Abstract
Chronic Pain syndromes are common after traumatic brain injury. This chapter discusses common etiologies for pain syndromes, both central and peripheral, common clinical presentations and treatment approaches to managing the tarumatic brain injury patient with a chronic pain syndrome.
Keywords
Central pain, Central pain syndrome, Pain syndrome, TBI, Thalamic pain
Traumatic brain injuries (TBIs) are a worldwide significant cause of mortality and morbidity. There are approximately 1.4 million TBIs each year in the United States seen by healthcare providers and an estimated 1–3 million more mild injuries that do not seek medical attention. The overall prevalence rate for TBI survivors experiencing disability in the United States is estimated at 3–5 million. Chronic pain syndromes are common after TBI, estimated to affect approximately 50%–80% of TBI survivors, the majority of whom suffer from chronic headache and back pain. There may be a negative correlation between pain reporting and injury severity, with mild TBI survivors reporting more pain than moderate to severe TBI survivors. This difference can be attributed to a variety of factors including attentional, insight, and awareness impairments in moderate to severe TBI survivors versus increased activity and cognitive strain in the mild TBI population. Pain that persists beyond the initial phase (3 months) of healing is considered a chronic pain syndrome, although the time frame when acute becomes chronic has been clinically defined and may be more arbitrary. Concurrent posttraumatic stress disorder, especially among veterans, is common.
Management of chronic pain syndromes after TBI clinically requires understanding of the incidence, physiology, and pathophysiology of central nervous system (CNS) injuries and their effect on pain perception and modulation, relevant anatomic considerations, and a thorough understanding of nonorganic factors that contribute to ongoing reporting of pain. Key tenets of good physiatric management of patients with centrally mediated pain include taking a thorough history from the patient and possibly their caretakers, a comprehensive physical examination, evaluation of objective testing, and then developing a plan of care that allows for treatment of the whole patient, with an emphasis on improving function and quality of life.
Definitions of Pain
The definition of pain is widely accepted as: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. The pain pathways can involve an external stimulus, peripheral sensory nociceptors, subcortical structures, and cortical pathways. In addition, individual psychological factors contribute to pain in the acute and chronic phases and may predominate in these later stages. Assessment of chronic pain involves consideration of factors in each of these areas. Localized tissue damage, the activation of cytokine mediated pathways, and changes in regional blood flow and metabolism have all been associated with physiologic changes after TBI. In regards to anatomic differences, acute painful stimuli generally activate somatosensory, insular, and cingulate cortical regions, whereas spontaneous pain and allodynia activate the prefrontal cortex and limbic regions.
Chronic pain is common after TBI and can be grouped into a few main subtypes: somatic and musculoskeletal injuries, peripheral nociceptive pain, and central and peripheral neuropathic pain syndromes. Nociceptive pain is pain generated from peripheral damaged tissues, whereas neuropathic pain is pain with a generator from either a peripheral nerve or from an aberrant signal from the CNS. The incidence of the peripheral nerve injuries in patients with concomitant TBI is estimated at 34%. Traumatic neuropathies most commonly affect the brachial plexus, followed by the radial, ulnar, and peroneal nerves. About 50% of patients with peripheral nerve lesions experienced neuropathic pain, and patients with traumatic peripheral neuropathies had significantly decreased quality of life reporting. Somatic and musculoskeletal injuries are vast and can include the spectrum of soft tissue injuries (including tendinous, ligamentous, and capsular injuries and joint instability), fractures (both clinically acute and late-diagnosed fractures), heterotopic ossification, and visceral injuries with referred pain. Centrally mediated neuropathic pain can present as either a headache syndrome or more peripheral pain syndromes and is described in more detail in the following sections ( Table 18.1 ).
