Left Facial Palsy Research Articles

Cerebral microbleeding in varicella-zoster viral meningitis: An early sign of vasculopathy?

A 75-year-old man undergoing chemotherapy for prostate cancer for 3 months presented with headache after having blisters in his left ear canal and auricle. His body temperature at presentation was 38°C. Neurologic examination revealed nuchal stiffness and left peripheral facial palsy. We also noted leukocytopenia (2,000/µL) and elevated serum C-reactive protein (8.51 mg/dL). CSF analysis showed no erythrocytes, elevated leukocytes (640/µL; 3% monocytes, 97% neutrophils), an increased protein level (473 mg/dL), and slightly decreased glucose level (51 mg/dL, serum glucose 120 mg/dL). Brain MRI and magnetic resonance angiography (MRA) on the day of admission were normal except for irregular gadolinium (Gd) enhancement of the cerebral sulci and basal meninges consistent with meningitis (figure, A–E). Upon noting Ramsay Hunt syndrome from the patient's clinical history and considering the known predominance of neutrophils in CSF in early cases of varicella-zoster virus (VZV) infection of the nervous system,1 we initiated treatment with IV acyclovir (ACV; 1,800 mg/day) for suspicion of VZV meningitis. The patient's symptoms then gradually improved. Existence of VZV within CSF was later confirmed by PCR testing and high anti-VZV immunoglobulin M (IgM) antibody index (1.68; normal range <0.8) results. Two weeks after ACV treatment initiation, follow-up MRI showed attenuated Gd enhancement of the meninges; unexpectedly, diffusion-weighted imaging (DWI) showed a small acute infarction of the right insula (figure, F), and T2-weighted imaging (T2*WI) showed microbleeding in the left anterior cingulate gyrus (figure, G) and the midbrain interpeduncular fossa (figure, H). MRA revealed no apparent narrowing or malformation of the arteries. Without risk factors for cerebrovascular disease such as arrhythmia, hypertension, or coagulation abnormality, our clinical and radiologic findings taken together with patient history suggested small-vessel vasculopathy associated with VZV infection; therefore, oral dexamethasone (DEX; 1 mg/day) was added to the original treatment. Both ACV and DEX were continued for 2 months until the CSF testing and the anti-VZV IgM antibody index returned to normal. No clinical or radiologic signs of relapse were detected during the therapeutic course.

Disseminated non-Hodgkin′s lymphoma presenting as unilateral parotid gland enlargement with facial nerve palsy

The head and neck is the most common area for the presentation of lymphoproliferative disorders. Primary involvement of salivary glands is uncommon. Non-Hodgkin's lymphoma constitutes a group of malignancies those arises from cellular components of lymphoid or extra nodal tissues. Here we report a case of a 70-year-old male patient who presented with left parotid gland enlargement with left facial nerve palsy and involvement of other nodal sites, which is rarely reported in the literature.

A Case of Associated Laryngeal Paralysis Caused by Varicella Zoster Virus without Eruption

We report a patient with significant weakness of the left soft palate, paralysis of the left vocal cord, and left facial nerve palsy. Although the patient showed no herpetic eruption in the pharyngolaryngeal mucosa and auricle skin, reactivation of varicella zoster virus (VZV) was confirmed by serological examination. She was diagnosed with zoster sine herpete. After treatment with antiviral drugs and corticosteroids, her neurological disorder improved completely. When we encounter a patient with associated laryngeal paralysis, we should consider the possibility of reactivation of VZV even when no typical herpetic eruption is observed.

Mumps, Cervical Zoster, and Facial Paralysis: Coincidence or Association?

The association of mumps with peripheral facial paralysis has been suggested, but its pathogenesis remains unclear. An 8-year-old girl simultaneously developed left peripheral facial paralysis, ipsilateral cervical herpes zoster, and bilateral mumps sialadenitis. Elevated anti-mumps and anti-varicella zoster virus IgM antibodies in serological testing indicated recent infection of mumps and reactivation of VZV. Molecular studies have provided mounting evidence that the mumps virus dysregulates the host's immune system and enables the virus to proliferate in the infected host cells. This dysregulation of the immune system by mumps virus may have occurred in our patient, enabling the latent VZV infection to reactivate.

