Neurology Flashcards
(171 cards)
1
Q
What are the types of stroke?
A
Ischaemia: cerebral infarction
Hemorrhagic: intracerebral or subarachnoid
2
Q
What are the types of neurological ischaemic events?
A
transient ischaemic attack (TIA)
cerebral infarction (ischaemic stroke)
3
Q
What are the types of neurological haemorrhagic events?
A
strokes:
intracerebral haemorrhage
subarachnoid haemorrhage
not a stroke:
subdural haemorrhage
extradural haemorrhage
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
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
6
Q
What timeframe of cerebral ischaemia counts as a TIA?
A
anything < 24 hours is a TIA, > 24 hours is a stroke
7
Q
Describe the onset of symptoms in a TIA?
A
symptoms are at maximal severity upon onset and last 5-15 minutes
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
9
Q
Where do TIAs occur?
A
90% occur in the internal carotid arteries (ICA)
10% are vertebral
10
Q
How many first strokes are preceded by a TIA?
A
15%
11
Q
What can a TIA foreshadow?
A
a stroke or an MI
12
Q
Who is more likely to suffer a TIA?
A
males, black people
13
Q
Why do black people have a higher chance of having a TIA?
A
they have a predisposition to hypertension and atherosclerosis
14
Q
What are the risk factors for a TIA?
A
age
hypertension
smoking
T2 diabetes
AF
combines contraceptive pill
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
16
Q
What is the differential diagnosis for a TIA?
A
hypoglycaemia
migraine aura
focal epilepsy
vasculitis
syncope
retinal bleed
17
Q
When can you differentiate between a TIA and a stroke?
A
not until after recovery
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
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
20
Q
What may be the cause of TIA symptoms but with a gradual onset?
A
demyelination
tumour
migraine
21
Q
What is an ABCD2 score?
A
assesses risk of stroke after a TIA
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
23
Q
What is another term for a cerebral infarction?
A
ischaemic stroke
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
25
What are the main risk factors for ischaemic stroke?
male
age
hypertension
smoking
diabetes
26
What are the main causes of ischaemic stroke?
- small vessel occlusion by thrombus
- atherothromboembolism
- cardioembolism
27
Why do clinical presentations of ischaemic stroke differ?
depends on the site of occlusion (i.e. is it ACA, MCA, PCA, etc)
28
What is the most common occlusion site of an ischaemic stroke?
middle cerebral artery
29
What is the presentation of an ischaemic stroke occurring due to a MCA occlusion?
- 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
30
If a patient with MCA occlusion causing ischaemic stroke has aphasia what does this suggest?
That the occlusion is left sided
31
What is the artery least likely to be involved in an ischaemic stroke?
anterior cerebral artery
32
What is the presentation of an ischaemic stroke occurring due to a ACA occlusion?
contralateral leg weakness and sensory loss
may observe behavioural abnormalities and incontinence
33
What is the presentation of an ischaemic stroke occurring due to a PCA occlusion?
- visual deficits (contralateral homonymous hemianopia or total blindness in one eye)
- contralateral hemiparesis
34
What does PCA occlusion cause visual deficits?
the PCA supplies the occipital lobe
35
What structures make up the brainstem?
midbrain
pons
medulla
36
How do brainstem infarcts present?
depends on site, but in general:
- *QUADRIPLEGIA*
- cerebellar signs
- vertigo, nausea, vomiting
- speech impairment
- facial numbness/ paralysis
- locked-in syndrome
- coma
37
What is a lacunar infarct?
small infarcts from occlusion of a single small perforating artery supplying a subcortical area
38
Where do lacunar infarcts occur?
internal capsule
basal ganglia
thalamus
pons
39
How do lacunar infarcts present?
Most asymptomatic, but can cause big problems if there are multiple of the small infarcts
sensory loss
unilateral weakness
ataxic hemiparesis
dysarthria
40
What investigations are carried out for cerebral infarcts?
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
41
Why are CT scans so useful in ischaemic strokes?
- distinguishes ischaemic vs hemorrhagic (vitally important for treatment!)
- shows site of infarct
- identifies conditions that may mimic stroke symptoms
42
How are ischaemic strokes managed?
- 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
43
Why is IV alteplase not suitable for everyone with ischaemic stroke?
