Neurology Flashcards
(139 cards)
1
Q
what are the differentials for headache?
A
cluster headache tension headache migraine medication over-use infective causes- meningitis/encephalitis subarachnoid haemorrhage trigeminal neuralgia temporal arteritis
2
Q
features of migraine?
A
severe, unilateral, throbbing headache
nausea
photophobia + phonophobia
visual aura - progressive, usually scotoma or hemianopic disturbance
3
Q
what are some of the triggers of a migraine?
A
tiredness stress alcohol COCP lack of food cheese, chocolate, red wine menstruation lack of food or dehydration bright lights
4
Q
what is the diagnostic criteria of a migraine?
A
1) headache lasting 4-72 hours
2) two of the following: unilateral, pulsating, moderate or severe intensity, aggravate by routine physical activity
3) includes nausea and/or vomiting, photophobia or phonophobia
4) not attributable to any other disorder
5
Q
why is COCP contra-indicated in patients with migraine with aura?
A
increases risk of stroke
6
Q
management of migraine?
A
Acute treatment:
5-HT receptor agonist (triptan) plus either paracetamol or NSAID
Prophylaxis:
Topiramate (teratogenic)
Propranolol
7
Q
features of a tension-type headache?
A
tight band around head pressure sensation bilateral lower intensity than migraine no aurua, N+V, or aggravation by physical routine
8
Q
management of tension-type headache?
A
acute treatment: aspirin, paracetamol, or NSAID
prophylaxis: acupuncture, low dose amitriptyline
9
Q
features of cluster headache?
A
pain occurs once or twice a day episodes last 15 mins to 2 hours clusters last 4-12 weeks intense sharp stabbing pain around one eye redness, lacrimation and lid swelling
10
Q
management of cluster headache?
A
100% oxygen
subcut triptan
prophylaxis: verapamil
11
Q
what is temporal arteritis?
A
large vessel vasculitis commonly affecting the temporal artery
12
Q
what condition is temporal arteritis associated with?
A
polymyalgia rheumatica
13
Q
symptoms of temporal arteritis?
A
headache jaw claudication tender, palpable temporal artery visual disturbances (secondary to anterior ishcamic optic neuropathy) PMR
14
Q
investigations of temporal arteritis?
A
ESR/CRP
temporal artery biopsy- histology shows skip lesions
15
Q
management of temporal arteritis?
A
high dose prednisolone immediately (before results of biopsy come back)
urgent opthalmology review
16
Q
features of trigeminal neuralgia?
A
unilateral headache
brief electric shock like pains
abrupt onset and termination
pain is evoked by light tough including washing, shaving, smoking etc.
17
Q
management of trigeminal neuralgia?
A
carbamazepine
18
Q
what is an indicator of medication over-use headache?
A
when the headache does not respond and worsens to migraine or other treatment
19
Q
symptoms of subarachnoid haemorrhage?
A
sudden thunderclap headache very severe nausea + vomiting meningism CN III palsy - (oculomotor nerve is compressed by growing or budding of posterior communicating artery (PcoA) aneurysm, midbrain injury, or increased intracranial pressure (ICP)) coma seizures
20
Q
pathophsyiology of subarachnoid haemorrhage?
A
rupture of berry aneurysms or AV malformation
21
Q
investigatons of subarachnoid haemorrhage?
A
CT head - hyperdensity in ventricular system
LP after 12 hours- xanthachromia (RBC breakdown)
CT intracranial angiogram - to identify vascular lesion
22
Q
management of subarachnoid haemorrhage?
A
remain on neuro intensive care
21 day course of nimodipine (Ca channgel blocker) - reduce vasospasm
Endovascular coiling or surgical clipping
Hydrocephalus treated with external ventricular drain
23
Q
complications of SAH?
A
Re-bleeding
vasospasm
SIADH
seizures hydrocephalus
24
Q
pathophysiology of subdural heamorrhage?
