For reprint orders, please contact [email protected]
Craniomandibular muscles,
intraoral orthoses and migraine
Elliot Shevel
Intraoral splints are effective in migraine prevention. In this review, changes in the quality of
life of migraineurs treated with a palatal nonoccluding splint were measured. Using the
Migraine Specific Quality of Life Instrument (Version 2.1), it was found that the palatal

nonoccluding splint significantly improved the quality of life of migraineurs. The role of the
craniomandibular muscles in the pathophysiology of migraine is also discussed.

Expert Rev. Neurotherapeutics 5(3), 371–377 (2005) Migraine is a common disorder with a life- Materials & method
Materials & method
time prevalence of 16% worldwide, and a last-year prevalence of 10% [1,2]. It may sig- In total, 152 patients, 117 female and 35 male, Discussion
nificantly diminish quality of life, even were admitted to the study. The inclusion between attacks, and impairs quality of life Expert opinion
more than diabetes, hypertension and osteo- • Age of onset of migraine before 50 years Five-year view
arthritis [3–5]. Although the pathogenesis of • Subjects with all or most of their own teeth, Key issues
migraine headache remains poorly under- and who did not wear a removable dental References
stood, current theories suggest a primary, possibly genetically determined, CNS dys- Affiliation
function to be involved. There is activation • History of migraine of 1 year or more, with of the trigeminovascular system at least one attack per week in the previous is comprised of the meningeal vessels, trigeminal nerve and trigeminal nucleus, in • Headache free between attacks particular the trigeminal subnucleus • A diagnosis of migraine without aura caudalis [8].
(i.e., group 1.1 in the guidelines laid down Tenderness and dysfunction of the crani- by the Headache Classification Committee omandibular muscles is a common finding of the International Headache Society) in migraine [9–15]. Intraoral interocclusal To make the diagnosis of migraine without orthoses, used in the treatment of cranio- aura, the following criteria must be met [27]: mandibular muscle dysfunction [16–21], arealso effective in preventing migraine A. At least five attacks fulfilling criteria B, C Their therapeutic muscle-relaxing effect is attributed to the fact that they encourage B. Headache attacks lasting 4–72 h (untreated the mandible to assume the physiologic rest or unsuccessfully treated) position, thereby altering habitual neu- C. Headache has at least two of the following The Headache Clinic, romuscular patterns within the mastica- characteristics: unilateral location, pulsat- Suite 256, P Bag X2600, tory muscles [21]. When a nonoccluding Houghton, 2014, South Africa ing quality, moderate or severe intensity palatal orthosis is worn, there is increased Tel.: +27 114 840 933 (inhibits or prohibits daily activities), Fax: +27 114 840 982 resting length and relaxation of the cranio- aggravated by walking up stairs or similar mandibular muscles [25,26]. This study routine physical activity determined the effect of wearing a nonoc- KEYWORDS:
D. During the headache at least one of the fol- craniomandibular, migraine, cluding palatal orthosis on the quality of lowing: nausea and/or vomiting, muscle dysfunction, orthosis life of migraineurs.
photophobia and phonophobia 2005 Future Drugs Ltd

Factors that could influence the frequency or intensity of • Role function restriction, which measures the percentage of migraine, such as pregnancy, the use of prophylactic migraine time that the patient can perform normal daily activities medication or ergot derivatives, a history of drug or alcohol • Role function prevention, which measures the percentage abuse, or serious illness were exclusion criteria. All participants productivity while working were fully informed of the nature of the project and their prior • Emotional function, which measures the percentage of consent was obtained.
emotional and relationship disability Patients completed the MSQ before the start of treatment The posture-modifying appliance (PMA) was fabricated using and again 12 months later. Participants were instructed to the maxillary cast of the subject. It consisted of a 3 mm thick continue using palliative medication whenever necessary.
acrylic resin reinforced with a chrome cobalt strip (FIGURE 1).
