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CCC > Primary care - Neurological > Flashcards

Primary care - Neurological Flashcards

1
Q

What is epilepsy?

A

Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures

  • general=both hemispheres
  • focal=one area within 1 hemisphere
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2
Q

What causes epilepsy?

A

2/3rd = idiopathic

1/3rd have identified cause:

  • Space-occupying lesion e.g. neoplasm
  • Head injury or cortical scarring from previous head injury
  • CNS infections
  • Stroke
  • Hippocampal sclerosis after febrile convulsion
  • Vascular malformations
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3
Q

What are some triggers of seizures?

A

Stress
Flashing lights
Alcohol/alcohol withdrawal

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4
Q

What are the common features of focal/partial seizures?

A

-focal motor/sensory (olfactory-smells, visual-flashing lights) /autonomic/psychic (change in mood/behaviour) symptoms

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5
Q

What is a focal/partial seizure?

3 types of focal/partial seizure?

A

Start in one area of one side of the brain. Often seen with underlying structural disease

3 types:
1. Without impairment of consciousness ‘simple’:

  1. With impairment of consciousness ‘complex’
    - most commonly temporal lobe
    - post-ictal confusion (headache, confusion, myalgia, temporary weakness, dysphasia)
  2. Focal to bilateral tonic-clonic seizure (2/3s progress to generalised seizure-convulsive)
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6
Q

What are generalised seizures?

What are the different types and how do they present?

What features are present for all of these?

A

Involve both hemispheres of the brain

  1. Tonic-clonic - LOC, stiff limbs (tonic) then jerk (clonic). Tongue biting, incontinence. Post-ictal confusion and drowsiness
  2. Absence seizures - brief (less than 10 sec) pauses e.g. stares into space for 5 seconds then resumes talking, common in childhood
  3. Myoclonic - sudden shock like jerk of limb/trunk/face
  4. Atonic - all muscles relax and drop to floor, no LOC
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7
Q

What investigations should you do in epilepsy? (bedside, bloods, imaging, special)

A

EPILEPSY

Bedside
-ECG-1st line for all adults
• arrhythmia or long QT

Bloods
-for acquired causes: FBC, U&E, LFTs, Glucose, Ca2+

Imagning
MRI - if new Dx in adults to exclude infective or vascular causes (do not do routinely)

Special tests
-EEG
•after 2nd seizure or 1st if considered necessary by neurologist
•should add to clinical diagnosis (cannot exclude epilepsy)

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8
Q

What are DVLA guidelines related to seizures?

A

Inform DVLA:
• 1st unprovoked seizure – stop driving for 6 months.
• Epileptic seizure – stop driving until seizure-free for 1 year.
• No HGV driving until seizure free and no meds for 10 years

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9
Q

What are 1st line treatment for focal/partial seizures?

A

1st line - carbamazepine or lamotrigine

2nd line - sodium valproate

Extra info:
Prescribe brand name - changing brand has 10% risk of worse seizure control

AEDs can only be prescribed following confirmed diagnosis (usually after second
seizure)

Patients on AEDs are entitled to free prescriptions

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10
Q

What are 1st line treatment for all generalised seizures?

A

Sodium valproate

second line is normally lamotrigine (unless absence)

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11
Q

What type of seizures should you AVOID carbamazepine in ?

A

Carbamazepine can worsen:
Absence
Myoclonic (if sodium valproate CI>2nd line levetiracetam)

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12
Q

Which anti-epileptic drug must be strictly avoided in pregnancy?
What should they take instead?

A

Sodium valproate is the most teratogenic (do not give if sexually active or pregnant)

Lamotrigine is preferred

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13
Q

What are the side effects of sodium valproate?

A

vALPROATE

Appetite increase - weight gain
Liver failure
Pancreatitis
Reversible hair loss - grows back curly
Oedema
Ataxia
Teratogenicity, thrombocytopenia, tremor
Encephalopathy
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14
Q

Which drug should you avoid if taking sodium valproate?

A

Aspirin - it displaces sodium valproate from its binding sites which increases the adverse effects

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15
Q

When is carbamazepine contraindicated?

A

AV node conduction abnormalities

Bone marrow depression

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16
Q

Define stroke and TIA - specifying the differences

A

Stroke = sudden onset of focal/global neurological disturbance lasting over 24 hours. Causes irreversible cell damage + death.

TIA = less than 24 hour neurological dysfunction caused by ischaemia

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17
Q

What heart diseases particularly predispose you to ischaemic stroke?

