Chapter 11- senses

Objectives

By the end of this section, you should be able to:

1. Classify sense organs into general or special and explain the differences.

2. Discuss how stimuli are converted into sensations and conditions involving general senses.

3. Describe general sense organs and their functions.

4. Describe the eye and its structures/functions.

5. Name/describe major visual conditions.

6. Discuss the ear and its role in hearing/equilibrium.

7. Name/describe major hearing impairments.

8. Describe the tongue and its sensory role in taste.

9. Describe the nasal cavity and its sensory role in smell.

10. Explain how senses are integrated in the brain.

Introduction to Senses

• The common sense organs you think of are: eyes, ears, nose, tongue.

• But there are millions of sensory receptors all over the body — in skin, internal organs, and muscles.

• These receptors detect stimuli like touch, pressure, temperature, pain.

• They’re located at the tips of sensory neuron dendrites.

• Sensory input is crucial for homeostasis and survival.

• External dangers: detected by sight or hearing.

• Internal dangers: detected by temperature changes, stretching, pain.

• Specialized receptors can alert the brain so corrective action can be taken.

Classification of Senses

General Senses

• Detected by simple microscopic receptors spread throughout body — skin, muscles, tendons, joints, internal organs.

• Responsible for: pain, temperature, touch, pressure, body position.

Special Senses

• Detected by receptors grouped in specific areas and tied to complex structures.

• Includes: smell, taste, vision, hearing, equilibrium.

Sensory Receptor Types

• Classified as encapsulated (covered by a capsule) or unencapsulated (“naked” endings).

• Also classified by mode (type of stimulus they respond to):

  1. Photoreceptors – light (vision)

  2. Chemoreceptors – chemicals (taste, smell)

  3. Pain receptors – injury

  4. Thermoreceptors – temperature changes

  5. Mechanoreceptors – position/shape change (touch, pressure, hearing)

Sensory Pathways

• All sense organs: must detect stimulus → convert it to nerve impulse → send to brain via specific pathways.

• For general senses, pathways involve conduction to:

  • Thalamus (cutaneous/skin receptors)

  • Cerebellum (proprioceptors)

General Sense Organs (Table 11-1)

Special Sense Organs (Table 11-2)

Distribution of General Sense Receptors

• Found in nearly all body areas but most in skin.

• Uneven distribution — why different body parts have different touch sensitivity.

• Two-point discrimination test measures sensitivity by detecting if two touches are felt as one or two points.

• Fingertips have close receptor spacing; back and torso have wider spacing.

• Proprioceptors are located in tendons/muscles to provide position/movement info.

Modes of Sensation

• Vibration, deep pressure, light pressure, pain, stretch, temperature — detected by various receptors.

• Proprioceptors: provide info on position/movement of body parts and muscle contraction.

Conditions Involving General Senses

• Third-degree burns: destroy receptors — loss of pain/touch in that area.

• Reduced blood flow (sitting with legs bent) → temporary receptor impairment (numbness).

• Other causes: diabetes, cardiovascular disease, stroke, spinal cord injury, brain injury.

Quick Check (p. 300)

1. Two major classifications of senses?

   • General senses, Special senses

2. Major modes of sensory cell function?

   • Photoreceptors, Chemoreceptors, Pain receptors, Thermoreceptors, Mechanoreceptors

3. Sensory pathway of general sense organs?

   • Receptors → Nerve impulse → Spinal cord → Thalamus (or cerebellum) → Brain interpretation

4. Two-point discrimination?

   • Ability to detect if two touches are separate or one; depends on receptor density.

5. Function of a proprioceptor?

   • Detect muscle tension/length, position/movement of body parts.

Special Senses – Vision

Function of Vision

• Detects color and intensity of light in our environment.

• When processed by the brain, allows us to:

  • Recognize outlines and depth of objects.

  • Analyze movement.

  • Determine distances.

Structure & Function of the Eye

The eyeball has three layers:

1. Fibrous layer

   • Sclera – white, tough fibrous tissue; gives shape & protection.

   • Cornea – transparent “window” of the eye; bends light for focusing.

     • Inflammation = keratitis.

     • Shape affects vision focus (can be reshaped with surgery).

