Headache is the most common physical symptom of TBI.

The prevalence of headache after TBI is approximately 58% to as high as 90%.

The International Headache Society (IHS) defines posttraumatic headache (PTH) as:

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  “When a new headache occurs for the first time in close temporal relation to trauma or injury to the head and/or neck, it is coded as a secondary headache attributed to the trauma or injury. This remains true when the new headache has the characteristics of any of the primary headache disorders classified in Part One of ICHD-3.”

  
  
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  “When a preexisting headache with the characteristics of a primary headache disorder becomes chronic or is made significantly worse (usually meaning a two-fold or greater increase in frequency and/or severity) in close temporal relation to such trauma or injury, both the initial headache diagnosis and a diagnosis of [PTH]. Headache attributed to trauma or injury to the head and/or neck (or one of its types or subtypes) should be given, provided that there is good evidence that the disorder can cause headache.”

This new headache or exacerbation of preexisting headache occurs within 7 days of trauma to the head.

If headache symptoms persist for less than 3 months, it is termed acute . If symptoms persist for greater than 3 months, the headache is termed persistent .

The IHS uses a 7-day window for diagnosis of posttraumatic headache, but PTH may develop beyond this window —commonly referred to as delayed onset.

PTH, although common in isolation, evaluation should be considered for other symptoms of postconcussive syndrome symptoms:

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  Fatigue, memory deficits, dizziness, insomnia, impaired concentration, irritability, blurred vision, anxiety, light, and sound sensitivity

Patients with preexisting headache and female gender are more likely to report PTH.

Severity of TBI is not felt to be related to the incidence of posttraumatic headache.

Posttraumatic seizures and intracranial hemorrhage do, however, correlate with increased severity of headaches reported at 36 months.

Migraine-type headache is the most common category of posttraumatic headache and accounts for approximately 35% of posttraumatic headache types.

Probable migraine type headaches account for approximately 25% of PTH.

Tension-type headaches account for approximately 20% and cervicogenic headache approximately 10%.

Often more than one headache type is identified.

The mechanisms of PTH are not fully understood but are hypothesized to occur through central and peripheral factors.

Proposed peripheral mechanisms include damage to cranial tissues such as arteries, dura mater, bone, muscle, cranial nerves, skin, and fascia, which creates an inflammatory state vis-a-vis release of cytokines and chemokines.

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  Activation of this cascade results in local monocyte and glial cell activation along with release of nociceptive neuropeptides resulting in spontaneous pain, hyperalgesia, and allodynia.

Proposed central mechanisms include damage to spinothalamic and thalamocortical pathways resulting in hyperexcitability of central neurons and a possible decrease in descending inhibitory pain control.

Psychological factors such as posttraumatic stress disorder, anxiety, and depression may also be associated with PTH. ^,

At this time, there are no US Food and Drug Administration–labeled medications approved for management of posttraumatic headache.

Some practitioners have successfully used treatment strategies focused on the primary headache.

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  This includes abortive and preventive migraine medications used off label.

Care should be taken when using these pharmacologic treatment strategies to avoid precipitating rebound or medication overuse headaches.

Understanding the initial mechanism of injury may be beneficial in decision making because the presence of occipital neuralgia, cervicogenic headache, or oculomotor or vestibular dysfunction may allow another treatment strategy.

Most common physical symptom after TBI

Either a new headache or exacerbation of existing headaches after trauma

May be part of a postconcussive syndrome; consider evaluation for other symptoms

Mechanisms not well understood; likely involves both central and peripheral mechanisms

Migraine-type headaches most common

Consider tailoring treatment strategies based on primary headache type

CRPS is a clinical syndrome that often occurs after trauma.

The hallmark of this disorder is pain and typically includes sensory, autonomic, motor, and trophic changes.

Gellman et al found that patients with severe TBI had a 12% incidence of CRPS (primarily in limbs with spasticity).

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  Among these patients, 75% had an injury to the affected limb.

CRPS has a peak incidence between 37 and 50 years of age.

CRPS affects women more commonly than men, at a ratio of 2:1 to 4:1

CRPS affects the upper extremities more commonly than lower extremities.

CRPS is a clinical diagnosis relying on a thorough clinical history and examination.

The International Association for the Study of Pain has adopted the Budapest Criteria for diagnosis of CRPS, in which there is a sensitivity of 0.99 and specificity of 0.68.

The diagnostic criteria are as follows:

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  “Continuing pain which is disproportionate to any inciting event.

  
  
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  At least one symptom in three of four of the following categories:

  
  
  
  
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    Sensory: Reports of hyperalgesia and/or allodynia.

    
    
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    Vasomotor: Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry.

    
    
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    Sudomotor/Edema: Reports of edema and/or sweating changes and/or sweating asymmetry.

    
    
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    Motor/Trophic: Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin).

  
  
  
  
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  Must display at least one sign at time of evaluation in two or more of the following categories:

  
  
  
  
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    Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint movement).

    
    
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    Vasomotor: Evidence of temperature asymmetry (>1°C) and/or skin color changes and/or asymmetry

    
    
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    Sudomotor/Edema: evidence of edema and/or sweating changes and/or sweating asymmetry

    
    
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    Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin).

  
  
  
  
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  There is no other diagnosis that better explains the signs and symptoms.”

