All of the nerve bundles are covered by the epineurium. Regeneration Is Incomplete, and axon regeneration may be inappropriate resulting in synkinesis. M There is an increase in calcitonin-related peptide expression, GAP43, and cytOskeletal proteins such as actin and tubulin.
Growth occurs at -1 mmfday; the fadal nerve should therefore be able to grow from the cerebellopontine angle to the periphery within 6 months. Favorable and unfavorable factors coindde with this regeneration: a:xons shrink, allowing new ones to grow around, and microglial cells proliferate, which can interfere with normal synaptic transmission. Sprouting axons maintain a responsiveness to trophic factors. Several neurotrophic factors are known to play a role in regeneration; for a more extensive review, the reader is referred to Tuszynski?
Regenerating a:xons travel through Bunger bands formed by Schwann cells that have lined the degenerating a:xons during wallerian degeneration: the Bunger bands serve as an endoneural tube. The basement membrane ofthe endoneurium helps to guide regeneration. Regenerating fibers have no known spedfidty during regeneration; however, the Schwann cell will ultimately myelinate them.
Nerve repair is therefore advocated as early as the injury occurs. Distal to the site of injury, nerve resorption with Schwann cell proliferation begins quickly and is very advanced by 48 hours.
This process is termed a:xolysis and myelinolysis, and occurs distal to the site of injury. Denervation at the muscle results in loss of muscle weight with a decrease in muscle fiber diameter. Early changes in the muscle occur at the cellular level within a week of denervation.
These cellular changes include increased mitochondria number, deoxyribonucleic add, satellite cells, and chromatin change.
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This represents the plastic state of denervated muscle. Over time, fibers disappear and are replaced by fat and connective tissue. The 2 Physiology of the Facial Nerve speed of contraction decreases, and spontaneous action potential known as fibrillations can be recorded. The number of motor end plates increase, and inhibitor substances decrease.
Prior to reinnervation, muscle viability is tested by volitional movement which if absent is tested by electromyography.
If electromyography shows no response, a muscle biopsy can be performed. The time at which muscle is no longer available to accept reinnervation is not well established. The literature includes case reports of reinnervation occurring after several years, but a "sooner the better" philosophy is advocated by the time course of the described degenerative and regenerative changes observed.
Muscle response can be elicited with voluntary contraction or it can be evoked with electrical signal. Electrophysiological testing provides both quantitative and qualitative measures of physiological degeneration and recovery following facial nerve injury.
These tests can be used to predict the degree of injury, the likelihood of recovery, and assist the surgeon in clinical decision making. A detailed discussion on the most commonly used tests is presented in Chapter 4. These tests include the following.
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Maximal Stimulation Test A maximal stimulation test uses electrical stimulation to compare muscle response between sides. Increasing current is used to rate facial movement in the 1 forehead and eyebrow; 2 periorbital area; 3 cheek, upper lip, and nasal ala; 4 lower lip; and 5 cervical and platysma area.
Testing is initiated 3 days after injury to account for wallerian degeneration. Electronystagmography Electronystagmography or evoked electromyography is an electrically evoked electromyelogram.
Electric current is applied to the facial nerve, and the latency and amplitude of the muscle response is recorded and compared with the contralateral normal side.
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Electromyography Electromyography measures voluntary muscle response. The motor unit response morphology provides further information. In addition to greutatea pierderii mișcării amplitude and latency of the muscle responses, denervation patterns fat burn burn ser as positive sharp waves or fibrillation can be recorded.
Reinnervation can be documented with polyphasic potentials.
The clinician can correlate this to known cellular responses to injury and expected recovery in the medical and surgical decision-making process. Nerve injuries that are grades I, II, and III are not amenable to nerve repair or graft Treatment is aimed at minimizing compression and intraneural pressure. Steroids and surgical decompression are routinely used, with the latter most often reserved for grade III injuries. Nimodipine, a calcium channel blocker, has been shown to accelerate facial nerve recovery in animal models.
Grade IV and V injuries result in partial or complete transection. Treatment is aimed at promoting neurotropism, the factors in nerve regeneration that influence the direction of regeneration, in addition to neurotrophic factors. Surgical repair with direct anastomosis or autologous neural interposition is the gold standard.
