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\def\makelabel##1{\upshape ##1}}% } {\end{list}\end{raggedright}} \newenvironment{specHead}[2]% {\vspace{20pt}\hrule\vspace{10pt}% \phantomsection\label{#1}\markright{#2}% \pdfbookmark[2]{#2}{#1}% \hspace{-0.75in}{\bfseries\fontsize{16pt}{18pt}\selectfont#2}% }{} \def\TheFullDate{2016-01-15 (revised: 15 January 2016)} \def\TheID{\makeatother } \def\TheDate{2016-01-15} \title{A Computed Tomography-Aided Clinical Report on Anatomical Variations of the Paranasal Sinuses} \author{}\makeatletter \makeatletter \newcommand*{\cleartoleftpage}{% \clearpage \if@twoside \ifodd\c@page \hbox{}\newpage \if@twocolumn \hbox{}\newpage \fi \fi \fi } \makeatother \makeatletter \thispagestyle{empty} \markright{\@title}\markboth{\@title}{\@author} \renewcommand\small{\@setfontsize\small{9pt}{11pt}\abovedisplayskip 8.5\p@ plus3\p@ minus4\p@ \belowdisplayskip \abovedisplayskip \abovedisplayshortskip \z@ plus2\p@ \belowdisplayshortskip 4\p@ plus2\p@ minus2\p@ \def\@listi{\leftmargin\leftmargini \topsep 2\p@ plus1\p@ minus1\p@ \parsep 2\p@ plus\p@ minus\p@ \itemsep 1pt} } \makeatother \fvset{frame=single,numberblanklines=false,xleftmargin=5mm,xrightmargin=5mm} \fancyhf{} \setlength{\headheight}{14pt} \fancyhead[LE]{\bfseries\leftmark} \fancyhead[RO]{\bfseries\rightmark} \fancyfoot[RO]{} \fancyfoot[CO]{\thepage} \fancyfoot[LO]{\TheID} \fancyfoot[LE]{} \fancyfoot[CE]{\thepage} \fancyfoot[RE]{\TheID} \hypersetup{citebordercolor=0.75 0.75 0.75,linkbordercolor=0.75 0.75 0.75,urlbordercolor=0.75 0.75 0.75,bookmarksnumbered=true} \fancypagestyle{plain}{\fancyhead{}\renewcommand{\headrulewidth}{0pt}} \date{} \usepackage{authblk} \providecommand{\keywords}[1] { \footnotesize \textbf{\textit{Index terms---}} #1 } \usepackage{graphicx,xcolor} \definecolor{GJBlue}{HTML}{273B81} \definecolor{GJLightBlue}{HTML}{0A9DD9} \definecolor{GJMediumGrey}{HTML}{6D6E70} \definecolor{GJLightGrey}{HTML}{929497} \renewenvironment{abstract}{% \setlength{\parindent}{0pt}\raggedright \textcolor{GJMediumGrey}{\rule{\textwidth}{2pt}} \vskip16pt \textcolor{GJBlue}{\large\bfseries\abstractname\space} }{% \vskip8pt \textcolor{GJMediumGrey}{\rule{\textwidth}{2pt}} \vskip16pt } \usepackage[absolute,overlay]{textpos} \makeatother \usepackage{lineno} \linenumbers \begin{document} \author[1]{Salah Eldeen} \author[2]{Mohamed Ali Seyed} \author[3]{Nazik A Elfadil} \affil[1]{ IBN sina national medical college} \renewcommand\Authands{ and } \date{\small \em Received: 16 December 2015 Accepted: 5 January 2016 Published: 15 January 2016} \maketitle \begin{abstract} Disease of the paranasal sinuses (PNS) is a global public health problem, with the only treatment option available being endoscopic surgery. Previous studies have suggested that anatomical variations of the PNS are common in different populations; however, there is little information available to verify this. Hence, the objective of the present study was to determine the prevalence of different anatomical variations of the PNS and nasal cavity among Sudanese patients who were referred by ear, nose and throat (ENT) surgeons for a computed tomography (CT)-aided study. The total number of patients eligible for the study was 557; of these, 51 were excluded, 317were in the study group, and 189 were controls. The CT images were carefully reviewed and discussed with the involvement of consultant radiologists, an anatomist, and an otolaryngologist. Our results showed that there was extensive pneumatization of the frontal sinus (FS) in 37% of cases, a rudimentary FS in 11%, and absence of the FS in 12%. In addition, the Keros classification showed the FS to be normal in 55%, type I in 27%, type IIin 10%, type III in 6%, and type IV in only 2% of patients. A large ethmoid bulla (EB) was found in 43% of patients, but the remaining 57% had a normal ethmoid sinus. Posterior ethmoid cells showed extensive pneumatization unilaterally in 5%, and bilaterally in 3% of patients; 92% were normal. Extensive pneumatization of the sphenoid was seen in 49%of patients, while the remaining 51% had a normal sphenoid. The sphenoid septum was attached bilaterally to the internal carotid artery in 6% and unilaterally in 21% of patients. Aseptate sphenoid sinus (more than one septum) was found in 33% of patients; the remaining 67%were normal. A bilateral hypoplastic maxillary sinus was seen in 23%, a unilateral hypoplastic maxillary sinus in 3%, extensive pneumatization in 17%, bilateral septation in 17%, unilateral septation in 19%, Haller cells in 33%, and normal anatomy in 67% of patients. To \end{abstract} \keywords{paranasal sinuses, anatomic variation, computed tomography, sudanese population.} \begin{textblock*}{18cm}(1cm,1cm) % {block width} (coords) \textcolor{GJBlue}{\LARGE Global Journals \LaTeX\ JournalKaleidoscope\texttrademark} \end{textblock*} \begin{textblock*}{18cm}(1.4cm,1.5cm) % {block width} (coords) \textcolor{GJBlue}{\footnotesize \\ Artificial Intelligence formulated this projection for compatibility purposes from the original article published at Global Journals. However, this technology is currently in beta. \emph{Therefore, kindly ignore odd layouts, missed formulae, text, tables, or figures.