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Year 4 Neurology and Special Senses > Neuro: Headaches > Flashcards

Neuro: Headaches Flashcards

1
Q

Where is the pain in a cluster headache?

A

Severe and unbearable unilateral headaches,
Usually around the eye

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2
Q

Over what time period do cluster headaches tend to occur?

A

Clusters of attacks - 3-4 a day for weeks-months followed by periods of remission

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3
Q

Typical demographics of a patient suffering from cluster headaches?

A

30-50 year old male smoker

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4
Q

Potential triggers of cluster headaches?

A

Alcohol
Strong smells
Exercise

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5
Q

Symptoms of cluster headaches?

A

Severe pain (unilateral, surrounding eye) - ‘suicide headache’
Unilateral:
Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating

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6
Q

Acute management of cluster headaches?

A

Triptans (e.g. sumatriptan 6mg injected subcutaneously)
High flow 100% oxygen for 15-20 minutes (can be given at home)

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7
Q

Drugs that can be used for cluster headache prophylaxis?

A

Verapamil
Lithium
Prednisolone (2-3 week course to break cycle of clusters)

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8
Q

Types of migraine?

A

Migraine with aura
Migraine without aura
Silent migraine - aura without headache
Hemiplegic migraine

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9
Q

How long to migraines typically last?

A

4 to 72 hours

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10
Q

Typical features of migraine?

A

Moderate to severe intensity
Pounding or throbbing in nature
Usually unilateral but can be bilateral
Discomfort with lights (photophobia)
Discomfort with loud noises (phonophobia)
With or without aura
Nausea and vomiting

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11
Q

What is aura (in relation to migraine)?

A

Visual changes associated migraine
- Sparks in vision
- Blurring vision
- Lines across vision
- Loss of different visual fields

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12
Q

A hemiplegic migraine can mimic a stroke which must be ruled out urgently, what are the symptoms?

A

Typical migraine symptoms
Sudden or gradual onset
Hemiplegia (unilateral weakness of the limbs)
Ataxia
Changes in consciousness

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13
Q

Common migraine triggers?

A

Stress
Bright lights
Strong smells
Certain foods (e.g. chocolate, cheese and caffeine)
Dehydration
Menstruation
Abnormal sleep patterns
Trauma

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14
Q

The course of a migraine can be broken down into 5 stages. These stages are not typical of everyone and they will vary between patients. Some patients may only experience one or two of the stages. The prodromal stage can involve several days of subtle symptoms such as yawning, fatigue or mood changes prior to the onset of the migraine. What are the 5 stages?

A
  1. Premonitory or prodromal stage (can begin 3 days before the headache)
  2. Aura (60 minuites)
  3. Headache stage (4-72 hours)
  4. Resolution (the headache can fade away or be relieved completely by vomiting or sleeping)
  5. Postdromal or recovery phase
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15
Q

Acute management of migraine?

A

Paracetamol
Triptans (e.g. sumatriptan 50mg as the migraine starts)
NSAIDs (e.g ibuprofen or naproxen)
Antiemetics if vomiting occurs (e.g. metoclopramide)

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16
Q

When are triptans used?

A

When the migraine starts to develop, abortative therapy

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17
Q

What class of drug are tripatans?

A

5HT receptor agonists (serotonin receptor agonists)

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18
Q

Mechanism of action of triptans?

A

Unclear which mechanism leads to effect on migraine, however they act on:
Smooth muscle in the arteries to cause vasoconstriction
Peripheral pain receptors to inhibit their acitivation
Reduce neuronal activity in the central nervous system

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19
Q

MIgraine prophylaxis?

A

Medications: propranolol, topiramate, amitryptiline
Accupuncture
Headache diary to avoid triggers
B2 supplementation (riboflavin)
Mensuration related: NSAIDs (mefanamic acid) or triptans

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20
Q

Why must patients using topiramate for migraine prophylaxis not get pregnant?

