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A Dávalos

Publications and source records attributed to A Dávalos.

At least 19 recordsLinked to original sources
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.

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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

Hemostatic markers of recanalization in patients with ischemic stroke treated with rt-PA.

OBJECTIVE: To determine whether pretreatment markers of coagulation and fibrinolysis are related to recanalization and functional outcome. METHODS: The authors included patients treated with IV rt-PA with occlusion on baseline transcranial Doppler (Thrombolysis in Brain Ischemia [TIBI] criteria) in whom recanalization within 6 hours was monitored. At baseline, the authors recorded data about demographics, vascular risk factors, the NIH Stroke Scale (NIHSS) score, early CT signs, etiology, blood glucose, and time to rt-PA. The authors also measured plasmatic markers of coagulation (fibrinogen, prothrombin fragments 1 + 2, Factor XIII, Factor VII) and fibrinolysis (alpha2-antiplasmin, Plasminogen Activator Inhibitor, Functional Thrombin Activatable Fibrinolysis Inhibitor [fTAFI]). A favorable outcome was defined as a modified Rankin score < 2 at 3 months. RESULTS: The authors studied 63 patients with a mean age of 67.3 +/- 12.5 years. The median NIHSS score was 16. Patients who recanalized had lower concentrations of alpha2-antiplasmin (87.5 +/- 18% vs 96.5 +/- 12.5%, p = 0.023) and fTAFI (91.7 +/- 26.7% vs 104.4 +/- 21%, p = 0.039). A multivariant logistic regression analysis showed that the level of alpha2-antiplasmin was the only predictive variable of recanalization (OR 0.95, 95% CI 0.91, 0.99, p = 0.038), while the NIHSS score was the only predictive variable of functional outcome (OR 0.81, 95% CI 0.72, 0.92, p = 0.001). CONCLUSION: Baseline levels of alpha2-antiplasmin were predictive of recanalization but were not related to the long-term outcome in patients treated with rt-PA within the first 3 hours.

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PubMed2005

Magnetic resonance imaging findings in pre-clinical Creutzfeldt-Jakob disease.

The diagnosis of probable Creutzfeldt-Jakob disease (CJD) requires compatible clinical manifestations, typical electroencephalographical findings, and 14.3.3 protein positive in cerebrospinal fluid. Actually, MRI findings are not necessary, but they may support this diagnosis. The authors report a patient with definitive diagnosis of CJD who showed in a first MRI study performed two years before the clinical onset of the disease the same hyperintensities in caudate nuclei that were found in the last MRI. The authors think that these findings could be useful in detecting asymptomatic patients who need more extensive study and following.

Aged↗
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.

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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.

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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.

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PubMed2004

Antioxidant activity of peptides derived from egg white proteins by enzymatic hydrolysis.

This work reports the antioxidant activity of peptides produced by enzymatic hydrolysis of crude egg white with pepsin. Four peptides included in the protein sequence of ovalbumin possessed radical scavenging activity higher than that of Trolox. The hydrolysate of egg white with pepsin for 3 h was previously found to exhibit a strong angiotensin I-converting enzyme (ACE) inhibitory activity in vitro. The combined antioxidant and ACE inhibition properties make it a very useful multifunctional preparation for the control of cardiovascular diseases, particularly hypertension. No correlation was found between antioxidant and ACE inhibitory activities. However, the peptide Tyr-Ala-Glu-Glu-Arg-Tyr-Pro-Ile-Leu, which was a strong ACE inhibitor (50% inhibitory concentration, 4.7 microM) also exhibited a high radical scavenging activity (oxygen radical absorbance capacity-fluorescein value, 3.8 micromol of Trolox equivalent per micromol of peptide) and delayed the low-density lipoprotein lipid oxidation induced by Cu2+ at a concentration of approximately 0.16 mg/mg of low-density lipoprotein. Present results support that antioxidant peptides and amino acids not only act individually, but also cooperatively and synergistically.

Amino Acid Sequence↗
PubMed2003

[Consensus review. Pharmacological neuroprotection in cerebral ischemia: is it still a therapeutic option?].

Our increasing knowledge concerning the pathophysiology of cerebral ischemia is leading to a considerable development of drugs that at various levels block or modify the chain of biochemical processes set off as a consequence of hypoperfusion of cerebral parenchyma. In this zone of ischemic penumbra, the interaction between the neuronal ischemia cascade, the response of the glia and changes in the microcirculation, determine the evolution towards either functional recovery of the ischemic fabric or it necrosis. In various types of animal models, the majority of neuroprotective drugs have been shown to have considerable efficacy. However, this has not been translated into human clinical practice. The identification of persistence of recoverable cerebral tissue, together with the development of new designs of clinical trails better adapted to preclinical experiences and to the features of the drugs concerned, may contribute to an improved applicability of the new drugs in human clinical practice.

Animals↗
PubMed2003

[Neuropsychological and behavioural impairments resulting from bilateral thalamic infarct].

