Auriculotemporal and Greater Auricular Nerve Blocks Have Roles in Patients with Ramsay Hunt Syndrome with Trigeminal Nerve Involvement -A Report of Two Cases

Total Page:16

File Type:pdf, Size:1020Kb

Auriculotemporal and Greater Auricular Nerve Blocks Have Roles in Patients with Ramsay Hunt Syndrome with Trigeminal Nerve Involvement -A Report of Two Cases Anesth Pain Med 2012; 7: 16~21 ■Case Report■ Auriculotemporal and greater auricular nerve blocks have roles in patients with Ramsay Hunt syndrome with trigeminal nerve involvement -A report of two cases- Department of Anesthesiology and Pain Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea Hyun Seung Jin, Woo-Seok Sim, and Hee-Jin Roe Ramsay Hunt syndrome (RHS) refers to herpes zoster infection of CN VIII or cervical spinal nerves are also involved in the the geniculate ganglion of the facial nerve. Cases complicated by disease process, in which symptoms and the clinical course are multicranial nerve involvement in the process of reactivation of the heavier and the prognosis worse, emphasizing the greater need virus, which are known to show virulent clinical course and worse prognosis, are not common in literature as in practice, and there for appropriate and earlier treatment. Although pain physicians has been only one reported case of suspected co-involvement of may actually encounter cases with multicranial nerve invol- the trigeminal nerve in Korean literature. Therefore, in cases of vement in RHS once in a while in practice, there has been RHS with severe rash over the face and neck, it is pertinent to give consideration to such multiple involvement in their early presen- only one such case report in Korean literature, where the tation. Facial nerve palsy and herpes related pain are the two authors finally concluded RHS was mistaken for a trigeminal worrisome complication, which could be alleviated by early treatment herpes zoster, rather than co-involement [1]. In search for with neural blockade in addition to oral medication. Especially, foreign literature related to Koreans, one article reported of a nerve blocks are known to decrease the extent of nerve infla- mmation or damage, thereby facilitating recovery and probably Korean patient with concurrent involvement of trigeminal and preventing postherpetic neuralgia. We report two rare cases of facial nerve, and another report by Korean authors evaluated Ramsay Hunt syndrome with trigeminal nerve involvement, where the clinical characteristics and prognosis of over 300 patients early implementation of blockade of somatic peripheral nerve with RHS and multicranial nerve involvement [2], but none of branches, in addition to the conventional treatment, promoted early recovery. (Anesth Pain Med 2012; 7: 16∼21) the articles discussed about the optimal treatment in such cases, especially related to somatic peripheral nerve blocks. Key Words: Herpes zoster, Polyneuropathy, Ramsay Hunt The goals of all treatment modalities of acute herpes zoster syndrome, Somatic peripheral nerve branch block. infection including RHS, are to reduce edema and infla- mmation of the involved nerves and associated pain, thus Ramsay Hunt syndrome (RHS) is herpes zoster infection of reducing central sensitization and thereby preventing posther- the geniculate ganglion, characterized by vesicular skin lesions petic neuralgia (PHN) or nerve palsy. Especially, the usefulness in the auricle of ear, external ear, palatal and tongue mucosa of neural blockade with local anesthetics with or without and associated pain, usually accompanied by facial nerve palsy. steroids, has been proven in numerous studies [3,4]. Cranial nerve (CN) VIII, and rarely cranial nerves other than The authors are presenting, with review of literature, two rare cases of RHS with co-involvement of the trigeminal Received: October 20, 2011. nerve, where early suspicion and diagnosis of multicranial Revised: October 24, 2011. nerve involvement, and early institution of blockade of specific Accepted: November 18, 2011. somatic peripheral nerve branches in the involved dermatome Corresponding author: Woo-Seok Sim, M.D., Ph.D., Department of Anesthesiology and Pain Medicine, Samsung Medical Center, combined with conventional treatments, were associated with Sungkyunkwan University School of Medicine, 50, Irwon-dong, good prognosis. Gangnam-gu, Seoul 135-710, Korea. Tel: 82-2-3410-0356, Fax: 82-2-3410-0361, E-mail: [email protected] 16 Hyun Seung Jin, et al:Somatic peripheral nerve block in Ramsay Hunt syndrome 17 examination revealed no specific abnormalities, and was CASE REPORTS prescribed with oral valacyclovir 1 g daily for 1 week under the impression of recurrent herpes zoster virus infection of the Case 1 trigeminal nerve. The skin lesion seemed to improve after the A 64-year-old man presented with a 3-day history of initiation of such treatment, but the pain did not subside, and right-sided headache and earache accompanied by vesicular starting from the 5th day of oral medication, the patient newly skin lesions. The pain was stinging in nature, and started from developed difficulty in mouth opening and lip movement on the right ear and surrounding temporal area that spread through the right side and blinking of the right eye (Fig. 