}} \end{textblock*} \let\tabcellsep& \par he paranasal sinuses (PNSs) are air-filled, mucosa-lined cavities that develop in the facial and cranial bones and communicate with the nasal airways. However, their function is not known, and has been the subject of much speculation. Some argue that they could be involved in decreasing the weight of the skull and others postulate that they may act as resonators for voice Durr DG et al \hyperref[b0]{1} . In lower animals, they are associated with a more acute sense of smell, and are largely lined by olfactory epithelium that has developed to increase the available surface area for smelling. However, in humans, olfaction is limited to a much smaller surface area, and the presence of the paranasal sinuses is probably a vestigial anachronism.\par The PNSs are clinically categorized into the following four paired types a) the frontal pair in the frontal bone. The posterior wall is located adjacent to the anterior cranial fossa. They are usually asymmetrical and occasionally absent. b) The maxillary pair in the maxilla. The superior wall forms the floor of the orbit and the medial wall is formed by the lateral wall of the nose. Inferiorly, the maxillary pairis related to the tooth-bearing area of the maxilla. c) The numerous ethmoid cells in the superior and lateral walls of the nose and the medial walls of the orbits. d) The sphenoid pair, located in the sphenoid bone where the sellaturcica projects into this space Koskenkorva T et al \hyperref[b1]{2} . Infection in the PNSs can cause headache because of obstruction to normal drainage as well as negative pressure created in the sinus. It has been reported that neoplasms growing in the sinuses also may cause obstruction for a prolonged period, and are therefore usually diagnosed at an advanced stage. \section[{Types of anatomical variations in the PNS: Variable pneumatization of the frontal sinus:}]{Types of anatomical variations in the PNS: Variable pneumatization of the frontal sinus:}\par Pneumatization of the frontal sinuses is highly variable and asymmetric. Although extensive pneumatization of the frontal sinuses is very common, aplasia and hypoplasia can be seen in up to 5\% of the population Ozpursoy OB et al \hyperref[b2]{3} . It is speculated that pneumatization may extend into the orbital plate of the frontal bone, resulting in development of the anterior ethmoids, and is associated with the absence of an T Type I: Single frontal recess cell above the agger nasi cells. Type II: Tier of cells in the frontal recess above the agger nasi cells. Type III: Single massive cell pneumatization cephalad to the frontal sinuses. Type IV: Single isolated cell within the frontal sinus. \section[{a) Variable pneumatization of the maxillary sinuses}]{a) Variable pneumatization of the maxillary sinuses}\par Four types of recesses are reported in the maxillary sinuses, as follows. (i) Palatine recesses, which extend medially into the hard palate from the inferior aspect of the maxillary antra Lanzieri CF et al \hyperref[b6]{8} . These recesses are bilateral and symmetric. (ii) Alveolar recesses, which are formed by extension of pneumatization into the superior alveolus and are seen more frequently in edentulous patients Bell GW et al \hyperref[b7]{9} . They are close to the roots of the premolar and molar teeth. (iii) Infraorbital recesses are the result of pneumatization along the roof of the maxillary sinus and are medial to the groove for the infraorbital nerve. These extensions are usually confused with infraorbital ethmoid air cells, i.e., Haller cells. (iv) Zygomatic recesses are the result of extension of pneumatization of the maxillary sinus roof into the zygomatic bone. \section[{b) Anatomical variation of the ethmoid sinuses}]{b) Anatomical variation of the ethmoid sinuses}\par The most notable anatomical ethmoid variations include the agger nasi cells, which are mostly seen in the anterior ethmoid air cells, and are extramural (i.e., not within the ethmoid bone). Because of variations in anatomic descriptions, the prevalence of these cells also varies widely in nature. For the purpose of coronal CT imaging in this study, agger nasi cells are defined as those located anterior to the superior end of the nasolacrimal duct, because they may cause narrowing of the frontal recess and cause predisposition to ipsilateral frontal sinus disease. The large ethmoid bullae are another variation of the ethmoid sinus; these may compromise the osteomeatal complex at the level of the infundibulum, hiatus semilunaris, or middle meatus. A third anatomical variation is the presence of infraorbital ethmoid Haller cells, which extend along the medial aspect of the orbital floor; they may be present as discrete air cells or drain into the infundibulum or maxillary sinus. These infraorbital cells may cause narrowing of the ethmoid infundibulum, resulting in ipsilateral maxillary sinus disease.