Peripheral Facial Nerve Palsy due to Spontaneous Internal Carotid Artery Dissection.

Purpose: To evaluate the findings of normal facial nerve, as seen on oblique sagittal MRI using a TMJ (temporomandibular joint) surface coil, and then to evaluate abnormal findings of peripheral facial nerve palsy. Materials and Methods: We retrospectively reviewed the MR findings of 20 patients with peripheral facial palsy and 50 normal facial nerves of 36 patients without facial palsy. All underwent oblique sagittal MRI using a TMJ surface coil. We analyzed the course, signal intensity, thickness, location, and degree of enhancement of the facial nerve. According to the angle made by the proximal parotid segment on the axis of the mastoid segment, course was classified as anterior angulation (obtuse and acute, or buckling), straight and posterior angulation. Results: Among 50 normal facial nerves, 24 (48%) were straight, and 23 (46%) demonstrated anterior angulation; 34 (68%) showed iso signal intensity on T1WI. In the group of patients, course on the affected side was either straight (40%) or showed anterior angulation (55%), and signal intensity in 80% of cases was isointense. These findings were similar to those in the normal group, but in patients with post-traumatic or post-operative facial palsy, buckling, of course, appeared. In 12 of 18 facial palsy cases (66.6%) in which contrast materials were administered, a normal facial nerve of the opposite facial canal showed mild enhancement on more than one segment, but on the affected side the facial nerve showed diffuse enhancement in all 14 patients with acute facial palsy. Eleven of these (79%) showed fair or marked enhancement on more than one segment, and in 12 (86%), mild enhancement of the proximal parotid segment was noted. Four of six chronic facial palsy cases (66.6%) showed atrophy of the facial nerve. Conclusion: When oblique sagittal MR images are obtained using a TMJ surface coil, enhancement of the proximal parotid segment of the facial nerve and fair or marked enhancement of at least one segment within the facial canal always suggests pathology of the facial nerve. The use of this modality, together with the coil, is, therefore, an effective complementary technique for the evaluation of a facial nerve.

The patient’s imaging features, especially the honeycomb pattern of ossific changes in the geniculate fossa, were virtually pathognomonic for ossifying hemangioma of the facial nerve.

Typical presentation of spontaneous internal carotid artery (ICA) dissection is an ipsilateral pain in neck and face with Horner's syndrome and contralateral deficits. Although rare, lower cranial nerve palsy have been reported in association with an ipsilateral spontaneous ICA dissection. We report three new cases of ICA dissection with lower cranial nerve palsies. The first symtom to appear was headache in all three patients. Examination disclosed a Horner's syndrome in two cases (1 and 2), an isolated XIIth nerve palsy in two patients (case 1 and 3) and IX, X, and XIIth nerve palsies (case 2) revealing an ipsilateral carotid dissection, confirmed by MRI and angiography. In all cases, prognosis was good after a few weeks. These cases, analysed with those in the literature, led us to discuss two possible mechanisms: direct compression of cranial nerves by a subadventitial haematoma in the parapharyngeal space or ischemic palsy by compression of the ascending pharyngeal artery.

Spontaneous internal carotid artery dissection is a rare condition that generally affects middle-aged individuals. Most cases of reported spontaneous internal carotid artery dissections are unilateral, but approximately 10%-20% involve bilateral internal carotid arteries. Spontaneous internal carotid artery dissection generally presents with neck pain, ischemic cerebral symptoms, and/or Horner's syndrome. Pulsatile tinnitus is present in around 5%-10% of spontaneous internal carotid artery dissection cases. However, this is generally accompanied by other major internal carotid artery dissection symptoms. Herein, we report a case of bilateral spontaneous internal carotid artery dissection that presented with unilateral pulsatile tinnitus of sudden onset as an isolated symptom. An otherwise healthy 50-year-old man visited a neurosurgical clinic complaining of right temporal pulsatile tinnitus that had begun 1 day prior. In addition to tinnitus, a thorough symptom interview revealed mild heavy-headedness. Magnetic resonance angiography showed bilateral extracranial internal carotid artery dissections and severe stenosis of the true lumen of the right internal carotid artery. No cerebral ischemic lesions were observed. Administration of 5 mg/day amlodipine and 100 mg/day aspirin was initiated. Following the 9th day after onset, the pulsatile tinnitus gradually improved. Around the 40th day after onset, the pulsatile tinnitus disappeared, and magnetic resonance angiography showed an improvement of the right internal carotid artery stenosis. Magnetic resonance angiographies at 5 and 9 months after onset revealed complete disappearance of the false lumen and slight stenosis of the right internal carotid artery at the entrance of the carotid canal. This case suggests that the sudden onset of isolated unilateral pulsatile tinnitus can be a clue to the diagnosis of spontaneous internal carotid artery dissection.

