Headache Flashcards
Headaches can be split into Primary and Secondary Types, what would be signs of a secondary headache? [6]
- Trauma
- First or worst ever headache
- Thunderclap onset
- A new daily & persistant headache
- A change in the headaches pattern or type
- Other symptoms such as jaw claudication, fevers, neuro signs/symptoms or worsened by position
What could cause a thunderclap headache [4]
- intracranial aneurysm (saccular ‘berry’ aneurysms)- accounts for around 85% of cases, conditions associated with berry aneurysms include hypertension, adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
- arteriovenous malformation
- pituitary apoplexy
- mycotic (infective) aneurysms
What causes most subarachnoid haemorrhages? [1]
Aneurysms
Do we order CT head or lumbar puncture to diagnose SAH?
- NCCT Head: acute blood, hyperdense/bright on CT in basal cisterns, sulci, ventricles
- If CTH within 6h and normal, dont do LP
- If CTH >6h and normal, do LP because LP should be at least 12h following onset of sx to allow development of xanthochromia.
Define a thunderclap headache? [2]
Describe a few other associated features with SAH.
Thunderclap headache: High intensity [1] peaking instantly or within 1-5 minutes of onset [1]
* nausea and vomiting
* meningism (photophobia, neck stiffness)
* coma
* seizures
* ECG changes including ST elevation may be seen- this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines
What types of CNS infection cause thunderclap headache [3]
If the patients headache comes with fever, rash or: [1]
Meningitis [1]
Encephalitis [1]
What is the triad of meningism [4]
Describe presentation of encephalitis [3]
What could raise [4] or lower Intracranial pressure [2]?
Headache, neck stiffness, and photophobia, often with nausea and vomiting.
Encephalitis- Altered mental state, seizures, focal neuro symptoms/signs
Raised ICP:
- Hydrocephalus
- Cerebral Abscess
- Glioblastoma/Meningioma
- Venous sinus infarct
Lowered ICP:
- Dural CSF leak either spontaneously or after LP
What are the specific signs of raised ICP? [6]
Progressively worse headache
Worse in morning/wakes them up
Worse on flat, valsalva (poop/cough/strain) or on exertion
Neurological symptoms
Seizures
Visual obscurations and pulsatile (whooshing) tinnitus
What indicates an intracranial hypotension [3] and how do we approach it? [2]
Headache appearing/worsening on standing and lessening/resolving on lying down [2]
Sagittal MRI of brain and spine will show an empty subarachnoid space [1]
Conservative: Bed rest, fluids, analgesia, caffeine [1]
Epidural Blood patch (to stimulate healing of a CSF leak) [1]
What is an epidural blood patch? [3]
A treatment for leaking CSF that causes lowered ICP [1]
Put some of the patients blood in their epidural space [1] which will cause irritation leading to healing of the leak [1]
What is Giant Cell Arteritis [3] and what about a headache would indicate it [2]?
Giant cell granulomatous inflammation of the arteries [1] causing narrowing which can cause an infarction [1] to the brain and/or optic nerve [1]
The headache is diffuse persistant and may be severe
What are the symptoms of giant cell arteritis? [4]
What is an associated condition [1]
- Diffuse, persistant and severe headache
- Jaw claudication (pathognomonic)
- Visual Disturbance eg blindness, diplopia
- Scalp Tenderness
Associated with PMR
GCA
Ix [5]
Dx [1]
Mx [1]
ESR/CRP/Platelets all elevated
Anemia, high ALP
Confirm with a temporal artery biopsy
Treat with prednisolone 60mg
What are the main types of Primary Headache? [4] + [3]
Indicate the most common cause of primary headache*
- Tension-Type*
- Migraine
- Medication Overuse Headache
- Trigeminal Neuralgia
And the Trigeminal Autonomic Cephalagias:
- Cluster headache
- Paroxysmal Hemicrania
- SUNA/SUNCT
TTH
Presentation [4]
Cause/mechanisms [1]
- Mild, bilateral
- Described as ‘tight band’
- Worse towards end of day
- Not aggravated by ADL
Mechanism
- Muscular due to persistent contraction
What are the subtypes of Tension Type headache? [2]
Episodic - <15 days a month
Chronic - >15 days a month
TTH
Approach [3]
Rx [3]
Second line [2]
Reassurance
Reduce psychological stress
Reduce analgesic over-use
Aspirin, paracetamol or NSAIDs
2nd line: TCA
Define Migraine? [4]
Describe subtypes [2]
Nature of headache [3]
Chronic episodic attacks [1] featuring phono/photophobia, functional disability and nausea. [3]
Types:
- Migraine with Aura (33%)
- Common migraine
Nature of headache: unilateral throbbing headache, 2-48h, less than 2x weekly
What triggers a migraine? [8]
- Barometric pressure/humidity.
- Sleep (lack or excess).
- Dietary intake, e.g. cheese, caffeine, alcohol.
- Stress (either excess or in periods of relief)
- Physical exertion.
- Loud noise.
- Bright light.
- Hormonal changes such as puberty, menses and menopause.
What is an “aura”? [4]
Describe visual [3], basilar [4], hemiplegic [1] and retinal auras [1]
A set of transient neurological symptoms [1] lasting 15-60 minutes.[1]
Can be of visual, sensory or motor type [1]
Often precedes headache [1]
Visual forms: - Foritifications (zigzags) - Flashing lights - Scintillating scotoma (migraine with occipital origin)
Basilar
- Bilateral visual symptoms
- Unsteadiness, vertigo,
- Dysarthria
- Limb paresthesia, LOC
Hemiplegic
- Unilateral paralysis persisting few days after headache settled
Retinal
- Unilateral visual loss reversible
What defines a Chronic Migraine? [3]
Headaches >15 days a month for >3 months [2]
Of which atleast 8 a month must be migraines [1]
Migraine management
2 approaches [7]
First line: simple analgesia, anti-emetics
Abortive:
- Triptan 5HT AGONIST & NSAIDs
- Adjunctive metoclopromide
Prophylactic: considered when headaches occur more than 3-4x a month.
