Peripheral Nerve Disorders/Nerve Injury Classification. NPTE Study Guide: Master the NPTE

Peripheral nerve injury: Etiology: acute traumatic injury or chronic repetitive trauma d/t compression and/or shear forces

-Classifications:

1. Neuropraxia: nerve injury that causes a transient and focal LOF (sensory or motor). Often related to compressive forces causing ischemia (eg, carpal tunnel syndrome). Nerve dysfunction can be rapidly reversed or persist for weeks to months. Positive prognosis is indicated if compression removed. It’s the mildest form of nerve injury d/t no nerve degeneration.

2. Axonotmesis: focal damage to axon and myelin & varying degree of peripheral nerve connective tissue (endoneurium, perineurium, epineurium). Seen w/ increased-duration & larger-amplitude compressive (crush injury) or traction forces. Prognosis is related to degree of connective tissue damage. Axonal regrowth occurs at about 1 to 3 mm/day or 1 in/month

3. Neurotmesis: severing of axon and myelin and all connective tissue structures. Complete loss of function; requires surgery

Neuroplasticity and peripheral nerve injuries:

—Axonal regeneration: axons that undergo regeneration will not remyelinate to pre-injury level. This can impact nerve conduction velocity, as well as speed and coordination of movement

—Collateral sprouting: intact axons can pick up denervated terminal targets (muscles). Often results in switching of muscle fiber type (from type 1 to type 2)

Types of peripheral nerve injuries:

—Mononeuropathy: involvement of single nerve (eg, CTS)

—Mononeuropathy multiplex: involvement of 2 or more nerves without clear pattern of polyneuropathy. Example: Patient with B/L CTS, left cubital tunnel, and right tarsal tunnel. Presentation is often related to other health conditions (eg, diabetes mellitus, renal disease, chronic alcoholism)

—Radiculopathy: involvement of nerve root(s)

—Plexopathy: involvement of brachial or lumbosacral plexus

Peripheral nerve disease: Polyneuropathy:

-Risk factors:

  1. DM, renal failure, alcohol abuse

  2. Systemic autoimmune disease. Examples: Sjögren syndrome (dry eyes or mouth), lupus

  3. Autoimmune diseases. Example: GBS

  4. Nutritional imbalances

  5. Hereditary. Example: Charcot-Marie-Tooth disorder

  6. Infections. Examples: hepatitis B or C, human immunodeficiency virus (HIV), Lyme disease

  7. Cancers

  8. Medications. Example: chemotherapy

  9. Toxins. Examples: radiation, pesticides

  10. Idiopathic onset. Occurs in approximately 25% of patients

-Pathological process:

1. Segmental demyelination: disease process that primarily impacts myelin. If treated, remyelination can occur (eg, GBS)

2. Axonal degeneration: disease that impacts axons to a greater degree than myelin. Progresses from distal to proximal (eg, neuropathy secondary to alcohol abuse)

3. Most polyneuropathic conditions impact both myelin and axons (eg, diabetic polyneuropathy). More chronic in nature. Acute & rapidly progressing polyneuropathic conditions that are typically related to toxins (poison) or autoimmune conditions

-Neuroplasticity and polyneuropathy:

1. Remyelination, axonal regeneration, and collateral sprouting are all possible if causative agent is treated

2. Treat and address early!

-Examination:

1. Sensory, motor, & autonomic symptoms (hair loss & vascular changes) occur in distal to proximal fashion (gloves & stocking). Make sure to test both small (pain, temperature) and large (proprioception, kinesthesia) neural fiber involvement because impairment may vary.

2. Screen for autonomic dysfunction: vasodilation and loss of vasomotor tone (dryness, warmth, edema, orthostatic hypotension)

3. Balance and fall risks. Balance difficulty with static posture; sensitive to eyes being closed and looking upward.