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Neurology and special senses (Y4) > 5- Neurology (Less acute: Headaches, Migraines, Facial droop) > Flashcards

5- Neurology (Less acute: Headaches, Migraines, Facial droop) Flashcards

1
Q

Differentials of headaches

A
  • Haemorrhage
  • Meningitis
  • Tumour
  • Glaucoma
  • GCA
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2
Q

types of headache

A

primary and secondary

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3
Q

Primary headache

A

due to the headache condition itself – will have normal clinical exam
- Non life-threatening or sight threatening

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4
Q

Secondary headache

A

due to another condition causing headache – will have a rash or neurological effect

1) Life-threatening
- SoL (tumour or haemorrhage)
- Meningitis

2) Sight threatening
- Giant cell arteritis
- Acute glaucoma

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5
Q

summary of primary vs secondary headache conditions

A
  • In red required urgent referral to ENT
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6
Q

red flags for headache

S

A

SNOOP
Red flags

  • S – Systemic signs and disorders – meningitis or hypertension
  • N – Neurological symptoms – glaucoma and SOL
  • O – Onset new or changed and patient over 50 – brain metastases
  • O – onset in thunderclap presentation – haemorrhage
  • P – papilledema, pulsatile tinnitus, positional provocation precipitated by exercise – raised ICP
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7
Q

exmaination for headache

A

Must perform pull peripheral and CNS examination and vital signs when pt presents with headache

Clinical examination
- Vital signs
o BP
o PR
o Temp
- Neurological examination (cranial and peripheral nerve exam, Glasgow-coma scale)
- Other relevant systems, guidance by history

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8
Q

zero to finals red flags for headache list

A
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9
Q

history taking for headache

A

FHistory taking
- Presenting complaint (HPC)
- SOCRATES
 Site
 Onset
 Character
 Radiate?
 Associated symptoms
 Timing (day/night)
 Exacerbating factors
 Severity
- Past medical history (PMH)
- Drug history (DH)
o Analgesic use (medication over use)
- Family history (FH)
- Social history (SH)

ENQUIRE ABOUT ALL RED FLAGS

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10
Q

investigations for headache

A

Investigations
- Clinical diagnosis
- Fundoscopy to look for papilledema
o Indicates raised intracranial pressure
 Brain tumour
 Benign intracranial hypertension
 Intracranial bleed
- If worried CT
- Lumbar puncture if we think meningitis

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11
Q

Primary heafahces

A
  • tension headache
  • migraine
  • medication overuse (sort of secondary cause)
  • cluster headache
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12
Q

Tension type headaches
Background

A

-** Due to tension in muscles of head and neck – occipitofrontalis**
- Unusual for >50 to have first onset
- F>M
- Common
- Teenagers and adults

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13
Q

RF for tension type headaches

A
  • Stress and mental tension are common triggers
  • Fatigue
  • Alcohol
  • Dehydration
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14
Q

presentation of tension-type headaches

A

Presentation
- Normal clinical examination
- Band like pattern of mild ache around head

Acronymn
- S – bilateral frontal, sometime occipital – radiates to neck
- Q – squeezing like a band – non pulsatile
- I – mild to moderate
- T – worse at end of day, can be recurrent >15 in a month is chronic
- A – stress, poor posture, lack of sleep
- R – simple analgesia
- S – possible slight nausea

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15
Q

management of tension headache

A

Management
- Reassurance
- Simple analgesia e.g. paracetamol and ibuprofen
- Reduce stress -relaxing activities e.g. exercise, yoga and massage
- Avoid dehydration
- Cut down on caffeine
- Change pillow

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16
Q

Cluster headaches

Background

A
  • Severe and unbearable unilateral headache, usually around the eye
  • Come in clusters of attacks and then disappear for a while
  • E.g. 3-4 attaks a day for weeks followed by pain-free lasting 1-2 years
  • Last between 15 mins and 3 hours
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17
Q

risk factors cluster headache

A

Risk factors
- M>F
- Smoking history= risk factor
- 1 in 1000
- Usually begins 30-50 years

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18
Q

Pathophysiology of cluster

A
  • Unknown
  • Hypothalamic activation with secondary trigeminal and autonomic involvement
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19
Q

cluster triggers

A

Triggers
- Alcohol
- Strong smells
- Exercise

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20
Q

presentation of cluster headaches

A

Presentation
- Excruciating- like an ice pick in the eye
o ‘Most intolerable pain’
o Suicidal headache
- Red swollen and watering eye
- Pupil constriction (miosis)
- Eyelid drooping (ptosis)
- Nasal discharge
- Facials sweating

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21
Q

management of cluster headaches

A

Management

Acute
- Triptans (e.g. sumatriptan)
- High flow 100% oxygen for 15-20 minutes

Prophylaxis
- Verapamil
- Lithium
- Prednisolone

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22
Q

Medication over-use headache (secondary headache)

