Internal Medicine study notes Neuro/brain/psych
Elevated intracranial pressure/ intracranial HTN o ICP>20 mm Hg
o Causes: trauma, space-occupying lesions, hydrocephalus, impaired CNS venous outflow
o Dx: diffuse headaches (worse in morning), N/V early in the day, vision changes, papilledema, CN deficit, somnolence, confusion, unsteadiness, cushings reflex (HTN and bradycardia)
o Dx: CT or MRI Cavernous sinus thrombosis
o Secondary to infection of the medial aspect of the face around the eyes and nose (can also be ethmoid or sphenoid sinus infections) o Sx: headache, low grade fever, periorbital edema, cranial nerve palsies
CN 3,4,5 (V1,V2, V3) all pass through the cavernous sinus and can be affected Headache d/t neuropathic pain d/t irritation of V1 and V2
Dx: MRI or CT w/ contrast of the orbits
Tx: IV broad=spectrum antibiotic; anticoagulation, glucocorticoid, or surgery may be indicated Acoustic neuroma/ vestibular schwannoma
o Typically unilateral
o Sx: sensorineural hearing loss Craniopharyngioma
o Tumor of the sella and suprasellar space
o Sx: headache, focal neurologic changes, visual problems; can cause central diabetes insipidus (decreased ADH) Headaches
o Dx: CT or MRI to exclude an intracranial mass lesion if the dx is unclear or the syndrome has recently started o Tension headache
Most common type Dx of exclusion
Tx: NSAIDs or other analgesics o Migraine headache
Precipitants: emotions, food (chocolate, red wine, cheese), menses
Sx: visual disturbance (flashes, sparks, stars, luminous hallucinations), photophobia, aura, N/V, headaches lasting 4-72 hrs (usually unilateral, pulsating quality)
Other possible sx: aphasia, numbness, dysarthria, weakness
Tx: IV antiemetics (chlorpromazine, Prochlorperazine, or metoclopramide) +/- NSAIDS or triptans for acute migraine headaches; triptans or ergotamine
Triptans must be started early in the course of the migraine before sx become severe in order to be of benefit Prophylactic (preventative) tx: propanolol (#1), calcium channel blockers, tricyclic antidepressants (amitriptyline),
SSRIs, botulinum toxin injections
o for pts with >3 migraine headaches/month o cluster headaches
M>F
Sx: frequent short duration high intensity headaches
Other possible sx: red tearing eye with rhinorrhea, horner syndrome Tx: triptans, ergotamine, 100% oxygen, prednisone, or lithium
o giant cell (temporal) arteritis
sx: visual sx (irreversible blindness), jaw claudication, scalp tenderness, headache; sx in other arteries (decreases arm pulses, bruits near clavicles, aortic regurgitation); systemic sx (muscle pain, fatigue, weakness)
dx: elevated ESR and CRP; biopsy of artery (most accurate) tx: high dose prednisone (started before biopsy)
o pseudotumor cerebri (benign/idiopathic intracranial HTN) communicating hydrocephalus; diagnosis of exclusion
a/w obesity, venous sinus thrombosis, vitamin A toxicity, medications (corticosteroids, OCPs), trauma
sx: headache (pulsatile, wake pt from sleep, a/w pulsatile tinnitus; worse lying flat/ better standing up); mimics a brain tumor d/t elevated ICP (N/V, transient visual obscurations, blurry vision), papilledema w/ diplopia from 6th cranial nerve (abducens) palsy
vision loss, sluggish pupillary reflexes to light, papilledema,
dx: CT or MRI to exclude an intracranial mass lesion (empty sella d/t downward herniation of archnocele d/t high CSF pressure, slit like ventricles), lumbar puncture showing increased pressure (w/o CSF disturbances)
note: papilledema is not a contraindication to an LP unless the pt has evidence of obstructive to noncommunicating hydrocephalus and/or space-occupying lesion +/- mass effect or midline shift
tx: weight loss, acetazolamide (decreased CSF production), steroids, repeated lumbar puncture (rapidly lower ICP); ventriculoperitoneal shunt if medical therapy not sufficient
Transient ischemic attack (TIA)/ stroke o #3 cause of death
o Causes: carotid stenosis, cardioembolism, lipohyalinosis, small-vessel disease, atheroembolism from carotid artery Ischemia (85%), bleeding (15%)
Embolic sources: carotid stenosis, heart (atrial fibrillation, valvular heart disease, DVT through patent foramen ovale) o Risk factors: HTN, diabetes, hyperlipidemia, smoking
Hypertensive stroke is most common in the putamen and adjacent internal capsule hemiparesis, semi-sensory loss, homonymous hemianopsia
o Sx: acute focal neuro deficits, amaurosis fugax
Amaurosis fugax: transient monocular blindness; “gray shade being pulled down over the eye” d/t ischemia to the retinal artery TIA: transient neuro deficit secondary to ischemia in a defined vascular territory that lasts <24 hr
MCA stroke (90%)
Sx: contralateral weakness/sensory loss, homonymous hemianopsia (loss of visual field on opposite side of stroke), eye deviation to side of lesion, aphasia, if speech center effected
o Speech center on same side as “handedness” (if right handed L. side dominant Left sided speech center) Anterior cerebral artery (ACA) stroke
Sx: personality/cognitive defects, urinary incontinence, weakness leg>arm Posterior cerebral artery (PCA) stroke
Sx: ipsilateral sensory loss of face & CN 9/10, contralateral sensory loss of limbs, limb ataxia
Cerebellar hemorrhage: ataxia, vomiting, occipital headache, gaze palsy (towards the lesion), facial weakness (opposite lesion)
Lacunar stroke
Occurs d/t microatheroma and lipohyalinosis (small vessel hyalinosis); type of ischemic stroke o RF: HTN, diabetes
o Most common in the posterior internal capsule pure motor stroke
Putamen hemorrhage: most common site of HTN hemorrhage; internal capsule lies adjacent to the putamen and is almost always involved hemiparesis; hemisensory loss, homonymous hemianopsia, stupor, coma; eye are deviated away form the paralytic side
o Dx: CT w/o contrast (best initial; differentiate ischemic from hemorrhagic stroke), MRI (most accurate) Determine etiology
carotid duplex U/S or MRA to evaluate for carotid artery stenosis
o tx: >70% stenosis + symptomatic cerebrovascular disease carotid endarterectomy > angioplasty w/ stenting
>80% stenosis, asymptomatic, good surgical candidates carotid endarterectomy o consider carotid surgery for 50-60% stenosis
o medical management with aspirin and statins <50% stenosis echocardiogram: damaged valves or thrombi
o tx: surgically repair/replace damaged valves; heparin warfarin to INR of 2-3 for thrombi EKG: assess for atrial arrhythmia (fibrillation or flutter)
o Holter monitoring if initial EKG is normal to r/o arrhythmia o Tx: warfarin to INR of 2-3 as long as arrhythmia persists o Tx:
Non-hemorrhagic stroke (ischemic stroke)
<3hr since onset thrombolytics (IV tPA)
>3hr since onset aspirin; if pt was already on aspirin add dipyridamole or change to clopidogrel hemorrhagic stroke: no treatment
control RFs: HbA1c<7%, control BP, LDL<100, smoking cessation Rankin score system for stroke
o Measures the degree of disability or dependence n the daily activities of stroke pts (or other neuro disability) o 0= no sx
o 1 - No significant disability. Able to carry out all usual activities, despite some symptoms.
o 2 - Slight disability. Able to look after own affairs without assistance, but unable to carry out all previous activities. o 3 - Moderate disability. Requires some help, but able to walk unassisted.
o 4 - Moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk unassisted. o 5 - Severe disability. Requires constant nursing care and attention, bedridden, incontinent.
o 6 - Dead.
