Histology · Year 1 · from Histology
Case 3: Peripheral Nerve Injury with Chromatolysis
Clinical Image
Source: Wikipedia - Chromatolysis - CC BY-SA 4.0
Case Presentation
A 28-year-old construction worker sustains a deep laceration to his forearm, severing the median nerve. He immediately loses sensation over the thumb, index, middle, and radial half of the ring finger (median nerve territory), and cannot flex these fingers or oppose his thumb. Surgical repair of the nerve is performed. Over the following weeks, the motor neurons in the spinal cord whose axons were severed undergo characteristic changes visible histologically: the Nissl bodies (aggregates of rough endoplasmic reticulum) appear to dissolve and disperse (chromatolysis), the nucleus moves from its central position to the cell periphery, and the cell body swells. This response represents the neuron shifting its metabolic priority from synaptic transmission to axon regeneration - upregulating proteins needed for axon regrowth while downregulating neurotransmitter synthesis. Because this is a peripheral nerve injury (PNS), regeneration is possible: Schwann cells proliferate and form bands of Bungner within their basal lamina tubes, guiding the regenerating axons. He gradually recovers motor and sensory function over 12-18 months.
Key Learning Points
- Nissl bodies represent aggregates of rough ER and ribosomes, responsible for the intense protein synthesis neurons require
- Chromatolysis (dispersal of Nissl bodies, peripheral nuclear displacement, cell swelling) is the neuronal response to axon injury
- The response reflects metabolic reprogramming: shifting from maintaining steady-state function to producing proteins for regeneration
- Peripheral nerves can regenerate because Schwann cells and their basal lamina provide guidance channels for regrowing axons
- Understanding the distribution of Nissl substance (present in soma and dendrites, absent from axon hillock and axon) helps explain why the cell body must provide all proteins for the axon
Summary: Neuronal Disorders
These cases illustrate how understanding neuronal structure informs clinical diagnosis:
| Disorder | Structure Affected | Histological Finding | Clinical Correlation |
|---|---|---|---|
| Alzheimer Disease | Microtubules/tau protein | Neurofibrillary tangles (hyperphosphorylated tau) | Axonal transport disruption, neuronal death, dementia |
| Rabies | Retrograde axonal transport | Negri bodies (viral inclusions in cytoplasm) | Virus travels from bite site to CNS via axonal transport |
| Peripheral Nerve Injury | Nissl bodies (protein synthesis) | Chromatolysis (Nissl dissolution, nuclear displacement) | Metabolic shift to regeneration; PNS can regenerate |
Knowledge of neuronal ultrastructure - Nissl bodies for protein synthesis, microtubules for transport, axon hillock as action potential initiation site - provides the foundation for understanding neurological disease.