Epilepsy and Seizure Activity in Athletes

Cervical Cord Neurapraxia (Transient Quadriplegia)

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  Overview: Transient neurologic episodes characterized by a temporary loss of motor or sensory function, or both. This is likely secondary to central cord contusion with or without associated ischemia. Most common with contact sports. Prevalence is estimated at 7 per 10,000 football participants.

  
  
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  Mechanism of injury: Varied mechanisms (usually hyperflexion, hyperextension, or axial loading of the neck) resulting in cervical cord contusion and decreased blood flow; suspected to be associated with spinal stenosis and the shape of the spinal canal. Degree of stenosis may be estimated using the Torg ratio (ratio of spinal canal width to vertebral body diameter). A ratio of <0.80 is considered indicative of “significant cervical stenosis”; this ratio has been shown to be an unreliable measure in larger athletes because of the relative vertebral body width yielding poor positive predictive value, and it has been replaced by magnetic resonance imaging (MRI) evaluation.

  
  
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  Symptoms: Bilateral sensory changes, motor changes, or combined sensorimotor deficits. Total body numbness may occur. Neck pain is usually absent.

  
  
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  Physical examination:

  
  
  
  
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    On the field

    
    
    
    
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      Assume cervical spine injury until proven otherwise. Follow cervical spine precautions and use cervical collar and spine board.

      
      
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      Athlete should be stabilized and transported to the nearest appropriate facility by EMS for further evaluation.

      
      
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      For football, remove the face mask, but helmet and shoulder pads should remain in place. According to the most recent position statement by the American College of Sports Medicine (ACSM), it is strongly advised to not remove an American football helmet and shoulder pads from an unconscious athlete or an athlete who has sustained a neck injury. If any of the criteria below are met, the helmet and the shoulder pads should be removed maintaining cervical spine precautions:

      
      
      
      
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        If the helmet and chin strap do not securely hold the head, such that immobilization of the helmet does not also immobilize the head

        
        
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        If the design of the helmet and chin strap is such that even after removal of the face mask, the airway cannot be controlled or ventilation provided

        
        
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        If after a reasonable period of time, the face mask cannot be removed to gain access to the airway

        
        
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        If the helmet prevents immobilization for transportation in an appropriate position

        
        
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        Standard guidelines for management of airway, breathing, and circulation must be followed.

      
      

    
    
    
    
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    Off the field

    
    
    
    
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      Thorough cervical spine and neurologic evaluation is necessary.

      
      
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      Pain and tenderness over the cervical spine is not associated with transient quadriplegia and should prompt consideration of other injuries such as fracture.

    
    

  
  
  
  
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  Diagnostics: Plain cervical spine trauma radiograph series should be obtained to rule out fracture or dislocation. Once a fracture is definitively ruled out, flexion and extension views may be obtained to check for ligamentous instability. CT to rule out occult facture. MRI should be obtained to evaluate spinal stenosis, spinal cord, and associated injuries.

  
  
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  Treatment: Initial treatment should focus on cervical spine immobilization, medical stabilization, and transport via EMS. The most recent Cochrane review recommends high-dose methylprednisolone within 8 hours of spinal cord injury because it has been shown to improve recovery of motor functions. However, controversy still exists, and additional research is needed. There is no role for steroids in athletes with transient quadriparesis who show resolution of symptoms. Systemic hypothermia, which is thought to decrease tissue metabolism and limit secondary hypoxic injury, has also been used but is still experimental and not part of routine care.

  
  
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  Prognosis and return to play (RTP): Temporary condition by definition, but both extent and duration of neurologic dysfunction factor in the overall prognosis; average rate of recurrence for players who return to football is 56%. Repeat episodes may be associated with cervical radiculopathy and myelopathy. Predisposition to permanent neurologic injury after an episode of cervical cord neurapraxia is controversial, but there are published case reports regarding the same; RTP decisions are made on an individual basis taking into account history of injuries, anatomical predisposition, and future risk of injury. Although discussing all possible scenarios is beyond the purpose of this text, we have enlisted a few examples here: If an athlete is asymptomatic without documented stenosis, it is generally accepted that he/she be allowed to RTP. If an athlete is asymptomatic with documented stenosis, significant controversy exists regarding RTP. Stenosis is more accurately defined by adequate cerebrospinal fluid around the cord as opposed to by absolute canal diameter. Opinions range from considering this as a relative contraindication to an absolute contraindication. Multiple episodes without documented stenosis should prompt serious consideration of discontinuing contact sports.

