Neurology Flashcards
non-dominant parietal lobe lesions (right brain for most)
hemispatial neglect (usually left)
dominant parietal lobe (left brain for most)
agraphia, acalculia
frontal lobe
personality changes
subthalamic nucleus
c/l hemiballismus
Broca aphasia
nonfluent aphasia
affects written language as well as speech, can’t produce words despite good comprehension
Wernicke aphasia
poor comprehention, word substitutions, meaningless words
Conduction aphasia
poor repetition of what’s heard
global aphasia
nonfluent speech, poor comprehension, poor repetition
Brown Sequard hemisection of spinal cord
All tracts on one side of the cord are affected
Dorsal column- ipsilateral loss of vibration and discrimination below the lesion
Corticospinal tract- ipsilateral spastic paresis (UMN) below the lesion
Anterior motor horn- ipsilateral flaccid paralysis (LMN) at level of lesion
Spinothalamic tract- contralateral loss of pain and temperature below the lesion
most common sites (n=2) for berry saccular aneurysms
Anterior communicating artery and posterior communicating artery
fasciculations and spastic paralysis
ALS (UMN and LMN)
impaired proprioception+ pupils do not react to light
tertiary syphilis (tabes doralis and argyle robertson)
bilateral loss of pain and temp below the lesion + hand weakness
syringomyelia
bilateral loss of vibration sense + spastic paralysis of legs then arms
B12 deficiency
bilateral loss of pain/temp below lesion + bilateral spastic paralysis below lesion+ bilateral flaccid paralysis at the level of the lesion
anterior spinal artery syndrome
everything but the dorsal column
contralateral hemiballismus
subthalamic nucleus lesion
hemispatial neglect syndrome
nondominant parietal lobe
poor comprehension
Wernicke’s area (MCA), this is receptive aphasia
poor vocal expression
Broca’s area (MCA). this is expressive aphasia
personality changes
frontal lobe lesions
agraphia and acalculia
dominant parietal lobe (usually left)
Where do the dorsal columns cross over?
medulla after ascending as medial lemniscus
where does the lateral corticospnial tract cross over
medullary pyramids
where does the spinothalamic tract cross over?
anterior white commisure
What are the four main longterm complications of bacterial meningitis in pediatric patients?
hearing loss
seizure disorder
intellectual disability
spastic paralysis
gram positive dipococci leading to meningitis
s. pneumoniae
gram negative diplococci leading to meningitis
=/- purpura
n. meningitidis
small pleomorphic gram negative coccobacilli leading to meningitis
h. influenzae type B
now rarer due to vaccine
gram positive rods and coccobacilli leading to meningitis
listeria
What medication should be given to close contacts of patients who have neisseria or h. influenzae meningitis?
rifampin or ciprofloxacin
Signs of increased ICP indicating CT before LP
focal neurologic deficits pupil asymmetry papilledema seizure suspicion of mass effect
AIDS patient with fungal meningitis
cryptococcal meningitis
treat with intrathecal amphoteriicin B
Reye syndrome organs affected labs symptoms/signs treatment
affects brain and liver
results in significant hypoglycemia
A reaction in children with viral infection who are given ASA
rash vomiting increased LFT headache lethargy
tx: supportive care
encephalitis
meningitis plus AMS
HSV
temporal lobe encephalitis
WNV
birds are reservoir, mosquitos are vector
Reye sydrome
virus + ASA
(brain and liver HEPATOENCEPHALITIS)
potential hypoglycemia
Brain abscess
MRI shows ring- enhancing lesion
poliomyelitis
detroys motor neurons
rabies
negri bodies
Toxoplasma gondii
