Post traumatic headache can occur after mild, moderate, or severe traumatic brain injury (TBI). The most common symptom is headache, which usually resolves within 3 months but can become chronic. Headaches occurring after TBI are often indistinguishable from primary headache disorders like tension-type headache or migraine. Post traumatic headache accounts for about 4% of all secondary headaches. Treatment involves both pharmacological and non-pharmacological approaches based on the type of headache, and may include abortive medications, prophylactic medications, nerve blocks, trigger point injections, and behavioral therapies. Managing any comorbid conditions is also important for optimal treatment of post traumatic headache.
2. Introduction
Post concussion syndrome (PCS) it is a symptom complex that includes
headache, dizziness, neuropsychiatric symptoms, and cognitive impairment after
TBI.
M/C symptom to occur is headache.
Can occur after mild, moderate, or severe TBI, usually resolving within the first
3 months, although a minority develop chronic headaches.
3. Introduction
More common after a mild TBI than more severe injuries.
Headaches occurs variably in 25% to 78% of persons following mild TBI.
Estimates of the relative causes of TBI are as follows: motor vehicle accidents
(45%), falls (30%), occupational accidents (10%), recreational accidents (10%),
and assaults (5%) in USA.
Evans RW: The postconcussion syndrome and the sequelae of mild head injury. In Neurology and Trauma, edn. 2. Edited by Evans RW. New York: Oxford University
Press; 2006:95–128.
4. Introduction
Overall, PTH accounts for approximately 4% of all secondary headaches.
No defining clinical features of PTHAs, other than onset after trauma,
distinctly separate them from other headache disorders.
5. Introduction
Athletes and military personnel.
PTH has been well characterized in soldiers who have sustained mTBI, and has
been estimated to occur in 97.8% of concussed soldiers returning during their
final 3 months of deployment.
A/w multiple somatic complaints with depressive symptoms.
Within any sport, females are prone to develop PTH.
Theeler BJ, Flynn FG, Erickson JC. Headaches after concussion in US soldiers returning from Iraq or Afghanistan. Headache 2010; 50:1262–1272.
6. Classification
According to ICHD 2, headache attributed to head & neck trauma include 7
different secondary headache syndromes
1. Acute PTHA
2. Chronic PTHA
3. Acute headache attributed to whiplash injury
4. Chronic headache attributed to whiplash injury
5. Headache attributed to traumatic intracranial hematoma
6. Postcraniotomy headache
7. Headache attributed to other head & neck trauma
7.
8.
9.
10.
11. Pathophysiology
The trigeminal nerve is the major peripheral nerve for transmitting pain stimuli
of the head.
It contains nociceptive afferents from the anterior scalp, anterior cranium,
face, mouth, teeth, temporomandibular joints, sinuses, cranial blood vessels,
and meninges.
Injury to any of these structures can cause headache.
12. Pathophysiology
The greater and lesser occipital nerves, which arise from the C2 and C3 cervical
spinal roots, convey nociceptive stimuli from the posterior head and scalp.
Painful stimuli from structures of the cervical spine are conveyed largely by the
cervical nerve roots.
13. Pathophysiology
The central processes of
trigeminal pain neurons and
cervical pain neurons converge
within the CNS in the upper
cervical spinal cord.
Pathways collectively is known
as the trigeminocervical
complex.
The trigeminocervical complex
helps explain why injury of
neck structures can cause
headache and vice versa.
14. Pathophysiology
Mild head injury are rarely cause identifiable underlying structural injury.
Number of neuronal biochemical and cellular changes induced by head
trauma.
Changes include widespread neuronal depolarization, indiscriminant release of
glutamate and other neurotransmitters, altered glucose and energy utilization,
and decreased magnesium levels.
15.
16.
17. Pathophysiology
DTI studies have discovered regions of associated axonal swelling in patients
with mild TBI.
SPECT/PET imaging can demonstrate structural and functional deficits.