\par The fourth and final variation is the fovea ethmoidalis. This asymmetric, low-lying ethmoid roof is a potential risk factor for intracranial injury during endoscopic surgery of the ethmoid air cells; focal dehiscence of the fovea ethmoidalis or cribriform plate may be posttraumatic or congenital Krmpotic et al \hyperref[b8]{10} . \section[{c) Anatomical variation of the sphenoidal sinuses}]{c) Anatomical variation of the sphenoidal sinuses}\par Sphenoid pneumatization is highly variable because the sphenoid sinuses can be hypoplastic or extensively pneumatized with aeration of multiple recesses. Lateral extension of pneumatization may occur into the lesser wing of the sphenoid above the optic nerve, or into the anterior clinoid processes inferior and lateral to the optic nerves. Pneumatization of the optic nerve may increase the risk of injury during endoscopic surgery in the region. Pneumatization into the greater wing may extend lateral to a line drawn between the pterygoid canal and foramen rotundum. These extensions excavate into the base of the pterygoid process and are referred to as pterygoid recesses. However, midline extensions may occur anteriorly into the nasal septum or posteriorly into the dorsum sellae. Another variation in the sphenoid sinus is septation. Vertical septations within the sphenoid may traverse the sinus obliquely and terminate posteriorly in the bony covering over the internal carotid artery, predisposing the vessel to injury Lund Sethi et al \hyperref[b9]{11} .\par Hence, an objective of the present study is to demonstrate the anatomical PNS variations that may occur in the Sudanese population. This study also intends to correlate sinus disease to anatomical variations of the PNS. \section[{II. Material and Methods}]{II. Material and Methods}\par Study design: This was a retrospective and descriptive hospital-based study that recruited557 patients. Study location: This study was conducted in the Department of Radiology of the Ear, Nose, and Throat (ENT) Hospital, and in the Antalia diagnostic Center of Alzytona Hospital between January 1, 2012 and January 1, 2015. \section[{Groups, inclusion and exclusion criteria:}]{Groups, inclusion and exclusion criteria:}\par The present study included 557 individuals. Of these, 368 were referred to the Radiology Department for a CT study of the PNS. We excluded 51 individuals for the following medical reasons: those who were diagnosed with nasal or sinus tumors and those who had a history of surgery of the nose or sinuses, as well as those who had congenital facial anomalies and dysmorphic syndromes. Finally, we included a total of 317 patients with PNS disease (Group B). The control group consisted of 189 randomly selected healthy individuals with no symptoms or signs of PNS (Group A). \section[{a) CT scan equipment}]{a) CT scan equipment}\par We used a Siemens Sensation 64-slice multidetector CT scanner (Siemens AG, Germany); this is the preferred modality for PNS imaging because it ethmoid bulla Momeni AK et al \hyperref[b3]{4} . Frontal cells are an additional reported variation of the frontal sinuses 5 demonstrated that these cells play a role in embryonic development of the sinuses, whereas Van Aleya et al \hyperref[b4]{6} reported that these cells encroach into the frontal recess or frontal sinuses. However, J.M. Delgaudio et al 7 classified these into the following four categories: provides a precise view of the anatomical structures. The PNS differ between patients, leading to anatomical variations in the general population. In this study, coronal reference views were used for data collection; in some cases, axial views were used for additional details. CT images were analyzed for the presence or absence of anatomical variations in the PNS and also for pathological conditions. \section[{b) Statistical analysis}]{b) Statistical analysis}\par The collected data were analyzed using SPSS version 16 software (IBM Analytics, USA). \section[{III. Results}]{III. Results}\par The results showed that there is a strong association between PNS anatomical variations and sinusitis in Sudanese patients. \section[{a) Anatomical variation of the frontal sinus (FS) in the}]{a) Anatomical variation of the frontal sinus (FS) in the}\par Sudanese population Individuals belong to Group B were characterized by the pneumatization of the FS in about 28\%, with a rudimentary FS in 10\%, and the absence of FS in 11\%. In addition, 51\% showed no PNS anatomical variation. Our study also indicated that extensive pneumatization of FS had the highest incidence rate in group B, at about 37\%, followed by a rudimentary FS in11\%, and absence of the FS in 12\%. However, nearly 40\% of group B showed no PNS anatomical variation (Table \hyperref[tab_0]{1}). The results indicated a strong correlation (P <0.05; chi-square between anatomical variation and PNS disease. \section[{b) Keros classification of the FS in the Sudanese population c) Anatomical variation of the ethmoid sinuses in the Sudanese population i. The ethmoid bulla (EB)}]{b) Keros classification of the FS in the Sudanese population c) Anatomical variation of the ethmoid sinuses in the Sudanese population i. The ethmoid bulla (EB)}\par In group B individuals, a large EB was present in about 43\%, but 57\% were normal. However, in group A, about 29\% had a large EB, and 71\% were normal (P<0.05). These results indicated a correlation between a large EB and ethmoiditis (Table \hyperref[tab_2]{3}). \section[{ii. Posterior ethmoid cells}]{ii. Posterior ethmoid cells}\par In group A, unilateral cells were seen in about 2\%, bilateral cells in 1\%, and normal anatomy in 96\% of patients. In group B, posterior ethmoid cells were extensively pneumatized unilaterally in 5\%, bilaterally in 3\%, and were normal in 92\% of patients (Table. 