Compression Of Cranial Nerves Research Articles

Sleep disturbance: A forgotten syndrome in patients with Chiari I malformation

IntroductionChiari type I malformation (CM-I) is characterised by caudal ectopia of the cerebellar tonsils through the foramen magnum. This is associated with brain stem, high spinal cord, and cranial nerve compression phenomena. The most frequent symptoms are occipital headaches and dizziness. Less well-known symptoms are sleep disorders and nocturnal respiratory abnormalities. SourcesMEDLINE and information from patients evaluated at the Neurosurgery and Clinical Neurophysiology Departments at Hospital Universitario Vall d’Hebron. DevelopmentReview article based on data obtained from MEDLINE articles since 1966, using combinations of the following keywords: “Chiari malformation” or “Arnold-Chiari malformation” and “sleep apnea” or “sleep disorders”. ConclusionsCM-I patients show a higher prevalence of sleep disorders than that observed in the general population. Some studies report a 50% prevalence of sleep apnea-hypopnea syndrome (SAHS), probably associated with sudden death in some cases. These results support analysing sleep respiratory parameters in these patients. Identifying SAHS symptoms may help optimise treatment, thereby improving quality of life and prognosis.

Sclerosing cavernous hemangioma of the cavernous sinus mimicking congenital fibrosis of the extraocular muscles

A girl with a clinical presentation suggestive of unilateral congenital fibrosis of the extraocular muscles type 3 at 2 years of age years later developed progressive ophthalmoplegia and an afferent pupillary defect. Reimaging revealed a lesion diagnosed as a sclerosing cavernous sinus hemangioma with focal calcification. Cavernous sinus hemangioma is a rare, benign vascular malformation whose growth causes cranial nerve compression. Although frequently missed on routine neuroimaging, characteristic radiologic findings distinguish it from lesions such as meningioma.

Headache associated with compression of the third cranial nerve by an aneurysm of the posterior communicating artery

Continuous unilateral pain in the orbital area may be a sign of an intracranial structural lesion. We report a case of a 64-yearold woman with continuous headache of moderate intensity at the region of the left eye bulb. There was a complete paralysis of the left third oculomotor nerve. The patient was admitted with headache, vomiting, palpebral ptosis, divergent strabismus of the left eye, diplopia when looking to the left, upwards and downwards and paralytic mydriasis on the left. The Angiography revealed a saccular aneurysm dilation in the internal carotid artery with origin at the origin of the left posterior communicating artery. A microsurgery was performed on the aneurysm of the left internal carotid artery and the aneurysm was occluded by clipping. On four months follow up the patient is asymptomatic, with a complete recovery of the third nerve palsy. There is still much controversy about microsurgical and endovascular therapy in cerebral aneurysms, this case represents the good outcome in a patient with paralysis of the oculomotor nerve after microsurgery occlusion of a posterior communicating aneurysm. In conclusion, all patients with a continuo pain in the orbital area need to be evaluated by angiography in order to display a intracranial aneurysm.

Purely Endoscopic Management of Vestibular Schwannomas

Introduction: Endoscopic resection of CPA tumors remains a scarcely reported entity. Several authors have described excellent results in utilizing endoscopy for MVD in cranial nerve compression syndromes, however, only a handful of reports currently exist describing CPA tumor resection in a purely endoscopic manner. This despite numerous articles indicating that endoscopy can improve visualization of neuro-vascular structures in the CPA. Among CPA tumors, vestibular schwannomas remain one of the most challenging tumors to resect and has rarely been described in a purely endoscopic technique. We report our results of resecting vestibular schwannomas in a purely endoscopic manner.

