2.1 Neuroanatomy & Neurophysiology

Understanding nervous-system structure and function lets physical therapists localize lesions and anticipate functional deficits—skills the NPTE neuromuscular domain tests heavily.

CNS vs. PNS

The regeneration difference is clinically pivotal: a crushed peripheral nerve may recover over months as the axon regrows along intact connective-tissue tubes, whereas a central cord or brain lesion relies on neuroplastic reorganization rather than true axonal regrowth.

Upper vs. Lower Motor Neuron Lesions

This is one of the most tested neuromuscular concepts. UMN and LMN lesions produce opposite pictures:

UMN spasticity patterns: the upper extremity tends toward a flexor synergy (shoulder adduction/internal rotation, elbow/wrist/finger flexion, forearm pronation); the lower extremity tends toward an extensor synergy (hip extension/adduction/internal rotation, knee extension, ankle plantarflexion/inversion). Conditions like ALS are notable because they show mixed UMN and LMN signs.

Spinal Cord Tracts and Decussation

Localizing whether a deficit is ipsilateral or contralateral depends on where each tract crosses.

Because the dorsal columns and corticospinal tract cross in the medulla, a spinal-cord lesion produces ipsilateral loss of proprioception/vibration and ipsilateral motor weakness below the level. Because the spinothalamic tract crosses almost immediately at the cord, a cord lesion produces contralateral loss of pain and temperature. This crossing pattern is exactly what creates the classic findings of Brown-Sequard (cord hemisection): ipsilateral motor and proprioceptive loss with contralateral pain/temperature loss.

Dermatomes and Myotomes

Key dermatome landmarks

Key myotomes

Memorizing the saddle anesthesia (S2-S4) pattern is important because, paired with bowel/bladder change, it signals cauda equina syndrome, a medical emergency.

Putting Localization Together

Localization on the NPTE is a two-question habit: Is this UMN or LMN? and Which side and which modality? The first question separates a central lesion (spasticity, hyperreflexia, positive Babinski) from a peripheral one (flaccidity, hyporeflexia, fasciculations, rapid atrophy). The second question uses the decussation rules to predict laterality: dorsal-column and corticospinal signs are ipsilateral to a cord lesion (because those tracts cross higher), while spinothalamic pain/temperature signs are contralateral.

Apply this to a worked case. A patient has right-leg spasticity and hyperreflexia, loss of right-sided proprioception, and loss of left-sided pain and temperature below a thoracic level. The spastic, hyperreflexic motor picture is UMN; the ipsilateral motor and proprioceptive loss with contralateral pain/temperature loss is the signature of a right cord hemisection (Brown-Sequard). No memorized list is needed—just the UMN/LMN distinction plus the three decussation rules.

The same logic distinguishes a cortical stroke (contralateral UMN signs, because the corticospinal tract has not yet crossed at the brain) from a peripheral neuropathy (LMN signs in a nerve distribution).

Cranial Nerve Quick Reference

Brainstem and cranial-nerve knowledge supports localization for stroke and TBI items. High-yield nerves for PT include CN V (trigeminal) for facial sensation and muscles of mastication, CN VII (facial) for facial expression (a central lesion spares the forehead; a peripheral Bell palsy does not), CN VIII (vestibulocochlear) for hearing and balance, CN IX/X (glossopharyngeal/vagus) for swallowing and the gag reflex (dysphagia screening), and CN XI (accessory) for the trapezius and sternocleidomastoid.

Pairing a deficit with its cranial nerve helps pinpoint a brainstem level and flags swallowing-safety concerns that change PT priorities.