CBL - Headache Flashcards

1
Q

What are the important components of the history in a patient with headache? [8]

A
  1. Aura
    • typically reversible visual, sensory or language symptoms
  2. Location
    • facial/retro-orbital/frontal/occipital/parietal; unilateral/bilateral, radiation/spread of pain
  3. Onset
    • thunderclap or gradual onset
  4. Severity
    • (can be scored out of 10)
  5. Associated symptoms
    • nausea/vomiting
    • photophobia
    • phonophobia
  6. Periodicity
    • frequency, duration; is the patient headache-free between attacks?
  7. Exacerbating/relieving factors
  8. Concerns, fears, anxieties about headaches and their underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the ‘red flag’ features in a patient with a headache? [8]

A
  1. Age >50 years at onset of headache symptoms;
  2. Thunderclap headache (i.e. headache reaches maximal intensity in <5 minutes)
  3. Focal/non-focal neurological deficit;
  4. Worsening of symptoms with posture (high/low CSF pressure headache), valsalva (coughing, straining during defecation) or physical exertion
  5. Early morning headaches
  6. Previous history of cancer (higher risk of metastatic tumour deposit)
  7. Systemic symptoms:
    • fever
    • weight loss
  8. Temporal artery tenderness/jaw claudication specifically suggestive of temporal arteritis in >65 years age group
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the symptoms of visual aura and how long do they typically last? [9]

A
  1. “Positive” symptoms:
    • flickering lights,
    • spots,
    • zig zag lines,
    • tingling
  2. “Negative” symptoms:
    • visual loss
    • numbness
  3. Symptoms characteristically evolve over 25 minutes and resolve within 60 minutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the typical symptoms of migraines? [6]

A
  1. can be unilateral or bilateral
  2. associated nausea
  3. photophobia (sensitivity to light)
  4. phonophobia (sensitivity to sound)
  5. interference with daily activities
  6. can get clustering of headaches around menstrual periods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the possible triggers for migraines? [5]

A
  1. stress
  2. alcohol
  3. caffeine
  4. hunger
  5. sleep deprivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical signs of raised intracranial pressure? [4]

A
  1. Papilloedema on fundoscopy
  2. Constriction of visual fields
  3. Enlargement of the blind spots
  4. Unilateral or bilateral 6th nerve palsy may be a false localising sign of raised ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the differential diagnoses for migraine? [3]

A
  1. Episodic headache without “red flag” features
  2. Tension-type headache
  3. Trigeminal autonomic cephalgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the pathogenesis of migraine [7]

A
  1. Migraines are considered a neurovascular disorder
  2. Attacks probably result from dysfunction within sensory brainstem nuclei
  3. The pain results from interactions between components of the trigeminovascular system:
    • the pain-sensitive cranial blood vessels,
    • the trigeminal nerve fibres that innervate them and
    • the cranial parasympathetic outflow
  4. The aura phase of migraine is associated with reduction blood flow in hemispheric regions contralateral to affected symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the management of a migraine under the following headings:

  1. lifestyle factors? [3]
  2. acute management? [3]
  3. prophylaxis? [3]
A
  1. Lifestyle factors
    • Advise patients to avoid triggers identified
    • Reduce caffeine and alcohol intake
    • Encourage regular meals and good sleep patterns
  2. Acute management
    • Analgesia
      • Paracetamol
      • Aspirin
      • Ibuprofen
    • Triptans
      • Highly selective 5-HT1 agonists
      • Can be given orally, subcutaneously or by nasal spray
    • Antiemetics
      • Prochlorperazine
      • Metoclopramide
      • For nausea
  3. Prophylaxis
    • Beta-blockers (e.g. propranolol)
    • Tricyclics (e.g. amitriptyline)
    • Anti-epileptic drugs (e.g. topiramate, sodium valproate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a sudden-onset or thunderclap headache? [2]

A
  1. high-intensity headache in which the time from onset of symptoms to reaching its maximal intensity is minutes.
  2. in most cases of subarachnoid haemorrhage (SAH) this only takes a few seconds and patients often describe the pain as the “worst headache of life”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the important components of the history of a patient with suspected thunderclap headache? [7]

A
  1. Location of pain;
  2. Severity of pain;
  3. Time to reach maximal intensity;
  4. What was patient doing at onset of pain?
  5. Associated features:
    • nausea,
    • vomiting,
    • photophobia,
    • neck stiffness
  6. Focal neurological deficit
  7. Exacerbating/relieving features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the red flag features in a typical thunderclap headache description and what do they suggest? [4]

