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Trigeminal Autonomic Cephalalgias Manjit S Matharu Headache Group, Institute of Neurology & The National Hospital for Neurology and Neurosurgery LondonUK.

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Presentation on theme: "Trigeminal Autonomic Cephalalgias Manjit S Matharu Headache Group, Institute of Neurology & The National Hospital for Neurology and Neurosurgery LondonUK."— Presentation transcript:

1 Trigeminal Autonomic Cephalalgias Manjit S Matharu Headache Group, Institute of Neurology & The National Hospital for Neurology and Neurosurgery LondonUK Third Biennial Hull-BASH Headache Meeting 23 rd January 2009

2 Trigeminal Autonomic Cephalgias Unilateral head pain, predominantly V 1Unilateral head pain, predominantly V 1 Very severe / excruciatingVery severe / excruciating Cranial autonomic symptomsCranial autonomic symptoms –Parasympathetic  –Sympathetic  Attack frequency and duration differsAttack frequency and duration differs Treatment responses differTreatment responses differ Cluster HeadacheCluster Headache Paroxysmal HemicraniaParoxysmal Hemicrania SUNCT (Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing)SUNCT (Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing) Cluster HeadacheCluster Headache Paroxysmal HemicraniaParoxysmal Hemicrania SUNCT (Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing)SUNCT (Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing)

3 Paroxysmal Hemicrania IHS CLASSIFICATION CRITERIA SevereSevere UnilateralUnilateral Orbital, supraorbital or temporal painOrbital, supraorbital or temporal pain 2-30 minutes duration2-30 minutes duration >5 attacks daily at least 50% of the time>5 attacks daily at least 50% of the time Associated symptoms:Associated symptoms: -Conjunctival injection -Lacrimation-Ptosis-Miosis -Eyelid oedema -Nasal congestion -Rhinorrhea -Forehead and facial sweating Stopped completely by indomethacinStopped completely by indomethacin

4 Trigeminal Autonomic Cephalgias Cluster Headache Paroxysmal Hemicrania SUNCT Attack frequency (daily)1-81-403-200 Duration of attack15-180mins2-30mins5-240secs Pain quality Sharp, throbbing Stabbing, burning Autonomic features+++ +++* Restless or agitated90%80%65%

5 Trigeminal Autonomic Cephalgias ClusterHeadache Paroxysmal Hemicrania SUNCT Migrainous features++ + Triggers Alcohol NTG Cutaneous +++ - ++-++- +++ Circadian periodicity70%45% Absent Episodic : Chronic90:1035:6510:90

6 Trigeminal Autonomic Cephalgias Cluster Headache Paroxysmal Hemicrania SUNCT Lifetime prevalence1/10001/50,000* F:M ratio1:2.5-7.21:11:1.5 Age Mean Range 30 6-67 37 5-68 48 19-75

7 Paroxysmal Hemicrania DIFFERENTIAL DIAGNOSIS Symptomatic Paroxysmal HemicraniaSymptomatic Paroxysmal Hemicrania Cluster headacheCluster headache SUNCT syndromeSUNCT syndrome Hemicrania continuaHemicrania continua Symptomatic Paroxysmal HemicraniaSymptomatic Paroxysmal Hemicrania Cluster headacheCluster headache SUNCT syndromeSUNCT syndrome Hemicrania continuaHemicrania continua

8 Symptomatic Paroxysmal Hemicrania Vascular ICA aneurysm Subclavian artery dilatation Parietal AVM MCA Stroke Occipital infarction Inflammatory or Infection Collagen vascular disease Ophthalmic herpes zoster Iatrogenic Surgical sympathectomy Tumours Pituitary tumours Frontal tumour Tuber cinereum hamartoma Sella turcica gangliocytoma Cavernous sinus meningioma Multiple parotid ca. Metastasis Non-Hodgkin’s lymphoma Pancoast syndrome Miscellaneous Essential thrombocythaemia Intracranial hypertension Maxillary cyst

9 Trigeminal Autonomic Cephalgias Pituitary and TACs Cittadini and Matharu, Neurologist 2009 Literature review of symptomatic TACs published between 1975-2007 Identified 37 symptomatic cases of CH 50% had typical presentation 33% poor response to treatments Cittadini and Matharu, Neurologist 2009 Literature review of symptomatic TACs published between 1975-2007 Identified 37 symptomatic cases of CH 50% had typical presentation 33% poor response to treatments CauseCH N=24 PH N=3 SUNCT N=10 Vascular lesions8 Tumours Pituitary tumour 12 73 10 7 Miscellaneous Idiopathic granulomatous hypophysitis 4141