A

It is teratogenic and can cause a cleft lip/palate

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21
Q

Differentials for patients presenting with a headache?

A

Tension headache
Migraine
Cluster headache
Secondary headaches
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Subarachnoid haemorrhage
Analgesic headache
Hormonal headache
Cervical spondylosis
Trigeminal neuralgia
Raised ICP (brain tumour)
Meningitis
Encephalitis

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22
Q

Key red flag symptoms for headaches?

A
  • Fever, photophobia, neck stiffness (meningitis or encephalitis)
  • New neurological symptoms (haemorrhage, malignancy or stroke)
  • Dizziness (stroke)
  • Visual disturbance (temporal arteritis or glaucoma)
  • Occipital headache with sudden onset (subarach)
  • Worse on coughing or straining (raised ICP)
  • Postural/changes with position (raised ICP)
  • Severe enough to wake pt from sleep
  • Vomiting (raised ICP, CO poisoning)
  • History of truama (intracranial haemorrhage)
  • Pregnancy (pre-eclampsia)
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23
Q

What examination can be used to assess whether a headache is secondary to raised ICP?

A

Fundoscopy - papilloedema indicated raised intracranial pressure which may be due to a brain tumour, benign intracranial HTN or and intracranial bleed)

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24
Q

How does tension headaches typically present?

A

Mild ache across the forehead and in a band-like pattern around the head.
This may be due to muscle ache in the frontalis, temporalis and occipitalis muscles.
Tension headaches comes on and resolve gradually and don’t produce visual changes.

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25
Q

What might tension headaches be associated with?

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

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26
Q

How are tension headaches managed?

A

Reassurance
Basic analgesia
Relaxation techniques
Hot towels to local area

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27
Q

Potential causes of secondary headache?

A

Infection, obstructive sleep apnoea or pre-eclampsia
Alcohol
Head injury
Carbon monoxide poisoning

28
Q

Sinusitis headache

A

Sinusitis causes a headache associated with inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses. This usually produces facial pain behind the nose, forehead and eyes. There is often tenderness over the affected sinus, which helps to establish the diagnosis.

Sinusitis usually resolves within 2-3 weeks. Most sinusitis is viral. Nasal irrigation with saline can be helpful. Prolonged symptoms can be treated with steroid nasal spray. Antibiotics are occasionally required.

29
Q

Analgesic Headache

A

An analgesic headache is a headache caused by long term analgesia use. It gives similar non-specific features to a tension headache. They are secondary to continuous or excessive use of analgesia. Withdrawal of analgesia important in treating the headache, although this can be challenging in patients with long term pain and those that believe the analgesia is necessary to treat the headache.

30
Q

Hormonal Headaches

A

Hormonal headaches are related to oestrogen. The produce a generic, non-specific, tension-like headache. They tend to be related to low oestrogen:

Two days before and first three days of the menstrual period
Around the menopause
Pregnancy. It is worse in the first few weeks and improves in the last 6 months. Headaches in the second half of pregnancy should prompt investigation for pre-eclampsia.

The oral contraceptive pill can improve hormonal headaches.

31
Q

Cervical Spondylosis headache

A

Cervical spondylosis is a common condition caused by degenerative changes in the cervical spine. It causes neck pain, usually made worse by movement. However, if often presents with headache.

It is important to exclude other causes of neck pain such as inflammation, malignancy and infection. It is also important to exclude spinal cord or nerve root lesions.

32
Q

What is the first line treatment of trigeminal neuralgia?

A

Carbamazepine

33
Q

How does trigeminal neuralgia present?

A

Intense facial pain
Comes on spontaneuosly
Last seconds to hours
Elecrticity-like shooting pain
Attacks often worsen over time

34
Q

What condition is trigeminal neuralgia associated with?

A

Multiple sclerosis

35
Q

Potential triggers of trigeminal neuralgia?

A

Cold weather
Spicy food
Caffieine
Citrus fruits

36
Q

Branches of trigeminal nerve?

