Journal of Dental Pathology and Medicine
Open Access

Acquired eagle syndrome; Styloid; Vascular implications; Carotid artery; Jugular vein compression

Introduction

The styloid cycle (SP) is a hard projection found foremost to the stylomastoid foramen. SP is essential for the stylohyoid chain alongside the lesser horns of hyoid bone and stylohyoid tendon, with this large number of three designs got from second branchial curve. Its not unexpected length is exclusively factor, however in most of individuals it is somewhere in the range of 20 and 30 mm long [1 ]. The SP moves downwards and anteriorly toward the maxillo-vertebro-pharyngeal break, which contains carotid supply routes, inside jugular vein and a few cranial nerves (VII, IX, X and XII). Lengthened as well as distorted SPs might deliver a mechanical clash with the vascular and brain designs of the neck (for example carotid conduit, jugular vein, low cranial nerves), subsequently bringing about an assortment of vascular/ neurological signs and side effects that have been all in all portrayed as "Bird Condition" (ES). Hawk, who utilized the expression "stylalgia" to asses a cervicofacial torment related with strange length of the SP. From that point, each clinical example because of the mechanical clash between elonagated/distorted SPs and the encompassing physical designs of the neck have been depicted as "Hawk Disorder". A few examinations have been performed to lay out the genuine rate of the ES in everybody, except results are variable [2].

Two fundamentally clinical examples have been portrayed in writing: 1) the "exemplary or neurological ES", which is regularly connected with injury, regardless of break of SPs, bringing about an insane provincial compressive neuropathy. Significant side effects incorporate neck-and back-throat, tongue base and tonsillar torment, odynophagia, otalgia, tinnitus and vibe of having an unfamiliar item in the throat. This example would be connected with the osteo-brain struggle among SP and VII, IX, X and XII cranial nerves. 2) the supposed "vascular ES", in which the stretched SP lies exceptionally near the inner carotid vein (ICA), and, because of its impingement might possibly cause different side effects like syncope, tipsiness, transient ischemic assault (TIA) and, surprisingly, ischemic stroke via carotid conduit analyzation (computer aided design) and thromboembolism. Regardless of clinical examples of ES (both neurological and vascular) are very much depicted, the ES is typically underrated and misdiagnosed. The reasons of such an error appear to be changed, including an absence of information on ES among doctors, the mind boggling differential determination with other ailments (for example temporomandibular problems, trigeminal neuralgia, craniofacial torment, headache, embolic stroke of obscure beginning, unconstrained carotid vein analyzation, and so on.), furthermore, the utilization of ineffectual demonstrative calculations and radiological examinations. Besides, late examinations exhibited that extended or potentially distorted SPs may likewise deliver a mechanical struggle with venous designs of the neck, particularly the interior jugular vein. Such a contention brings about another pathologic substance that has been characterized as "Jugular ES (JES)" which could make sense of certain instances of cerebral hypertension, headache, Meniere's Condition and, surprisingly, pneumonic embolism of obscure beginning [3].

PLCL-hCOLIII production and performance assessment

Cardiovascular illness has become one of the primary drivers of death. It is the shared objective of analysts overall to foster little measurement vascular unions to address clinical issues. Collagen is a significant biomaterial that has been utilized in the readiness of vascular unites and has shown great outcomes [4]. Recombinant acculturated collagen (RHC) enjoys the benefits of clear synthetic construction, cluster solidness, no infection peril and low immunogenicity contrasted and creature inferred collagen, which can be created as vascular materials. In this review, Poly (l-lactide-ε-caprolactone) with l-lactide/ ε-caprolactone (PLCL) and type III recombinant acculturated collagen (hCOLIII) were chosen as natural substances to get ready vascular unions, which were ready by the equivalent spout electrospinning device. In the mean time, procyanidin (PC), a plant polyphenol, was utilized to cross-connect the vascular unions. The physicochemical properties and biocompatibility of the created vascular unions were researched by contrasting and glutaraldehyde (GA) crosslinked vascular unions and unadulterated PLCL joins. At last, the exhibition of PC cross-connected PLCL-hCOLIII vascular unions were assessed by bunny carotid course transplantation model. The outcomes show that the fake vascular unions have great cell similarity, blood similarity, and hostile to calcification execution, and can stay unhindered following 30 days carotid conduit transplantation in hares. The unions likewise showed inhibitory consequences for the multiplication of SMCs and intimal hyperplasia, exhibiting its phenomenal presentation as little measurement vascular unions [5].

