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Phase 3a AW > Neuro ILAs > Flashcards

Neuro ILAs Flashcards

1
Q

What are the eye symptoms and signs in optic neuritis?

A
  • Blurred and cloudy vision
  • Discomfort on eye movement
  • Worse with heat

Signs:

  • Reduced direct and indirect response
  • Decreased visual acuity in one eye
  • Normal fundoscopy and eye movements
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2
Q

What is Marcus Gunn pupil?

A

A medical sign observed during the swinging-flashlight test whereupon the pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye

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3
Q

What is 6/6 for visual acuity?

A

It means you can see at 6 metres what you should see at 6 metres

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4
Q

What are the HELLP questions to ask for unilateral visual loss?

A

Headache associated? Do ESR in all cases >50 years for GCA

Eye movements hurt? Optic neuritis

Lights/ flashes preceding visual loss? Detached retina

Like a curtain descending? Amaurosis Fugax

Poorly controlled diabetes and vitreous haemorrhage

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5
Q

What are the vascular causes of unilateral visual loss?

A

Amaurosis fugax/ central retinal artery occlusion
Central retinal vein occlusion
Anterior Ischaemic Optic Neuropathy (ischaemia of posterior choroidal artery)

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6
Q

What are other causes of unilateral visual loss?

A
  • Optic neuritis
  • Retinal detachment (flashes/floaters)- Vitreous haemorrhage (associated with diabetic retinopathy, also see vitreous floaters)
  • Acute angle closure glaucoma
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7
Q

What are the causes of anterior ischaemic optic neuropathy?

A

Arteritic- Giant Cell Arteritis

Non-arteritic- atherosclerosis

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8
Q

What are the symptoms of GCA?

A

New-onset headache, malaise, jaw claudication, scalp tenderness, neck pain
Unilateral visual loss

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9
Q

What is GCA associated with?

A

Polymyalgia rheumatica

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10
Q

What are the tests for GCA?

A

ESR and CRP

Temporal artery biopsy

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11
Q

What is the treatment for GCA?

A

Prednisolone 60mg/24 hours

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12
Q

What are the symptoms of optic neuritis?

A 
Afferent pupillary defect
Subacute loss of vision
Colour vision is affected
Eye movements hurt
Exacerbated by heat or exercise
Risk of developing MS
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13
Q

What are the causes of optic neuritis except MS?

A

Inflammation of optic nerve

Syphilis
Leber’s optic atrophy
DM
Vitamin deficiency

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14
Q

What is the treatment of optic neuritis?

A

High dose methylprednisolone for 72 hours
(1000mg/24 hours IV)
Then Pred 1mg/kg PO for 11 days

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15
Q

What is retinal vein occlusion?

A

Second most common cause of blindness from retinal vascular disease (Diabetic retinopathy is first)

Causes= arteriosclerosis, hypertension, diabetes, polycythaemia, glaucoma

Less sudden than central retinal vein occlusion

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16
Q

How does central retinal vein occlusion present?

A

Sudden onset painless blurred vision in one eye

Can see dilatation of branch veins, multiple retinal haemorrhages and cotton wool patches

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17
Q

What investigations would you do?

A

History and examination
VEP/MRI (optic neuritis)
Fluorescein angiography (CRVO)
Tonometry- intraocular pressure measure (glaucoma)
USS- vitreous haemorrhage/ retinal detatchment

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18
Q

How is MS diagnosed?

A

The presence of multiple CNS lesions, which cause symptoms that

  • last longer than 24 hours
  • are disseminated in space (clinically or on MRI)
  • are disseminated in time (>1 month apart)
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19
Q

What are the typical features of MS?

A 
Visual loss (Optic neuritis)
Pyramidal weakness, spastic paraparesis
Sensory disturbance
Cerebellar symptoms (nystagmus / vertigo / tremor /ataxia / dysarthria)
Bladder involvement / sexual dysfunction
Lhermitte’s & Uhthoff’s phenomenon
Fatigue
Cognitive impairment
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20
Q

What are the signs in MS?

