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Management of Chronic Headaches
in Traumatic Brain Injury
Glen Zielinski, DC, DACNB, FACFN, CBIS Board Certified Chiropractic Neurologist
Fellow of the American College of Functional Neurology
Certified Brain Injury Specialist
Assistant Professor of Clinical Neurology, Carrick Institute for Clinical
Neuroscience
Clinic Director, Northwest Functional Neurology
www.northwestfunctionalneurology.com
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Concussion (Mild Traumatic Brain Injury) and the Team Physician: A Consensus Statement. Medicine & Science in Sports & Exercise. 2011.
• Concussion or mild traumatic brain injury (MTBI) is a pathophsyiological process affecting the brain induced by direct or indirect biomechanical forces.
• Concussions occur as a result of imparted linear and rotational accelerations to the brain. Because of modifying factors, there is currently no known threshold for concussive injury.
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The Current Status of Postconcussion Syndrome. Neuropsychiatry. 2011.
• Concussions are temporary disruptions of brain function that appear to be a very mild form of TBI.
• Cardiovascular disturbances, eye movement disturbances, slowed reaction times, and feeling ‘like in a fog’ are all compatible with the possibility of brainstem disturbance in some patients.
• The fact that with multiple concussions the individual may not fully recover does suggest that some underlying structural change in brain anatomy may occur, even with concussions.
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Biomechanics of Concussion. Clinical Sports Medicine. 2011.
• Many different head motions can occur from a concussion. This complex variety of responses makes each concussion unique.
• Two broad categories of forces, contact and inertial forces, occur during concussions.
• The primary cause of concussive injuries is the inertial/acceleration loading experienced by the brain at the moment of impact.
• Linear and rotational acceleration occur with every concussion.
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Biomechanics of Concussion. Clinical Sports Medicine. 2011.
• Brain tissue deforms more readily in response to shear forces compared to other biological tissue.
• Rapid head rotations generate shear forces throughout the brain causing tissue damage.
• If the head motion is constrained to exclude any rotational motion, it is difficult to produce traumatic unconsciousness.
• In comparison, introducing or allowing a rotational component after impact substantially increases the likelihood of an unconscious episode.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• The initiating event is stretching and disrupting of neuronal and axonal cell membranes, while cell bodies and myelin sheaths are less affected.
• Resulting membrane defects cause a deregulated flux of ions, including an efflux of potassium and influx of calcium.
• These events precipitate enhanced release of excitatory neurotransmitters, particularly glutamate.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• Binding glutamate to N-methyl-D-aspartate (NMDA) receptors results in further depolarization, influx of calcium ions, and widespread suppression of neurons with glucose hypometabolism.
• Increased activity in membrane pumps (to restore ionic balance) raises glucose consumption, depletes energy stores, causes calcium influx into mitochondria, and impairs oxidative metabolism and consequently anaerobic glycolysis with lactate production, which might cause acidosis and edema.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• Diffuse axonal injury, caused by shearing of fragile axons by acceleration/deceleration forces from the trauma, is the primary neuropathology of TBI.
• The severity of diffuse axonal injury is proportional to the deceleration force.
• MRI studies that use DTI show that the extent of DAI after mild TBI is related to postconcussion cognitive problems.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• Diffuse axonal injury with axolemmal disruption causes calcium influx, neurofilament compaction, and microtubule disassembly.
• Neurofilament compaction is an early event caused by calpain mediated proteolysis of neurofilament side arms or phosphorylation.
• Calcium influx triggers microtubule disassembly.
• Calcium homeostasis disruption results in calpain-mediated proteolytic degradation of essential cytoskeletal proteins, such as neurofilament proteins.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• Repeated blows to the head are especially detrimental for the brain, because the cerebral physiology is disturbed after mild brain trauma and concussions, which makes the brain more susceptible to further injury.
• Researchers argue that metabolic dysfunction, including reduced mitochondrial energy status in the brain with increased metabolic demands but decreased energy stores with a low ATP/DTP ratio and increased lactate/pyruvate ratio, may play a role.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• There are two main categories of brain damage due to trauma: focal damage and diffuse injury.
• Focal injury includes cortical or subcortical contusions and lacerations, as well as intracranial bleedings (subarachnoid hemorrhage and subdural hematoma).
