Neuro Flashcards
1
Q
how many people that have a stroke will die within a year?
A
1/4
2
Q
events that can create stroke inducing cardiac emboli
A
AF
Endocarditis
MI
any arrhythmia really
3
Q
factors that increase risk of CNS bleeds
A
hypertension
trauma
aneurysm rupture
anticoagulation
thrombolysis
4
Q
what could cause stroke in younger patients
A
carotid artery dissection - can be spontaneous or from neck trauma
sudden blood pressure drop by >40mmHg which can affect boundary zones between vascular beds
5
Q
differentials for stroke symptoms
A
head injury
hypo-hyperglycaemia
subdural haemorhage
Wernicke’s/Hepatic encephalopathy
Drug overdose (if comatose)
6
Q
modifiable risk factors for stroke
A
Hypertension
smoking
alcohol excess
heart diseae
poor DM control
hyperlipidaemia
7
Q
what is meningism?
A
it is the triad of nuchal rigidity, headache and photophobia
8
Q
general signs of stroke
A
meningism
severe headache
coma
carotid bruit
9
Q
non-modifiable risk factors for stroke
A
AF
Past TIA
IHD
Age
10
Q
what percentage of strokes are cerebral infarcts
A
50%
11
Q
what are the signs specific to a cerebral infarct
A
hemiparesis
hemiplegia
contralateral sensory loss
limbs are initially flacid but eventually become spastic
12
Q
what percentage of strokes are in the brainstem
A
25%
13
Q
what are the signs specific to brainstem infarcts
A
quadriplegia
locked in syndrome
disturbances of gaze and vision
14
Q
where is a lacunar infarct
A
in the basal ganglia, internal capsule, thalamus and pons
15
Q
what percentage of strokes are lacunar
A
25%
16
Q
what are the 5 syndromes of lacunar stroke
A
ataxic hemiparesis
pure motor
pure sensory
sensorimotor
dysarthria/clumsy hand
in all lacunar strokes except thalamic strokes the cognition/consciousness remains intact
17
Q
6 important points for the acute management of stroke
A
- protect the airway
- maintain homeostasis (glucose etc)
- screen swallow (nil by mouth until this is done)
- CT/MRI within 1hr
- antiplatelet agents (once haemorrhagic stroke is excluded)
- Thrombolysis if haemorrhagic stroke excluded and onset of symptoms was <4.5hrs ago
18
Q
what agent do you use to thrombolyse stroke patients
A
alteplase
19
Q
what should you do 24 hrs after you thrombolyse a stroke patient
A
CT head
to identify any bleeds
20
Q
what are 8 contraindications for thrombolysis of stroke patient
A
haemorrhage on CT
mild/non-disabling deficit
recent surgery or trauma
previous CNS bleed
arteriovenous malformations/aneurysms
if high INR
known clotting disorder
stroke or serious head injury in the last 3 months
HTN above 200 systolic
21
Q
primary prevention of stroke
A
- this is before any stroke occurs so it is control of risk factors
- treat hypertension
- control DM
- improve diet to reduce lipids
- treat cardiac disease
- quit smoking
- exercise more
- lifelong anticoagulation in AF or with prosthetic heart valve
22
Q
secondary prevention of stroke
A
this is after a stroke or TIA has occured and you want to prevent a second one
- control the risk factors as with primary prevention
- anticoagulate after CVA (2 weeks aspirin 300mg and then move onto long term anti-platelets like clopidogrel)
23
Q
A
24
Q
what is the CHA2DS2VASc score and what are the components
A
- it is a score designed to assess the risk of an AF patient for embolic stroke
- Congestive cardiac failure
- Hypertension
- Age (65-74) (2 points)
- Diabetes
- Stroke/TI/Thromboembolism previously (2 points)
- Vasular disease
- Sex Category (1 point if female)
- a score of 2 has an anual stroke risk of 2.2. but risk goes up with more points
25
stroke complications related to immobility
pressure sores
aspiration pneumonia
constipation
contractures
26
are TIAs usually haemorrhagic or embolic
usually embolic
27
what is the definition of TIA
incident of neurological ischaemia in which symptoms last less than 24 hours by which time they have completely resolved
28
why is prompt intervention with TIA so important
without intervention more than 1/12 patients will go on to have a stroke within a week
29
what is amaurosis fugax
it is when the retinal artery is occluded
this causes unilateral progressive vision loss
like a curtain descending
30
what is a crescendo TIA and what does it suggest
more than two TIAs in a week and it suggests some intraranial stenosis
31
what are 4 main causes of TIA
Atherothromboembolism (usually from the internal carotid)
cardioembolism (post MI or in AF)
Hyperviscosity
Vasculitis (rare)
32
what 3 things can cause hyperviscosity
polycythaemia
sickle cell
myeloma
33
differnetials for TIA
hypoglycaemia
migraine
focal epilepsy
hyperventilation
retinal bleeds
34
tests for TIA
FBC
U&E
ESR
Glucose
Lipids
CXR
ECG
Carotid doppler (to check for carortid artery stenosis)
Angiography CT
35
4 principles of treatment for TIA
control CVS risk factors
antiplatelet drugs
anticoagulation
carotid endarterectomy
36
what antiplatelets following TIA
aspirin 300mg following TIA for two weeks then switch to clopidogrel
37
how long is driving prohibited for after TIA
1 month at least
38
carotid endarterectomy
only if occlusion is \>70% and the operative risk is acceptable
