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Tuesday, November 29, 2005

Realities of a Educational Loans

Are you planning to take an Educational Loan. Please read this before you do so.
This is what applies the Medical field
But the worst off would be medical students. Given that they earn paltry sums until they complete their MDs, it makes sense to take a loan only if your dad owns a nursing home or is willing to shoulder your EMI burden for several years to come!

Little correction. They earn paltry even AFTER MD. Hope you know that the payment for MD graduates which Tamil Nadu Goverment now offers is Rs 10000. (Rs 8000 for MBBS and Rs 9000 for Diploma)

TNPSC 2005 - FAQ

1) For a candidate getting appointment in Service this time, will he be able to write TNPGMEE this time.
YES. There is no problem. It is your choice
2) What will be the first month salary for one who joins the forthcoming service. Whether Rs.8000 or Rs.13,500
The basic is 8000. With this you have DA and other allowances which will come around 14000. The exact amount will vary depending on the HRA and other minor differences from area to area
3) How much will it increase in one year (Increment)
The Increment for Basic is Rs 275. So you will get about Rs 400 to 450 rise per year
4) Period after which one is eligible to write Tamilnadu entrance. Whether 2 or 3 years
Please see See below "landmark judgments on that site
5) How much will be the stipend for a Service PG for master degree. (MD/MS)
Pay and DA. That will come around Rs 13000 by the time you are eligible for
6) How much will he be paid after finishing PG while in service
You will complete PG probably in 2012. By that time, you are eligible for 6 regular increments. One increment for is added for PG. So totally you have 7 increments. Now, your increment per year is about Rs 400. So that will come around Rs 3000. You will be getting Rs 17000 if you finish PG and Rs 16400 if you have not finished.

In addition your take home pay will be less by Some 2000 to 3000 (depends on how much you pay for Insurance, PF and Tax)


For more FAQs, please see

1. If I take a pg seat in tamil nadu in All India counselling, and not joining in the college, instead joining in service, what will happen? Please explain with regard to remaining fees, rules for writing the exam again and about TN exam

If you take a seat and DO NOT JOIN, then there is NO PROBLEM
If you join and leave, then that is called as DISCONTINUING the course

The candidates (including the candidates selected under the All India Quota) who discontinue the course on or before 25-5-2006 shall pay the sum as specified below by way of Demand Draft taken in favour of the Secretary, Selection Committee, Kilpauk, Chennai –10 payable at Chennai to the Deans of the respective Colleges.
  • For P.G. Diploma Courses Rs.20,000/-
  • For P.G. Degree / Five Year M.Ch. (Neuro-Surgery) Courses Rs.30,000/-
  • For MDS Course Rs.30,000/-

The Candidates (including the candidates selected under All India Quota) who discontinue the course on or after 25-5-2006 shall pay to the Deans of the respective Colleges the sum as specified below by way of Demand Draft taken in favour of the Secretary, Selection Committee, Kilpauk, Chennai- 10 payable at Chennai.
  • For P.G. Diploma Courses Rs.30,000/-
  • For P.G. Degree / Five Year M.Ch. (Neuro- Surgery) Courses Rs.60,000/-
  • For MDS Course Rs.60,000/-

The candidates who have joined Post Graduate Degree / Diploma / 5 years M.Ch Neuro-Surgery / MDS courses in any discipline and discontinued the courses on any grounds and if the discontinuance has resulted in a seat being wasted, they are eligible to apply only after a period of 2 years from the date of discontinuance of the course. If the candidate’s discontinuance does not result in a seat being wasted, he can apply for the next selection for which he/she is eligible.

2. After how many years can the batch which is going to be recruited, write the tamil nadu pg? Your batch Balamurugan sir said it is 2 yrs. Is it true?

Please see See below "Landmark judgments" on that site

3. What will be the probable date of result for service exam?

April 2nd week

4. What will be the probable date of counselling for service ? Will there be atleast one week between result and counselling?

May 2nd Week (depends upon the election)

5. I heard that the DA is increased from 50% to 70%. So my friends are telling that the starting pay will be aroung Rs.16,000. Is it true?

Close to that

Monday, November 21, 2005

A piece of advice for aspirants of TNPG

Please don't "over think" in Tamil Nadu PG........
Tamil Nadu PG (as well as TNPSC) Questions are from the same question bank that is followed for the MCQ Part of your theory exams by MGR Medical University. Eventually the level of the questions will be from I MBBS to III MBBS.

It is this reason why you have question like "Hypokalemia is " and the "nerve injured in Fracture Neck of Humerus is " Though these questions are cakewalk for you, they are apt question for the I MBBS Students.....

It is for the same reason that you get questions like a wave in JVP and Rowsing's sign (Final MBBS)

The most unfortunate aspect of this question bank is that of late they have introduced MCQs in MD and MS Exams also.... some times question from that Question Bank (PG level ) enter into the TNPG or TNPSC question paper and every one (except those with a diploma in that speciality) is in for trouble

So the best way is to Read the question carefully and clearly.... think once.... think once only (and if you don’t know, skip the question and proceed to the next) and mark the answer

Using your logic and abstract thinking where it is not warranted will land you in trouble

All the best

Wednesday, November 16, 2005

Hallucinations... Please don't be under an Illusion !!!!

Question from AIPG(All India PG) 2003 and the related discussion

105. All of the following are features of hallucinations, except:

1.It is independent of the will of the observer.
2.Sensory organs are not involved.
3.It is a vivid as that in a true sense perception.
4. It occurs in the absence of perceptual stimulus.

Ans. 2
Sensory ORGANS are NOT involved in Hallucination... Only SENSATIONS are involved.......... and only those hallucinations occuring in Delirium Tremens are as vivid as in true perception

Hence the answer can be only 3


my dear bruno its the choice 4 which is true in this regard AS THERE IS ALWAYS A FALSE SENSORY PERCEPTION IN HALLUCINATION

When You see scooter and think it as a Truck it is Illusion..............
Only when u see a truck WITHOUT there being a Scooter.. It is hallucination

Only when you hear drums without there being a bells is Hallucination

Coming to text book example

When you see a snake when there is a rope, it is Illusion
When you see a snake without there being a snake it is hallucination


Sad When u see ur roll number against Rank one in the merit list of all india
entrance, Wink Is It illusion Twisted Evil or hallucination Wink

I think...then, Wink its time to wake up!! Idea

When you get some rank.............. your roll number is in the result....... but you see it as rank 1...... it is Illusion

If you see your number as rank 1 even without writing the exam..... it is Hallucination

If it is time to wake up, it is hypnopompic !!
If it is time to go to sleep, it is hypnogogic !!

IN this question we have to SPOT A WRONG STATEMENT. Lets consider each options one by one.
1. This is a TRUE statement as hallucination are independent of observers will, basic part of defination.

2. This is a FALSE statement,SENSORY ORGANS ARE INVOLVED,not structurally but in functionaly(Ref Kaplan and Saddock's Comprehensive Text-book of Psychiatry,pg-810)Hallucination is a false SENSORY perception even in abscence of any perceptual stimulus.Had the sensory organ not been involved we couldnot have been able to type them in to auditory, visual , tactile and etc. types.NOTE THAT THE SENSORY ORGANS ARE NOT STRUCTUALLY INVOLVED BUT THEY ARE DEFINATELY INVOLVED IN A FUNCTIONAL MANNER.
Say for example, for an hallucination to be AUDITORY, observer must be aware that EARS are involved in hearing (true or imaginary), and when person tells that he/she can hear voices in EAR even in absence of any real voice, we term it as AUDITORY hallucination.So for hallucination to be auditory the person must hear them in his/her EARS. so only functional involvement and not structural.
Any perceptions that occur without involvement of sensations are termed as Extra-Sensorial Perceptions(ESP).

3.This is a TRUE statement as they can be vivd as true sense perception.For example person having auditory hallucination can tell very minute details with full description of what he seems to hear from voice, which is comparable to true sense perception.

4. This is a TRUE staement as they occur in abscence of any perceptual stimulus, a basic part of defination.

SO it is obvious that only 2 is a false statement. Hence 2 should be the answer.

quoting the prevoius post ..........they can be vivd as true sense perception.For example person having auditory hallucination can tell very minute details with full description of what he seems to hear from voice, which is comparable to true sense perception.

Thats the problem... only certain hallucinations are as vivid as in true perception........

And sensory organs are involved functionally....... that means the sensations are involved in the absence of a stimulus.......... this definiton of sensory organs is for Illusion where there is a stimulus and sensory organs are involved

Sir,what you want to tell is actually a part of EXTRA SENSORIAL PERCEPTION . If sensory organs are not involved,DO YOU MEAN TO SAY THAT A BLIND PERSON CAN ALSO EXPERIENCE VISUAL HALLUCINATIONS??
I dont agree with you, as you can get it confirmed from any of the psychiatrist close to you.

You can have hallucinations with your eyes closed........... but it is the illusion which needs your eyes............... Sensory organs are not needed for hallucination... only SENSATIONS are involved........... Just tell me whether you understand the difference between sensory organs and sensations or according to you both are same

Sir, there is no meaning of perception of sensations without any sensory organs, even though both dont mean to be same.
And a person can experience a VISUAL hallucination with CLOSED eyes,but NOT if the person is BLIND(congenital or acquired), which clearly indicates that sensory organs(here eyes in visual hallucinations) are involved in perception of hallucination(a false perception)in a functional manner of perception (EITHER TRUE OR FALSE)only without any structural or physiological changes.
THIS is a very clear fact to undrstand.Is not it??

I agree and understand that Visual cortex is involved in hallucination............ Thats clear to me.... but i am not understanding that eyes are involved............

Or let me ask you a question....... are impulses transmitted in optic nerve when a person is experiencing visual hallucination ?

Impulses are transmitted during illusion.... for example the eye sees and the optic nerve transmits a image of rope... and the brain interprets it as snake ......

Sir, I understand that there is no transmission of impulses through optic nerve(suggesting that no physiological changes occurs in reality)in visual hallucination.
But EYES(IN VISUAL HALLUCINATION) ARE INVOLVED FUNCTIONALLY FOR THE PERCEPTION OF HALLUCINATION.AND SINCE HALLUCINATION IS A FALSE PERCEPTION THERE OCCURS NO ASSOCIATED REAL PHYSIOLOGICAL CHANGES IN EYES.And as I had already mentioned in my previous post that a blind cannot perceive visual hallucination, suggesting eyes are involed merely for the function of perception, either true(where physiological changes do occur as in illusion)or false(as in hallucination where no actual physiological changes occurs).
The point lies in the fact that eyes (or any other sensory organ) are required by the observer for perception of visual(or any other sensory type) sensory organs are involved for functional perception without any true physiological changes in the sensory organs.

I hope this is the best possible way to explain the fact

Dear Dr. Bruno,

The hallucination examples are really great....

I enjoyed them a lot.


Sir, I understand that there is no transmission of impulses through optic nerve(suggesting that no physiological changes occurs in reality)in visual hallucination. Thats why we say that eyes are not involved........ visual cortex alone is involed in optic illusion..........



