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Year 3 Neuroscience > Headaches > Flashcards

Headaches Flashcards

1
Q

What is tension headache?

A

Generalised headache, feeling like a dull, ‘tight band’ around the head, with predilection for involving the frontal and occipital regions.

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2
Q

What are the types of tension headache?

A

Chronic (over 7 headache days/month) or episodic.

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3
Q

What is the pathophysiology of tension headache?

A
  • Pathophysiology is associated with raised CNV activity. CNV releases inflammatory agents that lead to sensitisation of peripheral trigeminal afferents to muscular contraction (unlike in migraines where the nociceptors are the meninges and blood vessels). This is called peripheral sensitisation.
  • As such, pain arises from pericranial muscle contraction.
  • Chronic tension headache also leads to central sensitisation, associated with generalised hyperalgesia
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4
Q

What is ‘pericranial’?

A

Periosteum of the skull.

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5
Q

What are the risk factors for tension headache? (x5)

A

Psychological stress, lack of sleep, missing meals, medication overuse/withdrawal, premenstrual.

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6
Q

What is the aetiology of medication overuse/withdrawal and headache?

A
  • Medication withdrawal: usually hypertension medication, antihistamines, caffeine, opiates, corticosteroids
  • Medication overuse: more than 15 days per month on a patient with pre-existing headache disorder, as a result of regular overuse of headache medication e.g., paracetamol, NSAIDs. Patients either develop a new type of headache or experience deterioration of a pre-existing headache
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7
Q

What are the symptoms and signs of tenson headache? (x4) Exclusions?

A
  • Generalised head pain: often bilateral, non-throbbing, predilection for involving the frontal and occipital regions. NOT worsened by physical activity.
  • Pericranial tenderness
  • Tenderness in other muscles such as SCM, trapezius, temporalis, lateral pterygoid and masseter
  • Photophobia and phonophobia uncommon
  • N&V EXCLUDES diagnosis.
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8
Q

What are the investigations for tension headache? (x3)

A
  • Investigations needed only to exclude other diagnoses
  • BLOODS: ESR should be normal. Raised in temporal arteritis differential
  • CT/MRI if suspicion of secondary headache disorders
  • LUMBAR PUNCTURE: if suspicion of meningitis
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9
Q

How is tension headache managed: Acute? Chronic?

A
  • ACUTE: simple analgesics
  • CHRONIC: antidepressants (amitriptyline) and muscle relaxants (tizanidine) have proven effective
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10
Q

What are the complications of tension headache?

A

Can progress to analgesia-overuse headache (also called rebound headache) due to chronic use of analgesics.

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11
Q

How are analgesia-overuse headaches managed?

A

Stop all medication. Will get worse before it gets better.

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12
Q

What is a migraine?

A

Severe episodic headache that may have a prodrome of focal neurological symptoms called aura and is associated with systemic disturbance.

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13
Q

What are the classifications of migraine? (x5)

A

Migraine with aura (classical migraine) and without aura (common migraine). There is also familial hemiplegic (migraine with aura including muscle weakness), ophthalmoplegic (pain around eye), and basilar (aka brainstem aura associated with headache originating from base of brain).

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14
Q

What is the pathophysiology of migraine? Aura?

A
  • Pathophysiology is associated with neurogenic inflammation of the first division of CNV, serotonin, and bradykinin.
  • First division of CNV innervates the large vessels and meninges.
  • In migraine, there is raised CNV activity resulting in release of inflammatory agents that lead to sensitisation of peripheral trigeminal afferents to the meningeal vessels and meninges (unlike in tension headache where the nociceptor is the pericranial musculature). This is called peripheral sensitisation.
  • As such, the pulsating, throbbing pain of a migraine is associated with the previously ignored stimuli of meningeal vessel pulsations being interpreted as painful.
  • Aura occurs before or at the same as the headache. It occurs as a result of cortical spreading depression (decreased neuronal activity) which is associated with intracranial vasoCONSTRICTION resulting in localised ischaemia. Meningeal vasodilation occurs AFTER this event – this dilation is what leads to the progression to headache.
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15
Q

What is the epidemiology of migraine: Prevalence? Gender? Age?