The neuropsychological characteristics of a patient with a bilateral thalamic infarct in the posterior communicating artery territory due to basilar artery thrombosis are described. MRI examination showed bilateral thalamic acute ischemic lesions in the zone anterior to the tuberothalamic branches. In the cognitive exploration, the patient showed verbal and visual memory disorders, impairment of the executive functions including inability to generate and make decisions and behavioural disorders including lack of inhibition, euphoria, and occasional aggressiveness. Two months later the patient had improved in the neuropsychological test scores but still suffered from severe recent memory loss, and certain behavioural disorders including lack of inhibition and euphoria. Other cases on thalamic infarcts with cognitive and behavioural impairments due to disconnection of the front subcortical pathways have been described in the literature.

Adult↗
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

Embolism in acute middle cerebral artery stenosis.

OBJECTIVE: To investigate the frequency of middle cerebral artery (MCA) stenosis in a series of nonselected patients and the coexistence of microembolic signals with stenosis. METHODS: MCA stenosis was sought by transcranial Doppler (TCD) in 387 patients admitted consecutively with acute ischemic cerebrovascular disease within the first 48 hours of the onset of symptoms and again at 6 months. TCD monitoring for microembolic signals was performed on all patients with MCA stenosis. RESULTS: MCA stenoses were found in 29 patients (7%), although in only 20 patients (5%) was the stenosis symptomatic. Microembolic signals were detected in five of 14 symptomatic stenoses (36%) monitored at the acute phase, but none were found in the chronic phase or in asymptomatic stenosis. Despite one third of symptomatic patients having had a further source of emboli, microembolic signals were detected only distally to the MCA stenosis. In the symptomatic group, 25% of stenoses had completely disappeared 6 months after stroke. Microembolic signal detection at the acute phase was associated with the subsequent disappearance of the stenosis. CONCLUSIONS: The frequency of symptomatic MCA stenosis in acute ischemic stroke was 5% in the population studied. Many stenoses are transient, and microembolic signals are often detectable at the poststenotic segment in the acute phase. The origin of at least 25% of symptomatic acute MCA stenoses may be embolic rather than atherosclerotic.

Adult↗
PubMed2001

Neuroprotective effect of aspirin by inhibition of glutamate release after permanent focal cerebral ischaemia in rats.

Aspirin reduces the size of infarcts after ischaemic stroke. Although this fact has been attributed to its anti-platelet actions, direct neuroprotective effects have also been reported. We have recently demonstrated that aspirin is neuroprotective by inhibiting glutamate release in 'in vitro' models of brain ischaemia, via an increase in ATP production. The present study was designed to determine whether the inhibition of glutamate release induced by aspirin might be protective in a whole-animal model of permanent focal brain ischaemia. Focal brain ischaemia was produced in male adult Fischer rats by occluding both the common carotid and middle cerebral arteries. Central and serum glutamate levels were determined at fixed intervals after occlusion. The animals were then killed and infarct volume was measured. Aspirin (30 mg/kg i.p. administered 2 h before the occlusion) produced a significant reduction in infarct volume, an effect that correlated with the inhibition caused by aspirin on ischaemia-induced increase in brain and serum glutamate concentrations after the onset of the ischaemia. Aspirin also inhibited ischaemia-induced decrease in brain ATP levels. Our present findings show a novel mechanism for the neuroprotective effects of aspirin, which takes place at concentrations in the anti-aggregant-analgesic range, useful in the management of patients with risk of ischaemic events.

Adenosine Triphosphate↗
PubMed2001

Atherosclerotic aortic arch plaques in cryptogenic stroke: a microembolic signal monitoring study.

BACKGROUND AND PURPOSE: To find out the prevalence of relevant atherosclerotic plaques in the aortic arch and their potential role as a source of embolism in cryptogenic stroke. METHODS: We performed a transoesophageal echocardiography (TEE) on 49 patients with cryptogenic stroke from a total series of 212 non-selected patients with acute ischaemic stroke studied prospectively by cranial computed tomography (CT), colour-duplex and transcranial Doppler (TCD) sonography with micro-embolic signal (MES) monitoring. Cryptogenic stroke was diagnosed in those patients without carotid or intracranial stenosis > 50%, nor lacunar or cardio-embolic strokes. We defined relevant plaques as those > or = 4 mm thick located in the ascending aorta or proximal arch. RESULTS: Twenty-three patients (46.9%) had atherosclerotic aortic plaques (AAP): 3 in the ascending aorta (in 1 > or = 4 mm), 11 in the proximal aortic arch (in 4 > or = 4 mm) and 9 in the descending aorta (in 5 > or = 4 mm). Hence, 5 patients (10.2%) had relevant plaques. Aortic plaques were significantly related to older age (p < 0.001) and male gender (p = 0.042). A carotid artery stenosis < 50% was found in 39% of patients with AAP and in 8% of those without AAP (p = 0.009). MES were detected in 3 patients with plaques > or = 4 mm thick, but not in those without AAP or with AAP < 4 mm thick (p = 0.006). CONCLUSION: Although few patients with cryptogenic stroke had relevant plaques in our non-selected population, our results support the hypothesis that relevant aortic plaques have embolic potential.

Aged↗
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↗