Neuro Flashcards
Define TIA
Rapid onset Neurological deficit of vascular origin that resolves spontaneously within 24 hours
Define stroke
Rapid onset Neurological deficit of vascular origin that does not completely resolves within 24 hours
What are signs and symptoms of stroke and TIA
Vision loss, vertigo, dizziness
Dysarthria, dysphagia
paralysis
Nausea and vomiting
What are investigations for TIA / stroke
Bedside: ECG, capillary glucose
Bloods: FBC, U&E, lipids, venous glucose, clotting, cardiac enzymes, G&S
Imaging: CT Head, carotid doppler
Consider swallow assessment
What score can you use to estimate risk of stroke following TIA
ABCD2
How do you manage TIA
Immediately: aspirin 300mg (unlesss CI)
Review and assessment by specialist
Ongoing management: clopidogrel 75mg PO OD + statin 80mg
Consider carotid artery endarterectomy
What are the two maain causes of stroke and what is their likelyhood
ischaemic 80%
haemorrhagic 20%
What classification is used for stroke
Bamford classification
How do you manage a haemorrhagaic stroke
SAH: Nimodipine (CCB for 21 days) + coiling or surgical clipping
How do you manage an ischaemic stroke
AFTER EXCLUDING HAEMORRHAGE:
- Aspirin 300mg PO (PR if impaired swallow)
- Consider thrombolysis with tPA if:
- Age < 80 yrs and < 4.5 hours from start of symptoms
- Age > 80 yrs and < 3 hours from start of symptoms
-Consider thrombectomy <6 hours from start of symptoms
How do you differentiate between haemorrhagic and ischaemic stroke
CT head - look for visible haemorrhage
what causes a SAH
spontaneous or traumatic head injury
85% are associated with Berry aneurysm (saccular) - RF HTN, PKD, Connective tissue disease, HTN, smoking
What are sx of SAH
thunderclap headache across back
nausea and vomiting
photophobia
neck stiffness
reduced consciousness
Long term mx of ischaemic stroke
First 2 weeks: 300 mg Aspirin (PR if impaired swallow)
After 2 weeks: change to 75 mg CLOPIDOGREL + Statin (e.g. atorvastatin 80mg)
— or ASPIRIN 75mg + DIPYRIDAMOLE + STATIN
If AF: warfarin / apixaban + statin
Alongside with:
o BP control
o Feeding assessment (screen for safe swallow withni 24h, otherwise NG tube)
o Anticoagulants (e.g. apixaban or warfarin) if co-existing AF
What are core symptoms of Parkinsons
bradykinesia + stooped, shuffling gait
hypertonia (leadpipe rigidity, cogwheeling)
pill-rolling tremor (resting tremor)
+ hypomimic face,
What are ix for suspected PD
CT/MRI head to esclude vascular causes
DaTScan (= dopamine transporter scan)
What is the general approach to managing PD
- MDT approach
- Disability UPDRS (uniified PD rating scale)
- Physiotherapy (postural exercised)
- Depression screen
What are medications for PD management
LEVODOPA + dopa decarboxylase inhibitor e.g. CO-CARELDOPA
Otherwise: MAO-B inhibitors (e.g. seleginine) , DA agonists (pramipexole, ropinirole)
What is indication for levodopa
motor symptoms
What are siide effects of levodopa
DOPAMINE
Dyskinesia
On/off phenomena
Psychosis
Arterial BP low
Mouth dry
Insomniia
N&V
EDS
What are Parkinson PLUS syndromes?
Multiple Systems Atriiphy
Progressive Supranuclear Palsy
Corticobasilar Degeneration
Dementiia with Lewy Bodiea
Features of Multiple Systems Atrophy
Autonomic dysfunction (postural hypotension, bladder dysfunction)
Cerebellar ataxia
Rigidity, tremor
Features of Progressive supranuclear palsy
Vertical gaze palsy
postural instability &T falls
Speech disturbance
Dementia (forgetfulness, personality change)
Fts of Corticobasilar degeneration
Unilateral parkinsonism
Aphasia
Astereognosis (cortical sensory loss > alien limb phenomenon)
Demenita wiith lewy bodies fts
VISUAL HALLUCINATIONS
Fluctuing cognition
Demenita > parkinsonism
How do you differntiate Parkinsonism from PD?