A

Background
- Long term analgesia use

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23
Q

medication over-use headache pathophysiology

A

Pathophysiology
- Regular use of analgesics leads to upregulation of pain receptors in the meninges e.g. codeine

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24
Q

risk factors for medication over-use headache

A

Risk factors
- F>M
- 30-40 yrs

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25
Q

Presentation of medication overuse headache

A
  • Similar nonspecific features of tension headache
  • Headache present on at least 15 days/month (constant)
  • Using regular analgesics at least 10 days/month)
    o Headache not responding
  • Occurs in pts with pre-existing headache disorder
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26
Q

Management of medication over-use headache

A

discontinue medication (headache worsens before improves)- resolves completely by 2 months

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27
Q

Hormonal Headache
background

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.

28
Q

hormonal headache management

A
29
Q

hormonal headache management

A
30
Q

rasied intracranial pressure e.g. SOL

A
  • Rarely occurs in absence of other suspicious historical or exam findings
  • Worse on leaning forward and coughing
  • On waking
31
Q

trigeminal neuralgia background

A

Can affect any branch of the trigeminal nerve
o Ophthalmic (V1)
o Maxillary (V2)
o Mandibular (V3)

32
Q

trigeminal neuralgia background

A

Can affect any branch of the trigeminal nerve
o Ophthalmic (V1)
o Maxillary (V2)
o Mandibular (V3)

33
Q

trigeminal neuralgia risk factors

A

trigeminal neuralgia

34
Q

TN triggers

A
  • Touching scalp e.g. combing hair
  • Eating spicy or citrus food
  • Caffeine
  • Cold weather
35
Q

pathophysiology of TN

A

Pathophysiology
- Most caused by compression of CN V due to loop of blood vessels
- 5% due to tumours/skull base abnormalities or AV malformations

36
Q

Presentation TN

A
  • Starts spontaneously and can last anywhere between a few seconds and hours
  • Like electricity
  • Attacks worsen over time
37
Q

TN management

A

Management
- First line: Carbamazepine
- Surgery to decompress or intentionally damage trigeminal nerve

38
Q

Temporal arteritis
Background

A

Giant cell arteritis
- Vasculitis of large and medium sized arteries of head
- Superficial **temporal artery commonly **involved.

39
Q

temporal arteritis risk factors

A

Risk factors
- F>M
- >50 years (most common >75 yrs)
- Polymyalgia rheumatica
- White

40
Q

temporal arteritis strongly associated with

A

polymyalgia rheumatica (think raised ESR)

41
Q

TA presentation

A
  • Unilateral headache typically around temple and forehead
  • Scalp tenderness when brushing hair
  • Jaw claudication
  • Blurred or double vision
  • Associated: fever, muscle aches, fatigue, weight loss, lossof appetite, peripheral oedema
42
Q

TA investigations

A

-Clinical presentation

Key finding
- Raised ESR

Biopsy
- Temporal artery biopsy (Multinucleated giant cells found)

Additional tests
- FBC- normocytic anaemia and thrombocytosis
- LFT may show raised ALP
- CRP raised
- Duplex US may show hypoechoic halo sign

43
Q

management of TA

A

Initial

  • Steroids -> to reduce risk of permanent slight loss
  • 40-60mg per day
  • Aspirin
  • PPI – for steroid
  • Referral to vascular surgeons, rheumatology, ophthalmology

Ongoing management

  • Continue high dose steroids into symptom resolve and then wean
44
Q

key additional measures for steroid use

A
45
Q

Complications of TA

A
  • Risk of irreversible loss of vision due to involvement of blood vessels supplying CN II (optic)
  • Cerebrovascular accident (stroke)
  • Relapse
  • Aortitis – AA or aortic dissection
  • Steroid related effects
46
Q

Migraines
Background

A
  • Complex neurological condition that cause headache and other symptoms
  • Occur in ‘attacks’ that often follow a typical pattern

Types of migraine
- Migraine without aura
- Migraine with aura
- Silent migraine (migraine with aura without a headache)
- Hemiplegic migraine

47
Q

migraine pathophysiology

A
  • Various theories
  • No simple explanation
  • Combination of: structural, functional, chemical, vascular and inflammatory factors
48
Q

5 stages of migraine

A

Can be broken down into 5 stages- not typical of everyone
* Premonitory or prodromal stage (can begin 3 days before the headache)
o The prodromal stage can involve several days of subtle symptoms such as yawning, fatigue or mood changes prior to the onset of the migraine.

