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🧠 COMPLETE LECTURE: Neurology & Special Senses (Pages 542-550)

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PAGE 542 - CHILDHOOD PRIMARY BRAIN TUMORS

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📌 What is a Brain Tumor?

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1. PILOCYTIC ASTROCYTOMA

• GFAP positive - GFAP stands for Glial Fibrillary Acidic Protein. Think of GFAP as the "name tag" that identifies astrocyte cells. When we stain the tumor tissue, these cells light up positive for GFAP, confirming they are astrocyte-type cells.
• Bipolar neoplastic cells with hairlike projections - Under the microscope, the cancer cells have two ends (bipolar) with long thin hair-like arms extending out.
• Rosenthal fibers - These are cork-screw shaped structures (like twisted fibers) seen inside the tumor cells. They are a hallmark finding. If you see "corkscrew fibers" in a microscopy question, think pilocytic astrocytoma.
• Eosinophilic - Eosinophilic means the structures stain pink-red with a standard H&E (hematoxylin and eosin) stain used in pathology labs.

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2. MEDULLOBLASTOMA

• Headaches (especially in the morning - because lying flat at night worsens pressure)
• Papilledema - Papilla = the optic disc (the back of the eye where the optic nerve enters). When intracranial pressure rises, it pushes on the optic nerve, causing swelling of the optic disc when you look into the eye with an ophthalmoscope. This is a CRITICAL sign of raised intracranial pressure.

• PNET (Primitive Neuroectodermal Tumor) - These cells are very primitive (undifferentiated). They haven't matured into specific cell types yet. "Neuroectodermal" means they come from the same embryonic origin as the nervous system (the ectoderm layer of the embryo).
• Homer-Wright rosettes - Under the microscope, the cells arrange themselves in circular patterns around a central pale area (neuropil, which is nerve fiber material). This rosette pattern is diagnostic. Named after the two doctors who described it.
• Small, round, blue cells surrounding central area of neuropil - These small, dark-staining (blue) cells arranged in circular clusters are the classic microscopic picture.
• Synaptophysin positive - Synaptophysin is a protein found in nerve cells at the synapse (connection point between nerves). When the tumor stains positive for synaptophysin, it confirms the cells have neuronal characteristics.

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3. EPENDYMOMA

• Perivascular pseudorosettes - "Peri" = around, "vascular" = blood vessel. The tumor cells arrange themselves around blood vessels in a spoke-wheel pattern. These are called pseudorosettes because they look like rosettes but are centered around a blood vessel rather than neuropil.
• Rod-shaped blepharoplasts - Blepharoplasts are tiny rod-shaped structures near the nucleus. They are modified cilia basal bodies (cilia are hair-like projections that cells use to move fluid). This tells us ependymal cells normally have cilia to circulate CSF.

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4. CRANIOPHARYNGIOMA

• It grows along the pituitary stalk - the pituitary stalk connects the hypothalamus (brain's hormone control center) to the pituitary gland. Compression here causes hormone deficiencies.
• Compression of optic chiasm - The optic chiasm is where the optic nerves from both eyes cross. It sits directly below the pituitary stalk. Compression here causes bitemporal hemianopia - you lose vision in both outer (temporal) fields. Imagine a horse with blinders covering the sides - you can only see straight ahead, not to the sides.
• Associated with pituitary adenoma - Sometimes confused with pituitary adenomas (benign tumors of the pituitary gland itself).
• High recurrence rate - These tumors come back even after surgery.

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5. PINEAL GLAND TUMORS

• Upward gaze palsy - The person cannot look upward. Ask them to look up - they cannot. The brain cannot send the signal.
• Convergence-retraction nystagmus - Nystagmus means rhythmic jerking of the eyes. Convergence = eyes turning inward. Retraction = the eyeballs actually jerk backward into the socket. This is an extremely bizarre-looking eye movement abnormality.
• Light-near dissociation - Normally when you shine a light in the eye, the pupil constricts (gets smaller). Also, when you look at something close up, the pupil constricts. In Parinaud syndrome, the pupil does NOT react to light, but it DOES constrict when looking at near objects. The two normally linked responses are dissociated (separated).

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PAGE 543 - HERNIATION SYNDROMES + UMN vs LMN

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BRAIN HERNIATION SYNDROMES

What is Herniation?

