Lower Motor Neuron Facial Nerve Research Articles

An Unusual Presentation of Lyme Neuroborreliosis

Back pain is a common symptom among patients presenting to the acute medical unit. We describe the case of a 55-year-old man with a brief history of fatigue and severe back pain, unresponsive to escalating doses of opiate analgesia. Blood tests and imaging studies were unremarkable and a functional diagnosis was considered. Several weeks into his admission he developed a lower motor neurone facial nerve palsy. He was treated with antibiotics for an incidental finding of a hospital-acquired pneumonia on imaging, which remarkably led to the resolution of his facial palsy and allowed a dramatic reduction in analgesia. This triggered further investigations; identifying Lyme neuroborreliosis as the cause of his symptoms.

Melkersson–Rosenthal syndrome with involvement of masticatory muscles

Melkersson–Rosenthal syndrome (MRS) is a rare syndrome of nknown aetiology characterised by a triad of relapsing orofacial wellings, recurrent lower motor neuron facial nerve palsy and fisured tongue [1–3]. Diagnosis is often difficult as incomplete forms re more common. Other clinical manifestations and associated disrders reported have included intraoral and ocular lesions, other ranial nerve palsies, migraine or autoimmune diseases [1–4]. In ome cases, the association between these symptoms and MRS emains uncertain and magnetic resonance imaging (MRI) is often a seful tool in identifying soft tissue and cranial nerve inflammation 3,5]. We report a patient with MRS who presented with recurrent rofacial swelling, bilateral facial diplegia and jaw muscle weakess. MRI confirmed inflammation of the masticatory muscles and he right trigeminal nerve. To the best of our knowledge, these linical findings have not been previously described.

Optimising treatment of Bell’s Palsy in primary care: the need for early appropriate referral

Bell’s palsy remains the most common cause of lower motor neurone facial nerve paralysis. While 71% experience complete spontaneous resolution, including 61% who demonstrate a complete palsy and 94% who demonstrate a partial palsy, the remaining 29% exhibit lifelong residual hemifacial weakness.1,2 In 55% of these cases, the deficit is moderate to severe. In addition to stigmatising facial asymmetry, other distressing and socially embarrassing sequelae include: facial spasms and mass-movement contractions (synkinesis); loss of oral competence; facial pain and paraesthesia; nocturnal corneal exposure; dry mouth and eyes caused by loss of parasympathetic innervation to the submandibular/sublingual salivary glands and lacrimal glands respectively; and intolerance to loud noise caused by involvement of the nerve branch to stapedius, resulting in loss of acoustic dampening. Unsurprisingly, anxiety and depression are common.3 Therapeutic targets for acute Bell’s palsy seek to reach these 29%, accepting that prognostic indicators of an incomplete or minimal recovery may be of some value but require further validation.4 As GPs are likely to see, on average, one acute case every 2 years, it is highly improbable that they will have sufficient expertise to know what to do in the event that acute medical management fails. Worse still, referral to a facial reanimation service is critically time dependent, with the reconstructive options dwindling as the months progress.5 This article explores this referral pathway, making a case for early referral in every patient failing to demonstrate evidence of resolution by around 6 weeks. Bell’s palsy is thought to occur as a …

Physiological utility of ultrasound biomicroscopy in the lacrimal drainage system

ObjectiveTo evaluate lacrimal sac (LS) pump failure in patients with lower motor neuron facial nerve palsy (FNP) using ultrasound biomicroscopy (UBM).MethodsThis was a prospective observational case series. Patients with unilateral...

