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Nerve Tracing in Juvenile Rats: A Feasible Model for the Study of Brachial Plexus Birth Palsy and Cocontractions?
Krister Jönsson1, Tomas Hultgren1, Mårten Risling2
1Department of Handsurgery Södersjukhuset, Karolinska Institutet Department of Clinical Science and Education, Södersjukhuset, Stockholm, Sweden.
Insights
Brachial plexus birth injuries can cause abnormal muscle co-contractions. This study in rat neonates suggests nerve injury may disrupt correct muscle reinnervation, potentially explaining these co-contractions.
Area of Science:
- Neuroscience
- Developmental Biology
- Orthopedic Surgery
Background:
- Brachial plexus birth injuries frequently lead to upper extremity motor deficits.
- Internal rotation contracture and muscle co-contractions are common sequelae, limiting functional recovery.
- A leading hypothesis suggests aberrant nerve regeneration causes co-contractions.
Purpose of the Study:
- To establish a rat model for investigating co-contractions in brachial plexus birth injuries.
- To explore the reinnervation patterns following crush injury to C5-C6 nerve roots.
- To test the hypothesis of misdirected nerve fiber regeneration.
Main Methods:
- Neonatal rats (5 days old) underwent crush injury to C5-C6 nerve roots.
- Following a 4-week healing period, the infraspinatus muscle was injected with Fluoro-Gold.
- Spinal cords were harvested and sectioned to analyze Fluoro-Gold and NeuN positive cell distribution.
Main Results:
- Fluoro-Gold uptake was greater on the uninjured side compared to the injured side.
- On the injured side, positive cells were more dispersed along the craniocaudal axis.
- The method successfully traced Fluoro-Gold from muscle through the neuroma.
Conclusions:
- The rat model is effective for studying brachial plexus injury and associated co-contractions.
- Neuromas in continuity impede proper motor neuron-muscle connections.
- Nerve crush injuries can lead to neuronal loss and aberrant reinnervation patterns.
Abstract:
Brachial plexus birth injuries cause diminished motor function in the upper extremity. The most common sequel is internal rotation contracture. A number of these patients also suffer from cocontractions, preventing the use of an otherwise good passive range of motion in the shoulder. One theory behind the co-contracture problem is that injured nerve fibers grow into distal support tissue not corresponding to the proximal support tissue, resulting in reinnervation of the wrong muscle groups. To further elucidate this hypothesis, we used rat neonates to investigate a possible model for the study of cocontractions in brachial plexus birth injuries. Five-day-old rats were subjected to a crush injury to the C5-C6 roots. After a healing period of 4 weeks, the infraspinatus muscle was injected with Fluoro-Gold. A week later, the animals were perfused and spinal cords harvested and sectioned. Differences in the uptake of Fluoro-Gold and NeuN positive cells of between sides of the spinal cord were recorded. We found a larger amount of Fluoro-Gold positive cells on the uninjured side, while the injured side had positive cells dispersed over a longer area in the craniocaudal direction. Our findings indicate that the method can be used to trace Fluoro-Gold from muscle through a neuroma. Our results also indicate that a neuroma in continuity somewhat prevents the correct connection from being established between the motor neuron pool in the spinal cord and target muscle and that some neurons succumb to a crushing injury. We also present future research ideas.
