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 »  Abstract
 »  Introduction
 »  Material and methods
 »  Results
 »  Discussion
 »  References

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Year : 2000  |  Volume : 48  |  Issue : 2  |  Page : 116-9

Frequency, clinical features and risk factors of lacunar infarction (data from a stroke registry in South India).


Department of Neurology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, 500082, India.

Correspondence Address:
Department of Neurology, Nizam's Institute of Medical Sciences, Panjagutta, Hyderabad, 500082, India.

  »  Abstract

Analysis of 893 patients of ischaemic stroke in the stroke registry of Nizam's institute of Medical Sciences, Hyderabad is presented. 16% of them had lacunar infarction. The mean age at presentation was 56.9 years and male to female ratio was 3.5:1. The common risk factors included hypertension(62%),diabetes(38%) and smoking(28%). Six percent had an underlying cardiac source of embolism and none had significant (>50%) extracranial carotid atherosclerosis. In 22% of patients, no obvious risk factors could be identified. The frequency of risk factors was similar in patients with lacunar and non- lacunar infarctions. However, patients with lacunar infarction had higher frequency of diabetes and absence of significant (>50%) extracranial carotid artery disease. Pure motor hemiparesis was the presenting syndrome in 45% patients. Ataxic hemiparesis and sensorimotor stroke accounted for 18% each and dysarthria-clumsy hand syndrome for 14%. This study suggests that the frequency, risk factors and clinical profile of lacunar infarction in our stroke registry is similar to most of the western stroke registries.

How to cite this article:
Kaul S, Venketswamy P, Meena A K, Sahay R, Murthy J M. Frequency, clinical features and risk factors of lacunar infarction (data from a stroke registry in South India). Neurol India 2000;48:116


How to cite this URL:
Kaul S, Venketswamy P, Meena A K, Sahay R, Murthy J M. Frequency, clinical features and risk factors of lacunar infarction (data from a stroke registry in South India). Neurol India [serial online] 2000 [cited 2017 Mar 25];48:116. Available from: http://www.neurologyindia.com/text.asp?2000/48/2/116/1563




   »   Introduction Top

Hypertension and diabetes mellitus are frequent risk factors associated with the development of lipohyalinosis and subsequent lacunar infarction.[1],[2],[3],[4] Acceptance of this hypothesis has led some cerebrovascular experts to recommend that no detailed evaluation of a patient is necessary when a diagnosis of lacunar infarction is made.[5],[6] However, the exclusive role of hypertension and diabetes in the genesis of lacunar infarction has been questioned,as these risk factors are not present in all the patients.[7] Other reported aetiologies include middle cerebral artery atherosclerotic disease[8],[9] embolism from a cardiac source[10],[11] and embolism or haemodynamic compromise from a carotid lesion.[12],[13],[14],[15] High incidence of lacunar stroke in certain geographical regions has been attributed to racial and ethnic factors.[16],[17] There is no literature on this subject from the Indian subcontinent. This study is aimed at determining the relative frequency, risk factors, clinical and radiological features of lacunar infarcts in patients with ischaemic strokes seen in a university hospital in south India.


