pt1 Week 5 - Neurological Review and Alterations in Special Sensory Function

Alterations in Special Sensory Function - ears, eyes

Diagnostic differentiation between conductive and sensorineural loss done with what (2)

tuning fork tests (Rinne and Weber tests)

audiometry - evaluate air conduction through external ear canal versus bone conduction through the mastoid process

Conductive Hearing Loss Primary Site of Lesion

External ear or middle ear cavity

Conductive Hearing Loss Pathophysiological Mechanism

Physical obstruction/mechanical defect blocking sound wave transmission to the inner ear

Conductive Hearing Loss Etiology (5)

Cerumen impaction, foreign bodies, tympanic membrane perforation/scarring, otitis media effusion, otosclerosis

Conductive Hearing Loss Conduction Test Profile

Impaired air conduction with preserved inner ear/bone conduction

Conductive Hearing Loss General Severity & Response

Mild to moderate deficit; frequently responds to medical or surgical removal of obstruction

Sensorineural Hearing Loss Primary Site of Lesion (3)

Inner ear (Organ of Corti/hair cells), Cranial Nerve VIII, or temporal auditory cortex

Sensorineural Hearing Loss Pathophysiological Mechanism

Failure of electrical transduction in sensory hair cells or neural impulse transmission along the auditory nerve

Sensorineural Hearing Loss Etiology (5)

Presbycusis (aging), ototoxic medications, acoustic trauma/loud noise, viral/bacterial infections, head trauma

Sensorineural Hearing Loss Conduction Test Profile

Equal impairment of both air and bone conduction

Sensorineural Hearing Loss General Severity & Response

Can cause severe to total deafness; may require hearing aids or cochlear implants

Cerumen Accumulation and Foreign Bodies relation to conductive loss

blockage of external auditory meatus prevents sound waves from reaching tympanic membrane

Tympanic Membrane Perforation and Scarring relation to conductive loss

Loss of tympanic membrane elasticity or integrity secondary to trauma or recurrent infections (such as chronic otitis media), » restricted membrane vibration

otosclerosis relation to conductive loss

inherited or acquired metabolic bone remodeling disorder where excessive bone growth fixes the stapes footplate to the oval window, preventing mechanical fluid displacement within the cochlea

Presbycusis

progressive, age-related sensorineural decline by the gradual loss of sensory hair cells and degenerative changes in the cochlea

Ototoxic meds causing sensorineural hearing loss (4)

agents that damage hair cells in the Organ of Corti or vestibular system

aminoglycoside antibiotics (e.g., streptomycin, vancomycin, neomycin), loop diuretics (e.g., furosemide), NSAIDS (e.g., high-dose aspirin, ibuprofen), and antineoplastic agents.

define Acoustic Trauma, causes which hearing loss

extremely loud noises/chronic occupational exposure to high-decibel noise » damages delicate hair cell microvilli due to excessive wave force.

sensorineural

Infections and Neurological Disorders cause what hearing loss + examples

sensorineural

viral infections (such as rubella, influenza, and herpes), bacterial meningitis, head trauma, or temporal lobe tumors that injure CN VIII

otosclerosis management

stapedectomy - remove stapes

membrane perforation treatment

tympanoplasty - repairs hole/tear

standard sensorineural loss treatment

sound-amplifying hearing aids are beneficial if functional hair cells remain

profound sensorineural loss treatment

if non-functional hair cells present

intact auditory nerve » cochlear implants surgically

Otitis media

inflammation or infection of the middle ear cavity

Otitis media common demographic

pediatrics

Over 70% of children experience at least one episode before age two

Otitis media etiology

bacterial pathogens (flu), streptococcus pneumoniae (pneumococci), beta-hemolytic streptococci, and staphylococci

Anatomical Predisposition of otitis media in Children

Eustachian (auditory) tubes are shorter, wider, and oriented more horizontally compared to adults, facilitating the migration of nasopharyngeal pathogens along the continuous mucosal lining

Otitis Media Pathophysiology*

infection » inflammatory response » exudate accumulation in middle ear » exudate exerts pressure against non-yielding tympanic membrane/structures

consecutive inflammatory edema blocks Eustachian tube » prevented normal fluid drainage to nasopharynx

immediate pain relief with otitis media

pressure rises » tympanic membrane bulges » eventual rupture » purulent discharge released into the external canal

otitis media manifestations

earache, red/bulging tympanic membrane on otoscopic exam, fever, fullness, mild CONDUCTIVE hearing loss

otalgia

earache

Mastoiditis, associated with what pathology

Spread of infection into the mastoid air cells of the temporal bone - chronic otitis media