1). He also the inner ear toward the mandible, and multiple papules and complained of tingling and numbness on the right side of the vesicles developed in the face along the mandibular nerve gingiva and tongue, and visited the neurology department, dermatome. The patient immediately visited otolaryngology and where Bell’s palsy due to herpes zoster virus, RHS was dermatology outpatient clinic, but the otolaryngological physical diagnosed. He was admitted to the neurology department, and the laboratory examination on admission showed slightly increase in neutrophil count and ESR, and right facial nerve lesion was observed in both nerve conduction and corneal reflex test. The aggravation of pain and development of new clinical symptoms such as facial nerve palsy seemed to be a sign of progression of the inflammation even after the previous 7-day oral valacyclovir treatment. This raised the possibility of zoster meningitis, encephalitis or multiple cranial nerve involvement including the trigeminal nerve, and a 7-day intravenous treatment with 650 mg of acyclovir every 8 hr was initiated. The cranial nerve magnetic resonance imaging (MRI) showed multiple enhancement around the fundus of internal auditory canal, labyrinth segment of the facial nerve, geniculate fossa, which were all compatible with his clinical RHS with right facial nerve involvement (Fig. 2). Steroid therapy was commenced with oral prednisolone 60 mg daily for 3 days and maintained on 50 mg daily for another 3 days. Fig. 1. This picture shows the skin lesion and facial paralysis on admission in the first patient. On hospital day 5, the movement of the right eyelid began to Fig. 2. This picture shows the two sections of cranial nerve MRI of the first patient, showing enhancement around the fundus of right internal auditory canal, the labyrinthine segment of facial nerve, and geniculate fossa. Arrows indicate the lesion. 18 Anesth Pain Med Vol. 7, No. 1, 2012 show improvement, whereas the persisting severe pain his admission. However, he had a history of hearing loss necessitated supplementation with carbamazepine 200 mg/d and immediately after admission, and the otolaryngologic exami- gabapentin 300 mg/d. After his discharge on hospital day 8, nation revealed a mild unilateral sensorineural hearing loss, prednisolone was tapered off, while oral carbamazepine and which improved quickly and returned to normal within 5 days gabapentin was maintained. However, the patient came to our of admission. Although the possibility of RHS could not be outpatient clinic due to unrelenting pain. At his first visit, totally ruled out, no further radiologic examination was taken, facial muscle movement and skin sensation had both improved and the treatment was focused on reducing the skin lesions to grade 4/5 by Medical Research Council (MRC) scale, and accompanying pain with antivirals and analgesics, since whereas his pain intensity was describe as 70−80/100 mm by apparent facial nerve palsy was absent throughout the course visual analogue scale (VAS). The most painful area was and the cochlear symptoms resolved. He was discharged after around the right side cheek and chin, which included intravenous injection treatment for 7 days with improvement of electric-shock like pain spreading from the auricle forward acute skin lesions, and was maintained thereafter on ibuprofen, Ⓡ accompanied by dull ache with pruritis of the same area, acetaminophen and codein (Mypol cap , Sungwon Adcock stabbing pain of the tongue, dull ache of the teeth and Pharm., Korea) every 8 h. He visited our clinic due to gingiva. Spontaneous pain and hyperalgesia was observed in all remaining pain, and at his first visit, his pain score on areas. He was taking carbamazepine 600 mg/d, amitriptylin 10 aggravation reached VAS 80−90/100 mm, and its relief of mg/day, pregabalin 150 mg/d, without a significant about 50% after the medication, was only transient. There was improvement in his pain. A stellate ganglion block (SGB) was no observable facial nerve palsy, while skin pigmentation given using 8 ml of 1% lidocaine, which resulted in a relief without vesicles were diffusely scattered around the ear auricle of pain to VAS 50/100 mm at 1-week follow up. Pain and right mandibular nerve dermatome, and crusted skin lesion persisting around the area ahead of the auricle, and below the remained in the external auditory canal. The most severe pain lower lip, raised suspicion of the involvement of the trigeminal was the earache, and all the above mentioned skin areas were nerve, and the cranial nerve MRI findings were reassessed, to accompanied by spontaneous pain and hyperalgesia. Concu- reveal an ill-defined signal change along the spinal nucleus of rrence of the trigeminal nerve lesion with RHS was suspected, trigeminal nerve suggesting a change following viral infection. and somatic and sympathetic nerve blocks were given During the following month, he was given 4 times of SGBs, alternatively, including a right SGB, a right greater auricular twice each of auriculotemporal nerve block (ATNB) and nerve block (GANB) using a mixture of 20 mg of triam- mental nerve block (MNB), to report a decreased pain score of cinolone in 5 ml of 0.375% ropivacaine, and a right mental VAS 30/100 mm.
