An intracranial aneurysm is a fairly common incidental finding at postmortem examination, with a prevalence ranging from 1 to 6 percent among adults in large autopsy series. Many of these aneurysms, however, are very small, and the prevalence of incidental intracranial aneurysms among adults undergoing cerebral angiography is between 0.5 and 1 percent.

Most intracranial aneurysms remain asymptomatic until they rupture and cause a subarachnoid hemorrhage.

Some of them grow to a large size and compress the neighborhood nerves and present with neuropathies.

 Pathology:

Saccular (Berry) aneurysms:

Approximately 85% of all spontaneous hemorrhages into the subarachnoid space arise from rupture of saccular aneurysms at the base of the brain. Such aneurysms are not congenital, but develop during the course of life. Cerebral aneurysms almost never occur in neonates and they are also rare in children. In those exceptional cases, there is usually a specific underlying cause for the aneurysm, such as trauma, infection or connective-tissue disorder.

The majority of intracranial aneurysms (80 to 85 percent) are located in the anterior circulation, most commonly at the junction of the internal carotid artery and the posterior communicating artery, the anterior communicating-artery complex, or the trifurcation of the middle cerebral artery.

It is largely unknown why only some adults develop aneurysms at arterial bifurcations and most do not. The once popular notion of a congenital defect in the muscle layer of the wall (tunica media) being a weak spot has not been accepted now. Any defect in the muscle layer is located not at the neck of the aneurysm, but somewhere in the wall of the aneurysmal sac.

A role of acquired changes in the arterial wall is likely because hypertension, smoking and alcohol abuse are risk factors for SAH in general. It may well be the influence of these factors that leads to local thickening of the intimal layer ( ‘intimal pads') in the arterial wall, distal and proximal to a branching site, changes that some investigators regard as the earliest stage in the formation of aneurysms. The formation of these pads, in which the intimal layer is inelastic, may cause increased strain in the more elastic portions of the vessel wall. Also, structural abnormalities in structural proteins of the extracellular matrix have been identified in the arterial wall at a distance from the aneurysm itself.

Aneurysms arising from the intracranial arteries are much more common than those arising from extracranial arteries of similar size. One possible reason for this discrepancy is that as compared with their extracranial counterparts, intracranial arteries have an attenuated tunica media and lack an external elastic lamina. On microscopical examination, the typical saccular, or berry, aneurysm has a very thin tunica media or none, and the internal elastic lamina is either absent or severely fragmented. Thus, the wall of the aneurysm is generally composed of only intima and adventitia, with variable amounts of fibrohyaline tissue interposed between these two layers.

Macroscopically, many intracranial aneurysms, especially those that rupture, have an irregular appearance, with one or more daughter sacs and variable wall thickness. The point of rupture is generally in the dome of the aneurysm.

Genetic Risk factors: Familial intracranial aneurysms are much more common than has generally been appreciated. According to several epidemiologic studies, 7 to 20 percent of patients with aneurismal subarachnoid hemorrhage have a first or second degree relative with a confirmed intracranial aneurysm. The familial aggregation of intracranial aneurysms was first described in 1954 by Chambers et al. Considerable evidence supports the role of genetic factors in the pathogenesis of intracranial aneurysms.

Recent studies have also indicated that the familial aggregation of intracranial aneurysms is not a matter of chance. Among first-degree relatives of patients with aneurismal subarachnoid hemorrhage, the risk of a ruptured intracranial aneurysm is approximately four times higher than the risk in the general population.

In most families with intracranial aneurysms, only two or three members are known to be affected, and the inheritance pattern is unclear. The two main lines of evidence are the association of intracranial aneurysms with heritable connective-tissue disorders and their familial occurrence. Of the numerous heritable connective-tissue disorders that have been associated with intracranial aneurysms, the most important are autosomal dominant polycystic kidney disease, Ehlers–Danlos syndrome type IV, neurofibromatosis type 1, and Marfan's syndrome. It is not known to what extent these specific heritable disorders are present in the population of patients with intracranial aneurysms.

As compared with sporadic intracranial aneurysms, familial aneurysms rupture at an earlier age, may be smaller when they rupture, and are more often followed by the formation of a new aneurysm.

Affected siblings are often in the same decade of life at the time of the rupture.