Cholesteatoma, associated with what pathology

eroding, cyst-like mass of epithelial cells and debris that forms in the middle ear following tympanic membrane perforation, produces enzymes that destroy the bony ossicles and surrounding bone - chronic otitis media

Cholesteatoma treatment

surgical excision

otitis media treatment*

Analgesic + antipyretic therapy (acetaminophen or ibuprofen) for comfort during the initial 48 hours; targeted antibacterial therapy if bacterial infection is confirmed; decongestants to encourage Eustachian tube drainage; and surgical insertion of temporary drainage tubes through the tympanic membrane for recurrent cases.

tympanostomy/myringotomy tubes use

temp drainage tubes through tympanic membrane for recurrent causes of otisis media

Otitis externa (swimmer’s ear)

infection of the external auditory canal and pinna

Otitis Externa Etiology (4)

predominantly bacterial origin, sometimes fungal

swimming (moisture create culture medium)

mechanical irritation from cleaning ear

frequent earphone/plugs

common bacteria causing swimmer’s ear

Pseudomonas aeruginosa

Otitis Externa general manifestations

Severe localized pain, purulent discharge, external canal swelling, and mild hearing deficit

classic diagnosis to distinguish otitis externa from media

pain is markedly exacerbated by movement of the pinna or pressure on the tragus

Otosclerosis

insidious chronic middle ear disorder by an abnormal imbalance between bone resorption and bone deposition

Otosclerosis development process*

excess spongy bone develop in middle ear, fixes stapes footplate to oval window, blocks mechanical transmission of sound to cochlear fluids » conductive hearing loss

Otosclerosis common demographic

genetic disposition

young adult female

Otosclerosis treatment (2)

stapedectomy (removal of the fixed stapes and insertion of a prosthetic replacement) or laser liberation of the ossicular chain (separates inner ear structures from diseased tissue)

Ménière's Syndrome

chronic disorder of inner ear labyrinth by intermittent, excessive accumulation of endolymph fluid (endolymphatic hydrops) within the membranous labyrinth

usually unilateral

Ménière's Syndrome Epidemiology

adults 30-50

Ménière's Syndrome etiology (3)

stress, conditions altering systemic blood flow (such as hypertension), and sudden barometric pressure changes

Ménière's Syndrome pathophysiology*

distension of the endolymphatic sac stretch the membranous labyrinth » interfered hair cell function in cochlea (hearing organ) and vestibule/semicircular canals (balance organs)

fluid buildup/rupture causes perilymph and endolymph to mix, triggering acute symptomatic attacks lasting minutes to hours. repeated can cause permanent sensorineural loss/equilibrium deficits

Ménière's Syndrome symptom triad

severe vertigo, tinnitus, unilateral sensorineural hearing loss (full sensation/pressure)

Severe Vertigo

Intense whirling sensation, loss of balance, and risk of falls

Tinnitus

Subjective roaring, ringing, or buzzing noise in the affected ear

Ménière's Syndrome associated signs

Autonomic disturbance (nausea, vomiting, sweating), inability to focus, and nystagmus

nystagmus

involuntary eye movements

Ménière's Syndrome diagnostics

Balance tests (rotary-chair, video head impulse), electronystagmography (ENG), electrocochleography (ECOG), and MRI to exclude acoustic neuromas.

Ménière's Syndrome management - meds (3) and lifestyle (4)

Pharmacological suppression during attacks using dimenhydrinate (antiemetic), diazepam (vestibular depressant), and antihistamines

Long-term management includes a low-sodium diet, mild diuretics, avoidance of triggers (smoking, alcohol, caffeine), and motion-desensitization exercise programs.

rods type of vision

dim light, black-and-white vision

cones location and type of vision

concentrated at the fovea centralis within the macula lutea

acute, sharp color vision

visual pathway*

optic nerve CN II » optic chiasm (medial nasal fibers cross to the contralateral hemisphere) » optic tract » Lateral Geniculate Nucleus of Thalamus » Visual Radiations » Primary Visual Cortex

Myopia (Nearsightedness)

eyeball too elongated/focal point too strong, light rays focused in front of retina

Myopia (Nearsightedness) correction

concave lenses

Hyperopia (Farsightedness)

eyeball too short, light rays focused behind retina

Hyperopia (Farsightedness) correction

convex lenses

Presbyopia

Age-related loss of lens elasticity, reducing accommodative capacity for near vision

Astigmatism

Irregular curvature of the cornea or lens causing uneven light refraction.

