BELL’S PALSY: SUATU TINJAUAN PUSTAKA

Bell’s palsy merupakan kelainan saraf fasialis yang paling banyak dijumpai. Gejala klinis bell’s palsy yaitu adanya lesi saraf fasialis akut tipe lower motor neuron yang terjadi secara tiba-tiba dan cepat. Sekitar 80% pasien sembuh spontan. Etiologi dan patofisiologi masih diperdebatkan. Kehamilan memiliki resiko tiga kali lipat terjadi bell’s palsy. Penegakkan diagnosis berdasarkan klinis. Terapi yang direkomendasikan yaitu pemberian steroid oral. Artikel ini merupakan sebuah studi pustaka.Kata kunci: Bell’s palsy, etiologi, diagnosis, penatalaksanaan ABSTRACTBell's palsy is the most common facial nerve disorder. The clinical symptom is acute lower motor neuron type facial nerve lesion that occurs suddenly and rapidly. About 80% of patients recover spontaneously. The etiology and pathophysiology are still being debated. Pregnancy has a threefold risk of developing Bell's palsy. Diagnosis based on clinical. The recommended therapy is oral steroid administration. This article was a literature review.Keyword: Bell’s palsy, diagnosis, etiology, treatment

Efficacy of surgical repair for the functional restoration of injured facial nerve

Background Early surgical repair to restore nerve integrity has become the most commonly practiced method for managing facial nerve injury. However, the evidence for the efficacy of surgical repair for restoring the function of facial nerves remains deficient. This study evaluated the outcomes of surgical repair for facial nerve lesions. Methods This retrospective observational study recruited 28 patients with the diagnosis of facial nerve injury who consecutively underwent surgical repairs from September 2012 to May 2019. All related clinical data were retrospectively analyzed according to age, sex, location of the facial nerve lesion, size of the facial nerve defect, method of repair, facial electromyogram, and blink reflex. Facial function was then stratified with the House-Brackmann grading system pre-operation and 3, 9, 15, and 21 months after surgical repair. Results The 28 patients enrolled in this study included 17 male and 11 female patients with an average age of 34.3 ± 17.4 years. Three methods were applied for the repair of an injured facial nerve, including great auricular nerve transplantation in 15 patients, sural nerve grafting in 7 patients, and hypoglossal to facial nerve anastomosis in 6 patients. Facial nerve function was significantly improved at 21 months after surgery compared with pre-operative function (P = 0.008). Following surgical repair, a correlation was found between the amplitude of motor unit potential (MUP) and facial nerve function (r = -6.078, P = 0.02). Moreover, the extent of functional restoration of the facial nerve at 21 months after surgery depended on the location of the facial nerve lesion; lesions at either the horizontal or vertical segment showed significant improvement(P = 0.008 and 0.005), while no functional restoration was found for lesions at the labyrinthine segment (P = 0.26). Conclusions For surgical repair of facial nerve lesions, the sural nerve, great auricular nerve, and hypoglossal-facial nerve can be grafted effectively to store the function of a facial nerve, and MUP may provide an effective indicator for monitoring the recovery of the injured nerve.

The Importance of Physical Therapy in the Treatment of Unilateral Congenital Bell Paralysis - A Case Report

Peripheral paralysis of facial nerve in the newly-born can be congenital and developed. In clinical sense, paralysis of facial nerve is characterised by paralysis of mimic face muscles that are controlled by a facial nerve. A female newly-born, delivered by Caesarean section was clinically diagnosed weakness on the right side of the face. Thirteen days after the birth the newly-born was examined by a physiatrist for the first time due to the weakness of the right facial side. During the first year of life a severe congenital lesion of facial nerve was diagnosed. Rehabilitation treatments were administered during the first year of life, with partial clinical improvement. The seriousness of facial nerve lesion has a significant influence on the degree of recovery. It is very important to identify the type of lesion by using efficient technology, since it is the only way to provide early and adequate therapy.