hypertensive encephalopathy
o Sx: altered mental status (confusion), severe HTN, increased ICP, and/or seizures
o Diff dx: drugs (cocaine, amphetamines), stroke, subarachnoid hemorrhage, meningitis, mass lesion, rebound HTN from meds (clonidine), pheochromocytoma
o Tx: decreased BP in ICU (goal 100-110 mmHg systolic) Hematomas/hemorrhages
o Note: hemorrhages appear as hyperdense areas on CT scan, whereas infarcts are hypodense parenchymal areas o Subarachnoid hemorrhage
d/t rupture of an aneurysm (usually anterior circle of Willis)
RFs of aneurysm: polycystic kidney diseases, smoking, HTN, hyperlipemia, high alcohol consumption
Sx: “worst headache of my life”; sudden onset severe headache, meningeal irritation (stiff neck, photophobia), fever, loss of consciousness (sudden increase in ICP), focal neurological complications
Dx: CT w/o contrast, LP (blood, xanthochromic CSF; may have elevated WBC)
WBC count should not exceed the normal ratio of 1 WBC for every 500-1000 RBCs; if elevated above this, consider meningitis
EKG: may have large or inverted T waves (d/t excessive sympathetic activity)
Angiography to determine the site of aneurysm (CT angiography, catheter angiography, or MRA) Tx: nimodipine (calcium channel blocker; prevents future ischemic stroke), embolization (coiling)> surgical clipping,
ventriculoperitoneal shunt if hydrocephalus occurs, seizure prophylaxis with phenytoin Syncope
o Transient LOC and postural tone w/ spontaneous recovery
d/t transient global decrease in cerebral perfusion (not regional hypoperfusion like TIA) o causes:
vasovagal: fainting d/t excessive vagal tone hypotension w/o reflex increase in HR or vasomotor tone; #1 cause of syncope prodromal sx: nausea, yawning, diaphoresis
triggers: micturition, defecation, coughing, emotion (stress or fear), pain tx: if young pt w/no PMhx then just reassurance & D/C home carotid sinus hypersensitivity
occurs in old men; triggers (pressure on carotic sinus)= turning head, tight collar, shaving neck over area dx: carotid massage to reproduce sx (auscultate 1st to ensure no bruits)
orthostatic hypotension: decrease >20mm Hg with postural changes
causes: diabetic neuropathy (autonomic insufficiency), other peripheral neuropathy (alcoholic, nutritional, amyloid), parkinsonism, idiopathic dysautonomia, hypovolemia, anti-HTN/ vasodilator drugs, neuro disorder (Shy-Drager syndrome) physical deconditioning, sympathectomy, acute dysautonomia (guillain-barre syndrome variant) cardiac disease: arrhythmias or outflow obstruction (aortic stenosis, hypertrophic obstructive cardiomyopathy)
arrhythmias #1 cause of cardiac induced syncope (usually bradycardia)
tachyarrhythmias: supraventricular tachycardia, with structural cardiac disease, atrial fibrillation a/w the wolf-Parkinson-white syndrome, atrial flutter with 1:1 AV conduction
cardiopulmonary disease: PE, pulmonary HTN, atrial myxoma, myocardial disease (massive MI), LV myocardial restriction or constriction, pericardial constriction/tamponade, aortic outflow tract obstruction (aortic valve stenosis, hypertrophic obstructive cardiomyopathy)
vascular disease (TIA, carotid stenosis): r/o with carotid artery U/S or duplex scanning
neurologic disorder (seizures, intracranial lesions); consider EEG or CT/MRI is hx suggest seizures or intracranial lesions seizures
o epilepsy: seizure of unclear etiology o partial seizures: focal to one part of the body
simple=intact consciousness, complex= loss of consciousness o absence (petit-mal) seizures
occurs in children
consciousness only briefly impaired; appears as if the person is staring into space tx: ethosuximide
o generalized tonic-clonic seizures
causes: electrolyte disturbances (hypo/hypernatremia, hypomagnesemia, hypocalcemia), uremia, hypoxia, hypoglycemia, CNS infection (encephalitis, meningitis, abscess), CNS anatomic abnormalities (trauma, stroke, tumor), hepatic failure, drug withdrawal (alcohol, barbiturate, benzodiazepine), cocaine toxicity
sx: phases of muscular rigidity (tonic) followed by muscle jerking (clonic)
dx: BMP (r/o metabolic disturbance), toxin screen, CT or MRI of head (r/o anatomic defect), electroencephalogram (EEG) EEG is only done if there is no other clear etiology of the seizure
o Status epilepticus
Tx: IV benzodiazepine (Lorazepam, diazepam) fosphenytoin> phenytoin phenobarbital neuromuscular blocking agent (succinylcholine, vecuronium, or pancuronium) + intubation+ general anesthesia (midazolam or propafol)
Phenytoin SE: hypotension & AV block (b/c also a class Ib antiarrhythmic) o Treatment
Treatment is not always necessary following a single seizures
Treatment indications: status epilepticus, abnormal EEG, family hx of seizures
1st choice= phenytoin, valproic acid, or carbamazepine; alternatives= gabapentin, topiramate, lamotrigine, oxcarbazepine, levetiracetam
if single agent not effective, try an alternative drug; if still not effective 2 drugs; if still not effective surgical correction of a seizure focus
treat until pt is seizure-free for 2 yrs, then test if discontinuation can be done via a sleep deprivation EEG driving restrictions: recommend that the patient find an alternate means of transportation
Tremors
o Physiologic
Causes: fear, anxiety, fatigue, metabolic (hypoglycemia, hyperthyroid, pheochromocytoma), toxic (alcohol withdrawal, valproic acid, lithium, methylxanthines=caffeine or theophylline)
o Essential tremor
Autosomal dominant (~1/3 of cases) Tremor occurs at rest and with intention
Exacerbated by intentional activity and caffeine, decreased by alcohol use Tx: propanolol
o Neurologic diseases: Parkinson’s, cerebellar disease, Wilson’s disease Meningitis
o Causes: infectious, medications, SLE, sarcoidosis, carcinomatosis
o Sx: headache, fever, N/V, stiff painful neck, malaise, photophobia, altered mental status (confusion, lethargy, coma), myalgias, seizures Increased ICP, kerning’s sign (unable to extend knees with hips flexed), brudzinski’s sign (passive flexion of neck causes thigh/leg
flexion)
N. meningitidis: Maculopapular rash w/ petechiae or purpura Varicella or HSV: vesicular lesions
Complications: seizures, coma, brain abscess, subdural empyema, DIC, respiratory arrest; deafness, brain damage, hydrocephalus o Acute: onset w/in hrs-days
Bacterial
Neonates (<3mo): GBS> E.coli >listeria monocytogenes; klebsiella spp. Kids (3mo-18yrs): Neisseria meningitidis > strep pneumoniae >H. influenzae Adults (18-50): Strep pneumo > N. meningitidis > H. influenzae
Elderly (>50 yo): Strep pneumo > N. meningitidis > listeria monocytogenes Immunocompromised: L. monocytogenes > gram (-) bacilli > strep pneumo Aseptic meningitis
Enterovirus, HSV, certain bacteria, parasites, fungi o chronic: onset w/in wks-months
mycobacteria, fungi, lyme dz, parasites
o differential diagnosis: meningitis, brain or epidural abscess, subarachnoid hemorrhage
bugs that cause meningitis: strep pneumo (#1), N. meningitidis (#2), GBS/strep agalactiae, listeria monocytogenes, H. influenzae; staph aureus or staph epidermidis following neuro procedures; enteroviruses, HSV 1 or 2, cryptococcus (HIV pts), TB, rocky mountain spotted fever
o dx: CSF exam (lumbar puncture), blood cultures
CT scan before lumbar puncture if focal neurologic signs or abnormal level of consciousness, papilledema Normal LP: WBC <5 (all lymphocytes or monocytes), glucose 50-75, protein <60
bacterial: elevated opening pressure, elevated WBC (PMNs) & protein, low glucose, gram stain usually positive aseptic/viral meningitis: increased lymphocytes, protein normal, glucose normal
HSV: normal/increased opening pressure, elevated WBC (lymphocytes), normal/elevated protein, normal glucose, high RBC count
o If HSV meningitis is suspected MRI (enhancement of the temporal lobes), HSV polymerase chain reaction analysis
TB: normal/increased opening pressure, increased WBC (monocytes), low glucose, high protein
Repeat LP in 48 hrs shows decreased glucose from last value; AFB culture takes 6-8 wks; MRI (enhancement of the basal region)
