Biomedical subjects

R Leira

Publications and source records attributed to R Leira.

At least 19 recordsLinked to original sources

PubMed2007

Testing the combination beta-blocker plus topiramate in refractory migraine.

OBJECTIVE: To test treatment combining a beta-blocker plus topiramate in migraine patients previously resistant to the two medications in monotherapy. PATIENTS AND METHODS: Those patients who had not responded to a beta-blocker and topiramate received combined treatment. RESULTS: Fifty-eight patients (47 women, age 25-76 years) received the combined treatment. Thirty-three (57%) met criteria for chronic migraine/medication overuse headache, 18 (31%) for migraine without aura and seven (12%) with aura. Ten (17%) discontinued due to adverse events. Among the 48 patients who tolerated the combination, 36 (75%, 62% of the total series) showed response (>50% reduction in frequency), while 12 (25%) did not. The number of days with headache/month decreased from 15.1 to 6.5 (-57%). Sixteen (44% of responders) showed an excellent (>75%) response. Eighteen patients (38%) experienced a total of 26 adverse events (mild-moderate). CONCLUSIONS: The combination of beta-blocker plus topiramate showed a benefit in around 60% of patients who had not previously responded to monotherapy. Adverse events led to discontinuation in one out of six patients. From these open results, it seems reasonable to recommend this combination, complementary in terms of mechanism of action, as a potential strategy in patients with refractory migraine.

Adrenergic beta-Antagonists↗

PubMed2006

New-onset hypertension and inflammatory response/poor outcome in acute ischemic stroke.

OBJECTIVE: To study the association of previously unknown high blood pressure (HBP) during the acute phase of stroke (new-onset hypertension) with the inflammatory response and clinical outcome. METHODS: We classified 844 patients with hemispheric ischemic stroke into three groups according to history of hypertension and presence of HBP within the first 24 hours after symptom onset: Group I (n = 412), normotensive patients; Group II (n = 265), chronic hypertensive patients; and Group III (n = 167), new-onset hypertensive patients. Interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and metalloproteinase 9 (MMP-9) were measured in blood samples obtained on admission. The influence of new-onset HBP and markers of inflammation on poor neurologic outcome at 3 months was evaluated by logistic regression analysis. RESULTS: New-onset HBP was found in 19.9% of patients. Patients in this group had higher plasma concentrations of IL-6, TNF-alpha, ICAM-1, VCAM-1, and MMP-9 than the other two groups. New-onset HBP was associated with poor outcome at 3 months (odds ratio [OR] 2.10; 95% CI 1.54 to 3.52; p < 0.0001) after adjustment for other prognostic factors. However, when markers of inflammation were included in the model, IL-6 (OR 1.01; 95% CI 1.00 to 1.03; p = 0.020) and MMP-9 (OR 1.01; 95% CI 1.00 to 1.01; p < 0.0001), but not new-onset HBP, were independently associated with poor neurologic outcome. CONCLUSIONS: New-onset high blood pressure in acute ischemic stroke, but not chronic hypertension, is associated with an inflammatory response and poor neurologic outcome.

Aged↗

PubMed2006

Micro- and macroalbuminuria predict hemorrhagic transformation in acute ischemic stroke.

BACKGROUND: Hemorrhagic transformation (HT) after cerebral ischemia seems to be related to the endothelial disruption secondary to the ischemic process. Albuminuria has recently been found to be a marker of chronic endothelial damage. OBJECTIVE: To investigate the relationship between albuminuria and HT in patients with acute ischemic stroke. METHODS: We studied 200 patients (51.5% men, age 72.5 +/- 8.5 years) with ischemic stroke within the first 24 hours of evolution. HT development was assessed on CT performed between days 4 and 7 of evolution and classified according to the ECASS II criteria. Urinary samples were collected within the first 3 hours after admission and the presence of albuminuria, which was considered to be present when the ratio albumin-to-creatinine was > or =30 mg/g creatinine, was determined by nephelometry within the first 24 hours of evolution. RESULTS: Forty-nine patients (24.5%) had albuminuria and 36 (18%) had HT on the second CT scan. After adjusting for potential confounders including a previous history of diabetes mellitus, hypertension and atrial fibrillation, stroke severity, the presence of early signs of ischemia and leukoaraiosis on the baseline CT scan, and IV anticoagulant treatment, logistic regression analysis showed that albuminuria was independently associated with HT (OR, 7.45; 95% CI 2.30 to 24.16). Moreover, albuminuria was also a significant and independent predictor of parenchymal hemorrhage type 1 and 2 (OR, 8.30; 95% CI 1.77 to 38.89). CONCLUSION: Albuminuria is an independent predictor of hemorrhagic transformation, and particularly of the most severe bleedings, in patients with acute ischemic stroke. Due to the small number of events, the predictive capacity of albuminuria should be confirmed in larger studies.

