syndrome. Right: T2-weighed conventional MRI showing a cerebral infarct in the genu of the right internal capsule in a patient with contralateral isolated central facial palsy.
Fig. 2. Left: T2-weighed conventional MRI showing a cerebral infarction in the posterior limb of the left internal capsule in a patient with pure motor hemiparesis. Right: the brain CT scan shows an intracerebral hemorrhage in the posterior limb of the right internal capsule in a patient with sensorimotor stroke.
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pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand, and atypical lacunar syndromes; neuroimaging variables in relation to the site of lesion (frontal, parietal, temporal, occipital, internal capsule, cerebellum, mesencephalon, pons, middle cerebral artery topography, and basilar artery topography); and outcome variables. Outcome data included cardiac events (myocardial infarction, heart failure, tachyarrhythmia), respiratory events (pulmonary embolism, atelectasis or respiratory infection), vascular events, infectious complications, and in-hospital mortality. 2.1. Statistical methods Demographic characteristics, vascular risk factors, clinical variables, and outcome data for patients with capsular hemorrhage were compared with those of the remaining 205 patients with non-capsular intracerebral hemorrhage. The same comparison was made between the groups of capsular infarction and the remaining 1349 patients with cerebral infarction as well as between the subtypes of capsular hemorrhage and capsular infarction. The student’s t-test and the chi-square (χ2 ) test (with Yate’s correction when necessary) were used for univariate analysis. Statistical significance was set at P < 0.05. To determine the independent predictive value of variables on hemorrhagic capsular stroke (versus capsular infarct and versus the remaining cases of intracerebral hemorrhage) and on capsular infarct (versus the remaining cases of cerebral infarction), statistically significant variables in the univariate analysis plus age (used as continuous variable with a constant odds ratio (OR) for each year) and sex, were studied in three multiple linear regression models, with a total of 8, 18, and 9 variables, respectively. Capsular hemorrhage or capsular infarct coded as absent: 0, present: 1, were the dependent variables. The level of significance to remain in the models was 0.15. The tolerance level was established as 0.0001. The maximum likelihood approach was used to estimate weights of the logistic parameters [14]. Odds ratios and 95% confidence intervals (CI) were calculated from the beta coefficients and standard errors. The hypothesis that the logistic model adequately fit the data was tested by means of the goodness of fit χ2 test [15]. The SPSS-PC+ [16] and BMDP [17] computer programs were used for statistical analysis.
3. Results Isolated capsular stroke accounted for 8.4% of all acute stroke patients in our stroke registry as well as for 10.5% (24/229) of intracerebral hemorrhages and 8.4% (124/1473) of ischemic stroke. The mean (S.D.) age of the patients was 71.2 (10.8) years and 59.5% were men. Main vascular risk factors included hypertension in 73% of patients and diabetes mellitus in 28.4%. In 39% of cases, a sudden (minute) stroke onset was recorded. Onset of neuro-
logical deficit occurred suddenly (minute) in 58 (39%) patients, acutely (hour) in 82 (55.5%), and subacutely (day) in 5 (3.5%). In the remaining three patients, onset of symptoms was unknown. Carotid artery stenosis was observed in one patient with capsular hemorrhage (4.2%) and in 10 patients with capsular infarction (8%). Eighty-seven percent of patients presented with a lacunar syndrome, mostly pure motor hemiparesis (59%) or sensorimotor stroke (12.5%). The location of lesions included the anterior limb in 12% of patients, genu in 3%, and posterior limb in 85% (Figs. 1 and 2). Absence of neurological deficit at hospital discharge was observed in 21% of patients. The mean length of stay was 15.5 days. The in-hospital mortality was 3.4%.
4. Hemorrhagic versus ischemic capsular stroke As shown in Table 1, there were no differences between both subtypes with regard to demographic data and vascular risk factors. However, capsular hemorrhages were more severe than capsular infarctions as shown by significantly higher percentages of patients with sudden onset, headache, nausea and vomiting, sensory symptoms, and altered consciousness on presentation, significantly higher in-hospital mortality and length of stay, and lower number of patients with lacunar stroke and free of functional deficit at discharge. The mortality rate in patients with capsular hemorrhage was 20.8% (five out of 24) compared to 0% in patients with capsular infarction. Spontaneous early intracerebral hemorrhage growth occurred in three of the five patients who died. In the multivariate analysis, limb weakness (OR = 32.38), sudden onset (OR = 8.62), and sensory symptoms (OR = 4.26) were independent factors significantly associated with capsular hemorrhage, whereas pure motor hemiparesis (OR = 0.07) was independently associated with capsular infarction (Table 2).
5. Hemorrhagic capsular stroke versus non-capsular hemorrhages Capsular hemorrhages presented more frequently as a lacunar syndrome, mainly in the form of pure motor hemiparesis and sensorimotor stroke, with hypertension, peripheral vascular disease, limb weakness, and speech disturbances being also significantly more frequent (Table 3). After multivariate analysis, only lacunar syndrome (OR = 21.30), dysarthria or aphasia (OR = 8.13), and peripheral vascular disease (OR = 6.56) were significantly associated with capsular hemorrhage (Table 2).