Recommended publications
  • Perioral Gustatory Sweating: Case Report
    The Journal of Laryngology & Otology (2012), 126, 532–534. CLINICAL RECORD © JLO (1984) Limited, 2012 doi:10.1017/S0022215112000229 Perioral gustatory sweating: case report S C KÄYSER1, K J A O INGELS2, F J A VAN DEN HOOGEN2 1Department of Primary and Community Care, Radboud University Nijmegen Medical Centre, and 2Department of Otorhinolaryngology/Head and Neck Surgery, Radboud University Nijmegen Medical Centre, The Netherlands Abstract Objective: Presentation of a case of perioral Frey syndrome. Design: Case report. Subject: A 72-year-old woman with hyperhidrosis around the mouth and chin. Results: This patient suffered from bilateral perioral gustatory sweating following a mandibular osteotomy; such a case has not previously been described. Possible pathophysiological hypotheses are discussed in relation to the anatomy and innervation of the salivary glands. Conclusion: Perioral gustatory sweating is a rare complication of osteotomy. Key words: Gustatory sweating; Frey Syndrome; Perioral; Hyperhidrosis Introduction perioral excessive sweating and flushing which only Frey syndrome, also known as auriculotemporal syndrome, is a occurred during (and not preceding) eating. Her complaints well-known complication of parotid surgery. Approximately had begun following bilateral osteotomy of the mandible in 24 per cent of patients undergoing parotidectomy experience 1960, at the age of 25 years. The indication for this procedure gustatory sweating, although the reported incidence varies had been prognathism. Her recovery had been complicated greatly.1 Frey syndrome appears following a latency period by inadequate bone healing and loss of the right and left of one to 36 months (or longer) after surgery.2,3 inferior alveolar nerves (Figure 1). The aetiology of Frey syndrome is explained by ‘aberrant The diagnosis of hyperhidrosis was made using the nervous regeneration’.
    [Show full text]
  • Facial Nerve Paralysis Due to Chronic Otitis Media: Prognosis in Restoration of Facial Function After Surgical Intervention
    http://dx.doi.org/10.3349/ymj.2012.53.3.642 Original Article pISSN: 0513-5796, eISSN: 1976-2437 Yonsei Med J 53(3):642-648, 2012 Facial Nerve Paralysis due to Chronic Otitis Media: Prognosis in Restoration of Facial Function after Surgical Intervention Jin Kim,1* Gu-Hyun Jung,1* See-Young Park,1 and Won Sang Lee2 1Department of Otorhinolaryngology, Inje University College of Medicine, Goyang; 2Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea. Received: December 21, 2010 Purpose: Facial paralysis is an uncommon but significant complication of chronic Revised: June 16, 2011 otitis media (COM). Surgical eradication of the disease is the most viable way to Accepted: July 6, 2011 overcome facial paralysis therefrom. In an effort to guide treatment of this rare Corresponding author: Dr. Won-Sang Lee, complication, we analyzed the prognosis of facial function after surgical treatment. Department of Otorhinolaryngology, Materials and Methods: A total of 3435 patients with COM, who underwent Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, various otologic surgeries throughout a period of 20 years, were analyzed retro- Seoul 120-752, Korea. spectively. Forty six patients (1.33%) had facial nerve paralysis caused by COM. Tel: 82-2-2228-3606, Fax: 82-2-393-0580 We analyzed prognostic factors including delay of surgery, the extent of disease, E-mail: [email protected] presence or absence of cholesteatoma and the type of surgery affecting surgical outcomes. Results: Surgical intervention had a good effect on the restoration of *Jin Kim and Gu-Hyun Jung contributed equally to this work.