   • Conjunctiva – thin mucous membrane lining eyelids and covering sclera; kept moist by lacrimal gland (tear production).

2. Vascular layer

   • Choroid – contains many blood vessels and pigment melanin to absorb stray light.

   • Ciliary muscle – controls lens shape for focusing.

   • Iris – colored part of eye; controls pupil size.

   • Lens – transparent structure behind iris; focuses light on retina.

3. Inner layer

   • Retina – contains photoreceptor cells (rods and cones).

     • Rods – vision in dim light, black/white.

     • Cones – vision in bright light, color (red, green, blue).

   • Macula lutea – yellow spot on retina.

   • Fovea centralis – sharpest vision, most cones.

   • Optic nerve – transmits visual info to brain.

Pupil Control (Figure 11-3)

• Dim light – radial muscles contract → pupils dilate → more light enters.

• Bright light – circular muscles contract → pupils constrict → less light enters.

• Controlled by autonomic nervous system.

Fluids of the Eye

• Aqueous humor – watery fluid in front of lens (anterior chamber); continuously made, drained, replaced.

• Vitreous humor – jelly-like fluid behind lens (posterior chamber); maintains shape.

• Glaucoma – if aqueous humor drainage is blocked → pressure increases → may cause blindness.

Quick Check (Vision)

1. Three layers of the eyeball: Fibrous, Vascular, Inner.

2. Function of melanin in eye: Absorbs stray light, prevents scattering for clear vision.

3. Pupil size regulation: Radial muscles (dilate), Circular muscles (constrict) under autonomic control.

4. Cornea vs. Lens: Cornea = fixed transparent window; Lens = adjustable focus.

5. Humors of the eye:

   • Aqueous humor = watery fluid in front of lens; maintains pressure, nourishes lens/cornea.

   • Vitreous humor = gel-like fluid behind lens; maintains shape of eye.

6. Rods vs. Cones:

   • Rods = night vision, black/white, sensitive to dim light.

   • Cones = day vision, color vision (red, green, blue).

Special Senses – Vision

Overview of Vision

• Vision detects color and intensity of light in the external environment.

• Light focused by the eyes and processed by the brain allows recognition of object outlines, analysis of depth, movement detection, and distance judgment.

• Vision is one of the most complex and precise senses.

• This section focuses on the anatomy and function of the eye.

Structure and Function of the Eye

The eyeball is a fluid-filled sphere with a wall made of three layers:

1. Fibrous Layer

• Made of tough fibrous tissue.

• Two main parts:

  • Sclera –

    • The “white” of the eye.

    • Dense bundles of collagen fibers give strength.

    • Forms most of the fibrous layer.

  • Cornea –

    • Transparent circle at the front of the fibrous layer.

    • Known as the “window” of the eye due to its transparency.

    • Keratitis – inflammation of the cornea, can cause loss of transparency.

    • Shape changes can affect ability to focus an image on the retina.

    • Shape can be altered with lasers or other instruments to improve vision without glasses or contact lenses.

• Conjunctiva –

  • Thin mucous membrane lining the eyelids and covering the front sclera.

  • Blood vessels seen in the sclera are actually in the conjunctiva.

  • Kept moist by tears from the lacrimal gland.

2. Vascular Layer

• Called vascular because it has a dense network of blood vessels.

• Contains the choroid –

  • Large amount of pigment melanin (dark pigment).

  • Absorbs stray light to prevent scattering and helps focus light on the retina.

• Iris –

  • Colored part of the eye.

  • Contains muscles that control the size of the pupil (opening in the center of the iris).

    • Pupil appears black because it’s a hole through which light enters.

    • Fibers arranged like spokes → dilate pupil (let in more light).

    • Circular fibers → constrict pupil (reduce light entry).

    • Pupil changes are under autonomic nervous control.

• Lens –

  • Transparent, located directly behind the iris.

  • Held in place by a ligament attached to the ciliary muscle (an involuntary muscle).

  • For distant vision → ciliary muscle relaxes, lens is flatter.

  • For near vision → ciliary muscle contracts, pulling choroid forward, causing lens to bulge and curve more for stronger focusing power.

3. Inner Layer

• Made up mostly of the retina – the innermost sensory layer of the eye.

