9.30.2010

ob/gyn seminar

ob/gyn notes


angiongenesis


mural cells- specialized cells that surround blood vessels

-pericytes, smooth muscle


angiogenic factors

vegf's, notch ligands


wet macular degeneration caused by hypoxia and vessel overgrowth that clouds vision - using antiVEGF is good treatment, also used for diabetic retinopathy


vegf family tyrosine kinase receptor expressed on blood and lymphatic vessels


notch - regulates sprouting angiogenesis, ligand is tethered to another cell membrane (jagged, delta like),

all vegf receptors regulated by notch


notch4 and delta ligand 4, - important for determining whats an artery and vein, delta ligand for is strongly expressed in tip cells the beginning of angiogenesis

notch blocks sprout initiation, keeps a stalk a stalk and tip cell is notch off, ^notch ligand

notch downregu vegfr2 and upreg vegfr1 (inhibitory), tip cells vegfr2 increased expression to increases ligand expression and decreases notch expression


vegf induces delta ligand 4, turns on ligand stimulates notch in neigboring cell.


macrophages can be a source of VEGF and can guide angiogenesis


avasatin - vegf inhibitor approved for some cancers (colon 6-9months longer life than chemo alone, breast very good in shrinking size but doesn't increase survival time etc)


avastin side effects

gi perf ~10% of patients (thought that regeneration of gut depends on angiogenesis)

htn crises

chf

nephrotic syndrome


dii4 blocking antibodies lead to paradoxical hypersprouting but lumens are collapsed so blood cant flow



Pregnancy

2000-2030 incidence expected to double

nyc 530k have it

265k don't know it

1/2 hispanic children will get diabetes


ethnicity - non hispanic whites type1

asians/hispanics type ii predominance


obesity major risk factor, ^portions, sedentary lifestyle


type I 10%

tyep II 90%

gestational carb intolerance (gestation diabetes 2-8%)

secondary diabetes - from injury to pancreas, steroid induced


symptoms - polyuria, phagia, dipsia


blood sugar >200 anytime is diabetic

fast >126 diabetic

100>126 suspect


screen - )GTT

75gm two hour test - 110-126F

140-199 PP = impaired


in pregnancy

OCT - 50gms (don't need fasting) - 1 hour 130-140 abnormal just postive screen

done 24-28wks, high risk pt done at first visit at city hospitals


high risk patient

asian/hispanic, hx of macrosomia, stillbirth, fam hx, obese, glucosuria


if OCT+?

3 hour OGTT

fasting 100gm 1,2,3 hour tests

at least 2/4 have to be abnormal

95 fasting

180 1 hour

155 2nd hour

140 3rd hour



HAPO hyperglycemia and adverse pregnancy outcomes big study

75gm OGTT @ 28wks any of the following lead to adverse outcomes

F=92

1hr 180

2hr 153


capillary blood glucose is unreliable, glycosylated hemoglobin not used


White Classification 1949

A gestational in pregnancy, A1normal fasting high Postprandial, A2 elevated need treatment

B onset >20 yrs duration <10yrs

C- onset 10-20 duration 10-19yrs

D - onset <10>20yrs benign retinopathy

F - nephropathy >500mg 25 hrs

R - proliferative retinopathy

H - ASHD(athersclerotic heart disease)

T-prior renal transplant


Pregnancy - diabetogenic state, insulin resistance and hyperinsulinemia

contrainsulin hormones - HPL, prolactin, progesterone, cortisol - increase gluconeogenesis, come from placenta. ~24 wks when placenta big enough to make hormones on its own why test is done then


throwing up - ketoacidosis, increased insulin, hypoglycemia


PMR perinatal mortality rate (used to compare health of populations)= IUFD +NND neonatal death = 1-3% in general pop

3-5% in diabetes

congential anomalies in diabetes, TGA, VSD, CoA, PDA, ASK, TOF

caudal regression - extremely rare, low low survival

CNS- spina bifida

risk incresed 252fold


Pathophys

hyperglycemia - free radicals, reduces arachidonic acid, ketone bodies, shifts Oxyhb curve, somatomedin inhibiting factors,

yolk sac may be primary targe site (4-6 weeks gestation).