6. Capsular infarcts versus non-capsular cerebral infarctions In patients with capsular infarct, there was a significantly higher occurrence of hypertension, diabetes, previous intrac-
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Table 1 Comparison of demographic features, vascular risk factors, clinical variables, and outcome between hemorrhagic and ischemic capsular strokes Data
Capsular hemorrhage, n = 24
Male sex Age (year)a
16 (66.7) 69.5 (11.4)
72 (58.1) 72.2 (10.7)
NS NS
21 4 1 2 1 1 2
87 38 16 8 4 14 21 4 5 6 7 4 2 32 17
(70.2) (30.6) (12.9) (6.5) (3.2) (11.3) (16.9) (3.2) (4) (4.8) (5.6) (3.2) (1.6) (25.8) (13.7)
NS NS NS NS NS NS NS NS NS NS NS NS NS NS NS
(75) (37.5) (20.8) (100) (66.7) (58.3) (37.5)
40 10 1 108 20 56
(32.3) (8.1) (0.8) (87.1) (16.1) (45.2)
<0.01 <0.01 <0.01 NS <0.01 NS <0.001
5 (21) 3 (12.5)
124 84 2 16 3 10 9
(100) (67.7) (1.6) (12.9) (2.4) (8.1) (7.3)
<0.001 <0.01 NS NS NS NS NS
Vascular risk factors Hypertension Diabetes mellitus Ischemic heart disease Atrial fibrillation Heart failure TIAs Previous cerebral infarct Previous intracerebral hematoma Chronic obstructive lung disease Peripheral vascular disease Obesity Alcohol abuse (>80 g per day) Chronic liver disease Hyperlipidemia Cigarette smoking (>20 per day) Clinical variables Sudden onset Headache Nausea, vomiting Limb weakness Sensory symptoms Dysarthria, aphasia Altered consciousness Lacunar syndrome Pure motor hemiparesis Pure sensory stroke Sensorimotor syndrome Ataxic hemiparesis Dysarthria-clumsy hand Atypical lacunar syndromes Outcome Respiratory events Infectious complications Absence of deficit at discharge Length of stay (day)a In-hospital mortality a
(87.5) (16.7) (4.2) (8.3) (4.2) (4.2) (8.3)
2 (8.3) 4 (16.7) 2 (8.3)
4 (16.7) 5 (20.8) 18 9 5 24 16 14 9
2 (8.5)
3 (12.5) 6 (25) 1 (4.2) 27.7 (19.9) 5 (20.8)
Capsular infarction, n = 124
1 (0.8) 3 (2.4) 30 (24.2) 12.6 (8.04)
P value
<0.05 <0.01 <0.05 <0.01 <0.01
Mean (S.D.).
erebral hematoma, and hyperlipidemia as well as a significantly lower frequency of atrial fibrillation, valvular heart disease, severe functional impairment at hospital discharge, length of hospital stay, and in-hospital mortality (Table 4). After multivariate analysis (Table 2), pure motor hemiparesis (OR = 132.45), dysarthria-clumsy hand syndrome (OR = 131.51), sensorimotor stroke (OR = 78.64), and atypical lacunar syndromes (OR = 56.74) were independent factors significantly associated with capsular infarct.
7. Discussion In our stroke registry, capsular strokes of ischemic origin are more frequent than capsular hemorrhages (84% versus 16%). On the other hand, approximately one out of each
12 patients with acute ischemic stroke and one out of each 10 patients with intracerebral hemorrhage had a capsular stroke. There are a few studies exclusively focused on capsular strokes because the internal capsule is a usual topography in the clinical series of lacunar syndromes [5,18–20]. Accordingly, in these studies, clinical data of patients with capsular stroke are analyzed together with other topographies that are characteristic of lacunar infarctions, particularly the basal ganglia, thalamus, and ventral part of the pons. By contrast, in the present study, we selected the internal capsule as the lesion location and investigated clinical features and outcome data of ischemic and hemorrhagic capsular strokes. Results of the multivariate analysis indicate that capsular hemorrhages may show differential clinical data as compared with the remaining intracerebral hemorrhages includ-
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Table 2 Independent predictive value of different variables on isolated capsular stroke in three logistic regression models β
Logistic regression models
S.E. (β)
Odds ratio (95% CI)
Hemorrhagic vs. ischemic capsular stroke Demographic, vascular risk factors, clinical variables, and lacunar syndromesa Limb weakness 3.4776 Sudden onset 2.1539 Sensory symptoms 1.4497 Pure motor hemiparesis −2.6584
1.4297 0.6639 0.6639 0.8614
32.38 (1.96–533.64) 8.62 (2.35–31.62) 4.26 (1.16–15.66) 0.07 (0.01–0.38)
Hemorrhagic capsular stroke vs. remaining intracerebral hemorrhages Demographic, vascular risk factors, clinical variables, and lacunar syndromesb Lacunar syndrome 3.0587 Dysarthria, aphasia 2.0952 Peripheral vascular disease 1.8810
0.7232 0.6007 0.7980
21.30 (5.16–87.90) 8.13 (2.50–26.38) 6.56 (1.37–31.35)
Ischemic capsular stroke vs. remaining cerebral infarcts Demographic, vascular risk factors, clinical variables, and lacunar syndromesc Pure motor hemiparesis 4.8862 Dysarthria-clumsy hand 4.8791 Sensorimotor stroke 4.3649 Atypical lacunar syndromes 4.0385 Sudden onset −0.5618 Atrial fibrillation −1.0003
0.4712 0.6126 0.5423 0.5899 0.2430 0.4122
132.45 (52.60–333.6) 131.51 (39.58–436.9) 78.64 (27.17–227.6) 56.74 (17.86–180.3) 0.57 (0.35–0.92) 0.37 (0.16–0.82)
a b c
β = −2.7327; S.E. (β) = 0.6902; goodness of fit χ2 = 10.5510; d.f. = 5; P = 0.0610. Area under the ROC curve = 0.903. β = −3.7524; S.E. (β) = 0.5365; goodness of fit χ2 = 0.7140; d.f. = 2, P = 0.6998. Area under the ROC curve = 0.810. β = −4.9689; S.E. (β) = 0.4573; goodness of fit χ2 = 1.0170; d.f. = 4; P = 0.9072. Area under the ROC curve = 0.929.