1. can only be given if patient presents within 4.5 hours
2. LOTS of contraindications
44
What surgery may be performed for ischaemic stroke?
patients may have mechanical thromboectomy (endovascular removal of thrombus)
45
Where do patients with ischaemic stroke go after immediate medical/ surgical treatment?
admitted to acute stroke unit for swallowing and feeding support and eventual rehabilitation
46
What are the types of haemorrhagic stroke?
intracerebral
subarachnoid
47
What is an intracerebral haemorrhage?
sudden bleeding into the brain tissue due to rupture of a blood vessel within the brain, leading to infarction due to oxygen deprivation
48
What happens to the ICP in an intracerebral haemorrhage?
pooling of blood within the brain causes raised ICP
49
What % of strokes are intracerebral haemorrhages?
approx. 10%
50
What is the mortality for an intracerebral haemorrhage?
up to 50% mortality
51
What are the risk factors for intracerbral haemorrhage?
hypertension
anticoagulation
thrombolysis
age
alcohol
smoking
diabetes
52
What are the main causes of intracerebral haemorrhage? Why do these have such an effect?
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
53
Describe the pathophysiology if increased ICP.
- 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)
54
How does intracerebral haemorrhage present?
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
55
What is meant by meningism?
clinical syndrome of symptoms including headache, photophobia, neck stiffness and seizures
56
How is intracerebral haemorrhage diagnosed?
same as ischaemic stroke, CT/ MRI essential
57
How is intracerebral haemorrhage managed?
- 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
58
How long after an intracerebral haemorrhage can you restart anticoagulants?
1-2 weeks on a case by case basis
59
Which patients with an intracerebral haemorrhage should you refer to neurosurgery?
hydrocephalus
coma
brainstem compression
60
What is a SAH?
subarachnoid haemorrhage
type of haemorrhagic stroke caused by spontaneous bleeding into the subarachnoid space
can be catastrophic
61
Describe the spaces between each layer of the meninges.
from outside to inside:
skull
extradural space
dura mater
subdural space
arachnoid mater
subarachnoid space
pia mater
brain
62
What is the typical age of a person with a SAH?
35-65
63
What % of strokes are SAHs?
5%
64
What is the mortality of SAHs?
50% of people die immediately
10-20% more die 1-2 weeks later due to rebleeding
65
How does a SAH affect people long term?
only 30-40% survive and half of those people will be left with significant disability
66
What are the major risk factors for a subarachnoid haemorrhage?
hypertension
known aneurysm (berry aneurysm)
previous aneurysmal SAH
other risk factors include smoking, alcohol, family history and bleeding disorders
67
What occurs if a berry aneurysm ruptures?
will usually result in a subarachnoid haemorrhage
but result can also be:
cerebral haematoma
subdural haematoma
and/or intraventricular haemorrhage
68
What conditions are associated with a berry aneurysm?
polycystic kidney disease
coarctation of the aorta
ehlers-danlos syndrome
marfans syndrome
69
What is the aetiology of subarachnoid haemorrhage?
- traumatic injury
- berry aneurysm rupture (70-80% of cases)
- arteriovenous malformation (15% of cases)
- 15-20% idiopathic
70
Where are most berry aneurysms found?
between the anterior cerebral artery and the anterior communicating artery in the circle of willis
71
Describe the pathophysiology of a subarachnoid haemorrhage.
- 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
What are the main complications of a subarachnoid haemorrhage?
rebleeding and hyponatraemia
73
how does a subarachnoid haemorrhage present?
- '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
What does retinal bleeding indicate in a SAH?
worse prognosis, with or without papilloedema
75
Where is a SAH thunderclap headache typically felt?
occipitally
76
What is the differential diagnosis for a subarachnoid haemorrhage?
- migraine/ cluster headache
- meningitis
- intracerebral haemorrhage
- cortical vein thrombosis
- carotid/ vertebral artery dissection
77
What are the investigations for a subarachnoid haemorrhage?
- 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
Why does a SAH cause xanthochromia?
yellow discolouration of CSF is due to presence of bilirubin due to breakdown of SAH
79
When can you do a lumbar puncture for SAH?
only after 12 hours of onset
80
How sensitive is brain CT in detecting SAH?
detects > 95% of SAH in the first 24 hours
81
How is a subarachnoid haemorrhage managed?
- 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
What are the surgical interventions for subarachnoid haemorrhage?