preeclampsia common in diabetics

polyhydramnios - baby is polyuric (just like adult, osmotic diuresis), another explanation is baby is big has big placenta and more fluid coming across

poly associated w/poorly controlled diabetes, control diabetes the fluid level can resolve


fetal demise - seen in both kinds of diabetes, big babies susceptible to fetal demise, mediated by fetal hypoxia


macrosomia - hard to deliver (shoulder dystocia), trunkal obesity, hyperinsulinemia causes IGF-1 big baby


neonatal complications

-resp distress syndrom

-hypoglycemia - when deliver diabetic do a heel stick and check sugar

-hypocalcemia - transport of calcium across cell membrane, mechanism unknown look for tetany

- hyperbilirubinemia due to hemolysis (earlier and more intense)

- polycythemia


A1c should be<6.5

fasting should be <95

2hr pp <120


monitoring -

glucometer

lab checks, bad because longer tube sits RBCs each sugar in tube,

glycosylated hemoglobin - very reliable

rbc life is 3months (half life is 6 weeks)

diet - 25-35kcal/kg

early dinner, ^fiber, no concentrate sugars, ^complex carbs, soluble fiber lowers lipids, keeps blood sugar steady

aim for glycemic index of 50%,

physical activity - walking is the safest activity, 15-30min 3x week, stair climbing is good

insulin treatment in pregnancy

NPH longer acting

R-regular short acting

0.7-0.9 units/kg, begin at half dose

newer one - lispro -very good because acts immediately

oral agents - not approved for pregnancy although used in clinics

glyburide - RCT on glyburide for GDM, used off label, starting in 3rd trimester, doesn't cross placenta

now initial agent, can be used in 1st trimester, no reports of teratogenesis

Metformin - used to treat PCOS and began to ovulate, less neonatal hypoglycemia, 1/2 need insulin as well, more preterms, FDA/ACOG not endorsed.


renal function -24hr urin, CrCl, protein, BP, retinal function, EKG

nodular glomerulosclerosis - kimmelsteil-wilson lesion (glycosylated protein), microalbuminuria

diabetes leading cause of dialysis/blindness


fetal surveillance

crown rump length, anomly scan/efw 3rd

msafp w/quad screen

fetal echo for pregestational diabetics

3rd tri nst and bpp because diabetes big cause of late term death (38-39 wks)


delivery timing and mode

deliver >38 wks if can

check L/S and PG if <38wks

may deliver earlier if big baby,

ripen cervix to avoid failed inductions

NPO no insulin that morning

IV fluids D5RL,10 u insulin

if active labor wont need insulin because muscle using it

SSI postparum, 6 weeks to go down pregestation levels

do a GTT if + residual diabetes, 50% will eventually get diabetes in 20yrs

IUDs in diabetics have higher risk of infection (intrauterine)

long term - GDM doesn't ^nephropathy, retinopathy, baby has increased risk of diabetes, ADHD, learning disabilities,

ob/gyn roles on...

can give methotrexate for terminating pregnancy for b-HCG levels upto 10,000-
but you CANNOT give methotrexate if-
baby has heartbeat
mom has severe pain
baby is >3cm

vulvar pain differential will mostly likely be
folliculitis
vulvovaginitis
bartholin's cyst

treatment for recurrent bartholin's
1. salt water bath
2. glandectomy
3. marsupialization (sewing it open)

do not use KY jelly for exam lubricant in an REI clinic because its spermicidal

getting an accutane prescription in NYS requires a pledge that you will not become pregnant or evidence you are on OCP

episiotomies - two types (midline and mediolateral)
mediolateral - worse healing more nerve damage
midline - faster better healing
LATEST ACOG GUIDELINES INDICATE EPISIOTOMIES ARE NOT HELPFUL, DO NOT CUT THEM.

Retained placenta - >30minutes and placenta has not delivered.
problem- could bleed to death
how to get it out?
-manual
-DnC

transfusion - 1 unit of pRBC increases Hct3points, Hgb1point

How to put in an IUD
obtain consent
insert speculum visualize cervix/os
clean w/betadyne
grasp cervix w/tenaculum
sound uterus (figure out how deep)
cock the IUD and put it in gently
cuts strings and foxswabs for any bleeding

>35 years old and metro/menorrhagia = endometrial biopsy

Hypertensive emergency in the OR?
1. labetalol push 20mg wait 10min, still high? 20mg push wait 10min still high?, 40mg wait 10min still high?, 40mg wait 10 still high?, 80mg push wait 10min still high?

