8.01.2011

multiple system atrophy vs parkinsons

multiple system atrophy - group of three overlapping neurodegenerative disorders

striatonigral degeneration - predominant parkinsonism

autonomic dysfunction (shy drager)

olivopontocereballar degeneration - predominant cerebellar ataxia



now categorized

MSA - P - predominant parkinson's - brady, rigid, post instability, tremor (can also get dystonia)

MSA - C - predominant cerebellar - nystagmus, dysarthria, impaired smooth pursuit,

dysphagia, increased urinary frequency, urgency, incomplete emptying

sleeping and breathing disorders (involuntary sighs/gasps)

cognitive function - typically spared

Raynaud's


Imaging - atrophy of putamen, pons, cerebellar peduncle (middle), "hot cross bun" sign -T2 hyperintense signal within pons (degeneration of transverse pontocerebellar fibers)


pathology - intracytoplasmic inclusions of alpha-synuclein, tau, ubiquitin


autonomic symptoms come from loss of neurons in the intermediolateral cell column or catechol C1 neurons of ventral lateral medulla


urinary symptoms can be result of loss of inhibitory pontine micturition neurons or Onuf's sacral nucleus (cause of erectile dysfunction in men)


KEY DIFFERENTIAL FOR MSA VS. IDIOPATHIC PARKINSON'S

response to L-dopa - MSA does not have sustained responses to L-dopa

MSA - C secondary to cerebellar, inf. olivary neucleus, basis pontins, pontine nuclei


Diagnosis is clinical. Levodopa dx MSA from idiopathic Parkinson's (above),

-must use HIGH dose to avoid false negative (lack of response)

-L-dopa can create false positive if trial doesn't last long enough (MSA can manifests after brief period of L-dopa responsiveness) trial period is 3 months

- use Ldopa w/carbidopa (peripheral decarboxylase inhbitor)

+ response is >30% increase in UPDRS score (unified parkinson disease rating scale

unilateral facial dystonias after L-dopa treatment suggest MSA over idiopathic parkinson




7.31.2011

mri notes

order MR if question about age of hemorrhage

(classically in child abuse cases)


hemorrhage on CT

white 2/2 Hgb/protein concentratino ~56 HU, anemic patient may appear isodense


hyper acute blood 0-72 hyperdense

Early subacute 3 days 1 week still hyperdense

Late subacute hypodense 1 week to months


MRI

2 factors affect MR: oxygenation state of hemoglobin, lysi of initially intact RBC


hyperacute 3-6hours - contains oxyhemoglobin (diamagnetic) - will not see it on GRE/SWI


acute 8-72 hrs - ^ deoxyhemoglobin (paramagnetic) will see on SWI/GRE


chronic hemorrhage - months to years, iron atoms deposited and cannot exit


hyper acute

oxy - isointense T1, bright on T2

acute 1-3 days

deoxy - iso on T1 dark on T2


subacute )3-7days)

bright on TI, dardk on T2

late 7-14 days bright bright - extracellular methemoglobin

chronic >14 days - dark dark T1T2


intracranial vasculature

digital subtractio angiography - gold standard, catheter angiography

do each vessel individually

bolus injection 100ml at 4-6ml/sec

large bore 18guage antecubital to get good cta


MRA/V

TOF - no contrast - moving spins experience different excitations (flow related), slow flow may appear as if vessel is occluded - can see >1.5mm on 1.5T

2D limitations - need adequate flow, aneurysms poorly visualized, underestimated because of slow moving spins

Phase contrast -

TRICKS - time resolved iagin of contrast kinetics: needs contast -time resolved imaging of contrast


giant aneurysm >2.5cm presents w/mass effect


http://www.youtube.com/watch?v=_OJ5qnErsTc&NR=1

7.15.2011

ipab

IPAB notes


the independent payment advisory board - us gov agency created in 2010 by ACA (affordable care act)


task

-reduce rate of growth in medicare to target levels w/o adversely impacting coverage/quality

priveleges

-IPAB has the ability to set medicare reimbursement rates independently, only congress has ability overrule IPAB decisions

thesis

-orginally MedPAC (medicare payment advisory commission) could advise congress on proper medicare spending but MedPAC could not legislate, however congress never made MedPAC's suggested cuts. it is believed congressional members were beholden to special interest groups from medical device/supply makers to keep spending high, IPAB was proposed as a way to remove power from congress with these financial conflicts of interest and put medicare spending policy decisions in the hands of healthcare policy experts