Churg-strauss syndrome presented with hearing impairment and facial palsy.

Churg-Strauss syndrome (CSS) is a rare systemic necrotizing vasculitis. Cranial nerve involvement is very rare in CSS. A 59-year-old woman had complained of both hearing impairments for eight months and left facial palsy for three months. Left facial and cochlear neuropathies were detected in electrodiagnostic studies. Paranasal sinus computed tomography (CT) showed chronic pansinusitis. Chest CT revealed eosinophilic infiltration in the right upper lobe. Tissue biopsy of the right inferior turbinate displayed necrotizing vasculitis with eosinophilic infiltration. She was diagnosed as CSS, based on the presence of eosinophilia, pulmonary infiltration, paranasal sinusitis, and biopsy containing blood vessels with extravascular eosinophils. She was treated with intravenous and oral steroids and azathioprine, showing relatively good prognosis on facial palsy and hearing impairment. We report a very rare case of CSS presented with hearing impairment and facial palsy.

Unusual natalizumab-associated progressive multifocal leukoencephalopathy starting in the brainstem

we report on a 45-year-old German patient with relapsingremitting (RR) multiple sclerosis (MS) who was started on natalizumab (NAT) therapy in November 2007, because of ongoing disease activity despite interferon therapy. She had never been treated with immunosuppressants before. After she tested positive for anti-JCV (John Cunningham Virus)antibodies for the first time, she decided to discontinue NAT treatment in July 2011 (after 49 NAT infusions). At this time point, as well as during NAT therapy, she was clinically stable (EDSS 3.5). Six weeks later in August 2011, she developed new brainstem symptoms, with left facial and trigeminal nerve palsy, double vision and mild dysphagia. On magnetic resonance imaging (MRI), a large brainstem-midbrain lesion was seen (Fig. 1D). The symptoms were initially interpreted as MS relapse and treated with corticosteroids. After transient improvement, she deteriorated again and was seen for the first time at our hospital. Progressive multifocal leukoencephalopathy (PML) was diagnosed in September 2011 after detection of JCV DNA (31 c/ml in CSF, 5 c/ml in serum; EDSS 7.0). Subsequently, she developed severe immune reconstitution inflammatory syndrome (IRIS), deteriorated clinically (EDSS 9.5), and had to be transferred to the intensive care unit (ICU) for several weeks. Finally, she stabilized after repeated courses of high-dose iv glucocorticosteroids (GC) and iv immunoglobulins (IVIgG, 5 days a 0.4 g/kg body weight), as well as concomitant therapy with mefloquine and mirtazapine. Six months later, she had improved, but still showed severe ataxia and brainstem symptoms (EDSS 6.0). Retrospective analysis of all available MRI scans identified a small new-initially asymptomatic-T2 brainstem lesion as the first MRI manifestation of this patient’s PML in November 2010, which slowly progressed over 41 weeks until clinical PML presentation (Fig. 1A–D). Several aspects in this report are unusual: (1) brainstem PML is rare and has been reported in association with NAT therapy in MS patients only once so far [1]; (2) the longlasting pre-symptomatic phase of 41 weeks and clinical manifestation of PML only 6 weeks after NAT was discontinued; and (3) clinical improvement after combined therapy with GC and IVIgG. In this patient, a new, asymptomatic, non-contrast-enhancing T2 lesion appeared in the brainstem in November 2010 (Fig. 1B). Notably, before the MRI lesion was rated as important, the patient decided to stop NAT therapy in July 2011 due to fear of PML. At this time and during NAT treatment, the lesion was completely asymptomatic. The patient developed new brainstem symptoms only 6 weeks after discontinuation of NAT and showed a large brainstem-midbrain lesion on MRI at that time. Detailed retrospective MRI analysis identified that this large lesion had progressed over time from the small brainstem lesion 41 weeks before. NATassociated PML with a pre-symptomatic course up to 24 weeks has been reported, but not in the brainstem so far [2]. More recently, Yousry and colleagues [3] identified common MRI patterns of NAT-associated PML, which help in the early diagnosis of PML. Except for the unusual initial localization in the brainstem and size (\ 3 cm), all J. Havla (&) R. Hohlfeld T. Kumpfel Institute of Clinical Neuroimmunology, Ludwig-Maximilians-University, Medical Campus Grosshadern, Marchioninistr. 15, 81377 Munich, Germany e-mail: joachim.havla@med.lmu.de