The appliance covered the hard palate, with the exception of the anterior part where the tip of the tongue normally touches As there was no significant statistical difference between the during speech.
results for males and females, they were combined, and the The PMA was adjusted for fit and overall comfort. Patients average pretreatment and post-treatment scores for each were told that the PMA should not interfere with the free parameter were calculated. Analysis of the data using the Stu- movement of the tongue during speech. They were asked to dent's t-test showed statistically significant improvement in all speak with the PMA in situ using the words listed in three parameters. Role function restriction improved from which are phonetically balanced and designed to test the whole 54.6 to 91% (p < 0.0001), role function prevention improved range of English sounds in various combinations from 45.4 to 84.8% (p < 0.0001) and emotional function was then removed and the part that the tongue had touched improved from 45.4 to 91.2% (p < 0.0001).
during speech indicated by the patient. The offending acrylicwas ground away and the process repeated, until the patient was no longer aware of any interference with tongue move- Migraine is considered to be a neurovascular syndrome, with ment. The final shape and thickness of the PMA was, in most abnormal neuronal excitability in the cerebral cortex, peripheral patients, very different to the original sensitization of the trigeminovascular system and pain due to (FIGURE 2). Subjects were instructed to wear the PMA day and night, but to remove it dilation of intracranial blood vessels [30–32]. The triptans were during tooth brushing, eating and drinking, and when playing developed as cranial vasoconstrictors to mimic the desirable contact sports. Subjects were requested to return for adjustment effects of serotonin [33,34], while avoiding its side effects [35]. An of the PMA if they experienced discomfort or speech difficulty.
important hindrance to the more widespread use of the triptansis the unsubstantiated perception that they have harmful Migraine specific quality of life measurement
vasoconstrictor effects [32].
The Migraine Specific Quality of Life Questionnaire (MSQ) Nociceptive input to the CNS is increased due to sensitiza- Version 2.1 was used to assess the efficacy of the PMA. The tion of peripheral sensory afferents, and the resultant barrage of MSQ is a 14-item, self-administered questionnaire, which nociceptive impulses results in sensitization of second- and measures three dimensions of headache-related quality of life third-order neurons in the CNS. In this way, sensitization may that are affected by migraine play a role in the initiation and maintenance of migraine Consequently, current research has focussed upon prejunctionaland presynaptic targets on nociceptive trigeminovascular neu-rons in an attempt to develop drugs that inhibit trigeminalnociceptive traffic and central sensitization withoutvasoconstrictor effects [32,37].
Central sensitization is induced by nociceptive afferent input from the intracranial dura mater travelling along thetrigeminovascular pain pathway [38]. It results in [39–41]: • A reduction of the threshold to cell depolarization • Cellular activity that continues after cessation of the peripheral nociceptive input • A spread of cellular activity to neighbouring cells Noxious stimulation of muscle afferents also increases the excitability of spinal cord neurons [42]. Persistent stimulationleads to cellular and molecular changes, which result in neuro- Figure 1. The posture-modifying appliance before adjusting
nal hyperexcitability, to the extent that pain is elicited by low- for speech.
threshold, normally non-noxious, stimuli [43–49]. After anincrease in central excitability produced by the activation of Expert Rev. Neurotherapeutics 5(3), (2005) Muscles and migraine
peripheral chemoreceptors, cells in the trigeminal nucleus cau-dalis that are normally nociceptive-specific begin to respond to Box 1. Phonetically balanced word list designed to test
low-threshold, primary afferent non-nociceptive mechano- the whole range of English sounds in various
receptors [50]. Repeated stimulation of a dorsal root produces, in some neurons, a prolonged heterosynaptic facilitation withan augmentation of the response to the conditioning root (homosynaptic potentiation) as well as to adjacent test roots (heterosynaptic potentiation) Restoring a patient's ability to function normally is now recognized as the primary treatment goal, rather than merely [52]. The results of this study show that relaxa- tion of the craniomandibular muscles by means of a PMA improves the quality of life of migraineurs. By reducing sen- sory input from the craniomandibular muscles, central sen- sitization is reduced. The probable mechanism is that intraoral splints may have therapeutic effects apart from • Volumetric analysis of the masseter and medial pterygoid those commonly attributed to the occlusal component [53].
muscles showed that the volume of masticatory muscles in This may be attributed to the fact that an intraoral appli- migraineurs is nearly 70% greater than in nonmigraineurs ance may encourage the mandible to assume the physiologic rest position, thereby altering habitual neuromuscular pat- terns within the masticatory muscles [54]. Further research has shown that when a nonoccluding palatal appliance isworn there is an increase in the interocclusal distance and, • Sensory afferents from the craniomandibular muscles consequently, in the resting length of the masticatory project to the trigeminal sensory nuclei, and in particular muscles [55,56].
