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Phase 2a BASICS > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the types of stroke?

A

Ischaemia: cerebral infarction

Hemorrhagic: intracerebral or subarachnoid

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2
Q

What are the types of neurological ischaemic events?

A

transient ischaemic attack (TIA)
cerebral infarction (ischaemic stroke)

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3
Q

What are the types of neurological haemorrhagic events?

A

strokes:
intracerebral haemorrhage
subarachnoid haemorrhage

not a stroke:
subdural haemorrhage
extradural haemorrhage

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4
Q

What is a TIA?

A

transient ischaemic attack

sudden onset of a brief episode of neurological deficit due to temporary, focal cerebral ischaemia

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5
Q

What is the main difference between a TIA and an ischaemic stroke?

A

There is no infarction (irreversible cell death) in a TIA

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6
Q

What timeframe of cerebral ischaemia counts as a TIA?

A

anything < 24 hours is a TIA, > 24 hours is a stroke

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7
Q

Describe the onset of symptoms in a TIA?

A

symptoms are at maximal severity upon onset and last 5-15 minutes

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8
Q

What happens if a patient has a TIA and receives no intervention?

A

1 in 12 patients who have a TIA without intervention will have a stroke within a week

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9
Q

Where do TIAs occur?

A

90% occur in the internal carotid arteries (ICA)
10% are vertebral

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10
Q

How many first strokes are preceded by a TIA?

A

15%

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11
Q

What can a TIA foreshadow?

A

a stroke or an MI

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12
Q

Who is more likely to suffer a TIA?

A

males, black people

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13
Q

Why do black people have a higher chance of having a TIA?

A

they have a predisposition to hypertension and atherosclerosis

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14
Q

What are the risk factors for a TIA?

A

age
hypertension
smoking
T2 diabetes
AF
combines contraceptive pill

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15
Q

Describe the aetiology of TIAs.

A

main cause: atherothromboembolism from carotid artery

can also be caused by:
cardioembolism in AF/ after MI/ valve disease
hyperviscosity
hypoperfusion

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16
Q

What is the differential diagnosis for a TIA?

A

hypoglycaemia
migraine aura
focal epilepsy
vasculitis
syncope
retinal bleed

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17
Q

When can you differentiate between a TIA and a stroke?

A

not until after recovery

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18
Q

How does a TIA present?

A

amaurosis fugax
aphasia
hemiparesis
hemisensory loss
hemianopia vision loss

if TIA is in the vertebral territory, may experience ataxia, vertigo, vomiting, loss of consciousness, tetraparesis, choking

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19
Q

What is amaurosis fugax?

A

sudden vision loss in one eye caused by temporary occlusion of the retinal artery
transient- only lasts minutes

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20
Q

What may be the cause of TIA symptoms but with a gradual onset?

A

demyelination
tumour
migraine

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21
Q

What is an ABCD2 score?

A

assesses risk of stroke after a TIA

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22
Q

What is ABCD2 based on and what do the scores suggest?

A

based on age, blood pressure, clinical features, duration of TIA, presence of diabetes

max score is 7

2 day risk of stroke is:
4.1% with a score 4-5
8.1% with score 6-7

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23
Q

What is another term for a cerebral infarction?

A

ischaemic stroke

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24
Q

How does an ischaemic stroke occur?

A
  • blood vessel to/in brain is occluded by a clot
  • ischaemia and infarction follow as a result
  • infarcted areas die resulting in focal neurological symptoms
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25
Q

What are the main risk factors for ischaemic stroke?

A

male
age
hypertension
smoking
diabetes

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26
Q

What are the main causes of ischaemic stroke?

A
  • small vessel occlusion by thrombus
  • atherothromboembolism
  • cardioembolism
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27
Q

Why do clinical presentations of ischaemic stroke differ?

A

depends on the site of occlusion (i.e. is it ACA, MCA, PCA, etc)

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28
Q

What is the most common occlusion site of an ischaemic stroke?

A

middle cerebral artery

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29
Q

What is the presentation of an ischaemic stroke occurring due to a MCA occlusion?

A
  • hemiplegia of contralateral side affecting lower part of face, arms, hand while mostly sparing the leg
  • contralateral sensory loss of same areas
  • contralateral homonymous hemianopia
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30
Q

If a patient with MCA occlusion causing ischaemic stroke has aphasia what does this suggest?

A

That the occlusion is left sided

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31
Q

What is the artery least likely to be involved in an ischaemic stroke?

