tension HA

migraine

Chronic Daily HA (rebound)

Increase ICP - "worst HA of my life" - bleeds

progressive HA - tumors

temporal arteritis - systemic vascular inflammation

70% for men

90% for women

unilateral

bilateral

frontal

occipital

temporal

eyes/sinuses

prodrome/aura

visual/neurological changes

tearing/rhinorrhea

photo/phonophobia

nausea/vomiting

other illnesses

sinusitis

dental disease

progressive HA

worst HA of my life

change in intensity, frequency

new, severe HA in adult

meningeal sxs

jaw claudation

AM HAs/HA that disturbs sleep

cough-induced HA

HA w/ focal neurologic sxs

post lumbar puncture HA

nuchal rigidity

fever

papilledema

pathologic reflexes or reflex asymmetry

altered state of consciousness

neurologic signs

neck mm tenderness, spasm,

relief of HA with pericranial mm massage

palpate temporal arteries for tenderness in older patients

TMJ exam

sinuses, tenderness over sinus cavities

migraine

HTN

Cluster

inflammatory

all usually unilateral

periodic, debilitating HA, associated with nausea/vomiting

tend to be localized

most will have an aura

NSAIDS, APAP

sleep

vasoconstrictors (ergots, caffeine)

imitrex

antipsychotic-related Rx

triptans (abortive)

antiemetics

beta blockers and Ca channel blockers

tricyclic antidepressants

gabapentin, other anticonvulsants

SSRIs in depressed patients

avoidance of triggers (chocolate, nitrites)

exercise

occur daily

worsens throughout the day

band-like

extra-cranial structures, with vasodilation pain secondary to inflammatory mediators

most will successfully self-medicate with OTCs

NSAIDS

tricyclic antidepressants

lifestyle changes

triptans

prophylaxis

you want to relieve the stress

wakes up with but gets better as the day goes on

gets better if you treat the sinusitis/chronic allergies

chronic use of sinus medications can cause rebound HAs and sinus problems

sinus cavities can erode cause serious problems

men > women

unilateral/transient/very severe, often incapacitating

non-throbbing, not worse with activity, patient often resteless, may pound on head

ipsilateral nasal congestion, lacrimation, redness, tearing, Horner's syndrome

30mins to 1.5 hours

1-8 per day

often ineffective

100% O2

triptans/ergotamine

Ca channel blockers

indomethancine - could cause bleed

intranasal 4% lidocaine

prophylaxis w/ beta blockers, CCB, tricyclics, anticonvulsants, Li, steriods

chronic daily HA that usually starts as a migraine but can originate as tension headache

REBOUND

involves daily dose of a HA med

sudden onset, lancinating facial pain

follows trigeminal nerve distribution

unbearable, even the wind can bring on pain

R/O with MS

gamma radial surgery

post herpetic neuralgia

sinusitis

dental pain

TMJ pain

a systemic vascular inflammatory condition

unknown cause

the inflammation causes tenderness of arteries

oral prednisone, relatively high dose to reduce inflammation and risk of thrombus/embolus

urgent opthamology consult

temporal artery biopsy before steriods take effect

brain: lung and breast

spinal cord: prostate, breast, lung

may lead to "spinal cord dysfunction"

back pain

distal paresthesia

sensory loss/weakness below level of tumor

loss of bladder/bowel control

can cause impinging and pain

progressive HA/nausea

sometimes vomiting

cranial nerve involvement

new onset seizures/sensorimotor changes

cognitive impairment

visual field changes

complete neuro exam

CT or MRI, with contrast

EEG

biopsy

arteriography

PET, SPECT, MRS

subdural hematoma

hydroencephalus

brain abscess

Progressive multifocal leukoencephalopathy

MS

cerebral infarcts

Alzheimer's disease

surgerical intervention

radiation/chemotherapy

corticosteroids (start prior to surgery)

anticonvulsants

pallative care

inflammation associated with multiple foci of demyelination in the CNS white matter

probably autoimmune basis

most common in young adults

f >> m

more prevalent in caucasians

more prevalent in northern latitudes

fatigue

weakness

tremor

diplopia

CSF: inc Protein, inc IgG w/ possible lymphocytosis

and EP

Common initial labs

TSH, Vit B12, ESR, ANA,

RPR, Serum ACE level, lyme titre

 dsDNA, anti-SSA, anti-SSB (for Sjogrens syndrome)

initial neurology referral with PCP FUs

treat sxs, individualize to minimize impairment

EXERCISE AND PERSERVATION OF FUNCTION BETWEEN EXACERBATIONS

use diease modifying drugs early

high dose steroids for acute exacerbations 

interferon beta

peptide immunomodulator

monoclonal AB

very expensive

roughly 30% reduction in plaques/sxs

cooling vests

PT

OT

aquatic therapy

autoimmune disease involving autoantibodies that block ACh receptors at the neuromuscular junction.