And as I had already mentioned in my previous post that a blind cannot perceive visual hallucination, Which book says so ?? Rolling Eyes May be persons who are congenitally blind may not experience visual hallucinations because thier cortex is not developed suggesting eyes are involed merely for the function of perception, either true(where physiological changes do occur as in illusion) Correct
or false(as in hallucination where no actual physiological changes occurs). No dear......... in this case eyes are not involved.... the cortex perceives images without there being a signal from eyes

The point lies in the fact that eyes (or any other sensory organ) are required by the observer for perception of visual(or any other sensory type) hallucination. No not needed, Hallucinations are the sensations which the observer perceives without the sense organs so sensory organs are involved organs are not involved.. the corresponding regions in the brain are involved for functional perception without any true physiological changes in the sensory organs. correct How are eyes involved without there being a physiological change........ obviously you know the fact.......but you are still confused between the difference between eyes and vision.......

I hope this is the best possible way to explain the fact Me too

Hi Bruno,
Is VISUAL CORTEX in Brain a sensory organ or not Question

Visual Cortex in Brain is not a sense organ...........................

In fact one book quotes brain as "senseless" because it has no sensory receptors....... and so we never experience pain when brian is handled

But another book says that brain is not "absolutely senseless" as Retina is said to an extension of brain..............

But Visual Cortex or for that matter any cortex is not a sense organ

Hi again,

If u r saying in HALLUCINATIONS sensory organ involvement is not there,then tell me WHY DO STRUCTURAL DISEASES OF SOME SENSORY ORGANS & CONDUCTING MECHANISM CONTRIBUTE TO THE FORMATION OF HALLUCINATIONS,eg. otitis media often may be associated with tinnitus or an irritative lesion of the visual cortex may produce hallucinoses or temporal lobe damage may show as auditory hallucinations. ALSO, HOW CAN A COCAINE ADDICT ABLE TO LOCALISE THE COCAINE BUGS OR TACTILE HALLUCINATIONS OEVR HIS BODY Question

Do reply back.

Otitis Media / Meniers with Tinnitus... This is not hallucination... In this case, there is transmission of some signals through the nerves!!!!!!! and the brain interprets this as sound and the SENSE ORGAN IS INVOLVED........Only if there is a tinnitus with NO ear pathology (or physiology), it is hallucination

Cocaine bugs...... the patient is able to localise, and there are no bugs........... Again there sense receptors in skin are normal.... there is no transmission in the peripheral nerves........ but the brain assumes that there is a sensory impulse from skin............. This is exactly the definition of hallucination........ Perception without stimulus..... and the perception can be localised too ....... you can see a lion on your right side or you can see a zebra on your left side, just one feet in front of you or 100 feet away when there is nothing in front

Go back to the previous examples

When You see scooter and think it as a Truck it is Illusion..............
Only when u see a truck WITHOUT there being a Scooter.. It is hallucination

Only when you hear drums without there being a bells is Hallucination

Coming to text book example

When you see a snake when there is a rope, it is Illusion
When you see a snake without there being a snake it is hallucination

Also seeing rank 1 against ur name without writing the exam is called as dreaming or extra sensory perception AND NOT HALLUCINATION. WAKE UP MATE.

It is given in all pharmacological books , No changes occurs in the cases I quoted.... If there is a change in the receptors and when the receptors are involved, we call them as Illusion!!!!

You are still confusing between Hallucination and Illusion !!!!

Can you give your definition of ILLUSION


Tinnitus is a sensation of noise caused by abnormal excitation of auditory apparatus, or its afferent pathways or the cortical area.

Tinnitus from Stedman

Tinnitus Aurium :
Sensation of sound in one or both ears associated with disease in the middle ear, inner ear or the central auditory apparatus

Tinnitus Cerebri :
Subjective sensation of noise in head rather than in ears

Only the latter type comes under hallucination........ and as Stedman says( not me ,Stedman) "heard in head" without involvement of ears.......... This is a typical Hallucination...... Appreciation of a sense without the involvemnt of the sense organ..........

When we appreciate something with the involvement of the sense organs, but there is misperception, we use the terminology ILLUSION

Do TINNITUS CEREBRI & TINNITUS AURIUM differ qualitatively ??? I mean to say whether a pt. can differentiate b/w. the two qualitatively ???

A patient cannot differentiate between the yellow discolouration caused due to hemolysis and the yellow discolouration due to Ca Pancreas !!!!

I just wanna know whether the two types of sensations (regarding tinnitus aurium & cerebri) different ? This is in context to the choice no.3 of the AIPGE question.

he question in AIPG 2003 doesnot ask whether the two sensations are different or not..........

The question was to find the wrong statement regarding hallucinations

The choice 2 given was "Sensory Organs are not involved"

But the fact is that in Hallucinations sensory organs are not involved and sensory organs are involved only in illusion

So Choice 2 is correct and we all know that choice 1 and 4 are also correct.... Hence the answer is Choice 3 which is wrong

Hi Bruno, Smile

I agree with u in all the points. Infact there was never any doubt in my mind about illusion,hallucination,delusion & dreaming (AIPGE rank 1 example). Smile
But the problem here is that even choice 3 is correct because as u urself indicated that true sensory perceptions & hallucinations cannot be differentiated clinically, implying that HALLUCINATIONS ARE AS VIVID AS TRUE SENSE PERCEPTIONS ( eg., as in the case of tinnitus cerebri & tinnitus aurium where qualitatively both of them could not be differentiated neither by the pt. nor the clinician ). No Doubt that it isn't true all the times but happens most of the times

Text books say that of all hallucinations, only the hallucinations occuring in alcoholics are as clear as in normal perceptions..... Others are not as clear !!!!!!!!!!!!

So that point is not true for all hallucinations in general

Hi mate !
Infact all the conditions under ORGANIC HALLUCINOSIS are as vivid, complex & well organised as in true sense perception.
The causes include : Hallucinogenic drugs( LSD, Psilocybin,mescaline,cocaine,cannabis,phencyclidine,so on & so forth...);
Alcohol ; Sensory deprivation ; Release hallucinations ; Migraine ; Epilepsy ; ICSOL ; Temporal arteritis ; Brain stem lesions(Peduncular hallucinosis).
What do u say

Though there is a big list of causes of organic hallucinations, please note that event though there is a big list for the incidence may not be big too........... (like secondary hypertension, for which we again have a big list of conditions like phaeochromocytoma, Cushing, THyroid Storm, Coarctaion etc but the incidence of primary hypertension is still great)

Any how, About the point that all ORAGANIC HALLUCNIATIONS are as clear and as vicid.............Reference Please !!!!!!!!!!!!!

Ahuja says that in Delirium tremens the hallucination are as clear as normal perception

Go thru ORGANIC HALLUCINOSIS in neeraj ahuja.
Also DELIRIUM TREMENS is not as uncommon as Secondary hypertension. Its much more commoner phenomenon.
Moreover its not the question about incidence of organic hallucinations but about whether the particular phenomenon is a part of a syndrome or not.

You might know that Hallucinations can be classified according to

1. Etiology
a. Organic
b. Non-organic/functional

2.Sensation affected
a. Visual
b. Auditory
c. Gustatory
d. Smell
e. Tactile

Types of Hallucination

a. Visual --> only this is as clear and vivid as normal........... This is an exception; not a rule
b. Auditory
c. Gustatory
d. Smell
e. Tactile
a. Visual
b. Auditory
c. Gustatory
d. Smell
e. Tactile

Now you can find that all the conditions listed under your list form a small part...... in fact in Schizo we have auditory hallucinations and in Temporal lobe epilepsy we have hallucinations of smell........ They are not as clear and as vivid as in normal perception

Hallucinations are as vivid and clear as in normal perception.... This is a wrong statement

A type of Hallucination (as an exception) is as vivid and clear as in normal perception... This only is a true statement

Please refer the question in AIPG 2003

Friday, November 11, 2005

About Court Case in Karnataka

PG Aspirants: Fight for our righte - Merit Vs Might: "Post Graduate Aspirants Group: Karnataka State Junior Doctors' Association (KSJDA)

Wednesday, November 9, 2005

Ethical dilemmas.

Ethical dilemmas.

From Journal of Post Graduate Medicine

Pandya SK
Department of Neurosurgery, Seth GS Medical College, Parel, Bombay.

Correspondence Address:
Department of Neurosurgery, Seth GS Medical College, Parel, Bombay.

How to cite this article:
Pandya SK. Ethical dilemmas. J Postgrad Med 1997;43:1-3

How to cite this URL:
Pandya SK. Ethical dilemmas. J Postgrad Med [serial online] 1997 [cited 2005 Nov 9];43:1-3. Available from:;year=1997;volume=43;issue=1;spage=1;epage=3;aulast=Pandya

:: Introduction Top

Dilemma: difficulty, impasse, perplexity, predicament, quandary.
All medical doctors face situations from time to time, where the proper course of action is not clear. We are tempted, then, to paraphase Hamlet: “To do, or not to do - that is the question ...”

Take the case of a patient with confirmed malignant cancer of the breast whose chest x-ray film shows a rounded metastatic deposit. She now presents with a history of a recent focal epileptic fit but without any neurological abnormality on examination. Computerised tomographic scan shows what is most probably a metastasis in the left parietal lobe over the motor strip. Are we justified in advising excision of the tumour, knowing that it might leave her hemiplegic and when her general prognosis as regards long-term survival is grim?
Under such circumstances, how do we arrive at a decision? What do we navigate by?

:: Guiding principles Top

Four fundamental ethical principles have received universal acceptance by medical professionals:
* non-maleficence - ‘primum, non nocere’: first of all, do no harm
* beneficence - whatever we do must be for the benefit of the patient;
* respect for autonomy - the patient has an absolute right to make decisions concerning his own well-being, on any test or therapy proposed for him and on measures for resuscitation, prolonged maintenance on a ventilator and other such events.
In order to make such decisions, the patient - and family - need to be adequately informed on the pros and cons of each step. It is the communication of such details, in a manner that is clearly understood, that forms the basis of informed consent.
Justice as with reference to fair distribution of scarce resources; respect for the rights of the patient and family in the context of the rights of society at large; the use of the least expensive means in investigation and therapy; and respect for morally acceptable laws. It also implies the overcoming of personal prejudices - as against homosexuals or chronic alcoholics.
Thoughtful application of these principles to specific instances often helps resolve dilemmas.