A

Prevalence is 6% in males and 15-20% in females (3:1). Usual onset is adolescence or early adulthood.

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16
Q

What are the risk factors for migraine? (x6)

A

Stress, exercise, lack of sleep, oral contraceptive pill, high altitude, and certain foods e.g., caffeine, alcohol, cheese, chocolate.

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17
Q

What are the symptoms of migraine? (x8)

A
  • POUND
  • P – pulsatile or pounding
  • O – 0 hours, or one day duration
  • U – unilateral (bilateral in 30%)
  • N – nausea/vomiting
  • D – disabling intensity
  • Photophobia
  • Phonophobia (loud noises)
  • May be preceded by aura that may include visual disturbance, flashing lights, spots, blurring, zigzag lines (fortification spectra – see photo), blindspots (called scotoma), or other sensory symptoms such as tingling or numbness in limbs.
18
Q

What would chronic headache of a similar character to migraine suggest?

A

Most migraine attacks are episodic. Chronic lasting several weeks suggest either analgesia-overuse headache or secondary headaches.

19
Q

What are the investigations for migraine?

A
  • Investigations needed only to exclude other diagnoses
  • BLOODS: ESR should be normal. Raised in temporal arteritis differential
  • CT/MRI if suspicion of secondary headache disorders
  • LUMBAR PUNCTURE: if suspicion of meningitis
20
Q

What must be ensured before lumbar puncture is performed?

A

Do not perform until space-occupying lesion has been excluded because can lead to herniation of cerebellar tonsils.

21
Q

How are migraines managed in A&E? (x4)

A
  • Rescue therapy: metoclopramide (dopamine antagonist), promethazine (antihistamine), ‘triptans’ (5-HT1 agonists)
  • IV antiemetic
  • High-flow oxygen (may provide effective acute treatment)
  • Offer IV corticosteroid such as dexamethasone to prevent recurrence
22
Q

How is migraine managed (when not presenting to A&E)? (x4)

A
  • NSAID such as naproxen (or paracetamol)
  • Antiemetics
  • Triptans may be used instead of or in addition to NSAID if severe symptoms
  • ADVICE: encourage hydration, regular meals and sleep, caffeine restriction, stress management, rest in dark room during episodes, beware of analgesia-overuse headaches
23
Q

How are migraines managed prophylactically? (x2, x3 and x1)

A
  • MENTSTRUAL CYCLE: magnesium oxide and triptan
  • AURA (or predominant depression): anticonvulsant (topiramate – anti-epileptic), TCA (amitriptyline), beta-blockers
  • HEMIPLEGIC/BASILAR: calcium-channel blocker
24
Q

What are the complications of migraine?

A

Can progress to analgesia-overuse headache due to chronic use of analgesics.

25
Q

What is the prognosis of migraine?

A

Usually, chronic.

26
Q

What is a cluster headache?

A

Unilateral headache attacks lasting 15-180 minutes, associated with autonomic symptoms secondary to parasympathetic hyperactivity and sympathetic hypoactivity.

27
Q

What are the types of cluster headache? (x2)

A
  • Episodic cluster: at least two periods of attacks lasting from 7 days to 1 year when untreated, separated by remission periods lasting at least 3 months
  • Chronic: attacks that occur for 1 year or longer without remission, or with remission periods lasting less than 3 months
28
Q

What is the epidemiology of cluster headache: Type? Gender? Age?

A

90% have episodic, 10% chronic. 3:1 male to female ratio. Onset is between 20 and 40.

29
Q

What are the risk factors cluster headache? (x5)

A

History of head trauma, heavy cigarette smoking, heavy alcohol intake, sleep apnoea, familial inheritance.

30
Q

What is the pathophysiology of cluster headache?