• Contains microscopic photoreceptor cells:

  • Rods –

    • Sensitive to dim light.

    • Give monochrome (colorless) vision in low light.

    • Function in night vision.

  • Cones –

    • Sensitive to bright light.

    • Allow color vision.

    • Three types: red, green, and blue.

    • Scattered throughout central retina; allow distinction between different colors in daylight.

• Macula lutea –

  • Yellowish area near retina’s center.

  • Has a small depression called the fovea centralis, which contains the highest concentration of cones and gives the sharpest vision.

• Ophthalmoscope –

  • A medical device that can view structures like the macula and fovea.

• Ganglion cells –

  • Sensitive to light and wavelengths but not used for detailed visual images.

  • Send information to the brain about day/night cycles, helping regulate the internal clock for daily, monthly, and seasonal rhythms.

Fluids of the Eye

• Eye contains two main fluids that fill hollow spaces:

  • Aqueous humor –

    • Watery fluid in the anterior chamber (in front of lens).

    • Constantly formed, drained, and replaced.

  • Vitreous humor –

    • Jelly-like fluid in posterior chamber (behind lens).

• Functions:

  • Maintain shape of the eye.

  • Refract (bend) light rays to focus them on retina.

• Glaucoma –

  • Blocked aqueous humor drainage increases internal pressure.

  • Can damage the eye and cause blindness.

Pupil Control (Figure 11-3)

• Dim light → radial muscles contract → pupil dilates → more light enters.

• Bright light → circular muscles contract → pupil constricts → less light enters.

• Typical light → balanced muscle action.

• Controlled by autonomic nervous system:

  • Sympathetic nerves stimulate dilation.

  • Parasympathetic nerves stimulate constriction.

Quick Check (Vision)

1. Three layers of the eyeball – Fibrous layer, Vascular layer, Inner layer.

2. Function of melanin – Absorbs stray light to prevent scattering and helps focus light on the retina.

3. Pupil regulation – Radial fibers dilate pupil, circular fibers constrict pupil; controlled by autonomic nerves.

4. Cornea vs. Lens – Cornea is a fixed transparent front layer; Lens changes shape for focusing.

5. Humors –

   • Aqueous humor (anterior chamber): watery, nourishes and maintains pressure.

   • Vitreous humor (posterior chamber): gel-like, maintains shape.

6. Rods vs. Cones –

   • Rods: dim light, black-and-white vision.

   • Cones: bright light, color vision (red, green, blue).

Visual Pathway

• Stimulus: Light is the stimulus for vision.

  • We detect brightness (intensity), color (wavelength), and also perceive images and movement.

• Light enters the eye through the pupil and is refracted (bent) so it focuses on the retina.

  • Refraction occurs as light passes through:

    1. Cornea

    2. Aqueous humor

    3. Lens

    4. Vitreous humor

• When light reaches the innermost layer of the retina (photoreceptor cells: rods and cones), these respond by producing a nerve impulse.

• Bipolar cells carry signals from photoreceptors to ganglion cells.

• Ganglion cells transmit impulses out of the retina through the optic nerve (cranial nerve II).

• At the optic disk (blind spot), no rods or cones are present because it’s the exit point of optic nerve fibers.

• The optic nerves travel to the visual cortex in the occipital lobe (Figure 11-6) for visual interpretation.

Conditions of Vision

Healthy vision depends on three main processes:

1. Image formation on the retina (refraction).

2. Stimulation of rods and cones.

3. Conduction of nerve impulses to the brain.

If any process fails → vision problems occur.

Refraction Conditions

Myopia (Nearsightedness)

• Eyeball is too long from front to back.

• Image focuses in front of retina.

• Retina receives fuzzy image.

• Corrected with glasses/contact lenses or refractive surgery (Figure 11-7 B & C).

Hyperopia (Farsightedness)

• Eyeball is too short from front to back.

• Image focuses behind retina.

• Produces fuzzy image.

• Corrected with glasses/contact lenses or surgery (Figure 11-7 D & E).

Astigmatism

• Unequal curvature of cornea or lens → distorted vision.

• Correctable with glasses or contacts.

Presbyopia

• Age-related loss of lens elasticity → inability to bulge for near vision.

