3.7.1 Appraise the International Classification of Headache Disorders
ICHD-3
The ICHD-3 is the third edition of the taxonomy of headache disorders.
It is almost entirely evidence-based - earlier editions were more expert opinion
Electronic and multi-language versions are available
Classification is hierarchical - with overarching diagnoses becoming increasingly subcategorised as you descend the levels
Group --> Type --> Subtype --> Subform
If more than one diagnosis - it should be listed in order of importance to the patient
Classification is important for research trials and physiological studies
Pros of ICHD-3
Easy to use
Flexible coding
Standardised
Clearly presented and can be followed
Empirically derived
Good validity
Cons:
Orofacial pain disorders not described
No consideration for psychosocial and behavioural factors
30% were not classifiable of headaches at a tertiary facility
ICD-11
Split into:
Chronic primary headache (Headache occurring at least every 15 days within 30 over a 3 month period)
Chronic migraine (unilateral throbbing and photo/phonophobia)
Chronic tension-type headache (bilateral pressing and tight)
Trigeminal autonomic cephalgias (autonomic features)
Temporomandibular disorder (Muscle pain mastication and orofacial pain)
Chronic burning mouth pain (Intraoral burning and dysaesthesia sensation)
Chronic primary orofacial pain (pain in mouth face with emotional distress)
Chronic secondary headache
Injury to head/neck
Cranial or cervical vascular
Intracranial
Withdrawal or substance
Infection
Dental pain
Neuropathic orofacial pain
TMD pain
3.7.2 Generally discuss accepted definitions of terms associated with headache syndromes
Chronic daily headache - Headache on at least 15 days per month for at least 3 months
These were defined as headaches that last more than4 hours. This was to distinguish true chronic headaches from more paroxysmal episodic conditions such as the TACs
3.7.3 Describe a taxonomy of orofacial pain
Facial pain has been separated from headaches in the latest ICD-11 - these are more commonly from musculoskeletal sources and transmitted through the second and third branches of the trigeminal nerve
Headache is pain above the orbitomeatal and/or nuchal ridge. Facial pain is below this line
Otherwise, these conditions are defined and classified as per headache disorders
ICHD-3 -
There are several axes of classification.
a) Syndromology: neuralgia or neuropathy
The division between, for example, trigeminal neuralgia and trigeminal neuropathy should be viewed as a pragmatic way of distinguishing conditions in which clinical presentations and treatment approaches differ while the two conditions cannot be classified on the basis of currently known pathology or pathophysiology. The same applies to painful conditions associated with the glossopharyngeal and intermedius nerves.
An important cause of cranial-nerve pain is herpes zoster. Despite the fact that trigeminal pain following herpes zoster probably leads to different types of pathological change in trigeminal pathways (ie, “irritable nociceptor” versus “deafferentation” type), available data are too limited to classify them as neuralgia versus neuropathy. Therefore the well-established term post-herpetic neuralgia is maintained.
b) Location: central or peripheral neuropathic pain
A lesion or undue activation of these nerves (peripheral neuropathic pain), or of their central pathways (central neuropathic pain), causes neuropathic pain in the face.
c) Aetiology: classical, idiopathic or secondary
The cause of a neuropathic pain may be clear, such as infection by Varicella zoster virus or a structural abnormality (eg, multiple sclerosis plaque) demonstrated by imaging: such pain is termed secondary, and attributed to the cause. In other cases no cause is apparent (termed idiopathic).
For the trigeminal, glossopharyngeal and intermedius neuralgias, the term classical is reserved for cases where imaging or surgery has revealed vascular compression of the respective nerve. Strictly speaking, classical neuralgias are secondary (to the neurovascular compression), but it is beneficial to separate them from other causes on the basis of the wider therapeutic options and potentially different nerve pathophysiology.
3.7.4 Describe the anatomy of the cranial and upper cervical nerves and the innervation of the scalp, sinuses and teeth
Anterior distribution of cervical nerves
Cervical plexus (C1 - C4)
Brachial plexu (C5 - T1)
Posterior distribution of cervical nerve
Suboccipital nerve (C1)
Greater occipital nerve (C2)
Third occipital nerve (C3)
The major sensory dermatomes of the head and
neck.