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1. CINGULATE (SUBFALCINE) HERNIATION under falx cerebri

• Contralateral lower extremity weakness - Contra = opposite side. If the right side herniates under the falx and compresses the left ACA, the patient has weakness in their LEFT leg.
• If it compresses the dominant hemisphere's ACA, it can also cause aphasia (inability to speak/understand language). The dominant hemisphere for language is usually the left.
• Arcuate fasciculus compression → aphasia - The arcuate fasciculus is a bundle of nerve fibers connecting Broca's area (speech production) to Wernicke's area (language comprehension). Damage here = aphasia.

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2. CENTRAL/DOWNWARD TRANSTENTORIAL HERNIATION

• Caudal = toward the tail/bottom
• The brainstem gets pulled downward
• This stretches and tears tiny arteries called "paramedian basilar artery branches" that penetrate the brainstem
• Duret hemorrhages = bleeding inside the brainstem caused by this stretching. These are longitudinal (vertical) hemorrhages in the pons and midbrain. They are usually FATAL because the brainstem controls breathing, heart rate, and consciousness.

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3. UNCAL TRANSTENTORIAL HERNIATION

• Ipsilateral blown pupil (ipsilateral CN III compression) - The third cranial nerve (CN III = oculomotor nerve) runs right next to where the uncus herniates. When the uncus herniates, it SQUEEZES CN III.
  • CN III normally keeps the pupil constricted (small). When compressed, the pupil DILATES widely and becomes non-reactive to light.
  • "Ipsilateral" = SAME side as the herniation. So if the RIGHT temporal lobe herniates, the RIGHT pupil blows.
  • This is the famous "blown pupil" - a fixed, dilated pupil. It's an EMERGENCY sign!
• Contralateral hemiparesis - The corticospinal tract (motor pathway from brain to body) is compressed on the OPPOSITE side, causing weakness of the opposite half of the body.

• Coma - Full loss of consciousness as the brainstem gets compressed.
• Kernohan phenomenon - This is a misleading/false localizing sign. The herniation is so severe that the opposite cerebral peduncle (motor pathway on the OPPOSITE side) gets pushed against the tentorium, causing:
  • Ipsilateral hemiparesis - Weakness on the SAME side as the herniation (misleading!)
  • Contralateral blown pupil (also misleading)
  • This is called a "false localizing sign" because the hemiparesis appears on the "wrong" side - it would make you think the lesion is on the side opposite to where it actually is.

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4. CEREBELLAR TONSILLAR HERNIATION INTO THE FORAMEN MAGNUM

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UMN vs LMN SIGNS (MOTOR NEURON TABLE)

Two Motor Systems

1. Brain (motor cortex) → sends signal down a long wire → spinal cord
2. Spinal cord → sends signal through another wire → muscle

• Lower motor neuron = everything LOWERED (↓ muscle mass, ↓ tone, ↓ reflexes, ↓ toes [toes point down = no Babinski])
• Upper motor neuron = everything UP (↑ tone, ↑ reflexes, ↑ toes [toes point up = Babinski positive])

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PAGE 544 - SPINAL CORD LESIONS

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1. POLIOMYELITIS

• Fecal-oral = you swallow virus from contaminated water/food
• The virus first replicates (makes copies of itself) in the throat and intestine lymphoid tissue
• Then enters the blood and from there travels to the nervous system (CNS)

• Asymmetric weakness - This is KEY. Unlike many other conditions that cause symmetric (both sides equal) weakness, polio causes random, asymmetric weakness. One leg may be paralyzed while the other is fine.
• Respiratory muscle involvement → respiratory failure - If the polio destroys the motor neurons that control breathing (diaphragm, intercostal muscles), the patient cannot breathe. Historically, these patients needed iron lungs!

• ↑ WBCs (lymphocytic pleocytosis) - Pleocytosis = increased white cells. Lymphocytic = they are lymphocytes (a type of immune cell). This is typical of viral infections in the CNS. In bacterial meningitis, you'd see neutrophils instead.
• Slight ↑ protein - Inflammation slightly raises the protein level in CSF.
• No change in CSF glucose - In viral infections, glucose stays normal. In bacterial meningitis, glucose drops (bacteria eat the sugar).