A

UMN signs: spastic paraparesis, brisk reflexes
Sensory signs
Cerebellar signs (eyes, gait, UL, speech)
Optic atrophy
Relative afferent pupillary defect
Internuclear opthalmoplegia (decreased adduction of ipsilateral eye, nystagmus on abduction of contralateral eye)

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21
Q

What are the investigations in MS?

A

MRI scan
LP-oligoclonal bands
Evoked potentials e.g. VEPs

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22
Q

What is the pathophysiology of MS?

A

-Inflammatory
-Focal loss of myelin, with relative preservation of axons.
Neurodegenerative
-Axonal loss may contribute to fixed and progressive deficits.

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23
Q

Give a differential diagnosis of blackouts?

A

Syncope
Epilepsy
Non-epileptic attacks

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24
Q

What is syncope?

A

Syncope is an abrupt and transient loss of consciousness associated with loss of postural tone that follows a sudden fall in cerebral perfusion.

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25
Q

What is neurogenic syncope?

A

Inappropriate activation of cardio-inhibitory and vasodepressor reflex leading to hypotension

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26
Q

What are the causes of neurogenic syncope?

A

Vasovagal syncope

Reflex syncope with specific precipitants

  • Micturition syncope
  • Cough syncope

Carotid sinus hypersensitivity

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27
Q

What are other causes of syncope?

A
  • Orthostatic syncope (autonomic failure)- primary (multisystem atrophy)
  • Secondary (diabetes, drugs)

Cardiac syncope

  • Arrhythmias
  • Valvular heart disease
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28
Q

What is a seizure?

A

Clinical manifestation of disordered electrical activity in the brain (paroxysmal discharge of cerebral neurones)

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29
Q

What is epilepsy?

A

Tendency to recurrent seizures

30
Q

How can you differentiate syncope from seizures from non-epileptic attack?

A 
Eye witness can be crucial
Trigger 			
Prodrome 
Description of the attack
Recovery - how long, any confusion or headache
Past medical/personal history
31
Q

What is a trigger for syncope?

A

Stress/fear, prolonged standing, heat, venepuncuture,

cough, micturition

32
Q

What is a trigger for a seizure?

A

Sleep deprivation, flashing lights, menstruation,

alcohol and alcohol withdrawal

33
Q

What is the prodrome for syncope?

A 
Hot, visual crowding and loss, feel faint, can
feel dizzy (looks pale)
34
Q

What is the prodrome for seizure?

A

Aura gustatory, auditory,
(partner, family friend may be able to tell when an attack is going to happen but this can also happen with non-epileptic attacks)

35
Q

What is the onset. duration, convulsions, colour and incontinence/ tongue biting for syncope?

A

Onset - Quick but can sometimes prevent faint if sit or lie down quickly
Duration – short (seconds to 1 minute)
Convulsions – rare, brief
Colour - pale
Incontinence/Tongue biting – rare (unless bladder full)

36
Q

What is the onset. duration, convulsions, colour and incontinence/ tongue biting for a seizure?

A

Onset - Can have an aura but not always. In tonic-clonic seizures goes rigid then clonic movements of limbs
Duration – 2 – 3 minutes
Convulsions – GTC seizure, focal motor fits, myoclonic jerks (on awakening), frontal lobe motor fits
Incontinence/Tongue biting – yes, tongue biting side of tongue

37
Q

What is the onset. duration, convulsions, colour and incontinence/ tongue biting for NEA?

A

Duration – can last for 30 minutes
Convulsions – Non-neuroanatomically accurate. Wild shaking. Arms flexing and extending. May lie completely still. Wax and wane, pelvic thrusting, eyes closed
Incontinence/Tongue biting – can have injury to self

38
Q

What is the recovery for

a) syncope
b) seizure
c) NEA

A

Syncope
Little or no confusion, quick recovery.

