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neuro Flashcards

1
Q

what are the 2 types of stroke

A

ischaemic- blocked artery - more common
haemorrhagagic- artery the breaks

Haemorrhagic can be further divided into Intracerberal haemorrhage- stays within the cerebrum and a SAH- occurs between the PIA mater and the Arachnoid mater

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2
Q

if symptoms resolved in 24 hours what I sit called

A

TIA

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3
Q

2 ways an ischeamic stroke can happen

A

endothelial cell damage

and embolism

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4
Q

describe endothelial cell damage

A

irritants damage endothelium, now a site of atherosclerosis- plaque forms.

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5
Q

describe embolism

A

when a blood clot breaks from one location and travels and becomes lodged in a vessel with a small diameter

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6
Q

what does lacunar stroke

A

damage to the middle cerebral artery and affects legs

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7
Q

what can shock lead to?

A

reduction in blood throughout the body

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8
Q

risk factors for stroke?

A

smoking
dm
heart disease
alcohol

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9
Q

is there recovery with embolic stroke?

A

no

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10
Q

is there recovery from a haemorrhage stroke or embolic?

A

haemorrhagic

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11
Q

What do we use to estimate the risk factor of strokes?

A 
CHA2DS2-VASc
) Congestive heart failure
- HTN 
- Age >75 (2 points) 
- DM 
- Stroke prior, TIA (2 points) 
- Vascular disease 
- Age 65-74 
- Female
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12
Q

Stroke tests:

A

) HTN

  • ECG - AF
  • Echo
  • Carotid doppler US - for stenosis
  • MRI/CT
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13
Q

how do we prevent strokes:

A
  • Stop smoking
  • Control BP
  • Move around/exercise
  • Hyperlipidaemia
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14
Q

What is TIA?

A

An ischaemic (usually embolic) neurological event with symptoms lasting <24hours MAY LEAD TO STROKE

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15
Q

Cause of TIA?

A

Atherothromboembolism from carotid

  • Cardioembolism
  • Hyperviscosity
  • Vasculitis
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16
Q

Tests for TIA

A

FBC, ESR, U&ES, glucose, lipids

  • CXR
  • ECG
  • Carotid doppler +/- angiography
  • CT/diffusion weighted MRI
  • Echocardiogram
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17
Q

treatment for TIA?

A

) Control CV risk factors

  • Antiplatelet drugs (aspirin, then clopidogrel)
  • Anticoagulation indications (if cardiac source of emboli)
  • Carotid endarterectomy is >70% stenosis
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18
Q

what is ABCD2 risk score

A

risk of stroke following suspected tia

  • Age >60
  • BP high
  • Clinical features (unilateral weakness 2, speech 1)
  • Dyration of symptoms (>1hr 2, <1hr 1)
  • DM
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19
Q

what makes up the ABCD2 Score?

A
  • Age >60
  • BP high
  • Clinical features (unilateral weakness 2, speech 1)
  • Dyration of symptoms (>1hr 2, <1hr 1)
  • DM
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20
Q

what is a subarachnoid haemorrhage?

A

Spontaneous bleeding into the subarachnoid space, often catastrophic

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21
Q

symptoms of SAH

A
  • Sudden onset excruciating headache (thunderclap)
  • neck pain as a result of irritation to meninges
  • Vomiting
  • Collapse
  • Seizures
  • Coma
  • Possible preceding sentinel headache
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22
Q

signs of SAH

A

Neck stiffness

  • Kernig’s sign (leg extension)
  • Retinal, subhyaloidand vitreous bleeds
  • Focal neurology at presentation may suggest site of aneurysm
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23
Q

cause if SAH

A

) Berry aneurysm rupture

  • trauma
  • Arteriovenous malformations - get tangled up
  • Encephalitis, vasculitis, tumour, idiopathic
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24
Q

Risk factors for SAH?

A

) Previous aneyrysmal SAH

  • Smoking
  • Alcohol misuse
  • High BP
  • Bleeding disorders
  • SBE
  • Family history
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25
Q

Places where berry aneurysms can occur?

A
  • Posterior communicating with internal carotid
  • Anterior communicating with anterior cerebral artery
  • Bifurcation of middle cerebral artery
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26
Q

tets for sah?

A
  • Urgent CT/MRI can show blood pool

- Consider Lumbar Puncture >12hr after headache (yellow due to Hb breakdown)

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27
Q

Treatment for SAH?

