ILAs 1 to 3 [03/11/20] Flashcards
What is the Marcus Gunn pupil, and how can it be assessed?
Relative afferent pupillary defect: slower response to dilate pupil in swinging light test.
What can a Marcus Gunn pupil be caused by?
Large retinal detachment, central retinal artery/vein pathology, optic nerve pathology.
How is visual acuity measured?
Snellen chart, first number viewing distance, second number is the distance an average eye can read it.
Allowed two goes per line.
What are the 5 main anatomical parts of vision that can have pathology?
Aqueous humour, vitreous humour, retina, vasculature, nerve
Describe the simple PP, Sx and Sx and what acute glaucoma can easily be confused by?
Drainage of the aqueous humour becomes blocked. Results in a rapid rise in IOP.
Sx: pain, red eye, N and V.
Confuse Sx often with migraine.
Sx of a vitreous haemorrhage
prevents light lens to retina: flashes/floaters, blurred vision
Sx of retinal detachment fundoscopy
Flashes, floaters, ‘curtain’ over part of vision [which is also seen vascular pathology].
Sx of anterior ischaemic optic neuropathy. What is AION? What should you think of causative?
Swollen optic disc, occlusion of th eposterior ciliary artery supplying had of the optic nerve.
THINK of GCA!
Sx of GCA
Jaw claudication, scalp tenderness, anorexia, anaemia, fatigue, age [over 70, though can be over], elevated ESR and CRP, no athersclerotic RFs
Central retinal artery occlusion on fundoscopy? Whose opinion should you ask as what could this be?
pale disc, cherry red spot at macula.
Occlusion of the central retinal artery [branch of the opthalmic artery] which supplies the whole retina.
Need urgent intervention.
Stroke opinion as consider a TIA.
Features and Sx of central retinal vein occlusion
Dilated of branch veins
Multiple retinal haemorrhage
Cotton wool patches [hard exudates].
Difference between papillitis and optic neritis?
Both inflammation of the optic nerve; if optic head then papillitis, if behind 2/3rds then ON
What does nerve damage look like fundoscopy?
Optic clonicity [optic enrve damage been awhile], usually more temporal. Normally paler beyond optic disc.
Papilloedema look like?
Disc margins distorted, haemorrhage lower area.
Something puhsing from the back centrally.
Swelling in this area of disc, means area is elevated.
Sx of optic neuritis
Reduced acuity over few days, pain moving eye, excerbated by heat and exercise, apparent pupillary defect, dyschromatopsia
Aetiology ON
Inflammation optic nerve, often associated with MS. can occur clinically isolated.
other causes: infection [Lyme’s, syphilis, HIV], B12 def., arteritis
Common course of ON
6w recovery vision
Tx of ON
steroids help reduce pain and hasten recovery
What in ON can lead to long term damage?
Neuromyleitis optica
Essential criteria for ON?
RAPD
15 year risk of developing MS if have ON?
40%
15 year risk ON is MRI normal 10y, abnormal 10y?
Normal then 11%, abnormal then 83%
Dx of MS
Multiple CNS lesion, whihc cause Sx that:
- last longer 24h
- dissminated in space
- dissiminated in time
typical features MS
- visual loss [ON, optic atrophy, LNO]
- pramidal weakness, spastic paresis
- sensory disturbances
cerebellar Sx [nystagmus/vertigo/tremor/ataxcia etc.] - bladder/sexual dysfunction
Lhermitte and Uhtoff’s phenomenon, fatigue, cognitive impairment, 3rd and 6th nerve palsy
Ix for MS
MRI scan
- T2 lesions found in four key areas [cortical/ventricular,/tenortorial/spinal cord]
LP
- unmatched oligoclonal bands
PP of MS
inflammatory, local loss myelin sheath, realtive preservation axons
neurodegenerative stage loss of axons and prgoressive fixed deficits
MS types
- benign MS
RRMS
SCR
PP [10-20%, older]
Tx acute episode
steroids [hasten recovery, thought not DMT after 6-9m]
DMT for chronic MS
sub-cut: e.g. Ib, Ga
oral e.g. figolimod
IV e.g. natalizumumab?
stem cell transplant
SE steroids
avascular necrosis, lowered blood sugar, cushings, OP, etc.