16 Syndrome in a Patient With Multiple Sclerosis

We read with interest the report of Connors et al (1) of a case of 16 syndrome with complete horizontal gaze paralysis and facial diplegia caused by a pontine hemorrhage. We describe a patient with multiple sclerosis (MS) who experienced an evolving eye movement disorder, which included internuclear ophthalmoplegia, one-and-a-half syndrome, eight-and-a-half syndrome, fifteen-and-a-half syndrome, and finally 16 syndrome. A 44-year-old man with a history of hypertension, heavy smoking, and a positive family history of cardiovascular disease complained of double vision upon awakening. Neurological examination revealed bilateral internuclear ophthalmoplegia (INO), which was attributed to a brainstem infarction given the sudden onset and patient’s vascular risk factors. Magnetic resonance imaging (MRI) of the brain and the intracranial vessels revealed several periventricular white matter lesions but no brainstem abnormality. Three days later, the patient developed drooping of the right corner of his mouth and complained of drooling. Examination revealed a right lower motor neuron facial nerve paresis in addition to bilateral INO. Repeat MRI revealed a nonenhancing lesion in the midline of the dorsal pons (Fig. 1). Two days later, he developed a complete right conjugate horizontal gaze palsy which, coupled with his left INO, produced a one-and-a-half syndrome. Concurrently, he also experienced bilateral facial paresis.FIG. 1: Axial fluid-attenuated inversion recovery (A) and sagittal T2 (B) MRI show an area of high signal (arrows) in the dorsal pons ventral to the fourth ventricle.Evaluation for stroke including extensive hematological tests, Holter cardiac monitoring, and transesophageal echocardiography was normal. Cerebrospinal fluid analysis for IgG, oligoclonal bands, and aquaporin-4 antibodies as well as visual evoked responses were normal. MRI of the cervical spinal cord revealed no lesions. On the 11th day of hospitalization, the patient developed bilateral horizontal gaze palsies with worsening of his facial diplegia. His clinical course in combination with the periventricular white matter lesions was highly suggestive of demyelinating disease. Treatment with methylprednisolone was begun, and 3 weeks later, he had recovered completely. Several follow-up MRIs were performed. The most recent MRI, 1.5 years after the onset of symptoms, revealed an increase in number and extent of the white matter hyperintensities (Fig. 2). Glatiramer acetate therapy was initiated.FIG. 2: Axial fluid-attenuated inversion recovery (A) and sagittal T2 (B) scans reveal several areas of high signal intensity in the periventricular region and corpus callosum.On occasion, a one-and-a-half syndrome can be accompanied by a facial paresis if the fascicle or nucleus of the seventh cranial nerve in the lower part of the dorsal pontine tegmentum is also affected. Eggenberger (2) designated this as eight-and-a-half (1.5 + 7) syndrome. As mentioned by Connors et al (1), variations of this syndrome caused by pathology of the dorsal pontine tegmentum have since been described including a combination of a one-and-a-half syndrome and a bilateral peripheral facial paresis which Bae and Song (3) designated fifteen-and-a-half (1.5 + 7 + 7) syndrome. Only 3 cases of isolated eight-and-a-half syndrome caused by MS have been described in the literature (4,5). In one of these cases (4), the eight-and-a-half syndrome was, as in our patient, the initial symptom of MS. A 16 syndrome caused by MS has not been reported previously.

Congenital cholesteatoma of petrous apex: Rare case report: Diagnostic and management challenge

A rare case of congenital cholesteatoma of petrous apex with facial nerve palsy and its successful management is reported. 49 year old female presented with progressive vertigo since 2 years. Patient developed tinnitus and hearing loss in the right ear since 7 months and right sided complete facial asymmetry since 6 months. She had normal right tympanic membrane and complete right lower motor neuron facial nerve palsy. She also had profound sensorineural hearing loss with positive Cerebellar signs. Magnetic resonance imaging and High resolution computed tomography with contrast temporal bone showed extensive bony destruction and petrous apex lesion. Facial nerve and vestibular cochlear nerve was compressed by abnormal soft-tissue present in the internal auditory meatus. Transmastoid translabyrinthine exploration was carried out for petrous apex lesion. Intra-operative extensive bony erosion was noted in the temporal bone. Erosion was extending upto Internal Acoustic Meatus compressing VII and VIII nerve bundle. Post-operatively patient was relieved of vertigo and tinnitus. Though hearing didn't improve, but there was an improvement in facial palsy. Congenital petrous apex cholesteatoma is very rare case. With no specific radiological signs congenital cholesteatoma is difficult to diagnose pre-operatively. It was a challenge to treat surgically such a rare case with extensive neurosurgical presentation without any neurological deficit. Patient showed improvement official nerve after the 1΍ year of surgery.

RECURRENT BILATERAL BELL’S PALSY- A RARE CASE REPORT AND REVIEW OF LITERATURE A CASE REPORT.

