Prognostic relevance of pathological sympathetic activation after acute thromboembolic stroke

OBJECTIVE: To evaluate the prognostic impact of early pathologic sympathetic activation after stroke. METHODS: The authors examined 112 consecutive patients (mean age, 69 years; 60 men) with their first brain infarction. A pathologic sympathetic activation was presumed if the initial norepinephrine level exceeds 300 pg/mL. In addition, involvement of the insular cortex, nighttime blood pressure changes, and several cardiovascular risk factors were determined. One-year outcome measures were mortality rate, cardiovascular and cerebrovascular events, and activities of daily living (Barthel index and Rankin score). RESULTS: Norepinephrine levels greater than 300 pg/mL, nighttime blood pressure increases, and insular involvement were associated with a lower Barthel index (p < 0.005) at the 1-year follow-up. By stepwise logistic regression analysis, insular infarction, serum norepinephrine concentration, right-sided infarction, and nighttime blood pressure increase were significant and independent predictors of an unfavorable functional outcome. Cox regression analysis showed a higher rate of cardiovascular and cerebrovascular events (hazard ratio, 2.9; 95% CI, 1.07; 6.83; p < 0.04) in patients with initially increased norepinephrine concentrations. CONCLUSIONS: The involvement of the insular cortex, the occurrence of a pathologic nighttime blood pressure increase, and an initially increased serum norepinephrine concentration are independent predictors of poor long-term outcome.     

Lateralization in autonomic dysfunction in ischemic stroke involving the insular cortex

Autonomic nervous system dysfunction is a common complication of ischemic stroke. Clinical and experimental data indicate hemispheric lateralization in the control of autonomic activity. The insular cortex has also been shown to play a crucial role in the central autonomic network. The aim of this study was to assess cardio-autonomic dysfunction in patients with ischemic insular versus non-insular cortex infarction, and to demonstrate a possible lateralization in autonomic activity mediated by the insular cortex. Sympathetic function was prospectively assessed by determining plasma norepinephrine and epinephrine in 15 patients with left-hemisphere (LH; four insular infarction), and 14 with right-hemisphere (RH) middle cerebral artery (MCA) stroke (five insular infarction). Systolic and diastolic blood pressure and heart rate were recorded during the first 5 days after stroke. Sympathetic activity was significantly higher in insular than in non-insular infarction (p < 0.05) with concomitantly elevated cardiovascular parameters in insular stroke patients. The pathological activation of the sympathetic nervous system was most excessive in RH-stroke involving the insular cortex (p < 0.05). Our data indicate a hemispheric lateralization in autonomic activity which is mediated by the right-sided insular cortex. Patients with RH stroke involving the insular cortex are most susceptible to develop cardio-autonomic dysfunction.     

24 hour ambulatory blood pressure variability and cardiac parasympathetic function 2 and 6 weeks after acute myocardial infarction

The aim of the study was to assess non-invasively circadian blood pressure rhythm as well as the influence of parasympathetic function 2 and 6 weeks after acute myocardial infarction treated with beta-blocking agents. Twenty-four patients with uncomplicated first myocardial infarction, and aged less than 60 years, underwent ambulatory blood pressure recordings every 15 min during the day (0900–2100 h) and every 30 min during the night (2100–0900 h), 2 and 6 weeks after infarction. The deep breathing test (6 breaths/min) was performed on each occasion. Normal circadian blood pressure rhythm was maintained with a nocturnal decline of 10 to 15%. Both for systolic and diastolic blood pressure a moderate increase was obtained after 6 weeks (107.8 ± 9.2 mmHg vs. 111.8 ± 10.3 mmHg; NS and 64.9 ± 4.5 mmHg vs. 68.8 ± 6.5 mmHg;p < 0.05). The respective blood pressure variations were significantly higher at that time (10.0 ± 2.4 mmHg vs. 13.6 ± 4.2 mmHg;p < 0.001 and 7.9 ± 1.7 mmHg vs. 11.7 ± 3.5 mmHg,p < 0.001). There was a close correlation (r=0.60,p < 0.005) between 24-h diastolic blood pressure variability and the results of the parasympathetic function test (deep breathing) 2 weeks after infarction. We conclude that the circadian blood pressure rhythm persists after acute myocardial infarction. The correlation between blood pressure variability and parasympathetic function early after infarction suggests a role for vagal control in post-infarction blood pressure variability.     