A
  1. Headache is of sudden-onset
  2. Neurological deficit:
    • e.g. generalised seizure followed by diplopia
  3. Worsening of headache with coughing
    • suggests raised intracranial pressure
  4. Neck stiffness and photophobia
    • suggest meningism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the differential diagnoses for a thunderclap headache? [6]

A
  1. SAH
  2. Intercerebral haemorrhage
  3. Cerebral venous sinus thrombosis
  4. Arterial dissection (vertebral or carotid)
  5. Bacterial meningitis
  6. Primary thunderclap or exertional headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the risk factors for subarachnoid haemorrhage?

  1. modifiable? [3]
  2. non-modifiable? [5]
A
  1. Modifiable:
    • Cigarette smoking
    • Hypertension
    • Alcohol excess
  2. Non-modifiable:
    • Previous SAH
    • Polycystic kidney disease
    • Connective tissue diseases e.g. Ehler’s Danlos, Marfan syndrome)
    • Arteriovenous malformations
    • Strong family history (>2 first-degree relatives)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a positive Kernig’s sign and what is it suggestive of? [2]

A
  1. When the hip and knee are flexed at 90° and subsequent extension at the knee is painful
  2. Headache, photophobia, neck stiffness and a +ve Kernig’s sign suggests meningism (irritation of the meninges)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the presentation of a CNIII nerve palsy? [3]

A
  1. Dilatation of pupil
  2. Eye is deviated down and out
  3. Ptosis
17
Q

What are the causes of CNIII nerve palsy? [3]

A
  1. Aneurysm of the posterior communicating artery
  2. Tumour compressing the parasympathetic fibres that supply pupillary constrictor muscles that run along the outside of the 3rd nerve
  3. An isolated, pupil-sparing, complete 3rd nerve palsy in a diabetic patient is likely to be due to small vessel ischaemia
18
Q

What investigations should you carry out on a patient with suspected subarachnoid haemorrhage? [4]

A
  1. Bloods
    • FBC
    • U&Es
    • LFTs
    • Glucose
    • Coagulation screen
    • CRP
  2. ECG
    • Check for ischaemic changes
  3. Non-contrast CT of brain
  4. Lumbar puncture
    • If history is suggestive of SAH but there is no blood on the CT brain scan, wait 12 hours and then perform a lumbar puncture
    • look for xanthochromia (yellow discolouration of CSF due to presence of bilirubin as a blood breakdown product)
19
Q

Describe the pathogenesis of subarachnoid haemorrhage [9]

A
  1. The circle of Willis is a collateral network of large arteries situated at the base of the brain within the subarachnoid space, and is surrounded by CSF.
  2. SAH occurs when blood extravasates into this space between the arachnoid membrane and the pia mater.
  3. The most common reason for SAH is trauma.
  4. 85% of spontaneous or non-traumatic SAH result from saccular or Berry aneurysms.
    • these are outpouchings of the intimal layer through the muscular wall of artery.
    • a congenital weakness within the muscular layer, which is later vulnerable to the effects of smoking or hypertension, is responsible for development of Berry aneurysms.
    • Rarer causes of aneurysmal SAH include polycystic kidney disease and connective tissue disease (e.g. Ehlers-Danlos syndrome, Marfan syndrome).
    • 90% of aneurysms develop in the anterior cerebral circulation, most commonly at the bifurcation of the anterior communicating artery and the anterior cerebral artery, the internal carotid artery and the posterior communicating artery and at the middle cerebral artery bifurcation.
  5. Those patients who have a non-traumatic SAH in whom an aneurysm cannot be found are describes as peri-mesencephalic SAH. In general, these patients have a more benign presentation and an improved outcome.
20
Q

What are the common sites for aneurysm formation [4]

A
  1. Anterior communicating artery (most common)
  2. Posterior communicating artery (associated with 3rd cranial nerve palsy)
  3. Basilar artery
  4. Posterior inferior cerebellar artery
21
Q

Describe the management of SAH [13]

A
  1. General measures
    • Fluid resuscitation
    • Analgesia
    • Prevent/treat vasospasm with nimodipine
  2. Definitive measures
    • Endovascular coiling
    • Neurosurgical clipping
  3. Manage complications
    • Rebleeding
    • Hydrocephalus
      • may need extra-ventricular drain
    • Seizures
      • treat with anti-epileptic drugs
    • Hyponatraemia
    • Vasospasm