Environmental Factors: Of the various environmental factors that may confer a predisposition to aneurismal subarachnoid hemorrhage, cigarette smoking is the only factor that has consistently been identified in all the populations studied, and it is also the most easily preventable. The estimated risk of an aneurismal subarachnoid hemorrhage is approximately 3 to 10 times higher among smokers than among nonsmokers. In addition, the risk increases with the number of cigarettes smoked, and patients who continue to smoke after an initial subarachnoid hemorrhage may be at especially high risk for the development of a new aneurysm.

It is unclear how cigarette smoking affects the development of aneurysms, but several hypotheses have been proposed. Cigarette smoking has been shown to decrease the effectiveness of 1-antitrypsin, the main inhibitor of proteolytic enzymes (proteases) such as elastase, and the imbalance between proteases and antiproteases in smokers may result in the degradation of a variety of connective tissues, including the arterial wall. In support of this hypothesis is the observation that patients with a genetically determined 1-antitrypsin deficiency may also be at increased risk for the development of intracranial aneurysms.

Hypertension is the most frequently studied risk factor for the development and rupture of intracranial aneurysms. Several studies have shown that hypertension is associated with an increased risk of aneurismal subarachnoid hemorrhage, as well as unruptured intracranial aneurysms. Although the data are inconsistent, taken together they suggest that hypertension poses a risk of aneurismal subarachnoid hemorrhage, but probably not as high a risk as that associated with cigarette smoking.

The incidence of aneurysmal subarachnoid hemorrhage, unlike other types of stroke, is higher among women than among men. Before the fifth decade of life, however, aneurismal subarachnoid hemorrhage occurs more frequently in men, suggesting the role of hormonal factors.

The use of low-dose oral contraceptives by premenopausal women does not increase and may even decrease  the risk of subarachnoid hemorrhage.

The risk of aneurismal subarachnoid hemorrhage is lower among postmenopausal women receiving hormone replacement therapy than among postmenopausal women not receiving such therapy, but not as low as the risk among premenopausal women. These data suggest that premenopausal women have a low risk of aneurismal subarachnoid hemorrhage, postmenopausal women have a relatively high risk, and postmenopausal women receiving hormone-replacement therapy have an intermediate risk.

A moderate-to-high level of alcohol consumption is an independent risk factor for aneurismal subarachnoid hemorrhage. Recent, heavy use of alcohol (binge drinking) in particular appears to increase the risk of subarachnoid hemorrhage.

The data on hypercholesterolemia as a risk factor for aneurismal subarachnoid hemorrhage are inconsistent.

Other causes of Aneurysms:

Septic aneurysms: Infected tissue debris entering the blood stream may lodge in the wall of cerebral arteries and lead to aneurysmal dilatation. The traditional term`mycotic aneurysms' refers only to fungi and should perhaps be discarded; after all, bacterial endocarditis is more common as an underlying condition than aspergillosis. Aneurysms associated with infective endocarditis are most often located on distal branches of the middle cerebral artery, but 10% of these aneurysms develop at more proximal sites, and rupture of a septic aneurysm causes an intracerebral hematoma in most patients, but some have a basal pattern of hemorrhage on CT that is very similar to that of a ruptured saccular aneurysm.

Septic aneurysms in patients with aspergillosis are usually located on the proximal part of the basilar or carotid artery. Rupture of such an aneurysm causes a massive SAH in the basal cisterns, indistinguishable from that of a saccular aneurysm. Aspergillosis is difficult to diagnose, but should particularly be suspected in patients undergoing long-term treatment with antibiotics or immunosuppressive agents.

Severely HIV-infected children may develop cerebral aneurysms secondary to generalized arteriopathy. In HIV-infected adults, aneurismal SAH can also be coincidental.

Aneurysms associated intracranial tumors: Aneurysms associated with tumor are usually incidental. It is suggested that neoplasm increases local blood flow which predispose to aneurysms. Some (meningoma) may have dysgenetic factors. Hormone factors are suggested because of high frequency of pituitary adenoma with aneurysms.
Cerebral metastases may in exceptional cases infiltrate the wall of an intracranial artery, and thus cause an aneurysm to develop, even >1 year after operation on the primary tumor.

Iatrogenic causes include radiation therapy, acrylate applied externally for microvascular decompression and operation for a superficial temporal artery-middle cerebral artery bypass, with the aneurysm at the site of the anastomosis.