• “Old-sightedness.”

• Corrected with reading glasses.

Cataracts

• Lens becomes hard, loses transparency, becomes “milky” (Figure 11-8).

• Caused by long-term UV exposure.

• Cloudy lens prevents proper focusing, especially in dim light (night vision issues in older adults).

• Progressive; can cause blindness.

• Treated surgically by removing lens and replacing with artificial implant.

Conjunctivitis

• Inflammation of conjunctiva (“pink eye”).

• Causes: infections, allergies, chemical irritants.

• Bacterial conjunctivitis (Figure 11-9) → mucous pus drainage; highly contagious.

• Pathogens: Staphylococcus, Haemophilus, Chlamydia trachomatis (can cause trachoma).

• Can damage cornea if untreated → impaired vision or blindness.

• May cause subconjunctival hemorrhage if trauma occurs.

Strabismus

• Eyes fail to align properly; binocular vision is disrupted.

• Convergent squint = eyes turn toward nose (“cross-eye”).

• Divergent squint = eyes turn outward.

• Can be caused by muscle weakness, paralysis, or nerve damage.

• If untreated, brain may ignore input from misaligned eye → permanent vision loss in that eye.

• Treatment: corrective surgery, therapeutic training, or corrective lenses.

Quick Check

1. Myopia vs Hyperopia – Myopia: image focuses in front of retina (eye too long). Hyperopia: image focuses behind retina (eye too short).

2. Part affected in cataracts – Lens.

3. Pink eye – Inflammation of conjunctiva, often infectious, sometimes allergic.

4. Strabismus – Misalignment of eyes; treated with surgery, training, or corrective lenses.

Conditions of the Retina

Damage to the retina can impair vision even if an image is well-focused, because if the sensory retinal cells are damaged or nonfunctional, vision cannot occur.

Retinal Detachment

• Definition: Separation of part of the retina from the underlying tissue that supports it.

• Causes:

  • Aging

  • Eye tumors

  • Sudden blows to the head (e.g., sports injury)

• Warning signs:

  • Sudden appearance of floating spots

  • Odd “flashes of light” that may last for weeks

• If untreated:

  • The retina can detach completely, causing total blindness in the affected eye.

• Treatment options:

  • Laser therapy – seals retina in place

  • Tight collar around the eyeball – increases pressure, using the vitreous humor’s pressure to keep the retina pressed against the rear wall of the eye.

Diabetic Retinopathy

• Cause: Diabetes mellitus (deficiency of insulin) → small hemorrhages in retinal blood vessels.

• Effect: Disrupts oxygen supply to photoreceptors.

• Body’s response: Builds new blood vessels (neovascularization) which can block vision and possibly detach retina.

• Prevalence: One of the leading causes of blindness in the U.S.

• Treatment: Laser therapy to seal hemorrhaging vessels; successful in many cases.

Glaucoma

• Definition: Excessive intraocular pressure from accumulation of aqueous humor.

• Process:

  • Increased pressure → pushes on retina → slows blood flow → degeneration of retinal cells → vision loss.

• Forms:

  • Acute – sudden onset, but rare.

  • Chronic – develops slowly over years; may be symptomless early on.

• Early signs: Gradual loss of peripheral vision (“tunnel vision”).

• Advanced signs: Blurred vision, headaches, halos around lights.

• If untreated: Leads to total permanent blindness.

• Prevention: Routine eye exams include glaucoma screening.

Retinal Degeneration

• General: Degeneration of retina → difficulty seeing at night or in dim light (nyctalopia or “night blindness”).

• Causes:

  • Vitamin A deficiency (needed to make photopigment in rods).

  • Photopigment deficiency → rods fail to function → poor dim-light vision.

• Age-related macular degeneration (AMD):

  • Progressive degeneration of the macula (central retina).

  • Leading cause of permanent blindness in older adults.

  • Cause is unknown, but risk increases after age 50.

  • Risk factors: Smoking, family history.

  • Macula degeneration affects the area needed for sharp, central vision.

Color Vision Deficiency

• Cause: Usually inherited; most often due to genes on the X chromosome producing abnormal photopigments in cones.

• Cone sensitivity:

  • Each cone type is sensitive to red, green, or blue light.

