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Clinical neuroscience Flashcards

1
Q

What is status epilepticus?

A

medical emergency which is defined as a seizure lasting > 5 mins or more than 3 seizures in 1 hour without regaining consciousness

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2
Q

What is the first aid management for seizures?

A
  • Asses - remove objects that can cause injury
  • Cushion - for the head
  • Time - time the duration
  • Identify - medical bracelet and cards
  • Over - when the seizure is over roll them into recovery position
  • Never - put anything in their mouth or try to restrain them
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3
Q

What is the A-E approach for?

A

secure airway

high flow O2

gain IV access and take blood

check blood glucose

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4
Q

what class of drugs are used in seizures?

A

benzodiazepines

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5
Q

which benzodiazepine is used in the hospital setting?

A

IV lorazepam

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6
Q

which benzodiazepine is used in the community?

A

PR diazepam

buccal midazolam

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7
Q

what do you give to a patient in established status epilepticus?

A

valproate

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8
Q

what do you give to a patient in refractory status epilepticus (45 mins after onset)?

A

induction of general anaesthesia

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9
Q

what are blackouts?

A

describe the event of temporarily losing consciousness and muscle strength as a result of disrupted blood flow to the brain, if a patient is standing up this leads to a fall

Also referred to as vasovagal episodes, fainting, syncope

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10
Q

what are the features of syncope?

A
  • Prolonged upright position before the event
  • Lightheaded before the event
  • Sweating before the event
  • Blurring or clouding of vision before the event
  • Reduced tone during the episode
  • Return of consciousness shortly after falling
  • No prolonged post-ictal period
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11
Q

what are the features of seizure?

A
  • Epilepsy Aura (smells, tastes or deja vu) before the event
  • Head turning or abnormal limb positions
  • Tonic Clonic Activity
  • Tongue Biting
  • Cyanosis
  • Lasts more than 5 minutes
  • Prolonged post-ictal period
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12
Q

what are the 2 categories of blackouts?

A 
primary syncope (simple faint) 
secondary syncope (underlying disease)
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13
Q

what are the causes of primary syncope?

A
  • dehydration
  • missed meals
  • standing in warm environment
  • vasovagal response to stimuli (pain, sight of blood)
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14
Q

what are the causes of secondary syncope?

A
  • Anaemia
  • Hypoglycaemia
  • Dehydration
  • Severe Haemorrhage
  • Infection
  • Anaphylaxis
  • Arrythmias
  • Valvular heart disease (aortic stenosis)
  • Hypertrophic obstructive cardiomyopathy
  • PE
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15
Q

what are the clinical features of someone who has experienced syncope (blackout)?

A
  • prodrome - warning that they will faint (pre-syncope)
  • hot or clammy
  • sweaty
  • heavy
  • dizzy and lightheaded
  • blurry vision
  • headache
  • groggy when regaining consciousness but no confusion
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16
Q

what causes a blackout/syncope

A

due to problems in the Autonomic Nervous System ability to regulate blood flow to the brain

vagus nerve receives a strong stimulus causes a stimulation of the parasympathetic nervous system

results in decreased blood pressure and cardiac output, leading to reduced blood pressure

reduced perfusion of the brain, leading a patient to lose consciousness

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17
Q

investigations for blackouts/syncope

A
  • Bedside - obs, lying and standing BP, dehydration, ECG (arrhythmia and long QT)
  • Bloods - FBC (anaemia), WCC/CRP (infection), glucose (hypoglycaemia), electrolytes (deranged)
  • 24 hour ECG if paroxysmal arrhythmia suspected
  • tilt table test
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18
Q

what is a TIA?

A

Brief period of neurological deficit due to a vascular cause, typically lasting less than an hour. A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction (tissue-based definition). Often called mini-stroke. No evidence of ischaemia on MRI.

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19
Q

clinical features of TIA

A
  • similar to stroke - sudden onset, resolves within 1 hour
  • unilateral weakness or sensory loss
  • aphasia or dysarthria (disordered speech)
  • ataxia, vertigo, or loss of balance
  • visual problems - loss of vision in one eye, diplopia, homonymous hemianopia (only see one half of the world from each eye)
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20
Q

pathophysiology of TIA

A
  • temporary reductions in cerebral blood flow result in ischaemia of cerebral tissue, leading to tissue dysfunction which presents the symptoms of a stroke
  • When blood flow is restored to the brain the symptoms disappear -TIA can be thought of as angina of the brain
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21
Q

what investigations are ordered for TIA?

A
  • MRI of head (not CT) - look for territory of ischaemia

- Carotid imaging - carotid US/doppler to look for atherosclerosis

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22
Q

what drug do we give to patients who have had a suspected TIA?

A

300 mg aspirin

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23
Q

what are the 2 types of stroke?

A

ischaemic and haemorrhagic

24
Q

what is an ischaemic stroke?