o tx: empiric antibiotics, steroids if cerebral edema (glucocorticoids decreased inflammation), vaccination; prophylaxis for close contacts (rifampin or ceftriaxone)
start antibiotics after LP &blood cx unless there are anticipated delays such as need for CT, then start immediately infants <3mo: cefotaxime + ampicillin + vancomycin (aminoglycoside if <4 wk old)
3mo-50 yo: (ceftriaxone or cefotaxime) + vancomycin
>50 yo: (ceftriaxone or cefotazime) + vancomycin + ampicillin immunocompromised: ceftazidime + ampicillin+ vancomycin
o cryptococcal meningitis tx: IV amphotericin B + flucytosine, followed by chronic suppression with oral fluconazole
lumbar puncture is still diagnostic if done 30min-2hrs after antibiotics If neisseria meningitidis is suspected, start antibiotics immediately Pneumococcus or meningococcus: 3rd gen cephalosporin + vancomycin Listeria (gram (+) rod): ampicillin
HSV: acyclovir + bacterial coverage until cx results are back
TB: 4 drug treatment (isoniazid+ rifampin + pyrazinamide + ethambutol or streptomycin) vaccines
all pt >65 yo :strep pneumo
Asplenic pt against encapsulated organisms: strep pneumo, n. meningitidis, H. influenzae meningococcus (n. meningitidis) vaccine: immunocompromised, dorm/military
o household & close contacts: rifampin (2x/day for 2 days) or 1x ciprofloxacin Supportive tx (analgesics, fever reduction) for aseptic meningitis; self-limited
Brain tumors
o Cerebellar tumor
Sx: ipsilateral ataxia (pt fall towards the side of the lesion), nystagmus, intention tremor, ipsilateral muscular hypotonia, marked difficulty in coordination and performing rapid alternating movements; obstruction of CSF flow ICP headaches, N/V, papilledema
Brain abscess
o Can be d/t distant infections (lung, teeth, heart, GI, bone) or d/t contiguous spread of infection (middle ear, mastoids, paranasal sinuses) o Agents: aerobic and anaerobic streptococci (69-70%) and bacteroides spp. 9anaerobes; 20-40%) are the most common; staph
aureus (10-15%)
o Sx: headaches, focal neurologic deficit
o Dx: CT scan (solitary/isolated ring-enhancing lesions) Neurologic lesions
o Upper motor neurons: weakness, spasticity/ clonus/ increased muscle tone, hyperreflexia, extensor plantar responses o Lower motor neurons: weakness, wasting, fasciculations
o Front lobe damage: apathy, inattention, disinhibition, labile affect Dominant front lobe: Broca (motor) aphasia
o Parietal lobe damage
Dominant parietal lobe damage: inability to read, write, name, or do math
Nondominant parietal lobe damage: ignoring one side of body, trouble with dressing o Temporal lobe damage: memory impairment, hyperaggression, hypersexuality
Dominant temporal lobe damage: Wernicke (sensory) aphasia o Occipital lobe damage: visual hallucinations/ illusions
o Signs of cerebellar dysfunction: intention tremor, ataxia, broad-based gait, dysmetria, difficulty with rapid alternating movements, nystagmus, dysarthria, scanning speech; muscle hypotonia can be seen pendular knee reflex
Cranial nerves o Locations Midbrain: CN 3,4 Pons: CN 5,6,7,8 Medulla: 9,10,11,12 o Trigeminal neuralgia
5th cranial nerve dysfunction sx: severe pain in the face (stabbing)
pain precipitated by: chewing, touching the face, speaking words where the tongue strikes the back of the front teeth tx: carbamazepine or oxcarbazepine; baclofen, lamotrigine; surgical decompression if not controlled by meds
postherpetic neuralgia
o d/t singles (herpes zoster reactivation); pain syndrome after resolution of the vesicular lesions o tx:
shingles prevention: zoster vaccine to all pt >60yo
incidence prevention following shingles: antherpetic meds (acyclovir, famciclovir, valganciclovir)
pain control: tricyclic antidepressants, gabapentin, pregabalin, carbamazepine, phenytoin, or antiepileptic meds; topical capsaicin disk herniation
o sx: pain at the site of compression, signs of nerve compression (if radiculopathy) o dx: x-ray, MRI
cervical fracture
o sx: can compromise innervation to the diaphragm if phrenic nerve interrupted o dx: tender to palpation, x-ray
syringomyelia
o fluid filled dilated central canal in the spinal cord; d/t tumor or severe trauma
o sx: capelike distribution of loss (across upper back and both arms); loss of pain/temp, reflexes; muscle atrophy o dx: MRI (most accurate)
o tx: surgical removal of tumor if present; drainage of fluid from the cavity anterior spinal artery infarction
o sx: loss of all function except for posterior column (positional and vibratory sensation intact); flaccid paralysis below lesion, loss of deep tendon reflexes at the level of lesion; spastic paraplegia several wks later, loss of pain & temp sensation, extensor plantar response subacute combined degeneration of the cord
o d/t vit B12 deficiency or neurosyphilis o sx: loss of positional and vibratory sensation spinal trauma
o sx: acute onset of limb weakness and/or sensory disturbance; sphincter function impaired; loss od DTRs at the level of injury, hyperreflexia below the level of injury
o tx: glucocorticoids brown sequard syndrome
o unilateral hemisection fothe spinal cord
o sx: loss of pain & temp on the contralateral side; ipsilateral loss of motor function & positional/vibratory sensation cauda equina syndrome
o sx: low back pain, saddle anesthesia, bowel or bladder dysfunction; possible lower extremity weakness & loss of reflexes d/t compression of multiple sacral nerve roots
o tx: surgical emergency brain abscess
o can spread from contiguous infection (sinuses, mastoid air cells, otitis media) or from any source of bacteremia o sx: headache, N/V, fever, seizures, focal neurological findings
o dx: MRI or CT (best initial; ring, contrast enhancing lesion with surrounding edema and mass effect), brain biopsy (most accurate) LP is contraindicated d/t risk of herniation
o Tx: empiric tx with penicillin + metronidazole+ (ceftriaxone or cefepime); vancomycin can be used instead of penicillin if pt has recent neurosurgery (increased risk of staph)
Treat 6-8 wks IV, followed by 2-3 mo orally Toxoplasmosis
o Most common CNS mass lesion in AIDs pt o Sx: headache, seizures, focal neurologic deficits
o Dx: CT or MRI (multiple enhancing lesions often in basal ganglia) o Tx: sulfadiazine + pyrimethamine
#1 causes of altered mental status in elderly= dehydration Normal pressure hydrocephalus
o d/t decreased CSF absorption at the arachnoid villi or obstructive hydrocephalus
o Sx: gait disturbance (broad-based shuffling gait, bradykinetic), dementia, urinary incontinence o Dx: CT or MRI (dilated ventricles)
o Tx: if repeated spinal taps cause improvement ventriculo-peritoneal shunts for definitive treatment Frontotemporal dementia
o Causes: Pick’s disease
May have a family hx of frontotemporal dementia
o Sx: prominent personality changes (euphoria, disinhibition, apathy), compulsive behaviors (peculiar eating habits, hyperorality), impaired memory
Intact visuospatial functions
o Dx: MRI (symmetrical frontal or temporal lobe atrophy) Multi-infarct dementia
o Sx: rapid onset dementia
o Dx: MRI (multiple areas of increased T-2 weighted density in the periventricular areas) Alzheimer’s disease
o Sx: visuospatial problems early (getting lost while driving), anterograde memory dysfunctionpersonality and behavioral changes hallucinations, changes in alertness
o Dx: MRI (normal or diffuse cerebral cortex atrophy) o Tx: donepezil (anticholinesterase inhibitor increases Ach) Dementia with lewy body
o Sx: fluctuating cognitive impairment with pronounced variation in attention and alertness, and bizarre visual hallucinations; motor features of parkinsonism (with poor response to dopaminergic agonist therapy); prominent or persistent memory impairment; deficits in attention, frontal-subcortical skills, and visuospatial ability
Progressive cognitive decline that interferes with normal social or occupational functions
Other features: repeated falls, syncope, transient LOC, neuroleptic sensitivity, systematized delusions Creutzfeldt-jakob disease