4). \section[{d) Anatomical variation of the sphenoid sinuses in the}]{d) Anatomical variation of the sphenoid sinuses in the}\par Sudanese population Among individuals belong to Group A, 44\% showed extensive pneumatization of the sphenoid sinuses, whereas 56\% had normal sphenoids. However, in group B, extensive pneumatization of the sphenoids was found in 49\%, and 51\% had normal sphenoids (Table \hyperref[tab_4]{5}).\par In addition, in group A, the sphenoid septum was attached bilaterally to the internal carotid artery in 16\%, and unilaterally artery in 39\% of patients. However, in group B, the sphenoid septum was attached bilaterally to the internal carotid artery in 6\%, and unilaterally in 21\% of patients (Table \hyperref[tab_5]{6}). In group A, a septate sphenoid sinus (more than one septum) was found in 41\% of patients and 59\% were normal. However, in group B, a septate sphenoid sinus was found in 33\% of patients and about 67\% were normal (Table \hyperref[tab_6]{7}). \section[{e) Anatomical variation of the maxillary sinuses in the Sudanese populations}]{e) Anatomical variation of the maxillary sinuses in the Sudanese populations}\par In group B, bilateral hypoplastic maxillary sinuses were observed in 23\% of patients, and unilateral hypoplastic maxillary sinuses were found in only 3\%, with extensive pneumatizationin 17\% (Table \hyperref[tab_7]{8}). Moreover, bilateral maxillary sinus septation was observed in 17\% and unilateral septation in 19\% of patients (Table \hyperref[tab_8]{9}). In group B, Haller cells were found in 33\% of patients, while 67\% had normal Haller cell anatomy. In group A, Haller cells were observed in only 15\% of patients and 85\% had normal Haller cell anatomy (Table \hyperref[tab_9]{10}). \section[{IV. Discussion}]{IV. Discussion}\par Anatomical variations of the PNS must be determined before performing any surgery in order to avoid the potential risks associated with functional endoscopic surgery (FESS) Abdullah et al \hyperref[b10]{12} . Before proceeding with endoscopic surgery, the radiographic details of the osteomeatal complex as well as the anatomy of the other Para nasal sinus must be thoroughly verified.\par In a previous study Nitinavakarn B et al 13 emphasized that CT of the PNS is usually required prior to any endoscopic sinus surgery because it demonstrates both the extent of disease and the anatomical variations that may predispose the patient to rhinosinusitis, as well as nearby vital structures so that iatrogenic injury can be avoided. Detailed knowledge of anatomical variations in the PNS region is critical for endoscopic sinus surgery as well for involvement by radiologists in the preoperative work-up. Prior knowledge of the anatomical variants and possible accompanying pathological influences are the key to the success of diagnostic and therapeutic management of PNS disease. Based on the Keros classification (13, 14), 64\% of group A individuals were normal, type I was seen in 19\%, type II in 9\%, type III in 6\%, and type IV in 2\%; in contrast, 55\%of individuals in group B were normal, type I was seen in 27\%, type II in 10\%, type III in 6\%, and type IV in 2\%, as shown in Table \hyperref[tab_1]{2}.\par Haller cells are ethmoid air cells that project beyond the limits of the ethmoid labyrinth into the maxillary sinus. They are considered to be ethmoid cells that grow into the floor of the orbit and may narrow the adjacent ostium of the maxillary sinus, especially if they become infected Stallman JS et al \hyperref[b12]{14} Furthermore, failure to diagnose this condition preoperatively can predispose the patient to orbital trauma and violation of the lamina papyracea during middle meatal antrostomy. The incidence of Haller cells in this study was 33\%, Lioyd GAS et a \hyperref[b13]{15} but reportedthe incidence as 15\%, which was less than that reported previously by palmer JN et al \hyperref[b14]{16} (45.9\%), Maru YK et al \hyperref[b15]{17} (36\%), and Laine FJ et al \hyperref[b16]{18} (6.8\%). Based on the above, it was clear that there is a strong association between maxillary sinusitis and anatomical variations of Haller cells (P <0.05).\par The EB is the air cell directly above and posterior to the infundibulum and hiatus semilunaris. Although it is the largest ethmoid air cell, excessive size and pneumatization can impair sinus ventilation and drainage. An EB sometimes grows to a size that completely fills the sinus in the middle turbinate. An excessively large EB is a potential cause of sinus infection, especially if pus, polyps, or cysts are present. However, Danese M et al \hyperref[b17]{19} reported that this variation is difficult to assess and that it may be over diagnosed. The authors also reported that when compared to other variations, an enlarged EB had a lower correlation with sinus disease.