   »   Material and methods Top

Patients registered in the stroke registry of Nizam's Institute of Medical Sciences between January 1993 to December 1997 formed the study material. The total population of the region during the study period was 2,60,89,074 (26.089 million). This hospital is a major neurological centre in Telangana region where patients are either referred by practising physicians or can get registered themselves. The patient population is fairly representative sample of the disease pattern in this region.
The diagnosis of ischaemic stroke was based on the clinical findings and brain computed tomographic (CT) scan. Every patient underwent an electrocardiographic (ECG) examination and transthoracic echocardiogram(TTE). When necessary, patients were subjected to transoesophageal echocardiography(TEE). In the early part of the study, carotid testing was done with doppler carotid flow studies. A haemodynamically significant lesion was identified when there was >5.0 kHz frequency shift on spectral analysis. Subsequently, patients were subjected to real time duplex B-mode ultrasonography of the carotid system. A potential embolic carotid source of stroke was defined as the presence of a haemodynamically significant lesion (>50%) or an ipsilateral severe heterogenous plaque on real time Bmode ultrasonography or a 4.0-5.0 kHz frequency shift on spectral analysis, measured with a 4.0MHz duplex doppler probe.[16]
Stroke subtyping was done according to the criteria adopted by 'stroke data bank' of National Institute of Neurological Disorders and Stroke (NINDS).[18] In particular, lacunar infarct was defined as a focal neurological deficit involving the carotid or vertebrobasilar territory which lasted for more than 24 hours and consisted of one of the following syndromes: pure motor hemiparesis, sensorimotor stroke, dysarthria-clumsy hand syndrome, ataxic hemiparesis or pure hemisensory stroke. In addition,a CT scan of brain following the event had to be without evidence of acute cerebral infarction or show only a low- density lesion of <1.5 cm diameter in a subcortical area of appropriate hemisphere. If there was a disparity between the clinical picture and CT scan done within 72 hours of onset, then the CT scan was repeated and, if necessary, magnetic resonance imaging (MRI) performed. Patients with non- lacunar, large vessel stroke included those with focal neurological deficit in the carotid or vertebrobasilar territory and included cortical or subcortical abnormalities which persisted for more than 24 hours. Additionally a CT scan following the event had to show an appropriate cortical,subcortical or combined lesion of > 1.5 cm diameter in the absence of an obvious cardioembolic source. For inclusion in the category of cardioembolic stroke, at least two of the following criteria were required to be fulfilled: a) sudden onset and maximal neurological focal deficit from the very beginning of the episode, b) brain CT scan showing an ischaemic lesion with features consistent with cardioembolism (haemorrhagic infarct or multiple cortical infarcts), c) presence of an acceptable potential cardiac source of embolism as defined previously by Kittner et al.[19] These criteria include history of valvular surgery, atrial fibrillation, atrial flutter or sick sinus syndrome with or without valvular heart disease, echocardiographic evidence of ventricular aneurysm, mural thrombus, cardiomyopathy, and left ventricular hypokinesis or akinetic region. Risk factor correlations were done between the CT findings and clinical features of lacunar and non - lacunar infarct. Cardioembolic strokes were excluded in this comparison. Chi-Square test was performed for assessing statistical significance. The level of significance was taken as p<0.05.


   »   Results Top

Of the 893 patients of ischaemic strokes,lacunar infarcts accounted for 16% (141 patients), cardioembolic infarcts 9%, and large vessel infarcts 75%. Mean age of the patients with lacunar infarction was 56.9 years (18-84 years). Fourteen patients(10%) were aged less than 40 years. The maximum frequency was in sixth decade. The male:female ratio was 3.5:1. Of risk factors, hypertension accounted for 62%, diabetes for 38%, smoking for 28% and cardioembolism for 6%. Twenty percent of patients had the presence of more than one risk factors. No obvious risk factor could be established in 22% of the patients. The difference in the frequency of various risk factors between patients with lacunar infarcts and non-cardiac, large vessel infarcts was not significant [Table I]. Even though diabetes was found in 53(38%) of patients with lacunar infarction, 36(62%) of them had associated hypertension. The difference in the frequency of diabetes as an isolated risk factor between the two groups was not significant(11% vs 7%).
Of the 141 patients with lacunar infarcts, 43% had pure motor hemiparesis, 18% ataxic hemiparesis, 18% sensorimotor stroke, 14% dysarthria-clumsy hand syndrome and 4% pure sensory stroke [Table II]. Initial CT scan of brain was normal in 26% of patients. Of the patients with pure motor stroke, 33% had infarct in the corona radiata and 29% had in the internal capsule (12% in the anterior limb and 17% in the posterior limb). In patients with sensorimotor stroke, the posterior limb of internal capsule was the site of infarct in 48%; lesions were equally distributed between the anterior limb of internal capsule and pons in patients with ataxic hemiparesis. In patients with dysarthria-clumsy hand syndrome, 25% of the lesions occured in corona radiata. Thalamus showed the lesion in 50% of patients with sensory strokes. Motor deficit was more severe in patients with sensorimotor stroke than in pure motor stroke.