39
what is the ABCD2 score
the ABCD2 score is a tool to stratify which patients are higher risk of having a stroke following TIA
40
what does a score of 4 or more in ABCD2 mean
it means they are high risk for a stroke and need asssessment by a specialist within 24hrs
41
what does a score of 6 or more in ABCD2 mean
it means that they are 35.5% likely to have a stroke in the next week
42
factors not on ABCD2 but that will increase risk of stroke following TIA
AF
\>1 TIA in a week
TIA while anticoagulated
43
what is the incidence of subarachnoid hemorrhage
9/100,000/yr
44
what is the typical age range for a subarachnoid haemorrhage
35-65
45
symptoms of subarachnoid haemorrhage
thunderclap headache
sudden onset
vomiting
collapse
seizures
coma often follows
46
What is strongly contraindicated in a EDH
LUMBAR PUNCTURE
47
signs of sub arachnoid haemorrhage
neck stiffness
kernig's sign
focal neurology (may indicate site)
48
what is kernig's sign
A sign indicating the presence of meningitis (inflammation of the meninges covering the brain and spinal cord). The test for Kernig sign is done by having the person lie flat on the back, flex the thigh so that it is at a right angle to the trunk, and completely extend the leg at the knee joint. If the leg cannot be completely extended due to pain, this is Kernig sign.
49
what are the causes of subarachnoid haemorrhage
* rupture of berry aneurysm (80%)
* encephalitis
* vasculitis
* tumour with invading blood vessels
* idiopathic
50
common sites of berry aneurysm rupture
junction of posterior communicating artery with internal carotid or aterior cerebral
bifurcation of the middle cerebral artery
51
8 risk factors for subarachnoid haemorrhage
previous aneurysmal SAH
smoking
alcohol misuse
bleeding disorders
family history
PKD
aortic coarctation
Ehlers Danlos Syndrome
hypertension
52
5 differentials of SAH
meningitis
migraine
intracerebral bleed
cortical vein thrombosis
dissection of carotid or vertebral artery
53
what is the treatment for rising ICP
IV mannitol
54
tests for suspected SAH
urgent CT detects \>95% of SAH within the first 24hrs
55
what to do if the CT is negative but the history is convincing for SAH
consider a lumbar puncture if there is no CI
this should be done 12hrs after headache onset to allow breakdown of the RBCs
therefore the positive sign is yellow CSF due to bilirubin
not red which could be confused with blood from traumatic LP
56
management for SAH
* refer all proven SAH to neurosurgery immediately
* CNS exam often
* GCS, repeat CT, EWS
* maintain cerebral perfusion
* hydration and BP
* nimodipine
* CCB that reduces vasospasm
* surgery
* surgical clipping of aneurysm
57
complications from SAH
re-bleeding is the most common cause of death
cerebral ischaemia due to vasospasm can cause permanent CNS deficit and is the commonest cause of morbidity
hydrocephalus due to blockage of arachnoid granulations
58
describe the mortality of SAH patients based on their signs
59
where does the bleeding come from in subdural haematoma
from bridging veins that connect the dural venous sinuses and the cortex
60
what happens in subdural haematoma
* bridging veins are vulnerable to deceleration injury
* this results in accumulating haematoma between the dura and the arachnoid
* this gradually raises the ICP
* this can lead to coning
61
what kind of event causes a subdural
* they are mostly from trauma
* trauma is often forgotten because it was so minor
* trauma can have been up to 9 months ago
* can occur without trauma
* in the case of low ICP the brain shrinks and bridging veins are vulnerable
* elderly patients and alcoholics with atrophy
62
three populations who are vulnerable to SDH
alcoholics
elderly
those on anticoagulant drugs
63
symptoms of a subdural haematoma
* fluctuating consciousness
* insidious intellectual or physical slowing
* sleepiness
* headache
* personality change
* unsteadiness
64
signs of SDH
rising ICP
seizures
localising neurological symptoms can occur amonth after injury
65
differentials for SDH
stroke
dementia
CNS masses
66
imaging for SDH
CT/MRI shows clot with or without a midline shift
crescent shaped collection of blood over one hemisphere (differentiates from extradural)
67
management of SDH
* reverse any clotting abnormalities urgently
* generally, lots over 19mm with 5mm midline shift need evacuating
* craniotomy or
* burr hole washout
* address the cause of the trauma
68
what natural history should make you think of extradural haematoma
beware any loss of consciousness following any head injury that initially caused no loss of consciousness
or
after an initial drowsiness following an injury seems to have resolved
lucid interval pattern is typical of extradural bleeds
69
what typically causes an extradural haemorrhage
suspect after any traumatic skull fracture
often it's a fractured temporal or parietal bone causing a laceration of the middle meningeal artery and/or vein
any tear in a dural venous sinus will also cause an extradural bleed
70
8 clinical features of EDH
* lucid interval
* hrs-days
* lowering GCS
* incresing ICP
* increasingly severe headache