\par The present study reported a pneumatized EB in 43.2\%, whereas Kang SJ et al \hyperref[b19]{20} found a large bulla unilaterally in 12.5\%, and bilaterally in 7.4\%. The presence of a large EB was strong evidence of maxillary sinusitis in our study (P<0.05). Preoperative evaluation of the anatomy of the sphenoid sinus by CT is a routine procedure and can direct surgical decision-making. Conchal pneumatization of the sphenoid sinus was seen in 2\%, pre sellar pneumatization in 21\%, sellar type in 54.7\%, and post sellar pneumatization in 22.3\% of patients. Lateral pneumatization of the greater wing of the sphenoid, leading to a capacious sinus, was reportedly seen in83\% of patients by Hamid O et al \hyperref[b20]{21} , whereas the frequency of pneumatization of the sphenoid sinus was 49.5\% in this study.\par Asymmetric septation of the sphenoid sinuses (more than one septum) is very important, especially when it shows considerable deviation. As it advances, it marks the line of the internal carotid artery, which may protrude into the posterior ethmoidal cell Zinreich SJ et al \hyperref[b21]{22} . However, the prevalence of septation in this study was about 33.5\%; the frequency of presence of a unilateral sphenoid septum was 20.5\%, and the septum was attached bilaterally to the internal carotid artery in 6.6\%. If the removal of a sphenoid septum is required, it should be done cautiously after CT is performed in order to prevent possible complications in case of attachment to the internal carotid artery or the optic nerve.\par The FSs are typically paired, asymmetric, and separated by a central intersinus septum, and have different degrees of pneumatization. Around 10 to 12\% of normal adults may have a rudimentary FS or even a complete lack of frontal bone pneumatization on one side. Around 4\% of the asymptomatic population has bilateral frontal sinus agenesis. In the present study, we found that extensive frontal sinus pneumatization occurred in 36.9\%.\par Agenesis of the paranasal sinuses is an uncommon clinical condition that appears mainly in the FS. Bilateral FS agenesis was seen in 11.7\%, and unilateral agenesis was seen in only three individuals (11.1\%) as reported by Pondé et al \hyperref[b22]{23} . The prevalence of bilateral absence of the FS has been reported to be only 3-4\%, but can be 10\% in some populations Aydinlioglu A et al \hyperref[b23]{24} . However, this frequency was significantly higher in some populations, including Alaskan Eskimos (25\% in males and 36\% in females) and Canadian Eskimos (43\% in males and 40\% in females), as reported by Som PM et al \hyperref[b24]{25} . The frequency of bilateral absence of the FS in this study was 11.7\%, which is identical to that in Aydinlio?lu's report, but lower than that reported for most other ethnic populations Binali Çakur et al \hyperref[b25]{26} .\par Bulla frontalis is a group of variants basically indicating air cells located cranial to agger nasi cells, and extending towards the frontal sinus; they can be isolated and protruding (type III) or not (type I). In the present study, bulla frontalis was found in 31.5\%.Frontal cells have been implicated as a cause of frontal recess obstruction. Follows 14.9\% had type I, 3.1\% had type II, 1.7\% had type III, and 2.1\% had type IV. The frontal cells in the present study, based on the Keros classification, showed the highest incidence for type I (26.5\%), followed by type II (10.4\%), type III (5.7\%) and type IV (1.6\%).\par Extensive maxillary sinus pneumatization (EMSP) was defined when the largest horizontal and/ orvertical dimension of the maxillary sinus was equal to or exceeded 90\% of the corresponding diameter of the orbit. In a study by Meyer TK et al \hyperref[b26]{27} , the prevalence of EMSP was found to be 8\% (7\% bilateral and 1\% unilateral). Extensive pneumatization was found in 17.3\% of our cases, Maxillary sinus hypoplasia is an anomaly of the paranasal sinuses occasionally encountered by otolaryngologists. However, the literature lacks a system by which the various types of maxillary sinus hypoplasia can be classified using computerized topographic imaging. The overall prevalence of maxillary sinus hypoplasia was 10.4\%. In the present study, we found that the incidence of a hypoplastic maxillary sinus was 26.5\%, whereas twice this percentage was reported by Bassiouny A et al \hyperref[b27]{28} Maxillary septa were found in 47\%, and appropriate imaging prior to performing sinus surgery seems justified, since complications and the success rate of sinus floor elevation are clearly related to the presence of septa. Bilateral maxillary septa were seen in 22.7\% of scans, whereas unilateral septa were seen in 13; the combined total percentage was 35.7\%. \section[{V. Conclusion}]{V. Conclusion}\par From the above results, we conclude that anatomical variations in patients have a great impact on the predisposition to inflammatory disease of the PNS, as these variations are largely found in patients with EB, Haller cells, variable pneumatization of the FS (hypo and hyper), frontal cells, and sphenoid sinuses with septation and pneumatization. Imaging of the PNS will aid in diagnosis in individual patients, and