Aged↗

PubMed2006

Hyperthermia is a surrogate marker of inflammation-mediated cause of brain damage in acute ischaemic stroke.

UNLABELLED: The influence of temperature on the outcome observed in experimental models of ischaemic stroke has not been definitively proved in patients with stroke. Interleukin-6 (IL-6) acts as important endogenous pyrogen, and it is an important regulator of spontaneous body temperature during cerebral ischaemia. The objective of this study was to determine, during the acute phase of cerebral ischaemia, the potential relationship between proinflammatory cytokines and hyperthermia as a cause of larger cerebral infarcts. PATIENTS AND METHODS: We studied 229 patients with a first-ever acute hemispheric infarction admitted within the first 24 h from onset of symptoms. On admission, axillary temperature was recorded and blood chemistry studies and cranial computed tomography were performed. We classified body temperature into two groups: hyperthermia (>or=37.5 degrees C) and normothermia (<37.5 degrees C). We determined proinflammatory markers [IL-6, tumour necrosis factor-alpha (TNF-alpha), intercellular adhesion molecule (ICAM-1) and vascular cellular adhesion molecule] on admission. Two outcome variables were evaluated: (i) infarct volume; (ii) Canadian Stroke Scale (CSS) at 3 months (CSS 7 good outcome). RESULTS: Patients with hyperthermia had higher infarct volume [46.5 (9.8-78.5) cm(3) vs. 19.1 (5.0-23.5) cm(3); P < 0.0001], as well as poor outcome at 3 months. Plasma levels of IL-6, TNF-alpha and ICAM-1 were significantly higher in the group of patients with hyperthermia than in the normothermic group. There was a significant correlation between body temperature on admission and infarct volume (r = 0.302; P < 0.0001), and between proinflammatory markers (IL-6 and TNF-alpha) and infarct volume. A significant association was also found between proinflammatory markers (IL-6, TNF-alpha, and ICAM-1) and poor outcome. However, after adjustment for potential confounders, hyperthermia was not independently associated with either larger infarct volume or with poor outcome at 3 months. CONCLUSIONS: Inflammatory mediators play a role in acute ischaemic brain damage independently of hyperthermia.

Acute Disease↗

PubMed2005

Predictors of good outcome in medium to large spontaneous supratentorial intracerebral haemorrhages.

OBJECTIVE: To determine potential predictors of good outcome in primary medium to large intracerebral haemorrhages (ICH) which could be useful for selecting patients for surgical procedures. METHODS: Subjects were 138 patients with spontaneous hemispheric ICH >20 ml. They were non-surgically treated and were admitted consecutively to 15 hospitals within the first 12 hours of symptom onset (mean (SD), 5.8 (3.1) hours). Haematoma volume was measured on computed tomography (CT) at admission. Stroke severity was assessed by the Canadian stroke scale (CSS). Good outcome was defined as modified Rankin score < or =2 at three months. RESULTS: At the end of the follow up period, 45 patients (32.6%) had good outcome. Baseline stroke severity, systolic and diastolic blood pressure, body temperature, and acute phase reaction biochemical markers (ESR, C-reactive protein, fibrinogen, neutrophil count) were significantly associated with good outcome in bivariate analyses. Of the initial CT scan variables, intraventricular contamination, deep location, mass effect, and greater ICH volume were related to poor outcome. On multiple logistic regression analysis, cortical location of bleeding (odds ratio 3.79 (95% confidence interval 1.2 to 12.01); p = 0.023), high CSS score (OR 2.3 (1.6 to 3.1); p<0.0001), and low fibrinogen concentrations (OR 0.92 (0.87 to 0.97); p = 0.001) were independent predictors of good outcome. These three factors correctly classified 85% of patients. CONCLUSIONS: Good outcome in medium to large ICH can be predicted on admission by three readily assessable factors (CSS score, ICH location, and fibrinogen levels). These predictors may be helpful in selecting patients for surgical treatment.

Aged↗

PubMed2004

Early neurologic deterioration in intracerebral hemorrhage: predictors and associated factors.

