David Goldemund

Serum inflammatory biomarkers in Parkinson's disease.

Numerous recent findings indicate the involvement of a neuroinflammatory reaction in the neurodegeneration in idiopathic Parkinsons disease (PD). We examined 29 consecutive patients with PD, ages 54-84 years, most of whom were moderately impaired (median UPDRS 19; Hoehn-Yahr 3; MMSE 28). A series of serum biomarkers were investigated, and their levels were correlated with the degree of the motor and cognitive impairment. There were no abnormalities of IL-6, acute phase proteins (C-reactive protein, serum amyloid A, alpha 1-antitrypsin, orosomucoid, ceruloplasmin, alpha 2-macroglobulin, transferrin, prealbumin) and factors of the complement system (C1q, C1-INH, C3, C4). A decrease in Mannan-binding lectin (MBL) levels was observed in six patients; an elevation of tumor necrosis factor-alpha (TNF-alpha) was found in 12 patients. No statistically significant correlation was found between the patients clinical state (neuropsychologic and motor, as expressed by UPDRS III, Hoehn-Yahr, and MMSE) and the immunomarker changes. Our results indicate that the inflammatory process may be reflected in the serum; nevertheless, further research is needed to elucidate the possible clinical implications.

Vascular pathology in patients with idiopathic Parkinson's disease.

To study the impact of brain vessel pathology on the clinical status of Parkinsons disease (PD), in 57 consecutive patients the clinical and neuropsychological data were compared with clinical MRI signs of vascular impairment and with the ultrasound brain vessel investigations. There was a significant correlation between clinical and cognitive status and intimomedial thickness, which is an indicator of large vessel impairment. Cognitive status was significantly related to the pulsatility index (an indicator of small vessel impairment). This study provides evidence that subclinical vascular pathology could influence the clinical status by contributing to motor and cognitive dysfunction in PD.

Safety of performing CT angiography in stroke patients treated with intravenous thrombolysis

Objective Exposure to contrast agents may cause nephrotoxicity. The safety of performing CT angiography without having knowledge of the baseline creatinine level in stroke patients treated with tissue plasminogen activator (tPA) has not been established. Methods This is an observational cohort study, with a historical control group to evaluate the safety of CT angiography performed before tPA treatment given within 3 h of symptom onset. The CT angiography group represents all patients treated with tPA between September/2003 and November/2007 who had CT angiography. The control group consists of all patients treated with tPA between January 1999 and August 2003 when CT angiography was not performed. The primary outcome was a creatinine increase in 24–72 h compared with baseline; the secondary outcome was a creatinine increase by ≥44 μmol/l in 24–72 h and the incidence of symptomatic intracerebral haemorrhage (sICH). Results Baseline parameters between the CT angiography group (164 patients, age 70±11; 91 male) and the control group (77 patients, age 67±11; 45 male) were similar. In the CT angiography group, the mean creatinine increase was −0.89 mmol/l and in the control group 2.2 mmol/l (p=0.42). A creatinine increase of ≥44 μmol/l occurred in five patients (3%) in the CT angiography group and in three patients (4%) in the control group (p=0.50). Also, in the CT angiography group, eight patients (5%) had sICH as compared with three patients (4%) in the control group (p=0.73). Conclusion Contrast agents given for CT angiography, performed in patients with normal and abnormal creatinine level, neither caused renal injury nor interfered with the safety of tPA treatment.

