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Yr 5 conditions > Neurology conditions > Flashcards

Neurology conditions Flashcards

1
Q

Difference between stroke and TIA in terms of length of symptoms?

A

Stroke –> Sx last over 24 hours

TIA –> Sx (focal neurological deficit) completely resolved by 24 hours

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2
Q

What scoring tool is used to assess the need for urgent hospital investigation (within 24 hours) following a TIA? What score indicates the need for urgent investigation?

A

ABCD2 score.
Score 4+: urgent TIA clinic appointment and appropriate investigaton
Score <4: investigate as an outpatient but must be done within 1 week.

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3
Q

Immediate management of TIA?

A

300mg aspirin once diagnosis confirmed (usually after CT has confirmed no haemorrhagic stroke).
Then low dose aspirin daily thereafter.

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4
Q

What is the name of the formal stroke classification system?

A

Oxford Stroke Classification aka the Bamford Classification

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5
Q

What are the 3 criteria involved in the Oxford Stroke Classification system?

A
  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
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6
Q

If a patient has all 3 features described in the Oxford Stroke Classification system, what type of stroke have they had?

A

Total Anterior Circulation Stroke (TACS) - involves middle and anterior cerebral arteries

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7
Q

If a patient has 2 of the 3 features described in the Oxford Stroke Classification system, what type of stroke have they had?

A

Partial Anterior Circulation Stroke (PACS) - involves smaller arteries of the anterior circulation e.g. upper or lower division of middle cerebral artery.

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8
Q

According to the Oxford Stroke Classification, how do lacunar strokes present?

A

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
These involve the small basilar arteries around the internal capsule, thalamus and basal ganglia

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9
Q

According to the Oxford Stroke Classification, how do posterior circulation strokes (POCS) present?

A

With 1 of the following:

  1. cerebellar or brainstem syndromes
  2. loss of consciousness
  3. isolated homonymous hemianopia
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10
Q

What scoring tool may be used to help identify possible strokes in the emergency department?

A

ROSIER tool.

Recognition Of Stroke In the Emergency Room. Score < 0 makes stroke unlikely.

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11
Q

What must always be excluded as a cause of sudden onset neurological deficit?

A

Hypoglycaemia

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12
Q

Although symptoms alone cannot differentiate between an ischaemic and haemorrhagic stroke, what features make a haemorrhagic stoke more likely?

A

Decrease in the level of consciousness: seen in up to 50% of patients with a haemorrhagic stroke
Headache is also much more common in haemorrhagic stroke
Nausea and vomiting is also common
Seizures occur in up to 25% of patients

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13
Q

What is first line radiological investigation for suspected stroke?

A

A non-contrast CT head scan. MRI may be used.
Up to 50% of ischaemic strokes won’t be visible on the initial CT. However, haemorrhagic strokes will be visible immediately as bright white blood and this therefore informs the clinician as to how to proceed with management.

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14
Q

Providing a patient with ischaemic stroke doesn’t have any contraindications to thrombolysis, how long after onset of symptoms can this be offered?

A

Within 4.5 hours.

3 if over 80

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15
Q

How is ischaemic stroke managed following thrombolysis (or otherwise if thrombolysis not appropriate)?

A

(If thrombolysis given, repeat CT head 24 hours post treatment then if no signs of bleeding)…
300mg aspirin for 2 weeks or until discharge

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16
Q

Long term management/secondary prevention of ischaemic stroke?

A

NICE recommend clopidogrel 75mg (and statin if cholesterol > 3.5mmol/L)
If clopidogrel contraindicated, low-dose aspirin plus MR dipyridamole.
If a patient has suffered a stroke/TIA in the carotid artery terrority, is not significantly disabled, and has significant carotid artery stenosis –> carotid artery endarterectomy.

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17
Q

How is haemorrhagic stroke managed?

A

Supportive management - don’t reduce blood pressure unless SBP > 185 as need to maintain cerebral perfusion.
Refer for neurosurgical input but many aren’t fit for surgery.

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18
Q

What are the most common causes of meningitis?

A

Adults and kids: Neisseria meningitides and streptococcus pneumoniae
Neonates: Group B strep

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19
Q

What drug should be given in the community prior to hospital if they are suspected of having meningitis with a non-blanching rash?

