Headache in Whiplash

Chapter 7 Headache in Whiplash


A Comprehensive Overview



The impact of headache associated with whiplash is significant but has thus far proven difficult to quantify.


Accessing data about whiplash-associated headache disorders is difficult at best. The National Accident Sampling System (NASS) lists only the top six injuries that have occurred in a crash resulting in a tow-away. This may not include a soft tissue injury such as a whiplash, let alone a resultant headache. And, of course, many such injuries do not result from a crash that results in a tow-away.


Acquiring data from emergency department records is also problematic. Post-whiplash headache may not appear in the first 24 or 48 hours, and even if it does, it may not be the chief complaint and may not be recorded clearly or prominently. Furthermore, not everyone involved in a car crash will present to the emergency department. Prevalence data of whiplash-associated headache are thus estimates and have been reported as varying from 32% to 80%.1 Whereas costs of whiplash have been estimated at $4.5 billion annually in the United States, the costs of whiplash-associated headache are unknown.



Taking a Headache History


Studies of doctors and patients have found that the best way to elicit history is to ask open-ended questions and allow the patient to tell their story. The American Migraine Communication Study, in particular, found this was especially important in taking a headache history.2 Ask patients to describe when their headaches began and how their headaches feel. Allow them to speak, uninterrupted, until they are finished. You will find that with most patients, this takes only about 2 minutes or less. Then you may begin to ask more specific questions to fill in the gaps of what you need to know.


Major historical features to cover in a headache history are frequency of headache, severity of pain, quality of pain, duration of headache, and degree of disability. Location of pain is also important; it is most important if it never changes. Associated headache features should also be determined, meaning presence of nausea, avoidance of light and/or sound, dizziness, difficulty with concentration due to head pain, or visual disturbances.


Frequency of headache may at first be daily. However, as recovery progresses, the headache disorder usually becomes intermittent, and it is important to see the frequency and duration of headache attacks. Headache diaries can be useful in this regard (Figure 7-1).



These may be as simple as a grid to record yes/no for headache, and estimated time of pain, or may be very complex, with room to record detail such as associated symptoms or treatments tried. The patient should use the diary format that best suits their needs. No diary will work if it is not used.


Many patients do not understand the term “quality of pain”; just ask them “What does the pain feel like?” Sometimes, it may be necessary to prompt with adjectives, such as squeezing, dull, sharp, or throbbing, but it is best to avoid this if possible, and allow patients to express it in their own terms. Severity of pain is often expressed in descriptive terms rather than a numeric scale. One person’s “3” may be another person’s “6.” A standard practice in headache medicine is to grade headache pain as none, mild, moderate, or severe. Others prefer a 0-10 pain scale such as the Visual Analogue Scale (VAS). Both scales are useful in the ongoing evaluation of headache to monitor progress of individual patients. Pain scales are subjective and not reliably reproducible between patients. If more objective measures are desired, it should be realized that current technology does not support objective measurement of the experience of pain. The best that can be done is the standardization of subjective reports, and for that, the Headache Impact Test (HIT-6) can be used.3 Although the HIT-6 is a measure based on subjective reporting by the patient, it is a standardized method that yields a numeric value and thus means the same thing to everyone. The Migraine Disability Assessment Scale (MIDAS), devised for measuring disability related to migraine headache, can also be adapted for other headache types and provides a quantifiable scale as well4 (Figure 7-2).



Degree of disability should be discussed with the patient. Are there things they are no longer able to do because of head pain? Are they avoiding social activities? Is it affecting home life? Are they able to work? Headache disorders have been socially stigmatized, and many patients will go to work with pain and simply be less productive, or even call in with the “flu” before they will admit disability due to headache pain.


Associated symptoms may or may not be present in whiplash-associated headaches. Nausea can be a concomitant of headache and does not in itself necessarily denote concussion. Whether or not nausea indicates concussion depends on timing, and on the presence of cognitive symptoms. Avoidance of light or sound, or aggravation of headache pain by bright light or noise, is a fairly common associated symptom. Dizziness is often reported in whiplash-associated headache. This may manifest as true vertigo, described as a spinning sensation, especially with head tilting or turning, or may manifest as dysequilibrium, in which there is a sense of feeling unsteady or off-balance.


