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Transcript of Headache
Cluster Migraine Two types Migraine with aura Migraine without aura Common mechanisms central sensitisation nociceptive stimulation for just 5 minutes can lead to an
increase in response in the trigeminocervical nucleus
for over an hour to other nociceptive stimuli, even if that simulation
is received from the C2 innervation.(Goadsby, 2005) cutaneous allodynia peripheral triggers triggers in the periphery can lead to activation of the
trigeminocervical nucleus. They can include:
trigger/tender points in muscles
other irritative structres like tumours etc Secondary headaches Any patient that presents with the “worst
headache of their life”. Focal neurological signs, particularly on the first
occurrence of the headache, including changes in
personality, mental status and level of consciousness. Headache precipitated or made worse by bending, sneezing, coughing
or exertion. This may indicate raised intracranial pressure. Vomiting
with headache may also be associated with raised intracranial pressure. Changes in the headache pattern of an existing
headache sufferer. Association of headache with fever, rash, nucal rigidity, lymphadenopathy, and particularly if for the first time, photophobia. New headaches in patients under 5 or
over 50 years of age. Multifactorial condition! the mix faulty energy metabolism Activation of trigeminocervical nucleus causes neurogenic inflammation Activated C fibres release pro-inflammatory substances
[Substance P and Calcitonin Gene Related Peptide
(CRGP) ]from the nociceptive nerve endings in the
periphery, which in turn causes vasodilation and
protein extravasation, i.e. further inflammation.
(Dalkara, Zervas et al. 2006) impaired energy metabolism in migraineurs (Lodi, Iotti et al. 2001; Lodi, Tonon et al. 2006), which will predispose to anaerobic metabolism. Anaerobic metabolism is toxic to neurones and the metabolic by-products associated with it such as lactic acid are able to activate nociceptive fibres. an impaired ability to habituate to sensory stimulation across all sensory modalities.(Schoenen 2006; Brighina, Palermo et al. 2009) thought to be due to impaired functioning of inhibitory networks in the cortex, and has been suggested that this dysfunction occurs in a manner similar to the GABA circuit down-regulation that occurs in sensory deafferentation.(Brighina, Palermo et al. 2009) further risk of forcing neurones into anaerobic metabolism immunological changes that predispose migraineurs to the activation of the inflammatory cascade triggers may be infections, foods or other environmental factors.(Longoni and Ferrarese 2006) management plan for the migraineur should include the identification and, as far as possible, the removal of the triggers - food diaries etc. Supplementation with co-enzyme q10 due to its antioxidant capabilities and involvement in oxidative phosphorylation.(Lodi, Tonon et al. 2006) Supplementation with other antioxidants. Supplementation with magnesium to reduce the likelihood of activation of NMDA receptors on nociceptive fibres.(Lodi, Tonon et al. 2006) Reduction of circulating adrenaline levels as adrenaline reduces the threshold to activation of C fibres via the alpha 1 receptors. Examples may be stress reduction or the reduction of caffeine intake. Ensuring good respiratory mechanisms through preservation of the lumbar lordosis and normal rib mechanics. Management of autonomic function to ensure optimum vascular supply to the brain. Lifestyle advice to ensure the patient only stimulates their nervous system within the tolerance of fatigue. repeated trains of TMS have been shown to improve the functioning of the inhibitory networks Brainstem dysfunction has also been implicated in migraine, both as a primary migraine generator, and through failure of brain stem pain inhibition mechanisms. Goadsby (2005) reports activation of the locus coeruleus and periaqueductal grey (PAG) in migraine without aura, and that these correspond to areas that have generated migraine-like symptoms in patients when stimulated electrically. dysfunction in the periaqueductal grey leads to disinhibition of the trigeminocervical nucleus. (Knight and Goadsby 2001) The PAG is involved in descending pain control mechanisms, along with the locus coeruleus and raphae nuclei. the notion of brain stem dysfunction is further supported by the presence of:
measured balance deficits, vestibular changes (Akdal, Dönmez et al. 2007; Akdal, Donmez et al. 2009; Asai, Aoki et al. 2009),
and subclinical cerebellar deficits in migraineurs. (Sandor, Mascia et al. 2001) Diagnostic Criteria for Migraine without Aura (The International Classification of Headache Disorders, 2nd edition. 2004)
Recurrent headache disorder manifesting in attacks lasting 4-72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia.