to the subnucleus caudalis. Subnucleus caudalis neurons, A limitation of this study is the lack of a placebo control including low-threshold mechanoreceptive, wide-dynamic group. There is, unfortunately, no remedy for this when range and nociceptive-specific neurons, are excited by the testing a physical intervention such as an intraoral appli- stimulation of craniomandibular muscle sensory ance, given the sensitivity of the intraoral structures. The possible placebo effect of the PMA cannot therefore be • The subnucleus caudalis also acts as a critical interneuronal measured, and its importance must remain the subject of relay site in craniofacial nociceptive reflex activity involving speculation. According to Occam's Razor, in science the sim- the craniofacial muscles [67–70].
plest theory that fits the facts of a problem is the one thatshould be selected. This is interpreted to mean that the sim- plest of two competing theories is preferable. If Occam's The following clinical findings have been determined: Razor is applied, then the most likely conclusion is that the • Pericranial muscle pain and tenderness are prominent PMA does have a beneficial nonplacebo effect. The possibil- features in migraine [71–73] ity of natural regression of the migraine in this group of • There is increased pericranial muscle electromyographic patients is minimal, given that all the subjects had been suf- activity in migraine fering for a long time frame without improvement until the PMA was fitted.
• Physical therapy can precipitate migraine attacks [76] Further corroborating evidence that the craniomandibular muscles play a role in the cascade of events in migraine pathogenesis is described below.
Treatment modalities that reduce craniomandibular muscletension are effective in the treatment of migraine and include: • Intraoral splints which reduce migraine intensity and • The middle meningeal artery, dura of the middle and ante- rior cranial fossae, and craniomandibular muscles, all receive • Biofeedback to induce muscle relaxation is widely used in sensory afferents from the mandibular division of the trigem- migraine prophylaxis. The positive treatment response to inal nerve. They all send sensory afferent input to the subnu- biofeedback/relaxation in migraine headache is not related to cleus caudalis, possibly enhancing central sensitization. The presence of changes in blood flow velocity [83].
middle meningeal artery and dura of the middle and anterior • Intramuscular trigger point injections are effective in the cranial fossae via its recurrent meningeal branch, and the treatment of acute migraine pain [84–86].
muscles via their individual branches [57,58].

findings suggest a relationship between migraine headaches onthe one hand and dysfunction of the craniomandibular muscleson the other. In this study, the quality of life of migraineurs wassignificantly enhanced by the use of an intraoral palatal nonoc-cluding appliance. This and other evidence, including anatomi-cal evidence, the projection of sensory afferents from the crani-omandibular muscles to the trigeminal subnucleus caudalis,clinical findings, treatment modalities designed to reduce mus-cle tension which also successfully treat migraine, and drug tri-als, provide a compelling argument that central sensitization inmigraineurs is enhanced by sensory input originating from thecraniomandibular muscles. Therefore, the best current treat-ment regimen must include assessment and treatment of thepericranial muscles.
Figure 2. Example of the posture-modifying appliance after adjusting
It is unlikely that this treatment regimen will gain much favor.
for speech.
The reason being that medicine is divided into different disci-plines, each with its own sphere of interest. While the general • Resection of the corrugator supercillii muscles in patients public may believe that these disciplines share information at who respond positively to botulinum toxin A injection the highest level, in reality they rarely communicate with each results in prolonged and effective migraine other. The excellent results achieved with the use of intraoral splints in migraineurs have been on record for many years. Inspite of this, intraoral splints are rarely mentioned in the headache literature – there is not a single article on the subject Preliminary studies indicate that drugs such as botulinum in Headache or Cephalalgia in at least the last 3 years. Unfor- toxin A, baclofen and tizanidine, which reduce skeletal mus- tunately, despite the excellent clinical results, splint therapy cle spasm and tone, may be useful in migraine for migraine is still regarded with scepticism. In the words of prophylaxis [90].
Max Planck (Nobel Prize Physicist, 1918), "A new scientific Sumatriptan was developed as a cerebral vasoconstrictor, but truth does not triumph by convincing its opponents and it has also been shown to act on skeletal muscle [91–93]. It cannot making them see the light, but rather because its opponents be excluded, therefore, that the triptans may be effective in eventually die, and a new generation grows up that is familiar migraine due to altered muscle metabolism.
with it". It is improbable, therefore, that, despite the provenefficacy of intraoral splints, their use will be widely adopted within the next 5 years. In the next 50 years. perhaps? Current theories suggest that a primary, probably geneticallydetermined, CNS dysfunction is involved in the initiation of the migraine headache, with activation of the trigeminovascular The author would like to express sincere thanks to Daniel system and sensitization of neurons in the CNS [6]. Clinical Shevel for his invaluable input in the writing of this review.
Key issues
• Migraine is a common disorder.