10 Trigeminal Autonomic Cephalgias Pituitary and TACs Levy et al, Brain 2005 84 pituitary tumour patients with headaches studied 9% had TACs Functioning adenomas more likely to cause TACs Investigate all TAC patients for pituitary tumours? Prevalence of pituitary tumours in TACs is unknown 1 in 10 of the population have an incidental pituitary micro- adenoma (< 1cm diameter) on routine MRI 1 in 500 have a macro-adenoma Levy et al, Brain 2005 84 pituitary tumour patients with headaches studied 9% had TACs Functioning adenomas more likely to cause TACs Investigate all TAC patients for pituitary tumours? Prevalence of pituitary tumours in TACs is unknown 1 in 10 of the population have an incidental pituitary micro- adenoma (< 1cm diameter) on routine MRI 1 in 500 have a macro-adenoma

11 Trigeminal Autonomic Cephalgias Pituitary and TACs Difficult to draw up definitive guidelines from retrospective reviews Pituitary imaging should be performed in: – –Atypical phenotype/abnormal examination – –Treatment resistant cases Do typical cases require neuroimaging? – –Increases likelihood of identifying incidental lesion Implication of data on pituitary lesions? – –Need prospective community based study in CH patients – –Carefully elicit symptoms related to pituitary disease in all TAC patients but only perform MRI scans of the pituitary and a basal pituitary hormone profile in: patients with atypical features (including pituitary related symptoms) abnormal examination poor response to appropriate treatments. Difficult to draw up definitive guidelines from retrospective reviews Pituitary imaging should be performed in: – –Atypical phenotype/abnormal examination – –Treatment resistant cases Do typical cases require neuroimaging? – –Increases likelihood of identifying incidental lesion Implication of data on pituitary lesions? – –Need prospective community based study in CH patients – –Carefully elicit symptoms related to pituitary disease in all TAC patients but only perform MRI scans of the pituitary and a basal pituitary hormone profile in: patients with atypical features (including pituitary related symptoms) abnormal examination poor response to appropriate treatments.

12 Paroxysmal Hemicrania DIFFERENTIAL DIAGNOSIS Symptomatic Paroxysmal HemicraniaSymptomatic Paroxysmal Hemicrania Cluster headacheCluster headache SUNCT syndromeSUNCT syndrome Hemicrania continuaHemicrania continua Symptomatic Paroxysmal HemicraniaSymptomatic Paroxysmal Hemicrania Cluster headacheCluster headache SUNCT syndromeSUNCT syndrome Hemicrania continuaHemicrania continua

13 Cluster Headache Vs Paroxysmal Hemicrania Trial of Indomethacin if: 1.Attack frequency > 5 daily 2.Attack duration < 30 minutes 3.Chronic subtypes FeatureCHPH Gender (M:F) 2.5-7:11:1 Duration (min) 15 - 180 2 – 30 Frequency (attacks/day) 1- 8 1 - 40 Indomethacin-+

14 Paroxysmal Hemicrania DIFFERENTIAL DIAGNOSIS Symptomatic Paroxysmal HemicraniaSymptomatic Paroxysmal Hemicrania Cluster headacheCluster headache Hemicrania continuaHemicrania continua SUNCT syndromeSUNCT syndrome Symptomatic Paroxysmal HemicraniaSymptomatic Paroxysmal Hemicrania Cluster headacheCluster headache Hemicrania continuaHemicrania continua SUNCT syndromeSUNCT syndrome

15 Hemicrania Continua Unilateral headacheUnilateral headache Forehead, temple, orbit and occiputForehead, temple, orbit and occiput Continuous, moderate painContinuous, moderate pain Exacerbations:Exacerbations: –lasting from 20 min to several days –accompanied by autonomic and migrainous features –occur in 75% Lack of precipitating factorsLack of precipitating factors Complete response to indomethacinComplete response to indomethacin Unilateral headacheUnilateral headache Forehead, temple, orbit and occiputForehead, temple, orbit and occiput Continuous, moderate painContinuous, moderate pain Exacerbations:Exacerbations: –lasting from 20 min to several days –accompanied by autonomic and migrainous features –occur in 75% Lack of precipitating factorsLack of precipitating factors Complete response to indomethacinComplete response to indomethacin