A. At least 5 attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated)
C. Headache has at least two of the following characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
D. During headache at least one of the following:
1. nausea and/or vomiting
2. photophobia and phonophobia
E. Not attributed to another disorder Diagnostic Criteria for Migraine with Aura (adapted from The International Classification of Headache Disorders, 2nd edition. 2004)
Recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5-20 minutes and last for less than 60 minutes. Headache with the features of migraine without aura usually follows the aura symptoms. Less commonly, headache lacks migrainous features or is completely absent.
A. At least 2 attacks fulfilling criterion B
B. Migraine aura fulfilling criteria 1 and 2 for one of the subforms 1.2.1-1.2.6, for example:
1. Aura consisting of at least one of the following, but no motor weakness:
A. fully reversible visual symptoms including positive features (eg, flickering lights, spots or lines) and/or negative features (ie, loss of vision)
B. fully reversible sensory symptoms including positive features (ie, pins and needles) and/or negative features (ie, numbness)
C. fully reversible dysphasic speech disturbance
2. At least two of the following:
A. homonymous visual symptoms and/or unilateral sensory symptoms
B. at least one aura symptom develops gradually over ≥5 minutes and/or different aura symptoms occur in succession over ≥5 minutes
C. each symptom lasts ≥5 and ≤60 minutes
C. Not attributed to another disorder migraine with aura the same mechanisms as MWOA plus: cortical spreading depression a slow travelling wave of neuronal and glial depolarisation in the cortex, which is followed by a long-lasting suppression of neural activity.(Buzzi and Moskowitz 2005) accompanied by increases in extracellular ions, neurotransmitter such as glutamate, and a temporary increase in cortical blood flow, which is followed by a longer period of decreased flow. what causes CSD to occur? high concentrations of excitatory amino acids and K+ ions, as well as energy failure.(Somjen 2001) failure to habituate to repeated sensory stimuli may cause sufficient elevation of excitatory amino acids and K+ to initiate CSD.(Dalkara, Zervas et al. 2006) Migraine Summary Multifactorial condition energy deficiencies failure of inhibitory mechanisms immunological changes brainstem dysfunction management needs to be multifactorial Cluster Headache CH is characterised by unilateral attacks of head pain with ipsilateral craniofacial autonomic disturbances. (Leone and Bussone 2009) Diagnostic Criteria for Cluster Headache (The International Classification of Headache Disorders, 2nd edition. 2004)
Attacks of severe, strictly unilateral pain which is orbital, supraorbital, temporal or in any combination of these sites, lasting 15-180 minutes and occurring from once every other day to 8 times a day. The attacks are associated with one or more of the following, all of which are ipsilateral: conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, eyelid oedema. Most patients are restless or agitated during an attack.
A. At least 5 attacks fulfilling criteria B-D
B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes if untreated
C. Headache is accompanied by at least one of the following:
1. ipsilateral conjunctival injection and/or lacrimation
2. ipsilateral nasal congestion and/or rhinorrhoea
3. ipsilateral eyelid oedema
4. ipsilateral forehead and facial sweating
5. ipsilateral miosis and/or ptosis
6. a sense of restlessness or agitation
D. Attacks have a frequency from one every other day to 8 per day
E. Not attributed to another disorder Pathophysiology peripheral? central? finding raised venous level of calcitonin gene related peptide, thought to suggest peripheral inflammation linked to intracranial lesions and removal of lesion removes the CH greater occipital nerve block has been shown to be effective in aborting a period of CH greater amount of research suggests a central cause circadian nature of CH, the relationship with sleep and the autonomic symptoms all point to the involvement of the hypothalamus in CH.(Holland and Goadsby 2007) the hypothalamus also involved in nociceptive regulation with pathways connecting both directly with the trigeminocervical nucleus(Leone and Bussone 2009) and indirectly via the periaqueductal grey, the raphae nuclei and the locus coeruleus.