2. hydralazine 5mg wait 5min, still high? 5mg wait 5min still high? 10mg, wait 5min still high? 20mg wait 5min still high?

3. call ICU need drip w/Ca channel blocker


1:370 is the risk for fetal loss during amniocentesis so when the risk of down's becomes greater than 1:370 amnio is indicated otherwise risk of loss of fetus supercedes

advice on marriage from patient
1. never take each other for granted
2. no sundown on anger
3. take care of yourself (keep looking good/attractive)



9.09.2010

OB/Gyn clinical notes

Pap smear starts @ 21 or new onset intercourse
Abnormal pap, LEEP- surgery for dysplastic cervix, increased risk for prematurity on successive pregnancy, cervical shortening.

gonorrhea, chlamydia - test with urine

>30 years old? Pap + HPV is very sensitive (can rule you out), if -/- don't repeat for 3 yrs

vaginal pH - low, blood, semen, rupture of membrane increases pH


three major infections in GU
yeast - cottage cheese, no change in pH
trichomoniasis -erythema, greenish yellow frothy, increases pH
bacterial vaginosis - grey spilled milk, increases pH
-whiff test - KOH tx and smells bad, or have sex without condom and alkaline sperm create bad smell, clue cells

bacterial vaginosis, trichomonas treated with metronidazole

"chandelier sign" - moving the cervix causes great pain, sing of peritoneal tenderness

acute cystitis - UTI
chronic cystitis (interstitial) disease of lining of bladder, chronic UTI w/neg culture, avoid acidic, citric, spice, tylenol

fetal heart rate monitoring
keep track of
1. rate
2. variability
3. accels/decels
4. uterine contractions

reactive heart rate should accelerate to
<32>10 bpm for 10 seconds x2 within 20 minutes
>32 weeks gestation? fhr accelerate>15 bpm for 10 seconds x2 within 20 minutes
late decelerations happen after uterine contraction, very bad, sign of fetal hypoxia, possible uteroplacental insufficiency

4 questions to ask every antepartum mother every morning?
1. any contractions/cramping?
2. any vaginal bleeding?
3. any fluid leakage? water break?
4. any fetal movments?

actinomyces is associated with IUD's, treatment is penicillin


Endometrial Cancer
US 40,000 cases annually, 4-5,000 deaths
typical clinical presentation is post-menopausal bleeding

risk factors
obesity - adipose contains aromatase (converts estrogen)
nulliparity
smoking is protective because nicotine by products induce clearance of estrogen, ^ binding
globulin
tamoxifen
HNPCC - hereditary nonpolyposis colorectal cancer - in young presentations

atypical hyperplasia - 30% go on to develop cancer

Diagnostics
Ultrasound - $1,800 good negative predictive value
Biopsy - $100's, 80-90% sens/spec
D&C better but con is surgery

Woman >35yrs w/menorrhagia? Sample.

Prognosis - Grade very important, higher grade lower prognosis, more than stage

Stage
Ia <1/2cm>
Ib >1/2cm invasion into myometrium
II stromal invasion
IIIa - serosa/tube/adnexal
b - vagina
c - nodes (pelvic, periaortic)
IV a bladder/rectal mucosa
b Distant

Treatment
surgery (uterus, nodes, bilateral salpingoopherectomy)
low risk? no further tx
intermediate risk? radiation (pelvic vs intracavitary brachytherapy)
high risk? chemo + radiation


Anesthesia in Labor-

somatic vs visceral pain

visceral pain - hard to localize, first stage of labor, well treated w/opioids
somatic pain - stage two in labor,

9.07.2010

more neuro clinical notes

Use SPECT to follow brain pathology

Choline uptake is increased in demyelination

Lactate is increased in stroke

NAA (n-acetylaspartic acid) increased in tumor becuase marker of cell turnover


Sinemet side effect is psychosis, dont stop suddenly because can cause NMS

avoid giving Sinemet with large protein meals (take an hour before or after a meal).


Parkinson 4 multisystem atrophy syndromes

1. nigrostriatal degeneration

2. olivopontocerebellar atrophy

3. Shy-Drager = parkinson's + dysautonomia

4. Parkinson's + LMN atrophy

all four have intracytoplasmic overlap, dont respond to Sinemet


Rounds:

localization related epilepsy is 2/2 trauma, creates a seizure nidus but can be controlled with meds.