Advances in understanding pituitary tumors

Pituitary tumors are common in the general population. Since neuroimaging techniques have improved, pituitary tumors are more often diagnosed incidentally. About 16.7% of the general population show changes in the pituitary gland. Predominantly, pituitary tumors are benign pituitary adenomas. Pituitary carcinomas or aggressive pituitary tumors are extremely rare. They might develop from benign adenomas. New genetic and epigenetic abnormalities help us to understand pituitary tumorigenesis and might lead to therapeutical targeting drugs in the future. Macroadenomas (>1 cm) can lead to visual field disturbances, compression of cranial nerves, hypopituitarism, and infiltration of the cavernous sinuses. The functional status of the pituitary tumor is important. About half to one third of all pituitary tumors are non-functioning pituitary adenomas. The other pituitary tumors show a specific pattern of hormone secretion. About 25% to 41% of all pituitary tumors are prolactinomas, acromegaly with production of growth hormone represents 10% to 15% of adenomas, Cushing's disease with production of adrenocorticotropic hormone accounts for 10%, and other hormonal characteristics are less common. Transsphenoidal resection and total adenomectomy are desirable. Radiosurgery has enriched the surgical treatment options. Surgical treatment is the intervention of choice except for prolactinomas, where pharmaceutical treatment is recommended. Pharmaceutical treatment consists of dopamine agonists such as cabergoline and somatostatin analogues that include octreotide and pasireotide; retinoic acid is of theoretical interest while peroxisome proliferator-activated receptor-gamma-ligands are not clinically useful. In acromegaly, pegvisomant is a further treatment option. Temozolomide should be considered in aggressive pituitary tumors. In general, pharmaceutical options developed recently have extended the repertoire of treatment possibilities of pituitary tumors.

Research progress on vertebrobasilar dolichoectasia.

Vertebrobasilar dolichoectasia (VBD) is a rare disease characterized by significant expansion, elongation, and tortuosity of the vertebrobasilar arteries. Current data regarding VBD are very limited. Here we systematically review VBD incidence, etiology, characteristics, clinical manifestations, treatment strategies, and prognosis. The exact incidence rate of VBD remains unclear, but is estimated to be 1.3% of the population. The occurrence of VBD is thought to be due to the cooperation of multiple factors, including congenital factors, infections and immune status, and degenerative diseases. The VBD clinical manifestations are complex with ischemic stroke as the most common, followed by progressive compression of cranial nerves and the brain stem, cerebral hemorrhage, and hydrocephalus. Treatment of VBD remains difficult. Currently, there are no precise and effective treatments, and available treatments mainly target the complications of VBD. With the development of stent technology, however, it may become an effective treatment for VBD.

Primary Optic Atrophy in Osteopetrosis

Osteopetrosis is a rare disorder of defective osteoclastic resorption of bone, resulting in abnormally dense bones. Two main forms are milder adult onset autosomal dominant form and severe infantile malignant autosomal recessive form. Both types of mutations lead to disturbances of acidification needed for normal osteoclast function. We report a rare ocular finding in a rare case of malignant variety of osteopetrosis. A five month old girl child diagnosed as malignant variety of osteopetrosis with failure to thrive on fundus examination revealed chalky white optic discs with sharply demarcated borders bilaterally. Cranial neuropathies are caused due to improper bone remodeling leading to narrowing of cranial nerve foramina and compression of nerves in skull foramina. Allogeneic hematopoietic stem cell transplantation is the only treatment known to significantly alter the course of disease. *Chintan Dedhia, Nilesh Parekh, Neepa Gohil, Hetal Patel, Yogesh Parmar

Outcome Of Unrelated Umbilical Cord Blood Transplantation For Children With Osteopetrosis: An Eurocord and Inborn Errors Working Party (IEWP)-EBMT Study