(Holland and Goadsby 2007) the pain matrix is activated in CH attacks anterior cingulate contralateral posterior thalamus ipsilateral basal ganglia bilateral insulae cerebellar hemispheres (Leone and Bussone 2009) hypometabolism in the prefrontal, orbitofrontal and perigenual anterior cingulate cortices both during the headache period and out of it, and hypometabolism in the cerebellopontine area multifactorial condition with failure of cortical and brain stem pain control, as well as hypothalamic systems that leads to an imbalance of pro- and anti-nociceptive inputs regulating the trigeminovascular system ouch! inhalation of 100% oxygen at 7 to 12 L/min via a nonrebreathing face mask is rapidly effective for most sufferers in the acute attack.(Cohen, Matharu et al. 2007) Treatment of Cluster Headache Oxygen has been shown to have a direct effect on the inhibitory projections from the brainstem to the central pain pathway.(Bussone 2008) several pharmaceutical treatments for CH. Subcutaneous sumatriptan has a rapid effect and high success rate during an attack.(Cohen, Matharu et al. 2007) Tension-Type Headache usually mild to moderate, pressure or muscle type pain lasting hours to days no neurological or constitutional symptoms usually bilateral and may extend into the neck peripheral and central mechanisms implicated infrequent form of TTH is primarily due to peripheral mechanisms central mechanisms coming to bear in the frequent and chronic forms of the condition (Bendtsen and Jensen 2009) main model for TTH is that tender/trigger points in peripheral muscles produce nociceptive activation, which in time will cause central sensitisation chronic TTH sufferers have lowered sensitivity thresholds, not only in the cranium, but in the periphery as well the generalised nature of these changes indicate that the sensitisation is central rather than peripheral.(Bendtsen 2000) there are signs of cerebellar/brain stem dysfunction and changes in TTH sufferers also: deviation of subjective visual vertical (a vestibular/otolithic sign) (Asai, Aoki et al. 2009), increased sway in stabilometry (Ishizaki, Mori et al. 2002) TTH sufferers show the same volumetric brain changes seen in many chronic pain conditions regions of the brain known to be involved in pain processing, namely the cingulate cortex, insula, and the orbitofrontal cortex and parahippocampus bilaterally. it is likely they are the consequence, rather than the cause of the chronic pain.(May 2009) Treatment of TTH removal of pain generators in the periphery and the removal of any triggering factors such as psychological stress, postural aberrancies etc. some studies have found cervical spine manipulation to be effective acupuncture, ultrasound and stretching may also be effective Nutritional therapies magnesium supplementation to decrease NMDA receptor activation omega 3 fatty acids to minimise peripheral inflammation Much of this applies to migraine
but in my experience is often present
in other headache types link between exposure to OKN stimulus and the development of headache in migrainuers (Drummond, P.D., Granston, A., 2004) Patients with vestibular dysfunction, migraine and/or anxiety may experience visual vertigo (VV), whereby symptoms are provoked by disorienting visual environments (Pavlou, Quinn etal 2011) visual dependency, both at a perceptual and a postural level, can be reduced with short-term graded OKS exposure in healthy subjects (Pavlou, Quinn etal 2011) there is also evidence that vestibular stimulation can reduce pain (Ramachandran, McGeoch et al. 2007; Ramachandran, McGeoch et al. 2007; Waisblat, Mercier et al. 2010) Summary Headaches are multifactorial conditions
and need to be treated as such As well as nutritional and physical therapies
brain based approaches need to be considered Vestibular stimulation has been found to be effective for pain relief Headache sufferers appear to have subclinical vestibular dysfunction Consider vestibular therapies such as
gaze stabilisation exercises
modified Brandt Darof exercises
graded optokinetic stimulation
saccade exercises AKDAL, G., DONMEZ, B., OZTURK, V. & ANGIN, S. 2009. Is balance normal in migraineurs without history of vertigo? Headache, 49, 419-25.
AKDAL, G., DÖNMEZ, B., ÖZTÜRK, V. & ANGIN, S. 2007. Balance in migraineurs. Neurology, 68, sA89
ASAI, M., AOKI, M., HAYASHI, H., YAMADA, N., MIZUTA, K. & ITO, Y. 2009. Subclinical deviation of the subjective visual vertical in patients affected by a primary headache. Acta Otolaryngol, 129, 30-5.
BENDTSEN, L. 2000. Central sensitization in tension-type headache--possible pathophysiological mechanisms. Cephalalgia, 20, 486-508.
BENDTSEN, L. & JENSEN, R. 2009. Tension-type headache. Neurol Clin, 27, 525-35.
BRIGHINA, F., PALERMO, A. & FIERRO, B. 2009. Cortical inhibition and habituation to evoked potentials: relevance for pathophysiology of migraine. J Headache Pain, 10, 77-84.