EtOH withdrawal seizures are always generalized.

Metallic taste are temporal lobe seizure


Beauty of phenytoin is you can get a quick level, the newer antiepileptic drugs take 3-4 days to get a level.


Tegretol 2x day

Depakote ER can be 1x day


SUDEP - sudden unexplained death in epilepsy patients (very rare), could be as a result of dangerous ictal arrhythmia


sickle cell causes acquired moyamoya disease


What is a potential problem of giving Demerol (meperidine)? metabolized to normoperidine which is epileptogenic and causes seizure in those with renal failure


anterior interosseous nerve - pure motor nerve (makes hand into knuckle ball pose)

posterior interosseous nerve - continuation of radial nerve


peroneal nerve fibers encircle tibial nerve fibers so most external nerve injuries produce peroneal signs


"usual state of health" is not a good term, instead use, "without significant symptoms"


malignant hypertension is diagnosed clinically


penumbra - surrounding the infarct, an area of ischemia, reason for autohypertensing and this ischemic area is what is conserved with tPa treatment,


autoregulation of cerebral blood flow is disturbed in stroke


Endogenous cannabinoid receptor ligand - anandamide (sanskrit for bliss)


A good marker of aphasia to follow in stroke is writing - its the most lagging function of language to recover, so when examining and someone seems all better, have them write


Diffusion weighted imaging

Senstivity 77%

Specificity 90+%

diffuse axonal injury - DAI - usually from head torsion, bad prognosis


Keppra is great because it has no DDI, but it can unmask psychosis

Fat emboli can cause psychosis


Alcohol/tobacco amblyopia - pallor @temporal margins on fundus


Nick sized decreasd sensation on chin in a women? Breast cancer.


SPAF trial - stroke prevention in atrial fibrillation - warfarin outperformed aspirin (aspirin outperformed placebo)


Conus syndrome - UMN syndrome (fecal bladder incontinence only)

Cauda equina - lower motor neurons (compression of cord from mass, central herniated disc, hematoma, inflammation, carcinoma)



Avonex, intramuscular 1x week

Betaseron subq 3x week


Heard in rounds, "placebo is expectation"


Three frontal lobe syndromes

1. lateral convexity - decreased executive functioning,

2. medial frontal - creates abulia

3. orbitofrontal - disinhibited, inappropriate (Phinease Gage)

9.06.2010

Neurology portfolio project on cognitive enhancement

Part I

Jim and Steve are good friends and love to play tennis against one another, probably because they are quite evenly matched. The games are very exciting for them and it helps balance their lives. They are both very competitive and are always trying one-up each other. To this end Jim’s wife purchases a lighter racket for his birthday, and with this new and improved racket Jim can now add a few extra mph on his serve, this edge has noticeable effects on his game and he begins to win more than the average number of matches with Steve. As they are walking back to the locker room one afternoon, Steve remarks about how Jim’s new racket has really helped his game and inquires about it.

At this point, please stop and consider whether you think is it fair for Jim and Steve to continue to play tennis even though Jim has a technical advantage by virtue of his lighter racket. Is it ethical for them to play if the object of the game is to win? Is it ethical for them to play if the object of the game is maximal competition?

Over dinner with his wife, Steve remarks that if he only had a lighter racket he might again be winning his share of matches against Jim. Soon they are on their way to the sporting goods store to buy a lighter racket and Steve’s wife asks why if the point of playing tennis with Jim is to have a fair competition should we have to buy a new racket, why can’t Jim just use the old racket and save us the money? Steve says that Jim will not stop using the new racket because Jim likes the elevated playing the racket provides and will not go back to a heavier racket, so the only answer is for Steve to get the new lighter racket too and level the playing field again. And this is exactly what happens. Now, Jim and Steve are having even closer matches with faster serves, and the competition and excitement has increased to the point where a few people come regularly to watch their games. In fact their most recent match on Friday went for 3 hours and as they were walking back to locker room Steve reflects on how tired the match made him and how they were both missing a lot of points because of their fatigue. The idea dawns on Steve that if he could become more accustomed to playing while being this tired it might give him an advantage against Jim. So for the next month Steve wakes up every morning and runs until he becomes as tired as he did that day on the court and over time he finds that it takes more and more running to make him that tired. The next time Jim and Steve play the match goes for 2.5 hours and it is very exciting, but it is clear to Jim, Steve and the ever growing number of spectators that Steve was not as tired during that match and even more, Steve appeared faster on his feet and these abilities allowed him to very clearly appear as the dominant tennis player. As they are walking back to the locker room Jim remarks about Steve’s superior speed and stamina.