A

AF
Infective endocarditis
Valve disease
Heart failure

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18
Q

What are some causes of stroke?

A
  • Most common is atherosclerotic plaque aetiology
  • Haemorrhage: aneurysm rupture, SAH,HTN, trauma
  • Carotid artery dissection (most common cause of ischimic stroke in young people)
  • Cerebral embolism (from AF, endocarditis, MI)
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19
Q

What is the most common cause of ischaemic stroke in young people?

A

Carotid artery dissection - usually caused by hitting their chin and hyperextending their neck, rupturing the carotid artery

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20
Q

What symptoms point more towards a bleed than ischaemia?

A

Meningism
Severe headache
Coma
Seizure

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21
Q

What does the anterior cerebral artery supply?

How would an anterior cerebral artery stroke present?

A

ACA supplies frontal + medial side of cerebrum
(medial side supplies legs (think homunculus)

-Contralateral leg weakness and sensory loss (lower limb>upper limb (FOOT DROP)

  • personality change/depression
  • urinary incontinance
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22
Q

What does the middle cerebral artery MCA supply?

How would an middle cerebral artery stroke present? (4)

A

-MCA supplies lateral side of cerebrum

  • Contralateral weakness and sensory loss (upper limb>lower limb) effecting ARMS more
  • Contralateral homonymous hemianopia
  • If DOMINANT HEMISPHERE then aphasia (e.g. left side for most people)
  • If NON DOMINANT HEMISPHERE then affects neglect (the patient will neglect the opposite side to the hemisphere)
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23
Q

How would a total anterior circulation stroke (TACS) present?
What artery occlusion normally causes this?

A

TACS (total anterior circulation stroke) includes the ACA and MCA

ALL 3 OF FOLLOWING

  1. Unilateral weakness (and or sensory) of face, arm, leg
  2. Higher cerebral dysfunction (dysphasia, visuospatial)
  3. Homonymous hemianopia (if involving optic radiation)

If partial, then 2/3 are present

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24
Q

How does a posterior circulation stroke (POCS) present? (6)

A

Either one of the following:

  • Cranial nerve lesions with contralateral motor/sensory deficit
  • Eye movement disorder (gaze palsy)
  • Isolated homonymous hemianopia (posterior cerebral artery)
  • Loss of conciseness
  • Cerebral/brainstem syndrome (coordination/ataxia)
  • Bilateral motor/sensory defect
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25
Q

Which vessels are occulded in POCS?

A

-posterior cerebral artery, basilar artery, vertebral artery or cerebellar artery

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26
Q

What symptoms are in cerebellar dysfunction?

A

DANISH

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech/Scanning dysarthria (monotonous voice) 
Hypotonia/hyporeflexia

*Think POCS

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27
Q

What are symptoms of partial anterior circulation syndrome (PACS)?

What vessel is occluded?

A

PACS (partial anterior circulation stroke) involves the ANTERIOR circulation

isolated higher cortical function
OR
any 2 of hemiparises, hemianopia, higher cortical function

normally occlusion of branch of MCA (midde cerebral artery)

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28
Q

Managment of acute stroke? (4)

A

ABCDEG assessment
FAST screen
ROSIER to confirm stroke diagnosis
URGENT CT HEAD (non contrast) WITHIN 1 HOUR

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29
Q

What is the acute management of an ischaemic stroke?

A

IF WITHIN 4.5 HOURS

  • Give ALTEPLASE thrombolysis once haemorrhage is excluded by CT (ischemia will look dark on CT). (0.9mg/kg max 90mg, 10% as a bolus)
  • Control BP (<180/110)
  • do CT 24 hours after to look for bleeds
  • Then if okay give 300mg aspirin within 24 hours

IF AFTER 4.5 HOURS

  • Give aspirin 300mg for 2 weeks
  • May need thrombectomy if within 6.5 hours
  • FIND CAUSE:
  • carotid USS, 24hr ECG for AF
  • angiogram (might need thrombectomy if PCA and within 24 hours)
  • if no cause found do echo (infective endo/mitral stenosis)
  • TREAT COMPLICATIONS (aspiration pneumonia-chest X ray)
  • ADMIT to stroke ward- NBM
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30
Q

What is alteplase?

A

Recombinant tPa- tissue plasminogen activator (helps break down clot)

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31
Q

What causes a unilateral progressive vision loss ‘like a curtain descending’?