The hypodense artery sign in acute cerebral infarction

A 77-year-old man was admitted with severe stenosis of both left anterior descending and circumflex coronary arteries and mitral valve regurgitation. He underwent mitral valve replacement and coronary artery bypass grafting (CABG). During the second postoperative day, sedation having been stopped, the patient presented a left hemiplegia and homolateral central facial paralysis.

Cosmetic appreciation of lateralization of peripheral facial palsy: ‘preference for left or right, true or mirror image?’

There have been several studies in the past depicting asymmetry in 'normal' human faces. Evidence supports the fact that the right hemisphere is superior in the recognition of emotions expressed by the human face and indicates a right hemispheric specialization for processing emotional information. The primary aim of this study is to determine whether there is a difference in cosmetic appreciation of a left peripheral facial palsy compared to a right peripheral facial palsy? Pictures of patients with a facial palsy with House-Brackmann II-VI were reversed as a mirror image and offered as a pair of pictures, together with the true image. Forty-two patients and 24 medical professionals familiar with facial palsy were asked to choose the most attractive photograph. The primary 'end' point was the most attractive side in the pictures chosen by medical professionals and patients. The secondary 'end' points consisted of the preferences for the mirror or true image, and influences of the House-Brackmann score and age. Medical professionals preferred the photographs from patients with a right and left peripheral facial palsy (PFP) in, respectively, a mean of 44 % (41-48 %) and 56 % (52-59 %) of the pictures (p = 0.02). When comparing mirror and true image, patients with a left-sided facial palsy chose their mirror and true image as most attractive in 90 and 10 %, respectively (p < 0.05). Patients with a right-sided facial palsy chose their mirror and true image in 30 and 70 %, respectively (p > 0.05). Subanalysis of patients with a PFP House-Brackmann score V and VI showed that medical professionals did not have a significant preference for a left nor right-sided facial palsy. Patients with a left-sided facial palsy chose their mirror image in all cases and patients with a right-sided palsy chose their mirror and true image in resp. 33 and 67 %. The House-Brackmann score (p = 0.52) and age (p = 0.73) of the patients did not influence preferences. This study, demonstrating that medical professionals find a right-sided facial palsy cosmetically less attractive than a left-sided, has clinical relevance. Patients, especially with a left-sided facial palsy, tend to choose for their mirror image, although this choice seems to be influenced by hemispheric specialization and familiarity.

RASH DECISIONS–DERMATOLOGICAL MANIFESTATIONS PRECEDING A PROGRESSIVE NEUROLOGICAL SYNDROME

We describe the case of a 72 year old woman who presented with sequential cranial nerve palsies preceded by irritation, pain and a vesicular rash in the sensory distributions of...

Ramsey Hunt syndrome — a case report

Case report: An 82-year-old woman with a history of hypertension and diabetes mellitus was presented to the Emergency Room (ER) because of left facial weakness of sudden onset and pain on the mastoid region. She had a history of a recent viral upper airway infection. On examination, she had a peripheral left facial nerve paralysis, with no other abnormalities. She was diagnosed with a Bell's Palsy and discharged from the ER with a prescription of prednisolon and recommendation for eye care measures.

Pure motor trigeminal neuropathy in a woman with tegmental pontine infarction

A 50-year-old woman presented with drowsiness, severe dysarthria, left facial palsy, and left hemiparesis. Diffusion-weighted MRI showed cerebral infarction in the left pontine tegmentum and right cerebellum and angiography revealed basilar artery occlusion. Altered consciousness and hemiparesis fully resolved following successful recananlisation of the basilar artery by emergent intra-arterial thrombolysis. However, about 8months later, obvious wasting of the left temporal and buccal area without sensory signs was detected. Electrophysiological evaluation revealed a chronic denervation process in the left masseter and temporalis muscles. We suggest that a small infarction in the trigeminal nucleus of the pontine tegmentum can cause an isolated trigeminal motor neuropathy with masticatory muscle atrophy.