Osteopetrosis (OP) is a genetic disease characterized by increased bone density due to osteoclast dysfunction, leading to life-threatening multi-systemic complications in early childhood. Haematopoietic stem cell transplantation (HSCT) is the only curative approach for most children with OP and can effectively prevent serious complications such as blindness, bone fractures, hydrocephalus and cranial nerve compression. Since timing of transplant is critical in OP, umbilical cord blood is an attractive stem cell source, due to its prompt availability.We analysed the outcomes of unrelated umbilical cord blood transplantation (UCBT) in 45 children with osteopetrosis transplanted in EBMT centers between 1996 and 2012, using data reported to Eurocord. Median age at UCBT was 6 months (1.1 month - 7.4 years). Donor-recipient pairs were matched at HLA-A and -B (antigen level) and DRB1 (allelic level) in 14 or HLA mismatched at 1 (n= 23) or 2 (n= 7) loci. Information on conditioning regimen was available for 42 patients; it was myeloablative (mostly busulfan-based) in 40 children and reduced intensity in 2 patients. GvHD prophylaxis consisted mainly of cyclosporine combined with either prednisolone (n= 20), or methotrexate (n=6), or mycophenolate mofetil (n=3). Anti thymocyte globulin (ATG) or alemtuzumab was given to 37/40 patients. Median number of infused total nucleated cell (TNC) and CD34+ was 13x107/kg and 3.4x105/kg, respectively. Median follow-up for survivors was 44 (range 4-144) months. Neutrophil recovery with donor chimerism was documented in 27/45 patients; 19/25 evaluable patients presented full donor engraftment, while 6 children presented mixed donor chimerism. Median time to neutrophil recovery was 20 (range 10-60) days. Eighteen patients experienced graft failure and 3/18 are alive at last follow up. Information on treatment post-graft failure was available 7/18 children: 6 patients underwent a second HSCT and 3 of them survived. Stem cell dose was associated with a trend for a better probability of donor engraftment: the cumulative incidence of donor engraftment was 46% in patients who received a CD34+ cell dose<2 x 105/kg, versus 71% in children receiving a CD34+ cell dose ≥2x105/kg (p = 0.09). Eleven patients developed grade II-IV acute graft-versus-host disease (aGvHD: n=6 grade II, n=4 grade III, n=1 grade IV) and 5 patients chronic GVHD (cGvHD: n=3 limited, n=2 extensive). Overall survival (OS) at 3 years was 45+8%. Twenty-four patients died after UCBT due to: infections (n=13), acute respiratory distress syndrome (n=2), veno occlusive disease (VOD), (n=2) hemorrhage (n=2), or other causes (n=5). VOD was observed in 7/26 evaluable patients. Stem cell dose and HLA disparity were the only predictors of superior outcome in univariate analysis. The 3-year probability of OS was 50% in patients who received grafts with a CD34+ cell dose >2x105/kg versus 0% in children receiving grafts with a CD34+ cell dose < 2x105/kg (p=0.001). According to HLA disparities, 3-year probability OS was 54% versus 58% versus 0% in patients receiving a 6/6, 5/6 and 4/6 HLA-mismatched graft, respectively (p=0.01). Interestingly, 4/4 children receiving a treosulfan-based myeloablative regimen achieved donor engraftment and 3 children are alive at last follow up.These data suggest that transplantation of unrelated UCB is a valid alternative for children with OP without a matched sibling or a suitable matched unrelated adult donor. The use of CB units mismatched at >1 HLA locus should be avoided due to worse survival. The incidence of primary graft failure was high and therefore the optimization of the conditioning regimen and/or the use of CB units containing a high TNC and CD34+ cell dose must be considered in this setting. The use of treosulfan-based conditioning regimens is worth further investigation, as well as the use of defibrotide prophylaxis to reduce the risk of VOD in this population of high risk patients. Disclosures:No relevant conflicts of interest to declare.