• It is characterized by moderate-to-severe pain, with associated symptoms such as nausea, vomiting, photophobia and phonophobia.
• Migraine is associated with changes in the trigeminovascular system.
• Tenderness and dysfunction of the craniomandibular muscles is a common finding in migraine.
• Intraoral orthoses are used to relax the craniomandibular muscles and restore them to normal function.
• This review studies the effect on migraineurs of wearing a nonoccluding palatal orthosis.
• Placebo-controlled studies are not feasible when intraoral orthoses are used.
• The effect was therefore measured by comparing pretreatment with post-treatment quality of life.
• Statistical analysis of the results showed a significant improvement in quality of life when the orthosis was worn.
Expert Rev. Neurotherapeutics 5(3), (2005) Muscles and migraine
Olesen J. Some clinical features of the acute appliance on muscular symptoms in Papers of special note have been highlighted as: migraine attack: an analysis of 750 patients. craniomandibular disorders: a preliminary Headache 18, 268–271 (1978).
study. J. Craniomandib. Pract. 19, 42–47 •• of considerable interest Cohen MJ. Psychophysiological studies of First suggestion in the literature that a
Rasmussen BK, Jensen R, Schroll M, headache: is there similarity between palatal appliance could bring about
Olesen J. Epidemiology of headache in a migraine and muscle contraction headache? improvement of myofascial pain
general population – a prevalence study. J. Headache 18, 189–196 (1978).
Clin. Epidemiol. 44, 1147–1157 (1991).
Bakal DA, Kaganov JA. Muscle contraction Olesen J. Classification and diagnostic Schwartz BS, Stewart WF, Lipton RB. Lost and migraine headache: psychophysiologic criteria for headache disorders, cranial workdays and decreased work effectiveness comparison. Headache 17, 208–215 neuralgias, and facial pain. First edition. associated with headache in the workplace. J. Cephalalgia 8(Suppl. 7), 19–33 (1988).
Occup. Environ. Med. 39, 320–327 (1997).
Block SL, Apfel M, Laskin DM. The use of Berger KW. Speech Audiometry Materials. Gerbaud L, Navez ML, Couratier P et al. a resilient rubber bite appliance in the Herald, OH, USA, 46–50 (1977).
Validation of the combined SF36/MSQOL treatment of MPD syndrome. J. Dent. Res. test of evaluation of quality of life in 57, A71 (1978).
Patrick DL, Hurst BC, Hughes J. Further migraine patients in France. Rev. Neurol. Campbell J. Extension of the development and testing of the migraine- 158, 719–727 (2002).
temporomandibular joint space by methods specific quality of life (MSQOL) measure. Headache 40(7), 550–560 (2000).
Michel P, Dartigues JF, Lindoulsi A, Henry derived from general orthopaedic Shows that cumulative evidence for the
P. Loss of productivity and quality of life in procedures. J. Prosthet. Dent. 7, 386–399 migraine-specific quality of life instrument
migraine sufferers among French workers: meets established criteria for validity,
results from the GAZEL cohort. Headache Greene CS, Laskin DM. Splint therapy for consistency and reproducibility. It
37, 71–78 (1997).
the myofascial pain-dysfunction syndrome: confirmed that quality of life testing is a
Osterhaus JT, Townsend RJ, Gandek B, a comparative study. J. Am. Dent. Ass. 84, valid tool for measuring treatment efficacy
Ware JE. Measuring the functional status 624–628 (1972).
in migraine.
and well-being of patients with migraine Lamey PJ, Steele JG, Aitchison T. Silberstein SD. Migraine pathophysiology headache. Headache 34, 337–343 (1994).
Migraine: the effect of acrylic appliance and its clinical implications. Cephalalgia Russell MB. Genetic epidemiology of design on clinical response. Br. Dent. J. 24(Suppl. 2), 2–7 (2004).
migraine and cluster headache. Cephalalgia 180, 137–140 (1996).
Wolff HG. Headache and Other Head Pain. 17, 683–701 (1997).
Matthews E. Treatment for the teeth- First Edition. Oxford University Press, NY, Edvinsson L. Aspects on the grinding habit. Dent. Record 62, 154–155 pathophysiology of migraine and cluster Goadsby PJ. Prejunctional and presynaptic headache. Pharmacol. Toxicol. 89, 65–73 Posselt U. Treatment of bruxism by bite trigeminovascular targets: what preclinical guards and bite plates. J. Canad. Dent. evidence is there. Headache Currents 1, 1–6 Goadsby PJ, Lipton RB, Ferrari MD. Migraine Assoc. 29, 773–778 (1963).