Bells palsy is a benign lower motor neuron facial nerve disorder. Recurrent unilateral Bells palsy is found in about 7% of the facial palsy cases . Alternating bilateral recurrent Bells palsy is relatively uncommon. A review of recent medical literature revealed very few case reports of bilateral recurrent Bells palsy, with none found in Asian neurology medical literature. We report a case of recurrent alternating bilateral Bells palsy ( 3 episodes) in a male patient aged 34 years , was treated conservatively and recovered completely. He is symptom free on follow up till date. We present this case because of its rarity.

Pancreatic adenocarcinoma presenting with sudden onset bilateral deafness secondary to metastatic leptomeningeal infiltration

Deafness is a very common problem in older persons. We present a case of metastatic adenocarcinoma of the pancreas with deafness being the patient's only reason for seeking medical attention. The patient had bilateral vestibulocochlear nerve palsies with associated lower motor neurone facial nerve palsies and a bulbar palsy. Magnetic resonance imaging of his brain was unremarkable. It was only on post-mortem histology that tumour infiltrating the leptomeninges was demonstrated. Leptomeningeal metastases are rarely associated with adenocarcinoma of the pancreas. A review of the literature reveals only two other case reports of mestatic pancreatic carcinoma presenting with deafness but both had demonstrable temporal bone lesions on MRI as opposed to the meninges.

Full recovery of a 13-year-old boy with pediatric Ramsay Hunt syndrome using a shorter course of aciclovir and steroid at lower doses: a case report

IntroductionReports on children with Ramsay Hunt syndrome are limited in the literature, resulting in uncertainty regarding the clinical manifestations and outcome of this syndrome. Treatment for Ramsay Hunt syndrome is usually with antivirals, although there is no evidence for beneficial effect on the outcome of Ramsay Hunt syndrome in adults (insufficient data on children exists). Here, we report a case of Ramsay Hunt syndrome occurring in a child who inadvertently received a lower dose of aciclovir and steroid administered for shorter than is usual. Our patient made a full recovery.Case presentationA 13-year-old African boy presented to our out-patients department with an inability to move the right side of his face for one week. He had previously been seen by the doctor on call, who prescribed aciclovir 200 mg three times per day and prednisone 20 mg once daily, both orally for five days, with a working diagnosis of Bell's palsy. After commencement of aciclovir-prednisone, while at home, our patient had headache, malaise, altered taste, vomiting after feeds, a ringing sound in his right ear as well as earache and ear itchiness. Additionally, he developed numerous fluid-filled pimples on his right ear. On presentation, a physical examination revealed a right-sided lower motor neuron facial nerve palsy and a healing rash on the right pinna. On direct questioning, our patient admitted having had chicken pox about three months previously. Based on the history and physical examination, Ramsay Hunt syndrome was diagnosed. Our patient was lost to follow-up until 11 months after the onset of illness; at this time, his facial nerve function was normal.ConclusionsThis case report documents the clinical manifestations and outcome of pediatric Ramsay Hunt syndrome; a condition with few case reports in the literature. In addition, our patient made a full recovery despite inadvertently receiving a lower dose of aciclovir and steroid administered for shorter than is usual.