   »   Discussion Top

The relative frequency of lacunar infarcts in our registry was similar to most of the stroke registries from western countries,[20],[21],[22] but was at variance with the reported high frequency (27-30%) from other Asian countries with predominant population of Chinese origin.[16],[17] This has been attributed to ethnic factors.
The frequency and pattern of clinical syndromes in this study was similar to that reported in previous registries from western countries.[20],[21],[22] Of the 17 patients with pure motor hemiparesis due to capsular lesion, the anterior limb was involved in about half, a site least expected to cause pure motor hemiparsis. Similar were the observations by others.[9],[23] The genesis of sensorimotor stroke based on lesions in the posterior limb of internal capsule has been equally puzzling and has been explained by interruption of the thalamo-cortical pathways.[24]
Advancing age is an important risk factor for lacunar infarction.[13],[20],[21],[22] The lower mean age and somewhat higher proportion of patients below 40 years of age in our study probably reflects the lower life expectancy in India compared to western studies (62.6% vs 77 years).[25] The frequency of diabetes was found to be higher than reported earlier in western registries.[20],[21],[22]
However,about two thirds of patients with diabetes had also associated hypertension. When considered as a lone risk factor, diabetes was still more common in lacunar infarctions than large vessel infarctions but the difference was not statistically significant. As diabetes is known to be associated with small vessel arteriopathy, it is reasonable to assume its role as a risk factor for lacunar infarction.[26]
Emboligenic cardiac disease is an unlikely risk factor for lacunar infarction,[27],[28] but it must be stressed that in a small percentage of our patients, high risk cardioembolic sources were found in the absence of other risk factors for stroke. In view of the therapeutic implications, the patients with lacunar stroke should be screened for any underlying cardiac disease, if other established risk factors are absent. However, artery to artery embolus is a very uncommon cause of lacunar stroke and we agree with the earlier suggestions that patients with lacunar infarcts may not require detailed evaluation of carotid arteries.[29],[30]
In conclusion, the frequency,risk factors and clinical profile of lacunar infarctions in our stroke registry is similar to that in most of the western registries.


 