Parkinsonism: symmetrical, rapid progression, poor response to levodopa
PD: asymmetrical, pprogressive, good response
What are the criteria for a diagnosis of epilepsy?
2 or more epileptic seizures
OR 1 seizure + epileptogenic markers (EEG or brain malformation)
What are signs of a tonic clonic seizure
- Behavioural arrest (stop writing and stop talking)
- Head and eyes turn to one side (the side they turn to is opposite to the side of the lesion)
- Stiffeniing (tonic)
- Shaking (clonic)
Ix for seizure
A>E (incl glucose)
ECG (cardiac cause)
MRI (structural cause)
once stabilised, discharge to first fit clinic
What is Alzheimers diisease
Most common form of dementia
WHat part of the brain does AD affect first
Hippocamppus
RF for AD
BIological:
- Age (1% at 60yo, doubles every 5 years)
- Genetics (although most gene mutations are sporadic)
- Head injury
- Vascular risk factors
Psychosocial:
- low IQ
-poor educational level
Four key pathophysiological elements of AD
- Cortical atropy
- plaque formation
- neurofibrillary tangle fpormation
- cholinerhgic loss
Four As in Alzheimers (features of middle progression of disease)
Amnesia
Aphasia (broca’’s - difficultuy finding the correct words)
Agnosia (usually visual - unable to recognie phases sso prosopagnosia)
Apraxia (unable tto complete skilled tasks such as dressing, despite normal motor function
+ mood change, abnormal behaviour, delusions and hallucinations
Management of AD
biosychosocial
BIO:
Anticholinesterases: aims to raise the ACh available
- donepezil
- galantamine
- rivastigmine
NMDA partial receptor agonist: Memantine
PSYCHOLOGICAL
structural group cognitive stimulation therapu
SOCIAL
explain diagnosis and signopost support
SINGLE CARE MANAGER
Every 6 month follow up
General: always wear ID, Dosset boxes, change gas to electricity, assistive technology around house.
Carers assessment etc
What must you do before giving anticholinesterases
ECG
side effects anticholinesterases
GI (N&V, diarrhoea, aanorexiia), fatigue, dizziness, headaches
Migraine tx
Acute: oral triptain + NSAID / paracetamol
Prophylaxis: topiramate / propanolol (only is >=2 attacks per month)
Mx cluster headache
Acute: 100% oxygen, SC triptain
Prophylaxis: verapamil
What is multiple sclerosis
autoimmune demyelinating disorder of CNS characterised by multiple plaques separate in time and place
Pathophys of MS
CD4 mediated destruction of oligodendrocytes > demyellination > neuronal death
Four types of MS
Relapsing remitting ( occasional flare causing worsening, otherwise stable)
Primary progressive (steady decline with no flares)
Secondary progressive (initial flares, then steady decline)
Progressive relapsing (steady decline with occasional flare)
MAARBURG VARIANT = very severe, very rapid
Symptoms of MS
Tingling
Eye (optic neuritis)
Ataxia (and other DANISH cerebellar signs)
Motor (spastic paresis)
What does optic neuritis present as
CRAP
Central scotoma
RAPD
Acuity drop
Pain on eye movement
What signs occur with MS
Lhemitte’s sgn (neck lflexion > electic shock in trunk and limbs)
Uhthoff0s sign (worsening of MS symptoms in increased temperatures)
Internuclear opthalmopledgia
What Ix are done with MS
Contrast MRI (gandolium enhanced, T2)
LP (IgG oligoclonal bands)
Blood antibodies
Evoked potnetials
What is acute and chronic management of MS
Acute attach: methylpred 1g IV/PO OD for 3 days
Chronic: DMARD (e.g. INF beta), biological (natalizumab) and SYMPTOMATIC MANAGEMENT
What meds can be given for symptomatic management of MS
Modafinil (fatigue)
SSRI (depression)
Amyltriptiline, gabapentine (pain)
Baclofen + gabapentine (spasticity)
oxybutynine ( urgency / freqwuency)
sildenafil (ED)