  • Most common deficiency: green-sensitive photopigment absent/nonfunctional.

  • Next: red-sensitive photopigment affected.

  • Rare: blue-sensitive deficiency.

• Pattern: X-linked → more common in males.

• Detection: Standardized color plates (e.g., Figure 11-11).

• Note: People with color vision deficiency still see colors but can’t distinguish between certain hues.

• Rare form: Blue color deficiency caused by mutation on nonsex chromosome (rarely distributed in humans).

Conditions of the Visual Pathway

• Damage or degeneration in the optic nerve, brain, or any part of the visual pathway can impair vision.

• Example: Pressure from glaucoma can damage the optic nerve.

• Diabetes can cause degeneration of the optic nerve.

Effects of Damage

• Visual pathway damage does not always cause total blindness.

• The specific location of damage determines the visual deficit.

• Sometimes only part of the visual field is lost.

Examples

1. Optic Nerve Neuritis

   • Often associated with multiple sclerosis (MS).

   • Causes partial visual field loss, sometimes affecting the center of vision.

   • This condition is called scotoma.

2. Cerebrovascular Accident (Stroke)

   • Stroke or brain injury can damage areas of the cerebrum that process visual information.

   • May result in acquired cortical color vision deficiency:

     • Person loses ability to distinguish any colors, not just one or two, unlike inherited color blindness.

     • Caused by damage to color-processing regions of the brain.

Quick Check

1. Progressive loss of central vision common with aging → Age-related macular degeneration (AMD).

2. How glaucoma harms retina → Increased intraocular pressure slows blood flow and degenerates retinal cells.

3. Nyctalopia & Vitamin deficiency → Nyctalopia = night blindness, caused by vitamin A deficiency affecting rod photopigment.

Hearing & Equilibrium (pp. 309–313)

Before “Ear”: the mode for hearing & balance (p. 309, first paragraph)

• The “trigger” for both hearing and equilibrium is a mechanical stimulus, so their receptors are mechanoreceptors.

• In hearing, sound vibrations → nerve impulses → perceived in the cerebral cortex as sound.

• In equilibrium, changes in position or movement of the body trigger impulses that produce sensations of balance.

Ear (section header + overview) (p. 309)

• The ear is more than the visible appendage; most functional parts lie deep in the temporal bone.

• Anatomical divisions (Fig. 11‑12):

  1. External ear

  2. Middle ear

  3. Inner (internal) ear

External Ear (p. 309–310)

Parts

• Auricle (pinna) = the external flap on the side of the head.

• External acoustic canal leads inward from the auricle.

Injury/skin notes (p. 309)

• Because the auricle is exposed over bone, it’s often bruised by blunt trauma.

• Bruising can cause blood and tissue fluid to collect between skin and cartilage; if untreated, the classic “cauliflower ear” may develop permanently.

• Skin behind the ear has many sebaceous (oil) glands; if they become infected, painful cysts can develop that must be drained.

Nodules on the helix (p. 309)

• In gout, urate crystal nodules called tophi can appear on the upper edge of the helix.

• A benign variant called a Darwin tubercle may also appear on the helix—no treatment needed.

Frank’s sign (p. 309)

• Oblique earlobe creases (Frank’s sign) in people >50 yrs may be related to coronary artery disease (controversial).

Landmarks & canal specifics (p. 309–310)

• Tragus: small projection just anterior to the canal opening (see Fig. 11‑12).

• External acoustic canal: a curving tube ~2.5 cm (1 in.) long; extends into the temporal bone and ends at the tympanic membrane.

Tympanic membrane (eardrum) (p. 309–310)

• The tympanic membrane (the eardrum) separates the external and middle ear.

• Sound waves traveling through the canal strike it and cause it to vibrate.

Ceruminous glands & earwax (p. 310)

• The canal’s outer one‑third has short hairs and ceruminous glands that secrete cerumen (earwax).

• Cerumen prevents drying/flaking of canal skin and traps dust, which is then carried outward as the canal’s epithelium grows toward the exterior.

Exam of the external ear (p. 310; Fig. 11‑13)

• An otoscope is used to view the external canal and the outer surface of the tympanic membrane.

