Acute HeadacheDiagnosis and Management

Dr Jas Dulay

Case presentation

• A 28-year-old woman presented with a 4-hour history of a bifrontal-temporal throbbing headache.

• The headache was initially mild and then progressed over about 1 hour to a severe intensity ( 10/10) the worst headache she had ever had, associated with nausea, vomiting, light and noise sensitivity.

• She had no visual symptoms, fever, or systemic symptoms.

• There was a history of occasional mild headaches relieved with Ibuprofen.

• No Past medical history . Observations were normal.

• The neurological examination was normal-including Fundi and neck exam(no neck stiffness).

• She was given sumatriptan 6 mg subcutaneously. The headache and associated symptoms resolved within 2 hours.

• Diagnosis?

Case presentationDiagnosis?

• SAH• TTH• Migraine headache• Medication overuse headache• IIH

Headache

• History from patient/ carer and examination

• Recognisable primary headache syndrome

• Evidence of CNS infection

• Acute onset headache syndrome– CT brain and CSF examination

– ? SAH

• Other causes of acute onset headache

Primary vs Secondary headache

• Migraine

• Tension type

• Cluster

Migraine

• 1. 1 in 7 people in the UK suffer from migraine.

• 2. M:F= 1:2

• 3.All age groups –commonly “productive years”

• 4. Migraine costs the UK more than £2 billion per annum.

• 5. The World Health Organisation has classified headache as a major health disorder and has rated migraine amongst the top 20 most disabling lifetime conditions.

• 6. A migraine attack can last for between 4 and 72 hours. However other migraine symptoms, such as mood changes and lethargy can last for longer as they can occur before or after the headache phase.

• 7. Sufferers experience an average of 13 attacks each year

• Ref: Migraine.org.uk

Pathophysiology

• Neurovascular– Neural events cause dilation of blood vessels

• A “dysfunction of brain-stem or diencephalic nuclei that are involved in sensory modulation of craniovascular afferents”

• – Goadsby et al NEJM 2002

Selected Diagnostic Criteria from International Headache Society Classification (ICHD-II)• 1.1 Migraine without aura

• Diagnostic criteria:

• A At least 5 attacks, 1 fulfilling criteria B–D

• B Headache attacks lasting 4–72 hours (untreated or unsuccessfully treated)

•• C Headache has at least two of the following characteristics:

• 1. unilateral location

• 2. pulsating quality

• 3. moderate or severe pain intensity

• 4. aggravation by or causing avoidance of routine physical activity (e.g walking or climbing stairs)

• D During headache at least one of the following:

• 1. nausea and/or vomiting

• 2. photophobia and phonophobia

• E Not attributed to another disorder

Migraine aura

• Migraine with aura or stroke?

• Visual, sensory,speech, motor(hemiplegic migraine)

• Usually marches, +ve or -ve

• Duration normally 10-30 mins, then headache

• Lasts less than 60 mins(except hemiplegic migraine)

Migraine - acute treatment

• ASA-900mg Paracetamol 1000mg

• NSAIDS-Ibuprofen/Naproxen

• Antiemetics-Domperidone/Metoclopramide

• Triptans

• Avoid opioids

• Prophylaxis:b-blockers Atenolol (BASH)• Amitriptyline,Topiramate,valproate

Mechanism of Action

• Triptans activate 5-HT (serotonin) receptor sites, causing

– cranial vasoconstriction

– peripheral neuronal inhibition

– inhibition of transmission through second-order neurons of the trigeminocervical complex

• Unclear which mechanism predominates

Triptans, the Treatment of Choice

• Many on the market now• Sumatriptan , almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan and zolmitriptan

• Advantages• Selective pharmacology, well established efficacy and safety, moderate side effects

• Disadvantages• Higher cost and C/I in CV disease

Triptans, cont.

• Side effects• Tingling, paraesthesias, warm sensations in chest, head, dizziness, neck pain, flushing, rare MI

• Contraindications• CAD, uncontrolled HTN, cerebrovasc dis, pregnancy, renal or liver dis, familial hemiplegic migraine, basilar migraine, Raynaud’s, MAO or ergots

• Efficacy: • 76% response rate at 10 mins after sumatriptan 6 mg Sc; 86-92% relief by 2 hours

Triptan Interactions

• Watch for rare possibility of serotonin syndrome if combining triptans and

SSRIs/SNRIs.