IPAB guidelines

-proposals must not involve "rationing" of care

-proposals must not raise medicare premiums

-proposals must not increase cost sharing (deductibles, copayments, coinsurance)

-proposals must not restrict benefits

-proposals must not alter eligibility criteria


who makes up IPAB

-15 members appointed by president, confirmed by senate

-composed of healthcare administrators, physicians, hospital managers, healthcare IT managers, consumer group representatives

-member salary 165,000

-total funding $15 million


notable organizations against IPAB

-pharmaceutical research and manufacturers of america -

-american hospital association

-american medical association - wants "working" physicians to be included as board members

-american academy of neurology - concerned reimbursements will be cut, believes there will not be physician representation on the IPAB board

-nursing home associations - IPAB would adversely impact their ability to lobby congress (this is as i understand it the whole purpose the board was created)


those for it

-medicare benficiaries stand to benefit, provided they can access care

-washington post editorial - reject criticism of IPAB essentially by saying that the current political system is failing greatly


numbers

-IPAB goal- decrease by $28 billion by 2019 - total medicare spending for this period will be 7 trillion!!, thus the savings will amount to 0.04% of total spending



my opinion is that this panel could probably be a benefit to healthcare reform and i support its formation. i understand opposition to IPAB probably stems from the loss of revenue and pre-existing political relationships between special interest lobbyists and congress. disrupting this channel of communication definitely adversely impacts these institutions' profit equilibrium and political position, and those who have spoken out against IPAB probably feel that their interests will be adversely impacted by IPAB proposals. but i happen to believe that congress would sell out the interests of physicians in order to maintain ties with private insurance and hospital lobbying groups who are more integral to their re-election, and because of the inherent instability that those relationships place on my standing as a future physician taken together with the good faith effort of our president and healthcare reform analysts comprising the IPAB (who may be more aligned with interests of office based/general practice physicians), i see more reason to support the formation of the IPAB then to maintain the status quo of medicare reimbursement defined in my eyes by annual emergency medicare reimbursement reduction stopgaps passed at the eleventh hour which continuously place the reimbursement system for physicians in precarious straits.

7.13.2011

chest radiology notes

pulmonary edema


cardiogenic

LV failure

valvular -

pulmonary veno-occlusive

12-19 pulmonary hypertension

20-25 interstitial edema (interlobular septa, bronchovascular bundle, subpleural compartment) - kerley lines (septal thickening), pleural effusion

>25 alveolar edema - (25mmhg is normal oncotic pressure of plasma)

batwing pattern, airbronchograms (ARDS), fluid leaks into the alveoli (50% begin in RUL because associated w/mitral regurg b/c r superior pulm vein right above mitral valve and it receives regurg jet _ this is the leading idea


non cardiogenic - high capillary perm - tends to be more permanent when onset (associated with high mortality) toxin

drug

trauma

sepsis


kerley A lines - long emanate from the hila, best seen in upper lobes

B lines short thick extend to pleural base

C lines fine very short, criss cross

no real difference between A B C, merely a historical note


rt pleural effusion predominates in CHF because patient sleeps rt side down! right usually larger than left

re-expansion pulmonary edema - re-exanpsion edema more sever w/chronic edema being drained,


some radiology notes

brain mra no contast

resolution is 3mm (CT angio is better than this)


petrous cavernouse supraclinoid -path of carotid


diffusion of water is restricted (restricted diffusion) in acute infarct (hi on dwi) cytotoxic edema, low on ADC,


dont have a use for contrast on T2 MR


T2 Flair good for fluid containing pathology


corpus callosal lesion

gbm

ms

lymphoma (likes periventricular white matter)




signs in chest radiology

butterfly pattern of cardiogenic pulmonary edema

air bronchogram - parencyhmal process (air blood pus cells tumor) - you can see bronchi,

bronchus cut off sign -atelectasis

veil sign - left lobe atelectsasis

golden s sign - right upper lobe atelectasis

comet tail and crow feet on CT - pleural fibrosis round atelectasis (need to have pleural disease)

juxtaphrenic peak sign - tenting of diaphragm upperwards in cases of upper lobe volume loss (atelectasis or surgical removal)