Clonazepam (tremor)
what blood antibodies would you find in MS
anti.MBP (myelin basic protein)
NMO-IgG (neuromyelitis optica)
what are good prognostic indicators in MS
female, young, sensory siigns at onsets, long interval in relapses, few MRI lesions
what are bad prognostic indicators in MS
male, older, motor signs at onset, short initerval in relapses, many MRI lesions, axonal loss
what is myasthenia graviis
autoimmune disorder characterised by insufficient functioning of acetylcoliine receptors
what is the most common antibody seen in MG
anti acetylcholine receptor antibody
what groups is MG most seen in
women:men=2:1
women typically in 20s, men in 60s
what are diseases associated with MG
thymic hyperplasia
thymoma
AI disease (PA. RhA, SLE)
what are signs and symptoms of MG
muscle fatiguabiliity - progressively weaker during periods of actvity and improviing after rest
- extraocular muscle weakness > diplopia, ptosis
- proximal myopathy (face, neck, limb girdle)
- dysphagia
what drugs exacerbate MG
penicillamines
lithium
phenytoin
What ix can you do for MG
single fibre EMG
repetitve nerve stimulation
serial pulmonary function tests
antibodies
TENSILON TEST
what iis management of MG
1st line symptomatic: long acting acetylcholinesterase inhibitors (pyridostigmine, neostigmine)
1sr line long term: immunupprssion (prednisolone, then azathioprinie)
final: thymectomy
what causes lambert eaton myasthenic syndrome
antibodies against presynaptic voltage gated calcium channel in peripheral nervous system
associated with SCLC, breast and ovarian canceer
what are symptoms of LEMS
- limb girlde weakness (affects lower limbs first)
- repeated muscle cpontractions may lead to increased muscle strngth
hyporeflexia
ANS sx
how do you manage LEMS
treat the cancer
immunosuppression with pred +- azathioprine
what is MND
umbrella term for debilitating chronic progressive diseases affecting MN
what are the four types of MND
Amylotrophic lateral sclerosis ALS
Primary lateral sclerosis
Progressive muscular atrophy
progressive bulbar palsu
what area of neuro system does ALS affect
corticospinal tracts
what are signs of ALS
mixed UMN and LMN
- inspection: wasting and fasciculations (incl tongue)
- tone: spastic
- power: weak
- reflexes: absent, +ve babinski
normal sensation!
what is MND management
MDT managhement (neurologist, physio, OT; dietician, GP, specialist nurse)
Meds:
- Riluzole (extends life by 3 months)
- SUPPORTIVE MX
what supportive MX can you consider for MND
Drooling - amyltriptiiiline, glycopyrolate
muscle cramps - quinine
spasticity - baclofen, botulinum
pain mx
NIV for respiratory failuyre
NG tube or PEG for dysphagia
HOW MUCH time off do bus drivers need to take followoing a seizure
10 years
how mych time off do you need to take following first / isolated seizure
6 months off if clear brain imaging, otherwise 1 year
how much time off if established epilepsy with multiple seizures
1 year off
left sided nystagmys means lesion is whre?
LEFT CEREBELLUM
what side do signs of a cerebellar lesiono present?
IPSILATERAL
is bacterial or viral meningitis moree common?
BACTERIAL men is more common!!
whaat is internuclear opthamoplegia due to
lesion in the medial longitudinal fasciculus in brainstem
whichh conncts CN6 to CN3 and 4
how does internuclear opthamoplegia pressent
weak adduction of IPSILATERAL eye
nystagmus of contralateral eye
what can caus internuclear opthamoplegia
MS
stroke
what is vertigo
sensation of movment between person and enviroonment
what is vertigo due to
sensory input mismatch (due to failure of vestibular system)
what territory is affected in facial weakness with forehead sparing on the left side?