:: Some common ethical dilemmas Top

Let us take examples from either end of the spectrum of life.
The treatment of infertility:
In a country where untold numbers of orphaned or discarded infants and children languish in unfeeling institutions where they are denied the attentions of parents and the company of siblings, is it fair for us to embark on such expensive techniques as in vitro fertilization?
On the other hand we have the plea of the barren wife who is willing to sacrifice almost everything to achieve the status of mother.
Possible resolution of dilemma:
Since it is the mother who comes to the doctor seeking treatment and since she has the right to decide on what should be done to and for her, the position of the orphaned children should not be allowed to intrude on the management of her problem.
Those in favour point to the legal sanction afforded to the termination of the life of the unborn foetus. Some have gone so far as to say that this is a welcome means for controlling our mushrooming population. Others have used it to get rid of female foetuses in their quest for the male child.
Many, however, remain troubled. Is this law morally acceptable? Are we ever justified in snuffing out life?
Possible resolution of dilemma:
This will depend on the beliefs and values cherished by the individual doctor. The doctor who holds life, as a sacred boon granted to an individual must refuse to perform or advice an abortion except in the specific instance where continuation of pregnancy may kill the mother. (Here, the operative principle is that the life of the mother is of greater concern than the life of the unborn foetus.)
Must we always strive to keep every baby alive, irrespective of costs?
Take two examples:
A premature newborn weighing 600 grams. Left to itself, it will perish. We can make extraordinary attempts to help it survive. In the process we may lead to a situation where the family is saddled with a severely handicapped individual with poor mental abilities.
A baby is born with meningomyelocele, paraplegia, incontinence of urine and severe hydrocephalus. A light applied to the head shows brilliant transillumination of the intracranial contents suggesting a paper-thin brain. It is possible to repair the skin over the exposed and damaged spinal cord and insert a shunt to drain the accumulated cerebrospinal fluid into the peritoneum. Survival is now assured but the family will bear the burden of looking after a mindless person who unknowingly passes urine and stools reflexly and will never understand, appreciate or communicate.
Possible resolution of dilemma:
The doctor must place the pros and cons of treatment in either instance before the parents. The doctor sympathetic to the social milieu in which the family exists and of the precarious economic circumstances of a particular family will emphasize the liabilities to the parents should treatment be preferred. I have, at times, gone a step further and told the parents that were the child in question mine, I would have decided against treatment.
If it is decided not to treat, should the patient’s life be terminated by a fatal dose of a drug? Some advocate stopping all feeds and supplying only water to take away thirst. The logic offered is that by this means we are not taking away life but allowing nature to take its own course. Is starvation to death not more cruel than instant death?
Possible resolution of dilemma:
Here, as often is the case with ethical dilemmas, the individual doctor’s conscience must dictate the course of action. Such a decision, however, must take into account the fact that the law of the land does not permit any doctor to kill the patient by any act of commission.
Admission to an intensive care unit:
The intensive care unit is already full of seriously ill patients, each of whom needs the special attention afforded in it. A fresh patient is brought to the clinic who also needs this specialized care. There is no other nearby centre that can take him. What is to be done?
Do we continue to treat existing patients and place this patient in a room or ward without special facilities for monitoring and treatment and, in the process, lose this patient? Do we shift the ‘least seriously ill patient’ out of the unit to make way for the new arrival and, in doing so, jeopardize the life of someone who may be on the way to recovery?
What if the new arrival is a ‘V.I.P.’?
A similar dilemma is posed when one has to select which of two patients is to be provided the only available ventilator.
Possible resolution of dilemma:
A new patient presenting to a clinic or hospital has not yet established the doctor-patient relationship with the consultant. Existing patients in the intensive care unit are already under his treatment and he is responsible for their welfare. His primary concern, then, must be for patients already in the unit. If, however, there if definite evidence that one of them can, without any risk, moved out of the intensive care unit to the half-way house of the semi-intensive care ward, such a transfer can be affected so as to take in the new patient.
Demand for euthanasia by a terminally ill patient in unremitting agony:
A patient with widespread cancer is in severe agony, which persists despite use of the maximal therapeutic doses of powerful drugs such as morphine. He begs to be relieved of pain and asks for the use of much larger doses, knowing that such doses will be fatal. Should one oblige?
Possible resolution of dilemma:
Here, as often is the case with ethical dilemmas, the individual doctor’s conscience must dictate the course of action. Such a decision, however, must take into account the fact that the law of the land does not permit any doctor to kill the patient by any act of commission.
Shutting off the ventilator:
The law, as it stands, does not allow one to take a brain-dead patient off the ventilator unless this patient is a donor of an organ such as the heart. What about the patient who is not suitable to offer an organ but whose relatives can no more afford the cost of an intensive care unit?
Should we insist on following the letter of the law so that we are not subject to prosecution under the Consumer Protection Act or the Indian Penal Code?
Possible resolution of dilemma:
The law, in this instance, is faulty. It is illogical to permit removal of the heart, lungs, kidneys, pancreas and other organs for transplantation into another patient and not allow switching off the ventilator. Senior lawyers consulted by us inform us that judges would, in all probability, rule in favour of the doctor, provided the procedure for the diagnosis of brain death before switching off the ventilator was foolproof.

:: Some personal guidelines Top

I have found the following additional guidelines useful. I pass them on for your consideration.
* The golden rule: Do unto others, as you would have others to do unto you. I have often found it helpful to ask myself, “Were I the patient, what course of action would I have wished the doctor to follow?”
* The patient comes first. The raison d’etre of our profession is the patient. We are here to serve him. The sick patient, often in physical pain and always in mental distress, deserves our fullest attention and calls for the best qualities of our mind and heart. His interests and decisions must prevail above all else except when the patient is non compos mentis. In the latter instance, the decisions of his family must prevail.
* The poor patient deserves special consideration He has nowhere else to go. He does not possess the means to command or demand. In our milieu he is often reduced to seeking help with bowed head and hands folded together. And he is ill. Medically malpractice against this group is particularly abhorrent.
* Ensure that your decisions and actions are scientific, humane, effective and in the best interests of the patient and his family. Record them. Once this is done, you need fear no individual, administrator or tribunal.

Ayurveda Drugs - Danger to Life - Poison which kills

The flip side of Ayurveda.

Thatte UM, Rege NN, Phatak SD, Dahanukar SA
Dept. of Pharmacology, Seth GS Medical College & KEM Hospital, Parel, Bombay, Maharashtra.

From Journal of Post Graduate Medicine

Correspondence Address:
Dept. of Pharmacology, Seth GS Medical College & KEM Hospital, Parel, Bombay, Maharashtra.

How to cite this article:
Thatte UM, Rege NN, Phatak SD, Dahanukar SA. The flip side of Ayurveda. J Postgrad Med 1993;39:179-82,182a

How to cite this URL:
Thatte UM, Rege NN, Phatak SD, Dahanukar SA. The flip side of Ayurveda. J Postgrad Med [serial online] 1993 [cited 2005 Nov 9];39:179-82,182a. Available from:;year=1993;volume=39;issue=4;spage=179;epage=82,182a;aulast=Thatte

"A 62 year old male patient was brought to the casualty in an unconscious state. A detailed history from relatives revealed that he was a known diabetic whose hyperglycemia was well controlled with insulin and glibenclamide. Five days earlier he had started an ayurvedic drug for psoriasis. He developed giddiness following ingestion of the drug, but ignored it. Subsequently, he became unconscious. He was diagnosed to be in hypoglycemic coma to which he ultimately succumbed."
While investigating the causes for such sudden hypoglycemia, the attending physician would naturally question, "Could the ayurvedic drug be responsible for the hypoglycemia?". This case was referred to the Adverse Reactions (Ayurvedic drugs) Monitoring Cell of the Ayurveda Research Centre of King Edward Memorial Hospital. On scanning available ayurvedic literature, no reference could be found describing metabolic actions of any of the constituents of this medication. Subsequent animal studies revealed, however, that in occasional mice a significant hypoglycemia occurred, reiterating the fact that the adverse interaction in the patient could have been due to the inadvertent co-administration of the ayurvedic agent and powerful hypoglycemic agents.
This case dramatically illustrates the sequel of self-administering 'ayurvedie' drugs and emphasises the fact that there is indeed a flip side to Ayurveda. We present in this brief article, the other side of Ayurveda.
A question that will arise at the outset is why read about adverse effects of ayurvedic drugs (let alone their uses or benefits) if we do not practice Ayurveda? The answer to this question is simple: over 80% of our population takes ayurvedic medicines - either self-prescribed or through a ‘Vaidya’. These same patients expect to be treated by our medicines while simultaneously taking ayurvedic medicines often leading to interactions of the type described above.
Another point to note is that a large number of herbal preparations are in the market under the label 1 ayurvedic Drugs'. Due to aggressive salesmanship and over-the-counter (OTC) availability, these drugs are prescribed by doctors and consumed by patients widely.
Hence, it is obvious, that at least in our country, we have to be aware of salient beneficial and adverse effects of commonly used ayurvedic drugs as much as of allopathic agents.
Ayurvedic drugs that one is likely to encounter in practice can be discussed under two broad categories: a) the traditional formulations including for example kadhas (decoctions), arishthas (decoctions containing alcohol) or gutis (pills) and b) the so called ayurvedic formulations which are a combination of different herbal extracts (sometimes aqueous, sometimes alcoholic). These plants are prescribed individually or together for a particular condition in ayurvedic texts. However, their fixed dose combination, as marketed, may not be mentioned therein. These herbal medicines are prescribed for a wide variety of non-specific conditions like improving vitality, anti-stress effects, boosting immunity and increasing appetite or memory!
Since, in this article we are discussing adverse reactions, we shall for the moment assume efficacy of these herbal preparations. It is an old adage of pharmacology that teaches us that if a drug is effective it is most likely to produce a side effect [1].
In fact, standard text-books of Ayurveda mention that ayurvedic drugs, if improperly used can be toxic. Charaka[2] states in the Sutrasthana of the Charaka Sarnhita - "A potent poison also becomes the best drug on proper administration. On the contrary, even the best drug becomes a potent poison if used badly".
Ayurvedic texts classify toxic plants (See into different categories depending on the part of the plant that is toxic. Subsequent research has revealed the exact chemical nature of the toxic alkaloid validating the knowledge laid down in ayurvedic texts.

