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Aacp paperwork

• Aim is provide comprehensive paperwork for • Compiled for ease of use in either office or • For adult and child • Axis 1 and Axis 11 considerations to help classify difficulty and treatment outcomes of • Medical and Dental History Office – Adult – Child • History of Pain Condition Surgery • Intraoral Examination • Differential Diagnosis of OFP • Records check Office/Surgery • TMJ Symptoms Review Sheet • Adjunct Paperwork Office/ Surgery – Pain diary – Sleep diary

Adult/Child Medical Dental History • Office Use data • History of Medications – Prescription. OTC, Homeopathic – Reason using them – Time of intake – Dosage – Everybody Lies • Dr R Kulich Tufts Adult/ Child Medical History • History of past Treatment – May give an indication of types of treatment that wil or wont – May indicate nature of chief complaint, eg neuropathic, • Systems Review – Organizes the medical conditions logical y – Al ows patterns/ relationships to be seen clearly – Can be important in later facial pain/ headache diagnosis • SSI • 3 questions are a quick screening tool for pain of TMD • Sensitivity/specificity >0.95 Adult/ Child Medical Dental History • Axis 11 psychosocial screening questionnaires • More indicative of treatment outcomes than Axis 1 pain • Are used to classify patients by difficulty of treatment • Are not meant to be used by dentists to diagnose anxiety or depressive disorders • Mandatory if pain present > 6mths • Or if previous unsuccessful treatment • Identify barriers to treatment response • Contributors to chronicity • Alternative targets for therapeutic intervention Adult/ Child Medical Dental History • Questions 1-9 • PHQ 9 for depression • Cutoffs at 5 mild • 10 moderate • 15 mod-severe • 20 severe • Levels of depression Adult/ Child Medical Dental History • Q 10-16 • GAD 7 for anxiety • Cutoffs 10 • 15 severe • Q 1-14 • PHQ15 for physical symptomms • 5 low • 10 medium • 14 high somatic symptom severity TMD Symptom Questionnaire • Q1-7 • Enables diagnosis of new headache disorder • Headache due to TMD • Requires temporal headache • And change in pain intensity with function • Q 8-14 establish presence of disc displacement • MRI required for definitive diagnosis of disc • CT for definitive Diagnosis of DJD • Exception is DDWOR with limited opening(<40mm) Adult/ Child Medical Dental Hisotry • JFLS • Asses global limitation of function of jaw • GCPS • Broken into Characteristic Pain Intensity (CPI) • Q1-5 • ≥ 50/100 is high intensity • Pain Disability Rating • Q 6-8 • No of days pain interferes with work • Measurement of disability Adult Medical Dental History • Please note Child form does not have comprehensive Axis 11 screeners • There is no reliable screening tool for Axis 11 disorders for children • The best tools at present have sensitivity/ spec around 0.4 so not included Adult/ Child Medical Dental History • Sleep Screening • Adult form has Epworth • Subjective screening tool for tiredness • And Berlin Questionnaire • Slightly less subjective than ESS Adult/ Child Medical Dental History • Child Screening has Pediatric Daytime Sleepiness Scale • Endorsed by ATS • Screens for sleepiness and negative sghool outcomes in middle school ages 11-15 • Has similar characteristics to ESS Adult/ Child Medical Dental History • History of missing teeth, premature birth, extractions and hypermobility given by Prof Guilleminault at recent conference as risk • Mostly unpublished data but reasonable Adult/ Child Medical Dental History • Pain Drawing • Useful to see – Overal pain experience – Referral patterns for myofascial pain in head and – Localized pain areas in the head may indicate localized problems – Widespread pain indicates the need for referral for further investigation History of Pain Condition • 1st job is to work out • WHO SHOULD NOT BE IN YOUR CHAIR • Screening for life threatening secondary causes of • Systemic symptoms • Neurologic signs or symptoms • Onset sudden • Onset> 40 • Pattern change History of Pain Condition • Systemic symptoms or disease • May be indicative of encephalitis, bacterial infection, cancer, HIV, immunotherapy – Fever – Weight loss – Arthralgias – Stiff neck – Rash History of Pain Condition • Neurological Signs or symptoms • Confusion, clumsiness, weakness, aphasia, numbness, dizzyness, visual problems • Need to rule out primary headache disorder eg migraine, basilar migraine • Or may be TIA, stroke, mass lesion, infiltrating lesion affect CNs, artereovenous malformations, thrombotic disease, malignancy, infections History of Pain Condition • Onset Sudden • Sudden onset severe general or localised headache • To be considered severe until proven otherwise • DD Subarachnoid or intracerebral bleed • Ruptured or unruptured aneurysm • Cerebral venous thrombosis • Carotid or vertebral artery dissection • Cerebral infarction • Encephalopathy • CNS infections History of Pain Condition Headaches brought on by a cough, sneeze, straining, Headache awakening from sleep rule out causes of increased intracranial pressure post traumatic headache can be due to fracture, hematoma, infection Positional headache Worse standing better lying may be CSF leak Worse lying better standing may be intracranial mass Headache in morning OSA, MOH, Tumour, Parafunction History of Pain Condition • Onset after 40 • New onset or change in pattern • Most migraines before 30yo • Ha in older no prior history may be tumour, vascular disease/ hormonal • ESR rules out giant cell arteritis • CBC (blood) anemia anad blood dyscrasias • T4 rule out thyroid disease History of Pain Condition • Pattern Change • 1st or worst headache • Change in frequency, • Severity, • Associated symptoms, • Quality • Warrant investigation History of Pain Condition • Location • Has it changed • Does it cross the midline • Does it change during the pain episode • Use 1 finger • Site is not always source • Is chief complaint stimulated by pushing History of Pain Condition • Onset • Was there an event associated with onset eg trauma physical/emotional • When • Time of day • Sudden or gradual History of Pain Condition • Quality • Types of pain eg burning sharp dull can be associated with different causes • This must be taken with caution • Musculoskeletal – Dull – Aching – Pressure – Depressing – Tight – Stiff – Can be sharp History of Pain Condition Diagnosis only after exclusion of al possible causes History of Pain Condition • Intensity • Subjective • Affected by emotional state and sleep status and medication (can increase or decrease it) • 0-10 where 0= no pain 10 = most extreme pain • VAS = 10cm line • Sensory changes may affect intensity • Can be related to intracranial disorder, neuropathic, or central pain History of Pain Condition • Frequency and Duration • Does pain occur in clusters • Are there periods of remission. How long • Normal pain is not continuous • Some headache disorders have characteristic durations of pain History of Pain Condition • Associated Symptoms • May aid diagnosis • Visual or sensory changes may go with • Drooping eyelids, conjuctival tearing may be associated with cephalalgias History of Pain Condition – Numbness – Hyperalgesia – Paraesthsia – Allodynia – dysesthesia – Increased by increasing ICP eg valsalva, physical activity, bending over – Sensitivity to light, sound – Nausea, vomitting Musculoskeletal pain – Flushing – Hyperalgesia – Can be referral – Worsens with function History of Pain Condition • Alleviating/ triggering • Jaw function yes/no • Posture • Sleep • Wind/touch/shaving/stress • How much medication and types • Massage/ PT Sleep Complaints Can you fall asleep Do you stay asleep Do you have trouble going back to sleep Do you wake often Do you wake with a fright Do you dream/ nightmare Do you snore/ stop breathing/ grind/ clench Do you go to the toilet Do you sleep talk/walk/act out dreams Do you wake with a headache/ dry throat/ sore neck/blocked nose/red eyes Do you feel good in the morning Do you nap during the day Do you consume alcohol, coffee, tea, soft drink, dairy gluten after 2pm and Intraoral Examination • Make sure that their dental examinations are • Do they have or need current BW x-rays • Check probing depths for perio/ root • Rule out dental/ periodontal/ mucogingival • Examine intraoral tissues including base of Intraoral Examination Check occlusal issues Correlative data only Unilateral x-bite >6 missing posterior teeth Interferences to CO Consider denture patients may have all/most of these examine/ palpate associated structures Temporal arteries Salivary and lymph glandss pontaneous flow, colour and consistency of saliva Refer when appropriate

Intraoral Examination • Muscle Palpation • Muscle Pain • Myalgia – Localized. Confined to site of palpation – Myofascial pain with spreading beyond site of palpation – Myofascial pain with refera lbeyond boundary of muscle – Record location of referral • 1kg pressure for 2 seconds for myalgia • 1kg for 5 seconds for spreading/referral Intraoral Examination • Myalgia • Provocation tests • Pain on opening jaw muscles • Pain on palpation of the temporalis and masseter • Lat Pterygoid only able to be tested by provocation…. Push jaw forwards against pressure • Buccinator in approximately position of Lat Pterygoid • Is often tender in cases without TMD • Always ask DOES THIS REPLICATE THE FAMILIAR PAIN Intraoral Examination – Height – Weight – BMI – Neck circumference – BP – O2 saturation (if sleep) Intraoral Examination • Cervical examination for middle age person • Normal CROM lateral is 65-75 degrees • Lateral tilt 35-45 degrees • Flexion 50-60 degrees • Extension 60-70 degrees • CROM decreases by 5 degrees extension and 3 degrees other movements over 10 years • Head on chest and move left and right = C1/C2 • Look symmetry and pain

