Neuro Flashcards
To learn the very basics
basic pathology of diabetic neuropathy
nerve damage caused by diabetes, because high triglycerides and high blood glucose damages the nerves.
basic pathology of stroke (2)
ischaemic = infarction/ischaemia due to disrupted blood supply
haemorrhagic = intracranial bleeding
Causes of ischaemic stroke i.e. due to disrupted blood supply- 4
Thrombosis, atherosclerosis, shock, vasculitis
what’s vasculitis
group of conditions that cause inflammation of the blood vessels such as autoimmune vasculitis
first-line treatment for vasculitis
no cure… Anti-inflammatory medications, notably glucocorticoids such as prednisone or methylprednisolone, are the most common first-line treatments.
does TIA have infarction?
no
TIA is temporary neurological dysfunction lasting what length of time
less than 24 hours
Presentation of stroke- fast
FAST
facial weakness
(arm) limb weakness
speech difficulties
(TIME)
other symptoms
visual field defects
sensory loss
ataxia/vertigo
the combined contraceptive pill carries a tiny increased risk of what
stroke
risk is higher in patients with migraines with aura
what tool/score gives a score for patients with stroke like symptoms
rosier
TIA treatment/management (3)
aspirin 300mg daily immediately
referral to specialist treatment within 24 hrs
MRI scan imaging
Immediate management for stroke (excludetwo things, then give this drug)
Obvs admittance as well
exclude hypoglycemia
immediate CT scan to exclude haemorrhage
aspirin 300 mg daily
when is thrombolysis with alteplase considered for management of stroke
when haemorrhage is excluded, within 4.5 hours of symptom onset
thrombolysis is used in ST elevation myocardial infarction, true or false
true
In which type of stroke is blood pressure usually treated
Blood pressure is treated aggressively in haemorrhagic stroke
But in ischaemic stroke, lowering blood pressure can worsen the ischaemia
We believe the stroke was related to the patient’s atrial fibrillation. What treatment do we give?
anticoagulation such as apixiban
after excluding haemorrhage, and finishing two weeks of aspirin
Following a stroke: what imaging do we do to assess for underlying causes? (2) -most common being atrial fibrillation, and carotid artery stenosis
carotid imaging like carotid ultrasound or CT/MRI angiogram
ECG
secondary prevention of stroke- 2 meds and 2 general health things
clopidogrel
atorvastatin (statin to lower cholesterol)
blood pressure/diabetes control
addressing other risk factors like obesity, smoking, exercise
what’s clopidogrel
an antiplatelet
presentation of parkinsons -triad
resting tremor
bradykinesia
rigidity-resisting passive movement
what disease does this gait describe- stooped, fascial masking, forward tilt, reduced arm swing, shuffling gait
parkinsons
pathophysiology of parkinson’s
progressive loss of dopaminergic neurons in pathway originating in the substantia nigra of the basal ganglia.
importance of dopamine in regulation of movement
it’s a key neurotransmitter.
no dopamine in parkinson’s leads specifically to what
Therefore no dopamine, = increase in antagonistic indirect pathway = bradykinesia and rigidity
formation of lewy bodies/ protein clumps in parkinsons- true or false
true
Is the tremour in parkinsons the same on both sides or unilaterally worse
asymmetrical and importantly, worse at rest
pill rolling tremor seen in what disease
parkinsons
initial symptoms of Parkinson’s, seen before the triad of resting tremor, rigidity, and bradykinesia? (5)
sleep disturbance like sleepiness, or shouting/kicking etc during REM
low mood
autonomic symptoms like: constipation, light headed, excessive sweating or salivation
Motor troubles with handwriting
cognitive impairment
one bedside investigation of Parkinson’s, as well as cognitive assessment, is checking the difference between lying and standing blood pressure
patient’s with PD have postural hypotension
Diagnosis of PD is based on what
By a specialist, based on history and neuro examination findings
management of PD (3)
levadopa = first line
and this is taken with:
COMT inhibitors to prolong levadopa action, and decreases dopamine action
MOA-B inhibitors inhibit breakdown of dopamine
response decreases with time
Anti-parkinsonian medications are ‘critical medications’ and are time-sensitive. Patients who miss doses or receive late doses could experience
freezing (akinesia).
