Neurology Brief Flashcards
1
Q
what is the new definition of a TIA
A
ischaemia without infarction
2
Q
what is as crescendo TIA
A
two or more TIAs within a week
carries high risk of developing into a stroke
3
Q
what is alteplase
A
tissue plasminogen activator
4
Q
management of stroke
A
- exclude hypoglycaemia
- immediate CT head to exclude haemorrhage
- aspirin 300mg stat and continued for 2 weeks
- alteplase if within 4.5 hrs of onset of symptoms
- monitoring for post thrombolysis complications
- repeated CT head
- monitoring for post thrombolysis complications
- admit to specialist stroke centre
- diffusion weighted MRI is gold standard imaging
- carotid ultrasound if carotid stenosis is suspected
5
Q
management of TIA
A
300mg aspirin daily
referred and seen within 24hrs by stroke specialist
start secondary prevention for cardiovascular disease
6
Q
management of carotid stenosis
A
endarterectomy to remove plaques
carotid stenting to widen lumen
7
Q
what is the secondary prevention of stroke
A
clopidogrel 75mg once daily
carotid endarterectomy or stenting in patients with carotid disease
treat modifiable risk factors
8
Q
what percentage of strokes are caused by intracranial bleeds
A
10-20%
9
Q
draw out the glasgow coma scale
A
10
Q
what causes subdural haemorrhage
A
rupture of bridging veins in the outermost meningeal layers between dura mater and arachnoid mater
11
Q
CT scan appearance of subdural haemorrhage
A
crescent shape and not limited by cranial sutures
12
Q
which population of patients is most likely to have a subdural haemorrhage
A
the elderly and alcoholics
they have atrophy and vessels are more likely to rupture
13
Q
which artery in which region is most likely to cause a extradural haemorrhage
A
middle meningeal artery in the temporo-parietal region
this can be associated with a fracture of the parietal bone
14
Q
CT appearance of an extradural haemorrhage
A
egg shaped and limited by cranial sutures
15
Q
Typical history is a patient with a traumatic head injury and ongoing headache.
They have a period of improved neurological symptoms and consciousness followed by a rapid decline over hours.
What sort of bleed is this?
A
extradural haemorrhage
16
Q
other features of a subarachnoid haemorrhage other than thunderclap headache
A
neck stiffness
photophobia
vision changes
neurological symptoms
17
Q
risk factors for subarachnoid haemorrhage
A
- hypertension
- smoking
- excessive alcohol consumption
- cocaine use
- family history
- black ethnicity
- female sex
- age 45-70
- sickle cell anaemia
- neurofibromatosis
- autosomal dominant polycystic kidney disease
- connective tissue disorders
18
Q
investigations for subarachnoid haemorrhage
A
CT head will show hyperattenuation in the subarachnoid space
LP will show raised red cells and xanthochromia
CT or MRI angiography to locate source of bleeding
19
Q
management of subarachnoid haemorrhage
A
- surgery
- coiling (endovascular)
- clipping (cranial surgery)
- Nimodipine
- CCB
- to prevent vasospasm and ischaemia following SAH
- LP or Shunt for hydrocephalus
- antiepileptic meds for seizures
20
Q
multiple sclerosis only affects the neurons of the _______ nervous system where the myelin is formed by ________
A
multiple sclerosis only affects the neurons of the central nervous system where the myelin is formed by oligodendrocytes
21
Q
internuclear opthalmoplegia presents how and how is it caused
A
- one eye lags behind the other
- the affected eye adducts minimally
- they have diplopia
*
22
Q
what is lhermitte’s sign
A
electric shock sensation when neck is stretched in patients with MS
23
Q
what are the two types of ataxia and what are the differences
A
- sensory ataxia - problem with proprioceptive sense
- results in positive rombergs
- can cause pseudoathetosis
- cerebellar ataxia
- result of problems with the cerebellum coordinating movement
- suggests cerebellar lesions
24
Q
what is a clinically isolated syndrome in MS
A
first episode of demyelination and neurological signs and symptoms
MS cannot be diagnosed at this point as the lesions are not ‘disseminated in time and space’
pts with clinically isolated syndrome may never have another episode or develop MS