  »   References Top

1.Fisher CM: Lacunes: small, deep cerebral infarcts. Neurology 1965; 15: 774-784.   Back to cited text no. 1    
2.Fisher CM: The arterial lesions underlying lacunes. Acta Neuropathol 1969; 12: 11-15.   Back to cited text no. 2    
3.Fisher CM: Lacunar strokes and infarcts: A review . Neurology 1982; 32: 871-876.   Back to cited text no. 3    
4.Weisberg LA: Diagnostic classification of stroke, especially lacunes. Stroke 1988; 19: 1071-1073.   Back to cited text no. 4    
5.Caplan LR, Stein RW: Small vessel disease. In: Caplan LR, eds. Stroke,Boston:Butterworth 1986; 167-177.   Back to cited text no. 5    
6.Fisher CM, Curry HB: Pure motor hemiplegia of vascular origin. Arch Neurol 1965; 13: 30-44.   Back to cited text no. 6    
7.Millikan C, Futrell N: The fallacy of the lacune hypothesis. Stroke 1990; 21: 1251-1257.   Back to cited text no. 7    
8.Adams HP, Damisio HC, Putman SF et al: Middle cerebral artery occlusion as a cause of isolated subcortical infarction. Stroke 1983; 14: 948-952.   Back to cited text no. 8    
9.Caplan L, Babikian V, Helgason C et al: Occlusive disease of the middle cerebral artery. Neurology 1985; 35: 975-982.   Back to cited text no. 9    
10.Pullicino P, Nelson RF, Kendall BE et al: Small deep infarcts diagnosed on computed tomography. Neurology 1980; 30: 1090- 1096.   Back to cited text no. 10    
11.Ghica J, Bogousslavsky J, Regli F: Infarcts in the territory the deep perforators from the carotid system. Neurology 1989; 39: 507-512.   Back to cited text no. 11    
12.Ringelstein EB, Zeumer H, Angelou D: The pathogenesis of strokes from internal carotid artery occlusion;Diagnostic and therapeutical implications. Stroke 1983; 14: 867-875.   Back to cited text no. 12    
13.Gorsselink EL, Peeters HPM, Lodders J: Causes of small deep infarcts detected by CT. Clin Neurol Neurosurg 1984;86: 271-273.   Back to cited text no. 13    
14.Aleksic SN, Georoge AE: Pure motor hemiplegia with occlusion of the extracranial carotid artery. J Neurol Sci 1973; 19: 331-339.   Back to cited text no. 14    
15.Rascol A, Clanet M, Manelfe C et al: Pure motor hemiplegia:CT study of 30 cases. Stroke 1982; 13: 11-17.   Back to cited text no. 15    
16.Davis LE, Xie JG, Zou AH et al: Deep cerebral infarcts in the people's republic of China. Stroke 1990; 21: 394-396.   Back to cited text no. 16    
17.Huang CY, Chan FL, Yu YL et al: Cerebrovascular disease in Hongkong Chinese. Stroke 1990; 21: 230-235.   Back to cited text no. 17    
18.Foulkes MA, Wolf PA, Price TR et al: Stroke Data Bank: Designs,methods and baseline characteristics. Stroke 1988; 19: 547-554.   Back to cited text no. 18    
19.Kittner SJ, Sharkness CM, Price TR et al: Infarcts with a cardiac source of embolism in the NINCDS Stroke Data Bank: Historical features. Neurology 1982; 32: 49-56.   Back to cited text no. 19    
20.Bamford J, Sandercock P, Jones L et al: The natural history of lacunar infarction: the Oxfordshire Community Stroke Project. Stroke 1987; 18: 545-551.   Back to cited text no. 20    
21.Bogousslavsky J, Van Melle G, Regli F: The Laussane Stroke Registry: analysis of 1000 consecutive patients with first stroke. Stroke 1988; 19: 1083-1092.   Back to cited text no. 21    
22.Mohr JP, Caplan LR, Melski JW et al: The Harward Cooperative Stroke Registry: A prospective registry. Neurology 1978; 28: 754- 762.   Back to cited text no. 22    
23.Rascol A, Clanet M, Manelfe C: Pure motor hemiplegia: CT study of 30 cases. Stroke 1982; 13: 11-17.   Back to cited text no. 23    
24.Groothius DR, Duncan GW, Fisher CM: The human thalamocortical sensory path in internal capsule. Evidence from a capsular hemorrhage causing a pure sensory stroke. Ann Neurol 1977; 2: 328-331.   Back to cited text no. 24    
25.The Human development report. Progress in survival. Oxford University press, New York. 1999; 168-170.   Back to cited text no. 25    
26.Boiten J, Lodder J: Lacunar infarcts. Pathogenesis and validity of clinical syndromes. Stroke 1991; 22: 1374-1378.   Back to cited text no. 26    
27.Lodder J, Bamford JM, Sandercock PAG et al: Are hypertension or cardiac embolism likely causes of lacunar infarction? Stroke 1990; 21: 375-381.   Back to cited text no. 27    
28.Loeb.C, Gandolfo.C, Mancardi GL et al: The lacunar syndromes: a review with personal contribution. In Lechner H, Meyer J.S. Ott E, eds. Cerebrovascular Disease: Research and Clinical Management Vol 1, Amesterdom: Elsevier 1986; 107-156.   Back to cited text no. 28    
29.Norrving B, Cronqvist S: Clinical and radiological features of lacunar versus nonlacunar minor stroke. Stroke 1989; 20: 59-54.   Back to cited text no. 29    
30.Tegler CH, Shi F, Morgan T: Carotid stenosis in lacunar stroke. Stroke 1991; 22: 1124-1128.   Back to cited text no. 30    

 

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