Deep brain stimulation for PD is reserved for who
It is reserved for those with severe symptoms refractory to medical management yet still fit with few co-morbidities.
Huntington’s pathology
autosomal, genetic error on chromosome 4, causing loss of striatum.
when do symptoms of huntington’s begin
age 30-50
How does harry Huntington present?
insidious, progressive worsening of symptoms: BASICALLY personality and cognitive problems, and chorea.
Followed by movement disorders like: weird posture, rigidity, eye movement difficulties, swallowing and speech difficulties
Death in Huntington’s is often due to what:
aspiration pneumonia, and suicide.
NB often falls etc due to frailty
Management of Huntington’s (3)
No cure/treatment. But can include:
tetrabenazine for chorea
anti-depressants e.g. SSRI’s
Speech and language therapy and physiotherapy
Life expectancy of someone with Huntington’s after diagnosis
10-20 years after onset of symptoms
Pathology of epilepsy
recurrent epileptic seizures of abnormal electrical activity from a specific focus that spreads throughout the brain
how do epileptic seizures manifest
usually they manifest with motor and sensory symptoms, and often associated with reduced consciousness levels
Seizures can either be motor or non-motor. But they are either classified as:
focal, generalised, or unknown origin
Are you conscious during a focal/partial seizure?
maybe, maybe not
generalised/tonic clonic seizures often affect what parts of the brain
both cerebral hemispheres
which type of seizure can have an aura
focal - like a premonition that something is about to happen
an absence seizure is a type of generalised seizure. Is it more often seen in children or adults?
children
what is seen in a tonic clonic seizure?
stiffening followed by intermittent jerking movements
could tinnitus and vision loss ever be aura for seizure? or not
yes
also unusual emotions, strange smells/sensations etc, abnormal behaviours, deja vu.
what investigations for epilepsy
EEG (electrodes placed on patient’s head)
MRI brain to detect tumour
why would you look at Capillary blood glucose in epilepsy
To identify hypoglycaemia, an important reversible cause of seizures
what 4 investigations can be considered in epilepsy to exclude important pathology
ECG
serum electrolytes
blood glucose (for hypoglycaemia)
blood and urine culture and lumbar puncture if sepsis, encephalitis or meningitis suspected
First line therapies for epilepsies
Lamotrigine or Levetiracetam- if men/can’t have children AND it’s generalised, then sodium valproate.
what does sodium valproate do
calms the brain by increasing GABA.
what’s status epilepticus
medical emergency when:
seizure lasts more than 5 mins, or multiple seizures when consciousness isn’t regained.
management of status epilepticus
ABCDE incl giving oxygen and inserting cannula, securing airway, and checking blood glucose
A benzodiazepine first-line, repeated after 5-10 minutes if the seizure continues
Second-line options (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate
Options for benzodiazepines are:
Buccal midazolam (10mg)
Rectal diazepam (10mg)
Intravenous lorazepam (4mg)
Myasthenia Gravis is an autoimmune condition that consists of fatigable fatigue. What does it affect?
The neuromuscular junction, because of acetylcholine receptor antibodies
Myasthenia gravis affects men and women at different ages:
typically affecting women under 40 and men over 60.
Myasthenia gravis is strongly linked with what tumour
thymoma, a thymus gland tumour
what causes cell damage at the post synaptic membrane in myasthenia gravis, further worsening symptoms?
acetylcholine receptor antibodies
muscle weakness in the face causes what symptoms in myasthenia gravis?
difficulty swallowing, fatigue in jaw when chewing, slurred speech, double vision, droopy eyelids/ptosis.
if we want to elicit symptoms in clinic of myasthenia gravis, what would we ask to do.
repeated blinking, and prolonged upward gazing
and check for thymoma scar
investigations: what antibody tests for myasthenia gravis?
AChR antibodies
also CT and MRI to look for thymoma
what happens in the endrophonium chloride test
blocks the cholinesterase enzymes that break down acetylcholine. If little rise = positive test.
