الفهرس 
Pathophysiology of Nervous System TraumaOnly 14 pages are availabe for public view
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Abstract
As the central and peripheral nervous system may be substantially exposed to injury due to trauma, it is the neurologist who should be trained and qualified to diagnose and treat these neurological conditions, and to be at the forefront of emergency team. Also to be qualified to treat post traumatic sequalea.
Traumatic brain injury
Traumatic brain injury (TBI) is a major cause of disability and death in most Western nations and consumes an estimated $100 billion annually in the United States alone. In the last 2 decades, the management of TBI has evolved dramatically, as a result of a more thorough understanding of the physiologic events leading to secondary neuronal injury as well as advances in the care of critically ill patients.
Traumatic brain injury (TBI) is a non degenerative, non congenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness.
Despite decades of research, there are still very few data to define the best practice for managing TBI in its early stages. Hypotension, hypoxia, hyper- and hypocapnia all remain potentially avoidable insults, which are associated with worse outcome after TBI. There is no single treatment, which has been, or is likely in the future, to improve dramatically the outcome for patients with TBI. Adherence to national and international guidelines may be associated with improved outcome.
TBI occurs when a sudden trauma causes damage to the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. A person with a mild TBI may remain conscious or may experience a loss of consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking. A person with a moderate or severe TBI may show these same symptoms, but may also have a headache that gets worse or does not go away, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation.
Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible. Because little can be done to reverse the initial brain damage caused by trauma, neurologist should try to stabilize an individual with TBI and focus on preventing further injury. Primary concerns include insuring proper oxygen supply to the brain and the rest of the body, maintaining adequate blood flow and controlling blood pressure. We should put in our consideration measures that prevent increased intracranial pressure, post traumatic epilepsy and electrolyte disturbance.
Imaging tests help in determining the diagnosis and prognosis of a TBI patient. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures or spinal instability. For moderate to severe cases, the imaging test is a computed tomography (CT) scan.
Moderately to severely injured patients receive rehabilitation that involves individually tailored treatment programs in the areas of physical therapy, occupational therapy, speech/language, psychology/psychiatry, and social support.
Traumatic spinal cord injury
Various types of injury can produce damage to the spinal cord. What constitutes appropriate management will differ, depending on the mechanism of injury. Osseous disruption is the most common mechanism of injury and includes fracture dislocation, flexion distraction–associated fractures, burst fractures, and wedge compression fractures. Another common clinical entity is an injury due to preexisting spondylosis. As spondylitic disease progresses, there is compromise of the spinal canal and/or neural foramina, which often is asymptomatic. When force is transmitted to the spinal column, these spondylitic abnormalities compress and deform either the spinal cord or the nerve roots, producing subsequent neurological injury.
If a spinal injury is suspected, immediate neck immobilization is vital. The usual technique is to pass a firm backboard beneath the victim. After the thoracic spine is immobilized, the cervical spine should be similarly restrained before it is moved. The usual emergency protocol of an ABC (airway, breathing, circulation) survey should be appropriately modified to consider the spinal cord–injured patient.
If the patient is awake and alert, a detailed and careful neurological examination is of paramount importance, both to establish the deficit that is present and to serve as a useful baseline to assess the success or failure of subsequent interventions. The extent of injury is defined by the ASIA American Spinal Injury Association (ASIA) Impairment Scale (modified from the Frankel classification).
Diagnostic imaging begins with the acquisition of standard radiographs of the affected region of the spine. Investigators have shown that computed tomography (CT) scanning is exquisitely sensitive for the detection of spinal fractures and is cost effective. However, a properly performed lateral radiograph of the cervical spine that includes the C7-T1 junction can provide sufficient information to allow the multiple trauma victim to proceed emergently to the operating room if necessary without additional intervention other than maintenance of full spinal immobilization and a hard cervical collar. In some centers, CT scanning has supplanted plain radiographs.
There are several types of treatment in the short term for a spinal cord injury. First, the spine in the area of the injured spinal cord is immobilized (held in place so it can’t move) to prevent further injury to the cord, Airway management in the setting of spinal cord injury, with or without a cervical spine injury, is complex and difficult. Because the cervical spines must be maintained in neutral alignment at all times. Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury. Because of the vital sign confusion in acute spinal cord injury and the high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made.
To reduce swelling in the spinal cord caused by injury, steroid medication is usually given during the first 24 hours following injury. Other medical treatment is often necessary, depending on complications that may develop. The use of steroid is still a controversy, but overall, the benefit from steroids is considered modest at best, but for patients with complete or incomplete quadriplegia, a small improvement in motor strength in one or more muscles can provide important functional gains.
Because traumatic injury to the spinal cord usually involves an injury to the bones and ligaments of the spine, surgery may be performed. The aim of some surgeries is to remove bone (this is called ”decompression”) that is pressing on or into the spinal cord. A surgeon may also want to stabilize or realign the spine in the area of the spinal cord injury when the vertebrae or ligaments have been damaged. Metal rods or cages and screws may be attached to normal vertebrae to prevent movement of fractured vertebrae and the vertebrae may be “fused” together using bone graft for the same reason.
