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The lipid-rich highly branched cell processes are incapable of sur- myelin material enables saltatory conduction of viving without contact to the cell body. The motor action potentials between nodes of Ranvier — the nerve cell has several short processes called den- unmyelinated axon between adjacent myelinated drites, which allow communication with other Schwann cells. The width of this internode distance nerve cells in the spinal cord. The cell can form new plays an important role for the velocity of impulse processes at any time if necessary. The axon is the conduction along the nerve.

As the potentials are longest process; it leaves the spinal cord to make conducted by saltatory conduction, that is leaping contact with a muscle. An axon consists of an axon over the myelin sheath of what is called an inter- cylinder, a fluid-filled neurilemma in which nutri- node, they reach the destination more quickly than ents, enzymes, chemical signals, and structural pro- by continually traveling along the axon as on an teins flow distally from the cell body. There is also a unmyelinated axon.

Each node of Ranvier has an reverse axoplasmic flow that transports information increased density of sodium channels compared from the periphery to the cell body Figure 3a. In the axon cylinder of the nerve, chemical substances are transported in a fluid axoplasmic flow from the cell body to the nerve ending and from there back to the cell body. The flow supplies the axon and the muscle with nutrients a. Problems in the axoplasmic flow damage the axon cylinder, which then dies back from distal to proximal end; the denervated muscle atrophies b.

The nodes of Ranvier 1. The basal lamina is preserved when a Schwann In the peripheral nerve are a number of axons that cell degenerates and a duplicate basal lamina is are bundled together by connective tissue septa, the formed by new Schwann cells. The basal lamina has perineurium. Within the fascicles the individual a crucial function in axonal regeneration because it axons are enveloped by the endoneurium; the entire degenerates very slowly after Schwann cell death.

After a nerve of the nerve Figure 4. These anatomical conditions lesion and axonal regeneration, demyelination, and alone can give rise to considerable problems when remyelination, the myelin sheath can regenerate but suturing the fascicle of a nerve, especially if part of the sheath will be thinner and the internode dis- the nerve is missing or must be resected. For exam- tances will be much smaller Figure 7.

These chan- ple, a proximal nerve ending with only two fascicles ges explain the slower conduction velocity of these must then be anastomized with five fascicles in nerves.

However, the slowdown does not necessari- the distal stump. Then unrelated nerve tracts are ly mean that clinical function must be poorer. The peripheral nerve consists of individual fascicles that sheathe the epineurium see also Figure 83 aberrant reinnervation with motor and sensory this is reversible explains the prompt effect of clini- function damage.

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Removing the blockage associated with morphological changes. External of the electrolyte channels caused by antibodies re- damage such as sharp or blunt trauma, ischemia, or stores the conductivity of the nerve and thus its inflammations can change either the insulating function. The level of severity of the damage also myelin alone Table 1 , the width of the nodes of determines the potential for regeneration.

Neura- Ranvier, or they can sever the axons and connective praxia first causes a loss of conductivity in the nerve; tissue coating. In the case of polyneuropathies, the damage is from metabolic diabetic and toxic chemotherapy noxa.

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They have a primary influ- Table 1 Classification of nerve injuries. The various ence on metabolism in the nerve cell or obstruct the traumatic lesions are designated as follows if certain axoplasmic flow. As the axon segments located furthest dis- praxia mesis mesis tal from the cell body are most poorly supplied, they are the first to be damaged.

The axon is responsible for conducting electric signals. A considerable acceleration of conduction velocity is possible through saltatory conduction a. Degenerating myelin sheaths or the naked axon can conduct electric stimulation only through slow continuous conduction b. The shorter and thinner internodes after remyelination slow down the originally faster conduction capacity of the nerve c this lesion has the best prognosis of all types of dam- electromyography EMG ; the muscle, which now age.

If the axon cylinder is sound, the demyelinated also shows trophic denervation, exhibits spontane- axon segment regains conductivity — although re- ous activity. By contrast, axonotme- sis means severe damage to the axon process and causes Wallerian degeneration of the nerve cell. The 1.

