Lectures : Neuro Flashcards

1
Q

Name grading scores used to predict prognosis and outcome in patients with subarachnoid haemorrhage?

A
  1. Hunt and Hess
  2. World Federation of Neurosurgeons
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2
Q

Definitive treatment for SAH

A
  • transfer to specialist neuro unit
  • analgesia and anti-emetic
  • metallic coils (radiological) / surgical clipping
  • ICP monitoring
  • BP management
  • Nimodipine po 60mg / 4hrly (within 48hrs)

Notes: Endovascular coiling

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3
Q

Complications of SAH

A
  • re-bleeding
  • subdural haemorrhage
  • global cerebral ischaemia
  • vasospasm
  • hydrocephalus
  • seizures
  • SIADH / cerebral salt wasting syndrome
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4
Q

What might be given to help reduce risk of re-bleeding in SAH?

A

Nimodipine po 60mg / 4hrly (within 48hrs)

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5
Q

What is used to pathologically classify brain tumours?

A
  • The WHO classification
  • based on cells affected
  • nerves —> schwannoma
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6
Q

The commonest primary brain tumour is glioma, this is further classified onto what the cells look like under a microscope. Name the cells:

A
  1. Astrocytes
  2. Oligodendrocytes (myelin sheath !)
  3. Ependymal cells (line ventricular system)
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7
Q

What genetic deletion is associated with oligodendroglioma?

A

1p 19q deletion

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8
Q

IDH1 mutation is associated with what type of brain tumour?

A

astrocytoma

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9
Q

In patients with glioblastoma what type of genetic change may be seen?

A

MGMT promotor methylation
- patients with methylation will respond better to chemotherapy.
- methylated - blocks

MGMT which would normally break down chemotherapy, does better with treatment

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10
Q

This is used to measure cancer patients ability to carry out ordinary tasks

A

Karnosfsky performance status

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11
Q

What is spectroscopy and why is it used?

A

Looks at chemical composition within defined area of brain.

N-ACETYL-ASPARTATE PEAK
- marker of cell turnover, if cells turning over suggests tumour

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12
Q

What drug is given to patients before brain surgery that will given a deep red hue to the patients tumour?

A

5 -ALA
- tumour lights up under UV light

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13
Q

Name of a chemotherapy that can be placed like wafers on the tumour and gently diffuses into the tumour

A

Gliadel

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14
Q

While chemotherapy does not tend to work that well on the brain given an example of a type of chemotherapy drug that does?

A

temozolamide
- works better in MGMT methylated patients

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15
Q

What two special tests/ signs might indicate meningitis?

A

KErnig sign
- knee extension is painful

Brudzinski sign
- neck flexion leads to knee flexion

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16
Q

What tools may be used for cognitive function assessment?

A
  1. MOCA - Montreal cognitive assessment
  2. Addenbrooke’s cognitive assessment
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17
Q

Presence of hypertension with bradycardia is known as what sign?

A

Cushing’s sign
- systolic BP
- decreased pulse
- decreased respiration

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18
Q

What monitoring is important in the treatment of HSV encephalitis?

A
  • renal
  • aciclovir may lead to crystal nephropathy
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19
Q

In immunocompromised patients, what are the likely viral causes of encephalitis?

A

HHV 6 –> Roseola

HHV 7 –> pityriasis rosea

HHV 8 –> Kaposi sarcoma in HIV individuals

EBV

CMV

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20
Q

Pathophysiology of viral encephalitis

A
  1. via cranial nerves –> HSV
  2. via peripheral nerves –> Rabies
  3. neuroinvasion from blood (in plasma e.g. flaviviruses, Japanese encephalitis) or by infecting leukocytes (HIV)
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21
Q

autoimmune encephalitis caused by what:

A

antibodies against NMDA receptor

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22
Q

How is the diagnosis of epilepsy made?

A
  • at least two unprovoked seizures occurring greater than 24 hours apart
  • one unprovoked seizure and increased probability of further seizures
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23
Q

What is an arteriovenous malformation?

A
  • abnormal connection of blood vessels
  • can be associated with seizures and epilepsy
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24
Q

What investigations are required for a suspected thunderclap headache?

