Cases reported "Facial Paralysis"

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1/48. Facial canal decompression leads to recovery of combined facial nerve paresis and trigeminal sensory neuropathy: case report.

    BACKGROUND: Trigeminal sensory neuropathy is often associated with facial idiopathic nerve paralysis (Bell's palsy). Although a cranial nerve viral polyneuropathy has been proposed as the usual cause, in many instances the etiology remains unclear. This case report of recovery of both trigeminal and facial neuropathy after surgical decompression of the facial nerve suggests an anatomic link. methods: A case of a 39-year-old woman presenting with recurrent unilateral facial paralysis is summarized. Her fifth episode, which did not spontaneously recover, was associated with retroorbital and maxillary pain as well as sensory loss in the trigeminal distribution. RESULTS: A middle cranial fossa approach for decompression of the lateral internal auditory canal, labyrinthine segment of the facial nerve and the geniculate ganglion was performed. The patient's pain and numbness resolved immediately postoperatively, and the facial paralysis improved markedly. CONCLUSION: This result implicates a trigeminal-facial reflex as hypothesized by others. It suggests that decompression of the facial nerve can lead to improvement in motor and sensory function as well as relief of pain in some patients with combined trigeminal and facial nerve dysfunction.
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2/48. Congenital facial neuropathy in oculoauriculovertebral dysplasia-hemifacial microsomia (Goldenhar-Gorlin syndrome).

    Four patients with clinical features of Goldenhar-Gorlin syndrome who showed facial paralysis on clinical examination are presented. The fourth case died following surgery for cleft lip. autopsy revealed hypoplasia of the right facial nerve in its intracranial segment, with small right facial nucleus in the brain stem. Nosological aspects of the Goldenhar-Gorlin syndrome are discussed. Peripheral facial paralysis, as a part of this syndrome, is reviewed in the light of clinical and pathological findings and in its relationship to cardiac anomalies. It is suggested that Goldenhar-Gorlin syndrome is a part of a so-called cardiofacial syndrome.
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keywords = nucleus
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3/48. One and one-half syndrome with supranuclear facial weakness: magnetic resonance imaging localization.

    OBJECTIVE: To provide clinicoanatomical correlation for a small pontine tegmental ischemic stroke producing the one and one-half syndrome associated with supranuclear facial weakness. DESIGN: Case report. SETTING: Tertiary care center. PATIENT: A 70-year-old man developed left-sided facial weakness sparing the forehead, a left internuclear ophthalmoplegia, and a complete left horizontal gaze palsy immediately after percutaneous transluminal coronary angioplasty. magnetic resonance imaging demonstrated a small lesion in the left paramedian aspect of the dorsal pontine tegmentum. MAIN OUTCOME AND RESULTS: Electromyographic findings were consistent with supranuclear facial involvement. The patient had nearly complete recovery after 1 year. CONCLUSIONS: To our knowledge, this is the first report of supranuclear facial weakness in association with the one and one-half syndrome. The location of the lesion provides evidence of the existence of corticofugal fibers that extend to the facial nucleus in the dorsal paramedian pontine tegmentum.
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4/48. facial nerve neurinoma presenting as middle cranial fossa and cerebellopontine angle mass: a case report.

    facial nerve neurinomas are rare. The tumours arising from the geniculate ganglion may grow anteriorly and superiorly and present as a mass in the middle cranial fossa. Only a few cases of facial nerve neurinomas presenting as middle cranial fossa mass have so far been reported. These tumours present with either long standing or intermittent facial palsy along with cerebellopontine angle syndrome.
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5/48. multiple sclerosis with caudate lesions on MRI.

    A 31-year-old woman displayed sleepiness and impairment of recent memory. T2-weighted MRI revealed high signal intensity lesions in the bilateral basal ganglia, thalamus, and brainstem. Although remission was achieved with corticosteroid therapy, she again displayed memory dysfunction and emotional disturbance one year later, at which time MRI disclosed new lesions in the right caudate nucleus and left frontal white matter. Corticosteroid therapy lead to improvement, and she suffered no recurrence on maintenance steroid therapy. These findings suggest that caudate lesions do occur in multiple sclerosis, the manifestations of which can be abulia and memory dysfunction, as in the present case.
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keywords = nucleus
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6/48. Ramsay Hunt syndrome: pathophysiology of cochleovestibular symptoms.