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SPINAL MUSCULAR ATROPHY (SMA)

• Congenital = present from birth (genetic disease)
• Autosomal recessive = you need TWO defective copies of the gene (one from each parent). If only one copy is defective, you're a carrier.
• SMN1 mutation = SMN1 is the "Survival Motor Neuron 1" gene. It makes a protein essential for motor neuron survival.
• snRNP assembly = snRNPs (small nuclear ribonucleoproteins) are tiny molecular machines that help process RNA messages in cells. Without the SMN protein, snRNP assembly is defective, meaning RNA processing fails in motor neurons specifically.
• LMN apoptosis = Apoptosis = programmed cell death. The lower motor neurons die off.

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AMYOTROPHIC LATERAL SCLEROSIS (ALS)

• Corticospinal tract = UMN tract going from motor cortex down the spinal cord
• Corticobulbar tract = UMN tract going from motor cortex to the brainstem (bulb = old term for medulla/brainstem)

• SOD1 = Superoxide dismutase 1 gene
• Superoxide dismutase is an enzyme that neutralizes free radicals (toxic oxygen molecules that damage cells)
• When SOD1 is mutated, free radicals accumulate and kill motor neurons
• "Usually idiopathic" = in most patients we don't know the cause
• "Familial form (less common)" = some families carry inherited mutations

• Flaccid limb weakness - floppy muscles
• Fasciculations - muscle twitching
• Atrophy - muscles waste away
• Bulbar palsy (dysarthria = slurred speech, dysphagia = difficulty swallowing)
• Tongue atrophy

• Spastic limb weakness - stiff muscles (both spastic AND flaccid, because BOTH neuron types die)
• Hyperreflexia - brisk reflexes
• Clonus - rhythmic involuntary jerking (when you rapidly dorsiflex the foot, it keeps bouncing)
• Pseudobulbar palsy - dysarthria, dysphagia, emotional lability (the patient cries or laughs uncontrollably without appropriate triggers - called "emotional incontinence")

• Riluzole = blocks glutamate activity (excitotoxicity = too much glutamate kills motor neurons)
• Edaravone = a free radical scavenger (mops up toxic oxygen molecules)
• Neither cures ALS - they only slow progression.

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TABES DORSALIS

• T pallidum = Treponema pallidum - the bacterium that causes syphilis
• 3° syphilis = tertiary syphilis - the stage that occurs years to decades after the initial infection
• Dorsal columns = the back part of the spinal cord. These carry sensation of proprioception (body position sense), vibration, and fine touch from the body to the brain.
• Demyelination = the myelin sheath (insulating cover around nerve fibers) is destroyed, slowing/blocking nerve signals

• Progressive sensory ataxia = the patient loses proprioception (sense of where their feet are in space). Without knowing where your feet are, you stagger and fall - classic ataxia.
• Impaired proprioception → poor coordination - Like walking blindfolded while not feeling your legs.
• Positive Romberg sign - Test: Have the patient stand with feet together. Normal: They can stand even with eyes closed (because proprioception maintains balance). In tabes dorsalis: They sway and fall when eyes are closed. Eyes OPEN = okay. Eyes CLOSED = falls. This means they're compensating for absent proprioception using vision.
• Absent DTRs (deep tendon reflexes) - Because the sensory arcs (dorsal roots) are destroyed, reflexes are absent.
• Shooting pain - "Lightning-like" shooting pains in the legs - called "lightning pains." Absolutely classic for tabes dorsalis.
• Argyll Robertson pupils - Famous finding. The pupil DOES NOT constrict to light (afferent pupil problem) BUT DOES constrict to accommodation (looking at near objects). Like a prostitute: "accommodates but doesn't react (to light)." This is the reverse of Parinaud syndrome.
• Charcot joints - Painless joint destruction! Because the patient can't feel pain, they keep using their damaged joints without feeling the damage. The joints become grossly deformed and destroyed.

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SUBACUTE COMBINED DEGENERATION (SCD)

• Dorsal columns (fine touch, vibration, proprioception) → positive Romberg sign, paresthesias (tingling sensations), impaired position and vibration sense
• Lateral corticospinal tract (UMN motor pathway) → UMN signs (hyperreflexia, Babinski)
• Spinocerebellar tract → ataxic (uncoordinated) gait

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ANTERIOR SPINAL ARTERY OCCLUSION

• Anterior 2/3 of the spinal cord
• It does NOT supply the dorsal columns (back part) - those are supplied by the posterior spinal arteries

• The front part of the cord dies
• The back part (dorsal columns) is SPARED

• Watershed = area at greatest risk of ischemia (blood supply shortage) because it's the farthest from the source
• Adamkiewicz artery = the major reinforcing artery to the ASA in the lower spine. This is why aortic aneurysm repair can cause ASA occlusion - the Adamkiewicz artery may be inadvertently ligated.