18. Greater white matter pathology predicted greater cognitive deficits,
suggesting DTI as an objective means for determining the relationship of
cognitive deficits to TBI.
19. Clinical features
PTHAs are highly heterogeneous.
Do not possess any unique clinical symptoms.
The current criteria for PTHA require onset of headache within 7 days of head
or neck trauma, but do not require the presence of any particular headache
characteristics.
20. Clinical features
72% of headaches are bilateral in location.
In one study, a frontal location was seen in 50%, followed by holocranial (18%),
hemicranial (13%), and bitemporal (10%).
Over 80% of PTHAs in civilian populations are nonthrobbing.
Lew HL, Lin PH, Fuh JL, et al. Characteristics and treatment of headache after traumatic brain injury: a focused review. Am J Phys Med Rehabil 2006;85(7):619–627.
21. Clinical features
70 – 96 % headaches developing after head trauma often possess the same
characteristics as primary headache disorders.
Major subgroups of headaches after trauma include tension-type headache,
migraine, cranial neuralgias, cervicogenic headaches, and MOH.
M/C are tension-type headache or migraine headache.
22. Clinical features
33% of PTHAs resemble tension-type headaches with a wide range of 6%-85%.
Bilateral and of mild or moderate severity.
Pressing or tightening in nature and not aggravated by routine physical activity.
May be accompanied by either light or sound sensitivity, but not nausea.
23. Clinical features
28% - 60% of PTHAs resemble migraine.
M/C form of PTHA after military-related mild head trauma.
Moderate or severe, unilateral or asymmetric, throbbing or pulsatile in quality,
aggravated by or cause avoidance of routine physical activity, and accompanied
by either nausea and vomiting or both light and sound sensitivity.
24. Clinical features
Last several hours to several days without treatment.
Visual aura might occur.
Not be distinguishable from idiopathic migraine by clinical features or by
responsiveness to treatment.
25. Clinical features
Rarely, head trauma can precipitate the development of trigeminal autonomic
cephalalgias.
Manifest as unilateral headache accompanied by prominent autonomic
manifestations.
26. Clinical features
Occipital neuralgia is probably the most common neuralgiform disorder
following head or neck injury
Typically presents with persistent, moderate, side-locked unilateral head pain
with episodes of brief, severe, lancinating pain radiating from the occipital area
to the side of the head.
Trigeminal neuralgia is rare.
27. Clinical features
Cervicogenic headaches occur when pain is generated or referred from a
source in the cervical spine, such as cervical discs, facet joints, or myofascial
structures. Located in posterior head. Unilateral/bilateral.
Typically have persistent or intermittent neck discomfort and headaches may
be precipitated by certain neck movements.
Neck or occipital tenderness with or without trigger points may be present.
28. Clinical features
Medication overuse headache, previously called analgesic rebound headache.
Analgesic overuse is defined as use of acute analgesics 15 or more days per
month for more than 3 months.
Of patients with PTHAs, 19% - 42% develop this secondary headache disorder.
M/C in patients with migraine.
29. Clinical features
Usually begins a number of hours after consuming the offending analgesic.
Typically the headaches worsen for 2 weeks after analgesic cessation and then
gradually improve over the next 4 to 6 weeks.
Opioids, combination medications, and triptans - potential to cause MOH
NSAIDS - less likely
Dihydroergotamine and antiemetics - unlikely to induce MOH.
30. CLINICAL EVALUATION
Comprehensive history
Focus on preinjury and postinjury headache pattern.
Physical examination
Brief cognitive assessment
Look for FND
Range of neck movement
Fundus examination
31.
32. Indication for Imaging
LOC greater or equal to 5 seconds
Altered mental status
FND
Progressively worsening headache pattern
Intractable headache
Persistent rhinorrhea
Headache induced by position
33. Other causes of headache after trauma
Dangerous Causes of Headache
CVT Cerebral aneurysm
Subdural / epidural hematoma Skull fracture
ICH Cervical vertebra fracture
SAH Cervical disc protrusion
Carotid or vertebral artery dissection
Carotid-cavernous fistula
34. Imaging
MR or CT angiogram - arterial dissection, aneurysm, vasospasm, or carotid-
cavernous fistula are considerations.