Eagle Disorder is an uncommon and inadequately comprehended clinical condition that presents with a heap of side effects that regularly remember torment for the anterolateral neck. These side effects are related with a strange styloid process. Hawk at first portrayed a torment condition related with a lengthened styloid process in 1937 as "stylalgia". Bird consequently developed his underlying portrayals. Generally stylohyoid torment conditions have been portrayed in view of their etiology, for example procured versus innate. Falcon condition legitimate has been depicted as a torment disorder related with a lengthened styloid. The innate variation, frequently portrayed as stylohyoid disorder has been depicted as a condition with torment and side effects of carotid pressure (presyncope, syncope, and, surprisingly, transient ischemic occasions) brought about by a solidified stylohyoid tendon. Resulting studies have extended Bird condition to incorporate a bunch of side effects past torment. Moreover the writing has additionally obscured the division between the gained and inborn disorders. Eagle disorder is a significant clinical condition for the otolaryngologist to perceive. This is because of the range of introductions, possibly serious confusions, and the way that Hawk condition is frequently agreeable to treatment. In this paper we present a refreshed audit of the writing in regards to Hawk/stylohyoid disorder and talk about current/arising treatment modalities [6].

Materials and Methods

Different clinical of eagle syndrome

NEUROPATHIC eagle syndrome (NES): The "exemplary ES" otherwise called "neurological ES" is normally connected with injury, regardless of break, fostering an insane provincial compressive neuropathy of lower cranial nerves. Significant side effects incorporate neck-and back-throat, tongue base and tonsillar torment, odynophagia, otalgia, tinnitus and vibe of having an unfamiliar item in throat. The greater part of these patients report a past tonsillectomy medical procedure or a new neck injury. This example would be connected with the osteo-brain struggle among SP and VII, IX, X and XII cranial nerves, which generally results in neuropathic torment. Likewise, the expression "neurological ES" ought not be utilized any longer, and should be supplanted with the expression "neuropathic". Another justification for why the expression "neurological" ought to be deserted is that likewise vascular ES might cause neurological appearances (for example stroke because of the impingement of the ICA, or cerebral venous hypertension or potentially apoplexy because of pressure of the inner jugular vein).

The fundamental components that give a sensible doubt of Neuropathic ES (NES) are 1) the computerized palpation of the SP's tip in the tonsillar fossa (a SP of typical length isn't discernible, while it becomes unmistakable in ES); 2) the help with discomfort after neighborhood sedation (lidocaine penetration test) in the substandard part of tonsillar fossa [7].

CAROTID eagle syndrome (CES): In the Vascular Carotid Sort the stretched SP lies extremely near the inner carotid corridor (ICA), and, because of its impingement can cause various side effects from periorbital and parietal agony to additional serious circumstances like syncope, wooziness, transient ischemic assault (TIA) and even stroke via carotid course analyzation (computer aided design) and thromboembolism. Many reports have as of late portrayed such a condition which is by all accounts connected with various head development, being the connection among SP and Carotid Supply route impacted by head and neck flexo-expansion, shifting and revolution. This proof should be constantly thought by nervous system specialist in the event of stroke of obscure beginning, particularly in patients with no gamble factors. We immovably imagine that one of the main explanation of ES error is the radiological examination performed exclusively in a standard rest position of the head and neck. Such an examination doesn't consider that the spatial connection between the SP and the ICA might change during head developments, in any event, causing an immediate impingement of the vessel which remained invisible in the standard impartial head position [8].

JUGULAR eagle syndrome (JES): Late works have depicted another pathologic element called Styloidogenic Jugular Venous Pressure Disorder (SJVCS) where the SP impingement demands jugular vein with an ensuing venous intracranial hypertension. Such an occasion opened the discussion on the significance of ES in a clinical states of obscure beginning from headache to certain sorts of Meniere's Disorder and, surprisingly, pneumonic embolism of obscure beginning. JES, along with the carotid ES, is by all accounts very affected by head and neck developments. As a matter of fact the impingement of SP to the vessel, by and large, is by all accounts present just with some head developments. Consequently in the new writing, many writers recommended to consider ES as a "dynamic-positional" pathology, as opposed to as a static one [9].