Internal carotid artery dissection after anterior cervical disc replacement: first case report and literature review of vascular complications of the approach

We report the case of a 41-year-old woman who underwent cervical total disc replacement at C4C5 and C5C6 levels and fusion at C6C7 level through an anterior right-side approach. After anesthesia recovery, the patient presented left hemiparesia and facial palsy due to large right hemispheric stroke. Diffusion-weighted magnetic resonance imaging was performed as soon as the patient developed neurologic symptoms of stroke and revealed a right internal carotid artery dissection. Digital substraction angiography, endovascular stenting, angioplasty and thrombectomy were performed. Six months after treatment, clinical examination showed mild left-arm spasticity. To the best of our knowledge, only two cases of internal carotid artery stroke without dissection or thrombosis are reported. In conclusion, although vascular complications are rare after anterior cervical spine procedure, internal carotid artery dissection can occur. Suspected risk factors are prolonged retraction of the carotid artery and neck extension.

Recurrent paraganglioma of occipito-temporal bone masquerading as temporal bone malignancy

A 33-year-old male patient presented with left facial nerve palsy, left earache along with left ear bloody discharge for last 4 months. He also had left vocal cord paralysis and impairment of hearing on left side. Contrast enhanced computed tomography (CECT) of temporal bone revealed enhancing mass present in left middle ear and mastoid and also involving left temporal and occipital bone causing destruction of bone, mimicking as temporal bone malignancy. Complete excision of tumor was done and biopsy came out to be paraganglioma. Patient had been operated previously for similar lesion 8 years ago. Paraganglioma with such extensive involvement of bone is not reported in literature and hence we describe this case to distinguish it from temporal bone malignancy. The tumor was not functional clinically as well as biochemically. DOI: http://dx.doi.org/10.3329/bjo.v19i1.12150 Bangladesh J Otorhinolaryngol 2013; 19(1): 58-64

Multimodal therapy including electroacupuncture for the treatment of facial nerve paralysis in a horse

Summary This Case Report describes a 5-year-old Standardbred gelding that was referred to the Equine Hospital of ONIRIS Veterinary School of Nantes, France for a surgical procedure under general anaesthesia. Anaesthesia was induced and maintained intravenously and the horse was placed in left lateral recumbency with a padded halter. On post operative Day 1, a post anaesthetic distal facial nerve branch paresis was diagnosed based on clinical signs. The horse was discharged on post operative Day 2 with medical treatment based on anti-inflammatory drug administration locally and systemically. The horse was re-examined 2 weeks after the surgery; the left partial facial paralysis was still present and associated with amyotrophy of the muscles supplied by the buccal branches of the facial nerve. In accordance with the owner, the horse was hospitalised to start an electrostimulation treatment. The horse was treated every day for the first 4 days, then every 2 or 3 days during the following 3 weeks, for a total of 11 sessions. At the end of the second week of treatment, the horse was able to normally prehend the food and atrophy seemed reduced. The horse was discharged from hospitalisation at the end of the third week of treatment with specific recommendations. One month after discharge from the hospital just a slight asymmetry could be noticed at rest. Six months later, the training season began and the horse was able to perform. Facial paralysis due to nerve compression is a well-known complication of anaesthesia. Gradual recovery of function over the weeks of treatment suggests that electroacupuncture may promote recovery and may hasten time of recovery.