o Fatal neurodegenerative disease d/t prions
Occurs on older pts (500-70 yo); most case sporadic, other familial or iatrogenic o Sx: rapidly progressive dementia, myoclonus
o Dx: EEG (periodic high voltage complexes; periodic synchronous bi or triphasic sharp wave complexes), brain biopsy (cortical spongiform changes)
o Tx: none; death usually occurs within 12 months Parkinson disease (paralysis agitans)
o Progressive neurodegenerative disease; mean age 70.5yo (pt >50-60 yo)
d/t dopamine depletion in the substantia nigra (basal ganglia) and in the nigrostriatal pathway to the caudate & putamen increased inhibition of the thalamus & reduced excitatory input to the motor cortex
o Secondary parkinsonism: antipsychotics (metoclopramide, prochlorperazine, reserpine, thorazine) & antiemetics are most common causes; repeated head trauma, encephalitis
o Sx: tremor (“pill rolling”, at rest & decreased with purposeful action, 5-7 Hz frequency, may be a sensation of internal tremulousness), bradykinesia, rigidity (asymmetric, increased resistance to passive movement; cogwheel rigidity d/t tremor superimposed on increased tone), postural instability (orthostatic hypotension d/t inability of pulse and BP to reset appropriately with movement), micrographia (small writing), limited facial expression (hypomimia)
Sx: parkinsonism, autonomic dysfunction (postural hypotension, abnormal sweating, dry mouth, dry skin, disturbance of bowel/bladder control, abnormal salivation or lacrimation, impotence, gastroparesis), widespread neuro signs (cerebella, pyramidal, or lower motor neuron)
Tx: intravascular volume expansion (fludrocortisone, salt supplementation, alpha-adrenergic agonists, application of constrictive garments to the lower body); note that anti-parkinson drugs are generally ineffective
Motor sx
Craniofacial: hypomimia (masked facial expression), decreased spontaneous eye blink rate, speech impairment (hypokinetic dysarthria, hypophonia, palilalia= involuntary repetition of syllables/words/phrases), dysphagia, sialorrhea= drooling
Visual: blurred vision, impaired contrast sensitivity, hypometric saccades, impaired vestibuloocular reflex, impaired upward gaze & convergence, eyelid opening apraxia
Musculoskeletal: micrographia (small handwriting), dystonia, myoclonus, stooped posture, camptocormia (severe anterior flexion of the thoracolumbar spine), kyphosis, scoliosis, difficulty turning in bed
Gait: shuffling, short stepped gait, freezing, festination (involuntary quickening of the gait) Nonmotor sx
Cognitive dysfunction and dementia, psychosis and hallucinations (paranoid psychosis; visual hallucinations most common), mood disorders (depression, anxiety, apathy/abulia), sleep disturbances (insomnia sleep initiation problems, frequent awakening, and early morning awakening), fatigue, autonomic dysfunction, olfactory dysfunction, pain and sensory disturbances, dermatologic findings (seborrheic dermatitis)
o Ambulia= loss of impulse/will/motivation to think, speak, and act
Dementia: subcortical; psychomotor retardation, memory difficulty, altered personality, problems with executive function (decision making or multi-tasking), memory retrieval, visuospatial misperception
o Cortical neuronal Lewy inclusion bodies filled with alpha synuclein+ amyloid plaques & neurofibrillary tangles (more common to Alzheimer’s disease)
o Dx: Based on clinical impression
Brain MRI to r/o structural lesions
Striatal dopamine transporter imaging (DaTscan) may be useful for pts where clinical diagnosis is unclear o Treatment
Dopamine agonists (pramipexole, ropinirole): best initial tx for severe parkinsonism Pergolide and cabergoline should NOT be used d/t risk of valvular heart disease Bromocriptine is also not frequently used d/t SE
Levodopa + peripheral decarboxylase inhibitor (carbidopa) is most effective for symptomatic treatment
Carbidopa inhibits aromatic AA decarboxylation; inhibits metabolism of levodopa in the peripheral circulation SE: “on/off” phenomena (episodes of too much dopamine and insufficient dopamine)
COMT inhibitor (Entacapone, tolcapone): extend the duration of levodopa/carbidopa by blocking the metabolism of dopamine MAO B inhibitors (Selegiline, rasagiline): block metabolism of dopamine; only MAO-B inhibitors are a/w the possibility of
retarding the progression of parkinsonism
mild symptomatic benefit; only used for early disease
Avoid tyramine-containing foods (wine, cheese); they precipitate HTN
Anticholinergic drugs (benztropine, trihexyphenidyl): used for young pts when tremor or rigidity is the predominant sx (mild disease)
SE: dry mouth, worsening prostatic hypertrophy, constipation Amantadine: used for early or mild PD or for problematic dyskinesia
Increases release of dopamine & NE from nerve endings; weak NMDA receptor antagonist; anticholinergic
Psychosis: quetiapine or clozapine (atypical neuroleptics); stop or reduce drugs causing psychosis in reverse order of potency (anticholinergic, amantadine, COMT inhibitors, and lastly dopamine agonists)
Choose antipsychotics with the least extrapyramidal sx (antidopaminergic)
Note: clozapine requires weekly or bi-weekly blood counts d/t risk of granulocytopenia (risk exponentially decreased with time; almost nothing >6mo)
Daytime sleepiness: sleep hygiene, modafinil, methylphenidate, or judicious use of coffee during the day Fatigue: amantadine, stimulants (methylphenidate, pemoline)
Depression: SSRI (SE possibly aggravates motor sx, adverse interaction with selegiline causing serotonin syndrome) Deep brain stimulation (electrical stimulation)
Dopamine agonist for pt <65, levodopa for pt >65 Multiple sclerosis
o Multiple neurologic deficits of the CNS; presents in 20-40s; insidious onset of intermittent neurologic deficits
o Sx: scattered motor & sensory deficits (paresthesias and numbness, weakness, gait disturbance, visual disturbances); optic neuritis blurry vision or visual disturbances (most common), painless loss of vision; diplopia, internuclear ophthalmoplegia; b/l trigeminal neuralgia; cognitive defects, mental status changes, emotional lability, dementia; spasticity (painful contracted muscles), hyperreflexia, fatigue, cerebellar deficits; scanning speech
Internuclear ophthalmoplegia: inability to adduct 1 eye with nystagmus in the other eye
o Dx: MRI ( demyelination plaques= white matter lesions surrounding the ventricles, corpus callosum, basal ganglia); lumbar puncture of CSF (elevated protein, <50-100 WBCs, oligoclonal bands/ elevated IgG, elevated myelin basic protein)
o Tx:
high dose steroids (glucocorticoids) for acute exacerbation (shorten duration)
prevent relapse & progression: 1st choice glatiramer acetate (copolymer 1) or interferon-beta; natalizumab (alpha-4 integrin inhibitor), mitoxantrone, azathioprine, cyclophosphamide, cyclophosphamide, methotrexate
glatiramer acetate: synthetic mixture of polypeptides containing random combinations of 4 AA found in myelin basic protein; induces suppressor T-cells to down regulate the T-cell mediated immune response to myelin antigens natalizumab SE: progressive multifocal leukoencephalopathy (PML; new multiple white matter hypodense lesions) interferon beta is best for the relapsing-remitting form of MS
immunosuppressive agents (cyclosporine, methotrexate, mitoxantrone, etc) can be used for the progressive form of MS (downhill course w/o clear-cut remissions)
Spasticity: baclofen, dantrolene, or tizanidine (central acting alpha agonist) Amyotrophic lateral sclerosis (ALS)
o Loss of upper and lower motor neurons o Onset age 20-40
o Sx: weakness starting distally & asymmetrically, difficulty chewing & swallowing, difficulty speaking, decrease in gag reflex; pooling of saliva in pharynx aspiration, weak cough, respiratory difficulties
Upper motor neurons: weakness, spasticity, hyperreflexia, extensor plantar responses Lower motor neurons: weakness, wasting, fasciculations
o Dx: electromyography (loss of neural innervation in multiple muscle groups), elevated CPK o Tx: riluzole (reduces glutamate buildup in neurons; may prevent progression)