A pilot study on systemic thrombolysis followed by low molecular weight heparin in ischemic stroke

Low molecular weight heparin (LMWH) administered immediately after intravenous thrombolysis (IT) may reduce the risk of arterial re‐occlusion. Its benefit, however, may not outweigh the risk of intracranial hemorrhage (ICH). We sought preliminary data regarding safety of this combined therapy in an open‐label, non‐randomized study. The patients received either a standard anticoagulation (AC) starting 24 h after IT (the standard AC group) or AC with 2850 IU of nadroparin, given every 12 h immediately after IT (the early AC group). Sixty patients received IT treatment: 25 in the standard AC group [mean age 66, median National Institutes of Health Stroke Scale (NIHSS) 13, 64% men] and 35 in the early AC group (mean age 68, median NIHSS 13, 69% men). Symptomatic ICH occurred in one patient (4%) in the standard AC group and three patients (8.6%) in the early AC group [odds ratio (OR) 1.8; 95%CI 0.2–12.8]. At 3 months, nine patients in the standard AC group (36%) and 16 patients in the early AC group (45.7%) achieved a modified Rankin scale 0 or 1 (OR 1.2; 95%CI 0.5–3.2). Our study suggests that treatment with LMWH could be associated with higher odds of ICH, although it may not necessarily lead to a worse outcome. This justifies larger clinical trials.

Impairment of brain vessels may contribute to mortality in patients with Parkinson's disease.

The effect of brain‐vessel pathology on mortality in 57 consecutive PD patients was studied.

Outcome of Patients With Negative CT Angiography Results for Arterial Occlusion Treated With Intravenous Thrombolysis

Background and Purpose— Stroke patients without evidence of arterial occlusion may not be suitable candidates for thrombolytic therapy. In our study, we investigated the outcomes of patients with negative CT angiography results for arterial occlusion. Methods— The study included patients treated within 3 hours after symptom onset with intravenous thrombolysis for significant neurological deficit between August 2003 and June 2007. All of the patients were documented with negative CT angiography results for arterial occlusion by independent reviews. Outcome measurements included modified Rankin score at 3 months, incidence of intracranial hemorrhage, and infarction volume on control CT. The predictors of unfavorable outcome (modified Rankin score, 2-6) were identified by multivariate logistic regression. Results— Altogether, 173 patients received intravenous thrombolysis; of those, 138 underwent CT angiography. The CT angiography results were negative for arterial occlusion in 39 (28%) of the patients: mean age, 71±10 years; 16 (41%) female; median baseline NIHSS, 11. At 3 months, modified Rankin score of 0 to 1 was achieved in 18 (46%) of the patients; 6 (15%) died; and 3 (8%) had symptomatic parenchymal hemorrhage. The median infarct volume was 1.5 cm3. The independent predictors of unfavorable clinical outcome were higher age (OR, 1.1; 95% CI, 1.01-1.27), and baseline NIHSS >12 (OR, 18.8; 95% CI, 1.4 to 261). One patient had encephalitis diagnosed. Conclusions— Negative baseline CT angiography is not uncommon. The risk of intracerebral hemorrhage after thrombolytic therapy for patients without evidence of arterial occlusion is similar to the risk carried in an unselected patient population. Given the prognosis, thrombolytic therapy seems justified; however, etiology other than stroke should be considered.

Influence of location of paresis on site of pneumonia in stroke

IntroductionStroke can cause unilateral paresis of the diaphragm. It is, however, unknown if diaphragm paresis can lead to post-stroke pneumonias. We aimed to evaluate whether the location of post-stroke paresis influenced the location of pneumonia.MethodsThis is a retrospective study of all patients admitted to stroke unit in 2006–2009 with a diagnosis of acute ischemic stroke or intracerebral hemorrhage who had hemiparesis or hemiplegia, and who were diagnosed with unilateral pneumonia based on chest radiogram.ResultsOf 1394 patients with a diagnosis of stroke, 64 (5%) patients met the study criteria. Of 35 patients with motor deficit on the left side, 18 (51%) developed pneumonia on the left and 17 (49%) on the right side (p=0.90). Of 29 patients with motor deficit on the right side, 17 (59%) developed pneumonia on the right and 12 (41 %) on the left side (p=0.51). Thus, of all 64 patients, 35 (55%) had pneumonia on the same side as the paresis and 29 (45%) on the contralateral side (p=0.60).ConclusionsThere was no significant occurrence of pneumonia on the side of paresis. Therefore, the side of paresis is not likely to be a helpful clinical marker of diaphragm paresis.