Major scalp innervation
- Supratrochlear (CNV1)
- Supraorbital (CNV1)
- Lessor occipital
- Greater occipital
- Third occipital
- Zygoma9cotemporal (CNV2)
- Auriculotemporal (CNV3)
- Greater auricular (C2,3)
B, buccal nerve; EN, external (dorsal) nasal nerve; IO, infraorbital nerve; IT,
infratrochlear; ST, supratrochlear nerve; M, mental nerve; SO, supraorbital nerve; Zf,
zygomaticofacial nerve; ZT, zygomaticotemporal nerve.
Adapted from: Simplified Facial
Rejuvenation. 1st ed. Heidelberg: Springer; 2008.
Innervation of nose
3 Cranial Nerves
CN 1 olfaction
CN 5 general sensation / Anterior V1 / Posterior V2
Glands : parasympathetic fibres in CN 7
Sympathetic nerve fromT1 spinal cord
4 Paranasal Sinuses
Frontal
a. Supraorbital and supratrochlear nerve
Ethmoidal
V1 --> anterior and posterior ethmoidal branches
V2 --> orbital branch from pterygopalatine ganglion
Lessor and greater palaytine nerve
Maxillary: most common site of chronic sinusitis
Infraorbital and alveolar branches of V2
Sphenoid
Posterior ethmoidal branch of V1
Orbital branch of V2 from pterygopalatine ganglion
Blood supply of spinal cord:
Arterial supply is through:
Anterior spinal artery
Posterior spinal artery
Segmental arterial supply from radicular / medullary arteries.
3.7.5 Describe potential neurobiological mechanisms for:
Headache
Tension-type
Pathophysiology
Peripheral sensitivity - pericranial myofascial tissues
Central - sensitisation of second-order neurone at the dorsal horn
Genetic basis
Relationship with psychological stress, anxiety and depression (descending inhibition)
Migraine
Pathophysiology
Cortical spreading depression - a wave of sustained depolarization (neuronal inactivation) moving through intact brain tissue. Likely triggers inflammatory responses
Hyperexcitable cortex - The lower threshold for occipital cortex excitations (?genetic)
Changes in periaqueductal grey over time with iron deposition
Increased white matter lesions
Activation of trigeminovascular complex (meningeal receptors)
Calcitonin Gene related peptide -
Facial Pain
Pathophysiology
PIFP does not have a specific cause however injury to the trigeminal nerve proximally or distally may lead to this disorder
Demyelination may initiate
Infectious causes can also be considered
Hyperactive central neuronal activity may contribute
Hypofunctioning dopaminergic pathways may also contribute
Orodental pain
Pathophysiology
Current mechanisms are controversial
Psychological factors play a role however are unlikely to be initiating factors
Deafferentation of the trigeminal sensory fibres is most likely mechanism but not confirmed
Reference: Bosch-Aranda, M. L., Vázquez-Delgado, E., & Gay-Escoda, C. (2011). Atypical odontalgia: a systematic review following the evidence-based principles of dentistry. CRANIO®, 29(3), 219-226.
Cluster headache
Pathophysiology
Reflex activation of the trigeminovascular system, which innervates cranial vessels and dura mater, synapse in the trigeminocervical complex.
Activation of the trigeminovascular system also activates the superior salivatory nucleus in the pons
Cells within this nucleus also control the parasympathetic autonomic vasodilator pathway.
Activation of the parasympathetic pathways may cause a further reflex arc back through the trigeminal autonomic reflex arc relayed through the sphenopalatine ganglion
3.7.6 Discuss the pathophysiology of trigeminal neuralgia
Types:
Idiopathic (10%) - Unknown - nothing found
Classic (60%) - Neurovascular compression in the trigeminal root entry zone
Secondary (30%) - Tumours or artery malformations / MS relationship
Pathophysiology
Disease-related e.g. MS
Peripheral - Progressive dystrophy of peripheral branches of trigeminal nerve evoked by compression syndrome
Allergic-immune reaction processes causing dystrophy
Possibly also changes to voltage-gated sodium channels with ectopic activity effects
Central - Peripheral factors cause change to afferent signal with pathological paroxysmal irritation focus with ectopic discharge
3.7.7 Discuss the pathophysiology of:
Post-traumatic headache
Pathophysiology is not clear. Theories include:
Impaired descending modulation
Neurometabolic changes (local cellular injury and unregulated ion-exchange neurotransmitter release)
Trigeminal sensory system activation - Neuroinflammatory CNS changes
Post-craniotomy headache
Pathogenesis is unclear
Meningeal inflammation
Nerve entrapment
Adhesion of muscle to the dura or other mechanisms
Neuroma formation
Destruction from drilling
Presenting features
Immediate postoperative headache may occur in up to 80% of craniotomy
Most resolve within 7 days
Unrelated to tumour size
More common in females
Up to 25% develop chronic (>3 months) headache
Posterior fossa procedures, sub occipital craniotomies for acoustic neuromas
Modification of operative procedure may help reduce risk
Factors that decrease the risk
Early NSAID use
The surgical technique to minimise muscle injury
Fat grafting with dura closure
Local anaesthetic use in wound
Perioperative gabapentinoid may help
Postoperative depression has an association with developing the headache
Management
Botox?