Peripheral Nerve Injury in Athletes

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  Overview of anatomy: The peripheral nervous system includes cranial nerves, spinal nerves and their roots and branches, peripheral nerves, and neuromuscular junctions.

  
  
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  Classification of injury: There are two primary classification systems: Seddon and Sunderland. Descriptions of each type, prognosis, and associated electrodiagnostic findings are compared in Table 38.1 (see also Fig. 38.1 ). Neuropraxia (grade I) is typically a demyelinating injury with good recovery. Axonotmesis (grades II–IV) involves axon disruption but with preservation of some degree of supporting structures (endoneurium, perineurium, and epineurium). The more supporting structures involved, the worse the outcomes. Neurotmesis (grade V) is complete disruption of both axons and supporting structures, with limited scope of recovery without surgical intervention.

  
  
  
  

  TABLE 38.1

  
  

  PERIPHERAL NERVE INJURY CLASSIFICATION

  
  

  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  
  

  Seddon	Sunderland	Pathology	Electrodiagnostic Findings	Prognosis
  Neuropraxia	I	Demyelination	Conduction block	Excellent, recovery typically 2–3 months
  Axonotmesis	II	Demyelination and axon loss	Axon loss	Good, but limited by distance to muscle
  Axonotmesis	III	II + endoneurium involvement	Axon loss	Fair, surgery may be required
  Axonotmesis	IV	III + perineurium involvement	Axon loss	Poor, surgery usually required
  Neurotmesis	V	IV + epineurium involvement	Axon loss	Poor, no spontaneous recovery and surgery required

   
  
  

  
  

  
  

  

  
  

  
  

  Peripheral nerve injury classification.

  
  
  
  
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  Mechanism of injury: Injuries can be subcategorized into acute, subacute, or chronic. Acute injuries may result from nerve compression, stretch/traction, or laceration and usually result from an unexpected fall or extrinsic force (e.g., tackle). Stretch/traction injuries are most common; most nerves can tolerate 10%–20% lengthening before structural damage occurs. Subacute or chronic injuries are best classified as overuse injuries resulting from repetitive microtrauma or compression.

  
  
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  Evaluation: History should elicit a specific time course and mechanism of injury. A detailed physical examination is essential and includes muscle bulk inspection, strength testing, deep tendon reflexes, and sensory examination. Provocative maneuvers should be performed, including neural tension testing (i.e., straight leg raise) and direct nerve percussion (i.e., Tinel’s sign). Equipment should be inspected for appropriate use and fit. In addition, a kinetic chain evaluation must be performed in search of a root cause for overuse injuries (i.e., a volleyball athlete with knee pain leading to shoulder overuse and subsequent suprascapular nerve injury).

  
  
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  Diagnostics:

  
  
  
  
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    Electrodiagnostic testing: Used to assess the neurophysiologic function of the peripheral nervous system, including nerve roots, plexus, and peripheral nerves; testing includes nerve conduction studies (NCS) and needle electromyography (EMG). Used as an extension of physical examination and can help clarify or confirm a suspected diagnosis; more specifically, it can help to define location, duration, severity, and prognosis of neuromuscular disorders. NCS are performed by placing electrodes on the skin and stimulating the nerve of interest with electrical impulses. NCS are divided into motor and sensory nerve testing and help to determine if there is dysfunction of the myelin sheath (slowed electrical impulse), axons (reduced amplitude), or a combination of both. EMG involves a needle electrode that is inserted into a muscle of interest and is able to analyze motor units and their recruitment. Moreover, EMG can detect muscle denervation and whether or not any re-innervation has occurred.

    
    
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    MRI: Useful as an adjunct in diagnosis and prognosis; may help with acute injuries in assessing soft tissue damage and deciding on surgical intervention. Normal peripheral nerves appear isointense compared with surrounding muscles, reveal a fascicular pattern, and are usually surrounded by a small rim of fat tissue. Nerve hyperintensity can be detected on T2-weighted MRI within 24 hours of a nerve injury. Focal demyelination reveals hyperintensity at the lesion site, whereas axonal injury with Wallerian degeneration reveals hyperintensity in the entire nerve segment distal to the lesion. Magnetic resonance neurography (MRN) refers to nerve-specific imaging using pulse sequences for optimal visualization. Axial T1-weighted and fluid-sensitive fat-suppressed T2-weighted images serve as the mainstay for interpreting peripheral nerve signal intensity, course, caliber, fascicular pattern, size, perineural fibrosis, and mass lesions. MRI can also identify masses that cause nerve compression.