Visual disturbances also occur in association with headache disorders. Some visual disturbances are intrinsic to the headache itself, which usually occurs in migraine headaches. Existing migraine headaches may be exacerbated by a whiplash injury and can certainly be exacerbated by head injury.5 However, visual blurring, double vision, or changes in visual processing can occur as a consequence of mild head trauma or whiplash in those who have never experienced migraine.6,7


Although not specific to headache, it is important to be certain that there have been no episodes of loss of consciousness, which could indicate a posttraumatic seizure disorder.


And, finally, at the conclusion of the patient encounter, it is useful to ask if the patient has additional issues or questions. Research done at UCLA in primary care indicates that it is more effective to ask, “Is there something else you want to address in the visit today?” than to ask, “Is there anything else you want to address in the visit today?” Surprisingly, this single word change brought out answers in an additional 40% of patients.8



Types of Headache That Might Be Encountered



Posttraumatic Headaches


The posttraumatic headache is defined as a headache following head trauma. There are a variety of grading systems for head injury. In terms of classifying posttraumatic headache, the International Classification of Headache Disorders, second edition (ICHD-2) of the International Headache Society (IHS) has divided posttraumatic headaches into acute and chronic and into mild and moderate-severe (Table 7-1). In this scheme, moderate or severe head injury requires loss of consciousness for more than 30 minutes, a Glasgow Coma score of less than 13, or posttraumatic amnesia for more than 48 hours. Mild head injury in the ICHD-2 requires all these: no loss of consciousness or loss of consciousness less than 30 minutes, a Glasgow coma score ≥13, and symptoms or signs diagnostic of concussion.9



Posttraumatic headaches occur in a high proportion of head-injured individuals. Motor vehicle collisions are the most common cause of head injuries, constituting 42%. Earlier estimates indicated that between 30% and 50% of those who sustained mild head injury would experience headache lasting 2 months or more; more recent data suggest acute posttraumatic headache affects up to 80%.10,11 Mild head injury is associated with an increased risk of chronic posttraumatic headache.12 Paradoxically, the severity of head injury is inversely proportional to the severity of posttraumatic headache.13 Posttraumatic headache results in more disability than the primary headaches do (migraine, tension-type headache, cluster headache, and others).14


There is no usual headache type that characterizes posttraumatic headache. The pain may be constant or intermittent, pulsating or non-throbbing, sharp or dull. In some patients, there may be more than one type of headache pain reported. Photophobia, phonophobia, nausea, and vomiting are fairly common in posttraumatic headache. The presence of double vision, anosmia, or other neurological abnormalities indicates a higher likelihood of chronic posttraumatic headache. Anosmia, memory loss, dizziness, irritability, depression, anxiety, and personality change occur in 20% to 25% of those with chronic posttraumatic headache.11


The exact pathogenic mechanisms of posttraumatic headache remain unclear. Historically, “chronic” posttraumatic headache had to last more than 2 months. More recently, the IHS ICHD-2 somewhat arbitrarily declared 3 months as the cut-off for chronic posttraumatic headaches.9 Approximately 20% of posttraumatic headaches will last more than 1 year, and a substantial number of these may become permanently chronic headache.15




Cervicogenic Headache: A Matter of Terminology


To many, the term “cervicogenic headache” simply means a headache arising from cervical structures. The term has a far richer, and more contentious, history. It is beyond the scope of this book to trace that history, but the reader should be aware that the term, when encountered in the literature, may carry differing connotations, depending on author and author’s background, date of publication, and country of origin.


There have been diagnostic criteria established by the IHS, as well as by the Cervicogenic Headache International Study Group (CHISG).9,19 The difficulty at present is that it has been determined that upper cervical and posterior head pain is common in primary headache disorders such as migraine, tension-type headache, and even trigeminal autonomic cephalgias. The mere existence of neck pain is not sufficient for a diagnosis of cervicogenic headache. Moreover, existing criteria do not adequately address biomechanical concerns.


The CHISG diagnostic criteria have, since 1998, been somewhat muddied by various reports of migraine symptom patterns. The criterion requiring unilateral neck pain has been eroded by several reports of migraine presenting with neck pain. There has also been a recent study describing reduced cervical range of motion in women with migraine, casting some lack of clarity on that criterion for cervicogenic headache.20 The IHS criteria have, in the revised version, been simplified to the point of a danger of lack of specificity. In the CHISG criteria, the underlying principle is that the diagnosis is not proved without invasive diagnostic anesthetic nerve blockade of C2, the “third occipital nerve,” or other suspected cervical structures, including facets.