• UMN signs below the lesion (corticospinal tract is anterior → affected) → spasticity, hyperreflexia
• LMN signs at the level of the lesion (anterior horn cells = LMN, sitting in the anterior cord) → flaccid weakness at that specific level
• Loss of pain and temperature sensation below the lesion (spinothalamic tract is anterior/lateral → affected)
• Dorsal columns are SPARED = proprioception, vibration, and fine touch remain intact! This dissociation between absent pain/temperature but preserved proprioception is the hallmark.

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PAGE 545 - BROWN-SEQUARD + FRIEDREICH'S ATAXIA + CEREBRAL PALSY

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BROWN-SEQUARD SYNDROME (Hemisection of Spinal Cord)

• SAME side as lesion = weakness + loss of fine touch/proprioception
• OPPOSITE side = loss of pain and temperature

• The sympathetic nerve pathway to the eye travels down through the cervical and upper thoracic spinal cord
• If the hemisection is above T1, this pathway is interrupted on the same side
• Horner syndrome = ipsilateral ptosis (droopy eyelid) + miosis (small pupil) + anhidrosis (no sweating on that side of face)

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FRIEDREICH'S ATAXIA

• Autosomal recessive = need 2 bad copies of the gene
• Trinucleotide repeat = a specific type of genetic mutation where a 3-letter DNA code (GAA) is repeated too many times. Normally, GAA repeats a few times. In Friedreich's, it repeats hundreds of times, expanding the gene and silencing it.
• Chromosome 9 = the gene is on chromosome 9
• Frataxin = the protein produced. It's an iron-binding protein that lives inside mitochondria (the energy factories of cells) and helps regulate iron. Without frataxin, iron builds up in mitochondria → oxidative damage → cell death.

• Lateral corticospinal tract → spastic paralysis
• Spinocerebellar tract → ataxia (unsteady walking)
• Dorsal columns → decreased vibratory sense, proprioception
• Dorsal root ganglia → loss of DTRs (absent reflexes)

• Staggering gait - ataxic, wide-based, uncoordinated walk
• Frequent falling
• Nystagmus - involuntary eye movements
• Dysarthria - slurred speech
• Pes cavus - high arched feet (characteristic foot deformity)
• Hammer toes - toes curled downward permanently
• Diabetes mellitus - frataxin also needed in pancreatic beta cells
• Hypertrophic cardiomyopathy (cause of death) - the heart muscle becomes abnormally thickened and stiff. Most Friedreich patients die from this cardiac complication.
• Presents in childhood with kyphoscoliosis - kyphoscoliosis = curved/bent spine (kypho = hunchback-type curve, scoliosis = sideways curve)

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CEREBRAL PALSY

• Prematurity (being born before 37 weeks) means the brain is not fully developed and fragile
• Low birth weight further increases vulnerability

• Periventricular = around the ventricles (fluid spaces in the brain)
• Leukomalacia = softening/death of white matter (white matter = myelinated nerve fiber tracts)
• In premature babies, the white matter around the ventricles is particularly vulnerable to ischemia (poor blood supply)

• Spasticity - stiff, tight muscles (UMN damage)
• Hyperreflexia - exaggerated reflexes
• Affects ≥1 limbs
• Persistence of primitive reflexes - Newborns have reflexes like the Moro reflex (startle) and grasp reflex that normally disappear at a few months. In CP, these persist abnormally.
• Abnormal posture
• Developmental delay in motor skills
• Neurobehavioral abnormalities (excessive docility or irritability)

• Muscle relaxants (eg, baclofen) - baclofen acts on GABA receptors in the spinal cord to reduce spasticity
• Botulinum toxin injections - Botox injected into spastic muscles temporarily paralyzes them, reducing spasticity
• Selective dorsal rhizotomy - surgical cutting of overactive sensory nerve roots to reduce spasticity