A

anterior cerebral artery

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32
Q

What is the presentation of an ischaemic stroke occurring due to a ACA occlusion?

A

contralateral leg weakness and sensory loss
may observe behavioural abnormalities and incontinence

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33
Q

What is the presentation of an ischaemic stroke occurring due to a PCA occlusion?

A
  • visual deficits (contralateral homonymous hemianopia or total blindness in one eye)
  • contralateral hemiparesis
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34
Q

What does PCA occlusion cause visual deficits?

A

the PCA supplies the occipital lobe

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35
Q

What structures make up the brainstem?

A

midbrain
pons
medulla

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36
Q

How do brainstem infarcts present?

A

depends on site, but in general:

  • QUADRIPLEGIA
  • cerebellar signs
  • vertigo, nausea, vomiting
  • speech impairment
  • facial numbness/ paralysis
  • locked-in syndrome
  • coma
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37
Q

What is a lacunar infarct?

A

small infarcts from occlusion of a single small perforating artery supplying a subcortical area

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38
Q

Where do lacunar infarcts occur?

A

internal capsule
basal ganglia
thalamus
pons

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39
Q

How do lacunar infarcts present?

A

Most asymptomatic, but can cause big problems if there are multiple of the small infarcts

sensory loss
unilateral weakness
ataxic hemiparesis
dysarthria

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40
Q

What investigations are carried out for cerebral infarcts?

A

CT scan ASAP

if diagnosis is uncertain then a diffusion-weighted MRI is more sensitive

may do blood tests to rule out hypoglycaemia, polycythaemia, vasculitis

ECG to check for AF/ MI

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41
Q

Why are CT scans so useful in ischaemic strokes?

A
  • distinguishes ischaemic vs hemorrhagic (vitally important for treatment!)
  • shows site of infarct
  • identifies conditions that may mimic stroke symptoms
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42
Q

How are ischaemic strokes managed?

A
  • exclude haemorrhagic stroke immediately, treating wrong type is catastrophic
  • if patient presents within 4.5hrs- treat with clot busting IV ALTEPLASE
  • immediate 300mg aspirin, which will continue daily for 2 weeks
  • life-long daily clopidogrel
  • warfarin in patients with AF
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43
Q

Why is IV alteplase not suitable for everyone with ischaemic stroke?

A
  1. can only be given if patient presents within 4.5 hours
  2. LOTS of contraindications
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44
Q

What surgery may be performed for ischaemic stroke?

A

patients may have mechanical thromboectomy (endovascular removal of thrombus)

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45
Q

Where do patients with ischaemic stroke go after immediate medical/ surgical treatment?

A

admitted to acute stroke unit for swallowing and feeding support and eventual rehabilitation

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46
Q

What are the types of haemorrhagic stroke?

A

intracerebral
subarachnoid

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47
Q

What is an intracerebral haemorrhage?

A

sudden bleeding into the brain tissue due to rupture of a blood vessel within the brain, leading to infarction due to oxygen deprivation

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48
Q

What happens to the ICP in an intracerebral haemorrhage?

A

pooling of blood within the brain causes raised ICP

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49
Q

What % of strokes are intracerebral haemorrhages?

A

approx. 10%

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50
Q

What is the mortality for an intracerebral haemorrhage?

A

up to 50% mortality

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51
Q

What are the risk factors for intracerbral haemorrhage?

A

hypertension
anticoagulation
thrombolysis
age
alcohol
smoking
diabetes

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52
Q

What are the main causes of intracerebral haemorrhage? Why do these have such an effect?

A

2 main causes: hypertension + secondary to ischaemic stroke

hypertension: gives stiff and brittle vessels that are prone to rupture and microaneurysms

ischaemic stroke: bleeding after repurfusion

other causes: head trauma, arteriovenous malformations, vasculitis

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53
Q

Describe the pathophysiology if increased ICP.

A
  • increased ICP puts pressure on the skull, brain and blood vessels
  • CSF obstruction causing hydrocephalus
  • causes a midline shift
  • tectorial herniation
  • coning (compression of brainstem)
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54
Q

How does intracerebral haemorrhage present?

A

similar to ischaemic stroke, but pointers towards intracerebral haemorrhage are:

  • sudden loss of consciousness
  • severe headache
  • meningism
  • coma

however these are not reliable for diagnosis and urgent CT is needed

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55
Q

What is meant by meningism?