    [Show full text]
  • The Impact of Misdiagnosing Bell's Palsy As Acute Stroke
    ORIGINAL RESEARCH ClinicalClinical Medicine Medicine 2019 2017 Vol Vol 19, 17, No No 5: 6:494–8 494–8 T h e i m p a c t o f m i s d i a g n o s i n g B e l l ’ s p a l s y a s a c u t e s t r o k e Authors: I s u r u I n d u r u w a , A N e g i n H o l l a n d , B R o s a l i n d G r e g o r y C a n d K a y v a n K h a d j o o i D Idiopathic Bell’s palsy can lead to a serious and, sometimes For many clinicians, acute stroke remains a concerning permanently, disfiguring and emotionally challenging facial diagnosis in patients presenting with facial palsy, but there are palsy. Early diagnosis and treatment with corticosteroids are key characteristics which facilitate differentiation of the two important, as they significantly improve recovery rates. Bell’s conditions, often without the need for further investigations. Our palsy is a benign condition that should be diagnosed and study aimed to explore whether clinicians could diagnose Bell’s ABSTRACT managed in primary care. Patients who self-present to the palsy in patients presenting with facial palsy at initial assessment emergency department should be managed and discharged and, if not, how often they sought a specialist opinion, as well as to without needing admission.
    [Show full text]
  • Facial Nerve Palsy 7 James M
    Facial Nerve Palsy 7 James M. Gilchrist Abstract Facial neuropathy is the most common cranial neuropathy, due to its extensive course and multiple sites of potential injury. The causes of facial neuropathy are many, but 70% are diagnosed as Bell’s palsy, an idiopathic syndrome but increasingly being associated with herpes simplex virus infection as the cause of the majority of cases. Ramsay Hunt syndrome (herpes zoster oticus) is the second most common cause. Facial neuropa- thy causes weakness of the muscles of facial expression on the ipsilateral side, and can be distinguished from a central, or upper motor neuron, caused by the involvement of forehead muscles. Taste, hearing, salivation, lacrimation, and sensation over the ipsilateral ear and the face may also be disturbed. Diagnosis can be confi rmed by electrodiagnostic testing or MRI but is often not necessary. Treatment is directed at the underlying cause. In cases of Bell’s palsy a short course of steroids has been shown effective, if started within 72 h of onset. Treatment with antiviral agents against herpes virus is probably best reserved for patients with severe or complete facial neuropathy or those with Ramsay Hunt syndrome. Keywords Antiviral agents • Bell’s palsy • Herpes simplex • Herpes zoster • Lyme • Ramsay Hunt syndrome • Seventh cranial neuropathy • Steroids J. M. Gilchrist , MD () Neurology , Warren Alpert Medical School of Brown University, Rhode Island Hospital , Providence , RI , USA e-mail: [email protected] K.L. Roos (ed.), Emergency Neurology, DOI 10.1007/978-0-387-88585-8_7, 133 © Springer Science+Business Media, LLC 2012 134 J.M. Gilchrist Introduction Pathophysiology and Pathogenesis The facial nerve, also known as the seventh cra- Facial nerve palsy cannot truly be understood nial nerve, is the most commonly diagnosed without at least some knowledge of the anatomy cranial neuropathy.
    [Show full text]
  • Facial Paralysis
    FACIAL PARALYSIS What is facial paralysis? Facial paralysis is caused by damage to the facial nerve, which controls the muscles of the face. Facial paraly- sis can occur with problems in the brain or with problems to the nerve after it has exited the brain. What are the symptoms of facial paralysis? Facial paralysis is manifested by loss of the normal blink reflex.Affected animals cannot protect their eyes ap- propriately, and they often withdraw their eyeballs into the socket as a reflex because they cannot blink. Facial paralysis can cause drooping of the face on one side and drooling. There can also be decreased tear produc- tion in the eyeball, resulting in dry eye. What causes facial paralysis? In the majority of cases, an underlying cause is not identified (idiopathic facial paralysis). Facial paralysis has been linked with low thyroid level. In some cases, facial paralysis is seen concurrently with problems in the vestibular system (system of balance). This may reflect a problem in the inner ear or in the brain. If the prob- lem is inside the brain, possible causes include cancer, infection, inflammation, and stroke. There are usually additional neurologic signs in animals with brain disease (e.g. difficulty walking, change in level of alertness, abnormalities with other cranial nerves). How is facial paralysis diagnosed? A full neurological exam is necessary to determine whether the symptoms reflect a problem inside or outside of the brain. If the problem is thought to be inside the brain, an MRI +/- spinal fluid analysis is recommended. If the problem is thought to be out- side of the brain, ruling out hypothyroidism is recommended.