DDx blackouts
syncope, epilepsy, NEA
Dx syncope
abrupt and transient loss of consciousness associated with loss postural tone follows sudden fall cerebral perfusion
3 main types of syncope
Neurogenic, orthostatic, cardiac
Define neurogenic syncope
Inappropriate activation of cardio-inhibotiry and vaso-depressor reflex leading to hypotension
Causes of neurogenic syncope
Vasovagal Reflex: - micturition - cough - carotid sinus hypersensitivity [stimulate baroreceptors e.g. when men shaving, or reaching for things]
Types and examples of orthostatic syncope
Autonomic failure
- primary [multi-system atrophy]
- secondary [diabetes, drugs]
Cardiac syncope causes
Arryhtmias [prolonged QT, bradycardias, exertional syncope]
Valvular heart disease
Seizure definition
Compare to epilepsy
Clinical manifestation of distorted electrical activity of the brain [paroxysmal discharge of cerebral neurones]
Epilepsy is just tendency for recurrent seizures
Compare triggers syncope to epilepsy
Syncope
- stress/fear, prolonged standing, heat, venepuncture, cough, micturition
Seizure
- sleep deprivaiton, flahsing ligths, menstruation, alcohol and alcohol withdrawal
Describe syncopal episode [onset, duration, convulsions, colour, intontience/tongue biting]
- onset = quick, but can sometimes prevent faint if lie down quickly
- duration = short [seconds to 1 minute]
- convulsaions = rare, but brief
- colour = pale
- incontience/tongue biting = rare [unless bladder full]
Seizure description
onset - can have aura, tonic-clonic episodes goes rigid then clonic movement limbs
duration - 2/3 mins
convulsions - GTC seizures, focal motor fits, myoclonic jerks [on awakwning], frontal lobe motor fits
incontinence/tongue biting - yes, biting lateral side tongue
NEA description
can last 30m, convulsions [non-neuroanatomically accurate], wild shaking, arms felxing and extending, may be completely still. Waxc and wane, pelvic thrusting, eyes closed. Incontinence/tongue biting can have injury to self.
Recovery from each
Syncope - little or no confusion, quick recovery
Seizure - confusion or headache, may not recognise family/friends, amnseia for few miutes, first mem in ambulance, needs rest [sleep 1/2 hours]
NEA - recovery rapid, can be very upset
Compare PMH/personal history of each
Syncope - previous faints, cardiac causes
[heart block, tachycardia like VT], obstructive lesions like aortic stenosis
Seizure - perinatal illness, educaitonal achievements, previous serious head injury/neurosurgery, neonatal seizures [prolonged], meningitis. If late onset [over 40], think stroke/tumours.
NEA - preivous unexplained medical Sx. PMH child abuse etc.
Ix of blackouts
Listen to heart [aortic stenosis] 12 lead ECG!!!!! blood tests [FBC] Brain imaging EEG if suspected syncope consider 24 hours tape, tilt table, autonomic function tests
types of EEG can do
inter-ictal EEG
provocation [photosensitivty, hyperventilation]
sleep dewprived EEG
prolonged EEG
vidoe-telemtry: useful NEA, preo-op assess, not useful frontal seziures
Accuracy of EEGs
false postiive rate 0.5-2%
false negative rate 50%
false negative rate repeat EEG 30%
false negative sleep deprived 20%
When should/shouldn’t you do imaging? What type best?
If focal onset, imaging
if over 25 and new onset, imaging
if suspected idiopathic generalised epilepsy imaging less useful [rarely abnormal]
MRi best, but CT emergency can do
Types of idiopathic generalised epilepsy
GTC, myoclonus, absences
What is the interictal marker of a seizure?