 Asymptomatic Intracranial Aneurysms:

The discrepancy between the prevalence of incidental intracranial aneurysms at autopsy and the incidence of aneurismal subarachnoid hemorrhage indicates that most aneurysms never rupture. With the widespread use of computed tomographic scanning and magnetic resonance imaging, many unruptured asymptomatic intracranial aneurysms can now be detected.

The natural history of such aneurysms is incompletely understood, but all the large studies have reported annual rupture rates of 0.5 to 2 percent.

The rate of rupture increases with the size of the aneurysm but appears to be unrelated to the age or sex of the patient or to the presence or absence of hypertension. Data suggest that only intracranial aneurysms that are 10 mm or larger in diameter carry a significant risk of subsequent rupture, but there is still considerable controversy about the size below which the risk of rupture is negligible.

Screening

The natural history of asymptomatic intracranial aneurysms is not well defined, and the benefits of screening have never been quantified. Screening for asymptomatic intracranial aneurysms appears to be warranted, because aneurismal subarachnoid hemorrhage has a dismal prognosis, whereas the treatment of most asymptomatic intracranial aneurysms is associated with a fairly low rate of morbidity (less than 5 percent) and mortality (less than 2 percent).

Screening has been suggested for patients at high risk for the development of an aneurysm.

The two groups of patients most commonly screened are those with a family history of intracranial aneurysms, and

those with autosomal dominant polycystic kidney disease.

In the absence of any clinical feature or biologic marker that can identify persons in whom intracranial aneurysms are most likely to develop, screening is generally recommended for asymptomatic members of families with two or more affected members. Although the extent of screening depends on the apparent inheritance pattern in a particular family, usually only first-degree relatives are screened. Using such a screening program, Detection rate is about 9 percent with affected family members.

Some investigators have suggested screening of persons even with only a single affected family member. However, the absolute lifetime risk of subarachnoid hemorrhage for persons with one affected first-degree relative is small (1 percent at the age of 50 and 2 percent at the age of 70), even though they have a risk of aneurismal rupture that is four times higher than that in the general population. Screening is therefore not recommended for such persons.

Approximately 5 to 10 percent of asymptomatic adults with autosomal dominant polycystic kidney disease who undergo screening are found to have saccular intracranial aneurysms. Clustering of intracranial aneurysms has been reported in several families with autosomal dominant polycystic kidney disease, and screening reveals asymptomatic aneurysms in 20 or 25 percent of the members of such families. Therefore, although screening for asymptomatic intracranial aneurysms in patients with autosomal dominant polycystic kidney disease remains controversial, most investigators agree that screening is indicated for those patients who also have family histories of intracranial aneurysms.

 Surgery:

Dott successfully wrapped a ruptured berry aneurysm in 1931. Dandy was the first to use a metal clip in 1944. Since then great strides have been made. The aim of the surgical intervention is to prevent a rebleed unless it is for hydrocephalus or intracerebral hematoma.

Pre-operative assessment: 

1) Duration since last bleed:

About 40% patients with ruptured aneurysms die following the first hemorrhage.40% of survivors will rebleed in the I year.25% will rebleed in 2 weeks, with the incidence markedly decreasing over the next 6wks. Beyond this, the rebleed rate is about 3% and death is about 2% per year The proponents of early operation (within 3 days) believe that overall mortality can be improved by correction of vasospasm by means of  induced vascular hypertension and cerebral perfusion in the presence of a secured aneurysms. They also claim, irritating blood products from the basal cisterns, which are presumed to be the cause for vasospasm can be removed during surgery. Others feel operative manipulation offset the overall management. 

Certainly it should not be delayed beyond the period of vasospasm. 

2) Clinical grades & dynamic trend: 

If the trend is toward a poorer grade, many believe the surgery should be delayed. If the trend is towards a better grade, surgery may be considered.

3) Age:

Generally patients above 60 years do not tolerate major cerebrovascular procedures as well as the younger do. However each patient should be considered with her or his prebleed life style and other factors.

4) Associated medical problems:

The systemic problems, such as diabetes must be corrected before surgery to a reasonable level.

5) Blood pressure:

Rise in blood pressure, assumed due to elevated catecholamines, is usual in SAH. A relentless increase may herald vasospasm and should alert the surgeon to possible operative complications Reasonable stabilization is advised before surgery. A stable blood pressure even on the higher side is preferable to unstable B.P.