ing the presence of lacunar syndromes, speech disturbances, and peripheral vascular disease. Five patients with capsular hemorrhage had a lacunar syndrome (21%) and pure motor hemiparesis was diagnosed in three of them. These findings are consisted with the study of Weisberg and Wall [2] who reported pure motor hemiparesis in seven of 10 patients as well as with other reports indicating that a small hematoma
of subcortical topography in the internal capsule, but also in the basal ganglia and more infrequently in the pons, may cause a lacunar syndrome [21–23]. Interruption of the corticolingual pathways in the internal capsule may explain the higher frequency of dysarthria [23–25]. On the other hand, the higher occurrence of peripheral vascular disease may be related to the higher percentage of hypertension (87.5%
Table 3 Comparison of demographic features, vascular risk factors, clinical variables, and outcome between hemorrhagic capsular stroke and the remaining intracerebral hemorrhages Data
Capsular hemorrhage, n = 24
Other intracerebral hematomas, n = 205
Male sex Age (year)a
16 (66.7) 69.5 (11.4)
106 (51.7) 72.2 (10.7)
Vascular risk factors Hypertension Peripheral vascular disease
21 (87.5) 4 (16.7)
118 (57.6) 7 (3.4)
<0.005 <0.05
Clinical variables Limb weakness Dysarthria, aphasia
24 (100) 14 (58.3)
153 (86.4) 62 (30.2)
<0.01 <0.01
Lacunar syndrome Pure motor hemiparesis Pure sensory stroke Sensorimotor syndrome Ataxic hemiparesis Dysarthria-clumsy hand Atypical lacunar syndromes Outcome Absence of deficit at discharge Length of stay (day)a In-hospital mortality a
Mean (S.D.).
5 (21) 3 (12.5) 2 (8.5)
1 (4.2) 27.7 (19.9) 5 (20.8)
12 6 3 3
(5.8) (2.9) (1.5) (1.5)
7 (3.4) 21.6 (24.5) 65 (31.7)
P value NS NS
<0.05 NS NS <0.05
NS NS NS
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Table 4 Comparison of demographic features, vascular risk factors, clinical variables, and outcome between capsular infarction and the remaining cerebral infarcts Capsular infarction, n = 124
Data Male sex Age (year)a Vascular risk factors Hypertension Diabetes mellitus Valvular heart disease Atrial fibrillation Previous intracerebral hematoma Hyperlipidemia Clinical variables Sudden onset Nausea, vomiting Limb weakness Altered consciousness Sensory symptoms Lacunar syndrome Pure motor hemiparesis Pure sensory stroke Sensorimotor syndrome Ataxic hemiparesis Dysarthria-clumsy hand Atypical lacunar syndromes Outcome Respiratory events Infectious events Severe deficit at discharge Length of stay (day)a In-hospital mortality a
Other intracerebral infarcts, n = 1349
P value
72 (58.1) 73.02 (12.6)
689 (51.1) 72.2 (10.7)
87 (70.2) 38 (30.6)
681 257 77 396 8 215
(50.5) (19.1) (5.7) (29.4) (0.6) (15.9)
<0.001 <0.005 <0.001 <0.001 <0.05 <0.01
713 96 1016 261 588
(52.9) (7.1) (75.3) (19.3) (43.6)
<0.001 <0.005 <0.05 <0.001 <0.001
298 128 67 38 14 15 36
(22.1) (9.5) (5) (2.8) (1) (1.1) (2.7)
<0.001 <0.001 NS <0.001 NS <0.001 <0.05
8 (6.5) 4 (3.2) 32 (25.8) 40 (32.3) 1 (0.8) 108 (87.1) 20 (16.1) 124 84 2 16 3 10 9
(100) (67.7) (1.6) (12.9) (2.4) (8.1) (7.3)
1 (0.8) 3 (2.4) 3 (2.4) 12.6 (8.04)
128 (9.5) 171 (12.7) 154 (11.4) 19.2 (24.9) 226 (16.8)
NS NS
<0.001 <0.001 <0.001 <0.01 <0.001
Mean (S.D.).
