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Neurology > Headache > Flashcards

Headache Flashcards

1
Q

What is the estimated prevalence for headache over the past year?

A

Half of adult population estimated

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2
Q

Pain sensitivity of cranial structures - what is pain sensitive?

A

Pain sensitive: cranial venous sinuses with afferent veins
Arteries at the base of their brain and their major branches
Arteries of the dura
Dura near the base of the brain and large arteries
Dural cranial and extracranial nerves
All extracranial structures

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3
Q

Neurotransmitters - headaches

Which neuromodulators and neuropeptides are involved?

A

Serotonin, dopamine, glutamate, oxytocin, noradrenalin

CGRP, PACAP, orexin, neurokinin A, Substance p

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4
Q

Headache classifications

A
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5
Q

What headaches are primary headaches?

A
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6
Q

Define migraine

A

Brain disorder caused by altered regulation (neurotransmitters) due to dysfunction of central brain stem functions, and therefore control of sensory afferents (pain sensitive structures)

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7
Q

Phenotype the headache

A

Presenting headache:
constant or episodic
Site: unilateral or bilateral/holocranic
Headache load: frequency/duration/severity
Character of pain: throbbing, stabbing etc
Precipitating factor
Previous history of headaches

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8
Q

… level of serotonin are associated with migraines

A

Low levels

Useful for proposing treatment (Triptan’s - serotonin agonist)

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9
Q

What to be wary of when taking sumatriptan?

A

High blood pressure, uncontrolled due to vasoconstriction affect

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10
Q

… hypersensitivity leads to the associated symptoms of migraine which include
Nausea, vomiting
Yawning

A

Dopamine hypersensitivity

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11
Q

Cortical spreading depression helps explain

A

Aura

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12
Q

Migraines are more common in who?

A

Females - more prevalent around menstruation

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13
Q

Are migraines increased or reduced during pregnancy?

A

Reduced - increase in oestrogen

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14
Q

Treatment for migraine

A

Lifestyle - avoid triggers, hydrate, reduce caffeine, alcohol
Regular meals
Good sleep hygiene
Exercise
Triptans - decrease CGRP release
NSAIDS - decrease prostaglandin secretion
Antiemetic - decrease dopamine sensitivity
Botox in small doses

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15
Q

Tension headache

A

Pain > 4 hours
No migraine features
Often bilateral
Prefers to be still

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16
Q

Migraine

A

Pain > 4 hours
+++ migraines features
Unilateral or bilateral
Prefers to be still

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17
Q

Cluster headache

A

Pain <4hours
Prominent autonomic symptoms
Side-locked
Agitated

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18
Q

Tension headache - common causes

A

Stress, anxiety, depression, lack of sleep, poor posture

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19
Q

Red flags in clinical assessment - headache

A
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20
Q

Giant cell arthritis:

A
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21
Q

Classification of headache

A
22
Q

Red flags in headaches

A
23
Q

Tension headaches

A 
Associated with stress
Symmetrical (30mins - 7hours)
Gradual onset
Band of pressure around forehead
Acute management - NSAID, paracetamol 
Prevention - stress relief (yoga, massage, cool flannel to forehead, acupuncture)
Prophylaxis such as amitriptyline
24
Q

Migraine

A

Migraine - unilateral, pulsating, associated with aura, N+V, photophobia, phonophobia
Risk factors such as FH, previous episodes, unavoidable exposure to trigger
Aura may precede headache (5-60min before)
4-72 hour lasting

25
Q

Management of headache (overview)

A

Propranolol over topiramate in women of childbearing ages (Reduced hormonal contraception effectiveness and teratogenic potential)
Propranolol - not in asthma, depression or vascular disease

26
Q

Temporal arteritis (also known as …)

A

GCA
Sudden onset unilateral localised headache with scalp tenderness
Jaw claudication and visual changes (partial or total visual loss in one or both eyes)
Risk factors include poly myalgia rheumatica, female and over 55 years old
To investigate, temporal artery biopsy which will show skip lesions in temporal arteritis - also useful to do bloods such as CRP and ESR

27
Q

GCA is a medical emergency ! How do we detect and manage?

A

Jaw claudication
Visual loss
Intermittent Diplopia (double vision)
Treat with prednisolone 60mg and aspirin 75mg and urgent rheumatologist review
If any visual symptoms - same day ophthalmology review essential
Temporal arteritis but no visual changes or jaw claudication, start on prednisolone 40mg and aspirin 75mg and refer to rheumatology within 3 days
Signs and symptoms resolve - continue prednisolone for 12-18 months
Give PPI and blue steroid card!

