OBSERVATIONS ON THE COURSE OF INTERNAL CAROTID ARTERY IN HUMAN CADAVERS
By
Dr. NIRMALA. D., M.B.B.S
A Dissertation submitted to the
Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore. In partial fulfillment Of the requirements for the degree of
Doctor of Medicine In Anatomy Under the guidance of
Dr. J. H. Sharieff, Ph. D Professor and H.O.D Department of Anatomy Govt. Medical College Mysore.
Department of Anatomy Government Medical College MYSORE 570001 2006
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES KARNATAKA
DECLARATION BY THE CANDIDATE
I here by declare that this dissertation entitled " OBSERVATIONS ON THE
COURSE
OF
INTERNAL
CAROTID
ARTERY
IN
HUMAN
CADAVERS" is a bonafide and genuine research work carried out by me under the guidance of Dr. J. H. Sharieff., Professor and Head of the Department of Anatomy, Govt. Medical College, Mysore.
Date: Place: Mysore
(DR. NIRMALA. D)
ii
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled " OBSERVATIONS ON THE COURSE OF INTERNAL CAROTID ARTERY IN HUMAN CADAVERS " is a bonafide research work done by Dr. Nirmala. D., in partial fulfillment of the requirement for the degree of the Doctor of Medicine in Anatomy.
Date:
(Dr. J. H. SHARIEFF, Ph. D) Professor & H. O. D Govt. Medical College Mysore
Place: Mysore
iii
ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE INSTITUTION
This is to certify that the dissertation entitled " OBSERVATIONS ON THE COURSE OF INTERNAL CAROTID ARTERY IN HUMAN CADAVERS" is a bonafide research work done by Dr, Nirmala. D., under the guidance of Dr. J. H. Sharieff., Professor and Head of the Department of Anatomy.
Seal & Signature Dr. J. H. Sharieff , Ph. D Professor & Head Department of Anatomy Government Medical College, Mysore.
Seal & Signature Dr. B. C. Vastrad, M. D Principal Government Medical College, Mysore.
Date: Place: Mysore
Date: Place: Mysore
iv
COPY RIGHT DECLARATION BY THE CANDIDATE I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall have the rights to preserve, use and disseminate this dissertation in print or electronic format for academic /research purpose.
Date: Place: Mysore
(Dr. NIRMALA. D)
© Rajiv Gandhi University of Medical Sciences, Karnataka.
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ACKNOWLEDGEMENT It is my great pleasure to acknowledge with deep sense of gratitude for the constant supervision and valuable encouragement offered by my respected teacher and guide Dr. J. H. Sharieff., Professor and Head of the Department of Anatomy, Govt. Medical College. Through out my work he has extended his valuable guidance with utmost patience and keen interest. I wish to express my thanks with due respect to Dr. C. M. Ramesh., Head of the Dept of Anatomy, JJM Medical College, Davangere and Dr. Shama Sunder., Head of the Dept of Anatomy, JSS Medical College, Mysore, for their kind gesture and co-operation by allowing me to collect the data of the specimens from their colleges. I gratefully acknowledge their support in completing my dissertation. I wish to thank with due respect and deep gratitude Dr. K. R. Dakshayani, Asst. Professor, Dept of Anatomy, Govt. Medical College, Mysore for her patience, suggestions and advice that helped me to a great extent. I wish to express my deep gratitude and regards to Dr. J. Poornima, & Dr. K. T. Chandrashekar, lecturers, for their kind co-operation & timely help. I extend my sincere thanks to Dr. Mudassir Azeez, Asst. Professor, Dept of Preventive & Social Medicine, Govt. Medical College, Mysore for the help rendered with respect to statistical analysis. I sincerely thank Sri William Raju & Sri Bhadrachala, dissection hall attenders, who helped in my study. I also thank dissection hall attenders of JJMMC & JSSMC, for their help in my study. I extend my heart felt thanks to my colleagues for their co-operation during my study.
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Last, but not the least, I extend my thanks to my family members who have stood by me as eternal source of inspiration & encouragement.
Date: Place: Mysore
(Dr. NIRMALA. D)
vii
LIST OF ABBREVIATIONS USED
•
ACA- Anterior cerebral artery
•
AO- After origin of ophthalmic artery
•
&- And
•
CC- Carotid canal segment of internal carotid artery
•
CV - Cavernous segment
•
C2,C3,C4 - Cervical vertebral 2nd ,3rd & 4th
•
CL - Clinoid segment
•
CCA - Common carotid artery
•
cm - centimeter
•
deg - Degree
•
ECA - External carotid artery
•
ECP - Extracranial portion
•
F - Female
•
ICA - Internal carotid artery
•
ICP - Intracranial portion
•
IJV - Internal jugular vein
•
M - Male
•
SD - Standard deviation
•
i.e., - that is
•
U - Unpaired
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ABSTRACT Background & Objectives: Blood supply to the brain is important to understand the etiology of cerebrovascular accidents. Brain is supplied by the carotid-vetebro-basilar system & internal carotid artery is an exclusive branch, which supplies the cerebral hemisphere. It's tortuous & unusual course with so many bends and kinks before its termination could reduce the blood supply causing ischaemia of the brain. Therefore the study of the entire course of ICA by dissection method is chosen to throw some light on the above lines. 1. To observe the length & diameter of different segments & to derive clinical significance of the same. 2. To evolve a proportion between straight course & angulated course. 3. To observe the bends & angulations in the course of ICA and to correlate them functionally. Methodology: The present study was undertaken on the 56 sagitally bisected formalin fixed head & neck specimens of adult human cadavers obtained from the dept of Anatomy of various medical colleges. The data was obtained on parameters like length, breadth & angles of different segments of ICA. Results: 1. Estimation of total length of ICA measured revealed higher values on the left side. 2. Estimation of diameter of ICA on both sides did not reveal any difference. 3. Measurement of the angles at IV bend of siphon exhibited more acuteness. 4. Additional bends were observed at the siphon part of ICA. 5. A small percentage of aneurysm was observed in the siphon part of ICA.
ix
6. A small percentage of kinks & bends were seen in cervical part of ICA. 7. A rare case of complete loop formation of cervical part of ICA was observed. Interpretation & results: The above observations revealed presence of more bends, kinks and acuteness in the angulations of the siphon part of ICA to be an adaptive feature to slow the blood flow and provide dampening effect to it.
Key words: Internal carotid artery; External carotid artery; Common carotid artery; carotid siphon; Carotido-vertebro-basilar system; carotid insufficiency; cerebrovascular ischaemia.
x
LIST OF TABLES
SL NO
TABLES
Page no
I
List of specimens studied.
24
II
Various segments of ICA studied.
28
III
Length (mean) of ICA on both the sides.
IV
Length of ICA.
V
Diameter of ICA on both the sides.
VI
Diameter (mean) of ICA.
VII
a) Diameter for the segments of ICP on both the sides. b) Mean diameter of individual segments of ICP. Length & diameter of the carotid siphon on both the sides.
VIII
32,33 34 36,37 38
39,40 41,42
IX
Length & diameter (mean) of the carotid siphon.
43
X
Measurement of angles at the bends.
44
XI
Angles (mean) at bends.
45
XII
Class interval for the angles measured at the bends in the intracranial part of the ICA. Variations in the course of ICA found in the study.
47 47
XIII
LIST OF FIGURES SL NO 1
FIGURES
Page no
Normal course of ICA.
6
2
Development of ICA.
8
3
Materials used.
23
4
Total specimens of the study.
5
Intracranial part of ICA to show the bends.
30
6
Mean length of ICA on both sides.
35
7
Mean diameter of ICA on both sides.
38
8
Mean diameter of individual segments of ICA.
40
9
Mean length & diameter of carotid siphon.
43
10
Mean angles at the bends.
46
11
Complete loop in the cervical segment.
48
12
Kink in the cervical segment (ECP).
13
Additional bend (kink) in the cavernous segment (ICP).
50
14
Aneurysm of clinoid segment (ICP).
51
15
Histology of ICA at cervical segment (ECP).
52
25,26,27
49,50
TABLE OF CONTENTS
Page No. 1.
INTRODUCTION
1
2.
OBJECTIVES
3
3.
REVIEW OF LITERATURE
4
4.
METHODOLOGY
23
5.
RESULTS
31
6.
DISCUSSIONS
55
7.
CONCLUSION
59
8.
SUMMARY
60
9.
BIBLIOGRAPHY
61
10.
ANNEXURE
69
INTRODUCTION
Internal Carotid Artery is one of the major source of blood supply to the brain. It is a branch of common carotid artery given in the neck. The ICA does not give any branches in the neck and enters the cranial cavity through the carotid canal in the petrous part of the temporal bone. Inside the cranial cavity it forms 'S' shaped curve while passing through cavernous sinus, lateral to the body of the sphenoid bone. This part is named as 'Carotid siphon'. The siphon may be simple or may have a double curve or transitional form, each condition occurring in about a third of cases examined by Moniz1 (1950). After carotid siphon it terminates by dividing into anterior and middle cerebral arteries, at the anterior perforated substance. The blood flow to the brain is conditioned by chemoreception and baroreception by carotid body & carotid sinus respectively. Further, from carotid foramen to its termination at the anterior perforated substance, the ICA has half dozen bends in its course well seen in lateral angiograms. It may be that these bends damp down the pulsations and give a more regular stream of blood for delivery to the brain.2 Moreover, the study of the course of ICA gains more significance from clinical point of view since exaggerated angulations and kinks of the vessel may lead to a serious condition known as carotid insufficiency syndrome with a manifestation of cerebral ischaemia. It is therefore worthwhile to explore the causative factors which are responsible for exaggeration of angulation such as osteophytes, ossification of ligaments and presence of additional foramina, etc., if any. Whether age has any role to play is also interesting to investigate with reference to coiling, angulations and kinks.
1
It is known fact that the blood flows at a greater pressure on the left ICA since CCA arises directly from the arch of aorta causing frequency of cerebral hemorrhages on the left side. In order to cut down more pressure, are there any differences in the pattern of the loop formation of right and left carotid siphon is worth investigating. Moreover it is also interesting to compare length and breadth proportion of carotid siphon with reference to total length and breadth of ICA.
2
OBJECTIVES
1. To observe the length and diameter of the different segments and to derive clinical significance of the same. 2. To evolve a proportion between straight course and angulated course. 3. To observe the bends and angulations in the course of ICA and to correlate them functionally and clinically.