A

TRIGEMINAL AUTONOMIC REFLEX: Nociceptive information from pain-sensitive structures in the face, particularly the dura mater and cerebral blood vessels, is carried to the brainstem via the trigeminal nerve to the trigeminocervical complex (TCC). Information is sent to the hypothalamus, thalamus and cortex via pain-processing pathways. Within the TCC, these afferent fibres activate the cranial parasympathetic system and causes the autonomic features seen in an attack. Neurotransmitters released at these PSNS synapses also cause further irritation to the trigeminal sensory nerve endings which potentiates the reflex further.

31
Q

What are the signs and symptoms of cluster headache? (x3 +5)

A
  • THREE CARDINAL SIGNS:
  • Trigeminal distribution of pain: strictly unilateral (though may switch sides between attacks), excruciating, sharp, sometimes described as pulsating, orbital, supra-orbital and/or temporal areas are affected. On average, 4 attacks per day.
  • Ipsilateral cranial autonomic symptoms: ptosis, conjunctival injection, LACRIMATION, rhinorrhoea, nasal stuffiness, eyelid and facial swelling, aural fullness, facial sweating, and redness.
  • Circadian/circannual pattern of attacks
  • ADDITIONAL SYMPTOMS:
  • Most patients become very restless or agitated during an acute attack, unlike people with migraine who often report motion sensitivity during attacks
  • N&V
  • Photophobia
  • Phonophobia
  • Aura seen in approximately 14% of patients.
32
Q

What are the investigations for cluster headache? (x3)

A
  • CT/MRI: eliminate secondary causes
  • ESR: exclude giant cell arteritis in patients over 50
  • PITUITARY FUNCTION TESTS: including TFTs, LH, FSH, cortisol may suggest secondary causes resulting from a pituitary oedema.
33
Q

What is trigeminal neuralgia? Characterised by? (x2)

A

Facial pain syndrome in the distribution of at least 1 division of the trigeminal nerve. It is characterised by (i) combination of sudden attacks of sharp, stabbing pain lasting up to 2 minutes or/and (ii) constant component of facial pain without associated neurological deficit.

34
Q

What is the sensory function of the trigeminal nerve?

A

The sensory function of the trigeminal nerve is to provide tactile, proprioceptive, and nociceptive afference to the face and mouth.

35
Q

What are the branches of the trigeminal nerve?

A

V1 ophthalmic, V2 maxillary and V3 mandibular.

36
Q

What is the aetiology of trigeminal neuralgia? (x6)

A
  • Nerve compression (85% of patients) at root by an aberrant vascular loop (usually superior cerebellar artery – see photo) or rarely by a tumour
  • Demyelinating disease such as MS
  • Brainstem lesions such as from amyloidosis or calcium deposition along the sensory pathway
  • Trauma to trigeminal nerve
  • Denervating procedure
  • Facial herpes zoster virus
37
Q

What is the pathophysiology of trigeminal neuralgia?

A

Disease is believed to arise from myelin loss.

38
Q

What is the epidemiology of trigeminal neuralgia: Gender? Age?

A

Higher in women. Increasing incidence with age.

39
Q

What are the different types of trigeminal neuralgia? (x6)

A
  • Classic trigeminal neuralgia (Type 1)
  • Atypical trigeminal neuralgia (Type 2)
  • Trigeminal neuropathic pain – secondary to injury
  • Trigeminal deafferentation pain – secondary to intentional denervating procedures
  • Symptomatic TN – where the pain is a symptom of an underlying pathology such as tumour
  • Post-herpetic TN – from outbreak of facial herpes zoster
40
Q

What are the signs and symptoms of trigeminal neuralgia?

A

Facial pain: excruciating, sharp and shooting in Type 1; aching and throbbing in Type 2. Mostly unilateral, though can be bilateral in symptomatic TN.

41
Q

What are the investigations for trigeminal neuralgia? (x3)

A
  • Diagnosis is usually clinical
  • INTRA-ORAL X-RAY: only required if dental cause of pain is suspected
  • MRI: considered if diagnostic uncertainty to demonstrate presence of abnormal vessel loop or identify other pathologies
  • TRIGEMINAL REFLEX TESTING: abnormal reflex is suggestive of symptomatic TN

Year 3 Neuroscience (14 decks)

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