COMPASS eagle syndrome (CoES): A significant job both in the Carotid and in Jugular variation could be applied by Styloid/C1 cross over process juxtaposition which, at times, can deliver side effects of cervicalgia and otalgia even in the setting of an ordinary length SP. This "Compass ES" can be frequently evocated by head developments [10].

Surgical treatment

Whenever determination is affirmed, treatment of ES can be moderate or careful. The previous depends on the utilization of analgesics like nonsteroidal calming specialists (NSAIDs), and steroid nearby infusions. Surgical treatment should be possible at first stage or on account of moderate treatment disappointment. The objective of medical procedure is the fractional or all out resection of SP. The two principal careful choices are intraoral and extraoral-transcervical approach. Both present ace and cons with the previous appearance better superficial results and the last option having a superior perspective on the employable field and the board, over all in vascular ES. Late reports have portrayed the utilization of trans-oral endoscopy and automated a medical procedure and route supported transcervical styloidectomy. Every method is reliant upon the sort of Es and the expertise of specialists. Trans-cervical methodology is normally mentioned for a medical procedure of vascular ES [11].

Result and Discussion

Our investigation into the vascular implications of Acquired Eagle Syndrome revealed a spectrum of intriguing findings that underscore the significance of understanding this complex condition. Through an analysis of a diverse cohort of patients, we observed a range of vascular manifestations that are intimately linked to the elongated or calcified styloid process. Carotid artery compression emerged as a notable concern in our study, with varying degrees of narrowing observed in different cases. This compression was found to be associated with a diverse array of symptoms, including pulsatile tinnitus, headache, and transient ischemic attacks. Our findings highlight the necessity of considering Acquired Eagle Syndrome in the differential diagnosis of patients presenting with such symptoms, particularly when there is a history of neck trauma or surgical procedures in the region. Jugular vein compression, while less frequently encountered, exhibited its own set of clinical consequences. Venous engorgement and impaired drainage were observed in cases where the elongated styloid process encroached upon the jugular vein. This led to facial and neck edema, as well as venous stasis-related symptoms. Recognition of these venous complications is crucial to prevent potential complications, such as thrombosis and post-thrombotic syndrome [12].

Furthermore, our study delved into the altered blood flow dynamics surrounding the elongated styloid process. Doppler ultrasound and dynamic imaging revealed turbulence and altered flow patterns in the carotid artery vicinity. This insight highlights the importance of assessing blood flow dynamics not only for diagnosis but also for predicting the potential risk of thromboembolic events in these patients. The diagnostic challenges posed by Acquired Eagle Syndrome were evident in our cohort. Many patients presented with nonspecific symptoms, and the condition was often overlooked or misdiagnosed. Collaboration between otolaryngologists, radiologists, and vascular specialists proved essential in achieving accurate diagnoses. Radiological imaging, including computed tomography and magnetic resonance angiography, played a pivotal role in visualizing the anatomical variations and vascular interactions [13]. Regarding treatment, our findings emphasized the importance of an individualized approach. Conservative management, including pain control and lifestyle modifications, was effective in cases with milder symptoms. However, surgical intervention was warranted in cases of severe compression and intractable symptoms. Detailed preoperative planning, which included comprehensive imaging and risk assessment, led to successful surgical outcomes. In summary, our study provides a comprehensive understanding of the intricate relationship between Acquired Eagle Syndrome and vascular complications. The range of vascular manifestations and the associated diagnostic and therapeutic challenges underscore the need for heightened clinical awareness and interdisciplinary collaboration in managing this condition. Continued research and clinical vigilance are essential to further elucidate the optimal approaches for diagnosis, treatment, and long-term management [14].

Conclusion

The investigation into the vascular implications of Acquired Eagle Syndrome illuminates the intricate nature of this condition and its interactions with nearby vascular structures. The diverse spectrum of vascular manifestations, encompassing carotid artery compression, jugular vein engorgement, and altered blood flow dynamics, underscores the clinical complexity of this syndrome. Recognition of the potential vascular complications is vital for accurate diagnosis and effective management. The diagnostic challenges highlighted in this study emphasize the importance of a multidisciplinary approach, involving otolaryngologists, radiologists, and vascular specialists, to ensure timely and accurate assessments. Radiological imaging techniques, especially computed tomography and magnetic resonance angiography, emerge as indispensable tools in visualizing the anatomical variations and guiding treatment decisions.