* vomiting
* confusion
* seizures
* hemiparesis
71
how do symptoms and signs of EDH progress if the bleeding continues
ipsilateral pupil may dilate
coma deepens
bilateral limb weakness develops
breathing may become deep and irregular (indicates brainstem compression)
72
differentials of EDH
epilepsy
carotid dissection
stroke
TIA
73
tests for suspected SDH
* CT head
* egg shaped bleed
* Skull x ray
* check for fracture lines crossing middle meningeal artery
* REMEMBER THAT A LUMBAR PUNCTURE IS CONTRAINDICATED
74
What is the management of EDH
urgent transfer to neurosurgery for clot evacuation and ligation of bleeding vessel
care of the airway
if ICP is high then IV mannitol
75
prognosis for EDH and indicators
excellent if prompt diagnosis and management
poor if coma, pupil abnormalities or decerebrate rigidity are present pre-op
76
what is the definition of epilepsy
this is the recurrent tendancy to spontaneous intermittent abnormal electrical activity in the brain manifesting in seizures
77
how do you know if a blackout is epilepsy or syncope
Syncope is a temporary loss of consciousness usually related to insufficient blood flow to the brain
epilepsy is an electrical disturbance of brain function
78
what is the definition of epileptic seizure
paroxysmal event in which changes of behaviour, sensation or cognitive decline are processes that are caused by excessive hypersynchronous neuronal discharges in the brain
79
how long does an epileptic seizure last generally
30-120 seconds
80
how long can a post ictal state last, when does it happen and how is it characterised
* 5-30 minutes after the seizure
* characterised by:
* drowsiness
* confusion
* nausea
* hypertension
* headache
81
what would an epileptic prodrome look like
it can last for hours or days before the seizure and it is a change in mood or behaviour
82
what portion of epileptic seizures are idiopathic
2/3
83
name three structural causes of epilepsy
cortical scarring due to a historic head injury
stroke
vascular malformation
84
what must an epilepsy history include
a detailed description from a witness of the seizure
85
broadly what are the two different types of seizures and what are the differences between them
* Focal seizures (AKA partial seizures)
* affects particular part of the body depending on the neurological origin of the seizure
* Generalised seizures
* originate from widespread electrical discharge that can't be localised
86
what are the three types of focal seizure and very briefly what are the differences
* without impairment of consciousness
* and no post-ictal symptoms
* with impairment of consciousness
* consciousness may be impaired at time of seizure or after an aura
* and there are commonly post-ictal seizures
* evolving to a bilateral convulsing seizure
* typically progresses to a convulsive generalised seizure
* this occurs in 2/3 patients with partial seizures
87
what are the four types of generalised seizures and briefly describe each of them
* absence seizures
* brief pauses \<10s - suddenly stops talking mid sentence before carrying on where left off
* commonly presents in childhood
* tonic clonic seizure
* there's loss of consciousness
* limbs stiffen then jerk
* commonly post ictal confusion and drowsiness
* myoclonic seizures
* sudden jerk of face, limb or trunk
* might be suddenly thrown to ground or have sudden disobedient limb.
* 'plate throwing epilepsy'
* atonic seizures
* no loss of consciousness
* sudden loss of muscle tone causing a fall
88
how many types of epilepsy are there and what is classification based on
* there are over 40 types
* classification is based on
* seizure type
* EEG findings
* other features
* age of onset
89
what is a provoked seizure
most people will have a seizure if provoked but this is not epilepsy
3-10% of provoked seizures recur
whereas 30-50% of unprovoked seizures occur
90
examples of seizure provocation
* anoxic seizures following syncope
* trauma
* haemorrhage
* alcohol or benzodiazepine withdrawal
* infection
* drugs (cocaine)
* metabolite imbalance
* glucose
* sodium
* calcium
91
Investigations of Epilepsy
* look for a provoking cause
* check metabolite levels
* hyper or hypoglycaemia
* hyper or hyponatraemia
* hypocalcaemia
* uremia
* Drug levels (are they compliant with their anti-epileptic)
* LP if infetion is suspected
* consider an EEG
* MRI to look for structural lesions
92
what type of activity should an epileptic patient not undertake
driving
swimming
heights
93
epilepsy and driving
the patient MUST contact the DVLA and not drive until they have been seizure free for \>1yr
94
1st line medical treatment for focal seizures
carbamazepine or Lamotrigine
95
1st line medical treatment for generalised tonic-clonic seizures
sodium valproate or Lamotrigine
96
1st line treatment for absence seizures
sodium valproate
2nd line is Lamotrigine
97
1st line medical treatment for myoclonic seizures
sodium valproate
2nd line is levetiracetam
98
what drug might worsen myoclonic seizures
carbamazepine
99
what is the first line medical treatment for atonic seizures
sodium valproate or lamotrigine
100
surgery for epilepsy?