OBJECTIVE: To identify potential predictors of and factors associated with early neurologic deterioration (END) in primary intracerebral hemorrhage (ICH). METHODS: Two hundred sixty-six patients with spontaneous supratentorial ICH admitted within 12 hours of stroke onset were investigated in a multicenter, prospective study. Sixty-one clinical, biochemical, and neuroimaging variables were registered on admission, and 37 clinical and neuroimaging variables were registered at 48 hours. The volumes of the ICH and peripheral edema on admission and at 48 hours were measured on CT scan. Stroke severity and functional outcome were evaluated with the Canadian Stroke Scale (CSS) and modified Rankin Scale. END was diagnosed when the CSS score decreased > or =1 points between admission and 48 hours. With use of logistic regression analyses, baseline variables that predicted END and factors measured after the early acute phase and associated with END were investigated. RESULTS: END occurred in 61 (22.9%) patients. Body temperature of >37.5 degrees C (odds ratio [OR] 24.5; 95% CI 4.8 to 125), neutrophil count (by 1,000-unit increase; OR 2.1; 95% CI 1.6 to 2.6), and serum fibrinogen levels of >523 mg/dL (OR 5.6; 95% CI 1.9 to 16.2) on admission were independent predictors of END. Among the factors recorded at 48 hours, early ICH growth (OR 4.3; 95% CI 1.3 to 14.5), intraventricular bleeding (OR 2.6; 95% CI 1.4 to 5.0), and highest systolic blood pressure (by 10-unit increase; OR 1.17; 95% CI 1.02 to 1.32) were associated with END in multivariate analyses. CONCLUSIONS: Clinical and biologic markers of the inflammatory reaction on admission are predictors of subsequent END, whereas early ICH growth, intraventricular bleeding, and high systolic blood pressure within 48 hours are factors associated with END in patients with spontaneous ICH.

Aged↗

PubMed2004

The clinical-DWI mismatch: a new diagnostic approach to the brain tissue at risk of infarction.

OBJECTIVE: To evaluate the usefulness of a mismatch between the severity of acute clinical manifestations and the diffusion-weighted imaging (DWI) lesion in predicting early stroke outcome and infarct volume. METHODS: One hundred sixty-six patients with a hemispheric ischemic stroke of <12 hours' duration were studied. The NIH Stroke Scale (NIHSS) score and the volume of DWI lesion were measured on admission and at 72 +/- 12 hours. Infarct volume was measured on T2-weighted or fluid-attenuated inversion recovery images at day 30. Early neurologic deterioration (END) was defined as an increase of > or =4 points between the two NIHSS evaluations. Thirty-eight patients received IV thrombolysis or abciximab. Clinical-DWI mismatch (CDM) was defined as NIHSS score of > or =8 and ischemic volume on DWI of < or =25 mL on admission. The adjusted influence of CDM on END, DWI lesion enlargement at 72 hours, and infarct growth at day 30 was evaluated by logistic regression analysis and generalized linear models. RESULTS: CDM was found in 87 patients (52.4%). Patients with CDM had a higher risk of END than patients without CDM because NIHSS < 8 (odds ratio [OR], 9.0; 95% CI,1.9 to 42) or DWI lesion > 25 mL (OR, 2.0; 95% CI, 0.8 to 4.9). CDM was associated with an increase of 46 to 68 mL in the mean volume of DWI lesion enlargement and infarct growth in comparison with non-CDM. All the effects were even greater and significant in patients not treated with reperfusion therapies. CONCLUSIONS: Acute stroke patients with an NIHSS score of > or =8 and DWI volume of < or =25 mL have a higher probability of infarct growth and early neurologic deterioration. The new concept of CDM may identify patients with tissue at risk of infarction for thrombolytic or neuroprotective drugs.

Aged↗

PubMed2004

[Spanish contribution to the clinical development of eletriptan: an analysis of controlled studies].