serious mm weakness

usually insidious onset

ptosis

diplopia

chewing and swallowing difficulty

respiratory difficulty

limb weakness

increased complaints of weakness at the end of the day

mm weakness and fatigability improving with rest

Anticholinergic challenge

Edrophonium test

Anticholineresterases

pyridostigmine (mestinon)

neostigmine (prostigmin)

Peripheral Arterial Occlusive Disease

very common

related to atherosclerosis of arteries

reduced perfusion of peripheral tissues

especially important to lower extremity LEAD

smoking

obesity

sedentary lifestyle

diabetes

HTN

hyperlipidemia

FHx

inspection: atrophy of calf mm, loss of extremity hair, thickened toenails

palpation of pulses from aorta to feet

ABI measurements with palpation or Doppler

ankle-brachial index of 0.8 or less

diminished or absent peripherial pulses, combined with suggestive sxs

**convincing history of intermittent claudication

possible arteriography (only if surgery is planned)

STOP SMOKING

antiplatelet drug

exercise promotes collateralization

reduce cardiovascular risk

surgical (vascular bypass, balloon angioplasty)

spinal cord compression

osteoarthritis

venous disease

peripheral neuropathy

buerger's disease

thromboangiitis obliterans

unique to smokers, generally middle aged

inflammatory reaction of small arteries leading to claudications sxs

sequential amputation common

affects upper extremities as well

Pain

Pallor

Paresthesia

Paralysis

Pulselessness

atherosclerotic vascular disease

hypercoagulable states

episodic, vasospastic ischemic attacks of the digits

digital vessels are overly reactive to cold temps, involves sympathetic activation

for primary: avoiding cold temps,

CCBs, possible digit sympathectomy

secondary: treat underlying disease

reticular, or fishnet pattern of blanching and bluish skin as a result of vasospasm

idiopathic, not dangerous

secondary can be related to vascular or autoimmune diseases

abdominal aortic aneurysm

a rupture or leak is a surgical emergency

temporal or takayasu's are forms of giant cell arteritis

a systemic vascular inflammatory condition, unknown cause

causes tenderness of arteries, especially temporal

can cause blindness

venous insufficiency, a loss of competance of venous valves as a result of pressure over a long time

possibly related to trauma, FHx

not equivalent to DVT

superficial veins become engorged and allow backflow of blood distally

painful, generally not a dangerous condition

associated with varicose veins

leg heaviness

exercise intolerance

pain or tenderness along the course of a vein

pruritis

burning sensations

restless legs

night cramps

edema

skin changes

paresthesias

improved by walking or by elevating legs

presence of varicosities on pathway of greater saphenous vein

darkened pigmentation, ulcers, esp above medial malleolus (venous stasis)

thrombosed veins (risk for DVT)

percussion pulse wave for mapping

a variety of stripping/sclerosing techniques often used

support stockings, avoidance of panty hose with higher up restriction

chronic condition due to imcompetent veins and leakage of blood into tissues

inflammatory reaction, swelling, pigmentation, ulcer

edema initially pitting, but may become woody

support stockings

stasis (flow)

vessel wall injury

hypercoagulation

angiography

V-Q scan ***

CT

D-dimer

peripheral ultrasonography for clots

limb enlargment due to decreased lymphatic drainage of an extremity

breast cancer treatment in US, filariasis worldwide most common causes

also vein stripping, surgery and insect bites

no, it can happen years later

often inresponse to mild trauma, overuse of limb, infection, etc.

bacterial or fungal infection of lymphatics, with cellulitis

red streaking, usually of extremity, enlarged proximal lymph nodes

patient is ill, with leukocytosis

give IV antibiotics empirically while awaiting blood cultures

elevate limb

encourage meticulous hygiene

treat all skin injuries promptly

aggressively treat any cellulitis that develops

avoid weight gain/lose weight

compression garments

pneumatic compression

PT

surgery of equivocable value

lymphangitis

lymphangiosarcoma

infection

amputation

bacterial

fungal or mycobacterium tuberculosis

viral

meningitis

encephalitis

space occupying infectious lesions of the CNS

prion diseases

bacteria

spirochetes

viruses

fungi

protozoa

prions

immunosuppression

cranial trauma

peds

streptococcus Group B

E. Coli

listeria monocytogenes

hemophilus influenza

(H. Flu)