Ipsilateral hippocampal atrophy is associated with long‐term memory dysfunction after ischemic stroke in young adults

Memory impairment after stroke in young adults is poorly understood. In elderly stroke survivors memory impairments and the concomitant loss of hippocampal volume are usually explained by coexisting neurodegenerative disease (e.g., amyloid pathology) in interaction with stroke. However, neurodegenerative disease, such as amyloid pathology, is generally absent at young age. Accumulating evidence suggests that infarction itself may cause secondary neurodegeneration in remote areas. Therefore, we investigated the relation between long‐term memory performance and hippocampal volume in young patients with first‐ever ischemic stroke. We studied all consecutive first‐ever ischemic stroke patients, aged 18–50 years, admitted to our academic hospital center between 1980 and 2010. Episodic memory of 173 patients was assessed using the Rey Auditory Verbal Learning Test and the Rey Complex Figure and compared with 87 stroke‐free controls. Hippocampal volume was determined using FSL‐FIRST, with manual correction. On average 10 years after stroke, patients had smaller ipsilateral hippocampal volumes compared with controls after left‐hemispheric stroke (5.4%) and right‐hemispheric stroke (7.7%), with most apparent memory dysfunctioning after left‐hemispheric stroke. A larger hemispheric stroke was associated with a smaller ipsilateral hippocampal volume (b=?0.003, P<0.0001). Longer follow‐up duration was associated with smaller ipsilateral hippocampal volume after left‐hemispheric stroke (b=?0.028 ml, P=0.002) and right‐hemispheric stroke (b=?0.015 ml, P=0.03). Our results suggest that infarction is associated with remote injury to the hippocampus, which may lower or expedite the threshold for cognitive impairment or even dementia later in life. Hum Brain Mapp 36:2432–2442, 2015. © 2015 Wiley Periodicals, Inc.     

Diverging lesion and connectivity patterns influence early and late swallowing recovery after hemispheric stroke

Knowledge about the recovery of oral intake after hemispheric stroke is important to guide therapeutic decisions, including the administration of enteral tube feeding and the choice of the appropriate feeding route. They aimed to determine the localization and connectivity of lesions in impaired recovery versus recovered swallowing after initially dysphagic stroke. Sixty‐two acute ischemic hemispheric stroke patients with impaired oral intake were included in a prospective observational cohort study. Voxel‐based lesion‐symptom mapping and probabilistic tractography were used to determine the association of lesion location and connectivity with impaired recovery of oral intake ≥7 days (indication for early tube feeding) and ≥4 weeks (indication for percutaneous endoscopic gastrostomy feeding) after stroke. Two distinct patterns influencing recovery of swallowing were recognized. Firstly, impaired recovery of oral intake after ≥7 days was significantly associated with lesions of the superior corona radiata (65% of statistical map, P < 0.05). The affected fibers were connected with the thalamus, primary motor, and supplemental motor areas and the basal ganglia. Secondly, impaired recovery of oral intake after ≥4 weeks significantly correlated with lesions of the anterior insula (54% of statistical map, P < 0.05), which was connected to adjacent operculo‐insular areas of deglutition. These findings indicate that early swallowing recovery is influenced by white matter lesions disrupting thalamic and corticobulbar projection fibers. Late recovery is determined by specific cortical lesions affecting association fibers. This knowledge may help clinicians to identify patients at risk of prolonged swallowing problems that would benefit from enteral tube feeding. Hum Brain Mapp 38:2165–2176, 2017. © 2017 Wiley Periodicals, Inc.     

