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Neurology Brief Flashcards

1
Q

what is the new definition of a TIA

A

ischaemia without infarction

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2
Q

what is as crescendo TIA

A

two or more TIAs within a week

carries high risk of developing into a stroke

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3
Q

what is alteplase

A

tissue plasminogen activator

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4
Q

management of stroke

A
  • exclude hypoglycaemia
  • immediate CT head to exclude haemorrhage
  • aspirin 300mg stat and continued for 2 weeks
  • alteplase if within 4.5 hrs of onset of symptoms
    • monitoring for post thrombolysis complications
      • repeated CT head
  • admit to specialist stroke centre
  • diffusion weighted MRI is gold standard imaging
  • carotid ultrasound if carotid stenosis is suspected
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5
Q

management of TIA

A

300mg aspirin daily

referred and seen within 24hrs by stroke specialist

start secondary prevention for cardiovascular disease

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6
Q

management of carotid stenosis

A

endarterectomy to remove plaques

carotid stenting to widen lumen

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7
Q

what is the secondary prevention of stroke

A

clopidogrel 75mg once daily

carotid endarterectomy or stenting in patients with carotid disease

treat modifiable risk factors

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8
Q

what percentage of strokes are caused by intracranial bleeds

A

10-20%

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9
Q

draw out the glasgow coma scale

A
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10
Q

what causes subdural haemorrhage

A

rupture of bridging veins in the outermost meningeal layers between dura mater and arachnoid mater

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11
Q

CT scan appearance of subdural haemorrhage

A

crescent shape and not limited by cranial sutures

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12
Q

which population of patients is most likely to have a subdural haemorrhage

A

the elderly and alcoholics

they have atrophy and vessels are more likely to rupture

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13
Q

which artery in which region is most likely to cause a extradural haemorrhage

A

middle meningeal artery in the temporo-parietal region

this can be associated with a fracture of the parietal bone

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14
Q

CT appearance of an extradural haemorrhage

A

egg shaped and limited by cranial sutures

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15
Q

Typical history is a patient with a traumatic head injury and ongoing headache.

They have a period of improved neurological symptoms and consciousness followed by a rapid decline over hours.

What sort of bleed is this?

A

extradural haemorrhage

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16
Q

other features of a subarachnoid haemorrhage other than thunderclap headache

A

neck stiffness

photophobia

vision changes

neurological symptoms

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17
Q

risk factors for subarachnoid haemorrhage

A
  • hypertension
  • smoking
  • excessive alcohol consumption
  • cocaine use
  • family history
  • black ethnicity
  • female sex
  • age 45-70
  • sickle cell anaemia
  • neurofibromatosis
  • autosomal dominant polycystic kidney disease
  • connective tissue disorders
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18
Q

investigations for subarachnoid haemorrhage

A

CT head will show hyperattenuation in the subarachnoid space

LP will show raised red cells and xanthochromia

CT or MRI angiography to locate source of bleeding

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19
Q

management of subarachnoid haemorrhage

A
  • surgery
    • coiling (endovascular)
    • clipping (cranial surgery)
  • Nimodipine
    • CCB
    • to prevent vasospasm and ischaemia following SAH
  • LP or Shunt for hydrocephalus
  • antiepileptic meds for seizures
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20
Q

multiple sclerosis only affects the neurons of the _______ nervous system where the myelin is formed by ________

A

multiple sclerosis only affects the neurons of the central nervous system where the myelin is formed by oligodendrocytes

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21
Q

internuclear opthalmoplegia presents how and how is it caused

A
  • one eye lags behind the other
  • the affected eye adducts minimally
  • they have diplopia
    *
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22
Q

what is lhermitte’s sign

A

electric shock sensation when neck is stretched in patients with MS

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23
Q

what are the two types of ataxia and what are the differences

A
  • sensory ataxia - problem with proprioceptive sense
    • results in positive rombergs
    • can cause pseudoathetosis
  • cerebellar ataxia
    • result of problems with the cerebellum coordinating movement
    • suggests cerebellar lesions
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24
Q

what is a clinically isolated syndrome in MS

A

first episode of demyelination and neurological signs and symptoms

MS cannot be diagnosed at this point as the lesions are not ‘disseminated in time and space’

pts with clinically isolated syndrome may never have another episode or develop MS

if lesions seen on MRI then they are more likely to progress to MS

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25
Q

what are the four different ways you can describe relapsing remitting MS

A
  • Active: new symptoms are developing or new lesions are appearing on MRI
  • Not active: no new symptoms or MRI lesions are developing
  • Worsening: there is an overall worsening of disability over time
  • Not worsening: there is no worsening of disability over time
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26
Q

what are the 4 different ways you can describe secondary progressive MS

A
  • Active: new symptoms are developing or new lesions are appearing on MRI
  • Not active: no new symptoms or MRI lesions are developing
  • Progressing: there is an overall worsening of disease over time (regardless of relapses)
  • Not progressing: there is no worsening of disease over time
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27
Q

how long do symptoms need to be progressive over before you can diagnose primeary progressive MS