3
REVIEW OF LITERATURE ANATOMY 3 ICA supplies blood to the fore brain with the exception of occipital lobe. The ICA arises from the bifurcation of CCA at the level of upper border of thyroid cartilage, i.e., at the level of intervertebral disc between C3 & C4 vertebra. Its course is divided into four parts - cervical, petrous, cavernous and cerebral parts. The cervical ICA ascends in the neck in front of the transverse process of upper three cervical vertebrae, and enters the carotid canal of the temporal bone. In the petrous bone, the artery curves anteromedially & then curves superomedially above the cartilage filling the foramen lacerum in the middle cranial fossa. Here it enters the cranial cavity & turns anteriorly through the cavernous sinus in the carotid groove on the side of the body of the sphenoid bone. It then curves up medial to the anterior clinoid process to emerge through the dural roof of the sinus. The ophthalmic artery arises from the ICA as it leaves the cavernous sinus, often at the point of piercing dura & enters the orbit through the optic canal. After piercing the dura mater, the ICA turns back below the optic nerve to run between the optic & oculomotor nerves. It reaches the anterior perforated substance at the medial end of the lateral cerebral fissure & terminates by dividing into large anterior & middle cerebral arteries. RELATIONS ICA is initially superficial in the carotid triangle, then passes deeper, medial to the posterior belly of the digastric muscle. The ECA is at first anteromedial, then curves back to lie superficial.3 a) Posteriorly the ICA adjoins the longus capitis, & the superior cervical ganglion lies between them. The superior laryngeal nerve crosses obliquely behind it.
4
b) The pharyngeal wall lies medial to the artery, which is separated by fat & pharyngeal veins from ascending pharyngeal artery & superior laryngeal nerve. c) Anterolaterally the ICA is covered by sternocleidomastoid. i)
Below the posterior belly of the digastric - the hypoglossal nerve & superior root of ansa cervicalis & the lingual & facial veins are superficial to the artery.
ii)
At the level of digastric - the ICA is crossed by stylohyoid & the occipital & posterior auricular arteries.
iii)
Above the level of digastric - it is separated from the ECA by the styloid process, stylopharyngeus, the glossopharyngeal nerve & the pharyngeal branch of vagus, the deeper part of the parotid gland.
d) Except near the skull, the IJV & vagus are lateral to it with in the carotid sheath. e) At the base of the skull, the glossopharyngeal, vagus, accessory & hypoglossal nerves lies between the ICA & IJV, which here has become posterior. f) Petrous part - ICA lies anterior to cochlea & tympanic cavity & separated from the latter by pharyngo-tympanic tube. Further anteriorly it is separated from trigeminal ganglion by the thin roof of the carotid canal, which is often deficient. ICA is surrounded by venous plexus & the carotid autonomic plexus, which is derived from the internal carotid branch of superior cervical sympathetic ganglion. g) Cavernous part- The abducent nerve is immediately inferolateral to the artery. Further laterally oculomotor, trochlear, ophthalmic & mandibular nerves are related. h) Cerebral part - Medially optic chiasma is related
5
Fig 1: Normal course of internal carotid artery4
Schaeffer JP5 (1953) has stated that, in its course in the neck ICA occasionally forms a marked curve - sigmoid internal carotid - especially in the old people, thereby bringing the vessel close to the tonsillar sinus. Lee McGregor6 (1986) in his synopsis of Surgical Anatomy has stated about the relation of the ICA to tonsil. ICA lies 2.5 cm behind & lateral to the tonsil separated from the pharynx by lax areolar tissue & fat, so that when the organ is pulled inwards with forceps prior to its removal, it is separated still further from the internal carotid artery
6
England MA, Wakely J7 (1991) have mentioned that the ICA is divided into four parts: cervical, intrapetrosal, intracavernous & supraclinoid. The latter two are referred to as the carotid siphon. A tumor in the hypophysial fossa may cause the curve of the carotid siphon to straighten. Harold Ellis8 (2002) has given that there are six bends in the intracranial course of ICA (readily appreciated by studying lateral carotid angiogram) which are believed to lessen the pulsating force of the arterial systolic pressure on the delicate cerebral tissues.
BRANCHES 1) No branches from cervical part. 2) Petrous part: a) Caroticotympanic artery b) Branches to pterygoid canal 3) Cavernous part: a) Inferoir hypophysial arteries b) Meningeal branch 4) Cerebral part: a) Superior hypophysial arteries b) Ophthalmic artery c) Posterior communicating artery d) Anterior choroidal artery e) Anterior cerebral artery f) Middle cerebral artery
7
DEVELOPMENT The first part the of ICA along with CCA develops from the third aortic arch; the remainder of the ICA is formed by cranial portion of dorsal aorta.9
Fig 2: Development of ICA9
8
VARIATIONS The length of the artery varies with the length of the neck & the point of carotid bifurcation. It may arise from the aortic arch & then lie medial to the ECA as far as the larynx, where it crosses behind it. The cervical position is normally straight, but may be very tortuous, in which case it lies closer to the pharynx than usual & very near the tonsil. Its absence also has been recorded.3 Much literature is available on the variations in the ICA. These have been classified as follows: a) Variations in development. b) Variations in position c) Variations in size & shape d) Variations in course e) Pathological changes.
a) Variations in development Tode10 (1787) first described agenesis of internal carotid artery. Fisher11 (1913) summarized seven cases of agenesis of ICA. He also presented a case of bilateral absence of ICA in which abnormally large basilar artery supplied the anterior & the middle cerebral arteries on both sides through the posterior communicating arteries. Other anomalies were present in this case & both carotid canals were absent. Da Silva G12 (1936) described findings in a disarticulated skull, presumably of a female between ages of 18 & 22. There was absence of carotid canal, which led him to surmise that the patient had absent ICAs.
9
Verbiest13 (1954) gave first radiologic demonstration of absence of ICA by angiographic study in a living patient. Fields WS, Bruetman ME, Weibel J14 (1965) uncovered one case of bilateral agenesis of ICA, while reviewing carotid angiograms in 1407 patients. Hills & Sament15 (1968) reviewed the findings in a 10 -week old infant who died because of severe cardiac anomalies. Both ICAs were absent at the base of the brain. The major circulation to brain was through large left vertebrobasilar arteries into the circle of Willis. Smith RR, Kees CJ, Hogg JD16 (1972) reported a case of unilateral agenesis of right ICA with a large carotid - cavernous anastomosis at the level of dorsum sellae. Teal JS, Rumbaugh CL, Bergeron RT, et al17 (1973) cited an incidence of subarachnoid hemorrhage associated with aneurysm in seven of 31 reported cases of absence of an ICA. Rosen IW, Mills DF, Nadel HI & Kaiserman DD18 (1975) presented a case report of angiographic demonstration of bilateral, congenital & total absence of ICAs in a patient with subarachnoid hemorrhage. The intracranial blood supply had been provided by communication between a hypertrophied basilar artery & circle of Willis through the posterior communicating artery. Absence of carotid canals substantiated the congenital nature of the anomaly. Servo A19 (1977) reported a case with congenital absence of left ICA associated with an aneurysm on the contralateral carotid siphon. Aneurysms were situated on the bifurcation of the right carotid siphon where hemodynamic forces may have initiated the aneurysmal process & favoured its growth. Of the reported cases of absence, 25% had an aneurysm on the contralateral side or on the basilar artery. The
10
normal incidence of intracranial aneurysms is only 2-4% only. As quoted by Servo A, Ferguson20 (1972) showed in model experiments & clinical studies that at the apex of bifurcation the arterial wall is subject to hemodynamic forces that distend the wall & initiate the development & growth of aneurysms. Janicki PC, Limbacher JP & Guinto FC.Jr., 21 (1979) reported a case of agenesis of the left ICA with a primitive transsellar communicating artery, connecting the intracavernous portion of the right & left ICAs. Tomography of the petrous bone showed an absent carotid canal on the left side, more indicative of agenesis than aplasia. Kishore PRS, Kaufman AB & Melichar FA22 (1979) reported two cases of arterial communication between the cavernous segments of the carotid arteries associated with unilateral agenesis of ICA. The intrasellar carotid anastomosis simulated pituitary microadenoma. An area of focal erosion in the floor of the sella in the region of the anomalous intrasellar artery was revealed in the poly tomography of the base of the skull. Handa J, Matsuda I, Nakasu S & Nakano Y23 (1980) reported a case of congenital absence of one ICA & they reported the absence of the bony carotid canal & the intracavernous portion of the ICA by CT & cavernous sinography respectively. Huber G24 (1980) reported a rare arterial anastomosis between the right & left ICAs at the base of the skull (transverse carotid anastomosis), with aplasia of the cervical part of the left ICA. In addition to the vascular anomaly o f the carotid artery there was an aneurysm of the anterior communicatuing artery and bilateral renal cysts. The condition was a complex malformation syndrome caused by defective regression of the third branchial artery.
11
Milder DG & Lance JW25 (1984) reported a case of a 13-year-old girl who consistently developed unilateral sensory & motor symptoms on hyperventilation, suggesting the diagnosis of hysteria. Investigations disclosed hypoplasia of one ICA & part of the circle of Willis, responsible for compromising blood flow to one hemisphere sufficiently to produce ischaemic deficit during hypocapnia. ICA hypoplasia may be associated with hypoplasia of the circle of Willis or intracranial aneurysm & has been related causally to intracranial collateral vessel formation. Worthington C, Olivier A, & Melanson D26 (1984) first reported a case of agenesis of ICA to be correlated with conventional as well as digital subtraction angiography, along with high resolution CT of skull which showed absent carotid foramen on right side. Kunishio K, Yamamoto Y, Sunami N, Asari S27 (1987) presented a case of agenesis of left ICA, CCA & the main trunk of ECA with multiple cerebral aneurysms. This case was diagnosed by angiography & computed tomography scanning & confirmed at operation. Quint DJ, Boulos RS, Spera TD28 (1989) reported two cases of congenital absence of the cervical & petrous ICA with intercavernous anastomosis. They opine that though this anomaly is associated with collateral flow to the involved vascular territory and neurological deficits are few; it is associated with high occurrence of intracranial aneurysms, about 24-34%; most likely to altered hemodynamics. Other reason could be secondary to some underlying congenital defect. Fuwa I29 (1994) reported a case of carotid rete mirabile in a 13-year-old girl. The right ICA gradually tapered at cavernous portion. A small sinuous arterial curve was seen around the liesion. The dilated ophthalmic artery was connected with small
12
arteries originating from maxillary artery. The left ICA was stenotic at supraclinoid segment. Pascual-Castroviejo I, Viano J, Pascual-Pascual SI & Martinez V30 (1995) described a paediatric case of facial haemangioma, associated with agenesis of ICA, cerebral cortical dysplasia & hypoplasia of the cerebral hemisphere on the same side of the angioma. They reasoned that hypoplasia of cerebral hemisphere was linked to lack of ipsilateral ICA, inspite of apparently good blood supply through the large anterior communicating artery. Sunada I, Inoue T31 (1996) reported a case of bilateral agenesis of ICA presenting as intracerebellar hemorrhage. Heth JA, Loftus CM, Piper JG, & Yuh W32 (1997) reported a case of a patient with transient ischaemic attacks who was evaluated by duplex scanning, which demonstrated total carotid occlusion. Arteriography revealed what appeared to be a classic "string sign" in the cervical carotid artery & a standard endarterectomy was planned. At surgery the ICA was found to be congenitally atretic, accounting for string appearance of the arteriogram. String sign is customarily thought to be an indicator of critical stenosis of ICA requiring carotid endarterectomy on an emergency basis to prevent occlusion of the vessel. Czarnecki EJ, Silbergliet R, Mehta BA & Sanders WP33 (1998) reported a case of absence of supraclinoid ICA & hypoplasia of ipsilateral ICA, along with hypoplastic carotid canals in association with intracranial aneurysms. A variety of collateral pathways supply the brain in such cases & there is strong association with intracranial aneurysms, probably secondary to hemodynamic stress on these collateral pathways. This increased prevalence of intracranial aneurysm formation could
13
however relate to a genetic predisposition linking the ICA anomaly with the development of the aneurysms. Chen CJ, Chen ST, Hsieh FY, Wang LJ & Wong YC34 (1998) reported symptomatic case of unilateral hypoplasia of the ICA with an intercavernous anastomosis. The symptoms were caused by occlusion of the proximal middle cerebral artery. The hemodynamic stress caused by the anomalous intercavernous anastomosis may have strained these suprasellar part of the hypoplastic ICA & caused elongation, calcification of the supraclinoid segment & occlusion of the proximal M1 segment. Hattori T, Kobayashi H, Inoue S, & Sakai N35 (1998) reported two cases of absent ICA associated with persistent primitive trigeminal artery. Mahadevan J, Batista L, Alvarez H, Bravo-Castro E, Lasjaunias P36 (2004) reported a case of symptomatic symmetrical, bilateral absence of the cavernous (both horizontal & clinoid segment) ICA & transdural vertebral artery segments with formation of a rete mirabile, which was diagnosed by angiography. A rete mirabile is an arterial network most often supplied by ECA branches, especially branches of maxillary artery. It is present in many species and does not appear as such during the development of the cranial circulation in man. It forms a rich plexus in the parasellar region from which the distal ICA arises, divides into its terminal branches & supplies the brain. They opine that extradural arteries are segmental in origin. The segments of fully developed ICA correspond to embryonic structures and each may be present or absent (segmental agenesis) independently or in association with the adjacent ones. Segmental agenesis does not usually compromise the blood supply to the brain & exceptionally described in children despite the embryonic nature of the disorder.