    
    
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    Ultrasound: Provides immediate, nonionizing, high-resolution, bedside assessment of peripheral nerves and surrounding tissues with ease of contralateral comparison; functional assessment is possible and can detect abnormal nerve motion and nerve entrapment with joint movement (subluxing ulnar nerve at the elbow). In addition, sonopalpation (transducer pressure) to the area of nerve dysfunction is useful for confirming typical symptoms. In long-axis view, peripheral nerves appear fascicular with hypoechoic fascicles surrounded by hyperechoic connective tissue. In short-axis view, peripheral nerves display a honeycomb or speckled appearance. With regard to nerve entrapment, ultrasound can demonstrate sudden flattening (notch sign) or gradual narrowing (dumbbell sign) at the compression site with proximal hypoechoic nerve swelling.

  
  
  
  
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  Treatment:

  
  
  
  
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    Surgical: Open, sharp traumatic injuries should be immediately repaired through surgical intervention. For open, blunt injuries, delayed repair after 2–3 weeks is recommended to allow scar formation and demarcation of healthy nerve ends. Closed injuries are usually initially treated conservatively. Axonotmetic versus neurotmetic lesions should be differentiated using serial examinations and electrodiagnostic studies after 3 weeks. Surgical exploration using intraoperative elec­trophysiologic monitoring is suggested if no recovery is seen after 3–4 months. At that time, neurotmetic lesions are repaired and axonotmetic lesions are treated conservatively.

    
    
    
    
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      “ Rule of three”: Immediate surgery within 3 days for clean and sharp injuries; early surgery within 3 weeks for blunt injuries; delayed surgery at 3 months for closed injuries

    
    
    
    
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    Conservative management: Includes a period of rest and avoidance of aggravating activities along with bracing and padding for protection of the injured region; a full kinetic chain evaluation should be performed to identify underlying faulty biomechanics predisposing to an overuse neuropathy. Physical therapy can aid in neuromuscular retraining and progressing back to appropriate sport-specific technique. Medications for symptomatic relief, including anti-inflammatory and neuromodulating agents (i.e., gabapentin), can be used for unpleasant dysesthesias.

  
  
  
  
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  Prognosis and recovery: Largely dependent on the type of nerve injury; most traumatic injuries are a combination of axonal and demyelinating pathologies, and prognosis depends on the predominant injury. Mechanisms of recovery include resolution of conduction block (failure of nerve propagation beyond the demyelinated segment), distal axonal sprouting, and axonal regeneration. Resolution of conduction block is typically the first mechanism to promote strength recovery. Recovery after an ischemic injury is quick, whereas demyelinating injuries take up to several months. With an incomplete axonotmesis injury, distal sprouting of intact motor axons starts within 4 days after an injury. In minor axonotmesis injuries, axons can traverse the segment of injury in 8–15 days and then regenerate at a rate of 1–5 mm/day. The regeneration rate is faster for more proximal lesions and after a crush injury, whereas it is slower for distal lesions and after a laceration injury. Even if axons are unable to grow across the injury site, sprouting of motor axons can re-innervate about 5 times their original muscle fiber territory. Moreover, recovery depends on muscle integrity when the nerve reaches it. Muscle remains viable for re-innervation until about 18–24 months after an injury, following which fibrosis develops. Therefore, recovery, including surgical repair, is poor if denervation persists beyond 1–2 years.

  
  
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  Optimal timing of electrodiagnostic testing: NCS can help immediately localize a lesion as conduction is absent across the injury site and is normal distally until Wallerian degeneration is complete as early as day 7. EMG in the first week can help determine whether an injury is complete or incomplete. Presence of even a single motor unit firing on EMG signifies at least partial axonal continuity of a nerve. Using NCS to achieve stimulation above and below an injury site can differentiate between neuropraxia and more severe axonotmesis and neurotmesis as early as day 7 for motor and day 11 for sensory nerves owing to completion of Wallerian degeneration. However, the most useful diagnostic information can be obtained 3–4 weeks after an injury when needle EMG reveals denervation abnormalities. Findings of re-innervation are first seen proximally, progressing distally. Paraspinal re-innervation can be seen as early as 6–9 weeks after an injury, followed by proximal and then distal muscles between 2 and 6 months.