Spasticity: baclofen
Respiratory distress/failure: CPAP, BiPAP, tracheostomy & ventilator maintenance Most common cause of death is respiratory failure
Charcot-marie-tooth disease
o Genetic; loss of motor and sensory innervation
o Sx: distal weakness & sensory loss, wasting in the legs (legs look like inverted champagne bottles), decreased DTRs, tremor foot drop o Dx: electromyography (most accurate)
Foot drop
o d/t damage in the common peroneal nerve or radiculopathy of any of the spinal roots that contribute to the peroneal nerve (L4-S2) o sx: high-stopping or “Steppage” gait d/t the inability to dorsiflex the foot
Restless leg syndrome
o More common middle age-older pt; pt with chronic kidney disease and/or iron deficiency anemia o Sx: uncomfortable sensation or urge to move the legs (“creepy and crawly” sensation)
worse at night or at rest; Worsened by caffeine relieved by moving the legs, massage, warming bed partner may complain of being kicked at night o Tx: dopamine agonists (pramipexole, ropinerole) Huntington disease
o Autosomal dominant; Hereditary CAG trinucleotide repeat on Chr. 4; onset age 30-50 yo
o Sx: choreaform movement disorder (dyskinesia), dementia, behavior changes (irritability, moodiness, antisocial behavior), mood disturbances (depression, apathy)
Movement disorder progression: “fidgetiness” /restlessness, dystonic posturing, rigidity, akinesia
Choreiform movements: facial grimacing, ataxia, dystonia, tongue protrusion, writhing movement of the extremities o Dx: clinical (movement, memory, mood changes); head CT or MRI (caudate nucleus atrophy enlargement of the lateral ventricles) o Tx: dyskinesia tetrabenazine; psychosis haloperidol or quetiapine
Tourette disorder
o Sx: vocal tics, grunts, coprolalia (involuntary swearing); motor tics (sniffing, blinking, frowning), obsessive-compulse behavior o Tx: neuroleptics (haloperidol, clonazepam, pimozide)
Facial (7th CN) nerve palsy/ bell palsy
o Causes: idiopathic, lyme disease, sarcoidosis, herpes zoster, tumors, stroke
o Sx: paralysis of the entire side of the face (except stroke will only have lower face paralysis b/c upper face innervated from both
hemispheres); difficulty eating, hyperacusis (sounds are extra loud d/t loss of stapedius muscle innervation), taste disturbances (CN7 detects taste in anterior 2/3 of tongue), difficulty closing the eye (especially at night) dryness corneal ulceration
Central facial paresis will still have forehead furrowing; bell’s palsy (peripheral 7th nerve palsy) will have absence of forehead furrows
o Dx: clinical; electromyography and nerve conduction studies (most accurate)
o Tx: self-resolving (60%); prednisone; taping eye shut & lubricants at night to prevent corneal ulcers Peripheral neuropathies
o Causes: diabetes mellitus (most common), uremia, alcoholism, paraproteinemia (monoclonal gammopathy of unknown significance=MGUS) o Sx:
Ulnar: wasting of hypothenal eminence, pain in 4th/5th fingers Radial: wrist drop
Median n: thenar wasting, pain/numbness in first 3 fingers
Lateral cutaneous nerve of thigh: pain/numbness of outer aspect of 1 thigh Occurs with pregnancy, obesity, sitting with crossed legs
Tarsal tunnel (tibial nerve): pain/numbness in ankle and sole of foot; worse with walking Peroneal: weak foot with decreased dorsiflexion and eversion
o Tx: 1st choice=pregabalin or gabapentin; TCA antidepressants, seizure meds (phenytoin, carbamazepine, lamotrigine) Acute inflammatory polyneuropathy (Guillain-barre syndrome)
o Autoimmune attack of myelin sheath in multiple peripheral nerves; no CNS involvement a/w infections, recent immunization, or pt with lymphoma, sarcoidosis, or SLE
associated infections: campylobacter jejuni (#1), herpes viruses, mycoplasma, hemophilus influenzae, HIV o Sx: weakness/ parestheisas in the legs that ascends toward the chest (ascending paralysis), loss of DTRs; respiratory muscle
weakness, autonomic dysfunction possible (hypo/hypertension, tachycardia) Note: sensation remains intact or is only slightly diminished
o Dx: clinical diagnosis; nerve conduction studies/electromyography (decrease in propagation/velocity of electrical impulses d/t demyelination), CSF (increased protein, normal cell count)
PFTs: decrease forced vital capacity and peak inspiratory pressure if diaphragm involved; earliest way to detect impending respiratory failure
Serial measurement of bedside vital capacity is used to monitor respiratory function o Tx: self-resoling; IVIG (children) or plasmapheresis (adults) to reduce severity and length of disease
Myasthenia gravis
o Antibodies against Ach receptors at the neuromuscular junction muscle weakness
o Sx: double vision, difficulty swallowing; ptosis, weakness with sustained activity, normal pupillary responses
o Dx: acetylcholine rector antibodies (best initial), edrophonium test (short acting acetylcholinesterase inhibitor; improvement in motor function that lasts a few minutes), electromyography (most accurate; decreased strength with repetitive stimulation); CXR/CT/MRI (look for thymoma or thymic hyperplasia)
o Tx: neostigmine or pyridostigmine (long acting acetylcholinesterase inhibitors) Acute exacerbation: IVIG or plasmapheresis
If not controlled: <60 yo thymectomy, >60 yo prednisone
Weaning off steroids: azathioprine, cyclophosphamide, or mycophenolate Schizophrenia
o Sx: hallucinations (auditory) Mini mental status exam for dementia
o <9 severe cognitive impairment, 10-20 moderate impairment, 21-24 mild impairment, 25-30= normal cognition
o orientation to time (5), orientation to place (5), registration (3), attention and calculation (5), recall (3), language (2), repetition (10), complex commands (6)
attention and calculation: serial sevens or sell “world” backwards language: naming a pencil and watch
neurocutaneous diseases o tuberous sclerosis
sx: neuro sx (seizures, progressive psychomotor retardation, slowly progressive mental deterioration), skin sx (adenoma sebaceum, shagreen patches, ash leaf patches), retinal lesions, cardiac rhabdomyomas
adenoma sebaceum: reddened facial nodules shagreen patches: leathery plaques on the trunk ash lead patches: hypopigmented areas tx: seizure control
o neurofibromatosis (von Recklinghausen disease)
sx: neurofibromas, 8th CN tumors, café au lait spots (cutaneous hyperpigmented lesions), meningioma and gliomas neurofibromas: soft, flesh colored lesions attached to peripheral nerves
tx: 8th CN lesions may need surgical decompression to help preserve hearing o sturg-weber syndrome
sx: port-wine stain of face, seizures, CNS (homonymous hemianopsia, hemiparesis, mental subnormality) dx: skull x-ray (calcification of angiomas)
tx: control seizures
Lhermitte Test (barber chair phenomenon): electrical sensation that runs down the back and into the limbs; d/t lesion of the posterior column or
caudal medulla
o The patient is sitting or standing and the examiner is behind them and introduces lower cervical flexion
A positive test results in production of an electrical “type” response or a “pins and needles” sensation near the end range of flexion
o Diff dx: multiple sclerosis, vit B12 deficiency, behcet’s disease, transverse myelitis, radiation myelopathy, compression of the spinal cord
(cervical spondylosis, disc herniation, tumor, Arnold-chiari malformation)
Spurling’s test: assess nerve root pain (radicular pain) in the neck
o Downward pressure on the top of the patients head in the neutral position, in neck extension, and with neck extended and tipped to the
affected side
Lumbar puncture
o Contraindications: acute head trauma, signs of elevated ICP, suspected subarachnoid hemorrhage
Near a clear CT/MRI in these settings; risk of uncal herniation death
o CSF analysis
Condition Cells Glucose (mg/dL) Protein (mg/dL) Pressure (mmHg)
Normal CSF 0-3 lymphocytes 50-100 20-45 100-200
Bacterial meningitis >1000 PMNs <50 ~100 >200
Viral/aseptic meningitis >100 lymphocytes Normal Normal/slightly increased Normal/ slightly increased