A

1 year

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28
Q

what will lumbar puncture detect in MS

A

oligoclonal bands

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29
Q

features of optic neuritis

A

central scotoma

pain on eye movement

impaired colour vision

RAPD

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30
Q

non MS causes of optic neuritis

A
  • Sarcoidosis
  • Systemic lupus erythematosus
  • Diabetes
  • Syphilis
  • Measles
  • Mumps
  • Lyme disease

however MS is the main cause

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31
Q

management of optic neuritis

A

urgent assessment by opthalmologist if acute loss of vision

treat with steroids

recovery takes 2-6 weeks

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32
Q

MS prognosis following first episode of optic neuritis

A

50% of patients with a single episode of optic neuritis will go on to develop MS over the next 15 years

changes on MRI can predict which patients do

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33
Q

management of MS

A
  • disease modifying drugs
    • mabs too complex for you to know about
  • treating relapses
    • methylprednisolone
      • 500mg orally daily for 5 days
  • symptomatic treatment
    • neuropathic pain
      • gabapentin
      • amitryptilline
    • depression
      • ssris
    • urge incontinence
      • anticholinergics such as tolterodine and oxybutynin
    • spasticity
      • baclofen
      • gabapentin
      • physio
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34
Q

what are the 4 types of motor neurone disease to know about

A
  • amyotrophic lateral sclerosis
  • progressive bulbar palsy
  • progressive muscular atrophy
  • primary lateral sclerosis
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35
Q

what percentage of motor neurone disease cases are inherited

A

5-10%

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36
Q

signs of lower motor neurone disease

A

muscle wasting

reduced tone

fasciculations

reduced reflexes

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37
Q

signs of upper motor neurone disease

A

increased tone or spasticity

brisk reflexes

upgoing plantar responses

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38
Q

what is the only drug licensed in the UK for ALS

A

rilzole can slow progression and extend survival by a few months in ALS

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39
Q

distinguish between parkinson’s tremor and benign essential tremor

A
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40
Q

describe multiple system atrophy

A
  • degeneration of basal ganglia leads to
    • parkinsons presentation
  • degeneration of other regions of the brain leads to
    • autonomic dysfunction
      • postural hypotension
      • constipation
      • abnormal sweating
      • sexual dysfunction
  • degeneration of cerebellum leads to
    • ataxia
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41
Q

what must be given with levodopa in parkinson’s and what are the combinations called

A
  • must be given with peripheral decarboxylase inhibitors such as carbidopa and benserazide
  • so
    • co-benyldopa is levodopa and benserazide
    • co-careldopa is levodopa and carbidopa
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42
Q

what are the different medical managements options for parkinson’s

A
  • levodopa
    • most effective
    • but becomes less effective over time
    • so reserve for late disease
  • COMT inhibitors
    • taken with levodopa to slow breakdown of levodopa in brain
  • dopamine agonists
    • less effective than levodopa
    • delay need for levodopa
    • then used in combo with levodopa
    • prolonged use causes pulmomary fibrosis
  • Monoamine oxidase-B inhibitors
    • MOB breaks down dopamine
    • inhibiting it increases circulating dopamine
    • delay need for levodopa
    • then used in combo with levodopa
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43
Q

what are COMT inhibitors used to treat, how do they work and give an example

A

used to treat parkinson’s

taken with levodopa to slow breakdown of levodopa in brain

example is entacapone

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44
Q

how are dopamine agonists used to treat Parkinsons and what are some examples

A
  • less effective than levodopa
  • delay need for levodopa
  • then used in combo with levodopa
  • prolonged use causes pulmomary fibrosis
  • e.g.
    • bromocryptine
    • pergolide
    • carbergoline
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45
Q