if there is a single, known epileptogenic focus then it can work
an example would be a tumour
carries risk of causing focal neurological defect
101
what is sudden unexpected death in epilepsy
this is more common in uncontrolled epilepsy
this may be related to nocturnal seizure-associated apnoea or systole
17% of epilepsy deaths are due to SUDEP
102
how much higher is mortality in epileptic population than in gen pop
3x higher
103
how many epilepsy related deaths are there in the UK every year
\>700
104
three considerations for epilepsy in pregnancy
there's a 5% risk of fetal abnormalities
sodium valproate is teratogenic so transition to other drugs is required
most AEDs are present in breast milk but lamotrigine is thought not to be harmful to infants
105
how long does syncope last and how long is recovery from syncope
lasts 5-30 seconds
recovery within 30s
106
what are non-epileptic seizures
these are psychogenic and situational
suspect if there's gradual onset, prolonged duration and abrupt termination
also characteristic are closed eyes that are resistant to opening
can coexist with true epilepsy
patient may have history of mental illness
CNS exam, MRI, CT and EEG are all normal
107
What is status epilepticus
* seizure lasting more than 30moinutes without intervening consciousness
108
what are the risks with status epilepticus
mortality
permanent brain damage
likelihood of both increase with the length of the attack
109
management of convulsive status epilepticus
secure airway and get anaesthetist support
oxygen
IV bolus of lorazepam to stop seizure
assess metabolite and drug levels
correct hypotension
correct metabolite levels
if seizures continue start phenytoin infusion
if seizure lasts more than 60-90mins anaesthetist may consider propofol infusion for paralysis
110
what is the mean age of onset of parkinson's
60
111
what is the prevalence of parkinson's at 85-95 years
3.5%
112
what is parkinsonism
* triad of
* resting tremor ('pill rolling')
* hypertonia
* bradykinesia - slow initiation of movement
113
what are two key features of parkinson's seen on examination
* cogwheel rigidity
* caused by rigidity and tremor together
* micrographia
114
what is the pathogenesis of parkinsons
loss of dopaminerfic neurons in the substantia nigra
this is associated with formation of lewy bodies in the basal ganglia, brain stem and cortex
most cases are sporadic but there are some genetic loci implicated in familial cases
115
clinical features of parkinson's
10 things
* the parkinsonism triad
* micrographia
* non motor symptoms
* autonomic disfunction
* constipation
* dribbling
* urinary frequency/urgency
* sleep disturbance
* reduced sense of smell
* neuropsychiatric complications
* depression
* dementia
* psychosis
* it is invariably worse on one side - if symmetrical then look for other causes
116
diagnosis of parkinson's
it is clinical and based on the triad
if there is a good response to dopaminergic therapy then this is supportive of the diagnosis
MRI to exclude structural pathology
117
what is a non-pharmacological option for treatment of parkinson's
deep brain stimulation
118
when should you start pharmacological treatment for parkinson's
when over 70 or when symptoms of parkinson's are seriously interfering with life
this is because efficacy decreases with time and SEs get worse with time
119
what are the 4 types of pharmacological treatment for parkinson's
levodopa
dopamine agonists
mono amine oxidase B inhibitors (MAO-B)
COMT inhibitors
120
what is the most important pharmacological treatment of parkinson's
describe how it is given and with what
levodopa
it is given with a dopa-decarboxylase inhibitor (carbidopa) in a combined drug called co-careldopa or co-beneldopa
carbidopa helps the dopa not be metabolised before it reaches the brain
121
what are the side effects of levodopa treatment
dyskinesia
dystonia
psychosis
hallucinations
nausea
vomiting
122
what is an example of a dopamine agonist used for parkinson's and why might they be used
ropinirole
can delay starting levodopa
123
what is an example of a MAO-B, why might they be used and how do they work
selegiline
they are an alternative to dopamine agonists early in PD
they prevent the breakdown of dopamine
124
what is an example of a COMT inhibitor, how does it work and what is a risk
tolcapone
stops the breakdown of levodopa
is hepatotoxic so close monitoring of LFTs is important
125
what is the most common type of headache
tension headache
126
if someone says it's the first headache of this type that they've ever had and it's the worst headache ever what should you be worried about
SAH
127
if someone complains of unilateral headache and eye pain what is it
a cluster headache or alternatively acute glaucoma
128
if a headache is initiated by a cough or is worse in the morning or on bending over what does it indicate
that it's related to high ICP
129
if there's persisting headache with scalp tenderness in the over 50s what should you suspect
giant cell arteritis
130
if there's headache with fever or neck stiffness what should you be concerned about
meningitis
131
two vital questions on taking a history of new headache
travel? malatia
pregnant? pre-eclampsia - especially if proteinuria and HTN
132
are cluster headaches more common in men or women
men
133
what is one modifiable risk factor for cluster headaches
smoking
134
clinical presentation of cluster headache
* rapid onset excruciating pain around one eye
* eye can become watery and bloodshot with lid swelling and lacrimation
* facial flushing
* pain is strictly unilateral and always affets the same side
* lasts from 15-180 minutes
* occurs once or twice a day and is often nocturnal
* clusters are 4-6 weeks and followed by periods of months to years between clusters
* sometimes it can be chronic and not episodic
135
treatment for acute attack of cluster headache
100% oxygen via non-rebreathe mask
SC sumatriptan
136
prevention of cluster headaches
avoid triggers like alcohol
verapamil might help (CCB)
137
what is the M:F for migraines
1:3
138
what % of people suffer with migraines
15%
139
which artery territory stroke do you sometimes get akinetic muteness
and what is it
ACA
motor components not that affected but they can't talk and they're almost unconscious with it
140
8 ACA territory stroke symptoms
* Leg Weakness
* Sensory disturbance in the legs (homonculi)
* Gait Apraxia
* Truncal Ataxia
* Incontinence
* Drowsiness
* Akinetic Mutism
* Decrease in spontaneous speech
* Stuporus state
141
6 MCA stroke symptoms