versus 57.6%) as compared with cerebral hematomas of other topographies. With regard to prognosis, significant differences in the mean length of stay, neurological impairment at discharge, and in-hospital mortality between capsular hemorrhages and other intracerebral hemorrhages were not observed. Significant predictors of ischemic capsular stroke as compared with the remaining ischemic strokes included pure motor hemiparesis, dysarthria-clumsy hand syndrome, sensorimotor stroke, and atypical lacunar syndromes. This may be explained by the fact that isolated internal capsule infarcts are usually lacunar infarctions responsible for a lacunar syndrome [26,27] and because this location is the habitual topography of this stroke subtype. On the other hand, sudden stroke onset and atrial fibrillation would be more characteristic features of cardioembolic stroke [3,28,29]. In the comparison of capsular hemorrhage with capsular infarct, limb weakness, sudden onset, and sensory symptoms were independent predictors of hemorrhagic capsular stroke. The high frequency of limb weakness (in 100% of cases of capsular hemorrhages) may be due to disruption of the pyramidal tract and the higher occurrence of sensory symptoms by the mass effect caused by the hematoma as well as by compression of the adjacent thalamocortical sensory projection. Sudden onset is also more characteristic
of capsular hemorrhage. This finding is in agreement with the study of Landi et al. [30] in which non-sudden onset of symptoms was found in 41% of lacunar infarcts. The more favorable prognosis of capsular infarcts in respect to the remaining ischemic strokes and to capsular hemorrhages was manifested by a shorter mean length of stay in hospital, lower number of patients with severe functional impairment at discharge, and by no case of death in the hospital. Ultra early intracerebral hemorrhage growth occurred in 38% of patients within 3 h of symptom onset [31]. Patients with hematoma growth had early neurological deterioration and increased mortality [32]. Risk factors for early hematoma growth included history of cerebral infarct, hypertension in the setting of hyperglycemia, and depressed level of consciousness [31]—factors that were all present in our patients. There appears to be no impact of hemorrhage location of the frequency of hematoma growth. Early hematoma growth results from persistent bleeding or rebleeding from a single arteriolar rupture or may result from bleeding into a “penumbra” of damaged and congested brain tissue immediately surrounding a hematoma [31]. In a previous study [10], we found that history of intracerebral hemorrhage was an independent predictor of lacunar infarction, which indirectly suggested that lacunar infarcts and subcortical intracerebral hemorrhages may have
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the same arterial pathological substrate. The present study confirms that capsular infarcts and capsular hemorrhages had an identical vascular risk factor profile. This finding may provide indirect evidence of a similar underlying small-vessel disease in both conditions. Changes induced by hypertension and by other vascular risk factors on small penetrating arteries may load to occlusion causing a capsular infarct or to arterial rupture causing intracerebral capsular hemorrhage.
Acknowledgements We thank Drs. E. Comes, M. Balcells, and M. Sánchez for their assistance in the study, and Dr. Marta Pulido for editing the manuscript and editorial assistance.
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Acute isolated capsular stroke A clinical study of 148 cases Adrià Arboix a,∗ , Mar´ıa Mart´ınez-Rebollar a , Montserrat Oliveres a , Luis Garc´ıa-Eroles b , Joan Massons a , Cecilia Targa a a
Acute Stroke Unit, Department of Neurology, Hospital del Sagrat Cor, Viladomat 288, E-08029 Barcelona, Spain b Intensive Care Unit, Hospital del Sagrat Cor, Viladomat 288, E-08029 Barcelona, Spain Received in revised form 29 October 2003; accepted 24 November 2003
Abstract 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. © 2003 Elsevier B.V. All rights reserved. Keywords: Capsular stroke; Capsular infarction; Lacunar infarct; Pure motor hemiparesis; Sensorimotor stroke
1. Introduction Isolated internal capsule stroke has been poorly investigated [1] and little is known about its natural history mainly regarding clinical presentation and outcome. Moreover, risk factor profile and prognostic differences between capsular infarcts and capsular hemorrhages are unclear. In case of a similar risk factor profile, then it may be suggested that both disorders may have the same underlying vascular pathology. This is important because although capsular stroke may be seriously disabling, the case fatality rate is low [2] and, therefore, informative autopsy studies are very rare. To contribute to the knowledge of acute isolated capsular stroke, a study based on data collected in a prospective stroke registry was designed with the following purposes: (1) to assess whether there were differences between hemorrhagic and ischemic capsular stroke with regard to risk factor pro∗
Corresponding author. Tel.: +34-93-4948940; fax: +34-93-4948906. E-mail address: [email protected] (A. Arboix).
0303-8467/$ – see front matter © 2003 Elsevier B.V. All rights reserved. doi:10.1016/j.clineuro.2003.11.003
file, clinical features, and outcome data, and (2) to compare capsular strokes with all other (non-capsular) strokes, that is, hemorrhagic capsular stroke versus the remaining intracerebral hemorrhages and capsular infarction versus the remaining ischemic strokes.