how do MOB inhibitors work and what are some examples

A
  • MOB breaks down dopamine
  • inhibiting it increases circulating dopamine
  • delay need for levodopa
  • then used in combo with levodopa
    • e.g.
      • selegiline
      • rasagiline
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46
Q

is benign essential tremor present or absent during sleep

A

absent

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47
Q

what are the key differential diagnoses of a tremor

name 6

A

parkinson’s disease

MS

huntington’s chorea

hyperthyroidism

fever

medications e.g. antipsychotics

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48
Q

managment of benign essential tremor

A
  • there is no need to treat unless causing functional or psychological problems
  • treatment options include
    • propanolol
    • primidone (barbiturate anti-epileptic medication)
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49
Q

what is the aim of epilepsy treatment

A

to be seizure free on the minimum anti-epileptic medications

ideally a monotherapy

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50
Q

describe generalised tonic clonic seizures

A
  • loss of consciousness
  • tonic episode
  • followed by clonic episode
  • there may be
    • incontinence
    • tongue biting
    • groaning
    • irregular breathing
  • prolonged post-ictal period
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51
Q

what is the management of tonic clonic seizures

A

first line: sodium valproate

second line: lamotrigine or carbamazepine

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52
Q

what are the 5 important types of generalized seizures

A
  1. absence seizures
  2. tonic clonic seizures
  3. myoclonic seizures
  4. atonic seizures
  5. infantile spasms
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53
Q

what are the three types of focal seizures

A
  • without impairment of consciousness
  • with impairment of consciousness
  • evolving to a bilateral, convulsive seizure
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54
Q

what features would localise a seizure to the temporal lobe

A

automatisms

dysphasia

deja vu

jamais vu

emotional disturbance

hallucinations of smell, taste or sound

delusional behaviour

bizarre associations - “Canned music at Tesco always makes me cry and then pass out”

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55
Q

what features would localise a focal seizure to the frontal lobe

A

posturing or peddling of the legs

jacksonian march

subtle behaviour disturbances

dysphasia

speech arrest

post-ictal todd’s palsy

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56
Q

what features would localise a focal seizure to the parietal lobe

A

sensory disturbance such as tingling numbness and pain

motor symptoms due to spread to pre-central gyrus

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57
Q

what features would localise a focal seizure to the occipital lobe

A

visual phenomena such as spots, lines and flashes

58
Q

is there loss of consciousness in a tonic clonic seizure

A

yes

59
Q

is ther loss of consciousness in atonic seizures

A

no

60
Q

what is the management of focal seizures

A

first line: carbamazepine or lamotrigine

second line: levetiracetam or sodium valproate

61
Q

what is the management of generalized tonic clonic seizures

A

first line: sodium valproate or lamotrigine

second line: carbamazepine, levetiracetam or topiramate

62
Q

what is the management of absence seizures

A

first line: sodium valproate

second line: lamotrigine

63
Q

what is the management of myoclonic seizures

A

first line: sodium valproate

second line: levetiracetam or topirimate

AVOID carbamazepine as it can worsen seizures

64
Q

what is the managment of tonic or atonic seizures

A

sodium valproate or lamotrigine

65
Q

what are infantile spasms? what is the prognosis? what is the management?

A

aka west syndrome

rare

starts at ~6 months of age

clusters of full body spasms

poor prognosis (1/3 die by 25)

difficult to treat

give prednisolone or vigabatrin

66
Q

side effects of carbamazepine

A

agranulocytosis

aplastic anaemia

enzyme inducer

67
Q

side effects of phenytoin

A

folate and vitamin D deficiency

megaloblastic anaemia (due to folate deficiency)

osteomalacia (due to vitamin D deficiency)

68
Q

side effects of ethosuxamide

A

night terrors

rashes

69
Q

side effects of lamotrigine

A

stevens johnson syndrome

DRESS syndrome

leukopenia

70
Q

what is the definition of status epilepticus

A

seizures lasting more than 5 minutes or more than three seizures in one hour

71
Q

management of status epilepticus

A
  1. secure airway
  2. oxygen and suction as required
  3. IV access
    • lorazepam 4mg bolus
      • repeat if no response after 10-20 minutes
    • U&E, LFT, FBC, glucose, Ca2+
  4. Thiamine IV if alcoholism or malnourishment suspected
  5. Glucose IV unless glucose known to be normal
  6. Correct hypotension wih IV normal saline
  7. If seizures continue start phenytoin IV infusion
  8. General anaesthesia if working on them for 60-90 minutes
72
Q

what are the 4 drugs used in neuropathic pain and what are their drug classes

A
  1. amitriptyline is a tricyclic antidepressant
  2. duloxetine is an SNRI antidepressant
  3. gabapentin is an anticonvulsant
  4. pregabalin is an anticonvulsant

try one at a time.

stop the one you’re using before you trial the next one.