A
collection of blood in the subdural space (in between the dura mater and the pia mater), most commonly due to tearing of the bridging veins due to high impact trauma (i.e. in the elderly after a fall)
25
presentation of subdural haemorrhage?
fluctuating consciousness
headache
personality change
Hx of trauma -> can be months ago as presents chronically
26
RF for subdural haemorrhage?
warfarin/antiplatelet
elderly
epileptics
alcoholics
27
investigations of subdural haemorrhage?
CT head - crescentic in shape, not restricted by suture lines and compress the brain - hyper/hypodense depending on how long
28
management of subdural haemorrhage?
conservative management if no symptoms
| if symptoms- craniotomy/burr-hole (neurosurgical decompresison)
29
what are the two locations that berry aneurysms present most commonly?
posterior communicating artery connects to internal carotid
| anterior communicating artery connects to the anterior cerebral
30
presentation of extra-dural haemorrhage?
patient initially loses consciousness
briefly regains - "lucid period"
then decreasing GCS due to expanding haematoma and brain herniation
fixed and dilated pupil due to compression of CN III
31
What happens during brain herniation?
temporal lobe herniates through the tentorium cerebelli - structure made of the dura mater near the base of the skull.
This compresses the CN III causing reduced parasympathetic innervation to the affected eye. This causes the pupil of the affected eye to be fixed and dilated, with no response to light.
32
causes of extradural haemorrhage?
trauma to parietal or temporal bone which commonly causes:
| tearing of the middle meningeal artery or a tear in the dural venous sinus
33
investigations of extradural haemorrhage?
CT head: biconvex hyperdense collection that is limited by the suture lines of the skull (due to tight adherence of the dura to the calvarium - causes the biconvex shape)
34
management of extradural haemorrhage?
urgent neurosurgical intervention - craniotomy/burr-hole to evacuate the haematoma
35
what is the scoring system used to evaluate the likelihood of TIA?
```
Age > 60
BP > 140/80
Clinical - unilateral weakness or speech impairement
Duration > 60 mins
Diabetes
(ABCD2 score)
```
36
Definition of TIA?
transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia (without acute infarction)
37
management of TIA?
300mg aspirin immediately
clopidogrel continued therapy
carotid artery endardectomy if able to tolerate
38
what symptoms does an anterior cerebral artery infarct result in?
contralateral hemiparesis
sensory loss
usually worse in the lower extremities than the upper limbs
39
what would a total anterior circulation infarct result in?
unilateral hemiparesis
homonymous hemianopia
higher cognitive dysfunction
40
what would a partial anterior circulation infarct result in?
2 of:
unilateral hemiparesis
homonymous hemianopia
higher cognitive dysfunction
41
which vessels does a lacunar infarct involve?
perforating arteries around the internal capsule, thalamus, and basal ganglia
42
how does a lacunar infarct present?
1 of:
unilateral weakness
pure sensory stroke
ataxic hemiparesis
43
how does a posterior circulation infarct present?
1 of:
cerebellar or brainstem syndrome
LOC
isolated homonymous hemianopia
44
which vessels are affected in a posterior circulation infarct/
vestibulobasilar arteries
45
what are cerebellar symptoms??
```
impaired co-ordination
slurred speech
unsteady gait
repetitive eye movements
difficulty with fine motor tasks
headahces
```
46
what features of a stroke are more common in haemorrhagic strokes than ischaemic?
LOC
N+V
headache
seizures
47
investigations of stroke?
CT head
| MRI
48
management of ischaemic stroke?
thrombolysis within 4.5 hours
300mg aspirin
antiplatelet therapy continued (clopidogrel)
medical thrombectomy - within 6 hrs
49
management of hemorrhagic stroke?
neurosurgery involvement
usually not operable - supportive management
stop antiplatelets and anticoagulants
50
what is thrombolysis?
tissue plasminogen activator - dissolves blood clots (alteplase)
51
what are some examples of thrombolysis agents?
streptokinase
| alteplase
52
what are some contra-indications to thrombolysis?
