Neuro Flashcards
What are the possible causes of unilateral vision loss?
Vascular -amaurosis fugax -central retinal vein occlusion -anterior ischaemic optic neuropathy (GCA) NON-Vascular -Optic neuritis -retinal detachment -acute angle closure glaucoma -vitreous haemorrhage
What’s the difference between vascular changes in vision compared to inflammatory causes?
- Vascular reaches height of problem quickly
- Vascular would be associated with CVD risk factors such as smoking, diabetes & obesity
- inflammatory causes blurring/loss of acuity w/ pain opposed to abrupt loss of vision
What would you see on examination of a n optic neuritis eye?
- reduced direct and indirect pupillary response
- decreased visual acuity and colour vision in one eye
- normal fundoscopy and movements
What is papilloedma generally a sign of?
-raised intracranial pressure
What may exacerbate symptoms of someone with multiple sclerosis?
- heat
- exercise
- infection
What is the epidemiology of MS?
- F>M predominance - effects more and earlier
- onset 20-40
- 30% of MS risk genetic
- closer to the equator risk lower
what’s the 3 stage model of MS pathophysiology?
- initiation
- propagation
- resolution
What happens during the initiation phase of MS pathophys?
T cells become primed to being autoreactive
- increased genetic risk
- environmental triggers - infectious agents similar to CNS antigens prime T cells to be autoreactive to oligodendrocytes
- leaky gut hypothesis - increased inflammation in gut may lead to increased activation of T cells that then pass the BB
- traumatic insult - 2x more likely to get MS if had a TBI
What happens during the propagation stage of MS pathophys?
once T cells are autoreactive
- BBB loss due to inflammation m
- plaque formation - killer cells, helper cells, B cells and microglia proliferate and aggregate
- plaques cause - demyelination, conduction block and axonal loss.
What happens during the resolution stage of MS?
- remyelination
- neuroplasticity
- axonal redundancy
Define relapse in terms of MS?
- acute onset Sx that must be experienced by patient (not incidentally found)
- confirmed by neuro exam
- lasts longer than 48 hours
- reaches nadir in subacute pattern - days to weeks
- plateaus - weeks to months
- complete resolution
What is uthoff’s phenomena?
Sx of MS get worse with heat i.e. bath, exercise, holidaying
What are common sites for plaques in MS? and what Sx would they cause?
- periventricular -
- spinal cord - parathesiae, weakness, numbness, bowel and/bladder incontinence
- brainstem - dysarthria, vertigo, hemiplegia (if massive lesion)
- cerebellar - ataxia, nystagmus, intention tremor
What is Lhermitte’s sign?
Electric shock felt through the body. indicative of spinal cord MS lesion.
What criteria would you use to diagnose MS? what are it’s requirements?
Macdonalds Criteria.
evidence of at least 2 lesions disseminated in time and space.
can be 2 clinical ones, can be 1 clincal + MR evidence of second lesion, can be 1 clinical + historical suggestion of previous episode of demyelination. bit of a maccies pic n mix.
What investigations would you do in suspected MS?
- MRI
- lumbar puncture - looking for oligoclonal bands
- maybe neurophysiology - VEP, NCS.
What MRI changes would be suggestive of MS?
- dawson’s fingers (corpus callosom)
- multiple sites of hyperintense lesions on T2 or multiple gadolinium enhancing lesions on T1
Describe the progression of MS?
- separate pathophys to inflammation
- not complete remyelination post relapse
- leads to steady decline in function over 10-15 years
- oligodendrocytes die so can no longer tropically support neurons that then subsequently die themselves.
What are the 4 types of MS?
- relapsing remitting (85%)
- secondary progressive - 10-15 years after onset of R&R
- progressive relapsing
- primary progressive - worsening of disease from onset minor improvements, plateaus maybe
What is the treatment for an acute MS rekapse?
- oral methylpred - if not to bad
- IV methylpred - if severe
When would an MS patient be eligible for immunomodulation therapy? What are the pros and cons of this?
- needs to have had 2 or more relapses within a 24 month period
- drugs decrease recovery time and reduce number of lesions
- drugs don’t slow progression of disability
What is the first line treatment for active MS? what is it’s MOA?
-interferon beta 1b - anti-inflammatory cytokine that reduces active inflammation
Name a second line biologic drug used to treat more active MS? briefly describe MOA.
- nataluzimab - monoclonal antibody that targets integrin on lymphocytes
- alemtuzumab - targets and kills T regulatory cells.
What is the definition of a TIA?
The rapid onset of focal neurological symptoms caused by a vascular injury that resolve completely within 24 hours (usually an hour) with no evidence of neuronal loss
What are risk factors for a TIA?
- atrial fibrillation
- Known Carotid stenosis
- smoking Hx
- Age
- high systolic BP
- diabetes
- CVD
- obesity
What investigations would you do for a suspected TIA?
