5.2 Headaches and Pain Flashcards by Mageed Ramadan

What examinations might you do as part of a headache presentation?

1) fundoscopy
2) cranial nerves
3) BP
4) temperature
5) HR
6) skin and neck

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Name three investigations you might do as part of a headache presentation

1) CT
2) MRI
3) inflammatory markers

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What differentiates a primary from a secondary headache?

A primary headache is not caused by underlying disease or structural problems and are therefore not dangerous.

Secondary headaches are caused by something external or an underlying disease and can be harmless or dangerous.

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Name three types of primary headaches and identify which are the more common

1) Migraine - common
2) Tension headache - common
3) Cluster headaches and trigeminal neuralgia

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List 4 causes of Secondary headaches

1) Head trauma
2) Med overuse
3) Cancer
4) Infection
5) Vascular

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Name six potential mechanisms of a headache

SIT RAT

1) Skeletal muscle tension
2) Arterial dilatation
3) Traction on arteries
4) Traction or dilation on venous sinuses
5) Inflammation
6) Referred pain

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Name a potential cause for extracranial and intracranial

a) arterial dilation
b) inflammation

extracranial - migraine
intracranial - hypertension, infection

extracranial temporal arteritis
intracranial -meningitis

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Which mechanism of a headache might occur post lumbar puncture?

Traction or dilation on venous sinuses (when patient sits up)

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Name three things which may cause traction on arteries

1) raised intracranial pressure (ICP)
2) tumour
3) hemorrhage

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What may cause reffered pain that presents as a headache?

Disease of ears /sinuses/c-spine

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How does the prevalence of migraines in M vs F change pre and post puberty?

Name one other non-modifiable predisposing factor

Pre-puberty: M=F

Post-puberty: 1:3 (M:F)

Genetics are a strong component

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What is a migrane?

Recurrent, unilateral headaches +/- aura

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How commonly are auras experienced in migraines?

Which types of auras are most commonly experienced?

20% have auras, usually visual (photophobia) or sensory

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Name six possible precipitating factors for a migraine

Foods, alcohol, emotion, menses, bright light, OCP

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Name the two hypothesized theories explaining the pathogenesis for migraines?

1) Vascular Theory
2) Central Neural Circuitry

BUT theory is unclear

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Describe the 4 stages of a migraine

PAHR:

1) Prodromal fatigue: vague change in mood/appetite
2) Aura phase
3) Headache phase
4) Resolution

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What kinds of management are provided for acute and chronic migraines?

Acute: analgesia, triptans, antiemetic (prevents vomiting)

Chronic: precipitant avoidance, beta blockers/topiramate, acupuncture

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Describe the following features of a tension headache:

a) Time it lasts
b) Sensation
c) Intensity variation throughout the day?
e) frequency

a) 30 min-7 days
b) bilateral pressure, rarely systemic upset and no aura
c) worse during the day
d) ranges from infrequent attacks to daily pain

* most common type of headache in primary care

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How are tension headaches managed?

Lifestyle: stress, alcohol, exercise, mood, med abuse, reassurance

Medication: OTC (paracetamol, ibuprofen), use low dose amitriptyline if experienced for >2days/week

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Compare 5 differences between a migraine and tension headache

Where?

M- unilateral
T- bilateral

Feeling?

M- pulsatile
T- tight band pressure

Aura?

M- yes
T- no

Triggers

M- yes
T- stress

Responsiveness to migraine meds

M- responsive
T- limited response

Describe the sensation and typical frequency of a cluster headache

How common is it?

Bouts of severe orbital pain lasting 15 min-3 hours that occurs frequently- daily for several weeks

Uncommon (M:F 6>1)

How might a cluster headache affect one’s routine differently from a migraine?

Makes patients restless- often wake people during the night

Name 3 symptoms that someone with a cluster headache is likely to experience

Name 2 symptoms/signs which are occasionally experienced

Likely: Conjunctival injection, lacrimation and nasal blockage

Occasionally: ptosis and horner’s syndrome

How are cluster headaches managed?