Do you think Steve’s early morning running is fair? Does Steve have an ethical duty to disclose to Jim about how his early morning running is helping his tennis game? Is it just for Steve to maintain this advantage if Jim is unaware about the physiological benefits of running?

Because they are such good friends, Steve tells Jim his about how his early morning running is enhancing his speed and stamina. At home, Jim realizes that if he is ever going to be competitive with Steve again he too will have to make early morning running a regular habit. Well, Jim is very competitive so he decides to run, and he runs until he is extremely tired. In fact Jim’s runs starts earlier and finish later than Steve’s. While having dinner with his son, the medical student, Jim complains about how his muscles are very sore from all this running. His son remarks that if he eats more protein his muscles will recuperate faster and he may be able to increase the benefit he receives from all this running. Jim follows the advice of his son and increases the caloric content of his diet, his increased fat and protein intake has a very noticeable effect on both his early morning running and his grocery bill. When Jim and Steve play their match it goes on for 3.5 hours and is very exciting, the level of their play has elevated greatly and many spectators at the tennis club now watch their match. In set 15 of the last game of the match in front of a not insignificant crowd, Jim hits a drop shot and as Steve advances for the return he pulls his calf muscle and fails the return, losing the match to Jim.

Later in the doctor’s office Steve asks his physician why his muscle gave out on him, and after his physician explains this he recommends ibuprofen to help ease his pain with his joints so that he can get back to his early morning running sooner. The physician also makes the recommendation that Steve should be consuming more calories given the extent of his physical activity. Later, when Steve goes to buy some choice beef cuts from Nikolas his favorite butcher in Greek town, Nikolas pulls him aside and says that his ancestors from the home country ate the testicles of the bull to derive its strength and that Steve should too. And so with the reader’s suspension of disbelief, Steve’s oral ingestion of bovine sex steroids undeniably augments his strength and stamina. Later on the tennis court in an unequivocal demonstration of physical superiority Steve enjoys a resounding defeat of Jim, this time in front of local news media coverage.

If most would agree that the increased ingestion of dietary protein by both Jim and Steve to create a competitive advantage is ethical, wouldn’t it also be ethical to consume the bull’s testosterone? If not, what is the difference? If so, then can one argue it is unethical to consume purified or synthetic testosterone for the same reasons? Finally if it is wrong for Steve to eat the bull’s testosterone for a competitive advantage, is it also wrong for him to be taking ibuprofen a synthetic compound designed for the same purpose with a different albeit less potent effect? Why?

Part II

Steve and Jim’s friendly tennis game functions as an instructive metaphor for the relentless competition faced by those alive in the world. At each step in the escalation of their game, one is confronted with ethical considerations concerning the disparity in the relative playing field, whether technological, physiological, or otherwise. For most of us the stakes of competition are much greater than those of friendly tennis matches and so these ethical considerations of competition take on greater significance. Survival is not easy and methods that can confer a competitive advantage inevitably become widespread phenomena. This reality has important ethical implications for the direction of medicine because as medicine slowly unveils the natural world, the field will be faced with continued pressure to do more and more with that understanding. Currently when we use the word “medicine”, we typically mean the capability to reverse, slow, or eliminate disease and restore ourselves to a previous level of health. Health, the goal of “medicine”, derives from the verb, heal, derived from Anglo-German heilen, or to make whole, an interesting insight into the ancestry of this discipline. In the context of medicine the concept of health or whole is informative when we are less than whole, but it does not inform us as to the absolute value of a “whole”. Should medicine only be concerned with making “wholes”, but not defining them? I contend that we in medicine do not have the luxury of that ignorance.