• Focal injury is due to severe direct impact on the brain and is thus mainly seen in severe cases of TBI.
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The Neuropathology and Neurobiology of Traumatic Brain Injury. Neuron. 2012.
• Diffuse injury is caused by stretching and tearing of the brain tissue and does not need any skull fracture or direct impact or crush injury to the brain surface and is therefore also seen in cases with mild TBI.
• The main form of diffuse injury is called diffuse axonal injury (DAI), which is due to acceleration/deceleration forces that lead to shearing of axons.
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Updated clinical practice guidelines for concussion/mild traumatic brain injury and persistent symptoms. Brain Injury. 2015.
• In post-traumatic headaches, a focused headache history should be performed in order to identify the headache sub-types that most closely resemble the patients symptoms.
• Perform a neurologic exam and
• musculoskeletal exam including cervical spine examination.
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Updated clinical practice guidelines for concussion/mild traumatic brain injury and persistent symptoms. Brain Injury. 2015.
• In patients with persistent vision and vestibular dysfunction, evaluation should include a thorough neurologic examination that emphasizes vision, vestibular, balance and coordination and hearing.
• If symptoms of benign positional vertigo are present, the Dix-Hallpike Maneuver should be used for assessment.
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Objectively Assessing Balance Deficits After TBI: Role of Computerized Posturography. Journal of Rehabilitation Research & Development. 2007.
• Balance impairment, or postural instability, is a common source of residual physical disability after severe traumatic brain injury (TBI).
• There is an association between early balance deficits after TBI and late functional recovery.
• Computerized Posturography Testing safely and effectively assists the diagnosis of balance impairments and provides quantitative data to track changes over time and/or assess the efficacy of treatment interventions.
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Dizziness after traumatic brain injury: Overview and measurement in the clinical setting. Brain Injury. 2006
• Dizziness can be further explained in relation to a definition of vestibular function as the ‘neural sensory– motor interaction that leads to the maintenance of balance (motor function) and the perception of motion of objects relative to oneself (sensory function) as part of the larger and global function of orientation’.
• In recent years, vestibular rehabilitation has emerged as an accepted and effective means of treating dizziness and vestibular disorders. It involves exercises and activities designed to enhance central nervous system compensation to vestibular system dysfunction.
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A Brief Vestibular/Ocular Motor Screening (VOMS) Assessment to Evaluate Concussions. American Journal of Sports Medicine. 2014.
• Researchers have reported that vestibular impairments are common after a concussion and may delay recovery from this injury.
• The vestibulo-ocular system maintains visual stability during head movements, whereas the vestibulospinal system is responsible for postural control.
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A Brief Vestibular/Ocular Motor Screening (VOMS) Assessment to Evaluate Concussions. American Journal of Sports Medicine. 2014.
• Because these 2 functional vestibular networks do not share identical neuronal circuitry, it is possible to have impairments of the vestibulo-ocular system without impairments of the vestibulospinal system.
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A Brief Vestibular/Ocular Motor Screening (VOMS) Assessment to Evaluate Concussions. American Journal of Sports Medicine. 2014.
• The Vestibular/Ocular Motor Screening Assessment (VOMS)
• – 1. Smooth pursuit
• – 2. Horizontal/Vertical saccades
• – 3. Convergence
• – 4. Horizontal vestibular ocular reflex (VOR)
• – 5. Visual motion sensitivity (VMS)
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A Brief Vestibular/Ocular Motor Screening (VOMS) Assessment to Evaluate Concussions. American Journal of Sports Medicine. 2014.
• The VOMS appears to assess distinct vestibular and ocular motor symptoms, which are unrelated to current clinical balance measures.
• The VOMS may help clinicians to identify patients for vestibular and ocular referrals and more targeted treatment, thereby enhancing recovery from this injury.
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Impaired Eye Movements in Post-Concussion Syndrome Indicate Suboptimal Brain Function Beyond the Influence of Depression, Malingering or Intellectual Ability. Brain. 2009.
• Our results indicate that eye movement function is impaired in post concussion syndrome (PCS), the deficits being unrelated to the influence of depression or estimated intellectual ability.
• The majority of eye movement deficits in the PCS group were found on measures relating to motor functions executed under both conscious and semi-conscious control (directional errors; poorer visuospatial accuracy; more saccades and marginally poorer timing and rhythm keeping in memory-guided sequences; smaller number of self-paced saccades; deficits in OSP).