* Contralateral arm and leg weakness
* Contralateral sensory loss
* Hemianopia
* Aphasia
* Dysphasia
* Facial Droop
142
PCA stroke symptoms
* Contralateral homonymous hemianopia
* cortical blindness with bilateral involvement of the occipital lobe branches
* visual agnosia
* Can’t interpret visual information, but can see
* Prosopagnosia
* dyslexia, Anomic aphasia, colour naming and discrimination problems
* Headaches unilateral
143
as strokes get older how does there appearance change on CT
the infarcted area gets darker
144
what is MCA syndrome stroke
this is where the mca stroke is so big that all the oedema causes compression of the rest of the brain
it can lead to herniation and is very dangerous
145
what is almost never a feature of ischaemic stroke and what is the exception
bad headache
the exception is in posterior cerebral artery strokes
146
posterior circulation strokes symptoms
* Motor deficits such as hemiparesis or tetraparesis and facial paresis
* Dysarthria and speech impairment
* Vertigo, nausea, and vomiting
* Visual disturbances
* Altered consciousness
147
what part of the brain will be affected by posterior circulation strokes
the brainstem
can be devastating and has high mortality
148
why can you detect change so quickly with MRI
MRI gives basically a map of water content of tissue
water changes in the brain happen rapidly in response to injury so you can sometimes see change within minutes
149
what are warning syndromes
small infarcts in the small cerebral arteries
in people who are vasculopaths
they have transient motor symptoms that go away and come back repeatedly before persisting
warning syndrome occurs over a couple of days - 'very odd and looks like a seizure'
it's less self contained than a TIA
150
when would clot retrieval be indicated in stroke patients
this only works for clots in larger arteries
151
what does the modified rankin scale assess
the degree of disability or dependence in the daily activities of people who experience stroke
0-5
5 being worst, 0 being no symptoms
152
characteristic CT signs for ruptured berry aneurysm on circle of willis
spider sign
153
what are the classic presentations of migraines
* visual or other aura lasting 15-30 minutes followed by 1hr unilateral throbbing headache
* isolated aura with no headache
* episodic severe headache without aura - may be premenstrual usually unilateral with nausea, vomiting and photophobia/phonophobia
* maybe allodynia where all stimuli cause pain even brushing hair/wearing glasses
154
what is an aura
* Visual: chaotic melting and jumbling of lines and dots, with or without hemianopia
* Somatosensory: paraesthesia spreading from fingers to face
* Motor: dysarthria and ataxia
* Speech: dysphasia and paraphasia
155
how frequently do people with migraines have triggers
50%
156
what are the triggers for migraines
* CHOCOLATE
* Chocolate
* Hangovers
* Orgasms
* Cheese/caffeine
* Oral contraceptive
* Lie ins
* Travel
* Exercise
157
what two things are associated with migraine
family history and obesity
158
diagnosis of migraines
clinical and is based on the history
* the diagnostic criteria if there aer no aura are
* \>5 headaches lasting 4-72hrs with nausea/vomiting or photo/phonophobia
* AND any 2 of:
* unilateral
* pulsating
* impairs or is worsened by usual activity
159
6 differentials for migraine
Cluster headaches
high BP
intracranial pathology
sinusitis
otitis media
TIA can mimic migraine aura
160
last resort treatment for chronic migraine
12 weekly botulinum toxin type A injections
161
prophylactic treatment for migraines
how much can it reduce attack frequency in patients
propanolol
this can achieve 50% reduction in attack frequency in most patients
162
treatment during a migraine attack
triptans combined with either NSAIDs or paracetamol
anti-emetics for nausea
163
when would a triptan be contraindicated
IHD, Coronary spasm and uncontrolled HTN
164
non-pharma treatment for migraines
acupuncture
avoid identified triggers
ensure that it's not analgesic rebound headache
165
what are worsening headaches in pregnancy associated with
pre-eclampsia
166
what percentage of MS patients develop progressive disability
\>80%
167
what is the concordance in identical twins of MS
\>30%
168
what is the geographical distribution of MS
there is increasing incidence at latitude
adult migrants take their risk with them
children migrants acquire the risk of the region in which they settle
169
what is the mean age of onset of MS
30
170
what is the M:F
1:3
171
what is the presentation of MS
~20% of people present with unilateral optic neuritis (pain on moving the eye ± vision loss)
corticospinal tract and bladder invovlement are also common
symptoms may worsen the heat
can be sensory, motor, sexual/GU, GI, Eye, cerebellar and the presentation depends on site of the lesion
172
Tests for MS
* MRI - sensitive but not specific
* but it's the most useful since we can use it to exclude other causes of pathology
* CSF
* looking for oligoclonal bands of IgG that are not present in serum
* Evoked potentials
* you would see visual, auditory or somatosensory delays
173
diagnosis of MS
* this is made using the McDonald criteria
* if the presentation is dead on then it may be enough to diagnose clinically
* if there are fewer attacks and fewer clinical lesions then it's likely the diagnosis needs to be confirmed with MRI, CSF and Evoked Potentials
174
progression of MS
* most patients follow relapsing remitting course followed by secondary progressive disease
* 10% of patients have absence of relapses and this is called primary progressive MS
* small minority of patients experience no progressive disablement at all
175
what are poor prognostic signs in MS
older men
motor signs at onset
many early relapses
many MRI lesions
176
what are 4 principles of managing MS
lifestyle advice
monoclonal antibodies
treating relapses
treating symptom control
177
lifestyle advice for MS
regular exercise
stopping smoking
avoiding stress
178
Monoclonal antibodies for MS
alemtuzumab (anti T-Cell)
179
treating relapses in MS
methylprednisolone shortens acute relapses but must be used less than 2x a year due to SE
180
treating symptom control in MS
use 4 main symptoms
* spasticity
* baclofen or gabopentin
* tremor
* Botulinum toxin A injections every 12 weeks
* urinary urgency/frequency
* potential for self-catheterisation
* fatigue
* CBT
* exercise
181
what is the prevalence of MND
6/100,000 people
182
what is the M:F of motor neuron disease
3:1
183
what can distinguish MND from MS and polyneuropathies?