A

) Fluids and maintaining cerebral perfusion

  • Nimodipine- CCB stops vasospasms
  • Endovascular coiling or surgical clipping
  • Catheter or CT angiography before intervention
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28
Q

complications of SAH?

A

) Fluids and maintaining cerebral perfusion

  • Nimodipine
  • Endovascular coiling or surgical clipping
  • Catheter or CT angiography before intervention
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29
Q

What is a haemtoma?

A

The accumulation of leaked blood inside the body within tissue planes. collection of blood

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30
Q

what is a haemorrhage?

A

The leakage of blood from a blood vessel due to lack of integrity in the vessel wall or clotting mechanism. ACTIVE BLEEDING

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31
Q

What does a SAH make

A

a pool of blood which applies pressure on skull, brain tissue and blood vessels

  • blood irritates the meninges
  • leads to inflammation and scarring
  • obstruction of csf outflow
  • leads to hydrocephalus
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32
Q

Talk about the meninges

A

protective layer of the brain
Dura
Arachnoid- contains subarachnoid space contains csf
Pia

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33
Q

what is a subdural haemorrhage

A

bleeding below the dura mater

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34
Q

what happens in subdural space?

A

venous drainage

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35
Q

what causes a subdural haematoma

A

rupture of bridging veins that can happen due to brain atrophy, alcohol abuse and head trauma

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36
Q

what does a subdural haematoma cause?

A

1) Gradual rise in ICP
2) Shift in midline structures away from side of clot
3) Eventual tentorial herniation and coning

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37
Q

risk factors for a subdural haematoma?

A
  • Elderly (atrophy makes bridging veins more vulnerable)
  • Falls (epilepsy, alcoholics)
  • Anticoagulation
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38
Q

symptoms of a subdural haematoma?

A 
- Fluctuating level of consciousness
\+/- 
- Insidious physical/intellectual slowing 
- Sleepiness 
- Headache 
- Personality change 
- Unsteadiness
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39
Q

what does a ct/mri shhow about a subdural haematoma?

A

Clot +/- midline shift, crescent shaped collection of blood over 1 hemisphere

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40
Q

Treatment of a subdural haematoma?

A
  • Reverse clotting abnormalities

- Craniotomy/burr hole washout on >10mm or with midline shift >5mm

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41
Q

What is Extra dural?

A

above the dura closest to the skull

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42
Q

what is a common symptom that should make you think extradural haematoma

A

Lucid interval - deteriorating consciousness after any head injury that initially produced no loss of consciousness/drowsiness

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43
Q

what causes extradural haematoma?

A
  • Fractured temporal/parietal bone causing laceration of middle meningeal artery after trauma to temple just lateral to eye
  • Any tear in a dural venous sinus
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44
Q

name some more clinical features of extradural haematoma

A 
lucid interval
increase headache 
vomitin g 
confusion 
seizure
45
Q

if an extradural haematoma happens what is the main cause of death?

A

respiratory arrest

46
Q

differential diagnosis of extradural haematoma

A

epilepsy

co poisoning

47
Q

what is the tests for extradural haematoma

A

lp
ct-biconvex lens
XR- fracture lines crossing middle meningeal vessels

48
Q

management fo extradural haematoma?

A

Clot evaluation +/- ligation of the bleeding vessel

49
Q

What is epilepsy?

A

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

50
Q

what are convulsions?

A

The motor signs of electrical discharges

51
Q

what are the elements of a seizure?

A

Prodrome-Change in mood or behaviour hours or days before
Aura- Implies a focal seizures often from the temporal lobe - flashing lights and smells
Post-ictal- Dysphasia following a focal seizure in the temporal lobe, headache confusion
–

52
Q

structural cause of epilepsy?

A

Cortical scarring
Stroke
Hippocampal sclerosis

53
Q

non-structural cause of epilepsy?

A

Tuberous sclerosis
sarcoidosis
SLE

54
Q

What is a focal seizure?

A

Originating within networks linked to one hemisphere and often seen without underlying structural disease

55
Q

What is a generalised seizure?

A

(abnormal electrical activity causing a seizure begins in both halves (hemispheres) of the brain at the same time)

56
Q

Give 3 provoking causes for seizures

A
  • Trauma
  • Stroke
  • Haemorrhage
  • Increased ICP
  • Alcohol/benzodiazepine withdrawal
  • Metabolic disturbance
  • Infection
  • High temp
  • Drugs
57
Q

Give 2 tests for epilepsy

A
  • EEG
  • MRI
  • Drugs screen, LP
58
Q

What are the non-pharmacological treatment options for epilepsy?