High Response Rates and Prolonged Survival in Patients With Corticotroph Pituitary Tumors and Refractory Cushing Disease From Capecitabine and Temozolomide (CAPTEM)

Rarely, corticotrophic pituitary tumors take on an aggressive form characterized by rapid growth, invasion into local structures, compression of cranial nerves, and possible spread to distant sites. When conventional surgery, radiation therapy, and hormones fail to control progression and symptoms, alternative therapies are needed. A novel chemotherapeutic regimen of capecitabine and temozolomide (CAPTEM), originally designed in our laboratory, demonstrated dramatic antineoplastic effects against corticotrophic pituitary tumors. We present a case series of 4 patients with aggressive, adrenocorticotrophic hormone--producing pituitary tumors who had previously depleted all surgical, radiation, and hormonal therapies and were then treated with CAPTEM. Dramatic clinical improvements in neurological deficits and Cushing symptoms were evident in all patients after treatment was initiated. Confirmed by radiographic imaging, 2 of 4 patients demonstrated complete regression of disease, 1 patient had a 75% regression, and the fourth patient has ongoing stable disease for > 4.5 years at the time of this writing. Immunohistochemical analysis of patients' tumor samples showed low O-methyguanyl methyltransferase expression and adequate levels of mismatch repair enzymes (MLH-1, MSH-2, MSH-6, and PMS-2), which are important for the in vivo efficacy of CAPTEM. This is the first report of prolonged antitumor response to and radiographic complete remissions as a result of CAPTEM in patients with aggressive pituitary tumors who had exhausted all other therapies.

Hypertension in patients with cranial nerve vascular compression syndromes and comparison with a population-based cohort

Although essential arterial hypertension (AH) represents a major health issue, its underlying causes remain unknown. An intriguing hypothesis is that AH in some cases may be caused by vascular compression of the rostral ventrolateral medulla (RVLM). Because hemifacial spasms (HFSs) are caused by vascular compression of the seventh cranial nerve in close proximity to the RVLM, one would, if this hypothesis is correct, expect to find a positive association between the occurrence of AH and chronic HFSs. Such a positive association would not be expected in patients with trigeminal neuralgia (TN), since TN is caused by vascular compression of the fifth cranial nerve, which is not close to the RVLM. In view of this background, the authors conducted a retrospective population-based study to investigate how the occurrence of AH in patients with either HFSs or TN compares with the prevalence of AH in the general population, when adjusted for sex and age. The general population was represented by participants of the Nord-Trøndelag Health Study 3 (HUNT3). The prevalence of AH in the authors' patients with HFSs was significantly higher than in a sex- and age-adjusted sample from the general population; this was not true for the patients with TN. The authors suggest that the data provide supporting evidence to the theory that compression of the RVLM may be one cause of AH.

Teaching Neuro Images : Compression of the eighth cranial nerve causes vestibular paroxysmia

A 55-year-old man reported having recurrent spontaneous attacks of rotatory vertigo lasting 1–5 seconds and occurring up to 10 times daily and often associated with attacks of right ear tinnitus for more than 3 years. Caloric testing showed a right peripheral vestibular deficit. Cervical vestibular myogenic potentials showed impaired function of the right saccule. An audiogram was normal. MRI (figure, A and B) showed that the eighth nerve was in contact with the anterior inferior cerebellar artery. Vestibular paroxysmia was diagnosed.1,2 Carbamazepine resolved the symptoms but the patient discontinued it due to side effects. The symptoms recurred, and surgery was performed. Intraoperatively, compression of the eighth nerve was found (figure, C and D). He has had no further symptoms and takes no medication. These findings support the view that vascular compression of the root entry zone of the eighth cranial nerve can cause vestibular paroxysmia. The authors thank Dr. Jennifer Linn for evaluation of the MRI scans.

Vertebrobasilar And Bilateral Carotid Dolichoectasia: A Rare Entity

Dolichoectasia is a term used to describe marked widening, tortuosity and elongation of an artery. Intracranial vertebral and basilar arteries are most commonly involved. Vertebrobasilar dolichoectasia is usually asymptomatic. Both vertebrobasilar and bilateral carotid dolichoectasia has been reported very rarely in the literature. Cranial nerve compression and cerebral ischemia findings are frequently seen in symptomatic patients. We reported a 67-year-old female, without medical or family history for cerebrovascular disease, presented with vertebrobasilar and bilateral carotid dolichoectasia and subarachnoid hemorrhage, manifesting as reduced level of consciousness and weakness, and left

Chiari type I malformation caused by craniometaphyseal dysplasia.