| Pain Syndrome | Causes | Manifestations | Treatment |
|---|---|---|---|
| Peripheral nociceptive pain syndrome | Damage to tissues: Crush injuries Visceral injuries Fractures Sprains Strains Hematoma Abrasions Wounds Burns Heterotopic ossification | Typically occurs at or near the site of injury | Reduction of inflammation Relative rest Stretching Myofascial release Modalities including ice and heat Immobilization or mobility to improve healing |
| Peripheral neuropathic pain syndrome | Damage (trauma or autoimmune/disease process specific to the peripheral nervous system | Typically follows a more distal to proximal progression (length-dependent process) | Rule out chronic impingement requiring surgical intervention Medication Desensitization techniques Modalities |
| Central neuropathic pain syndrome | Damage to central nervous system, usually thalamus | More distal than proximal, may occur focally or globally, does not follow dermatomal distribution | Medications Desensitization Cortical stimulation Complementary and alternative medicine |
Posttraumatic Headaches
By far, the most common centrally mediated pain syndrome after TBI is posttraumatic headache. The incidence of posttraumatic headache varies; the most widely accepted definition is from the International Classification of Headache disorders (ICHD). The ICHD-Beta 3 defines posttraumatic headache as occurring within 7 days of trauma or the ability to sense and report headache after trauma. It is usually classified as tension-type headache or migraine. The 7-day cutoff may underestimate the number of TBI survivors who experience headaches, which has been reported as up to 71% in the first year. The anatomy of headache involves modulation of a complex series of excitatory and inhibitory neuronal networks, involving changes in afferent input to the trigeminocervical nucleus as well as changes in modulation of nociceptive inputs as excellently summarized by Bogduk.
Diagnostic criteria for posttraumatic headaches rely exclusively on patient reporting, and thus the clinician should document the location, duration, onset, radiation, associated symptoms, and ameliorating and exacerbating factors with each visit. Pain-related behaviors and the consistency of those behaviors should also be observed and documented. In addition, headache logs and standardized questionnaires are more likely to be used in specialty headache centers as part of the evaluation process. Serial administration of standardized headache questionnaires such as the Migraine Disability Assessment score can be useful in determining the impact on quality of life. Factors associated with prolonged headaches include history of prior headaches, less severe injury, female gender, and history of psychiatric disorder. This comprehensive assessment helps to document changes in headache character over time and also aids in the detection of inconsistencies, which may represent manifestations of secondary gain.
Although these approaches can be helpful in treating mild TBI survivors, unique challenges exist for patients with moderate to severe injuries. Difficulty with alertness, attention, verbal expression, insight/awareness, and agitation may make it difficult to understand for certain whether a patient is in pain as well as make it difficult to understand the specific characteristics of the painful condition, such as subtleties of any ameliorating or exacerbating factors. Observation of pain-related behaviors, correlation between physical movements and worsening agitation, fluctuations in vital signs, and any asymmetry on physical examination can be a clue to the clinician to pursue further diagnostic studies.
International Classification of Headaches (ICHD-Beta 3) taxonomy delineates a few different headache syndromes. The first is acute headache attributable to moderate or severe injury to the head and must include one of the following: (1) loss of consciousness for >30 min; (2) Glasgow Coma Scale score <13; (3) posttraumatic amnesia lasting >24 h; (4) alteration in the level of awareness for >24 h; (5) imaging evidence of a traumatic head injury, such as intracranial hemorrhage and/or brain contusion. Acute headache caused by mild TBI involves lack of inclusion into the moderate or severe category, plus one of the following: (1) transient confusion, disorientation, or impaired consciousness; (2) loss of memory for events immediately before or after the head injury (anterograde or retrograde amnesia); (3) two or more other symptoms suggestive of mild TBI: nausea, vomiting, visual disturbances, dizziness and/or vertigo, impaired memory and/or concentration. Chronic headache is defined as symptom duration lasting more than 3 months.
The awareness of the morbidity of blast-related injury after military deployment has led to more research into the prevalence of headache in this population. Military veterans with history of deployment-related TBI report more frequent, persistent headaches than age-matched controls.