In fact, in Ayurveda, there is a separate science which deals with toxicological aspects and is known as Vishagarvajrodhika tantra' (toxicology)[3].
There are enough grounds to conjecture that some knowledge regarding toxicity of plants was obtained through observation of behaviour of insects and animals towards these plants. Plants, which were never infested with insects, were considered dangerous: these were later shown to contain repellants like anthraquinone, naphthalene or nimbidine. Plants like vinca or nerium from which animals steer clear have later been shown to contain toxic materials. Aconitum does not allow any other plant in its vicinity! An interesting feature about ancient ayurvedic physicians worth noting, and perhaps emulating, is their ability to improvise on information they had, using whatever facilities were at hand. Thus, for example, when the physicians discovered that a particular plant was visciously toxic and perhaps fatal, they evolved ways by which the toxic components could be destroyed and converted them not only to safe but further therapeutically useful entities! The story of Aconitum heterophyllum is illustrative in this respect. The roots of this plant are considered toxic (they contain an alkaloid aconitine) and following ingestion of roots, the toxicity manifests in the form of tingling numbness of mouth and throat, abdominal pain, loss of muscle power, visual and auditory disturbances and finally clonic convulsions [4]. However, aconite forms an important constituent of ayurvedic formulations. The aconite used in the formulations is not a crude agent but one, which is processed. This processing involves boiling of roots with 2 parts of cow's urine (7 hours per day) for 2 consecutive days. The roots are then thoroughly washed with water and boiled with 2 parts of cow's milk for the same duration. These are washed again with lukewarm water, cut into pieces, dried and ground. It has been shown that aconite becomes safe only after this elaborate process and all the steps are 6 essential for complete detoxification[6],[7].
Besides toxicology, ayurvedic pharmacology describes in some detail the side effects that can occur with different therapeutically useful drugs. Further, it also describes ways (which also include manufacturing techniques) to minimise these side effects. Just like we, for example, would advise that NSAIDs should not be taken on an empty stomach, Ayurveda gives instructions regarding time of drug administration, the relationship with food, type of food which should be avoided/permitted with the drug etc. The do's and don'ts are clearly enunciated. For example, amalki (amla, Emblica officinalis) should be avoided at bedtime to prevent harmful effects on teeth [8]. Chyavanprash contains large quantities of Amla - one wonders whether the package insert with any Chyavanprash mentions this precaution! Similarly, pippali (Piper longum) used in asthma should be avoided in patients with peptic ulcer disease and should be consumed with milk [9].
Tribhuvankirti is a combination of several plants which is very commonly used to treat a "cold in the head" and fever. There are clear instructions in Ayurveda that because it contains aconite [Table - 1] it should be used cautiously. When used, it should be taken with tulsi (holy basil) juice, ginger juice or honey[8].
Guggul is derived from the resin of Commiphora mukul [11] and is used in a variety of diseases including hypercholestrolemia (in fact gugglulip has been introduced into the market for this condition) and arthritis[12]. Ayurveda specifies that guggul should be used cautiously in patients with peptic ulcer disease. While on guggul therapy the patient is advised to avoid sour food, alcohol and heavy exercise[13],[14].
The subject of teratogenecity also figures in Ayurveda. Thus, certain plants like Terminalia hebula (harda) are to be avoided in pregnancy. This is a constituent of a large number of OTC preparations. It is a powerful purgative and is supposed to stimulate GI motility and would therefore be contraindicated in pregnancy[15]! This fact is not sufficiently publicised.
Apart from plants, Ayurveda also includes metals in its formulary. Thus, several preparations containing metals like mercury, lead and copper are available readily in the market on OTC basis. These metals have to be deligently processed before they are suitable for human consumption and there is again a long list of do's and don'ts regarding their use. Unfortunately, there are no quality control methods to standardise such metal containing drugs and to find out whether processing of metal is done appropriately so as to render it nontoxic. This thus increases the probability of toxic effects.
The case history of a 70-year-old male patient referred to the ADR monitoring cell illustrates the relevance of being aware of these. This patient was taking a 'herbo-mineral' preparation 'Mahayograj Guggul' in the dose of 4 tablets three times a day, for the complaints of joint pains for well over two years. He got relief from the arthritis but developed symptoms of lead poisioning including severe anaemia with classic basophilic stippling of the RBCs. The case was referred to the ADR cell with the query whether Mahayograj Guggul could lead to this problem. As this preparation contains lead, our centre adviced immediate withdrawal of the preparation.
This particular preparation is prescribed for rheumatoid arthritis in ayurvedic texts[13] and contains several plants and metals as shown in .

Ayurvedic textbooks recommend a special pharmaceutical process to detoxify the metals. The lead in this preparation has to be processed by first heating over a fire till it glows. It should then be cooled by dipping into a mixture of sesame oil, buttermilk, cow's urine and a decoction of three plants, viz. amia (E.officinalis), beheda (T. bellerica) and harda (T. chebula). After repeating this procedure thrice, the lead is heated the fourth time following which it is dipped into a churna (powder) made of the rind of tamarind and Piper longum. This lead is then mixed with arsenic sulphide and wrapped in a betel leaf and warmed in a crucible to a fixed temperature. This process is repeated thirty times before nagabhasma or processed lead is ready for use[16]. In addition, in the doses that this patient was taking the drug he would have consumed a phenomenal 414 mg lead per day for more than 2 years leading to lead toxicity. There are two points to note in this case. Firstly, Ayurveda definitely reconimends Mahayogiraj Guggul for rheumatoid arthritis but has cautioned about duration of therapy, which was overlooked. Secondly, as there are no quality control procedures in existence, there is rio way to know whether the lead in this formulation had been processed in the complex way it should have been.
This brings us to the second group of the 'herbal' formulations marketed under the label 'Ayurvedic'. All doctors are aware that such preparations are available, many may be prescribing them and some will come across patients self-medicating themselves with these drugs. What exactly are these drugs and what do we know about them? Most doctors prescribe these agents, in spite of lack of sufficient clinical studies (using the randomised controlled clinical trial model) proving their efficacy in comparison to allopathic drugs, in the utopian misconception that "never mind if they are ineffective, they will be safe!"
What adverse effects can occur with such formulations? The most glaring are possible drug interactions with the usually co-administered allopathic drugs. Several plants have been shown to alter bio-availability of allopathic drugs[17].
Similarly when used in combination with allopathic drugs they may alter their pharmacodynamics. The example in the diabetic patient described earlier is illustrative. Further, such herbal preparations may produce toxicity, often unexpectedly, per se.
A very herbal remedy is the need to conduct safety studies on them. Protagonists for this believe that with the changing ecological environment, use of pesticides, new manufacturing techniques, modern formulations and combinations of herbs not prescribed in ayurvedic texts, the need for looking at ayurvedic herbal drugs as new drug entities cannot be ignored. This is being seriously considered by the office of the Drugs Controller of India and an amendment to the laws governing manufacture and sale of ayurvedic drugs is on the anvil.
Opponents feel however that herbal remedies are natural remedies and are beyond conventional toxicity studies. Further developmental costs would be formidable.
Is there a via media? Perhaps incorporation of any or all of the methods summarised in [Table:3] would optimise use of ayurvedic drugs.
The Adverse Drug Reaction monitoring cell for Ayurvedic Drugs has been set up at the Ayurveda Research Centre of King Edward Memorial Hospital, Mumbai with several aims. Alongwith documenting anecdotal case reports suggestive of adverse effects to ayurvedic drugs, (please see ADR reporting card) we also, where necessary conduct studies in animals to confirm or rule out the cause and effect relation between the drugs and side effects reported. Further we give information related to ayurvedic drugs.
In conclusion we can reiterate that in view of the fact that we are
a) not using ayurvedic drugs only in the form as described in standard texts,
b) making over-the-counter formulations without much heed to the need for individualisation,
c) giving ayurvedic drugs in combination with allopathic agents which have a narrow therapeutic margin,
d) using raw plant material that is possibly polluted by environmental and ecological devastation,
e) not having good quality control methodologies,
We must beware. We must not wait for a thalidomide- like tragedy in Ayurveda to shake us out of our complacence that ayurvedic drugs are safe!

:: References Top

1. Melmon KL, Morrelli HE. Drug Reactions. In: Clinical Pharmacology. Basic Principles in Therapeutics, 2nd ed. New York: Macrinillan Publ Co; 1978, pp 968. Back to cited text no. 1
2. Samhita C. Sutrasthanam In: Sharma PV, editor. Charak Samhita Varanasi: Chaukhamba Orientalia; 985; 1:126. Back to cited text no. 2
3. Dahanulkar SA, Thatte UM. Historical survey of the evolution of Ayurveda. In: Ayurveda Revisited. Mumbai: Popular Prakashana; 1989; 10-27. Back to cited text no. 3
4. Franklin CA, In: Modi's Medical Junspiudence and Toxicology, 21st ed. Mumbai: NM Tripathi Pvt. Ltd; 1988, pp 279. Back to cited text no. 4
5. Sastri A. In: Sri Vagbhatacharya’s Rasaratna Samuchchaya, 6th ed. Varansi: Chawkhamba Sanskrit Series office; 1978, pp 590. Back to cited text no. 5
6. Sen SP, Khosla RL. Effect of Sodhana on the toxicity of aconite (vatsnava). Current Med Pract 1968; 12:694. Back to cited text no. 6
7. Thorat S, Dahanulkar SA. Can we dispense with ayurvedic Somskaras? J Postgrad Med 1991; 37:157-159. Back to cited text no. 7
8. Gogate VM. Emblica officinalis. In: Drvyaguna Vigyan. 1st ed. Pune: Continental Prakashan; 1962, pp 350. Back to cited text no. 8
9. Swami B. Tribhuvankirti. In: Rasadarpan - part 1, 3rd ed. Patiyala: Swami Publication; 985, pp 393. Back to cited text no. 9
10. Sukh Dev. A modern look at an age old ayurvedic drug gugguiu. Science Age 5:13-18. Back to cited text no. 10
11. Satyavati GV. Gum guggul (Commiphora mukul) - the success story of an ancient insight leading to a modern discovery. Ind J Med Res 1988; 87:327-335. Back to cited text no. 11
12. Gogate VM. In: ayurvedic Materia Medica. Pune: Continental Prakashan; 1981, pp 289-290. Back to cited text no. 12
13. In: Bhavaprakash Nighantu Karpooradi vargu. Varanasi: Chaulkhamba Sanskrit Samsthan; 1969, pp 205. Back to cited text no. 13
14. Gogate VM. Terminalia chebula. In: Dravyaguna Vigyan, 1st ed. Pune: Continental Prakashan; 1982, pp 436 Back to cited text no. 14
15. Gune G. In: Ayurvediya Aushadhi Gunadharma Shastra, Siddhaushadhi, part IV, 2nd ed. Ahmadnagar: Mohan Mandir; 1934; 8-9. Back to cited text no. 15
16. Dahanulkar SA, Kapadia AB, Karandikar SM. Influence of trikatu on rifampicin bioavailability. Indian Drugs 1982; 271-273. Back to cited text no. 16
17. Back to cited text no. 17

Doctor bashing and why the Indian medical profession must evolve.

Doctor bashing and why the Indian medical profession must evolve.