Opposing opinions in the headache field have arisen, pointing out emerging evidence of trigeminal pathways within the cervical spinal cord, as well as other areas of diagnostic uncertainty due to symptom overlap between various headache syndromes. Again, it is not the scope of this book to debate these issues in detail. This trigeminocervical complex and its role in headache and neck pain will be discussed in further detail later in this chapter.



Pre-existing Headache Syndromes Exacerbated by Whiplash


A pre-existing headache syndrome is prone to worsening when subjected to a whiplash injury. The argument has been made, in fact, that whiplash headache is solely due to a transitory worsening of a pre-existing primary headache.21 This conclusion was based on the logic that both the collision group and the matched controls had the same long-term prognosis (at 1 year), and that therefore the headaches were primary headaches, with worsening most likely induced by the stress of the accident situation. Given that this study was conducted in Lithuania by the same investigators who did the original Lithuanian study, it would be reasonable to conclude that there might be some bias present.22


A retrospective records review of 2,771 headache patients, looking for correlation with trauma, found a trauma history in 1.3% of migraine patients, 1.5% of tension-type headaches, and 15% of cervicogenic/neck-associated headaches. The majority of the traumatic incidents were believed to include a whiplash action. Some of the headaches occurred remote to the trauma history. This data set suggests that worsening of migraine, if present, is not likely to be long-lasting on the basis of whiplash injury.23 Anecdotally, many headache experts will state that pre-existing headache disorders will be exacerbated by whiplash injuries. Unfortunately, this population is often excluded from study populations, and thus, many questions remain.



Temporomandibular Dysfunction


Temporomandibular dysfunction, also called temporomandibular joint disorder (TMJD) can occur as the sequelae of whiplash injury, even without direct trauma to the jaw. If the individual does not see the collision coming, for example, and has the mouth open, perhaps in conversation, the forces involved in a whiplash can cause sudden forcible closure of the jaw. In lateral collisions, there is increased risk of direct trauma to the jaw.


Either bruxism, which is clenching or grinding, or frank temporomandibular dysfunction can exacerbate or trigger any co-occurring headache type. There are two types of temporomandibular disorders recognized by the American Academy of Orofacial Pain: myogenous temporomandibular disorder (TMD) and arthrogenous TMD. Myogenous TMD is due to bruxism, clenching, or both, and lacks evidence of joint pathology. Arthrogenous TMD is secondary to some level of articular disorder and may include disc derangement or degeneration. Symptoms may overlap, and some individuals may have both conditions.


TMD occurs more frequently in women, with a 4 to 1 ratio reported.24 In the setting of trauma, there has often been a tendency to attribute TMD primarily to personality factors rather than to sequelae of trauma, similar to the tendency to dismiss chronic TMD in nontrauma patients as a function of personality factors or psychiatric disorders.


Clearly, not everyone with TMD is depressed. There is a study that shows no difference in pain levels between depressed TMD patients who received intervention for depression and nondepressed individuals with TMD.25 Most significantly, it has recently been discovered that individuals with TMD are more likely to have an abnormality in the serotonin transporter gene, which indicates that there may be an inherited predisposition to abnormal pain processing in at least some TMD patients.26


Arthrogenous TMD often results in the popping, clicking, and loss of parafunction often associated with TMD, such as inability to fully open the jaw. This can result in a variety of symptoms, not always listed as the cardinal diagnostic features. These include ear pain, tinnitus, a sense of fullness in the ear, hyperacusis (hypersensitivity to ordinary sound levels), and dizziness.


Both patients with myogenous TMD and arthrogenous TMD should be monitored for signs and symptoms of a worsening condition, heralded by increasing or new sounds generated by the use of the jaw, decreased jaw range of motion, decreased function, and increasing pain. Onset of new ear symptoms may also be a clue.


The National Institute of Dental and Craniofacial Research in a 1996 consensus statement recommended that treatment measures for TMD should be reversible when at all possible, citing the lack of universally accepted, scientifically based diagnostic guidelines and the need for further study. The use of stabilization splints (night guards, bite splints), although used widely, remains controversial.