Ptosis in patients with hemispheric strokes

BACKGROUND: Cerebral ptosis is considered rare; it has been reported with unilateral, usually right hemispheric lesions. However, the frequency of cerebral ptosis in patients with strokes has not received systematic study. OBJECTIVE: To determine the frequency of ptosis in patients with acute hemispheric stroke and to identify stroke features associated with ptosis. METHODS: Eyelid function was studied in 64 consecutive patients with acute hemispheric stroke and 40 age-matched subjects with no known neurologic disease. All underwent comprehensive neuro-ophthalmologic and general neurologic examination within 48 hours of admission, including measurement of palpebral fissures, marginal reflex distance, and range of upper lid movement. Only patients who could cooperate with eyelid testing were included. Brain CT scans were obtained for all patients who had had strokes. RESULTS: Twenty-four (37.5%) of the patients with strokes had neurogenic ptosis, which was bilateral in 10 and unilateral in 14. None of the control subjects had neurogenic ptosis. All patients with strokes with ptosis had a hemiparesis. Rightward gaze deviation and upgaze paresis were more common (p < 0.05) in the patients with ptosis compared with others who had had strokes. CT evidence of right-sided hemispheric cortical infarction was more common in patients with strokes with ptosis (p < 0.05). In five patients with large hemispheric infarction, complete bilateral or asymmetric ptosis was the first sign of imminent herniation, preceding pupillary dilation and ocular motor deficits. CONCLUSIONS: Ptosis occurs frequently in patients with hemispheric strokes, especially in association with right hemispheric lesions. Complete bilateral ptosis is usually caused by large infarctions and may be a premonitory sign of an impending herniation.     

Atrial natriuretic peptide response to postural change and medication in familial dysautonomia

Circulating atrial natriuretic peptide (ANP) was assayed before and after postural change and exercise in 54 patients with familial dysautonomia (FD) and 20 controls. ANP levels were compared with blood pressure, heart rate, plasma catecholamines and parameters of renal function. Compared with controls supine FD subjects had elevated blood pressures, heart rates and ANP levels (39 ± 4 pg/ml vs. 23 ± 3 pg/ml,p < 0.01). With the erect posture and exercise in FD subjects, blood pressure fell below control values, with ANP lowered. In FD subjects, blood pressure was correlated with ANP levels when supine and when erect and with heart rate post exercise. In controls, ANP levels did not correlate with other parameters. In FD patients on metoclopramide, supine and erect blood pressure and ANP levels were higher. FD subjects treated with fludrocortisone, had elevated supine and erect noradrenaline (p < 0.05 andp = 0.06); and those on diazepam had lower erect and post exercise noradrenaline (p < 0.05), but ANP levels were similar. In conclusion, sympathetic denervation may increase FD patients' responsiveness to other regulators of cardiovascular integrity, such as ANP. In addition, circulating ANP and catecholamines in FD subjects appear to be influenced by commonly used medications, such as metoclopramide.     

The relation between aortic arch branching types and the location of large vessel occlusion in cardioembolic stroke

Cardiac embolism is the leading etiology of ischemic strokes. There are arguments about the left–right propensity of cardioembolic strokes. This study aimed to reveal the relationship between the different aortic arch types and the location of large vessel occlusion (LVO) in cardioembolic stroke. We retrospectively identified all patients with acute ischemic stroke admitted to our comprehensive stroke center who had medium- to high-risk cardioembolic sources according to the TOAST classification. Only those with LVO and available images of the aortic arch were included. Patients were classified into 3 groups according to the aortic arch types: Type I (n = 44), Type II (n = 105), Type III (n = 36). The thrombus was divided into large thrombus or small thrombus based on the location of LVO. Overall, left-sided strokes (50.8%) were almost equal to right-sided (49.2%). There was a growing tendency for the percentage of left-sided infarcts with advancement of the aortic arch types either in the total cases or in the atrial fibrillation cases, with no statistical difference between the 3 aortic arch types. In type III aortic arch, left-sided strokes (69.0%) were twice than right-sided (31%) in large thrombus (P < 0.05), while right-sided strokes (85.7%) were more common than left-sided (14.3%) in small thrombus (P < 0.05). Conversely, in type Ⅰ and II aortic arches, left-sided strokes were more common than right-sided in small thrombus, while right-sided strokes were more common than left-sided in large thrombus (P < 0.05). The left–right propensity of cardioembolic stroke is related to the proximity of clot lodging in different aortic arch types.     

