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Neurology > Primary and secondary headache syndromes > Flashcards

Primary and secondary headache syndromes Flashcards

1
Q

What is the most common cause of episodic headache?

A

Migraine

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2
Q

What are some triggers of migraine?

A

Sleep deprivation
Diet (E.g. Caffeine, Chocolate)
Stress
Hormonal changes
Physical exertion
Oral contraceptive
Hunger

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3
Q

Describe the pathophysiology of migraine without aura

A
  1. Triggers cause changes in the brain which causes release of serotonin
  2. Blood vessels constrict and dilate
  3. Chemicals including substance P irritate nerves and blood vessels, causing pain
  4. This causes sensitisation of trigeminal neurones, making normally innocuous stimuli (E.g. Movement, light and sound perception) painful and uncomfortable
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4
Q

Describe the pathophysiology of migraine with aura

A
  1. Cortical spreading depolarisation in the migraine centre of the brain (dorsal raphe nucleus, locus coeruleus)
  2. Activation of the trigeminal vascular system causes dilation of blood vessels
  3. Release of substance P, neurokinin A, CGRP
  4. This causes sensitisation of trigeminal neurones, making normally innocuous stimuli (E.g. Movement, light and sound perception) painful and uncomfortable
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5
Q

How will a migraine present?

A

Unilateral throbbing headache, occasionally preceded by an aura, associated with nausea, vomiting, photophobia and photophobia

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6
Q

What is a migraine prodrome?

A

A condition occurring 24-48 hours before the onset of a migraine headache, affecting 1 in 10 migraine sufferers

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7
Q

What are some symptoms of migraine prodrome?

A
  • Mood changes
  • Behavioural changes
  • Yawning
  • Hunger
  • Cravings
  • Fatigue
  • Hyperactivity
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8
Q

What is a migraine aura?

A

A fully reversible visual, sensory, motor or language symptom, lasting 20-60 minutes associated with migraine onset

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9
Q

What are some aura symptoms?

A

Scotoma
Central fortification
Hemianopic loss

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10
Q

What are the diagnostic criteria for migraine without aura?

A
  • At least 5 attacks
  • 4-72 hours
  • 2 of: moderate/severe, unilateral, throbbing pain, worst movement
  • 1 of: autonomic features, photophobia/phonophobia
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11
Q

What are some forms of atypical migraine ?

A
  • Acephalgic - no headache
  • Basilar - very nauseating, vertigo
  • Retinal, opthalmic
  • Hemiplegic (familial/sporadic)
  • Abdominal - more common in young children
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12
Q

What are some non-pharmacological management options for migraine?

A
  • Set realistic goals
  • Education - avoid triggers
  • Headache diary
  • Relaxation/stress management
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13
Q

What are some acute pharmacological management options for migraine?

A

NSAIDS (Taken as early as possible)
Triptans (5HT agonist)
Anti-emetic is gastroparesis

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14
Q

What are some examples of triptans?

A

Rizatriptan
Eletriptan
Sumatriptan

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15
Q

What are some prophylactic management options for migraine?

A
  • Amitriptyline
  • Propranolol
  • Topiramate
  • Acupuncture
  • Relaxation exercises
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16
Q

What are some other pharmacological management options for chronic migraine

A

Botulinum toxin
Anti-calcitonin gene related peptide (Anti CGRP)

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17
Q

How do anti-CGRP drugs work?

A
  • CGRP is a protein that triggers receptors which open up pain pathways related to the start of migraine
  • Anti-CGRP agents designed to stop this action
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18
Q

What are some examples of anti-CGRP drugs?

A

Atogepant
Rimgepant

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19
Q

What is a tension headache?

A

An attacks headache (usually bilateral) which is pressing or tightening in quality and of mild to moderate intensity lasting minutes to days

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20
Q

What are some associations with tension headache?

A
  • Stress
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
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21
Q

How does tension headache usually present?

A
  • Bilateral non-throbing headache
    • Episodic or chronic
    • Pressing tingling quality
    • Mild to moderate
  • Absence of N+V
  • Absence of photophobia or phonophobia
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22
Q

What are some possible clinical signs of tension headache?

A

They may be associated with tenderness of the scalp muscles, as their contraction is the primary source of the pain

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23
Q

How are tension headaches managed?

A
  • Simple analgesics
  • Relaxation physiotherapy
  • Reassurance
  • Anti-depressants (Dothiepin, amitriptyline)
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24
Q

What is intercranial pressure?