Gandhi JS

From Journal of Post Graduate Medicine

How to cite this article:
Gandhi JS. Doctor bashing and why the Indian medical profession must evolve. J Postgrad Med 2002;48:155-155

How to cite this URL:
Gandhi JS. Doctor bashing and why the Indian medical profession must evolve. J Postgrad Med [serial online] 2002 [cited 2005 Nov 9];48:155-155. Available from:;year=2002;volume=48;issue=2;spage=155;epage=155;aulast=Gandhi

I read with interest the comments by Dr. Pandya on the harassment and violence inflicted on doctors in India.[1] Indeed, in one of the recent issues of the British Medical Journal a Pakistani doctor reports similar events in his country.[2] It is clear even in Britain that doctors no longer have the kudos that their predecessors commanded implicitly as part of their professional role. Certainly in the UK this loss of faith in the medical profession has resulted from large malpractice scandals incriminating senior doctors during the last decade. We saw over the nineties the Bristol paediatric cardiac surgery scandal, the Alder Hey revelations, the Dr Shipman affair, and an array of ignominious ends to otherwise admirable careers. It was undoubtedly the case in these instances that patient care had been substandard. The General Medical Council responded briskly by establishing new mechanisms to monitor the performance of consultants (who hitherto had worked with relative impunity) and by forming bodies such as the National Institute of Clinical Excellence to audit clinical practices. The British people also changed their view of doctors, and there is presently a rising trend of complaints against health professionals and the system of the National Health Service (NHS). For the time being in Britain we are only more aware of the medicolegal aspects of our practice (so that clinical care is improving), but it may be that soon we will work in the litigious culture found in North America.
The spate of aggression against doctors in the subcontinent must also prompt a timely reassessment of the doctor’s role in Indian society. As observed by Dr Pandya and others, frequently the anger and distrust expressed by patients and relatives against doctors stem from poor communication rather than negligence. Patients and relatives feel alienated and powerless. In Indopakistani culture, anger can easily be vented in a fanatic manner that involves injury or murder, and it seems that the current vogue is to channel this destructive force towards the medical profession. Although I suspect there may be political issues that have led to the persecution of individual Indian doctors, surely it is now up to the Indian profession as a whole to actively redeem itself in the eyes of the public. Unlike in Britain, the Indian state is unlikely to show interest in the plight of its doctors, and changes to improve patient care and restore public confidence must arise from within the profession.
As a symbolic step, undergraduate curricula in India must now include teaching on communication between doctor and patient in earnest. On speaking to doctors who have qualified in India and now work in the NHS, the recurrent opinion I encounter is that there is a gross lack of such training. Moreover, the importance of good communication needs to be reiterated throughout postgraduate training. Indian doctors must also now be provoked to create a system to handle complaints from patients and relatives that gives people dignity, and minimises the dishonesty and inefficiency that Indians themselves admit riddles their existing institutions. Control of the quality of patient care is warranted especially in India, where healthcare is primarily in the private sector and patients are potentially vulnerable to serious iatrogenic blunders. Cynics will quickly say that the corruption cannot be erased, but surely every effort will help in reducing the actual burden of dishonesty that is sparking frustration and violence. If there is no accountability or audit in the profession, then barbarism will persist and probably worsen. The minutiae of how such a system of audit can be conceived, formed, financed, and run is not a matter for a bystander such as myself to contemplate. And armchair analyses and cynicism will not suffice, because if the chair is kept too warm too long Indian doctors will inevitably attain the status given to unreliable politicians.

:: References

1. Pandya SK. Doctor patient relationships: The importance of the patient’s perceptions. J Postgrad Med 2001;47:3-7. Back to cited text no. 1
2. Shafqat S. New hazard of medicine. BMJ 2002;324:1045. Back to cited text no. 2

Monday, November 7, 2005

The Truth About the Male and Female Brain.

Simon Baron-Cohen is the director of the autism research center at Cambridge University and the author of "The Essential Difference: The Truth About the Male and Female Brain." at
New York Times

The Male Condition : Published: August 8, 2005 : Cambridge, England

TWO big scientific debates have attracted a lot of attention over the past year. One concerns the causes of autism, while the other addresses differences in scientific aptitude between the sexes. At the risk of adding fuel to both fires, I submit that these two lines of inquiry have a great deal in common. By studying the differences between male and female brains, we can generate significant insights into the mystery of autism.

So was Lawrence Summers, the president of Harvard, right when he remarked that women were innately less suited than men to be top-level scientists? Judging from current research, he was and he wasn't. It's true that scientists have documented psychological and physiological differences between male and female brains. But Mr. Summers was wrong to imply that these differences render any individual woman less capable than any individual man of becoming a top-level scientist.

In fact, the differences that show up in brain research reflect averages, meaning that they emerge only when you study groups of males and females and compare the two groups' averages on particular psychological tests or physiological measures. The evidence to date tells us nothing about individuals - which means that if you are a woman, there is no evidence to suggest that you could not become a Nobel laureate in your chosen area of scientific inquiry. A good scientist is a good scientist regardless of sex.

Nonetheless, with brain scanning, we can discern physiological differences between the average male and the average female brain. For example, the average man's cerebrum (the area in the front of the brain concerned with higher thinking) is 9 percent larger than the average woman's. Similar, though less distinct, overgrowth is found in all the lobes of the male brain. On average, men also have a larger amygdala (an almond shaped structure in the center of the brain involved in processing fear and emotion), and more nerve cells. Quite how these differences in size affect function, if at all, is not yet known.

In women, meanwhile, the connective tissue that allows communication between the two hemispheres of the brain tends to be thicker, perhaps facilitating interchange. This may explain why one study from Yale found that when performing language tasks, women are likely to activate both hemispheres, whereas males (on average) activate only the left hemisphere.

Psychological tests also reveal patterns of sex difference. On average, males finish faster and score higher than females on a test that requires the taker to visualize an object's appearance after it is rotated in three dimensions. The same is true for map-reading tests, and for embedded-figures tests, which ask subjects to find a component shape hidden within a larger design. Males are over-represented in the top percentiles on college-level math tests and tend to score higher on mechanics tests than females do. Females, on the other hand, average higher scores than males on tests of emotion recognition, social sensitivity and language ability.

Many of these sex differences are seen in adults, which might lead to the conclusion that all they reflect are differences in socialization and experience. But some differences are also seen extremely early in development, which may suggest that biology also plays a role. For example, girls tend to talk earlier than boys, and in the second year of life their vocabularies grow at a faster rate. One-year-old girls also make more eye contact than boys of their age.

In my work I have summarized these differences by saying that males on average have a stronger drive to systemize, and females to empathize. Systemizing involves identifying the laws that govern how a system works. Once you know the laws, you can control the system or predict its behavior. Empathizing, on the other hand, involves recognizing what another person may be feeling or thinking, and responding to those feelings with an appropriate emotion of one's own.

Our research team in Cambridge administered questionnaires on which men and women could report their level of interest in these two aspects of the world - one involving systems, the other involving other people's feelings. Three types of people were revealed through our study: one for whom empathy is stronger than systemizing (Type E brains); another for whom systemizing is stronger than empathy (Type S brains); and a third for whom empathy and systemizing are equally strong (Type B brains). As one might predict, more women (44 percent) have Type E brains than men (17 percent), while more men have Type S brains (54 percent) than women (17 percent).

What of Mr. Summers's other claim, that such sex differences are innate? We know that culture plays a role in the divergence of the sexes, but so does biology. For example, on the first day of life, male and female newborns pay attention to different things. On average, at 24 hours old, more male infants will look at a mechanical mobile suspended above them, whereas more female infants will look at a human face.

It has also been found that the amount of prenatal testosterone, which is produced by the fetus and measurable in the amniotic fluid in which the baby is bathed in the womb, predicts how sociable a child will be. The higher the level of prenatal testosterone, the less eye contact the child will make as a toddler, and the slower the child will develop language. That is connected to the role of fetal testosterone in influencing brain development.

Males obviously produce far more prenatal testosterone than females do, but levels vary considerably even across members of the same sex. In fact, it may not be your sex per se that determines what kind of brain you have, but your prenatal hormone levels. From there it's a short leap to the intriguing idea that a male can have a typically female brain (if his testosterone levels are low), while a female can have a typically male brain (if her testosterone levels are high). That notion fits with the evidence that girls born with congenital adrenal hyperplasia, who for genetic reasons produce too much testosterone, are more likely to exhibit "tomboy" behavior than girls with more ordinary hormone levels.

What does all this have to do with autism? According to what I have called the "extreme male brain" theory of autism, people with autism simply match an extreme of the male profile, with a particularly intense drive to systemize and an unusually low drive to empathize. When adults with Asperger's syndrome (a subgroup on the autistic spectrum) took the same questionnaires we gave to non-autistic adults, they exhibited extreme Type S brains. Psychological tests reveal a similar pattern.

And this analysis makes sense. It helps explain the social disability in autism, because empathy difficulties make it harder to make and maintain relationships with others. It also explains the "islets of ability" that people with autism display in subjects like math or music or drawing - all skills that benefit from systemizing.

People with autism often develop obsessions, which may be nothing other than very intense systemizing at work. The child might become obsessed with electrical switches (an electrical system), or train timetables (a temporal system), or spinning objects (a physical system), or the names of deep-sea fish (a natural, taxonomic system). The child with severe autism, who may have additional learning difficulties and little language ability, might express his obsessions by bouncing constantly on a trampoline or spinning around and around, because motion is highly lawful and predictable. Some children with severe autism line objects up for hours on end. What used to be dismissed by clinicians as "purposeless, repetitive behavior" may actually be a sign of a mind that is highly tuned to systemize.

One needs to be extremely careful in advancing a cause for autism, because this field is rife with theories that have collapsed under empirical scrutiny. Nonetheless, my hypothesis is that autism is the genetic result of "assortative mating" between parents who are both strong systemizers. Assortative mating is the term we use when like is attracted to like, and there are four significant reasons to believe it is happening here.

FIRST, both mothers and fathers of children with autism complete the embedded figures test faster than men and women in the general population.

Second, both mothers and fathers of children with autism are more likely to have fathers who are talented systemizers (engineers, for example).

Third, when we look at brain activity with magnetic resonance imaging, males and females on average show different patterns while performing empathizing or systemizing tasks. But both mothers and fathers of children with autism show strong male patterns of brain activity.

Fourth, both mothers and fathers of children with autism score above average on a questionnaire that measures how many autistic traits an individual has. These results suggest a genetic cause of autism, with both parents contributing genes that ultimately relate to a similar kind of mind: one with an affinity for thinking systematically.

In order to fully test this theory, we still need to do a lot of work. The specific genes involved must be identified. It is a theory that may be controversial and perhaps unpopular among those who believe that the cause of autism is largely or totally environmental. But controversy is not a reason not to test it - systematically, as we might say

The Syllabus for Anatomy in MBBS Course

The Syllabus for Anatomy in MBBS Course
A) GENERAL Anatomy

I) Descriptive terms
Terms used for describing the position of the body, Anatomical planes, Commonly used terms in Gross Anatomy , Terms used in Embryology, Terms related to limbs, for hollow organs, for solid organs, to indicate the side, for describing muscle, for describing movements

II) General Osteology
Definition, Nutrition & Morphological Classification, Distribution and Functions of bone Appendicular, Axial.
Diaphysis, Metaphysis, Epiphysis, Types of epiphysis
Primary centres, Secondary centers, Law of ossification, Epiphyseal plate, Blood supply of long bone
Definition, Types, structure, Distribution, Nutrition

III) General Arthrology
Classification, Synarthrosis, Amphiarthrosis, Diarthrosis.
Cartilaginous. Primary, Secondary
Synovial - Axis of movement, Structure of typical synovial joints
Classification of synovial joints, according to the shape ,axes of movement and morphology
Simple, Compound ,Complex joints,Blood supply & nerve supply.