A

amaurosis fugax = TIA of retinal artery

can get this with a stroke

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32
Q

What is the acute management of a haemorrhagic stroke? (4)

A
  • prothrombin and vitamin K to normalise clotting
  • refer to neurosurgeons
  • control BP aim for 130-140 (amlopopine/IV labetolol)
  • nill by mouth and treat complications (aspiration pneumonia)
  • refer to stroke ward
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33
Q

What must be assessed in all stroke patients?

A

Swallow assessment

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34
Q

What does a CT head look like in acute/chronic ischaemia?

A

Acute - thrombus/embolus may be visible as hyper-dense segment of a vessel

Chronic - hypo-dense (dark) area with negative mass effect (midline shift towards infarct)

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35
Q

acute management of TIA? (3)

A
  1. ABCDEG ASSESMENT
  2. IMMEDIATELY GIVE 300mg ASPIRIN (daily until TIA clinic then reduce to 75mg clopidergrol)
  3. URGET REFERAL TO TIA CLINIC within 24 hours or ASAP if they take anticoags or have bleeding disorder

(-if happened a week ago-TIA clinic in 7 days)

(carotid imaging: if >50% stenosis do endardectomy)

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36
Q

How do you differentiate between extradural and subdural haematoma on CT head?

What about SAH?

A

Both have positive mass effect-push brain away

Extradural haematoma

  • lens shape of bleeding (eggstradural) (confined by suture lines)
  • Usually arterial (needs pressure to tear dural away from skull)
  • can’t cross sutures of skull
  • can cross midline

Subdural haematoma

  • crescent shape of bleeding (not confined by suture lines of dura-because its under dural)
  • Sliver - venous bleed between dura and arachnoid
  • can cross sutures of skull
  • can’t cross midline

subarachnoid-loss of sulk and gyrus

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37
Q

What is the difference in onset between sub-dural and extradural haematoma?

How do the pattern of consciousness differ?

A

-Sub-dural haematoma is SLOWER (Subdural Slow)
you tend to get fluctuation in conciseness/confusion over several DAYS

  • Extra-dural is faster (hours) (Extradural Emergency)
  • ‘Talk and die’ lucidity sequelae. LOC>full recovery>rapid neuro degeneration and LOC
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38
Q

What is motor neurone disease?

A

A group of neurological disorders affecting neurones in spinal cord, brainstem and motor cortex

Affects upper and lower motor neurons

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39
Q

What are UMN signs?

A 
Weakness
Spasticity
Hypertonia
Hyperreflexia i.e. brisk reflexes
Upgoing plantar reflex
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40
Q

What are LMN signs?

A

Weakness
Hypotonia
Hyporeflexia
Fasciculation

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41
Q

What symptoms never appear in motor neurone disease?

A

Eye movement problems

Sensory loss

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42
Q

What is amyotrophic lateral sclerosis (ALS)?

A

Presents as UMN in legs and LMN signs in arms

It may be familial - associated with Ch21

50% of cases of MND

43
Q

What is the prognosis of MND?

A

Rapidly progressive

Death usually results from ventilatory failure 3-5 years post-diagnosis

44
Q

What are the types of MND?

A

Amyotrophic lateral sclerosis (ALS)
Bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

45
Q

What is the difference between progressive muscular atrophy and primary lateral sclerosis?

A

Progressive muscular atrophy - only LMN affected

Primary lateral sclerosis - only UMN affected

46
Q

What is the only licensed drug for MND?

A

Riluzole - prolongs life by 3 months; requires LFT monitoring

47
Q

What is the pathophysiology of Parkinson’s disease?

Managment of parkinsons disease?

A
  • Loss of dopaminergic neurons in substantia nigra (part of the basal ganglia-motor function)
  • Therefore, there is a deficiency of dopamine and relative excess of ACh

Managment

  • bio (meds and interactions)
  • psycho (sleep, depression)
  • social (managing at home)
48
Q

What is the extrapyramidal triad of Parkinsonism?

What are other symptoms to ask about in Parkinson’s history?

A

PARKINSONISM

  1. Tremor (70% patients)
    - ‘pill-rolling’, 4-6Hz
    - resting tremor
    - unilateral
  2. Rigitity
    - cogwheel rigidity of wrist
    - lead piping rigidity
  3. Bradykinesia
    - mask-like face, slow to initiate movement, shuffling/festinating gait (leaning forward), decreased arm swing

Parkinsonism can be caused by PD, or other causes

Other questions

  • hand writing changed? (micrographia)
  • how is your sleep?
  • how is your mood (depression)
  • any voice changes? (quiet voice)
  • Urinary symptoms (FUNI)? (luti)
  • Has your sex life been affected?
  • Have you had any falls?
49
Q

What are the 4 causes of parkinsonism?