The rehabilitation process following a spinal cord injury typically begins in the acute care setting. In the acute phase physical therapists focus on the patient’s respiratory status, prevention of indirect complications (such as pressure sores), maintaining range of motion, and keeping available musculature active.
As the patient becomes more stable, they may move to a rehabilitation facility or remain in the acute care setting. The patient begins to take more of an active role in their rehabilitation at this stage and works with the rehabilitation team to develop reasonable functional goals.
Traumatic peripheral nerve injury
Common etiologies of acute traumatic peripheral nerve injury (TPNI) include penetrating injury, crush, stretch, and ischemia. Management of TPNI requires familiarity with the relevant anatomy, pathology, pathophysiology, and the surgical principles, approaches and concerns.
There are two commonly used classification schemes for peripheral nerve injury: the Seddon and the Sunderland. The Sunderland classification is more complex, but more useful. It is important for the clinical neurophysiologist to be familiar with these classification schemes because they are in widespread use in the surgical community.
Seddon divided injuries into neurapraxia, axonotmesis and neurotmesis, In neurapraxia , the nerve is intact but cannot transmit impulses . In axonotmesis, the axon is damaged or destroyed, but most of the connective tissue framework is maintained. In neurotmesis, the nerve trunk is disrupted and not in anatomical continuity. Most of the connective tissue framework is lost or badly distorted. Sunderland’s classify nerve injury into five degrees (1) neurapraxia, (2) loss of continuity of the axons without breaching the endoneurial sheath of the nerve fibers, (3) loss of continuity of nerve fibers, (4) involvement of the perineurium and the fasciculi, and (5) loss of continuity of the nerve trunk.
Electrodiagnostic study is paramount in the evaluation of nerve injuries. Needle EMG can demonstrate whether the injury is complete or incomplete at any time after injury. Nerve conduction studies are required to differentiate demyelination from axon loss; they yield the maximal information in this regard approximately 10 days after the injury. Nerve conduction studies should be bilateral to allow side-to-side comparisons of amplitude.
In the early management of peripheral nerve injury, control of pain is the most pressing consideration. The pain is typically neuropathic, characterized by burning and dysesthesias, and requires medications which are specific for neuropathic pain, such as tricyclic antidepressants, serotonin reuptake inhibitors, anti-convulsants such as carbamazepine, phenytoin, and lamotrigine, gabapentin and pregabalin, antiarrhythymics, baclofen and others. Although traditional analgesics are not regarded as first-line drugs for treating neuropathic pain, agents such as non steroidal anti-inflammatory drugs, tramadol, and opioids may be useful.
Surgical repair of TPNI is done at varying time intervals after the injury, and there are a number of considerations in deciding whether and when to operate.
In neurapraxia, the compound muscle and nerve action potentials on stimulating distal to the lesion are maintained indefinitely; stimulation above the lesion reveals partial or complete conduction block. Complete nerve injuries that are predominantly neurapraxic can be expected to recover favorably over the course of weeks to months. When such cases do not recover as expected, patients should undergo follow-up electrodiagnostic testing, which may show the presence of significant secondary axonal loss suggesting that the initial testing was done too early, before the electrophysiologic abnormalities had fully evolved.
The picture in axonotmesis and neurotmesis depends on the time since injury. The optimal timing for an electrodiagnostic study depends upon the clinical question being asked. Although conventional teaching usually holds that an electrodiagnostic study should not be done until about 3 weeks after the injury, in fact a great deal of important information can be obtained by studies done in the first week.
Proximal nerve injuries are problematic because the long distance makes it difficult to reinnervate distal muscles before irreversible changes occur. Decision making regarding exploration must occur more quickly, and exploration using intraoperative nerve action potential recording to guide the choice of surgical procedure is often useful.
Patients with weakness and deformity after nerve injury should be considered for physical and occupational therapy evaluation. Function may be improved significantly by the use of the appropriate assistive devices such as cock-up wrist splints (for radial nerve injuries) and AFO splints (for foot DROP with peroneal or sciatic nerve injuries). Additionally, consider tendon transfer to improve residual function, depending on the precise pattern of residual injury and functional limitation.
Whiplash injury
Whiplash is the most common injury associated with motor vehicle accidents and is a common cause of chronic disability. Whiplash injury may occur as a result of hyperextension of the lower cervical vertebrae in relation to a relative flexion of the upper cervical vertebrae, which produces an S-shape of the cervical spine at the time of impact.
a wide variety of clinical manifestations including neck pain, neck stiffness, arm pain and paresthesias, problems with memory and concentration, and psychological distress. This group of symptoms and signs are collectively termed WAD. The QTF developed a classification system includes 5 grades for WAD based on severity of signs and symptoms.
The diagnosis of whiplash remains clinical. The mechanism of injury must be elicited. There are no specific neuropsychological studies or electrophysiological tests that can diagnose whiplash injury.
Injury most often is not identified radiographically in the acute phase. The most common radiographic findings associated with whiplash injury are preexisting degenerative disease or slight loss of the normal lordotic curve of the cervical spine. MRI is not indicated because of high false positive results. CT and MRI are generally reserved for patients with suspected disc or spinal cord injury, fracture, or ligamentous injury. CT and MRI may also be indicated in patients with long term persistent arm pain, neurologic deficits, or clinical signs of nerve root compression.