IV) General Myology
Definition, types: Origin, Insertion, Morphological classification
Actions of muscles, nerve supply
Functional classification, Prime movers, Fixators, Antagonists, Synergists
BURSA, Structure, Functions,types:
LIGAMENTS, Types & functions,Sprains

V) Integument

a) SKIN -
Introduction : Surface area
Types :Thin, Thick, hairy, Functions, innervation
Structure :
Epidermis, Dermis, Appendages

Distribution of fat, functions

Features, Modifications, Functions

VI) General Angiology

Arteries: Muscular, Elastic; Arterioles; Capillaries: Sinusoids, Veins - Anastomosis: End arterial; Vasa vasorum, nerve supply of blood vessels

Lymphatic system
Lymph vessels, Central lymphoid tissue, Peripheral lymphoid organs, Circulating lymphocytes - T and B lymphocytes

VII) General Neurology
Structure of nervous tissue,
Neurons:Synapses :Structural – type, Functional types
Classification of neurons : According to polarity and According to relative lengths of axons and dendrites:
Neuroglia:Nerves :Cranial – Spinal, Structure of typical spinal nerve
Autonomic nervous system :Sympathetic :Sympathetic ganglia, postganglionic fibres
Parasympathetic :Cranial outflow, sacral outflow

Level 2: Mechanical properties of bones.
synthesis, histogenesis, growth of Cartilage,Factors limiting range of movement,
Kinesiologically: Sellar, Ovoid, Joint position: Loose-packed, Close-packed
Number and diameter of fibres, Range of contraction, Active insufficiency,Passive insufficiency, shunt, swing, spin
Adventitious bursae - Housemaid’s knee, Clergyman’s knee, Student’s elbow, Weaver’s bottom, Porter’s shoulder
Clinical correlation, significance of Langer’s lines, Tension lines, flexure lines Transplant
Collateral circulation, Functional end arteries, Arteriosclerosis,

Level 3: Effect of hormones on bony growth, Wolff’s law, Surface topology of articular surfaces, Spin, Swing, Cartilage Grafts, Kinesiology, Body liver system,SKIN grafts,Ischaemia, Infarct,Bursitis


REGIONS : Mammary gland, Axilla, Cubital fossa, Fascial spaces of the hand
Relations and functional importance of individual structures, Dupuytren’s contracture, Hand as a functional unit – grips, Nerve injury, carpal tunnel syndrome, Clavipectoral fascia; Salient features about carpals;

Shoulder girdle; Shoulder joint; Elbow; Radioulnar joints; Wrist; Carpometacarpal joint of thumb; Bones taking part
Classification of joints, Movement with muscles causing movements,
midcarpal joint, metacarpophalangeal joints,
interphalangeal joints
Fall on the outstretched hand

Level 2Axilla: Collaterals Lymph nodes (breast) Axillary sheath cervico-axillary canal, Abscess drainage, Palm: comparative Anatomy (thumb, palmaris brevis), position of rest and of function, collaterals, Fascial spaces: Surgical significance

Identification; Anatomical position; Parts; Joints formed; Development; identification of individual carpals in and articulated hand)
Clavicle: Line of force transmission, commonest site of FRACTURE
Humerus: fractures -
Carpals, Metacarpals, Phalanges: Carpal tunnel syndrome, FRACTURE scaphoid
Surgical approaches, Subluxation of head of radius, carrying angle

Muscles of upper limb, attachment, Nerve supply, Actions
Applied aspects: Volkmann’s ischaemic contracture
Quadrangular and triangular spaces, Triangle of auscultation

ANGIOLOGY: Axillary, Brachial, Radial, Ulnar Arteries, veins, lymphatics
Commencement, Termination, Main area of distribution and drainage, Anastomosis –
Applied aspects, Artery : Damage to vessels, Raynaud’s disease, Veins: Thrombosis, Lymphatics: Lymphangitis (red streaks), lymphadenitis,

A. Nerves
Axillary, median, ulnar, musculocutaneous, radial, Origin, course, distribution, Root value

B. Plexus: Brachial
Applied aspects: Nerve injury at various sites - Tendon reflex - Winging of scapula, Erb’s palsy, Klumpke’s palsy, Crutch palsy, ulnar paradox


REGION: boundaries, major contents; Gluteal, femoral triangle; Adductor canal, compartments of thigh, leg; Popliteal fossa, Adductor canal , Sole, Arches of foot,; Gluteal IM injections
Femoral hernia
blood supply to head of femur; FRACTURE neck of femur, mechanics movement of joints; hip and knee, Trendelenburg test; Knee joint : derangement, injuries to cruciate ligaments, menisci; (tear - bucket handle type); Ankle : Sprain
mechanism of venous return, varicose veins
Applied aspects of Adductor canal, popliteal aneurysms

OSTEOLOGY: Identification, region, anatomical position; parts, joints formed,
For tarsals - identification of individual tarsals in an articulated foot.

Level 2
Applied aspects: Bony specialization for bipeds, walking and transmission of weight,
FRACTURE , femoral torsion, neck shaft angle, bone grafts

Hip, knee, ankle, subtalar, Tibiofibular
Hip joint : dislocation, congenital, traumatic, surgical approaches to joints (anatomical basis), traumatic effusion, bursitis

Attachments, nerve supply, actions of: Muscles of lower limb
calf pump, antigravity muscles

Artery: Femoral, profunda femoris, popliteal, dorsalis pedis, Commencement, termination, main area of supply, course, relations & applied
Vein: Venous drainage of lower limb, long and short saphenous veins, Communication and valves. Varicose
Lymphatics: Inguinal group of lymph nodes

Lever 2 :intermittent claudication, clinical significance of anastomosis: around knee, venous thrombosis

a. Plexus: Lumbar and sacral, Location, Formation, Distribution
b. Nerves: Root value of sciatic, femoral, obturator, tibial, common peroneal nerves; Origin, course, distribution; sciatica, foot drop

Level 2 :Pes cavus, equinovarus, clawing of toes


i) Anterior abdominal wall
Rectus sheath, quadrants and regions, Testes, epididymis, spermatic cord, scrotum
Level 2: Surgical incisions of abdomen types of inguinal herniae
Peritoneum, Lesser Omentum, Omental Bursa, Epiploic Foramen, Testes
Morphology, blood supply, lymphatic drainage

Definition, beginning, end, course and contents, coverings, vasectomy

ii) Abdominal organs : Morphology relations blood supply, lymphatics nerve supply & applied Anatomy of following organs
stomach, spleen , liver :,biliary apparatus, pancreas, small intestine,large intestine and vermiform appendix,kidneys, ureters,suprarenal glands

Level 2: peptic ulcer ,Splenic circulation, splenic vascular segments,liver , biopsy, Support of liver ,Gall stones ,Duct system of pancreas ,Surgical approach to kidney , stones (Renal), Ureter,Sites of constrictions, Hydronephrosis, pheochromocytoma

Level 3: Gastroscopy, Achlorhydria,Splenectomy ,liver transplant,Pancreatitis, diabetes,Renal transplant,Stones in ureter, Cushing’s disease

iii) Pelvic Viscera :- Morphology, relations, blood supply nerve supply & applied Anatomy
urinary bladder & urethra, uterus, ovaries and uterine tubes, prostate, rectum and anal canal, urogenital diaphragm (ugd)

Level 2: Supports and micturition, stones in bladder ,Ovarian cyst, enlargement complications, Fistula, Fissure, piles

Level 3: cystoscopy, Hysterectomy,cancer, Supports of rectum

iv) Perineum – Ischiorectal fossa, pudendal canal, perianal spaces Urogenital diaphragm, male urethra, penis – perineal pouches

Level 2: Ischiorectal hernia

v) Myology
Anterior abdominal wall, Rectus sheath, Psoas major, Quadratus lumborum, Thoracoabdominal diaphragm, pelvic diaphragm, Thoracolumbar fascia, perineal spaces & muscles

Level 3: Psoas abscess

vi) Osteology
Level 2: Pelvis - types
(various diameters), lumbar vertebrae, anatomical basis of disc prolapse, nerve compression
Level 3: Sacralization, Lumbarization
Movements of lumbar vertebrae, lumbosacral, sacroiliac, sacrococcygeal joints

vii) Angiology :- Origin, course, termination, relations, branches & applied Anatomy of
Level 2: portasystemic communications
Level 3: Portasystemic communications in detail; Development

viii) Neurology, lumbar plexus, sacral plexus

i) Thoracic wall,Thoracic inlet
Boundaries and contents
THORACIC OUTLET, Boundaries and contents, major openings and levels,
Typical intercostal space, Boundaries and contents, muscles Atypical intercostal space, Movements of respiration
Level 2: importance and minor openings in outlet, Accessory muscles of respiration
Level 3: Applied aspects: Barrel chest, pectus excavatum, rickety rosary

ii) Mediastinum
Divisions and major contents

Level 2: Mediastinitis, mediastinoscopy
Boundaries and contents:
Level 2 : Superior mediastinal Syndrome, Course, relation and branches / area of drainage
Level 3: Coarctation of aorta, aneurysm, developmental anomalies

Pleural reflections, recesses, innervation
Level 2: importance of recesses
Level 3: pleural effusion
Gross description including lobes, fissures and bronchopulmonary segments
Level 2: relations, blood supply, nerve supply
Level 3: Postural drainage, surgical importance, of bronchopulmonary segments, foreign body inhalation

iv)Pericardium & heart
Divisions of pericardium and sinuses
Level 2: referred pain
Level 3: Pericardial effusion
Anatomical position, location, surfaces and borders, interior of all chambers, conducting system of heart ; vessels of heart
Level 2: Relations, nerve supply - foramen ovale, patent IV septum, over-riding aorta, referred pain, functional end arteries - coronaries
Level 3: PDA, Fallot’s tetralogy, etc.