2. Patients and methods Between January 1986 and December 1995, data of 2000 acute stroke patients admitted consecutively to the Department of Neurology of Sagrat Cor Hospital of Barcelona, were collected prospectively in a stroke registry [3]. The Department of Neurology has 25 beds and an acute stroke unit. Intensive care unit beds are also available. Our institution is an acute-care 350-bed teaching hospital in the city of Barcelona serving a population of approximately 250 000. Subtypes of stroke were classified according to the Cerebrovascular Study Group of the Spanish Neurological Society [4], which is similar to the National Institute of Neuro-
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logical Disorders and Stroke Classification [5], and are those used by our group in previous studies [6,7]. Subtypes of stroke included transient ischemic attack (TIA) (n = 239), atherothrombotic stroke (n = 452), lacunar stroke (n = 374), cardioembolic infarction (n = 347), infarction of undetermined origin (n = 224), infarction of unusual cause (n = 76), intracerebral hemorrhage (n = 229), subarachnoid hemorrhage (n = 35), spontaneous subdural hematoma (n = 23), and spontaneous epidural hematoma (n = 1). Definitions of cerebrovascular risk factors and lacunar syndromes (pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand, and atypical lacunar syndromes) were those used in previous studies [8–12]. Lacunar syndrome was diagnosed in 440 patients (pure motor stroke 222, pure sensory stroke 72, sensorimotor stroke 59, ataxic hemiparesis 17, dysarthria-clumsy hand 25, and atypical lacunar syndrome 45). Atypical lacunar syndromes included isolated dysarthria in 24 patients, hemichorea/hemiballismus in five, unilateral (n = 2) or bilateral (n = 3) paramedian thalamic infarction, pure motor hemiparesis with transient subcortical aphasia in four, pure motor hemiparesis with transient internuclear ophthalmoplegia in four, and isolated hemiataxia in three. For the purpose of this hospital-based prospective study, 148 patients who presented on neuroimaging studies an isolated internal capsule ischemic or hemorrhagic lesion located in the anterior limb and/or genu and/or posterior limb of the internal capsule without extension into the thalamus or the basal ganglia (Figs. 1 and 2) that can be correlated to a focal neurological deficit of more than 24 h duration were included. A total of 124 patients had an acute isolated internal capsule infarct (maximum volume of infarct <15 mm) in the vascular territory of the perforating cerebral arteries, therefore secondary to a presumed small-vessel disease. The remaining 24 patients had capsular hemorrhages (Fig. 2). Isolated capsular topography was defined according to tem-
plates of the vascular territories defined by Ghika et al. [13]. The study was approved by the institutional review committee. All patients were admitted to the hospital within 48 h of the onset of symptoms. On admission, demographic characteristics, salient features of clinical and neurological examination and results of routine laboratory tests (blood cell count, biochemical profile, serum electrolytes, urinalysis), chest radiography, and twelve-lead electrocardiography were recorded. Neurological examination was performed every day after admission to the hospital. In all patients, brain computed tomography (CT) scan was performed within the first week of hospital admission. Overall, 22.1% of patients were studied by MRI and angio-MRI. Other investigations included Doppler ultrasonography of the supra-aortic trunks in 14.5%, arterial digital subtraction angiography in 16.2%, two-dimensional echocardiography in 15.5%, and lumbar puncture in 4.8%. For each patient, demographic data, vascular risk factors, clinical features, neuroimaging findings, and outcome were recorded. Variables were dichotomized as present versus absent and included the following: demographic data (age, sex); anamnestic findings (history of hypertension, diabetes, myocardial infarction or angina, rheumatic heart disease, congestive heart failure, atrial fibrillation, smoking habit (>20 cigarettes per day), alcohol abuse (>80 g per day), intermittent claudication, TIA, previous cerebral infarction, hyperlipidemia, nephropathy, cirrhosis or chronic liver disease, chronic obstructive pulmonary disease (COPD), and age of 85 years or older), clinical variables (sudden onset of symptoms (minute), acute onset (hour), subacute onset (day), headache, dizziness, seizures, nausea or vomiting, altered consciousness (drowsy, stuporous, comatose), limb weakness (hemiparesis or hemiplegia, Babinski’s sign not mandatory), sensory symptoms, hemianopia, aphasia or dysarthria, ataxia, cranial nerve palsy, lacunar syndrome,
Fig. 1. Left: the brain CT scan shows a cerebral infarction in the anterior limb of the left internal capsule in a patient with a dysarthria-clumsy hand syndrome. Right: T2-weighed conventional MRI showing a cerebral infarct in the genu of the right internal capsule in a patient with contralateral isolated central facial palsy.
Fig. 2. Left: T2-weighed conventional MRI showing a cerebral infarction in the posterior limb of the left internal capsule in a patient with pure motor hemiparesis. Right: the brain CT scan shows an intracerebral hemorrhage in the posterior limb of the right internal capsule in a patient with sensorimotor stroke.
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pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria-clumsy hand, and atypical lacunar syndromes; neuroimaging variables in relation to the site of lesion (frontal, parietal, temporal, occipital, internal capsule, cerebellum, mesencephalon, pons, middle cerebral artery topography, and basilar artery topography); and outcome variables. Outcome data included cardiac events (myocardial infarction, heart failure, tachyarrhythmia), respiratory events (pulmonary embolism, atelectasis or respiratory infection), vascular events, infectious complications, and in-hospital mortality. 2.1. Statistical methods Demographic characteristics, vascular risk factors, clinical variables, and outcome data for patients with capsular hemorrhage were compared with those of the remaining 205 patients with non-capsular intracerebral hemorrhage. The same comparison was made between the groups of capsular infarction and the remaining 1349 patients with cerebral infarction as well as between the subtypes of capsular hemorrhage and capsular infarction. The student’s t-test and the chi-square (χ2 ) test (with Yate’s correction when necessary) were used for univariate analysis. Statistical significance was set at P < 0.05. To determine the independent predictive value of variables on hemorrhagic capsular stroke (versus capsular infarct and versus the remaining cases of intracerebral hemorrhage) and on capsular infarct (versus the remaining cases of cerebral infarction), statistically significant variables in the univariate analysis plus age (used as continuous variable with a constant odds ratio (OR) for each year) and sex, were studied in three multiple linear regression models, with a total of 8, 18, and 9 variables, respectively. Capsular hemorrhage or capsular infarct coded as absent: 0, present: 1, were the dependent variables. The level of significance to remain in the models was 0.15. The tolerance level was established as 0.0001. The maximum likelihood approach was used to estimate weights of the logistic parameters [14]. Odds ratios and 95% confidence intervals (CI) were calculated from the beta coefficients and standard errors. The hypothesis that the logistic model adequately fit the data was tested by means of the goodness of fit χ2 test [15]. The SPSS-PC+ [16] and BMDP [17] computer programs were used for statistical analysis.