if lesions seen on MRI then they are more likely to progress to MS
25
what are the four different ways you can describe relapsing remitting MS
* Active: new symptoms are developing or new lesions are appearing on MRI
* Not active: no new symptoms or MRI lesions are developing
* Worsening: there is an overall worsening of disability over time
* Not worsening: there is no worsening of disability over time
26
what are the 4 different ways you can describe secondary progressive MS
* Active: new symptoms are developing or new lesions are appearing on MRI
* Not active: no new symptoms or MRI lesions are developing
* Progressing: there is an overall worsening of disease over time (regardless of relapses)
* Not progressing: there is no worsening of disease over time
27
how long do symptoms need to be progressive over before you can diagnose primeary progressive MS
1 year
28
what will lumbar puncture detect in MS
oligoclonal bands
29
features of optic neuritis
central scotoma
pain on eye movement
impaired colour vision
RAPD
30
non MS causes of optic neuritis
* Sarcoidosis
* Systemic lupus erythematosus
* Diabetes
* Syphilis
* Measles
* Mumps
* Lyme disease
however MS is the main cause
31
management of optic neuritis
urgent assessment by opthalmologist if acute loss of vision
treat with steroids
recovery takes 2-6 weeks
32
MS prognosis following first episode of optic neuritis
50% of patients with a single episode of optic neuritis will go on to develop MS over the next 15 years
changes on MRI can predict which patients do
33
management of MS
* disease modifying drugs
* mabs too complex for you to know about
* treating relapses
* methylprednisolone
* 500mg orally daily for 5 days
* symptomatic treatment
* neuropathic pain
* gabapentin
* amitryptilline
* depression
* ssris
* urge incontinence
* anticholinergics such as tolterodine and oxybutynin
* spasticity
* baclofen
* gabapentin
* physio
34
what are the 4 types of motor neurone disease to know about
* amyotrophic lateral sclerosis
* progressive bulbar palsy
* progressive muscular atrophy
* primary lateral sclerosis
35
what percentage of motor neurone disease cases are inherited
5-10%
36
signs of lower motor neurone disease
muscle wasting
reduced tone
fasciculations
reduced reflexes
37
signs of upper motor neurone disease
increased tone or spasticity
brisk reflexes
upgoing plantar responses
38
what is the only drug licensed in the UK for ALS
rilzole can slow progression and extend survival by a few months in ALS
39
distinguish between parkinson's tremor and benign essential tremor
40
describe multiple system atrophy
* degeneration of basal ganglia leads to
* parkinsons presentation
* degeneration of other regions of the brain leads to
* autonomic dysfunction
* postural hypotension
* constipation
* abnormal sweating
* sexual dysfunction
* degeneration of cerebellum leads to
* ataxia
41
what must be given with levodopa in parkinson's and what are the combinations called
* must be given with peripheral decarboxylase inhibitors such as carbidopa and benserazide
* so
* co-benyldopa is levodopa and benserazide
* co-careldopa is levodopa and carbidopa
42
what are the different medical managements options for parkinson's
* levodopa
* most effective
* but becomes less effective over time
* so reserve for late disease
* COMT inhibitors
* taken with levodopa to slow breakdown of levodopa in brain
* dopamine agonists
* less effective than levodopa
* delay need for levodopa
* then used in combo with levodopa
* prolonged use causes pulmomary fibrosis
* Monoamine oxidase-B inhibitors
* MOB breaks down dopamine
* inhibiting it increases circulating dopamine
* delay need for levodopa
* then used in combo with levodopa
43
what are COMT inhibitors used to treat, how do they work and give an example
used to treat parkinson's
taken with levodopa to slow breakdown of levodopa in brain
example is entacapone
44
how are dopamine agonists used to treat Parkinsons and what are some examples
* less effective than levodopa
* delay need for levodopa
* then used in combo with levodopa
* prolonged use causes pulmomary fibrosis
* e.g.