ENTÉRATE DE CÓMO CAMBIA EL CEREBRO CUANDO SE LESIONA UN NERVIO

<p>Desde hace algunos años el grupo de investigación de Neurofisiología Comportamental de la Universidad Nacional de Colombia ha venido evaluando los cambios que ocurren en el sistema nervioso central luego de la lesión de un nervio periférico. Específicamente trabajamos con el modelo de lesión del nervio facial en roedores para evaluar las modificaciones funcionales y estructurales que ocurren en la corteza sensoriomotora primaria luego de la lesión. Al lesionarse el nervio facial, el cerebro entra en un programa de reorganización que incluye cambios electrofisiológicos en las neuronas de la corteza motora que comandan los movimientos faciales (M1). En este sentido, las células de la corteza motora cerebral se vuelven más excitables y modifican su respuesta ante estímulos sensoriales. La reorganización tras la lesión también incluye cambios morfológicos en M1: las células piramidales de la corteza motora retraen su árbol dendrítico y disminuye la densidad de sus espinas dendríticas. En asociación con estos cambios, las células de M1 disminuyen transitoriamente su inmunorreactividad para NeuN (marcador específico de núcleos neuronales) y aumentan la expresión de GAP43 (proteína de crecimiento axonal). Esto indica, posiblemente, un cambio metabólico celular en asociación con la búsqueda de nuevas dianas sinápticas. Finalmente, hallamos que la glía circundante en M1 (tanto astrocitos como microglía) se activa de manera muy temprana luego de lesiones del nervio facial. Esto podría indicar que el remodelamiento estructural y funcional hallado en las neuronas corticales es el resultado de la interacción entre la activación de la glía circundante y las células piramidales de M1 (aunque se necesitan muchos experimentos adicionales que así lo demuestren).</p><p> </p><p>Abstract</p><p>Our research group (Neurofisiología Comportamental, Universidad Nacional de Colombia) has evaluated changes in the central nervous system induced by peripheral nerve injuries. We have characterized facial nerve lesion-induced structural and functional changes in primary motor cortex pyramidal neurons (M1) in rodents. Following the lesion, M1 neurons modified their spontaneous basal firing frequency: they become more excitable. Moreover, we found changes in evoked-activity with somatosensory stimulation after facial nerve lesion. Morphologically, it was found that facial nerve lesion induced long-lasting changes in the dendritic morphology of M1 pyramidal neurons. Dendritic branching of the pyramidal cells underwent overall shrinkage and dendrites suffered transient spine pruning. Additionally, we evaluated the reorganization processes in the central nervous system by using both neuronal and glial markers. Decreased NeuN (neuronal nuclei antigen) immunoreactivity and increased GAP-43 (growth-associated protein 43) immunoreactivity were found M1 after facial nerve lesion. In addition, we also observed astrogliosis and microglial activation sourrounding M1 early after facial nerve injury. Taken together these findings suggest that facial nerve lesions induce widespread reorganization in M1 including neuronal shrinkage, axon sprouting as well as astrocytic and microglia activation. These results suggest that facial nerve injuries elicit active remodeling due to pyramidal neuron and glia interaction (although additional experiments that demonstrate it are needed)</p>

Layer 5 Pyramidal Neurons’ Dendritic Remodeling and Increased Microglial Density in Primary Motor Cortex in a Murine Model of Facial Paralysis

This work was aimed at characterizing structural changes in primary motor cortex layer 5 pyramidal neurons and their relationship with microglial density induced by facial nerve lesion using a murine facial paralysis model. Adult transgenic mice, expressing green fluorescent protein in microglia and yellow fluorescent protein in projecting neurons, were submitted to either unilateral section of the facial nerve or sham surgery. Injured animals were sacrificed either 1 or 3weeks after surgery. Two-photon excitation microscopy was then used for evaluating both layer 5 pyramidal neurons and microglia in vibrissal primary motor cortex (vM1). It was found that facial nerve lesion induced long-lasting changes in the dendritic morphology of vM1 layer 5 pyramidal neurons and in their surrounding microglia. Dendritic arborization of the pyramidal cells underwent overall shrinkage. Apical dendrites suffered transient shortening while basal dendrites displayed sustained shortening. Moreover, dendrites suffered transient spine pruning. Significantly higher microglial cell density was found surrounding vM1 layer 5 pyramidal neurons after facial nerve lesion with morphological bias towards the activated phenotype. These results suggest that facial nerve lesions elicit active dendrite remodeling due to pyramidal neuron and microglia interaction, which could be the pathophysiological underpinning of some neuropathic motor sequelae in humans.