• Prenatal magnesium sulfate for high-risk pregnancies (premature labor) - this neuroprotective agent reduces the incidence and severity of CP

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PAGE 546 - CRANIAL NERVE LESIONS & FACIAL NERVE

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COMMON CRANIAL NERVE LESIONS

CN V Motor Lesion (Trigeminal Nerve - Motor Branch)

CN X Lesion (Vagus Nerve)

CN XI Lesion (Accessory Nerve)

• Sternocleidomastoid (SCM) muscle = turns the head to the opposite side. If RIGHT CN XI is damaged, the patient can't turn head to the LEFT.
• Trapezius muscle = shrugs the shoulder. Damage = the shoulder on the same side droops.

CN XII Lesion (Hypoglossal Nerve)

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FACIAL NERVE LESIONS - Bell's Palsy

• CN VII = the facial nerve. Controls all muscles of facial expression.
• Bell's palsy = sudden, unilateral (one-sided) facial paralysis
• HSV reactivation = HSV (Herpes Simplex Virus) lies dormant in the geniculate ganglion of CN VII. When reactivated (stress, illness), it inflames the nerve → Bell's palsy.
• Treatment: Glucocorticoids (prednisone) to reduce inflammation, +/- acyclovir (antiviral against HSV)
• Most patients recover function (the nerve grows back)
• Aberrant regeneration can occur = nerve fibers grow back to the wrong muscles, causing synkinesis (involuntary movements - e.g., eye closes when patient smiles)

• Lyme disease (tick bite → Borrelia burgdorferi bacteria)
• Ramsay Hunt syndrome = herpes zoster (shingles) affecting CN VII's geniculate ganglion → triad of: ipsilateral facial paralysis + otalgia (ear pain) + vesicles near the auditory canal
• Sarcoidosis (inflammatory disease)
• Tumors (e.g., parotid gland tumor - parotid gland surrounds CN VII)
• Diabetes mellitus

UMN vs LMN Facial Palsy - the KEY Distinction

• Patient has a stroke in right motor cortex → LEFT lower face weakness, but forehead is FINE on both sides → UMN lesion (central = stroke)
• Patient has Bell's palsy → RIGHT entire face including forehead is paralyzed → LMN lesion (peripheral)

• Incomplete eye closure - the eye on the affected side can't close fully
• Dry eyes (CN VII carries parasympathetic fibers to lacrimal gland for tears)
• Corneal ulceration - because the eye can't close, the cornea dries out and can ulcerate
• Hyperacusis - abnormal sensitivity to loud sounds. CN VII innervates the stapedius muscle in the middle ear (dampens loud sounds). When paralyzed, even normal sounds feel painfully loud.
• Loss of taste sensation to anterior tongue - CN VII carries taste from the front 2/3 of tongue via the chorda tympani nerve branch.

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PAGE 547 - EAR ANATOMY & OTOLOGY

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AUDITORY ANATOMY

External (Outer) Ear

• Pinna = the visible ear structure you see on the side of the head
• Auditory canal = the tube going from the pinna to the eardrum
• Tympanic membrane = the eardrum. Sound waves hit it and make it vibrate.
• Nerve supply from multiple nerves visible in the diagram: Lesser occipital nerve (C2), Mandibular nerve (V3/auriculotemporal branch), Facial nerve (VII) sensory branch, Vagus nerve (X auricular branch), Greater auricular nerve (C2, C3)

Middle Ear

• Malleus (hammer) = attached to the eardrum; vibrates first
• Incus (anvil) = the middle bone
• Stapes (stirrup) = the last bone, rests in the oval window of the inner ear
• This mechanical chain amplifies sound (like a lever system) before passing it into the fluid-filled inner ear
• The Eustachian (pharyngotympanic) tube connects the middle ear to the back of the throat - equalizes pressure (hence your ears "pop" when you swallow on a plane)

Inner Ear

• Cochlea = the snail-shaped hearing organ, filled with fluid (endolymph)
• Basilar membrane runs through the cochlea. Different frequencies of sound cause different parts of this membrane to vibrate.
• Tonotopy = each location on the basilar membrane responds to a specific frequency (like different piano keys responding to different notes)
  • Low frequency at apex (top of cochlea's spiral) - the membrane here is wide and flexible = responds to low-pitched sounds
  • High frequency at base (bottom/entrance) - the membrane here is thin and rigid = responds to high-pitched sounds
• Specialized hair cells sit on the basilar membrane. When the membrane vibrates, hair cells bend → generate electrical signals → auditory nerve (CN VIII) → brainstem → brain