Facial onset sensory motor neuronopathy: not always a slowly progressive disorder

Facial onset sensory motor neuronopathy (FOSMN) is a rare disorder characterized by sensory deficits in the trigeminal territory associated with weakness and wasting of facial muscles [1]. Symptoms usually spread to neck and upper limb (UL) muscles. Usually, the disease duration is slowly progressive [1, 2]. In past reports, temporary response to intravenous immunoglobulin (IVIG) or plasmapheresis (PE) in some patients suggested an inflammatory pathogenesis [2, 3]. More recently, pathologic studies indicated a neurodegenerative mechanism [4]. We describe a rapidly progressive case of FOSMN mimicking amyotrophic lateral sclerosis (ALS). A 70-year-old man presented to our hospital with left UL weakness. He reported a 1-month history of paraesthesia and numbness in left side of face with loss of taste. Two weeks later, numbness involved scalp and neck. At the admission, neurological examination revealed moderate wasting of temporal and masseter muscles, especially the left ones. Fasciculations were present in facial and proximal limb muscles. He had also moderate weakness of neck flexors and trunk muscles, and slight weakness of left arm abductors and flexors. Pinprick and temperature sensation were reduced in the left trigeminal nerve territory. His general laboratory workup including serum lipoproteins, hormones and autoantibodies was unrevealing. Genetic testing for Kennedy’s disease was negative. Cerebrospinal fluid (CSF) analysis revealed 95 mg/dL protein with no oligoclonal bands. Nerve conduction studies (NCS) were normal, needle electromyography (EMG) revealed fibrillations in the left trapezius muscle and denervation-reinnervation changes in the muscles of the upper and lower limbs. Blink reflex showed delayed responses bilaterally. Motor evoked potentials showed an increase of central conduction time. MRI of the brain and spinal cord appeared normal with no evidence of syrinx or malignant roots infiltration. Because of the CSF protein increase, IVIG (2 g/kg in 5 days) was administered. Few weeks later, the patient experienced a subjective improvement in left UL muscle strength, however his overall condition at neurological examination remained unchanged. Two months after disease onset, facial pain increased, becoming continuous and stabbing. Left facial nerve palsy with severe weakness of neck flexors and moderate involvement of proximal and distal left UL muscles was evident. After 9 months the patient’s clinical condition continued to worsen, despite a five PE protocol. Common analgesics, pregabalin, amitriptyline, carbamazepine, tapentadol and tramadol were used in order to treat pain, with poor results. Weakness spread up to the territory of both facial nerves E. Barca (&) M. Russo A. Mazzeo C. Terranova A. Toscano P. Girlanda Department of Neurosciences, University of Messina, Messina, Italy e-mail: emanuelebarca@hotmail.com

Alternating Progression of Pontine Infarction: A Case Report

We report a patient with rapid progression of crossed pontine infarction. A 59-year-old man noticed occipital headache and dizziness suddenly. Neurological examination showed medial longitudinal fasciculus syndrome on the left side. Brain magnetic resonance imaging (MRI) revealed acute isolated lesion in the left lower midbrain tegmentum. Four hours later, he developed coma, ataxic respiration and quadriparesis with left peripheral facial nerve palsy. MRI disclosed extensive midbrain lesion and alternating lesions in the left upper and the right middle pons . T1-hyperintense lesions existed at the periphery of the basilar artery (BA). Brain magnetic resonance angiography disclosed tapered occlusion at the mid-pontine level of the BA. Arterial walls were irregular in the left vertebral artery and BA. Alternating branch atheromatous occlusion due to BA dissection could contribute to the pathogenesis of crossed pontine infarction. doi: http://dx.doi.org/10.4021/jnr181w

Infantile inflammatory pseudotumor of the facial nerve as a complication of epidermal nevus syndrome with cholesteatoma

The first reported case of facial paralysis due to an inflammatory pseudotumor (IPT) of the facial nerve as a complication of epidermal nevus syndrome (ENS) is herein presented. A 10-month-old female patient was diagnosed with ENS at 3 months of age. She was referred to us because of moderate left facial paralysis. Epidermal nevi of her left auricle extended deep into the external ear canal. Otoscopy revealed polypous nevi and cholesteatoma debris filling the left ear. Computed tomography showed a soft mass filling the ear canal, including the middle ear, and an enormously enlarged facial nerve. Surgical exploration revealed numerous polypous nevi, external ear cholesteatoma, and tumorous swelling of the facial nerve. The middle ear ossicles were completely lost. The facial paralysis was improved after decompression surgery, but recurred 5 months later. A second operation was conducted 10 months after the first. During this operation, facial nerve decompression was completed from the geniculate ganglion to near the stylomastoid foramen. Histological diagnosis of the facial nerve tumor was IPT probably caused by chronic external ear inflammation induced by epidermal nevi. The facial paralysis gradually improved to House-Blackmann grade III 5 years after the second operation.