– current understanding and treatment. N. Quayle AA, Gray RJM, Metcalfe RJ, Kimball RW, Friedman AP, Vallejo E. Effect Engl. Med. J. 346, 257–270 (2002).
Guthrie E, Wastell D. Soft occlusal splint of serotonin in migraine patients. Neurology Lipchik GL, Holroyd KA, Talbot F, Greer therapy in the treatment of migraine and 10, 107–111 (1960).
M. Pericranial muscle tenderness and other headaches. J. Dent. 18, 123–129 Lance JW, Anthony M, Hinterberger H. exteroceptive suppression of temporalis The control of cranial arteries by humoural muscle activity: a blind study of chronic Lapeer GL. Reduction of the painful mechanisms and its relation to the migraine tension-type headache. Headache 37, sequelae of migraine headache by use of the syndrome. Headache 7, 93–102 (1967).
368–376 (1997).
occlusal diagnostic appliance: an Raises the possibility that pericranial
hypothesis. J. Craniomandib. Pract. 6, Humphrey PPA, Feniuk W, Perren MJ, muscle tenderness is present early in
82–86 (1988).
Beresford IJM, Skingle M, Whalley ET. migraine without aura, and thus may
As early as 1988, Lapeer suggested that
Serotonin and migraine. Ann. NY Acad. Sci. contribute to the etiology.
"further research into occlusal splint
600, 587–598 (1990).
Steele JG, Lamey PJ, Sharkey SW, Smith therapy as an adjunct to relieving or
Bendtsen L. Sensitization: its role in GMR. Occlusal abnormalities, pericranial aborting the painful sequelae of migraine
primary headache. Curr. Opin. Investig. muscle and joint tenderness and tooth wear headaches is necessary".
Drugs 3, 449–453 (2002).
in a group of migraine patients. J. Oral Lamey PJ, Barclay SC. Clinical Elucidated the concept that nociceptive
Rehabil. 18, 453–458 (1991).
effectiveness of occlusal splint therapy in input to the CNS may be increased due to
activation or sensitization of peripheral

Lous I, Olesen J. Evaluation of pericranial patients with classical migraine. Scot. Dent. tenderness and oral function in patients J. 32, 11–12 (1987).
with common migraine, muscle Young P. A cephalometric study of the Ramadan NM, Buchanan MS, Stare H, contraction headaches, and combination effect of acrylic test palatal piece thickness Pearlman H. Peripheral and central headache. Pain 12, 385–393 (1982).
on the physiologic rest position. J. targets for acute migraine therapy: early clinical trial results. Headache Cur. 1, Tfelt-Hansen P, Lous I, Olesen J. Philippine Dent. Ass. 19, 5–15 (1966).
7–12 (2004).
Prevalence and significance of muscle Minagi S, Shimamura M, Sato T, Natsuaki tenderness during common migraine N, Ohta M. Effect of a thick palatal Malick A, Burstein R. Peripheral and attacks. Headache 21, 49–54 (1981).
central sensitization during migraine. Funct. Neurol. 15(Suppl. 3), 28–35 Wenzel R, Dortch M, Cady R, Lofland JH, Sessle BJ, Hu JW, Amano N, Zhong G. Diamond S. Migraine headache Convergence of cutaneous, tooth pulp, Woolf CJ, Salter MW. Neuronal plasticity: misconceptions: barriers to effective care. visceral, neck and muscle afferents onto increasing the gain in pain. Science 288, Pharmacotherapy 24, 638–648 (2004).
nociceptive and non-nociceptive neurones 1765–1768 (2000).
Greene CS, Laskin DM. Splint therapy for in trigeminal subnucleus caudalis (medullary dorsal horn) and its Coderre TJ, Katz J. Peripheral and central the myofascial pain-dysfunction syndrome: implications for referred pain. Pain 27, hyperexcitability: differential signs and a comparative study. J. Am. Dent. Ass. 84, 219–235 (1986).
symptoms in persistent pain. Behav. Brain 624–628 (1972).
Sci. 20, 404–419 (1997).
