Sensory Systems
Usually weeks 4-5 of a medical physiology course, right after synapsesEvery sense runs the same three-step program: a receptor converts one form of energy into a graded receptor potential, the receptor potential sets an action-potential frequency, and a dedicated pathway delivers that code to a dedicated patch of cortex. The exam tests the program in general (adaptation, receptive fields, labeled lines) and then in each special sense, where it lives at the lesion: which pathway crosses where, which visual-field cut goes with which structure, and which hearing test separates conductive from sensorineural loss. Learn the general rules first — the special senses are the same rules with better props.
This guide is the frame. The exams are written from your lectures— drop this unit's slides on the dashboard to get flashcards and board-style questions from your own course, and quiz them all semester (a course whose exams re-test earlier units rewards nothing more than early, repeated self-testing). The physiology playbook has the weekly loop.
Free30 study kits/mo · 1 diagram deck · 1 board-graded quiz · 2 tutor Qs/wk
Pro $20/mono monthly cap (5 kits/day) · 10 diagram decks · See plans →
Lectures you file for this course live under Physiology → My Lectures in your library — pick it from the Module box as you upload, or from any card's Move menu afterwards.
AI-authored study notes, not faculty-reviewed and not medical advice. Verify every mechanism against your course materials and faculty; programs differ in emphasis.
High-Yield Pearl
For any sensory lesion question, ask three things in order — which receptor feeds this pathway, where does the pathway cross, and what does the other side of the body lose — and the pattern names the lesion.
What the exam asks
Mechanisms, curves, and what happens when each one fails.
- Transduction and the receptor potential. A sensory receptor is tuned to one ADEQUATE stimulus (light, stretch, a chemical, heat) and converts it into a graded RECEPTOR POTENTIAL — usually a depolarization from opening non-selective cation channels. The receptor potential is not an action potential: its size scales with stimulus strength, and where it reaches the first node or the axon's trigger zone it sets the FIRING RATE of the afferent. Bigger stimulus → bigger receptor potential → higher action-potential frequency. Intensity is also coded by population: a stronger stimulus recruits more receptors, including less sensitive ones.
- Labeled lines, receptive fields, and lateral inhibition. The labeled-line principle: the sensation perceived depends on WHICH pathway fires, not on what fired it — press on a closed eye and you 'see' light. A neuron's receptive field is the patch of skin (or retina) whose stimulation changes its firing; small, dense fields (fingertips, lips, fovea) give fine two-point discrimination, large sparse fields (the back) give poor discrimination. Lateral inhibition — the most-active pathway suppressing its neighbors through interneurons — sharpens edges and localizes a stimulus more precisely than the raw receptive fields would allow.
- Adaptation — tonic vs phasic receptors. Under a constant stimulus, receptor potentials decline. SLOWLY adapting (tonic) receptors keep firing for as long as the stimulus lasts and report its magnitude: Merkel discs (sustained pressure, texture), Ruffini endings (skin stretch), muscle spindles, and nociceptors. RAPIDLY adapting (phasic) receptors fire at onset (and often offset) and then fall silent — they report CHANGE: Meissner corpuscles (light touch, flutter), Pacinian corpuscles (vibration, whose onion-like lamellae dissipate a sustained deformation), and hair follicle receptors. That is why you stop feeling your clothes but never stop feeling a burn.
- The two somatosensory pathways — and where each crosses. Dorsal column–medial lemniscus (DCML): fine touch, vibration, two-point discrimination, conscious proprioception. First-order axons ascend IPSILATERALLY in the dorsal columns (fasciculus gracilis from the legs, cuneatus from the arms), synapse in the nucleus gracilis/cuneatus of the medulla, and second-order axons cross there to form the medial lemniscus. Anterolateral (spinothalamic) system: pain, temperature, crude touch. First-order axons synapse in the dorsal horn, and second-order axons cross within a segment or two through the anterior white commissure. Both relay in the thalamic ventral posterolateral (VPL) nucleus (the face uses VPM) and end in the primary somatosensory cortex of the postcentral gyrus, mapped as the sensory homunculus — legs medial, face and hand lateral.