Craniometaphyseal dysplasia is a rare genetic condition characterized by progressive thickening of bones in the skull and metaphyseal abnormalities in the long bones. This disorder often causes progressively symptomatic cranial nerve compression, but in rare cases foramen magnum stenosis may lead to quadriplegia. Chiari I malformation with craniometaphyseal dysplasia is extremely rare. The authors report on a 25-year-old woman with myelopathy due to Chiari I malformation along with craniometaphyseal dysplasia. There are only four previous case reports of this condition. The authors present here the fifth case report of this rare condition and summarize its characteristics.

Delayed Pneumocephalus-Induced Cranial Neuropathy

Pneumocephalus is a common occurrence after cranial surgery, with patients typically remaining asymptomatic from a moderate amount of intracranial air. Postsurgical pneumocephalus rarely causes focal neurological deficits; furthermore, cranial neuropathy from postsurgical pneumocephalus is exceedingly uncommon. Only 3 cases have been previously reported that describe direct cranial nerve compression from intracranial air resulting in an isolated single cranial nerve deficit. The authors present a patient who developed dysconjugate eye movements from bilateral oculomotor nerve palsy. Direct cranial nerve compression occurred as a result of postoperative pneumocephalus in the interpeduncular cistern. The isolated cranial neuropathy gradually recovered as the intracranial air was reabsorbed.

Hemifacial spasm and jugular foramen syndrome caused by diametrically opposite aneurysms on the vertebral artery

Vertebral artery (VA) aneurysms commonly occur on a fusiform segment of the artery and have unusual appearances and characteristics [1]. They commonly present with symptoms of cranial nerve compression secondary to related dolichoectasia, mass effect or subarachnoid hemorrhage. In the setting of a VA aneurysm, hemifacial spasm occurs when the VA is ectatic or fusiform, while individual lower cranial nerve palsies have been reported in saccular and fusiform cases [1]. A simultaneous occurrence of these two clinical syndromes related to an aneurysmal VA has not been described. A 50-year-old lady presented with left-sided hemifacial spasm of 2-year duration and nasal regurgitation and altered phonation of 1-year duration. Both the symptoms were insidious in onset and were progressive. There was no history of facial pain or numbness, tinnitus or vertigo. Her neurological deficits included left sided IX, X nerve palsies. Examination of the other cranial nerves was normal. MRI of the brain showed a mildly ectatic vertebro-basilar artery (VBA) on the left side with compression on the VII–VIII nerve complex (Fig. 1a). Digital subtraction angiogram (DSA) revealed an ectatic left VA with a ventrolaterally pointing, distal 12 9 8 9 6 mm sized saccular aneurysm and a small blister aneurysm (3 9 3 mm) directed dorsomedially (Fig. 1b, c). At surgery via a far lateral craniectomy, the saccular aneurysm directed toward the jugular foramen was found arising proximal to origin of the posterior inferior cerebellar artery (PICA) which was draped on the aneurysm (Fig. 2a). It was clipped with a 10-mm angled ring clip, with the ring enclosing the VA (Fig. 2b). The clipped aneurysm was then opened and decompressed. The dorsally directed blister aneurysm compressing the facial nerve at its exit from the pons (Fig. 2b) was wrapped with muscle and dura. Teflon was interposed between the nerve and the ectatic VA segment. The risk of rupturing the nearby blister aneurysm and narrowing the ectatic VA precluded reconstruction of the VA with clips. Postoperatively, the patient was relieved of her hemifacial spasm, while her lower cranial nerve palsy remained status quo. An aneurysmal etiology is noted in 0.3–0.6 % of all cases of hemifacial spasm. The postulated pathogenesis is related to the compression of the root entry zone (REZ) of the facial nerve by the pulsations of the aneurysm. In 7.5–21 % of the cases an ectatic VBA is the causative factor [2]. A Pubmed search revealed 12 cases of VA aneurysms presenting with hemifacial spasm. One report describes Foville’s syndrome secondary to a dissecting VA aneurysm [3]. Our first-of-its-kind report demonstrates the simultaneous occurrence of hemifacial spasm and jugular foramen syndrome due to the mass effect of two aneurysms on an ectatic VA loop. Microsurgical clipping and debulking are performed for VA aneurysms causing brainstem compression and neurological deficits [4], while endovascular coiling is an optional in other cases [5]. In our case, the complex nature of the contiguous aneurysms on the VA segment and the need for decompression precluded endovascular intervention. S. V. Furtado (&) S. Thakar N. A. Saikiran A. S. Hegde Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences (SSSIHMS), EPIP Area, Whitefield, Bangalore 560066, Karnataka, India e-mail: sunilvf@gmail.com