- endovascular coiling (preferred)
- surgical clipping if angiography has shown aneurysm
83
What is a subdural haematoma?
bleeding into the subdural space (between dura and arachnoid mater)
84
What vessels are responsible for subdural haematoma?
the bridging veins which run from the cortex to venous sinuses (they are vulnerable to deceleration injury)
85
What causes a subdural haematoma?
burst bridging veins usually caused by head injury but can also be caused by dural metastases
86
Describe the time between head injury and presentation with subdural haematoma to A&E.
there is a massive latent interval lasting weeks to months between injury and presentation
87
Describe the prognosis of subdural haematoma.
very treatable
88
Who do you see subdural haematoma most often in?
- babies (shaken baby syndrome)
- brain atrophy (dementia, elderly, alcoholics)
- people on anticoagulants
89
Why does brain atrophy make you more susceptible to a subdural haematoma?
- veins are more susceptible to rupture
- these people are also more accident prone and at risk of falls (along with epileptics)
90
Describe the pathophysiology of subdural haematoma.
- 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
How does subdural haematoma present?
- fluctuating levels of consciousness
- drowsiness
- headache
- confusions
- physical and intellectual slowing
- personality change
- unsteadiness
- raised ICP
- seizures
- anisocoria
- hemiparesis
92
What is important to remember in patients with subdural haematoma?
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
What are the investigations for subdural haematoma?
- CT scan: CRESENT SHAPED HAEMATOMA
crosses the suture line and shows midline shift
- MRI
94
What do different densities of subdural haematoma mean on CT?
acute - hyper dense (bright)
subacute - isodense
chronic - hypotenuse (darker than brain)
95
How is subdural haematoma managed?
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
What is an extradural haematoma?
bleeding into the extradural space (space between dural mater and skull)
97
What is the most common cause of an extradural haematoma?
trauma to the temple:
- fracture to temporal/ parietal bone
- rupture of middle meningeal artery
98
Describe the progression of symptoms in an extradural haematoma.
- initial drowsiness/ unconsciousness after trauma
- then recovery and lucid interval, maybe lasting hours
- then rapid deterioration
99
Describe the epidemiology of extradural haematoma.
- 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
Describe the pathophysiology of extradural haematoma.
after lucid interval:
- rise in ICP
- pressure on brain
- midline shift
- tentorial herniation
- coning
101
What is the presentation of extradural haematoma?
- 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
What investigations are done for extradural haematoma?
CT SCAN:
- shows lemon shaped haematoma
- doesn't cross suture lines
- unilateral
- shows midline shift
SKULL X-RAY
- may see fracture lines
103
How is an extradural haematoma managed?
- stabilise patient
- urgent surgery: clot evacuation, ligation of bleeding vessel
- IV mannitol
- airway care (intubation, ventilation)
104
What is a migraine?
recurrent throbbing headache often preceded by an aura
associated with vomiting, nausea and vision changes
105
What is the most common cause of episodic headache?
migraine
106
What are the risk factors for migraine?
- 3 times more likely in females
- 90% have onset before 40 yrs old
- genetics and family history
- adolescent age
107
Describe the aetiology of migraine.
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
How does migraine present?
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
How are migraines classified?
either with or without aura
110
What are the conditions that need to be met to diagnose migraine?
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
How is migraine diagnosed?
usually made clinically but may have extra tests to rule out other causes of headache
112
How is migraine managed?
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
What types of headaches are classified primary?
migraine
cluster
tension
drug overdose
114
What is a secondary headache? Give examples.
due to underlying causes
- GCA (giant cell arteritis)
- infection
- SAH
- trauma
- cerebrovascular disease
- eye/ ear/ sinus pathology
115
What is a cluster headache?
episodic headache lasting from 7 days to 1 year with pain free periods in between that last approx. 4 weeks
116
What is the most disabling primary headache?
cluster headaches
116
What is the most disabling primary headache?
cluster headaches
117
Describe the epidemiology of cluster headache/
- 4 times more common in males
- onset usually 20-40 years
118
What are the risk factors for cluster headache?
smoking
alcohol
male
genetics
119
Describe the type of pain experienced in cluster headache?
- 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
What are the symptoms of cluster headache aside from pain?
- watery bloodshot eye
- facial flushing
- rhinorrhea (blocked nose)
- miosis (pupillary constriction) +/- ptosis (in 20%)
121
How is cluster headache diagnosed?
5 or more similar attacked confirms diagnosis
122
How is cluster headache managed?
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
How is tension headache classified?
episodic: < 15 days per month
chronic: > 15 days per month for at least 3 months
124
What is the aetiology of tension headache?
no known organic cause, but can be triggered by:
- stress
- sleep deprivation
- bad posture
- hunger
- anxiety
- eyestrain
- noise
125
What is the clinical presentation of tension headache?