  • Aura (lasting up to 60 minutes)

* Headache stage (lasts 4-72 hours)

* Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping)

* Postdromal or recovery phase

49
Q

migraine triggers

A

Triggers
- Stress
- Bright lights
- Strong smeels
- Certain food e.g. choc, cheese, caff
- Dehydration
- Menstruation
- Abnormal sleep patterns
- trauma

50
Q

presentation of migraine

A

Headache
* Mod to severe intensity
* Pounding or throbbing in nature
* Usually unilateral, can be bilateral
* Photophobia
* Phonophobia
* With or without aura
* N + V

Aura- visual changes associated with migraine
* Sparks in vision
* Blurring vision
* Lines across vision
* Loss of different visual fields

51
Q

management of migraines

A

Self management
- Dark quiet room
- Sleep

Other options
- Paracetamol
- Triptans e.g. sumatriptan 50mg as the migraine starts
- NSAIDS e.g. ibuprofen or naproxen
- Antiemetics e.g. metoclopramide

52
Q

prophylaxis for migraines

A

1) Keep a headache diary to identify triggers

2) Avoid triggers

3) Long term preventative medication
- Propranolol
- Topiramate- teratogenic – cleft lip/palate
- Amitriptyline

3) Acupuncture

4) Supplementation with vitamin B (riboflavin) may reduce frequency and severity

5) If triggered by menstruation
NSAIDs e.g. mefenamic acid
Triptans e.g. frovatriptan or zolmitriptan

53
Q

Triptans

A

Used to abort migraines when symptoms start to develop.
MOA: 5HT receptor agonists
- Cause vasoconstriction of the smooth muscle in arteries
- Inhibit action of pain receptors
- Reduce neuronal activity of CNS

54
Q

prognosis of migraines

A

Migraines tend to get better over time and people go into remission from their symptoms

55
Q

Hemiplegic Migraine

A

Hemiplegic migraines can mimic stroke. It is essential to act fast and exclude a stroke in patients presenting with symptoms of hemiplegic migraine.
Symptoms of a hemiplegic migraine can vary significantly. They can include:
* Typical migraine symptoms
* Sudden or gradual onset
* Hemiplegia (unilateral weakness of the limbs)
* Ataxia
* Changes in consciousness

56
Q

branches of the facial nerve

A
  • Temporal
  • Zygomatic
  • Buccal
  • Marginal mandibular
  • Cervical
57
Q

UMN lesions

A

Causes
* Stroke
* Tumours
* Pseudobulbar palsies
* MND

Presentation
* Forehead sparing -> due to each side of the forehead having UMN innervation by both sides of the brain
* Usually unilateral
* Rarely unilateral: pseudobulbar palsies, MND

58
Q

LMN lesions

A

Causes
1) Bells palsy
2) Ramsay hunt
3) Infection
- Otitis media
- HIV
- Lyme
4) Systemic
- Diabetes
- Sarcoidosis
- Leukaemia
- MS
- G-B syndrome
5) Tumours
- Acoustic neuroma
6) Trauma
- Direct nerve trauma
- Basilar fracture

Presentation
Non-forehead sparing -> each side of the forehead only has LMN from one side of the brain

59
Q

Bells palsy

A
  • Common condition
  • Idiopathic
  • Unilateral LMN facial nerve palsy

Description: an unexplained episode of facial muscle weakness or paralysis. It begins suddenly and worsens over 48 hours. This condition results from damage to the facial nerve (the 7th cranial nerve). Pain and discomfort usually occur on one side of the face or head.

60
Q

Bells palsy management

A

For those presenting within 72h of symptoms:
- Prednisolone
- In general antivirals not recommender by NICE, but may. Offer some benefit
- Supportive: lubricating eye drop/ tape eyelids at night to prevent exposure keratopathy

Prognosis
- Full recovery over several weeks, may take 12 months

61
Q

Ramsay-Hunt Syndrome

A

Occurs when a shingles outbreak affects the facial nerve near one of your ears. In addition to the painful shingles rash, Ramsay Hunt syndrome can cause facial paralysis and hearing loss in the affected ear
- Caused by varicella zoster virus (VZV)

62
Q

presentation of ramsay-hunt syndrome

A

Presentation
- Unilateral LMN facial nerve palsy
- Painful vesicular rash in the ear canal, pinna and around the ear on the affected side
- Rash can extend to the anterior 2/3 of the tongue and hard palate

63
Q

management of R-H syndrome

A

Management
Ideally within 72 hours
- Prednisolone
- Acyclovir
- Supportive
o Lubricating eye drops

64
Q

Bells or Stroke?

A

Bells palsys - forehead furrowing lost

65
Q

Bells or Stroke?

A

stroke - forehead has been spared

66
Q

pathophysiology of forehead sparing in stroke

A

Dual cortical input (due to loss of contralateral input)- ipsilateral input for muscle fibres of the upper part (not lower) of the face can be saved-> therefore if stroke can furrow both eyebrows.

Neurology and special senses (Y4) (52 decks)

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