Intraoral Examination • Mandibular Range of Motion • Vertical norm = 40-55mm • Max opening + overbite • Lateral = 7mm • Active mouth opening = unassisted • Passive = assisted mouth opening • Record pain and joint noises during opening • Deviation and deflection • Provocation tests- hard/soft end feel Intraoral Examination • Cranial Nerve Eval • 1 Olfactory camphor, coffee, vanilla • 2 Optic Visual aacuity, visual field P • 3 Occulomotor Pearl, eyelid elevation, • 4 Trochlear Downward gaze in

Intraoral Examination Intraoral Examination • 5 Trigeminal Light touch to face, muscles of mastication, Downward gaze in Facial expressions, corneal reflex, taste to ant 2/3 Hearing, nystagmus on EO tests, caloric testing (COWS) Intraoral Examination • 9 Glossopharyngeal gag, taste to post 1/3 Speech, palatouvula • 11 Accessory SCM and traps against • 12 Hypoglossal Tongue bulk, strength • Make sure to record deficits position and size on

Differential Diagnosis • Axis 1 structural • Axis 11 psychosocial • Can change during course of lifetime in each • Record need for MRI/ MRA/ med CT pr if Differential Diagnosis • Intracranial – Acute ischaemic cerebrovascular disease – Intracranial haemorrhage traumatic/ nontraumatic – Unruptured vascular formation – Venous thrombosis – CSF pressure high/low – Chiari Malformation – Neoplasm – Infection – Noninfectious inflammatory disesase Differential Diagnosis • Acute Ischaemic Cerebrovascualr Disease • Pain mild-mod • Nothing pathognomic about qualilty, severity, location • Person>50 • Neurologic deficits and related to time of head pain • Different headache from familiar • Vertebral and basilar artery more likely to cause pain • Diplopia, weakness, vision obscured, numbness, altered cognition, dysarthria, aphasia ataxia Differential Diagnosis • TIA deficits resolve in 20min-24 hrs • Vascular risk factors, (diabetes, coronary disease HBP, High cholesterol, nicotine) • Can use CT esp if acaute bleed • MRI (diffusion weighted) better • DD • migraine, • Older migraineur new neurologic symptoms considered to have vascular issue until proven • Usual y treated with vasoactive drugs

Differential Diagnosis Intracranial Haemmorhage Epi or subdural haemotoma Epidural haematoma after blunt trauma Pain and change in cognition rapid RAPID surgical drainage High Suspicion after Trauma Subdural haematoma can be acaute, subacute, chronic Older > risk due to falls and fragile veins Trauma may be minimal/ indirect Symptoms several hours to days after. Pain not always chief CO Anticogulants, NSAIDs increae risk Neurologoical deficit, personality change, somnolence, visual disturbance, hemiparesis, hemisensory changes, visual field disturbance May be surgical y treated but usual y monitored Differential Diagnosis • Nontraumatic • Intracerebral haemmorhage • Acute neurologic deficits • Related to HBP, neoplasm arteriovenous • Occurs in brain parenchyma • Can cause coma, death • Effect dependent on cause and size and resultant destruction of cerebral tissue • Can be compression of CV 111 Differential Diagnosis • Subarachnoid hemorrhage • Characteristic HA • Sudden onset thunderclap headache • Max intensity seconds to 1 minute • Eg stopped in middle of sentence, hit by baseball • Nausea, vomiting, stiff neck, loss of • Send to emergency via ambulance • Head CT, lumbar puncture (blood)

Differential Diagnosis • Arteritis • Initial presentation can be severe unilateral temporal headache • Giant cell aerteritis (temporal A) may lead to blindness • Occlusion of carotid artery • To be ruled out in al especial y women >50 with new/ persistent headache 1 or both temples worse with cold and with jaw claudication (tiredness, pain on chewing), pain combing hair, polymyalgia rheumatica, stiff/sore neck, shoulders, proximal arms • Tests ESR (>90), biopsy • High dose sterids • Enlarged tender temporal arteries reduced pulsatility Differential Diagnosis • Carotid or Vertebral Artery Pain • Ipsilateral pain in neck, face, head • Neurological symptoms/ TIA/ stroke • May be associated with pulsatile tinnitus or Horner Syndrome (ptosis, annihydration, constriction of pupil, red conjunctiva, enopthalmours) • due to sympathetic fibres on Carotid Artery • May be trauma (surfing, chiro, blunt trauma), spontaneous, arterial damage (fibromusculr dysplasia, migraine) • Listen for bruits over orbit or temporal bone • Refer to neurologist Differential Diagnosis • Unruptured Vascular Malformation • Saccular aneurysms, arteriovenous malformations, dural arteriovevenous fistulae, venous cavernous • May be present long term and silent or nonspecific • May mimic migraine/TTH and respond to same • Any age • May be pulsatile tinnitus, family history • May use MRA/ CTA Differential Diagnosis Venous Thrombosis Pain may be acute severe- subacute- chronic Severe new headache with visual disturbances