Right (contralateral) MIDDLE CEREBRAL ARTERY stroke
what is a high stepping gait due to
LMN lesion (peripheral nerve lesion causing FOOT DROP)
what does high stepping / neuropathic gait look like
patient takes HIGH STEPS to bypass their foot drop
What is a STOMPING GAIT due to
sensory neuropathy (defect in proprioception)
what does a STOMPING GAIT look like
Patient takes HIGH STOMPING STEPS
to maximise their proprioception
What is an antalgic gait due to
due to pain on affected side
what does an ANTALGIC GAIT look like
limping
stance phase is relatively shorter than swing phase
what is a HEMIPLEGIC gait due to
STROKE or other UMN lesion
how does HEMIPLEGIC gait present
FLEXION HYPERTONIA in UL (flexed arms and wrist)
EXTENSOR HYPERTONIA in LL (circumduction of leg)
spasticity
distal weakness, central power retained > foot drop
why does hemiplegic patient have leg circumduction
due to EXTENSOR HYPERTONIA in LL and the foot drop
what is a diplegic gait due to
Cerebral palsy
Describe diplegic gait
tiptoe walking
foot adduction
what is another name for a waddling gait
trendlenburg gait
what is a waddling gait due to
defective hip abductor medhanisms (superior gluteal nerve damage / muscle abscess or inflammation, radiculopathy)
describe waddling gait
sound side sags – patient leans away from side of lesion as they walk
what is an ataxic gait also known as
cerebellar gait
what occurs in ataxic / cerebellar gait?
broad stance
wide staggering steps
sways at rest (titubatin)
sways towards side of lesion
explain the vestibular system
Semicircular canals contain endolymph fluid
With movement, the endolymph fluid moves around on the stereocilia (which detect the movement)
the vestibular nerve then takes these inputs into the cerebellum
What is the anatomical categories of conditions you can divide vertigo into
PERIPHERAL (vestibular system / vestibular nerve)
CENTRAL (cerebellum)
what are vestibular system causes of vertigo? list
- BPPV
- Menieres
- vestibular neuritis
What occurs in BPPV
cristals displace into semicircular canals > move with head movement > provoke NYSTAGMUS (accelerating towards affected side) and VERTIGO
what is classic BPPV presentation
positional vertigo
provoked by head movement
very brief (lasts seconds to minutes)
Hallpike maneuvre confirms it
What maneuvre confirms BPPV
Hallpike maneuvre
what maneuvre resolves BPPV
Epley maneuvre
What is pathophysiology of menieres
excess endolymph in canal
whar are 3 key symptoms of menieres
recurrent vertigo (starts spontaneously, stops after few hours)
unilateral tintinnus
unilateral sensorineural hearing loss
how do you manage meniere’s diease
histamines, benzos
intratympanic gentamycin (via grommet) if recurrent
what is vestibular neuritis
inflammation of vestibular nerve due to viral infection
lasts for weeks
how doess vestibular neuritis present
spontaneouss onset vertigo
constant
worsened by head movement
balance affected, risk of falls
what is illness course of vestibular neuritis
self resolves within weks
how do you maage vestibular neuritis
usually self resolving
may need to give chlorperazinr / cyclizine if nausea
what is GBS
Ascending polyneuropathy (radiculopathy) caused by demyelination post-infection / vaccine
How long before GBS and what infections precede it
HHV, HIV, campylobacter
1-3 weeks
What are sx of GBS
Progressive ASCENDING symmetrical limb weakness (lower then upper)
Progressive ASCENDING parasthesia
for 4 weeks, then recovery
in extreme cases; CN may be involved (dysarthhia, dysphagia, facial weakness)
Resp muscle involvement ( T2RF)
signs of GBS
LMN ascending signs
flaccid paralysis
areflexia
lack of sensation
ix of GBS
Bloods (incl anti ganglioside antibodies)
CT > LP (high protein)
MRI spine
NERVE CONDUCTION STUDIES (reduced velocity)
EMG
how do you manage GBS
admit for surveillance
support body cortical functions and ventilation if necessary
what are signs of a cerebellar lesion
DANISH D
Dysdiadocokinesia
Ataxia
Nystagmus
Intention tremor
Staccato speech
Hypotonia
Dysmetria
How are the cerebellar vs vestibular causes of nystagmus?