Pseudotumor cerebri Normal Normal Normal >200
Guillain-barre syndrome 0-100 lymphocytes Normal >100 Normal
Cerebral hemorrhage Blood (RBC) Normal >45 >200
Multiple sclerosis Normal/ slightly increased lymphocytes Normal Normal/slightly increased normal
Sleep disorders
o Circadian rhythm disorders
Delayed sleep phase syndrome: inability to fall asleep at “normal” bedtimes such as 10pm-midnight; pt cannot fall asleep until 4-5am but have normal sleep if they are allowed to sleep until late morning; pt c/o insomnia and excessive daytime sleepiness
Dx: sleep hx and sleep diary
Advanced sleep phase disorder: inability to stay awake in the evening (usually after 7pm) making social functioning difficult; c/o
early morning insomnia d/t early bedtime
Head and neck Meniere’s disease
o Distention of the endolymphatic compartment of the inner ear Triggers: alcohol, caffeine, nicotine, food high in salt
o Sx: sense of ear fullness, vertigo (20 min-24 hr), low-frequency sensorineural hearing loss, tinnitus; vertigo can cause N/V and postural instability; symptoms wax & wane; nystagmus during an acute attack
o Tx: salt restricted diet (2-3g /day); if persistant diuretics, antihistamines, anticholinergics Otosclerosis/otospongiosis
o Abnormal remodeling of the otic capsule (bony overgrowth of the stapes) stapes footplate becomes fixed to the oval window causing loss of piston action
Age 20-30, F>M, possible autoimmune o Sx: Conductive hearing loss
o Dx: PE, CT (may show lucent or sclerotic focus in the temporal bone near the oval window)
Rinne test (bone conduction> air conduction), Weber test (sound lateralizes to the affected ear; sound is perceived as louder b/c ambient noise of the room is perceived less on that side, so bone conduction seems louder)
o Tx: hearing amplification or surgical stapedectomy Presbycusis
o Elderly pts (>50yo)
o Sx: sensorineural hearing loss (starts as symmetric high-frequency hearing loss)
Difficulty hearing in corwsed or noisy environments; trouble hearing high-pitched noises or voices Medication induced ototoxicity
o Sx: bilateral sensorineural hearing loss (reversible or permanent), and/or tinnitus o Drugs: aminoglycosides, loop diuretics (furosemide), chemotherapeutic agents, aspirin Serous otitis media (non-infectious effusion)
o Most common middle ear pathology in pts with HIV
o Auditory tube disfunction d/t HIV lymphadenopathy or obstructing lymphomas
o Sx: middle ear effusion w/o signs of inflammation dull tympanic membrane that is hypomobile, conductive hearing loss o Dx: pneumatic otoscopy
Ramsay Hunt syndrome
o Herpes zoster infection in the ear
o Sx: facial nerve palsy (bell’s palsy), vesicles in the auditory canal and auricle Malignant otitis externa
o Elderly pts w/poorly controlled diabetes; pseudomonas aeruginosa infection o Sx: ear pain & drainage, granulation tissue seen w/in the ear canal
Complications: osteomyelitis of the skull base, destruction of the facial nerve o Dx: CT or MRI
o Tx: ciprofloxacin presbyopia
o normal aging (starts age 40, peaks age 60)
o loss of elasticity in the lens lack of accommodation of the lens difficulty focusing in near objects Optic neuritis
o Age 20-45 yo; F>M; a/w multiple sclerosis
o Sx: rapid impairment of vision in 1 eye (rarely b/l) and pain on eye movement (retrobulbar pain); marked changes in color perception; afferent pupillary defect and filed loss (usually with central scotoma)
Papilledema
o d/t increased ICP
o Sx: transient loss of vision that lasts a few seconds with changes in head position, morning headaches Central retinal vein occlusion
o RFs: coagulopathy, hyperviscosity, chronic glaucoma, atherosclerotic RFs (age, HTN, diabetes) o Sx: sudden painless unilateral loss of vision
o Dx: disk swelling, venous dilation and tortuosity, retinal hemorrhages, cotton wool spots Central retinal artery occlusions
o d/t embolism ischemia of the inner retina
RFs: carotid artery disease, endocarditis, cardiac valvular disease, long bone fracture, hypercoagulable conditions, vasculitis, atrial myxoma
Recall ophthalmic artery is the first intracranial branch of the internal carotid artery; supplies blood to eye via central retinal artery (supplies inner retina) and ciliary branches (supplies choroids and anterior portion of globe)
o Sx: sudden painless loss of vision in 1 eye; commonly a/w amaurosis fugax before the occlusion
o Dx: ophthalmoscopy (pallor of the optic disc, cherry red fovea, boxcar segmentation of blood in the retinal veins; diffuse ischemia retinal whitening and cherry red spots)
o Tx: ocular massage and high flow oxygen Amaurosis fugax
o Retinal emboli
a/w atherosclerosis, CV disease, HTN
o Sx: monocular transient visual loss; “like a curtain falling down”
o Dx: ophthalmoscopy (zones of whitened edematous retina following the distribution of the retinal arterioles) Choroidal rupture
o d/t blunt ocular trauma
o dx: ophthalmoscopy (central scotoma, retinal edema, hemorrhagic detachment of the macula, subretinal hemorrhage, crescent-shaped streak concentric to the optic nerve)
Vitreous hemorrhage`
o Causes: diabetic retinopathy (#1)
o Sx: sudden loss of vision and onset of floaters o Dx: fundus is hard to visualize
o Tx: conservative (upright position during sleep which enhances settling of hemorrhage) Retinal detachment
o Most common age 40-70 yo; usually the inciting event is months before retinal detachment (myopia or trauma retinal breaks fluid seeps in an separates the retinal layers)
May be a/w metabolic disorder (DM), trauma (including ocular surgery), vascular disease, myopia, or degeneration
o Sx: loss of vision, photopsia (flashes of light) with showers of floaters (spots in the visual field); “a curtain coming down over my eyes” o Dx: fundoscopy (elevated retina with folds and/or a tear)
o Tx: laser therapy and cryotherapy (create permanent adhesions between the neurosensory retina, retinal pigment epithelium, and choroid) Diabetic retinopathy
o Diabetic retinopathy occurs before nephropathy
o Background/simple retinopathy: microaneurysm, dot and blot hemorrhages, hard exudates, retinal edema o Per-proliferative retinopathy: cotton wool spots
o Proliferative/malignant retinopathy: neovascularization o Eventual blindness
o Tx: argon laser photocoagulation to prevent complications Hypertensive retinopathy
o initally focal spasm of arterioles then progressive sclerosis and narrowing
o Dx: fundoscopy (AV nicking, copper wiring or silver wiring, exudates and hemorrhages) Acute angle-closure glaucoma
o Seen in elderly pts (age 55-70); usually occurs following pupillary dilation (ex. In a dark movie theatre, during times of stress, or due to drug intake)
o Sx: acute onset of sever eye pain, visual loss, halos around lights, headache, N/V
Eye is red with a hazy/steamy cornea; fixed dilated pupil that is nonreactive to light; anterior chamber is shallow ith inflammatory changes; tonometry (increased intraocular pressure)
o Dx: tonometry (elevated intraocular pressure)
o Tx: medical emergency; narcotics for pain control, decrease intraocular pressure (mannitol, acetazolamide, timolol, or pilocarpine); laser peripheral iridotomy for permanent cure
Avoid atropine (dilates the pupil and worsen the glaucoma)
Timolol (topical beta blocker) and acetazolamide (carbonic anhydrase inhibitor) reduce the production of aqueous humor Pilocarpine opens the canals os Schlemm to allow drainage of aqueous humor
Open angle glaucoma
o Sx: gradual loss of peripheral vision (over years) tunnel vision; central vision is spared o Dx: elevated intraocular pressure, cupping of the optic disk
o Tx: beta-blocker (timolol eye drops), laser trabeculoplasty, surgical trabeculectomy Sympathetic ophthalmia/ “spared eye injury”
o Immune mediated inflammation of ene eye (the sympathetic eye) after a penetrating injury to the other eye
d/t the uncovering of “hidden antigens” (some antigens are contained w/in the eye are protected from immunologic recognition by natural barrier; breaking the barrier results in release of these antigens autoantibodies and cell mediated immunity)