Predisposing factors, dehydration, oral controceptive, postpartum, prothrombotic blood dyscrasias, neoplasms, mild-mod head trauma, local Refer to neurologist Modify predisposing factors/ 6mths anticoagulant therapy Signs of increased intracranial pressure – Nausea – Vomitting – Pappil edema – Seizures – Neurologic deficits Differential Diagnosis CSF pressure change Nonspecific headache in any region, but commonly hoocephalic daily headache, intermittent visual disturbances, pulsatile tinnitus Worsens with valsalva, supine Associated with nausea, vomiting, visual problems, neurologic deficits, blindness Watch for extraoccular movement abnormalities Especially diplopia, early papil edema Young obese females OC/ tetracycline Beware of papil edema and bilateral abduces paralysis Normal MRI, lumbar puncture pressure > 200-250mmHg Treat with modification of risk factors, acaetazolamide ( dec CSF), steroids (dec edema), multiple lumbar puncture Differential Diagnosis • Low CSF • Increaed headache standing and decreased with supine within minutes (Effect decreases with time) • Neck pain/stiffness, tinnitus, hyperaccusia, photophobia, nausea, paresthesia of neck, arms • May be iatrogenic (dural/lumbar puncture) • Spontaneous (meningeal diverticulae, connective tissue disease, weakened dura mater • Traction on dura mater and sensitive pain sensitive vasculature on standing due to sagging brain • MRI with gadolinium • Treatment bed rest 2-3 days no head elevation • Mild OTC analgesics, caffeine, theophyl ine, epidural blood patch • Headache gone 48-72 hours after treatment Differential Diagnosis • Chiari Malformation • Herniation of cerebel ar tonsils3-5mm below FM • May include hydocephalus, myelomeningocele, sysssringomeliaspinal cord cavitations, distortion of contents of middle and posterior cranial fossa, flattening pons, kinking of brainstem • May cause traction or compression of CN • Headaches, hemifacial spasm, coughing, inability to speak, dysphagia, nystagmus, weakness of limbs • Can be congenital/ acquired • May require surgical decompression Differential Diagnosis • Neoplasm • Headaches in approx 50% of cases • Primary presenting symptom in 20% • May have focal neurologic symptoms or seizure • May be due to increased ICP, or meningitis • Weight loss, personality changes, weakness, numbness, trouble walking, visual disturbances, progressive neurologic disturbances • New headache plus above needs investigation Differential Diagnosis • Infection • Bacterial meningitis, lymphocytic meningitis, encephalitis, brain abscess, subdural epyema • Holocephalic headache associated with fever, arhtralgias, stiff neck, photophobia, nausea, altered consciousness, • Can occur within minutes to hours • Menigitis patients have stiff necks, cant flex • Positive Kernig and Brudzinski sign • HSV most common cause of nonepidemic viral encephalitis, also fungal and HIV • Blood cultures, CSF testing Differential Diagnosis • Noninfectious Inflammatory Disease • Neurosarcoidosis • Aseptic meningitis • May be severe headache with or just after IHS classification 17% of women and 6% of men in the US have migraine 5 attacks of Idiopathic recurring headache lasting 4-72 hours 70% as migraine without aura 30% as migraine with aura Usually unilateral, but bilateral in 40% Most commonly occur on wakening Both photophobia and phonophobia must be present 2 major theories of causation, that the migraine begins central y and then activates the peripheral branches of the trigeminal nerve Or that the peripheral braches of the trigeminal system are activated and the central involvement of the trigeminal system is a form of central sensitization, explaining the allodynia experienced on he facial skin. Familial Hemiplegic migraine related to mutations in 3 different ion Phases of a Migraine – The Prodrome Phase – Occurs in 30% of migraineurs – Occurs equal y in migraine with and without aura – Starts from hours to days prior to a migraine attack – Changes in mood or behaviour – Depression, craving for special foods, yawning – Aura – A series of idiopathic recurring neurologic symptoms – Develop gradually over 5-20 minutes, but <1hr – Onset of headache within 60 mins of aura abating – Not all auras are fol owed by a migraine – Visual Disturbances fortification pattern, photopia, scotoma – Adults may have sensory symptoms such as unilateral paresthesias, numbness, tingling,unilateral weakness, aphasia and speech disturbances – Aura symptoms are reversible • Nausea/ vomitingPhase 3 – The Headache Phase – Throbbing moderate to severe headache – 2-4 of – Usual y unilateral, throbbing headache – Photophobia and phonophobia – Nausea and vomiting – Pain aggravated by routine physical exercise – Pain in adults may present as a headache, or pain in the teeth, masticatory muscles,or the middle or lower third of • Phase 4 • Termination • Phase 5 • Postdrome – May be exhausted/ confused/ fatigued – Loss of appetite and aching muscles – Dul diffuse aching headache for 1-2 days Episodic Versus Chronic Migraine • Chronic Migraine – p> 80% have a Past history of migraine – Transformation of an acute episodic migraine to a daily attack – Typical y a slow process – Headaches increase in frequency – Intensity declines – Periodic superimposed attacks of migraine – 15 days/ month for >3months without MOH =chronic migraine – Photophobia/ phonophobia/ GIT features are absent – Similar to TTH – Migraineurs taking triptans and other analgesics are susceptible – Status migranosus migraine>3days Migraine Therapy 1. Patient Education and Recognition of migraine triggers Migraine Therapy 2. Nonpharmacologic • Biofeedback training • Cognitive behavioural therapy • Psychotherapy • Exercise programme • Dietary modification • Migraine and TMD comorbid conditions • To treat migraine the TMD needs to be treated • And vice versa Migraine Therapy 3. Abortive Therapy Use a Phase Specific concept Stratified Care approach Start with OTC analgesics, eg paracetamol, NSAIDs, fiorinal , caffeine to abort migraine in the prodrome or aura period Use a stronger rescue medicine in the late stage Major rescue medications are 5HT receptor agonists – Injectable – Quickest:- average to relief 41minutes – Short ½ life so recurrence commmon – Max al owance 2 x 6mg subcutaneous injections in 24 hrs – Oral – Usually 50-100 mg – Nasal Spray – For use in patients with nausea and vomitting – Comparable efficacy to oral dose, but bitter taste – Triptans have cardiovascular side effects, but not likely at the dose used for migraine treatment Migraine Therapy 4. Prophylactic Therapy If headaches are control ed at 6 months t aper or withdraw medication for a trial – Suppress peripheral beta adrenergic receptors that promote vasodilation – Propanolol and atenolol most common – Should not be used in asthmatics or people with depression or Raynauds disease – Antidepressants – TCA – Efficacy only established for amitriptyline – Start at 10mg titrate to 25-75 mg at bedtime – SSRI – Major side effect bruxism – NSAIDS – Use at times when migraine most likely to be triggered, eg the week before menses – Need to take NSAID before and not after PG formation – Calcium Channel Blockers – Not as effective as beta blockers – Anticonvulsants – For use in people who cannot take other classes of prophylactiv drugs – Oeriodic liver function and monitoring of blood levels recommended – Botox – Just approved by FDA for chronic migraine Tension Type Headache • 74% of the population may experience this 1/year • Dull non-pulsatile tightness felt in the occipital, parietal, temporal and frontal regions • 90% of the time it is bilateral, mild-moderate • 30 minutes-72hours • Photophobia or phonophobia, but not both • Etiology unclear • TTH is NOT the same as pain from referral of myofascial trigger points, headache associated with sleep bruxism or with sleep apnoea(?) Tension type Headache Management • Identify triggers (headache diary) • Reduce caffeine, alcohol and headache medications. • Avoid stressors • No evidence based protocol for best medications • TTH can be secondary, and the cause of the headache needs to be identified. • Treat the cause of the tension, eg TMD, OSA, bruxism (Okeson and Leeuw 2011) Cluster Headache • Presentation • Male:female 3-4:1 , 0-09-0.32% • Onset between 20-40 years • Attacks occur in clusters over weeks or months • 15-180 minutes • May occur every few days to 8x/day • Attacks occur in clusters from 2weeks- few Cluster Headache • May be precipitated by alcohol, nitroglycerine, • Precipitating factors do not initiate an attack during remission • May be related to changesin the posterior • Episodic >1 month of headache free days/ year • In 10% attacks may become chronic= >1 year with no remission or remission <1 month • Often misdiagnosed as dental/ sinus/ TN pain Cluster Headache • Pain is boring, there's a hot poker in my eye, my eyebal is being pushed out • Rarely throbbing • Rapid onset • Builds to a peak in 10-15 minutes • Unilateral centred around orbit or the Cluster Headache • Autonomic symptoms due to parasympathetic
overactivity and always accompany the pain
• Ipsilateral lacrimation
• Conjunctival injection
• Ptosis and miosis
• Pain in the distribution of the carotid artery, eg maxil ary
posterior teeth and anterior temporalis region
• 50% may have ipsilateral posterior cervical tenderness
• Ipsilateral forehead and facial sweating/ pal or
• Bradycardia, ataxia,vertigo,syncope,hypertension,
• Increased gastrointestinal acid