* bromocryptine
* pergolide
* carbergoline
45
how do MOB inhibitors work and what are some examples
* MOB breaks down dopamine
* inhibiting it increases circulating dopamine
* delay need for levodopa
* then used in combo with levodopa
* e.g.
* selegiline
* rasagiline
46
is benign essential tremor present or absent during sleep
absent
47
what are the key differential diagnoses of a tremor
name 6
parkinson's disease
MS
huntington's chorea
hyperthyroidism
fever
medications e.g. antipsychotics
48
managment of benign essential tremor
* there is no need to treat unless causing functional or psychological problems
* treatment options include
* propanolol
* primidone (barbiturate anti-epileptic medication)
49
what is the aim of epilepsy treatment
to be seizure free on the minimum anti-epileptic medications
ideally a monotherapy
50
describe generalised tonic clonic seizures
* loss of consciousness
* tonic episode
* followed by clonic episode
* there may be
* incontinence
* tongue biting
* groaning
* irregular breathing
* prolonged post-ictal period
51
what is the management of tonic clonic seizures
first line: sodium valproate
second line: lamotrigine or carbamazepine
52
what are the 5 important types of generalized seizures
1. absence seizures
2. tonic clonic seizures
3. myoclonic seizures
4. atonic seizures
5. infantile spasms
53
what are the three types of focal seizures
* without impairment of consciousness
* with impairment of consciousness
* evolving to a bilateral, convulsive seizure
54
what features would localise a seizure to the temporal lobe
automatisms
dysphasia
deja vu
jamais vu
emotional disturbance
hallucinations of smell, taste or sound
delusional behaviour
bizarre associations - "Canned music at Tesco always makes me cry and then pass out"
55
what features would localise a focal seizure to the frontal lobe
posturing or peddling of the legs
jacksonian march
subtle behaviour disturbances
dysphasia
speech arrest
post-ictal todd's palsy
56
what features would localise a focal seizure to the parietal lobe
sensory disturbance such as tingling numbness and pain
motor symptoms due to spread to pre-central gyrus
57
what features would localise a focal seizure to the occipital lobe
visual phenomena such as spots, lines and flashes
58
is there loss of consciousness in a tonic clonic seizure
yes
59
is ther loss of consciousness in atonic seizures
no
60
what is the management of focal seizures
first line: carbamazepine or lamotrigine
second line: levetiracetam or sodium valproate
61
what is the management of generalized tonic clonic seizures
first line: sodium valproate or lamotrigine
second line: carbamazepine, levetiracetam or topiramate
62
what is the management of absence seizures
first line: sodium valproate
second line: lamotrigine
63
what is the management of myoclonic seizures
first line: sodium valproate
second line: levetiracetam or topirimate
AVOID carbamazepine as it can worsen seizures
64
what is the managment of tonic or atonic seizures
sodium valproate or lamotrigine
65
what are infantile spasms? what is the prognosis? what is the management?
aka west syndrome
rare
starts at ~6 months of age
clusters of full body spasms
poor prognosis (1/3 die by 25)
difficult to treat
give prednisolone or vigabatrin
66
side effects of carbamazepine
agranulocytosis
aplastic anaemia
enzyme inducer
67
side effects of phenytoin
folate and vitamin D deficiency
megaloblastic anaemia (due to folate deficiency)
osteomalacia (due to vitamin D deficiency)
68
side effects of ethosuxamide
night terrors
rashes
69
side effects of lamotrigine
stevens johnson syndrome
DRESS syndrome
leukopenia
70
what is the definition of status epilepticus
seizures lasting more than 5 minutes or more than three seizures in one hour
71
management of status epilepticus
1. secure airway
2. oxygen and suction as required
3. IV access
* lorazepam 4mg bolus
* repeat if no response after 10-20 minutes
* U&E, LFT, FBC, glucose, Ca2+
4. Thiamine IV if alcoholism or malnourishment suspected
5. Glucose IV unless glucose known to be normal
6. Correct hypotension wih IV normal saline
7. If seizures continue start phenytoin IV infusion
8. General anaesthesia if working on them for 60-90 minutes
72
what are the 4 drugs used in neuropathic pain and what are their drug classes
1. amitriptyline is a tricyclic antidepressant
2. duloxetine is an SNRI antidepressant
3. gabapentin is an anticonvulsant
4. pregabalin is an anticonvulsant
try one at a time.
stop the one you're using before you trial the next one.
