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3rd Year Medicine UoM > Neurology > Flashcards

Neurology Flashcards

1
Q

what is an extra-dural haematoma?

A

aka epidural haematoma
traumatic brain injury can cause an artery to haemorrhage (usually middle meningeal artery)
blood builds up between skull and dura

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2
Q

how is an acute rise in ICP managed?

A

1) heavy sedation +/- paralysis
2) manitol (osmotic diuretic - draws water across BBB into circulation)
3) hyperventilation - decreased PaCO2
4) CSF drainage
5) barbiturates = phenobarbitone - into coma
6) surgical treatment
- decompressive craniectomy (decreases ICP by 15%, if open dura as well, decrease ICP by 70%)

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3
Q

what are the common benign brain tumours?

A
  • meningioma 20%
  • pituitary tumour 5%
  • neural sheath tumour (vestibula schwannema) 5%
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4
Q

how does a tension like headache present?

A 
bilateral, band like headache
mild-moderate pain 
lasting ~30  mins 
no vomiting or nausea 
may have slight photo OR phonophobia (not both)
scalp muscle tenderness 
possible due to head/neck muscle tension
not worsened with daily activities
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5
Q

how does a subdural haematoma present?

A

traumatic injury AND seizures, incontinence, neurological decline
occurs slowly (veins leak slower than arteries) - can present days - months after injury
fluctuating levels of consciousness for a period of time is typical as the haematoma contracts and expands due to osmotic effect

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6
Q

what is the monro kellie doctrine?

A

increase in components in the cranium will cause displacement of other components = compliance
compliance phase ends when no more components to displace and then ICP begins to raise

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7
Q

in relation to migraines, which medication can cause an overuse headache?

A

triptans
analgesia
treated with cessation

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8
Q

how do you define chronic/episodic cluster headaches?

A 
chronic = remission < 7 months in 12 months 
episodic = 1 every other day up to 8 a day = remission ? 1 month
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9
Q

how are cluster headaches treated?

A 
acutely = oxygen and nasal/subcutaneous triptans 
prophylaxis = verapamil, prednisolone
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10
Q

what are syndromes causing familial brain tumours?

A

neurofibromatosis
von hippel lindau syndrome
tuberous sclerosis

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11
Q

how is a subdural haematoma treated?

A

IF <10MM, NON-EXPANSILE, NO SIG. NEUROLOGICAL DEFICITS

1) observe, monitor GCS, imaging
2) prophylactic anti-epileptics (phenytoin, phenobarbital)
3) correction of coagulopathy
4) ICP lowering regime

IF >10MM, EXPANSILE AND W/ NEURO DEFICITS

1) Surgery!
- burr hole drainage (saline washout and suction of clot)
- craniotomy and duraotomy (removal of clot)

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12
Q

what maintains cerebral perfusion

A

CP = mean arterial BP - ICP

raise in ICP means need a raise in arterial BP to maintain cerebral perfusion

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13
Q

how do you classify an acute or chronic headache?

A

occurring on <15 days a month = ACUTE

occurring on >15 days/month for 3 consecutive months = CHRONIC

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14
Q

how is a tension type headache treated?

A

stress relief
aspirin/ibruprofen
drink water - to rule out dehydration

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15
Q

what does the prophylactic treatment of migraines include?

A

1ST LINE
1) beat blocker (propranolol) or topiramate (anti-epileptic- teratogenic)
2) Amitriptyline
3) oestrogen patches for women with menstrual related migraines
2ND LINE
1) Antiepilpetics = sodium valproate/topiramate
2) antihypertensive medication may help some.
3) 12 weekly Botox injections = last resort

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16
Q

features of MRI?

A

magnetic waves
more expensive
takes longer, noisier
better spatial resolution of soft tissue lesions
better identifying between normal/abnormal tissues

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17
Q

what are the diagnostic criteria for migraines?

A

If no aura present:

1) 5+ headaches lasting 4-72 hours
2) with nausea/vomiting (or photo/phono phobia)
3) and 2 of the following
- throbbing/pulsating
- made worse by routine activities
- unilateral

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18
Q

what is 1st investigation for suspected cranial haematoma?

