Consequences of Nerve Cell Damage: What Doesn't Happen?

When a neuron is damaged, it loses its ability to perform its normal functions. Here is what **will not happen** (i.e., functions that are impaired or lost):

Lost Functions

• **Signal Transmission:** Cannot generate or propagate action potentials (electrical signals) to other neurons, muscles, or glands.
• **Signal Reception:** Cannot receive/integrate synaptic input (neurotransmitters) from other neurons.
• **Structural Integrity:** Cannot maintain axonal/dendritic architecture; Wallerian degeneration distal to injury.
• **Self-Repair (CNS):** Adult CNS neurons **cannot regenerate** axons effectively (inhibitory environment: Nogo, MAG, OMgp; glial scar). PNS neurons *can* regenerate (~1 mm/day) if cell body intact and endoneurial tubes preserved.
• **Neurotransmitter Synthesis/Release:** Impaired synthesis, vesicular packaging, calcium-triggered exocytosis.
• **Trophic Support:** Cannot provide/receive neurotrophic factors (NGF, BDNF) → atrophy of target tissues.

Resulting Clinical Deficits

• **Sensory:** Numbness, paresthesia, pain (neuropathic), loss of proprioception.
• **Motor:** Weakness, paralysis, atrophy, fasciculations, spasticity (UMN).
• **Autonomic:** Orthostatic hypotension, gastroparesis, neurogenic bladder, anhidrosis.
• **Cognitive/Behavioral:** Memory loss, executive dysfunction, personality change (cortical).
• **Special Senses:** Vision/hearing loss (cranial nerve/optic nerve damage).

Neuroplasticity & Recovery

• **CNS:** Functional reorganization (vicariation), synaptic strengthening, compensatory strategies – **not true regeneration**.
• **PNS:** Axonal regeneration possible; surgical repair if gap > few mm.
• **Rehabilitation:** PT/OT/speech drives plasticity.