A

PARKINSONISM

1) Parksinson’s disease (asymmetrical, good treatment responce)
2) Parkinson plus syndromes
3) Drug induced (metoclopramide, antipsychotics, lithium)
4) Other (vascular, post infection, tumour)

50
Q

What are the parkinson plus syndromes (4) and how can you differential between them and PD?

A

1) Multiple system atrophy (autonomic symptoms, hyotension, cerebellar signs, poor dopamine treatment response)
2) Supra nuclear palsy (Ocular paresis-cant look up)
3) Corticobasal degeneration (apraxia, alien limb)
4) Lewy body dementia
- visual hallucinations
- fluctuating consciousness
- dementia (<1 year)

51
Q

Describe a Parkinsonian gait

A

Parkinsonian gait

  • Hesitant - difficulty initiating + turning
  • Shuffling - small steps
  • Festinating - walks faster and faster to not fall over
  • Lack of arm swing
  • Stooped posture
  • Unsteadiness
52
Q

What sign is seen with glabella tap in Parkinson’s?

A

Myerson’s sign - blinking fails to cease with tapping on forehead

53
Q

What is often used as 1st line for parkinson’s?

A

1st line drug for Parkinson’s disease:

  • Levodopa+dopa decarboxylase to prevent peripheral dopamine conversion(gold standard if affecting Q of Life or late disease)
  • Dopamine receptor agonist, given to younger patients with parkinsons (save levodopa for later) (bromocriptine, pramipexole, ropinirole)
  • Monoamine oxidase B inhibitors e.g. Selegiline (less effective but less side effects )
54
Q

What type of drug are Sinemet and Madopar?

A

Levodopa = dopamine precursor

55
Q

How do you diagnose PD?

A

Diagnosing parkinsons disease

1) confirm parkinsonism (bradykenisia, rigidity, tremor)
2) exclude other causes (if palsy or cerebellar signs)
3) supporting evidence (e.g. responds to treatment)

56
Q

What are some side effects of levodopa?

What does this mean in terms of prescribing it?

A
  • Dyskinesia
  • Dystonia (painful)
  • Psychosis
  • Nausea + vomiting

The efficacy reduces over time, which requires much larger doses –> more side effects.

Start levodopa late i.e. over 70 years old or when Parkinson’s seriously affects life

57
Q

What are some side effects of dopamine agonists?

A

Dopamine agonists: bromocriptine, pramipexole ropinirole

  • Compulsive behaviour e.g. gambling, hypersexuality, hallucinations
  • Ergot derived drugs (older type) e.g. bromocriptine can cause fibrosis (heart, lungs)
58
Q

driving advise for TIA/stroke?

A
  • dont drive for 1 month

- inform DVLA if drive for job

59
Q

differentials/stroke mimics?

A

• Hypoglycaemia
• Hyponatraemia
• Hypercalcaemia
• Migraine with aura (sensory or visual) (can also mimic raised ICP
○ You can get aura without headache
○ Headache not present in thrombolytic stroke and is present in heamorragic
• Epilepsy (Todds palsy)
• Black out/syncope
• MS
• Subdural haemorrhage (headache, trauma)
•Beauty parlour syndrome (vertigo diplopia insufficiency)

60
Q

What type of dysphagia is Wernikes?
How are the patients feeling?
What part of brain effected?
Explain it to a patient

A
  • Wernikes (rernikes) is receptive dysphagia (comprehension)
  • patient is happy as has no insight (like Byron in the video) may get annoyed if people don’t understand
  • left temporal cortex effected
  • Filing cabinet has been mixed up
61
Q 
What type of dysphagia is Brocas?
How are the patients feeling?
What can be useful for these patients?
What part of brain effected?
Explain it to a patient
A
  • Brocas is expressive (fluency)
  • Patient is frustrated as they can’t find the words and have insight (Sarah in vid)
  • These need pointy board at hospital
  • Left frontal cortex effected
  • Filing cabinet has stiff doors-cant get words out (articulation)
62
Q

Lesion at optic chiasma symptoms and common cause?