also provide a deeper understanding of the manifestations of the disease. In addition, CT topographical imaging of the PNS and anatomical variations enables endoscopic surgeons to be fully prepared for FESS, thus decreasing the risk of complications. This study may alert the endoscopic nasal surgeon to the importance of defining anatomical variations, and the significant impact of these variations on patient care, there by reducing iatrogenic complications of morbidity and mortality. \section[{VI. Recommendations}]{VI. Recommendations}\par The authors propose the following recommendations for the improvement of current treatment options available for PNS. \section[{List of Figures}]{List of Figures}\begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-2.png} \caption{\label{fig_1}A}\end{figure} \begin{figure}[htbp] \noindent\textbf{}\includegraphics[]{image-3.png} \caption{\label{fig_2}A}\end{figure} \begin{figure}[htbp] \noindent\textbf{12}\includegraphics[]{image-4.png} \caption{\label{fig_4}Figure 1 : 2 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{345}\includegraphics[]{image-5.png} \caption{\label{fig_5}Figure 3 : 4 :Figure 5 :A}\end{figure} \begin{figure}[htbp] \noindent\textbf{9}\includegraphics[]{image-6.png} \caption{\label{fig_6}Figure 9 :A}\end{figure} \begin{figure}[htbp] \noindent\textbf{78}\includegraphics[]{image-7.png} \caption{\label{fig_7}Figure 7 : 8 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{1} \par \begin{longtable}{P{0.85\textwidth}} 1. Collaboration between endoscopic nasal surgeons\\ and radiologists is very important in proper\\ diagnosis and interpretation of scans of the sinuses.\\ 2. Establishment of a standard protocol for CT\\ scanning of the nose, paranasal sinuses, and skull\\ base, including window specifications, thickness of\\ cuts, and views to increase the precision of\\ detection of pathology and anatomical variations.\\ 3. Regularly scheduled combined radiology and ENT\\ academic meetings are recommended to bridge the\\ gap between radiologists and ENT surgeons, and to\\ provide exchange of knowledge and experience\\ with the aim of improving medical services.\\ VII.\end{longtable} \par \caption{\label{tab_0}Table 1 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{2} \par \begin{longtable}{P{0.24366666666666667\textwidth}P{0.068\textwidth}P{0.06516666666666666\textwidth}P{0.221\textwidth}P{0.09066666666666667\textwidth}P{0.034\textwidth}P{0.036833333333333336\textwidth}P{0.09066666666666667\textwidth}} Sample\tabcellsep Normal\tabcellsep Karos I\tabcellsep \multicolumn{3}{l}{Frontal sinus karos classification Karos II Karos III Karos IV}\tabcellsep \multicolumn{2}{l}{Total}\\ Group A*\tabcellsep 64\%\tabcellsep 19\%\tabcellsep 9\%\tabcellsep 6\%\tabcellsep 2\%\tabcellsep \tabcellsep 100\%\\ No. of cases\tabcellsep (121)\tabcellsep (36)\tabcellsep (17)\tabcellsep (11)\tabcellsep (4)\tabcellsep \tabcellsep ( N= 189)\\ Group B*\tabcellsep 55\%\tabcellsep 27\%\tabcellsep 10 \%\tabcellsep 6\%\tabcellsep 2\%\tabcellsep \tabcellsep 100\%\\ No. of cases\tabcellsep (174)\tabcellsep (86)\tabcellsep (32)\tabcellsep (19)\tabcellsep (6)\tabcellsep \tabcellsep ( N= 317)\\ \multicolumn{2}{l}{ses/ control prevalence \%}\tabcellsep \tabcellsep \tabcellsep Chi -square\tabcellsep \tabcellsep \multicolumn{2}{l}{p-value}\\ 27.7 / 16.8 \%\tabcellsep \tabcellsep \tabcellsep \tabcellsep 147.474\tabcellsep \tabcellsep <\tabcellsep 0.05\end{longtable} \par \caption{\label{tab_1}Table 2 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{3} \par \begin{longtable}{P{0.22471264367816093\textwidth}P{0.17586206896551723\textwidth}P{0.28821839080459766\textwidth}P{0.16120689655172413\textwidth}} Sample\tabcellsep Normal ethmoid bulla\tabcellsep Size of Ethmoid bulla Large ethmoid bulla\tabcellsep Total\\ Group A*\tabcellsep 71\tabcellsep 29\tabcellsep 100\%\\ No. of cases\tabcellsep (134)\tabcellsep \%(55)\tabcellsep ( N= 189)\\ Group B*\tabcellsep 57\%\tabcellsep 43 \%\tabcellsep 100\%\\ No. of cases\tabcellsep (181)\tabcellsep (136)\tabcellsep (N = 317)\end{longtable} \par \caption{\label{tab_2}Table 3 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{4} \par \begin{longtable}{} \end{longtable} \par \caption{\label{tab_3}Table 4 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{5} \par \begin{longtable}{P{0.21135135135135136\textwidth}P{0.11486486486486487\textwidth}P{0.38135135135135134\textwidth}P{0.14243243243243245\textwidth}} Sample\tabcellsep Normal\tabcellsep Pneumatization of sphenoid sinus Pneumatization of sphenoid sinus\tabcellsep Total\\ Group A*\tabcellsep 56\%\tabcellsep 44\%\tabcellsep 100\%\\ No. of cases\tabcellsep (106)\tabcellsep (83)\tabcellsep (N= 189)\\ Group B*\tabcellsep 51 \%\tabcellsep 49 \%\tabcellsep 100\%\\ No. of cases\tabcellsep (162)\tabcellsep (155)\tabcellsep (N= 317)\end{longtable} \par \caption{\label{tab_4}Table 5 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{6} \par \begin{longtable}{P{0.1804245283018868\textwidth}P{0.09622641509433963\textwidth}P{0.3408018867924528\textwidth}P{0.10023584905660378\textwidth}P{0.13231132075471697\textwidth}} Sample\tabcellsep \tabcellsep \multicolumn{3}{l}{Sphenoid Septum Attached Laterally internal carotid