o Sx: anterior uveitis, panuveitis, papillary edema, or blindness Cataracts
o Progressive thickening of the lens
Caused by oxidative damage that occurs with aging o Sx: gradual blurred vision and glare
o Tx: lens extraction (phacoemulsification, extracapsular or intracapsular cataract extraction) Uveitis
o a/w HLA B27-related conditions
o Sx: blurred vision, moderate pain, conjunctival injection, constricted pupils; hypopyon in severe anterior uveitis; keratic precipitates (“mutton fat”) and iris nodules may be present
macular degeneration
o RF: Pt >50 yo (age related), smoking
o Degeneration and atrophy of the outer retina, retinal pigment epithelium, bruch’s membrane, and choriocapillaries
o Sx: painless progressive and unilateral or bilateral loss of central vision (burring of central vision); intact peripheral fields and navigational vision; distortion of straight lines (lines appear wavy)
o Dx: drusen deposits in the macula intraocular foreign body
o RF: high-velocity injuries (drilling, grinding, etc)
o Dx: pen light exam with topical anesthetic; if no gross abnormalities fluorescein application followed by a slit lamp> wood’s lamp exam; if no abrasion or foreign body seen with high suspicion CT or ultrasonography of orbit
MRI contraindicated! (can dislodge the foreign body d/t strong magnetic field) Allergic conjunctivitis
o Acute HSR reaction d/t environmental exposure to allergens
a/w personal/family hx of asthmas, seasonal rhinitis, atopic ermatitis, food allergies, urticaria o Sx: intense itching, hyperemia, tearing, and conjunctival edema and eyelid edema; photophobia, burning sensation
o Tx: self-limited w/in 24hrs, decrease exposure to allergens, avoid rubbing eyes, topical antihistamines, artificial tears, cool compresses Atopic keratoconjunctivitis
o Severe form of ocular allergy
o Sx: itching, tearing, thick mucus discharge, photophobia, blurred vision Toxic conjunctivitis
o d/t direct damage to ocular tissues from drugs after prolonged use (aminoglycosides, glaucoma drops, artificial tears, contact lens solution) Herpes simplex keratitis
o RF: excessive sun exposure, outdoor occupation, fever, immunodeficiency (HIV) o Sx: pain, photophobia, blurred vision, tearing, redness; can cause corneal blindness
Corneal vesicles and dendritic ulcers
o Dx: clinical; epithelial scrapings (multi-nucleated giant cells) o T: oral or topical antiviral tx
Bacterial keratitis
o RF: contact lenses, corneal trauma, foreign body
o Sx: cornea appears hazy with a central ulcer and adjacent stromal abscess; hypopyon may be present Herpes simplex retinitis
o Sx: rapidly progressing b/l necrotizing retinitis (acute retinal necrosis syndrome); starts as keratitis and conjunctivitis with eye pain rapidly progressive visual loss & blindness
o Dx: fundoscopy (widespread pale peripheral lesions and central necrosis of the retina) CMV retinitis
o Occurs in HIV pts o Sx: painless loss of vision
o Dx: fundoscopy (fluffy or granular retinal lesions located near the retinal vessels and associated hemorrhages) Herpes zoster ophthalmicus
o d/t varicella-zoster virus reactivation in the trigeminal ganglion travels to the ophthalmic branch to the forehead and eye mostly in elderly or immunosuppressed
o sx: fever, malaise, burning/itching sensation in the periorbital region; vesicular rash in the distribution of the cutaneous branch of the 1st division of the trigeminal nerve
o dx: conjunctivity and dendriform corneal ulcers
o tx: high dose acyclovir (started w/in 72hrs after eruption) to recues the development of complications Postoperative endophthalmitis
o Occurs w/in 6 wks of surgery; infection within the vitreous of the eye
o Sx: eye pain, decreased visual acuity; swollen eyelids and conjunctiva, hypopyon (pus in the eye), corneal edema and infection o Dx: sent vitreous for gram stain and culture
o Tx: intravitreal antibiotics or vitrectomy Xanthelasma
o a/w primary biliary cirrhosis
o bilateral cholesterol-filled soft yellow plaques on the medial aspects of the eyelids; benign; lipid-filled macrophages in the dermis Hordeolum/stye
o agent: staphlococci
o purulent infection of one of the glands of the eyelids (abscess located over the upper or lower eyelid) stye=small external hordeolum involving Zeis’s or Moll’s glands
o tx: frequent hot compresses, incision and drainage if unresolved within 48 hrs after starting tx; antibiotics against staph chalazion
o chronic sterile granulomatous inflammatory lesion of the meibomian glands
painful swelling that progresses to a nodular rubbery lesion (hard painless lid nodule)
persistent or recurrent chalazion can be d/t meibomian gland carcinoma (sebaceous carcinoma) basal cell carcinoma=most common malignancy of the lid margin & may appear similar to chalazion o dx: histopathologic exam to r/o malignancy
o tx: incision and drainage blepharitis
o choric inflammatory condition involving b/l lid margins o sx:
anterior blepharitis: crusty discharge clinging to the lashes posterior blepharitis: hyperemic lid margins with telangiectasias episcleritis
o infection of the episcleral tissue between the conjunctiva and sclera
o sx: acute onset mild-moderate discomfort, photophobia, watery discharge; diffuse or localized bulbar conjunctival injection dacrocystitis
o usually pt >40 yo
o infection of the lacrimal sac d/t obstruction of the nasolacrimal duct agents: staph aureus, beta-hemolytic strep
o sx: pain, swelling, tenderness, redness in the tear sac area (medial canthal region); mucous or pus can be expressed; may have fever or leukoctyosis
Nasal polyp
o a/w chronic rhinitis, post-nasal drainage, asthma, aspirin (or NSAID) exacerbated respiratory disease (bronchospasm)
o sx: bilateral nasal obstruction & discharge, anosmia (decreased smell decreased taste); bilateral grey glistening mucoid masses in the nasal cavities
Leukoplakia
o Whitish patch or plaque that can not be scraped off; can’t be characterized as any other disease (dx of exclusion) a/w chronic irritation to the oral mucosa d/t smoking, alcohol, or ill-fitting dentures
complications: squamous cell carcinoma Oral ulcers
o Gingivostomatitis d/t HSV1
Multiple vesicular intraoral lesions that have a red border Oral candidiasis
o Risk factors: diabetes
o Whitish plaques that can be scraped off with a tongue depressor Temporomandibular joint (TMJ) dysfunction
o Hx of nocturnal teeth grinding
o Sx: “ear pain” (d/t proximity of joint; pain worse with chewing), audible clocks or crepitus with jaw movement o Tx: nighttime bit guard, surgery
Thyroid cancer
o Papillary thyroid cancer
Most common thyroid malignancy; epithelial origin
Slow infiltrative local spread to other parts of the thyroid and lymp nodes
Dx: histology (psammoma bodies; large cells with ground glass cytoplasm and pale nuclei with inclusion bodies and central grooving; hurthle cells may be present)
o Follicular thyroid cancer Epithelial origin
Encapsulated; invasion of tumor capsule and blood vessels distinguishes it from follicular adenoma Early hematogenous spread to lung, brain, and bone
o Medullary cancer of the thyroid
C-cell origin; Secretion of calcitonin o Lymphoma of the thyroid
Increased risk from hashimoto’s thyroiditis
Sx: rapid enlargement of the thyroid gland, compressive sx (dysphagia, voice change)
Dx: CT scan of neck (enlargement of the thyroid gland around the trachea; “doughnut sign”), thyroid U/S (pseudocystic pattern), reduced radioactive iodine uptake; core needle biopsy
Epiglottitis
o d/t infection with Haemophilus influenzae or steptococcus pyogenes
o sx: high grade fever, severe sore throat, odynophagia (painful swallowing), droolin, progressive airway obstruction stridor
o tx: prevention with Hib vaccine; Peritonsillar abscess
o Complication from tosillitis
o Sx: fever, chills, sore throat; “hot potato voice”, deviation of the uvula; unilateral lymphadenopathy