contracted by eating meat or infected soil, litter boxes
affecting heart/liver/eye
Diagnosis: CD4
contra-indications for triptans
prinzmetal angina, CHF, pregnancy
Treat tension HA
NSAIDs
ergots
sumitriptan
relaxation
Treat cluster HA
100% O2 (6L/min on rebreather mask for 20+ min) and sumatriptan or dihydroergotamine (DHE 45)
migrrane HA
sumatriptan (or other triptan), dihydroergotamine (DHE 45), NSAIDs, and/or antiemetics (chlorpromazine, perchlorperazine, metaclopramide) in varying combinations based on severity, nature of symptoms and patient history
What agents can be used for migraine prophylaxis
CCB (verapamil)
Beta-blockers: propanolol, metoprolol
TCAs:amitriptyline, nortriptyline (good choice if comorbid depression, insomnia, pain syndrome)
NSAIDs: naproxen (good choice if menstrual migraine, comorbid osteoarthritis or other pain that could benefit from NSAIDs)
Anticonvulsants:valproic acid (good if history of bipolar disorder), topiramate, gabapentin
characteristic features of idiopathic intracranial hypertension
young obese woman
- HA- daily, pulsatile, possible n/v, possible retroocular pain -worse with eye movement
- papilledema
- most worrisome sequela is vision loss due to CNII compression
- CT scan is normal
- CSF pressure is elevated >200 mmH2o in non-obese patient, >250 mm H2O in obese patient
Treat IIH
confirm absence of other pathology with CT and MRI of head to r/o central venous thrombosis
discontinue any inciting agents (eg excess vitamin A, accutane, tetracyclines)
weightloss if obese
acetazolamide is first line
invasive treatment options:
- serial lumbar punctures
- optic nerve sheath decompression
- lumboperitoneal shunting (CSF shunt)
HA made worse by foods containing tyramine
migraine
HA in obese woman with papilledema
IIH
HA with jaw muscle pain when chewing
temporal arteritis aka giant cell arteritis
HA with periorbital pain, ptosis, miosis
cluster
HA with photophobia and/or phonophobia
migraine
HA with B/L frontal/occipital pressure
tension HA
HA with lacrimation and/or rhinorrhea
cluster
elevated ESR
giant cell arteritis
“worse HA of my life”
SAH
headache and extraocular muscle palsies
cavernous sinus thrombosis
scintillating scotomas prior to HA
migraine with aura
HA before or after orgasm
postcoital cephalalgia
HA Responsive to 100% O2 supplementation
cluster HA
frontal HA made worse by bending over
sinus HA
trauma to head- headache begins days after the event, persists for over a week and does not go away
subdural hematoma
treat neonatal meningitis empirically with which antibiotics?
ampicillin and gentamicin
part of the brain implicated in coma
reticular activating system
TIA definition
transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction
Pure motor hemiparesis lacunar syndrome
-weakness of face, arm, leg on one side of body
-absent sensory or cortical signs (aphasia, neglect, apraxia, hemianopsia)
MC (50% of lacunar strokes)
pure sensory lacunar stroke syndrome
- sensory defect (numbness) of the face, arm, leg on one side of the body
- absent motor or cortical signs
Ataxic hemiparesis lacunar syndrome
- ipsilateral weakness and limb ataxia out of proportion to the motor defect, possible gait deviation to the affected side
- absent cortical signs
Sensorimotor stroke lacunar syndrome
- weakness and numbness of the face, arm, leg on one side of the body
- absent cortical signs
dysarthria clumsy hand syndrome lacunar stroke syndrome
facial weakness, dysarthria, —
- dysphagia, and slight weakness and clumsiness of one hand
- absent sensory or cortical signs
- least common
bacterial meningitis plus purpura (what organism?)