• Changes seen with an otoscope give useful information:

  • Otitis media: eardrum becomes red, inflamed, and bulges outward as pus/fluids collect in the middle ear.

  • Swimmer’s ear (external otitis): inflammation from moisture/bacteria/fungi in the canal lining.

  • Perforations of the eardrum and foreign bodies are readily seen.

• HEALTH & WELL‑BEING – Swimmer’s Ear (p. 310):

  • Common in athletes; bacterial or fungal; associated with prolonged water exposure.

  • Involves external canal (and often auricle); ear is tender, red, swollen.

  • Treatment: usually antibiotics and analgesics.

Middle Ear (p. 310)

• A tiny epithelium‑lined, air‑filled cavity in the temporal bone (Fig. 11‑12).

• Contains three auditory ossicles:

  • Malleus (hammer): handle attaches to inside of the tympanic membrane; head attaches to incus.

  • Incus (anvil): bridges malleus → stapes.

  • Stapes (stirrup): base presses against the oval window (a membrane covering a small opening).

• Oval window separates the middle ear from the inner ear.

• Function: Eardrum vibrations are transmitted & amplified by the ossicles; stapes motion at the oval window moves inner‑ear fluid.

Auditory (Eustachian) tube & infections (p. 310–311)

• Auditory/Eustachian tube connects the throat to the middle ear (Fig. 11‑12).

• The epithelial lining of throat, auditory tubes, and middle ear is one continuous membrane, so throat infections can spread and cause otitis media (see Fig. 11‑13C).

(Additional) Function of the auditory tube (p. 311, top)

• A healthy auditory tube equalizes air pressure between the middle ear and the outside.

• If pressures are unequal, the tympanic membrane may remain stretched, which can be painful and reduces its ability to vibrate.

Inner Ear (p. 311)

Bony & membranous labyrinth

• The inner ear is a complex bony labyrinth (odd‑shaped space in the temporal bone) filled with perilymph and divided into: vestibule, semicircular canals, cochlea (Fig. 11‑14A).

• Vestibule lies adjacent to the oval window, between semicircular canals and cochlea.

• A balloonlike membranous sac (membranous labyrinth) is suspended in perilymph, following the bony labyrinth like a “tube within a tube”; it contains endolymph (thicker fluid).

Hearing (mechanism) (p. 311–312; Fig. 11‑14B, 11‑15)

• Sound waves → tympanic membrane vibrates → ossicles transmit/amplify → stapes moves at oval window → perilymph moves → endolymph in the membranous labyrinth moves.

• Vibrations reach the spiral organ (organ of Corti) inside the cochlea.

• Ciliated hair cells on the spiral organ are bent by endolymph movement, generating nerve impulses.

• Impulses travel via the cochlear nerve to the auditory area of the cerebral cortex → hearing.

Equilibrium (p. 312–313)

Static equilibrium (vestibule; Fig. 11‑16)

• Mechanoreceptors for balance are in the saclike membranous labyrinth of the vestibule and in the three semicircular canals.

• Inside the vestibule are two structures, each a patch of sensory hairs coated with a thick glob of heavy gel—each patch is a macula.

• Bending the head lets gravity shift the heavy gel, bending the hair‑cell cilia → nerve impulse.

• The brain interprets this as our “sense of gravity” or static equilibrium (head position at rest).

Dynamic equilibrium (semicircular canals; Fig. 11‑17)

• The three canals are half‑circles set at right angles to each other.

• Each has a dilated area, the ampulla, that contains a crista ampullaris.

• Crista ampullaris: sensory cells with hairlike cilia embedded in a flaplike cupula.

• When head movement changes speed or direction, endolymph flow displaces the cupula, bending hair cells → nerve impulse.

• Because each canal is angled in a different plane, the brain compares input from all three cristae to determine direction of movement.

Vestibular pathways (p. 312)

• Nerves from vestibular maculae and cristae join to form the vestibular nerve.

• The vestibular nerve joins the cochlear nerve to form CN VIII (vestibulocochlear nerve).

• Impulses travel to the cerebellum and medulla oblongata, and ultimately to the cerebral cortex.