water bottle shaped heart - pericardial effusion (blood, fluid,etc)

oreo cookie sign - pericardial effusion on lateral radiograph, seen best with patient who has lot of fat

dense calcification in radiograph in center of heart aortic stenosis


reverse 3 sign - coarctation


continuous diaphragm sign - 3 things

- pneumomediastinum/pericardium/peritoneum


air crescent sign - invasive aspergillosis (necrotic consolidation) not an aspergilloma (classically)


deep sulcus sign - deep costophrenic angle in supine patient, classic sign of pneumothorax

scimitar sign - - sign of hypogenic lung syndrome lung will be bi-mono lobed (lung malformation) associated with abberant pulmonary venous return


hampton's hump - wedge shaped opacity sign of infarct from PE

westermark's sign - oligemia (shift in perusion) enlargement of ipsi pulmonary artery


fallen lung sign - ct sign of pneumothorax


halo sign - frquently see in bleeding met (angiosarc) and aspergillos

reverse halo - high density surround normal lung - classically described in COP (cryptogenic organizing pneumonia) - not pathognomonic though, resolves w/steroids


crazy aving - alveolar proteinosis

6.21.2011

some excerpts from lao-tzu

the ancient masters looked ordinary

but their wisdom was profound

they didn't deviate from the truth

the clever couldn't persuade them

the beautiful couldn't seduce them

the rich couldn't corrupt them

they considered life and death

to be insignificant matters

unhindered, their minds could soar

to the edges of the unknown,

beyond time and space, and plunge

past the beginning and the end

they could take the most menial positions

and find contentment in their work

the ancient masters

slept without dreaming

woke without concerns

their food was spare and simple

their breath went deep

they didn't hold on to life

they faced death free of concepts

emerging without desire

going back without resistance

they didn't trouble their minds

searching for what their end was

they received life as a gift

and handed it back gratefully

there was no limit to their freedom


the sage dreams, but he knows it to be a dream in the same way as he knows the waking state to be a dream. established in the state of supreme reality, he detachedly witnesses the three other states, waking dreaming and dreamless sleep, as pictures superimposed onto it. for the sage all three states are equally unreal. most people are unable to comprehend this, because for them the standard of reality is the waking state. whereas for the sage the standard is reality itself


When a drunk falls from a wagon

he won't be killed, no matter

how fast the wagon is moving

his body is like other men's

but the way he falls is different

life and death mean nothing to him

thus fear can't enter his heart

he meets all circumstances

like an infant, without a thought

unconscious that he is falling

he falls softly, and his bones

bend like the branches of a tree


the mature person is like a good archer

when he misses the bull's eye

he turns around and seeks

the reason for his failure in himself


you can't talk about the ocean

with a frog who lives in a well

he is bounded by the space he inhabits

you can't talk about ice

with an insect who was born in June

its life is bounded by a single season

you can't talk about the Tao

with a person who thinks he knows something

he is bounded by his own beliefs

5.29.2011

random clinical snippets

have been away from posting clinical pearls received for the month because i was on surgery and the hours did not allow for even 45 minute blocks of time to write and copy, i will have to transpose those notes at a later date. lost ten lbs during that rotation, was sleep deprived, unshaven and had a constant facial/stress rash the whole time, had a great time though haha!

so to get caught up, now on last rotation, pediatrics, having a great time as well- totally different culture than surgery, medicine, ob/gyn, neuro. the hospital is more tolerable as well, art and paintings on the wall, and more windows with larger rooms. after this the clinical year will be over. it was
definitely fatiguing, but well worth the effort.

three bugs of neonatal meningitis
-E. coli
-GBS
-L. moncytogenes (need ampicillin to cover this)
meningitic doses are 100mg/kg - start w/cefotaxime until culture rules out.
dont want to use ceftriaxone in newborn because this drug can spike bilirubin.