Avellis syndrome as presenting manifestation of ulcerative colitis

We described a 41-year-old woman presenting with subacute onset of left hemihypesthesia, left facial palsy, dysphagia and dysgeusia. A cranial T2-weighted magnetic resonance imaging revealed bilateral inhomogeneous medullary hyperintensities. The clinical manifestations conformed to Avellis syndrome, and were linked to the diagnosis of ulcerative colitis which was proved by serological findings and pathological evidence on rectosigmoid mucosa. She recovered favorably under conservative medical treatment with complete remission over one month of follow-up. Brainstem syndromes are rarely associated with neurological complications of ulcerative colitis and can be the presenting manifestation beyond gastrointestinal symptoms.

帯状疱疹ウイルス再活性化による脳梗塞および脳動脈瘤を発症した後天性免疫不全症候群（AIDS）の1例

A 35-years-old right-handed man admitted to our hospital with a worsening of dysarthria, left facial palsy and left hemiparesis for 2 days. Acquired immunodeficiency syndrome (AIDS) was diagnosed when he was 28 years old. At that time, he also was treated for syphilis. After highly active antiretroviral treatment (HAART) was introduced at the age of 35 years old, serum level of human immunodeficiency virus (HIV) was not detected, but the number of CD4+ T cells was still less than 200/μl. He had no risk factors of atherosclerosis including hypertension, diabetes and hyperlipidemia. He had neither coagulation abnormality nor autoimmune disease. Magnetic resonance imaging (MRI) showed acute ischemic infarction spreading from the right corona radiate to the right internal capsule without contrast enhancement. Stenosis and occlusion of intracranial arteries were not detected by MR angiography. Although argatroban and edaravone were administered, his neurological deficits were worsened to be difficult to walk independently. Cerebrospinal fluid (CSF) examination showed a mild mononuclear pleocytosis (16/μl). Oligoclonal band was positive. The titer of anti-varicella zoster virus (VZV) IgG antibodies was increased, that indicated VZV reactivation in the central nervous system (CNS), although VZV DNA PCR was not detected. Therefore, acyclovir (750 mg/day for 2 weeks) and valaciclovir (3,000 mg/day for 1 month) were administered in addition to stroke therapy. He recovered to be able to walk independently 2 month after the admission.Angiography uncovered a saccular aneurysm of 3 mm at the end of branch artery of right anterior cerebral artery, Heubner artery, 28 days after the admission. We speculated that VZV vasculopathy caused by VZV reactivation in CNS was involved in the pathomechanism of cerebral infarction rather than HIV vasculopathy in the case.

Alternating Progression of Pontine Infarction: A Case Report

We report a patient with rapid progression of crossed pontine infarction. A 59-year-old man noticed occipital headache and dizziness suddenly. Neurological examination showed medial longitudinal fasciculus syndrome on the left side. Brain magnetic resonance imaging (MRI) revealed acute isolated lesion in the left lower midbrain tegmentum. Four hours later, he developed coma, ataxic respiration and quadriparesis with left peripheral facial nerve palsy. MRI disclosed extensive midbrain lesion and alternating lesions in the left upper and the right middle pons . T1-hyperintense lesions existed at the periphery of the basilar artery (BA). Brain magnetic resonance angiography disclosed tapered occlusion at the mid-pontine level of the BA. Arterial walls were irregular in the left vertebral artery and BA. Alternating branch atheromatous occlusion due to BA dissection could contribute to the pathogenesis of crossed pontine infarction. J Neurol Res. 2013;3(1):42-45 doi: https://doi.org/10.4021/jnr181w