Brain injury and repair
What happens to the brain after injury - from the initial cascade to long-term neuroplastic change - and what rehabilitation does to support recovery.
When the brain is injured, recovery is not simply “growing back” lost tissue. It is a dynamic, months-long process of inflammation, rewiring, and compensation - one that rehabilitation can powerfully shape.
The injury cascade
Within minutes to days of stroke, TBI, or hypoxia, a cascade unfolds:
- Primary injury - direct cell death in the affected area (infarct core in stroke; contusion in TBI).
- Ischaemic penumbra / peri-lesional zone - surrounding tissue is stressed but potentially salvageable.
- Glutamate excitotoxicity - dying neurons release excess glutamate, over-stimulating and killing neighbouring cells (hours to days).
- Inflammation - microglia and immune cells arrive; short-term inflammation clears debris but prolonged inflammation harms surviving tissue.
- Oedema - swelling increases pressure; large bleeds or injuries may need surgery.
What recovery looks like
Recovery occurs on several timescales simultaneously:
| Phase | Timeframe | What’s happening |
|---|---|---|
| Spontaneous recovery | Days to weeks | Oedema resolves; penumbral tissue restabilises; diaschisis (shut-down of connected regions) reverses |
| Synaptogenesis | Weeks to months | New synaptic connections form; surviving axons sprout |
| Cortical remapping | Months to years | Adjacent or contralateral areas take on functions of damaged regions |
| Learned compensation | Ongoing | Different strategies and circuits achieve former goals |
The role of rehabilitation
Rehabilitation doesn’t just wait for spontaneous recovery - it actively drives neuroplastic change:
- High repetition - practice frequency drives long-term potentiation (LTP), the synaptic strengthening mechanism underlying memory and skill learning.
- Task specificity - the brain rewires most efficiently for the exact task practiced; walking on a treadmill is more useful for gait than leg presses.
- Errorless learning vs trial-and-error - depends on the type of deficit; explicit tasks benefit from some error, while amnesic memory tasks benefit from minimising errors.
- Emotional engagement - dopamine released during rewarding, meaningful activity boosts synaptic plasticity; bored, disengaged practice produces less change.
- Intensity - more hours of active practice per day is consistently associated with better outcomes; passive treatments (massage, passive range of motion) without active movement add little to cortical remapping.
Factors that slow recovery
- Poor sleep - glymphatic clearance and memory consolidation are both reduced.
- Alcohol - suppresses neuroplastic signalling; significantly slows recovery.
- Untreated depression and apathy - reduce participation in rehab; directly impair dopaminergic plasticity pathways.
- Sedating medication - some anticonvulsants and benzodiazepines interfere with LTP in animal models; minimising them where safe is often worthwhile.
- Chronic pain - consumes attentional and cortical resources that could support plasticity.
A hopeful framing
Recovery is lifelong - neuroplasticity doesn’t stop after six months. Gains made at two years can still occur; they simply require ongoing active practice. This is why maintaining rehab intensity at home, through activities and daily routines, matters long after formal sessions end.