3. Results Isolated capsular stroke accounted for 8.4% of all acute stroke patients in our stroke registry as well as for 10.5% (24/229) of intracerebral hemorrhages and 8.4% (124/1473) of ischemic stroke. The mean (S.D.) age of the patients was 71.2 (10.8) years and 59.5% were men. Main vascular risk factors included hypertension in 73% of patients and diabetes mellitus in 28.4%. In 39% of cases, a sudden (minute) stroke onset was recorded. Onset of neuro-
logical deficit occurred suddenly (minute) in 58 (39%) patients, acutely (hour) in 82 (55.5%), and subacutely (day) in 5 (3.5%). In the remaining three patients, onset of symptoms was unknown. Carotid artery stenosis was observed in one patient with capsular hemorrhage (4.2%) and in 10 patients with capsular infarction (8%). Eighty-seven percent of patients presented with a lacunar syndrome, mostly pure motor hemiparesis (59%) or sensorimotor stroke (12.5%). The location of lesions included the anterior limb in 12% of patients, genu in 3%, and posterior limb in 85% (Figs. 1 and 2). Absence of neurological deficit at hospital discharge was observed in 21% of patients. The mean length of stay was 15.5 days. The in-hospital mortality was 3.4%.
4. Hemorrhagic versus ischemic capsular stroke As shown in Table 1, there were no differences between both subtypes with regard to demographic data and vascular risk factors. However, capsular hemorrhages were more severe than capsular infarctions as shown by significantly higher percentages of patients with sudden onset, headache, nausea and vomiting, sensory symptoms, and altered consciousness on presentation, significantly higher in-hospital mortality and length of stay, and lower number of patients with lacunar stroke and free of functional deficit at discharge. The mortality rate in patients with capsular hemorrhage was 20.8% (five out of 24) compared to 0% in patients with capsular infarction. Spontaneous early intracerebral hemorrhage growth occurred in three of the five patients who died. In the multivariate analysis, limb weakness (OR = 32.38), sudden onset (OR = 8.62), and sensory symptoms (OR = 4.26) were independent factors significantly associated with capsular hemorrhage, whereas pure motor hemiparesis (OR = 0.07) was independently associated with capsular infarction (Table 2).
5. Hemorrhagic capsular stroke versus non-capsular hemorrhages Capsular hemorrhages presented more frequently as a lacunar syndrome, mainly in the form of pure motor hemiparesis and sensorimotor stroke, with hypertension, peripheral vascular disease, limb weakness, and speech disturbances being also significantly more frequent (Table 3). After multivariate analysis, only lacunar syndrome (OR = 21.30), dysarthria or aphasia (OR = 8.13), and peripheral vascular disease (OR = 6.56) were significantly associated with capsular hemorrhage (Table 2).
6. Capsular infarcts versus non-capsular cerebral infarctions In patients with capsular infarct, there was a significantly higher occurrence of hypertension, diabetes, previous intrac-
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Table 1 Comparison of demographic features, vascular risk factors, clinical variables, and outcome between hemorrhagic and ischemic capsular strokes Data
Capsular hemorrhage, n = 24
Male sex Age (year)a
16 (66.7) 69.5 (11.4)
72 (58.1) 72.2 (10.7)
NS NS
21 4 1 2 1 1 2
87 38 16 8 4 14 21 4 5 6 7 4 2 32 17
(70.2) (30.6) (12.9) (6.5) (3.2) (11.3) (16.9) (3.2) (4) (4.8) (5.6) (3.2) (1.6) (25.8) (13.7)
NS NS NS NS NS NS NS NS NS NS NS NS NS NS NS
(75) (37.5) (20.8) (100) (66.7) (58.3) (37.5)
40 10 1 108 20 56
(32.3) (8.1) (0.8) (87.1) (16.1) (45.2)
<0.01 <0.01 <0.01 NS <0.01 NS <0.001
5 (21) 3 (12.5)
124 84 2 16 3 10 9
(100) (67.7) (1.6) (12.9) (2.4) (8.1) (7.3)
<0.001 <0.01 NS NS NS NS NS
Vascular risk factors Hypertension Diabetes mellitus Ischemic heart disease Atrial fibrillation Heart failure TIAs Previous cerebral infarct Previous intracerebral hematoma Chronic obstructive lung disease Peripheral vascular disease Obesity Alcohol abuse (>80 g per day) Chronic liver disease Hyperlipidemia Cigarette smoking (>20 per day) Clinical variables Sudden onset Headache Nausea, vomiting Limb weakness Sensory symptoms Dysarthria, aphasia Altered consciousness Lacunar syndrome Pure motor hemiparesis Pure sensory stroke Sensorimotor syndrome Ataxic hemiparesis Dysarthria-clumsy hand Atypical lacunar syndromes Outcome Respiratory events Infectious complications Absence of deficit at discharge Length of stay (day)a In-hospital mortality a
(87.5) (16.7) (4.2) (8.3) (4.2) (4.2) (8.3)
2 (8.3) 4 (16.7) 2 (8.3)
4 (16.7) 5 (20.8) 18 9 5 24 16 14 9
2 (8.5)
3 (12.5) 6 (25) 1 (4.2) 27.7 (19.9) 5 (20.8)
Capsular infarction, n = 124
1 (0.8) 3 (2.4) 30 (24.2) 12.6 (8.04)
P value
<0.05 <0.01 <0.05 <0.01 <0.01
Mean (S.D.).
erebral hematoma, and hyperlipidemia as well as a significantly lower frequency of atrial fibrillation, valvular heart disease, severe functional impairment at hospital discharge, length of hospital stay, and in-hospital mortality (Table 4). After multivariate analysis (Table 2), pure motor hemiparesis (OR = 132.45), dysarthria-clumsy hand syndrome (OR = 131.51), sensorimotor stroke (OR = 78.64), and atypical lacunar syndromes (OR = 56.74) were independent factors significantly associated with capsular infarct.