Background/Aims: The conventional systemic corticosteroid treatment for acute peripheral facial nerve palsy in patients with type 2 diabetes mellitus can induce hyperglycemia, and an alternative local therapy may be necessary. Our purpose in this study is to evaluate therapeutic effects of stellate ganglion block (SGB) on facial nerve palsy in patients with type 2 diabetes mellitus. Methods: A total of 361 cases of acute peripheral, chronic peripheral, acute central and chronic central facial nerve palsy treated with SGB or conventional therapy were included in this retrospective study. The facial nerve function score (Sunnybrook Facial Grading System) obtained at before and after treatment in non-SGB and SGB groups was used to assess the outcome. Furthermore, the blood glucose level in acute peripheral facial nerve palsy was measured. Results: The facial nerve function score in the SGB group was higher than that in the non-SGB group after treatment in peripheral facial nerve palsy, while the blood glucose level in the non-SGB group increased and was higher than that in the SGB group during the treatment in acute peripheral facial nerve palsy. Conclusions: Our findings suggest that SGB has better therapeutic effect than conventional treatment on acute and chronic peripheral facial nerve palsy in patients with type 2 diabetes mellitus.

Duplex Scan Findings in Patients with Spontaneous Cervical Artery Dissections

Carotid artery dissections have long been associated with compromise of the structural integrity of the arterial wall from heritable connective-tissue disorders, hypertension, and trauma. However, an association between spontaneous internal carotid artery dissection and tortuous or redundant carotid anatomy has not been fully explored. Patients with CTA confirmed spontaneous cervical internal carotid artery dissections were compared to a group of age and sex matched controls who also received CTA of the neck. Patients with trauma or aortic dissections were excluded. Five radiologists reviewed the CTA images to evaluate internal carotid artery tortuosity (reported as loops, kinks or coils), retrojugular and retropharyngeal courses of the internal carotid artery, presence of fibromuscular dysplasia and presence of atherosclerotic disease. Baseline data collected included demographic characteristics (sex, age, smoking history) and cardiovascular comorbidities. A total of 83 cervical internal carotid artery dissection and their age and sex matched controls were included in this study. 46% of patients were female in each group and mean age was 49.2±10.6 years. The presence of any carotid tortuosity was 53% (N.=44) and 34% (N.=28) in the per-patient analysis of dissection and control groups, respectively (P=0.02). Loops were reported in 22% (N.=18) of dissection patients and 8% (N.=7) of controls (P=0.03). Retrojugular course of the internal carotid artery were seen in 23% (N.=38) of dissection patients and 9% (N.=15) of controls (P=0.0009) in the per-vessel analysis. Our study suggests that there is an association between the presence of tortuous carotid artery anatomy and spontaneous carotid artery dissection. This finding emphasizes the importance of the presence of tortuous arteries on CTA imaging to increase the index of suspicion for a potential dissection.

