Published online before print November 21, 2002, doi: 10.1161/01.STR.0000042001.93827.2C
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(Stroke. 2002;33:2735.)
© 2002 American Heart Association, Inc.
Letters to the Editor |
Progressive Stroke, Lacunae, and Systemic Blood Pressure
Department of Neuroradiology, University of Turin, Turin, Italy
To the Editor:
We read with great interest the article by Steinke and Ley and the editorial by Caplan in the June issue of Stroke.1 Among 941 patients with stroke, Steinke and Ley identified 92 patients with prevalent motor deficit; motor performances further deteriorated in 22 of these patients, and a prevalence of deep (lacunar) lesions was found on these latter patients. The conclusion, which gives the title to the article, is that lacunar stroke is the major cause of progressive motor deficits. Some observations could be made. The strict inclusion criteria of Steinke and Ley allowed selection of only a minimal number of the screened patients. Such a situation is highly "at risk" for selection biases; for example, the exclusion of patients with "minor motor or predominantly other deficits" may rule out the whole population of patients with embolic occlusion of small pial branches of the middle cerebral artery, or may overestimate relatively rare conditions such as basal ganglia infarctions as a major consequence of an embolic occlusion of the main trunk of the middle cerebral artery, with an efficient leptomeningeal collateral circulation. Moreover, the European Stroke Scale baseline is different between groups: the 22 patients with progressive courses had more limited neurological deficits and less frequent consciousness impairment, due to smaller infarctions as demonstrated on neuroimaging studies. In this setting, a worsening clinical course is more easily appreciated in the less severely affected patients, because of the "saturation effect" of the upper end of the scale.
The possibility of these biases is not avoidable in such a work but must be discussed. While considering these criticisms, the conclusions drawn by Steinke and Ley are correct in the sense that patients with progressive motor deficits caused by stroke typically have mild deficits at the admission and develop prevalently deep lesions. What is to be noticed is that, because of the already mentioned biases, this population does not necessarily match the "canonical" definition of patients with lacunar infarctions.2
These criticisms extend in part to the editorial.3 In the comments, Caplan focuses some critical point on the meaning and the physiopathology of the "progressing stroke" in a fascinating, global vision of the problem. Apart from systemic disease, such as febrile diseases and worsening due to the mass effect of hematomas or large middle cerebral artery–posterior fossa infarctions, a series of data point out that clinical worsening is strongly linked to the presence of a lacunar infarction or to an occlusion of large extracranial arteries.4,5 The possible management of these patients includes vessel recanalization and increased collateral circulation mainly by increasing systemic blood pressure.
These statements raise some questions. First, since "penetrating arteries are widely considered to be end arteries with little potential of for collateralization," any effort to improve collateral circulation is expected to fail. Surprisingly, some works suggest that this is not true, by demonstrating that an increased hematic volume had a beneficial effect on these patients.6 Different mechanisms, other than collateralization, must be considered to explain these data.7 Second, if it is obvious that the increased blood pressure improves the collateral circulation through Willis arteries or leptomeningeal collaterals if the large extracranial vessels are occluded, why couldn’t the same collateral leptomeningeal branches play a role in the embolic occlusion of smaller vessel, meaning the first- and second-order branches of the pial arteries? Unfortunately, the clinical course in these patients, with a maximal deficit at the beginning, followed by a more or less relevant improvement, made this statement very difficult to be demonstrated. The goal of the restoring collateral circulation in this case is not to avoid worsening but to improve recovery. By the way, a moderate anticoagulation and an increase of the systemic blood pressure have an immediate beneficial effect both on the collateral circulation and on the recanalization of vessels occluded by emboli during intracranial endovascular procedures; unfortunately, this treatment, almost routinely used by the majority of interventional neuroradiologists, has been very rarely published and analyzed.8 It is interesting to note that a proposed trial on the effect of an increased blood pressure on stroke was based on similar considerations.9
Concluding, a different view may be proposed. A raising of the systemic blood pressure may have a beneficial effect on the brain ischemic tissue, regardless the involved vascular territories—perforators or pial vessels. This effect is more easily demonstrated on the particular subtype of deep infarctions that causes a clinical worsening. Those infarctions, whose physiopathology is not yet known, appear as lacunae on neuroimaging studies.
References
- Steinke W, Ley SC. Lacunar stroke is the major cause of progressive motor deficits. Stroke. 2002; 33: 1510–1516.
[Abstract/Free Full Text] - Fisher CM. Lacunes: small, deep cerebral infarcts. Neurology. 1965; 15: 774–784.