73
Q

what are the five branches of the facial nerve

A

temporal

zygomatic

buccal

marginal mandibular

cervical

74
Q

what are the functions of the facial nerve

A
  • motor
    • to the muscles of facial expression
  • sensory
    • to anterior 2/3 of the tongue
  • parasympathetic
    • to the submandibular and sublingual salivary glands
    • lacrimal gland - tear production
75
Q

how do you distinguish an upper motor neurone lesion and alower motor neurone lesion facial nerve palsy

A
  • upper motor neurone lesion the forehead is spared - stroke
  • lower motor neurone lesion the forehead is not spared - bell’s palsy
76
Q

how long is recovery from bells palsy

A

majority make full recovery within several weeks but may take up to 12 months

a third are left with residual weakness

77
Q

what is the management of bell’s palsy?

A

if patients present within 72 hours of developing symptoms give prednisolone for 10 days

they may also need lubricating eye drops as they are at risk of exposure keratopathy

78
Q

what is ramsay-hunt sundrome

A
  • caused by VZV
  • presents as
    • unilateral lower motor neurone facial nerve palsy
    • painful, tender, vesicular rash in the ear canal and pinna
    • rash may extend to anterior 2/3 of the tongue
79
Q

what is the management of ramsay hunt syndrome

A

prednisolone

aciclovir

they also require lubricating eye drops as they are at risk of exposure keratitis

80
Q

what is papilloedema

A

swelling of the optic disc secondary to raised ICP

optic nerve sheath is continuous with the arachnoid mater so CSF can flow in and cause optic disc to swell

81
Q

fundoscopic changes in papilloedema

A

blurring of optic disc margin

loss of venous pulsation

engorged retinal veins

haemorrhages around optic disc

82
Q

what are the most common cancers that metastasize to the brain

A

lung

breast

renal cell carcinoma

melanoma

83
Q

what are the three types of glioma from most to least malignant

A

astrocytoma (glioblastoma multiforme is the most common astrocytoma)

oligodendroglioma

ependymoma

84
Q

how are gliomas graded

A

grade 1-4

with grade 1 being most benign (possibly curable with surgery)

and grade 4 being most malignant (glioblastomas)

85
Q

what are meningiomas

A

tumours of meninges

mostly benign

however neurological symptoms from mass effect

86
Q

what are acoustic neuromas

A
  • tumours of schwann cells surrounding auditory nerve
  • occur at cerebellopontine angle
  • slow growing but eventually produce symptoms and become dangerous
  • usually unilateral
  • if bilateral then neurofibromatosis type 2
  • symptoms
    • hearing loss
    • tinitus
    • balance problems
87
Q

what is the inheritence pattern of huntington’s chorea

A

autosomal dominant

88
Q

what chromosome is the huntington’s mutation on

A

chromosome 4

89
Q

what is the management of huntington’s

A
  • no medication can slow or reverse progression
  • treatment is supportive
  • medications to suppress disordered movement
    • antipsychotics (e.g. olanzapine)
    • benzodiazepines (e.g. diazepam)
    • dopamine depleting agents (e.g. tetrabenazine)
  • depression can be treated with SSRIs
90
Q

what age are patients most likely to present with myasthenia gravis

A

Myasthenia gravis affects men and women at different ages. Typical patients are either a woman under the age of 40 or a man over the age of 60.

91
Q

what important thing is myasthenia gravis linked with

A
  • thymus tumour
  • 10-20% of MG patients have a thymoma
  • 20-40% of patients with a thymoma develop myasthenia gravis
92
Q

what is the pathophys of myasthenia gravis

A
  • 85% of pts with MG have acetylcholine receptor antibodies
  • these block the receptor and stop acetylcholine binding to postsynaptic NMJ receptors
  • these antibodies also activate the complement system
  • leading to damage of the postsynaptic membrane
  • the other 15% of cases are caused by
    • muscle specific kinase (MuSK) antibodies
    • LRP4 antibodies
  • LRP4 and MuSK are important for the production of the acetylcholine receptors
93
Q

85% of pts with myasthenia gravis have antibodies against

A

acetyl choline receptors

94
Q

15% of patients with myasthenia gravis have antibodies against

A

MuSK

LRP4

these proteins are important for creation and organisation of acetylcholine receptors