Brachial Plexus and Cervical Root Injuries (“Stingers/Burners”)

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  Overview: Transient neurologic injury accompanied by burning pain in the upper extremity believed to be the result of unilateral nerve traction or compression, generally involving C5 or C6 levels or the superior trunk of the brachial plexus ( Fig. 38.2 ); unclear if this results from brachial plexus or cervical root injury. One of the most common injuries in sports medicine; up to 65% of college football athletes have reported such an injury in their career

  
  

  
  

  
  

  

  
  

  
  

  Brachial plexus schema.

  
  
  
  
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  Proposed mechanisms of injury: Neck extension with lateral bending, resulting in a compression injury; distraction of the shoulder from the head and neck causing nerve traction; or direct blow to the supraclavicular region at Erb’s point (where the brachial plexus is most superficial), causing compressive injury

  
  

  Cervical stenosis predisposes to stingers and may contribute to more complicated mechanisms.

  
  
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  Presentation: Symptoms include unilateral, transient burning pain or numbness with or without weakness starting from the neck/shoulder and commonly radiating in a C5 or C6 distribution. A circumferential rather than dermatomal pattern may be present. Symptoms in lower extremity or bilateral upper extremities should prompt consideration of central cord injury. Care should be taken to distinguish this condition from transient quadriplegia, which may present with bilateral sensory changes, motor changes, or combined sensorimotor deficits. Typically not associated with neck pain or limited range of motion (ROM); symptoms generally last from seconds to minutes; if symptoms last longer or if there is cervical pain or limited ROM, cervical spine MRI should be strongly considered before RTP. Up to 10% have a neurologic deficit lasting from hours to weeks.

  
  
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  Physical examination: Athletes frequently leave the field shaking their arm and hand and may elevate the arm to decrease the neural tension. Initial evaluation should focus on the cervical spine for any evidence of fracture (bony tenderness [particularly midline], deformity, or swelling). If initial evaluation is normal, assess ROM. Conduct a complete neurologic examination, including strength, sensory, and muscle stretch reflex testing. The time of onset and severity of weakness may vary. C5 and C6 are the most common levels affected. Most common sites of weakness are deltoid, biceps, supraspinatus, and infraspinatus, resulting in weak shoulder abduction, elbow flexion, and external rotation of upper arm. Percussion of Erb’s point may elicit radiation of pain. A Spurling maneuver has been shown to recreate symptoms in 70% of cases—good specificity but variable sensitivity. Contralateral examination should be normal. If bilateral symptoms are present, full cervical precautions should be initiated, and the athlete must be transported to an appropriate medical facility for further evaluation and imaging. Shoulder examination must also be performed to rule out other injuries.

  
  
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  Diagnostics: Diagnosis based on physical examination. Radiographs usually normal; consider MRI for prolonged symptoms or recurrent stingers. EMG may be appropriate if symptoms persist beyond 3 weeks. The role of EMG in RTP decisions is controversial because EMG findings may remain abnormal long after clinical symptoms have resolved.

  
  
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  Treatment: Athletes should be removed from play until completely asymptomatic. Immediate supportive treatment includes rest and use of a sling. More chronic symptoms may necessitate anti-inflammatory medications, physical therapy, and occasionally, nerve root blocks. Prevention of recurrence is central to treatment. Rehabilitation should be instituted for neck and shoulder strengthening.

  
  
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  Preventative equipment: To limit excessive neck extension and lateral flexion, high-riding shoulder pads and neck rolls may be considered, but efficacy is debatable. Straps that connect the helmet and shoulder pads are not recommended. Evaluate tackling technique.

  
  
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  Prognosis and RTP: Decision is clinical. Athletes may return to full contact when they have pain-free, full ROM of the neck and shoulder, and normal neurologic examination, including normal symmetric strength. Longer rest periods are indicated for symptoms lasting >15 minutes and for recurrent stingers in the same season. Continue to evaluate for delayed weakness during the same event and for the next 2 weeks. Repetitive or prolonged episodes warrant additional diagnostic testing. Chronic and recurrent stingers have been associated with cervical disk disease, spinal stenosis, and/or neural foraminal narrowing. Prolonged time to symptom resolution (particularly >3 weeks) and recurrent stingers over a short period of time have poorer prognosis. Some experts advocate that if cervical foraminal stenosis is discovered, the athlete should discontinue contact sports.