    [Show full text]
  • Chapter 105 – Brain and Cranial Nerve Disorders Episode Overview 1
    CrackCast Show Notes – Brain and Cranial Nerve Disorders – August 2017 www.canadiem.org/crackcast Chapter 105 – Brain and Cranial Nerve Disorders Episode Overview 1. List the name, function and pathologic features of the cranial nerves 2. List 6 differential diagnosis for facial pain / trigeminal neuralgia 3. Trigeminal neuralgia - describe its diagnosis and management 4. Facial nerve paralysis: List 6 differential diagnoses for facial (CN VII) paralysis 5. Describe the facial weakness deficit associated with Bell’s Palsy and list 3 other associated symptoms 6. List 4 components of treatment of Bell’s Palsy, and list the symptoms that would make you suspect Lyme Disease 7. Differentiate between herpes zoster ophthalmicus and herpes zoster oticus 8. Describe the symptoms of vestibular schwannoma and diagnostic test of choice 9. What is the pathophysiology of diabetic mononeuropathy, and which nerves are usually involved? 10. What is Uhthoff's phenomenon? 11. List 10 clinical symptoms of Multiple Sclerosis and describe its diagnosis. Describe the typical CSF findings in a patient with MS. 12. Describe the management of an acute MS exacerbation and the usual management of a patient with relapsing-remitting MS who presents with a flare Wisecracks: 1. Cerebral Venous Thrombosis Bounceback: What are the key pearls? a. List four risk factors for cerebral venous thrombosis. b. What CT findings may be seen in cerebral venous thrombosis? What is the most common CT finding? 2. Which cranial nerve is most commonly injured in trauma? 3. What syndrome is associated with bilateral acoustic neuromas? 4. How is diabetic mononeuropathy treated? Rosen’s in Perspective What are three things I can guarantee you feel a little queasy when pimped about? Well we’ve got you covered here for Cranial Nerve problems, Cerebral Venous Thrombosis and Multiple Sclerosis.
    [Show full text]
  • Facial Palsy – a Case Report
    Shawna Rekshmy D’dharan et al /J. Pharm. Sci. & Res. Vol. 8(10), 2016, 1206-1209 Facial Palsy – A Case Report Shawna Rekshmy D’dharan Intern, Saveetha Dental College Dr.M.P.Santhosh Kumar * Reader, Department Of Oral and Maxillofacial Surgery Saveetha Dental College and Hospital,Velappanchavadi, Chennai Tamilnadu 600077, India Abstract Facial nerve paralysis (FNP) is the most common cranial nerve disorders and it results in a characteristic facial distortion that is determined in part by the nerves branches involved. We report a case of 54-year-old female patient who came to department of oral and Maxillofacial Surgery with right hemifacial palsy since 7 years. On clinical examination, there was lack of movement of the right forehead and eyebrows, involuntary blinking of the right eye, inability to close the right eye completely and hyperkinesia of the right cheek. After series of investigations, no definitive etiology could be traced out, hence considered as unilateral bell’s palsy of the right side. Patient has been taking vitamin B complex once daily for the past one year and reported with an improvement of symptoms, hence no other interventions were made to treat this condition. In this article, we discuss the differential diagnosis of facial nerve paralysis, etiology, clinical features and treatment modalities for bell’s palsy. Keywords-Facial palsy, Bell’s Palsy, Facial nerve, Hemifacial paralysis, Unilateral facial paralysis INTRODUCTION sudden, with facial muscle weakness progressing over Facial nerve paralysis is classified as central type or hours to days. peripheral type, depending on the level of nerve injury. Bell’s palsy is diagnosed only by exclusion of all other Central type results in paralysis of the lower part of the possible causes.