Posselt U. Treatment of bruxism by bite Amano N, Hu JW, Sessle BJ. Responses of neurons in feline trigeminal subnucleus Dubner R. Neural basis of persistent pain: guards and bite plates. J. Canad. Dent. caudalis (medullary dorsal horn) to sensory specialization, sensory modulation, Assoc. 29, 773–778 (1963).
cutaneous, intraoral, and muscle afferent and neuronal plasticity. In: Progress in Pain Young P. A cephalometric study of the stimuli. J. Neurophysiol. 55, 227–243 Research and Management. Jensen TS, effect of acrylic test palatal piece thickness Turner JA, Weisenfeld-Hallin Z (Eds). on the physiologic rest position. J. IASP Press, WA, USA, 77–91 (1997).
Philippine Dent. Ass. 19, 5–15 (1966).
Matthews B. Peripheral and central aspects of trigeminal nociceptive systems. Philos. Trans. R. Hu JW, Sessle BJ, Raboisson P, Dallel R, Minagi S, Shimamura M, Sato T, Natsuaki Soc. Lond. Biol. Sci. 19, 313–324 (1985).
Woda A. Stimulation of craniofacial muscle N, Ohta M. Effect of a thick palatal afferents induces prolonged facilitatory appliance on muscular symptoms in Tsai C. The caudal subnucleus caudalis effects in trigeminal nociceptive brain-stem craniomandibular disorders: a preliminary (medullary dorsal horn) acts as an neurones. Pain 48, 53–60 (1992).
study. J. Craniomandib. Pract. 19, 42–47 interneuronal relay site in craniofacial nociceptive reflex activity. Brain Res. 826, Jensen TS. Mechanisms of neuropathic 293–297 (1999).
pain. In: Pain 1996, an Updated Review. Shankland WE. The trigeminal nerve. Part Campbell JN (Ed.). IASP Press, WA, USA, IV: the mandibular division. J. Tsai CM, Chiang CY, Yu XM, Sessle BJ. 77–86 (1996).
Craniomandib. Pract. 19, 153–161 (2001).
Involvement of trigeminal subnucleus caudalis (medullary dorsal horn) in Jensen TS. Recent advances in pain Asfat R. A review of the neurovascular craniofacial nociceptive reflex activity. Pain research: implications for chronic headache. supply of the mandible. S. Afr. Dent. J. 57, 81, 115–128 (1999).
Cephalalgia 21, 765–769 (2001).
414–416 (2002).
Cairns BE, Sessle BJ, Hu JW. Gracely RH, Lynch SA, Bennett GJ. Lamey PJ, Burnett CA, Fartash L, Clifford Temporomandibular-evoked jaw muscle Painful neuropathy: altered central TJ, McGovern JM. Migraine and reflex: role of brain stem NMDA and non- processing, maintained dynamically by masticatory muscle volume, bite force, and NMDA receptors. Neuroreport 12, peripheral input. Pain 51, 175–194 (1992).
craniofacial morphology. Headache 41, 1875–1878 (2001).
Gottrup H, Nielsen J, Arendt-Nielsen L, 49–56 (2001).
Steele JG, Lamey PJ, Sharkey SW, Smith G. Jensen TS. The relationship between The volume of masticatory muscles in
Occlusal abnormalities, pericranial muscle sensory thresholds and mechanical migraineurs is nearly 70% greater than in
and joint tenderness and tooth wear in a hyperalgesia in nerve injury. Pain 75, nonmigraineurs (p < 0.0001).
group of migraine patients. J. Oral Rehabil. 321–329 (1998).
Yamakami Y. Characteristics of responses in 18, 453–458 (1991).
Gottrup H, Andersen J, Arendt-Nielsen L, the trigeminal subnucleus caudalis and Jensen K, Tuxen C, Olesen J. Pericranial Jensen TS. Psychophysical examination of adjacent reticular formation evoked by the muscle tenderness and pressure-pain patients following operation for cancer stimulation of the masseter muscle. Showa threshold in the temporal region during mammae. Pain 87, 275–284 (2000).
Shigakkai Zasshi 9, 130–135 (1989).
common migraine. Pain 35, 65–70 (1988).