A

caused by blockages in arteries, leading to reduced perfusion to brain tissue that results in its ischaemia and infarction, which can lead to necrosis

25
Q

risk factors for ischaemic stroke

A 
increased atherosclerosis 
-existing CVD
- previous stroke or TIA
CAD
- hypertension
- diabetes
- smoking
- alcohol

increased blood coagulation

  • AF
  • vasculitis
  • thrombophilia
  • combined contraceptive pill
26
Q

differentials for ischaemic stroke

A

head injury
hypoglycaemia
intracranial tumour
wernicke’s encephalopathy

27
Q

causes of cerebral infarction (ischaemic stroke)

A
  • reduced blood supply to brain
    • thrombus/embolus formation - AF
    • atherosclerosis
28
Q

clinical presentation of stroke in anterior cerebral artery

A

sudden onset weakness and numbness of ipsilateral leg

29
Q

clinical presentation of stroke in middle cerebral artery

A
  • weakness/numbness in hands and arms
  • weakness/numbness in face - droop
  • speech changes
30
Q

clinical presentation of stroke in posterior cerebral artery

A
  • visual disturbances

- motor dysregulation (tremor and abnormal gait)

31
Q

clinical presentation of lacunar stroke

A

weakness of entire side of body

32
Q

what are the 3 types of ischaemic stroke

A

thombotic
embolic
hypoxic

33
Q

how does an ischaemic stroke happen

A

result of an blood clot (embolism or thrombus) causing occlusion of a cerebral artery

leads to reduced blood flow of cerebral tissue, leading to it’s ischaemia and infarction

without oxygen the brain tissue cannot generate ATP

neuronal pumps unable to maintain ion gradients leading to sodium remaining in neurons

leads to continual depolarisation which results in large scale glutamate release which is neurotoxic in large concentrations and thus leads to neuronal death

results in cerebral swelling as water is drawn into neurons as a result of their increased osmolarity

leads to raised ICP

34
Q

in ischaemic stroke, what neurotransmittter is released in large concentrations and leads to neuronal death

A

glutamate (due to sodium remaining in neurones)

35
Q

investigations for ischaemic stroke

A
  • bedside - Rosier tool for stroke recognition in ED
  • blood sugar - check for hypoglycaemia
  • ECG (arrhythmia, AF)
  • echocardiogram
  • thrombophilia screen
  • CT head - shows as an area of low density, no bright white areas (blood), therefore thrombolysis is needed
  • MRI NOT USED
36
Q

management of ischaemic stroke (cerebral infarction)

A
  • Send to specialist stroke centre
  • 300mg aspirin for 3 weeks
  • thrombolysis - alteplase to degrade clot (must do CT prior)
37
Q

what is altepase?

A

tissue plasminogen activator - activates plasminogen to break down clots

38
Q

what is intracranial haemorrhage and what are the 4 types?

A

Intracranial haemorrhage is bleeding within the skull.

There are 4 broad types of intracranial haemorrhage:
epidural 
subdural
subarachnoid 
intraparenchymal (intracerebral)
39
Q

what is an epidural/extradural haemorrhage?

A

rupture of the Middle Meningeal Artery causing bleeding between the skull and outside of the dura mater. This rupture is typically caused by a fractured temporal or parietal bone. This bleeding leads to the formation of a haematoma which can compress the brain.

40
Q

what is the most common cause of extradural haemorrhage?

A

damage at the pterion

middle meningeal artery lies beneath

lateral blow to the head

41
Q

why is extradural haemorrhage so dangerous to clinicians?

A
  • talk and die syndrome
  • lateral blow to head - lose consciousness
  • patient appears well with no neuro sx
  • however, can undergo rapid neuro decline as haematoma compresses intracranial contents as it increases in size
42
Q

what is the clinical presentation of a rapid neuro decline in extradural haemorrhage

A
  • Severe Headache
  • Vomiting
  • Confusion
  • Seizures
  • Pupil Dilation
  • Reduced GCS
  • Coma
43
Q

what are the investigation for extradural haemorrhage

A
  • bedside - monitor GCS
  • bloods - FBCs (transfusion), clotting
  • immediate CT head
44
Q

what investigation must you not do in a patient with suspected extradural haemorrhage

A

lumbar puncture

45
Q

how does an extradural haematoma appear on CT head

A

lemon shaped

46
Q

what is the surgical management for extradural haematoma?

A

Surgical evacuation of the clot and ligation of the bleeding vessel

47
Q

what are the layers and spaces of the brain/meninges

A 
skull 
epidural space 
dura mater
subdural space 
arachnoid mater
subarachnoid space
pia mater
48
Q

what is a subdural haematoma?

A

This occurs when there is a bleed between the Dura Mater and Arachnoid Mater, causing blood to accumulate underneath the dura.

49
Q

risk factors for subdural haemorrhage

A
  • Elderly - Cerebral Atrophy, making the bridging vessels more likely to rupture due to more movement
  • Alcoholics - Cerebral Atrophy, making the bridging vessels more likely to rupture due to more movement
  • Anticoagulation - Increases the risk of bleed, an elderly person on anticoagulants is therefore at a higher risk of bleeding
50
Q

what ruptures in a subdural haematoma

A

bridging veins between dura and arachnoid

51
Q

clinical features of subdural haemorrhage

A
  • Sx
    • Fluctuating Consciousness
    • Sleepiness
    • Headache
    • Unsteadiness
    • Vomiting (Raised ICP)
  • signs
    • raised ICP
    • signs of head trauma or injury
52
Q

pathophys of subdural haemorrhage

A
  • The bleeding underneath the dura causes a haematoma to form which compresses the brain, leading to it’s dysfunction.
  • This causes a gradual rise in ICP, which can eventually lead to herniation and coning if left untreated.
53
Q

investigation for suspected dural haemorrhage

A

CT head

54
Q

what would a CT head scan show for a patient with subdural haemorrhage

A

sickle/banana shaped haematoma - not restricted by suture lines of dura

55
Q

what colour do acute vs chronic bleeds appear on CT

A

acute bleeds brighter

56
Q

management for subdural haematoma

A

1st Line - Burr Hole Craniostomy allows for irrigaiton/evacuation of the haematoma, reducing ICP

2nd Line - Craniotomy, allowing removal of the haematoma

Revision (20 decks)

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