axillary temp should be 1 degree higher than rectal

Glycogen storage disorder type 1 (von gierke's) here is some next level pimping courtesy of the liver fellow - whats the difference between von gierke's type 1a 1b and 1c?
1a - lack of the G-6-phosphatase
1b - lack of transporter - get IBD like symptoms
1c - lack of cofactor in the transporter
clinical significance? in 1b you get neutropenia, won't get that in other types
clinical presentation of von gierke's - obese, overfed, ^triglycerides, 60-70% hepatic adenoma, small percentage of this population goes onto HCC

indications for intestinal transplant
-tpn dependent (lifestyle issue)
-good post op care
-no social contraindication (sex drugs and rock'n'roll stuff)
-loss of vascular access
-intestinal failure associated w/liver disease
-recurrent sepsis
contraindications
-cant be immunosuppressed (cancer)

KVO abbreviation for keep vein open - run fluid at low rate so you don't have to hep lock the IV

when dealing with an oppositional teenager be concrete - "if you don't take your insulin, you will lose you limbs, go blind, then die"

methylmalonic aciduria - give metronidazole to decrease proprionic acid (made by enteric flora), proprionic acid is substrate used to make more methylmalonic acid

Serious bacterial infxn
-uti, bacteremia, menin
gitis

Oragel - not good for teething babies, can cause methemoglobinemia

baby physcial exam pointers:
increased fontanelle size associated with hypothyroid
posterior closes in 1st six months, anterior closes 1.5 yrs
nasal septal polyps think associated w/cystic fibrosis
ear pits (dimples anterior to tragus) associated w/sensorineural hearing loss -not associated w/renal anomalies

Heart exam: most babies have a systolic ejection murmur best ascultated at the left sternal border, its called peripheral pulmonic stenosis, it goes away in 6 months

Vaginal bleedi
ng from a neonate- everythings ok! the babies baby endometrium has responded to maternal hormones.
hip dysplasia increased risk in females because they are more sensitive to hormone relaxin, get sonograms upto 4-5 months then switch to x-ray b/c neonatal skeleton will have calcified to the point where it can be visualized.


now for my favorite thing ever! the asymmetric tonic reflex, this primitive reflex is elicited by turning the babies head to one side, and the baby will pose his arms just as seen in the picture below- its also aptly referred to as the fencer's reflex-





i could not get enough of this, its so cute. ok babies are cute.

primitive reflexes should be gone by 4 months.

medical metaphor-
open a book and read a page, how often do you know what it is about? you need to read the pages leading upto the current page to get any idea of the story. so it is with patients, you must get the history!

pelvic inflammatory disease can lead to tuboovarian abscess which can lead to fitz hugh curtis abscess.
3 things you can never miss in ER
1. ectopic pregnancy
2. ovarian torsion
3. appendectomy

lower abdominal pain w/vaginal bleeding is rule out ectopic until proven otherwise.

ovarian torsion - radiates to groin, intermittent and sudden
sti's - fevers, discharge, dyspareunia

kids can get abd pain in UTI's

doing an abdominal/intracavitary ultrasound to rule out ectopic pregnancy? need to document two things
1. +/- intrauterine pregnancy
2. if +, document fetal heart rate if possible

tip- aminoglycosides increase botulinum levels and can precipitate botulinum toxicosis

maternal lupus can have maternal antibodies that cause complete heart block in neonate, may also present w/cutaneous lesions

bowel viral gastroenteritis can lead to secondary lactose intolerance (transient), as well as strip the gut of disaccharidases therefore don't give fruit juices because just make it worse because of osmotic diarrhea, also don't give cold fluids (i don't know why i just wrote that down)

allergic eosinophilic gastroenteritis is non IgE mediated - its secondary to multiple food allergies, can have patient on inhaled steroid but swallow it!! don't inhale.

milk protein allergy: presents young and this one is IgE mediated, bloody stools

oral allergy - from eating raw fruits can get swelling tingling in mouth, allergic to skins/pollens etc and this is IgE mediated

an adverse reaction to MMR vaccine is usually an allergy to the gelatin in which it is carried.
egg allergy? no flu or yellow fever vaccine

UTI's
risk: boys >> girls for first 18months because of increased bladder pressures, then girls >> boys in risk from thereafter

patient was a 20 year old female w/neuropsychiatric lupus complicated by episodes of immune mediated thrombocytopenia, before giving IVIG you have to check... IgA levels, bone marrow biopsy before giving steroids to make sure not a hematological malignancy

3 stages of whooping cough - only worth treating if you catch it in the catarrhal phase - use a macrolide (not erythromycin because can lead to pyloric stenosis vis a vis its gastric activity)
1. catarrhal phase (low grade)
2. paroxysmal (whooping stage)
3. convalescent stage


viral gastroenteritis? BBRAT diet
bread banana rice apples toast - only good for 24 hours

5.11.2011

asymptomatic carotid notes

Carotid atherosclerotic disease

Symptomatic or asymptomatic?