in MND there is no sphincter loss and no sensory loss
184
what distinguishes MND from myasthenia gravis
MND never affects eye movements
185
what are the four clinical patterns of MND and which is the most common
* Amyotrophic lateral sclerosis (ALS) 80%
* Progressive bulbar palsy 10-20%
* Progressive muscular atrophy
* Primary lateral sclerosis
186
what happens in progressive bulbar palsy
this only affects cranial nerves IX-XII and is a disease of these nuclei
LMN lesion of the tongue causes flaccid fasciculation of tongue (like a sack of worms)
speech can be quiet, horse or nasal
187
where are neurons lost in ALS
motor cortex and the anterior horn of the cord so this combines UMN and LMN symptoms
188
what is median age of onset in MND
60
189
presentation of MND
* stumbling spastic gait
* foot drop
* weak grip
* shoulder abduction is hard (hair washing)
* UMN signs
* spasticity
* brisk reflexes
* upward plantars
* LMN signs
* wasting
* fasciculation
* areflexia
190
what is the prognosis of MND
poor
half of patients survive less than 3 years post diagnosis
involve palliative care from diagnosis
191
Members of the MDT for MND
neurologist
palliative nurse
hospice
physio
speech therapist
dietician
social services
192
what is the only medicine shown to improve survival in MND and what does it do
riluzole
it is an inhibitor of glutamate
193
symptomatic treatment of MND - 3
* excess saliva
* positioning
* oral care
* suctioning
* botulinum toxin A may help
* dysphagia
* blend food
* gastrostomy
* communicative difficulty
* augmentative and alternative communication equipment
194
4 non-infective causes of meningitis
* paraneoplastic
* drug side effects
* autoimmune
* vasculitis
* SLE
195
10 clinical features of meningitis: divide into early and late
* Early
* headache
* fever
* leg pain
* cold hands and feet
* abnormal skin colour
* Late
* meningism
* kernig's sign
* seizures
* Petychial rash (non-blanching could be only 1 or 2 spots)
* shock
196
what is the mortality of bacterial meningitis when treated
5%
197
what percentage of patients have permanent effects from bacterial meningitis
20%
198
4 potential complications from bacterial meningitis
amputation
hearing loss
seizures
brain damage
199
what is the immediate treatment for suspected bacterial meningitis
IM benzylpenicillin
200
Management of suspected meningitis
Ix and Mx proceed in parallel
take blood cultures
begin empirical Abx early with ceftriaxone (can cros BBB)
if they are immunocompromised or \>60 give amoxicillin too
give dexamethasone - steroid - helps reduce incidence of neuro sequelae
201
when is a definitive diagnosis of meningitis given
* later when a lumbar puncture is done - wait until patient is stable
* Lumbar puncture
* microscopy
* gram stain
* culture
* viral PCR
202
in suspected meningitis if the gram stain is -ve diplococci what is the causative organism likely to be
neisseria meningitidis
203
in suspected meningitis if the gram stain is +ve diplococci what is the causative organism likely to be
strep pneumoniae
204
what would the CIs for LP be in Meningitis
any evidence of shock
petychial rash
raised ICP
abnormal clotting
205
Gram -ve rods that can cause meningitis
Haemophilus influenzae B
E.coli
206
Gram positive rods that can cause meningitis
Listeria
207
gram +ve cocci that can cause meningitis
group B strep
208
3 viruses that can cause meningitis
enterovirus
herpes simplex virus
varicella zoster virus
209
5 differential diagnoses of meningitis
migraine
flu or other viral illness
sinusitis
brain abscess
malaria
210
Public health for meningitis
if it's neisseria meningitis then close contacts need to be notified immediately
they have a 1/300 chance of developing meninigits
they should be given Abx prophylactically
reduces risk and prevents onward transmission
211
abx prophylaxis for meningitis high risk
ciprofloxacin or rifampicin
212
6 signs and symptoms of encephalitis
bizarre behaviour or confusion
falling GCS
fever
headache
focal neuro signs
seizures
213