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Impaired Eye Movements in Post-Concussion Syndrome Indicate Suboptimal Brain Function Beyond the Influence of Depression, Malingering or Intellectual Ability. Brain. 2009.
• Importantly, the PCS group also had poorer performance on several eye movement functions that are beyond conscious control and indicative of subcortical brain function (slowed velocity of self-paced saccades and indications of longer saccade durations of self-paced saccades, anti-saccades and larger amplitude memory-guided saccades).
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CLINICAL EVALUATION AND INTERVENTION
VOMS TESTING:
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Eye movement parameters: 1. Pursuits: Observe the eyes as they pursue your finger moving in cardinal planes of gaze. Pursuits that consist of multiple small jerks to catch the target in all planes of gaze to a particular side (saccadic pursuit), may indicate a lesion on that side, primarily in the parietal lobe.
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2. Saccades: Have the patient hold their eyes on your index finger held to the side, then rapidly look at your other index finger held directly in front of their nose. Observe for eyes that are slow to engage the saccade (the rapid eye movement), or for eyes that stop short of the target and must perform a second saccade.
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The frontal lobe initiates saccades in the opposite direction. Dysfunctional saccades moving to the right implies a lesion in the left prefrontal cortex and associated pathways down to the R pontomedullary brainstem (and vice versa).
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3. Vergence:
Have the patient focus on your finger as you bring it towards their nose.
Observe for convergence insufficiency, convergence spasm, withdrawal responses, and autonomic events.
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Convergence insufficiency implies a lesion in the ipsilateral midbrain and associated pathways
Convergence spasm implies otolithic dysfunction
Autonomic events imply any or all of the above
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4. Vestibulo-ocular reflexes:
Have the patient focus on your nose, slowly move the head to the side
Rapidly move the head back to neutral (Halmagyi head thrust test)
Eyes should remain locked on your nose
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Observe for any secondary eye movement immediately after the head thrust
Secondary eye movement opposite the direction of head thrust indicates failure of the horizontal VOR mechanism
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Assess in RALP and LARP planes:
R anterior: turn head L, put head into extension, rapid thrust back to neutral while patient looks at your nose
L posterior: Head L, bring head back, rapid thrust back to neutral
LARP = the opposite directions
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Impairment of VOR pathways implies damage to the vestibular nerve, the cerebellum, or the brainstem
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5. Visual motion sensitivity:
Test the ability to cancel the horizontal VOR mechanisms.
Fixate on target (hold up sheet with small print), rotate patient and assess for failure of visual acuity
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Chronic Post-traumatic Headaches
•TBI frequently involves headaches that prove refractory to treatment
•These generally involve cervicogenic pain referral from hypertonicity of suboccipital musculature and hypomobility of upper cervical segments
•These are extremely common in whiplash injuries
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Chronic Post-traumatic Headaches
• Primary tissue healing is complete within 12 weeks of injury
• When symptoms persist beyond this threshold, we must at least consider that the driving force for these may no longer be exclusively structural
• Are the hypertonicity and mobility restriction direct causes of the headaches, or are they consequences of another physiological process?
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Postural Reflexes
• Automatic body movements reflect a overlay of several "synergies" -- The main ones discussed in the classic literature are ones related to body positioning alone (basic postural reflexes), and ones related to vestibular input (labyrinthine or vestibular spinal reflexes).
• When we stand or move, our body tends to automatically assume particular postures based on the combination of these responses.
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Postural Reflexes
• Tonic Neck reflex (TNR)
• The Tonic neck reflex describes the automatic positioning of the limbs in response to a movement of the head on trunk (neck). The tonic neck reflex can be observed in animals that have both been decerebrated as well as had their vestibular system eliminated.
• When the head is rotated in the yaw axis (around the up-down axis of the body), there is an increase in the extensor tone on the two limbs on the side in the direction of rotation, and a decrease in extension and flexion on the opposite side.
• There are also similar reflexes elicited when the head is rolled towards one shoulder.
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Postural Reflexes
• The Vestibulospinal Reflex (VSR)
• The purpose of the vestibulospinal reflex (VSR) is to stabilize the body. The VSR is an assemblage of several reflexes named according to the timing (dynamic vs. static or tonic) and sensory input (canal, otolith or both).