Symptomatic -
-focal neurological symptoms
-refer to appropriate distribution
-1+ TIA/Stroke
-w/in last six months

*vertigo and syncope not generally caused by carotid stenosis


Asymptomatic
-trials have established CEA for asymptomatic men w/ ICA stenosis >60% w/life expectancy >5yrs with perioperative risk of death <3%.
Woman? medical management

aspirin recommended for all having CEA

Three trials VA, ACAS, ACST
1993 -VA - absolute risk reduction was 1% over 4 year follow up
444 men w/50-99% stenosis (assessed w/arteriogram)
randomized to aspirin or aspirin + CEA, mean 48 month follow-up
results
-decreased stroke/TIA
stroke or TIA decreased 8 vs 20.6%
pertinent negative: no difference in ipsilateral stroke
no different in combine stroke/death at 4 years (41 v 44%)

1995- ACAS - absolute risk reduction was 3% over 2.7yrs
1662 adults w/60-99% stenosis to ASA325 vs ASA+CEA
end point was ipsi infarction or death in perioperative period
results
-ipsi stroke/peri stroke or death 5 v 11 @ median f/u 2.7
Men had ARR of 8% women 1.4% 2/2 periop complications
-subgroup analysis - less effective in women (but not significant)

ACST - absolute risk reduction 3.1% over 3.4 yrs
3120 patients w/>60% asymptomatic, there was an immediate surgery and versus deferral group vs medical management.
-@3.4 yrs - CEA perioperative death/stroke was 3.1% w/in 30 days
-immediate > deferral @5yrs 6.4 v 11.8 for strokes and periop death
-ARR >men

4.03.2011

Please take five minutes...

and follow along this gorgeous piece of music!! so beautifully written, every note is perfectly placed. perfectly timed



brain repair after stroke

Here is a very interesting grand rounds at UCSD about brain repair after stroke


principles of brain repair from grand rounds

1. brain repair is time sensitive - stroke physiology is a sequence of cellular events, have to time treatments accordingly (sequence growth factors, or if give NMDA blockers early kill recovery)
2. brain repair is experience dependent - need exposure to the lost function, task specific rehabilitation + repitition that leads to increase in behavioral recovery
3. have to optimize patient selection type, many therapies are $$, and there are many variables that modify outcome (age, handedness, genetics, medications, timing of events...)
4.value of domain specific endpoints - less global endpoints may be needed to understand repair issues because global recovery may be too broad to measure whats working

4.02.2011

List of all neuro programs



This link was taken from student doctor network, it is a google map with every neurology program listed, nice to get a bird's eye view. Thanks to Dandelionwine for making it

original link

American Academy of Neurology practice bulletin regarding prescription of "neuroenhancement" in well adults

practice of medicine traditional goals or obligations

1. prevent and diagnose disease or injury

2. cure/treat the disease or injury

3. reduce suffering

4. educate

5. help patients die in peace and dignity

6. reassure the well


ethically more complicated behaviors

1. participating in executions

2. participating in interrogations

i add these

3. use of medicine as a direct coercive force

4. research and experimentation with complicated ethical questions

5. profit motivated medicine


role is divided into

core domain

-these are obligatory

secondary domain

-considered ethically permissible


AAN describes prescribing medication for the purpose of neuroenhancement at best to fall into the category of secondary domain and at worst ethically impermissible


reasons prescribing for enhancement may be considered permissible

-improves well being (similarly to plastic surgery)

-benefits > risks



issues worth considering before prescribing-

-prescriptions will be "off-label" until medications are specifically designed and approved for the purpose of enhancement

-"off label" use should be based on

1. plausible rationale

2. based on available evidence

3. consistent w/standard of care (unfortunately very little clinical evidence to inform this use)

-before prescribing must inform patient

1. not FDA approved for this use

2. side effects

3. risks (short term and long term)

4. alternatives to not taking the medication


Ethical considerations before prescribing

-Thorough assessment of patient

e.g. - just because a patient is requesting neuroenhancement does not mean they are well, have to do a full work up for existing pathology. the request itself may be evidence of existing condition or the patient's interpretation of their symptoms

thus the request for neuroenhancement is still a "chief complaint"

-Beneficence and nonmaleficence

the putative benefits of enhancement (increased competitiveness, intelligence etc) are difficult to quantify and thus difficult to compare to the risks of treatment. thus clearly stating treatment goals will help the physician

-Distributive justice

drugs unlikely to be covered by third party payers, will remain in the domain of the rich, so consider the effects of limited access on society.

