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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 dating astatic jt 30 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 flying solo dating 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.
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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.
This represents the plastic state of denervated muscle. Over time, fibers disappear and are replaced by fat and connective tissue.
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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.
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A detailed discussion on the most commonly used tests is presented in Chapter 4. These tests include the following. Maximal Stimulation Test A maximal stimulation test uses electrical stimulation to compare muscle response between sides.
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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.
Electromyography Electromyography measures voluntary muscle response. The motor unit response morphology provides further information. In addition to the amplitude and latency of the muscle responses, denervation patterns such 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 dating astatic jt 30 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.