73
what are the five branches of the facial nerve
temporal
zygomatic
buccal
marginal mandibular
cervical
74
what are the functions of the facial nerve
* motor
* to the muscles of facial expression
* sensory
* to anterior 2/3 of the tongue
* parasympathetic
* to the submandibular and sublingual salivary glands
* lacrimal gland - tear production
75
how do you distinguish an upper motor neurone lesion and alower motor neurone lesion facial nerve palsy
* upper motor neurone lesion the forehead is spared - stroke
* lower motor neurone lesion the forehead is not spared - bell's palsy
76
how long is recovery from bells palsy
majority make full recovery within several weeks but may take up to 12 months
a third are left with residual weakness
77
what is the management of bell's palsy?
if patients present within 72 hours of developing symptoms give prednisolone for 10 days
they may also need lubricating eye drops as they are at risk of exposure keratopathy
78
what is ramsay-hunt sundrome
* caused by VZV
* presents as
* unilateral lower motor neurone facial nerve palsy
* painful, tender, vesicular rash in the ear canal and pinna
* rash may extend to anterior 2/3 of the tongue
79
what is the management of ramsay hunt syndrome
prednisolone
aciclovir
they also require lubricating eye drops as they are at risk of exposure keratitis
80
what is papilloedema
swelling of the optic disc secondary to raised ICP
optic nerve sheath is continuous with the arachnoid mater so CSF can flow in and cause optic disc to swell
81
fundoscopic changes in papilloedema
blurring of optic disc margin
loss of venous pulsation
engorged retinal veins
haemorrhages around optic disc
82
what are the most common cancers that metastasize to the brain
lung
breast
renal cell carcinoma
melanoma
83
what are the three types of glioma from most to least malignant
astrocytoma (glioblastoma multiforme is the most common astrocytoma)
oligodendroglioma
ependymoma
84
how are gliomas graded
grade 1-4
with grade 1 being most benign (possibly curable with surgery)
and grade 4 being most malignant (glioblastomas)
85
what are meningiomas
tumours of meninges
mostly benign
however neurological symptoms from mass effect
86
what are acoustic neuromas
* tumours of schwann cells surrounding auditory nerve
* occur at cerebellopontine angle
* slow growing but eventually produce symptoms and become dangerous
* usually unilateral
* if bilateral then neurofibromatosis type 2
* symptoms
* hearing loss
* tinitus
* balance problems
87
what is the inheritence pattern of huntington's chorea
autosomal dominant
88
what chromosome is the huntington's mutation on
chromosome 4
89
what is the management of huntington's
* no medication can slow or reverse progression
* treatment is supportive
* medications to suppress disordered movement
* antipsychotics (e.g. olanzapine)
* benzodiazepines (e.g. diazepam)
* dopamine depleting agents (e.g. tetrabenazine)
* depression can be treated with SSRIs
90
what age are patients most likely to present with myasthenia gravis
Myasthenia gravis affects men and women at different ages. Typical patients are either a woman under the age of 40 or a man over the age of 60.