Self-care measures for myogenous TMD causing myofascial pain include the use of moist heat, avoidance of chewing gum, and in marked cases, a soft diet. Self-awareness of clenching, which can be difficult to reinforce, is important in order to reduce this behavior. Physical therapy or relaxation training measures may be of assistance. For a discussion of manual techniques used in the treatment of TMD, see Chapter 6.



Low Pressure Headaches


Low pressure headaches associated with cerebrospinal fluid (CSF) leaks can occur in the setting of head and neck trauma. Acute CSF leaks are infrequent, but they present in a relatively straightforward fashion for those diagnosticians who retain a high index of suspicion. Low pressure headaches are typically diffuse, dull headaches that become worse within 15 minutes of sitting or standing and that generally are accompanied by at least one of the following: neck stiffness, tinnitus, hypacusia, nausea, or photophobia.


The condition that may well be more common in the setting of whiplash is the low pressure headache due to a subacute CSF leak. This will present with essentially the same symptoms as the acute CSF leak headache but is less likely to be affected by position. There is considerable symptom overlap between low pressure headaches, also known as intracranial hypotension, and whiplash-associated headache. An interesting study, noting this overlap, looked at 66 patients with chronic whiplash-associated disorder and performed radioisotope cisternography in all in search of a CSF leak. A surprising 56% (37) were positive. Symptoms in the positive group were—in addition to headache—dizziness, memory loss, visual impairment, and nausea. Symptoms were markedly improved after epidural blood patch, and half were able to return to work.27


The work-up of low pressure headache should begin with cranial MRI with contrast. Pachymeningeal enhancement can be seen in intracranial hypotension but is not always present. If clinical suspicion persists, the next diagnostic study to be pursued is either myelography or cisternography. Lumbar puncture will need to be performed for either of these studies, and it is essential that an opening pressure be measured. A pressure of less than 60 mm H2O in the sitting position is diagnostic of intracranial hypotension.9 Low pressure headaches tend to be resistant to medication and are treated with an epidural blood patch.



Headache with Autonomic Symptoms


Although infrequent, sometimes headache syndromes with autonomic features can be seen in the setting of either posttraumatic or whiplash-associated headaches. Both cluster headache and hemicrania continua have been reported.28,29


Hemicrania continua is an infrequently seen headache, manifesting with a baseline underlying headache of mild to moderate severity with superimposed exacerbations of severe pain. Exacerbations often center in the temporal and orbitofrontal regions. There may be stabbing pains. The headache is “side-locked,” meaning that it does not switch sides. Typically, there are associated autonomic features, which include nasal congestion, eyelid edema, tears, conjunctival injection, and ptosis. Often, ocular discomfort will be present, reported as a gritty sensation or foreign body sensation. There may be associated features of nausea, photophobia, and phonophobia.


Classically, hemicrania continua has been held to be so dramatically responsive to indomethacin that an absolute response to indomethacin was felt to be diagnostic. More recently, however, there have been reports of indomethacin-unresponsive hemicrania continua. Patients may respond to other nonsteroidal anti-inflammatory agents.


Cluster headache can also occur as a consequence of trauma, and has been reported in the setting of whiplash as well as head injury.29 Cluster headache is a severe headache, sometimes colloquially known as “the suicide headache” because of the excruciating nature of the pain that occurs during attacks. Cluster headache is so named because of the periodicity of headache attacks, which often occur in clusters. Headaches tend to be relatively short, usually lasting 30 to 60 minutes, although they may last up to 3 hours. It is common for cluster headache sufferers to experience two or three attacks per day; up to eight attacks per day have been noted. Often, one of the attacks will occur at night and may correlate with the first rapid eye movement (REM) period of sleep.


The pain in the cluster headache attack is unilateral and focuses in the orbital region or the temporal region. The pain, which may be described as constant, stabbing, burning, or throbbing, is always severe or very severe. Most cluster headache sufferers feel restless or agitated during attacks. There may or may not be associated nausea, photophobia, or phonophobia. The characteristic autonomic features of cluster headache are tears and conjunctival injection on the same side as the headache, which occur in 80% of cases, and nasal congestion or clear drainage, also ipsilateral, which occurs in 75% of cases. Other autonomic symptoms that may be seen are forehead sweating, eyelid edema, ptosis, and pupillary constriction. The prevalence of head trauma in cluster headache has been reported ranging from 5% to 37%. The onset of cluster headaches may be somewhat remote to the occurrence of whiplash or head trauma.

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Mar 13, 2017 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Headache in Whiplash

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