A

The pressure exerted by the cranium onto brain tissue, CSF and intracranial circulating blood volume

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25
Q

What are some possible causes of raised ICP?

A
  • Mass efect (E.g. tumour)
  • Brain swelling (E.g. due to ischaemia)
  • Increase in central venous pressure (E.g. Venous sinus thrombosis)
  • Problems with CSF flow
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26
Q

What are some abnormalities of CSF flow that can cause raised ICP?

A

Obstructive hydrocephalus - Masses, chiari syndrome

Increased production - Choroid plexus papilloma

Decreased absorption (Communicating hydrocephalus) - SAH, Meningitis, malignant meningeal disease

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27
Q

What is the normal ICP?

A

7-15mmHg

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28
Q

What is the Monroe-Kellie doctrine?

A

A compensatory mechanism for expanding masses:
- Immediate: decrease in CSF volume by moving it out of FM, decrease in blood volume by squeezing sinuses

- Delayed: decrease in ECF
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29
Q

Calculation for cerebral perfusion pressure

A

MAP - ICP

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30
Q

Calculation for cerebral blood flow

A

CPP ÷ Cerebral vascular resistance

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31
Q

What are some mechanisms that can allow for auto regulation of cerebral blood flow?

A

Pressure auto regulation - arterioles dilate or constrict in response to changes in BP or ICP

Metabolic autoregulation - arterioles dilate in response to chemicals e.g. CO2

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32
Q

Wha are some early sigs of raised ICP?

A
  • Decreased level of consciousness
  • Headache
  • Pupillary dysfunction +/- papilloedema
  • Changes in vision
  • Nausea and vomiting
33
Q

What are some later signs of raised ICP?

A
  • Coma
  • Fixed, dilated pupils
  • Hemiplegia
  • Bradycardia → Cushing’s triad
  • Hyperthermia
  • Increased urinary output
34
Q

What are some symptoms of venous sinus thrombosis?

A
  • Progressive headache
  • Visual changes
  • Seizures
  • Focal neurological deficits
35
Q

What are some risk factors for venous sinus thrombosis?

A
  • Oral contraceptives
  • Dehydration
  • Clotting disorders
36
Q

How is venous sinus thrombosis diagnosed?

A

CT/MR venography

37
Q

How does giant cell arteritis present?

A
  • Unilateral headache
  • Systemic features (Malaise, polymyalgia)
  • Very high ESR
  • In those over 55
38
Q

How is GCA treated?

A

Rapid symptom relief with steroids (60-80mg prednisolone per day)

39
Q

How is GCA diagnosed?

A

Confirm with temporal artery biopsy (-ve result does not exclude diagnosis)

40
Q

What is normal pressure hydrocephalus?

A

Idiopathic disease of the elderly, possibly due to decreased brain elastance

41
Q

How does normal pressure hydrocephalus present?

A

Hakim’s triad:
- Abnormal gait
- Urinary incontinence
- Dementia

42
Q

What investigations are required in normal pressure hydrocephalus?

A

LP, lumbar drain test, lumbar infusion studies

43
Q

How is normal pressure hydrocephalus managed?

A

VP shunt, medium-low or low-pressure valve

44
Q

What is idiopathic intercranial hypertension?

A

Condition characterized by increased intracranial pressure (pressure around the brain) without a detectable cause (Probably results from reduced CSF resorption)

45
Q

Who is most at risk of idiopathic intercranial hypertension?

A

Typically develops in younger, overweight female patients, many of whom have polycystic ovaries

46
Q

How does idiopathic intercranial hypertension present?

A
  • Headache
  • Double vision, visual blurring
  • Tinnitus
  • Radicular pain
  • Morning N+V
  • Papilloedema → 25% severe/permanent visual loss
47
Q

What investigations are required in idiopathic intercranial hypertension?

A
  • No ventricular dilation → normal CT
  • LP, CT/MR head, CTV, fundoscopy +/- opthalmology review
48
Q

How is idiopathic intercranial hypertension managed?

A
  • Weight loss
  • Carboanhydrase inhibitors - acetazolamide, topiramate
  • Ventricular atrial/lumbar peritoneal shunt
  • Monitor visual fields and CSF pressure
49
Q

How is raised ICP initially managed?

A
  • Maintain head in midline to facilitate blood flow
  • Loosen tube ties, collars etc.
  • HoB 30-45 degrees elevation
  • Avoid gagging, coughing etc.
  • Decrease environmental stimuli
  • Treat hyperthermia
  • Maintain fluid balance and electrolytes
  • Maintain normocarbia
50
Q

What medical treatment is required in raised ICP?