6) Study of the angiography:

Discussion with the radiologist helps, as also presence of the surgeon during angiography. The site, size, walls, configuration, the number aneurysms must be studied which will help the surgeon in deciding the optimal approach.

Length of supraclinoid carotid gives a clue on required frontal lobe retraction at surgery. State of cross circulations, asymmetry of circle of Willis, anomalous anterior cerebral artery, carotid basilar anastamosis, aplasia of one carotid or vertebral must be studied.

In the absence of ophthalmic artery, meningo orbital artery (superior orbital branch of middle meningial artery) may be the primary blood supply to retina and warn the surgeon while drilling the lesser wing at surgery. 

7) Local physiological & anatomical assessment:

Local pathological changes  clot, vasospasm, edema & hydrocephalus can be studied with CT and or MRI along with angio. When hydrocephalus (10%) or hematoma (10%)requires surgical intervention to save life, it is prudent that the aneurysms should be secured at the same sitting. 

8) Associated conditions:

a) Reports suggest that 1-2% of aneurysms are associated with AVM and 5% of AVM are associated with aneurysm. Ideally both must be treated in one sitting which is not possible always. Generally, aneurysms is the assumed culprit and treated first.

b) Carotid stenosis (associated with aneurysms) may be treated first if the aneurysm has not bleed. In the presence of bleed, aneurysms gets the priority. Of course, ideal will be if both can be treated simultaneously.

c) In Moyamoya disease, the aneurysms represent a false one and may disappear without surgery.

d) Aneurysms associated with tumor are usually incidental. It is suggested that neoplasm increases local blood flow which predispose to aneurysms. Some (meningoma) may have dysgenetic factors. Hormone factors are suggested because of high frequency of pituitary adenoma with aneurysms. Treatment is directed to symptomatic tumor. 

e) Aortic stenosis and polycystic kidney are the only 2 congenital anomalies with correlation with aneurysms. They may have congenital origin, but they also cause high BP which may be a factor.

f) Connective tissue diseases such as fibromuscular dysplasia, Ehler Danlos syndrome, Marfan's, Lupus erythematosis, have sporadic association Ehler Danlos lack collagen and the adventitia and elastic are ineffective. 

g) Familial aneurysms and need to screen the family members are still unanswered.

h) Aneurysms detected during pregnancy are treated as any other. 

i) Mycotic aneurysms carries higher (80%) mortality because of their  fragility.

CT-documented rebleeds have been reported. Septic aneurysms can be obliterated by surgical or endovascular treatment, but they usually resolve after adequate antibiotic therapy.

j) Aneurysms in cancer patients are due to oncotic emboli, destroying the wall of the artery. Cancer gets the priority in treatment. 

k) Traumatic ones are fragile and normally at distal anterior cerebral and intracavernous int. carotid and need surgical intervention. 

9) Special Tests:

Special tests such as PET, Isotope Scan, Doppler provide information on CBF and during temporary occlusion. 

10) In case of multiple aneurysms:

Ideally all the aneurysms on one side are attended to simultaneously.

If it is  not possible, the aneurysms which have bled, shall get the priority.

The following will help to decide the aneurysms which one has bled ,
a) History and clinical exam.

b) EEG 

c) Isotope scan-Rapid flow suggest perfusion; Static flow suggest infarct. 

d) CT & MRI-reveals midline shift, hemotoma and SAH.

e) Cerebral angiography-from displacement of vessels due to clot, from contour of the aneurysms with nipple like protrusion, from seepage of contrast. 

Largest, in the absence of above, is assumed to be the one which has bled.

Care must be taken with thickened bands of archnoid which cross the origins of the middle cerebral and anterior cerebral arteries.

Anterior circulation:
The optic nerve is the landmark in this region. It should be identified early at exposure. 

Posterior communicating Artery:

It originates from the inferior wall of the supraclinoid  IAC just distal to the anterior clinoid process and exits from the carotid cistern , runs medially (hidden from the surgeon in a subfrontal approach) to enter  the interpedunclar cistern to join the posterior cerebral artery. In 10% of the patients it is absent or hypoplastic. Its branches supply the optic chiasm and tract, mammilary bodies, hypothalamus and inferior thalamus.