A

clinical syndrome of symptoms including headache, photophobia, neck stiffness and seizures

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56
Q

How is intracerebral haemorrhage diagnosed?

A

same as ischaemic stroke, CT/ MRI essential

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57
Q

How is intracerebral haemorrhage managed?

A
  • STOP ANTICOAGULANTS IMMEDIATELY and reverse effects with a clotting factor replacement
  • control of blood pressure with IV drugs
  • reduce ICT with mechanical ventilation and IV mannitol
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58
Q

How long after an intracerebral haemorrhage can you restart anticoagulants?

A

1-2 weeks on a case by case basis

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59
Q

Which patients with an intracerebral haemorrhage should you refer to neurosurgery?

A

hydrocephalus
coma
brainstem compression

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60
Q

What is a SAH?

A

subarachnoid haemorrhage

type of haemorrhagic stroke caused by spontaneous bleeding into the subarachnoid space

can be catastrophic

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61
Q

Describe the spaces between each layer of the meninges.

A

from outside to inside:

skull
extradural space
dura mater
subdural space
arachnoid mater
subarachnoid space
pia mater
brain

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62
Q

What is the typical age of a person with a SAH?

A

35-65

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63
Q

What % of strokes are SAHs?

A

5%

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64
Q

What is the mortality of SAHs?

A

50% of people die immediately
10-20% more die 1-2 weeks later due to rebleeding

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65
Q

How does a SAH affect people long term?

A

only 30-40% survive and half of those people will be left with significant disability

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66
Q

What are the major risk factors for a subarachnoid haemorrhage?

A

hypertension
known aneurysm (berry aneurysm)
previous aneurysmal SAH

other risk factors include smoking, alcohol, family history and bleeding disorders

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67
Q

What occurs if a berry aneurysm ruptures?

A

will usually result in a subarachnoid haemorrhage

but result can also be:
cerebral haematoma
subdural haematoma
and/or intraventricular haemorrhage

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68
Q

What conditions are associated with a berry aneurysm?

A

polycystic kidney disease
coarctation of the aorta
ehlers-danlos syndrome
marfans syndrome

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69
Q

What is the aetiology of subarachnoid haemorrhage?

A
  • traumatic injury
  • berry aneurysm rupture (70-80% of cases)
  • arteriovenous malformation (15% of cases)
  • 15-20% idiopathic
70
Q

Where are most berry aneurysms found?

A

between the anterior cerebral artery and the anterior communicating artery in the circle of willis

71
Q

Describe the pathophysiology of a subarachnoid haemorrhage.

A
  • tissue ischaemia: less blood reaches tissue due to bleeding so less oxygen and nutrients can reach tissue causing cell death
  • raised ICP due to fast flowing arterial blood pumped into cranial space
  • space occupying lesion puts pressure on brain
  • blood irritates the meninges causing meningism symptoms and can obstruct CSF outflow causing hydrocephalus
  • vasospasm causes by irritation by blood leading to ischaemic injury
72
Q

What are the main complications of a subarachnoid haemorrhage?

A

rebleeding and hyponatraemia

73
Q

how does a subarachnoid haemorrhage present?

A
  • ‘thunderclap’ sudden excruciating headache
  • sentinel headache
  • nausea and vomiting
  • collapse
  • loss of consciousness
  • seizures
  • vision changes
  • coma and drowsiness
  • meningism
  • retinal, subhyaloid, vitreous bleeds
  • increased bp
74
Q

What does retinal bleeding indicate in a SAH?

A

worse prognosis, with or without papilloedema

75
Q

Where is a SAH thunderclap headache typically felt?

A

occipitally

76
Q

What is the differential diagnosis for a subarachnoid haemorrhage?

A
  • migraine/ cluster headache
  • meningitis
  • intracerebral haemorrhage
  • cortical vein thrombosis
  • carotid/ vertebral artery dissection
77
Q

What are the investigations for a subarachnoid haemorrhage?

A
  • brain CT asap, ‘star-shaped sign’ shows blood in ventricles
  • if normal ICP do a lumbar puncture, xanthochromia (yellow discolouration of CSF) confirms SAH
  • MR/ CT angiography to establish source of bleeding and for patients needing surgery
78
Q

Why does a SAH cause xanthochromia?

A

yellow discolouration of CSF is due to presence of bilirubin due to breakdown of SAH

79
Q

When can you do a lumbar puncture for SAH?