“Sixteen and a half”: a novel pontine neuro-ophthalmological syndrome

Two neuro-ophthalmological syndromes due to paramedian pontine infarction have previously been described. The ‘‘one and a half’’ syndrome was first reported and named by Miller Fisher [1], and consists of horizontal gaze palsy combined with an ipsilateral inter-nuclear ophthalmoplegia (INO) resulting in loss of all horizontal eye movements except abduction of the contralateral eye. The causative lesion is usually within the ipsilateral pontine tegmentum and is due to involvement of the abducens nucleus plus the medial longitudinal fasciculus (MLF), or alternatively to involvement of the MLF plus the paramedian pontine reticular formation (PPRF). These structures lie in close proximity to the nucleus and intra-axial fasiculus of the facial nerve. Consequently, ipsilateral fascicular lower motor neurone facial nerve palsy may accompany the ‘‘one-and-a-half’’ syndrome. This situation was named the ‘‘eight and a half syndrome’’ by Eggenberger [2], who reported 3 cases of this syndrome that had occured secondary to ischaemic stroke. In continuation of this concept, we here describe the ‘‘sixteen and a half syndrome’’, which is the ‘‘one and a half’’ syndrome with an additional 7th and 8th cranial nerve (vestibulo-cochlear nerve) palsy. A 78-year-old right-handed man presented with sudden onset of incomplete right upper limb paresis, horizontal diplopia and ataxia. This was shortly followed by complete right lower limb paresis. There was associated nausea and vomiting. Examination revealed a left-sided lower motor neurone facial nerve palsy and dysarthria with loss of conjugate gaze to the left and loss of adduction of the left eye. Abduction of the right eye was accompanied by horizontal nystagmus. Convergence was spared. The patient also complained of new-onset left-sided hearing loss. The patient and his family were certain that his hearing before this event had been normal. Magnetic resonance imaging (MRI) with diffusion-weighted sequences revealed an area of restricted diffusion consistent with an acute infarct. The lesion extended beyond and lateral to the paramedian pontine territory supplied by the anteromedial group of pontine perforating arteries, and dorsally to the fourth ventricle and the region of the facial colliculus (Fig. 1a, b). Pure tone audiometry showed no detectable hearing in the left ear. Brainstem auditory evoked potential testing showed no reproducible wave I, wave III or wave V after left ear stimulation. Waves I, III and V from right ear stimulation were of low amplitude with normal absolute and interwave latencies. Eight months later, the Weber test lateralized to the right ear, and the Rinne test revealed absent air-conducted and bone-conducted sound perception in the left ear. Our patient had an ‘‘eight and a half’’ syndrome plus additional ipsilateral hearing loss. We name this clinical entity the ‘sixteen and a half syndrome’. Hearing loss has not previously been described in association with either ‘‘one and a half’’ or ‘‘eight and a half’’ syndrome. A clinical series of 20 cases of ‘‘one and a half’’ syndrome noted G. Cummins R. Dunne K. O’Rourke (&) T. Lynch Dublin Neurological Institute, Mater Misericordiae University Hospital, 57 Eccles St., Dublin 7, Ireland e-mail: killian.orourke@gmail.com

Necrotising otitis externa: an unusual cause of cranial nerve palsy in a diabetic haemodialysis patient

We present an unusual case of necrotising otitis externa (NOE) causing a lower motor neurone facial nerve palsy in a patient with diabetes mellitus and receiving maintenance haemodialysis for end-stage renal disease (ESRD). Pseudomonas aeruginosa is the most common pathogen isolated in NOE, although our case involved the non-typical pathogens Aspergillus flavus and Proteus mirabilis. We discuss the need for diagnostic rigour and the importance of considering atypical infective pathology in patients with ESRD or diabetes mellitus. We review NOE with reference to causative agents, imaging strategies, prognostic indicators and treatment.

Acquired facial palsy with hypertension secondary to Guillain–Barre syndrome

Most cases of facial nerve paresis are idiopathic (Bell's palsy). However, rare and potentially dangerous conditions may present in this manner. We report 2 children presenting with unilateral lower motor neuron facial nerve palsy and hypertension. A diagnosis of Guillain-Barre syndrome was made in both; literature linking facial nerve palsy in childhood with hypertension and Guillain-Barre syndrome is reviewed.

Bell’s palsy in Mosul

Objective: To study the incidence, sex, age, and seasonal distribution of Bell’s palsy in Mosul.Methods: A prospective study of patients with Bell’s palsy from outpatient and private neurological clinic and Neurophysiological Unit in Ibn Sena Teaching Hospital in Mosul conducted between September 2001 to August 2003. The patient's age, sex and time of occurrence of Bell’s palsy were recorded.Result: the total number of the patients was 469, male patients were 207 and females were 262. The higher number of cases was recorded in the cold months, adult affected more than other age groups.Conclusion: Bell’s palsy is the commonest cause of lower motor neuron facial nerve palsy; herpes simplex has been claimed as a cause of the condition.Keywords: Bell’s palsy; facial nerve; facial nerve paralysis.

Facial Nerve Palsy Complicating Kawasaki Disease

The diagnosis of Kawasaki disease, the most common cause of pediatric acquired heart disease, is difficult and often delayed for children whose age falls outside the typical range of 6 months to 5 years, especially in those with incomplete Kawasaki disease and atypical features. Delayed diagnosis is associated with an increased incidence of coronary artery pathology. Here we describe 2 cases of lower motor neuron facial nerve palsy complicating Kawasaki disease. In both cases the diagnosis of Kawasaki disease was not made acutely, and both patients developed extensive coronary artery lesions. These cases highlight the importance of considering Kawasaki disease in children with unexplained prolonged fever at any age, particularly those without full diagnostic criteria and with unusual features.