streptococcus pneumoniae

GNR

listeria monocytogenes

fever

HA

malaise

nausea, vomiting, anorexia

rash

invasion

exposure

colonization

meningeal signs: nuchal rigidity, brudzinski sign, kernig sign, straight leg raise

progressively worsens, quickly

changes in mental status

LP

papilledema

progressive decline in level of consciousness

focal neurologic deficit

draw blood first for C&S

Start IV steroid and antibiotic therapy

get a CT scan

if CT scan shows no elevated ICP, then do a LP

obtain cell count, gram stain and C&S of CSF

cell count: 0-5 lymphocytes

protein: 15-45 mg/dL

glucose: 50-70% of blood glucose level

opening pressure: 70-180 mmHg H2O

cloudy or grossly purulent

organisms are seen on direct exam 75% of the time

CSF Protein is >45

Glucose is <40

opening pressure is markedly elevated

<5: 3%

>60: 30%

25% overall 

Hemophilus influenza, type B vaccine

(begin at 2 months old)

meningococcal vaccine 

more benign, serious but rarely fatal

self limiting -- about 2 weeks

relatively common

can takes several days to weeks for sxs to appear 

person to person

direct contact, skin to skin 

HA

fever

stiff neck

may have viral prodrome

changes in consciousness and localizing neurologic signs are rare 

inc. WBCs (mostly leukocytes)

increased protein

normal to slightly elevated glucose

normal to slightly elevated opening pressure 

CSF

CXR

TB skin test

syphilis/HIV serology

blood bacterial and viral cultures

PCR of virus from the CSF  

mycobacterium tuberculosis

lymes disease

syphilis 

fungal 

increased WBCs

increased protein

decreased glucose

moderately elevated opening pressure 

culture (diagnostic)

multiple drug therapies for meningial TB

antifungal therapy for cryptococcal 

mainly salivary, from bites

scratches

inhalation

infected organ transplants 

10 days to 1 year

usually 1-2 months 

tingling feeling at the site of innoculation

progresses to anxiety, agitation, delirium

spasms of the throat and frothing at the mouth at the sight of water (hydrophobia), coma and death 

they usually die, even if treated

its too late 

test the vector (if you can find him he has to be quarantined)

visualize cytoplasmic inclusions in neurons in hair-bearing regions of the skin

serology - only if patient hasn't been vaccinated 

start txt even before you have the test results back

you get very painful and expensive shots on day 0, 3, 7, 14 and 28 

cysticercosis

toxoplasmosis

abscesses 

flu like syptoms or an acute encephalitis

only 1 in 150 have a serious disease from this 

caused by the larval form of Taenia solium (which is a pork tapeworm)

its caused by eating their eggs, usually from undercooked pork

associated with pica and poor handwashing 

seizures

large infections

extensive brain swelling leads to herniation

and death 

antihelminthic drugs with steroids

albendazole or praziquantel are drugs of choice

eating raw beef

oral fecal contamination

(handling litter from a cat box)

transmitted in utero in the third trimester 

asymptomatic infection

respiratory disease

CNS infection

(ring enhancing lesions)

seizures, mental status changes, fever, focal neurologic defects

ocular infections

mental retardation

learning disabilities

growth retardation

eye infections and blindness

fetal death in utero 

Serology IgM and IgG may be detected in the CSF and serum

tissue biopsy

MRI demonstrates ring enhancing lesions 

trimethoprim sulfamethoxazole with pyrimethamine

long term prophylaxis may be needed for immunosuppressed patients 

caused by any number of bacteria

infection starts at a non-CNS site and spreads to the CNS

or it may occur from direct innoculation 

fever

drowsiness

HA

focal neurological defects (<50%)

seizures 

indolent to fulminant

75% have sxs for 2 weeks or less

you have to look for the source

(lung, ear or sinus disease) 

CBC (WBC only elevated 10% of the time)

CT or MRI

Aspiriation biopsy of abscess - draining 

early 1-3 days

late 4-9 days

early capsule formation 10-13 days

late capsule formation >14 days 

surgical drainage

antibiotic therapy

intrathecal administration of drugs may be required for adequate penetration into tissues

treat underlying cause of infection 

40-60%

factors:

delayed diagnosis

ventricular rupture

fungal infection

coma

multiple and deep inoperable abscesses

inappropriate antibiotics 

a prion

 protein infectious cause (protein mutates)

a progressive encepalitis 

there isn't one

not good 

Cruetzfeldt-Jakob disease

bc the Kuru tribe was into eating eachother's brains