A

only after 12 hours of onset

80
Q

How sensitive is brain CT in detecting SAH?

A

detects > 95% of SAH in the first 24 hours

81
Q

How is a subarachnoid haemorrhage managed?

A
  • once SAH proven, immediate neurosurgery referral
  • re-examine the CSF often
  • IV fluids to maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
  • nimodopine- calcium agonist to reduce vasospasm and cerebral ischaemia
  • surgery
82
Q

What are the surgical interventions for subarachnoid haemorrhage?

A
  • endovascular coiling (preferred)
  • surgical clipping if angiography has shown aneurysm
83
Q

What is a subdural haematoma?

A

bleeding into the subdural space (between dura and arachnoid mater)

84
Q

What vessels are responsible for subdural haematoma?

A

the bridging veins which run from the cortex to venous sinuses (they are vulnerable to deceleration injury)

85
Q

What causes a subdural haematoma?

A

burst bridging veins usually caused by head injury but can also be caused by dural metastases

86
Q

Describe the time between head injury and presentation with subdural haematoma to A&E.

A

there is a massive latent interval lasting weeks to months between injury and presentation

87
Q

Describe the prognosis of subdural haematoma.

A

very treatable

88
Q

Who do you see subdural haematoma most often in?

A
  • babies (shaken baby syndrome)
  • brain atrophy (dementia, elderly, alcoholics)
  • people on anticoagulants
89
Q

Why does brain atrophy make you more susceptible to a subdural haematoma?

A
  • veins are more susceptible to rupture
  • these people are also more accident prone and at risk of falls (along with epileptics)
90
Q

Describe the pathophysiology of subdural haematoma.

A
  • bleeding from bridging veins into the subdural space
  • forms a haematoma
  • the bleeding then stops
  • weeks/ months later the haematoma starts to autolyse
  • this causes a massive increase in oncotic and osmotic pressure, sucking water in and enlarging the haematoma
  • gradual rise in ICP over a number of weeks
  • midline shift away from side of clot causing tensorial herniation and coning
91
Q

How does subdural haematoma present?

A
  • fluctuating levels of consciousness
  • drowsiness
  • headache
  • confusions
  • physical and intellectual slowing
  • personality change
  • unsteadiness
  • raised ICP
  • seizures
  • anisocoria
  • hemiparesis
92
Q

What is important to remember in patients with subdural haematoma?

A

due to the latency period it is likely that the patient won’t remember the head injury, so don’t discount subdural haematoma in patients who don’t have any head injury in their history

93
Q

What are the investigations for subdural haematoma?

A
  • CT scan: CRESENT SHAPED HAEMATOMA
    crosses the suture line and shows midline shift
  • MRI
94
Q

What do different densities of subdural haematoma mean on CT?

A

acute - hyper dense (bright)
subacute - isodense
chronic - hypotenuse (darker than brain)

95
Q

How is subdural haematoma managed?

A

surgery:
- depends on clot size, chronicity and clinical picture
- clot evacuation to remove haematoma
- craniotomy
- burr hole washout

IV mannitol to decrease ICP

reverse clotting abnormalities

address cause for trauma (falls/ abuse)

96
Q

What is an extradural haematoma?

A

bleeding into the extradural space (space between dural mater and skull)

97
Q

What is the most common cause of an extradural haematoma?

A

trauma to the temple:
- fracture to temporal/ parietal bone
- rupture of middle meningeal artery

98
Q

Describe the progression of symptoms in an extradural haematoma.

A
  • initial drowsiness/ unconsciousness after trauma
  • then recovery and lucid interval, maybe lasting hours
  • then rapid deterioration
99
Q

Describe the epidemiology of extradural haematoma.

A
  • mostly young people aged 20-30
  • rare in small children due to plasticity of skull
  • rare in > 60s as dura is tightly adhered to skull
  • more common in males
100
Q

Describe the pathophysiology of extradural haematoma.

A

after lucid interval:
- rise in ICP
- pressure on brain
- midline shift
- tentorial herniation
- coning

101
Q

What is the presentation of extradural haematoma?

A
  • short episode of drowsiness/ unconsciousness
  • then lucid “I feel fine” interval
  • rapid deterioration after hours/ days involving:
    rapidly declining GCS
    vomiting
    seizures
    hemiparesis
    UMN signs
    ipsilateral pupil dilation
    coma
    death from respiratory arrest
102
Q

What investigations are done for extradural haematoma?

