The three classification slides are easier to remember as a map than as a numbered list. ICHD-3 groups secondary headache by cause: head/neck trauma; cranial or cervical vascular disease; non-vascular intracranial disease; a substance or its withdrawal; infection; a disorder of homoeostasis; and disorders of the cranium, neck, eyes, ears, nose/sinuses, teeth or other facial/cervical structures. A final part covers painful cranial neuropathies and other facial pain ^[15].

Secondary does not automatically mean dangerous, and primary does not mean “no biology”; the practical point is to look actively for a causative disorder whenever the history, examination or time course is atypical.

TTH general diagnostic criteria: ^[5]

Episodic TTH:

• ≥10 episodes of headache, each lasting 30 min – 7 days
• ≥2 of the following:
  • Bilateral location
  • Pressing/tightening (non-pulsating) quality
  • Mild to moderate intensity
  • Not aggravated by routine physical activity
• Both of the following:
  • No nausea or vomiting
  • No more than one of photophobia or phonophobia ^[6]

Chronic TTH (CTTH):

• ≥15 headache days per month for ≥3 months ^[6]

The mechanism involves peripheral and central sensitization. The initial trigger is pericranial myofascial tissue (PMT) tenderness—muscle tension in the head and neck generates nociceptive input. In episodic TTH, peripheral mechanisms dominate. In chronic TTH, central sensitization at the level of the spinal horn/trigeminal nucleus caudalis (SH/TNC) takes over, meaning the brain's pain processing becomes dysfunctional even without ongoing peripheral nociceptive input.

A model for pathophysiology of CTTH: PMT → brainstem interneurons (BI) → motor nuclei (MN) → SH/TNC (spinal horn/trigeminal nucleus caudalis). In CTTH, central sensitization at SH/TNC level becomes an important driver of pain rather than pain being explained by peripheral muscle tension alone ^[5].

Reading the two diagrams: nociceptive input from pericranial myofascial tissues reaches second-order neurons in the trigeminal nucleus caudalis/upper cervical dorsal horn. Repeated input can sensitise this central relay; descending limbic/brainstem control, stress and mood then alter gain, while motor output and muscle strain feed back into the peripheral input. The treatment diagram therefore places stress management and tricyclics mainly on central modulation, physical therapy mainly on peripheral contributors, and relaxation across both. It is a bidirectional model, not proof that every TTH is caused by “tight muscles.”

This is why amitriptyline works for CTTH—it modulates central pain processing, not peripheral muscle tension.

Aim: prevent TTH from becoming CHRONIC ^[5]

Acute/Abortive Treatment:

Prophylactic Treatment (for CTTH):

Long-term prophylactic treatments for TTH: ^[5]

Slide 10 reads “amitriptyline: reduce daily headache duration 11 → 8 hours” ^[5]. The previous note's “118 hours” was an image-reading error. Treat the 3-hour reduction as the result of the cited study/figure, not a guaranteed individual effect.

The remaining preventive list is lecture-era rather than a hierarchy of equally supported choices. Persistent/chronic TTH warrants confirmation of the phenotype, an overuse review, management of sleep/stress and comorbidity, and an individualised preventive plan.

Migraine is a neurovascular disorder of the brain; common, chronic, incapacitating. Attacks of (1) severe headache, (2) autonomic nervous system dysfunction, (3) in some, aura involving neurologic symptoms. ^[5]

Key epidemiological facts: ^[5]

• 10% general population (6% males, 15% females); 2010 global prevalence 14.7%
• From age 16, 2–3 times more frequent in females
• Peak incidence: age 14-16 for females, age 10-12 for males
• In women ~age 40: highest prevalence (24%)
• 90% onset before age 50 → new headache after 50 is NOT migraine until proven otherwise

Two main types: ^[5]

1. Migraine without aura (75%)

2. Migraine with aura (1/3 of migraineurs)

• Migraine patients defined as having ≥2 attacks with aura or ≥5 attacks without aura
• Up to 33% migraineurs experience both types of attack
• Up to 42% may have migraine aura without headache (acephalgic migraine)

Aura symptoms: one or more transient focal neurological symptoms ^[5]

1. Visual (99%) — the classic scintillating scotoma, zigzag lines, fortification spectra

2. Sensory (31%) — tingling, numbness, typically spreading over minutes

3. Aphasic (18%) — difficulty with speech

4. Motor (6%) — rare; when present, consider familial hemiplegic migraine

• Gradual development over > 4 min, or several symptoms in succession
• Usually last 5-60 min (motor symptoms may last longer)
• Aura nearly always precedes headache (follows or accompanies aura within 60 min)

The last line is older slide wording: aura can precede, accompany or occur without headache. Current ICHD-3 focuses on reversibility, gradual spread/succession and typical duration rather than requiring aura to come first ^[15].

Why does aura develop gradually? Because it reflects cortical spreading depression (CSD)—a slowly propagating wave of neuronal/glial depolarization across the cortex (~3 mm/min). The gradual spread of CSD across the visual cortex produces the expanding scotoma. This is fundamentally different from a TIA/stroke, where onset is sudden.