A

) Relaxation, CBT

  • Surgical resection
  • Vagal nerve/deep brain stimulation
59
Q

when should we start a person on anti-epileptic drugs?

A

After 2 or more seizures/high risk of recurrence

60
Q

Pharmacological treatment for focal seizures?

A

1) Carbamazepine or lamotrigine

2) Levetiracetam, oxcarbazepine, or sodium valproate

61
Q

Pharmacological treatment for generalised tonic-clonic seizures? (1st/2nd line)

A

1) Sodium valproate or lamotrigine
2) Carbamazepine, clobazam, levetiracetam or topiramate
- -

62
Q

what is dementia?

A

A neurodegenerative syndrome with progressive declines several cognitive domains

usual presentation: Memory loss over months/years

63
Q

How do we diagnose dementia?

A
  • History
  • Cognitive testing (AMTS)
  • Examination for physical cause
  • Medication review
64
Q

What tests do we do in dementia?

A
  • Bloods for reversible/organic causes
  • MRI can identify reversible pathologies or underlying vascular damage
  • PET functional imaging - shows how organs and tissues are working
  • EEG
  • HIV, syphilis, autoantibodies
65
Q

give 3 subtypes of dementia?

A

1) Alzheimer’s disease -The cumulative effect of many small strokes.
CLINICALLY PRESENTS:
Sudden onset and stepwise deterioration, we look for:
- High BP
- Past strokes
- Focal CNS signs

2) Vascular dementia

3) Lewy body dementia- presents as:
- Fluctuating cognitive impairment
- Detailed visual hallucinations
- Parkinsonism

66
Q

When should we suspect Alzheimers disease?

A

->40
- Persistent, progressive, global cognitive impairment
however if you have downs syndrome you’ll have it earlier

67
Q

Symptoms of Alzheimers?

A
  • Visuo-spatial skill affected
  • Memory loss
  • Verbal abilities affected
  • Executive function (planning) effected
  • Anosognosia - impairs a person’s ability to understand and perceive his or her illness
  • Irritability later
68
Q

what accumulates in Alzheimers disease?

A

beta-amyloid peptide- a degradation product of amyloid precursor protein, this leads to a loss of neurotransmitter ACh

69
Q

What parts of the brain are most vulnerable to neuronal loss in AD?
(HATS)

A
  • Hippocampus
  • Amygdala
  • Temporal neocortex
  • Subcortical nuclei
70
Q

How do we manage Alzheimers disease?

A
  • Acetylcholinesterase inhibitors
  • Antiglutamatergic treatment
  • Antipsychotics (severe non-cognitive only)
  • BP control
71
Q

What is the extrapyramidal triad of Parkinson’s?

A
  • Tremor- worse at rest often involves pill rolling
  • Hypertonia
  • Bradykinesia
72
Q

2 cause of Parkinson’s

A
  • Parkinson’s disease

- Drugs, trauma, encelophathy, toxicity, HIV

73
Q

Pathogenesis of parkinsons disease?

A
  • Loss of dopaminergic neurons in the substantial nigra

- Associated with Lewy bodies in the basal ganglia, brainstem, cortex

74
Q

how do we treat parkinsons disease?

A
  • Symptom control
  • Deep brain stimulation (dopamine responsive)
  • Surgical ablation of overactive basal ganglia circuits
  • Postural exercises and weightlifting
75
Q

medications we can give in Parkinsons disease

A
  • Levodopa
  • Dopamine agonists
  • Apomorphine
  • Anticholinergics
  • MAO-B inhibitors
  • COMT inhibitors
76
Q

give 4 things we need to know in a headache history?

A

) Types/number

  • Time
  • Pain
  • Associations
  • Triggers
77
Q

what is the most common type of headache?

A

tension

78
Q

give 2 symptoms of a tension headache?

A

bilateral

non pulsatile

79
Q

how do we treat tension headache?

A

message

antidepressants

80
Q

what are the symptoms of cluster headache and who are they more common in?

A 
men and smokers
) Rapid onset excruciating pain around one eye that may become watery ad bloodshot with lid swelling
- Lacrimation 
- Facial flushing 
- Rhinorrhoea - runny nose
81
Q

how do we treat an acute cluster headache?

A
  • 100% O2

- Sumatriptan

82
Q

preventative treatments of a cluster headache?

A
  • Avoid alcohol
  • Corticosteroids short term
  • Verapamil
83
Q

what is the classical presentation of a migraine?