Impaired cognition and hemispatial neglect in a woman with neck pain

MRI brain (Fig. 1A-C Images in Neuroscience: Question) revealed multiple subcentimeter gadolinium-enhancing foci throughout the leptomeninges and cortex. Cerebrospinal fluid (CSF) analysis revealed pleomorphic lymphocytosis with a low CSF/blood glucose concentration ratio (0.2, normal range > 0.6). Although infective processes, including tuberculosis (TB) are possible, the suspicious lesion behind the left ventricle (Fig. 1D Images in Neuroscience: Question) made cerebralmetastases from lung cancer themost likely diagnosis. Cerebral metastases from haematological dissemination usually results in a single or few nodules, which typically seed to the grey– white matter junction and are surrounded by oedema. This case is unusual, as there are numerous nodules throughout the leptomeninges and cortex andnoevidence of perilesional oedemaormass effect. Such ‘‘miliary’’metastatic tumoursor carcinomatousencephalitis are rare and usually present in patients with known systemic disease. Carcinomatous meningitis occurs in 5% of systemic malignancies and should be suspected in patients with aseptic meningitis, especially when underlying lung, breast or gastrointestinal tumours are present. Here, it is difficult to determine whether tumour cells spread from the brain parenchyma to the CSF or visa versa. Once in the subarachnoid space, however, dissemination to multiple meningeal sites overlying the brain and spinal cord is inevitable and there may be spread to the underlying parenchyma. Carcinomatous meningoencephalitis is characterized by cranial or spinal root neuropathies due to leptomeningeal disease in combination with focal neurological deficits or altered mental state attributable to cortical disease. Compression of cranial nerves as they exit the brainstem frequently presents as ophthalmoplegia or facial weakness, while aqueductal obstruction may result in hydrocephalus. Spinal root involvement presents as neck or back pain associated with compressive radiculopathies. Cortical involvement results in headache or altered mental state and disruption of the blood–brain barrier typically manifests as focal deficits, seizures or encephalopathy. In leptomeningeal disease CT scans are usually unremarkable and calcification or microhaemorrhage of cortical nodules is

Neurological manifestations of phaeochromocytomas and secretory paragangliomas: a reappraisal

ObjectiveTo determine the frequency and range of neurological manifestations of phaeochromocytomas and secretory paragangliomas.MethodsA retrospective review of case notes of patients admitted to Auckland Hospital from 1985 to 2011 with...