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OTITIS EXTERNA

• Pseudomonas aeruginosa = gram-negative bacteria that thrives in moist environments
• Associated with water exposure (swimmer's ear) - water in the ear disrupts the protective acid environment → bacteria overgrow
• Ear canal trauma/occlusion (eg, cotton buds, hearing aids) also predisposes

• Otalgia that worsens with ear manipulation - pain in the ear that gets WORSE when you pull on the ear or press the tragus (the little cartilage flap in front of the ear canal)
• Pruritus = itching
• Hearing loss
• Discharge

• Osteomyelitis = infection/inflammation of bone. Here, the infection spreads from the ear canal into the surrounding skull bones.
• Presents with severe otalgia and otorrhea (discharge)
• May lead to cranial nerve palsies (e.g., CN VII - facial palsy) as infection spreads
• Physical exam shows granulation tissue (healing tissue overgrowth) in the ear canal

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OTITIS MEDIA

• The eustachian tube connects the middle ear to the throat
• In children, this tube is shorter, more horizontal, and floppier → bacteria from throat can travel up more easily
• After a cold/upper respiratory infection, bacteria ascend through a dysfunctional eustachian tube → middle ear infection

• Fever
• Otalgia (ear pain) - hence children pull on their ears
• Hearing loss (conductive - because fluid blocks sound transmission through ossicles)

• Bulging, erythematous (red) tympanic membrane - fluid and pus behind the eardrum pushes it outward
• The eardrum may RUPTURE - releasing pus and suddenly relieving pain

• The mastoid is the bony prominence behind the ear (you can feel it)
• It contains air cells connected to the middle ear
• If otitis media is untreated, infection spreads into mastoid air cells → mastoiditis
• Presents with post-auricular pain (behind the ear), erythema (redness), swelling
• May push the ear forward (due to swelling behind it)
• Serious complication: brain abscess (infection can spread intracranially)

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PAGE 548 - HEARING LOSS & VERTIGO

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CAUSES OF HEARING LOSS

Noise-Induced Hearing Loss

• Stereocilia = the tiny hair-like projections on hair cells in the cochlea. Sound vibrations bend these hairs, generating electrical signals.
• Loud noise physically breaks these delicate hairs
• High-frequency loss first - because high-frequency vibrations are processed at the base of the cochlea (the entrance), this area receives the most mechanical stress from noise
• Sudden extremely loud noises (explosion, gunshot) can cause immediate hearing loss due to tympanic membrane rupture too

Presbycusis

• Presbycusis = "old hearing" (presbys = old, Latin)
• Sensorineural = the nerve/hair cell mechanism is damaged (vs. conductive = mechanical problem)
• Bilateral and symmetric = affects both ears equally
• High frequencies lost first (hair cells at cochlear base die first with age)
• Low-frequency hearing (at apex) is preserved longer = the patient can still hear low voices/rumbles

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DIAGNOSING HEARING LOSS: WEBER AND RINNE TESTS

Weber Test (Tuning Fork on Vertex of Skull)

• Normal: Sound heard equally in both ears = no lateralization
• Conductive hearing loss (one ear): Sound LOCALIZES to the affected ear (louder on bad side). Why? In conductive loss, the mechanical pathway is blocked (e.g., fluid in middle ear). But bone conduction bypasses this. Also, the affected ear is relatively quiet (less ambient noise reaches it), so it "catches" the bone-conducted vibration better.
• Sensorineural hearing loss (one ear): Sound LOCALIZES to the UNAFFECTED ear. The damaged cochlea/nerve can't process the signal as well, so sound seems louder in the good ear.