- Pain — two fibers, referral, and descending control. Nociceptors are free nerve endings. Aδ fibers (thinly myelinated) carry fast, sharp, well-localized first pain; C fibers (unmyelinated) carry slow, burning, poorly localized second pain. Visceral pain is REFERRED to skin whose afferents converge on the same dorsal horn neurons — the heart to the left arm and jaw, the diaphragm to the shoulder (C3–C5), the early appendix to the periumbilical region. Pain is modulated centrally: large-fiber touch input inhibits dorsal horn transmission (the gate-control idea behind rubbing a bruise), and the periaqueductal gray drives descending opioid, serotonergic, and noradrenergic suppression — the substrate of opioid analgesia.
- The eye as an optical instrument. The cornea does most of the eye's refracting; the lens adds an ADJUSTABLE amount. For near vision the ciliary muscle CONTRACTS (parasympathetic, via CN III), the zonular fibers slacken, and the elastic lens rounds up to add power — accommodation, paired with pupillary constriction and convergence (the near triad). Refractive errors: myopia (eye too long — image falls in front of the retina, corrected with a diverging lens), hyperopia (eye too short — image behind the retina, converging lens), astigmatism (unequal corneal curvature, cylindrical lens), and presbyopia (the lens stiffens with age and accommodation fails, usually noticed after about 40).
- Phototransduction — photoreceptors hyperpolarize to light. In the DARK, cGMP holds cation channels open in the photoreceptor outer segment; the resulting 'dark current' keeps the cell depolarized (about −40 mV) and releasing glutamate continuously. Light isomerizes 11-cis retinal in rhodopsin → activated rhodopsin activates the G protein transducin → phosphodiesterase breaks down cGMP → channels close → the photoreceptor HYPERPOLARIZES and glutamate release falls. The signal is the decrease. Rods (rhodopsin, peripheral retina) are exquisitely sensitive — night vision — with poor acuity because many converge on one ganglion cell; cones (three opsins, concentrated in the fovea) give color and high acuity in bright light. Retinal is vitamin A, which is why deficiency presents as night blindness first.
- The visual pathway and its lesions. Nasal retinal fibers (carrying the TEMPORAL visual fields) cross at the optic chiasm; temporal retinal fibers stay ipsilateral. So: an optic nerve lesion blinds one eye; a chiasm lesion (classically a pituitary adenoma pressing from below) produces bitemporal hemianopia; anything behind the chiasm (optic tract, radiations, occipital cortex) produces a CONTRALATERAL homonymous hemianopia. The optic radiations split: inferior fibers loop through the temporal lobe (Meyer's loop — lesion gives a contralateral SUPERIOR quadrantanopia) and superior fibers run through the parietal lobe (inferior quadrantanopia). An occipital stroke often spares the macula because of dual blood supply. The pupillary light reflex runs CN II in, pretectal nuclei, Edinger-Westphal and CN III out — to BOTH pupils, which is why light in one eye constricts both (the consensual response).
- Hearing — impedance matching and a tonotopic membrane. The middle-ear ossicles and the large tympanic membrane funnel sound onto the small oval window, overcoming the air-to-fluid impedance mismatch. In the cochlea, a pressure wave travels along the basilar membrane, which is narrow and stiff at the BASE (high frequencies peak there) and wide and floppy at the APEX (low frequencies) — the tonotopic map preserved all the way to auditory cortex. Hair cells sit on it with stereocilia bathed in ENDOLYMPH, a K+-rich fluid held about +80 mV positive: deflection toward the tallest stereocilium pulls tip links open, K+ flows IN down that combined gradient, and the hair cell depolarizes and releases glutamate. Inner hair cells carry most of the signal to the cochlear nerve; outer hair cells change length (prestin) to amplify quiet sounds — the source of otoacoustic emissions used in newborn screening.
- Balance — canals for rotation, otoliths for tilt. The three semicircular canals detect ANGULAR acceleration: when the head turns, endolymph lags and bends the cupula over the hair cells in each ampulla, exciting the canal on the side toward which the head turns. The otolith organs detect LINEAR acceleration and head tilt — the utricle (horizontal) and saccule (vertical), whose hair cells are weighted by calcium carbonate otoconia. The vestibulo-ocular reflex counter-rotates the eyes to keep an image steady on the retina as the head moves; nystagmus is that reflex's visible sawtooth when the input is unbalanced.
- The chemical senses. Taste (sweet, sour, salty, bitter, umami) reaches the brainstem's solitary nucleus via CN VII (anterior two-thirds of the tongue), IX (posterior third), and X, then relays through the thalamus. Olfactory receptor neurons are true neurons that regenerate throughout life; their G-protein (cAMP) receptors project through the cribriform plate to the olfactory bulb, and olfaction is the one sense that reaches cortex without a thalamic relay first. Losing smell is an early sign in Parkinson disease and a classic consequence of anterior skull base fracture and viral illness.