MR or CT venogram - in patients with possible cerebral vein thrombosis.
Cervical spine MRI - suspected cervicogenic headaches
35. Role of Lumbar puncture
Positional headache.
Low CSF pressure which can caused by dural tear.
36. Screening of comorbid condition
Concurrent medical & psychological conditions that can exacerbate headaches.
Common comorbidities include
Sleep disorders Posttraumatic stress disorder (PTSD)
Psychosocial stressors Depression
Alcohol or drug abuse Anxiety
Concurrent physical injuries (e.g, explosive blast injuries with amputation, eye
injury, hearing loss, or polytrauma)
Van Reekum R, Cohen T, Wong J. Can traumatic brain injury cause psychiatric Disorders? J Neuropsychiatry Clin Neurosci 2000;12(3):316–327
37. Screening of comorbid condition
Critical to identify and treat comorbidities to most optimally.
Comorbid conditions may limit headache treatment options or provide
therapeutic opportunities.
To select treatment that simultaneously benefit one or more comorbid
condition.
.
38. Treatment
Challenging and rewarding.
Treatment is based on treatments for phenomenologically similar headaches.
Goal
Abort headache attacks Reduce disability
Decrease headache frequency Prevent chronicity
39. Treatment
The goal is to achieve complete relief or nearly complete relief as rapidly as
possible by abortive agents.
Patients who experience
2 or more moderate-severe headache attacks/week.
3 or more days of impaired activities/month over a period of several months.
Despite use of abortive medications are good candidates for headache
prophylactic agents.
40. Treatment
Prophylactic medications require a minimum of 4 weeks to take effect.
Should begin with low dose to minimize S/E & gradually increased over weeks
or even months.
41.
42. Alternative treatment for acute attacks
Opioid medications are generally not highly effective for most headache types
and should not be used as first-line headache abortive agents.
IV or oral corticosteroids (eg, prednisone 60 mg daily for 5 days),
IV Valproaic acid
IV Magnesium
43.
44.
45.
46.
47. Nonpharmacologic Therapies
1) Behavioural therapies
Uncontrolled studies of cognitive behavioural therapy, relaxation therapy, and
biofeedback have shown favourable results in PTHA
2) Life style modification like healthy meal, sleep, exercise patterns, to avoid
triggers for headache, to avoid caffine overuse, smoking, alcohol.
Gurr B, Coetzer BR. The effectiveness of cognitive-behavioral therapy for post-traumatic headaches. Brain Inj 2005;19(7):481–491.
48. Nonpharmacologic Therapies
3) Physical modalities
Physical therapy, osteopathic manipulation therapy, acupuncture.
More useful as an adjuncts to medical therapy particularly in patients with
suspected cervical sources of pain.
49. Injections & Procedures
Nerve blocks
Occipital nerve blocks - occipital neuralgia.
One case series showed an 80% response rate of PTHA following occipital nerve
blockade.
Other Common sites include auriculotemporal nerve, supraorbital nerve,
supratrochlear nerve, sphenopalatine ganglion.
Blocking a single nerve unilaterally or bilaterally or blocking multiple nerves.
Hecht JS. Occipital nerve blocks in postconcussive headaches: a retrospective review and report of ten patients. J Head Trauma Rehabil 2004;19(1):58–71.
50. Arch Phys Med Rehabilitation 2004;85:1013-6.
We present a case wherein a man in his late twenties with posttraumatic headache
obtained more than 17 months of relief with SPG pulsed-mode radiofrequency
lesioning.
SPG pulsed-mode radiofrequency is a nonablative, neural lesioning method that
may be useful in the treatment of posttraumatic headache.
51. Injections & Procedures
Headaches secondary to C2-C3, C3-C4 facet joint dysfunction can be treated
with facet joint blocks or cervical medial branch blocks for cervicogenic
headache.