What treatment for myasthenia gravis? (3)
pyridostigmine = cholinesterase inhibitor
immunosuppression like prednisolone
thymectomy even when no thymoma
respiratory failure in myasthenia gravis = (2)
immunoglobulins and ventilation
pathophysiology of motor neuron disease
progressive degeneration of all motor neurons- upper and lower
Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes
is this lower or upper neuron disease
lower
so basically reduced, + fasciculations
Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex
is this upper or lower
upper
increased everything incl. brisk reflexes
What can slow the progression of the disease and extend survival by several months in ALS? (ALS is the most common type of motor neuron disease).
Riluzole
breathlessness worsened by anxiety in motor neuron disease- what might we give?
benzodiazepine (depressant)
why would you give an anti-muscarinic for motor neuron disease
excessive saliva
what for muscle spasticity (upper) do you give, in motor neuron disease?
baclofen
how does baclofen work?
muscle relaxant by reducing nerve transmission
what is a subarachnoid haemorrhage?
haemorrhage between the arachnoid mater, and the pia mater.
Difference in clinical presentation of the haemorrhages?
extra-dural
sub-dural
sub-arachnoid
Extra-dural- lucid interval, then unconsciousness
Sub-dural- Gradual deterioration
Sub-arachnoid- Thunderclap headache/ sudden onset of symptoms
Pathology of different haemorrhages?
Extradural = middle meningeal artery
Sub-dural = rupture of bridging veins
Sub-arachnoid = rupture of berry aneurysm
Management for haemorrhages
cocaine use is associated with what type of haemorrhage
sub-dural
typical history of sub-arachnoid haemorrhage?
sudden onset occipital headache during strenuous activity like heavy lifting or sex
what additional symptoms for arachnoid haemorrhage? (4)
1) neck stiffness
2) photophobia
3) vomiting
4) neurological symptoms like visual changes, dysphasia, focal weakness, seizures etc).
First line investigations in haemorrhage
CT head (normal doesn’t exclude subarachnoid haemorrhage)
lumbar puncture to check for bilirubin (looks yellow)
then:
CT angiography to find exact source of bleeding
why use nimodipine after subarachnoid haemorrhage?
calcium channel blocker used to prevent vasospasm - narrowing of arteries causing brain ischaemia
treatment of hydrocephalus
lumbar puncture, external ventricular drain
ventriculoperitoneal shunt
Myelin covers the axons of neurones and helps electrical impulses travel faster. Myelin is provided by cells that wrap themselves around the axons:
Oligodendrocytes vs Schwann cells, which for central vs peripheral nervous system
Oligodendrocytes in the central nervous system
Schwann cells in the peripheral nervous system
Multiple sclerosis: does it affect oligodendrocytes, or Schwann cells
oligodendrocytes, because it affects the central nervous system.
Recurring episodes of optic neuritis could be what condition
MS
Lesions in MS are uniform, true or false
False
Lesions vary in location, and so affected sites and symptoms change over time
optic neuritis- unilateral or bilateral reduced vision that develops over what time period?
hours or days- important to know- not like REALLY sudden, and it’s unilateral
optic neuritis causes relative afferent pupillary defect, and a central blind spot called a scotoma. Is this painful or painless?
painfull
how to treat optic neuritis
high dose steroids
There is:
relaxing-remitting
primary progressive
secondary progressive.
What’s the difference between primary and secondary progressive?
secondary = used to be relaxing remitting, but now it’s simply progressing
Diagnosis for MS is based on history of lesions changing location over time, where other causes are excluded. What are the two investigations that can support the diagnosis?
MRI scans to demonstrate typical lesions
Lumbar puncture can detect oligoclonal bands in CSF.
