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MD4001 > Headaches > Flashcards

Headaches Flashcards

1
Q

What proportion of the population have tension headache at any time ?

A

40%

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2
Q

What proportion of neurological referrals do headaches account for ?

A

30%

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3
Q

Identify the most common headache types.

A
  • Tension/muscular
  • Migraine
  • Analgesia overuse
  • Systemic illness
  • Cervicogenic
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4
Q

Identify the most serious headache types.

A
  • Subarachnoid Haem
  • Meningitis
  • Tumours
  • Other SOL
  • Temporal arteritis
  • Strokes (including CV sinus thrombosis)
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5
Q

Identify questions to ask about a headache history.

A
  • How long?
  • Position on head?
  • Character (not intensity)?
  • Frequency? When?
  • Diurnal variation?
  • Change in character?
  • Nausea/vomiting?
  • Postural?
  • Other neurological symptoms?
  • PMH, FH
  • Medicines
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6
Q

Identify the timeline, and clinical features of tension headaches.

A

TIMELINE
• Could have been there for weeks, months, years
• Constant, or worse towards evening

CLINICAL FEATURES
• “tightness”, “pressure” all around the head, or on top of the head
• Rarely with nausea

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7
Q

Identify the main treatments for tension headaches.

A

• Reassurance
• Explain the muscles
around the head (in a band, when all of them are under tension, feels painful)
• Reduce analgesia (because patients with tension headaches often take a lot of analgesia which may contribute to headache)
• Use relaxation exercises
• Low dose amitriptyline
• Won’t go away overnight

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8
Q

Identify the timeline, and clinical features of migraines.

A

TIMELINE
• With or without aura, if with then spreads over minutes (most migraine with aura tends to be unilateral)
• Unilateral or bilateral, usually hours-days (common migraine is bilateral without aura)

CLINICAL FEATURES
• Most headache with nausea will be migraine
• Photophobia, phonophobia, gut symptoms
• Pulsating, sharp
• Maybe exacerbated by physical activity
• Often family history
• Triggers (e.g. foods, alcohol, beginning or end of working week, periods)

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9
Q

Are there any epidemiological groups which are especially susceptible to migraines ?

A

• More common in women, especially mid-

cycle, at period and menopause (oestrogen)

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10
Q

What is the mechanism of migraines ?

A

Mechanisms unclear, vascular and neural theories, spreading depression of Leao (2- 5mm/min) (in animals, can stimulate cortex and see change of electrical activity over surface of cortex, which is thought to correlate with development of aura)

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11
Q

Why might you ask a patient to keep a diary ?

A

In migraine, to help decide pattern and treatments

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12
Q

Identify the type of aura which may arise in migraines.

A

Commonest: visual aura (flashing light and blind spot which gradually enlarges, usually jagged, and usually black and white)

Can be more complex and involve weakness, spreading numbness, dysphasia (in such cases, difficult to distinguish from stroke)

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13
Q

Describe migraine treatments.

A

ACUTE (if occasional)
• Triptans – agonists at 5HT- 1b and 5HT-1d receptors (rizatriptan, and other triptans)
• Aspirin, paracetamol
• Anti-nausea (prochlorperazine, metoclopramide), to stop N/V

PROPHYLACTIC (if using too many triptans, switch to prophylactic) (if >2/month)
• Beta blockers (e.g. propranolol)
• Low dose amitriptyline
• Pizotifen (5HT-2a and 2c antagonist, antihistamine, anticholinergic), can induce weight gain

  • Topiramate (anti-epileptic)
  • Sodium valproate (anti-epileptic)
  • Candesartan (ARB inhibitor)
  • Flunarazine (Calcium channel blocker)
  • Lisinopril (ACEi)
  • Methysergide (can cause retroperitoneal fibrosis, don’t use for more than three months at a time)

Sometimes, prophylactic works well for few weeks then stops working because get used to it. At that point, stop propranolol and get into low dose amitriptyline, then when bring back propranolol it will work again. Can cycle treatments.

OTHER
• Botulinum toxin injection into muscles of back of neck (usually every 90 days)
• Anti-CGRP monoclonal antibodies, erenumab, licensed in 2018 for >4 migraines/month UK, (s/c monthly injection), must have tried at least 3 other prophylactics
• Acupuncture

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14
Q

Identify any drugs that women with migraine and aura should NOT use.

A

Women with migraine and aura should not use combined OCP, because much increased risk of stroke (esp estrogen containing pill, progesterone only pill probably safer)

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15
Q

Identify the main clinical features of triG neuralgia.

A

• Shooting pain in one or more divisions of V
• Extremely painful, maybe triggered by cold or
eating

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16
Q

What is a cause of triG neuralgia ?

A

• In younger people consider demyelination (and MS), older people (more common), often abberant blood vessel touching V

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17
Q

Describe treatment for triG neuralgia.

A

Rx Carbamazepine (anti-epileptic), gabapentin (anti-epileptic), injection (into triG ganglion), surgery (if due to aberrant blood vessels touching CNV, can put bit of sponge between them)

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18
Q

What are the main clinical features of TriG autonomic Cephalgia ? What are its main types ?

A
  • (rare) Recurrent pain in trigeminal distribution with autonomic features (eye watering, nasal congestion, redness eye)
  • Commonest of these headaches is cluster headache: unilateral (striking circadian rhythm, same time of day, clustering in periods usually few weeks)
  • Other type is Paroxysmal hemicranias (women>men), shorter, more frequent attacks, responds well to indomethacin, affects one half of the face
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19
Q

Are cluster headaches especially frequent in one epidemiological group ? paroxysmal hermicranias ?