A

IV/IM Benzylpenicillin
Adults and 10+: 1.2g
1-9 years: 600mg
<1 year: 300mg

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20
Q

What investigations are important to order in suspected meningitis?

A

Blood culture and Lumbar puncture for CSF (ideally before starting Abx but treatment should not be delayed).
Bloods - Meningococcal PCR –> quicker result than blood cultures
Viral PCR testing

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21
Q

How is bacterial meningitis managed?

A

IV Abx (usually cefotaxime +/- amoxicillin)
Steroids (to reduce hearing loss and neuro damage) - usually dexamethasone
Notifiable disease! - inform public health - they will advise on Post-exposure prophylaxis for close contacts

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22
Q

What are the common causes of viral meningitis?

A

Herpes simplex virus, enterovirus, varicella zoster virus

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23
Q

How does CSF analysis help to determine if the cause of a meningitis is bacterial or viral?

A

Bacterial: cloudy CSF, high proteins, low (<0.5) glucose compared to blood, high neutrophils + WCC count
Viral: clear CSF, proteins mildly raised or normal, normal (0.6-0.8) glucose compared to blood, high lymphocyte + WCC

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24
Q

How can delirium be defined?

A

An acute and fluctuating disturbance in level of consciousness, attention and global cognition.

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25
Q

What are the symptoms of acute confusional state/delirium?

A 
Reduced and fluctuating level of consciousness;
Disorientation (time/person/place);
Inattention;
Illusions/hallucinations;
Altered personality;
Mood disorders;
Speech disorders (slurred speech/aphasic error/chaotic pattern);
Lacking insight.
Sx often worse at night.
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26
Q

What differentiates delirium and dementia?

A

The changes in delirium are more acute in onset whereas the decline/impairment is more gradual over months-years in dementia.
Also, consciousness unimpaired and attention preserved in dementia - not the case in delirium

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27
Q

As well as describing a ‘thunderclap headache/worst headache of life’ (often occipital), what features may someone with a subarachnoid haemorrhage have?

A

Features of meningism such as photophobia and neck stiffness.
Visual disturbances. Focal neuro deficit.

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28
Q

What is the first line investigation in suspected subarachnoid haemorrhage?

A

Non-contrast CT head

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29
Q

What features of CSF analysis following lumbar puncture indicate subarachnoid haemorrhage (if CT head is negative)?

A

Xanthochromia - yellow appearance to the CSF

Red cell count will be raised

30
Q

What is classed as status epilepticus?

A

Tonic Clonic Seizure lasting > 5 minutes, OR

Two or more seizures without full recovery (GCS = 15) in between (over any time period, usually within an hour or so)

31
Q

How is status epilepticus managed?

A

A-E approach (emphasis on securing the airway and giving high-flow O2)
In hospital: gain IV access and give IV lorazepam 0.1mg/kg repeated after 10 mins if seizure continues
In community: Buccal/IM midazolam or rectal diazepam.

If seizures continue, consider phenytoin or phenobarbital IV, with ICU input and consider the need for intubation and ventilation

32
Q

What are the features of a subdural haematoma on CT head?

A
  • Crescentric hyperdense mass (blood collection) +/- midline shift
  • May cross sutures and extend into the interhemispheric fissure and over tentorium
  • acute collection = hyperdense
  • subacute = isodense (consider MRI)
  • chronic = hypodense
33
Q

Which patients with subdural haematoma are the neurosurgical team likely to offer rapid surgical evaluation via craniotomy? (either with Burr hole (1st line) or large flap (2nd line))

A

Acute SubDural Haematoma that is symptomatic and >1cm at the thickest point with associated mass effect

34
Q

Damage to which vessels is most commonly associated with subdural haematoma?

A

Bridging veins between the brain and dura

35
Q

Damage to which vessel is most commonly associated with extradural haematoma?

A

Damage to middle meningeal artery (often following trauma to ptrerion leading to tempoparietal skull fracture)

36
Q

What are the features of a extradural haematoma on CT head?

A
  • Biconvex (lenticular) shape (adjacent to skull)
  • Uniform density with sharply defined edges
  • Blood in EDH does not cross suture lines
37
Q

What are the indications for surgical treatment of extradural haematoma? (emergency craniotomy with evacuation of clot)

A
  • Any symptomatic EDH.