Cluster Headache Management • Abortive • Oxygen 7-10l/minute for 15minutes • Effective in 70% of patients within 5 • minutes (CDB 2008 weak evidence only) • Triptans sumatriptan 6mg subcutaneously/ • zolmitriptan 10mg intranasal (CDB 2010) • often terminates attacks within 5 minutes • Dihydroergotamine (DHE-45) • Most effective • Injectable< IM< Nasal spray for speed of onset Cluster Headache Management Verapamil 120-480mg/day Start at 80mg and titrate to 160mg tid-qid C.I. cardiac conditons Lithium Carbonate Especial y effective in the chronic cluster headache patient Monitor toxicity through blood tests Ergotamine Tartrate Useful in nocturnal attacks when taken at bed time Divided doses up tp 4mg/day Radiofrequency Ablation of the pterygo-palatine ganglion Only in those refractory to pharmacologic management Occipital nerve stimulation last line of chhoice Paroxysmal Hemicrania • Shorter attacks than CH • 2-30 minutes/ more frequent • Female>male • Unilateral predominantly periorbital • Autonomic symptoms as per CH • Episodic = attacks from 7 days- 1 year with pain free periods of 1 month • Attacks>1 year withotu remission or remisison < 1 month= Chronic • 100% responsive to indomethacin • Short-lasting Unilateral Neuralgiform headache attack with Conjunctival injection and Tearing • Unilateral supraorbital / orbital/ temporal stabbing or • Lasts 5-240 seconds with 3-200 attacks /day • Includes autonomic symtoms • If only 1 of tearing or conjunctival injection is presenet, or if there are other autonomic symptoms = SUNA • Short-lasting Unilateral Neuralgiform headaches with cranial Autonomic Symptoms Differential Diagnosis SUNCT/SUNA • TN • SUNCT attacks more likely to be located in V1 • SUNCT/SUNA less likely to have a cutaneous trigger • SUNCT/ SUNA less likely to have a refractory period SUNCT/ SUNA not responsive to high-flow oxygen like CH SUNCT/SUNA not responsive to indomethacin like PH SUNCT/SUNA treated with lamotrigine/ topiramate/ Secondary Headache Disorders • Headaches secondary to another medical condition • Can include – Temporal arteritis – Post traumatic Headache – Medication Overuse Headache – Mountain Sickness – Headache Related to TMD – Phaeochromocytoma ( neuroendocrine tumour of medulla of the – Intracranial hypertension – Intracranial Infection – Intermittent hyprocephalus – Glaucoma – Optic neuritis Headache Related to TMD • A Headache that is affected by jaw movement, function or • Can replicate headache with provocation testing of the masticatory system • Must hav • Headache of any type in the temple AND • Headache modified with jaw movement, function or • Must be able to stimulate familiar headache with palpation of temporalis muscles or vertical lateral or protrusive movements of the mandible • Headache is not better accounted for by any other headcahe diagnosis Medication Related Headache Medication related headache may be due to medication overuse, or the
side effects of a prescribed medication
MOH is a subset of chronic daily headache
Overuse is defined as the use for more than 3 months of at least one
acute treatment medication
Ergotamine, triptans, and/or opioids used on 15 or more days/month or
simple analgesics
The headaches worsen (usual y in frequency) with the medication
May account for ½ the cases of CDH, and is the most common form of
secondary chronic daily headache.
The headache initial y worsens when the medications are withdrawn,
and then improves
Neuropathic Pain Episodic or continuous Trigeminal Neuralgia Episodic unilateral pain in the distribution of 1 or more division of CNV Brief electric shock like pains 155/1 000 000 Precipitated by nonpainful stimuli trigger zone) or may be spontaneous Pain may last seconds to minutes Refractory period May get fusion of paroxysms May have remission for days to years which decrease with time Pain does not usual y disturb sleep No neurological deficits V11 and V111 most common V1 only 1-2% RHS>LHS, does not cross miudline May be bilateral in 3-5% Average age of onset = 50 years • Demyelination or loss of myelin sheath • Most commonly from compression of trigeminal nerve root by blood vessel at level of entry into pons • Leads to spontaneous neve firing and ephaptic cross talk of nerve • May also be related to – Compressive tumours – Arteriovenous malformations – Saccular aneurysm – MS increases OR for TN x 20- beware of bilateral TN or TN early onset – Infarction of brainstem – Angioma – Genetic eg Charcot-Marie Tooth Disease – Demyelination does not explain al of the characteristics of TN • Triggering may explain – Light touch trigger zone – Amplification (spreading response beyond original area_ – Stop mechanism (lasting pain response and abrupt stop) – May have ectopic pacemakers sites at points of demyelination that are hyperexcitable and fire with little or – Some sites may have continuous firing for dull background – Ephaptic transmission or crosstalk amplifies transmission – Hyperpolariztion explains both stop and refractory period TN Classification • >85% are classical TN with Microvascular compression • Symptomatic or secondary caused by verifiable lesion ( tumour, • Must use imaging and CN