16 Paroxysmal Hemicrania TREATMENTS N=77 Indomethacin: Oral Indomethacin trialOral Indomethacin trial –25mgs tds –50mgs tds –If high index of suspicion: 75mgs tds –Lower doses for 3 days; maximum dose for 7 days Indotest (Intramuscular indomethacin)Indotest (Intramuscular indomethacin)Indomethacin: Oral Indomethacin trialOral Indomethacin trial –25mgs tds –50mgs tds –If high index of suspicion: 75mgs tds –Lower doses for 3 days; maximum dose for 7 days Indotest (Intramuscular indomethacin)Indotest (Intramuscular indomethacin)

17 Paroxysmal Hemicrania INDOTEST N=77 Time Indomethacin 50mgs intramuscularly 8.2+4.2 hr Indomethacin 100mgs intramuscularly 11.1+3.5 hr Time Adapted from Antonaci et al. Headache 1998;38:122-8

18 Paroxysmal Hemicrania TREATMENTS N=77 IndometacinIndometacin Persistence of efficacy 23% develop GI side effects with chronic treatment Other NSAIDS: Aspirin, naproxen, piroxicamOther NSAIDS: Aspirin, naproxen, piroxicam COX-II Inhibitors: Celecoxib, RofecoxibCOX-II Inhibitors: Celecoxib, Rofecoxib TopiramateTopiramate VerapamilVerapamil Greater occipital nerve injectionGreater occipital nerve injection IndometacinIndometacin Persistence of efficacy 23% develop GI side effects with chronic treatment Other NSAIDS: Aspirin, naproxen, piroxicamOther NSAIDS: Aspirin, naproxen, piroxicam COX-II Inhibitors: Celecoxib, RofecoxibCOX-II Inhibitors: Celecoxib, Rofecoxib TopiramateTopiramate VerapamilVerapamil Greater occipital nerve injectionGreater occipital nerve injection

19 SUNCTSUNCT Short-lasting Unilateral Neuralgiform attacks with Conjunctival injection and Tearing

20 SUNCT IHS CLASSIFICATION CRITERIA Unilateral orbital, supraorbital or temporal painUnilateral orbital, supraorbital or temporal pain Stabbing or pulsating painStabbing or pulsating pain 10-240 seconds duration10-240 seconds duration Attack frequency from 3-200/dayAttack frequency from 3-200/day Pain is accompanied by conjunctival injection and lacrimationPain is accompanied by conjunctival injection and lacrimation Unilateral orbital, supraorbital or temporal painUnilateral orbital, supraorbital or temporal pain Stabbing or pulsating painStabbing or pulsating pain 10-240 seconds duration10-240 seconds duration Attack frequency from 3-200/dayAttack frequency from 3-200/day Pain is accompanied by conjunctival injection and lacrimationPain is accompanied by conjunctival injection and lacrimation

21 Trigeminal Autonomic Cephalgias Cluster Headache Paroxysmal Hemicrania SUNCT Attack frequency (daily)1-81-403-200 Duration of attack15-180mins2-30mins5-240secs Pain quality Sharp, throbbing Stabbing, burning Autonomic features+++ +++* Restless or agitated90%80%65%

22 Trigeminal Autonomic Cephalgias ClusterHeadache Paroxysmal Hemicrania SUNCT Migrainous features++ + Triggers Alcohol NTG Cutaneous +++ - ++-++- +++ Circadian periodicity70%45% Absent Episodic : Chronic90:1035:6510:90

23 Trigeminal Autonomic Cephalgias Cluster Headache Paroxysmal Hemicrania SUNCT Lifetime prevalence1/10001/50,000* F:M ratio1:2.5-7.21:11:1.5 Age Mean Range 30 6-67 37 5-68 48 19-75

24 SUNCT DIFFERENTIAL DIAGNOSIS Secondary causesSecondary causes –Posterior fossa pathology –Pituitary tumours Trigeminal neuralgiaTrigeminal neuralgia Primary stabbing headachePrimary stabbing headache Paroxysmal hemicraniaParoxysmal hemicrania

25 SUNCT Vs Trigeminal Neuralgia FeatureSUNCTTN Gender (M:F) 1.5:11:2 Site of pain V1V1V1V1 V 2/3 Duration (secs) 5-240<5 Autonomic features ProminentSparse Refractory period AbsentPresent Trigeminal Vascular loop 7%47-90%