Spike or sharp wave
Juvenile myoclonic epilepsy on EEG
interictal EEG shows a normal background with frequent generalised polyspike and wave discharges
PP of seizures
Normal brain, spread electrical acitvity limited
during seizure, prolonged depolairization group neurones, whihc spreads out to adjacent neurones
Failure of GABA neurotransmitter
Type of epilepsy
Focal [has focus]
- simple partial
- complex partial
- secondary generalised tonic-clonic
Idiopathic generalised
Epielspy [generalised from outset]
- myoclonic jersk
- typical absence
- primary generalised tonic-clonic
PP of NEA
often mansifestation of stress
- situations that is intolerable or unaccepetable to a peron and over whihc they have no control
- may be asssociation abuse childhoo
may occur pts epilepsy
- commonly have other medically unexplained Sx
Early signs of a stroke
- may have none
- hyperdensw MCA
- hloss grey white matter differntiation and sulcal effacement
- hypodense basal ganglia
4 main clinical syndromes with stroke
- total canterior circulation infarction
- partial anterior ciruclation infarction
- lacunar stroke
- posterior circulation infarct
Complications of stroke
- raised ICP: cerebral oedema, haemorrhage
- aspiration
- pressure sores
- depression
- cognitive impairment
- other medical problems
Raised ICP signs
HTN, new neurology, GCS
High risk after a TIA?
- risk of stroke in first 48 hours
What should be done within 2 hours of stroke [NICE]?
Endarectomy
- symptomatic disease [incl. stroke/TIA]
- 50-90% stenosis
NNT to prevent major stroke in symptomatic stenosis 70-99%
6%
How to manage stroke anaphylasxis?
Clopidogrel
What is ABCD2 score?
Risk of stroke following TIA
ABCD2 stand for?
Age [over 60], BP [over 140/90], cf [unilateral weakness or speech impairment w/o weakness], duration Sx [over 60m, or 18-59 mins], diabetes
How to Mx a TIA?
Antiplatelets, 72 hour tape, Dopplers
Options for ischaemic [stress ischaemic] stroke with clear recent onset time?
Thrombolysis, thrombectomy
When thrombolysis allowed?
4.5 hours of Sx onset
Benefits of thrombolysis?
Improves chance of independance on discharge
Benefit decrease with longer Sx duration
Risk thrombolysis
Risk of death the same
However, haemorrhage 1 in 20 as reaction. Reaction to rTPA.
When thrombectomy offered?
mechanical retrieval of clot ig clot is seen in proximal anterior circulation and thromblysis
- offered within working hours
Outside of time window/following care what should be offered?
300mg aspirin for 14d or until discharge; switch to 75mg long-term. IPCO for all pts with reduced mobility.
Secondary prevention aftercare?
Cholesterol, anti-hypertensives, diet, alcohol, smoking, exercise
Driving advice?
must not drive for 1m, if ongoing Sx then can drive if safe.
Ix of haemorrhagic stroke
History and examination
bloods [FBC, UE, LFT, CRP, TFT, coag, lipid]
CT head
stop anticoag, antiplatelet, may drug increase risk
- reverse anticoagulation vitamin K/ Beriplex
- aggressive BP control: under 140 systolic
How to manage AF acronym?
CHADS2VASc
CHADS2VASc acronym stand for?
congestive HF, HTN, age [over 75], DM, stroke [TIA/systemic amoblism], vascular disease, age 65-74
If 1 then oral anticoag consiedered
If 2 and over, then oral anticoag recommended
HASBLED for?
- assess 1 year risk of major bleeding in pts taking anticoag with AF
- HTN, abnormal liver/renal function, stroke, INR, elderly, drugs/alcohol, blacking
Surgical Mx stroke
Extracranial carotid stenosis
Decompressive hemicraniotomy
PCI
Risk if PCI
Risk hyrocephalus, so EVD/posterior fossa decompression
Mx of haemorrhagic stroke
- ABCDE [monitor envinroment, regular neuro obs [GCS/pupils]
- BP [140-160 acutely, over 130/80 long term]
- Bleeding tendency [coagulation/ less platelets/ medication]
- Underlying malformation [?AVM]
- Neurosurgery [superficial clots, CSF obstruction = hydrocephalus etc.]
Reversal of anticoagulation
warfarin [beriplex, vitamin K] heparin [protamine] LMWH apixiban/rivaoraixban etc. Dabigatran
