3.5 Peripheral Neuropathies & Upper vs Lower Motor Neuron Signs

Upper vs Lower Motor Neuron Lesions

The motor pathway has two parts. The upper motor neuron (UMN) runs from the brain (motor cortex) down through the spinal cord. The lower motor neuron (LMN) runs from the anterior horn of the spinal cord (or a cranial nerve nucleus) out to the muscle. A lesion's location produces a distinct, predictable sign pattern — and the NPTE-PTA tests whether you can read it.

Note that ALS is the great exception — it damages both UMN and LMN, so a single patient can show spasticity and hyperreflexia alongside atrophy and fasciculations. When an item lists mixed signs, think ALS.

A quick reasoning shortcut: "hyper" everything (tone, reflexes, Babinski) = UMN; "hypo/flaccid" plus atrophy and fasciculations = LMN. Spinal shock immediately after an SCI is a temporary period of flaccidity and areflexia even though the lesion is UMN, which can briefly mask the eventual UMN picture.

Bell's Palsy

Bell's palsy is an acute lower motor neuron lesion of the facial nerve (cranial nerve VII), often idiopathic or viral. It causes sudden, one-sided facial weakness, and — because it is an LMN lesion — the entire half of the face, including the forehead, is affected. (A central/UMN facial lesion, such as a stroke, spares the forehead because the upper face has bilateral cortical input.) Findings include inability to close the eye, drooping mouth, loss of the nasolabial fold, drooling, and difficulty with facial expression. Most cases recover spontaneously within weeks to months.

PTA-implemented care: gentle facial-muscle exercises and neuromuscular re-education, soft-tissue and massage techniques, biofeedback, and patient education. Eye protection is critical — because the eye may not close, the patient is taught about lubricating artificial-tear drops, an eye patch, or taping the lid during sleep to prevent corneal drying and abrasion.

Carpal Tunnel Syndrome (CTS)

Carpal tunnel syndrome (CTS) is compression of the median nerve beneath the transverse carpal ligament at the wrist — the most common entrapment neuropathy. Symptoms include paresthesia and numbness in the thumb, index, middle, and the radial half of the ring finger, often worse at night, plus thenar (thumb base) weakness and atrophy in advanced cases. Provocative tests:

• Phalen test: sustained wrist flexion reproduces symptoms within 60 seconds.
• Tinel sign: tapping over the median nerve at the wrist causes tingling.
• Carpal compression test: direct pressure over the carpal tunnel provokes symptoms.

Conservative PTA-implemented care: neutral-wrist night splinting, median nerve and tendon gliding exercises, ergonomic and activity-modification education (neutral wrist posture, frequent breaks from repetitive gripping/keyboarding), and modalities within the plan of care.

Diabetic Peripheral Neuropathy

Diabetic peripheral neuropathy is nerve damage from chronically elevated blood glucose, producing a symmetrical, distal stocking-glove sensory loss that begins in the feet. The danger is loss of protective sensation — a patient cannot feel an injury, blister, or ill-fitting shoe, which can progress silently to ulceration and amputation. A 10-gram Semmes-Weinstein monofilament is the standard screen for protective sensation.

Essential PTA education:

• Inspect the feet daily, including the soles, using a mirror or a caregiver if needed.
• Check inside shoes for foreign objects before wearing; never go barefoot.
• Wear well-fitting, protective footwear and seamless socks.
• Avoid extreme heat (hot water, heating pads, hot foot baths) on insensate skin.
• Report any new redness, blister, callus, or skin breakdown promptly.

Balance and gait training also matter, because impaired distal sensation raises fall risk and a positive Romberg sign is common.

Putting It Together

The exam frequently hands you a cluster of signs and asks for the lesion type or the safe intervention. Read tone, reflexes, atrophy, and fasciculations first to classify UMN vs LMN; then layer the specific entrapment or neuropathy. For insensate skin, the highest-priority answer is almost always protect the skin and educate, not apply heat.

Other High-Yield Peripheral Lesions

A few additional patterns appear regularly. Erb's palsy (upper trunk, C5-C6) produces the "waiter's tip" posture — arm adducted, internally rotated, forearm pronated — while Klumpke's palsy (lower trunk, C8-T1) produces a clawed hand from intrinsic weakness. Radial nerve injury (often a humeral shaft fracture or "Saturday night palsy") causes wrist drop from extensor paralysis; the PTA may apply a cock-up wrist splint and train compensatory function. Common peroneal (fibular) nerve injury at the fibular head causes foot drop, addressed with an ankle-foot orthosis (AFO) and gait training to prevent tripping.

Complex Regional Pain Syndrome

Complex regional pain syndrome (CRPS) — historically reflex sympathetic dystrophy — can follow trauma or nerve injury and presents with disproportionate burning pain, allodynia (pain to light touch), swelling, temperature and color changes, and trophic skin changes. PTA-implemented care favors pain-free active movement, desensitization, edema control, and stress-loading/weight-bearing within tolerance; aggressive, painful stretching is counterproductive and can worsen symptoms. As always, the PTA reports increasing pain, new sensory loss, or skin breakdown to the supervising PT and adjusts only within the established plan of care.