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Headache Dr Viviana Elliott Consultant Physician Acute Medicine

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Headache. Dr Viviana Elliott Consultant Physician Acute Medicine. Aims. To provide a practical approach to the diagnosis and management of patients presenting with headache. Objectives. To be able to understand the causes of headache To be able to classify headaches in clinical practice - PowerPoint PPT Presentation

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HeadacheDr Viviana Elliott

Consultant Physician Acute Medicine

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Aims• To provide a practical approach to the diagnosis

and management of patients presenting with headache

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Objectives• To be able to understand the causes of headache• To be able to classify headaches in clinical

practice• To be able to organise a management plan for

patients presenting with headache• To be able to identify headache that you can’t

miss

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Headache

• 2.5 % of new emergency attendance• 15 % will have a serious cause

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Which structures in the head ache?

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Pain sensitive structures• Dura• Arteries• Venous sinuses• Para-nasal sinuses• Eyes• Tympanic membranes • Cervical spine

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Classification of headaches• Primary headache• Secondary headache

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Primary headache

• Migraine • Cluster headache• Tension Headache

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Secondary Headaches• Head Trauma• CNS infection• Vascular disease• Intracranial pressure disorders• Other common causes of headache

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Head trauma• Subdural• Extradural

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CNS infection• Meningoenchephalities• Cerebral abscess

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Vascular disease• Subarachnoid haemorrhage (SAH)• TIA/Stroke• Subdural- extradural- intracerebral haemorrhage• Arterial dissection• Cerebral Venous sinus thrombosis (CVST)• Giant cell arteritis (GCA) and vasculitis

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Intracranial pressure disorders• Tumours• Idiopathic intracranial hypertension• Intracranial hypotension• Hydrocephalus • Intermittent ( eg Colloid cyst)

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Other common headaches• Sinusitis• Glaucoma• Hyponatraemia• Toxins: alcohol excess and withdrawal• Drugs: calcium channel blockers and nitrates• Coital migraine/cephalgia

50% previous migraineExclude SAH

40 -80 mg Propanolol before intercourse

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History taking• The most important investigation in the evaluation of

headaches is HISTORY• First question to answer ourselves is whether it is a

PRIMARY or SECONDARY headache syndrome.• Any important red flags in history or examination to

consider investigation for a secondary headache

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History• Onset• Frequency• Periodicity• Duration• Time to maximum intensity• Time of the day• Recurrence• One type or more than one headaches• Life style

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Primary HeadachesFeatures Tension Migraine Cluster

Painlocation

Bilateral Unilateral orbilateral

Unilateral ( around eye , above eye along the side of the head/face

Pain quality Pressing/ tightening (non pulsating)

Pulsating (throbbing)

Variable ( sharp, burning, throbbing or tightening)

Pain intensity Mild or moderate Moderate to severe

Severe or very severe

Effect on activities Not aggravated by routine activities or daily living

Aggravated by, or causes avoidance of routine activities or daily living

Restlessness or agitation

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Features Tension Migraine Cluster

Other symptoms None Usual sensitivity to light and/or sound or nauseas and /or vomitingAuraSymptoms can occur with or without headache and: - are fully reversible - develop over at least 5‘-Las 5-60’Typical aura includes visual symptoms such as flickering lights, spots or lines and or partial loss of vision; sensory symptoms such as numbness and/ or pins and needles; and/ or speech disturbance

On the same side as the headache:-Red and or watery eye-Nasal congestion and/or runny nose-Swollen eyelid-Forehead and facial sweating-Constricted pupil and/or drooping eyelid

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Features Tension Migraine Cluster

Duration 30’ to continuous 4-72 hours 15’ to 180 ‘

Frequency < 15 per month < 15 per month 1 every other day to 8 per day with remission > 1 month

Diagnosis “Episodic tension headache”

“Episodic migraine”( with or without aura)

“Episodic cluster headache”

Frequency 15 per month for more than 3 months

15 per month for more than 3 months

1 every other day with continuous remission < 1 month in a 12 month period

Diagnosis “ Chronic tension headache”