Koltzenburg M. Painful neuropathies. Arvidsson J, Raappana P. An HRP study of Anttila P, Metsahonkala L, Mikkelsson M et Curr. Opin. Neurol. 67, 307–316 (1998).
the central projections from primary sensory neurons innervating the rat masseter muscle. al. Muscle tenderness in pericranial and Yamamura H, Malick A, Chamberlin NL, Brain Res. 20, 111–118 (1989).
neck-shoulder region in children with Burstein R. Cardiovascular and neuronal headache. A controlled study. Cephalalgia responses to head stimulation reflect central Shigenaga Y, Sera M, Nishimori T et al. 22, 340–344 (2002).
sensitization and cutaneous allodynia in a The central projection of masticatory Clifford T, Lauritzen M, Bakke M, Olesen rat model of migraine. J. Neurophysiol. 81, afferent fibers to the trigeminal sensory J, Moller E. Electromyography of 479–493 (1999).
nuclear complex and upper cervical spinal cord. J. Comp. Neurol. 22, 489–507 (1988).
pericranial muscles during treatment of Woolf CJ, Shortland P, Sivilotti LG. spontaneous common migraine attacks. Sensitization of high mechanothreshold Luo P, Wong R, Dessem D. Projection of Pain 14, 137–147 (1982).
superficial dorsal horn and flexor motor jaw-muscle spindle afferents to the caudal Burnett CA, Fartash L, Murray B, neurones following chemosensitive primary brainstem in rats demonstrated using Lamey PJ. Masseter and temporalis afferent activation. Pain 58, 141–155 (1994).
intracellular biotinamide. J. Comp. Neurol. 17, 63–78 (1995).
muscle EMG levels and bite force in Woolf CJ, Thompson SW, King AE. migraineurs. Headache 40, 813–817 Prolonged primary afferent induced Luo P, Dessem D. Inputs from identified alterations in dorsal horn neurones, an jaw-muscle spindle afferents to Blau JN, MacGregor EA. Migraine and the intracellular analysis in vivo and in vitro. J. trigeminothalamic neurons in the rat: a neck. Headache 34, 88–90 (1994).
Physiol. 83, 255–266 (1988–89).
double-labeling study using retrograde HRP and intracellular biotinamide. J. Lamey PJ, Barclay SC. Clinical Comp. Neurol. 27, 50–66 (1995).
effectiveness of occlusal splint therapy in Expert Rev. Neurotherapeutics 5(3), (2005) Muscles and migraine
patients with classical migraine. Scott. Med. Vasudeva S, Claggett AL, Tietjen GE, Freitag FG. Preventative treatment for J. 32, 11–12 (1987).
McGrady AV. Biofeedback-assisted migraine and tension-type headaches: do Lamey PJ, Steele JG, Aitchison T. relaxation in migraine headache: drugs having effects on muscle spasm and Migraine: the effect of acrylic appliance relationship to cerebral blood flow velocity tone have a role? CNS Drugs 17, 373–381 design on clinical response. Br. Dent. J. 24, in the middle cerebral artery. Headache 43, 137–140 (1996).
245–250 (2003).
Emre S, Erdem SR, Tuncer M. Does Shankland WE. Nociceptive trigeminal Tfelt-Hansen P, Lous I, Olesen J. serotonin relax the rat anococcygeus muscle inhibition–tension suppression system: a Prevalence and significance of muscle via 5-HT7 receptors? Naunyn Schmiedebergs method of preventing migraine and tension tenderness during common migraine Arch. Pharmacol. 362, 96–100 (2000).
headaches. Compend. Contin. Educ. Dent. attacks. Headache 21, 49–54 (1981).
Boska MD, Welch KM, Schultz L, Nelson 23, 105–108 (2002).
Hay KM. Pain thresholds in migraine. J. Effects of the anti-migraine drug Shankland WE II. Migraine and tension- Practitioner 222, 827–833 (1981).
sumatriptan on muscle energy metabolism: type headache reduction through Hay KM. The treatment of pain trigger relationship to side-effects. Cephalalgia 20, pericranial muscular suppression: a areas in migraine. J. Roy. Coll. Gen. Pract. 39–44 (2000).
preliminary report. J. Craniomandib. Pract. 26, 372–376 (1981).
Gobel H, Krapat S, Dworschak M, Heuss 19, 269–278 (2001).
Guyuron B, Varghai A, Michelow BJ, Davis D, Ensink FB, Soyka D. Exteroceptive Shankland WE. Nociceptive trigeminal J. Corrugator supercilii muscle resection suppression of temporalis muscle activity inhibition–tension suppression system: a and migraine headaches. Plast. Reconstr. during migraine attack and migraine method of preventing migraine and tension Surg. 106, 429–434 (2000).
interval before and after treatment with headaches. Compend. Contin. Educ. Dent. sumatriptan. Cephalalgia 14, 143–148 Guyuron B, Tucker T, Davis J. Surgical 22, 1075–1080 (2001).
treatment of migraine headaches. Headache Quayle AA, Gray RJM, Metcalfe RJ, 43, 302–303 (2003).