causes of encephalitis
* it is usually viral
* mainly HSV
* varicella zoster
* west nile (ask about travel)
* Non-viral causes
* any bacterial meningitis
* autoimmune or paraneoplastic
214
What is the mortality of untreated viral encephalitis
70%
215
Ix of suspected encephalitis
* MRI head
* is there meningeal involvement? meningoencephalitis
* LP and viral PCR
216
encephalitis management
* start IV acyclovir within 30 minutes of patient arriving as empirical treatment for HSV
* supportive therapy in ICU if necessary
* symptomatic treatment like phenytoin for seizures
217
what is the name of the bacteria that causes tetanus
clostridium tetani
218
tetanus presentation - 9 things
* trismus - lockjaw
* risus sardonicus - grin of hypertonic facial muscles
* respiratory compromise
* generalised spasms
* pain
* hypertension
* tachycardia
* arrhythmia
* fever
219
how many people does rabies kill every year
35-50 thousand globally
220
what is the incubation period of rabies
min two weeks - max years
221
what is the prodromal presentation of rabies - 6 things
headache
malaise
odd behaviour
agitation
fever
paraesthesia at bite site
222
what are the two forms of rabies disease
furious rabies
paralytic rabies
223
what are some features of furious rabies
hyperactivity and terror (e.g. hydrophobicity)
224
what happens in paralytic rabies
flaccid paralysis of bitten limb --\> coma --\> death
225
treatment following bite
wash wound for more than 15 minutes with soap and water
post exposure prophylaxis with vaccine and rabies Ig
226
what is the incubation period of varicella zoster virus
14-21d
227
what does VZV do once it is in the body
infiltrates the respiratory mucosa
replicates in lymph nodes
disseminates to the skin forming virus containing vesicles which are chickn pox
remains in sensory nerve roots
reactivation (shingles) is dermatomal
228
chicken pox prodrome
lasts 1-2 days
fever
malaise
headache
abdo pain
229
what type of rash from chicken pox and how long does it last
pruritic
macular before becoming vesicular
lasts around 48hrs
230
when are you contageous with chicken pox
1-2 days pre rash and 5 days post rash
231
what is the presentation of shingles
macular rash becoming vesicular in dermatomal distribution
disseminated infection in the immunosuppressed
infectious until scabs appear
232
treatment for shingles
what if pregnant
ora acyclovir for uncomplicated chicken pox/shingles in adults
needs to be taken within 48hrs of onset of rash
IV acyclovir if pregnant
233
what is a coup and a centre coup
coup is a brain bruise at the site of impact
centre coup is the one at the opposite side of the impact
234
what is diffuse axonal injury following head injury and what are the consequences
this is a clinicopathological syndrome of widespread axonal damage (including to the brainstem)
it usually involves acceleration and deceleration of head
mild --\> recovery of consciousness ± long term deficit
severe --\> unconscious from impact and may remain so or conscious with severe disability
235
initial features of chronic traumatic encephalopathy
5 things
* irritability
* impulsivity
* aggression
* depression
* memory loss
*
236
later features of Chronic Traumatic Encephalopathy
dementia
gait and speech problems
parkinsonism
237
clinical findings in chronic traumatic encephalopathy
3 things
* Atrophy of many nuceli
* Enlarged ventricles with a fenestrated cavum septum
* Tau positive neurofibrillary astrocytic tangles
238
in general what do you treat seizures with in the acute setting
lorazepam ± phenytoin
239
what is giant cell arteritis
* aka temporal arteritis
* granulomatous arteritis of the aorta and larger vessels like the extracranial branches of the carotid arteries
240
which arteries does giant cell arteritis typically affect
temporal
opthalmic
facial
occipital
carotid
241
what is the M:F of giant cell arteritis and at what age does it affect
M:F is 1:2
consider it in those over 50
incidence increases with age
242
how does temporal arteritis present?