[Free Full Text] - Caplan LR. Worsening in ischemic stroke patients: is it time for a new strategy? Stroke. 2002; 33: 1443–1445. Editorial
[Free Full Text] - Yamamoto H, Bogousslavsky J, van Melle G. Different predictors of neurological worsening in different causes of stroke. Arch Neurol. 1998; 55: 481–486.
[Abstract/Free Full Text] - Mohr JP, Caplan LR, Melski JW, Goldstein RJ, Duncan GW, Kistler JP, Pessin MS, Bleich HL. The Harvard Cooperative Stroke Registry: a prospective registry. Neurology. 1978; 28: 754–762.
[Abstract/Free Full Text] - Frey J. Hemodilution therapy for lacunar stroke: treatment results in 10 consecutive cases. J Stroke Cerebrovasc Dis. 1992; 2: 136–145.
- Caplan LR, Hennerici M. Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Arch Neurol. 1998; 55: 1475–1482.
[Abstract/Free Full Text] - Pelz DM, Lownie SP, Fox AJ. Thromboembolic events associated with the treatment of cerebral aneurysms with Guglielmi detachable coils. AJNR Am J Neuroradiol. 1998; 19: 1541–1547.[Abstract]
- Rordorf G, Cramer S, Effird J, Schwamm LH, Buonanno F, Koroshetz WJ. Pharmacological elevation of blood pressure in acute stroke: clinical effects and safety. Stroke. 1997; 28: 2133–2138.
[Abstract/Free Full Text]
Department of Neurology, Marien-Hospital Düsseldorf, Düsseldorf, Germany
Response
We appreciate the comments of Drs Bergui and Bradac regarding our article on progressive motor deficits in acute stroke.1 We agree that the application of strict inclusion criteria for the study population may have introduced a certain selection bias. However, in order to study the pathogenesis of further worsening of a relevant initial hemiparesis, it seemed methodologically adequate to exclude hemiplegic and comatose stroke patients as well as those with minimal motor or predominantly other neurological deficits. This approach provided a relatively homogeneous patient population for the investigation of stroke types in progressive motor deficits. Although we restricted the analysis to patients with a distinct clinical syndrome and course according to predefined criteria, all types of strokes were included in the final study population without selection bias. In contrast, definitions of stroke progression including decreasing level of consciousness and nonneurological causes of deterioration lead to more heterogeneous study populations in other recent studies, although with a main focus on large middle cerebral artery infarctions.2–4 Our study indicated lacunar infarction as the predominant stroke type in patients with worsening of motor hemiparesis. However, adequate interpretation of this result requires consideration of the inclusion criteria for our study population.
Drs Bergui and Bradac found a "saturation effect" in our study leading to easier assessment of worsening of the hemiparesis, if the initial deficit was less severe. Although our patients with progressive impairment of motor function started with a higher average modified European Stroke Scale (ESS) motor score (20.3 versus 15.9 points in patients without progression), motor deficits were nevertheless significant in both patient groups with regard to a possible maximum ESS motor score of 42 points (no paresis). Accordingly, the different clinical course of our study populations does not indicate methodological bias but actually reveals differences in stroke pathogenesis. This is also discussed in the accompanying editorial5 by Dr Caplan, who suggests distinct hemodynamic conditions such as hypoperfusion caused by occlusive disease of small penetrating and large arteries with possible distal embolization as significant mechanisms for worsening of neurological deficits. Defining the underlying pathophysiology is mandatory in view of potential therapeutic strategies for the prevention of disability from progressive motor deficits.
References
- Steinke W, Ley SC. Lacunar stroke is the major cause of progressive motor deficits. Stroke. 2002; 33: 1510–1516.
[Abstract/Free Full Text] - Wijdicks EF, Diringer MN. Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome. Mayo Clin Proc. 1998; 73: 829–836.[Medline] [Order article via Infotrieve]
- Toni D, Fiorelli M, Gentile M, Bastianello , Sette G, Saccetti ML, Argentino C, Pozzilli C, Fieschi C. Progressing neurological deficit secondary to acute ischemic stroke. Arch Neurol. 1995; 52: 670–675.[Abstract]
- Davalos A, Cendra E, Teruel J, Martinez M, Genis D. Deteriorating stroke: risk factors and prognosis. Neurology. 1990; 40: 1865–1869.
[Abstract/Free Full Text] - Caplan LR. Worsening in ischemic stroke patients: is it time for a new strategy? Stroke. 2002; 33: 1443–1445. Editorial.
[Free Full Text]
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