26 SUNCT DIFFERENTIAL DIAGNOSIS Stabbing or jabbing painStabbing or jabbing pain Ophthalmic trigeminal distributionOphthalmic trigeminal distribution Last a few seconds (rarely up to 1 minute)Last a few seconds (rarely up to 1 minute) Occurs at irregular intervalsOccurs at irregular intervals Site of pain varies from attack to attackSite of pain varies from attack to attack Spontaneous attacks onlySpontaneous attacks only Autonomic features absentAutonomic features absent Attacks subside with indomethacinAttacks subside with indomethacin Primary Stabbing Headache

27 SUNCT INVESTIGATIONS MRI (including pituitary views) Pituitary hormone profile Trial of indomethacin

28 SUNCT TREATMENTS DosesNumberEfficacyLamotrigine100-400mg/d2568% Topiramate50-400mg/d2152% Gabapentin600-3600mg/d2245% IV lidocaine 1.3-3.3 mg/kg/hr 11100% Greater occipital nerve injection 863% Cohen et al. Migraine Trust Symposium, September 2006

29 SUNCT TREATMENTS Cohen, Matharu, Goadsby. IHS, 2007 Topiramate in SUNCT Cross-over RCT of topiramate 50 bd vs placebo Primary endpoint was reduction in attack frequency by 50% Secondary endpoint was reduction in ‘attack load’ N=5 Results Beneficial in 2 – one had complete cessation of attacks, and one had a 71% reduction in attack load. Placebo response in one Two had no benefit

30 SUNCT TREATMENTS Hypothalamic Stimulator Leone M, Ann Neurol 2005.

31 Trigeminal Autonomic Cephalgias PATHOPHYSIOLOGY Cluster Headache PET Study May et al, Lancet 1998 Ipsilateral hypothalamic activation in CH

32 Trigeminal Autonomic Cephalgias PATHOPHYSIOLOGY Paroxysmal Hemicrania PET Study Matharu et al, Ann Neurol 2006 Contralateral hypothalamic activation in PH

33 Trigeminal Autonomic Cephalgias PATHOPHYSIOLOGY SUNCT fMRI Studies May et al, Ann Neurol 1999Cohen et al, Cephalalgia 2004Sprenger et al, Pain 2005 Hypothalamic activation in SUNCT

34 Functional Neuroimaging of Primary Headaches Headache Phase Episodic and Chronic Migraine Spontaneous Episodic Migraine Weiller et al, Nature 1995 Spontaneous Episodic Migraine Afridi et al, Arch Neurol 2005 Chronic Migraine Matharu et al, Brain 2004 Specific dorsal rostral pontine activation in migraine

35 Trigeminal Autonomic Cephalgias PATHOPHYSIOLOGY Hemicrania Continua PET Study Matharu et al, Headache 2004 Posterior HypothalamusDorsal Rostral Pons

36 Primary headaches can be pathophysiologically differentiated on the basis of distinct patterns of brain activationPrimary headaches can be pathophysiologically differentiated on the basis of distinct patterns of brain activation Dorsal pontine and hypothalamic activation are markers of migrainous symptoms and cranial autonomic features, respectivelyDorsal pontine and hypothalamic activation are markers of migrainous symptoms and cranial autonomic features, respectively These structures that likely play a pivotal role in the pathophysiology of primary headache syndromesThese structures that likely play a pivotal role in the pathophysiology of primary headache syndromes Primary headaches can be pathophysiologically differentiated on the basis of distinct patterns of brain activationPrimary headaches can be pathophysiologically differentiated on the basis of distinct patterns of brain activation Dorsal pontine and hypothalamic activation are markers of migrainous symptoms and cranial autonomic features, respectivelyDorsal pontine and hypothalamic activation are markers of migrainous symptoms and cranial autonomic features, respectively These structures that likely play a pivotal role in the pathophysiology of primary headache syndromesThese structures that likely play a pivotal role in the pathophysiology of primary headache syndromes Activation pattern in primary headaches Functional Neuroimaging of Primary Headaches MigraineCHSUNCTPHHC Posterior hypothalamus Dorsal rostral pons

37 “Pain is a more terrible lord of mankind than even death itself” Albert Schweitzer “Pain is a more terrible lord of mankind than even death itself” Albert Schweitzer


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