evaluation • Must be differentiated from – dental pain, – sinus disease – Head and neck neoplasms and infections – Postherpetic neuralgia – Persistent idiopathic facial pain – Headache associated with TMD – SUNCT/SUNA – Jabs and Jolts • Medical • Anticonvulsants • Tegretol (carbamazepine) most effective • Initial response 70% decreases to 20% after 5-16 years • Start 100mg/day • Increase by 100mg every 2 days to max of 1200mg/day in divided dose can be 2-4 x/day as needed • Side-effects drowsiness, dizzyness, nausea, anorexia, feel foggy. Aplastic anaemia and trnsient leukopenia • Need to monitor blood levels and kidney function • Gabapentin (neurontin) • Minimal side-effects cf carbamazepine • No RCTs • Pregabalin (lyrica) • Also used • Personal experience is that carbamezepine is most • If unwanted side effects use in a reduced dosage in a cocktail with other medication types or other • Best to let GP deal with medication • Oxcarbazepine (trileptal) • Ketoanalogue of carbamazepine • No bone marrow or hepatic toxicity • Start at 150mg twice daily • Increase as tolerated to 300-600mg twice daily up to max of 2400mg/day • Same side effects as carbamazepine except is an increased risk of hyponatremia (low sodium- cerebral edema, headache, confusion, seizures, • Other anticonvulsants • Lamotrigine (lamictal) • For rerfractory cases especially related to MS • 100-400mg daily • Stevens Johnson type rash can be associated with this, as wel as diplopia, ataxia, dizzziness, headache, GIT • Topiramate ( topamax) • Start at 25mg bd • Increase by 100 mg/day every 1-2 weeks aiming for 100- 400 mg dasily in 2 doses • Anorexia, weight loss, somnolence, anxiety fatigue • Other Medications • No others have evidence ( Cochrane Data Base) • Others used include • Baclofen centrally acting muscle relaxant GABA • Reduce carbamazepien 25% before adding • 5mg tid increase by 5-10 mg every 2-3 days • Max dose 80mg/day • Clonazepam • Benzodiazepine with anticonvulsant effects • Start 0.5-1mg/day in divided dose • Increase by 0.5-1mg every 3-7 days to max of • Dental Management • Make sure that patient is dental y fit. • Check for dental causes eg TA/ TMD/ root fracture • Local Anaesthetics • LA in the trigger zone wil temporarily remove the pain of TN • As LA is a membrane stabilizing agent it may help to decrease the number and severity of the events • There have been some reports that the adrenaline in some LA agents can upregulate pain in TN • Patients with TN are at risk for exacerbation of the TN after complex dental procedure, and especial y RCT • Discuss with GP if can increase anticonvulsant therapy levels prior to and just after dental visits • Topical Agents • Applied via a neurosensory stent • Avoids GI 1st pass effects • Systemic absorption depends on the vascularity of the area • Can use any med that can be used systemical y in a PLO gel • Lignocaine • Amytriptyline • To be made by a compounding pharmacy TN Surgical Therapy – MVD – Stereotactic radiosurgery (Gamma Knife) Delayed onset of pain relief and 61- 90% recurrence 10-27% – Neurectomy 50-64% short term only – Cryotherapy short term 6-12 months can have AFP and sensory deficits – Alcohol injection Higher recurrence fewer side effects than above. SE include hypo and paraesthesia, dysesthesia, fibrosis, necrosis, reactivation of Herpes Zoster Pain relief<1year – Near Gasserian Ganglion – Radiofrequency thermocoagulation – Percutaneous glycerol – Bal oon microcompression Immediate pain relief 91-100%, 2-5% recurrence at 18months, 19% at 5 years and 32% at 20 years Pretrigeminal Neuralgia • Continuous dull achy pain sometimes • Diagnosis is dull tooth-ache like pain normal neurologic and dental exam and normal CT or Glossopharyngeal Neuralgia • Similar character of pain to TN • In distribution of glossopharyngeal nerve and auricular and pharyngeal branches of vagus • Location ear, base of tongue, tonsil ar fossa, below • Unilateral, seconds up to 2 minutes • Provoked by swal owing, chewing, talking or yawning • Comorbid with TN in 10-12% • Normal CN evaluation • MRI with contrast to exclude symptomatic GN Nervus Intermedius Neuralgia • Rare • Unilateral paroxysms of pain in inner ear • Last seconds to minutes • Trigger zone in posterior wall of auditory canal • Disorders of lacrimation, salivation, taste sometimes present • Often associated with Herpes Zoster • Rx medical as per TN • Can resect nervus intermedius or chorda tympani Other Neuralgias • Painful Opthalmoplegia – Orbital pain with paralysis of 1 or more cranial nerves – 111, 1V, V1 – Pain relief within 72 hours of steroid therapy • Superior Laryngeal Neuralgia – Severe paroxysmal pain in throat, submandibular area, – Duration minutes to hours – Triggered by swallowing, straining the vboice, turning the – Trigger point on lateral of throat over the hypothyroid Continuous Neuropathic Pain • Idiopathic Trigeminal