Relapses of MS can be treated with what
steroids
500mg orally
or 1g intravenously daily for 3-5 days
Urge incontinence in MS can be treated with
antimuscarinic medications
What is the analgesic ladder?
non-opioid meds such as paracetamol vs NSAIDs
weak opioids such as codeine and tramadol
strong opioids such as morphine, oxycodone
Guillain-Barre pathology?
neuropathy of the peripheral nervous system triggered by an infection
Is Guillain barre symmetrical or asymmetrical, and is it sensory or motor?
symmetrical, ACUTE ascending weakness and sensory weakness… a tingle in my toes.
also reduced reflexes
symptoms within how many weeks of infection (e.g. gastroenteritis) , and what recovery time
4 weeks
recovery period = months to years
investigation of guillain barre
lumbar puncture - showing raised protein count normal cell count and normal glucose
nerve conduction studies showing reduced signal through the nerves
management of guillain barre
supportive care
VTE prophylaxis - as pulmonary embolism is leading cause of death
IV immunoglobulins
How long can recovery take for Guillain barre syndrome?
months to up to 5 years.
Important characteristics of a cluster headache
sudden onset, severe, unbearable, UNILATERAL pain behind one eye
How long do cluster headaches last?
15 mins-3 hours (pain peaks abt 15 mins)
3-4 a day
(importantly) Visible signs of a cluster headache?
red, swollen, watering eye and nasal discharge
NB cluster headaches very much involve the eye, with miosis, ptosis, pupil constriction, facial swelling
Acute management of cluster headache
triptans like sumatriptan and high flow oxygen
Prophylaxis for cluster headache (suppress not eliminate factors causing a cluster headache)
prednisolone and verapamil
Do tension headaches have any visual changes?
no
Management for acute migraine? (zig zags)
sumatriptan and NSAIDs analgesics
Prophylaxis for migraine?- first line and second line
1) propranolol (beta blocker that slows heart rate)
2) topiramate (espc. when propranolol is contraindicated e.g. in asthma)
when propranolol is contraindicated as prophylaxis for migraine
asthma
pathology of idiopathic intracranial hypertension
high pressure of unknown cause around the brain causing symptoms such as vision changes and headaches.
3 main symptoms of intracranial hypertension
headache
blind spot
peripheral vision loss
can also get double vision
Chief sign of intracranial hypertension
bilateral papilledema
What exacerbates the symptoms of intracranial hypertension?
worse in the morning
worse leaning forward
worse when coughing/sneezing
If intracranial hypertension is caused by an increase CSF, what is the management?
acetazolamide = this reduces CSF production, and also helps with the headaches
also diuretic = excrete more fluid
what tumour causes bitemporal hemianopia
pituitary adenoma causing optic chiasm compression
lesions affecting the flocculondular lobe =
vertigo and nystagmus
raised intra-ocular pressure causes what affect on the optic disc
cupping
High protein vs high glucose in lumbar puncture meaning?
high protein = viral
high glucose = bacterial
fever, altered mental status, seizures, focal neurological deficits, vomiting, neck stiffness.
We know neck stiffness is often meningitis, but what two other things could it be?
encephalitis and brain abscess
espc after infection or brain injury
Encephalitis pathology-
It means inflammation of the brain. Could be viral most commonly, or autoimmune next commonly.
Most common viral causes of encephalitis
herpes simplex virus HSV
also VZV associated with chicken pox.
Why do we ask about vaccinations with encephalitis
measles, mumps, rubella, polio viruses can cause
Presentation of encephalitis (4)
(Knowing it starts with flu like symptoms)
Altered mental status and behaviour
Fever
Focal seizures
Focal neurological symptoms
3 Investigations to help diagnose encephalitis?
1) lumbar puncture if GCS above 9- send CSF for viral PCR testing
2) MRI scan after lumbar puncture to visualise brain
HIV testing is recommended in all patients with encephalitis
Management of encephalitis (1 and support)
aciclovir treats HSV and VZV. IT IS STARTED EMPIRACALLY in suspected encephalitis until results are available.
ganciclovir treats CMV (cytomegalovirus)
Then just supporting them recover.
Acute management of MS? (2)
glucocorticosteroids like prednisolone
or
IV methylprednisolone
What benefit/when do you use natalizumab in MS?
It’s a disease modifying therapy (DMT) that blocks leukicytes in the brain therefore decrease in inflammation. For relaxing and remitting, given by injection by nurse.