A
  1. URGENT IMMEDIATE CT BRAIN

IF CT unremarkable for cause

  • LP and CSF examination (12hrs post headache)

Why the 12hr gap?

  • if there is blood in CSF not picked up by CT
  • this will break down to bilirubin
  • bilirubin can be picked up on a xanthochromia test
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25
Q

Management of headache caused by low CSF pressure?

A
  • lie flat (1 -2 weeks?)
  • IV fluids 8hrly or 2-3L oral fluids in 24 hours
  • gives time for brain to heal dura
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26
Q

Red flags for glaucoma

A

loss of vision and halo effect

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27
Q

Give example of neuropeptides involved in the trigemino cervical complex pathway of migraine genesis:

A

CGRP
- calcitonin gene related peptide

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28
Q

Management for episodic migraine

A
  1. Triptans AND/OR Aspirin OR NSAIDs should be 1st line therapy
  2. Triptan + NSAID + anti-emetic
    1. after aura!
    2. given as one off
  3. ensure adequate hydration
  4. Rest
  5. Don’t use strong painkillers
29
Q

When should migraine suffers be evaluated for use of preventive therapy:

A
  • if getting more than 2-3 episodes a month
  • or if episodes are severe
30
Q

Chronic headaches are defined as what frequency of headaches:

A
  • more than 15 days a month
    • for more than 3 months
    • at least 8 days in the month have features of migraine
    • triggers!
31
Q

Treatment of cluster headaches
- Acute treatment

A
  • Sumatriptan - injection / nasal spray
  • high flow oxygen
32
Q

Treatment of cluster headaches
- short term prevention

A
  • greater occipital nerve blocks
  • prednisolone 60-80mg/day 3-5 days and taper off (counsel on side effects and lansoprazole)
  • should not be used more than twice a year
33
Q

Treatment of cluster headaches

long term prevention

A
  • verapamil
  • topiramate
  • lithium
  • gamma core device
34
Q

Management of neuralgia :

A

Carbamazepine (usually responsive)

35
Q

Define multiple sclerosis

A
  • multifocal , upper motor neuron disorder
  • multiple sclerotic lesions
  • relapsing or progressive
  • dissemination in time and space
36
Q

radiographic feature of demyelination seen in multiple sclerosis

A

Dawson’s fingers

37
Q

How is the diagnosis of multiple sclerosis made:

A

Poser 1983

  • 2 attacks with objective clinical evidence
  • attacks occurring at different times

MRI may also be used

Macdonald criteria

38
Q

Management of MS

A
  1. Relapsing treatment
    1. 500mg Methylprednisolone for 5 days
  2. Relapse prevention
    1. specialist stuff
    2. e.g. interferons
  3. Slowing progression
  4. Neural repair
    1. re-myelination? stem cells?
39
Q

Define Parkinson’s disease

A
  • progressive reduction of dopamine
  • in basal ganglia of brain
  • leads to disorder of movements

Key features
1. Resting tremor (4-6hz)
2. Cog wheel rigidity
3. Bradykinesia

40
Q

What histopathological features are present in Parkinson’s disease:

A
  1. Lewy Body Depositions
    • composed mainly of alpha synuclein protein
  2. Diminished substantia nigra
41
Q

Appearance of substantia nigra in Parkinson’s disease:

A

lighter

42
Q

Parkinson’s tremor vs benign essential tremor

A

Parkinson’s tremor
–> asymmetrical
–> 4-6hz
–> worse at rest
–> improves with intentional movement
–> no changes with alcohol

Benign essential tremor
–> symmetrical
–> 5-8hz
–> improves at rest
–> worse with intentional movement
–> improves with alcohol

43
Q

Summarise the Parkinson’s plus syndromes which also exist:

A
  1. Multisystem atrophy
  2. Dementia w/ lewy bodies
  3. Progressive supranuclear palsy
  4. Corticobasal degeneration
44
Q

Management of Parkinson’s disease

A
  1. Levodopa
    a) synthetic dopamine
    b) usually combined with peripheral decarboxylase inhibitors
    –> carbidopa or benserazide
    –> prevents breakdown of levodopa before entering brainCombination drugs are:
    • Co-benyldopa (levodopaandbenserazide)
    • Co-careldopa (levodopaandcarbidopa)
45
Q

Main side effect of high levels of dopamine:

A

Dystonia –> excessive muscle contraction

Chorea –> abnormal involuntary movements jerking

Athetosis –> involuntary twisting movements

46
Q

What is the role of COMT inhibitors:

A

e.g. entacapone
- COMT enzyme metabolises L-dopa in both body and brain.

