Cerebral palsy

Cerebral palsy is not a single disease but a group of conditions sharing persistent disturbances of motor function, muscle tone, and coordination. The cause is brain injury during fetal development, birth, or the early postnatal period — hypoxia-ischaemia, infection, haemorrhage, or extreme prematurity. According to WHO, incidence is approximately 2–3 cases per 1,000 live births and has remained stable despite advances in perinatal medicine. Clinical presentation ranges from mild coordination disorders to severe spastic tetraplegia with epilepsy and cognitive deficits. Traditional rehabilitation — physiotherapy, botulinum therapy, orthopaedic surgery — has limited effect, particularly in children older than 6 years when neuroplasticity begins to decline. Cell therapy is considered a complementary approach targeting not the symptoms but the underlying pathogenic mechanisms: chronic neuroinflammation, oxidative stress, and deficient remyelination.

Cerebral palsy is classified by topography and the character of motor involvement. Spastic forms account for approximately 80% of cases — increased muscle tone, hyperreflexia, and characteristic postural patterns (scissor gait, equinus foot deformity). Dyskinetic CP manifests as involuntary movements: athetosis, chorea, dystonia. The ataxic form features impaired coordination and balance with relatively preserved tone. A significant proportion of patients show mixed phenotypes. Functional severity is graded internationally on the GMFCS (Gross Motor Function Classification System) from level I (independent ambulation with minimal limitation) to level V (full dependence on care). Cell therapy is most clearly indicated at GMFCS levels II–IV, where rehabilitation potential remains and can be amplified by neuroprotection. At level I the effect is less perceptible because baseline function is already high; at level V the therapy serves a supportive role for quality of life and reduction of secondary complications.

Pathophysiologically, cerebral palsy is a static lesion that triggers dynamic cascades. In children born preterm, periventricular leukomalacia is most common — death of oligodendrocytes in maturing white matter zones, followed by cystic degeneration. In term infants who suffered acute hypoxia-ischaemia, the basal ganglia and thalamus are typically affected. After the primary event, the brain tissue maintains a chronic inflammatory state for years: activated microglia secrete pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) that sustain oxidative stress, excitotoxicity, and inhibit remyelination. This explains why a single insult sustained at 32 weeks of gestation continues to influence neurons decades later — the brain literally lives in a state of smouldering neuroinflammation. It is precisely this component that the immunomodulatory capacity of mesenchymal stem cells targets.

Contemporary cerebral palsy management is multidisciplinary, and each component has defined limits. Botulinum toxin reduces local spasticity for 3–4 months but does not modify contracture progression and provides no systemic neuroprotective effect. Selective dorsal rhizotomy is effective in carefully selected patients with spastic diplegia and normal cognition, but it is an irreversible neurosurgical procedure. Intrathecal baclofen via an implanted pump controls severe spasticity but requires regular refills and carries infectious risks. Orthopaedic procedures — tenotomies, osteotomies — correct established deformities but do not prevent their recurrence. Concurrently, ongoing physiotherapy, occupational therapy, speech therapy, and intensive motor rehabilitation programmes (CIMT, HABIT, Bobath, Vojta) are pursued. All these modalities address consequences, but none modifies the primary pathogenic mechanism — chronic neuroinflammation and the brain's deficient endogenous regenerative programmes.

Mesenchymal stem cell and exosome therapy is conceived not as an alternative but as a complement to standard care. After systemic administration, MSCs migrate towards injury zones via chemokines released by damaged tissue (the SDF-1/CXCR4 axis, VCAM-1, ICAM-1). Most infused cells do not engraft long-term, but over the course of several weeks they function as a "biological factory" of paracrine factors: switching microglia from a pro-inflammatory M1 phenotype to a regenerative M2 phenotype, activating endogenous neural stem cells of the subventricular zone, supporting angiogenesis in zones of chronic ischaemia, and transferring functional mitochondria into neurons with metabolic dysfunction. This biochemical milieu opens a temporary window of enhanced neuroplasticity that must be exploited through intensive physical rehabilitation — without it, the effect of cell therapy is substantially diminished.

The Hanshi United programme for cerebral palsy is built around these principles. The standard protocol comprises three procedures at 15–20 day intervals: each session is a combined administration of umbilical-cord-derived mesenchymal stem cells (UC-MSC) intrathecally for direct CNS impact and intravenously for systemic immunomodulation. Between procedures and after the course, nasal exosomes may be used at home — this delivery route bypasses the blood-brain barrier through the olfactory nerve. The course is accompanied by mandatory intensive rehabilitation: physiotherapy 5–6 days per week, occupational therapy, speech therapy, and where indicated correction of epileptiform activity. A decision on a repeat course is taken at 6 months on the basis of objective scales — GMFM-66/88, FMS, MACS — and analysis of functional progress. The academic board reviews each case individually and does not accept patients with active malignancy, uncontrolled epilepsy, severe coagulopathy, or current acute infections.