• the term VSR usually also implies motor output to skeletal muscle below the neck
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Postural Reflexes
• 1. When the head is tilted (rolled) to one side, both the canals and otoliths are stimulated.
• 2. The vestibular nerve and vestibular nucleus are activated.
• 3. Impulses are transmitted via the lateral and medial vestibulospinal tracts to the spinal cord.
• 4. Extensor activity is induced on the side to which the head is inclined, and flexor activity is induced on the opposite side.
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Postural Reflexes
• The Vestibulocollic Reflex (VCR)
• The vestibulocollic reflex acts on the neck musculature in order to stabilize the head.
• Reflex head movement counters the movement sensed by the otoliths or semicircular canals. The neural pathways mediating this reflex are as yet uncertain.
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Cervical Reflexes
• The Cervicoocular Reflex (COR)
• The COR consists of eye movements driven by neck proprioceptors.
• As the COR can supplement the VOR under certain circumstances it becomes relevant when considering recovery from vestibular lesions. Normally, the gain of the COR is very low, but the COR is facilitated when the vestibular apparatus is injured.
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Cervical Reflexes
• The Cervicospinal Reflex (CSR)
• The cervicospinal reflex, also known as the tonic neck reflex (TNR), is defined as changes in limb position driven by neck afferent activity. Analogous to the COR which interacts with the VOR, the CSR can supplement or interfere with the VSR.
• Two pathways are thought to mediate these reflex signals, an excitatory pathway from the lateral vestibular nucleus and an inhibitory pathway from the medial part of the medullary reticular formation.
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Cervical Reflexes
• Their activity leads to extension of the limb on the side to which the chin is pointed and flexion of the limb on the contralateral side.
• Vestibular receptors influence both of these systems by modulating the firing of medullary neurons in a pattern opposite to that elicited by neck receptors.
• The interaction between the effects on the body of vestibular and neck inputs tend to cancel one another when the head moves freely on the body so that posture remains stable.
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Cervical Reflexes
• The Cervicocollic Reflex (CCR)
• The cervicocollic reflex is a cervical reflex that stabilizes the head on the body.
• Afferent sensory changes caused by changes in neck position, create opposition to that stretch by reflexive contractions of neck muscles.
• Like the COR, the CCR may be facilitated after labyrinthine loss.
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Effect of gaze direction on neck muscle activity during cervical rotation. Experimental Brain Research, 2005.
• Control of the neck muscles is coordinated with the sensory organs of vision, hearing and balance. For instance, activity of splenius capitis (SC) is modified with gaze shift. This interaction between eye movement and neck muscle activity is likely to influence the control of neck movement.
• Right SC and left SCM EMG increased with rotation to the right.
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Effect of gaze direction on neck muscle activity during cervical rotation. Experimental Brain Research, 2005.
• The data is consistent with previous human studies which have reported increased neural drive to the neck rotator muscles (SCM, SC) in association with voluntary horizontal shift of gaze in the direction to which neck muscles rotate.
• The interrelationship between eye position and neck muscle activity may affect the control of neck posture and movement.
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Cervico-ocular coordination during neck rotation is distorted in people with whiplash-associated disorders. Experimental Brain Research, 2012.
• People with whiplash-associated disorders (WAD) not only suffer from neck/head pain, but commonly report deficits in eye movement control. Recent work has highlighted a strong relationship between eye and neck muscle activation in pain-free subjects. It is possible that WAD may disrupt the intricate coordination between eye and neck movement.
• Electromyographic activity (EMG) of muscles that rotate the cervical spine to the right (left sternocleidomastoid, right obliquus capitis inferior (OI), right splenius capitis (SC) and right multifidus (MF)) was recorded in nine people with chronic WAD. Three main differences were observed in WAD.
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Cervico-ocular coordination during neck rotation is distorted in people with whiplash-associated disorders. Experimental Brain Research, 2012.
• First, the superficial muscle SC was active with both directions of cervical rotation in contrast to activity only with right rotation in pain-free controls.
• Second, activity of OI and MF varied between directions of cervical rotation, unlike the non-direction-specific activity in controls.
• Third, the effect of horizontal gaze direction on neck muscle EMG was augmented compared to controls.