Guthrie E, Wastell D. Soft occlusal splint Guyuron B, Kriegler JS, Davis J, Amini SB. therapy in the treatment of migraine and Elliot Shevel, BDS, Dip, MFOS, MB, BCh Comprehensive surgical treatment of other headaches. J. Dent. 18, 123–129 The Headache Clinic, Suite 256, P Bag X2600, migraine headaches. Plast. Reconstr. Surg. Houghton, 2014, South Africa 115(1), 1–9 (2005).
Tel.: +27 114 840 933Fax: +27 114 840 [email protected]

Source: http://www.headclin.co.za/uploads/ftp/DrShevelPublications/EXPERT_REVIEW_OF_NEUROTHERAPEUTICS.pdf


AGGIORNAMENTI IN MEDICINA VETERINARIA :questioni di clinica medica degli animali da compagnia  Diagnosi caso 1: Il cane magro con il "pancione": un segno, tante cause Grazie alla raccolta anamnestica, la visita clinica e le indagini collaterali è stato possibile raggiungere la diagnosi di sospetto: epatite cronica di origine tossica causata dall'ingestione di parti velenose di Cycas Revoluta. Le epatiti croniche del cane, sono processi flogistici che si sviluppano principalmente a livello del parenchima epatico, con il conseguente innalzamento dei valori delle transaminasi. Si tratta di patologie che si riscontrano soprattutto in cani di età adulta (4-7 anni) ad eccezione delle forme ereditarie da accumulo di rame che possono insorgere anche in soggetti più giovani; risultano maggiormente interessate le femmine, e, pur potendo interessare tutte le razze, esiste maggiore predisposizione per Bedlington Terrier, Dalmata, Labrador Retriever, Whest Highland White Terrier, Dobermann e Spaniel. Dal punto di vista sintomatologico, i cani affetti da epatite cronica possono presentarsi asintomatici o con segni clinici del tutto aspecifici, quali poliuria e polidipsia, anoressia/disoressia, dimagramento, abbattimento e intolleranza agli sforzi, vomito, diarrea e nei, casi gravi, ascite, coagulopatie ed encefalopatia epatica. La visita clinica del paziente raramente porta al riscontro di qualche reperto indicativo ad eccezione di uno scadimento delle condizioni generali del soggetto, o condizioni più eclatanti come ittero o ascite. Anche le alterazioni di laboratorio risultano non sempre indicative: si riscontrano di norma aumenti delle transaminasi , meno costanti aumenti di fosfatasi alcalina e γ-glutamiltransferasi; nelle fasi avanzate è poi possibile evidenziare tutte le alterazioni indicative di un malfunzionamento epatico, come ipoalbuminemia, riduzione dei valori dell'urea, aumento degli acidi biliari, abbassamento del fibrinogeno. Tra le alterazioni ematologiche che si possono incontrare, ci sono lieve anemia, leucocitosi e piastrinopenia (da consumo, in associazione a coagulopatia) oltre all'aumento dei tempi coagulativi (tempo di protrombina (PT), e tempo di tromboplastina parziale, PTT). La diagnostica per immagini, ed in particolare l'ecografia addominale, può solo completare il quadro ma non fornisce la diagnosi di certezza, in quanto possono sia essere evidenziate alterazioni nella struttura epatica, soprattutto in caso di cirrosi, ma non necessariamente soggetti affetti da epatite cronica presentano alterazioni dell'ecostruttura rilevabili all'esame. Lo strumento diagnostico più indicato in caso di tali patologie, è rappresentato dall'esame istopatologico di un campione prelevato tramite biopsia (ovviamente va ricordato che, in caso di patologia avanzata, in cui fossero comparsi deficit coagulativi, quest'ultima risulta controindicata). Nel presente caso l'esame bioptico ed istopatologico non è stato eseguito in quanto il proprietario non ha dato il suo consenso alla procedura perché preoccupato degli elevati rischi anestesiologici dovuti alla grave condizione clinica del suo cane.


More than twenty years ago, four college students asked each other: What if we could offer children from under-resourced communities individualized attention before they enter kindergarten, giving them the critical academic and social skills—the ‘jumpstart'—they need to succeed? The idea took hold and by 2015, Jumpstart had trained more than 40,000 college students and community volunteers, preparing over 87,000 children for kindergarten success. Jumpstart's program is replicated across the country in 14 states and the District of Columbia. We leverage partnerships with higher education institutions, Head Start, community-based preschools, and school districts to create sustainable solutions in order to close the kindergarten readiness gap.