14
b) Variations in position; Malacarne37 (1784) reported earliest case of absence of common carotid artery. Seidel38 (1965) in an angiogram showed lateral position of obliterated left external carotid artery. Several branches arising from ICA were identified as superior thyroid artery, lingual artery, external & internal maxillary artery, occipital & superficial temporal arteries. Lie39 (1968) reported two similar cases & assumed that lateral position of external carotid artery would be due to excessive migration o f the embryonic external carotid trunk. Handa J, Matsuda M, & Handa H40 (1972) reported a case where ECA arose lateral instead of medial to the ICA. The ICA was normal & although lingual & maxillary artery crossed it, it showed no strangulation or constriction. Bryan NR, Drewyer RG & Gee W41 (1978) presented a case of separate origins of the left ICA & ECA from the aorta. They opine that in about one half of cases, absence of CCA is associated with additional major vascular anomalies. These are double aortic arch, right aortic arch, cervical arch, aberrant right subclavian artery & persistent proatlantal artery. The most common associated anomaly is the cervical aortic arch. This is most likely based on atresia of third & fourth branchial arch plus persistence of the ductus caroticus on the involved side. Roberts LK, Gerald B42 (1978) reported a case of bilateral absence of CCA resulting in separate origins of both ICA & ECA. This has been shown to be a developmental possibility. Marimoto T, Nitia K, Kazekawa K & Hashizume K43 (1990) reported a case of a rare developmental anomaly of the cervical ICA. The nonbifurcating carotid
15
artery gave origin to all of the branches normally supplied by ECA & thereafter continued as the ICA. Kaneko K, Akita M, Masuta E, Imai M & Sowa K44 (1996) reported anomalous left CCA in which the left superior thyroid, lingual & facial arteries arose from CCA from a common trunk. The occipital & ascending pharyngeal arteries arose from ICA. The left carotid body was observed to be located at the level of intervertebral disc between the C2 & C3, at the same level as right carotid body. They assumed that the artery above the level of carotid body was ICA: there was no specific ECA and all branches of ECA arose from the ICA.
c) Variations in size & shape: Olivier A, Scotti G, Melancon D45 (1977) reported a case of hypoglossal nerve palsy due to compression by a tortuosity (an anomaly similar to fenestration) of the ICA at the level of C2. Killien FC, Wyler AR, & Cromwell LD46 (1980) reported a case of duplication of cervical part of ICA, which was described angiographically. They opine that duplication & fenestration are presumably the result of anomalous fusion of primitive vessels or plexus, and hence, the duplicated ICA presumably results from fusion of carotid plexus into two channels instead of one, duplication of ICA may simulate a dissection at angiography. Tanaka & Matsumoto47 (1981) reported a case of fenestration of cervical part of ICA. Hasegawa T, Kashihara K, Ito H & Yamamoto S48 (1985) described two cases of fenestration of cervical ICA that was revealed by angiography.
16
Findlay JM, Chui M & Muller PJ49 (1987) reported a case of subarachnoid hemorrhage with left anterior cerebral - anterior communicating artery aneurysm in a 28 year old woman. Also they identified fenestration of the right supraclinoid ICA with an associated accessory middle cerebral artery. Boerman RH, Padberg GWAM, Wondergem J & Gittenberger de Groot50 (1991) reported a case where angiography showed the common carotid arteries originating just above the aortic valves as a cause of stroke. An atheromatous obstruction of the ICA was also present. They speculate that the origin of the vessels close to the heart, where blood velocity is highest, may have resulted in higher velocity of blood in CCAs & damage to the vessel wall at the level of carotid bifurcation. Chess MA, Barsotti JB, Ja-kwei Chang, Ketonen LM & Per-Lennart Westesson51 (1995) described a case of duplication of left ICA from a point of 1 cm distal to the origin to the proximal petrous segment where the vessel reunited. They opined that identification of these entities is important, especially in patients who require surgical intervention involving the ICA. Koenigsberg RA, Zito JL, Patel M, Swartz JD, Goldofsky E, & Zahtz G52 (1995) presented a case of 61 year old woman examined because of unilateral nonpulsatile tinnitus involving the right ear. CT scanning showed a soft tissue mass in the hypotympanum. Angiographically, the mass was identified as a fenestrated or duplicated ICA associated with persistence of the stapedial artery. They opine that this case serves as an important embryologic link in demonstrating simultaneous development of the aberrant ICA with a normal - position adult ICA. Manglaa S, Teitelbauma GP53 (1999) reported a case where digital subtraction angiography of both CCAs in a 73 year old man was performed and right
17
ICA demonstrated a short segment division of the petrous segment into four channels. The fenestration was approximately 1 cm long. The ICA was equal in diameter above and below the fenestration. Goto Y, Yoshida K, Oshimoto T, Wataya T, Hojo M, Chin M, Yamagata S54 (2003) described two cases of fenestration at the extracranial ICA that were initially suspected of the dissection of ICA on MRA/I. Both angiography & CT angiography (CTA) disclosed the fenestration, which located at C2 vertebral levels. To confirm the fenestration at extracranial ICA is important in such an occasion that mimics the dissection of ICA especially in patients of cervical pain, mass & other related symptoms. Khan N, Schinzel A, Shuknecht B, Baumann F, Ostergaard JR, Yonekawa Y55 (2004) reported two children with moya moya angiopathy & bilateral dolichoectatic ICAs in combination with iris hypoplasia with bilateral fixed pupils and a history of patent ductus arteriosus. Authors propose the combination of these defects could be a not yet recognized clinical syndrome of probable genetic etiology.
d) Variations in course: Kelly56, 57 (1924& 1925) described 150 patients with pulsation or swelling of the lateral wall of the pharynx, apparently due to a kink in the ICA in the neck. For kinking of the ICA two causes have been postulated by Kelly57 (1925). The vessel is formed from the third aortic arch and from dorsal aorta; hence in the embryo, it is normally kinked. As the heart recedes into the thorax, the ICA is stretched and the kink is eliminated. Failure of this developmental process might account for persistence of the kink. The other cause suggested is elongation and tortuosity of the artery because of arteriosclerotic changes.
18
Myerson MD, Ruben H & Gilbert JG58 (1934) described an incidence of 1% of ectopy of the ICA based on petrous bone studies. A pinpoint dehiscence of ICA may be present in 1% of the population. In rare cases, other vessel anomalies can be associated with deviant cervical or intracranial vessel divisions. Parkinson J, Bedford DE & Almond S59 (1939) described 40 patients who presented with a pulsatile swelling in the neck, proved due to a kink in the CCA. Hsu & Kistin60 (1956) reported two patients with a kinking of ICA; one among them had previously a transient hemiparesis. Quattelbaum JK, Upson ET, Neville RL61 (1959) described three cases in which the development of hemiplegia was associated with a kink in the ICA. Metz H, Murray-Leslie RM, Bannister RG, Bull JWD, Marshal J62 (1961) reexamined 1000 angiograms & 16% of them showed kinking of the internal carotid artery. The kinking was present in every decade and there was a strong suggestion that recurrent cerebrovascular episodes were commoner in patients with kinks than in a normal control group. Lapayowker MS, Leibman EP, Ronis ML & Safer JN63 (1971) described a vestibular line drawn vertically on an anteroposterior arteriogram through the lateral aspect of the vestibule. Any part of ICA that lies lateral to this line is considered to be aberrant. Aberrant ICA presentation in the middle ear has been documented by Glasscock ME III, Dickins JR, Jackson CG, Wiet RJ (1980) 64 & Sinnreich AI, Parisier SC, Cohen NL, Berreby M65 (1984) & others. Approximately 45 cases have been reported with the vast majority of these patients being female & exhibiting this anomaly on the right side. The patients mean age was 25 years.
19
Glasscock ME III, Seshul M, & Seshul MB, sr66 (1993) reported a case of bilateral aberrant intratympanic carotid artery presentation. In addition there was unilateral duplication of the cervical and petrous portion of one ICA such that the duplicated portion rejoined the normal ICA in its petrous portion. Moreano EH, Paperella MM, Zelterman D, Goycoolea MV67 (1994) studied 1000 human temporal bones and detected a carotid canal dehiscence (7.7%), and a microdehiscence (7.4%) of the carotid canal in 15.1% of all bones. Saleem SM, Wani AM68 (1998) reported two young adult patients who had extracranial carotid artery anomalies in the form of abnormal loops and aneurysms, demonstrated angiographically. These were probably congenital in origin and presented as ischaemic cerebrovascular accidents or slowing of circulation at these sites. Ridder GJ, Fradis M & Schipper J69 (2001) reported 33-year old woman referred for unclear otoscopic finding. The high-resolution tomography showed an aberrant course of right ICA, which passed through the low part of the eardrum and the middle ear in a rectangular course and was covered by a thin bony lamella. On MRA, a distinctly caliber of the ICA with a lateral displacement on the right was seen.
e) Pathological changes: Sacher M, Som PM, Shugar JM & Leeds NE70 (1986) presented a case of acromegaly, which was associated with aneurysmal dilatation of the ICAs & their branches. A CT was taken which showed the enlarged cavernous portions of ICAs prolapsed into sella turcica & enlarged it along with other manifestations of acromegaly. The sellar CT appearance gave the term "kissing intrasellar arteries".