Autonomic control of the heart and renal vascular bed during autonomic dysreflexia in high spinal cord injury

Autonomic function and hemodynamics were studied in nine spinal cord injured (SCI) subjects, at rest and during peripheral afferent stimulation, bladder percussion. Nine able-bodied subjects were studied for comparison during unstimulated conditions. Spontaneous baroreceptor reflex sensitivity was calculated from recordings of ECG and intraarterial blood pressure. An index of sympathetic activity was provided by measuring total body noradrenaline (NA) spillover by isotope dilution technique. Renal vascular resistance was calculated from PAH-clearance. SCI subjects had lower total body NA spillover (1011 ± 193 vs 2261 ± 328 pmol/min, P < 0.01), but similar baroreceptor reflex sensitivity and hemodynamics compared to able-bodied subjects at rest. In SCI group, during bladder percussion, mean arterial pressure increased (79 ± 5 vs 113 ± 8 mm Hg, P < 0.01), whereas heart rate was reduced during the first minute of the manoeuvre (62 ± 2 vs 56 ± 2 bpm, P < 0.05). Baroreceptor reflex sensitivity remained unchanged. Total body NA spillover and renal vascular resistance increased by 332 % (from 1004 ± 218 pmol/min, P < 0.05) and 55 % (from 0.078 ± 0.011 mmHg/ml/min, P < 0.05), respectively. SCI subjects demonstrated lower total body sympathetic outflow but normal baroreceptor reflex sensitivity at rest, suggesting a balanced autonomic output to the heart. Bladder percussion caused a substantial increase in renal vascular resistance and blood pressure, which was partly due to marked generalised sympathetic activation. This activation was counterbalanced by an increased vagal activity as evidenced by reduction of the heart rate. Received: 6 March 2002, Accepted: 28 August 2002 Correspondence to Sinsia A. Gao, MD     

Optimizing the risk estimation after a transient ischaemic attack – the ABCDE⊕ score

Background and purpose: The risk of stroke after a transient ischaemic attack (TIA) can be predicted by scores incorporating age, blood pressure, clinical features, duration (ABCD‐score), and diabetes (ABCD2‐score). However, some patients have strokes despite a low predicted risk according to these scores. We designed the ABCDE+ score by adding the variables ‘etiology’ and ischaemic lesion visible on diffusion‐weighted imaging (DWI) –‘DWI‐positivity’– to the ABCD‐score. We hypothesized that this refinement increases the predictability of recurrent ischaemic events. Methods: We performed a prospective cohort study amongst all consecutive TIA patients in a university hospital emergency department. Area under the computed receiver‐operating curves (AUCs) were used to compare the predictive values of the scores with regard to the outcome stroke or recurrent TIA within 90 days. Results: Amongst 248 patients, 33 (13.3%, 95%‐CI 9.3–18.2%) had a stroke (n = 13) or a recurrent TIA (n = 20). Patients with recurrent ischaemic events more often had large‐artery atherosclerosis as the cause for TIA (46% vs. 14%, P < 0.001) and positive DWI (61% vs. 35%; P = 0.01) compared with patients without recurrent events. Patients with and those without events did not differ with regard to age, clinical symptoms, duration, blood pressure, risk factors, and stroke preventive treatment. The comparison of AUCs [95%CI] showed superiority of the ABCDE+ score (0.67[0.55–0.75]) compared to the ABCD²‐score (0.48[0.37–0.58]; P = 0.04) and a trend toward superiority compared to the ABCD‐score (0.50[0.40–0.61]; P = 0.07). Conclusion: In TIA patients, the addition of the variables ‘etiology’ and ‘DWI‐positivity’ to the ABCD‐score seems to enhance the predictability of subsequent cerebral ischaemic events.     