Triptans
Non-pharm - TENS, physiotherapy, acupuncture, CBT, stress management techniques, supportive neck collars
GON blocks and nerve stimulation (Strong evidence)
Radiofrequency or cryoablation (though the risk of pain aggravation)
Post-dural puncture headache
The theory is reduced CSF pressure with loss of cushioning of the brain in the intracranial fluid. Also possibly stretch on blood vessels within the brain
Munroe-Kelly doctrine - Secondary dilatation of the venous system
3.7.8 Perform a cranial nerve examination and fundoscopy / TMJ / cervical spine
3.7.11 Detail the critical factors for assessing life-threatening headache
Red flag headache features include:
Epidemiology
New-onset headache over 50 yo
Presentation
Subacute and/or progressive headaches that worsen over time
New or uncharacteristic headache
Any headache of maximum severity at onset
Increase in headache severity or frequency
Associated symptoms
Persistent headache precipitated by valsalva
Systemic features e.g. headache, myalgias, weight loss
Related illness e.g. history of cancer
Neurological signs
Seizures
3.7.12 Demonstrate awareness of potential causes of headache that may be overlooked on initial assessment including:
Idiopathic intracranial hypertension (Pseudotumour cerebri syndrome or BIH)
General
Requires all CAUSES of raised ICP to be excluded
More common in women and obesity
OCP is a risk factor
Symptoms
Headache
Visual loss (peripheral initially then later central)
Tinnitus (often pulsatile)
Nausea and vomiting
Diagnosis
Neuro-ophthalmological work up
Examination of the fundi for papilledema and visual field testing
MRI brain and MRI venography
Possibly LP - with CSF with opening pressures
Treatment
Medication - Acetazolamide
LP to lower pressure
Stenting of transverse sinus stenosis (previously CSF shunt)
Weight loss
Low CSF pressure (intracranial hypotension)
(Spontaneous intracranial hypotension)
General
Secondary headache caused by CSF leak or CSF-venous fistula involving the nerve root sheath
Female predominant in 40-50s
Pathophysiology
Possibly the hydrostatic indifference point (where the upper and lower CSF pressures are equal) moves lower down
Etiology
Traumatic, post-traumatic. Can be dural leaks of fistulae
Presentation
Abrupt onset daily persistent orthostatic headache that improves in the supine position
People can often report the exact date and time this began
Location is usually bifrontal/occipital or upper cervical but can be everywhere
Can present with neurological symptoms like tinnitus, photophobia, dizziness etc.
Diagnosis
MRI findings
Myelography can be considered
Treatment
Epidural blood patch can be effective
Post-craniotomy headache
(As above)
General
Occurs in 2/3rds of patients undergoing a craniotomy
Pathophysiology
Trauma to tissue, muscles, bone or meninges
Nerve injury
Debris from drilling bone irritating internal structures of meninges
Muscle adherence to dura mater
Formation of neuroma in surgical scar
Central sensitisation
Aberrant nerve regeneration
Risk factors
Neurosurgery > 4 hrs
Craniectomies
Assessment
Continuous, pulsatile or pounding pain of variable intensity within 7 days of surgery
Therapy
Similar to other headaches
Nothing specific
Reference: Subbarao BS, Fernández-de Thomas RJ, Eapen BC. Post Craniotomy Headache. [Updated 2021 Aug 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482297/
Pathology in the eyes and ears
Ophthalmologic - Consider
Acute narrow-angle glaucoma (Headache, vision changes, nausea and vomiting. Eye red)
Corneal abrasions/Foreign body (generally identified history. Watch for keratitis)
Giant cell arteritis (older, with PMR)
Intraocular tumours (Rare cause)
Optic neuropathy (usually with colour loss)
Dry eye (often tearing and redness)
Orbital vascular lesions (worse with Valsalva type factors)
Reference: Fiore, D. C., Pasternak, A. V., & Radwan, R. M. (2010). Pain in the quiet (not red) eye. American family physician, 82(1), 69-73.