20
Ishikawa T, Nakamura N, Houkin K & Nomura M71 (1997) reported a case of fatal subarachnoid hemorrhage caused by blister-like aneurysm of superior wall of the ICA. When the lesion was pathologically observed, the blister-like aneurysm appeared to be a laceration of the carotid wall based on degeneration of the internal elastic lamina. Liera EC, Bendixen BH, Kardon RH & Adams HP., jr72 (1998) reported a case of brief transient Horner's syndrome as a primary feature of carotid artery dissection. The MRI showed the dissection of the right ICA extending from the bulb to the base of the skull, leaving a lumen of 2 mm at the narrowest point. Norris JW, Beletsky V, Nadareishvili ZG73 (2004) gave a commentary on sudden neck movement & cervical artery dissection. By their recent Canadian survey it was found dissection of the cervical arteries was one of the most common causes of stroke in patients less than 45 years of age. Among them 28% was carotid artery dissection & 72% was vertebrobasilar artery dissections. Most (81%) of dissections were associated with sudden neck movement, ranging from therapeutic neck manipulation to a vigorous game of volleyball, but some occurred during mild exertion such as lifting a pet dog or during a bout of coughing. Jorden JA, Lewis M, Rollins N & Roland PS74 (2000) presented a case of ICA aneurysm involving high, cervical, petrous & cavernous portions of the artery with absence of petrous portion of the contralateral artery. Sinnreich et al65, had the largest series, reporting 23 aneurysms of the petrous portion of the contralateral ICA. Most aneurysms are congenital, such as the region in which primordial vessels involute or in a region in which the vessels make a sharp turn, such as the petrous portion of the ICA.
21
Robertson WC, Pettigrew LC75 (2003) reported a child with Horner's syndrome after the reported application of the birthing forceps to the head & neck during vaginal delivery. MRI & angiograaphy confirmed that proximal ICA showed injury caused by dissection. Payton TF, Siddiqui KM, Sole DP & Mckinley DF76 (2004) presented a case of 11-year-old male who had dissection of his left ICA following injury. Though this is rare, it remains an important cause of cerebrovascular accidents in children.
22
METHODOLOGY The present study was undertaken on the 56 sagitally bisected formalin fixed head & neck specimens of human cadavers obtained from the dept. of Anatomy of Govt. Medical College, Mysore, JJM Medical College, Davangere & JSS Medical College, Mysore. The specimens belonged to the adult group consisting of male and female subjects. The following materials were used to calculate the different parameters; a) Scale
g) Colour chalk pieces
b) Thread
h) Marking pencil
c) Divider
i) Flexible plastic wire
d) Protractor
j) Chisel mallet
e) White sheet
k) Dissection set
Fig 3: Materials used.
23
The sagittal sections were separated into right & left groups & further divided into paired & unpaired categories. Out of the 56 specimen, 44 were paired & 12 were unpaired. Paired specimens were numbered from 1-22. 17 pairs were from male cadavers -------------------------1 M-17 M(R & L) 5 pairs were from female cadavers-------------------------18 F-22 F(R & L) Among the remaining 12 unpaired specimens: 5 belonged to right side--------------------------------------1U R - 5 U R 7 belonged to left side----------------------------------------1U L - 7 U L
TABLE I: List of specimens studied.
1. PAIRED
2. UNPAIRED
TOTAL
SEX
No of specimen
RIGHT
LEFT
MALE
34
17
17
FEMALE
10
5
5
NOT KNOWN
12
5
7
56
27
29
The ICA was exposed in the cervical part by clearing the superficial relations to it. The intracranial portion of ICA was exposed by opening the carotid canal using a chisel & mallet & further traced the horizontal segment of ICA within the carotid canal till the anterior clinoid process. Due to limitation of space for exposure of cervical part, the length of ECP was measured by introducing flexible plastic wire into the artery from the portion of the carotid canal segment till it reached the origin of ICA in the neck. The level was marked on the wire & subsequently measured on the scale.
24
Fig 4: Total specimens of the study.
25
Fig 4: Total specimens of the study (Contd.)
26
Fig 4: Total specimens studied. (Contd.)
27
The following parameters were worked out: 1. LENGTH: - was measured from the bifurcation of CCA into ICA & ECA in the neck to the level of anterior clinoid process. Length of ICP was measured by placing the thread along the curved course of the artery. The different segments of intracranial portion of ICA were demarcated by marking with colored chalk pieces & their length was measured by approximating the thread along their course. The length of the thread was measured by using scale. The intracranial part was divided into five segments as against one continuous ECP segment. The details of intracranial part of ICA segment are furnished below in table. TABLE II: Various segments of ICA studied. ECP
From the origin of ICA till the vertical portion of carotid canal segment(till I bend)
ICP
From the horizontal portion of carotid canal segment to the level of the anterior clinoid process •
CC - horizontal portion of carotid canal segment to the level of the anterior clinoid process
•
LA - from foramen lacerum to its anterior curve along the lateral surface of the body of the sphenoid bone
•
CV - from its anterior curve to the acute superior curve
•
CL - from the superior curve to the origin of the ophthalmic artery
•
AO - after the origin of ophthalmic artery till its termination at carotidoclinoid foramen
28
2. DIAMETER: - The external diameter of the artery was measured using the divider for various segments and the distance between the two points of divider was measured using a scale. The diameter was measured at six levels: •
ECP-External part/cervical segment
•
CC - Carotid canal segment
•
LA - Lacerum segment
•
CV - Cavernous segment
•
CL - Clinoid segment
•
AO -After origin of ophthalmic artery
3. ANGLES: - The ICA shows four bends after it enters the carotid canal. •
I BEND-Between the vertical portion of carotid canal segment & its horizontal portion. (Measurement not done due to limitation of exposure of this part of the artery).
•
II BEND- Between the horizontal portion of carotid canal & lacerum segments
•
III BEND - Between the lacerum & cavernous segments.
•
IV BEND - Acute bend between cavernous & clinoid segment. For measuring the angles - the impression of the curve of artery was outlined
on a white paper using lead pencil. The angle was measured using a protractor. The angle at first bend was not measured due to limitation of exposure. Angles at II, III & IV bend were measured & the findings were noted.
Statistical tool used: - paired 't' test was used to analyze the observations.
29
Fig 5: Intracranial part of ICA showing bends.
•
I BEND-Between the vertical portion of carotid canal segment & its horizontal portion.
•
II BEND- Between the horizontal portion of carotid canal & lacerum segments
•
III BEND - Between the lacerum & cavernous segments.
•
IV BEND - Acute bend between cavernous & clinoid segment.
30
RESULTS The various parameters measured are: 1. Length of ICA - ICP, ECP & TOTAL length. 2. Diameter of ICA - for ICP, segments of ICP & ECP. 3. Length & diameter of carotid siphon. 4. Angles measured at II, III & IV bend.
31
1 M 2 M 3 M 4 M 5 M 6 M 7 M 8 M 9 M 10 M 11 M 12 M 13 M 14 M 15 M 16 M 17 M 18 F 19 F 20 F
NO
CC
1.5 2.1 2 2.1 1.9 2.3 2 1.6 1 1.9 1.6 2.3 1.1 1.5 2.2 1.5 2.6 2.2 1.1 2.7
1.1 1.2 2.1 1.5 1.9 1.9 1.7 1.5 1 1.3 1.7 0.8 1.1 1 0.7 1.3 1.3 1 1.1 1
1.2 1.5 1.6 2 1.5 2.2 1.7 2.2 0.9 1.3 1.6 1.5 1.9 1.4 1.9 1.8 1.5 2 1.3 1.4
0.9 0.9 0.6 1.2 1.3 1.1 1.1 1.3 * 0.6 0.5 0.7 0.5 1.2 0.4 1 0.9 0.7 0.8 0.7
0.7 0.8 0.5 1.2 0.9 0.4 * 0.8 * 0.8 0.9 0.6 0.5 0.9 0.9 0.9 0.5 * 0.7 0.7 5.4 6.5 6.8 8 7.5 7.9 6.5 7.4 2.9 5.9 6.3 5.9 5.1 6 6.1 6.5 6.7 5.9 5 6.5
7.6 8.4 8.1 8 8.5 8.8 9.2 10.4 11.3 7.5 8 8.5 8.3 9.2 9.2 8.8 8.1 6.7 7.6 7.2
RIGHT SIDE (length in cm) Segments of ICP ICP ECP LA CV CL AO 13 14.9 14.9 16 16 16.7 15.7 17.8 14.2 13.4 14.3 14.4 13.4 15.2 15.3 15.3 14.8 12.6 12.6 13.7
TOT AL CC
32
1.6 2.3 3 2.4 1.1 1.9 1.9 1.5 1 1.6 1.2 1.4 1.2 1.4 1.5 1.2 1.9 1.5 0.6 1.9
1.3 1.9 1.2 1.4 1.3 2.1 1.2 1.8 1 0.7 1.7 1.5 1.1 1.1 1.2 1.2 1.2 1.5 1.3 1.4
1.2 1.8 1.7 3 1.6 1.7 1.5 1.5 1.2 1.4 1.6 1.9 1.8 2.1 1.4 1.6 1.3 1.8 1.7 1.2
0.6 0.3 0.7 0.7 * 0.5 1 0.8 1 0.5 0.8 0.5 0.5 1.2 0.7 1.5 0.8 0.6 0.5 0.6
0.4 1 0.5 1.2 * 0.6 0.8 1 0.4 0.7 1.2 0.9 0.7 0.6 1 0.6 0.3 0.7 0.6 0.5
LEFT SIDE Segments of ICP LA CV CL AO
TABLE III: LENGTH of ICA on both the sides.
5.1 7.3 7.1 8.8 4 6.8 6.6 6.6 4.6 4.9 6.5 6.2 5.3 6.4 5.8 6.1 5.5 6.1 4.7 5.6
ICP
6.2 12.5 6 6.8 8.4 8.1 10.4 6.6 10.5 9.5 10.5 8.2 7.4 * 11 9.4 8.6 7 9 8.9
ECP
(length in cm)
11.3 19.8 13.1 15.6 12.4 14.9 17 13.2 15.1 14.4 17 14.4 12.7 * 16.8 15.5 14.1 13.1 13.7 14.5
TOT AL
1.6 1.8 2 1.5 2.7 2.5 2.3 * *
CC
1.1 1.5 1.5 2.2 1.2 1.1 1.3 * *
1.4 2.8 1.4 2.3 1.2 2.5 1.2 * *
0.3 0.8 0.3 0.7 0.8 1.2 0.4 * *
0.7 1.4 0.9 0.2 * 0.3 0.5 * *
TOTAL 14.516 1.39752
9.8 9.7 8.1 * 6.7 * 6.3 * *
14.9 15 14.2 * 12.6 * 12 * *
1.8 1.9 1.9 1.8 1.8 1.3 1.25 1.6 2.1
CC
MEAN SD
TOT AL
33
Rt. side Vs Lt. side t = 0.57 p > 0.05(NS)
5.1 5.3 6.1 6.9 5.9 7.6 5.7 * *
RIGHT SIDE (length in cm) Segments of ICP ICP ECP LA CV CL AO
RIGHT SIDE ICP ECP MEAN 6.2 8.4 SD 1.06626 1.16619 * - Data not available Statistical analysis: ICP Vs ECP t = 10.43 p < 0.001(HS)
21 F 22 F 1 U 2 U 3 U 4 U 5 U 6 U 7 U
NO
1.2 1.7 1.8 1.1 1.6 0.75 1 0.7 0.9
0.2 0.6 0.5 0.1 0.6 1 0.3 0.5 1.2
0.7 1 0.5 0.7 0.9 0.9 0.4 * *
ICP Vs ECP t = 7.47 p < 0.001(HS)
LEFT SIDE ICP ECP 5.93275 8.81428 1.11517 1.69786
1.7 1.3 2.7 1.4 0.6 2.8 1.45 1.1 1.3
LEFT SIDE Segments of ICP LA CV CL AO
TABLE III: LENGTH of ICA on both the sides. (Contd.)