脑梗死静脉溶栓治疗后出血性转化临床分析

目的探讨急性脑梗死患者溶栓治疗后出血性转化(hemorrhagic transformation,HT)的危险因素以及继发HT患者的溶栓后并发症。方法回顾性分析62例经静脉溶栓治疗的急性脑梗死患者的临床资料,结合文献选择溶栓后继发HT的危险因素,包括年龄、性别、高血压、糖尿病、心功能不全史、脑卒中史、有无早期CT缺血改变、是否大面积脑梗死、是否心源性脑栓塞、发病至溶栓时间、溶栓药物、溶栓前NIHSS评分、溶栓前血糖水平、溶栓后3d内最低纤维蛋白原水平、血小板计数、肌酐水平等进行分析,对单因素分析法发现有统计学差异的危险因素进一步行Logistic回归分析。结果单因素分析发现,与无HT组相比,继发HT组年龄较大(P<0.01),溶栓前血糖水平(P<0.05)、溶栓后6h和12h的收缩压和舒张压较高(均P<0.05),大面积脑梗死发病至溶栓时间>3h、有早期CT缺血改变的患者比例高(均P<0.05)。Logistic多因素回归分析发现高龄(OR:1.129,P<0.05)、溶栓时间>3h(OR:2.592,P<0.05)、早期CT有缺血改变(OR:1.728,P<0.05)是继发HT的危险因素。继发HT组出现颅外出血并发症(52.2%vs 20.5%,χ2=6.637,P<0.05)、重度脑水肿(30.4%vs 5.1%,χ2=5.567,P<0.05)和脑疝形成(26.1%vs 2.6%,P<0.05)的比例更高。结论急性脑梗死患者静脉溶栓后HT的发生率高,高龄、发病至溶栓时间>3h和早期CT缺血改变是HT的危险因素。     

Cardiovascular effects of human insular cortex stimulation.

Recent investigations indicate a site of cardiac representation within the left insular cortex of the rat. Moreover, the results of lesion studies suggest left-sided insular dominance for sympathetic cardiovascular effects. It is unclear whether similar representation exists within the human insular cortex. Five epileptic patients underwent intraoperative insular stimulation prior to temporal lobectomy for seizure control. On stimulation of the left insular cortex, bradycardia and depressor responses were more frequently produced than tachycardia and pressor effects (p less than 0.005). The converse applied for the right insular cortex. We believe this to be the first demonstration of cardiovascular changes elicitable during insular stimulation in humans, and of lateralization of such responses for a cortical site. In humans, unlike the rat, there appears to be right-sided dominance for sympathetic effects. These findings may be of relevance in predicting the autonomic effects of stroke in humans and in the explanation of sudden unexpected epileptic death.     

Ambulatory blood pressure in patients with Parkinson's disease without and with orthostatic hypotension

Non-invasive ambulatory recordings of blood pressure and heart rate were performed using a Spacelabs device during day and night periods in patients with Parkinson's disease with (n = 19) or without orthostatic hypotension (n = 19). In patients with orthostatic hypotension, the average systolic and diastolic blood pressure during the night (137 ± 5/80 ± 3 mmHg) was higher (p < 0.05) than during the day period (121 ± 3/76 ± 2 mmHg). In patients without orthostatic hypotension, a decrease in blood pressure was recorded during the nocturnal period. In patients with orthostatic hypotension, the blood pressure variability was higher (p < 0.05) during the day (systolic: 14.6 ± 1.3%; diastolic: 16.5 ± 1.0%) than during the night (systolic: 9.1 ± 0.8%; diastolic: 10.8 ± 1.1%). The blood pressure load (percentage of values above 140/90 mmHg) during the night was significantly higher than during the day for both systolic (41.2 ± 8.1 vs. 19.6 ± 4.7%) and diastolic blood pressure (24.9 ± 6.9 vs. 16.3 ± 4.9%). There was a decrease in heart rate in both groups during the night. A fall of 25 mmHg or more in systolic blood pressure after meals occurred in ten patients with orthostatic hypotension and in one patient without orthostatic hypotension. These results indicate that orthostatic hypotension in Parkinson's disease is associated with specific modifications of ambulatory blood pressure including loss of circadian rhythm of blood pressure, increased diurnal blood pressure variability and post-prandial hypotension.     