    [Show full text]
  • The Mandibular Nerve - Vc Or VIII by Prof
    The Mandibular Nerve - Vc or VIII by Prof. Dr. Imran Qureshi The Mandibular nerve is the third and largest division of the trigeminal nerve. It is a mixed nerve. Its sensory root emerges from the posterior region of the semilunar ganglion and is joined by the motor root of the trigeminal nerve. These two nerve bundles leave the cranial cavity through the foramen ovale and unite immediately to form the trunk of the mixed mandibular nerve that passes into the infratemporal fossa. Here, it runs anterior to the middle meningeal artery and is sandwiched between the superior head of the lateral pterygoid and tensor veli palatini muscles. After a short course during which a meningeal branch to the dura mater, and the nerve to part of the medial pterygoid muscle (and the tensor tympani and tensor veli palatini muscles) are given off, the mandibular trunk divides into a smaller anterior and a larger posterior division. The anterior division receives most of the fibres from the motor root and distributes them to the other muscles of mastication i.e. the lateral pterygoid, medial pterygoid, temporalis and masseter muscles. The nerve to masseter and two deep temporal nerves (anterior and posterior) pass laterally above the medial pterygoid. The nerve to the masseter continues outward through the mandibular notch, while the deep temporal nerves turn upward deep to temporalis for its supply. The sensory fibres that it receives are distributed as the buccal nerve. The 1 | P a g e buccal nerve passes between the medial and lateral pterygoids and passes downward and forward to emerge from under cover of the masseter with the buccal artery.
    [Show full text]
  • An Unusual Finding of the Auriculotemporal Nerve: Possible Risk Factor During Preauricular Skin Incisions
    Case Report An unusual finding of the auriculotemporal nerve: possible risk factor during preauricular skin incisions Joe Iwanaga1,2,3, Samuel L. Bobek4, Christian Fisahn1,5, Ken Nakamura3, Yoshihiro Miyazono3, R. Shane Tubbs1 1Seattle Science Foundation, Seattle, WA 98122, USA; 2Department of Anatomy, 3Dental and Oral Medical Center, Kurume University School of Medicine, Kurume, Fukuoka 830-0011, Japan; 4Swedish Maxillofacial Surgery, 5Swedish Neuroscience Institute, Swedish Medical Center, Seattle, WA 98122, USA Correspondence to: Joe Iwanaga. Seattle Science Foundation, 550 17th Ave, James Tower, Suite 600, Seattle, WA 98122, USA. Email: [email protected]. Abstract: The auriculotemporal nerve (ATN) is a branch of the mandibular nerve and has been implicated for some migraines and its role in Frey’s syndrome is well known. An adult cadaver was found to have a duplicated ATN. The anterior trunk ascended as the superficial temporal artery and gave off the branches to the temporomandibular joint, parotid gland, external acoustic meatus and temporal region and communicated with a posterior trunk of the ATN. The posterior trunk ascended via the subcutaneous tissues 1 mm anterior to the auricle and gave off the branches to the anterior auricular region, temporal region and communicated with the anterior trunk. Such a duplicated ATN might be injured with preauricular skin incisions. Knowledge of such an anatomical variation might assist surgeons in iatrogenic injury of the ATN. Keywords: Auriculotemporal nerve (ATN); infratemporal fossa; Frey’s syndrome; mandibular nerve Submitted Aug 09, 2016. Accepted for publication Aug 17, 2016. doi: 10.21037/gs.2016.09.02 View this article at: http://dx.doi.org/10.21037/gs.2016.09.02 Introduction Case presentation The auriculotemporal nerve (ATN) is one of the branches During the dissection of a cadaver that was 87-year-old at of the mandibular division (V3) of the trigeminal nerve.
    [Show full text]
  • (Ear) Surgery Under Local Anaesthesia
    OPEN ACCESS ATLAS OF OTOLARYNGOLOGY, HEAD & NECK OPERATIVE SURGERY LOCAL AND REGIONAL ANAESTHESIA TECHNIQUES FOR OTOLOGIC (EAR) SURGERY Alexander Bien, Richard Wagner, Eric Wilkinson The logistics of performing otologic (ear) ing devices would still be needed. Again, surgery in developing countries and in this returns to the issue of safety. humanitarian settings are challenging. Im- plementing the use of local anaesthesia to Another reason is that of recovery time and perform middle ear and mastoid surgery in turnover; the ability to perform more cases such situations has many advantages. in a shorter amount of time. Time is of the essence in the humanitarian setting, even This article will outline the rationale for more so than in a Western medical setting. local anaesthesia in otologic surgery as well A humanitarian mission may be limited to a as educate the reader about local anesthetic certain number of days or even daylight agents and the anatomy of the ear that hours. The capacity to perform even one allows local anaesthesia to be an effective additional case in any given day may trans- means under which to perform otologic late into the benefit of many - depending on procedures. the duration of the outreach - more patients. No time needs to be allotted for the reversal Rationale for Local Anaesthesia of anaesthesia and the monitoring needs during recovery are minimal - limited Performing otologic procedures under local primarily to observation. Most, if not all, of anaesthesia - as opposed to general anaes- these concerns are eliminated with the use thesia - has many advantages in a humani- of purely local anaesthetic.