neisseria meningitidis
reye syndrome
virus+aspirin (brain + liver)
brain abscess
MRI with ring-enhancing lesion
poliomyelitis
destroys motor neurons
rabies
negri bodies
HSV
temporal lobe encephalitis
normal CSF pressure
50-180
normal CSF WBC
normal CSF glucose
40-70
normal CSF protein
20-45
treatment for trigeminal neuralgia
carbamazepine phenytoin gabapentin valproic acid surgical decompression
treatment for someone with htn and recurrent migraine
propanolol or CCB (like nifedipine)
sudden onset of severe HA, vomiting, meningismus
subarachnoid hemorrhage
patient taking warfarin falls and bumps his head
subdural hematoma
brief loss of consciousness following head trauma; rapid clinical deterioration hours later
epidural hematoma
elderly patient with mild headache for 2 weeks, now becoming lethargic
SDH
patient with unilateral hemiparesis and BP 220/130 mm Hg
stroke- parenchymal hemorrhage
ruptured intracranial aneurysm
SAH
ruptured AVM
parenchymal hemorrhage or SAH
biconvex- shaped hematoma
epidural hematoma
crescent-shaped hematoma
subdural hematoma
Imaging appropriate for suspected intracranial hemorrhage
CT of head without contrast
faster and cheaper than MRI
First line med for absence seizures
ethosuximide
what drugs are used to treat status epilepticus
ABC
IV/IM benzodiazepine (diazepam, lorazepam)
If that doesn’t work, use phenobarbital (intubate first, as respiratory depression may occur)
phenytoin or fosphenytoin to help prevent immediate recurrence
treat eclampsia with…
magnesium sulfate
+/- benzodiazepine (eg diazepam, lorazepam)
c-section after the seizure
Adverse effects of phenytoin:
Phenytoin Has Given MDs Frustation
Peripheral neuropathy Hirsutism Gingival hyperplasia Megaloblastic anemia due to decreased folate absorption Drug- induced lupus SJS Fetal hydantoin syndome
anti-epileptics that are teratogens
phenytoin
carbamazepine
valproic acid (spina bifida- ppx with 4mg folic acid)
what drugs cause SJS
seizure drugs: ethosuximide, lamotrigine, carbamazepine, phenytoin, phenobarbital
antibiotics: sulfonamides, PCNs
Allopurinol
Agranulocytosis
carbamazepine
clozapine
colchicine
PTU, methimazole
Hepatotoxic anti-epileptics
valproid acid
carbamazepine
Which drugs induce CYP450
Coronas, Guiness, and PBRs incude chronic alcoholism
Carbamazepine Griseofulvin Phenytoin Barbiturates Rifampin St. Johns wort Chronic alcoholism
Focal sensory or motor deficit with NO loss of consciosness
simple partial seizure
Focal sensory or motor deficit with impaired consciousness (commonly localized to temporal lobe on EEG)
complex partial seizure (temporal lobe a common site)
Involves both hemispheres of brain with a pattern of neuromuscular activation: tonic, clonic, tonic- clonic, myoclonic, atonic. Loss of consciousness present with postictal period
generalized convulsive seizure
characterized by a brief (few seconds) impairment of consciousness. spike and wave on eeg, no post-ictal stage
absence seizure
characteristic features of amyotrophic lateral sclerosis
weakness but with normal sensation
initial presenting symptoms are
-asymmetric limb weakness (80%), in hands, fingers, shoulder girdle, lower extremity (foot drop), or pelvic girdle
dysarthria or dysphagie (bulbar dysfunction) (20%)
UMN si/sx: movement stiffness, slowness and incoordination; spasticity and hyperreflexia (spastic paralysis); slowed rapid alternating movements; gait disorder
Bulbar UMN si/sx: dysarthria, dysphagia, pseudobulbar affect (inappropriate laughing, crying, yawning)
Lower MN si/sx: weakness, gait disorder, reduced reflexes (flaccid paralysis), muscle atrophy, fasciculations
cognitive deficits: frontotemporal executive dysfunction
neuromuscular respiratory failure after months to years (average survival from time of diagnosis is 3-5 years)
How do you diagnose ALS?
Electromyogram shows widespread denervation and motor block
What is the one FDA- approved drug for ALS?
Riluzole, which decreases glutamate- induced excitotoxicity in the CNS (excess can be toxic to the brain)
Multiple sclerosis
progressive demyelination of brain and spinal cord
women ages 20-40
sx: vision abnormalities
paresthesias
sensory deficits
weakness in the face, limbs, eyes, diplioia, ptosis, urinary urgency, incontinence, retention
over time, progresses
worse with stress and overheating
Eye findings:
Unilateral optic neuritis (inflammation of the optic nerve), causing acute onset eye pain worse with movement and central vision loss. Afferent pupillary defect (Marcus Gunn pupil)
Internuclear ophthalmoplegia (damage to medial longitudinal fasciculus)- ipsilateral eye cannot adduct on lateral gaze (away from the MLF lesion- the injured side cannot adduct on lateral gaze) The eye contralateral to the lesion experiences nystagmus normal convergence (medial rectus muscle functional)
CSF:
increased protein
increased WBC count
oligoclonal bands
MRI of brain and orbits
MRI of spinal cord
look for asymmetric demyelinating lesions
Still, MS is a clinical diagnosis
Neuromyelitis optica (NMO)
bilateral optic neuropathy
lesions in cervical spinal cord
usually spares the brain
positive NMO-IgG
How do we treat MS?