- Propanolol
- Anti-epileptics topiramate 5HT ANTAGONIST
- Tricyclic Antidepressants Amitripytyline
- Acupuncture
- Botulinum toxin A
What should we be aware of in pregnant women with migraines? [2]
Dont give antiepileptics to those of child-bearing age as they’re teratogenic
Treat pregnant women with paracetamol or propanolol/Amitriptyline prophylactically
Define a medication overuse headache? [2]
Headache >15 days a month [1] developed or worsened on regular symptomatic medications [1]
What causes a medication overuse headache? [5] List the duration of time used to induce such a headache
- Triptans
- Ergots
- Opiods
More than 10 days a month
Or simple analgesics used more than 15 days a month
Also caffeine overuse
Where do Trigeminal Autonomic Cephalagias present with pain?
In the orbital, supraorbital and temporal regions
What do SUNA/SUNCT stand for? [2]
What are the autonomic symptoms that accompany Trgimenial autonomic cephalalgias [3]
Short Lasting Unilateral Neuralgiform headache
With either Autonomic symptoms
Redness, lacrimation, lid swelling
Horner’s syndrome
Nasal congestion
Cluster headache
- Clinical features [5]
- Unilateral sharp/throbbing pain
- Rapid onset and 15 min-2h minutes duration
- Incredibly severe
- Often comes with migranous symptoms such as nausea, aura and photo/phonophobia
- Patient restless and agitated
Also remember Autonomic symptoms with all TACs
Why are cluster headaches so named?
Triggers [1]
Pattern [1]
They are episodic, occuring in clusters [1] typically lasting 1-3 months with anything from 1-8 a day during an attack [1]
The bouts may be triggered by alcohol [1] and may feature continuous background level pain
They may show circadian rhythmicity with bouts coming the same time every year and attacks the same time each day [1]
How do you treat a cluster headache?
Acute [2]
Abortive
Prevention [2]
Acute: 100% O2, injectable sumatriptan,
Abortive: steroids, greater occipital nerve blockade (depomedrone)
Prevention: Verapamil, lithium, methylsegide for prevention
Describe a paroxysmal hemicrania? [5]
Unilateral sharp/throbbing pain Rapid onset, duration 2-30 minutes Very severe Possible continuous background pain 2-40 attacks per day without circadian rythm
How do we treat Paroxysmal Hemicrania?
SE [2]
Prophylactic Indomethacin (An NSAID) systemic upset, nephrotoxic
Describe SUNCT? [5]
Unilateral Stabbing/pulsing pain Short 10-240 second duration Triggered by wind/cold/touch/chewing 3-200 attacks a day Comes with conjunctival injection (red eye) and tears
How do we treat SUNCT? [1]
Lamotrigine prophylactically (an anti-epileptic, same for SUNA)
Describe Trigeminal Neuralgia [4]
Unilateral stabbing pain [1] unlike TACs its to the maxillary/mandibular regions [1] 5-10 second duration Also triggered by wind/cold/touch/chew 3-200 a day Unlikely to have autonomic symptoms
How do we treat Trigeminal Neuralgia? [3]
Gabapentin for pain relief
Carbamazepine prophylactic
Surgical vascular loop decompression
Name a tricyclic antidepressant and what headaches its used for? [3]
Amitriptyline
- Prophylaxis of Tension Type Headaches
- Prophylaxis of Migraines
How do you differentiate the types of TACs?
Frequency
Duration
Pain characteristic
Frequency:
CH = 1-8 PH = 1-40 SUNCT = 3-200
Duration:
CH = 15-180 mins PH=2-30mins SUNCT = 5-240 seconds
I.e. frequency and duration are inversely proportional
Pain is sharp and throbbing in CHs & PHs but stabbing/pulsing or burning in SUNCT
All have a very severe pain
CH most likely to show circadian rythmicity
Summary of Treatments for Headache Types: Thunderclap TTH Migraine MOH Trigeminal neuralgia Cluster headache Paroxysmal hemicrania SUNA/SUNCT
Thunderclap - Probably SAH - Coiling/clipping
Tension Type Headache - Aspirin/NSAID/Paracetamol + Amitryptiline
Migraine - Aspirin/NSAID/Triptan + Propanalol/Anti-epileptic/Amitryptiline
Medication Overuse Headache - Use less meds
Trigeminal Neuralgia - Carbamazepine
Cluster Headache - 100% O2/SC Sumatriptan + Verapamil
Paroxysmal Hemicrania - Prophylactic Indometacin NSAID
SUNA/SUNCT - Anti-epileptic Lamotrigine
SAH
Further investigation and management
After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
* CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
* +/- digital subtraction angiogram (catheter angiogram)
Management of a confirmed aneurysmal subarachnoid haemorrhage
supportive
* bed rest
* analgesia
* venous thromboembolism prophylaxis
* discontinuation of antithrombotics (reversal of anticoagulation if present)
* vasospasm is prevented using a course of oral nimodipine
* intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
* most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
Complications of aneurysmal SAH [5]
- re-bleeding - happens in around 10% of cases and most common in the first 12 hours, if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged, associated with a high mortality (up to 70%)
- hydrocephalus- temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
- vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset, ensure euvolaemia (normal blood volume)- consider treatment with a vasopressor if symptoms persist
- hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
- seizures