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Inaccurate Saccades and Enhanced Vestibulo-Ocular Reflex Suppression during Combined Eye-Head Movements in Patients with Chronic Neck Pain: Possible Implications for Cervical Vertigo. Frontiers in Neurology, January 2017.
• In patients with chronic neck pain, the internal commands issued for combined eye-head movements have large enough amplitudes to create accurate gaze saccades; however, because of increased neck stiffness and viscosity, the head movements produced are smaller, slower, longer, and more delayed than they should be.
• VOR suppression is disproportionate to the size of the actual gaze saccades because sensory feedback signals from neck proprioceptors are non-veridical, likely due to prolonged coactivation of cervical muscles.
• The outcome of these changes in eye-head kinematics is head-on-trunk stability at the expense of gaze accuracy. In the absence of vestibular loss, the practical consequences may be dizziness (cervical vertigo) in the short term and imbalance and falls in the long term.
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Adaptation of the cervico- and vestibulo-ocular reflex in whiplash injury patients. Journal of Neurotrauma, January 2008.
• The aim of this study was to investigate the underlying mechanisms of the increased gains of the cervico-ocular reflex (COR) and the lack of synergy between the COR and the vestibulo-ocular reflex (VOR) that have been previously observed in patients with whiplash-associated disorders (WAD).
• Reduced neck mobility yielded an increase in COR gain.
• Adaptation of both the COR and VOR was observed in healthy controls, but not in WAD patients.
• The lack of adaptation of the two stabilization reflexes may result in a lack of synergy between them. These abnormalities may underlie several of the symptoms frequently observed in WAD, such as vertigo and dizziness.
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• Is the persistent increase in suboccipital tone in chronic post-traumatic headaches secondary to trauma?
•Or is it the result of failed integration of postural, vestibular, and cervical reflexes?
•How would you assess the difference?
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•Another layer: head tilt
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Ocular Tilt Reaction
• The Ocular tilt reaction (OTR), comprises skew deviation, head tilt and ocular torsion involving structures of the inner ear responsible for maintenance of balance of the body
• Including the semicircular canals, utricle and saccule
• Normally, a body tilt (along with the initial head tilt) to the right causes a shift of the subjective visual vertical (SVV) to the left resulting in reflex, compensatory orientation of the head to left to realign the SVV to the true vertical.
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• In mTBI, there are myriad ways to impair the pathways associated with the normal ocular tilt response, resulting in a pathological ocular tilt reaction.
• These mechanisms involve damage to the central projections of the vestibular system at various levels.
• Pathologic OTR = eye elevation on the side opposite the head tilt
• The consequent change in cervical muscle tone that structurally maintains the tilt will not respond to structural therapy that does not address the vestibular impairment
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Treatment Parameters
• Assess Pursuits: • Rehabilitate with X2 viewing in the direction of the
impaired pursuit
• = pursuit coupled with contraphasic head movement
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Treatment Parameters
• Assess Pursuits: • Manipulate on the side opposite the deficient pursuit
• only when pursuit findings have normalized
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Treatment Parameters
• Assess Saccades: • Examine latency, velocity, and accuracy • Rehabilitate with saccades crossing the nose in the
direction of the impaired saccade
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Treatment Parameters
• Assess Saccades: • Move from short to longer ones as accuracy improves • Rehabilitate velocity with gap microsaccade stimulus
(Focus Builder app)
• Manipulate on the side to which the saccade is most impaired (i.e. saccadic hypometria to R = manipulate R body)
• Only after saccade parameters have normalized
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Treatment Parameters
• Assess Horizontal Vestibulo-ocular Reflex: • Halmagyi head thrust
• Assess with head returning rapidly to neutral from either side, observe for presence and direction of corrective saccades
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Treatment Parameters
• Assess Horizontal Vestibulo-ocular Reflex: • A deficient R VOR will show a correction from R to
neutral
• Rehabilitate with X2 viewing first, then Halmagyi into saccades, then Halmagyi into optokinetic stimulus (Optodrum app)
• Manipulate on the side of the deficient VOR • Only after the VOR parameters have normalized
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Treatment Parameters
• Assess VOR – COR integration: • Perform saccades to lateral targets
• Observe for cervical substitution • With significant cervical substitution, rehabilitate the
opposite VOR prior to addressing cervical hypertonicity in that direction
• This holds for pursuits as well
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