Facial nerve palsy associated with atomoxetine-induced hypertension

Rehabilitation Therapy of Neurological Training of Facial Paralysis

Facial nerve palsy is the most common cranial nerve disorder. There is no consensus on a single diagnostic tool deemed as the 'gold standard' for distinguishing between idiopathic (Bell's palsy) and symptomatic causes. The diagnosis is one of exclusion and most often made on physical examination. In the present study, we describe the etiological background of peripheral facial palsy in N = 509 patients and evaluate the relevance of cerebrospinal fluid (CSF) analysis and magnetic resonance imaging (MRI) in differential diagnosis. We carried out a retrospective data analysis of 509 patients with the clinical diagnosis of peripheral facial palsy admitted to our emergency unit between January 2006 and January 2017. All patients were seen clinically; their CSF was analyzed and MRI was performed. Of N = 526 patients with isolated facial palsy, 17 patients were excluded because they did not consent to CSF analysis. Of the remaining N = 509 patients, 383 patients (75.2%) were diagnosed with idiopathic facial palsy. In the remaining 126 patients (24.8%), the following etiologies for facial palsy could be found: Ramsay-Hunt-Syndrome (N = 34), Lyme Neuroborreliosis (N = 32), other viral/bacterial central nervous system (CNS) infections (N = 8), neoplasias (N = 18), autoimmune disease (N = 12), otogenous processes (N = 6), or other etiologies (N = 16). Analysis of the CSF showed 85% sensitivity for Ramsay-Hunt-Syndrome and 100% for Lyme Neuroborreliosis and other viral/bacterial CNS infections. CSF analysis proved a reliable diagnostic tool for identifying these subgroups. MRI with contrast compounds, as performed in 409 patients, was the most important tool in diagnosing neoplasias (88% sensitivity) and otogenous processes (83% sensitivity). MRI with contrast-enhancing compounds did not reveal additional information concerning inflammatory facial nerve lesions when performed the same day as hospital admission. Although peripheral facial palsy was predominantly idiopathic (75.3%) in our cohort, the disease was caused in approximately 25% of the patients by factors which require specific treatment. In the present study, CSF analysis proved to be the leading method for the diagnosis of Ramsay-Hunt-Syndrome, Lyme Neuroborreliosis, and other CNS infections. These subgroups made up approximately 15% of our cohort. To detect these subgroups reliably, routine use of CSF analysis in peripheral facial palsy may be advisable, whereas MRI proved to be useful for exclusion of otogenic and neoplastic processes with a sensitivity of 83% and 88%. We found that the use of MRI with contrast-enhancing compounds does not provide additional diagnostic information on the day of hospital admission. Hence, the potential benefits of routine use of MRI in patients with facial nerve palsy should be weighed against health care cost factors.

Spontaneous internal carotid artery (ICA) dissection is not an infrequent cause of headache and acute neurologic deficits in the younger population. Angiography has been the imaging modality of choice for both diagnosis and follow-up. The use of magnetic resonance imaging, (MRI), in conjunction with angiography, is described in three patients shown to have ICA dissection. Our clinical findings suggest that MRI may provide a less expensive, non-invasive, diagnostic and particularly a follow up modality in patients with headache and signs suggestive of ICA dissection.

BackgroundSudden onset of unilateral weakness of the upper and lower muscles of one side of the face is defined as peripheral facial nerve palsy. Peripheral facial nerve palsy is often idiopathic and sometimes it could be due to infectious, traumatic, neoplastic, and immune causes. This study aimed to report the clinical manifestation, evaluation, and prognosis in children with peripheral facial nerve palsy.Methods57 children under 18 years of age diagnosed with peripheral facial nerve palsy at Çukurova University, Balcalı Hospital, between January 2018 and September 2021, were included in the study.ResultsThe mean age of the children at the time of diagnosis was 9.6 ± 7, 4 years. Thirty-two (56.1%) of the patients were female and 25 (43.9%) were male. A total of 57 patients were diagnosed with peripheral facial nerve palsy and categorized into many groups by etiology: idiopathic Bell’s palsy in 27 (47.5%), infectious in 11 (19.2%), traumatic in 6 (10.5%), and others (due to congenital, immune, neoplastic, Melkersson–Rosenthal syndrome, drug toxicity, and iatrogenic causes) in 13 (22.8%). Forty-six of the children achieved full recovery under oral steroids within 1–7 months. Four patients with acute leukemia, myelodysplastic syndrome, Mobius syndrome and trauma did not recover and two patients (schwannoma, trauma) showed partial improvement. Five patients could not come to follow-up control.ConclusionPeripheral facial nerve palsy is a rare condition in children with different causes. It could be idiopathic, congenital, or due to infectious, traumatic, neoplastic, and immune reasons. So, when a child presents with facial palsy, a complete clinical history and a detailed clinical examination are recommended. Giving attention to the red flag is very important. Peripheral facial nerve palsy in children is considered to have a good prognosis.