Acute:

O2
triptan

Prophylaxis:

specialist advice
avoidance of triggers (alcohol, nicotine)
verapamil

List 3 presentations of a brain tumour

1) visual problems 2) vomiting 3) seizures Not commonly headaches

Name 4 types of secondary headaches

1) Temporal arteritis 2) Trigeminal neuralgia 3) Toothache 4) Med overuse headache 5) Meningitis 6) Sinusitis 7) Subarachnoid hemorrhage 8) Raised ICP

Name two things which may cause raised ICP

Tumour or idiopathic intracranial hypertension

Name 7 red flags for a secondary headache

1) Worsening headache with FEVER 2) Sudden onset headache reaching max intensity in 5 MIN 3) PERSONALITY change 4) Impaired level of CONSCIOUSNESS 5) Recent (typically within 3 month) HEAD TRAUMA 6) ORTHOSTATIC headache (changes with posture) 7) NEW ONSET: cognitive dysfunction, neurological deficit

If a headache is triggered by exercise, cough, valsalva or sneeze, what should you think?

RED FLAG!! Secondary headache

Is neck pain or cluster/tension headaches more common?

Neck pain! (Esp in elderly)

What is the most common cause of a headache seen in clinical practice?

Medication overuse (\> brain tumour)

Is a tension headache or temporal arteritis more common?

Tension headache

# Define 'chronic pain' Give 4 examples

Pain which persists beyond the natural healing time– usually \> 3months Commonly * Back pain / shoulder pain / neck pain / pelvic or abdominal pain * Phantom limb

How might 'healing with plasticity' influence one's healing process? (compared to normal healing)

Can lead to hyperalgesia and allodynia, which manifests into chronic pain

List 4 things that inflammation may alter (in terms of neurons/APs)

1) Ion channels on neurons 2) Sensitivity of neurons/receptors 3) Decreases the threshold for firing 4) Alters the trigger for firing

List 4 'central NS' alternations that may occur as a result of chronic pain

1) Spontaneous firing from dorsal horn 2) altered descending inhibition 3) Personality/perception 4) Psychology

Describe CRPS and its associations

COMPLEX: varied and dynamic clinical presentation REGIONAL: non-dermatomal distribution of symptoms PAIN: out of proportion to the precipitating events SYNDROME: constellation of signs and symptoms Linked to the sympathetic nervous system and usually involves a single limb (No correlation between injury and degree of CRPS)

Compare the two types of complex regional pain syndrome, which is more common?

Type 1: no identifiable lesion Type 2: after a nerve injury

Name one example of type 2 CRPS

Causalgia: severe burning pain in a limb following injury to a peripheral nerve

What triad of symptoms may CRPS may present with?

1) Autonomic 2) Sensory; pain may be spontaneous, hyperalgesia, allodynia 3) Motor: weakness, tremor, dystonia, myoclonus

Describe the pain distribution associated with CPRS

Spontaneous, hyperalgesia, allodynia

List 4 signs associated with a CRPS?

1) Distal edema 2) Skin temp and color changes 3) Altered sweating 4) Bone changes (periarticular osteoporosis, joint stiffness)

What are the 3 hypotheses explaining the mechanism behind CRPS?

1) Neurogenic inflammation 2) Autonomic dysfunction 3) Neuroplastic changes in the CNS

How is CRPS managed? (incl pharmacological and non pharmacological)

Pharmacological: Steroids, analgesia, neuropathic meds, sympathetic nerve blocks Non pharmacological: physio, occupational therapy, psychotherapy (CBT)

Explain the general mechanism of CPRS

Name structures of the head and neck which contain pain receptors for: * 4 vessels * 2 general nerves * 2 Muscle locations * 6 other structures

Vessels: extracranial arteries, MMA, large veins, venous sinuses Cranial and spinal nerves Head and neck muscles Meninges, falx cerebri, parts of brainstem, eyes, teeth and lining of mouth

What is thought to be the cause behind tension headaches and cluster headaches?

Tension headaches: activation of peripheral nerves in the head and neck muscles Cluster headaches: over activation of the trigeminal nerve and hypothalamus in the brain (but exact cause is unknown)

What is the mechanism of action for triptan?

Blocks serotonin receptors and constricts blood vessels \*treats migraines