Rinne Test (Air vs. Bone Conduction)

• AC (Air Conduction): Tuning fork in front of the ear
• BC (Bone Conduction): Tuning fork on the mastoid process behind the ear
• Normal: AC > BC (air conduction is better than bone conduction)
• Conductive loss: BC > AC (bone conduction bypasses the blocked middle ear, so it's relatively better)
• Sensorineural loss: AC > BC (still, because both pathways are reduced but the ratio is preserved - the inner ear/nerve itself is damaged, not the mechanical pathway)

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CHOLESTEATOMA

• Keratinized squamous epithelium = the type of cells that make up skin. These cells do not belong in the middle ear.
• Usually acquired (not congenital - not present at birth)

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VERTIGO

• Vertigo = you feel like the world is spinning, or you are spinning. Like just getting off a merry-go-round.
• Lightheadedness = feeling faint, like you might pass out - very different mechanism (usually cardiovascular)

Peripheral Vertigo

• Inflammation of the vestibular nerve (the balance part of CN VIII)
• Usually viral

• "Semicircular canal debris → episodic vertigo lasting ≤1 minute provoked by certain head movements"
• Inside the semicircular canals (which detect head rotation), tiny calcium carbonate crystals called otoliths (or otoconia, or "canaliths") normally sit on a membrane in the utricle. When they break loose and roll into a semicircular canal, they create false spinning signals.
• Lasts LESS than 1 minute when triggered by position change
• Dix-Hallpike maneuver = the diagnostic test (lay patient back with head tilted to one side - triggers brief vertigo and nystagmus if BPPV)
• Epley maneuver = treatment (series of head movements that roll the crystals back to where they belong)

• "Endolymphatic hydrops (↑ endolymph in inner ear)"
• Hydrops = fluid buildup. Too much endolymph (the fluid inside the inner ear)
• Triad: Vertigo + Sensorineural hearing loss + Tinnitus ("men wear vests" = vertigo, sensorineural hearing loss, tinnitus)
• Tinnitus = ringing in the ears

• Mixed horizontal-torsional nystagmus (never purely torsional or vertical)
• Suppressible with visual fixation (ask patient to stare at a point - nystagmus decreases)

Central Vertigo

• Nystagmus of ANY direction - can be purely vertical, purely horizontal, or direction-changing
• NOT suppressible with visual fixation - staring at a point doesn't stop the nystagmus
• Neurologic findings = diplopia (double vision), ataxia (uncoordinated movements), dysmetria (inability to judge distances precisely in movement)

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PAGE 549-550 - OPHTHALMOLOGY

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EYE ANATOMY

1. Sclera = the white, tough outer protective coat
2. Choroid = middle layer, filled with blood vessels (supplies nutrition to retina)
3. Retina = the inner layer containing photoreceptors (rods and cones) - the "film" of the camera

• Fovea = the central point of the retina with the highest density of cones. This is where you have maximum sharp color vision.
• Macula = the area surrounding the fovea. Contains high-density cones.
• Optic disc = where the optic nerve exits the eye (and where retinal vessels enter). Has no photoreceptors = the "blind spot."
• Vitreous chamber = filled with vitreous humor (gel-like fluid). Maintains shape of eyeball.
• Lens = transparent focusing structure, suspended by zonule fibers from the ciliary body. Can change shape (accommodation) to focus on near vs. far objects.
• Iris = colored ring with muscles controlling pupil size: dilator muscle (mydriasis, sympathetic) and sphincter muscle (miosis, parasympathetic)
• Ciliary body = muscular ring behind the iris that produces aqueous humor and controls lens shape

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CONJUNCTIVITIS

Allergic

• Itchy, bilateral - both eyes itch. Itching is the hallmark of allergic conjunctivitis.

Bacterial

• Purulent discharge = thick yellow-green pus discharge
• Treat with antibiotics (e.g., topical fluoroquinolones)

Viral

• Most common - usually adenovirus
• Sparse mucous discharge (watery/stringy, not thick pus)
• Swollen preauricular node = the lymph node in front of the ear is swollen. This is characteristic of adenoviral conjunctivitis.
• Increased lacrimation = watery, teary eyes
• Self-resolving - no specific treatment needed

Neonatal Conjunctivitis (Ophthalmia Neonatorum)

• Eyelid swelling, exudative discharge after vaginal birth - the baby's eyes get infected as it passes through the birth canal
• Must detect bacterial causes with NAAT (nucleic acid amplification test) to prevent blindness
• Maternal prenatal screening and treatment reduces incidence