Initial treatment include early mobilization may lead to improved outcomes and that rest and motion restriction may hinder recovery. Patients received high dose of steroid therapy had significantly fewer total sick days, and fewer disabling symptoms compared to those who didn’t received steroids.
Patients with chronic neck pain, not necessarily motor vehicle related, suggest that exercise and mobilization may improve long-term outcomes. Many other therapeutic interventions have been suggested including cervical radiofrequency neurotomy, temperomandibular joint treatment, cervical traction, intraarticular corticosteroids, and botulinim toxin.
Muscular injury
Muscular pain and injury occur when the musculotendinous contractual unit is exposed to single or recurrent episodes of biomechanical overloading. Myofascial pain is characterized by muscles that are in a shortened or contracted state with increased tone and stiffness and containing trigger points.
Myofascial pain may appear acutely following an identifiable incident of macro-trauma or may develop over a longer period of time in a more insidious manner due to recurrent or cumulative micro- traumatic injuries.
Patients with MPS may complain of muscle weakness that appears to be related to pain avoidance, rather than actual loss of muscle power as demonstrated by a manual muscle exam. Abnormalities of autonomic function include changes in skin temperature and sweating.
The diagnosis of MPS requires a physician history and thorough general physical, neurological, and musculoskeletal examinations. The neurologist must determine whether muscular symptoms are primary or secondary to another biomechanical, neurological, visceral, or referred source in order to formulate a treatment plan.
Treatment of MPS includes short-term rest, supplemented by pharmacological therapies aimed directly at the dysfunctional muscle to assist healing. Successful treatment often depends upon cooperative patient behaviors such as exercise, stretching, or pacing. When MP is secondary to a neuropathic pain generator, medical therapies should probably be initiated at the causative neural lesion.
Physical treatments of the involved muscle may provide adjunctive pain relief in these cases, and perhaps also prevent long-term changes that may induce a primary self-sustaining MPS by recruiting local and central neurophysiological mechanisms. Pharmacotherapy includes nonsteroidal anti inflammatory drugs, opioid and nonopioid analgesics, muscle spasmolytics, and tricyclic antidepressants. Topical analgesics such as the 5% lidocaine patch may also be used.
When musculoskeletal pain due to injury persists for more than 6 weeks, responsibility for rehabilitation and recovery should be transferred from the therapist to the patient, if possible. A patient specific exercise protocol should be prescribed to optimize support, protection, and movement across the injured and dysfunctional sites within the kinetic chain.
Sports injury
Injury to the nervous system may occur with essentially any sport and may involve multiple levels of the nervous system, including peripheral nerves, brachial and lumbar plexi, spinal roots, spinal cord, brain stem, and cerebrum.
Although neurological injuries are common place in sport, neurologists have not been at the forefront of providing oversight and guidance in sports related neurological injuries.
Concussion is the most visible aspect of sports neurology, and sadly, neurologists have not been leading the discussions in managing this disorder, nor in developing universally accepted oversight and guidelines for this condition. Concussion occurs when rotational or angular acceleration forces are applied to the brain, resulting in shear strain of the underlying neural elements. Concussion is graded as 1 (mild), 2 (moderate), and 3 (severe).
The decision about when to return to play in sports related concussion has to be taken by the neurologist. The importance of this issue involves the potential ability to prevent more severe brain injuries by identifying the patient at higher risk.
High altitude neurological trauma
High altitude neurological trauma occurs when unclamitized patient ascend to high altitude, it is type of physical trauma and it include multiple types of injuries such as high-altitude headache (HAH), acute mountain sickness (AMS) and high-altitude cerebral edema (HACE). HAH and AMS are common complications and have become public health problems. In contrast, HACE is rare, but potentially fatal.
The symptoms of high altitude trauma include headache, insomnia, dizziness, lassitude, fatigue, or gastrointestinal symptoms such as anorexia, nausea, or vomiting and may be impaired speech control.
Prevention and therapy of AMS and HAH are identical, because most patients with AMS also have headache. Mild AMS is treated with rest, and analgesics or antiemetics may be added. Moderate or severe AMS is treated with supplementary oxygen, and the patients should descend. The symptoms of AMS generally resolve after a descent of 500–1000 m.
Oral acetazolamide reduced the severity of AMS by 74% in a controlled small-scale study. Dexamethasone has been as effective as or superior to acetazolamide in several controlled studies. Prophylactic intake of oral aspirin (1 g) reduced the incidence of headache when exercising during high-altitude exposure.
High-altitude cerebral edema is defined as the onset of ataxia, altered consciousness, or both in a subject with AMS or HAPE. Associated signs include papilledema, retinal hemorrhage, encephalopathy, cranial nerve palsy, focal neurological deficits, and, rarely, seizures.
Magnetic resonance imaging revealed signs of a vasogenic edema of the supratentorial water matter that especially affected the splenium of the callosal body. The treatment for HACE is immediate descent in conjunction with supplementation of oxygen and the administration of dexamethasone.