A

non contrast CT scan

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19
Q

what are triptans?

A

strong serotonin agonist - causes vasoconstriction
used to treat migraines
shouldn’t be used more than 10 days a month
CI = IHD, HTN, recent lithium, SSRIs, vasospasms
rare SE - arrhythmias, angina, MI
can take a second dose if needed, must take 2 hours apart

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20
Q

what are routine measures to control raised ICP?

A

1) head up tilt (30-40 degrees)
2) prevent hypertension - use vaso-suppressins
3) sedate - decrease metabolic demands
4) keep neck straight and free
5) maintain euvolemia and normal osmolar state
6) maintain normal PaCO2 ( can raise cerebral blood volume and vasodilation)

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21
Q

what is a subarachnoid haemorrhage?

A

bleeding into the subarachnid space - between the arachnoid and pia matter

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22
Q

how does a migraine present?

A

mainly women
can present as:
aura lasting 15-30 mins followed by unilateral, throbbing headache
OR
isolated aura without headache
OR
episodic severe headaches without aura. usually premenstrual
headache associated with nausea, vomiting, prodrome (precedes headache by hours/days = cravings, yawning, mood/sleep changes), allodynia (all stimuli cause pain e.g. wearing glasses, hair brush)
throbbing pain can last hours - 3 days

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23
Q

how does a subarachnoid haemorrhage present?

A 
thunderclap severe headache
vomiting
seizures 
confusion
decreased consciousness
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24
Q

how do cluster headaches present?

A

unilateral, very severe headache - occurring around the eye and side of face.
associated with agitation, restlessness.
occurring on same side as headache: red, watery eye, swollen eye, nasal congestion and runny nose, sweating, droopy eyelid and constricted pupil
lasting 15-80 minutes

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25
Q

what is considered pathological ICP?

A

persistently > 20 mmHg

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26
Q

how may auras associated with migraines present?

A
  • visual; sincillating scotoma - chaotic, jumbling, partial loss of vision - in one eye or half of visual field in both eyes
  • somatosensory - paraesthesis spreading from fingers to face
  • motor - dysarthria (unclear speech) and ataxia (basilar migrain)
  • speech = dysphasia or paraphasia
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27
Q

what is a subdural haematoma?

A

disruption of bridging veins travelling to the dural venous sinuses- leads to a bleed
blood builds up inbetween dura and arachnoid mater

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28
Q

what are common triggers for migraine?

A

CHOCOLATE
chocolate, hangovers, orgasms, cheese, caffiene, oral contraceptive, lie-ins, alcohol, travel, exercise
loud sounds, flickering lights, menstruation

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29
Q

how are brain tumours classified?

A

primary/secondary
malignant/benign
supertentorial (mostly adults)/infratentorial (children)

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30
Q

when should prophylactic treatment be considered for migraines?

A

if >2 headaches a month

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31
Q

what are causes for raised ICP?

A 
raised brain/tissue volume (lesion/tumour/oedema)
raised CSF (obstruction to drainage, increased production, decreased absorption)
raised blood volume ( obstruction etc)
32
Q

when is botox indicated for treatment of migraines?

A

if patient has tried 3 different migraine preventative medication, each for 3 consecutive months

33
Q

what are features of CT scan?

A
  • multiple X ray images
    radiation exposure
    quick, comfortable
    shows different densities
34
Q

how does an epidural haematoma present?

A

patient regains consciousness from a traumatic head injury

lucid period begins and then slowly deteriorates - loosing consciousness

35
Q

how common are primary malignant brain tumours and which are the most common type?

A

represent 58% of brain tumours

  • glioblastoma multiforme (GBM) . Gliomas can range from agressive, rapid tumours to slowly progressing, indolent tumours. (25% cases)
  • anaplastic astrocytoma (20% )
36
Q

what are symptoms of ICP?

A

new onset headache in patient > 50 YO
vomiting
seizures
visual problems - transient visual loss on changing positions/ standing/bending over
headache progressively worsening, wakes patient from sleep. is present on waking up
headache precipitated by valsalva manoeuvre (e.g. cough/sneeze)
papilloedema, enlarged blind spots, restricted visual fields
pronator drift
HTN
bradycardia
resp depression

37
Q

what is contraindicated in patients who suffer migraines?