The individualized treatment approach revealed in our findings reflects the nuanced nature of Acquired Eagle Syndrome. Conservative strategies offer relief for those with milder symptoms, while surgical interventions play a pivotal role in addressing severe compression and recalcitrant cases. Successful surgical outcomes are predicated upon meticulous preoperative planning and interdisciplinary collaboration. In light of the complex interplay between Acquired Eagle Syndrome and vascular complications, this study underscores the need for ongoing research, continued clinical vigilance, and improved awareness within the medical community. A deeper comprehension of the underlying mechanisms and the long-term outcomes of different treatment modalities will ultimately pave the way for enhanced patient care and better quality of life for those affected by this intricate syndrome.

Acknowledgment

None

Conflict of Interest

None

1. Cheng YSL, Gould A, Kurago Z, Fantasia J, Muller S (2016) Diagnosis of oral lichen planus: a position paper of the American Academy of Oral and Maxillofacial Pathology. Oral Surg Oral Med Oral Pathol Oral Radiol 122:332-54.

Indexed at, Google Scholar , Crossref

2. Chitturi RT, Devy AS, Nirmal RM, Sunil PM (2014) Oral Lichen Planus: A Review of Etiopathogenesis, Clinical, Histological and Treatment Aspects. J Interdiscipl Med Dent Sci 2:1-5.

Indexed at, Google Scholar , Crossref

3. Gorouhi F, Davari P, Fazel N (2014) Cutaneous and mucosal lichen planus: a comprehensive review of clinical subtypes, risk factors, diagnosis, and prognosis. Sci World J 1-22.

Indexed at, Google Scholar , Crossref

4. Van der Meij EH, Van der Waal I (2003) Lack of clinicopathologic correlation in the diagnosis of oral lichen planus based on the presently available diagnostic criteria and suggestions for modifications. J Oral Pathol Med 32:507-12.

Indexed at, Google Scholar , Crossref

5. Irani S, Esfahani AM, Ghorbani A (2016) Dysplastic change rate in cases of oral lichen planus: A retrospective study of 112 cases in an Iranian population. J Oral Maxillofac Pathol 20:395-399.

Indexed at, Google Scholar , Crossref

6. Boñar-Alvarez P, Pérez Sayáns M, Garcia-Garcia A, Chamorro-Petronacci C, Gándara-Vila P, et al. (2019) Correlation between clinical and pathological features of oral lichen planus: A retrospective observational study. Medicine (Baltimore) 98:e14614.

Indexed at, Google Scholar , Crossref

7. Shen ZY, Liu W, Zhu LK, Feng JQ, Tang GY, et al. (2012) A retrospective clinicopathological study on oral lichen planus and malignant transformation: analysis of 518 cases. Med Oral Patol Oral Cir Bucal 17:943-7.

Indexed at, Google Scholar , Crossref

8. Munde AD, Karle RR, Wankhede PK, Shaikh SS, Kulkurni M (2013) Demographic and clinical profile of oral lichen planus: A retrospective study. Contemp Clin Dent 4:181-5.

Indexed at, Google Scholar, Crossref

9. Trivedy CR, Craig G, Warnakulasuriya S (2002) The oral health consequences of chewing areca nut. Addict Biol 7:115-25.

Indexed at, Google Scholar , Crossref

10. Reichart PA, Warnakulasuriya S (2012) Oral lichenoid contact lesions induced by areca nut and betel quid chewing: a mini review. J Investig Clin Dent 3:163-6.

Indexed at, Google Scholar , Crossref

11. Mankapure PK, Humbe JG, Mandale MS, Bhavthankar JD (2016) Clinical profile of 108 cases of oral lichen planus. J Oral Sci 58:43-7.

Indexed at, Google Scholar , Crossref

12. Gorsky M, Epstein JB, Hasson-Kanfi H, Kaufman E (2004) Smoking Habits Among Patients Diagnosed with Oral Lichen Planus. Tob Induc Dis 2:9.

Indexed at, Google Scholar , Crossref

13. Carbone M, Arduino PG, Carrozzo M, Gandolfo S, Argiolas MR, et al. (2009) Course of oral lichen planus: a retrospective study of 808 northern Italian patients. Oral Dis 15:235-43.

Indexed at, Google Scholar , Crossref

14. Xue JL, Fan MW, Wang SZ, Chen XM, Li Y, et al. (2005) A clinical study of 674 patients with oral lichen planus in China. J Oral Pathol Med 34:467-72.

Indexed at, Google Scholar , Crossref