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It uses up the nutrients stored in its axo- plasm and the myelin dissolves and degenerates. The interruption of continuity of the axon cylinder The axon looses conductivity within 4—10 days. The leads to massive changes in the entire nerve cell. Fol- nerve can then regain function only if it resprouts lowing the lesion, other nerve cells withdraw their over the entire degenerated segment. As long as dendrites from the surface of the damaged cell and trophic substances are still available in the distal isolate it from the synaptic cluster in the central nerve segment, the membrane potential of the adja- nervous system CNS.

In the cell body, the Nissl cent muscle fiber is not changed.

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When the sub- bodies degenerate tigrolysis , the body itself swells stances are lacking, the muscle membrane potential and its nucleus becomes marginal. These changes becomes unstable, resulting in spontaneous depo- are signs of increased metabolic activity used by the larization. Slight percussion along the course of the nerve eliciting a Tinel sign allows the progress of reinnervation or formation of a neuroma to be followed using simple clinical means. For example, demyelinating lesions prevent voluntary muscle activation by blocking conduction. The re- sult is atrophy due to inactivity.


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Since the muscle still has an intact axon and the axoplasmic flow is sup- plied by trophic factors, it is not subject to denerva- tion atrophy and shows no spontaneous activity in EMG. This situation changes dramatically if the axon of the nerve is also severed. This then quickly leads to denervation atrophy and the muscle devel- ops the EMG signs of spontaneous activity.

To re- store the nerve-muscle bundle, the sprouting nerve Figure 6 Normal and regenerating nerve. The 4 Axoplasm of the axon cylinder, 5 Endoneural interstitium further distal the lesion and thus the shorter the with collagen fiber, 6 Normal nerve, 7 Schwann cell, 8 Myelin distance, the more favorable the reinnervation re- sheath coating, 9 Node of Ranvier, bordering an internode, sult usually is. Peripheral to the degenerate, with the result that denervated muscle proximal axon Figure 7 axoplasm is exuded from fibers are found next to innervated ones in the mus- the stump, which first forms a growth bud, from cle.

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The intact axons immediately begin to innervate which axon sprouts branch out to grow toward the these denervated muscle fibers. To do so, the nerve periphery. The severed axon breaks down and it and sprouts small nerve fibers either from its terminal the myelin are cleared away by macrophages. The individ- which are the indispensable conduction pathways to ual nerve fiber forms a motor unit with the muscle the sensory target organ or muscle during the regen- fiber attached to it, which can expand considerably eration and reinnervation process Figure 6.

The in size during such reinnervation processes. The growth rate is different in one extremity from prox- activation of the motor unit is accompanied by elec- imal to distal end, and is about 5—1 mm per day. If tric discharge of the muscle fibers that can be re- access to the pathways in the periphery is blocked corded with an EMG needle in an electromyogram. Important for diagnostics is that a motor unit.

This affects nerve conduction velocity find the right conduction pathway to the periphery. Usually this exact readaptation is not suc- from such aberrant regeneration. The ability to per- cessful, as sequelae after severe facial nerve pareses ceive an object with eyes closed is based on a chain show. Aberrant regeneration can result in synkine- of events called stereognosis. This starts with taking sis. This is expressed, for example, in that nerve fi- in and transmitting information to the brain from bers that previously supplied the orbicularis oculi sensory and pressure receptors in the skin, where muscle now grow to the orbicularis oris muscle and pattern recognition is carried out on the basis of a innervate it.

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Every time the patient closes his eyelid, screening process. If the skin receptors are incor- this movement is linked with a synchronous muscle rectly reinnervated after a nerve lesion, inadequate contraction at the corner of the mouth. Synkinesis regions of the sensory cortex are addressed and pat- such as this is especially problematic after nerve terns arise that cannot be perceived by any familiar damage to the arm. Even with optimal surgical screen. Everyday activities such as buttoning a shirt nerve reconstruction and regeneration of the sen- can become problematic.

Visual input can lessen the sory and motor nerves, synkinesis can be so pro- sensory deficit, but not overcome the motor effects nounced that use of the hand is impaired.