- Carotid doppler
- ECG - 24 hour tape
- BP
- bloods - lipid profile
- Echo
What management would you do for a TIA?
Treat underlying risk factors
- anti-HTN
- if AF - rivaroxaban or warfarin if contraindicated
- carotid endarterectomy
- PFO closure if clinically significant
- statins probs anyway
- aspirin anyway
What must you tell a patient who has had a TIA?
No driving for a month
What is the definition for a complete ischaemic stroke?
An acute onset of focal neurological symptoms lasting longer than 24 hours due a disturbance in cerebral blood flow that has led to neuronal death!
What are some non-modifiable risk factor for having a stroke?
- Gender (M>F)
- Age
- genetic predisposition
- Previous stroke or TIA
What is a penumbra?
Brain tissue that surrounds the necrotic core of a stroke that remains viable for hours after the original vascular insult. Saving this is the target of acute stroke therapies like thrombolysis or thrombectomy.
How would you differentiate between an embolic stroke vs a carotid stroke?
-embolic stroke is more likely to have infarctions that cross vascular territories because the source of the clot is lower than the carotids.
What are the 3 pathophysiologic mechanisms for an ischaemic stroke?
- carotid disease
- embolic disease
- hypoperfusion
How does AF cause an increase risk of stroke? by how much?
5x increase risk
3x more likely to be severe
-incoordination of contraction of the atria
-causes blood stasis and clot formation (usually in the left atrial appendage)
-micro clots break off thrombus and go tot he brain
What are the causes of embolic stroke?
- AF
- suboptimal anticoagulation of mechanical heart valves
- LV thrombus post MI
- PFO ????
- subacute bacterial endocarditis vegetative growth
What are the 2 carotids diseases that can cause stroke?
- MAINLY atherosclerotic disease
- carotid dissection
What can cause cerebral hypo-perfusion and thus stroke?
- iatrogenic
- sepsis
- vasculitis
- major carotid stenosis predisposes
What are the 4 sub groups of stroke dependent on the Bamford classification? What is groups criteria?
- Total Anterior Circulation Stroke (TACS)
3/3 - unilateral weakness of arms and legs, hemianopia, higher cortical dysfunction - Partial Anterior Circulation Stroke (PACS)
2/3 unilateral weakness of arms and legs, hemianopia, higher cortical dysfunction - Lacunar syndrome (LACS)
-pure sensory, pure motor, pure sensori-motor or ataxic hemiparesis - Posterior Circulation Stroke (PACS)
1/4 - cranial nerve palsy + contralateral sensory or motor deficit, cerebellar dysfunction, bilateral sensory/motor dysfunction, isolated homonymous hemianopia.
What is thrombolysis?
- a recanalising treatment that aims to restore blood from to brain tissue surrounding the ischaemic core of a stroke.
- Done with Alteplase - tissue plasminogen activator (0.9mg/kg over 60 mins) 0 thrombolytic
What are the indications for thrombolysis?
- CONFIRMED (by CT) ischaemic stroke (rule out haemorrhagic acutely)
- presents to hospital within 4.5 hours of onset of symptoms or last seen well
What are contraindications for thrombolysis?
- BP <185
- on warfarin INR<1.7 or any NOAC or recent LMWH
- stroke is too severe or not severe enough
- prior ICH or known active cancer
- known bleeding source/coagulopathy
- really low or high BM
- stroke within last 6 weeks
- unsecured brain aneurysm
What’s the outcomes of thrombolysis?
1/10 - better outcome
1/20 - outcome is no better that it would have been without
1/30 - worse outcome
Other than thrombolysis what is the other acute stroke therapy?
- thrombectomy
- available up to 6 hours post onset or symptoms or last seen well
- must be functioning well before stroke and be a severe stroke
- however, it’s a limited resource
What’s the most important factor to manage in stroke primary and secondary prevention?
BLOOD PRESSURE
- 130/80 or less
- 120 if DM
- 140-50 if bilateral carotid stenosis
what 3 responses are measured using the GCS?
Eye /4 verbal /5 motor /6 lowest score 3 normal = 15
What meds would you give someone post stroke?
- 300mg aspirin for 2 weeks then clopidogrel life long
- anti-coag if AF HASBLED/CHADSVASC score
- Anti-HTN - long term target of 130/80
- Statin therapy - 40% reduction in non-HDL
What are the reversal agents for what anti-coagulants?
- Vitamin K for Warfarin
- Protamine for Heparin (artially for LMWH)
- Beriplex for NOACs
- Idarucizumab for Dabigatran
What is the classical triad of Parkinson’s disease?
- Cog-wheel rigidity
- Bradykinesia
- resting tremor
ALL ASYMMETRICAL
All PRESENT
IMPORTANT
Other than the classical triad, what other symptoms may people with parkinson’s disease have?