5.6 6.5 7.4 5.1 6.9 6.75 4.4 3.9 5.5
ICP
14.8 15.6 17.8 14.9 18.3 16.45 11.4 12.7 11.9
TOT AL
TOTAL 14.73035 2.1226
9.2 9.1 10.4 9.8 11.4 9.7 7 8.8 6.4
ECP
(length in cm)
TABLE IV: Length (mean) of ICA a. Length of ICP measured ICP(cm)
RIGHT
LEFT
MEAN
6.2
5.923
MIN
5
4
MAX
8
8.8
ECP(cm)
RIGHT
LEFT
MEAN
8.4
8.814
MIN
6.3
6
MAX
11.3
12.5
b. Length of ECP measured
c. Total length of ICA measured(ICP + ECP) ICA(cm)
RIGHT
LEFT
MEAN
14.516
14.730
MIN
12
11.3
MAX
17.8
19.8
34
Fig 6: Mean length (cm) of ICA on both right & left sides.
16 14 12 10 8
Right Left
6 4 2 0 ICP
ECP
TOTAL
35
1 M 2 M 3 M 4 M 5 M 6 M 7 M 8 M 9 M 10 M 11 M 12 M 13 M 14 M 15 M 16 M 17 M 18 F 19 F 20 F
NO 0.3 0.4 0.35 0.4 0.4 0.35 0.3 0.4 * 0.25 0.35 0.45 0.3 0.45 0.35 0.45 0.4 0.4 0.3 0.3 0.44 0.5 0.44 0.46 0.56 0.47 0.5 0.46 0.483 0.38 0.41 0.57 0.57 0.58 0.46 0.59 0.5 0.49 0.46 0.42
0.6 0.5 0.5 0.5 0.6 0.6 0.6 0.5 0.5 0.45 0.4 0.55 0.6 0.6 0.45 0.7 0.55 0.55 0.5 0.5
0.4 0.5 0.45 0.5 0.6 0.4 0.5 0.5 * 0.4 0.4 0.6 0.6 0.6 0.5 0.6 0.55 0.5 0.5 0.4
0.4 0.5 0.45 0.45 0.6 0.5 0.6 0.5 0.45 0.35 0.4 0.6 0.6 0.55 0.5 0.6 0.5 0.5 0.5 0.5
CC
0.5 0.6 0.45 0.45 0.6 0.5 0.5 0.4 0.5 0.45 0.5 0.65 0.75 0.7 0.5 0.6 0.5 0.5 0.5 0.4
RIGHT SIDE (Diameter in cm) Ave Segments of ICP ICP LA CV CL AO 0.45 0.6 0.55 0.575 0.6 0.6 0.6 0.5 0.6 0.45 0.6 0.5 0.6 0.6 0.4 0.6 0.65 0.6 0.6 0.5
ECP CC
36
0.42 0.62 0.62 0.55 0.5 0.5 0.6 0.6 0.5 0.5 0.5 0.5 0.5 0.5 0.6 0.5 0.525 0.6 0.5 0.4
0.4 0.6 0.5 0.55 0.5 0.45 0.6 0.6 0.5 0.5 0.5 0.6 0.5 0.5 0.6 0.5 0.5 0.5 0.5 0.4
0.475 0.55 0.55 0.55 0.3 0.5 0.6 0.5 0.5 0.45 0.5 0.65 0.5 0.6 0.6 0.5 0.5 0.55 0.5 0.4
0.4 0.5 0.42 0.5 * 0.5 0.6 0.6 0.5 0.5 0.5 0.6 0.5 0.6 0.6 0.5 0.525 0.6 0.5 0.5
0.25 0.4 0.4 0.4 * 0.35 0.45 0.4 0.3 0.35 0.4 0.4 0.4 0.3 0.5 0.35 0.4 0.3 0.4 0.3
0.389 0.534 0.498 0.51 0.43 0.46 0.57 0.54 0.46 0.46 0.48 0.55 0.48 0.5 0.58 0.47 0.49 0.51 0.48 0.4
LEFT SIDE (Diameter in cm) Ave Segments of ICP ICP LA CV CL AO
TABLE V: DIAMETER of ICA on both the sides.
0.45 0.62 0.52 0.6 0.6 0.6 0.6 0.6 0.6 0.5 0.5 0.4 0.5 0.4 0.5 0.55 0.6 0.6 0.6 0.5
ECP
RIGHT SIDE ICP 0.48155 0.057900
0.4 0.4 0.4 0.6 0.5 0.525 0.5 * * 0.39 0.44 0.425 0.55 0.48 0.49 0.48 * *
ECP 0.543 0.070533
0.25 0.3 0.35 0.45 0.4 0.5 0.4 * *
0.45 0.5 0.45 0.5 0.5 0.45 0.5 * *
0.4 0.5 0.45 0.7 0.5 0.5 0.5 * *
0.45 0.5 0.475 0.5 0.5 0.5 0.5 * *
CC
MEAN SD * - Data not available Statistical analysis: ICP Vs ECP t = 4.71 p < 0.001(HS)
21 F 22 F 1 U 2 U 3 U 4 U 5 U 6 U 7 U
NO
RIGHT SIDE (Diameter in cm) Segments of ICP Ave ICP LA CV CL AO 0.4 0.5 0.5 * 0.5 * 0.5 * *
0.4 0.6 0.6 0.5 0.6 0.6 0.4 0.45 0.55
CC
37
MEAN SD
ECP 0.4 0.55 0.6 0.4 0.55 0.6 0.4 0.4 0.6
0.45 0.55 0.6 0.4 0.5 0.575 0.4 0.45 0.5
ICP Vs ECP t = 4.71 p < 0.001(HS)
LEFT SIDE ICP 0.486758 0.061621
0.4 0.55 0.6 0.4 0.6 0.65 0.45 0.4 0.5
0.3 0.4 0.5 0.3 0.45 0.5 0.3 0.3 0.4
ECP 0.546206 0.077432
0.39 0.53 0.58 0.4 0.54 0.585 0.39 0.4 0.51
LEFT SIDE (Diameter in cm) Segments of ICP Ave ICP LA CV CL AO
TABLE V: DIAMETER of ICA on both the sides. (Contd.)
0.55 0.65 0.65 0.5 0.55 0.7 0.4 0.5 0.5
ECP
TABLE VI: Diameter (mean) of ICA a. Diameter if ICP measured ICP(cm)
RIGHT
LEFT
MEAN
0.481
0.486
MIN
0.39
0.389
MAX
0.59
0.585
ECP(cm)
RIGHT
LEFT
MEAN
0.543
0.546
MIN
0.4
0.4
MAX
0.65
0.7
b. Diameter of ECP measured
Fig 7: Mean diameter (cm) of ICA on both right & left sides
1 0.9 0.8 0.7 0.6 0.5 0.4 0.3 0.2 0.1 0
Right Left
ICP
ECP
38
TABLE VII (a): Mean diameter for the segments of intracranial part of ICA on both the sides.