Level 2: Identification of T1, T9, T10, T11, T12, vertebrae and atypical ribs - 1, 2, 11, 12. relations, attachments, ossification
Level 3: FRACTURE ribs, flail chest, compression FRACTURE of vertebra


i) Regions and organs, fasciae of the neck triangles of neck

Level 2 Spaces and spread of infections, axillary sheath , Relations of contents, Damage to accessory nerve, sialogram, approach to gland, bidigital palpation of submandibular gland, Dangerous area of face, squint

Level 3: surgical neck incisions, external jugular vein - air embolism, LN biopsy, JVP, pulse, Frey’s syndrome

Thyroid, Parathyroid, Parotid, Submandibular, sublingual, Pituitary
Morphology, capsule, relations, nerve supply, blood supply

Muscles, nerve supply - blood supply

scalp,palate,tongue,larynx, pharynx, orbit, eyeball,styloid apparatus,nasal cavity, ear ,internal ear ,middle ear ,external ear ,meninges

ii) Osteology
Identification, anatomical position, parts, foramina in the skull, structures passing through them, norma basalis, verticalis, frontalis, lateralis, occipitalis and interior of cranial cavity
Foetal skull; Mandible: Age changes
Level 2: Fontanelles, Dental formula
Level 3: Fractures of the skull, Age of dentition, cervical rib, disc herniation

iii) Arthrology
Level 2: Dislocation

iv) Myology
Sternomastoid, Digastric, Mylohyoid, Hyoglossus, Muscles of facial expression, mastication, larynx, pharynx, tongue, palate and, Extra-ocular muscles
Level 2 Relations, development
Level 3 facial nerve palsy

v) Angiology
Origin, parts, course, relations, branches of:
Subclavian, Internal carotid, External carotid, Vertebral, Lingual, Facial, Maxillary
Level 2: Sub-branches, distributions
Level 3: Subclavian steal syndrome, Subclavian-axillary anastomosis
External and internal Jugular veins, venous drainage of face

Names, locations, drainage, classification
emissary veins, cavernous sinus, lymphatic drainage of head face neck

vi) Neurology
Cranial nerves,Nucleus, course, relations, branches, distribution, reflex pathways & applied Anatomy , plexus: Cervical, Brachial, parasympathetic ganglia, cervical sympathetic chain


Gross features: Extent (child / adult), enlargements, conus medullaris,
filum terminale, spinal meninges Tracts Ascending and Descending

Level 2: Spinal segments, vertebral correlation, significance of enlargements
nuclei of grey matter at upper & lower cervical, mid-thoracic, Lumbar & sacral levels
Clinical correlation of lesions

Level 3: anomalies,lamination, syringomyelia, PID, tumours, TB, trauma, dislocation, myelography

Gross features: Motor decussation: Sensory decussation: Inferior olivary nucleus Cranial nerve nuclei

Level 2: Tuber cinereum, pontobulbar body, Order of neurons, Details of nuclei and organisation of white matter
Level 3: medullary syndromes-Bulbar palsy, increased ICT, Arnold-Chiari malformation,

iii) PONS
Cross sections at the level of:
¨ Facial colliculus, Trigeminal nucleus
General features: Peduncles, Floor of the fourth ventricle
Level 2: Relations
Level 3: Tumours, pontine haemorrhage

Gross features: Division, Lobes, relations, internal structure -
Level 2: connections of,cerebellar cortex and intracerebellar nuclei,
white matter classification, Purkinje neuron,
Level 3: dysfunction,-dysequilibrium, ataxia, hypotonia
Nuclei: Names of nuclei and important connections
Peduncles : Important tracts in the peduncles
Functions : Of archicerebellum, paleocerebellum & neocerebellum

General features :
relations, contents of interpeduncular cistern, connections of red nucleus
Level 2: Weber’s syndrome, Benedikt’s syndrome
Level 1 :T.S. at inferior colliculus, TS at superior colliculus

Surfaces, borders, major sulci, gyri, poles, lobes, major functional areas, interior - gray and white matter
Gray - cortex - granular / agranular, striate, Basal nuclei - names, White matter - classification with examples; Components of limbic lobe
Level 2: handedness, Connections of limbic lobe

Dorsal thalamus Epithalamus Metathalamus Hypothalamus Subthalamus
Boundaries, parts, relations (gross), cavity, major nuclei, gross connections
Parts, boundaries, foramina, correlation with parts of brain
Level 2: Choroid fissure, recesses, Queckenstedt’s test
Level 3: Hydrocephalus, VA shunt
Circle of Willis, subarachnoid space, arteries, veins
Level 2: blood brain barrier, Hemiplegia
Level3: End arteries, CSF formation

Cerebral and spinal meninges, folds of dura, contents of subarachnoid spaces, arachnoid villi and granulations, direction of flow of CSF , lumbar puncture Cisterns, Definition, terminology, cisterna magna

Level 2: cisternal puncture, Queckensted’s test, vertebral venous plexus, choroid plexus
Extracerebral and intracerebral communication, CSF block,
Level 3: Epidural space



i) Microscope,
Light microscope: parts, magnification, resolution,Electron microscope,
Level 2 Micro techniques, H and E staining
Level 3: Polarizing microscope, phase contrast, scanning EM

ii) Cytology
Cell,Cytoplasm and nucleus,Cytomembranes,Unit membrane, Cell organelles
Mitochondrial DNA, mitochondrial myopathy

Level 2 Specialisations of cell surface, Sarcoplasmic reticulum of muscle, Primary and secondary lysosomes, residual bodies, Effect of colchicine and anticytotic drugs on spindles preventing mitosis, Endocytosis, exocytosis, movement of microvilli; Cell mitotic activity
Level 3 Lysosomal storage disease
NUCLEUS - Structure, nuclear envelope, chromatin, Barr body, nucleolus

iii) Epithelial
Definition, Classification, Structure of various types & subtypes of epithelia
Level 2: Nutrition, Renewal, Innervation,
Level 3: Metaplasia;
Surface modifications,Cilia; Microvilli; Stereocilia; Cell junction and junctional complexes;
Glands, Classification; Unicellular and Multicellular; Exocrine, Endocrine, Amphicrine. Exocrine: Simple, Compound; Apocrine, Merocrine, Holocrine; Tubular, alveolar, tubuloalveolar; Serous; Mucous ; Mixed

iv) Connective tissue, classification, structure, fibres, ground substance,
loose areolar tissue, adipose tissue
Level 2 : Glycosaminoglycans
Level 3 : Scurvy, oedema, inflammation

v) Bone & Cartilage
Bone, Compact, Cancellous, Developing bone; ossification, Woven, lamellar bone
Cartilage, Classification, types, Perichondrium, functions
Level 2: Growth: Interstitial, Appositional; Bone callus, Osteomalacia , Osteoporosis , Osteoma
Level 3: Chondroma

vi) Muscle
Skeletal muscle Plain muscle Cardiac muscle Intercalated disc, syncitium; Sarcomere, I and A bands, myofibrils, myofilaments,; Sarcoplasmic reticulum,
Level 2: Innervation, Red fibres, white fibres
Level 3: Hypertrophy, Hyperplasia ,Rigor mortis , Myasthenia gravis

vii) Nervous
Neurons, types; Neuroglia, types; Myelinated nerve fibre LS; Non-myelinated nerve fibre; Peripheral nerve ; Nodes of Ranvier; Synapses;

viii) Vessels
Large sized artery Medium sized artery, Arteriole; Capillary, Sinusoid; Medium sized vein;
Level 2: Atherosclerosis, Aneurysm, Infarcts, clotting
Lymphoid tissue
T cells, B cells; Mucosa Associated Lymphoid Tissue; Humoral immunity, Cell mediated immunity; Lymph node section; Thymus, spleen , Tonsil
Level 2: Blood-thymus barrier, Open and closed circulation in the spleen
Level 3: Organ transplantation, Graft rejection, Autoimmune disease


Basic organization, salient features, Identification
Structure and function correlation, individual features

i) Integumentary system
SKIN - Types; Epidermis and dermis; various cells, Appendages of SKIN
Level 2: Renewal of epidermis
Level 3: Albinism, melanoma, Acne

ii) Alimentary system
a) Oral tissues
Lip, Tongue, taste buds, Papillae; Tooth, Developing tooth, Salivary glands
Level 2: Striated duct, ion transport
b) GI Tract
Basic organization - 4 layers; Oesophagus with glands Stomach - Fundus, Chief cells, Parietal cells, intrinsic factor; Stomach - Pylorus Duodenum Brunner’s glands; Small intestine - with Peyer’s patch, Appendix, Large intestine
Level 3: Pernicious anaemia, ulcer, gastritis, Hirschsprung’s disease or megacolon
c) Glands
Pancreas: Exocrine, islets of Langerhans; liver , Hepatic lobule, portal lobule,; portal acinus; Gall bladder
Level 2: liver as an endocrine gland
Level 3: Diabetes mellitus, Cirrhosis of liver , liver regeneration, Chalones

iii) Respiratory system
Olfactory mucosa; Epiglottis; Trachea, Lung, Bronchus, bronchiole, alveolar duct, sac, alveoli, pulmonary type I and II cells
Level 2: Double spirally arranged bronchial smooth muscle
Level 3: Bronchial asthma, Hyaline membrane disease, heart failure cells

iv) Urinary system
Basic organization; Nephron - Parts, podocytes, Collecting system; kidney - Cortex, Medulla Ureter; Urinary bladder, Urethra
Level 2: Juxtaglomerular apparatus

v) Male reproductive system
Basic organization; Gonads, Tract, Accessory glands; Testis; Epididymis ; Vas deferens; Prostate ; Penis; Seminal vesicle
Level 2: Stages of spermatogenesis
Level 3: Immotile sperm
Female reproductive system
Basic organization; Gonads, Tracts, Accessory glands; ; Ovary - with corpus luteum; Fallopian tube; Uterus ; Cervix; Vagina, Mammary gland Active , Passive
Level 2: Stages of maturation of ovarian follicle , Phases of menstruation
Colostrum, IgA, Placenta : Maternal unit, Foetal unit, Umbilical cord: Wharton’s jelly

vi) Endocrine system: Pituitary; Adenohypophysis; Neurohypophysis; Thyroid ; Follicular, parafollicular cells; Parathyroid ; Chief cells, oxyphil cells; Adrenal; Pancreas; Testis ; Ovary
Level 2: Hypothalamo-pituitary Portal system
Level 3: Pheochromocytoma
vii) Nervous system
A. Central
Basic organization; Cerebrum; Cerebellum; Spinal cord; Cervical; Thoracic; Lumbar;
B. Peripheral
Sensory ganglia; Autonomic ganglia (sympathetic ganglion); Peripheral nerve
Special senses
I. Visual: Eyeball
Cornea ; Sclerocorneal junction ; Canal of Schlemm; Lens ; Retina ; Optic nerve
Level 3: Kerattoplasty, eye donation, glaucoma, retinal detachment
2. Auditory:
Internal ear ; Cochlea ; Semicircular canals; Vestibule;
3. Olfactory
Nasal cavity
4. Gustatory
Tongue with taste buds