A

Visual or other aura lasting 15-30 mins followed within 1hr by unilateral, throbbing headache

  • Isolated aura with no headache
  • Episodic severe headaches without aura, often premenstrual, usually unilateral with N&V +/- photophobia/phonophobia
84
Q

what is a prodome?

A

Precedes headache by hours/days

  • Yawning
  • Cravings
  • Mood/sleep change
85
Q

what are the three types of aura?

A
  • Visual - chaotic distorting, jumbling, dots, zigzags, lines
  • Somatosensory - paraesthesiae spreading from fingers to face
  • Motor - dysarthria and ataxia, ophthalmoplegia, hemiparesis
  • Speech - dysphasia, paraphasia
86
Q

triggers for a migraine

A

CHOCOLATE

  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese/caffeine
  • Oral contraceptives
  • Lie-ins
  • Alcohol
  • Travel
  • Exercise
87
Q

diagnostic criteria of a migraine if no aura?

A
  • 5 or more attacks
  • Lasting 4-72 hours
  • N&V
  • Or P/P
  • Any 2 of unilateral, pulsating, impairs/aggravated by routine activity
88
Q

2 preventative treatments for migraines?

A
  • Avoid triggers
  • Ensure analgesic rebound headache not there
  • Propranolol or topiramate
89
Q

treatment for an acute migraine attack?

A

Oral triptan and NSAID/paracetamol

Anti-emetics

90
Q

2 non pharmacological treatments for migraines?

A
  • Hot/cold packs
  • Rebreathing into bag
  • Acupuncture
91
Q

What is a multiple sclerosis

A

Inflammatory plaques of demyelination in the CNS disseminated in space and time (multiple sites, >30d between attacks)

poorly myelinated leads to axonal loss
occurs more in females

MS is an autoimmune disease- T cell mediated

92
Q

how does MS present?

A
  • Usually monosymptomatic
  • Unilateral optic neuritis
  • Numbness/tingling in limbs, leg weakness
  • Brainstem/cerebellar symptoms (diplopia, ataxia)

a hot bath and exercise makes it worse

93
Q

how do we diagnose ms?

A
  • 2 or more attacks/relapses
  • 2 or more clinical lesions
  • Exclusion of other conditions
94
Q

what does csf show in ms?

A

Oligoclonal bands of IgG on electrophoresis that are not present in the serum (CNS inflammation)

95
Q

what does mri show in ms?

A

plaque detection

96
Q

how do we manage MS?

A
  • Lifestyle advice (avoid stress)
  • Disease modifying drugs
  • Treat relapses
  • Symptom control
97
Q

what disease modifying drugs duo we give in ms?

A
  • Dimethyl fumarate
  • Alemtuzumab (monoclonal antibody against T cells)
  • Natalizumab (monoclonal antibody against VLA-4 receptors that allow immune cells to cross the BBB)
98
Q

What is motor neurone disease?

A

A cluster of neurodegenerative diseases characterised by a selective loss of neurons

99
Q

where is the selective loss of neurones in motor neurone disease

A
  • motor cortex
  • cranial nerve nuclei
  • anterior horn cells
100
Q

how do we distinguish mnd from myasthenia grevis

A

MND never affects eye movements

101
Q

what are 4 clinical patterns of MND?

A
  • ALS/amyotrophic lateral sclerosis
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Primary lateral sclerosis
102
Q

name 4 presentations of MND?

A
  • stumbling spastic gait
  • foot drop
  • weak grip
  • umn and lmn signs
103
Q

diagnostic test for mnd?

A

LMN and UMN signs in 3 regions

104
Q

what treatments do we give in MND?

A
  • Antiglutamatergic drugs
  • symptoms control
  • pallative care
105
Q

what is meningitis

A

inflammation of the meninges

106
Q

3 causes of meningitis

A

) Meningococcus

  • Pneumococcus
  • Haemophilus influenzae
  • Listeria monocytogenes
107
Q

features of meningitis

A 
headache 
leg pain 
cold hands and feet
later=
neck stiffness 
photophobia
108
Q

tests for meningitis?

A
  • ) U&E, FBC, glucose, coagulation
  • ) Blood culture, throat swabs, serology
  • ) LP usually after CT
  • ) CSF for MC&S, gram stain, protein, glucose, virology/PCR, lactate
  • ) CXR for TB
109
Q

treatment for meningitis?

A
  • ) IV fluids and resus
  • ) <55 cefotaxime IV (or ceftriaxone)
  • ) >55 cefotaxime and ampicillin IV
  • ) Aciclovir if viral suspected

osmosis cards (2 decks)

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