A

combined contraceptive pill = CI in patients with migraine AND aura or >35 YO with migraines.
increases risk of CV events - mainly ischaemic stroke

38
Q

when should a headache patient receive a 2WW suspected cancer referral?

A

1) headaches with features of raised ICP
2) headaches with new onset seizures
3) headache with neurological deficit
4) headache with sig. history of malignancy (metastasis)
5) vomiting without any other explanation

39
Q

how are migraines managed/treated?

A

first line = NSAIDs, antiemetics (domperidone, prochlorperizine)
second line = triptans (sumatriptan, zolmitriptin)

40
Q

what is giant cell arteritis?

A

AKA temporal arteritis

  • common form of vasculitis in patients aged 50+
  • usually affects extra cranial branches of the carotid
41
Q

how does temporal arteritis present?

A 
headache (occipital or temporal areas_
blurring of vision 
sudden blindness 
sensitive scalp 
polymyalgia rheumatica 
systemic symptoms = low grade fever, lethargy, weakness, weight loss
42
Q

how is temporal arteritis treated?

A

once diagnosed it is an emergency

  • high dose steroids immediately to prevent sudden blindness from opthalmic artery occlusion
  • temporal biopsy can be performed once on steroids
43
Q

how is temporal arteritis diagnosed?

A

raised ALP, ESR, CRP and maybe platelets
non invasive- 3T MRI
biopsy = gold standard

44
Q

what are categories of syncope?

A

reflex syncope
(neurally mediated - sudden decrease in BP and HR in response to a trigger e.g. vasovagal syncope)

cardiogenic syncope
(LOC due to decrease in cardiac output e.g. arrhythmias)

orthostatic hypotension 
(LOC after standing up due to sudden drop in BP e.g. hypovolaemia, medication, autonomic failure)

TIA/stroke

45
Q

what are the differentials for loss of consciousness? (LOC)

A

syncope

or seizures

46
Q

how is a seizure defined?

A

a transient occurrence of signs or/and symptoms due to abnormal excessive neurological activity in the brain

47
Q

what is syncope? what are its characteristics?

A

LOC due to cerebral hypoperfusion

1) rapid onset
2) short duration
3) spontaneous and complete recovery

48
Q

how can you distinguish between a seizure or a syncope?

A

BEFORE
syncope will usually have an immediate before trigger (e.g. exercise, emotion) and a pre-syncope warning e.g. dizziness, visual tunnelling.
syncope patients will become pale, seizure patients will become blue (Cyanosis)
DURING
seizures are longer usually
tongue biting and incontinence are more associated with seizures.
both have convulsions
AFTER
seizures will have confusion/fatigue lasting hours. syncope will recover immediately with no lasting effects

49
Q

syncope without presyncopal symptoms raises suspicion of …??

A

cardiogenic syncope

50
Q

how does NEAD present? (non epileptic attack disorder)

A

similar to a tonic-clonic seizure with continuous limb shaking but with suggestive elements:

  • gradual onset, prolonged duration and abrupt termination
  • closed eyes and resistance to being opened
  • rapid breathing
  • episodes of motionless unresponsiveness
  • variable maintenance of unconsciousness
  • side to side head motion
  • pelvic thrust/ back arching
  • change in emotion when waking
51
Q

how are seizures classified ?

A

generalised - starts in one point but rapidly spreads bilaterally leading to simultaneous onset of widespread electrical discharge with no localising feature referring to a single hemisphere

focal - (aka localised/partial seizure) only affecting one network/ hemisphere of the brain. - often seen with underlying structural disease. different features will localise it to a different hemisphere e.g. temporal/occipital.

52
Q

what are the types of generalised seizures?

A

absence seizures = brief pauses < 10 seconds. presents in childhood

tonic-clonic seizure = loss of consciousness. muscles stiffen (tonic) and jerk (clonic). post-ictal drowsiness and confusion

myoclonic seizure = sudden jerking of muscles. brief

atonic (akinetic) seizure = sudden loss of muscle tone causing a fall. no LOC

53
Q

what are the types of focal seizure??