Differential diagnosis of posttraumatic headache involves probing into contributing and potential external factors. The presence of intracranial bleeding or mass lesion is typically ruled out with CT scan of the head in the initial management of TBI. The presence of an intracranial lesion should prompt neurosurgical consultation. Typically, a negative CT scan with persistent symptoms is followed by MRI to rule out any other mass or demyelinating process.
The presence of cervicogenic headache due to instability and/or pain from the cervical joints and associated ligaments, as well as the potential for trigger-point associated referred pain patterns, should be considered. Palpation of the posterior cervical musculature should also be assessed, as it can contribute to headache reporting, and patients with chronic tension-type headaches have lower pain thresholds for trigger points than patients without chronic headache. Orthopedic spinal injuries affecting spinal stability should be evaluated, as these injuries can contribute to chronic headache symptoms via referred pain pathways.
Assessment of the patient’s psychological milieu is imperative. Often traumatic events are associated with attributing premorbid symptoms to the event. Teasing out the presence or absence of symptoms before the TBI is an important clinical strategy. Malingering and other forms of secondary gain constitute a minority of cases of chronic headache; there is some evidence to suggest that societal factors influence persistent symptom reporting.
The course of posttraumatic headache is variable and unpredictable, although the overall prognosis is generally good. The most common presentation resembles tension-type headache and/or migraine or a mixture of headache syndromes and is most commonly reported in the temporal region (see Table 18.2 ). Eighty percent of patients improve over time; however, the duration of improvement can vary widely up to 6 months. Approximately 20% of patients report infrequent headaches at 1 year after their injury, with 5% of patients reporting persistent daily headache. Clinical worsening of headache presentation may be attributable to changes in environmental factors, including referred pain from musculoskeletal disorders, an increase in activity, increased depression, frustration or negative impact related to changes in social participation and fulfillment of societal roles, or medication overuse headaches.
| Common Types of Primary Headache | Clinical Manifestations |
|---|---|
| Migraine headache | May or may not be accompanied by aura or prodrome Female predominance Deep pulsating pain or throbbing Sound/light sensitivity Nausea and vomiting are common |
| Tension-type headache | Typically described as bitemporal, dull ache Female predominance Nausea and vomiting are rare Not associated with aura May last several days |
| Cluster headache (the most common of the trigeminal autonomic cephalgias) | Unilateral, stabbing pain, usually around the eye Sudden onset Male predominance Nausea and vomiting are rare |
The current clinical guidelines for treatment recommend identification of the most closely associated headache type and treatment of headaches based on the headache type. Posttraumatic tension-type headaches should be treated according to clinical practice guidelines for tension-type headaches in the non-TBI population, whereas migraine-type posttraumatic headaches should be treated according to clinical practice guidelines for migraine-type headaches in the non-TBI population. The medications recommended by the Ontario Neurotrauma Foundation Guidelines for mild TBI and persistent symptoms are given in Table 18.3 .