Quick Check (p. 313) — Answers

1. Tympanic membrane (eardrum).

2. Because the auditory (Eustachian) tube connects throat ↔ middle ear, infections spread and cause otitis media.

3. Perilymph (bony labyrinth) and endolymph (membranous labyrinth).

4. Maculae (vestibule) for static equilibrium; crista ampullaris (ampullae of semicircular canals) for dynamic equilibrium.

Hearing and Equilibrium Conditions

Hearing Conditions (p. 313–314)

Two broad categories

• Conduction impairment: blocking of sound conduction through the external and/or middle ear along the conduction pathway to the inner ear’s sensory receptors.

• Nerve impairment: insensitivity to sound because of inherited or acquired nerve damage.

Common causes of conduction impairment

• Blockage of the external auditory canal is the most obvious cause:

  • Waxy buildup of cerumen (see Fig. 11‑13D).

  • Foreign objects, tumors, or other matter in the external or middle ear.

• Otosclerosis (inherited bone condition):

  • Causes structural irregularities in the stapes that impair conduction.

  • Often appears during childhood or early adulthood.

  • Commonly associated with tinnitus (“ringing in the ear”).

• Otitis (ear infection) → temporary conduction impairment:

  • The auditory (Eustachian) tube connects the throat to the middle ear, so bacterial or viral throat infections can spread and produce otitis media (see Fig. 11‑13C).

  • Otitis media often produces swelling and pus formation that blocks sound conduction through the middle ear.

  • Severe cases may cause permanent damage to middle-ear structures.

  • Infectious organisms that invade the temporal bone can be difficult to treat and may cause redness, inflammation, and swelling of the mastoid process, sometimes pushing the auricle away from the skull; hearing loss can complicate severe cases.

Common forms of nerve impairment

• Presbycusis:

  • Progressive hearing loss associated with aging.

  • Results from degeneration of nervous tissue in the inner ear and the vestibulocochlear nerve.

• Noise‑induced hearing loss (after chronic exposure to loud noises):

  • Damages receptors in the spiral organ.

  • Because different sound frequencies stimulate different regions of the spiral organ, the impairment is often limited to certain frequencies.

  • In presbycusis, the part that degenerates first is stimulated by high‑frequency sounds → older adults commonly cannot hear high‑pitched sounds.

• Prevention note: Regardless of age, protecting yourself from loud and constant noises can reduce hearing loss over time.

Equilibrium Conditions (p. 314)

• Often characterized by vertigo (spinning sensation), disorientation, falling, dizziness, and/or lightheadedness.

• Some anxiety disorders can produce these symptoms too, but they are not true equilibrium diseases.

• Causes include infection or inflammation of the inner ear, head injuries, nerve damage, or unknown causes.

• Temporary equilibrium impairment can occur when the brain receives conflicting sensory information about body movement from multiple senses (vision, balance, proprioception, etc.) — as in motion sickness.

• Ménière disease:

  • Chronic inner ear disease of unknown cause.

  • Characterized by tinnitus, progressive nerve deafness, and vertigo.

Quick Check (p. 314) — Answers

1. Two basic categories: Conduction impairment and nerve impairment.

2. Tinnitus: Ringing in the ear, commonly associated with otosclerosis and also with Ménière disease.

3. Progressive nerve‑impairment hearing loss in older adults: Presbycusis.

Taste (Gustation) (p. 314–315)

What taste lets us do

• Our sense of taste (gustation) lets us chemically analyze food before we bite or swallow it.

Sense organs & cells

• Taste buds are the sense organs of taste.

• They contain supporting cells and chemoreceptors called gustatory cells, which generate the nerve impulses ultimately interpreted by the brain as taste (see Fig. 11‑18).

Nerve pathway

• Taste impulses from taste buds travel primarily through two cranial nerves — CN VII (facial) and CN IX (glossopharyngeal) — to the taste area of the cerebral cortex.

Locations of taste buds

• A few are in the lining of the mouth and on the soft palate, but most are on the tongue within small elevations called papillae.

• About 10–15 large circumvallate papillae form an inverted “V” at the back of the tongue and contain the most taste buds.

Microscopic structure & how taste is triggered

• Each taste bud opens to the surface through a taste pore into a trenchlike moat around the papilla that is filled with saliva (Fig. 11‑18B, C).