Neuropathic Pain • Atypical Facial Pain/ Peripheral painful trigeminal traumatic neuropathy/ Atypical odontalgia • Diagnosis by exclusion of al other conditions • Begins with partial or complete deafferentation, eg pulp extirpation • Negative symptoms = sensory loss or decrease • Positive symptoms may be processesof regeneration and • Dysesthesia, paresthesia, hyperalgesia • 3-7% of RCT may end with AO • Postimplant neurosensory disturbance = 0.6-36% • Dull aching persistent pain, often with history of multiple dental AO versus Pulpal pain • No local pathologies or radiographic findings • Constant pain in tooth with no known source or pathology • Local provocation does not consistently alter the pain • Toothache is unchanging cf pulpal pain which resolves or • Repeated dental therpies fail to resolve the pain • Response to local anaesthesia is equivocal (peripheral + • Pain must have been present for >4 months • No referred pain • May be a history of trauma or deafferentation • Rx TCAs gabapentin, pregabalin, tramadol, topical lidocaine Postherpetic Neuralgia • Normal recovery from herpes zoster = 3-4 weeks • Some have irreversible damage to skin and sensory • Infrequent in general population but 50-75% in older • Painn develops in aacute phase and recurring or persisting for >3 months • Burning with brief stabbing with hyperalgesia and allodynia • Risk factors age, female, prodrome, severe rash and pain • Rx high dose gabapentin, carbamazepine +clomipramine and desipramine, and tramadol, topical lignocaine Anesthesia Dolorosa • Painful area of anaesthesia or dysesthesia • Arises after damage to CNV, ganglion, or nuclear • Most common after surgical therapies for TN • Bal oon microcompression, MVD and gamma knife surgery not typical y associated with it • Accompanied by increased sensitivity to pain and temperature in one or more divisions of the trigeminal • Treatment anecdotal TCAs, and anticonvulsants • Microsurgical repair effective in only 1/7 Central Post Stroke Pain • Pain, dysesthesia, impaired sensation to pinprick and temperature (>50%) • Due to a lesion of the spinothalamic pathway not the trigeminal nerve • Most commonly a vascular lesion • Pain usually in half of the body contrlateral to the • Also caused by MS, syringobulbia, trauma, neurosurgical lesions, tumour, vascular malformations, some inflammatory disorders • Rx amitriptylene, lamotrigine Complex Regional Pain Syndrome • CRPS 1 was called reflex sympathetic dystrophy and CRPS11- causalgia • Persistent burning pain with allodynia and hyperalgesia • At some stage there is swelling, changes in blood flow, and/or abnormal sudomotor activity • CRPS1 symptoms are disproportionate to a mild injury • CRPS 11 there is evidence of nerve damage preceding the • For diagnosis must have ¾ reported and 2/4 at time of evaluation of sensory, vasomotor, sudomotor/edema, and motor/trophic changes • Usually in upper and lower extremities Burning Mouth Syndrome (BMS) • Probably neuropathic but with peripheral and central • Burning of the mucosa/ dysgeusia/ xerostomia with no pathology/abnormalities • Primary (neuropathic) or secondary • Prevalence 0.7-15% • Rare under 30yo, most common in postmenopausal • Bilateral symmetric distribution, often anterior 2/3rds of tongue, dorsum and lateral surface, anterior hard palate and mucosa of lower lip • 17-33% link onset to upper respiratory tract infection, dental procedure, or medication • In 50% pain decreases with distraction oral intake or stimulation • Pain increases – during the day – With stress/ fatigue – Acidic/ hot/spicy food • May be associated with reduced salivary gland function/altered composition • May be autonomic involvement • Behavioral approaches • Topical therapies including anxiolytics, analgesic, antimicrobials, artificial sweeteners, LLLT • Systemic therapies – Antidepressants, aniolytics, anticonvulsants – Antioxidants – Atypical analgesics – Histamine receptor antagonists – Salivary stimulants – Dopamine agonists – Herbal supplements Clonazepam 1st line treatment • Mental Nerve Neuropathy • Numbness, paresthesia and rarely pain in distribution of mental nerve • Most commonly after dental procedures • LA, implants, RCTs, dental pathology • If no dental cause known considered a red flag • Investigate for systemic malignancy • Other causes MS, bisphosphonates, vagal and hypoglossal paralysis, leukemic vasculitis Occlusal Dysesthesia • Uncomfortable/incorrect bite • Usually plus emotional distress • History of repeated /failed dental procedures • From complex restorative to orthodontic • Occlusal hyperawareness • SNRI improved symptoms in 5/6 patients TMDs Radiography Traumatic TMJ hypoplasia Adaptational condylar change Degenerative condylar change Osseonecrosis/ DJD secondary to radioation for Pleiomorphic adenoma Close fracture of condylar neck

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