artery}\\ \tabcellsep Normal\tabcellsep Unilateral\tabcellsep Bilateral\tabcellsep Total\\ Group A*\tabcellsep 45\%\tabcellsep 39\%\tabcellsep 16\%\tabcellsep 100\%\\ No. of cases\tabcellsep (85)\tabcellsep (74)\tabcellsep (30)\tabcellsep ( N= 189)\\ Group B*\tabcellsep 73 \%\tabcellsep 21 \%\tabcellsep 6 \%\tabcellsep 100\%\\ No.of cases\tabcellsep (231)\tabcellsep (67)\tabcellsep (19)\tabcellsep ( N= 317)\end{longtable} \par \caption{\label{tab_5}Table 6 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{7} \par \begin{longtable}{P{0.24208860759493672\textwidth}P{0.34430379746835443\textwidth}P{0.10759493670886076\textwidth}P{0.1560126582278481\textwidth}} Sample\tabcellsep \multicolumn{3}{l}{Septate sphenoid sinus (more than one septum)}\\ \tabcellsep Yes\tabcellsep No\tabcellsep Total\\ Group A*\tabcellsep 41\%\tabcellsep 59\%\tabcellsep 100\%\\ No.of cases\tabcellsep (77)\tabcellsep (112)\tabcellsep (N=189)\\ Group B*\tabcellsep 33\%\tabcellsep 67 \%\tabcellsep 100\%\\ No. of cases\tabcellsep 10.4\tabcellsep (12)\tabcellsep (N=317)\end{longtable} \par \caption{\label{tab_6}Table 7 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{8} \par \begin{longtable}{P{0.85\textwidth}} 35\\ Volume XVI Issue VI Version I\\ Medical Research\\ Global Journal of\end{longtable} \par {\small\itshape [Note: A]} \caption{\label{tab_7}Table 8 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{9} \par \begin{longtable}{P{0.2351063829787234\textwidth}P{0.07635933806146572\textwidth}P{0.12056737588652483\textwidth}P{0.08640661938534278\textwidth}P{0.15271867612293144\textwidth}P{0.0743498817966903\textwidth}P{0.09645390070921986\textwidth}P{0.008037825059101654\textwidth}} \tabcellsep \tabcellsep \multicolumn{4}{l}{Anatomical variation of maxillary sinus}\\ Sample\tabcellsep Normal\tabcellsep \multicolumn{2}{l}{Expensively}\tabcellsep Bi Hypoplastic\tabcellsep UniHypoplastic\tabcellsep Total\\ Group A*\tabcellsep 54\%\tabcellsep 17 \%\tabcellsep \tabcellsep 28\%\tabcellsep 2 \%\tabcellsep 100\%\\ Group B*\tabcellsep 57\%\tabcellsep 17 \%\tabcellsep \tabcellsep 23\%\tabcellsep 3\%\tabcellsep 100\%\\ \multicolumn{2}{l}{Cases/ control prevalence \%}\tabcellsep \tabcellsep \tabcellsep Chi -square\tabcellsep \tabcellsep p-value\\ 61.5/37.4 \%\tabcellsep \tabcellsep \tabcellsep \tabcellsep 278.079\tabcellsep \tabcellsep <\tabcellsep 0.05\\ Conclusion\tabcellsep \tabcellsep \tabcellsep \tabcellsep \multicolumn{2}{l}{Very strong evidence}\\ Sample\tabcellsep \multicolumn{2}{l}{Normal}\tabcellsep \multicolumn{3}{l}{Maxillary sinus septa Bi Septate UniSeptate}\tabcellsep Total\\ Group A*\tabcellsep 74\%\tabcellsep \tabcellsep \tabcellsep 12\%\tabcellsep 14\%\tabcellsep 100\%\\ No. of cases\tabcellsep \multicolumn{2}{l}{(140)}\tabcellsep \tabcellsep (23)\tabcellsep (26)\tabcellsep (189)\\ Group B*\tabcellsep 64\%\tabcellsep \tabcellsep \tabcellsep 17\%\tabcellsep 19\%\tabcellsep 100\%\\ No.of cases\tabcellsep \multicolumn{2}{l}{(203)}\tabcellsep \tabcellsep (54)\tabcellsep (60)\tabcellsep (317)\end{longtable} \par \caption{\label{tab_8}Table 9 :}\end{figure} \begin{figure}[htbp] \noindent\textbf{10} \par \begin{longtable}{P{0.36210762331838564\textwidth}P{0.07623318385650224\textwidth}P{0.27062780269058295\textwidth}P{0.030493273542600896\textwidth}P{0.11053811659192823\textwidth}} Sample\tabcellsep Yes\tabcellsep Haller cells No\tabcellsep \tabcellsep Total\\ Group A*\tabcellsep 15\%\tabcellsep 85\%\tabcellsep \tabcellsep 100\%\\ No. of cases\tabcellsep (28)\tabcellsep (161)\tabcellsep \tabcellsep (189)\\ Group B*\tabcellsep 33\%\tabcellsep 67\%\tabcellsep \tabcellsep 100\%\\ No. of cases\tabcellsep (105)\tabcellsep (212)\tabcellsep \tabcellsep (317)\\ Cases/ control prevalence \%\tabcellsep \tabcellsep Chi -square\tabcellsep \multicolumn{2}{l}{p-value}\\ 61.5/37.4\%\tabcellsep \tabcellsep 113.834\tabcellsep <\tabcellsep 0.05\\ Conclusion\tabcellsep \tabcellsep Very strong evidence\tabcellsep \end{longtable} \par \caption{\label{tab_9}Table 10 :}\end{figure} \footnote{© 2016 Global Journals Inc. (US)} \backmatter \subsection[{Acknowledgements}]{Acknowledgements}\par The authors express special thanks to the Dental Research Center, Tehran University of Medical Sciences, and Tehran, Iran. The study did not receive any financial support. Author Disclosure Statement No competing financial interests exists. \begin{bibitemlist}{1} \bibitem[ J Radiol ()]{b18}\label{b18} \textit{}, \textit{J Radiol} 1997. 78 p. . \bibitem[Aydinlioglu et al. ()]{b23}\label{b23} ‘Absence of frontal sinus in Turkish individuals’. A Aydinlioglu , A Kavakli , S Erdem . \textit{Yonsei Med J} 2003. 44 p. . \bibitem[Maru and Gupta ()]{b15}\label{b15} ‘Anatomic varaitions of the bone in sinonasal CT’. Y K Maru , V Gupta . \textit{Indian J Otolaryngol Head Neck Surg} 2001. 53 p. . \bibitem[Ponde et al. ()]{b22}\label{b22} ‘anatomic variations of the frontal sinus’. J M Ponde , P Metzger , G Amaral , M Machado , M Prandini . \textit{Miniumum invasive Neurosurg} 2003. 46 p. . \bibitem[Kang et al. ()]{b19}\label{b19} ‘Anatomical structures in the maxillary sinus related to lateral sinus elevation: a cone beam computed tomographic analysis’. S J Kang , S I Shin , Y Herr , Y H Kwon , G T Kim , J H Chung . \textit{Clin Oral Implants Res} 2003. 