A

-Lesion at optic chiasma causes bitemporal hemianopia

63
Q

Lesion at optic tract symptoms?

A
  • Lesion at optic tract -leads to contralateral homonymous hemianopia
    e. g. right optic tract lesion= lose left side of both eyes
64
Q

Important questions to ask in a TIA/stroke history?

A
  • Memory loss
  • Visual loss- amorosos fujax (curtain falls down Eyesite)
  • Diplopia-double vision
  • Facial weakness (2/3rds FOREHEAD SPARED)
  • Speech problems (slurring, cant find) dysarthria, dysphasia
  • Swallow problems (dysphagia)
  • Sensory change (numbness/tingling)
  • Arm weakness
  • Bladder/bowel weakness
65
Q

Acute treatment of migraine

A

MIGRAIN (acute)
acute: triptan + NSAID or triptan + paracetamol
(nasal triptan if age 12-17)

66
Q

What is the prophylaxis for migraine? When is this indicated?

A

MIGRAINE (prophylactic)

-prophylaxis (if 2+ attacks a month): propranolol (not in asthma) or topiramate (not in pregnancy or on pill)

67
Q

A patient has ACUTE ONSET confabulation and confusion, what artery is their stroke likely to be?

A

Posterior cerebral artery (memory problems causes confabulation)

68
Q

A patient has ACUTE ONSET speech affected, what artery is their stroke likely to be?

A

Middle cerebral artery (most likely their left i think)

69
Q

Women presents with ACUTE ONSET right sided leg weakness and numbness, what artery is their stroke likely to be?

A

left anterior cerebral artery (supplies foot-think homunculus)

70
Q

What do you give in the community if suspected bacterial meningitis?

A

In the community, give IM benzylpenicillinbefore urgent hospital transfer

71
Q

If someone is allergic to clopidegrol and needs it long term after a stroke what do you give?

A

Give aspirin and dipyramidole if allergic to clopidergrol

72
Q

If you’ve had a stroke, how long should you not drive for?

A

STROKE AND DRIVING

  • no driving for 1 month
  • if HGV driver no driving for 1 year
73
Q

What is malignant MCA syndrome

A

-build up of oedema> midline shift> increased ICP

74
Q

How would a posterior cerebral artery (PCA) stroke present?

A

PCA stroke

  • contralateral hemianopia with MACULAR SPARING
  • contralateral loss of temperature and pain (damage to thalaumus)
75
Q

How does a vertebrobasiclar artery stroke present?

A

Vertebrobasiclar stroke

  • reduced conciousness
  • cerebellar signs (DANISH)
  • quadraplegia/hemiplegia
76
Q

What is second line treatment for PD?

A

Apomorphine (injection) used in advanced parkinsons disease>1st dose gives significant postural hypotension so monster

77
Q

?What artery lesion would cause ‘locked in syndrome’

A

Basilary artery> no blood to pons>locked in syndrome

basilar artery strokes dont affect higher cerebral function

78
Q

What are symptoms of a lacunar stroke?

A

Lacunar stroke, one of the following: (small perforating arteries around hypothalamus, internal capsule, BG)

  • ataxic hemiparesis
  • pure sensory
  • pure motor (e.g. dysarthria)
  • sensori-motor

NO LOSS OF HIGHER CEREBRAL FUNCTIONS (dysphasia)

79
Q

What type of stroke is a thrombectomy useful for?

A

thrombectomy provides benefit for anterior circulation strokes (within 24 hours)

80
Q

Face and arm weakness-what artery?

A

Face and arm wekaness= Middle cerebral artery (FAM)

81
Q

Secondary prevention of stroke- how do you manage cause/risk factors?

A 
STROKE- MANAGE CAUSE/RISK FACTORS 
· Echo and carotid USS (look for AF)
· Control HTN 
	▪ If haemorrhagic-keep low 
        ▪ If thrombolytic- stop hypertensives to aid with reperfusion 
· Control diabetes
· Check thyroid (AF)
· Control cholesterol  if cholesterol >3.5
	▪  Atorvastatin 80mg (LFTs at baseline 3 and 12 months) 
	▪ Diet and weight 
	▪  Exercise 
	▪ Smoking and alcohol
82
Q

Secondary prevention of stroke- how do you prevent further disease for ischemic stroke?
What about if it was due to AF?