acute- corticosteroids in high doses for a few days
Maintenance- avoid stress
treat with interferon- beta
glatiramer
natalizumab is 3rd line
Alzheimer Disease characteristics
progressive memory loss loss of executive function disinhibition personality changes delusions
a diagnosis of exclusion
Alzheimer- cholinesterase inhibitors
donepezil
galantamine
rivastigmine
may slow progression of disease
memantine (NMDA inhibitor)
Dementia with Lewy bodies
similar to parkinsonism
Dementia
Parkinsonian features (bradykinesia, tremor, cogwheel rigidity, festinating gait)
visual hallucinations
episodes of syncope (repeated falls)
Frontotemporal dementia (aka Pick disease)
dementia plus inappropriate social behavior
dementia plus progressive aphasia (difficulty understanding what is said, difficulty speaking)
Normal pressure hydrocephalus
arachnoid granulations fibrose and can’t absorb CSF
Wacky (cognitive impairment or dementia)
Wet (urinary incontinence)
Wobbly (gait disturbance- magnetic gait, short steps, low to the ground)
Dx: MRI, dilation of ventricles
Tx: ventricular shunting so that extra CSF goes to the peritoneum
Myasthenia gravis
antibodies bind acetylcholine receptors at neuromuscular junction
may be associated with
thymoma
thymus neoplasm
thyrotoxicosis
more common in young adult women
weakness that worsens throughout the day, ptosis, diplopia, dysarthria, dyspnea, dysphagia
symptoms improve with Tensilon test (edrophonium, which stimulates the AChR, and is very short-acting)
nerve stim, EMG
Treatment for MG
anticholinesterase- neostigmine, pyridostigmine
thymectomy
immunosuppression: prednisone, azathioprine
plasmapheresis
IVIG
Lambert- Eaton syndrome
antibodies against presynaptic voltage- gated calcium channels
associated with small cell lung cancer
paraneoplastic syndrome
Treat LES
treat underlying cancer
cholinesterase inhibitors- pyridostigmine
immunosuppressants
plasmapheresis
Guillain- Barre syndrome (acute inflammatory demyelinating polyradiculopathy), classic presentation
symmetric muscle weakness that progresses over days to 4 weeks (2 avg)
usually beginning in distal legs, but may begin in arms or facial muscles in 10% of cases
- respiratory paralysis requiring mechanical ventilation in 30% of cases.
- facial muscle weakness and/or oropharyngeal weakness in 50% which may include bilateral facial muscle paralysis
- autonomic dysfunction in 70% of patients (tachycardia)
- absent or depressed deep tendon reflexes
- little if any change in sensation
- no fever at the onset of symptoms
- GBS may be preceded by campylobacter jejuni diarrheal illness (about 20% of cases), HIV, CMV, EBV, mycoplasma, other viral infection, immunization (rare)
How is diagnosis of GBS made in a patient with ascending muscle paralysis and preserved sensation?
characteristic clinical presentation
CSF shows albuminocytologic dissociation (elevated protein and normal WBCs)
Electrodiagnostic studies such as nerve conduction studies and EMG, which show evidence of demyelination
Prognosis of GBS
death despite ICU care in 5%
prolonged disease with delayed or incomplete recovery in 5-10%
relapse in 10%
spontaneous regression and complete recovery by 1 year in 80-90%
Treatment of GBS
hospitalization for respiratory monitoring including vital capacity, BP monitoring, cardiac monitoring (telemetry), and daily abdominal auscultation for ileus
30% of patients require mechanical ventilation
20% of patients require ICU monitoring for autonomic dysfunction
Plasmapheresis or IVIG are equally effective at shortening time to independent walking by 50%, while combining the 2 offers no additional benefit
Steroids are NOT recommended in treating GBS.
How do we diagnose Bell’s palsy?
First, make sure it is LMN facial muscle paralysis (the whole face is involved, and this actually looks worse than stroke)
rule out Lyme disease by history: tick bite, heart block, arthritis, vertigo, hearing loss
rule out otitis media by inspecting the TM
rule out stroke by looking for other defects
acute onset (1-2 days), with progressively weakening weakness for 3 weeks, leading to recovery within 6 months
Anything other than this particular presentation warrants CT and/or MRI, and screening blood tests to rule out other pathology (Lyme, zoster, AIDS, sarcoid, tumors, diabetes).