| Headache Type | First-Line Therapy | Second-Line Therapy | Third-Line Therapy |
|---|---|---|---|
| Tension type Unclassified type | Amitriptyline or nortriptyline 10 mg PO QHS, increasing 10 mg every 1–2 weeks as necessary/tolerated to a dose of 50–100 mg PO QHS. Choose amitriptyline if concomitant sleep issues | Gabapentin 100–300 mg PO QHS, increasing by 100–300 mg every 5 days as needed to a maximum of 600 mg PO TID | |
| Migraine type | Amitriptyline or nortriptyline 10 mg PO QHS, increasing 10 mg every 1–2 weeks as necessary/tolerated to dose of 50–100 mg PO QHS Or Nadolol 20 mg PO BID and increasing by 20 mg every 5 days as necessary/tolerated to 30–80 mg PO BID or Propranolol 20 mg PO TID and increasing by 20 mg every 5 days as necessary/tolerated to a maximum of 80 mg PO TID | Topiramate starting at 12.5 mg PO QHS and increasing by 12.5 mg PO QHS weekly as necessary/tolerated to a maximum of 100 mg PO QHS Or Gabapentin 100–300 mg PO QHS and increasing by 100–300 mg every 5 days as necessary/tolerated on a TID schedule to a maximum of 600 mg PO TID | Verapamil 40 mg PO TID and titrating to 80 mg PO TID as necessary/tolerated Or Pizotifen 0/5 mg PO QHS and increasing by 0.5 mg every week to a maximum dose of 3.0 mg PO QHS Or Flunarizine 5 mg PO QHS and increasing to 10 mg PO QHS after 10–14 days |
In addition to oral therapies, botulinum toxin is an effective treatment for chronic migraine and tension-type headaches. It may be a useful agent in patients with medication noncompliance. Botox should be considered when first- or second-line medications are unable to effectively manage chronic migraine headaches. The US Food and Drug Administration indications for botulinum treatment are for patients experiencing more than 15 days of headaches per month for more than 4 h per day. It has been shown to have long-lasting and reproducible long-term effectiveness with repeat treatments, typically 155 units injected over 31 areas. Other future treatment options may include antibodies to neuropeptide calcitonin gene-related peptide, which are currently being studied in animal models and Phase II clinical trials.
Medication overuse headaches should be considered in those headaches that persist. Medication overuse headaches are defined as headaches occurring more than 15 days per month with use of simple analgesics more than 15 days/month or a combination analgesic more than 10 days per month for 3 months or more. If this diagnosis is made, withdrawal of medication is the recommended treatment. However, there are no evidence-based clinical practices that have been shown to be more effective than others. Special considerations regarding TBI include safety of nonsteroidal antiinflammatory drugs or triptans in the setting of any recent intracranial hemorrhage.
Several nonmedication modalities have been shown to be effective for the treatment of posttraumatic headache. Mindfulness therapy is a meditative therapy with emphasis on focusing on individual aspects of body function while blocking out distracting thoughts. It was studied in chronic episodic migraineurs and led to a statistically insignificant reduction in headaches compared with standard therapy. Another small study in tension-type headaches showed a benefit of mindfulness therapy.
Group-based acceptance and commitment therapy, a form of psychotherapy that recognizes the current difficult situation at hand and attempts to move forward toward a desired goal, significantly reduced disability and anxiety, in a mix of patients with chronic tension-type and migraine-type headaches. In addition, yoga has been shown to be of benefit in the reduction of symptoms of chronic migraine in addition to conventional therapies.
Transcranial magnetic stimulation treatments were observed to reduce chronic migraine headache-related frequency and intensity as efficaciously as Botox, although the effect was reduced after 8 weeks, whereas the Botox-related effect persisted for about 12 weeks. Acupuncture has been generally accepted as an effective treatment for chronic headache and has been shown to decrease headache intensity. Overall, the use of complementary and alternative medicine (CAM) in the setting of chronic migraine has been shown to reduce moderate mental distress in women with chronic headache but not in men. The use of CAM is higher in the population with chronic headache than in the general population and is growing, and it is estimated to have been utilized in approximately 30% of the general population in the last 12 months.
Overall, a multidisciplinary and holistic approach to posttraumatic headache offers patients the best possible prognosis. Patients should be counseled regarding sleep hygiene, adequate hydration, environmental modulation, and stress management as a foundation for using other therapeutic interventions. In general, this prognosis is very good. Most patients with TBI with posttraumatic headaches see resolution or a significant reduction of their headaches within 6 months. The management of persistent, chronic headache is best achieved with a calculated, comprehensive approach that involves the identification of medical, musculoskeletal, psychiatric, and environmental factors that may be contributing to the persistence of posttraumatic headaches and then targeting therapies to help reduce symptom burden, with a focus on improving functional status.
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