91
what important thing is myasthenia gravis linked with
* thymus tumour
* 10-20% of MG patients have a thymoma
* 20-40% of patients with a thymoma develop myasthenia gravis
92
what is the pathophys of myasthenia gravis
* 85% of pts with MG have acetylcholine receptor antibodies
* these block the receptor and stop acetylcholine binding to postsynaptic NMJ receptors
* these antibodies also activate the complement system
* leading to damage of the postsynaptic membrane
* the other 15% of cases are caused by
* muscle specific kinase (MuSK) antibodies
* LRP4 antibodies
* LRP4 and MuSK are important for the production of the acetylcholine receptors
93
85% of pts with myasthenia gravis have antibodies against
acetyl choline receptors
94
15% of patients with myasthenia gravis have antibodies against
MuSK
LRP4
these proteins are important for creation and organisation of acetylcholine receptors
95
do myasthenia gravis symptoms change during the day
typically symptoms are minimal in the morning and worst at the end of the day
96
important examination points for myasthenia gravis
* repeated blinking will exacerbate ptosis
* prolonged upward gazing will exacerbate diplopia on further eye movement testing
* repeated abduction of one arm will lead to unilateral weakness when comparing both sides
* check for thymectomy scar
* test forced vital capacity
97
diagnosis of myasthenia gravis
* test directly for antibodies
* ACh-R antibodies (85%)
* MuSK antibodies (10%)
* LRP4 antibodies (\<5%)
* CT or MRI of the thymus
* Endrophonium test
* this is a cholinesterase inhibitor
* if it relieves symptoms then it establishes diagnosis
98
treatment for myasthenia gravis
* acetylcholinesterase inhibitors
* neostigmine
* pyridostigmine
* immunosuppression
* prednisolone
* azathioprine
* thymectomy
* works even in patients without a thymoma
* rituximab
99
myasthenic crisis is often triggered by
respiratory tract infection
this leads to progressive weakness of the muscles of respiration
patients may require NIV or BiPAP
may require intubation and ventilation
medical treatment is IV immunoglobulins and plasma exchange
100
what is lambert eaton syndrome
it's like myasthenia gravis but it's because of small cell lung cancer and autoantibodies against voltage-gated calcium channels in the **presynaptic terminals** of the neuromuscular junction
REMEMBER IN MG IT'S POST-SYNAPTIC RECEPTORS THAT ARE TARGETTED
101
Presentation of lambert eaton syndrome
* more gradual onset than myasthenia gravis
* affects proximal muscles most
* most notably proximal leg muscles
* also eye muscles causing diplopia and ptosis
* pts may also get dry mouth, blurred vision, impotence and dizziness due to autonomic dysfunction
* reflexes improve after a short period of strong muscle contraction
* post-tetanic potentiation
102
treatment for lambert eaton syndrome
* treat small cell lung cancer
* amifampridine releases more acetylcholine
* other options
* IV Ig
* immunosuppressants (prednisolone or azathioprine)
* plasmapheresis
103
how do you get charcot marie tooth disease
it is inherited autosomal dominant the majority of the time
symptoms usually appear before 10yrs old but can be delayed until 40 or later
104
causes of peripheral neuropathy
* ABCDE
* Alcohol
* B12 deficiency
* Cancer, Chronic kidney disease, Charcot-marie tooth
* Diabetes, Drugs
* Every vasculitis
105
name 3 drugs that cause peripheral neuropathy
isoniazid
amiodarone
cisplatin
106
classical features of charcot marie tooth
* high foot arches (pes cavus)
* distal muscle wasting (inverted champagne bottle legs)
* weakness in the lower legs (particularly ankle dorsiflexion)
* weakness in the hands
* reduced reflexes
* reduced muscle tone
* peripheral sensory loss
107
what is charcot marie tooth
inherited disease that affects the peripheral sensory and motor nerves
there are many different types
normally presents before age 10 but can be later
108
what is the management of charcot marie tooth
* there is no treatment for underlying disease
* management is supportive with input from
* neurologists
* physio
* OT
* podiatrists
* orthopaedic surgeons
109
what is the presentation of guillain barre syndrome
* symmetrical ascending weakness
* reduced reflexes
* peripheral loss of sensation or neuropathic pain
110
clinical course of guillain barre syndrome
* symptoms start within 4 weeks of preceding infection
* symptoms progress upwards
* symptoms peak at 2-4 weeks
* there is a recovery peeriod that can take months to years
111
what criteria are used to diagnose guillain barre syndrome
* the brighton criteria
112
what is the treatment for guillain barre syndrome?