Otalgic causes - Consider
Auricular cellulitis
Auricular trauma
Foreign body in ear
Herpes zoster (Ramsay Hunt Syndrome)
Acute otitis externa
Space-occupying lesions
General
The most common presenting sign is a headache
Worst symptom in 50% of cases
Risk factors
Trauma
HIV infection
Diabetes
Malignancy
Tuberculosis
Presentation
Dull and constant
Occasionally throbbing in nature
Intracranial pressure rising maneuvers often cause pain to worsen
Headaches with nausea and vomiting should be a red flag
Abnormal neurology with headache is also a concern
May be associated with seizures
Behavioural changes may be noted
Vascular disease
General Types
Cerebral ischaemic events
Non-traumatic intracranial haemorrhage
Unruptured vascular malformation
Arteritis (e.g. giant cell)
Cervical carotid or vertebral artery disorder
Pituitary apoplexy
Presentation
Acute in onset
Usually throbbing or thunderclap peaking rapidly
Not always associated with other symptoms and signs
Types with detail
Subarachnoid haemorrhage (Aneurysm rupture in 85%)
CNS vasculitis (Headache is insidious but commonly stroke is the outcome)
Cervical artery dissection (Stroke in young people. Avg onset 44yrs. Headache and neck pain. Headache can be insidious but hard to differentiate otherwise)
Cerebral venous thrombosis (More common in young and female. Usually other clotting risk factors. Severe headache otherwise non-specific)
Reference: Lu J, Liu W, Zhao H, Headache in cerebrovascular diseases
Stroke and Vascular Neurology 2020;5:doi: 10.1136/svn-2020-000333
Sinus pathology (Headache attributed to disorder of the nose and paranasal sinuses)
General
The presence of nasal autonomic symptoms is a hallmark differentiating these conditions
Chronic sinus pathology has been shown to be linked with persistent headaches
Diagnosis criteria/features - Acute
Headache in temporal relationship with the onset of rhinosinusitis
Worsened with rhinosinusitis
Worse with pressure
Unilaterality
Diagnostic criteria/features - Chronic
Headache developed in temporal relation to chronic rhinosinusitis
Headache waxes and wanes in parallel with the degree of sinus congestion
Headache exacerbated by pressure over paranasal sinuses
Unilateral - headache is also unilateral
Temporomandibular dysfunction
Three main types
Structural
Congenital malocclusion
Post-traumatic
Ankylosis (e.g. RA, OA)
NB: Only 3-5 % of TMJ patients have surgically amenable lesions
Dental
Occlusal disorders (malocclusion, bruxism)
Secondary muscle spasm (can be helped with splints, Physio, TCAs. Regular analgesics and relaxants have pitfalls)
Myofascial pain of masticatory muscles
Common
Multifactoral triggers
Depression and personality disorder traits
Associations with tension myalgia (fatigue, fragmented sleep)
72% have oral habits (e.g. clicking)
Treatments
Attend to mechanical disorder / correct malocclusion (Dental review)
Arrest abnormal habits
Relaxant therapy (physical, psychological)
Pain therapies - but be careful
Botox in refractory cases
Surgical consideration
(Avoid SSRIs because of risk yawning triggering)
Tricyclics and anti-inflammatories (if suitable)
Diet and healthy lifestyle
3.7.13 Distinguish between the clinical features of the following PRIMARY chronic daily headache syndromes
Migraine (with and without aura)
Epidemiology
17% of females and 6 % of males (In US)
Incidence of general migraine peaks at 5 yo in males and 12-13 in females
Incidence of migraine with aura is a bit older (12-13 M 14-15 F)
Lower socioeconomic status is associated with migraine
Symptoms
Headache, throbbing, unilateral, nausea, photophobia, phonophobia, worse with movement
One-third of patients do NOT have throbbing pain
Theories
Vascular was thought to be the cause as 'throbbing' no known it is not that simple - called a neurovascular condition
Cortex is hyperexcitable and migraine patterns are genetically determined
Modern imaging suggests vascular changes are NOT linked to pain
Pathophysiology
Cortical spreading depression - a wave of sustained depolarization (neuronal inactivation) moving through intact brain tissue. Likely triggers inflammatory responses
Hyperexcitable cortex - Lower threshold for occipital cortex excitations (?genetic)
Changes in periacqueductal gray over time with iron deposition
Increased white matter lesions
Differential diagnosis features
Less than 15 days = episodic
Greater than 15 days = chronic (8 of the 15 days must be clearly migrainous)
Less than four hours - short duration
Cluster headache