Our understanding of this natural world has progressed such that in our current time medicine has achieved a limited but effective ability to reliably predict and modify certain biological outcomes through applying our collective model of human physiology. In neurology, an increased understanding of nervous function has powerful implications not only for restoring health, but public policy, ethics, and ultimately our progression as a species. In light of the fact that all of modernity has derived from the increased neurocognitive capabilities of Homo sapiens we must turn our attention to advances currently being made in this field and ask ourselves one simple and real question. Is it ethical to take a pill that makes you smarter? It’s a complicated question and the subject of great debate. The issue cannot be ignored in light of data suggesting the pervasive use of psychostimulants. Maher reports that 1/5 of the readership of Nature had used a cognitive enhancing drug at one time. Consider that 350,000 individual prescriptions for modafinil were written in 2003 in the US, a time when the incidence of narcolepsy, its indicated use, was 135,000. Outram’s review indicates that on college campuses stimulant use has consistently hovered around 3-4%.

In expanding on the ethics of using medicine to enhance human cognitive performance I would like to address three issues. First, I would like to define what we mean when we say “smarter” by reviewing the current understanding of neuro-cognitive function. Next I will outline the current and well-established battle lines that frame the debate from an ethical standpoint. Finally I will register my opinion on the ethics of cognitive enhancement in well persons.

Lanni et al divide neurocognitive performance into three primary dimensions: memory, attention, and creativity. They indicate in their review1 that a multitude of distinct molecular pathways govern the magnitude of these functions. Memory is categorized as either implicit or explicit; the former (also called procedural, or non-declarative memory) consists of learned habits, motor functions, and feelings whereas the latter (also called declarative memory) relates to the verbal reconstitution of facts or ideas that can be called into consciousness. Currently, the mechanism by which an explicit memory is encoded into long term memory (a phenomenon called long-term potentiation) involves increased synaptic connectivity and neurotransmission within the neural pathway governing the subjective experience of that memory through plastic changes secondary to gene transcription via NMDA signaling and ultimately CREB modulation. It is thought that these gene products are proteins that help stabilize the synaptic connectivity responsible for a memory and that repetition enhances this effect. Certain compounds that have shown efficacy in enhancing memory formation and recall include acetylcholinesterase inhibitors, AMPAkines, NMDA modulators, adenosine blockade (caffeine), signal transduction enhancers (phosphdiesterase inhibitors), and CREB modulators (still preclinical).

Human attention is normally divided into two functional categories; a tonic overall attention “tone”, and a second “dynamic” attention (selective). There is also an evolving idea of networks of attention, of which three have been named; an alerting network (maintains cognition), an executive network (controls cognitive process and analyses), and an orienting network (directs the executive network/enhances its function). The effort of attention has been described as the interplay of many cortical and subcortical areas, including the lateral prefrontal cortex, anterior cingulate gyrus, and basal forebrain with multiple neurotransmitters, chief among which are cholinergic and catecholaminergic. Since the development of the blockbuster drug methylphenidate in 1944[source], most of the drugs developed have interacted with the catecholaminergic system (norepinephrine and dopamine).

Human creativity remains probably the most elusive cognitive function, but it is no less a capability. Many original theories on creativity relate this function to increased hemispheric asymmetry. Right hemispheric activity has classically been related to increased creativity. It may be that creativity is an epiphenomenon involving the frontal cortical functions of working memory and attention. Some investigations have related increased creativity with increased frontal lobe activity as well decreased left hemisphere inhibition of right hemispheric structures. Aside from hallucinogens, psychotropic drugs, and other dissociative compounds, there has not been much interest in generating compounds that increase creative thinking. In fact Lanni et al comment that many creative thinkers in history have displayed impulsive and disorganized traits, and they hypothesize that modern agents such as methylphenidate and amphetamines may in fact stifle creativity by activating the frontal cortex and reducing the cognitive flexibility associated with creativity.

Part III

Authors such as Schermer, Mehlman, Goodman, and Outram have closely assessed the ethical implications of taking “smart pills”. The subject has also gained attention from the President’s Council on Bioethics, in their 2003 report headed by Leon Kass, Beyond Therapy. In these works, the ethical objections to the use of these drugs are normally divided into the following categories;

1. Issues of risk and safety. Since no drug is without side effects, will adverse effects outweigh benefits?

2. Issues of coercion. If an efficacious agent is identified, will others be forced to follow suit in order to remain competitive? What will become of those who abstain?

3. Issue of distributive justice. Who gets it? What about those without access to “smart pills”, what will become of them?