Anterior Choroidal Artery: 

It arises few mms distal to P.com.artery and runs laterally, following the optic tract posteriorly. It is duplicated in about 30% of patients. It gives off  'uncal artery' which supplies the uncus, part of amygdala, and anterior hippocampus. The main trunk supplies the choroid plexus and anastomoses distally. In its course through the carotid cistern it supplies, through perforating branches, to inferior chiasm, parts of optic tract & globus pallidus, the genu of the internal capsule, part of cerebral peduncle, red nucleus, the subthalamus and thalamic nuclei and further distally, to lateral geniculate body, the internal capsule and the optic radiations. Obviously loss of this vessel is devastating.

Middle Cerebral Artery:

The ICA bifurcates at a variable distance from the anterior clinoid. The middle cerebral, from the origin to bifurcation is termed the 'M1'segment which gives off the superior lateral and the inferior medial perforating branches (lenticulo-striate) at its proximal part. The lenticulo-striate branches supply the anterior commisure, the putamen, the lateral globus pallidus, the superior internal capsule and the head and body of the caudate nucleus. The surgeon must look for these during archnoid dissection. The 'M2'segment is distal to the bifurcation. In about 20% of the patients there is a trifurcation instead of bifurcation. The orbitofrontal, pre-frontal, angular and posterior temporal arteries arise proximally from 'M2' and supply the cortex.

Anterior Cerebral Artery:

Anomalies are common, especially in patients with aneurysms. The 'A1' segment extends from the carotid bifurcation to the anterior communicating artery and the rest is termed the 'A2' segment. 

Typically one A1 is dominant. The proximal perforators postero inferiorly and distal perforators close to the anterior communicating artery, and  perforators from the anterior communicating artery (typically from the  inferior side of the neck of the aneurysm) supply the infundibulum, optic chiasm, fornix, internal capsule, striatum and hypothalamus. In 25% of the patients the communicator has various anomalies.

The recurrent artery of Heubner usually arise close to A.Com.Art. from A1 or A2 segment and runs parallel to the anterior cerebral artery laterally along the inferior frontal lobe and at risk during resection of the rectus gyrus. It supplies parts of caudate nucleus, the putamen, the globus pallidus,and internal capsule.

Posterior circulation: 
Vertebral Artery:

It is the 1st branch of the subclavian and enters the transverse foramen of C6. At C3 it turns laterally and enters the foramen at C2 and exits  through the foramen of C2 behind atlantoaxial joint and lies along the  posterior arch of C1. It penetrates the dura at foramen magnum, goes laterally and then ventrally to join the contralateral artery to form the basilar artery.

In 15%, one artery is dominant. In addition to the posterior inferior  cerebellar artery and anterior spinal artery, it gives off perforators  to the to medulla and occasional posterior spinal artery and few  meningeal branches.

Posterior Inferior Cerebellar Artery:

It is quite variable. In about 10%, it is absent. In about 50% it arises from the proximal vertebral artery. It loops along the lateral medulla and turns superiorly to complete the caudal loop. It then passes superiorly as a cranial loop and then crosses the cerebellar tonsil. The artery supplies the choroid plexus of the 4th ventricle, cerebellar tonsil, vermis and cerebellar hemisphere.

Basilar artery:

The vertebral arteries join along the anterior surface of the medulla, close to the pontomedullary junction. The artery is deviated to the side of the smaller vertebral artery. It extends along the ventral surface of the pons and terminates in the interpeduncular cistern into posterior cerebral arteries. In about 50%, the tip is at the level of the posterior clinoid. In 15%, the labyrinthine or the internal auditory artery arises  from the basilar artery. The perforating arteries from the trunk project  posteriorly. The anterior cerebellar artery and superior cerebellar artery are the major branches.

Anterior Inferior cerebellar Artery:

In most, it arises from the proximal basilar. Typically the right and left arteries arise at the same level. It runs inferiorly and laterally to the IAM. The labyrinthine artery arises from AICA in about 85% of the patients. It also supplies the pons, middle cerebellar peduncle, flocculus, tegmentum and cerebellar hemisphere.

Superior Cerebellar Artery:

In 85% of the patients, the left and right ones arise from the basilar as a single trunk. At its origin, it is separated from the posterior cerebral artery by the 3rd nerve. It supplies the superior the superior aspect of the cerebellar hemispheres, the superior cerebellar peduncle, the dentate nucleus and a portion of the middle cerebellar peduncle. 