Treat Bell’s Palsy
eye care
-artificial tears hourly while awake, lubricating ointment qHS, patch over eye at night
glucocorticoids in medium doses
+/- valacyclovir
benign essential tremor
idiopathic, but can be familial
fixed oscillation of hands or head
treat (alcohol makes it better) beta blockers benzodiazepines primidone thalamotomy deep brain stimulation
Chorea
rapid flinching distal limb and facial movements
associated with hyperthyroidism, huntington, lupus, levodopa use, rheumatic fever
Athetosis
writhing, snakelike movements
associated with cerebral palsy, encephalopathy, huntington disease, wilson disease
Dystonia
sustained contractions of proximal limb or trunk
associated with neuroleptic drug use, wilson disease, parkinson, huntington, encephalitis
treatment: levodopa/carbidopa, botulinum toxin
Hemiballismus
flinging movements of extremities
associated with stroke (subthalamic nucleus lesion)
treatment: haloperidol
Tics
brief, repetative, involuntary movement or sound
associated with tourette, OCD, ADHD
Treatment:DA antagonists
pimozide
tetrabenazine
fluphenazine
Lots of Bad Stuff Kills Glia
common mets to the brain
Lung cancer Breast cancer Skin cancer- melanoma Kidney- RCC GI tract tumors- colon cancer
MGM Studios: most common brain tumors in adults
Metastasis
Glioblastoma
Meningioma
Schwannoma
Animal Kingdom, Magic Kingdom, Epcot
common brain tumors in children
Astrocytoma
Medulloblastoma
Ependymoma
How to treat a brain tumor
resection radiation chemotherapy corticosteroids anticonvulsants
How to treat mets to the brain
full body imaging
surgical resection
palliative radiation
Prognosis:
depends on tumor- glioblastoma is aggressive and offers 6 month survival
Neurofibromatotis type 1
von Recklinghousen disease
Autosomal dominant, NF1 gene on chromosome 17
at least 2 of the following:
>5 cafe au lait spots 1 neurofibromas axillary or inguinal freckling optic glioma >1 iris hamartoma (Lisch nodules) bone lesions first- degree relative with NF1
NF2
AD, chromosome 22
b/l acoustic schwannomas
Stages of sleep (N1, N2, N3) awake- beta awake, relaxed- alpha N1-theta N2- Sleep spindles, K complexes N3- delta waves REM- beta waves
N1: fast delta, light sleep
N2: intermediate, sleep spindles and K complexes, decreasing frequency, increasing amplitude
45% of sleep is N2 sleep
N3, deep sleep, slow delta waves
REM every 1-2 hours, beta waves, low voltage, high frequency
increases N2 sleep, decreases N3 sleep
Benzodiazepines
helps you go to sleep, but you don’t get good rest
can reduce night terrors, and nocturnal enuresis, which occur during N3
nightmares versus night terrors
nightmares occur during REM sleep, the patient who appears to awaken is actually awake
night terrors occur during non-REM (Stage 3) sleep, and may appear to awaken but not really awaken, can be difficult to arouse, and is usually able to fall asleep right after the episode
Narcolepsy- requirements for diagnosis
cataplexy only in narcolepsy and is virtually diagnostic when present
other causes of excessive daytime sleepiness are ruled out, overnight polysomnogram (to rule out OSA and periodic limb movement disorder)
rule out sedating medications as a cause
multiple sleep latency test- when given 4-5 opportunities to nap every 2 hours, narcolepsy patients fall asleep in less than 8 minutes
How do we treat narcolepsy?