Triad of signs of Horner’s
1) Decreased sweating
2) Drooping eyelids
3) Decreased pupil size
Horner’s: lesion is on the parasympathetic or sympathetic?
sympathetic
what do we use to diagnose Horner’s?
eyedrops
apraclonidine: to reverse pupillary constriction, because it has agonistic effect on alpha-2-receptors
what tumour commonly causes Horner’s? With what symptoms?
Pancoast tumour- with cough and weight loss
so do CXR
What’s a Pancoast tumour?
cancer starting in apex of the lung
Is there a cure for Horner’s?
no
just treat underlying condition e.g. cancer
lesion for Horner’s is on what side of the sympathetic system?
ipsilateral side to the symptom
What is giant cell arteritis?
inflammation of arteries in the temples
Key complication of giant cell arteritis?
Vision loss, which is often irreversible. Therefore emergency.
Symptoms of giant cell arteritis? incl headache, (3)
UNILATERAL HEADACHE
scalp tenderness
jaw claudication
blurred/double vision
Management of giant cell arteritis?
prednisolone 40-60mg daily
Management of giant cell arteritis WITH jaw claudication?
500-1000mg daily methylprednisolone
Over what length of time would you wean a patient off steroids in giant cell arteritis?
Over 1-2 years
How to diagnose giant cell arteritis? (3)
Based on:
1) clinical presentation
2) Raised inflammatory markers, particularly ESR
3) Temporal artery biopsy showing multinucleated giant cells
What’s ESR?
a blood test
Narcolepsy pathology?
Loss of orexin signalling cells in the hypothalamus. So low levels of orexin in CSF.
Most cases of narcolepsy are due to
Autoimmunity.
Cataplexy is often seen in narcolepsy. (as well as excessive daytime sleepiness, hallucinations when emerging from REM, and sleep paralysis).
What is cataplexy?
sudden muscle weakness triggered by strong emotions like laughter or surprise.
head falls forward, jaw drops, knees buckle. lasts 30 secs to 2 mins
Manage narcolepsy?
1) anti-depressants or sodium oxybate for cataplexy
2) modafinil (central nervous system stimulant) first line for excessive stimulants
Investigate narcolepsy how? 1)
CSF orexin levels
Best: multiple sleep latency test
Theory of sleep: what builds up throughout the day, at and threshold leads to sleepiness?
adenosine
Caffeine is an antagonist to what receptors?
adenosine receptors
melatonin comes from where
pineal gland
cauda equina is neuropathy of what
nerve roots
meaning numbness, peeing problems and sexual dysfunction
is cauda equina syndrome bilateral or ipsilateral
bilateral
is cauda equina an acute emergency, or chronic
emergency because if left untreated, = permanent paralysis
how quickly do you need to do surgery for cauda equina
8 hours
investigate cauda equina =
MRI to check for compression
treat cauda equina how
lumbar decompression surgery and analgesia
fever, neck stiffness and altered mental state = what
triad of symptoms for meningitis
also rash
investigate/diagnose meningitis how?
Lumbar puncture for CSF findings, and blood culture for infection
why photophobia in meningitis
irritation of the meninges around the diaphragma sellae
when does meningitis become encephalitis
when the irritation of the brain occurs, because limited bacteria can get through the blood brain barrier
irritation of brain = focal neurological signs, and seizures, vomiting etc.
management of meningitis
dexamethasone, IV
meningitis vs encephalitis- which is more likely to have aphasia, behaviour change, visual disturbance
encephalitis
management of encephalitis (3)
antibiotics
anti-convulsant
corticosteroids
what condition does riluzole treat
motor neuron disease
pathology of cavernous sinus thrombosis
infection spreads from nearby areas such as nose (sinusitis) to the cavernous sinus- the space behind the eyes and underneath the brain. A blood clot develops to stop the infection from spreading. Retrograde flow of venous blood leads to an increase in pressure.
what nerve is compressed in cavernous sinus thrombosis?
oculomotor nerve
why could the brain be damaged in cavernous sinus thrombosis
because blood to the brain is disrupted
treat cavernous sinus thrombosis how?