The syndrome of combined polar and paramedian thalamic infarction

BACKGROUND: Occlusion of the polar or the paramedian arteries of the thalamus usually leads to distinct infarcts with specific clinical and imaging correlates. However, vascular variation is such that in up to one third of humans, the polar artery is missing and its territory taken over by the paramedian arteries. OBJECTIVE: To provide attention to the corresponding stroke syndrome of combined polar and paramedian thalamic infarction. METHODS: We studied combined polar-paramedian thalamic infarction in 12 patients (6 right-sided lesions, 3 left-sided lesions, and 3 bilateral lesions) who were selected from 208 consecutively registered patients with thalamic strokes in the Lausanne Stroke Registry. RESULTS: The clinical manifestation included executive dysfunction, apathy, and memory impairment in all patients, with eye movement disturbances in 10 patients (5 with right-sided lesions, 2 with left-sided lesions, 3 with bilateral lesions); acutely impaired consciousness in 11 patients (5 with right-sided lesions, 3 with left-sided lesions, 3 with bilateral lesions); aphasic disturbances in 8 patients (2 with right-sided lesions, 3 with left-sided lesions, 3 with bilateral lesions), including nonfluent aphasia in 1 patient (with left-sided lesions); dysarthria in 5 patients (4 with right-sided lesions, 1 with bilateral lesions); constructional apraxia in 5 patients (with right-sided lesions); mild hemiparesis in 4 patients (2 with right-sided lesions, 2 with left-sided lesions); dyscalculia in 3 patients (1 with left-sided lesions,1 with right-sided lesions, 1 with bilateral lesions); limb dystonia or asterixis in 2 patients (1 with right-sided lesions, 1 with bilateral lesions); mild hemisensory loss in 2 patients (1 with right-sided lesions, 1 with left-sided lesions); hemiataxia in 1 patient (with right-sided lesions); and ideomotor apraxia in 1 patient (with left-sided lesions). Follow-up showed severely disabling, persistent amnesia in 7 patients (4 with right-sided lesions, 3 with bilateral lesions) and persistent eye movement dysfunction in 5 patients (2 with right-sided lesions, 1 with left-sided lesions, 2 with bilateral lesions). The most common etiology appeared to be cardioembolism, followed by artery-to-artery embolism and presumed small-artery disease. CONCLUSIONS: Key features of this syndrome included amnesia preceded by a period of altered consciousness, and vertical eye movement disturbances. The severe and persistent amnesia may be due to coexisting damage to the anterior and dorsomedial nuclei.     

颈动脉超声应用筛查颈动脉狭窄及脑卒中高危因素分析

目的分析广西壮族自治区梧州市角嘴社区颈动脉超声应用筛查颈动脉狭窄结果及脑卒中的高危因素。方法选择2013年1月~2015年3月广西壮族自治区梧州市角嘴社区5789名居民为研究对象,对其采用问卷调查及体格检查,统计分析颈动脉超声检查的结果及脑卒中高危因素。结果调查的5789名居民中,≥60岁居民内膜增厚发生率26.65%,斑块形成率为13.67%;40~60岁居民内膜增厚发生率9.20%,斑块形成率为4.42%。≥60岁居民的内膜增厚发生率和斑块发生率均比40~60岁居民高(P0.05)。男性内膜增厚发生率27.89%,斑块形成率为11.38%,女性内膜增厚发生率8.06%,斑块形成率为7.37%。男性内膜增厚发生率和斑块发生率均比女性居民高(P0.05)。居民的脑卒中高危因素分析表明,吸烟史、高血压病、明显超重或肥胖、缺乏运动所占比例高,分别为14.32%、16.02%、16.02%、35.13%,与其他因素相比差异具有统计学意义(P0.05);高血压病、明显超重或肥胖、缺乏运动与脑卒中的发生关联较大(P0.05)。结论广西壮族自治区梧州市角嘴社区脑卒中高危人群的干预的重点方向应为降低血压、控制饮食和多运动。通过开展颈动脉血管超声检查,实现居民脑卒中前期患者的早发现、早干预、早治疗。     