INTRODUCTION: Eletriptan is a recently marketed second-generation triptan with a potent agonist activity on 5-HT1B/ 1D receptors. Our aim has been to analyze the specific results from the Spanish participation in phase IIIa and IIIb clinical trials vs placebo and compare them with the results obtained in the global clinical development of eletriptan. PATIENTS AND METHODS: Analysis of the results obtained in 40 centers in Spain (358 patients) vs global sample 4,677 patients) for the first migraine attack in 6 controlled clinical trials with eletriptan 40 mg, eletriptan 80 mg and placebo. This ad hoc analysis was carried out for those treatment groups with more than 50 patients, which reduced the final number of patients from Spain to 250. RESULTS: The proportion of patients with relief at 2 hours (main endpoint) in the Spanish sample was 22 %, 59 % and 67 % for placebo, eletriptan 40 mg and eletriptan 80 mg, respectively. These values were significantly higher (p < 0.05) than those of placebo and similar to those from the total sample. The proportion of pain free patients at 2 hours in the Spanish sample was 10 %, 36 % and 41 % for placebo, eletriptan 40 mg and eletriptan 80 mg, respectively. These values were significantly better than those for placebo (p < 0.05) and about 15 %-20 % higher than those from the total sample. Recurrence rate in the Spanish sample was 50 %, 16 % and 25 % for placebo, eletriptan 40 and eletriptan 80 mg, respectively, and did not differ from that of the total sample. Sustained relief for the two eletriptan doses was 46 % for both eletriptan 40 and eletriptan 80, this being significant (p < 0.05) over placebo (11 %) for the Spanish sample and similar to that of the global sample. The results for other efficacy parameters, such as need of rescue medication, functional response at 2 hours, complete response for pain-freeness and acceptability followed a similar pattern. Eletriptan was, in general, well-tolerated. Adverse events were slight-moderate in intensity, transient and were not different, either in profile or proportion, from those from the global sample. CONCLUSIONS: These results confirm eletriptan 40 mg and 80 mg as an excellent option for the symptomatic treatment of migraine in our setting.

Clinical Trials, Phase III as Topic↗

PubMed2003

Combined therapy for migraine prevention? Clinical experience with a beta-blocker plus sodium valproate in 52 resistant migraine patients.

The aim was to explore whether combining a beta-blocker and sodium valproate could lead to an advantage in efficacy in patients with migraine previously resistant to the two medications in monotherapy. Fifty-two patients (43 women) with a history of episodic migraine with or without aura, and previously unresponsive to beta-blockers and sodium valproate in monotherapy, were treated with a combination of propranolol or nadolol and sodium valproate in an open-label fashion. Eight patients (15%) discontinued due to adverse events. Fifteen (29%) did not respond. The remaining 29 cases (56%) showed response (> 50% reduction in migraine days). The response was excellent in nine (17%). From this open trial, combination therapy with a beta-blocker and sodium valproate appears to be a good migraine preventative in some previously resistant migraine cases. Controlled trials are now necessary to determine the true advantage in efficacy of this combination in difficult to treat migraineurs.

Adrenergic beta-Antagonists↗

PubMed2003

Topiramate for patients with refractory migraine: an observational, multicenter study in Spain.

INTRODUCTION: The efficacy of current preventive migraine treatments is limited. In addition, tolerability problems are not infrequent. OBJECTIVES: To check our experience with topiramate in the treatment of patients with refractory migraine. PATIENTS AND METHODS: We offered treatment with topiramate to patients with the diagnosis of International Headache Society (IHS) migraine who had not responded to or tolerated beta-blockers, amitriptyline, flunarizine and/or valproate. This series is made up of 115 patients (88 women), between 16 and 81 years. Most of them (n=79) fulfilled the Silberstein et al. criteria for transformed migraine. The parameters analyzed were "response" (reduction in migraine frequency>50%), excellent response (>75%) and tolerability. RESULTS: After 3 months, the maintenance doses of topiramate ranged from 25 to 400 mg, though most patients took 100 mg. Twenty-four (21%) patients withdrew due to adverse events, mostly cognitive difficulties, that had already occurred with doses as low as 25-50 mg, while 26 (23%) found topiramate ineffective. The remaining 65 (56%) patients responded, 34 with excellent response. Sixteen patients (10 obese) lost weight (3-13 kg). CONCLUSIONS: Topiramate seems to be a good therapeutic option for about half of the patients with refractory migraine. In these patients response is usually excellent. Intolerance due to adverse events appears in one-fifth of the cases early and at low doses.

Adolescent↗

PubMed2003

[Experimental headache models].

The use of experimental models is so common in most diseases, such as stroke, epilepsy or brain injury, that it does not seem to be necessary to justify in the study of experimental headache models. However, the study of these models was not been possible until 10-15 years ago. Two main reasons made it possible: first, increased basic knowledge about disease mechanisms in the last decade, a requirement necessary before models can be developed and validated; second, the publication of the headache classification of the International Headache Society in 1988 which has permitted an exact diagnosis, avoiding interobserver variability. This review examines the use of animal models to study the neurogenic inflammation described by Moskowitz and those used to study the vascular hypothesis. We have also examined the use of animal experiments to study the neurobiological basis for pain. Finally, we have explored the experimental human headache models not only in sufferers but also in healthy volunteers.