Neural conduits with neurotrophic factors have been employed and continue to be investigated with the goal of establishing a milieu similar josie gibson 21 day fat burner recenzii that seen in injury patterns where the endoneurium is preserved and facial motor outcomes are superior. This process is known as synkinesis. The physiology of synkinesis is not completely understood. Aberrant axonal regeneration, nuclear hyperexcitability, and ephaptic transmission have been proposed as mechanisms of synkinesis formation.
The nerve does not maintain a topographic distribution from the facial nucleus to the peripheral muscle. Therefore, disruption of individual fibers can result in regeneration patterns where axons innervate the incorrect peripheral muscle group.
Recent experimental evidence 15 16 The Facial Nerve has shown that this process may occur beyond the site of lesion. In the case josie gibson 21 day fat burner recenzii nuclear hyperexcitability, during recovery postsynaptic cells may become more receptive to neurotransmitters from other peripheral muscle axons or with incomplete myelination allow for aberrant contactmediated cross talk as seen josie gibson 21 day fat burner recenzii ephaptic transmission. U References 1.
Kellman RM. Fadal nerve manual. Chapter 3. Physiology and pathophysiology. Amj Otol;10 1 PubMed 2. Sunderland S. Nerve and Nerve Injuries, 2nd ed. London, Churchill Uvingstone; 3. Nissl f. Uber die Veranderugen am facialskem des Kaninchen nach Ausreissung der Nerven. Allg Z Psychiatr ; 4. Kreutzberg GW. Degeneration and regeneration. In: Miehlk A. Surgery of the Facial Nerve.
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Philadelphia: W. Saunders; 5. Choi D, Dunn LT. Acta Neurochir Wien ; 2 PubMed 6. Disorders of Peripheral Nerves. Philadelphia: FA Davis; 7. Tuszynski MH. Neurotrophic factors. In: Tuszynski Pierde greutatea rapidă atunci când obez, Kordower j, eds.
CNS Regeneration. San Diego: Academic Press; 8. Fu SY, Gordon T. The cellular and molecular basis of peripheral nerve regeneration. Mol Neurobiol;14 PubMed 9. Sdence ; PubMed May M. The Fadal Nerve, 2nd ed. New York: Thieme; Smitson C, Hadlock TA Nimodipine and acceleration of functional recovery of the facial nerve after crush injury.
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Moran Cj, Neely jG. Patterns of facial nerve synkinesis.
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Laryngoscope ; 12 pt 1 PubMed Sadjadpour K. Postfacial palsy phenomena: faulty nerve regeneration or ephaptic transmission? Brain Res ;95 : Choi D, Raisman G.
After facial nerve damage, regenerating axons become aberrant throughout the length of the nerve and not only at the site of the lesion: an experimental study. Fayad and Pred H. The normal histology of the facial nerve needs defining before discussing the histopathology.
The facial nerve is composed ofneurons, 7, of which are myelinated and innervate the nerves of facial expression.
Three thousand of the nerve fibers are somatosensory and secretomotor and make up the nervus intermedius. The nerve fibers, containing microfilaments and microtubules, are surrounded by a multilayered myelin sheath.
The fibers are in tum surrounded by endoneurium that encompasses each fiber but also surrounds groups of fibers to form fascicles. In the temporal bone, a tough perineurium surrounds the entire nerve and is cushioned from surrounding tissues and structures by the epineurium Fig. Sitting atop the nerve at the external genu where the nerve makes a sharp tum posteriorly, at the junction of the meatal and tympanic segments, is the geniculate ganglion that carries autonomic fibers from the greater superficial petrosal nerve.
The chorda tympani nerve, which carries taste and glandular secretory fibers, is an integral part of the facial nerve extending from the geniculate ganglion area to the descending mastoid segment, where it leaves the facial nerve to cross the middle ear.
The fibers are not recognizable within the nerve unless it has been divided proximal to the geniculate ganglion. In this case, they can be seen a as a discrete bundle of fibers near their exit from the tympanic segment Fig.
These can generally be classified as idiopathic, inflammatory, and neoplastic. We describe the various pathologies in each of these categories and provide histopathological examples. Idiopathic Bell palsy or idiopathic facial paralysis is a unilateral, sometimes recurrent facial nerve paralysis that usually spontaneously recovers. In a few cases, it may become permanent or result in partial impairment or synkinesis.