A Rare Association of Deaf Mutism, Syndactyly and Squamous cell carcinoma of the Temporal bone

Malignant tumours of the temporal bone are rare, the majority being squamous cell carcinoma. We here report a rare syndromic complex of squamous cell carcinoma of the temporal bone, deaf-mutism & syndactyle in a 12 year old male child, presented in Department of Otorhinolaryngology, Hamidia Hospital, Bhopal, with one month history of mass in left external auditory canal & lower motor neuron facial nerve palsy on a background of left chronic suppurative otitis media since childhood.

Reliability of the “Sydney,” “Sunnybrook,” and “House Brackmann” facial grading systems to assess voluntary movement and synkinesis after facial nerve paralysis

To investigate the extent of within-system reliability and between-system correlation for the "Sydney" and "Sunnybrook" systems of grading facial nerve paralysis, and to examine the interobserver reliability and agreement of the "House Brackmann" grading system. A fixed-effects reliability study in which 6 otolaryngologists viewed videotapes of patients with facial nerve paralysis. University and medical Centers. Patients with unilateral lower motor neurone facial nerve dysfunction greater than 1 year after onset, none of whom had undergone surgical reanimation procedures. Intervention Twenty-one patients with facial nerve paralysis were videotaped while they performed a protocol of facial movements. Six otolaryngologists viewed the videotapes and scored them with the Sydney and Sunnybrook systems, and then gave a House Brackmann grade. The 3 systems of grading facial nerve paralysis were evaluated and compared with the use of intraclass correlation coefficients, Pearson's weighted kappa, and percentage exact agreement values. The Sydney and the Sunnybrook systems had good intrasystem reliability and high intersystem association for the assessment of voluntary movement. Grading of synkinesis was found to have low reliability both within and between systems. The House Brackmann system had substantial reliability as shown by weighted kappa but had a percentage exact agreement of 44%. For clinical grading of voluntary movement, there is good correlation between ratings given on the Sydney and Sunnybrook systems, and within each system there is good reliability. The assessment of synkinesis was far less reliable within, and less related between, systems. Although the reliability of the House Brackmann system was found to be high, examination of individual grades revealed some wide variation between trained observers.

One-and-a-Half Syndrome With Facial Diplegia: The 15 1/2 Syndrome?

We recently examined a 67-year-old man who demonstrated findings consistent with a unilateral one-and-a-half syndrome and a bilateral lower motor neuron facial palsy (1 1/2 + 7 + 7 = 15 1/2). The patient had the sudden onset of dizziness, nausea, and blurring of vision. He smoked heavily and had a history of diabetes mellitus. Examination disclosed a complete right horizontal conjugate gaze palsy and a right adduction deficit. Oculocephalic stimulation did not improve the defective eye movements. Convergence was relatively spared. Vertical ocular movements and alignment were normal and ptosis was absent. The pupils were equal in size and normally reactive to light and a near stimulus. The remainder of the neurologic examination was normal. One day later, a bilateral lower motor neuron facial palsy abruptly developed, including bilateral flattening of the nasolabial fold and absent forehead wrinkling. Brain computed tomography was normal. FLAIR and T2-weighted brain magnetic resonance imaging disclosed high signal in the lower pontine tegmentum, findings considered typical of stroke (Fig. 1). A facial nerve conduction and blink reflex study confirmed a bilateral lower motor neuron facial palsy.FIG. 1: Axial FLAIR (A), axial T2-weighted (B), sagittal T2- weighted (C), and diffusion-weighted (D) magnetic resonance images show increased signal (arrow) consistent with ischemic stroke in the paramedian dorsal pontine tegmentum bilaterally.When last examined 2 months after the onset of symptoms, the patient showed only a minimal deficit in right horizontal gaze. Horizontal gaze palsy in one-and-a-half syndrome may result from lesions in the abducens nucleus, in the abducens nerve and the medial longitudinal fasciculus, or in the pontine paramedian reticular formation (PPRF) (1,2). Isolated PPRF lesions are associated with retained vestibulo-ocular movement. If the vestibulo-ocular movement is abolished, the lesion lies rostral or caudal to the PPRF (5,6). Because our patient showed limitation of oculocephalic abduction toward the right side, we presume that the lesion lies in the abducens nucleus or fascicle rather than in the PPRF (2-7). More rapid resolution of ipsilateral adduction compared with abduction favors involvement of the abducens fascicle rather than the nucleus. An alternative hypothesis is that these findings reflect the relative vulnerability of abducens motor neurons innervating the lateral rectus (2). The one-and-a-half syndrome is rarely an isolated finding (7), being usually associated with cranial nerve palsies (facial in 75%), hemiplegia (30%), or hemihypesthesia (35%) (3,4). A lower motor neuron facial nerve palsy is the most commonly associated finding, resulting from involvement of the genu of the intraaxial fasciculus of the facial nerve in the pontine tegmentum (2,4). Although the combination of a one-a-a-half syndrome and an ipsilateral seventh nerve palsy has been described ("eight-and-a-half syndrome" (2)), we are unaware of a previous description of a one-and-a-half syndrome with bilateral seventh nerve palsies, as our patient had. We attribute these findings to a bilateral tegmental pontine lesion involving the right abducens nucleus or fasciculus, bilateral or right medial longitudinal fasciculus, and bilateral intraaxial fasciculi of the facial nerve (Fig. 2). The histopathologic studies of Fisher (8) showing terminal bifurcation of a single paramedian artery to supply the dorsal pontine tegmentum bilaterally could explain why occlusion of a single vessel would produce these findings.FIG. 2: Schematic axial section through the caudal pons. The shaded area represents the site of the lesion that involves the right abducens nucleus, both medial longitudinal fasciculi, and both seventh (facial) nerve fasciculi.Jong Seok Bae, MD Hong Ki Song, MD Department of Neurology; Seoul Medical Center and College of Medicine, Hallym University; Seoul, Korea; E-mail: [email protected]