Cataracts

progressive opacity or clouding of normally clear crystalline lens that impairs light transmission to the retina

cataracts causes (5)

age-related protein denaturation, metabolic disorders (e.g., chronic hyperglycemia in Diabetes Mellitus), prolonged UV light exposure, ocular trauma, congenital infections (such as maternal rubella or toxoplasmosis).

cataracts pathophysiology

Structural protein degradation within the lens fibers causes aggregation and progressive clouding

cataracts manifestations

Insidious, painless onset of blurred vision across the visual field that becomes progressively darker over time.

difficulty with glare and night driving

cataracts management

Outpatient surgical replacement (phacoemulsification)

phacoemulsification

treatment for cataracts

ultrasonic oscillations to fragment the degenerated lens material for aspiration, then insertion of a clear artificial intraocular lens (IOL).

Glaucoma*

elevated intraocular pressure from excessive accumulation of aqueous humor in the anterior cavity » optic nerve atrophy and irreversible visual field loss

normal IOP

10 and 20 mmHg

pathological IOP

IOP > 24 mmHg

Aqueous humor pathway *

secreted by the ciliary processes into the posterior chamber, flows through the pupil into the anterior chamber, and drains through the trabecular meshwork into the Canal of Schlemm for reabsorption into venous circulation.

Acute (Narrow-Angle / Closed-Angle) Glaucoma - Incidence & Onset

Less common; sudden, acute emergency onset

Acute (Narrow-Angle / Closed-Angle) Glaucoma - Anatomical Pathology

Angle between cornea and iris is pathologically narrowed; iris shifts anteriorly, completely blocking fluid outflow

Acute (Narrow-Angle / Closed-Angle) Glaucoma - Etiology

Aging, anatomical narrow angle, trauma/scar tissue; triggered by pupil dilation (mydriasis)

mydriasis

abnormal or persistent dilation (enlargement) of the pupil of the eye that fails to constrict normally in bright light

Acute (Narrow-Angle / Closed-Angle) Glaucoma - manifestations

Sudden, severe ocular pain, eye redness, cloudy cornea, severe headache, nausea, rapid visual loss

Acute (Narrow-Angle / Closed-Angle) Glaucoma - treatment

Emergency medical lowering of IOP followed by surgical/laser iridotomy (creating a drainage hole in iris)

Chronic (Open-Angle / Wide-Angle) Glaucoma - Incidence & Onset

Most common form (90%); insidious, slow, asymptomatic onset after age 50

Chronic (Open-Angle / Wide-Angle) Glaucoma - Anatomical Pathology

Degenerative trabecular meshwork thickening and Canal of Schlemm obstruction; slow fluid drainage decline

Chronic (Open-Angle / Wide-Angle) Glaucoma - causes (3)

Age-related degeneration, genetic predisposition, diabetes

Chronic (Open-Angle / Wide-Angle) Glaucoma - manifestations (3)

Painless elevation of IOP; insidious loss of peripheral vision (tunnel vision); "cupping" of optic disc

Chronic (Open-Angle / Wide-Angle) Glaucoma - treatment

Lifetime topical eye drops (beta-blockers, miotics); laser trabeculoplasty or trabeculectomy if drops fail

Retinopathy

vascular damage affecting the microcirculation of the retina, leading to tissue ischemia and visual impairment.

predominantly secondary to chronic systemic diseases

Diabetic Retinopathy and progression

hyperglycemia damages retinal capillary endothelial cells

Early non-proliferative changes include microaneurysms, flame hemorrhages, and hard lipid exudates.

ischemia worsens: proliferative stage neovascularization occurs—the growth of fragile, abnormal new blood vessels that easily rupture, bleed into the vitreous humor, and create fibrous traction leading to retinal detachment

Hypertensive Retinopathy

elevated blood pressure causes retinal arteriolar narrowing, arteriolosclerosis ("copper-wiring"), flame-shaped hemorrhages, and ischemic cotton-wool spots (nerve fiber layer infarctions).

Retinopathy diagnostic

dilated fundoscopy (back of eye fundus exam)

Retinopathy treatment

strict control of underlying hypertension and blood glucose, laser photocoagulation (to cauterize leaking vessels and destroy ischemic tissue), intravitreal anti-VEGF (vascular endothelial growth factor) injections to suppress abnormal neovascularization

Retinal Detachment

pigmented layer of the retina separates from the underlying sensory layer and vascular choroid

Retinal Detachment pathophysiology

tear/hole in retina allows vitreous humour to seep behind retinal layer and separates it from vascular choroid » ischemia and irreversible blindness if untreated

Retinal Detachment manifestations

painless onset.

sudden appearance of dark floaters, flashes of light (photopsia), followed by a progressive, dark curtain-like shadow advancing across the visual field (scotomas).

Retinal Detachment treatment

Immediate surgical reattachment (such as scleral buckling, pneumatic retinopexy, or vitrectomy) to restore retinal apposition to the choroid before permanent receptor necrosis occurs