4. Issues of cheating. If you create a work while cognitively enhanced, does it truly belong to you?

Safety

If there were no side effects from using cognitive enhancing drugs, it would be very difficult to argue against their use. This is obviously not so. For example a stimulant used for the treatment of ADHD, methylphenidate, is also a commonly used study aid among students of all ages. The drug can cause loss of appetite, dry mouth, mood lability and jitteriness. This compound also has high abuse potential. Donepezil, a cholinesterase inhibitor developed to aid the symptoms of Alzheimer’s dementia, has been shown to increase working memory in non-demented controls. Here the trade-off is nausea, vomiting, diarrhea, and insomnia. So in constructing an ethical framework for the judicious use of cognitive enhancing substances what should inform our cost/benefit analysis? Cakic supports the notion that ethical objections to cognitive enhancing substances because they are dangerous hinges completely on the side effect profile. In his review he comments that large proportions of the world’s population safely use caffeine (a widely recognized cognitive enhancer). Yet by virtue of its milder side effect profile there are not the same ethical objections to its use. What about those compounds with side effects? Arguably a well person taking a drug for a non-medical purpose that results in a side effect that makes him unwell cannot be condoned. Really? This notion must be challenged. Why should a regulatory body prohibit an informed citizen form taking risks with his health in pursuit of his own end if that body does not absorb the cost of the associated risk (in the case of an insured patient)? This is exactly what a professional football player does every time he steps on the playing field. Yet when that same player chooses to use anabolic steroids and we question the ethical nature of that decision, we cannot argue against that act from the perspective of safety because the act may be no more or less safe than playing the game in the first place. I believe it is ethical to use compounds with side effect profiles if their use is informed and the cost of the use is not born by the collective.

Coercion

The objection to cognitive enhancement from the standpoint of coercion essentially states, “If one attains a competitive advantage by taking a drug, the other now must take it in order to remain competitive, and therefore the other has been coerced.” In exploring the issue of coercion, Goodman argues that the use of cognitive enhancing drugs would be ethical by distinguishing their use according to the following dimension: Would using cognitive enhancing substances aid outcomes that are zero sum or non-zero sum? For example it could be argued that professional sports are zero sum outcomes because there is only one victor and thus the use of performance enhancing substances are unfair to the competitor not using them, and hence their use is coercive to others. But, Goodman supports enhancement if the activity involved is non-zero sum. As an example of a non-zero sum outcome he cites is a graduate seminar where everyone can contribute, but no outcomes are affected by the actions of the other, and hence an individual cannot be coerced. I do not believe in Goodman’s dichotomy between zero sum and non-zero sum activity as a method of distinguishing the ethical use of cognitively enhancing substances. All activity is zero sum because each decision carries an opportunity cost. If we choose a non-zero sum activity we forego engaging in competitive behavior and have to some degree become less competitive, a strict application of opportunity cost. Furthermore, if one argues that coercive behavior is unethical for zero sum activity, than all adaptive, disruptive innovative behavior is unethical if it forces others to change, whether I’m a caveman who objects to the use tools or an accountant who refuses to use a keyboard for fear of developing carpal tunnel. Arguing against the use of cognitively enhancing substances from the standpoint that it may coerce others is tenuous in that it potentially implicates all competitive activity as unethical.

Distributive Justice

If efficacious cognitive enhancers continue to be developed, the issue of distributive justice becomes germane if only the rich have access to the benefits of the use of these drugs. I believe from a technical standpoint overcoming this ethical objection will prove far easier than other current issues of distributive justice that plague our world; food, water, medicine, education, and freedom. If cognitive enhancement comes about through neuro-modulation using small molecule mediators, providing these compounds on a grand scale is well within the reach of current manufacturing capabilities, whether or not there will be political will for widespread dissemination becomes the crux of the debate. An ethical framework for cognitive enhancement must be inclusive to all members of society, but if creating them is going to necessitate distribution asymmetry, should these drugs be developed in the first place? It is easy to imagine a scenario in which individuals seek to withhold such compounds and their benefits from others for reasons having to do with policy, defense, and state. This issue is not easily resolved, and there is no ethically defensible position of selective distribution, yet we must ask the central question, would we allow our enemies to have them? Policymakers are faced with the challenge of expanding the myriad complicating factors in search of an answer that balances ethical conduct and practical concern.