A

Cluster headache: More common in men

Paroxysmal hermicranias: More common in women

20
Q

Describe treatment of TriG autonomic Cephalgia.

A
  • Triptans
  • Oxygen
  • High dose verapamil (up to 960mg/day, high dose) (Calcium channel blocker)
  • Indomethacin for P Hemicrania
21
Q

Describe timeline of medication overuse headache.

A
  • Present for >15 days/month

* If using simple analgesia >15days/month, or >10 days for other acute e.g. triptans

22
Q

Describe clinical features of medication overuse headache.

A

• Worsened while analgesia has been used

23
Q

How do we treat medication overuse headache ?

A

Uncertain whether abrupt cessation, or gradual cessation is better for treatment

Can use amitriptyline low dose to help them get past initial stage of cessation of other treatment.

24
Q

Describe timeline of thunderclap headache.

A

• Instant or rapidly appearing (<60 seconds)

25
Q

Descirbe clinical features of thunderclap headache.

A

Must consider SAH (worst headache anybody every head, can throw up and potentially lose consciousness, photophobia, and neck stiffness from meningism from blood into Subarachnoid space), but can be exertional (coital cephalgia).

26
Q

Describe management of thunderclap headache.

A

• Requires urgent investigation:

  • CT head (looking for blood),
  • Lumbar Puncture (if no blood in CT) after 12 hours (more likely to pick up any blood or altered blood), look for bilirubin (Xanthochromia, yellowing of CSF, which should be gin clear) and oxyhaemaglobin)
  • MRI or CT angiogram if it has three weeks or more since onset of headache (unlikely to pick up anything in CSF)
27
Q

Describe the clinical features of the headache associated with raised ICP.

A
  • Headache usually mild
  • Diurnal variation, worse in morning, often gone by lunchtime
  • May be corse with cough, straining
  • Often also mild nausea
  • Neurological features (e.g. numbness or difficulty with speech)
  • Look for papilloedema in eye
28
Q

What are some causes of raised ICP ?

A

• Tumours, absess, CSF blockage (causing hydrocephalus)

29
Q

Describe management of raised ICP.

A

• Urgent referral and scan

30
Q

Describe the main features of papilloedema in ophthalmoscopy.

A
  • Elevated disc margin
  • Inflammation around it
  • Bleeding (hemorrhagic papilloedema)
31
Q

Identify the main clinical features of meningitis.

A
  • Fever
  • Photophobia
  • Neck stiffness
  • Altered consciousness
  • Petechial rash (if bacterial)
32
Q

What is the aetiology of meningitis ?

A

• Most meningitis is viral, but cannot distinguish clinically

33
Q

Define temporal arteritis.

A

Inflammation (AI disease) of arteries, usually around temporal arteries in side of the head

34
Q

Describe epidemiology of temporal arteritis.

A

Never <50 years of age

35
Q

Describe clinical features of temporal arteritis.

A
  • Maybe features of polymyalgia (aching, esp in proximal muscles, first thing in the morning)
  • Jaw claudication
  • Tender temporal arteries (clinical diagnosis based on this)
  • Danger of blindness (can get infarcts of retina due to compromise of blood supply)
36
Q

Describe management of temporal arteritis.

A
  • Can use ultrasound or temporal artery biopsy (sample error, can sample bit of artery without it but other bits contain it)
  • Use steroids early (due to dangers of blindness) (so try to get diagnosis early)
37
Q

Describe diagnosis of temporal arteritis.

A
  • Clinical diagnosis based on tender temporal arteries

- Raised ESR (above 30) also means possible inflammation

38
Q

Identify the main clinical features of cerebral venous sinus thromboses.

A
  • Headache, often severe
  • Often seizures
  • Maybe bilateral, haem
39
Q

Are any epidemiological groups more vulnerable to cerebral venous sinus thrombosis ?

A

Often female, on OCP

40
Q

Identify any investigations which should be undertake if suspecting a cerebral venous sinus thrombosis.

A

MRI/MRV

41
Q

When might low ICP occur ?

A

After lumbar puncture

BUT can occur spontaneously (esp if leak from cyst at base of spine)

42
Q

Identify the main clinical features of low ICP.

A
  • Headache on standing (pounding severe headache with vomiting), eased with lying
  • Blood patch (blood out of vein of arm and inject into subarachnoid space, so patching up leak in dura) from post LP headache
43
Q

Identify some causes of early morning headaches.

A
  • Obese (may have sleep apnoea)
  • History of snoring
  • Maybe COPD
  • Headache in morning
  • Diagnosis sleep apnoea with CO2 retention
44
Q

Describe investigations and treatment for a common cause of early morning headache.

A

May confirm diagnosis by sleep studies and oxygen saturation levels overnight. Treated with positive airway P ventilation.

45
Q

TRANSIENT GLOBAL AMNESIA

  • What is it
  • When does it occur
  • Clinical features
A

What it is: Thought to be a variant of migraine (NOT a stroke)

  • When does it occur: often arises during stress/exposure to cold
  • Clinical features: period of amnesia where the patient is unable to lay down any new memory, keep repeating the same question over and over again (usually only occurs once)
46
Q

How long do transient global amnesias last ? How is diagnosis performed ?

A

Few minutes to hours

Clinical diagnosis

MD4001 (74 decks)

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