headache
jaw claudication
scalp tendernes
non-specific malaise
acute blindness in one eye
ESR may be raised
243
what is it when arteritis presents with acute blindness in one eye
this is irreversible blindness
it's called arteric ischaemic optic neuropathy (AION)
urgent medical emergency to prevent blindness in the other eye
244
diagnosis of temporal arteritis
temporal artey biopsy is the goldstandard
you will see necrotising arteritis
245
what is AION
arteric ischaemic optic neuropathy
this is sudden painless monocular visual loss
the optic disk becomes swollen and pale with haemorrhages at the margin
this is diagnostic of GCA since you don't see these changes elsewhere
246
treatment for temporal arteritis
prompt corticosteroids like prednisolone
normally a dramatic response in 48hrs
guide treatment using CRP and ESR
247
what are the autoantibodies against in myasthenia gravis and which immune cells are implicated
the antibodies are against nicotinic acetylcholine receptors on the post synaptic side of the neuromuscular junction
both T and B cells are involved
248
muscle groups affected by myasthenia gravis in order of most commonly affected to least
extraocular
bulbar (swallowing/chewing)
face
neck
limb girdle
Evil Boys Find No Love
249
4 signs of myasthenia gravis
ptosis
diplopia
myasthenic snarl on smiling
voice fades on counting to 50 (dysphonia)
250
8 things that can make myasthenia gravis symptoms worse
pregnancy
infection
over treatment
change of climate
emotion
exercise
beta blockers
opiates
251
associations between myasthenia gravis and other diseases
RA and SLE
women under 50 it's associated with thymic hyperplasia
men over 50 it's associated with thymic atrophy and thymic tumour
252
Ix of myasthenia gravis
* raised anti-AChR antibodies present in 90%
* If anti AChR abs are -ve then look for anti-MuSK (muscle specific tyrosine kinase)
* neat test for clinic: ptosis improves by \>2mm after ice application to eyelid for more than 2mins (NOT DIAGNOSTIC)
253
treatment for myasthenia gravis
* anticholinestarase e.g. pyridostigmine
* has cholinergic side effects
* immunosuppression
* treat relapses with prednisolone
254
what is myasthenic crisis and how do you treat it
* it is life threatening weakness of resp muscles during a relapse
* difficult to differentiate from cholinergic crisis (which you can get from over treatment)
* monitor their FVC
* ventilate if necessary
* treat with plasmapheresis (removes AChR antibodies in blood)
* identify and treat the trigger of the relapse
255
what is the incidence of GBS
1-2/100,000 per year
256
how does GBS present
a few weeks after an infeciton a symmetrial ascending muscle weakness starts
257
5 triggers for GBS
campylobacter jejuni
CMV
Mycoplasma
HIV
EBV
258
what about GBS is unusual for neuropathies
proximal muscles may be more affected than distal
259
treatment for GBS
ventilate if necessary
IV Ig
plasma exchange
steroids have no role
260
prognosis for GBS
Good
~85% make a full or nearly full recovery
10% are unable to walk alone at 1 yr
mortality is 10%
261
262
what mode of inheritance is huntington's
AD inheritance
263
what are the symptoms of huntington's chorea
* early
* irritability
* depression
* incoordination
* progresses to
* chorea
* death
* seizures
* death within 15 years of diagnosis
264
what is the genetic basis of Huntington's
expansion of CAG repeats on chromosome 4
number of repeats correlates with severity of disease
\<26 repeats is normal
\>40 is full penetrance
265
triggers for trigeminal neuralgia
washing affected area
shaving
eating
talking
266
symptoms of trigeminal neuralgia
paroxysmal intense stabbing pain that lasts seconds in the trigeminal nerve distribution
it is unilateral
typically affects mandibular or maxillary divisions
267
who is most affected by trigeminal neuralgia
generally it's men \>50
268
causes of trigeminal neuralgia
* compression of the trigeminal root by:
* aneurysmal intercrania vessels
* tumour
* MS
* skull base malformations
269
Ix
MRI needed to exclude dangerous secondary causes
270
Treatment for trigeminal neuralgia
* anti-convilsant medication
* carbamazepine
* phenytoin
* Lamotrigine
271
what percentage of people over 80 have dementia
20%
272
initial Ix of dementia
AMTS
MSE to identify anxiety, depression or hallucinations
273
name 4 types of dementia
alzheimers
vascular dementia
lewy body dementia
fronto-temporal dementia
274
what percentage of dementia is vascular dementia
25%
275
what is vascular dementia
it is the cumulative effect of many small strokes
it has a sudden onset and a stepwise deterioration
look for signs of arteriopathy (HTN, past strokes, focal CNS signs)
276
what is lewy body dementia
there's fluctuating congnitive impairment
they have detailed visual hallucinations
later they get parkinsonism
histology is characterised by lewy bodies in the brainstem and neocortex
277
fronto-temporal dementia
frontal and temporal atrophy with loss of \>70% of spindle neurons
executive impairment
behavioural/personality change
disinhibition
hyperorality
emotional unconcern
episodic memory and spatial orientation are preserved until later stages
278
7 clinical features of alzheimers
* impairment of
* visuo-spatial skill
* memory verbal abilities
* executive function
* anosogosia
* lack of insight
* irritability
* mood disturbance
* psychosis
* agnosia
279
most vulnerable parts of the brain in alzheimers
hippocampus
amygdala
temporal neocortex
subcortical nuclei
280
three risk factors for alzheimers
* 1st degree relative with AD
* down's syndrome
* inevitable
* homozygosity for ApoE allele E4 on chr 19
* increases risk x12
281
what is mean survival from diagnosis of unequivocal alzheimer's symptoms
7yrs
282
what is the management of Alzheimers
* acetylcholinesterase inhibitors like donepezil
* these can cause heart block and peptic ulcer disease
* discontinue if no improvement
* do not use in mild disease
* BP control
283
what occurs on a cellular and molecular level in alzheimers
* accumulation of beta-amyloid peptide
* results in
* neuronal damage
* neurofibrillary tangles
* more amyloid plaques
* loss of Ach