A

Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)

37
Q

What drugs can cause medication overuse headaches?

A

Medication overuse can lead to chronic headache which resolves when the drug is withdrawn. Examples of drugs which can cause this problem are:
1. Paracetamol, aspirin or NSAIDs used for 15 days per month or more
2. Triptans, opioids or ergot preparations for 10 days a month or more

38
Q

What should a comprehensive headache history include?

A

A comprehensive headache history should include:
1. Mode of onset
2. Duration
3. Nature of headache - sharp, dull, throbbing
4. Site of headache - localised, variable, generalised
5. Pattern and timing. - including time of day, relation to menstruation
6. Provoking and relieving factors e.g. coughing, posture
7. Associated symptoms including aura
8. Drug history - particularly analgesic usage

39
Q

Headache red flag symptoms?

A
  1. Thunderclap headache
  2. Associated fever
  3. Meningism +/- non blanching skin rash.
  4. Raised intracranial pressure – headache on waking and worse on lying down, worse on coughing, papilloedema
  5. New neurological deficit
  6. New cognitive dysfunction
  7. Personality change
  8. Impaired or deteriorating conscious level
  9. Recent head injury
  10. New onset headache in elderly - giant cell arteritis
  11. Significant change in pattern of chronic headache
  12. History of malignancy or impaired immunity
  13. Postural headaches – i.e. worse on lying, worse on standing (e.g. post LP headache)
40
Q

What is idiopathic intracranial hypertension? (IIH)

A

Idiopathic intracranial hypertension, also known as pseudotumor cerebri, is a syndrome with signs and symptoms of increased intracranial pressure but where a causative mass or hydrocephalus is not identified.

41
Q

Who is typicall affected by IIH?

A

MIddle aged pts
Female
Obese

42
Q

What conditions is IIH associated with?

A

Endocrine: adrenal insufficiency, cushings disease, hypoparathyroidism, hypothyroidism, excessive thyroxine replacement in children
Drugs: Doxycyline
Chronic Renal failure
SLE
Hyperbitaminosis A (peads)
Dural venous sinus stenosis or web

43
Q

How does IIH present?

A

Headaches
Visual problems (transient or gradual loss)
Pulse-synchronous tinnitus
Photopsia
Eye pain
+/-Papilodema (may be unilateral, bilateral, absent)
Normal neurological examination (sometimes CN6 nerve palsy)
Normal CSF composition with elevated opening pressure

44
Q

Management of IIH?

A

Treatment options include CSF letting, acetazolamide and lumboperitoneal shunts. In patients with progressive visual deterioration, optic nerve fenestration may be required to preserve vision.

45
Q

What is GCA/temporal arteritis?

A

Giant cell arteritis is a systemic vasculitis of the medium and large arteries. It typically presents with symptoms affecting the temporal arteries and is also known as temporal arteritis.

46
Q

Which patients are at risk of GCA?

A

PMR
White
Female
Over 50

47
Q

How does GCA present?

A

The main presenting feature is a headache:

Severe unilateral headache typically around temple and forehead
Scalp tenderness my be noticed when brushing hair
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly

There may be associated systemic symptoms such as:

Fever
Muscle aches
Fatigue
Weight loss
Loss of appetite
Peripheral oedema

48
Q

GCA investigations and findings?

A

A definitive diagnosis is based on:

Clinical presentation
Raised ESR: usually 50 mm/hour or more
Temporal artery biopsy findings (may be false negative - skip lesions)

Additional Investigations

Full blood count may show a normocytic anaemia and thrombocytosis (raised platelets)
Liver function tests can show a raised alkaline phosphatase
C reactive protein is usually raised
Duplex ultrasound of the temporal artery shows the hypoechoic halo sign

49
Q

Management of GCA?