```
uncertainty of stroke onset
hypertension
heparin treatment in last 48hrs
INR>1.7
Hx of haemorrhagic stroke in last 3 months
known intracranial neoplasm
internal bleeding within last 6 weeks
```
53
differential diagnosis of seizures?
epilepsy disorder
NEAD/pseudoseizures
syncope with secondary jerk movements
primary cardiac/respiratory presenting as anoxic seizure
acute electrolyte inbalance (hyponatraemia, hypocalcaemia, hypomagnesaemia)
alcohol withdrawal
febrile (in peads)
54
presentation of generalised tonic clonic seizures?
aura: deja vu, abdominal sensation, premonition, fear, strange smells
tonic-clonic: rigidity followed by rapid repetitive jerking, complete loss of consciousness
incontinence
tongue biting
long recovery period - confusion and drowsiness lasting several hours
55
what are the different types of generalised seizures?
tonic clonic
tonic
clonic
typical absence (petit mal)
56
what are the features of absence seizures?
Precipitated by hyperventilation or stress:
| absences for a few seconds with no memory, associated with rapid recovery
57
what are the features of a temporal lobe seizure?
```
Hallucinations
Epigastric/emotional
Automatisms (lip smacking, plucking, grabbing)
Deja vu
HEAD
```
58
what are the features of frontal lobe focal seizures?
head/leg movements
| jacksonian march
59
what is a typical feature of a parietal lobe focal seizure?
paraesthesia
60
what is a typical feature of an occipital lobe focal seizure?
floaters/flashes in the vision
61
investigations of suspected epilepsy?
```
EEG
MRI
seizure blood tests- BM, FBC, U+E, LFT etc
ECG
collateral history
```
62
management of epilepsy with generalised seizures?
first line: sodium valproate
| second line: carbamazepine, lamotrigene
63
management of focal seizures?
first line: carbamazepine, lamotrigene
| second line: sodium valproate
64
contraindications to sodium valproate?
child bearing age- teratogenic (use cautiously)
acute porphyrias
severe hepatic dysfunction
65
S/E of sodium valproate?
```
alopecia with curly hair re-growth
anaemia
impaired conc.
agitation
behavioural changes + hallucinatoins
```
66
management of status epilepticus?
1) ABCDE
2) BUCCAL DIAZEPAM OR RECTAL MIDAZOLAM
3) IV LORAZEPAM
4) IV PHENYTOIN
5) > 60 MINS - MIDAZOLAM IV + GA
67
what is the MOA of sodium valproate?
increases GABA secretion
68
pathophysiology of MS?
autoimmune demyleination of the myelin sheath, leading to the formation of white matter plaques
69
RF for MS?
```
genetic
EBV exposure
HHV6
Low levels of Vit D + sunlight
female
```
70
presentation of MS?
Visual: optic neuritis, uhthoff's phenomena
Sensory: numbness, pins/needles, trigeminal neuralgia, Lhermitte's syndrome
Motor: spastic weakness
Cerebellar: tremor + ataxia
Other: urinary incontinence, sexual dysfunction
71
what are the different types of MS?
relapsing-remitting: most common
primary progressive
secondary progressive - 75% of patients will move onto secondary progressive within 35 years of onset
progressive-relapsing
72
investigations of MS?
MRI- periventricular plaques
CSF- oligoclonal bands+ increased IgG
visual evoked potentials- delayed but well preserved wave form
73
what is the diagnostic criteria for MS?
demonstration of two different lesions disseminated in time and space
74
management of acute relapse of MS?
IV methylprednisolone
75
management of MS long term?
```
Beta-interferon (DMARD- anti-lymphocyte monoclonal antibody)
glatiramer
natalizumab
symptom control:
spasticity: baclofen or diazepam
```
76
pathophysiology of parkinsons?
loss of dopaminergic neurones from the pars compacta of the substantia nigra in the midbrain that project to the striatum of the basal ganglia. Characterized by the presence of lewy body eosinophilic inclusion proteins.
77
features of parkinsons?
triad: bradykinesia, cog-wheel + lead pipe rigidity and (pill-rolling) tremor
```
additional symptoms:
mask like faces
depression
dementia
pyschosis
impaired olfaction
fatigue
postural hypotension
```
78
investigations of parkinsons?
usually clinical
| SPECT can help differentiate between essential tremor and parkinsons
79
management of parkinsons?