BUSSONE, G. 2008. Cluster headache: from treatment to pathophysiology. Neurol Sci, 29 Suppl 1, S1-6.
BUZZI, M. G. & MOSKOWITZ, M. A. 2005. The pathophysiology of migraine: year 2005. J Headache Pain, 6, 105-11.
COHEN, A. S., MATHARU, M. S. & GOADSBY, P. J. 2007. Trigeminal Autonomic Cephalalgias: Current and Future Treatments. Headache: The Journal of Head and Face Pain, 47, 969-980.
DALKARA, T., ZERVAS, N. T. & MOSKOWITZ, M. A. 2006. From spreading depression to the trigeminovascular system. Neurol Sci, 27 Suppl 2, S86-90.
Drummond, P. D. and A. Granston (2004). "Facial pain increases nausea and headache during motion sickness in migraine sufferers." Brain 127(Pt 3): 526-34.
GOADSBY, P. J. 2005. Migraine pathophysiology. Headache, 45 Suppl 1, S14-24.
HOLLAND, P. & GOADSBY, P. J. 2007. The hypothalamic orexinergic system: pain and primary headaches. Headache, 47, 951-62.
ISHIZAKI, K., MORI, N., TAKESHIMA, T., FUKUHARA, Y., IJIRI, T., KUSUMI, M., YASUI, K., KOWA, H. & NAKASHIMA, K. 2002. Static stabilometry in patients with migraine and tension-type headache during a headache-free period. Psychiatry Clin Neurosci, 56, 85-90
KNIGHT, Y. E. & GOADSBY, P. J. 2001. The periaqueductal grey matter modulates trigeminovascular input: a role in migraine? Neuroscience, 106, 793-800.
LEONE, M. & BUSSONE, G. 2009. Pathophysiology of trigeminal autonomic cephalalgias. Lancet Neurol, 8, 755-64.
LODI, R., IOTTI, S., CORTELLI, P., PIERANGELI, G., CEVOLI, S., CLEMENTI, V., SORIANI, S., MONTAGNA, P. & BARBIROLI, B. 2001. Deficient energy metabolism is associated with low free magnesium in the brains of patients with migraine and cluster headache. Brain Res Bull, 54, 437-41.
LODI, R., TONON, C., TESTA, C., MANNERS, D. & BARBIROLI, B. 2006. Energy metabolism in migraine. Neurol Sci, 27 Suppl 2, S82-5
LONGONI, M. & FERRARESE, C. 2006. Inflammation and excitotoxicity: role in migraine pathogenesis. Neurol Sci, 27 Suppl 2, S107-10.
MAY, A. 2009. New insights into headache: an update on functional and structural imaging findings. Nat Rev Neurol, 5, 199-209.
Pavlou, M., C. Quinn, et al. (2011). "The effect of repeated visual motion stimuli on visual dependence and postural control in normal subjects." Gait & Posture 33(1): 113-118.
Ramachandran, V. S., P. D. McGeoch, et al. (2007). "Can vestibular caloric stimulation be used to treat Dejerine-Roussy Syndrome?" Med Hypotheses 69(3): 486-8.
Ramachandran, V. S., P. D. McGeoch, et al. (2007). "Rapid relief of thalamic pain syndrome induced by vestibular caloric stimulation." Neurocase 13(3): 185-8.
SANDOR, P. S., MASCIA, A., SEIDEL, L., DE PASQUA, V. & SCHOENEN, J. 2001. Subclinical cerebellar impairment in the common types of migraine: a three-dimensional analysis of reaching movements. Ann Neurol, 49, 668-72.
SCHOENEN, J. 2006. Neurophysiological features of the migrainous brain. Neurol Sci, 27 Suppl 2, S77-81.
SOCIETY, I. H. 2004. The International Classification of Headache Disorders, 2nd edition. Cephalalgia 24 1-160.
SOMJEN, G. G. 2001. Mechanisms of spreading depression and hypoxic spreading depression-like depolarization. Physiol Rev, 81, 1065-96.
Waisblat, V., F. J. Mercier, et al. (2010). "[Effect of rocking motion on labor pain before epidural catheter insertion in the sitting position]." Annales francaises d'anesthesie et de reanimation 29(9): 616-20. References