A
  • Diuretics - hypertonic saline
  • Barbiturate coma
  • Antiepileptics
51
Q

What are some surgical options for managing raised ICP?

A
  • Surgical decompression
  • Other surgical treatment - remove mass lesions, CSF diversion
52
Q

What are trigeminal autonomic cephalgias?

A

Primary headache syndromes characterized by severe short-lasting headaches accompanied by paroxysmal facial autonomic symptoms

53
Q

What are some autonomic features of trigeminal autonomic cephalgias?

A

Ptosis
Miosis
Nasal stuffiness
Nausea/vomiting
Tearing
Eye lid oedema

54
Q

What investigations are required in trigeminal autonomic cephalgias?

A

Those with new onset unilateral cranial autonomic features require imaging - MRI brain and MR angiogram

55
Q

What are some examples of trigeminal autonomic cephalgias?

A

Cluster headache
Paroxysmal hemicrania
Hemicrania continua
SUNCT (Short-lasting Unilateral Neuralgiform headache with Conjunctival injection and Tearing)

56
Q

Who is most at risk of cluster headache?

A
  • More common in 30s-40s, more common in men
57
Q

How does cluster headache present?

A
  • Recurrent, sudden, unilateral periorbital headaches (Worst pain anyone can feel)
  • Headaches last 15 minutes to 3 hours, occurring once or twice a day in cycles of 4-12 weeks occurring at the same time each day (Alarm clock headache)
  • Autonomic symptoms - watery and bloodshot eye, lacrimation, rhinorrhoea, miosis, ptosis, lid swelling, and facial flushing
  • Behaviour - Agitated, can lead to suicide
58
Q

How are acute attacks of cluster headaches managed?

A
  • High flow O2 100% for 20 mins
  • Subcutaneous or nasal triptan
  • Steroids (reducing course over 2 weeks)
59
Q

What can be used for cluster headache prophylaxis?

A

Verapamil

60
Q

What is paroxysmal hemicrania?

A

A severe debilitating unilateral headache usually affecting the area around the eye

61
Q

Who is most at risk of paroxysmal hemicrania?

A

More common in 50s-60s, more common in women

62
Q

How does paroxysmal hemicrania present?

A
  • Severe unilateral headache
  • Unilateral autonomic features
  • 10-30 mins duration
  • 1-40 a day
63
Q

How id paroxysmal hemicrania managed?

A

Absolute response to indomethicin

64
Q

What is hemicrania continua?

A

Hemicrania continua describes a continuous, fluctuating, pain present on one side of the head

65
Q

Who is most at risk of hemicrania continua?

A

More common in 50s-60s, more common in women

66
Q

How does hemicrania continua present?

A
  • Severe unilateral headache
  • Unilateral autonomic features
  • Constant duration
67
Q

How is hemicrania continua managed?

A

Absolute response to indomethicin

68
Q

What is SUNCT?

A

Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing

69
Q

How does SUNCT present?

A
  • Unilateral neuralgiaform headache
  • Short-lived (15-120 secs)
  • Conjunctival injections
  • Tearing
70
Q

How is SUNCT managed?

A
  • Lamotrigine
  • Gabapentin
71
Q

What is trigeminal neuralgia?

A

Long-term pain disorder that affects the trigeminal nerve

72
Q

Who is most at risk of trigeminal neuralgia?

A

More common in elderly (>60 years) women

73
Q

What are some possible triggers of trigeminal neuralgia?

A

Stimulation of one or more trigger zones in the face (E.g. Washing, shaving, a cold wind and chewing)

74
Q

What is the theorised cause of trigeminal neuralgia?

A

Possibly caused by trigeminal nerve compression

75
Q

How does trigeminal neuralgia present?

A
  • Severe stabbing unilateral stabbing facial pain - occurs in the distribution of CN V
  • Attacks last 1-90 secs
  • Episodes occur many times a day with a refractory period after each
  • Bouts of pain may last weeks-months
  • Spontaneous remissions last months or years before (almost invariable) recurrence
76
Q

What is the main investigation of trigeminal neuralgia?

A

MRI brain

77
Q

What are the medical management options of trigeminal neuralgia?

A
  • Carbamazepine (1st line)
  • Gabapentin
  • Phenytoin
78
Q
A

Neurology (28 decks)

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