Spontaneous dissections of the internal carotid arteries are uncommon but are not rare. They constitute a fairly common cause of ischemic stroke in young patients (young in terms of the age at which strokes generally occur). The common presenting manifestations are (1) unilateral headaches followed after a period of delay by focal cerebral ischemic symptoms or (2) unilateral headaches and ipsilateral incomplete Horner's syndrome. These may or may not be associated with subjective or objective bruits. In rare instances, spontaneous dissections of the internal carotid arteries may present as lower cranial nerve palsies and cause dysphonia, dysarthria, dysphagia, and numbness of the throat. Affected patients may initially present to the otolaryngologist or be referred to one. This article describes eight patients with spontaneous dissections of the internal carotid arteries and lower cranial nerve palsies, and the pertinent literature is reviewed.

Key words: Bell's palsy, brainstem glioma, magnetic reso- nance imaging Introduction Facial palsy of the peripheral type is generally seen in the pain clinic and is often treated with a stellate gang- lion block. The most common cause of peripheral facial nerve palsy is Bell's palsy, although its etiology remains controversial. The diagnosis of Bell's palsy is usually made by exclusion of other conditions such as herpes zoster oticus (Ramsay Hunt syndrome), trauma (including skull base fracture and surgery), otitis media, and neoplasm [1]. Isolated peripheral facial nerve palsy of neoplastic origin is uncommon. We herein describe a case of peripheral facial nerve palsy which was initially diag- nosed as Bell's palsy but was later found to be caused by an intrinsic brain stem tumor. Case report A 9-year-old boy presented to the Pediatric Depart- ment of our University Hospital in August 1990 with left facial weakness. His mother noticed the hyperemic conjunctiva and lacrimation of his left eye at the end of June. Consultation with the ophthalmologist revealed no abnormality in his left eye and the hyperemia im- proved with conservative therapy. In July, facial asym- metry became obvious. He was diagnosed as having Bell's palsy by a pediatrician in August and was referred to. our pain clinic. Address correspondence to: K. Kodama Received for publication on May 31, 1993; accepted on January 6, 1994 Upon examination, the patient had a left facial nerve palsy of the peripheral type (score of the facial paresis was 24/40), however, no other neurological deficits were seen. An audiogram failed to reveal a hearing abnormality. Although repeated stellate ganglion block was given, his facial palsy progressed slowly over a 2- month period, suggesting an etiology other than Bell's palsy. Magnetic resonance imaging (MRI) in September demonstrated a tumor in the left pons and brachium pontis extending into the left cerebellopontine angle (Fig. 1). The lesion was seen as a hypointense and hyperintense area on T1- and T2-weighted images, re- spectively. He was admitted to the Neurosurgical De- partment on September 29. The positive neurological findings on admission were Bruns' nystagmus, absence of left corneal reflex, decreased gag reflex, and mild trunkal ataxia, in addition to left facial nerve palsy. He underwent a wide suboccipital decompressive craniec- tomy, and biopsy of the tumor indicated low-grade glioma. In spite of postoperative radiation (60 Gy) and chemotherapy including Ranimustine and tumor necro- sis factor, he died due to tumor progression 17 months from the time of his initial symptom. Discussion Eighty percent of peripheral facial nerve palsy cases represent idiopathic or Bell's palsy, of which approxi- mately 20% can be demonstrated to have a specific etiology [2]. Peripheral facial nerve palsy with neoplas- tic origin is uncommon, and is estimated to be the cause in approximately 5% of all cases [3]. The diagnosis of Bell's palsy is unjustified unless an accurate history is taken along with a careful examina- tion of the ear and central nervous system (CNS). The differential diagnosis of neoplastic facial palsy is vast

Spontaneous bilateral internal carotid artery dissection has frequently been described in the literature as a cause of stroke. In more than half of the patients with internal carotid artery dissection, recanalization occurs early after the event and is unusual later than 6 months after onset of the dissection. We describe a patient with ischemic stroke due to left internal carotid artery occlusion in the extracranial segment. The patient was treated with anticoagulants and early vessel recanalization did not occur. Ten months later, he developed contralateral internal carotid occlusion in the intracranial tract, which was followed by early complete recanalization. Anticoagulation therapy was continued and, 16 months after the initial event, the left internal carotid artery unexpectedly also reopened.