    Ramsay Hunt's hypothesis that herpes zoster oticus results from reactivation of the varicella zoster virus (VZV) in the geniculate ganglion is supported by the detection of viral genome in archival temporal bones of normals and Ramsay Hunt patients by the polymerase chain reaction. Ramsay Hunt syndrome is characterized by the presence of cochleovestibular symptoms in association with facial paralysis. VZV has also been demonstrated in the spiral and/or vestibular ganglion. Two cases are reported in which cochleovestibular symptoms outweighed the facial nerve symptoms, presumably representing VZV reactivation in the spiral and/or vestibular ganglion. From these observations and the known dormancy of VZV in non-neuronal satellite cells, it is argued that the cochleovestibular symptoms in Ramsay Hunt syndrome may result from VZV transmission across the nerves inside the internal auditory canal and that prompt treatment with an antiviral-corticosteroid combination might be justified in the management of any acute non-hydropic cochleovestibular syndrome.
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7/48. Cranial polyneuritis and bell palsy.

    In view of the specific nature of the clinical and neurologic findings in bell palsy and other acute benign cranial neuritides, the neural component of cutaneous herpes simplex, the predilection of the herpesvirus for sensory nerves, and intrinsic behavior and immunologic interreactions of the herpesvirus within ganglion cells, it is suggested that (1) the entity that has been termed "idiopathic facial paralysis" be recognized as an acute benign cranial polyneuritis; and (2) other acute benign cranial neuritides be recognized as formes frustes of bell palsy.
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8/48. Chronic varicella-zoster virus ganglionitis--a possible cause of postherpetic neuralgia.

    Postherpetic neuralgia (PHN) is dermatomal distribution pain that persists for months to years after the resolution of herpes zoster rash. The cause of PHN is unknown. Herein, we report clinical, molecular virological, and immunological findings over an 11-year period in an immunocompetent elderly woman with PHN. Initially, blood mononuclear cells (MNCs) contained varicella-zoster virus (VZV) dna on two consecutive occasions. Random testing after treatment with famciclovir to relieve pain did not detect VZV dna. However, the patient was reluctant to continue famciclovir indefinitely and voluntarily stopped drug treatment five times. pain always recurred within 1 week, and blood MNCs contained many, but not all, regions of the VZV genome on all five occasions. Immunological analysis revealed increased cell-mediated immunity to VZV. Chronic VZV ganglionitis-induced PHN best explains the recurrence of VZV dna in MNCs whenever famciclovir was discontinued; the detection of only some regions of the viral genome in MNCs, compared to the detection of all regions of the VZV genome in latently infected ganglia; the increased cell-mediated immunity to VZV; and a gratifying clinical response to famciclovir. The presence of fragments of VZV dna in MNCs likely represents partial degradation of viral dna in MNCs that trafficked through ganglia during productive infection.
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9/48. blepharospasm hemifacial spasm and tremors possibly due to isolated caudate nucleus lesions.

    Isolated caudate nucleus lesions have only rarely been documented to cause focal extrapyramidal dysfunction. Two cases with possible infarcts in the head of left caudate nucleus presenting with contralateral tremors and blepharospasm with hemifacial spasm are reported. The possible mechanisms for such a presentation are discussed.
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ranking = 0.33624924425826
keywords = nucleus
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10/48. Automatic-voluntary dissociation: an unusual facial paresis in a patient with probable multiple sclerosis.

    A patient with multiple sclerosis is described who presented with a unilateral loss of voluntary function of his lower face muscles. However, in an emotional situation, there was strong involuntary innervation of these muscles: automatic-voluntary dissociation. The subcortical afferents to the facial motor nucleus are discussed. It is hypothesized that cortical disinhibition of midbrain nuclei underlies the accentuated involuntary innervation.
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keywords = nucleus
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