Pain associated with CRPS is often described as burning, continuous, and exacerbated by movement, stress, or pressure.

Temperature changes and swelling may be seen in the affected limb.

The pain may not follow a specific dermatome or peripheral nerve distribution and often has more distal than proximal involvement.

If the symptoms develop after an injury not identifiable as trauma to a specific nerve, it is classified as CRPS type I (previously known as reflex sympathetic dystrophy ).

If symptoms develop after damage to a peripheral nerve, it is classified as CRPS type II (previously known as causalgia ).

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  CRPS type II symptoms may initially be confined to a specific peripheral nerve distribution but can become more diffuse over time.

Additional diagnostic testing may be performed but is not required for making the diagnosis and should be directed at excluding other possible diagnoses.

These studies have been used in the past to support a diagnosis of CRPS:

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  Triple phase bone scan: The uptake phase may demonstrate a characteristic pattern of subcutaneous blood pool changes.

  
  
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  Radiography may demonstrate patchy bone demineralization.

  
  
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  Sudomotor testing, which is not commonly available, may reveal side-to-side asymmetry.

The pathophysiology of CRPS is not well understood but is believed to stem from peripheral and central sensitization mechanisms and abnormal coupling of peripheral nociceptive afferents and sympathetic efferent neurons.

The treatment of CRPS in patients with TBI is similar to that of non–brain-injured individuals.

The mainstay of treatment of CRPS is a gradual and progressive rehabilitation program that uses pharmacology, physical therapy, and pain interventions, if necessary.

Initial therapy should be focused on reactivation of the affected extremity, contrast baths, desensitization/contrast textures, mirror-box therapy, and graded motor imagery.

As the patient’s symptoms improve, careful progression from low-intensity stimuli, such as isometric strengthening, to more intense stimuli, such as aerobic conditioning and movement therapies, is recommended.

Sympathetic plexus blocks have been shown to be beneficial for short-term pain relief and may help by interrupting sympathetic coupling/outflow that likely occurs in CRPS. ^,

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  Although these blocks may provide short-term benefit, they are unlikely to completely manage symptoms of CRPS in isolation.

  
  
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  The combination of physical and/or occupational therapy with multimodal care may improve outcomes.

There are relatively few randomized controlled trials designed to evaluate the efficacy of spinal cord stimulation in CRPS, but spinal cord stimulation and dorsal root ganglion stimulation have been used as a treatment option for refractory CRPS.

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  Symptom improvement in CRPS with spinal cord stimulation tends to be greatest in the first year, with subsequent reduction in pain relief by year five. ^,

Clinical diagnosis by Budapest Criteria; additional diagnostic testing is not required

Pathophysiology not well understood; involves central and peripheral mechanisms and may involve abnormal coupling of peripheral nociceptive afferents and sympathetic efferent neurons

Treatment should include therapy disciplines with inclusion of sensitization exercises.

Evidence for various pharmacologic and interventional treatment strategies in CRPS is limited, and clinical practice is often based on extrapolation of data from other neuropathic pain conditions.

Myofascial pain arises from the muscles and/or fascia and can be associated with taut bands of skeletal muscle called trigger points .

There are no accepted diagnostic criteria for this disorder, and a broad differential should be considered before making the diagnosis.

After headache, the neck, shoulders, back, and limb are the most frequent sites of pain in brain injury, which in part may be myofascial in nature.

Causes of myofascial pain may be varied and should be fully evaluated.

In the acute setting of TBI, consider the mechanisms involved and potential for unrecognized bony, ligamentous, or tendinous injury.

Chronically consider:

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  Deconditioning related to prolonged hospitalization and recovery may alter patient mobility and contribute to pain.

  
  
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  Alterations in biomechanics, postural changes, and heterotopic ossification may contribute to patient discomfort over time.

  
  
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  In the setting of TBI, spasticity may be an additional contributor to patient discomfort.

Treatment for myofascial pain may include physical therapy for stretching, posture training, massage, myofascial release, and modalities such as heat, ultrasound, and transcutaneous electrical nerve stimulation.

Medication options: Begin with over-the-counter NSAIDs and/or acetaminophen.

If symptoms are refractory to these treatments, consideration may be given to SNRIs, such as duloxetine.

If clinical examination suggests spasticity, then medications such as baclofen and tizanidine should be considered.

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  Diazepam may serve a role in the treatment of spasticity, but risks and benefits should be considered carefully in light of risks of sedation and dependence.

If trigger points are found on exam (taut bands of muscle that produce a characteristic radiating pain when palpated), consideration may be given for trigger point injection or dry needling.

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  This injection involves identifying the trigger point and inserting a needle into the area of pain, often resulting in a muscle twitch or spasm, which may reduce pain for a period.

Pain arising from muscles/fascia; may be associated with trigger points

No diagnostic criteria; consider a broad differential prior to making this diagnosis

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  In the acute setting, consider bone, ligament, or tendon injury.

  
  
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  Chronically, consider effects of deconditioning, biomechanical changes, spasticity, and heterotopic ossification.

Treatment should include physical therapy and therapeutic modalities.

Medication, if necessary, should primarily be with NSAIDs and/or acetaminophen.

Trigger points, if present, may be amenable to treatment with trigger point injections.