Trigger point injections are very useful in cervicogenic headache.
Occipital neurolysis, occipital nerve decompression surgery, and implantation
of occipital nerve stimulator are potentially useful treatments but studies are
required.
55. Trial based therapy
Use of melatonin in children with persistent PTH at doses of 3 to 10 mg has
demonstrated positive effects in up to 75% of participants in one study
population.
Kuczynski A, Crawford S, Bodell L, Dewey D, Barlow KM. Characteristics of post-traumatic headaches in children following mild traumatic brain injury and their
response to treatment: a prospective cohort. Dev Med Child Neurol. 2013;55(7):636-641.
56. 30/M, fell down from
motorcycle.
LOC for 30 minutes
Confusion and amnesia for 7
days
Disequilibrium and vertigo,
holocranial throbbing
headache with photo and
phonophobia with associated
nausea,vomiting after he was
discharged.
Started on ibuprofen &
paracetamol.
All symptoms improved in 6
weeks. He joined job in 2
months.
57. A 35-year-old male army officer
Hit his helmeted head on the roof of a military vehicle after it was struck by an
explosive device in Iraq.
Multiple prior concussions from intramural football and a parachute injury.
Left retro-orbital, dull, constant pain, worsening with movement, associated
with photosensitivity, phonosensitivity, nausea, and blurred vision.
Chronic neck and low back pain, poor balance, poor concentration,
forgetfulness, difficulty making decisions, slowed thinking, anxiety, depressed
mood, difficulty falling or staying asleep, repeated disturbing memories,
nightmares, and angry outbursts.
58. Cervical tenderness on examination with C-spine MRI showing degenerative
changes with normal MRI brain.
Treated with zolmitriptan 5mg for acute attacks, prednisolone for 10 days,
nortryptiline 10mg bedtime.
Gabapentin maximum dose was added gradually followed by botulinum toxin (
bilateral frontalis, corrugators, temporalis, splenius capitis, midcervical
paraspinal, lumbar paraspinal areas).
Behaviour therapy was continued for PTSD during this period.
59. References
1. Jay c. Erickson et al., Posttraumatic headache, continuum lifelong learning neurol
2010;16(6):55–78.
2. Bert b. Vargas et al., Posttraumatic headache, curr opin neurol 2012, 25:284–289.
3. Raquel langdon et al., Posttraumatic headache, pediatric annals, vol. 47, no. 2, 2018.
4. Mark obermann et al., An update on the management of posttraumatic headache,
therapeutic advances in neurological disorders, 2015, vol. 8(6) 311– 315
5. Francis x. Conidi et al., Understanding posttraumatic headache, part 2: management
and treatment, practical neurology, september 2017.
1)An inverse relationship exists between the severity of head injury and incidence of PTHA.
1)Headaches tend to occur more frequently and are more likely to persist after mild head injury compared to moderate or severe head injury.
1)Of 377 patients with severe head trauma, only 4% to 23% had headaches 1 year later.
International classification of headache disorders
A number of risk factors for developing chronic PTHA have been identified.
These include female sex, lower educational level, low socioeconomic status, prior history of headaches, mild severity of head trauma, short duration of posttraumatic amnesia, and medication overuse.
In comparison to extracranial injuries (ECI), such as a bone fracture, mTBI patients are more likely to have persistent symptoms after 3 months
The current classification criteria for PTHAs do not include the characteristics or accompanying features of the pain or the specific cause of injury (eg, blunt impact, explosive blast).
Moreover, the time criteria are somewhat arbitrary and not based on pathophysiologic mechanisms.
The central processes of trigeminal pain neurons and cervical pain neurons converge within the CNS in the upper cervical spinal cord.
Pathways collectively is known as the trigeminocervical complex.
2) A number of neuronal biochemical and cellular changes induced by head trauma have been identified and may contribute to the development of PTHAs in the absence of identifiable structural injury.
Early studies demonstrated that biomechanical injury results in ionic flux and hyperacute indiscriminate glutamate release.