28
Q

What is given in GCA?

A

Prednisolone 60mg
Aspirin 75mg
Urgent rheumatology review (+/- ophthalmology if visual changes)

29
Q

Cluster headache - overview

A

Severe pulsating periorbital pain - autonomic symptoms such as Lacrimation, Ipsilateral eyelid oedema, ptosis, rhinorrhea, conjunctival injection and sweating
Pain tends to be short lived and is relieved by physical activity
Patients during an episode appear restless and pace during episodes
Long periods of time without any headache, and then suddenly have a cluster (episodic)
Chronic cluster headache - do not go longer than a month without
Acute treatment - 100% high-flow O2 mask through a non-rebreathe mask for at least 20 mins
SC/Nasal triptans in acute attacks
If first attack, refer to neuro for diagnosis for prophylactic treatment such as verapamil
Stop smoking and reduce alcohol

30
Q

Cluster headache management

A

Acute treatment - 100% high-flow O2 mask through a non-rebreathe mask for at least 20 mins
SC/Nasal triptans in acute attacks
If first attack, refer to neuro for diagnosis for prophylactic treatment such as verapamil
Stop smoking and reduce alcohol

31
Q

Severe pulsating periorbital pain - autonomic symptoms such as Lacrimation, Ipsilateral eyelid oedema, ptosis, rhinorrhea, conjunctival injection and sweating
Pain tends to be short lived and is relieved by physical activity
Patients during an episode appear restless and pace during episodes
What headache is this?

A

Severe pulsating periorbital pain - autonomic symptoms such as Lacrimation, Ipsilateral eyelid oedema, ptosis, rhinorrhea, conjunctival injection and sweating
Pain tends to be short lived and is relieved by physical activity
Patients during an episode appear restless and pace during episodes
Long periods of time without any headache, and then suddenly have a cluster (episodic)
CLUSTER HEADACHE

32
Q

Trigeminal neuralgia - overview

A

Unilateral facial pain that’s described as a shooting pain in territory of trigeminal nerve (cheek/jaw)
Irritation of the nerve = makes it worse (Cold air, closing jaw, touch)
Autonomic symptoms also
Attacks = few seconds to several minutes
May have remission for a long time
Caused by compression of the trigeminal nerve (intracranial mass, MS, aneurysm, stroke, trauma, iatrogenic)
Management - carbamazepine

33
Q

No red flags in trigeminal neuralgia, treat with…

A

Carbamazepine

If red flags, refer to secondary care

34
Q

Subarachnoid haemorrhage, also known as…

A

Thunder clap headache
Sudden onset severe headache with reduced cognition/consciousness
Meningism

35
Q

Thunder clap headache is called….

A

Subarachnoid headache
‘Thunder clap headache’
Sudden onset severe headache with reduced cognition/consciousness
Meningism

36
Q

Subarachnoid headache - 2 types?

A

Traumatic - head injury
Spontaneous - absence of trauma
RF for spontaneous = PKD, Ehlers-Danlos syndrome and neurofibromatosis as they cause intracranial aneurysms (berry aneurysms) to develop

37
Q

RF for spontaneous subarachnoid haemorrhage?

A

= PKD, Ehlers-Danlos syndrome and neurofibromatosis as they cause intracranial aneurysms (berry aneurysms) to develop

38
Q

PKD, Ehlers-Danlos syndrome and neurofibromatosis are all risk factors for subarachnoid haemorrhage - why?

A

= PKD, Ehlers-Danlos syndrome and neurofibromatosis as they cause intracranial aneurysms (berry aneurysms) to develop

39
Q

Investigations in subarachnoid haemorrhage

A

CT head - hyperdense areas, indicative of an acute bleed
12 hours later - Lumbar puncture can be done to confirm if CT was negative
Positive lP = Xanthochromic and a normal or raised opening pressure
Can do a CT intracranial angiogram to visualise the source of the bleed such as the aneurysm
High risk of re bleeding - so refer to neurosurgeons if confirmed diagnosis

40
Q

Venous Sinus thrombosis - overview

A

Less common than other headache causes - half of patients with this will have sagittal sinus thrombosis
Cerebral infarction can happen
Risk factors - history of sinusitis, meningitis, facial cellulitis, otitis media, dehydration, pregnancy, COCP

41
Q

Risk factors for venous sinus thrombosis

A

Risk factors - history of sinusitis, meningitis, facial cellulitis, otitis media, skull fracture, dehydration, pregnancy, COCP

42
Q

Presenting signs and symptoms in …

A

venous sinus thrombosis

43
Q

venous sinus thrombosis - signs and symptoms?

