الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 149 |  |  |
| | | from | 149 | | |
Abstract
The peripheral nervous system is one of three major components of the entire nervous system
The peripheral nervous system consists of those structures containing nerve fibers or axons that connect the CNS to motor, sensory, somatic and visceral end organs. This includes the cranial nerves (III–XII), spinal nerves, cervical, brachial and lumbosacral plexus and nerves of the extremity. These nerves are mostly mixed nerves (motor and sensory).
In the peripheral nervous system, excluding the cranial nerves, they have their origin as a spinal nerve that is formed by the union of ventral and dorsal roots. The ventral root is largely formed by efferent fibers that innervate somatic musculature, but also contain some pre-ganglionic autonomic fibers that innervate blood vessels, smooth muscle and glandular epithelium. The dorsal root contains most of the afferent fibers from the somatic and visceral system.
Microanatomy of the peripheral nerves consists of axons of neurons whose cell bodies are located either in the spinal cord (anterior horn cells) or in the dorsal root ganglia. The axons within nerve trunk are sarranged in fascicles by means of connective tissue.
Peripheral nerve injury can be classified according to their severity into neuropraxia, neurotmesis and axonotmesis. In neuropraxia no surgical intervention is needed and the patient has to be followed up. If it is axonotmesis or neurotmesis then the patient may be in need for surgical intervention either early or late.
The diagnosis of peripheral nerve injury is done by means of the medical history and neurological examination. Imaging studies such as plain X ray, Computed tomography and Magnetic resonance imaging together with electrodiagnostic studies (which include electromyography and nerve conduction velocity) and ultrasound are essentially useful.
The timing of nerve repair depends very much on available facilities as well as the experience of the surgeon, but in general, if there is an open injury with a clean sharp nerve transection, immediate repair can be done. But if there is an open injury with a blunt nerve transection then delayed nerve exploration is indicated after repair and/or healing of other wounded tissues. On the other hand, if there is a closed injury follow up by clinical assessment and electrophysiological studies is indicated 3 months and if there is failure of recovery then surgical exploration is indicated.
The type of nerve repair could be neurolysis if the nerve is in continuity and not damaged, but, if the nerve is severely damaged and no action potential could be elicited across the site of injury, resection of the affected part is done together with anastomosing the two nerve stumps either directly or through any suitable nerve conduits
Direct nerve repair yields the best results and nerve autografts remain the gold standard treatment for nerve gaps. Conduits have a limited role in small gaps <3 cm for sensory nerves, but this may expand in the future with improvements in conduit design.
Clinical options exist for partially bypassing damaged peripheral nerve pathways using nerve transfers may be expanded in the future
The biological roadblocks to early and complete recovery remain Wallerian degeneration, slow axonal regeneration, and the effects of chronic axotomy on denervated muscles. Translational research therapies address some of these barriers and future advances in surgical care may come from enhancing axonal regrowth, electrically stimulating the distal motor target after injury, and most powerfully delaying or avoiding Wallerian degeneration.