95
Q

do myasthenia gravis symptoms change during the day

A

typically symptoms are minimal in the morning and worst at the end of the day

96
Q

important examination points for myasthenia gravis

A
  • repeated blinking will exacerbate ptosis
  • prolonged upward gazing will exacerbate diplopia on further eye movement testing
  • repeated abduction of one arm will lead to unilateral weakness when comparing both sides
  • check for thymectomy scar
  • test forced vital capacity
97
Q

diagnosis of myasthenia gravis

A
  • test directly for antibodies
    • ACh-R antibodies (85%)
    • MuSK antibodies (10%)
    • LRP4 antibodies (<5%)
  • CT or MRI of the thymus
  • Endrophonium test
    • this is a cholinesterase inhibitor
    • if it relieves symptoms then it establishes diagnosis
98
Q

treatment for myasthenia gravis

A
  • acetylcholinesterase inhibitors
    • neostigmine
    • pyridostigmine
  • immunosuppression
    • prednisolone
    • azathioprine
  • thymectomy
    • works even in patients without a thymoma
  • rituximab
99
Q

myasthenic crisis is often triggered by

A

respiratory tract infection

this leads to progressive weakness of the muscles of respiration

patients may require NIV or BiPAP

may require intubation and ventilation

medical treatment is IV immunoglobulins and plasma exchange

100
Q

what is lambert eaton syndrome

A

it’s like myasthenia gravis but it’s because of small cell lung cancer and autoantibodies against voltage-gated calcium channels in the presynaptic terminals of the neuromuscular junction

REMEMBER IN MG IT’S POST-SYNAPTIC RECEPTORS THAT ARE TARGETTED

101
Q

Presentation of lambert eaton syndrome

A
  • more gradual onset than myasthenia gravis
  • affects proximal muscles most
    • most notably proximal leg muscles
    • also eye muscles causing diplopia and ptosis
  • pts may also get dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction
  • reflexes improve after a short period of strong muscle contraction
    • post-tetanic potentiation
102
Q

treatment for lambert eaton syndrome

A
  • treat small cell lung cancer
  • amifampridine releases more acetylcholine
  • other options
    • IV Ig
    • immunosuppressants (prednisolone or azathioprine)
    • plasmapheresis
103
Q

how do you get charcot marie tooth disease

A

it is inherited autosomal dominant the majority of the time

symptoms usually appear before 10yrs old but can be delayed until 40 or later

104
Q

causes of peripheral neuropathy

A
  • ABCDE
    • Alcohol
    • B12 deficiency
    • Cancer, Chronic kidney disease, Charcot-marie tooth
    • Diabetes, Drugs
    • Every vasculitis
105
Q

name 3 drugs that cause peripheral neuropathy

A

isoniazid

amiodarone

cisplatin

106
Q

classical features of charcot marie tooth

A
  • high foot arches (pes cavus)
  • distal muscle wasting (inverted champagne bottle legs)
  • weakness in the lower legs (particularly ankle dorsiflexion)
  • weakness in the hands
  • reduced reflexes
  • reduced muscle tone
  • peripheral sensory loss
107
Q

what is charcot marie tooth

A

inherited disease that affects the peripheral sensory and motor nerves

there are many different types

normally presents before age 10 but can be later

108
Q

what is the management of charcot marie tooth

A
  • there is no treatment for underlying disease
  • management is supportive with input from
    • neurologists
    • physio
    • OT
    • podiatrists
    • orthopaedic surgeons
109
Q

what is the presentation of guillain barre syndrome

A
  • symmetrical ascending weakness
  • reduced reflexes
  • peripheral loss of sensation or neuropathic pain
110
Q

clinical course of guillain barre syndrome

A
  • symptoms start within 4 weeks of preceding infection
  • symptoms progress upwards
  • symptoms peak at 2-4 weeks
  • there is a recovery peeriod that can take months to years
111
Q

what criteria are used to diagnose guillain barre syndrome

A
  • the brighton criteria
112
Q

what is the treatment for guillain barre syndrome?