IV Ig
plasma exchange
supportive care
VTE prophylaxis
if respiratory failure then intubation and ventilation
113
prognosis in guillain barre syndrome
80% fully recover
15% are left with neurological disability
5% will die
114
which type of neurofibromatosis is more common
NF1
115
what chromosome is the NF1 gene found on
chromosome 17
116
what is the NF1 gene
chomosome 17
codes for 'neurofibromin' a tumour suppressor protein
117
what is inheritance pattern of NF1
Autosomal dominant
118
what is the criteria for diagnosing NF1
* CRABBING: must have 2 of the 7
* Cafe-au-lait spots (6 or more)
* Relative with NF1
* Axillary or inguinal freckles
* BB- Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
* Iris hamartomas (lisch nodules) 2 or more
* Neurofibromas (2 or more)
* Glioma of the optic nerve
119
complications of NF1
migraines
epilepsy
renal artery stenosis causing hypertension
scoliosis
vision loss (optic nerve gliomas)
malignant peripheral nerve sheath tumours
gastrointestinal stromal tumour
brain tumour
increased risk of cancer
120
on which chromosome is the NF2 gene found
chromosome 22
121
what is the protein that the NF2 gene codes for called and what does it do?
merlin
it is a tumour suppressor protein that's important in schwann cells
122
what is the inheritance of NF2
autosomal dominant
123
what happens in NF2
* acoustic neuromas
* hearing loss
* tinnitus
* balance problems
* schwannomas in the brain and spinal cord
* symptoms based on location
NB bilateral acoustic neuromas almost always means NF2
124
what is tuberous sclerosis
* genetic condition characterised by the development of hamartomas
* these are benign growths of the tissue they originate from
* they cause problems based on their location
* classically arise from
* skin
* brain
* lungs
* heart
* kidneys
* eyes
125
what are the mutations in tuberous sclerosis
* tuberous sclerosis is caused by mutations in one of the following:
* TSC1 on chromosome 9: codes for hamartin
* TSC2 on chromosome 16: codes for tuberin
hamartin and tuberin interact with each other to control the size and growth of cells
126
skin signs in tuberous sclerosis
ash leaf spots: depigmented skin in ash leaf shape
shagreen patches: thickened, dimpled, pigmented patches
angiofibromas: small papules over nose and cheeks
subungual fibromata: painless fibromas in nail bed that displace the nail
cafe-au-lait spots: light brown pigmented lesions on skin
poliosis: isolated patch of white hair on head, eyebrows, eyelashes or beard
127
neurological features of tuberous sclerosis
epilepsy
learning disability and developmental delay
128
what is the clasical presentation of tuberous sclerosis
a child presenting with epilepsy found to have skin features of tuberous sclerosis. It can also present in adulthood
129
what is the management of tuberous sclerosis
upportive with monitoring and treating complications such as epilepsy. There is no treatment for the underlying gene defect
130
how long does sinusitus take to resolve
normally resolves within 2-3 weeks
131
what are the three branches of the trigeminal nerve
Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)
132
how long do migraines last
4-72 hours
133
what are the 5 stages of migraine
* Premonitory or prodromal stage (can begin 3 days before the headache)
* Aura (lasting up to 60 minutes)
* Headache stage (lasts 4-72 hours)
* Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping)
* Postdromal or recovery phase
134
what are triptans
5HT receptor agonists (seretonin receptor agonists)
135
acute management of migraines
paraetamol
triptans (50mg as the migraine starts)
NSAIDs
antiemetics (e.g metoclopramide) if vomiting occurs
136
migraine prophylaxis
avoid known triggers
propanolol
topirimate (teratogenic and must not get pregnant)
amitriptyline
137
how are cluster head aches spread out over time
come in clusters of attacks and then disappear for a while
For example, a patient may suffer 3 – 4 attacks a day for weeks or months followed by a pain-free period lasting 1-2 years.
Attacks last between 15 minutes and 3 hours.
138
symptoms of cluster headache
* typically unilateral
* extremely severe pain
* red swollen watering eye
* pupil constriction
* eyelid drooping
* nasal discharge
* facial sweating
139
acute management of cluster headaches
* Triptans (6mg injected subcut)
* 100% high flow oxygen for 15-20 minutes
140
cluster headache prophylaxis
* Verapamil
* Lithium
* Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)