A

Visual symptoms or jaw claudication: 60mg prednisolone PO OD
Otherwise 40mg prednisolone PO OD

Review response within 48hrs (should be rapid and significant)

Also: aspirin 75mg to prevent CVA and decrease visual loss, PPI to cover steroids

Taper off steroids gradually once symptoms resolved (can take several years)

50
Q

Refferals in GCA?

A

Vascular surgeons for a temporal artery biopsy in all patients with suspected GCA
Rheumatology for specialist diagnosis and management
Ophthalmology review as an emergency same day appointment if they develop visual symptoms

51
Q

GCA complications?

A

Early neuro-ophthalmic complications:

Vision loss
Cerebrovascular accident (stroke)

Late:

Relapses of the condition are common
Steroid related side effects and complications
Cerebrovascular accident (stroke)
Aortitis leading to aortic aneurysm and aortic dissection

52
Q

NICE Criteria for 1 hour head CT

A

• GCS <13 on initial assessment
GCS <15 2 hours after the trauma
• Suspected open or depressed skull fracture
• Evidence of basal skull fracture (e.g. panda eyes, mastoid bruising, rhinorrhoea)
• Post-event seizure
New focal neurology
• More than 1 episode of vomiting

53
Q

NICE criteria for 8 hour head CT?

A

If a patient has experienced loss of consciousness or amnesia since the trauma they should receive a CT
head within 8 hours if they also have one of the following:
Age >65.
• Bleeding//clotting disorders.
Dangerous mechanism of injury (e.g. hit by car, fall from >1m).
More than 30min retrograde amnesia from the event.

54
Q

What is meant by post traumatic headache?

A

New Tension like headache occuring within 7 days of injury or regaining consciousness
Managed with basic analgesia
May persist beyond 2 months - chronic

55
Q

Potential complications of sinusitis?

A

Rare

Osteomylitis, cellulitis, meningitis

56
Q

What is intracranial venous thrombosis?

A

Intracranial venous thrombosis refers to occlusion of venous vessels in the cranial cavity.

57
Q

How does intracranial venous thrombosis present?

A

Presentation is variable but common symptoms include headache, confusion/drowsiness, impaired vision, and nausea/vomiting.

Other signs include seizures, reduced consciousness, focal neurological deficits, cranial nerve palsies, and papilloedema.

58
Q

Risk factors for intracranial venous thrombosis?

A

Risk factors are similar to those for venous thromboembolism and include: hormonal factors (the pill, pregnancy, and the peri-partum period), prothrombotic haematological conditions, systemic disease (such as dehydration or sepsis), and local factors (skull abnormalities, trauma, or local infection).

59
Q

Investigations for ?intracranial venous thrombosis and their gindings?

A

Non-contrast CT reveals a hyperdensity in the affected sinus.

CT venogram is used to look for a filling defect (‘the empty delta sign’).

The most common form of dural venous thrombosis affects the superior sagittal sinus.

Cavernous sinus thrombosis is less common. It is typically caused by spreading sinus infection and presents with chemosis, exophthalmos, and peri-orbital swelling.

60
Q

Mainstay of therapy for Intracranial Venous Thrombosis?

A

LMWH

61
Q

After how long would you expect complete remission from GCA?

A

2 years

62
Q

If a patient experiences headaches secondary to raised ICP with visual field defects, what would you expect the visual fields to show?

A

Enlarged blind spots and constricted fields

63
Q

How can IIH cause problems with the GI system

A
64
Q

Concerns re:headaches in pregnancy?

A

Dural sinus thrombosis
Pre-eclampsia

65
Q

Which type of primary headache has charecteristic autonomic symptoms?

A

Cluster headache

66
Q

If a patient with migraines has not benefiited from three oral phrophylaxis options for three month each, what can be trialed

A

Botox injections

fremanezumab

67
Q

What type of headache is classically worse on standing up than on lying flat

A

Low CSF headaches can occur due to spontaneous intracranial hypotension (not necessarily post-LP) and are classically worse on standing and improve when lying flat

Year 4 Neurology and Special Senses (24 decks)

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