• Chemicals dissolved in saliva stimulate gustatory hairs of gustatory cells.

• All taste qualities can be detected in all tongue areas that contain taste buds.

Primary tastes (and updates)

• Originally, physiologists listed four “primary” taste sensations: sweet, sour, bitter, salty — detecting sugars, acids, alkalines, and sodium ions dissolved in saliva.

• The list has expanded:

  • Metallic (detect metal ions).

  • Umami (savory/meaty; detects the amino acid glutamate).

  • The list continues to grow.

• People vary: some sense a larger number of tastes; “experts” and “supertasters” are said to detect dozens of discrete tastes in items like wine, coffee, tea, and other foods/beverages.

Smell (Olfaction) (p. 315)

Where the receptors are

• Chemoreceptors for smell (olfaction) are in a small area of epithelial tissue in the upper part of the nasal cavity (Fig. 11‑19).

• Because the location is somewhat hidden, we often sniff forcefully to smell delicate odors.

How the receptors work

• Each olfactory cell has multiple sensory cilia that detect different chemicals and trigger a nerve impulse.

• To be detected, chemicals must dissolve in the watery mucus lining the nasal cavity.

Sensitivity and adaptation

• Olfactory receptors are extremely sensitive and respond quickly even to very slight odors.

• They also adapt; odors that are noticeable at first may not be sensed after a short time due to decreased receptor sensitivity (adaptation).

Neural pathway & perception

• After stimulation, impulses travel through olfactory nerves in the olfactory bulb and olfactory tract of cranial nerve I.

• They then enter thalamic and olfactory centers of the brain, where they are interpreted as specific odors.

• The cortical areas for olfaction are closely associated with memory and emotion centers (including the limbic system), so we may retain vivid, long‑lasting memories tied to smells.

Quick Check (p. 315) — Answers

1. Primary tastes humans can perceive: sweet, sour, bitter, salty, plus the newly added umami and metallic (and the list is expanding).

2. Why odors fade: Adaptation — receptor sensitivity decreases after a short time.

3. Smell pathway: Olfactory receptor cells → olfactory nerves in olfactory bulb/tract (CN I) → thalamic & olfactory brain centers, where odors are interpreted.

Integration of Senses (p. 316)

Big picture

• Remember: sensations are perceived in the brain. Signals from individual receptors are sent to the brain, where some are amplified, others dampened, and many are integrated with other sensory signals and memories to produce our conscious perceptions.

Example: flavor is a combo sense

• What we call flavor often results from combined sensory input: taste (gustatory) + smell (olfactory) + touch & pain receptors (texture, spiciness) + temperature.

• Nasal congestion or odors from foods in the mouth can dull flavor by interfering with olfactory receptor stimulation (Fig. 11‑19).

• Some foods seem different because of texture; others stimulate pain (spicy foods → “hot”), and some mints trigger temperature receptors to produce a “cool” sensation—these all add to flavor.

Smell & memory

• Smell sensations are often powerful memory triggers.

Subconscious sensory processing

• Some sensory info is processed subconsciously; you can’t “feel” your blood pH or oxygen saturation, but your brain monitors them constantly.

Maintaining posture & balance

• We often combine equilibrium with vision and proprioception to maintain posture and balance during changing circumstances.

Aging changes

• With age, structural degeneration reduces function:

  • Mechanoreceptors in the ear become less sensitive.

  • Lenses become less able to adjust visual focus.

  • Taste and smell often decline.

• These changes can lead to isolation if sensory contact with the outside world fades; caring health professionals should recognize this and assist older adults so they can enjoy life.

Science Applications — Senses (p. 316 sidebar)

• Santiago Ramón y Cajal (1852–1934) is regarded as a founder of modern views of nervous system organization; he uncovered much about sensory cortex centers and retinal structure, made discoveries across the nervous system, and received a Nobel Prize (1906).

• Knowledge of sensory systems supports professions like optometrists, ophthalmologists, otologists, audiologists, and others who assess and treat sensory conditions.

• Many fields make indirect use of sensory neuroscience: artists, musicians, architects (visual perception; sound perception in performance/hall design), and aerospace professionals (spatial orientation, motion sickness).