16.4 The Sensory and Motor Exams

Spinal Cord and Sensory/Motor Exams

Organization of spinal cord regions

The spinal cord is organized into gray matter and white matter, each with distinct roles in processing and transmitting neural signals.

Gray matter contains neuron cell bodies and is divided into functional regions:

• The dorsal (posterior) horn receives sensory input from peripheral nerves, including pain, temperature, and touch signals.
• The ventral (anterior) horn houses motor neuron cell bodies that innervate skeletal muscles and drive voluntary movement.

White matter surrounds the gray matter and contains ascending and descending tracts of myelinated axons:

• The dorsal columns (cuneate and gracile fasciculi) carry ascending sensory information related to proprioception and fine touch.
• The lateral corticospinal tract carries descending motor commands from the primary motor cortex to control voluntary movements.

These sensory and motor pathways are organized somatotopically within the spinal cord. Each spinal cord level corresponds to a specific dermatome (a region of skin receiving sensory innervation from one spinal nerve) and a specific myotome (a group of muscles innervated by one spinal nerve). For example, the C5 dermatome covers the lateral upper arm, while the C5 myotome includes the deltoid muscle.

Effects of spinal cord injuries

Spinal cord injuries produce sensory and/or motor deficits that depend on the level and severity of damage.

Complete transection severs the cord entirely at a given level:

• All sensation and voluntary movement below the injury is lost. If the injury is in the thoracic or lumbar region, the result is paraplegia (loss of lower limb function). Cervical injuries cause tetraplegia (loss of all four limbs).
• Spinal shock occurs immediately after injury: reflexes below the level of damage are temporarily lost because descending input from the brain is suddenly cut off. Reflexes typically return over days to weeks, often becoming exaggerated.

Incomplete injuries damage only part of the cord, producing characteristic patterns:

• Anterior cord syndrome damages the front portion of the spinal cord. Motor function and pain/temperature sensation are lost below the injury (because the corticospinal tract and anterior spinothalamic tract run anteriorly), but proprioception and vibration sense are preserved because the dorsal columns remain intact.
• Brown-Séquard syndrome results from a hemisection (damage to one lateral half of the cord). On the same side as the injury (ipsilateral), motor function, proprioception, and vibration sense are lost because the lateral corticospinal tract and dorsal columns are damaged before they cross. On the opposite side (contralateral), pain and temperature sensation are lost because the spinothalamic tract fibers have already crossed to the other side before ascending.

Upper vs. lower motor neuron diseases

Distinguishing upper motor neuron (UMN) from lower motor neuron (LMN) lesions is one of the most important skills in the neurological exam, because the clinical signs are essentially opposite.

Upper motor neuron diseases affect neurons in the brain or descending tracts within the spinal cord. Examples include stroke, multiple sclerosis, and amyotrophic lateral sclerosis (ALS). Clinical features of UMN lesions:

• Spasticity: increased muscle tone and resistance to passive movement, caused by loss of inhibitory signals from the brain
• Hyperreflexia: exaggerated deep tendon reflexes (e.g., a brisk patellar reflex), because descending inhibition of the reflex arc is removed
• Positive Babinski sign: the big toe extends upward when the sole of the foot is stroked, indicating corticospinal tract damage
• Weakness with loss of fine motor control, though muscles do not waste away as quickly

Lower motor neuron diseases affect motor neurons in the ventral horn of the spinal cord or in peripheral nerves. Examples include poliomyelitis and spinal muscular atrophy. ALS affects both UMNs and LMNs, which is why patients can show a mix of signs. Clinical features of LMN lesions:

• Flaccid paralysis: decreased muscle tone and weakness, because the motor neuron connecting to the muscle is damaged or destroyed
• Hyporeflexia or areflexia: diminished or absent deep tendon reflexes (e.g., absent Achilles reflex), because the reflex arc itself is interrupted
• Muscle atrophy: visible loss of muscle mass from denervation and disuse
• Fasciculations: spontaneous muscle twitches visible under the skin, caused by dying motor neurons firing irregularly

Significance of neurological reflexes

Reflexes are a fast, reliable way to test the integrity of specific spinal cord segments and motor pathways during the neurological exam.

Deep tendon reflexes test the spinal reflex arc at specific levels:

Reflexes are graded on a 0 to 4+ scale: 0 means absent, 1+ is diminished, 2+ is normal, 3+ is brisker than normal, and 4+ indicates hyperreflexia (often with clonus). Asymmetry between sides is just as significant as the absolute grade.

Babinski reflex tests the corticospinal tract. You elicit it by stroking the lateral sole of the foot from heel to toe with a blunt object. A positive response (the big toe extends upward while the other toes fan out) indicates a UMN lesion. In healthy adults, the normal response is plantar flexion (toes curl downward). A positive Babinski sign is actually normal in infants under about 2 years old, because their corticospinal tracts are not yet fully myelinated.

Hoffmann's sign is the upper-extremity equivalent. You flick the nail of the patient's middle finger downward. If the thumb and index finger flex in response, that's a positive Hoffmann's sign, suggesting a UMN lesion in the cervical spinal cord or brain.

Sensory and Motor Integration

Sensory and motor systems don't work in isolation. Sensory receptors in the skin, muscles, and joints detect stimuli (touch, stretch, temperature) and convert them into electrical signals that travel along peripheral nerves to the spinal cord.

Spinal reflexes like the stretch reflex allow rapid, automatic responses without waiting for input from the brain. When a muscle is suddenly stretched (as when a reflex hammer taps a tendon), sensory neurons signal the spinal cord, and motor neurons fire back to contract that muscle almost instantly.

Proprioception, the sense of body position and movement, is critical for coordinating motor actions. Receptors in muscles (muscle spindles), tendons (Golgi tendon organs), and joints continuously feed position data to the spinal cord and brain, allowing you to adjust movements in real time.

The neurological examination systematically tests both sensory and motor pathways to pinpoint where in the nervous system a problem might exist. By combining findings from dermatome testing, myotome strength testing, and reflex assessment, a clinician can often localize a lesion to a specific spinal cord level or distinguish between central and peripheral damage.