avoid drugs that cause sleepiness
schedule naps 1-2 times daily for 10-20 minutes
Modafinil, a stimulant, can be used first-line
support group attendance
if cataplexy, venlafaxine, fluoxetine, or atomoxetine
Insomnia meds
melatonin valerian antihistamines (diphenhydramine, doxylamine) trazodone TCAs (amitriptyline, doxepin) benzodiazepines zolpidem/zaleplon eszopiclone ramelteon
Melatonin for insomnia
non-addictive, OTC, vivid dreams, safe for
Valerian for insomnia
OTC herbal, no evidence
Antihistamines for insomnia (diphenhydramine, doxylamine)
used by patients first-line, associated with poor sleep quality, not for long-term use, anticholinergic side effects (avoid in the elderly)
Trazodone for insomnia
antidepressant, decreases sleep latency, small risk of priapism
TCAs (amitriptyline, doxepin) for insomnia
antidepressant, small risk of arrhythmia (obtain EKG prior to use), anticholinergic side effects (avoid in the elderly)
Benzodiazepines (temazepam, lorazepam, clonazepam, diazepam, chlordiazepoxide) for insomnia
addictive, short-term only (
zolpidem/zaleplon for insomnia
act at the benzo receptor, short- term only (
eszopliclone for insomnia
may be used longterm
ramelteon for insomnia
non-addictive because it works at melatonin receptors instead of GABA/benzo receptors, avoid if hepatic insufficiency, longterm studies are lacking
Resless legs
parasthesias compel patient to have voluntary, spontaneous, continuous leg movements that temporarily relieve the sensations, discomfort is worse at rest/evening/during sleep, spiders or ants on/in feet/calf muscles, usually primary idiopathic disorder
May be secondary to iron deficiency, ESRD, diabetic neuropathy, Parkinson, pregnancy, rheumatic disease, varicose veins, caffeine intake
Treat: pramipexole, ropinirole (or levodopa/carbidopa), iron replacement, avoid caffeine, clonazepam qHS, gabapentin (if the DA agonists aren’t working), opioids
What is the next step after a brain tumor has been identified on CT or MRI?
full body CT and bone scan to look for the primary tumor
Causes of syncope
reflex syncope (BP and HR drop) Vasovagal- associated with emotional stress, trauma, pain, sight of blood, prolonged standing situational- associated with micturition, defecation, coughing, GI stimulation
carotid- sinus hypersensitivity: associated with head turning, shaving, tight collar
cardiogenic- exertion, palpitations, chest pain, SOB
orthostatic
cerebrovascular- associated with prolonged loss of consciousness, seizures, neurologic deficits
no identifiable cause (20% without known cause)
syncope versus seizure
seizure: hx of seizure, prodrome of dejavu, postictal confusion, tongue lacerations
more likely syncope: lightheadedness or sweating, prolonged standing
nonspecific: brief limb jerking, urine incontinence
CBC (anemia), electrolytes, BUN/Cr (arrhythmia), glucose (hypoglycemia)
volume status
pulse-ox and ECG (cardiogenic)
evaluate meds
in patients over 40, rule out carotid sinus hypersensitivity
consider
- serial cardiac enzymes, ECGx3, especially if >45yo, DM, smoker, prior MI or >2-3 risk factors
- echo (murmur, exertional syncope, hx of heart disease)
- cardiac stress test
- bilateral carotid duplex especially if >65yo, CAD, PVD, bruit
- 24hr Holter monitor especially if abnormal SCG, palpitations, heart disease, FHx of sudden death
- CT head w/o contrast and EEG is neuro sx, new seizure, HA
Persistent vegetative state versus coma
PVS:
normal sleep cycles
inability to perceive and interact with environment
preserved autonomic function for >1 month
Coma:
history, pupils, ocular motility, motor function
normal response to cold caloric testing (intact brain stem)
conjugate eye deviation towards ice water, followed by nustagmus in the opposite direction
no eye deviation indicates CN3, or 6 involvement, suggestive of brainstem damage
deviation without nystagmus indicates cerebral hemispheres damaged or suppressed
Doll’s eye oculocephalic reflex test
normal when the eyes are fixed on a particular point
DDx for patient presenting unconscious
AEIOUTIPS
Alcohol Epilepsy/environment Insulin OD/Opioids Uremia Trauma Infection Psychogenic Stroke
3 things you can give empirically to an unconscious patient
thiamine, glucose, naloxine
tilt table test results suggestive of orthostatic hypotension
measurements taken while patient is standing:
increase in HR greater than or equal to 20BPM
decrease in SBP greater than or equal to 20
drop in DBP more than or equal to 10 mmHg
What are the elbows doing in decorticate posturing?
flexing
what pathogens most commonly cause otitis media
s. pneumo
h. influenzae
m. catarrhalis
s. pyogenes
viruses
si/sx of aom
ear pain decreased hearing fever bulging TM with decreased mobility poor light reflex \+/- bloody discharge
when is it reasonable to observe without abx in aom?