What the Lashley aura sequence shows (slide 17): a small paracentral positive visual phenomenon enlarges over approximately 10 minutes into a curved zigzag/fortification border, with an area of missing vision (negative scotoma) trailing behind it. That progressive migration across the visual field is classic for aura. It is a pattern clue, not permission to dismiss a first, purely negative, abrupt, unusually prolonged or persistent deficit—those require urgent assessment for retinal or cerebral ischaemia.

Migraine Without Aura:

• A: ≥5 attacks fulfilling B-D
• B: Duration 4-72 hours (untreated)
• C: ≥2 of:
  • Unilateral
  • Pulsating
  • Moderate or severe
  • Aggravated by routine physical activity
• D: ≥1 of:
  • Nausea ± vomiting
  • Photophobia AND phonophobia
• E: Not better accounted for by another diagnosis ^[6]

Migraine With Aura:

• A: ≥2 attacks
• B: ≥1 fully reversible aura symptom (visual/sensory/motor/speech/brainstem/retinal)
• C: ≥2 of:
  • At least one aura symptom spreads gradually over ≥5 min
  • Each aura lasts 5-60 min
  • At least one is unilateral
  • Aura accompanied or followed within 60 min by headache ^[6]

Dysfunction of brainstem pathways that normally modulate sensory input: ^[5]

1. Trigeminovascular input from meningeal vessels
2. Trigemino-autonomic reflex (exaggerated in TACs)
3. Modulation of trigeminovascular nociceptive input from dorsal raphe nucleus, locus ceruleus, magnus raphe nucleus
4. Reduced cerebral blood flow (oligemia) during migraine aura, preceded by a phase of focal hyperemia

The diagrams' working model, explained from first principles:

1. Trigger phase: Internal or external triggers (stress, hormonal changes, foods) activate genetically susceptible brainstem nuclei (especially the dorsal raphe, locus ceruleus, and trigeminal nucleus).

2. Cortical Spreading Depression (CSD): A wave of neuronal/glial depolarization propagates across the cortex. This is the substrate of the aura. CSD activates trigeminal nociceptive afferents in the meninges.

3. Trigeminovascular system activation: meningeal/dural afferents travel through the trigeminal ganglion to the trigeminocervical complex, then ascend to thalamic and cortical pain networks. Activation releases CGRP (calcitonin gene-related peptide) and other signalling molecules.

The main source of CGRP is cell bodies in trigeminal ganglia. ^[5]

4. CGRP signalling and vascular change: the older slide depicts vasodilation and “neurogenic inflammation” as the initiating mechanism. Modern teaching is broader: migraine is a disorder of distributed sensory-processing networks with trigeminovascular/CGRP signalling; vascular dilatation and peripheral inflammatory phenomena may accompany an attack but are not a complete cause of migraine.

5. Central sensitization: Prolonged nociceptive input leads to sensitization of second-order neurons in the trigeminal nucleus caudalis → allodynia (pain from normally innocuous stimuli like touching the scalp), throbbing quality, worsening with movement.

6. Autonomic pathways: trigeminal input can recruit the superior salivatory nucleus and parasympathetic outflow through the pterygopalatine ganglion, producing lacrimation and nasal congestion. Nausea/vomiting involve wider brainstem and hypothalamic networks rather than this reflex alone.

FHM genes cause increased neuronal excitability and susceptibility to cortical spreading depression. All 3 genes are implicated in ION TRANSPORT: ^[5]

Why this matters for exams: FHM is the proof-of-concept that migraine is a channelopathy. All three mutations converge on the same final common pathway: increased cortical excitability → lowered threshold for CSD → migraine. The examiner may ask you to name the FHM genes or explain how they relate to CSD.

Neurostimulation devices: ^[5]

• Transcranial magnetic stimulation (TMS): approved for acute treatment of migraine with aura (2014); now also for acute and prophylactic treatment
• External trigeminal nerve stimulation: approved for acute treatment of migraine with/without aura AND preventive treatment of episodic migraine

Device authorisation and evidence vary by product and jurisdiction; the slide's generic word “approved” should not be read as a class-wide recommendation.

Migraine-like symptoms may be caused by: ^[5]

• Arteriovenous malformations (AVM)
• Internal carotid dissection
• Epilepsy
• MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes)
• CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarction and leucoencephalopathy)

Why this list matters: If a patient presents with "migraine" plus unusual features (stroke-like episodes, early dementia, maternal inheritance pattern, or young stroke), think of these secondary mimics.

The slide states that 3 or more criteria “diagnose” TA with 91.2% specificity and 93.5% sensitivity: ^[5]

1. Age at onset ≥50 years
2. New headaches
3. Abnormalities of temporal artery at clinical examination (tenderness, decreased pulsation, nodularity)
4. Raised ESR (≥50 mm/hr)*
5. Abnormal findings on biopsy of temporal artery (granulomatous inflammation with giant cells)

*Raised CRP ( > 5 mg/L) is another, currently used, clinically useful laboratory parameter ^[5]

Critical correction: these are classification criteria, developed to separate established vasculitis cases for research; they are not a stand-alone diagnostic rule. The 2022 ACR/EULAR criteria explicitly warn against use before a clinician has diagnosed medium/large-vessel vasculitis and excluded mimics ^[20]. A normal inflammatory marker lowers probability but does not by itself exclude GCA.