NO
RIGHT SIDE (Diameter) Segments of ICA (in cm) CC LA CV CL AO
LEFT SIDE (Diameter) Segments of ICA (in cm) CC LA CV CL AO
1M
0.6
0.4
0.5
0.4
0.3
0.42
0.4
2M 3M 4M 5M 6M 7M 8M 9M 10M 11M 12M 13M 14M 15M 16M 17M
0.5 0.5 0.5 0.6 0.6 0.6 0.5 0.5 0.45 0.4 0.55 0.6 0.6 0.45 0.7 0.55
0.5 0.45 0.45 0.6 0.5 0.6 0.5 0.45 0.35 0.4 0.6 0.6 0.55 0.5 0.6 0.5
0.6 0.45 0.45 0.6 0.5 0.5 0.4 0.5 0.45 0.5 0.65 0.75 0.7 0.5 0.6 0.5
0.5 0.45 0.5 0.6 0.4 0.5 0.5 * 0.4 0.4 0.6 0.6 0.6 0.5 0.6 0.55
0.4 0.35 0.4 0.4 0.35 0.3 0.4 * 0.25 0.35 0.45 0.3 0.45 0.35 0.45 0.4
0.6 0.5 0.55 0.5 0.45 0.6 0.6 0.5 0.5 0.5 0.6 0.5 0.5 0.6 0.5 0.5
18 F 19 F 20 F 21 F 22 F 1U
0.55 0.5 0.5 0.45 0.5 0.45
0.5 0.5 0.4 0.4 0.5 0.45
0.5 0.5 0.4 0.4 0.4 0.4
0.4 0.3 0.3 0.25 0.3 0.35
0.5 0.5 0.4 0.4 0.55 0.6
0.55 0.5 0.4 0.4 0.55 0.6
2U 3U 4U
0.5 0.5 0.45
0.5 0.5 0.5 0.45 0.5 0.47 5 0.5 0.5 0.5
0.62 0.62 0.55 0.5 0.5 0.6 0.6 0.5 0.5 0.5 0.5 0.5 0.5 0.6 0.5 0.52 5 0.6 0.5 0.4 0.4 0.6 0.6
0.47 5 0.55 0.55 0.55 0.3 0.5 0.6 0.5 0.5 0.45 0.5 0.65 0.5 0.6 0.6 0.5 0.5
0.7 0.5 0.5
0.45 0.4 0.5
0.5 0.6 0.6
0.4 0.55 0.6
0.4 0.6 0.65
5U 6U 7U
0.5 * *
0.5 * *
0.5 * *
0.6 0.5 0.52 5 0.5 * *
0.4 * *
0.4 0.45 0.55
0.4 0.4 0.6
0.45 0.4 0.5
CL 0.458 6538 0.087 447
AO 0.367 307 0.066 285
LEFT SIDE CC LA 0.052 0.510 534 344 0.069 0.072 3584 431
MEA N SD
RIGHT SIDE CC LA 0.522 0.499 074 0.066 0.063 98 7307
CV 0.522 0.092 3343
* - Data not available
39
0.4
0.25
0.5 0.42 0.5 * 0.5 0.6 0.6 0.5 0.5 0.5 0.6 0.5 0.6 0.6 0.5 0.52 5 0.6 0.5 0.5 0.45 0.55 0.6
0.4 0.4 0.4 * 0.35 0.45 0.4 0.3 0.35 0.4 0.4 0.4 0.3 0.5 0.35 0.4
0.4 0.5 0.57 5 0.4 0.45 0.5
0.3 0.45 0.5
0.3 0.4 0.3 0.3 0.4 0.5
0.3 0.3 0.4
CV 0.511 2068 0.082 2632
CL 0.513 214 0.065 336
AO 0.375 0.068 718
TABLE VII (b): Mean diameter of individual segments of ICP
MEAN(cm)
RIGHT
LEFT
CC
0.522
0.525
LA
0.499
0.510
CV
0.522
0.511
CL
0.458
0.513
AO
0.367
0.375
Fig 8: Mean diameter (cm) of individual segments of ICP on both right & left sides
0.6 0.5 0.4 RIGHT LEFT
0.3 0.2 0.1 0 CC
LA
CV
CL
40
AO
0.5 0.6 0.45 0.45 0.6 0.5 0.5 0.4 0.5 0.45 0.5 0.65 0.75 0.7 0.5 0.6 0.5 0.5 0.5 0.4
0.4 0.5 0.45 0.5 0.6 0.4 0.5 0.5 * 0.4 0.4 0.6 0.6 0.6 0.5 0.6 0.55 0.5 0.5 0.4
0.3 0.4 0.35 0.4 0.4 0.35 0.3 0.4 * 0.25 0.35 0.45 0.3 0.45 0.35 0.45 0.4 0.4 0.3 0.3 2.8 3.2 2.7 4.4 3.7 3.7 2.8 4.3 0.9 2.7 3 2.8 2.9 3.5 3.2 3.7 2.9 2.7 2.8 2.8
0.4 0.5 0.416 0.45 0.533 0.416 0.433 0.433 0.5 0.366 0.416 0.566 0.55 0.583 0.45 0.55 0.483 0.466 0.433 0.366
0.7 0.8 0.5 1.2 0.9 0.4 * 0.8 * 0.8 0.9 0.6 0.5 0.9 0.9 0.9 0.5 * 0.7 0.7
1.2 1.5 1.6 2 1.5 2.2 1.7 2.2 0.9 1.3 1.6 1.5 1.9 1.4 1.9 1.8 1.5 2 1.3 1.4
1M 2M 3M 4M 5M 6M 7M 8M 9M 10M 11M 12M 13M 14M 15M 16M 17M 18 F 19 F 20 F
0.9 0.9 0.6 1.2 1.3 1.1 1.1 1.3 * 0.6 0.5 0.7 0.5 1.2 0.4 1 0.9 0.7 0.8 0.7
Ave diam eter
RIGHT SIDE Leng LENGTH (in cm) DIAMETER (in cm) th CV CL AO CV CL AO
NO
41
1.2 1.8 1.7 3 1.6 1.7 1.5 1.5 1.2 1.4 1.6 1.9 1.8 2.1 1.4 1.6 1.3 1.8 1.7 1.2
CV
0.6 0.3 0.7 0.7 * 0.5 1 0.8 1 0.5 0.8 0.5 0.5 1.2 0.7 1.5 0.8 0.6 0.5 0.6
CL
0.4 1 0.5 1.2 * 0.6 0.8 1 0.4 0.7 1.2 0.9 0.7 0.6 1 0.6 0.3 0.7 0.6 0.5
AO
0.475 0.55 0.55 0.55 0.3 0.5 0.6 0.5 0.5 0.45 0.5 0.65 0.5 0.6 0.6 0.5 0.5 0.55 0.5 0.4
CV
0.4 0.5 0.42 0.5 * 0.5 0.6 0.6 0.5 0.5 0.5 0.6 0.5 0.6 0.6 0.5 0.525 0.6 0.5 0.5
CL
0.25 0.4 0.4 0.4 * 0.35 0.45 0.4 0.3 0.35 0.4 0.4 0.4 0.3 0.5 0.35 0.4 0.3 0.4 0.3
AO
2.2 3.1 2.9 4.9 1.6 2.8 3.3 3.3 2.6 2.6 3.6 3.3 3 3.9 3.1 3.7 2.4 3.1 2.8 2.3
LEFT SIDE Leng LENGTH (in cm) DIAMETER (in cm) th
TABLE VIII: LENGTH & DIAMETER of the carotid siphon on both the sides.
0.375 0.483 0.456 0.483 0.3 0.45 0.55 0.5 0.433 0.433 0.466 0.55 0.466 0.5 0.566 0.45 0.475 0.483 0.466 0.4
Ave diam eter
* - Data not available Statistical analysis
MEAN SD
5U 6U 7U
0.25 0.3 0.35 0.45 0.4 0.5 0.4 * * 2.4 5 2.6 3.2 2 4 2.1 * *
1.7 1.3 2.7 1.4 0.6 2.8 1.45 1.1 1.3
CV
42
0.7 1 0.5 0.7 0.9 0.9 0.4 * *
AO
LENGTH 2.92931 0.78416
0.2 0.6 0.5 0.1 0.6 1 0.3 0.5 1.2
CL
0.45 0.55 0.6 0.4 0.5 0.575 0.4 0.45 0.5
CL
0.3 0.4 0.5 0.3 0.45 0.5 0.3 0.3 0.4
AO
2.6 2.9 3.7 2.2 2.1 4.7 2.15 1.6 2.5
LEFT SIDE (of siphon) DIAMETER 0.462 0.06715
0.4 0.55 0.6 0.4 0.6 0.65 0.45 0.4 0.5
CV
LEFT SIDE Leng LENGTH (in cm) DIAMETER (in cm) th
Diameter No difference
RIGHT SIDE (of siphon) DIAMETER 0.462 0.067306
0.4 0.4 0.4 0.6 0.5 0.525 0.5 * *
Length Rt. Vs Lt. t = 0.93 p > 0.05(NS)
LENGTH 3.0666 0.82275
0.4 0.5 0.45 0.7 0.5 0.5 0.5 * * 0.35 0.4 0.4 0.583 0.466 0.508 0.466 * *
0.7 1.4 0.9 0.2 0.3 0.5 * *
1.4 2.8 1.4 2.3 1.2 2.5 1.2 * *
21 F 22 F 1U 2U 3U 4U
0.3 0.8 0.3 0.7 0.8 1.2 0.4 * *
Ave diam eter
RIGHT SIDE Leng LENGTH (in cm) DIAMETER (in cm) th CV CL AO CV CL AO
NO
TABLE VIII: LENGTH & DIAMETER of the carotid siphon on both the sides. (Contd.)
0.383 0.5 0.566 0.366 0.516 0.575 0.383 0.383 0.466
Ave diam eter
TABLE IX: Carotid siphon The length & diameter (mean) of the carotid siphon were measured a. the length(mean) measured Length(cm)
RIGHT
LEFT
3.06
2.92
MIN
2
2.1
MAX
5
4.9
MEAN
b. the diameter(mean) measured Diameter(cm)
RIGHT
LEFT
MEAN
0.462
0.462
MIN
0.366
0.3
MAX
0.583
0.575
Fig 9: Mean length & diameter (cm) of the carotid siphon.
3.5 3 2.5 2 1.5 Right Left
1
diameter
0
length
0.5
43
TABLE X: Measurement of ANGLES at the bends.
NO 1M 2M 3M 4M 5M 6M 7M 8M 9M 10 M 11 M 12 M 13 M 14 M 15 M 16 M 17 M 18 F 19 F 20 F 21 F 22 F 1U 2U 3U 4U 5U 6U 7U
II BEND RIGHT LEFT 119 142 129 116 139 65 87 112 110 112 111 116 154.5 139 158 117.5 132.5 146.5 130 115 58 113 126 119 127 159 139 133 99 120 143 120 117.5 127 137 137 136.5 144 131.5 110 120 124.5 111 108 110 110 103.5 153 133 123 89 104 158.5 117.5 * 98 * 119
ANGLES (in degrees) III BEND RIGHT LEFT 139 150 119 86 130 135 56 47 35 45 47 66.5 97 100.5 138 138 133 142 81 152 60 97 123.5 118 86 101.5 117 61 135 148 133 135 116 132 108 65 143.5 136.5 162 134 117 132.5 118.5 132 142 81 57 131.5 142 105 60 134 129 130 * 140 * 140
IV BEND RIGHT LEFT 61 90 66 54 44 41.5 18.5 5 14 * 14.5 35.5 63.5 34 32.5 53 * 108.5 22.5 78 18 48 21 43 50 25 18.5 22 38.5 65 33 13.5 76 91 45 14 70 96.5 81 71 101 36 2 56.5 25 49 29 24 72 35 66.5 14 54 72 * 51 * 59
II III IV RIGHT LEFT RIGHT LEFT RIGHT LEFT AVE 122.57407 121.37931 108.31481 114.34482 43.73076 49.46428 SD 22.74427 18.48921 35.21640 32.5461 25.50930 27.20870 * - Data not available Statistical analysis Rt. Vs Lt. Rt. Vs Lt. Rt. Vs Lt. t = 0.29 t = 17.86 t = 1.15 p > 0.05(NS) p < 0.001(HS) p > 0.05(NS)
44
TABLE XI: Angles (mean) at bends a. Angle measured at II bend II bend(deg)
RIGHT
LEFT
MEAN
122
121
MIN
58
65
MAX
158.5
159
III bend(deg)
RIGHT
LEFT
MEAN
108
114
MIN
35
45
MAX
162
152
IV bend(deg)
RIGHT
LEFT
MEAN
43.73
49.46
MIN
2
5
MAX
101
108.5
b. Angle measured at III bend
c. Angle measured at IV bend
45
Fig 10: Mean angles at the bends
140 120 100 80 Right Left
60 40 20 0 II bend
III bend
IV bend
46
TABLE XII: CLASS INTERVAL for the angles measured at the bends in the intracranial part of the ICA (in degrees). Minimum value - 0°, Maximum value - 168°, Class interval - 42
RANGE II BEND (in deg) RIGHT LEFT 0 0 0°-42° 1 1 43°-84° 12 19 85°-126° 14 9 127°-168° 27 29 TOTAL
III BEND RIGHT LEFT 1 0 6 6 10 6 10 17 27 29
IV BEND RIGHT LEFT 13 12 12 12 1 4 0 0 26 28
II BEND: Angle measured at the angulation between the carotid canal part & lacerum segment of the ICA. III BEND: Angle measured at the angulation between the lacerum & cavernous segment of the ICA. IV BEND: Angle measured at the angulation between cavernous & clinoid segment of the ICA.
VARIATIONS were found in the course of the artery. TABLE XIII: To show the VARIATIONS in the course of ICA found in the study. NO 1 2 3 4
LIST OF VARIATIONS Complete loop in the cervical segment (ECP) Kink in the cervical segment (ECP) Aneurysm in ICP Additional bend in cavernous part (ICP)
47
NO 1 6 2 2
% 1.785 10.714 3.571 3.571
Fig 11: Complete loop in the cervical segment (ECP)
48
Fig 12: Kink in the cervical segment (ECP)
49
Fig 12: Kink in the cervical segment (ECP)
Fig 13: Kink in the cavernous segment/ carotid siphon (ICP).