age 6 mos-2 yrs + U/L AOM w/o otorrhea + mild illness + appropriate fu available + abx started promptly if symptoms worsen
or
age> or = 2 yrs + UL or BL AOM wo otorrhea + mild illness + appropriate fu available + abx can be started promptly if symptoms worsen
with agreement between caregiver and provider
abx started if improvement not seen between 48-72 hours
consider treating if painful
what medications do you use to treat AOM?
amoxicillin for 10 days
amoxicillin + clavulanic acid
cephalosporin -cefdinir
tympanic tubes if recurrent
complications of AOM
mastoiditis meningitis hearing loss sigmoid sinus thrombosis brain abscess ruptured TM labyrinthitis bullous myringitis (vesicular inflammation of TM, more painful than usual AOM, large, reddish vesicles seen on exam)
What is the treatment fo bullous myringitis?
mycoplasma pneumoniae a common organism, treat with oral macrolide
topical analgesics
diagnostic features of mastoiditis
- symptoms days to weeks after AOM
- erythema, edema, tenderness behind ear
- external ear displaced
- diagnosis made from CT scan of mastoid process
swimmer’s ear- otitis externa
s. aureus
pseudomonas
s. epidermidis
associated with water in the ear
painful swollen ear, white discharge, red and swollen ear canal
pinna tenderness, normal TM
Treat otitis externa
topical- polymixin, neomycin, fluoroquinolone, hydrocortisone
oral- cephalosporins, fluoroquinolone
BPPV
feeling of rotational movement 2/2 otolith
brief episodic vertifo occurs with vertain movements, nystagmus
Dix hallpike exacerbates nystagmus
CT, MRI
TSH
Tx: Epley menauver
acute labyrinthitis
acute onset vertigo, n/v, nystagmus
single episode lasing days to weeks
preceded by viral URI
horizontal nystagmus suppressed with visual fixation, with fast phase away from affected side
abnormal head thrust test- patient unable to maintain visual fixation when examiner rapidly turns patient’s head to affected side
absence of neurologic defects
preserved ambulation
typically subsides spontaneously within weeks
corticosteroid taper improves recovery
symptomatic tx with scopolamine, metoclopramide, etc in the first 48 hours
vestibular rehabilitation exercises can be helpful
MRI if >60, HA, focal neuro signs, vascular risk factors or sustained vertigo inconsistent with acute labyrinthitis (vestibular neuritis)
Meniere disease
aka endolyphatic hydrops
caused by distention of endolymphatic compartment of inner ear
acute vertigo lasting hours n/v decreased hearing ear fullness tinnitus low frequency hearing loss
assoc with depression
Tx: anticholinergics antiemetics antihistamines salt restriction thiazide diuretics surgical decompression (obliteral vestibular apparatus with gentamicin)
acoustic schwannoma
3rd MC brain tumor in adults
compression of CN VIII with b/l tumors
hearing loss dizziness tinnitus ul facial palsy decreased sensation sensorineural hearing loss
dx with MRI
tx surgical excision
hearing loss
conductive (wax, orosclerosis)- air should be better than bone conduction in the Rinne test
sensorineural (presbycusis)
Weber test- equal hearing on both sides versus, sound heard better in the ear where bone conduction is faster = conductive
sound heard better in the ear where conduction was slower= sensorineural hearing loss
Cholesteatoma
overgrowth of desquamated keritin debris within the middle ear space that may eventually erode the ossicular chain and external auditory canal, leading to conductive hearing loss
causes: neg middle ear pressure (chronic retraction pocket) from eustachian tube dysfunction or direct growth of epithelium through a TM perforation
commonly associated wtih chronic middle ear infection
Tx: surgical removal, tympanomastoidectomy, reconstruction of ossicular chain
Ramsay Hunt syndrome
herpes zoster oticus (reactivation of herpes in the ear)
i/l facial paralysis ear pain vesicles in auditory canal/auricle tinnitus vertigo abnormal taste perception
tx: narcotic analgesia for pain relief
oral steroids to decrease inflammation
antiviral therapy with valacyclovir (highest efficacy), famciclovir, acyclovir
meniere triad of symptoms
vertigo, tinnitus, hearing loss
ACUTE LABYRINTHITIS
HEARING LOSS, VERTIGO, NAUSEA, VOMITING
What is Todd’s paralysis?
postictal hemiparesis lasting about 15 hours (but not more than 24 hours)