A

ISCHEMIC STROKE- PREVENT FURTHER DISEASE

  1. 300mg Aspirin for 2 weeks/until discharge (or 600mg rectal if no swallow)
    * stop warfarin/DOAC for 2 weeks> can bleed on top of ischemia
  2. Aspirin and clopidogrol 75mg (1-3 months)
  3. Lifelong clopidogrel 75mg (opposite to MI)

IF CAUSED BY AF: give anticoagulation DOAC/warfarin if (but start 2 weeks after)

83
Q

What complications could you get from stroke?

A

STROKE COMPLICATIONS
○ Stroke rehabilitation
- Vision changes
- Swallowing
- Speech and language therapist SALT
- Nutrition and hydration (PEG feed long term)-dietition
- Pain
- Mobility
- Pressure areas(tissue viability nurses-pressure sores)
- Continence-Community continence team
- Emotional and psychological-Psychological support
- Neglect/inattention of other side of lesion (dog bowl)

84
Q

When would you arrange follow up for stroke?

A

STROKE FOLLOW UP

- 6 months at GP then annually

85
Q

How would a temporal lobe siezure present?

A

TEMPORAL LOBE SEIZURE (head)
H-hallucinations (smell/taste/sound)
E-emotional disturbance (anger/panic/elation/derealization)
A-automatisms (assosiated with impaired awareness)
>lip smacking/chewing/swallowing
>fumbling/fiddling/grabbing
D-deja/jamais vu/dysphasia (wernikes temporal area)

86
Q

How would a frontal lobe siezure present?

A

FRONTAL LOBE SIEZURE (motor symptoms-pre-central gyrus)
Impaired inhibition
Speech arrest (Brokas area frontal lobe)
Motor features-peddling of legs
-jacksonian march (spreading focal motor seize with RETAINED awareness)

87
Q

How would a parietal lobe siezure present?

A 
PARIETEL SIEZURE (post central gyrus) 
-sensory disturbances: tingling/numbless/ pain (rare)
88
Q

How would a occipital lobe siezure present?

A

OCCIPITAL LOBE SEIZURE

-visual phenomena (riots/lines/flashes)

89
Q

How do anti epileptic drugs affect contraception?

A

Anti-epileptic drugs are P450 enzyme INDUCERS so they make progesterone-only contraception unreliable.

Oestrogen-containing contraceptives lower lamotrigine levels so need increased dose.

90
Q

How do you commence anti epileptic drugs

A
  • Start low and increase dose until siezures stopped or max dose reached
  • Then if no effect, switch to second drug, introduce slowly and withdraw only when fully established on 2nd drug
91
Q

Indications for stopping AED?

A
  • if patient has been seizure free >2 years

- dose reduced slowly 2-3 months

92
Q

What is drug of choice for absence siezures?

A

Ethosuximide is drug of choice for absence siezires (or sodium val)

93
Q

What visual changes would you expect in a pituitary gland tumour?

A

Pituitary gland tumour causes tunnel vision (bitemporal hemionopia)

94
Q

What is a lacunar syndrome?

A

Lacunar syndrome

  • pure sensory
  • pure motor
  • sensori-motor
  • ataxic hemiparises
95
Q

What is multi system atrophy?

A 
Multi system atrophy is a triad of: 
-Impotence 
-Urinary retention 
-Postural hypotension 
(with poor response to Levodopa)
96
Q

What is cause of valvular AF?

A

Mitral stenosis (increased after load> increase pressure> affects pacing>AF> risk of stroke

97
Q

What is a risk of hairdresser hair washing/cyropractic manipulation? (in terms of stroke)

A

Vertebral artery dissection (presents with posterior stroke)

98
Q

What test would show a patent foramen ovale?

A

Bubble echocardiogram (see if the bubbles pass between atria)

99
Q

Which patients with carotid stenosis should have carotid endarterectomy? (according to NICE)

A

Stenosis 50-99% can have carotid endarterectomy

100
Q

What is malignant MCA syndrome?

Whats diagnostic investigation?

A
  • Cerebral odema and raised ICP following stroke

- URGENT HEAD CT

101
Q

What is the BP aim for haemorrhagic stroke?

A

-control BP aim for 130-140 (amlopopine/IV labetolol)

102
Q

What is the only DOAC that has a reversal agent?

A

Dabigatran>idarucizamab

103
Q

Young + atonic siezure: what would you think?

A

lennox-gastaut

104
Q

Young + myoclonic siezure: what would you think?

A

Juvenile myoclonic epilepsy

CCC (15 decks)

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