Worth drilling · 40 concepts
Each with the one fact that identifies it. Your course's slides are the authority; use this to check your list against.
- 1Adequate stimulus — the energy form a given receptor is most sensitive to
- 2Receptor potential — graded potential at the sensory ending; its size sets the afferent's firing rate
- 3Labeled-line principle — the pathway activated, not the stimulus, determines the sensation perceived
- 4Receptive field — the area whose stimulation changes one sensory neuron's firing
- 5Lateral inhibition — the most-active pathway suppresses its neighbors, sharpening contrast and localization
- 6Two-point discrimination — finest where receptive fields are smallest and densest (fingertips, lips)
- 7Slowly adapting receptor — tonic; keeps firing through a sustained stimulus and reports its magnitude
- 8Rapidly adapting receptor — phasic; fires at onset and offset and reports change
- 9Pacinian corpuscle — onion-layered, rapidly adapting; vibration and deep pressure
- 10Meissner corpuscle — rapidly adapting dermal-papilla receptor; light touch and flutter on glabrous skin
- 11Merkel disc — slowly adapting; sustained pressure and texture
- 12Dorsal column–medial lemniscus — fine touch, vibration, proprioception; crosses in the medulla
- 13Spinothalamic tract — pain and temperature; crosses within a segment or two in the cord
- 14Ventral posterolateral nucleus — thalamic relay for body sensation on its way to cortex
- 15Postcentral gyrus — primary somatosensory cortex, mapped as the sensory homunculus
- 16A-delta fibers — thinly myelinated; fast, sharp, well-localized first pain
- 17C fibers — unmyelinated; slow, burning, poorly localized second pain
- 18Referred pain — visceral and skin afferents converge on the same dorsal horn neurons
- 19Periaqueductal gray — midbrain source of descending opioid pain suppression
- 20Accommodation — ciliary muscle contracts, zonules slacken, the lens rounds up for near vision
- 21Presbyopia — age-related stiffening of the lens; near focus fails
- 22Myopia — eye too long; image focuses in front of the retina; diverging lens corrects it
- 23Hyperopia — eye too short; image focuses behind the retina; converging lens corrects it
- 24Rods — rhodopsin-rich peripheral photoreceptors; night vision with poor acuity
- 25Cones — fovea-concentrated photoreceptors; color and sharp vision in bright light
- 26Fovea — cone-only pit at the center of the macula; point of sharpest vision
- 27Optic disc — where the optic nerve leaves the eye; no photoreceptors, the blind spot
- 28Dark current — cGMP-gated cation influx that keeps photoreceptors depolarized in the dark
- 29Transducin — G protein activated by light-struck rhodopsin; turns on phosphodiesterase
- 30Bitemporal hemianopia — optic chiasm compression, classically by a pituitary adenoma
- 31Homonymous hemianopia — lesion behind the chiasm; the contralateral field is lost in both eyes
- 32Meyer's loop — temporal-lobe optic radiations; lesion gives a contralateral superior quadrantanopia
- 33Consensual light reflex — light in one eye constricts both pupils (CN II in, CN III out)
- 34Basilar membrane — tonotopic: stiff base for high pitch, floppy apex for low pitch
- 35Endolymph — K+-rich, positively charged cochlear fluid; K+ entry depolarizes hair cells
- 36Outer hair cells — prestin-driven cochlear amplifier; the source of otoacoustic emissions
- 37Semicircular canals — detect angular (rotational) acceleration via the cupula
- 38Otolith organs — utricle and saccule; linear acceleration and head tilt
- 39Vestibulo-ocular reflex — eyes counter-rotate to hold gaze steady as the head turns
- 40Olfactory receptor neurons — regenerating neurons whose path reaches cortex without a thalamic relay
Practice it
Active recall over the drill list — flip and claim, match the pairs, produce the answers cold, fill in the diagram, or read the curves like the exam does.
Every concept on the drill list, one card at a time — the name up front, the fact that identifies it on the flip. Claim each card honestly and the deck learns what to lead with next time. Progress lives in this browser only.
What everyone misses
The distinctions that lose points on this material, year after year.
- Photoreceptors HYPERPOLARIZE to light. Every other receptor in the course depolarizes to its stimulus, so students assume light depolarizes rods and cones. The reverse is true: the dark current keeps them depolarized, light closes the cGMP-gated channels, and the signal is a DROP in glutamate release. Any answer choice in which light 'opens sodium channels in the rod' is the trap.