Seizure
Confusion or headache. May not recognize family or friends for a few minutes. May have amnesia. First memory in ambulance/A&E. Needs to rest/sleep for 1-2 hours after. Can take several hours for full recovery.

Nonepileptic attacks (pseudoseizure/dissociative seizure)
Recovery is atypically quick for a prolonged generalized fit. Can be very upset
39
Q

How is the PMH/ personal history different for syncope/seizures/ NEA?

A

Syncope
Previous faints
Cardiac causes include bradycardias (heart block), tachycardias (eg VT) and obstructive lesions eg aortic stenosis.

Seizure
Perinatal illnesses, education achievements, previous serious head injury/neurosurgery, neonatal seizures (prolonged), meningitis. If late onset (age >40) think stroke or tumours

Nonepileptic attacks
Previous unexplained medical symptoms. Past history of childhood trauma

40
Q

How would you investigate a blackout?

A 
Listen to heart (aortic stenosis)
12 lead ECG- long QT syndrome
Blood tests (FBC)
Brain imaging
EEG

If suspect syncope cause consider
24 hr tape
Tilt table
Autonomic function tests

41
Q

How is an EEG useful for recurrent blackouts?

A

Video telemetry can rule out a NEA

Different types- inter-ictal, provoked, sleep-deprived, prolonged and video telemetry

42
Q

What is the false negative rate in an EEG?

A

50%- about 50% of patients with epilepsy will have a normal first interictal EEG

However this reduces to 30% after repeat EEG

False negative rate is 20% after sleep-deprived EEG

43
Q

What is the role of imaging in diagnosing seizures?

A

Do it if-

  • Focal onset needs imaging
  • If over 25 and new onset seizure needs imaging
  • If suspected Idiopathic Generalized Epilepsy (GTC, Myoclonus, absences) does not need imaging because very rarely abnormal
  • Imaging ideally MRI but CT in emergency /semi-urgent situation
44
Q

What does an interictal EEG show in a patient with epilepsy?

A

The interictal marker of a seizure focus is the spike or sharp wave
Juvenile Myoclonic Epilepsy:
Interictal EEG shows a normal background with frequent generalized polyspike and wave discharges.

45
Q

What is the pathophysiology of seizures?

A

In the normal brain the spread of electrical activity is limited.
During a seizure there is a prolonged depolarization of a group of neurones, which spreads to adjacent or connected neurones
There is a failure of inhibitory (GABA) neurotransmission

46
Q

What are the types of seizures?

A

Focal (has a focus)
-Simple partial (aura)
-Complex partial
Secondary generalized tonic-clonic

Idiopathic Generalized
Epilepsy (generalized from outset)
-Myoclonic Jerks
-Typical absence
-Primary generalized tonic-clonic
47
Q

What is the pathophysiology of NEA?

A

Often a manifestation of stress
-a situation that is intolerable or unacceptable to a person and over which they have no control

May be associated with history of abuse in childhood
May occur in patients with epilepsy
Commonly have other medically unexplained symptoms

48
Q

What is the chance of having a seizure after already having one?

A

under 50%

49
Q

When do you start treatment in epilepsy?

A

Most neurologists now start antiepileptics following a second epileptic seizure. NICE guidelines suggest starting antiepileptics after the first seizure if any of the following are present:

  • the patient has a neurological deficit
  • brain imaging shows a structural abnormality
  • the EEG shows unequivocal epileptic activity
  • the patient or their family or carers consider the risk of having a further seizure unacceptable
50
Q

What is the treatment for generalised TC seizures?

A

Generalised tonic-clonic seizures
1st line: sodium valproate
second line: lamotrigine, carbamazepine

51
Q

What is the treatment for absence seizures?

A

Absence seizures* (Petit mal)
sodium valproate or ethosuximide
sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy

52
Q

What is the treatment for myoclonic seizures?