- bilateral head pain (like a rubber band)
- non pulsatile
- mild moderate intensity
- +/- scalp tenderness
126
How is tension headache diagnosed?
from history
127
How is tension headache managed?
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
What is trigeminal neuralgia?
unilateral pain in one or more trigeminal branches
129
What patients are most likely to experience trigeminal neuralgia?
20 times more likely in patients with MS
130
What triggers trigeminal neuralgia?
eating
shaving
talking
brushing teeth
131
Describe the pain felt in trigeminal neuralgia.
unilateral
electric shock type pain lasting seconds/ minutes
132
How is trigeminal neuralgia treated?
carbamazodine (anticonvulsant)
surgery possible as last resort
133
What is giant cell arteritis?
inflammation of the arteries within the head
134
How is a diagnosis of giant cell arteritis confirmed?
- 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
How is giant cell arteritis treated?
- corticosteroids (prednisolone)
- if any sign of amaurosis fugax, high dose IV methylprednisolone STAT
136
What is epilepsy?
the recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain manifesting in seizures
137
What is the diagnostic criteria for epilepsy?
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
What are the causes for seizures?
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
What is eclampsia?
a severe complication of pre-eclampsia that causes seizures during pregnancy
140
Describe the aetiology of epilepsy.
- 2/3 idiopathic/ genetic
- cortical scarring (trauma, cerebrovascular disease, infection)
- tumours/ space-occupying lesions
- strokes
- alzheimers
- alcohol withdrawal
141
What are the risk factors for epilepsy?
- family history
- premature babies, especially if small
- abnormal cerebral blood vessels
- drugs (e.g. cocaine)
142
Describe the stages of an epileptic seizure.
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
What is Todd's palsy?
temporary weakness after focal seizure
144
What does tongue biting during a seizure imply?
that the seizure is epileptic, tongue biting very uncommon in non-epileptic seizures
145
What does dysphagia following a seizure imply?
it was a temporal lobe seizure
146
What does Todd's paralysis following a seizure imply?
that it was a motor cortex seizure
147
How are epileptic seizures classified?
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
How does a tonic seizure look?
- rigid, stiff limbs
- will fall to floor if standing
149
How does a clonic seizure look?
rhythmic muscle jerking
150
What is a tonic clonic seizure?
- combination of tonic and clonic
- stereotypical "shaking" seizures due to mix of on/ off rigidity and muscle jerking
- up gazing eyes and incontinence
151
What is a myoclonic seizure?
isolated jerking of a limb/ face/ trunk
"disobedient limb"
152
What is an atonic seizure?
complete opposite to tonic seizure, loss of muscle tone = floppy
153
What is an absence seizure?
- 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
What is the major difference between primary generalised and partial epileptic seizures?
primary generalised is bilateral and always includes loss of consciousness, partial are confined to one region but can progress to secondary generalised
155
What is a simple partial/ focal seizure?
- 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
What is a complex partial seizure?
- 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
What is a partial seizure with secondary generalisation?
seizures that start focally and then spread widely throughout the cortex
158
Describe the presentation of a temporal lobe seizure.
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
Describe the presentation of a frontal lobe seizure.
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
Describe the presentation of a parietal lobe seizure.
parietal lobe= sensation
- sensory disturbances, e.g. tingling, numbness
161
Describe the presentation of an occipital lobe seizure.
occipital lobe= vision
- visual phenomenon, e.g. spots, lines, flashes
162
How can you distinguish epileptic vs non-epileptic seizures?
- 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
What are the signs that a seizure is epilepsy and not syncope?
tongue biting
head turning
muscle pain
loss of consciousness
cyanosis
post-cital symptoms
164
How is epilepsy diagnosed?
- 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
How is epilepsy managed?
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
What is the main considering when prescribing sodium valproate?
it is highly tetragenic
167
What are the most common origins for a brain tumour?
most common: non small cell lung cancer
others:
small cell lung cancer
breast
melanoma
renal cell carcinoma
GI cancer
168
Give 5 examples of primary brain tumours.
astrocytoma
oligodendroglioma
ependyma
meningioma
schwannoma
craniopharyngioma
169
What is Wernicke's encephalopathy?
depletion of thiamine (vitamin B1)
170
What are the symptoms of Wernicke's encephalopathy?
classic triad of:
confusion
ataxia
ophthalmoplegia
