الفهرس 
ABSTRACTOnly 14 pages are availabe for public view
 |  | from | 213 |  |  |
| | | from | 213 | | |
Abstract
Summary
Stroke is the second most common cause of death and the third most common cause of disability all over the world. TPA is the only FDA approved treatment for ischemic stroke. TPA was found to greatly eliminate stroke patients disability through its thrombolytic action. Recently, studies pointed to the crucial role of TPA in neuroplasticity participating in the recovery of ischemic stroke patients.(405)
The aim of this study is to assess the impact of treating stroke patients with TPA on their serum level of BDNF as a marker of neuroplasticity.
The study was conducted on 26 patients with ischemic stroke eligible for receiving rTPA treatment (within 4.5 hours from stroke onset) (patient group) and 21 patients with ischemic stroke having contraindications for treatment with rTPA (within 12 hours from stroke onset) (control group). The mean age for patients was 59±13.55 years and for controls 62.76 ±13.97 years. There was no statistically significant difference between patients and controls regarding age or sex.
Eligible Patients for rTPA received intravenous (i.v.) rTPA (0.9 mg/kg, Actilyse, Boehringer Ingelheim).
All included patients were subjected to the following:
History taking regarding: stroke risk factors (DM, HTN, AF, smoking, drug abuse, family history or past history of stroke).
Clinical assessment including: BMI and neurological assessment using the NIHSS at the onset of stroke and at day 7 from the onset.
Laboratory investigations including: Random blood sugar, complete blood count (WBC, PLT and HCT), lipid profile (cholesterol, TG, LDL and HDL) and uric acid.
Serum BDNF measurement at the onset of stroke and at day 7 from the onset using commercial sandwich-ELISA kits (Human BDNF ELISA Kit , SUNLONG BIOTECH ).
Radiological assessment including: C.T. or MRI brain at the onset of stroke and at day 7 from stroke onset. Infarction site and size were assessed using the pure ellipsoid model of ABC/2.
Cardiovascular assessment using echocardiography to assess the presence of valvular disease, ejection fraction , left atrium dilatation and cardiomyopathy.
Carotid and vertebrobasilar duplex to detect atherosclerosis or stenosis of the carotid and vertebrobasilar arteries.
The results of our study were summarized in the following:
rTPA treated patients were found to have significantly more increase in BDNF serum level (from day 1 to day 7) than controls.
Female patients had a significantly higher serum level of BDNF than male patients at the onset of stroke.
Smokers had a significantly lower serum level of BDNF than non smokers at the onset of stroke.
There was no statistically significant difference in BDNF serum level at the onset of stroke between subjects with and without DM or HTN
There was no statistically significant difference between abuser and non-abusers in BDNF serum level at the onset of stroke.
There was no statistically significant difference between subjects with and without a past or family history of stroke in BDNF serum level at the onset of stroke.
There was no statistically significant difference in BDNF serum level at the onset of stroke between subjects with and without valvular heart diseases, AF or cardiomyopathy.
There was no statistically significant difference between subjects with ejection fraction < 45% and subjects with ejection fraction ≥ 45% difference in BDNF serum level at the onset of stroke.
There was no statistically significant difference in BDNF serum level at the onset of stroke between subjects with and without carotid atherosclerotic changes.
There was no statistically significant correlation between BDNF serum level measured at the onset of stroke and either age, BMI, or blood pressure (systolic & diastolic).
There was no statistically significant correlation between BDNF serum level measured at the onset of stroke and either RBS, cholesterol, LDL, HDL, TG, platelets, HCT, WBCs or uric acid.
There was no statistically significant correlation between BDNF serum level measured at day 7 from stroke onset and either NIHSS or infarction size at day 7
There was no statistically significant correlation between BDNF serum level measured at day 7 form stroke onset and door to needle time.
Conclusion
TPA improves neuroplasticity (through increasing BDNF) in patients with acute stroke in addition to its role as a thrombolytic therapy.
Female patients had a significantly higher serum level of BDNF than male patients.
Smokers had a significantly lower serum level of BDNF than non smokers.
No effect of either age, BMI, HTN, DM, drug abuse, past or family history of stroke, valvular heart diseases, AF, cardiomyopathy, decreased ejection fraction, carotid atherosclerotic changes, RBS, cholesterol, LDL, HDL, TG, platelets, HCT, WBCs or uric acid, on BDNF serum level measured at the onset of stroke.
No effect of door to needle time on BDNF serum level measured at day 7 form stroke onset.
No effect of BDNF serum level measured at day 7 form stroke onset on NIHSS or infarction size at day 7.