I) General Embryology

i) Introduction: Stages of human life phylogeny
Ontogeny, Trimester, Viability,
Terms of reference: e.g. Cranial, Rostral, Caudal, Dorsal, Ventral, Lateral, Medial, Median, Planes of section
Level 3: The law of recapitulation, "Critical period", malformations, USG, Amniocentesis Chorionic Villus Biopsy, Fetoscopy, etc Teratology History of Embryology

ii) Gametogenesis: Menstrual cycle other reproductive cycles, Germ cell Transport and Fertilisation, Sperm capacitation, Methods of contraception, SEX determination
Level 3: Teratogenic influences; Fertility and Sterility, Surrogate motherhood; Social significance of “SEX -ratio”,
iii) Cleavage, Blastocyst, Cytotrophoblast, Syncytiotrophoblast
Implantation: Normal sites, Abnormal sites,; Placenta praevia, Extra-embryonic Mesoderm and Coelom; Bilaminar disc - Prochordal plate
Level 2: “abortion”; Decidual reaction, Chorionic Gonadotropins - Pregnancy test,

iv) Primitive streak Notochord, Neural tube and its fate Neural crest cells
- their fate, Development of somites, Intra-embryonic coelom, Foetal membranes :Chorionic villi, Amnion, Yolk sac, Allantois
Level 2: Congenital malformations, Nucleus pulposus, Sacrococcygeal teratomas, Neural tube defects, Anencephaly
Level 3: Signs of pregnancy in the first trimester, Role of teratogens, Alpha-fetoprotein levels

v) Folding of the embryo: Derivatives of germ layers,
Pharyngeal arches
Level 2: Thalidomide tragedy, Estimation of Embryonic Age - Superfoetation & superfoecundation

vi) Fetal membranes: Formation Functions, fate of: Chorion ; Amnion; Yolk sac; Allantois; Decidua; Umbilical cord; Placenta - Physiological functions; Foetomaternal circulation, Placental barrier, Twinning: monozygotic, dizygotic
Level 2: Placental hormones, Uterine growth, Parturition, Estimation of fetal age,

Level 3: Types of cord attachments, Chorion villus biopsy and Amniocentesis;
Uses of amniotic membranes, Trophoblastic tumours - Rh incompatibility, Haemolytic disease of newborn,

II) Systemic Embryology

i) Cardiovascular System - Venous System; heart - Chambers - Septa - Truncus -
Aortic arches - Fetal circulation - Changes at birth, ASDs, VSDs, PDA, Fallot’s Tetralogy.
Level 2: Veins, abnormalities, Surgical corrections
ii) The Respiratory System: Development of Larynx, Trachea, Bronchi, Lungs; Tracheo-oesophageal Fistula
Level 2: malformations
Level 3: Respiratory Distress Syndrome; Premature births
iii) The Alimentary System: Foregut: Oesophagus, Stomach, (Lesser sac); Duodenum - Hepatobiliary apparatus, Pancreas, spleen, Portal vein; Midgut : Rotation and Fixation, Caecum and Appendix, Meckel’s diverticulum; Hindgut : Cloaca; Rectum and Anal Canal
Level 2: Malformation - Tracheo-oesophageal fistulae; Congenital Hypertrophic Pyloric Stenosis; Atresia; Omphalocele, Hernia; Malformations - Fistulae, Situs inversus; Nonrotation; Mixed rotation of gut

iv) The Urogenital System, Development of Kidneys and Ureters; Cloaca - Urinary Bladder and Urethra; Suprarenal gland; Genital System - Testis and Ovary; Ducts and associated glands; External genital organs, Mesonephric and paramesonephric ducts, Uterine tube, Uterus and vagina
Level 2: congenital malformations; Ambiguous genitalia and Hermaphroditism ; Remnants and Vestiges of Ducts and Tubules

v) Integument : Development of mammary gland, SKIN & appendages

vi) Pharyngeal arches, nerves, muscles, cartilage, development of face, palate

vii) Endocrine : Glands, Adrenal, Thyroid, Parathyroid, Pituitary

viii) The Nervous System: Neural Tube: Spinal Cord and brain i.e., Forebrain, Midbrain and Hindbrain, Hypophysis cerebri; Neural Crest : Peripheral Nervous System,
Level 2: correlation Spina bifida; Anencephaly, Hydrocephalus, Retinal detachment; glaucoma; Coloboma iris,
Level 3: Myelination of tracts shortening of spinal cord, Neural Tube Defects
Organs of the special senses - eye and ear
ear - Internal ear -; External and middle ear - anomalies of the ear


i) Introduction – Mendelism, Laws Genetic code
Level 2: Evolution, Eugenics and Polygenic inheritance, Radiation and mutation , SEX chromatin, Population genetics

ii) Cytogenetics
Structure and function of chromosomes, Cell cycle, Cell divisions, Spermatogenesis, Oogenesis
iii) Molecular genetics (Normal)
Gene, Genetic code, Structure and types of DNA, Structure of RNA

iv) Inheritance: Single gene inheritance, Multifactorial inheritance, Polygenic inheritance, Mitochondrial inheritance, Pedigree charts with symbols

Genetic basis of variation

Mutation, Polymorphism, Multiple allelism
Level 2: Types, Factors influencing mutational load

Developmental genetics
chromosomes; Lyon’s hypothesis; Hermaphroditism and pseudohermaphroditism; teratogenesis

Gonadal dysgenesis, Adrenogenital syndrome Androgen insensitivity

Level 3: Counselling

Pedigree charting
Chromosomal basis of disease: Numerical, Structural abnormalities Down’s, Cri-du-chat, Turner’s, Klinefelter’s
Level 2: Dermatographics
Level 3: Counselling

Prenatal diagnosis
Maternal Serum Sampling; Fetal USG; Fetal Amniocentesis; Fetal Chorion Villus Sampling
Level 2: (cordocentesis); Foetoscopy
Level 3: Eugenics


I) Introduction
Principles of plain radiograms and CT scan.
Identification of gross anatomical features in plain and contrast radiographs.
Identification of gross anatomical features in normal CT scan especially of the Abdomen and Head-Face-Neck-brain regions.
Diagnostic procedures. Technical details (e.g. dye) are not necessary.
Level 2 :Estimation of age if epiphyseal line seen.

Shoulder region Hip region
Arm Thigh
Elbow region Knee region
Fore arm Leg
Wrist and hand Ankle region

Plain X-ray Plain X-ray
Ba meal Ba swallow
Ba meal follow through Bronchogram
Ba enema CT mediastinum
Oral cholecystogram High resolution CT lung
Intravenous urogram
Ascending pyelogram
Abdominal Aortogram
CT abdomen

X-ray skull plain
Carotid angiogram
Vertebral arteriogram
CT Scan brain
Plain X-ray cervical region

G) SURFACE Anatomy


i) Upper Limb
NERVES: Radial nerve, Median nerve, Ulnar nerve, Axillary nerve,
Musculocutaneous nerve
VESSELS: Axillary artery, Brachial artery, Radial artery, Ulnar artery, Superficial
and deep palmar arches

ii) Lower Limb
NERVES: Femoral, Sciatic, Common peroneal nerves
VESSELS: Great saphenous & Small saphenous veins; Femoral, Popliteal & Dorsalis pedis arteries

ORGANS: 9 regions and projection of organs in them; Stomach, Duodenum, Caecum, Appendix, Ascending,, transverse and descending colon, Pancreas, liver , Gall bladder, spleen , Kidneys (ventral and dorsal)
Abdominal aorta

heart and valves, Lungs, fissures and hilum; Pleurae, Trachea

ORGANS: Parotid gland & duct
Middle meningeal artery, Facial artery
Pterion, Bregma, Reid’s base line, Suprameatal triangle
Thyroid gland
Common carotid artery, External carotid artery, Internal carotid artery, Internal jugular vein, Trachea

vi) brain : Lateral sulcus, Central sulcus, Median longitudinal fissure, Superior sagittal sinus, Sigmoid sinus, transverse sinus

II) LIVING Anatomy :

Clavicle, Spine of scapula, Inferior angle, Coracoid process, Epicondyles of humerus, Olecranon process of ulna; Head and styloid processes of radius and ulna, Heads of metacarpals (knuckles), Pisiform, Hook of Hammate

Shoulder girdle, Shoulder joint, Elbow joint, Radio-ulnar joints, Wrist joint, 1st carpo-metacarpal joint, MP and IP joints

Principle of testing: Trapezius, Serratus anterior, Latissimus dorsi, Pectoralis major, Deltoid, Biceps Brachii, Brachioradialis, Brachialis, Extensors at the elbow, Supinators, Wrist extensors, Wrist flexors, Small muscles of the hand

NERVES: Dermatomes, Ulnar
Ulnar nerve thickening in Leprosy

VESSELS (PALPATION OF): Axillary artery, Brachial artery, Radial artery
OTHERS: Axillary groups of lymph nodes; Anatomical snuff-box (boundaries)

(BONY) LANDMARKS (PALPATION OF): Anterior superior iliac spine, Iliac crest, Tubercle of the iliac crest, Ischial tuberosity, Greater trochanter, Adductor tubercle, Head and neck of fibula, Lateral and medial malleoli, Tibial tuberosity, Subcutaneous surface of tibia, Patella
JOINTS (DEMONSTRATION OF MOVEMENTS): Hip , Knee , Ankle , Subtalar Joints
MUSCLES (DEMONSTRATION OF ACTION): Hip-Flexors, Extensors, Abductors, Adductors
Knee: Flexors, Extensors,
Ankle: Dorsiflexors, Plantar flexors
Subtalar: Invertors, Evertors
NERVES: Dermatomes, Sciatic, Tibial, Common peroneal, Femoral, Obturator
Thickening of common peroneal nerve in Leprosy

VESSELS (PALPATION OF): Femoral, Popliteal, Dorsalis pedis, Posterior tibial
OTHERS: Ligamentum patellae, Inguinal lymph nodes
TENDONS: Semitendinosus, Semimembranosus, Biceps femoris, Iliotibial tract

(BONY) LANDMARKS (PALPATION OF): Anterior superior iliac spine, Pubic tubercle
MUSCLES (DEMONSTRATION OF ACTION): Obliques, Transversus abdominis, Rectus abdominis
NERVES: Dermatomes
OTHERS: Enlarged liver , spleen , kidneys, Abdominal quadrants and regions; Position of superficial and deep inguinal rings; Renal angle; McBurney’s point;
Level2: Murphy’s sign

iv) THORAX (BONY) LANDMARKS(PALPATION OF): Sternal angle, Counting of rib spaces, locating thoracic spines
NERVES: Dermatomes
OTHERS: Apex beat, Apices of the lungs, Triangle of auscultation

v) HEAD FACE NECK - (BONY) LANDMARKS(PALPATION OF): Nasion, Glabella, Inion, Mastoid process, Suprameatal triangle, Zygoma, Zygomatic arch, Angle of mandible, Head of mandible,
MUSCLES (DEMONSTRATION OF ACTION): Of Mastication, Of Facial expression
Cranial nerves (I to XIII) testing
(PALPATION OF): Superficial temporal artery, Facial artery
(PALPATION OF): Symphysis menti, Hyoid bone, Thyroid cartilage, Cricoid cartilage, Tracheal rings, Suprasternal notch, Transverse process of atlas, Spine of C7
(DEMONSTRATION OF MOVEMENTS): Atlanto-occipital joint, Cervical joints
(DEMONSTRATION OF ACTION): Sternocleidomastoid, Neck flexors and extensors
(PALPATION OF): Common carotid artery, External carotid artery
OTHERS: Thyroid gland, Cervical lymph nodes, (Horizontal and vertical), Midline structures in the neck

NOTE :- Level 2 and 3 mentioned in the above syllabus includes the topics " desirable to know" (level-2) and " Nice to know" ( level-3. The remaining topics fall under the group " Must Know" ( level-1.)

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