Animals↗

PubMed2002

Molecular signatures of brain injury after intracerebral hemorrhage.

BACKGROUND: The mechanisms of cellular death in the tissue surrounding an intracerebral hemorrhage (ICH) are not defined. OBJECTIVE: To investigate the relationship of markers of excitotoxicity and inflammation to brain injury after ICH. METHODS: A total of 124 consecutive patients with spontaneous ICH admitted within 24 hours of stroke onset were prospectively investigated. The volumes of the initial ICH, peripheral edema on days 3 to 4, and the residual cavity at 3 months were measured on CT scan. Glutamate, cytokines, and adhesion molecules were measured in blood samples obtained on admission. Stroke severity and neurologic outcome were evaluated with the Canadian Stroke Scale. RESULTS: Poor neurologic outcome at 3 months (Canadian Stroke Scale < 7) was observed in 53 patients (43%). Stroke severity and glutamate concentrations (by each increment of 10 micromol/L, odds ratio 1.23; 95% CI 1.09 to 1.41), but not the initial volume of ICH, were independent predictors of poor outcome. In the multiple linear regression analyses, tumor necrosis factor-alpha concentration was correlated (r = 0.83, p < 0.0001) with the volume of perihematoma edema, and glutamate concentrations were correlated (r = 0.78, p < 0.0001) with the volume of the residual cavity. These same results were observed when lobar (n = 58) and deep (n = 66) ICH were analyzed separately. CONCLUSIONS: High plasma levels of proinflammatory molecules within 24 hours of intracerebral hemorrhage onset are correlated with the magnitude of the subsequent perihematoma brain edema, whereas poor neurologic outcome and the volume of the residual cavity are related to increased plasma glutamate concentrations.

Aged↗

PubMed2002

Headache as a surrogate marker of the molecular mechanisms implicated in progressing stroke.

The mechanism for headache in patients with acute ischaemic stroke are not completely understood. We analysed the relationship between headache and the early worsening of neurological symptoms in patients with acute ischaemic stroke, and we studied the possible biochemical mechanisms implicated. Headache at the onset of ischaemic stroke predicted progression with a sensitivity, specificity, and positive predictive value of 56%, 99%, and 98%, respectively. CSF concentrations of glutamate, Interleukin-6, and NO-m were significantly greater in patients with progressing stroke than in patients with nonprogressing stroke, and these biochemical markers were also significantly higher in patients with headache than in those without headache. Results of this study suggest that headache at the onset of ischaemic stroke is an independent predictor of neurological worsening and we hypothesize that headache might be a surrogate marker of the molecular mechanisms involved in neurological worsening after acute stroke.

Acute Disease↗

PubMed2001

Efficacy and safety of metamizol vs. acetylsalicylic acid in patients with moderate episodic tension-type headache: a randomized, double-blind, placebo- and active-controlled, multicentre study.

We assessed the efficacy and safety of oral single doses of 0.5 and 1 g metamizol vs. 1 g acetylsalicylic acid (ASA) in 417 patients with moderate episodic tension-type headache included in a randomized, double-blind, placebo- and active-controlled, parallel, multicentre trial. Eligibility criteria included 18-65 years of age, history of at least two episodes of tension-type headache per month in the 3 months prior to enrollment, and successful previous pain relief with a non-opioid analgesic. Treatment arms were metamizol 0.5 g (n = 102), metamizol 1 g (n = 108), ASA 1 g (n = 102) and placebo (n = 105). The analgesic efficacy of 0.5 and 1 g metamizol vs. placebo was highly statistically significant (alpha: 0.025; one-sided) for sum of pain intensity differences, maximum pain intensity difference, number of patients with at least 50% pain reduction, time to 50% pain reduction, maximum pain relief and total pain relief. A trend towards an earlier onset of a more profound pain relief of 0.5 and 1 g metamizol over 1 g ASA was noticed. All medications including placebo were almost equally safe and well tolerated.

Adolescent↗

PubMed2001

An open preference study with sumatriptan 50 mg and zolmitriptan 2.5 mg in 100 migraine patients.