    [Show full text]
  • ANATOMY of EAR Basic Ear Anatomy
    ANATOMY OF EAR Basic Ear Anatomy • Expected outcomes • To understand the hearing mechanism • To be able to identify the structures of the ear Development of Ear 1. Pinna develops from 1st & 2nd Branchial arch (Hillocks of His). Starts at 6 Weeks & is complete by 20 weeks. 2. E.A.M. develops from dorsal end of 1st branchial arch starting at 6-8 weeks and is complete by 28 weeks. 3. Middle Ear development —Malleus & Incus develop between 6-8 weeks from 1st & 2nd branchial arch. Branchial arches & Development of Ear Dev. contd---- • T.M at 28 weeks from all 3 germinal layers . • Foot plate of stapes develops from otic capsule b/w 6- 8 weeks. • Inner ear develops from otic capsule starting at 5 weeks & is complete by 25 weeks. • Development of external/middle/inner ear is independent of each other. Development of ear External Ear • It consists of - Pinna and External auditory meatus. Pinna • It is made up of fibro elastic cartilage covered by skin and connected to the surrounding parts by ligaments and muscles. • Various landmarks on the pinna are helix, antihelix, lobule, tragus, concha, scaphoid fossa and triangular fossa • Pinna has two surfaces i.e. medial or cranial surface and a lateral surface . • Cymba concha lies between crus helix and crus antihelix. It is an important landmark for mastoid antrum. Anatomy of external ear • Landmarks of pinna Anatomy of external ear • Bat-Ear is the most common congenital anomaly of pinna in which antihelix has not developed and excessive conchal cartilage is present. • Corrections of Pinna defects are done at 6 years of age.
    [Show full text]
  • Dr. E. Anitha Dr. K. Sujatha* INTERNATIONAL JOURNAL OF
    ORIGINAL RESEARCH PAPER Volume - 10 | Issue - 01 | January - 2021 | PRINT ISSN No. 2277 - 8179 | DOI : 10.36106/ijsr INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH A RARE VARIATION OF AURICULOTEMPORAL NERVE IN RELATION WITH MAXILLARY ARTERY- A CADAVERIC STUDY Anatomy MBBS, M.D., Assistant Professor, Department Of Anatomy, Government Stanley Dr. E. Anitha Medical College, Chennai - 600001. MBBS, D.A,M.D., Professor And HOD Of Department Of Anatomy, Government Dr. K. Sujatha* Stanley Medical College, Chennai – 600001. *Corresponding Author ABSTRACT Auriculotemporal nerve is a branch of posterior division of the mandibular nerve. It carries sensory, secretomotor and sympathetic bres. Clinical knowledge about this nerve, its course and relationship with adjacent vessels are important for performing neurosurgery and facio- maxillary surgeries. Aim of the present study was to observe the origin of this nerve, its relation to adjacent vessels and its communication to other branches of mandibular nerve. We studied 35 cadavers of both male and female of South Indian populations which were used for routine dissection for teaching 1st year MBBS medical graduates. During the study, we found a rare variation of auriculotemporal nerve, having 3 roots, encircling the maxillary artery instead of the middle meningeal artery. Knowledge of such rare variation will denitely help the surgeons to plan their surgery and prevent injuries to both nerve and the vessel. KEYWORDS Auriculotemporal Nerve (ATN), Mandibular Nerve, Maxillary Artery, Middle Meningeal Artery, Inferior Alveolar Nerve (IAN). INTRODUCTION of auriculotemporal nerve and its communication with the inferior The Auriculotemporal nerve is a branch of posterior division of the alveolar nerve. Gulekon et al, in their study have reported 4 roots of mandibular nerve.
    [Show full text]