Ipsilateral weakness caused by ipsilateral stroke: A case series

IntroductionThere are few reported cases of ipsilateral weakness following ischemic or hemorrhagic stroke. In these rare cases, ipsilateral weakness is typically the result of damage to uncrossed components of the corticospinal tract (CST) which were recruited in response to previous CST injury.Patients and methodsWe report a series of six cases of acute ipsilateral weakness or numbness following a hemorrhagic or ischemic stroke from three medical institutions in Saudi Arabia.ResultsThree of these patients presented with right-sided weakness caused by an ipsilateral right hemispheric stroke, while two exhibited left-sided symptoms and one had only left-sided numbness. In all six cases, the ipsilateral corona radiata, internal capsule, basal ganglia, insula, and thalamus were involved. No concomitant opposite hemisphere or brainstem lesion in none of the patients was evident. Two patients had previous strokes affecting the brainstem and left corona radiata, respectively. Complete stroke workup to reveal the cause of stroke was carried out, however no functional MRI was performed.ConclusionIschemic or hemorrhagic stroke may indeed result in ipsilateral weakness or numbness, though in very rare cases. We assume that the most likely mechanism of their ipsilateral weakness subsequent to the ipsilateral stroke was a functional reorganization favoring CST pathways within the ipsilateral hemisphere.     

Visually evoked blood flow responses and vasoneuronal coupling in partial epilepsy

OBJECTIVES: Increased metabolic demand is coupled with increased regional blood flow. The decreased vasoreactivity in epileptic patients however, prompts an impact of epileptic dysfunction on vasoneuronal coupling. MATERIAL AND METHODS: Blood flow velocities during visual stimulation were monitored by TCD in both posterior cerebral arteries in 20 epileptic patients and 20 control persons, response-amplitudes (RA) and pulsatility indices (PI) were analyzed. RESULTS: The RAs were significantly smaller in patients than in controls (28.4 +/- 5.7% vs 38.4 +/- 10.2%; P < 0.001). RAs were larger in the right side and these right-sided responses were significantly smaller in patients with right-sided vs left-sided epileptic foci (27.9 +/- 5.5% vs 36.1 +/- 4.5%; P < 0.005). The PI during stimulation was significantly larger in patients than in controls (0.92 +/- 0.11 vs 0.74 +/- 0.15; P < 0.001). CONCLUSION: Our data suggest an impaired vasoneuronal coupling in focal epilepsy, and support the view that the right hemisphere might be more important for color processing.     

Muscle sympathetic nerve activity during postural change in healthy young and older adults

Recent evidence suggests that during orthostatic stress the reflex increase in muscle sympathetic nerve activity may be diminished in older adults. To test this hypothesis, we measured muscle sympathetic nerve activity, plasma noradrenaline concentrations, heart rate, and arterial blood pressure in twelve young (mean, 25 years; range, 19–29 years) adults and 14 older (mean 64 years; range, 60–74 years) healthy adults, while supine and during upright sitting. Supine control levels of muscle sympathetic nerve activity were higher in the older subjects (35 ± 1 vs. 25 ± 1 bursts/min,p < 0.05), but there were no differences in plasma noradrenaline concentrations, heart rate or arterial pressure. Despite higher supine control levels in the older group, the absolute unit increases in muscle sympathetic nerve activity in response to upright sitting (p < 0.05 vs. control) were not different in the two groups (7 ± 1 vs. 7 ± 1 bursts/min), nor were the increases in plasma noradrenaline concentrations. Heart rate did not increase above supine control in response to sitting in either group. Arterial pressure increased slightly (p < 0.05, supine vs. control), but there were no age-related differences. These results indicate that, contrary to recent findings, the reflex increases in muscle sympathetic nerve activity and plasma noradrenaline concentrations and regulation of arterial pressure during this natural orthostatic stress are well preserved in older healthy men and women.     