50
Fig 14: Aneurysm in the clinoid segment/carotid siphon (ICP).
51
Fig 15: Histology of the cervical segment of ICA (specimen with loop formation).
52
RESULTS (Contd.) 1) LENGTH: In the present study, •
The total length (mean) of ICA was found slightly more on the left side, in comparison to right side.
•
The mean length of ICP of ICA was found to be more on the right and less on the left side.
•
The mean length of ECP of ICA measured more on the left and less on the right side.
(Ref table IV)
2) DIAMETER: •
The mean diameter of ICP & ECP did not show any difference between right & left side.
•
The mean diameter of individual segments of ICP also did not show any major difference between the right & left side.
(Ref table VI)
3) CAROTID SIPHON: •
The mean length of the carotid siphon showed negligible difference with higher values on the right side.
•
The mean diameter of the carotid siphon did not reveal any side difference. [Ref table VII (b)]
4) ANGLES: •
Measurement of angles of ICP showed acuteness of angulation on the right side in the IV bend.
•
The angles measured at the II & III bend on both the sides depicted obtuseness. (Ref table XII)
53
5) VARIATIONS: •
A complete loop formation was observed in cervical part (ECP) on left side in only one specimen.
•
The kinking of the cervical part (ECP) of ICA was found in six specimens.
•
The aneurysms were found in the clinoid segment of ICP in two specimens.
•
The additional bend (kink) in cavernous segment of ICP was observed in two specimens.
(Ref table XIII)
6) HISTOLOGICAL examination of ICA with loop formation was studied. No atherosclerotic changes or any other pathological changes could be observed. A huge sub intimal clot was seen on the right-sided ICA, which was a postmortem change.
54
DISCUSSION
It is a known fact that blood flows at a greater pressure in the left ICA since left CCA arises directly from the arch of aorta causing frequency of cerebral hemorrhages on the left side. Anatomic asymmetry between the two internal carotid arteries is considered secondary to the circulatory requirements placed by respective ipsilateral carebral territories fed by each vessel. This could lead disproportionate segmental blood flow to both ACAs. Extracranial & intracranial ICA asymmetry has also been identified in fetuses in support of above hypothesis.77 In the present study the total length of ICA on left side was more than the right side. Moreover, the left ECP segment particularly showed greater length in comparison to the right ECP segment. Probably this suggests a means of accommodating increased blood flow from the arch of aorta, forming a lengthy column of blood. Thoma78 (1893) accounted three mechanical reasons for the differentiation of vessels: 1. That the increase in size of lumen of a blood vessel is directly related to the rate of blood flow. 2. That the growth in the thickness of vessel wall is directly dependent on the tension to which it is subjected. 3. That an increase of blood pressure above a certain limit provides a direct stimulus for formation of capillaries. However in the present investigations, no difference could be seen in the diameter of ECP & ICP segments of ICA. This is indicative of the fact that other than
55
the increased diameter, the internal carotid arteries are adapting to other mechanical modes like tortuosity & bends for slowing down the rate of blood flow. The blood from ICA has to reach the brain at a favourable optimum pressure. To achieve this condition the other alternative for the ICA is to undergo kinks (angulations) to provide dampening effect to the flow of blood: since the vital tissues like brain and retina cannot withstand the blood flow at high pressure. Moreover the central branches of cerebral arteries are end arteries, thin walled and more susceptible for rupture leading to bizarre of localized cerebrovascular insults. In the present study four angulations were observed. The degree of angulation showed progressive acuteness from II to IV bend. (Refer table XII). In other words, the degree of acute angulation is seen in the carotid siphon, which extends between cavernous and clinoid segments. This observation strongly suggests that the pressure of the blood is definitely slowed down before the intracranial ICA becomes intradural ICA. The dampening effect to the flow of blood is very essential to protect the end arteries of the brain since the flow of blood at higher pressure increases the chances of cerebral hemorrhages. It is a well known fact that the left sided blood flow is comparatively at high pressure since the left ICA arises directly from arch of aorta. In the light of above established feature, in the present study no difference could be observed in the degree and frequency of kinking or angulations to provide more dampening effect to the blood flow on the left side.
56
In the present study, while estimating the class interval of angles, following observations were made in the siphon segment of ICA: 1. Great range of acuteness in the angle of bends was observed. 2. Total no of specimen which showed the acute angulation were maximum at the IV bend with no significant side difference. 3. At the II & III bend (refer table XII) the range and the number of obtuse angulations were more in contrast to negligent number of acute angulations. These observations suggest that the siphon part is mechanically & structurally adapted to provide decreased flow of blood as well as dampening effect. From the clinical point of view it is worth to remember about the effects of exaggeration of the degree and frequency of angulations in the siphon part of ICA; since it definitely adds to chances of carotid insufficiency. In the present investigation few interesting variations were also observed like complete loop formation, kink in the cervical segment of ICA and additional bends in the cavernous part of ICA. All the above observations are of greater importance from the clinical point of view. Kelly57 (1925) has enumerated the various causes for kinking of ICA. The vessel is formed from the third aortic arch and from dorsal aorta; hence in the embryo, it is normally kinked. As the heart recedes into thorax the ICA is stretched and the kink is eliminated. Failure of this developmental process might therefore account for persistence of the kink. The other cause suggested is elongation & tortuosity of the artery because of arteriosclerotic changes. Coiling & even complete loop of ICA occurs in 5-15% of patients in unselected angiographic series. This observation is thought to be at least partially developmental in related to either age or hypertension.79
57
Huber G24 (1980) observed the complete loop of ICA on right side along with intracranial ICA anastomosis. In the present investigation unilateral complete loop formation of ICA on left side is similar to the above documentation. The reason seems to be embryological as opined by Kelly57 (1924). Functionally these variations are perhaps preferential mechanical modes of adaptation for slowing down the blood flow. However the possibility of the pathological cause in terms of atherosclerotic changes are ruled out by the histological observations. (Fig 14) The kink in the cervical (ECP) segment of ICA that was observed in 6 specimens also appears to be an embryological cause for bringing about the mechanical adaptations to slow down the rate of blood flow. The additional bend or the kink observed in the cavernous (siphon) part was found in 2 specimens. This feature gains more significance since these bends are additional to the normal number of bends which are responsible for slowing of rate of blood flow and dampening effect of blood flow in the siphon part. These additional bends in the cavernous part have to be ruled out by angiographic studies since they may form the root cause for the carotid insufficiency and cerebral ischaemia. Aneurysms were seen in only 4% of the specimen studied and it was located in siphon part. The clinical significance of aneurysm is associated with the surgical clipping of the vessel. In this context the relation of the nerves gaining entry into cavernous sinus through their dural neuropores gain more importance and this needs thorough investigation in future.
58
CONCLUSION
The observations made on the course of ICA revealed the siphon part to adapt itself mechanically in the form of angulations, bends and kinks, and loop formation to slow down the blood flow. This is a protective measure to safeguard the neural tissue from the aftereffects of arterial rupture and provide dampening effect to the blood flow. The cause for such mechanical adaptation appears to be primarily embryological and secondarily functional. However the exaggeration in these adaptive measures in terms of additional bends calls for immediate attention.
59
SUMMARY In the present study the observations made on the course of ICA revealed certain mechanical adaptations to promote slowness and dampening effect to the blood flow. This appears to be very essential from the functional point of view since the central branches of ICA are end arteries and thin walled. The adaptations were seen in the form of bends or angulations, kinks and complete loop formation. They were seen more in the siphon part of ICA (cavernous and clinoid segment). This appears to be a sure modification of the carotid siphon to slow down the speed of the blood flow. Eventhough the asymmetry in the blood flow of internal carotid arteries is proved fact, no correlation could be observed in the present study with reference to the diameter of ICA and the more number of angulations and kinks on the left side. The predominance of acuteness in the angulations of the siphon part of ICA probably suggests dampening effect to the blood flow between the intracranial part of ICA and intradural part of ICA. The causes for variations like complete loop formation; kinks and additional bends appear to be more embryological and functional. However the possibility of pathology for the above variations is ruled out by histological observations. Small percentage of aneurysms encountered in the clinoid part of ICA draws attention from the clinical point of view since the cranial nerves entering the cavernous sinus through the dural neuropores form the potential sites of danger during clipping and this aspect needs further investigation
60
BIBLIOGRAPHY 1. Lima PA. Cerebral angiography. London: Oxford University Press; 1950. (Cited by Ranson SW, editor. The Anatomy of the nervous system. 10th ed. Philadelphia: WB Saunders Company; 1959. p.85-86.)
2. Last RJ. Anatomy Regional & Applied. 7th ed. Singapore: Longman Singapore Publishers Pte Ltd; 1986. p.396
3. Standring S (editor-in-chief), Ellis H, Healy JC, Johnson D, Williams A, Collins P, et al. Gray's Anatomy. 39th ed. Spain: Elsevier Churchill Livingstone Ltd; 2005. p.295-297.
4. Moore KL, Dalley AF II. Clinically oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 898.
5. Schaeffer JP, editor. Morris' Human Anatomy. 11th ed. McGraw-Hill Book Company, Inc; 1953. p.657.
6. Decker GAG, du Plessis DJ, editors. Lee McGregor's synopsis of Surgical Anatomy. 12th ed. Indian edition. Bristol: John Wright & Sons Ltd; 1986. p.190.
7. England MA, Wakely J. A Colour Atlas of the Brain and Spinal cord. Indian edition. England: Wolfe publishing Ltd; 1991. p.53,61.
8. Ellis H. Clinical Anatomy. 10th ed. Oxford OX2 0EL, UK: Blackwell publishing company; 2002. p.318-321.
9. Sadler TW. Langman's Medical Embryology. 9th ed. Philadelphia, USA: Lippincott Williams & Wilkins; 2004. p.257.
10. Tode. Medizinisch Chirurgische Bibliothek (Kopenhegan) 1787; 10: 408. (Cited in Lie.)
61
11. Fischer AGT. A case of complete absence of both internal carotid arteries, with a preliminary note on the developmental history of the stapedial artery. J Anat 1914:48: 37-46.
12. Da Silva G. Bilateral agenesis of the cranial route of the internal carotid arteries. Rev ottorrinolaringol 1936 (por); 4:425-438.
13. Verbiest H. Radiologic findings in a case with absence of the left internal carotid artery and compression of several cranial nerve roots in the posterior fossa by the basilar artery. Med Contemp 1954;71:601-9.
14. Fields WS, Bruetman ME, Weibel J. Collateral circulation of the brain. Baltimore: Williams & Wilkins; 1965. p. 211-212.
15. Hills J, Sament S. Bilateral agenesis of the internal carotid artery associated with cardiac & other anomalies. Neurology (Minneap) 1968; 18:142-146.
16. Smith RR, Kees CJ, Hogg ID. Agenesis of the internal carotid artery with an unusual primitive collateral. J Neurosurg 1972 Oct;37:460-462.
