19.2 Sensation & Movement

19.2 Sensation & Movement

Quick Answer: Sensation is the transduction of physical energy into neural signals; perception is the brain's interpretation. Each sensory modality follows a receptor → pathway → cortex route, and each motor act is planned, executed, and refined by parallel systems.

Sensory Systems

Vision. Rods (scotopic, high sensitivity, no color, peripheral retina) and cones (photopic, color, high acuity, fovea) transduce light via photopigment bleaching (rhodopsin in rods, photopsins in cones). Signals flow: retina → optic nerve (CN II) → optic chiasm (nasal fibers cross) → optic tract → lateral geniculate nucleus of the thalamus → optic radiations → primary visual cortex (V1) in the occipital lobe. The pathway is retinotopically mapped, so lesions produce predictable field defects (e.g., a left optic tract lesion yields a right homonymous hemianopia).

Hearing. Sound vibrations enter the external canal, vibrate the tympanic membrane, and are amplified by the ossicles (malleus, incus, stapes) at the oval window. Cochlear hair cells of the organ of Corti transduce mechanical energy; CN VIII carries signals to cochlear nuclei → superior olivary complex → inferior colliculus → medial geniculate body → primary auditory cortex (A1), superior temporal gyrus (areas 41/42). Tonotopic organization is preserved throughout.

Vestibular. Semicircular canals detect angular acceleration; otolith organs (utricle, saccule) detect linear acceleration and gravity. The vestibular branch of CN VIII projects to vestibular nuclei and the cerebellum, driving the vestibulo-ocular reflex (stabilizes gaze during head motion) and postural reflexes.

Somatosensation. Fine touch, pressure, vibration, and proprioception travel the dorsal column–medial lemniscus pathway; pain, temperature, and itch travel the spinothalamic tract. Both terminate in the somatosensory cortex (S1), organized as a sensory homunculus. Two-point discrimination is the ability to perceive two distinct points pressed on the skin; it is finest where receptor density is highest (fingertips, lips) and reflects cortical magnification. Sensory adaptation is the decreased firing of a receptor to a constant stimulus — why we stop noticing our clothes or a steady smell. Proprioception integrates muscle spindle, Golgi tendon organ, and joint receptor input to sense limb position without vision; its loss (as in tabes dorsalis from neurosyphilis) causes sensory ataxia.

Taste (gustation). Five basic qualities — sweet, salty, sour, bitter, umami — via taste receptor cells in taste buds. CN VII (anterior two-thirds of tongue), IX (posterior one-third), and X (epiglottis) carry taste to the solitary nucleus → thalamus → gustatory cortex (insula).

Smell (olfaction). The only modality that initially bypasses the thalamus. Olfactory receptor neurons (CN I) in the nasal epithelium project through the cribriform plate to the olfactory bulb → piriform cortex → amygdala and entorhinal cortex. A fracture of the cribriform plate can sever these fibers and cause anosmia.

Motor Systems

Voluntary movement is planned in the supplementary motor area and premotor cortex, executed by the primary motor cortex (precentral gyrus), and refined by the basal ganglia and cerebellum.

The pyramidal system (corticospinal and corticobulbar tracts) provides direct, volitional control. Upper motor neurons (UMN) originate in the cortex; lower motor neurons (LMN) live in the anterior horn or cranial nerve nuclei. UMN lesions produce spasticity, hyperreflexia, Babinski sign, and weakness; LMN lesions produce flaccidity, hyporeflexia, fasciculations, and atrophy.

The extrapyramidal system (basal ganglia, substantia nigra, subthalamic nucleus) modulates tone, posture, and involuntary movement. The direct pathway facilitates movement (D1 receptors); the indirect pathway suppresses it (D2 receptors). Dopamine from the substantia nigra pars compacta shifts the balance toward the direct, movement-promoting pathway.

The cerebellum coordinates timing and accuracy. It receives copies of motor plans (via pontine nuclei) and sensory feedback (via spinocerebellar tracts), compares them, and corrects error through cerebello-thalamo-cortical loops. Cerebellar lesions cause dysmetria (past-pointing), intention tremor, ataxia, and dysdiadochokinesia (impaired rapid alternating movements) — without primary weakness.

Reflexes

The stretch reflex (myotatic) is monosynaptic: muscle spindle stretch → Ia afferent → alpha motor neuron → contraction (e.g., patellar reflex). The gamma loop maintains spindle sensitivity during voluntary movement. The Golgi tendon organ reflex is disynaptic and inhibitory, protecting against excessive force by relaxing the contracting muscle. Withdrawal and crossed-extension reflexes coordinate limb withdrawal from a painful stimulus with contralateral leg extension to maintain balance — a polysynaptic, spinally mediated pattern that does not require brain input.

Motor unit recruitment follows the size principle: smaller, low-threshold motor units (slow-twitch, fatigue-resistant) are recruited first; larger, high-threshold units (fast-twitch, powerful but fatigable) join as force demands increase. This orderly recruitment smoothly scales force output.

Neurotransmitters

Dopaminergic degeneration in the substantia nigra causes Parkinson disease (bradykinesia, rigidity, resting tremor, postural instability). Excess mesolimbic dopamine activity is implicated in psychosis. Cholinergic deficits in the basal forebrain characterize Alzheimer disease.