Understanding factors influencing patients' preference will improve guidance to make rational choices in expanded symptomatic migraine treatment. The objective of this open-label, cross-over study was to explore patients' preferences for sumatriptan 50 mg vs. zolmitriptan 2.5 mg tablets, focusing on factors influencing this preference. One hundred consecutive migraine patients attending our clinics were asked to treat three attacks with each medication and then fill out a preference questionnaire. Ninety-four migraineurs completed the trial and 42 (44%, 95% CI 34-58%) reported that they preferred zolmitriptan 2.5 mg over sumatriptan 50 mg tablets and 27 (29%, 20-38%) preferred sumatriptan 50 mg. The remaining 25 (27%, 18-36%) did not show any preference. For the initial treatment of the attacks, there were more patients needing just one tablet of zolmitriptan 2.5 mg compared with sumatriptan 50 mg (67 vs. 39%). The reasons for preference among those 69 patients who had shown preference for either of the two triptans were: a faster onset of action (speed of onset) (73%), a longer duration of the effects (39%), fewer adverse events (35%) and lower price (13%). Only one-quarter of the studied migraine population thought that sumatriptan 50 mg and zolmitriptan 2.5 mg were equivalent, which suggests that most migraine patients differentiate between triptans. A faster onset of action (speed of onset) was the most important reason for preference.

Adult↗

PubMed2001

Predictors of deteriorating cerebral infarct: role of inflammatory mechanisms. Would its early treatment be useful?

The development of neurological deterioration in the hours following the stroke onset occurs in somewhat more than 1 in 3 cerebral infarcts and is associated with an increase in morbidity and mortality. This early deterioration (0--48/72 h) entails the conversion of the ischemic penumbra area in an irreversible lesion, a process that is mediated as much by hemodynamic changes in the local cerebral circulation as by biochemical mechanisms. Late neurological deterioration (3--7 days) is more frequently associated with systemic causes. Knowledge of the various clinical, biochemical and imaging markers associated with neurological deterioration is consequently of fundamental importance. For their repercussion in clinical practice, we classify these predictors of deteriorating cerebral infarct into nonmodifiable, modifiable and possibly modifiable. The reduction in cerebral blood flow in a particular cerebral zone causes very early cerebral damage as a consequence of a significant liberation of neuroexcitatory amino acids, followed by an excessive entry of calcium into the interior of cells; this process causes lipid peroxidation, disintegration of the cellular membranes, nuclear destruction and neuronal death. Moreover, ischemia and posterior reperfusion induce an inflammatory response leading to further cellular destruction. It is therefore conceivable that therapeutic interventions aimed at decreasing proinflammatory cytokines and cell adhesion molecules might result in better outcome in this population.

Cerebral Infarction↗

PubMed2001

Neurological deterioration in acute lacunar infarctions: the role of excitatory and inhibitory neurotransmitters.

BACKGROUND AND PURPOSE: The mechanisms involved in the neurological deterioration of acute lacunar strokes are unknown. Although accumulating evidence suggests that glutamate release plays a role in the progression of territorial infarctions, it remains to be established whether excitotoxicity also participates in lacunar stroke progression. We investigated whether excitatory and inhibitory amino acid concentrations in blood predict subsequent progressive motor deficits in lacunar infarctions. METHODS: We studied 113 consecutive patients with lacunar infarct, defined by clinical and computed tomography/magnetic resonance imaging criteria, within the first 24 hours after stroke onset. Neurological deterioration was defined as a decrease of >/=1 points in the motor items of the Canadian Stroke Scale in the first 48 hours after admission. Glutamate, glycine, and GABA were determined by high-performance liquid chromatography in plasma samples obtained on admission. Predictive values, sensitivity, specificity, and accuracy of specific glutamate and GABA concentrations and glutamatexglycine/GABA index for progression of lacunar stroke were calculated. RESULTS: Twenty-seven patients (23.9%) had neurological worsening. Plasma concentrations of glutamate (253+/-70 versus 123+/-73 micromol/L, mean+/-SD) were higher and those of GABA (140+/-63 versus 411+/-97 nmol/L) were lower in the progressing group than in the nonprogressing group (both P<0.001). Glutamate concentrations >200 micromol/L and GABA levels <240 nmol/L had a positive predictive value for neurological deterioration of 67% and 84%, respectively. A excitotoxic index >106 had a positive predictive value of 85%. CONCLUSIONS: These findings suggest that an imbalance between the glutamate and GABA concentrations may play a role in the pathophysiology of progressing lacunar infarctions.

Acute Disease↗

PubMed2000

[Rizatriptan].

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Dose-Response Relationship, Drug↗