Surgical instrumentation:
1) A binocular dissecting microscope with its superb magnification, clearer stereoscopic images, and improved illumination is a must, needless to say. It makes it possible for a smaller exposure with less brain retraction. Micro instruments along with bipolar forceps, lyla retractors and fine tipped suckers are essential for fine dissection.  

2) Clips: Generally, shorter clips have more closing pressure, the pressure is more near the shank.  

(a) Yasargill's clips are cross action clips and popular. Their small shank do not obscure vision.
(b) Sugita's clips are some what similar and comes in various angles.
(c) Heifetz clips have broader wings with an internal spring action and are preferred for thin, friable walls by some.
(d) less commonly malleable clips are used. 
(e) Temporary clips differ from permanent clips with their closing pressure not exceeding 25-40 gm.
(f) Fenestrated and the right angled ones are ideal for larger aneurysms with a broad neck, especially at the internal carotid and basilar tree. 

3) Other agents:

Protective coatings include muscle, fascia, gelatin, cotton and synthetic agents such as methylmethacrylate, EDH adhesive (bioband) come handy when surgeon is faced with unclippable aneurysm. Cotton is the only one with proven effect.

Surgical Technique: click for intraoperative videos

(a) Saccular aneurysms must be considered for clipping these days, whatever the size is, as they are not ideal for interventional radiology as it stands today. Broad neck, calcification at the neck, presence of intraluminal thrombus are more common in giant aneurysms and make clipping a difficult proposition. Angled, fenestrated, strong and extra strong clips are required. It is unusual that a single will suffice. 

Three basic systems of clip application are often used. 
 

(1) Piggyback or booster clip is a second clip placed so as to increase and reinforce the closing pressure of the primary clip.

(2) Tandem clipping involves application of 2 or more clips across the neck usually with short blades across the distal neck. With progressive distal application of these clips, a neck can be fashioned and occluded.

(3) Picket fence or parallel clipping is a system wherein clips are applied parallel to one another usually perpendicular to the plane of neck, lined up like a picket fence. It is wise to expose the proximal artery such as carotid or vertebral before dissection. Temporary proximal occlusion or aspiration of the sac or the use of an encircling silk ligature to narrow the neck may make clip occlusion possible. Rarely hypothermia (down to 16 degree c) and cardiopulmonary by pass in selected cases may be useful. 

(b) Fusiform aneurysms have no neck and not amenable for clipping. Excision and anastomosis with graft is ideal. But proximal (Hunterian ligation) or trapping are more commonly used with or without bypass.

Interventional radiology has largely replaced the need of these measures. When such measures are contemplated without bypass, the following pre op tests help to assess the viability of such procedures.

1) Mata's test - Common carotid is compressed at bed side for 10 mts. and the pt is examined clinically for a deficit (unreliable and uncomfortable).

2) Temp. occlusion (at surgery) for 30 mts and the pt is observed with or without EEG. This reveals only pts who are immediately intolerant and is of no help in the rest.

3) During angiography a cross circulation may be assessed with contra-lateral compression. 70% of those with giant aneurysms will show filling of opposite AC & MC and are good candidates. 25% of them fill only AC and ligation may be considered with some risk.

4) Carotid artery pressure determinations are reliable. Both carotids are exposed and the clamp applied. The pressure of the carotid stump distal to the clamp is measured. If the reduction of the pressure is not more than 50% when compared to the unclamped one the procedure is safe.

5) Ideal is Xenon study with temp clamping. If the CBF is more than 40ml/mt/100gm the procedure is safe. Less than 20 ml it is not safe. In between it is probably safe if the reduction is less than 25%. Crutch field clamp is ideally used. 

Post operative care:
Absolute bed rest with head kept flat and close surveillance of electrolytes is warranted. Some prefer to institute, 'triple H' (Hypervolemic, hypertensive, hemodilution) treatment for 2-3 days. Anti-convulsants are routinely given as the incidence of post op fits is next only to that of abscess.

It is wise to repeat angiogram in cases where there is doubt of complete occlusion. If facilities available an intra operative angiogram may be arranged. If done, brain swelling must be anticipated. 

Whatever discussed above is for some one at the bottom of the learning curve. As they go up in the curve, they form their own principles and technique, after all, medicine is an ever changing field!!.