“Chronic migraine”( with or without aura)

“ Chronic cluster headache”

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Features Tension Migraine ClusterAcute Treatment

AspirinNSAIDParacetamol

Oral triptan and NSAID or triptan and paracetamolMonotherapy : oral triptan , NSAID, aspirin (900 mg) or paracetamol.Add anti-emetic if nauseas or vomiting

Oxygen 100% at a 12 litres per minute with no reb-reathing mask and a reservoir bag ( arrange home oxygen or ambulatory oxygen) or nasal triptan

Prophylaxis 10 sessions of acupuncture over 5-8 weeks ( chronic tension headache)

Topiramte (risk of malformation in pregnant woman) or propanpolol . If unsuitable or uneffective 10 sessions of acupuncture over 5-8 weeks or Gabapentin 1200 mg/d

Verapamil with specialist advice and ECG monitoring.

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Note on treatment of migraine• All treatments should take into account the

person’s preference, co morbidities, risk of adverse events and the impact of the headache on their quality of life.

• People who are on another form of prophylaxis eg amitriptyline and who’s migraine is well controlled should continue with the same treatment

• Continue prophylaxis for 6 months• Riboflavin 400 mg once a day may reduce the

frequency and intensity of the migraines for some people.

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Atypical Aura in Migraine that needs imaging

• Motor weakness or• Double vision or• Visual symptoms affecting only one eye• Poor balance• Decrease level of consciousness

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Menstrual related migraine

• Migraine that occurs 2 days before and 2 days after the start of menstruation in at least 2 out of 3 consecutive menstrual cycles

• Diagnose menstrual related migraine using a headache diary for at least 2 menstrual cylces

• Treatment if no response with standard acute treatment consider frovatriptan (2.5 mg bd) or zolmitriptan (2.5 mg bd or tds) on the days that the migraine is expected.

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Medication overuse headacheHeadache developed or worsened while taking thefollowing drugs for 3 months or more:• triptans, opioids, ergots or combination analgesic

medication on 10 days per month or more.• Paracetamol, aspirin or an NSAID either alone or

in combination, on 15 days per month or more

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Treatment• Advice to stop ( abruptly) overused medication for

a month.• Advice that headache will be worse before it

improves ( withdrawal ). Close follow up and support.

• Consider prophylaxis for primary headache• No need for admission• Referral to specialist only if use of strong opioids ,

relevant co-morbidities or unsuccessful attempts

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Important headaches that you can’t miss (Secondary headache)

• GlioMe

Acute SAH

Cerebral Venous thrombosis

Glioma

Temporal arthritis

Meningitis

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“SNOOP – T” Red flags for secondary headaches• Systemic symptoms ( fever weight loss) or Secondary risk factors: systemic disease, cancer or HIV• Neurological symptoms +/- abnormal signs ( confusion impair alertness or consciousness and focal sign)• Onset: sudden, abrupt or split of a second or worsening and progressive• Older

new onset and progressive headache specially in middle age, > 50 years ( giant cell arthritis)

• Previous headache history first headache or different ( significant change in attack frequency,

severity or clinical features• Triggered Headache by Valsalva, exertion or sexual intercourse

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Bacterial Meningitis• High level of suspicious if fever and altered

consciousness!!!• Acute bacterial meningitis is an important fatal

medical emergency- early recognition saves lives!!• Prompt initiation of antibiotics• Confirm diagnosis & pathogen with CSF analysis via

lumbar puncture• Still obtain CSF even if antibiotics commenced eg

Polymerase Chain Reaction (PCR) for bacteria DNA

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Subarachnoid haemorrhage• Commonest potentially life threatening acute severe headache 1-3% headaches presenting to A&E• 1/3 present with acute onset of severe headache as only

symptom!• Headache characteristics - Acute or Abrupt Thunderclap”