Deafness in a Young Musician: A Case of Missed Diagnosis

Hearing loss in a young adult can be devastating and prompt diagnosis and treatment of the cause are vital. This case report is of a young musician presenting to the ENT surgeons with deafness and a lower motor neurone facial nerve palsy which was given a presumptive diagnosis of infective pathology but subsequent investigations indicated this was an uncommon presentation of Wegener's Granulomatosis. Treatment involved systemic Cyclophosphamide followed by steroids and Azathioprine. Two years after commencing therapy the disease remains under control but the patient is left with bilateral hearing aids and a grade 3 facial nerve palsy. Diagnosis and treatment of this multi-system disease are discussed.

SKULL BASE MENINGIOMA IN CHILDHOOD

Meningiomas are rare in childhood and they constitute 1.5% of intracranial meningiomas. We report a case of a left middle cranial fossa meningioma in a 11‐year‐old boy who presented with left‐sided facial weakness and deafness. Neurological examination showed left lower motor neuron facial nerve palsy with sensori‐neural deafness of his left ear.Computed tomography demonstrated a contrast enhancing extra‐axial tumour in the left middle cranial fossa with calcification. Magnetic resonance imaging confirmed the presence of an extra‐axial tumour measuring 3 × 3.5 × 2.7 cm. The mass was isointense to gray matter on T1‐weighted images, with a markedly hypointense rim on T2‐weighted images. The lesion exhibited homogeneous enhancement with gadolinium. It eroded the petrous base, extending into the left internal auditory meatus and cerebello‐pontine cistern. The preoperative diagnosis was trigeminal schwannoma.Intraoperatively, a firm tumour was seen arising from the middle cranial fossa attached to the petrous temporal bone. Near‐total excision of tumour was achieved. The histological diagnosis was xanthomatous meningioma. The patient recovered uneventfully without additional neurological deficit. He underwent linac radiosurgery for the 1 cm tumour remnants in the internal acoustic meatus and the left cerebellopontine angle. Follow‐up MRI scans 14 months after radiosurgery showed shrinkage of the remaining tumour. At follow up 20 months after operation the child was well and had resumed his education.Conclusion: While surgery remains the main therapeutic modality, complete excision is not always possible in skull base meningiomas as it carries significant postoperative morbidity. Radiosurgery is a valuable complementary measure for local control in case of residual or recurrent tumour.

Non-communicating arachnoid cyst of the temporal bone presenting as facial nerve paralysis in an infant

Non-communicating arachnoid cyst of the lateral temporal bone is a rare conditon. We present a case of a non-communicating arachnoid cyst of the temporal bone in an infant who presented with a lower motor neuron facial nerve paralysis. The patient was treated by surgical excision of the cyst.