-conflict of interest

"avoid financial arrangements that influence patient care", inform patients of conflict of interest (stock, financial incentives etc...)

-Liability

courts will probably analyze injury claims for neuroenhancement similarly as they do other cosmetic procedures - courts may or may not be more aggressive

case: Zalazar v Vercimack - expert witness testimony is not needed to prove causation for cases involving informed consent elective medical procedures because "there is no medical issue that requires explanation for the jury".

refrain from guaranteeing an outcome



The following are a couple of selected key practice guidelines put forth by the AAN

1. prescriptions of meds for "neuroenhancement" are not legally obligatory, not prohibited and legally permissible in the US

2. prescriptions of meds for "neuroenhancment" are not ethically obligatory or prohibited and therefore are permissible

3. there is limited evidence of efficacy and safety info for these agents

4. liability is uncertain and may favor the plaintiff

5. refusal to prescribe is both ethically and legally permissible

6. informed consent applies for the prescription of "neuroenhancing" meds

7. ending prescriptions for "neuroenhancement" after they have been initiated is both legally and ethically permissible


Reference:

Larriviere D, Williams M, Rizzo M, Bonnie R. "Responding to requests from adult patients for neuroenhancments, Guidance of the Ethics, Law and Humanities Committee" 2009. American Academy of Neurology. www.neurology.org

4.01.2011

The macula speaks softly but carries a big stick.

In the OR today I saw a vitrectomy- the removal of the vitreous fluid from the posterior chamber of the eye, a surgical treatment for retinal detachment. As I observed this surgery and saw the macula live and very clearly for the first time something hit me (not a scalpel). It is surprising how humble a structure the macula is, especially considering how powerful it is. It is a square centimeter or so (no bigger than your pinky nail) but it receives all the light from the world that will eventually be processed into "sight". Without the macula one is essentially blind (peripheral vision will be spared, but try crossing the street using only your peripheral vision). It is really so small and so simple appearing, at least grossly, it almost looks indistinguishable any square centimeter of tissue, but it is oh so much more talented! As I was looking at this through the ophthalmologist lens, I found it amazing to consider that this little bit of mild mannered tissue catches light! Not only that it transforms it into a patterned electrical signal. How marvelous! This little bit, this tiny tiny bit of tissue can even sort wavelengths of light, weigh and average the intensity of the inputs and send it off in a ordered pattern that will eventually be critical for survival. Think about what that means in the most basic sense, electromagnetic fields can be sensed by carbon based tissues. How gorgeous! Even more so to consider that this little piece tissue came about organically, spontaneously. It is fun to speculate how this came about, why should sensing light matter to ocean life (where photoreceptors have been presumed to originate)? Theories abound, but the truth remains unknown. So it is that a structure appearing so small to the naked eye makes it possible to view the ends of the cosmos. There is lesson in there somewhere...

ophtho notes last day

glaucoma (cannot be prevented, but goal is to prevent losing eyesight within their lifetime)


epi

2nd most common cause of blindness in world (cataract #1)

asymptomatic!! like htn

glaucoma - no longer just increased intraocular pressure, need nerve damage now for definition



look for donut hole in optic nerve


sensitivity of IOP w/pressure of >21mmHg is 50%!!!!


narrow angle

pressure lowering drug - acetazolamide, timolol

laser iridotomy - putting a hole in the iris to assist in aqueous flow


open angle treatment

-prostaglandins, beta blocker, alpha agonist.

-drainage shunts can be placed

exfoliative glaucoma is when the iris sheds cells and pigment (during pupillary constriction/dilation) and blockes aqueous outflow.



family history

sibling odds ration 3.7

parents odds ratio 2.2


nasal field defect can clue you in to glaucoma because very rare to find neurological cause of nasal field defect