100 p. . \bibitem[Nitinavakarn et al. ()]{b11}\label{b11} ‘Anatomical variations of the lateral nasal wall and paranasal sinuses: A CT study for endoscopic sinus surgery (ESS) in Thai patients’. B Nitinavakarn , S Thanaviratananich , N Sangsilp . \textit{J Med Assoc Thai} 2005. 88 p. . \bibitem[Al-Mujaini and Wali ()]{b10}\label{b10} ‘and Mazin Alkhabori Functional Endoscopic Sinus Surgery: Indications and Complications in the Ophthalmic Field’. Abdullah Al-Mujaini , Upender Wali . \textit{Oman Med J} 2009. 24 (2) p. . \bibitem[Ahuja et al. ()]{b20}\label{b20} ‘Carotid cavernous fistula and false aneurysm of the cavernous carotid artery: complications of transsphenoidal surgery’. A Ahuja , L R Guterman , L N Hopkins . \textit{Neurosurgery} 1992. 31 (4) p. . \bibitem[Lloyd et al. ()]{b13}\label{b13} ‘Computed tomography in the preoperative evaluation of functional endoscopic sinus surgery’. Gas Lloyd , V J Lund , G K Scadding . \textit{Journal of Laryngology and Otology} 1991. 105 p. . \bibitem[Meyer et al. ()]{b26}\label{b26} ‘Coronal computed tomography analysis of frontal cells’. T K Meyer , M Kocak , M M Smith , T L Smith . \textit{Am J Rhinol} 2003. 17 p. . \bibitem[Som et al. ()]{b24}\label{b24} ‘Crista gallipneumatization is an extension of the adjacent frontal sinuses’. P M Som , E E Park , T P Naidich , W Lawson . \textit{AJNR Am J Neuroradiol} 2009. 30 p. . \bibitem[Palmer and Kennedy ()]{b14}\label{b14} \textit{Cummings Otolaryngology Head \& Neck Surgery}, J N Palmer , D W Kennedy . 2005. Mosby: Elsevier. p. . (Revision Endoscopic Sinus Surgery. 4th ed) \bibitem[Sethi et al. ()]{b9}\label{b9} ‘Endoscopic anatomy of sphenoid sinus and sellaturcica’. Lund Sethi , D S Stanley , R E Pillay , PK . \textit{J. Laryngol. Otol} 1995. 109 p. . \bibitem[Krmpoti?-Nemaníc et al. ()]{b8}\label{b8} \textit{Endoscopic paranasal sinus surgery. The most important anatomic variations of the main paranasal sinus and accessory paranasal sinus}, J Krmpoti?-Nemaníc , I Vinter , D Jalsovec . 1993. 41 p. . \bibitem[Van Alyea ()]{b4}\label{b4} ‘Ethrnoid Labyrinth anatomic study’. O E Van Alyea . \textit{Arch Otolayngol} 1939. 29 p. . \bibitem[Ozgursoy et al. ()]{b2}\label{b2} ‘Hidden unilateral agenesis of the frontal sinus: human cadaver study of a potential surgical pitfall’. O B Ozgursoy , A Comert , Yorulmazi , I Tekdemir , A Elhan , B Kucuk . \textit{Am J Otolaryngol} 2010. 31 p. . \bibitem[Momeni et al. ()]{b3}\label{b3} ‘Imaging of chronic and exotic sinonasal disease: review’. A K Momeni , C C Roberts , F S Chew . \textit{AJR Am J Roentgenol} 2007. 189 p. . \bibitem[Durr et al. ()]{b0}\label{b0} ‘Impact of rhinosinusitis inhealth care delivery: the Quebec experience’. D G Durr , M Y Desrosiers , C Dassa . \textit{J Otolaryngol} 2001. 30 p. . \bibitem[Danese et al.]{b17}\label{b17} \textit{Influence of naso-sinusal anatomic variants on recurrent, persistent or chronic sinusitis. X-ray computed tomographic evaluation}, M Danese , B Duvoisin , A Agrifoglio , J Cherpillod , M Krayenbuhl . (in 112 patients) \bibitem[Koskenkorva and Kristo ()]{b1}\label{b1} ‘It's normal--structural and functional variations of nose and paranasal sinuses’. T Koskenkorva , A Kristo . \textit{Duodecim} 2012. 128 p. . \bibitem[Bell et al. ()]{b7}\label{b7} ‘Maxillary sinus disease: diagnosis and treatment’. G W Bell , B B Joshi , R I Macleod . \textit{British Dental Journal Br Dent J} 2011. 210 p. . \bibitem[Delgaudio et al. ()]{b5}\label{b5} ‘Multiplanar computed tomographic analysis of frontal recess cells: effect on frontal isthmus size and frontal sinusitis’. J M Delgaudio , P A Hudgins , G Venkatraman , A Beningfield . \textit{Archives of Otolaryngology-Head and Neck Surgery} 2005. 131 (30) p. . \bibitem[Çakur et al. ()]{b25}\label{b25} ‘Nurhan Bay?nd?r Durna Aplasia and Agenesis of the Frontal Sinus in Turkish Individuals: A Retrospective Study Using Dental Volumetric Tomography Int’. Binali Çakur , A Muhammed , Sumbullu . \textit{J Med Sci} 2011. 8 (3) p. . \bibitem[Lanzieri ()]{b6}\label{b6} ‘Paranasal Sinuses and Nasal Cavity’. C F Lanzieri . \textit{Clinical Magnetic Resonance Imaging}, R R Edelman, J R Hesselink, M B Zlatkin, J V Crues (ed.) (Saunders-Elsevier, Philadelphia) 2006. 64 p. . \bibitem[Zinreich et al. ()]{b21}\label{b21} ‘Paranasal sinuses CT imaging requirements for endoscopic surgery’. S J Zinreich , D W Kennedy , A E Rosenbaum , B W Gayler , A J Kumar , H Stammberger . \textit{Radiol} 1987. 163 p. . \bibitem[Stallman et al. ()]{b12}\label{b12} ‘The incidence of concha bullosa and its relationship to nasal septal deviation and paranasal sinus disease’. J S Stallman , J N Lobo , P M Som . \textit{AJNR Am J Neuroradiol} 2004. 25 (9) p. . \bibitem[Laine and Smoker ()]{b16}\label{b16} ‘The ostiomeatal unit and endoscopic surgery: anatomy, variations, and imaging findings in inflammatory diseases’. F J Laine , W R Smoker . \textit{AJR Am J Roentgenol} 1992. 159 (4) p. . \bibitem[Bassiouny et al. ()]{b27}\label{b27} ‘ZakiY Maxillary sinus hypoplasia and superior orbital fissure asymmetry’. A Bassiouny , W J Newlands , H Ali . \textit{The Laryngoscope} 1982. 92 (4) . \end{bibitemlist} \end{document}