A

CN6 - reduced eye abduction

44
Q

How to diagnosis venous sinus thrombosis?

A

MR venogram

Raised intracranial pressure - MRI brain or CT head non-contrast

45
Q

There are several red flags that are essential to determine in the history that may indicate a serious underlying cause of headache that requires further investigation. These can be remembered by the mnemonic ‘HEADACHE PAINS’:

A

H - Head injury (any history of trauma?)
E - Eye pain +/- autonomic features
A - Abrupt onset (i.e. thunderclap headache)
D - Drugs (analgesia overuse or since new drug started)
A - Atypical presentation or progressive headache
C - Change in the pattern or recent-onset new headache
H - High fever and systemic symptoms
E - Exacerbating factors (worse on lying/standing, sneezing, coughing, exercise)
P - Pregnancy or puerperium
A - Age (onset > 50 years)
I - Immunosuppressed (e.g. systemic therapy, HIV)
N - Neoplasia (current or past history of cancer)
S - Swollen optic discs (papilloedema)

46
Q

Low-risk features

There are a number of features that act as indicators that the cause of headache is unlikely to be secondary to a serious underlying disorder. The presence of all these features is usually a good indicator that further investigations (e.g. imaging) are not required.

A

Age ≤ 50 years
Presence of typical features of primary headaches
History of similar headache
No abnormal neurologic findings
No concerning change in usual headache pattern
No high-risk comorbid conditions
No new or concerning findings on history or examination

47
Q

Some of the major findings on clinical examination that would be considered high risk include;

A 
Focal neurological deficits
Global reduction in consciousness
Cranial nerve neuropathy
Seizure activity
Meningism (headache, neck stiffness, photophobia)
Fever
Presence of papilloedema
48
Q

Examples of possible imaging modalities include:

A

CT head (without contrast): useful in acute situations to quickly screen for major pathology (e.g. bleeding, space-occupying lesion)
CT head (with contrast): may be requested if there is a concern of a metastatic deposit or infective cause
CT angiography: this uses contrast and assesses the cerebral vessels. Essential if there is concern about a vessel abnormality (e.g. dissection, aneurysm)
CT venogram: this is utilised if there is suspicion of a cerebral venous thrombosis
MRI head: provides a very detailed assessment of the brain and surrounding structures to assess for secondary causes of headache

49
Q

Lumbar puncture

A lumbar puncture involves the insertion of a spinal needle into the subarachnoid space to take a sample of cerebrospinal fluid (CSF). The CSF can then be analysed for a variety of components to enable a formal diagnosis. Examples include:

A

Subarachnoid haemorrhage: analyse for breakdown products of blood (e.g. bilirubin, xanthochromia)
Meningitis: analyse for microscopy, culture and sensitivity with a viral PCR
IIH: check the opening pressure, which will be elevated

50
Q

It is estimated that among patients who present to A&E with a ‘thunderclap headache’ only …% will have a subarachnoid haemorrhage.

A

It is estimated that among patients who present to A&E with a ‘thunderclap headache’ only 8% will have a subarachnoid haemorrhage.

51
Q

The most concerning of these causes is a subarachnoid haemorrhage. However, other causes of a ‘thunderclap headache’ can include:

A 
Arterial dissection
Cerebral venous thrombosis
Reversible cerebral vasoconstriction syndrome
Intercerebral haemorrhage
Meningitis
Pituitary apoplexy
52
Q

Exacerbating and relieving factors

This involves establishing what make the headache better and what makes the headache worse. It is important to determine whether there are any features of a low or high-pressure headache that refers to changes in intracerebral pressure:

A

Low-pressure headache: worse on sitting or standing. Known as an orthostatic headache. Results from not enough CSF (e.g. a leak). Other features include dizziness, tinnitus, and visual changes.
High-pressure headache: worse or lying down, bending over or straining. Typically worse in the early morning. May be associated with nausea, vomiting, visual changes and low consciousness (depending on acuity and severity). Results from any cause of a raised intracranial pressure (e.g. tumour, IIH, abscess).

Neurology (32 decks)

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