•• Almotriptan , eletriptan , frovatriptan , or naratriptan may be used with MAOIs.

• Use Zolmitriptan 2.5mg dose if given with cimetidine –cytochrome p450 1A2

• Avoid using eletriptan or DHE with other medications that are broken down by CYP3A4(e.g Clarithromycin)

• Use rizatriptan (Maxalt) 5mg dose if given with propranolol (Inderal).

TTH

• Episodic vs Chronic(>15days/mo)

• Featureless headache

• m/s abnormalities

• Treatment:

• regular exercise,physio,relaxation therapy

• Limited NSAIDS-Ibuprofen,Naproxen(250-500 bd-break cycle 3/52)

• Amitriptyline

• Treat concurrent depression

• Cognitive therapy

• Care with medication overuse headache(MOH)

Cluster headache-(TAC)• International Classification of Headache Diseases 2004• Severe unilateral pain lasting 15-180 minutes untreated.• At least one of the following, ipsilaterally:-• • Conjunctival injection and/or lacrimation• • Nasal congestion and/or rhinorrhoea• • Eyelid oedema• • Forehead and facial sweating• • Miosis and/or ptosis• • A sense of restlessness or agitation

• Frequency between one on alternate days to 8 per day.• Not attributable to another disorder• Smoking/Alcohol

• Treatment- oxygen, triptan(sumatriptan s/c, nasal),lignocaine(1ml-10%)

• Prophylaxis- verapamil 80 tds +,Pred 60 mg 2-5 days

CLUSTER HEADACHE

• The underlying pathophysiology of CH is incompletely understood

• The periodicity of the attacks suggests the involvement of a biologic clock within the

hypothalamus (which controls circadian rhythms), with central disinhibition of the

nociceptive and autonomic pathways—specifically, the trigeminal nociceptive

pathways.

• Positron emission tomography (PET) have identified the posterior hypothalamic gray

matter as the key area for the basic defect in CH.

• Functional hypothalamic dysfunction has been confirmed by abnormal metabolism

based on the N-acetylaspartate neuronal marker in magnetic resonance

spectroscopy.

Case

• A 60 year old man presented to the emergency department with nausea and vomiting after sudden onset of headache two days previously that had radiated to his cervical spine.

• PMH migraine since childhood

• He had associated dizziness and had fallen twice.

• On examination, he had blood pressure 180/88 mm Hg, Glasgow coma score 15, normal reactive pupils, and no other signs or focal neurology.He still had a 6/10 headache

• Blood tests showed a mild neutrophilia and mildly raised C reactive protein. His clotting and all other blood tests were normal

• What investigation next?

CT head

Acute onset headache‘thunderclap headache’

• Sudden headache of unusual severity reaching maximum intensity in a few seconds(<1min)

• Of patients with thunderclap headache 11-25% have SAH

• BMJ 2012;345:e8557 doi: 10.1136/bmj.e8557

Subarachnoid haemorrhagea few background details

• Women > men, 1.6:1

• ADPKD in only 2% of SAH

• 50% mortality, of survivors 30% dependent

• Only 70% say onset instantaneous

• GCS affected in 50%

Subarachnoid haemorrhageinvestigations

• CT brain

• Negative in 2-10% of SAH

• After a few days MRI superior

• CSF

• 12 hrs post onset in CT negative

• Spectrophotometry required - bilirubin

Subarachnoid haemorrhagegeneral management

• Refer to neurosurgical unit(GCS ready!)

• Attention to feeding and fluids

• Do not treat hypertension unless end organ damage

• Pain relief

• Compression stockings

• Nimodipine 60 mg 4 hrly for 3 weeks

• BMJ

• 2010;341:c5204 • Variables included in each of three proposed rules For each rule, patients

should be investigated if one or more of the variables are present

• Rule 1

• Age >40 Complaint of neck pain or stiffness Witnessed loss of consciousness Onset with exertion

• Rule 2

• Arrival by ambulance Age >45 Vomiting at least once Diastolic blood pressure >100 mm Hg

• Rule 3

• Arrival by ambulance Systolic blood pressure >160 mm Hg Complaint of neck pain or stiffness Age 45-55

High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study

The Ottawa SAH rule

• Investigate if 1 or more high-risk variables present:

• 1. Age >40 y

• 2. Neck pain or stiffness

• 3. Witnessed loss of consciousness

• 4. Onset during exertion

• 5. Thunderclap headache (instantly peaking pain)

• 6. Limited neck flexion on examination

• JAMA. 2013;310(12):1248-1255

Algorithm for approachingheadache in the ED

• History from patient/ carer and examination

• Recognisable primary headache syndrome

• Evidence of CNS infection

• Acute onset headache syndrome• CT brain and CSF examination

• ? SAH

• Other causes of acute onset headache

Acute onset headache‘thunderclap headache’

• Vascular disorders• Subarachnoid haemorrhage• Intracerebral haemorrhage• Venous sinus thrombosis• RCVS

• Infections• Meningitis / encephalitis

• Primary headache disorders• Crash migraine• Exertional or coital headache(HASA)• Cluster headache

• Rare causes• Pituitary apoplexy• Cervical artery dissection

TCH - Venous sinus thrombosis

• Headache onset usually sub acute but 10% of CVST present as TCH

• CT normal in over 50% presenting as headache and raised ICP

• MRI (V) investigation of choice

• OCP,IBD,post partum• Anticoag >=6 mo

RCVS

• RCVS affects patients of all ages and has a female preponderance.

• Recurrent thunderclap headaches or cryptogenic stroke, especially post partum /vasoactive drugs.

• Removal of precipitants such as vasoactive substances, lowering of blood pressure when highly increased(PRES), control of seizures

RCVS• Diagnostic criteria for Reversible Cerebral Vasoconstriction

Syndrome:

• • Acute and severe headache (often thunderclap) with or without focal deficits or seizures

• • Uniphasic course without new symptoms more than 1 month after clinical onset

• • Segmental vasoconstriction of cerebral arteries shown by indirect (eg, magnetic resonance or CT) or direct catheter angiography

• • No evidence of aneurysmal subarachnoid haemorrhage

• • Normal or near-normal CSF (protein concentrations <100 mg/dL, <15 white blood cells per µL)

• Complete or substantial normalisation of arteries shown by follow-up indirect or direct angiography within 12 weeks of clinical onset

• Lancet Neurol 2012; 11: 906–17

Previous names for reversible cerebral vasoconstriction syndrome

• Isolated benign cerebral vasculitis

• • Acute benign cerebral angiopathy

• • Reversible cerebral segmental vasoconstriction

• • Call or Call-Fleming syndrome

• • CNS pseudovasculitis

• • Benign angiopathy of the CNS

• • Post-partum angiopathy

• • Migraine angiitis

• • Migrainous vasospasm

• • Primary(idiopathic) thunderclap headache*

• • Cerebral vasculopathy

• • Vasospasm in fatal migrainous infarction

• Calabrese LH et al Ann Intern Med 2007; 146: 34–44.

RCVS

TCH – idiopathic thunderclapheadache

• Has been referred to as benign vascular headache, crash migraine, benign sexual (coital) headache type II

• Onset over 30 seconds, may last days

• 1/3 get recurrence with precipitants e.g. exercise, sexual activity

• 40% have history of migraine

• May have abnormal angiograms with alternating constriction and dilatation(RCVS)

Headache associated with sexualactivity (= coital headache)

• Usually men, usually bilateral• Type 1 – dull pain, increasing in intensity as sexual excitement increases –

associated with tensing of the face, neck, and shoulders• Type 2 – vascular type, onset at orgasm, usually fades by 2 hrs• 25-50% have had migraine or family history of migraine

Differentiated from SAH by duration of headache?(4-11% of SAH occurs during sexual activity)

• Usually no vomiting, meningism, focal symptoms• CT scan if first presentation• Responds to ß blockers

Related to benign exertional headache• Type 3 – like low pressure headache after LP - ? Due to dural tear

TCH - pituitary apoplexy

• Sudden infarction or haemorrhage into pituitary gland – usually adenoma

• Uncommon

• Headache, opthalmoplegia

• CT may be normal

TCH – cervical artery dissection

• Headache common presenting symptom in ICA dissection

• Headache and Horner’s think dissection

• 15% of ICA dissections may present as TCH

Other important Causes of headache

• GCA

• Glaucoma

• CO

• IIH