- cognitive and mood changes
- sleep disorders (20 years receding REM SD)
- later autonomic dysfunction
What is thought to be the main causative protein in parkinson’s disease?
Alpha Synuclein
What environmental exposures increase your risk of having PD?
- head injury, emotional stress, shy and depressed personality type
- rural living: farming activity, well water drinking, exposure to pesticide, herbicide, insecticide
- heavy metal exposure - lead, maganese, mercry
ALL EXHIBIT A DOSE EFFECT
What are some protective factors of PD?
- Smoking
- Alcohol
- Coffee
- measles as a child
- NSAID usage CCB
What is the basic pathophysiology of parkinson’s disease?
- degeneration of the dopaminergic neurones in the substantia nigra reducing the ability/stopping completely an individual with parkinson’s ability to initiate movement
- degeneration is caused by cytoplasmic proteinaceous inclusions of alpha synuclein in these neurones
Describe the tremor seen in parkinson’s.
- 4-6Hz pill rolling tremor
- present mainly at rest
- worse on destraction
- can affect upper and lower limbs
Describe the Bradykinesia of parkinson’s.
- Decrements over usage
- has to be asymmetrical
- Variable in nature
Describe the rigidity seen in Parkinson’s.
- increased tone across the whole ROM
- worse on activation manoeuvres - get them to tap other hand and testing limb becomes more rigid.
Describe the gait seen in parkinson’s.
- Stooped posture
- short stride length
- shuffling
- Poor turning
- Freeze in doors
What are some complications of PD?
- sleep disturbances - could be dopamine side effects, could be PD meds wearing off over night, could be insomnia due to concurrent anxiety
- Psychosis - Dopamine therapy could trigger psychotic Sx, proving factors UTI, new drug (anticholinergic, MOAi, dopamine agonist)
- Impulse control disorder - spectrum from pathological gambling to punding
What things in a history would make you think it was likely PD?
Asymmetrical
Slowly progressive
Display excellent response to Levodopa
Average age of onset around 60 (but wide range)
What things in a history would make you think it wasn’t PD?
- Neuropsychiatric disorders when they present - LBD
- Prominent falls and postural instability early on - MSA
- Have abnormal eye movements -PSP
- Have early onset autonomic features - MSA
- Have ataxia - unequivocal cerebellar abnormalities
- Have a structural abnormality explain their symptoms le a fatty stroke of their basal ganglia - vascular Parkinson’s won’t have decrement in movements
- PD Sx restricted to the legs for <3 years - NPH
What investigations would you perform in suspected PD?
- L-dopa trial - if good response probably PD, if bad or responds and tails off probs not PD
- DAT Scan - Dopamine Active Transported - visualises how much dopamine is getting transported around the brain - good for young people with odd Px
What medication treatment would you give for PD?
FIRST LINE
-Levo-dopa - needs to be given with a dopamine decarboxylase inhibitor - Co-benaldopa/co-careldopa to prevent peripheral L-dopa metabolisation causing dopamine side effects
SECOND LINE ADJUNCTS
-Dopamine agonists - ropinerol - higher risk of Hallucinations, most improvement with off time & Motor Sx & ADL
-MAO-Bi- rasagiline
-COMT
What causes dyskinesia PD?
- post synaptic hypersensitivity to dopamine due to chronic dopamine deficiency
- involuntary fidgety movements (dyskinesia) seen at the height of dopamine transmission
What non-pharmacological treatment is available for PD?
- Psychological support - PD A&D + life adjustment for chronic illness for family as well as pt
- Deep brain stimulation of the sub nig
- OT - Cueing for walking assistance - bypasses needs for basal ganglia activation of movement by accessing premotor, parietal and cerebellar corticies
How do you treat trigeminal neuralgia?
-carbamazepine
How do you manage migraine acutely?
- Triptan - as soon as recognise one coming on
- NSAIDS
- Coedine
- Anti-emetics
What can you give to prophylatically treat migraine?
- Beta blockers
- topiramate
- amitriptiline
Tx for a partial seizure?
-Carbamazepine
2nd line - lamotrigine
Tx for GTCS?
- Valporate
- give carbamazepine if child bearing age
Tx for Absence?
Ethosuximide
valporate
Tx for myoclonic?
-Valporate or Keppra (leviteracetam)
When does a seizure become status?
1 seizure lasts for 15 mins
or
multiple seizures without recovery in between
What is the management for status?
- ABCDE
- O2, airways + IV access
- buccal midaolam or rectal diazepam
- IV lorazepam/diazepam
- IV phenytoin if seizures continue
What in MG is the pathophysiology and Tx?
- autoimmune destruction of nicotinic acetylcholine receptors
- pyridostigmine - 1st
- prednisolone to induce remission - 2nd
- may need chronic immunosuppresion from mycophenelate- 3rd
- Thymectomy if indicated
