Search This Site

Wednesday, November 9, 2005

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
www.jpgmonline.com


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: http://www.jpgmonline.com/article.asp?issn=0022-3859;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 http://www.jpgmonline.com/viewimage.asp?img=jpgm_1993_39_4_179_598_1.jpg) 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 http://www.jpgmonline.com/viewimage.asp?img=jpgm_1993_39_4_179_598_2.jpg .





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
www.jpgmonline.com


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: http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2002;volume=48;issue=2;spage=155;epage=155;aulast=Gandhi

Sir,
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
CARTILAGE
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
RETINACULA & APONEUROSES

V) Integument

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

b) SUPERFICIAL FASCIA
Distribution of fat, functions

c) DEEP FASCIA
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

B) REGIONAL Anatomy

I) UPPER LIMB
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;

ARTHROLOGY
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

OSTEOLOGY
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 -
Colles’ FRACTURE , Smith’s FRACTURE
Carpals, Metacarpals, Phalanges: Carpal tunnel syndrome, FRACTURE scaphoid
Surgical approaches, Subluxation of head of radius, carrying angle

MYOLOGY:
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,

NEUROLOGY:
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

II) LOWER LIMB

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

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

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

ANGIOLOGY
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

NEUROLOGY
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

III) ABDOMEN

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

SPERMATIC CORD
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
ARTHROLOGY
Movements of lumbar vertebrae, lumbosacral, sacroiliac, sacrococcygeal joints

vii) Angiology :- Origin, course, termination, relations, branches & applied Anatomy of
PORTAL VEIN
Level 2: portasystemic communications
Level 3: Portasystemic communications in detail; Development
INFERIOR VENA CAVA,ABDOMINAL AORTA,INTERNAL ILIAC ARTERY

viii) Neurology, lumbar plexus, sacral plexus


IV) THORAX
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
SUPERIOR AND POSTERIOR MEDIASTINA, LIST OF STRUCTURES
Boundaries and contents:
Level 2 : Superior mediastinal Syndrome, Course, relation and branches / area of drainage
Level 3: Coarctation of aorta, aneurysm, developmental anomalies

iii)Pleura
Pleural reflections, recesses, innervation
Level 2: importance of recesses
Level 3: pleural effusion
LUNGS
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
heart
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.

v)Osteology
IDENTIFICATION and parts of VERTEBRAE , RIBS - and STERNUM
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

V) HEAD-FACE NECK

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

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

FACE
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
TM JOINT
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
ARTERIES
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
VEINS
External and internal Jugular veins, venous drainage of face

VENOUS SINUSES
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



VI) NEUROANATOMY

i) SPINAL CORD
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

ii) MEDULLA OBLONGATA
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

iv) CEREBELLUM
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

v) MIDBRAIN
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

vi) CEREBRUM
CORTEX, WHITE MATTER, BASAL NUCLEI, LIMBIC LOBE
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

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

x) MENINGES
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


C) MICROANATOMY

I) GENERAL HISTOLOGY

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


II) SYSTEMIC HISTOLOGY

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;
Sacral;
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

D) DEVELOPMENT Anatomy

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

E) GENETICS

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

F) RADIOLOGICAL Anatomy

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.

II) UPPER LIMB – X-Ray of III) LOWER LIMB
Shoulder region Hip region
Arm Thigh
Elbow region Knee region
Fore arm Leg
Wrist and hand Ankle region
Foot



IV) ABDOMEN V) THORAX
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
Cystogram
Ascending pyelogram
Abdominal Aortogram
Hystero-salpingogram
Myelogram
CT abdomen



VI) HEAD-FACE
X-ray skull plain
Carotid angiogram
Vertebral arteriogram
CT Scan brain
NECK
Plain X-ray cervical region

G) SURFACE Anatomy

I) SURFACE MARKING:

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

iii) ABDOMEN
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

iv) THORAX
heart and valves, Lungs, fissures and hilum; Pleurae, Trachea


v) HEAD FACE NECK
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 :

i) UPPER LIMB
(BONY) LANDMARKS(PALPATION OF):
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

JOINTS (DEMONSTRATION OF MOVEMENTS):
Shoulder girdle, Shoulder joint, Elbow joint, Radio-ulnar joints, Wrist joint, 1st carpo-metacarpal joint, MP and IP joints

MUSCLES (DEMONSTRATION OF ACTION)
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)

ii) LOWER LIMB
(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

iii) ABDOMEN
(BONY) LANDMARKS (PALPATION OF): Anterior superior iliac spine, Pubic tubercle
JOINTS (DEMONSTRATION OF MOVEMENTS): Intervertebral
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
JOINTS (DEMONSTRATION OF MOVEMENTS): Intervertebral
MUSCLES (DEMONSTRATION OF ACTION): Respiratory movements
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,
JOINTS (DEMONSTRATION OF MOVEMENTS): Temporomandibular joint
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.)

Maharashtra MBBS Students Transfer

Maharashtra UNIVERSITY OF HEALTH SCIENCES

No. MUHS / EO / 71 /3097 / 2005 Date : 08/09/2005

Academic Notification No. 04/2005

Sub :- Students Transfer from one recognised College to other recognised College.