7. Discussion In our stroke registry, capsular strokes of ischemic origin are more frequent than capsular hemorrhages (84% versus 16%). On the other hand, approximately one out of each
12 patients with acute ischemic stroke and one out of each 10 patients with intracerebral hemorrhage had a capsular stroke. There are a few studies exclusively focused on capsular strokes because the internal capsule is a usual topography in the clinical series of lacunar syndromes [5,18–20]. Accordingly, in these studies, clinical data of patients with capsular stroke are analyzed together with other topographies that are characteristic of lacunar infarctions, particularly the basal ganglia, thalamus, and ventral part of the pons. By contrast, in the present study, we selected the internal capsule as the lesion location and investigated clinical features and outcome data of ischemic and hemorrhagic capsular strokes. Results of the multivariate analysis indicate that capsular hemorrhages may show differential clinical data as compared with the remaining intracerebral hemorrhages includ-
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Table 2 Independent predictive value of different variables on isolated capsular stroke in three logistic regression models β
Logistic regression models
S.E. (β)
Odds ratio (95% CI)
Hemorrhagic vs. ischemic capsular stroke Demographic, vascular risk factors, clinical variables, and lacunar syndromesa Limb weakness 3.4776 Sudden onset 2.1539 Sensory symptoms 1.4497 Pure motor hemiparesis −2.6584
1.4297 0.6639 0.6639 0.8614
32.38 (1.96–533.64) 8.62 (2.35–31.62) 4.26 (1.16–15.66) 0.07 (0.01–0.38)
Hemorrhagic capsular stroke vs. remaining intracerebral hemorrhages Demographic, vascular risk factors, clinical variables, and lacunar syndromesb Lacunar syndrome 3.0587 Dysarthria, aphasia 2.0952 Peripheral vascular disease 1.8810
0.7232 0.6007 0.7980
21.30 (5.16–87.90) 8.13 (2.50–26.38) 6.56 (1.37–31.35)
Ischemic capsular stroke vs. remaining cerebral infarcts Demographic, vascular risk factors, clinical variables, and lacunar syndromesc Pure motor hemiparesis 4.8862 Dysarthria-clumsy hand 4.8791 Sensorimotor stroke 4.3649 Atypical lacunar syndromes 4.0385 Sudden onset −0.5618 Atrial fibrillation −1.0003
0.4712 0.6126 0.5423 0.5899 0.2430 0.4122
132.45 (52.60–333.6) 131.51 (39.58–436.9) 78.64 (27.17–227.6) 56.74 (17.86–180.3) 0.57 (0.35–0.92) 0.37 (0.16–0.82)
a b c
β = −2.7327; S.E. (β) = 0.6902; goodness of fit χ2 = 10.5510; d.f. = 5; P = 0.0610. Area under the ROC curve = 0.903. β = −3.7524; S.E. (β) = 0.5365; goodness of fit χ2 = 0.7140; d.f. = 2, P = 0.6998. Area under the ROC curve = 0.810. β = −4.9689; S.E. (β) = 0.4573; goodness of fit χ2 = 1.0170; d.f. = 4; P = 0.9072. Area under the ROC curve = 0.929.
ing the presence of lacunar syndromes, speech disturbances, and peripheral vascular disease. Five patients with capsular hemorrhage had a lacunar syndrome (21%) and pure motor hemiparesis was diagnosed in three of them. These findings are consisted with the study of Weisberg and Wall [2] who reported pure motor hemiparesis in seven of 10 patients as well as with other reports indicating that a small hematoma
of subcortical topography in the internal capsule, but also in the basal ganglia and more infrequently in the pons, may cause a lacunar syndrome [21–23]. Interruption of the corticolingual pathways in the internal capsule may explain the higher frequency of dysarthria [23–25]. On the other hand, the higher occurrence of peripheral vascular disease may be related to the higher percentage of hypertension (87.5%
Table 3 Comparison of demographic features, vascular risk factors, clinical variables, and outcome between hemorrhagic capsular stroke and the remaining intracerebral hemorrhages Data
Capsular hemorrhage, n = 24
Other intracerebral hematomas, n = 205
Male sex Age (year)a
16 (66.7) 69.5 (11.4)
106 (51.7) 72.2 (10.7)
Vascular risk factors Hypertension Peripheral vascular disease
21 (87.5) 4 (16.7)
118 (57.6) 7 (3.4)
<0.005 <0.05
Clinical variables Limb weakness Dysarthria, aphasia
24 (100) 14 (58.3)
153 (86.4) 62 (30.2)
<0.01 <0.01
Lacunar syndrome Pure motor hemiparesis Pure sensory stroke Sensorimotor syndrome Ataxic hemiparesis Dysarthria-clumsy hand Atypical lacunar syndromes Outcome Absence of deficit at discharge Length of stay (day)a In-hospital mortality a
Mean (S.D.).