A

CT SCAN:
- shows lemon shaped haematoma
- doesn’t cross suture lines
- unilateral
- shows midline shift

SKULL X-RAY
- may see fracture lines

103
Q

How is an extradural haematoma managed?

A
  • stabilise patient
  • urgent surgery: clot evacuation, ligation of bleeding vessel
  • IV mannitol
  • airway care (intubation, ventilation)
104
Q

What is a migraine?

A

recurrent throbbing headache often preceded by an aura

associated with vomiting, nausea and vision changes

105
Q

What is the most common cause of episodic headache?

A

migraine

106
Q

What are the risk factors for migraine?

A
  • 3 times more likely in females
  • 90% have onset before 40 yrs old
  • genetics and family history
  • adolescent age
107
Q

Describe the aetiology of migraine.

A

no known definite causes, but there are triggers

triggers: CHOCOLATE
C- chocolate
H- hangovers
O- orgasms
C- cheese
O- oral contraceptives
L- lie-ins
A- alcohol
T- tumult (loud noises)
E- exercise

108
Q

How does migraine present?

A

three stages: prodrome, aura and headache

prodrome (days before attack)
yawning, cravings, mood/ sleep changes

aura (part of attack, occurs before headache)
visual disturbance, somatosensory (pins and needles, paraethesia)

throbbing headache lasting 4-72 hours

109
Q

How are migraines classified?

A

either with or without aura

110
Q

What are the conditions that need to be met to diagnose migraine?

A

At least 2 of:
- unilateral pain
- throbbing pain
- moderate to severe intensity
- motion sensitivity

plus at least 1 of:
- nausea, vomiting
- photophobia, phonophobia

There also must be a normal examination and no attributable cause

111
Q

How is migraine diagnosed?

A

usually made clinically but may have extra tests to rule out other causes of headache

112
Q

How is migraine managed?

A

Treatment:
- triptans e.g. sumatriptan
- NSAIDS e.g. naproxen
- anti-emetic e.g. prochlorperazine
- avoid opioids and ergotamine

Prevention:
- required if > 2 attacked per month or require acute meds > 2 times per week
- beta blockers, e.g. propanolol
- TCAs (tricyclic antidepressants) e.g. amitryptyline
- anti-convulsant, e.g. topiramate

113
Q

What types of headaches are classified primary?

A

migraine
cluster
tension
drug overdose

114
Q

What is a secondary headache? Give examples.

A

due to underlying causes

  • GCA (giant cell arteritis)
  • infection
  • SAH
  • trauma
  • cerebrovascular disease
  • eye/ ear/ sinus pathology
115
Q

What is a cluster headache?

A

episodic headache lasting from 7 days to 1 year with pain free periods in between that last approx. 4 weeks

116
Q

What is the most disabling primary headache?

A

cluster headaches

116
Q

What is the most disabling primary headache?

A

cluster headaches

117
Q

Describe the epidemiology of cluster headache/

A
  • 4 times more common in males
  • onset usually 20-40 years
118
Q

What are the risk factors for cluster headache?

A

smoking
alcohol
male
genetics

119
Q

Describe the type of pain experienced in cluster headache?

A
  • rapid onset of excruciating pain, classically round the eye/ temple/ forehead
  • pain is unilateral and localised to one area
  • crescendos over a few minutes and lasts 15-160 minutes
  • occurs once or twice daily around the same time of day
120
Q

What are the symptoms of cluster headache aside from pain?

A
  • watery bloodshot eye
  • facial flushing
  • rhinorrhea (blocked nose)
  • miosis (pupillary constriction) +/- ptosis (in 20%)
121
Q

How is cluster headache diagnosed?

A

5 or more similar attacked confirms diagnosis

122
Q

How is cluster headache managed?

A

acute:
- analgesics are helpful
- 50L 100% oxygen for 15 minutes via non-rebreather mask
- triptans (e.g. sumatriptan)

prevention:
- verapamil (CCB) - 1st line prophylaxis
- prednisolone
- reduce alcohol and stop smoking

123
Q

How is tension headache classified?

A

episodic: < 15 days per month
chronic: > 15 days per month for at least 3 months

124
Q

What is the aetiology of tension headache?

A

no known organic cause, but can be triggered by:
- stress
- sleep deprivation
- bad posture
- hunger
- anxiety
- eyestrain
- noise

125
Q

What is the clinical presentation of tension headache?