Current diagnostic approach: assess cranial ischaemic symptoms urgently; obtain FBC/platelets, ESR and CRP; and arrange prompt objective confirmation through a fast-track pathway. Depending on local expertise, this may be temporal/axillary artery ultrasound (EULAR's preferred first imaging test), a long-segment temporal-artery biopsy, and/or large-vessel imaging. Do not delay glucocorticoid treatment when vision is threatened while waiting for testing [21,22].

Most frequent facial neuralgia, prevalence: 3-6 per 100,000 ^[5]

• Incidence ↑ with age, ~70% patients > 60 yrs at onset
• Clinical hallmark: paroxysms of pain, very intensive, almost exclusively unilateral in a trigeminal distribution
• Typical: in second or third division (~5% first division)
• ~3% bilateral → suggesting a secondary origin

Trigger spots and typical triggers: ^[5]

• Touching/washing face, shaving, brushing teeth, chewing
• Sensory stimulation of cheek, chin, lip, tongue
• Stereotypic pain attacks usually many times per day, for weeks or months, then suddenly stop
• Subsequent pain-free periods for months or years
• Disease course: pain attacks tend to become more frequent over years, & remission periods shorter

Why the pain is paroxysmal: TN pain results from ectopic impulse generation in demyelinated trigeminal nerve fibers. The demyelination (often at the root entry zone where peripheral myelin transitions to central myelin) allows ephaptic transmission—one nerve fiber "short-circuits" to adjacent fibers, creating a burst of synchronized activity perceived as excruciating pain. Touch triggers fire Aβ fibers that cross-excite pain-carrying fibers through these ephaptic contacts.

Idiopathic TN (primary TN): normal neurological & MRI examination, no cause detectable ^[5]

Most common identifiable cause: compression of trigeminal nerve root by an aberrant loop of a blood vessel (60-90%) in neurosurgical and neuroradiological series ^[5]

Current terminology: classical TN requires neurovascular compression with morphological change of the trigeminal root; secondary TN is due to another disease such as MS or a tumour; idiopathic TN has neither demonstrated root change nor a secondary cause after adequate investigation. Mere vessel-nerve contact is common and must be interpreted with the nerve's anatomy and the symptomatic side ^[18].

MRI for detection of neurovascular contact: ^[5]

• Sensitivity (50-95%)
• Specificity (65-100%)
• False +ve (7-15%)
• False -ve (10%)

Up to 15% patients: an underlying cause can be identified (symptomatic TN): ^[5]

• Multiple sclerosis — especially young patients, bilateral
• Structural lesions mainly in pontine region:
  1. Vestibular/trigeminal schwannoma, meningiomas
  2. Epidermoid or other cysts
  3. Vascular brainstem lesions: pontine infarctions, angiomas, AVM

Features more common in symptomatic TN:

• Bilateral involvement
• Abnormal trigeminal reflex
• Trigeminal sensory deficits

MRI brain scan is the investigation of choice for trigeminal neuralgia ^[5]. Current guidance supports MRI in the diagnostic work-up because clinical features cannot reliably exclude secondary disease; use high-resolution trigeminal sequences with vascular imaging where available ^[18].

This was directly tested in the 2022 Fourth Summative MCQ Q59: A 79-year-old woman with short-lasting sharp lightning pain over her right cheek, multiple daily attacks lasting 30-40 seconds → Answer: MRI brain scan (not CT, not PET, not SPECT) ^[1].

Why MRI, not CT? MRI provides superior soft tissue resolution to:

1. Detect neurovascular contact/compression at the trigeminal root entry zone
2. Exclude MS plaques in the pons
3. Exclude CPA tumours (schwannoma, meningioma)
4. CT cannot reliably visualize the trigeminal nerve or vascular loops

• Sudden severe headache, “worst headache in my life” → urgent CT; LP depends on scan timing/quality and residual suspicion as above. Once confirmed, discuss urgently with a specialist neurosurgical centre, obtain CTA and secure the culprit aneurysm by coiling or clipping when appropriate ^[16]. The older lecture's blanket “tranexamic acid + anticonvulsant” bundle is not a universal modern prescription.
• SAH complications: rebleeding, hydrocephalus, vasospasm (delayed cerebral ischaemia)
• Consider enteral nimodipine in confirmed SAH; dosing, contraindications and haemodynamic management follow the specialist protocol ^[16].

• CNS infection imaging indications: altered mental state + fever, acute severe headache, first seizure with fever, immunocompromised + new neurological signs ^[12]

• ICA dissection → retroorbital pain + Horner's syndrome
• VA dissection → occipital pain + vertebrobasilar symptoms
• Can cause SAH intracranially if dissecting aneurysm ruptures ^[9]