Cerebellar = Closee
- fast phase towards lesion
- maximal looking towards lesion
Vestibular cause (v= far away)
- fast phase AWAY from lesion
- Maximal looking away froom lesion
what are the MOTOR SX CLASS in MS?
UPPER MOTOR NEURON ONLY
what are the types of stroke according to Bamford
TACS - total anterior crc
PACS - partial anterior circ
POCS - poosterior circ stroke
LACS - lacunar anterior circ stroke
what is TACS
hemiparesis + hemisensory deficit
homonymous hemianopia
hgher cortical dysfunctiono (dysphagia, neglect, apraxia)
what is PACS
2/3 TACS
what is POCS
any of:
- cerebellar syndrome
- brainstem stroke
- homonymous hemianopia
what is brainstem stroke
locked in
what is Lacunar stroke
pure motor / pure sensory / mixed sensorymotosr / dysarthraia / clumsy hand / ataxic hemiparesis
when do you do thrombolysis AND thrombectomy in stroke?
when they present <4.5 hours from onset with OCCLUDED PROXIMAL ANTERIOR CIRC
what is imaging of choice for MS lesions
MRI with CONTRAST
How does a frontal lobe seizure present
JACKSONIAN march
How does a temporal lobe sseizure present
aura
lip smacking
clothes pucking
How does a occipital lobe seizure present
visual changes
How does a prietal lobe seizure present
sensory defect
side effects of valproatw
VALPROATE
Vomiting and naussea
Anorexia
Liver failure
Pancreatitis
Retention on weight
Oedema
Alopeca
Teratogenicity and tremors
Enzyme inhib
what is the progressison of AD
EARLY: failing memory, wandering, irritability
MIDDLE: four As
LATE: fully dependent, incontinent, primitive reflexes, EPSE
what is prosopagnosia
inabiity to recognise faces
typically occurs in AD
How does a tension headache present
bilateral headache, like a tight band
how do you mx a tension headache
aspirin
paracetamol
NSAID
How does a migraine present
unilateral, throbbing, severe headache
lasts 4-72 hours
may be precded by aura
better in dark and quiet
when do you give migraine prophylaxis
if 2 or more attacks per month
what do you give for migraine prophylaxs
Topiramate (NOT if childbearing age)
Propanolol
What do you givee for migraine mx
oral triptan + NSAID/paracetamol
how does a cluster headache present
intense pain around the eye
watering eye
occurs repeatedly (e.g. every day for 3 months
how do you manage cluster headache acutely
0xygen + SC triptan
how does temporal arteritiss prsent
headache
jaw claudication
tender scalp
how do you manage temporal arteitis
prednsolone
list 4 cause of non-dangerous headachr
tension headache
Clusster headache
migrainee
medication overuse
what kinds of signs can occur with MS
UMN
sensory
cerebellar
NEVER LMN
trigger for MS
EBV exposure
Northern countries
Low vit D
what is RAPD
Relative affeerent puipillary defect
pupil is more constricted when light is shone in contralateral eye compared to directly in it
where is the lesion in RAPD
in the optic nerve
what chromosome is NF1
chr 17
waht chromosome is NF2
Ch22
susmmarise NF1
- neurofibromas (neurocutaneeous)
- cafe au lait spots (>5, >15mm)
- Lisch nodules on iris (hamartomas)
frecking on skin folds
scoliosi s
intellectual disability
summarise NF2
bilateral vestibular schwannomas
meningioma
glioma
thereby presents with:
- sensorineural hearing loss
- tintinnus
- imbalance
- headache
- facial weakness