A

IV Ig

plasma exchange

supportive care

VTE prophylaxis

if respiratory failure then intubation and ventilation

113
Q

prognosis in guillain barre syndrome

A

80% fully recover

15% are left with neurological disability

5% will die

114
Q

which type of neurofibromatosis is more common

A

NF1

115
Q

what chromosome is the NF1 gene found on

A

chromosome 17

116
Q

what is the NF1 gene

A

chomosome 17

codes for ‘neurofibromin’ a tumour suppressor protein

117
Q

what is inheritance pattern of NF1

A

Autosomal dominant

118
Q

what is the criteria for diagnosing NF1

A
  • CRABBING: must have 2 of the 7
    • Cafe-au-lait spots (6 or more)
    • Relative with NF1
    • Axillary or inguinal freckles
    • BB- Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
    • Iris hamartomas (lisch nodules) 2 or more
    • Neurofibromas (2 or more)
    • Glioma of the optic nerve
119
Q

complications of NF1

A

migraines

epilepsy

renal artery stenosis causing hypertension

scoliosis

vision loss (optic nerve gliomas)

malignant peripheral nerve sheath tumours

gastrointestinal stromal tumour

brain tumour

increased risk of cancer

120
Q

on which chromosome is the NF2 gene found

A

chromosome 22

121
Q

what is the protein that the NF2 gene codes for called and what does it do?

A

merlin

it is a tumour suppressor protein that’s important in schwann cells

122
Q

what is the inheritance of NF2

A

autosomal dominant

123
Q

what happens in NF2

A
  • acoustic neuromas
    • hearing loss
    • tinnitus
    • balance problems
  • schwannomas in the brain and spinal cord
    • symptoms based on location

NB bilateral acoustic neuromas almost always means NF2

124
Q

what is tuberous sclerosis

A
  • genetic condition characterised by the development of hamartomas
  • these are benign growths of the tissue they originate from
  • they cause problems based on their location
  • classically arise from
    • skin
    • brain
    • lungs
    • heart
    • kidneys
    • eyes
125
Q

what are the mutations in tuberous sclerosis

A
  • tuberous sclerosis is caused by mutations in one of the following:
    • TSC1 on chromosome 9: codes for hamartin
    • TSC2 on chromosome 16: codes for tuberin

hamartin and tuberin interact with each other to control the size and growth of cells

126
Q

skin signs in tuberous sclerosis

A

ash leaf spots: depigmented skin in ash leaf shape

shagreen patches: thickened, dimpled, pigmented patches

angiofibromas: small papules over nose and cheeks

subungual fibromata: painless fibromas in nail bed that displace the nail

cafe-au-lait spots: light brown pigmented lesions on skin

poliosis: isolated patch of white hair on head, eyebrows, eyelashes or beard

127
Q

neurological features of tuberous sclerosis

A

epilepsy

learning disability and developmental delay

128
Q

what is the clasical presentation of tuberous sclerosis

A

a child presenting with epilepsy found to have skin features of tuberous sclerosis. It can also present in adulthood

129
Q

what is the management of tuberous sclerosis

A

upportive with monitoring and treating complications such as epilepsy. There is no treatment for the underlying gene defect

130
Q

how long does sinusitus take to resolve

A

normally resolves within 2-3 weeks

131
Q

what are the three branches of the trigeminal nerve

A

Ophthalmic (V1)

Maxillary (V2)

Mandibular (V3)

132
Q

how long do migraines last

A

4-72 hours

133
Q

what are the 5 stages of migraine

A
  • Premonitory or prodromal stage (can begin 3 days before the headache)
  • 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
134
Q

what are triptans

A

5HT receptor agonists (seretonin receptor agonists)

135
Q

acute management of migraines

A

paraetamol

triptans (50mg as the migraine starts)

NSAIDs

antiemetics (e.g metoclopramide) if vomiting occurs

136
Q

migraine prophylaxis

A

avoid known triggers

propanolol

topirimate (teratogenic and must not get pregnant)

amitriptyline

137
Q

how are cluster head aches spread out over time

A

come in clusters of attacks and then disappear for a while

For example, a patient may suffer 3 – 4 attacks a day for weeks or months followed by a pain-free period lasting 1-2 years.

Attacks last between 15 minutes and 3 hours.

138
Q

symptoms of cluster headache

A
  • typically unilateral
  • extremely severe pain
  • red swollen watering eye
  • pupil constriction
  • eyelid drooping
  • nasal discharge
  • facial sweating
139
Q

acute management of cluster headaches

A
  • Triptans (6mg injected subcut)
  • 100% high flow oxygen for 15-20 minutes
140
Q

cluster headache prophylaxis

A
  • Verapamil
  • Lithium
  • Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)

Finals (19 decks)

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