This is notified to all concerned that, the University has framed the Rules governing transfer for 1st year passout candidates of MBBS / BDS / BAMS / BUMS / BHMS / OT / PT / B.Sc. (HLS) Courses. The said rules are available on the University Website. The students desirous of transfer to another College shall have to apply to the University in the prescribed form along with necessary fee, before cut off date for respective faculties.

The applications for student transfer may be submitted on or before cut off date mentioned below along with necessary documents and D.D. of Rs. 500/- drawn in favour of 'Registrar, Maharashtra University of Health Sciences, Nashik' from any Nationalised Bank, payable at Nashik.

Applications received after cut off date shall stand rejected.

For student transfer rules and application form, refer Direction No. 03/2002, which is available on the Website.

Maharashtra UNIVERSITY OF HEALTH SCIENCES

Mhasrul, Dindori Road, Nashik – 422 004.

Phone: 0253-2539190 - 94 / EPABX: 0253-2539100, 300 / Fax: 0253-2539195

E-mail: academic at muhsnashik.com / Web: www.muhsnashik.com

Internship transfer in Maharashtra

Maharashtra UNIVERSITY OF HEALTH SCIENCES

No. MUHS / EO / 54 /3098 / 2005 Date : 08/09/2005

Academic Notification No. 03/2005

Sub :- Internship Transfer from one affiliated College to other affiliated College.

This is notified to all concerned that, the University has framed the Rules governing Internship Training Programme for final year passout candidates of MBBS / BDS / BAMS / BUMS / BHMS / OT / PT / B.Sc. (HLS) Courses. The said rules are available on the University Website. The students desirous of transfer to another College for doing Internship Training Programme shall have to apply to the University in the prescribed form along with necessary fee, before cut off date for respective faculties.

The applications for internship transfer may be submitted on or before cut off date mentioned below along with necessary documents and D.D. of Rs. 1000/- drawn in favour of 'Registrar, Maharashtra University of Health Sciences, Nashik' from any Nationalised Bank, payable at Nashik.

Applications received after cut off date shall stand rejected.

For internship transfer rules and application form, refer Internship Training Programme of respective Faculty, which is available on the Website.

Maharashtra UNIVERSITY OF HEALTH SCIENCES

Mhasrul, Dindori Road, Nashik – 422 004.

Phone: 0253-2539190 - 94 / EPABX: 0253-2539100, 300 / Fax: 0253-2539195

E-mail: academic at muhsnashik.com / Web: www.muhsnashik.com

Saturday, November 5, 2005

Where Does a Post Plabber Stand?

Author: bindasnikhilg, Posted on Wednesday, November 02 @ 11:32:06 IST by RxPG at http://www.rxpgonline.com/article1492.html

This is basically a message to all UK bound doctors, please read this, these thoughts have given me strength and i hope it helps you somehow! I am yet to leave for UK but this is based on general views of doctors at UK.

The joy of a hard working doctor has no bounds on clearing the PLAB1.

Wishes of congratulations come from all corners; the excitement of having cleared one step of an important exam takes time to sink in.

Then the person starts enquiring about books and possible dates, coaching, places where he can stay.

This leads him to contact all people at UK known to family and friends. Then the real picture starts emerging. Some people reply and some regular contacts seem to vanish into thin air ;-)

Still he doesn’t loose hope, he sits for hours together on the computer, sending letters to consultants at UK requesting for clinical attachment. For every negative reply he gets, he sends 3 more requests for clinical attachment. His spirits are high in spite of the odds.

Then comes the time to book his PLAB Part 2 seat, book his coaching, he gets ready to battle the UK winter, shopping tops the 'TO DO' list.

All is set, the big days arrives he leaves his homeland for so called greener pastures, while there at UK he slogs it out at the coaching centre, he may have been a king back home but the bitter reality starts staring him straight into his eye.

He clears the PLAB Part 2, there is joy, the emotional burden which he was carrying on his shoulders eases and the vigour and vitality returns. After a long wait for criminal verification is over, he starts clinical attachment with full enthusiasm.

This attachment gets over; he tries for another and another.

His resources, his stores are getting depleted, then he feels the crunch, he has no job, no security and nothing to fall back on in case he returns, all seems dark but that ray of hope is still shining in the distance.

Months pass, but that first job is still a mirage.

Where does he go from there, what should he do?

My advice to all is don’t stretch yourself till you feel your going to snap, man is like an elastic band which can only be stretched to a certain extent.

Realise this fact that you have tried your best, in case you don’t succeed it is not your failure; it just goes to show that the system could not accommodate you in the time frame you had set for yourself.

At this stage instead of loosing hope, gather yourself and arise from this situation, find solutions (in fact i would suggest all of you to plan your trip in such a way that even if you have to return back to your country, you do so in such a way that you give yourself enough time to plan for something else without giving yourself too much time to sit and dissect what went wrong at UK).

I hope and pray that whoever tires their level best at UK gets what they want but in case you don’t, please don’t feel dejected, be like the phoenix which arose from its ashes to fly higher than before.

Failure is all in your mind, if you believe you have failed then you have failed, if you believe that you have learnt something from the experience of staying at UK and have returned out of your own free will you can consider yourself a WINNER of sorts.

One article I had read had the caption, "end of Indian holiday”, what I believe is that if you consider it a holiday then I guess it doesn’t matter as one day every holiday has to end, and just in case you have one bad holiday you can make up for it by having another one.

TargetPG on FaceBook