- Acute asymptomatic EDH >30 mL volume or with >5 mm of midline shift.

38
Q

What is Multiple Sclerosis?

A

An inflammatory disease of the CNS characterised by multiple episodes of demyelination separated in time and space.

39
Q

Which chromosomal locus is consistently associated with susceptibility to MS?

A

HLA-DRB1

40
Q

What are the 3 types of MS?

A

Relapsing and Remitting MS (RRMS): characterised by periods of exacerbation of symptoms (relapses) followed by unpredictable periods of stability (remission). The severity and frequency of relapses varies greatly between patients, but on average occur once or twice per year. This clinical pattern often develops into secondary-progressive multiple sclerosis (SPMS), with progressive disability unrelated to relapses.

Secondary-progressive MS (SPMS): a period of relapse is followed by relentless progression producing ever-increasing disability

Primary-progressive MS (PPMS): patients relentlessly deteriorate from outset without a proceeding history of relapses or recovery.

41
Q

What symptoms may someone with MS experience?

A

Symptoms of visual, sensory, motor, coordination, bladder or sexual dysfunction with or without disturbance in cognition or mood
FATIGUE ++

42
Q

What are the investigation of choice for MS and what do these show?

A

MRI T2-weighted image: hyperintensity especially in periventricular region and corpus callosum that reflects white matter change

CSF analysis:

  • Mild lymphocytic pleocytosis
  • Normal glucose
  • Normal to mildly elevated protein
43
Q

What drug is given to help manage an acute relapse of MS?

A

5 day course of Methylprednisolone - shortens relapse duration but no effect on recovery from relapse or frequnecy of future relapses or overall disease progression

44
Q

What is the aim of management of MS?

A

There is no cure for multiple sclerosis. The overall aims of treatment are to:
1. Modify the course of the disease and manage symptoms (e.g. baclofen for spasticity, oxybutynin for unstable bladder, amantidine for fatigue), in order to improve quality of life.
2. Treatment is aimed at reducing the frequency and duration of relapses (new immunomodulators may help with this) and at preventing or slowing disability.
MDT support with PT/OT input and specialist MS nurse

45
Q

What is the classical triad in Parkinson’s disease?

A

Resting tremor
Rigidity (“cogwheel”)
Bradykinesia

46
Q

What is the pathophysiology behind Parkinson’s disease?

A

Part of the basal ganglia called the substantia nigra produces a neurotransmitter called dopamine. Dopamine is essential for the correct functioning of the basal ganglia. In Parkinson’s disease, there is a gradual but progressive fall in the production of dopamine.

47
Q

What are the medication options for Parkinson’s disease?

A

Co-carledopa (containing synthetic dopamine, levodopa, and a peripheral decarboxylase inhibitor, carbidopa) or Co-benyldopa (containing synthetic dopamine, levodopa, and a peripheral decarboxylase inhibitor benserazide).
Dopamine agonists such as bromocriptine or perogolide (less effective than levodopa but usually used before levodopa to delay its need).
Monoamine Oxidase-B Inhibitors such as selegiline or rasagiline (less effective than levodopa but usually used before levodopa to delay its need).

48
Q

What is dementia?

A

A progressive global decline in cognitive function, without impairment of consciousness. It is typically defined as a syndrome secondary to one or more of multiple causes, rather than a diagnosis in its own right.

49
Q

To meet ICD-10 criteria, how long do the symptoms of dementia have to present for?

A

> = 6 months

50
Q

What are the different causes of dementia?

A 
Alzheimer's disease (~50%)
Vascular dementia (~25%)
Dementia with Lewy Bodies (~15%)
Fronto-temporal dementia (~5%)
Mixed dementia
Parkinson's disease
51
Q

What are the 5 A’s of Alzheimer’s disease?

A

Amnesia - memory loss
Agnosia - inability to recognise familiar objects/tastes/sounds etc
Aphasia - inability to express oneself through speech
Anomia - inability to remember the names of things
Apraxia - misuse of objects due to failure to correctly identify them

52
Q

What drugs are licensed for use in Alzheimer’s disease?