Potassium efflux, and sodium and calcium influx, occur due to damage to lipid membrane.
Initial ionic flux and depolarization can then trigger voltage- or ligand-gated ion channels, creating a diffuse ‘spreading depression-like’ state that may be the biological substrate for very acute post-concussive impairments.
2) Do not possess any unique clinical symptoms that clearly distinguish them from nontraumatic headache disorders.
If premorbid headaches existed, the preexisting headache type (ie, migraine) is usually magnified after head injury.
Most children who sustain a mTBI recover within a few weeks.
autonomic manifestations, such as conjunctival injection, lacrimation, ptosis, miosis, eyelid edema, rhinorrhea, or facial sweating abnormalities
MOH develops in susceptible patients when frequent use of acute analgesic medication is continue over a prolonged period of time.
1)The patient becomes trapped in a cycle of escalating headaches and increasing medication use.
BESS An error is defined as opening the eyes, lifting the hands off of the hips, stepping, stumbling or falling out of position, lifting the forefoot/heel, abducting the hip by >30 degrees, or failing to return to test position in under 5 seconds.
Designed for objective measure of assessing static postural stability after mild TBI and to assist in return to sports play decisions.
triggered by moving to an upright posture and relieved by lying back to supine position.
In an analysis of 10 studies, the prevalence of major depression after TBI was 44%.
The incidence of PTSD appears to be inversely related to the severity of the injury. In one study, the incidence of PTSD was 27% among patients who had less than 1 hour of loss
of consciousness compared to only 3% among those who were unconscious for more than 12 hours
All these comorbid conditions are risk factors for prolonged recovery of headache.so need to be addressed.
1)To date, no randomized, controlled clinical trials evaluating the efficacy of any therapies for PTHAs have been done. No US –FDA approved medication.
2)Classify headache.
Most practitioners do not initiate prophylactic therapy in the acute or early subacute stage because many patients with PTHAs experience spontaneous resolution in the first month or two after injury.
many practitioners would agree that patients who continue to experience frequent headache more than 2 months after the injury are appropriate candidates for prophylactic therapy.
3) until the frequency of headaches decreases, side effects develop, or the highest target dose is reached
3) Switching prophylactic agents prematurely, without first titrating up the dose or treating for a minimum of 6 weeks, should be avoided.
.
Lamotrigine is another option for neuralgiform headache, being well tolerated with minimal adverse cognitive side effects, but the dose must be slowly titrated up to minimize the risk of a serious mucocutaneous reaction.
A good musculoskeletal exam looking for trigger points, tenderness over the spinous processes, and decreased range of motion should be part of the initial evaluation.
Trigger points of the head and neck are often associated with various headache disorders.
a combination of physical medicine and trigger point injections may help to lower the patient’s headache frequency.
Cessation of analgesic medication inevitably results in worsening daily headaches for about 2 weeks followed by a gradual improvement back to an episodic headache pattern within 6 weeks.
Sleep-inducing medication and adequate hydration may be helpful during the withdrawal period.
Counselling has to be done on same visit when patient has been advised for medical management which increase the effectiveness of medication.
No RCT have evaluated the effectiveness of any of these approaches for PTHAs, but evidence supports their use in other headache disorders. Can be used as an adjunct to pharmacological treatments.
1) Life style modifi
Have not been fully evaluated for PTHA
3) Typical anesthetics include bupivacaine (0.25% to 0.75%) or lidocaine (2%), with volumes ranging from 0.5 to 2cc per site.
can be given alone, combined with each other and/or with a steroid, usually triamcinolone.
Moderate to severe injury with positive images findings.
Improved completely in 6 weeks.
Prognosis is good for headache after moderate to severe injury.
Learning points
Headache onset after multiple bouts of mild head injury
Persistent of chronic headache despite mild severity of head injury
Presence of PTSD, insomnia, neck and back pain exacerbated headache syndrome
Multidisciplinary approach for chronic headache.