Levodopa + carbidopa
dopamine agonist (bromocriptine, ropinirole)
MAO-B inhibitor (selegiline)
Amantadine
80
SE of levodopa?
```
dyskinesia
dry mouth
constipation
palpitations
anorexia
psychosis
drowsiness
```
81
SE of dopamine receptor agonist (i.e. bromocriptine, ropinirole)
```
hallucinaitons
dyskinesia
dry mouth
control disorders
nausea
orthostatic hypotension
somnolence
```
82
mechanism of action of MAO-B inhibitors (e.g. selegiline)
inhibits the breakdown of dopamine secreted by the dopaminergic neurones
83
signs of UMN lesion?
no muscle atrophy
weakness and spasticity
hyperreflexia
babinski positive
84
signs of LMN lesion?
```
muscle atrophy
flaccid paralysis
no plantar response
absent tendon reflexes
fasiculations
```
85
what are the different types of MND?
```
amyotrophic lateral sclerosis
primary lateral sclerosis
progressive muscular atrophy
progressive bulbar palsy
psudeobulbar palsy
```
86
how does amyotrophic lateral sclerosis typically present?
mixture of UMN and LMN signs
fasiculations begin in one distal limb and move upwards
focal weakness
brisk reflexes and spasticity
87
how does primary lateral sclerosis present?
```
UMN signs only -
increased reflexes
spasticity
babinski positive
usually begins in the legs
```
88
how does progressive muscular atrophy present?
LMN signs only
affects distal muscles before proximal
must have absence of LMN
89
how does progressive bulbar palsy present and why?
```
palsy of the tongue, muscles of chewing/swallowing, facial muscles
fasiculating tongue
dysphagia
dysarthria
emotional incontinence
loss of gag reflex
due to LMN palsy of CN IX-XII
```
90
how does pseudobulbar palsy present and why?
UMN lesion of CN V-XII
spastic tongue
exaggerated gag reflex and jaw jerk
91
management of MND?
```
patient education
riluzole
non-invasive ventilator therapy
diazepam and baclofen for spasticity
speech and language therapist
NG tube
```
92
MOA of riluzole?
prevents stimulation of glutamate receptors - prolongs life in MND by 3 months
93
what is the genetic mutation in huntingtons?
autosomal dominant with complete penetrance mutation in the huntingtin gene on chr 4 - CAG trinucleotide repeat which causes malfunction of GABA from substantia nigra
94
key features of huntingtons?
```
chorea - excessive rapid movements
saccadic eye movements
personality changes
dystonia
intellectual impairement
myoclonus
```
95
management of huntingtons?
no management
| only symptom control- MOA-I terabenazine
96
pathophysiology of GBS?
molecular mimicry autoimmune condition where antibodies against the myelin sheath are produced following a gastroenteritis type infection (commonly campylobacter)
97
presentation of GBS?
ascending weakness of all four limbs
few paraesthesia signs
areflexia
cranial nerve involvement
urinary retention and diarrhoea - autonomic involvement
diaphragm involvement = respiratory complications
98
investigations of GBS?
LP - rise in protein and normal WCC
| nerve conduction studies
99
management of GBS?
electrophoresis
IV immunoglobulins
ventilatory support
100
what is myasthenia gravis?
autoimmune condition characterized by loss of acteylcholine receptors at the neuromuscular junction
101
features of MG?
```
progressive weakness throughout the day
worse in the evenin
difficulty chewing
diplopia
ptosis
proximal muscle weakness
```
102
which drugs may exacerbate MG?
BB
lithium
phenytoin
antibiotics
103
investigations of MG?
single fibre electromyography
CT throax - associated with thymoma
anti-cholinergic receptor autoantibodies
104
management of MG?
long acting anticholinesterase inhibitors - pyridostigmine
prednisolone- immunosuppresion
thymectomy
105
what is a myasthenic crisis?
worsening of muscle weakness leading to respiratory failure and severe bulbar weakness, requiring intubation and life support
106
management of myasthenic crisis?
plasmapheresis
| IV immunoglobulins
107
what is radiculopathy?
compression of nerve root as it exits the spinal cord
108
causes of encephalitis?