A
  • bilateral head pain (like a rubber band)
  • non pulsatile
  • mild moderate intensity
  • +/- scalp tenderness
126
Q

How is tension headache diagnosed?

A

from history

127
Q

How is tension headache managed?

A

avoidance of triggers and stress relief

symptomatic relief: aspirin, paracetamol, ibuprofen, no opiates

limits analgesics to < 6 days per month to avoid drug-induced headaches

128
Q

What is trigeminal neuralgia?

A

unilateral pain in one or more trigeminal branches

129
Q

What patients are most likely to experience trigeminal neuralgia?

A

20 times more likely in patients with MS

130
Q

What triggers trigeminal neuralgia?

A

eating
shaving
talking
brushing teeth

131
Q

Describe the pain felt in trigeminal neuralgia.

A

unilateral
electric shock type pain lasting seconds/ minutes

132
Q

How is trigeminal neuralgia treated?

A

carbamazodine (anticonvulsant)
surgery possible as last resort

133
Q

What is giant cell arteritis?

A

inflammation of the arteries within the head

134
Q

How is a diagnosis of giant cell arteritis confirmed?

A
  • temporal artery biopsy shows granulomatous non-caseating inflammation of intima and media with skip lesions
  • raised ESR/ CRP
  • normocytic normochromic anaemia of chronic disease
135
Q

How is giant cell arteritis treated?

A
  • corticosteroids (prednisolone)
  • if any sign of amaurosis fugax, high dose IV methylprednisolone STAT
136
Q

What is epilepsy?

A

the recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain manifesting in seizures

137
Q

What is the diagnostic criteria for epilepsy?

A

must have had one of:
- at least 2 unprovoked seizures occurring more than 24 hours apart
- one unprovoked seizure and a probability of future seizures ( >60% within 10 years)
- diagnosis of an epileptic syndrome

138
Q

What are the causes for seizures?

A

pneumonic: VITAMIN DE

V- vascular
I- infection
T- trauma
A- autoimmune
M- metabolic
I- idiopathic (epilepsy)
N- neoplasms
D- dementia and drugs
E- eclampsia

139
Q

What is eclampsia?

A

a severe complication of pre-eclampsia that causes seizures during pregnancy

140
Q

Describe the aetiology of epilepsy.

A
  • 2/3 idiopathic/ genetic
  • cortical scarring (trauma, cerebrovascular disease, infection)
  • tumours/ space-occupying lesions
  • strokes
  • alzheimers
  • alcohol withdrawal
141
Q

What are the risk factors for epilepsy?

A
  • family history
  • premature babies, especially if small
  • abnormal cerebral blood vessels
  • drugs (e.g. cocaine)
142
Q

Describe the stages of an epileptic seizure.

A

PRODROME:
- precedes seizure hours/ days before
- mood/ behaviour changes, “weird feeling”

AURA:
- part of seizure, patient is aware
- strange feeling in gut, de ja vu, strange smells, flashing lights
- often implies a partial seizure

ICTAL EVENT: the seizure

POST-ICTAL: period after the seizure
- headache, confusion, myalgia, tongue biting
- Todd’s palsy following focal seizure in motor cortex
- dysphagia following temporal lobe seizure

143
Q

What is Todd’s palsy?

A

temporary weakness after focal seizure

144
Q

What does tongue biting during a seizure imply?

A

that the seizure is epileptic, tongue biting very uncommon in non-epileptic seizures

145
Q

What does dysphagia following a seizure imply?

A

it was a temporal lobe seizure

146
Q

What does Todd’s paralysis following a seizure imply?

A

that it was a motor cortex seizure

147
Q

How are epileptic seizures classified?

A

PRIMARY GENERALISED (40%):
- tonic
- clonic
- tonic clonic, aka “grand mal”
- myoclonic
- atonic
- absence, aka “petit mal”

FOCAL/ PARTIAL (60%):
- simple
- complex
- secondary generalised tonic clonic

148
Q

How does a tonic seizure look?

A
  • rigid, stiff limbs
  • will fall to floor if standing
149
Q

How does a clonic seizure look?

A

rhythmic muscle jerking

150
Q

What is a tonic clonic seizure?

A
  • combination of tonic and clonic
  • stereotypical “shaking” seizures due to mix of on/ off rigidity and muscle jerking
  • up gazing eyes and incontinence
151
Q

What is a myoclonic seizure?