Influence of antiplatelet pre‐treatment on the risk of intracranial haemorrhage in acute ischaemic stroke after intravenous thrombolysis

Background: Pre‐treatment with antiplatelet agents (AP) is present amongst 30% of acute stroke patients. Previous studies have shown conflicting results on the effect of these drugs regarding haemorrhagic transformation after thrombolytic therapy. The hypothesis that pre‐treatment with AP may increase the risk of cerebral haemorrhage (ICH) after intravenous tissue plasminogen activator (tPA) was assessed. Methods: Retrospective study of consecutive prospectively registered patients with acute ischaemic stroke treated with iv tPA (n = 235) in the last 5 years. Baseline characteristics and prior AP therapy were registered on admission. Computed tomography (CT) scan was performed on admission and 24–36 h after tPA. ICH was classified according to the ECASS II criteria into haemorrhagic infarction and parenchymal haematoma (PH). Symptomatic intracerebral haemorrhage (SICH) was defined as a worsening of ≥ 4 points in the NIHSS score during the first 36 h in any haemorrhage subtype. Results: Seventy‐two (30.6%) patients were pre‐treated with AP (55 aspirin, 14 clopidogrel, 2 aspirin + clopidogrel, 1 triflusal). PH was observed in 33 (14.1%) patients (PH1 13, PH2 12, PHr 8) of whom 16 were symptomatic. Male gender (78.8% vs. 21.2%, P = 0.036), prior AP therapy (54.5% vs. 26.9%, P = 0.001), stroke severity (median NIHSS, 17 vs. 12, P = 0.005) and early CT signs of infarction (12.5% vs. 2.1%, P = 0.004) were associated with PH. The adjusted odds ratios of PH for patients pre‐treated with AP therapy was 3.5 (1.5–7.8, P = 0.002) and for SICH 1.9 (0.6–5.9, P = 0.2). Conclusions: Pre‐treatment with AP is associated with an increased risk of PH after intravenous thrombolysis in patients with acute ischaemic stroke.     

Expression of stromal‐cell‐derived factor‐1 (SDF‐1): a predictor of ischaemic stroke?

Background and purpose: Platelet stromal‐cell‐derived factor‐1 (SDF‐1) plays a pivotal role in angiogenesis and the regeneration of ischaemic tissue through the regulation of haematopoietic progenitor cells and is upregulated at the sites of vascular injury and platelet activation. Thus, SDF‐1 has recently been discussed as a predictor in ischaemic diseases such as acute myocardial infarction. However, no clinical data pertinent to the investigation of the platelet SDF‐1 expression in patients with stroke are available. Methods: We consecutively evaluated 196 patients who were admitted to the stroke unit with symptoms suspected for stroke. Surface expression of the platelet activation markers (P‐selectin and GPIb) and the expression of platelet‐bound SDF‐1 were determined by two‐colour whole blood flow cytometry. Results: Patients with transient ischaemic attack (TIA) as well as with ischaemic stroke showed similar levels of SDF‐1 expression on hospital admission compared with patients with non‐ischaemic (NI) events and with 30 healthy controls (TIA (mean fluorescence intensity ± SD): 31.5 ± 18.2 vs. NI: 26.4 ± 15.7; P = 0.361; stroke: 28.7 ± 19.8 vs. NI; P = 0.943; control: 26.1 ± 11.3; P > 0.05 compared with all). Platelet SDF‐1 expression showed a trend with the severity of stroke according to National Institute of Health Stroke Scale score (r = 0.125; P = 0.085), but significantly correlated with the peak levels of C‐reactive protein (r = 0.218; P = 0.002) and with the levels of platelet activation (P‐selectin: r = 0.389; P = 0.001). Multifactorial analysis of covariance revealed a significant influence on platelet SDF‐1 expression by smoking (P = 0.019). Conclusions: Platelet SDF‐1 surface expression did not show any significant difference in patients with TIA and ischaemic stroke compared with patients with NI events. Thus, single biomarker evaluation of platelet SDF‐1 surface expression is not helpful to predict ischaemic stroke.