Recurrent Spontaneous Attacks of Dizziness

This article describes the common causes of recurrent vertigo and dizziness that can be diagnosed largely on the basis of history. Ninety percent of spontaneous recurrent vertigo and dizziness can be explained by six disorders: (1) Ménière disease is characterized by vertigo attacks, lasting 20 minutes to several hours, with concomitant hearing loss, tinnitus, and aural fullness. Aural symptoms become permanent during the course of the disease. (2) Attacks of vestibular migraine may last anywhere from minutes to days. Most patients have a previous history of migraine headaches, and many experience migraine symptoms during the attack. (3) Vertebrobasilar TIAs affect older adults with vascular risk factors. Most attacks last less than 1 hour and are accompanied by other symptoms from the posterior circulation territory. (4) Vestibular paroxysmia is caused by vascular compression of the eighth cranial nerve. It manifests itself with brief attacks of vertigo that recur many times per day, sometimes with concomitant cochlear symptoms. (5) Orthostatic hypotension causes brief episodes of dizziness lasting seconds to a few minutes after standing up and is relieved by sitting or lying down. In older adults, it may be accompanied by supine hypertension. (6) Panic attacks usually last minutes, occur in specific situations, and are accompanied by choking, palpitations, tremor, heat, and anxiety. Less common causes of spontaneous recurrent vertigo and dizziness include perilymph fistula, superior canal dehiscence, autoimmune inner ear disease, otosclerosis, cardiac arrhythmia, and medication side effects. Neurologists need to venture into otolaryngology, internal medicine, and psychiatry to master the differential diagnosis of recurrent dizziness.

The role of autonomic nervous system in the pathophysiology of hemifacial spasm

Objectives: Despite the vascular compression of the seventh cranial nerve has been verified by the microvascular decompression surgery as the cause of hemifacial spasm (HFS), the mechanism of the disease is still unknown. We believe that the autonomic nervous system in adventitia of the offending artery may contribute to the HFS. To prove our hypothesis, we performed an experiment in SD rats.Methods: Moller’s HFS model was adopted and the abnormal muscle response (AMR) wave was electrophysiologically monitored. With randomization, some HFS rats underwent exclusion of the offending artery or removal of the ipsilateral superior cervical ganglion. Some HFS rats with negative AMR following exclusion of the offending artery were dripped with norepinephrine onto the neurovascular conflict site.Results: With exclusion of the offending artery, AMR disappeared in 14 (70%) of the 20 HFS rats, while in three (30%) of the 10 from sham operation group (P<0·05). With ganglionectomy, AMR disappeared in 12 (75%) of the 16 HFS rats, while in two (25%) of the eight from the sham operation group (P<0·05). With norepinephrine drip, AMR reappeared in four (67%) of the six from those offending-artery-excluded HFS rats, while in zero of the six from normal-saline-dripped group (P<0·05).Discussion: The neurotransmitter releasing from the autonomic nervous endings in the worn adventitia of the offending artery may induce an ectopia action potential in those demyelinated facial nerve fibers expanding to the neuromuscular conjunction and trigger an attack of HFS.

The Association of Anterior Inferior Cerebellar Artery in IAC with Tinnitus and Hearing Loss

Objective: Tinnitus is a common disorder, but the etiology of this disorder remains unknown. The objective of this study was to assess the correlation between anatomic type and the thickness of the anterior inferior cerebellar artery (AICA) loop with tinnitus, using 3D-fast imaging employing steady state acquisition magnetic resonance image (MRI). Method: Seventy-four patients with tinnitus and 82 asymptomatic controls were included in this study. Otologic symptoms, which were measured based on the results of a pure tone audiometry, were reviewed. We evaluated the position and thickness of the AICA vascular loop in 3D-FIESTA MRI using 2 scoring systems. The first system was Chavda classification based on the anatomic location of the AICA loop. The second scoring system was used to measure the thickness of the AICA loop. The AICA loops were classified into 2 groups based on thickness, thinner than adjacent facial nerve and thicker than the facial nerve. Results: Ears with type I, II AICA loops showed significantly higher rates of tinnitus than those with type III. There was no association between the type of AICA loop and subtype of tinnitus (pulsatile, nonpulsatile). There was no association between the type of tinnitus and hearing loss. Ears with thinner AICA loop had a higher rate of tinnitus than those with thicker AICA loop. Conclusion: The type I, II and thinner AICA loop was significantly correlated with tinnitus. Compression of VIIIth cranial nerve by AICA loops at a cerebellopontine angle and impaired blood flow through thevessel may be the pathophysiology of tinnitus.