antibiotics immediately
and
anticoagulants like heparin
and
corticosteroids for swelling/inflammation
Korsakoff syndrome is a complication of what, and is characterised by what
Wernicke’s encephalopathy- where is becomes dementia, so it’s characterised by irreversible deficits in anterograde and retrograde memory
Wernicke’s encephalopathy pathology
alcohol blocks thiamine- B12
manage wernicke’s encephalopathy how
replace thiamine via IV very quickly
triad for wernickes encephalopathy
ataxia
nystagmus
confusion
so eyes, gait, confused
thiamine deficiency can impair processes like
the utilisation of carbs for energy therefore affects all organs
affects synthesis of neurotransmitters, and myelination etc.
we know alzheimer’s is associated with amyloidosis (build up of amyloid plaques and tau proteins. It’s also seen with the loss of what
cholinergic neurons
manage Alzheimer’s how
cholinesterase inhibitors (because reduced acetylcholine causes some symptoms).
Give three examples of cholinesterase inhibitors
donepezil, rivastigmine, galatamine
Biggest presenting complaint of glaucoma
peripheral vision loss
All symptoms of glaucoma (5)
headache
blurry vision
halo’s around lights
fluctuating pain
does the pupil cup in open angle or acute angle closure glaucoma?
acute angle closure
In glaucoma, what’s causing damage to the optic nerve?
raised-intraocular pressure
How to surgically treat glaucoma?
laser trabeculoplasty
or
trabeculectomy surgery
Which eye drops treat inflammation in glaucoma?
prostaglandin eye drops
Why use beta blockers in glaucoma?
Inhibits production of aqueous humour
Do you treat guillain barre or myasthenia gravis with cholinesterase inhibitor like pyridostigmine?
MG
Normal pressure hydrocephalus: what does ‘wet, wacky, wobbly’ mean?
dementia
urine problems
difficulty walking
pathology behind normal pressure hydrocephalus?
Increased CSF, leading to increased ICP (NB- the CSF looks normal, but ventricles are enlarged).
4 examples of things that would block flow/absorption of CSF, thus leading to normal pressure hydrocephalus
subarachnoid haemorrhage
meningitis
head injury
surgical complications
Treat normal pressure hydrocephalus how? (2)
1) therapeutic lumbar puncture
2) shunt CSF from brain to abdomen
which type of dementia has hallucinations, is rapidly progressive, and has parkinsonian symptoms?
Lewy body dementia
lewy body protiens in parkinsons vs lewy body dementia?
dementia = throughout brain,
vs
parkinsons = just deposited in the substantia nigra
(if physical symptoms before cognitive decline, then it’s Parkinson’s!)
Which type of dementia has loads of hallucinations? (also mainly affecting motor skills and judgement).
vascular
NB stepwise with lots of cerebrovascular infarcts
lumbar spinal stenosis is narrowing therefore compression of spinal nerves in the lumbar region. What symptoms?
pain, discomfort especially during physical activity. Claudication in thigh and buttock.
When lumbar spinal stenosis (which would cause claudication) is caused by a tumour, what symptoms also?
weight loss, night sweats and other systemic symptoms
When lumbar spinal stenosis (which would cause claudication) is caused by a herniated lumbar disc, what is it:
exacerbated by?
relieved by?
exacerbated by flexion
relieved by extension
what usually causes coma?
toxic metabolic state
depressed respiration during coma is usually caused by what
drug over dose
Cushing’s triad
increased intracranial pressure = decrease in heart rate, increase in blood pressure, irregular breathing
how would we correct clotting issues in a haemorrhage of the brain
platelet transfusions
vitamin k if warfarin previously used
why would you give tetrabenazine to someone with Huntington’s
it inhibits dopamine uptake
where do you place the tuning fork in rinne test, and what does it test?
bone conduction
anterior and posterior
where do you place the tuning fork in weber’s test, and what does it test?
Sensio neural hearing loss, middle of forehead
negative Rinne means whats
means bone conduction is greater than air conduction
would a positive or negative Rinne mean that sound is greater in the bad ear?
negative
What’s the meaning of the acronym, FOSSIT?
feeling of something stuck in throat
What’s the meaning of the acronym, FOSSIT?
feeling of something stuck in throat