A

Myoclonic seizures
sodium valproate
second line: clonazepam, lamotrigine

53
Q

What is the treatment for focal seizures?

A

Focal** seizures
carbamazepine or lamotrigine
second line: levetiracetam, oxcarbazepine or sodium valproate

54
Q

What anti-epileptic should not be given to pregnant women?

A

Sodium valproate- associated with neural tube defects
Carbamazepine thought to be the least teratogenic
Always give folic acid 5mg per day to pregnant women with epilepsy well before pregnancy to minimise the risk of neural tube defects.

55
Q

What are the early signs of a stroke?

A
  • May be none
  • Hyperdense middle cerebral artery
  • Loss of grey white matter differentiation & sulcal effacement (superficial cortical infarction)
  • Hypodense basal ganglia (deep vessels)
56
Q

What are the complications of a stroke?

A

Raised ICP
-Cerebral oedema
-Haemorrhage
Signs:hypertension, new neurology, GCS

  • Aspiration
  • Pressure sores
  • Depression
  • Cognitive impairment
  • Other medical problems
57
Q

What are the risks of thrombolysis?

A

Haemorrhage (1 in 20)

Reaction to rTPA (uncommon)

58
Q

What is CHADS-VASc?

A 
Congestive heart failure
Hypertension
Age >75 years
DM
Prior Stoke or TIA or TE

Vascular disease
Age 65-74 years
Sex category

Risk of stroke in AF
2 or more- give apixaban

59
Q

What is the HAD-BLED score? (risk of major bleed)

A

Risk of major bleeding with anticoagulation

Hypertension (systolic >160mmHg)

Abnormal renal function

Abnormal liver function

Age >65 years

Stroke in past

Bleeding

Labile INR
s

Taking other drugs as well

Alcohol intake at same time

60
Q

When is the risk of stroke after TIA highest?

A

48 hours

61
Q

When does NICE recommend endarectomy for carotid stenosis?

A 
Symptomatic disease (i.e. stroke/TIA)
50-90% stenosis
62
Q

What is ABCD2 score?

A

Age >60 years
Blood pressure systolic >140 and/or diastolic >90mmHg
Clinical features- 2 unilateral weakness, 1 speech disturbance w/o weakness
Duration 2 if >60 mins, 1 if 10-59
Diabetes

63
Q

What arteries are involved in a total anterior circulation infarct?

A

involves middle and anterior cerebral arteries

all 3 of the above criteria are present

64
Q

What arteries are involved in a partial anterior circulation infarct?

A

involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery

2 of the above criteria are present

65
Q

What is the Bamford classification for stroke?

A
  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
66
Q

What arteries are involved in a lacunar infarct?

A

involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

67
Q

What arteries are involved in a posterior circulation infarct?

A 
involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
68
Q

What is the immediate management of an ischaemic stroke?

A

CT- rule out haemorrhage

Offer thrombolysis in <4.5 hour onset and the patient hasn’t had a previous intracranial haemorrhage

Give aspirin 300mg ASAP and antiplatelet therapy should be continued

69
Q

What is the immediate management of a TIA?

A

Immediate antithrombotic therapy:
-give aspirin 300 mg immediately, unless contraindicated e.g. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)

70
Q

What do you do if a patient has had a suspected TIA in :

  • the past 7 days
  • over a week ago
A

7 days- arrange urgent assessment (within 24 hours) by a specialist stroke physician

Over 7 days- refer for specialist assessment as soon as possible within 7 days

71
Q

How would you manage a haemorrhagic stroke?

A

The vast majority of patients however are not suitable for surgical intervention. Management is therefore supportive as per haemorrhagic stroke.

Anticoagulants (e.g. warfarin) and antithrombotic medications (e.g. clopidogrel) should be stopped to minimise further bleeding. If a patient is anticoagulated this should be reversed as quickly as possible.

Phase 3a AW (7 decks)

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