A 
simple partial (without impairment of consciousness)
complex partial (with impairment of consciousness)
secondarily generalised (occurs in 2/3 focal seizures)
54
Q

what are provoked seizures?

A

many situations will push anyone to a seizure. they rarely (3-10%) recur and so would not be classified as epileptic. only recur if damage is irreversible

55
Q

what are causes for provoked seizures?

A

trauma, stroke, haemorrhage, rasied ICP, alcohol/benzodiazepine withdrawal, metabolic disturbance, hypoxia, infection (encephalitis, meningitis), raised temp, drugs (cocaine, TCA)

56
Q

what are unprovoked seizures ?

A

seizures which are caused by a natural phenomena in the body e.g. congenital defect, genetics, neurological problems

57
Q

how does vasovagal syncope present?

A

aka convulsive syncope
can present with <15 seconds of convulsions shortly after LOC
usually patient is upright and LOC is preceded by tunnelling of vision or dizziness
LOC is typically very brief and patient quickly returns to baseline

58
Q

what is epilepsy?

A

a recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as convulsions/seizures.

59
Q

what are features of epilepsy?

A
  • patients may experience a prodrome for hours/days before seizure, causing a change in mood or behaviour. an aura may imply a focal seizure in temporal lobe. it may include a strange feeling (gut feeling/ deja vu) or strange smells/lights
  • post-ictally there may be headache, confusion, myalgia, temporary weakness or dysphasia
60
Q

what are causes for epileptic seizures?

A
  • 2/3 cases = idopathic
  • structutal = cortical scarring e.g. from head injury years ago, developmental, SOL, stroke, vascular malformations.
  • others = SLE, sarcoidosis, Tuberous sclerosis
61
Q

what are the rules regarding driving for seizure patients?

A

must contact DVLA and need to be > 1 year seizure free before can drive again

62
Q

should seizure patients be referred?

A

yes, within 2 weeks

63
Q

what investigations should be performed for a seizure patient?

A

rule out provoking factors (LP, drug levels, FBC, Uand E)
MRI scan of brain
EEG

64
Q

when are anti-epileptic drugs started? (AED)

A

after 2nd seizure

65
Q

when shoud AEDs be started after the first seizure?

A
  1. patient has neurological deficit
  2. brain imaging shows structural abnormalities
  3. EEG reading shows unequivocal epileptic activity
    4) family or patient refuse to take the risk of 2nd seizure
66
Q

what is the treatment for tonic clonic generalised seizures?

A

1st line = sodium valproate

2nd line = lamotrigine, carbamazepine

67
Q

what is the treatment for myoclonic generalised seizures?

A

1st line = sodium valproate

2nd line = clonazepam, lamotrigine

68
Q

what is the treatment for absence seizures?

A

1st line = sodium valproate or ethosuximide

69
Q

what is the treatment for focal seizures?

A

1st line = carbamazepine or lamotrigine

2nd line = levetiracetam, oxcarbazepine or sodium valproate

70
Q

what is status epilpeticus?

A

a dangerous condition in which epileptic seizures follow on from each other and the patient fails to regain consciousness between them

71
Q

how is status epilepticus treated?

A

benzodiazepines
IV lorazepam is commonly used
if IV access not obtained can use buccal midazolam

72
Q

what is a common complication post-op which may cause provoked seizures?

A

hyponatraemia

73
Q

what % of the ppln are affected by epilepsy?

A

0.5-1%

74
Q

what is the pathophysiology of epileptic seizures?

A

a disruption in the normal balance between inhibitory and excitatory currents or neurotransmission in the brain resulting in hypersynchronous neural discharge

75
Q

what is the MoA of sodium valproate?

A

increases GABA activity

76
Q

what is the MoA of carbamazepine ?

A

binds to sodium channels-increasing their refractory period

77
Q

what is the MoA of lamotrigine

A

sodium channel blocker

3rd Year Medicine UoM (9 decks)

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