How is paralysis treated in a rat? - briefly
Paralytic deficits in rats are addressed through a combination of pharmacological agents (e.g., neuroprotective drugs, anti‑inflammatory compounds), targeted physical rehabilitation (including treadmill training and limb‑supported exercise), and advanced interventions such as stem‑cell grafts, viral‑mediated gene delivery, or electrical stimulation to promote neural regeneration and functional recovery.
How is paralysis treated in a rat? - in detail
Paralysis in laboratory rodents is addressed through a combination of pharmacological, surgical, and rehabilitative interventions designed to restore neural function or mitigate secondary damage.
Initial assessment includes neurological scoring and electrophysiological testing to determine the extent and location of motor deficits. Based on these data, treatment proceeds in three overlapping phases.
Pharmacological management
- Administration of anti‑inflammatory agents (e.g., dexamethasone, methylprednisolone) within the first hours after injury to reduce edema and cytokine‑mediated damage.
- Neuroprotective compounds such as riluzole or N‑acetylcysteine are given to limit excitotoxicity.
- Analgesics (buprenorphine, meloxicam) are provided to control pain and prevent stress‑induced worsening of motor outcomes.
Surgical and regenerative strategies
- Microsurgical decompression of compressed spinal segments when applicable.
- Implantation of biodegradable scaffolds seeded with neural progenitor cells or mesenchymal stem cells to promote axonal regrowth.
- Gene‑therapy vectors delivering neurotrophic factors (e.g., BDNF, NT‑3) are injected intrathecally to enhance survival of damaged neurons.
- In cases of complete transection, peripheral nerve grafts or autologous muscle‑derived stem cell sheets are used to bridge the gap.
Rehabilitation and functional training
- Daily passive range‑of‑motion exercises to maintain joint flexibility and prevent contractures.
- Treadmill locomotor training with body‑weight support to stimulate central pattern generators and improve stepping patterns.
- Electrical stimulation of hindlimb muscles (functional electrical stimulation) to reinforce synaptic connections and improve muscle mass.
- Enriched environment housing, including climbing structures and tactile cues, to encourage voluntary movement and neuroplastic adaptation.
Outcome monitoring relies on weekly behavioral scores (e.g., Basso, Beattie, and Bresnahan locomotor rating), imaging (MRI for lesion volume), and histological analysis of axonal regeneration. Successful protocols typically combine early anti‑inflammatory treatment, targeted delivery of growth‑promoting factors, and intensive locomotor training, resulting in measurable improvements in hindlimb function within 4–6 weeks post‑injury.