A

AChesterase inhibitors –> Donepezil, galantamine, rivastigmine (n.b. cholinergic side effects) for mild-to-moderate Alzheimer’s
NMDA antagonists –> Memantine for moderate Alzheimer’s when an AChesterase inhibitor is contra-indicated or not tolerated; or for severe Alzheimer’s

53
Q

What score on the Mini Mental State Examination (MMSE) e.g. MoCA suggests possible dementia?

A

<24/30

54
Q

How can epilepsy and seizures be defined?

A

Epilepsy is an umbrella term for a condition where there is a tendency to have seizures. (2+ seizures)
Seizures are transient episodes of abnormal electrical activity in the brain. There are many different types of seizures.

55
Q

What are some common triggers for seizures?

A

Sleep deprivation
Alcohol (alcohol intake AND alcohol withdrawal)
Drug misuse
Physical/mental exhaustion
Flickering lights –e.g. on TV/video games )(cause primary generalised epilepsy only)
Infection / metabolic disturbance

56
Q

What are the features of primary generalised seizures (40% all seizures)?

A

Abnormal electrical discharge involves the entire brain. They begin in BOTH hemispheres simultaneously. Associated with LOC from the onset.
May be generalised tonic-clonic seizures (aka Grand-mal), absence seizures (aka petit mal), atonic seizures, myoclonic seizures

57
Q

What are the features of partial (focal) seizures (around 50-60% of seizures?

A

Abnormal electrical discharge originates from discrete regions of the brain. They begin in ONE hemisphere. Often occurs due to an underlying structural abnormality.
Can be simple partial (patient fully conscious) or complex partial (decreased awareness)

58
Q

What is a prodrome to a seizure?

A

The symptoms preceding a seizure by hours to days such as change in mood or behaviour.

59
Q

What is an aura relating to a seizure?

A

Part of the seizure of which the patient is aware and may precede its other manifestations. Can be an odd feeling in the gut or flashing lights or strange smells.

60
Q

When should a patient be offered an EEG?

A

After a 2nd seizure

61
Q

When should a patient be started on AED treatment?

A

If there has been 2+ seizures in a 2 year period

62
Q

What are the 1st and 2nd line drugs for generalised tonic-clonic seizures?

A

1st line: Sodium valproate

2nd line: Lamotrigine or carbamazepine

63
Q

What are the 1st and 2nd line drugs for focal seizures?

A

1st line: Lamotrigine or carbamazepine

2nd line: Sodium valproate or Levetiracetam

64
Q

What is the 1st line drug for absence seizures?

A

Sodium valproate or ethosuximide

65
Q

What are the 1st and 2nd line drugs for atonic seizures (aka drop attacks)?

A

First line: sodium valproate

Second line: lamotrigine

66
Q

What is the 1st line drug for myocloninc seizures?

A

Sodium valproate

67
Q

What are the red flag symptoms for headache and what may each symptoms indicate?

A

Photophobia, neck stiffness, fever (meningitis/encephalitis)
New neurological symptoms (haemorrhage, malignancy or stroke)
Dizziness (stroke)
Visual disturbance (temporal arteritis or glaucoma)
Sudden onset occipital headache (subarachnoid haemorrhage)
Worse on coughing or straining (raised intracranial pressure)
Postural, worse on standing, lying or bending over (raised intracranial pressure)
Severe enough to wake the patient from sleep
Vomiting (raised intracranial pressure or carbon monoxide poisoning)
History of trauma (intracranial haemorrhage)
Pregnancy (pre-eclampsia)

68
Q

What is the classical presentation of a tension headache?

A

Mild ache across the forehead in a band-like pattern

69
Q

What muscles are implicated in tension headache?

A

Frontalis temporalis and occipitalis

70
Q

What are the typical features of the headaches in migraine?

A 
Last 4-72 hours
Pounding or throbbing in nature
Usually unilateral but can be bilateral
Photophobia, phonophobia
May have an aura
May be associated nausea and vomiting
71
Q

What are the options for acute medical management of migraines?

A

Paracetamol
Triptans (e.g. sumitriptan 50mg as the migraine starts)
NSAIDs
Antiemetics (if vomiting occurs)

72
Q

What are the options for migraine prophylaxis?

A

Avoid triggers!
Propanolol
Topiramate (not in pregnancy!)
Amitriptyline

Yr 5 conditions (16 decks)

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