1. Chlamydia trachomatis serotypes D-K (most common neonatal)
   • Onset 5-14 days after birth (later onset because it's intracellular)
   • Treat with erythromycin or azithromycin
2. Neisseria gonorrhoeae
   • Onset 2-5 days after birth (earlier)
   • Prophylaxis: erythromycin eye drops at birth
   • Treat with ceftriaxone
   • If untreated → rapid corneal destruction → BLINDNESS

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REFRACTIVE ERRORS

Myopia (Nearsightedness)

• The eyeball is elongated (too long)
• Light from distant objects converges BEFORE reaching the retina → blurry distance vision
• Near objects are fine (the eye can accommodate)
• Correct with CONCAVE (diverging) lens - a concave lens spreads light rays apart so they focus farther back, landing on the retina

Hyperopia (Farsightedness)

• The eyeball is too short
• Light from near objects focuses BEHIND the retina
• Distance vision may be OK, near is blurry
• Correct with CONVEX (converging) lens - brings the focus point forward onto the retina

Astigmatism

• Normally the cornea is a perfect sphere (like a basketball)
• In astigmatism, the cornea is shaped more like a football - curved more in one direction
• Different meridians of the cornea have different curvatures → light focuses at different points for different axes → distorted, blurry vision at all distances
• Correct with CYLINDRICAL lens - a lens with different curvature in different planes, compensating for the irregular cornea

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LENS DISORDERS

Presbyopia

• Accommodation = the ability to change the lens shape to focus on near objects (ciliary muscles contract → zonule fibers relax → lens becomes more convex/rounded)
• With age, the lens hardens and loses elasticity → can't round up for near focus
• Patients need reading glasses or magnifiers
• Can result in glare, loss of red reflex, and increased nearsightedness at night

Cataract

• Opacification = the transparent lens becomes cloudy/opaque (like a frosted window)
• Normally the lens is crystal-clear. In cataract, proteins denature and aggregate → cloudiness
• Causes blurry, foggy vision, glare, halos around lights
• Acquired risk factors: increasing age (most common), tobacco smoking, alcohol overuse, excessive sunlight (UV radiation), prolonged glucocorticoid use, diabetes mellitus, trauma, infection
• Congenital risk factors: galactosemia and galactokinase deficiency (accumulation of galactitol in lens), trisomies (13, 18, 21), Marfan syndrome, Alport syndrome, myotonic dystrophy, NF2
• TORCH infections (Toxoplasma, Rubella, CMV, Herpes/HIV) in utero
• Treatment: surgical replacement with an artificial lens (IOL = intraocular lens)

Lens Dislocation (Ectopia Lentis)

• Marfan syndrome: mutations in fibrillin (a component of zonule fibers) → weak zonules → lens dislocates UPWARD and OUTWARD
• Homocystinuria: lens dislocates DOWNWARD and INWARD
• High-yield exam distinction!

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AQUEOUS HUMOR PATHWAY

• Aqueous humor = a clear fluid (different from vitreous humor) that fills the anterior and posterior chambers of the eye (in front of the lens)
• It is continuously produced and continuously drained - this balance determines intraocular pressure (IOP)
• If drainage is blocked → IOP rises → glaucoma (damage to optic nerve from pressure)

• β-blockers (eg, timolol) - block sympathetic stimulation of ciliary epithelium
• α2-agonists (eg, brimonidine) - also decrease aqueous production
• Carbonic anhydrase inhibitors (eg, acetazolamide) - carbonic anhydrase is needed for fluid production; blocking it reduces aqueous formation

• Trabecular meshwork → canal of Schlemm → episcleral vasculature
• Think of it as a drain screen (trabecular meshwork) → pipe (canal of Schlemm) → blood vessels
• Enhanced (increased drainage) by: Muscarinic agonists (M3) like carbachol and pilocarpine (these contract the ciliary muscle, which opens the trabecular meshwork → better drainage → lower IOP)

• Fluid drains through the uvea (iris + ciliary body) and sclera directly
• Enhanced by: Prostaglandin agonists (eg, latanoprost, bimatoprost) - these increase uveoscleral drainage
• This is actually the MOST commonly prescribed class for glaucoma (first-line eye drops)

1. REDUCING aqueous production (β-blockers, α2-agonists, carbonic anhydrase inhibitors)
2. INCREASING aqueous drainage (prostaglandin agonists increase uveoscleral flow; muscarinic agonists increase trabecular flow)

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SUMMARY TABLE - Key Memory Points