  • Entacapone is taken with L-dopa (and decarboxylase inhibitor) to slow breakdown of L-dopa
    • extending duration of levodopa!
47
Q

What is the name of enzyme which breakdowns neurotransmitter dopamine

A

monoamine oxidase B
- more specific to dopamine
- thus monoamine oxidase-B inhibitors will be used to increase circulating dopamine.

48
Q

What condition is important to consider in a patient with cerebrovascular risk factors and Parkinsonism type symptoms:

A
  • Vascular Parkinsonism
    • predominant gait and postural instability
    • tremor less prominent
    • poor levodopa responsiveness
49
Q

Side effects of dopamine agonists

A
  1. Impulse control disorders: pathological gambling, binge eating and hypersexuality
  2. Somnolence: strong desire to fall asleep
  3. Confusion, hallucinations
50
Q

Examples of MAO-B inhibitors

A

Increase amount of dopamine available for receptors in the striatum.

Rasagiline and Selegiline

51
Q

MAO-B inhibitor associated with hallucinations, confusion and insomnia

A

Selegiline

52
Q

Drug which prevents reuptake of dopamine at synapses

A

Amantadine

Used only for the management of levodopa-induced dyskinesia

53
Q

What are 3 other drug induced movement disorders important to be aware of:

A
  1. Akathisia
    • motor restlessness
  2. Tardive Dyskinesia
    • smacking of lips
    • facial grimacing
    • lateral jaw movements
    • choreiform (jerking) or athetoid (slow involuntary writhing of fingers) movements
  3. Dystonia’s
    • Torticollis
    • oculogyric crisis
54
Q

What is the precursor for dopamine and how is this converted to dopamine:

A
55
Q

2 broad categories of dopamine agonists:

A
  1. Ergot-based (not used as much)
    • pergolide, cabergoline

Adverse effects of Ergot based drugs
- pulmonary, pericardial and retroperitoneal fibrosis

  1. Non-ergot
    • pramipexole, ropinirole
56
Q

Treatment of essential tremor:

A
  • B-blockers
    • propranolol
57
Q

Treatment of dystonia:

A
  • botulinum toxin injections
    • weaken affected muscle
58
Q

Absent seizure AEDs

A

1st line - ethosuximide

2nd line - sodium valproate

59
Q

Focal seizure AED

A

1st - Carbamazepine, sodium valproate, levetiracetam

60
Q

Generalised seizu

A
61
Q

Common side effect of levetiracetam

A

behavioural problems

62
Q

Common side effects of carbamazepine

A

Steven Johnson Syndrome

Behavioural problems

63
Q

Common side effects of nitrazepam

A

drowsiness

64
Q

Common side effects of vigabatrin

A

visual field defects

65
Q

Common side effects of topiramate

A

weight loss

66
Q

Name the 6, cytochrome P450 hepatic enzyme inducers:

A

‘Randy’s car smokes and goes poot poot’

  • Rifampicin
  • Carbamazepine
  • Spironolactone
  • Griselfulvin
  • Phenytoin
  • Phenobarbituate
67
Q

Describe the 3 categories of AEDs and what this means in terms of prescribing:

A

Category 1 —> should not switch between brands

—> carbamazepine

—> phenobarbital

—> primidone

Category 2 —> clinical judgement whether to switch or not

—> sodium valproate

—> lamotrigine

—> perampanel

Category 3 —> can switch between different versions

—> levetiracetam

—> gabapentin

68
Q

Scoring system for myelopathy

A

mJOA scoring system