SUNCT/SUNA
Paroxysmal hemicrania
Hypnic headache
Primary stabbing headache
Longer than four hours - long duration
Chronic migraine
Chronic tension-type headache
Hemicrania continua
New daily persistent headache
Associated conditions
Epilepsy (benign rolandic epilepsy, benign childhood epilepsy)
Familial dyslipoproteinaemias
Hereditary haemorrhagic telangiectasia
Tourette syndrome
Hereditary essential tremor
Hereditary cerebral amyloid angiopathy
Depression
Anxiety
Asthma
Patent foramen ovale
Stroke (migraine with aura is a risk factor for stroke particularly cerebellar)
Transformed (Chronic) migraine
Definition
Headache (tension-type or migraine-like) on >15 days/month for > 3 months
Occurring in a patient who has had >5 attacks of migraine with or without aura
On >8 days/month for > 3 months
Risk factors
Attack frequency
Acute medication overuse
Duration of disease
Obesity and snoring
Stressful life events
Female gender
Lower education and socioeconomic status
Head injury
Factors to REVERT from chronic to episodic migraine
Adherence to migraine prophylactic drugs
Withdrawal of overused migraine abortive drugs
Physical exercise
Absence of cutaneous allodynia
Lower baseline headache frequency
Cluster headache and variants
Referred Neuralgias and Vascular Fascial pain
Neuralgia (clues from history)
Vascular (often from associated symptoms - vasomotor, visual, flushing)
Cluster (Rhinorrhoea, lacrimation, conjunctival injection)
Cluster headache
Usually male in 3rd or 4th decades
Headache is severe and usually unilateral
Throbbing - cranial/orbital/facial
Associated conjunctival redness, eye-watering & lacrimation
The attack may last 30 minutes to 4 hours - several times a day over a 6-8 week period
Can be transient Horner's syndrome - persists in 10% of cases
Cluster headache may be precipitated by trauma
High rates of suicide
SUNCT syndrome
Short lasting, Unilateral, Neuralgiform headache with Conjunctival injection and Tearing
Attacks of moderate or severe unilateral headache pain lasting seconds to minutes at least once a day with lacrimation and red eye
Often a series of stabs
(Another option is SUNA - which does NOT have conjunctival injection and lacrimation)
Paroxysmal Hemicrania
Attacks of severe, unilateral pain that is orbital, supraorbital, temporal or any combination of these
2-30 mins
Several times a day
Ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, mitosis, ptosis and/or eyelid oedema.
Responds to indomethacin
Hemicrania Continua
Persistent, unilateral headache with ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, mitosis, ptosis, restlessness and agitations. SENSITIVE TO INDOMETHACIN
3.7.14 Distinguish between the clinical features of the following SECONDARY chronic daily headache syndromes
Medication-related
Medication overuse headache - Regular use of acute or symptomatic medication on 10 or more (opioid/triptan) or 15 (simple analgesia) or more days per month. Usually resolves when medication overuse is stopped
Multiple substances possible, not just medications
Medication-induced side effects (Headache attributed to substance or its withdrawal) - Difficult to prove irrefutably. Headache needs to occur temporally and then cease with avoidance/removal of the substance
Post-traumatic
Headache attributable to neck injury or whiplash
Pathophysiology
Malfunction of descending serotonergic pain inhibitory system
Neurochemical dysregulation
Activation of the trigeminal system by vertebrae C2 to C5 afferents by the convergence of trigeminal and cervical afferents in the spinal dorsal horn and consecutive sensitisation of CNS
Psychological factors also heavily contribute
Management
Proper patient education
Support of normal movement
Avoiding immobilisation
Resumption of work
Targeted physiotherapy
Reference: Obermann, M., Naegel, S., Bosche, B., & Holle, D. (2015). An update on the management of post-traumatic headache. Therapeutic advances in neurological disorders, 8(6), 311–315. https://doi.org/10.1177/1756285615605699
Disorders of intracranial pressure
Increased intracranial pressure
Usually associated with other neurological symptoms and papilloedema/neck stiffness
Headache in the morning, visual obscuration, vomiting with little nausea
Causes include Idiopathic ICH, ICH due to metabolic, toxic, or hormonal causes, hydrocephalus, chromosomal problem (e.g. Down syndrome)
Decreased intracranial pressure
Orthostatic headache often with neck pain, tinnitus, hearing and photophobia, and nausea.