HSV-1
| VZV
109
feautres of encephalitis?
```
fever
headache
psychiatric symptoms
seizures
vomiting
focal lesions
```
110
investigations of encephalitis?
CSF: increased lymphocytes + protein
PCR for HSV
CT/MRI: medial temporal and inferior frontal changes
111
management of encephalitis?
IV aciclovir
112
most common organisms to cause meningitis in children?
neisseria meningitidis
strep pneumoniae
haemophilus influenza
113
most common organisms to cause meningitis in adults?
neisseria meningitidis
| strep pneumoniae
114
signs and symptoms of meningitis?
```
headache
fever
nause and vomiting
photophobia
drowsiness
seizures
kernigs sign
purpura rash
```
115
management of meningitis?
IM benzylpenicillin
IV cefotaxime +/- amoxicillin
if meningiococcal septicaemia - IV cefotaxime or benzylpenicillin
116
what prophylaxis is given to relatives of patients with meningitis?
oral ciprofloxacin or rifampicin
117
What are the 4 different types of dementia?
alzheimers
frontotemporal
lewy body
vascular
118
pathophysiology of alzheimers?
deposition of beta-amyloid plaques and neurofibrillary tangles of tau protein causin widespread cortical atrophy
119
features of alzheimers?
```
memory lapse
difficulty in finding words
wandering
apraxia
planning problems
psychiatric symptoms
```
120
what is the diagnostic criteria for alzheimers?
deficits in 2 or more cognitive areas, insidious onset, no disturbance in consciousness, no other identifiable causes
121
management of alzheimers disease?
Ach inhibitor - rivastigmine, NMDA antagonist- memantine
management of symptoms-
diazepam if agressive, antipsychotics for psychotic symptoms
122
pathophysiology of lewy body dementia?
deposition of lewy bodies (alpha synuclein cytoplasmic inclusions) in the brainstem and neo-cortex
123
features of lewy body dementia?
well formed hallucinations
fluctuating attention
parkinsonism - bradykinesia, tremor, rigidity
124
management of lewy body dementia?
acetylcholinesterase inhibitors - donepazil, rivastigmine
AVOID anti-parkinson meds and anti-psychotics associated with parkinson symptoms (chlorpromazine, metoclopramide, haloperidol) as can make symptoms worse
125
pathophysiology of frontotemporal dementia?
presence of pick bodies (aggregations of tau protein)
126
features of frontotemporal lobe dementia?
```
inapropriate behaviour
loss of empathy
lack of insight
personality changes
loss of inhibition
loss of vocabulary
```
127
macroscopic changes seen in picks disease?
atrophy of the frontal and temporal lobes
128
microscopic changes seen in picks disease?
pick bodies
neurofibrillary tangles
senile plaques
129
management of frontotemporal dementia?
alleviate symptoms/agitation
| stop aggrevating drugs such as Ach inhibitors or CNS drugs
130
which tumours most commonly spread to the brain?
```
lung (most common)
breast
bowel
melanoma
kidney
```
131
which type of malignancy is the most common in the brain?
glioblastoma multiforme
132
what is a glioblastoma?
malignant tumour of the glial tissue of the nervous system- including: oligodendrocytes, astrocytes, microglia etc.
133
what is seen on histology of glioblastoma?
pleomorphic tumour cells with necrotic areas
134
management of glioblastoma/
surigcal removal
post-op chemotherapy/radiotherapy
dexamethasone - treat oedema
135
which type of tumour is second most common in the brain?
meningioma (arise from dura mater, usually benign)
136
what is a vestibular schwannoma?
benign tumour arising from the eighth cranial nerve, often within the cerebellopointine angle
137
symptoms of vestibular schwannoma?
unilateral hearing loss, facial nerve palsy, tinnitus (however can be bilateral if tumour is bilateral)
138
which type of malignancy is the most common paediatric cranial tumour?
craniopharyngioma
139
what is tested for brain death?
fixed pupils that do not respond to light
no corneal reflex
no response to supraorbital pressure
no cough reflex
no gagging reflex
no observed respiratory effort in response to deconnection of the ventilator