Complications: airway obstruction, spear to the parapharyngeal space involvement of the carotid sheath o Tx: aspiration of the abscess, IV antibiotics
Retropharyngeal abscess
o Sx: sore throat, fever, difficulty swallowing (dysphagia), pain with swallowing (odynophagia), pain with certain neck movements (extension), trismus (inability ot open the mouth normally)
o Complication: spread of infection to mediastinum acute necrotizing mediastinitis “danger space” of infection is between the alar and prevertebral fasciae o dx: CT or lateral x-ray of neck
o tx; IV broad-spectrum antibiotics, urgent drainage of the abscess infectious mononucleosis
o sx: fever, pharyngitis, posterior cervical lymphadenopathy, malaise, splenomegaly; risk of splenic rupture (avoid contact sports until the physical exam is normal no splenomegaly)
o dx: atypical lymphocytosis, positive heterophile antibody test diphtheria
o sx: pseudomembranous pharyngitis, low grade fever, unilateral nasal discharge, pharyngitis, cervical lymphadenopathy cardiovascular
ECG interpretation
o Inferior surface: Leads II, III, aVF; supplied by right coronary artery
o Anterior surface: leads V2-V4; supplied by left anterior descending coronary artery (LAD) o Lateral surface: leads I, aVL, V5 & V6; supplied by left circumflex artery
o Posterior surface: R waves in leads V1 & V2
o Horizontally: 1 small box= 0.04 sec , each large box=0.2 sec (200 ms) if paper speed is 25 mm/sec o Vertically: 1 small box=10mm=1mV
o Steps: rate, rhythm, axis, intervals, P wave, QRS complex, ST segment, T wave, overall interpretation o Heart rate
Counting boxes from R-R interval (300/ # big boxes): 300, 150, 100, 75, 60, 50 If irregular rhythm: count # QRS complexes x 6
Divide by 6 b/c standard ECG displays 10 sec of time to get 60 sec (bpm) o Rhythm:
Sinus rhythm:
P wave upright in leads I, II, aVF, and V4-V6; negative in aVR. Negative or biphasic in III and V1 o Most important: up in I & aVF, down in aVR
P waves before every QRS complex If QRS <0.12 sec, then rhythm is supraventricular
If the QRS is wide (ie, >0.12 sec), then the rhythm is either supraventricular with aberrant conduction, pre-excitation, or ventricular pacing, or it is of ventricular origin
o Axis: direction and magnitude of various complexes
Normal between -30 to 90 degrees (directed downward/ inferior and to the left) Left axis deviation: between -30 to -90
Right axis deviation: between 90 and 180
Between -90 and -180 is either extreme L or R deviation Determining axis
If the QRS complex is positive (upright) in both leads I and II, then the axis falls between -30 and 90o, and the axis is normal.
If the QRS complex is positive in lead I but negative in lead II, then the axis is leftward (-30 to -90o). If the complexes are negative in lead I and positive in aVF, then the axis is rightward (90 to 180o). If the complexes are negative in both I and II, then the axis is extreme (180 to -90o).
Another method of axis determination is to find the lead in which the complex is most isoelectric; the axis is directed perpendicular to this lead. As an example, if the QRS is isoelectric in lead 3 which is directed at 120o, then the electrical axis is either 30o or -150o.
A third method is to determine the frontal lead in which the QRS is of the greatest positive amplitude. The axis is parallel to this lead.
o P wave: atrial depolarization
duration <0.12 sec (3 small boxes) and amplitude <0.25 (2.5 small boxes)
Right atrial depolarization before L atrium Notched in limb leads & biphasic in V1
o PR interval: measured from the beginning of the P wave to the first part of the QRS complex; represent atrial depolarization and conduction through the AV node and the His-Purkinje system
Normally 0.12-0.2 sec (3-5 small boxes)
Short PR interval: wolff-parkinson-white syndrome Long PR interval: 1st degree AV block
Shorter at faster HR d/t sympathetic enhancement of AV node conduction o QRS: ventricular depolarization
Total time <0.06-0.10 sec (1.5-2.5 small boxes)
Long QRS interval: bundle branch block, ventricul preexcitation, ventricul pacing, ventricular tachycardia Q wave: initial negative deflection (septal depolarization); seen in leads I, aVL, V4-V6
R wave (L. ventricle myocardium depolarization): first positive deflection Small R wave in V1= initial septal depolarization
Should progress in size across V1-V4/V6 (precordial leads)
S wave (terminal depolarization of the high lateral wall): negative deflection following the R wave R’ wave: second positive deflection
Lower case letters are used for small amplitude waves <0.5mV Atrial repolarization is hidden within QRS complex
o ST segment
J point: initial part of the ST segment; intersection of the end of the QRS complex and the beginning of the ST segment Normally isoelectric
o T wave: ventricular repolarization; begins at the epicardial surface and spreads to the endocardium (opposite of depolarization; last to depolarize is 1st to repolarize)
Slow upstroke with rapid downstroke; in same direction as the major deflection of the QRS o QT interval: measure of ventricular repolarization
Corrected for heart rate (QTc) using Bazett’s formula: QTc= QT interval/ (square root of RR interval in sec) Normal <0.44 sec (M), <0.45-0.46 sec (F)
Note that QRS prolongation will increase QT time and therefor does not signify problems with ventricular repolarization, but with depolarization
o U wave: may be repolarization of the His-Purkinje system, or late repolarization of the mid-myocardial M cells May be seen, esp V2-V4
Amplitude usually <0.2 mV
more evident during hypokalemia or bradycardia; occurs with QT interval prolongation or QT or JT interval shortening (digoxin, hypercalcemia)
o hypertrophy
right atrial hypertrophy: large diphasic P wave with a tall initial component in V1
Left atrial hypertrophy: large diphasic P wave with a wide terminal component in V1 (2nd part of wave going down is larger than the first upward wave)
Right ventricular hypertrophy
R wave >s wave in V1; R wave gets progressively smaller from V1-V6 S wave persists in V5 & V6
Right axis deviation with slightly widened QRS Left Ventricular Hypertrophy
Hypertrophy of the L. ventricle produces QRS complexes that are exaggerated in amplitude (both height and depth), especially in the chest leads
o Larger S (downward) in V1, large R in V5 (more excessive depolarization away from V1, towards V5 which lies over the L. ventricle)
Criteria: o Sokolow + Lyon S V1+ R (V5 or V6) > 35 mm o Cornell criteria SV3 + R avl > 28 mm in men SV3 + R avl > 20 mm in women o Framingham criteria R avl > 11mm, R V4-6 > 25mm S V1-3 > 25 mm, S V1 or V2 + R V5 or V6 > 35 mm, R I + S III > 25 mm o Any precordial lead (V1-V6) >35 mm
Dysrhythmias/ conduction disturbances o Premature atrial complexes (PACs)
Premature activation of the atria originating form a site other than the SA node RFs: tobacco, alcohol, caffeine, stress
Dx: EKG (early P wave) Treatment
Asymptomatic: avoid reversible risk factors Symptomatic: beta-blocker
o Premature ventricular contractions (PVCs)
Wide QRS (>120 ms), bizarre morphology, compensatory pause
More common in pt with cardiac pathology; increased frequency after MI Tx: observation
not treated with antiarrhythmic agents unless they occur very frequently, are sustained, or induce hemodynamic compromise
o beta blockers (#1) for symptomatic patients; amiodarone 2nd line check magnesium and phosphate levels
o Supraventricular tachycardia
Tx: direct current (DC) cardioversion if sx or hemodynamic instability; antiarrhythmics (adenosine, metoprolol, procainamide) Ventricular tachycardia/fibrillation
Tx: immediate defibrillation; antiarrhythmics (lidocaine, procainamide, amiodarone); maintain K+>4 mEq/L and Mg >2 mEq/L o atrial fibrillation
abnormal irregular heart rhythm with chaotic generation of electrical signals in the atria of the heart; disordered atrial depolarization
rapid ventricular response w/ HR>110
paroxysmal is self-limiting; persistent >7 days, permanent >1 yr impulses come from the pulmonary veins