Headache on standing with improvement when lying down
No visual changes on change of posture and minimal nausea
Causes include: post lumbar / dural puncture, spontaneous leak
Headache referred from other structures
Tension-type headache
Similar triggers to migraine - some overlap
Stress
Menstruation
Strong odours
Sleep fragmentation / sleep lack
Weather change
Missing meal
Exertion
Dehydration
Similar triggers to migraine
65% Photophobia in tension headache
65% sonophobia in TH
75% neck pain in patients with migraine!
More kinesiophobia in migraine
Key differences
Cervicogenic headache
This is said to be problematic terminology. The likely anatomical location of nociception is the cervical spine - likely the zygapophyseal joints through pathogenesis is unclear. Management similar to tension-type headaches
3.7.15 Recognise the clinical features of
Trigeminal neuralgia
A brief shock-like pains
Abrupt in onset and termination
Limited to a distribution of one or more of the trigeminal nerve
Triggered by innocuous stimuli
Pain may become more severe over time
No neurological deficits!
Can cause muscle movements - Tic doloureux
May have some mild autonomic features
Following paroxysm - usually a quiescent time where it cannot be triggered again
Other cranial neuralgias
Glossopharyngeal neuralgia
Unilateral brief stabbing pain abrupt in onset and termination in the glossopharyngeal, auricular and/or pharyngeal branches of the vagus nerve
Pain can be in the ear, tongue, tonsillar fossa, or below the angle of the jaw
Worsened by yawning, swallowing, talking, or coughing
Treatment is commonly surgical - glossopharyngeal and upper vagal root section
Occipital neuralgia
Unilateral brief stabbing pain abrupt in onset and termination in the distribution of the greater, lesser and/or third occipital nerves- often with dysaesthesia and tenderness
Geniculate neuralgia (Nervus intermedius neuralgia)
Same but felt in the ear
Lancinating pain of the 7th cranial nerve
Treatment similar to trigeminal neuralgia
Post-herpetic neuralgia
Preceding vesicles (commonly but not always)
Older age at onset
Constant
Can have sensory triggers
Treatment: Antivirals, steroids, TCAs, anticonvulsants, gabapentin or pregabalin
“Burning mouth” syndrome
Condition of older women (50-70)
Etiology/pathophysiology remains unclear
Primary and Secondary types (nutritional deficiencies, dental-related trauma, hormonal (menopause), endocrine (diabetes).
Presentation
Tongue is most common site followed by hard palate, gingiva and lower lips
Pain is worst in the mornings
Relaxation, chewing gums, drinking cold drinks can all help
Usually symmetrical and bilateral
Pain worsens over the day
Xerostomia may play a role with reduced salivary gland secretion noted
Treatment
No consensus on cause so treatment is difficult
Addressing psychosocial is important as patients often don't feel validated
Simple measures such as avoiding triggers (e.g. acids) and helping to relieve dry mouth (e.g. crushed ice and gum)
Capsaicin can be trialled but epigastric pain is often a problem
Topical clonazepam has been trialled but the minimal benefit
Low dose TCA and oral clonazepam can be trialled
Psychological therapy is essential
3.7.16 Apply a differential diagnosis approach to determining the anatomical origin of 'atypical' facial pain
Start with: What is TYPICAL facial pain?
Cranial arteritis
Cluster headache
Post-herpetic neuralgia
Trigeminal neuralgia
Etc.
What is Atypical facial pain?
Atypical facial pain (Now persistent idiopathic facial pain) is a persistent facial pain that does not have the characteristics of cranial neuralgias and is not attributable to another disorder
Presenting features
Facial pain occurs daily and persists throughout the day
Limited to one particular side of the face at onset, deep and poorly localised, no sensory or neurological deficits. Investigations do not show a cause.
Commonly occurs in areas of the trigeminal nerve but does not fit other criteria
Usually unilateral without autonomic features
Duration is long-lasting most of the day
Often may have a triggering event
Epidemiology / Risk factors
Females more commonly
Often psych or mood disorder
Ill-defined pattern
Sometimes related to sinuses
Cause
Likely neuropathic pain
Maxillary artery migraine variant
Diagnostics
ICH3 requires more than 2 hrs per day over more than 3 mths
Lots of terms - all unhelpful generally (myofascial pain, facial arthromyalgia, somatodynia, atypical odontalgia etc)
Post-traumatic Trigeminal pain
Usually from dental surgery
80% recover within one year
Rarely a posterior fossa tumour or vertebral artery aneurysm
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