17. Teal JS, Rumbaugh CL, Bergeron RT, et al. Congenital absence of the internal carotid artery associated with cerebral hemiatrophy, absence of the external carotid artery, and persistence of the stapedial artery. Am J Roentgenol Rad Ther Nucl Med 1973;118:534-545.
18. Rosen IW, Mills DF, Nadel HI & Kaiserman DD. Angiographic demonstration of congenital absence of both internal carotid arteries. J Neurosurg 1975;42:478482.
19. Servo A. Agenesis of the left internal carotid artery associated with an aneurysm on the right carotid siphon. J Neurosurg 1977 May; 46:677-680.
20. Ferguson GG. Physical factors in the initiation, growth and rupture of human intracranial saccular aneurysms. J Neurosurg 1972;37:666-677.
62
21. Janicki PC, Limbacher JP, Guinto FC, jr. Agenesis of the internal carotid artery with a primitive transsellar communicating artery. Am J Radiol 1979 Jan;132:130-2.
22. Kishore PRS, Kaufman AB, Melichar FA. Intrasellar carotid anastomosis simulating pituitary microadenoma. Radiology 1979 Aug;132:381-383.
23. Handa J, Matsuda I, Nakasu S & Nakano Y. Agenesis of an internal carotid artery, angiographic, tomographic and computed tomographic correlation. Neuroradiology 1980;19:207-211.
24. Huber G. Intracranial carotid anastomosis and partial aplasia of an internal carotid artery. Neuroradiology 1980;20:207-212.
25. Milder DG, Lance JW. Intermittent claudication of one cerebral hemisphere. Neurology (Cleveland) 1984;34:692-4.
26. Worthington C, Olivier A, & Melanson D. Internal carotid artery agenesis: correlation by conventional & digital subtraction angiography & by computed tomography. Surg Neurol 1984;22:295-300.
27. Kunishio K, Yamamoto Y, Sunami N, Asari S. Agenesis of the left internal carotid artery, common carotid artery and main trunk of the external carotid artery associated with multiple cerebral aneurysms. Surg Neurol 1987;27:177-181.
28. Quint DJ, Boulos RS, Spera TD. Congenital absence of the cervical and petrous internal
carotid
artery
with
intercavernous
anastomosis.
AJNR
1989
Mar/Apr;10:435-439.
29. Fuwa I. A pediatric case of carotid rete mirabile. Stroke 1994;25:1268-1270. 30. Pascual-Castroviejo I, Viano J, Pascual-Pascual SI & Martinez V. Facial hemangioma, agenesis of the internal carotid artery & dysplasia of cerebral cortex: case report. Neuroradiology 1995;37:692-695.
63
31. Sunada I, Inoue T. Bilateral internal carotid artery agenesis. J Neurol Neurosurg Psychiatry 1996;61:206-7.
32. Heth JA, Loftus CM, Piper JG, & Yuh W. Hypoplastic internal carotid artery mimicking a classic angiographic "string sign". J Neurosurg 1997 Mar;86:567570.
33. Czarnecki EJ, Silbergliet R, Mehta BA & Sanders WP. Absence of the supraclinoid internal carotid artery in association with intracranial aneurysms. Neuroradiology 1998;40:11-14.
34. Chen CJ, Chen ST, Hsieh FY, Wang LJ & Wong YC. Hypoplasia of the internal carotid artery with intercavernous anastomosis. Neuroradiology 1998;40:252-254.
35. Hattori T, Kobayashi H, Inoue S & Sakai N. Persistent primitive trigeminal artery associated with absence of internal carotid artery. Surg Neurol 1998;50:352-5.
36. Mahadevan J, Batista L, Alvarez H, Bravo-Castro E, Lasjaunias P. Bilateral segmental regression of the carotid & vertebral arteries with rete compensation in a western patient. Neuroradiology 2004;46:444-449.
37. Malacarne V. Osservzioni sopra alcone arterie del corpo umano nello statto preternaturale. Osservature Chir (Torino) 1784;2:119.
38. Seidel K. Arteriographische Boebachtung einer seltenen carotisanomalie. Fortschr Roentgenstr 1965 Sep;103:390-391.
39. Lie TA. Congenital anomalies of the carotid arteries. Amsterdam: Excerpta Med Found; 1968. p.19-20.
40. Handa J, Matsuda M, Handa H. Lateral position of the external carotid artery. Radiology 1972 Feb;102:361-362.
64
41. Bryan NR, Drewyer RG, Gee W. Separate origins of the left internal & external carotid arteries from the aorta. Am J Roentgenol 1978 Feb;130:362-365.
42. Roberts LK, Gerald B. Absence of both common carotid arteries. Am J Roentgenol 1978 May:130: 981-982.
43. Marimoto T, Nitia K, Kazekawa K, & Hashizume K. The anomaly of a nonbifurcating cervical carotid artery. J Neurosurg 1990;72:130-132.
44. Kaneko K, Akita M, Masuta E, Imai M & Sowa K. Unilateral anomalous left common carotid artery: a case report. Anat-Anaz 1996 Oct;178(5):477-80
45. Olivier A, Scotti G, Melancon D. vascular entrapment of the hypoglossal nerve in the neck. J Neurosurg 1977;47:472-5.
46. Killien FC, Wyler AR & Cromwell LD. Duplication of the internal carotid artery. Neuroradiology 1980;19:101-2.
47. Tanaka M, Matsumoto S. Fenestration of the internal carotid artery. Nuerol Med Chir (Tokyo) 1981;22:291-4.
48. Hasegawa T, Kashihara K, Ito H, Yamamoto S. Fenestration of internal carotid artery. Surg Neurol 1985;23:391-5.
49. Findlay JM, Chui M, Muller PJ. Fenestration of the supraclinoid internal carotid artery. Can J Neurol Sci 1987 May;14(2):159-61.
50. Boerman RH, Padberg GWAM, Wondergem J, & Gittenberger de Groot AC. Anomalous origin of the common carotid arteries as a cause of stroke. Clin Neurol Neurosurg 1991;94(4):317-319.
51. Koenigsberg RA, Zito JL, Patel M, Swartz JD, Goldofsky E, & Zahtz G. Fenestration of internal carotid artery: a rare mass of the hypotympanum associated with persistence of the stapedial artery. AJNR 1995 Apr;16:908-910
65
52. Chess MA, Barsotti JB, Ja-kwei Chang, Ketonen LM & Per-Lennart Westesson. Duplication of the extracranial internal carotid artery. AJNR 1995 Aug;16:1545-47.
53. Manglaa S, Teitelbauma GP. Multichannel fenestrations of the petrous segment of the internal carotid artery. AJNR 1999(4);20:590-592.
54. Goto Y, Yoshida K, Oshimoto T, Wataya T, Hojo M, Chin M, Yamagata S. Fenestration of the extracranial internal carotid artery: report of two cases. No To Shinkei 2003 Jul;55(7):623-8.
55. Khan N, Schinzel A, Shuknecht B, Baumann F, Ostergaard JR, Yonekawa Y. Moya moya angiopathy with dolichoectatic internal carotid arteries, patent ductus arteriosus & pupillary dysfunction: a new genetic syndrome? European Neurology 2004;51:72-77.
56. Kelly AB. Proc R Soc Med 1924;17:1. 57. Kelly AB. J Laryng 1925;40:15. 58. Myerson MD, Ruben H, Gilbert JG. Anatomic studies of the temporal bone. Arch Otolaryngol 1934;20:195-210.
59. Parkinson J, Bedford DE, Almond S. Brit Heart J 1939;1:345. 60. Hsu I, Kistin AD. Arch Inter Med 1956;98:712. 61. Quattlebaum JK, Upson ET, Neville RL. Ann Surg 1959;150:824. 62. Metz H, Murray-Leslie RM, Bannister RG, Bull JWD, Marshal J. Kinking of the internal carotid artery in relation to cerebrovascular disease. The Lancet 1961;1:424-426.
63. Lapayowker MS, Leibman EP, Ronis ML & Safer JN. Presentation of the internal carotid artery as a tumor of the middle ear. Radiology 1971;98:293-97.
66
64. Glasscock ME III, Dickins JR, Jackson CG, Wiet RJ. Vascular anomalies of the middle ear. Laryngoscope 1980;90:77-88.
65. Sinnreich AI, Parisier SC, Cohen NL, Berreby M. Arterial malformations of the middle ear. Otolaryngol Head Neck Surg 1984;92:194-206.
66. Glasscock ME III, Seshul M, & Seshul MB, sr. Bilateral aberrant internal carotid artery: a case presentation. Arch Otolaryngol Head Neck Surg 1993 Mar;119:335-339.
67. Moreano EH, Paparella MM, Zelterman D, Goycoolea MV. Prevalence of carotid canal dehiscence in the human middle ear: a case report of 1000 temporal bones. Laryngoscope 1994;104:612-8.
68. Saleem SM, Wani AM. Extracranial carotid artery anomalies presenting as ischaemic strokes. JK Practitioner 1998 Jan-Mar;5(1):52-4.
69. Ridder GJ, Fradis M, & Schipper J. Imaging case study of the month: Aberrant internal carotid artery in the middle ear. Ann Otol Rhinol Laryngol 2001;110:8924.
70. Sacher M, Som PM, Shugar JM & Leeds NE. Kissing intrasellar carotid arteries in acromegaly: CT demonstration. J Comput Assist Tomogr 1986 NovDec;10(6):1033-1035.
71. Ishikawa T, Nakamura N, Houkin K & Nomura M. Pathological consideration of a 'blister-like" aneurysm at the superior wall of the internal carotid artery: case report. Neurosurgery 1997 Feb;40(2):403-406.
72. Liera EC, Bendixen BH, Kardon RH & Adams HP., jr. Brief, transient Horner's syndrome can be the hallmark of carotid dissection. Neurology 1998;50:289-290.
67
73. Norris JW, Beletsky V, Nadareishvili ZG. Commentary (on behalf of the Canadian stroke consortium): Sudden neck movement & cervical artery dissection. JAMC 2000 Jan 11;163(1):38-40.
74. Jordan JA, Lewis M, Rollins N & Roland PS. Congenital internal carotid artery aneurysm with absence of the petrous portion of the contralateral internal carotid artery. Annals of Otol Rhinol & Laryngol 2000 Dec;109(12):1167-69.
75. Robertson WC, Pettigrew LC. Congenital Horner's syndrome and carotid dissection. Journal of Neuroimaging 2003 Oct;13(4):367-370.
76. Payton TF, Siddiqui KM, Sole DP & Mckinley DF. Traumatic dissection of internal carotid artery. Pediatric Emergency Care 2004 Jan;20(1):27-29.
77. Viken BL, Wechsler LR. Transcranial Doppler Ultrasonography. 2nd ed. USA: Butterworth-Heinemann;1999. p. 319.
78. Le Gros Clark WE. The tissues of the body. 6th ed. Oxford, Great Britain: The Clarendon Press; 1975. p. 217.
79. Osborn AG. Diagnostic Cerebral Angiography. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 63.
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ANNEXURE
Stastical tool used - Paired 't' test =X1 - Χ2 SD/√n
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Where X1 &X2 are means n is no of observations.
