scholarly journals First Autologous Cell Therapy of Cerebral Palsy Caused by Hypoxic-Ischemic Brain Damage in a Child after Cardiac Arrest—Individual Treatment with Cord Blood

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
A. Jensen ◽  
E. Hamelmann

Each year, thousands of children incur brain damage that results in lifelong sequelae. Therefore, based on experimental evidence, we explored the therapeutic potential of human cord blood, known to contain stem cells, to examine the functional neuroregeneration in a child with cerebral palsy after cardiac arrest. The boy, whose cord blood was stored at birth, was 2.5 years old and normally developed when global ischemic brain damage occurred resulting in a persistent vegetative state. Nine weeks later, he received autologous cord blood (91.7 mL, cryopreserved,5.75×10e8mononuclear cells) intravenously. Active rehabilitation (physio- and ergotherapy) was provided daily, follow-up at 2, 5, 12, 24, 30, and 40 months. At 2-months follow-up the boy’s motor control improved, spastic paresis was largely reduced, and eyesight was recovered, as did the electroencephalogram. He smiled when played with, was able to sit and to speak simple words. At 40 months, independent eating, walking in gait trainer, crawling, and moving from prone position to free sitting were possible, and there was significantly improved receptive and expressive speech competence (four-word sentences, 200 words). This remarkable functional neuroregeneration is difficult to explain by intense active rehabilitation alone and suggests that autologous cord blood transplantation may be an additional and causative treatment of pediatric cerebral palsy after brain damage.

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
A. Jensen ◽  
E. Hamelmann

Intracranial laceration due to traumatic birth injury is an extremely rare event affecting approximately one newborn per a population of 4.5 million. However, depending on the mode of injury, the resulting brain damage may lead to lifelong sequelae, for example, cerebral palsy for which there is no cure at present. Here we report a rare case of neonatal arterial ischemic stroke and cerebral palsy caused by fetal traumatic molding and parietal depression of the head during delivery caused by functional cephalopelvic disproportion due to a “long pelvis.” This patient was treated by autologous cord blood mononuclear cells (45.8 mL, cryopreserved, TNC2.53×10e8) with a remarkable recovery. Active rehabilitation was provided weekly. Follow-up examinations were at 3, 18, 34, and 57 months. Generous use of neonatal head MRI in case of molding, craniofacial deformity, and a sentinel event during parturition is advocated to enhance diagnosis of neonatal brain damage as a basis for fast and potentially causative treatment modalities including autologous cord blood transplantation in a timely manner.


Cytotherapy ◽  
2018 ◽  
Vol 20 (5) ◽  
pp. S114
Author(s):  
A. Saha ◽  
L. Xu ◽  
P. Scotland ◽  
S. Buntz ◽  
R. Franczak ◽  
...  

2010 ◽  
Vol 19 (3) ◽  
pp. 351-358 ◽  
Author(s):  
Pedro M. Pimentel-Coelho ◽  
Elizabeth S. Magalhães ◽  
Laudelino M. Lopes ◽  
Leonardo C. deAzevedo ◽  
Marcelo F. Santiago ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
R. Schneider ◽  
C. Stumpf ◽  
A. Yilmaz ◽  
G.H. Wasmeier ◽  
C. Schlundt ◽  
...  

Background: Overall prognosis in comatose survivors of Cardiopulmonary resuscitation is poor and the degree of hypoxic brain damage is usually the most important prognostic factor. Elevation of the neuron-specific enolase (NSE) as measured with 72 hours after admission has been identified as a predictor of neurologic outcome, and a threshold level of 33 ng/ml has been proposed as a highly specific cut-off value, above which neurologic outcome will be unfavourable. Therapeutic hypothermia is a new concept to improve neurologic outcome in patients after resuscitation, and the prognostic relevance of elevated NSE levels in patients treated by hypothermia has not yet been assessed. Methods: Mild therapeutic hypothermia (33–34°C) was applied via an intravenous cooling catheter for 24 hours in 38 consecutive patients admitted after successful on-site resuscitation following out-of-hospital cardiac arrest (28 male, 10 female, age 38 – 83 years, mean age 64.4±12.7 years). 72 hours after admission, NSE level was measured. Clinical and neurologic outcome was assessed at 1 and 4 weeks. Results: Out of 38 patients, 4 patients died within the first 72 hours. In 2 additional patients, NSE measurement was impossible because of haemolytic serum. NSE levels displayed a wide range (9.8 ng/ml − 720 ng/ml). Of the 32 patients available for analysis, 17 patients suffered severe ischemic brain damage or died during the further course (NSE 11.0 –720 ng/ml, mean 150.4±185.9 ng/ml). 15 patients recovered and had favourable neurologic outcome (NSE 9.8 – 47.9 ng/ml, mean 21.1±11.9 ng/ml). Using the recommended threshold value of 33 ng/ml, the sensitivity for ischemic brain damage was 76.5%, specificity was 80.0%, and the positive predictive value was 81.3%. Conclusions: Based on prior experience in patients without therapeutic hypothermia, a cut-off level of 33 ng/ml has been recommended as a highly specific threshold above which neurologic outcome in patients resuscitated for out-of-hospital cardiac arrest will be poor. Our data demonstrate, however, that favourable outcome can be achieved even for higher NSE levels in patients who are treated with therapeutic hypothermia. Thus, the prognostic value of NSE in these patients must be reconsidered.


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