5 (21) 3 (12.5) 2 (8.5)
1 (4.2) 27.7 (19.9) 5 (20.8)
12 6 3 3
(5.8) (2.9) (1.5) (1.5)
7 (3.4) 21.6 (24.5) 65 (31.7)
P value NS NS
<0.05 NS NS <0.05
NS NS NS
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Table 4 Comparison of demographic features, vascular risk factors, clinical variables, and outcome between capsular infarction and the remaining cerebral infarcts Capsular infarction, n = 124
Data Male sex Age (year)a Vascular risk factors Hypertension Diabetes mellitus Valvular heart disease Atrial fibrillation Previous intracerebral hematoma Hyperlipidemia Clinical variables Sudden onset Nausea, vomiting Limb weakness Altered consciousness Sensory symptoms Lacunar syndrome Pure motor hemiparesis Pure sensory stroke Sensorimotor syndrome Ataxic hemiparesis Dysarthria-clumsy hand Atypical lacunar syndromes Outcome Respiratory events Infectious events Severe deficit at discharge Length of stay (day)a In-hospital mortality a
Other intracerebral infarcts, n = 1349
P value
72 (58.1) 73.02 (12.6)
689 (51.1) 72.2 (10.7)
87 (70.2) 38 (30.6)
681 257 77 396 8 215
(50.5) (19.1) (5.7) (29.4) (0.6) (15.9)
<0.001 <0.005 <0.001 <0.001 <0.05 <0.01
713 96 1016 261 588
(52.9) (7.1) (75.3) (19.3) (43.6)
<0.001 <0.005 <0.05 <0.001 <0.001
298 128 67 38 14 15 36
(22.1) (9.5) (5) (2.8) (1) (1.1) (2.7)
<0.001 <0.001 NS <0.001 NS <0.001 <0.05
8 (6.5) 4 (3.2) 32 (25.8) 40 (32.3) 1 (0.8) 108 (87.1) 20 (16.1) 124 84 2 16 3 10 9
(100) (67.7) (1.6) (12.9) (2.4) (8.1) (7.3)
1 (0.8) 3 (2.4) 3 (2.4) 12.6 (8.04)
128 (9.5) 171 (12.7) 154 (11.4) 19.2 (24.9) 226 (16.8)
NS NS
<0.001 <0.001 <0.001 <0.01 <0.001
Mean (S.D.).
versus 57.6%) as compared with cerebral hematomas of other topographies. With regard to prognosis, significant differences in the mean length of stay, neurological impairment at discharge, and in-hospital mortality between capsular hemorrhages and other intracerebral hemorrhages were not observed. Significant predictors of ischemic capsular stroke as compared with the remaining ischemic strokes included pure motor hemiparesis, dysarthria-clumsy hand syndrome, sensorimotor stroke, and atypical lacunar syndromes. This may be explained by the fact that isolated internal capsule infarcts are usually lacunar infarctions responsible for a lacunar syndrome [26,27] and because this location is the habitual topography of this stroke subtype. On the other hand, sudden stroke onset and atrial fibrillation would be more characteristic features of cardioembolic stroke [3,28,29]. In the comparison of capsular hemorrhage with capsular infarct, limb weakness, sudden onset, and sensory symptoms were independent predictors of hemorrhagic capsular stroke. The high frequency of limb weakness (in 100% of cases of capsular hemorrhages) may be due to disruption of the pyramidal tract and the higher occurrence of sensory symptoms by the mass effect caused by the hematoma as well as by compression of the adjacent thalamocortical sensory projection. Sudden onset is also more characteristic
of capsular hemorrhage. This finding is in agreement with the study of Landi et al. [30] in which non-sudden onset of symptoms was found in 41% of lacunar infarcts. The more favorable prognosis of capsular infarcts in respect to the remaining ischemic strokes and to capsular hemorrhages was manifested by a shorter mean length of stay in hospital, lower number of patients with severe functional impairment at discharge, and by no case of death in the hospital. Ultra early intracerebral hemorrhage growth occurred in 38% of patients within 3 h of symptom onset [31]. Patients with hematoma growth had early neurological deterioration and increased mortality [32]. Risk factors for early hematoma growth included history of cerebral infarct, hypertension in the setting of hyperglycemia, and depressed level of consciousness [31]—factors that were all present in our patients. There appears to be no impact of hemorrhage location of the frequency of hematoma growth. Early hematoma growth results from persistent bleeding or rebleeding from a single arteriolar rupture or may result from bleeding into a “penumbra” of damaged and congested brain tissue immediately surrounding a hematoma [31]. In a previous study [10], we found that history of intracerebral hemorrhage was an independent predictor of lacunar infarction, which indirectly suggested that lacunar infarcts and subcortical intracerebral hemorrhages may have
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the same arterial pathological substrate. The present study confirms that capsular infarcts and capsular hemorrhages had an identical vascular risk factor profile. This finding may provide indirect evidence of a similar underlying small-vessel disease in both conditions. Changes induced by hypertension and by other vascular risk factors on small penetrating arteries may load to occlusion causing a capsular infarct or to arterial rupture causing intracerebral capsular hemorrhage.
Acknowledgements We thank Drs. E. Comes, M. Balcells, and M. Sánchez for their assistance in the study, and Dr. Marta Pulido for editing the manuscript and editorial assistance.
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