Issues of Cheating

Goodman explores two examples of chemically enhanced performances; that of baseball star Raphael Palmeiro’s anabolic steroid use, and the Beatles’ use of psychotropic drugs. Goodman argues that the two activities are sufficiently different to warrant separate ethics, consistent with the observed public outrage of Palmeiro’s steroid use when compared to the tacit approval of the presumed increased musical creativity of the Beatles. What explains this differential treatment? Are the accomplishments of the enhanced truly their own depending on the activity? The President’s Council on Bioethics (PCB) argues that for us to arrive at an ethics of enhancement in sports, we need to define what the ethos of the sport is. Traditionally is has been framed as victory, or a reward, as a matter of dessert based on merit. Schermer picks up this point and asks what is it we want to praise about sports? He suggests in contrast to the PCB that the result (winning or losing) does not matter, but what matters in sports is not simply performance but a display of a type of human excellence not currently subject to enhancement and a much harder term to define. Schermer summarizes the current state of surreptitious steroid use in professional sports by positing that as long as their remains external rewards (money, fame…) from playing sports well, cheating behaviors may or may not be ethical but they are rational. He also argues that in enhancement in professional sports, “…causes spectators to miss out on display of natural efforts that gives sports moral meaning.” I agree with Schermer’s summary and would ask anyone who watches sports why they do, is it for the demonstration of human excellence or for the homeruns and KO’s? If it is the former reason, faster times and bigger hits do not increase or decrease the drama of the trial of the human spirit that defines excellence in sports, and likely competing while enhanced against unenhanced opponents decreases this relative human excellence, I would argue it is unethical to use in this way. However, if one watches sports for the latter reason, then it is ethical for the players to take these substances if it increases the pleasure of those spectators who seek these goods. Whether or not it is ethical to lie about taking them is a separate issue.

Schermer also asks a very important question that relates to this notion of human excellence. What is the value of effort? Who is more deserving of credit, a less gifted student who works very hard to earn average marks or a brilliant student who takes a pill and gets the same mark with almost no work? This idea is central to the main critique against cognitive enhancement. If you enhance, you potentially cheat yourself of the value of hard work. What is the value of hard work? Mehlman summarizes this point beautifully by stating that it is not that cognitive enhancing drugs make the activities easier, it is that by virtue of the ease they are less meaningful. Mehlman suggests that if we are threatened by shortcuts, which “smart pills” could easily provide we fail to experience the fulfillment of achievement, an experience critical to ego function and maintenance of willed and intended action. This lack of ego driven function may alter the experience of improvement resulting from goal directed behavior to a phenomenon that happens to us. Mehlman asks if we move to this point, will our achievements be our own? Goodman comments on this notion of “achievements happening to us” and by stating that our current notion of goal directed achievement is a cultural entity and that many artists, innovators, scientists, and leaders in previous cultures attributed their accomplishments to forces not their own. Johann Sebastian Bach commonly signed his finished compositions, SDG, standing for soli Deo gloria, “the glory of God alone” stating his belief that all achievement came from God regardless of whatever pills, balms, foods, spells or muses were used to aid in the creation. If Bach were alive today would he inform us that we are misattributing our accomplishments to ourselves apriori?

Conclusion

Debating the ethics of the use of cognitive enhancing substances has great relevance to the field of neurology because likely any advances will come from the investigators in this specialty. I believe that if we are to create an ethical framework for dealing with these compounds we must more fully explore the aforementioned issues surrounding safety, coercion, and justice. However, I agree with Goodman, that the central issue regarding the ethics of these drugs will rest in defining what is the value of an accomplishment and what is the value in the process of accomplishing. We must seek to understand what is the value of “hard work”. My chemistry professor emphasized on the very first day of lecture, “If you learn only one thing in this class, please let it be that the universe does not permit free lunches.” I believe this statement of cosmic accounting can be applied broadly; these compounds are not inherently good or bad but in their use. There is some inherent meaning to struggle and hard work that the use of “smart pills” threatens to compromise. We must recognize that their use should not allow us an “easier” path. If their use threatens the integrity of the human struggle by creating the illusion of doing more with less, or getting something for nothing, we have foolishly deceived ourselves, and we will bear the cost of that folly. However, if we recognize that while these drugs may alter our neuro-cognitive functioning they necessarily cannot leverage the value of human struggle, then by holding true to this ethic and with proper humility we may yet more ably pioneer uncharted territories.

References

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