A

isolated jerking of a limb/ face/ trunk
“disobedient limb”

152
Q

What is an atonic seizure?

A

complete opposite to tonic seizure, loss of muscle tone = floppy

153
Q

What is an absence seizure?

A
  • common in childhood but usually goes by adulthood, but increased risk of developing generalised tonic-clonic seizures as an adult
  • will go pale and “stare blankly” for a few seconds
  • often suddenly stop talking mid sentence and do not realise they have had an attack
154
Q

What is the major difference between primary generalised and partial epileptic seizures?

A

primary generalised is bilateral and always includes loss of consciousness, partial are confined to one region but can progress to secondary generalised

155
Q

What is a simple partial/ focal seizure?

A
  • no effect on consciousness or memory
  • awareness unimpaired but will have focal, motor, autonomic or psychic symptoms depending on affected lobe
  • no post-ictal symptoms
156
Q

What is a complex partial seizure?

A
  • memory/ awareness affected at some point
  • most commonly arises from temporal lobe- affects speech, memory and emotion
  • post-octal confusion is common if temporal lobe, whereas recovery is swift if frontal lobe affected
157
Q

What is a partial seizure with secondary generalisation?

A

seizures that start focally and then spread widely throughout the cortex

158
Q

Describe the presentation of a temporal lobe seizure.

A

temporal lobe= memory, understanding speech, emotion
- aura (deja vu, auditory hallucinations, funny smells, fear)
- anxiety, out of body experiences
- automatisms, e.g. lip smacking

159
Q

Describe the presentation of a frontal lobe seizure.

A

frontal lobe= motor, thought processing
- motor features, e.g. posturing, peddling movements of leg
- Jacksonian march: seizures march up and down motor homunculus
- post-octal Todd’s palsy: starts distally in a limb and works its way upwards to face

160
Q

Describe the presentation of a parietal lobe seizure.

A

parietal lobe= sensation
- sensory disturbances, e.g. tingling, numbness

161
Q

Describe the presentation of an occipital lobe seizure.

A

occipital lobe= vision
- visual phenomenon, e.g. spots, lines, flashes

162
Q

How can you distinguish epileptic vs non-epileptic seizures?

A
  • non-epileptic are entirely sensational, e.g. metabolic disturbances, or related to syncope
  • non-epileptic seizures are longer with closed eyes and mouth
  • non-epileptic do not occur during sleep or involve tongue biting or incontinence
  • there are pre-ictal anxiety symptoms in non-epileptic, e.g. they know it is going to happen
163
Q

What are the signs that a seizure is epilepsy and not syncope?

A

tongue biting
head turning
muscle pain
loss of consciousness
cyanosis
post-cital symptoms

164
Q

How is epilepsy diagnosed?

A
  • EEG
    not diagnostic but supports diagnosis, may help to determine type of epileptic syndrome
  • MRI/ CT head
    used to rule to other potential causes, e.g. space occupying lesions
  • bloods: FBC, U+Es, LFTs, blod glucose
    rule out metabolic disturbances
  • genetic testing if suspected genetic cause, e.g. juvenile myoclonic epilepsy
165
Q

How is epilepsy managed?

A

medication is only started after the second epileptic episode

PRIMARY GENERALISED SEIZURES:
sodium valproate for ALL MEN and women who are unable to child bear

for women age 15-45:
- generalised tonic-clonic = lamotrigine
- absence = ethosuximide
- myoclonic = levetriacetam/ topiramate

PARTIAL SEIZURES:
everybody is given lamotrigine/ carbamazepine

acute management for a seizure lasting > 5 mins is benzodiazepines (e.g. diazepam) IV or rectally

166
Q

What is the main considering when prescribing sodium valproate?

A

it is highly tetragenic

167
Q

What are the most common origins for a brain tumour?

A

most common: non small cell lung cancer

others:
small cell lung cancer
breast
melanoma
renal cell carcinoma
GI cancer

168
Q

Give 5 examples of primary brain tumours.

A

astrocytoma
oligodendroglioma
ependyma
meningioma
schwannoma
craniopharyngioma

169
Q

What is Wernicke’s encephalopathy?

A

depletion of thiamine (vitamin B1)

170
Q

What are the symptoms of Wernicke’s encephalopathy?

A

classic triad of:
confusion
ataxia
ophthalmoplegia

Phase 2a BASICS (6 decks)

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