Instantaneous 50%Seconds< minute 25%1-5 minutes 20%Over 5 minutes zero

• “Worse ever” : more likelihood• Transient lost of consciousness or epileptic seizure

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CT Brain ASAP !( sensitivity decreases with time)

• First 12 hs 96 – 100%• Within 24 hs 92 – 95 %• Within 48 hs 86 %• At 5 days 58 %• At 7 days 50 %• After 2 weeks 30 %• After 3 weeks almost nil

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Chronology of CSF abnormality in CSF• 12 hs should elapse before CSF analysis for

xanthochromia –immmediate centrifugation– Red cell lysis in the CSF to billirubin and

oxyhaemoglobin

•Xanthochromia reliably present >12 hs and up to 2 weeks of SAH

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Management of SAH• Call a friend : Neurosurgery• Analgesia & anti-emetics• Reduce secondary ischemia

Nimodipine 60 g 4 hrly• Supportive care to reduce brain insult

Adequate hydration > 3 lts of saline daily Avoid hypotension Avoid hypoxia• Early Neurovascular MDT• Complications: Hydrochephalus

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Giant Cell arteritis

• Affects large/medium size arteries• Microscopically infiltration of lymphocytes, macrophages,

histiocytes and multinucleates giant cells• Vessel are tender, red, firm and pulsless with scalp

sensitivity• Risk of blindness if not treated

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Presentation• Rare before 50• Female > male• Insidious onset• Often associated with jaw claudication on chewing• Headache localised to the superficial occipital or

temporal arteries, throbbing and worse at night• 75% raised CRP and ESR• Diagnostic biopsy with in 2 weeks• Prednisolone 60 mg

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Cerebral Venous Sinus ThrombosisHeadache presentation

• Acute/ subacute progressive “headache plus” syndromePapilloedema “ idiopathic intracranial hypertension” mimicSymptoms of raised ICP

VI nerve palsy Focal signs Seizures Enchephalopathy

• Acute Thunderclap – SAH like presentationCT –ve, CSF negative -Consider specially if raised CSF OP

• New daily persistent headache• Isolated headache !!!

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CVST: appropriate investigations

• D-Dimer level?Abnormal in 96% with enchephalopathyNormal in ¼ with isolated headache

• Brain MRI/MRV (T2)Sinus occlusion

Venous haemorrhage Venous infarction• CT venogram

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CVST: management- anticoagulation• Low molecular weight heparin or IV Heparin• 3-6 months Warfarin• Thrombolisis?• Treatment of comorbidities, seizures and increased

ICPConsider Anticardiolipin antibody syndrome,Thrombotic & Homocystein screenCancer CNS and ENT infectionSystemic inflammatory disease/Behcets

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Carotid dissection

A hemorrhage into the wall of the carotid artery,separating the intima from the media and leading toaneurysm formation. Suspect in• Blunt trauma? Post RTA• Rotational forces? Manipulation• Spontaneous

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Acute Cervical arterial dissectionInternal carotid artery dissection (ICAD)• Unilateral headache/face pain + neck +/- Contra lateral stroke or TIA

Vertebral artery dissection (VAD)• Occipital-nuchal headache +/- posterior circulation TIAs

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CAD Investigations• MRI Brain and neck & MRA

(Carotid & vertebral) Crescent shaped intramural haematoma & vessel occlusion Identifies ischemic brain tissue > clearly• CT brain & CTA of cervical vessels Tapering lumen, vessel occlusion• Rarely Catheter angiogram Intimal flap +/- double lumen path gnomonic seen in <10 %

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Management of carotid artery dissection

• “Ring a friend” neurology• Aspirin vs anticoagulation

3-6 month therapy

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Conclusions• Remember that history is the most important clue• Describe a classification useful in clinical practice

Primary headache (migraine – cluster - tension)

Head TraumaCNS infection Vascular diseaseIntracranial pressure disorders

• Remember “SNOOP – T” • Don’t miss: Brain tumours, Giant arteritis, carotid

dissection, meningitis and SAH !

Snoop-T

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Questions?