**2. Plasma growth factor functions**

of improve levels of certain plasma growth factors depending on the platelet or mononuclear

An emerging medical field of application is undoubtedly neurology, especially those processes of anoxic or hypoxic ischemic origin, including cerebral palsy. The immunomodulatory and proangiogenic effect that plasma growth factors have on neurogenesis opens up a surprising range of treatment possibilities together with neurorehabilitation with the aim of improving functional capacity in these patient with the aim of improving functional capacity in these patients, especially in the cognitive area: language, memory, ability to perform complex tasks, etc., using a technique that is minimally invasive, easy to reproduce and with

predominance of the product finally obtained [3, 4].

124 Cerebral Palsy - Clinical and Therapeutic Aspects

a very low economic cost [4–6] (**Figure 1**).

**Figure 1.** Effects of growth factors in neural tissue.

*PDGF* (*platelet-derived growth factor origin*): promotes angiogenesis via macrophages by a mechanism of chemotaxis, having a significant mitogenic activity on neurons, microglia cells, making both proliferation and remyelination and facilitates the formation of type 1 collagen [5, 7].

*TGF-beta* (*transforming growth factor-beta*): induces differentiation of neural stem cells.

*FGF* (*fibroblast growth factor*): enables the proliferation and differentiation of neural stem cells.

*IGF-1* (*insulin-like growth factor 1*): it induces a potent mitotic effect on neural progenitor stem cellularity.

*VEGF* (*vasculo-endothelial growth factor*): enables chemotaxis and differentiation neural cells promoting blood vessel air permeability.

*Ectodermal growth factor* (*EGF*): great proapoptotical capacity, chemotaxis on neural and glial cells.

*BDNF* (*brain-derived neurotrophic factor*): produces proliferation, differentiation and neuronal chemotaxis on microglial and oligodendrocitarial cellularity and remyelination thereof.

*HGF* (*hepatocyte growth factor*): induces cell proliferation and differentiation, chemotaxis, angiogenesis and extracellular matrix synthesis (**Table 1**).



**4. Plasma growth factors (PRP) in cerebral palsy**

tates the survival and neuronal differentiation [2, 3, 7].

of the PI3K/Akt anti apoptotic signaling pathway [2].

tablishing the normal functional circuit of the same.

final reconnection of the affected axon.

skeletal muscle ischemia [2, 3, 7].

PRP produces a release of cellular signaling molecules only or in combination that have been shown to produce both neuroprotective and anti apoptotic effect on the neuron and adult neural stem cells repairing neural tissue. Plasma growth factors constitute support that facili-

Plasma Growth Factors in Cerebral Palsy http://dx.doi.org/10.5772/intechopen.80369 127

It has been shown that application of autologous plasma growth factors had a neuroprotective and antifibrotic effect, improving nerve regeneration probably induced by the activation

We do not yet have enough studies to evaluate effect of angiogenesis in the nerve repair. Administration of autologous PRP rich in VEGF and IGF-1 accelerates the regeneration of the neuromuscular junction owing to the increase of angiogenesis. Intramuscular injections of PRP would increase the angiogenesis and produces reperfusion after the induction of a severe

The main function of PRP has been showed in a rat brain sample, where application of plasma growth factors induced both the increase in the number and the growth of axons. The PRP has been used in a model of acute cerebral nerve injury in rabbits, as a culture medium to neurological stem cells reporting beneficial effects on axonal count, myelination and electrophysiological functionality. PRP could increase both the thickness of the myelin and amount of axons, producing an increase in functional activity at the date of latency associated with improvement in the thickness of the myelin. PPR could contribute significantly to the two key events for a proper axonal regeneration: angiogenesis and the establishment of an optimal microenvironment for the differentiation, immunomodulation and cell division [1–3, 5, 6].

It has been objectified an anti-inflammatory activity of PRP, aiming that b-amyloid expresses cytokines inhibited when astrocytes are cultivated with autologous growth factors, that could be explained by suppression of NFkB in astrocytes with the activation of the Cyclooxygenase and the expression of tumor necrosis factor in the brain. Several studies have reported that plasma growth factors like IGF-1, PDGF and TGF-B, could inhibit the NFkB on the tenocytes, synovial cells, fibroblasts, chondrocytes and change the macrophages from phenotype M1 to M2 [2, 6, 7].

The growth factors would produce neurogenesis phenomena through 3 ways: first inhibiting the inflammatory process that would difficult the anatomical and physiological neuronal recovery; secondly improving the migration and proliferation of stem neuronal cells at the site of the lesion and finally stimulating its differentiation toward mature neuronal mass rees-

The lesion of a neuron actives macrophages and mononuclear cells like Monocytes that phagocyte the myelin residues, stimulating by autocrine way the nerve growth factor (NGF), that facilitates the recruitment of Schwann cells to the area of the lesion, their differentiation and proliferation join to the vasculo-endothelial growth factor producing remyelination and

**Table 1.** Summary of the proteins in the platelet alpha granules.