- The two somatosensory pathways cross at different levels. DCML crosses in the MEDULLA; spinothalamic fibers cross within a segment or two of entry. So a hemisection of the cord produces ipsilateral loss of vibration and proprioception (fibers not yet crossed) with contralateral loss of pain and temperature (fibers already crossed) — Brown-Séquard. Students who remember 'everything crosses' can't solve the lesion question; the level of crossing IS the question.
- Accommodation: the ciliary muscle CONTRACTS to see near. The intuitive picture — a muscle squeezing the lens fat — gets the zonules backwards. Ciliary muscle contraction moves the ciliary body inward, RELAXING zonular tension, and the lens rounds up on its own elasticity. At rest (distance vision) the zonules are taut and the lens is flat. Presbyopia is the lens losing that elasticity, not a weak muscle.
- Base is high pitch, apex is low. Students picture the wide, 'big' end handling high frequencies. The base of the basilar membrane is narrow and STIFF, so it resonates with high frequencies; the apex is wide and floppy, resonating with low ones. It matters clinically: noise and ototoxic drugs damage the base first, so high-frequency hearing is lost first.
- Adaptation is a design feature, not fatigue. A Pacinian corpuscle that stops firing under steady pressure hasn't run out of anything — its capsule dissipates the sustained deformation so the ending signals only change. Tonic receptors (Merkel, spindles, nociceptors) are built to keep reporting. Questions that ask which receptor signals ongoing tissue damage want the non-adapting nociceptor.
- Meyer's loop is superior; the parietal radiations are inferior. The loop dips through the TEMPORAL lobe and carries the inferior retinal fibers — which see the SUPERIOR visual field — so a temporal lesion causes 'pie in the sky.' Parietal lesions take the superior retinal fibers and cause an inferior quadrantanopia. Flip either and you've chosen the distractor.
Clinical correlations
Where this unit shows up again — in clinic, on rotations, and on the boards.
- Brown-Séquard syndrome. A stab wound hemisects the cord: ipsilateral weakness and loss of vibration and proprioception below the lesion, contralateral loss of pain and temperature starting a level or two below. It is the cleanest bedside demonstration of where the DCML and spinothalamic pathways cross, and the reason every sensory exam tests them separately.
- Pituitary adenoma and the chiasm. A patient bumps into door frames on both sides and has headaches: a pituitary mass rising from the sella compresses the crossing nasal fibers at the chiasm — bitemporal hemianopia — often alongside hormonal symptoms (galactorrhea, acromegaly, or hypopituitarism). Formal visual fields and an MRI of the sella follow.
- Conductive vs sensorineural hearing loss. Weber (fork on the forehead) lateralizes TO the affected ear in conductive loss and AWAY from it in sensorineural loss. Rinne (mastoid then air) shows bone conduction louder than air conduction in conductive loss; in sensorineural loss air stays louder than bone. Cerumen, otitis media, and otosclerosis are conductive; presbycusis, noise, and aminoglycoside or cisplatin toxicity damage hair cells — high frequencies first.
- Benign paroxysmal positional vertigo. Brief spinning with head turns or rolling over in bed: otoconia dislodged from the utricle drift into the posterior semicircular canal and make it respond to gravity. The Dix-Hallpike maneuver reproduces vertigo with torsional nystagmus; the Epley maneuver rolls the debris back out — canal physiology used as treatment.
- Referred cardiac and visceral pain. Crushing chest pressure radiating to the left arm and jaw, shoulder-tip pain from blood under the diaphragm, periumbilical pain from an early appendix that later localizes to the right lower quadrant as the parietal peritoneum is irritated — each is dorsal-horn convergence, and each is a vignette you must not mistake for a local problem.
- Diabetic peripheral neuropathy. Stocking-glove numbness with lost vibration sense and absent ankle reflexes: long axons fail first. Losing protective sensation is why screening uses a monofilament and why foot ulcers go unnoticed; small-fiber involvement adds burning pain even as sensation fades.
- Vitamin A deficiency and night blindness. Without retinal, rods can't regenerate rhodopsin, so dim-light vision fails first; progressive deficiency dries the conjunctiva (Bitot spots, xerophthalmia). It remains a leading preventable cause of childhood blindness worldwide and is seen in fat-malabsorption states.