neuro top tier Flashcards
what investigation can be done to assess type of stroke
what does this affect
CT stroke - allows you to see if haemorrhagic.
if not (=embolic) then lytic medicine given so embolus broken down and damage reduced. but if it is haemorrhagic, then lytic medicine should be avoided as this would increase the bleed
effect on ischaemia to broca’s area
expressive dysphasia (motor)
effect on ischaemia to wernicke’s area
receptive dysphasia (sensory) - misinterpret own speaking and you think it is wrong \+ can't understand other people's communication
is someone more likely to recover from a large ischaemic (embolic) or haemorrhagic stroke?
haemorrhagic
in haemorrhagic- the axons are disturbed (lenticular striate arteries cross internal capsule) but cell bodies are not affected- so necrosis. so as the haemorrhage resolves (With macrophages ), the pressure on axons decreases allowing recovery
with embolic blockage- there is necrosis of cell bodies. these are unable to regenerate and so are non-recoverable
in terms of the motor homunculus- which areas are supplied to which arteries (and so which areas would suffer from a stroke blockage in this artery)
anterior cerebral arteries = medial of cerebrum and homunculus
– lower limb
middle cerebral arteries = lateral of cerebrum
– upper limb and face
which is more common, embolic or haemorrhagic stroke?
85% embolic
15% haemorrhagic
which side of the brain is more likely to be affected by embolus from heart / carried in heart and why
right brain
R common carotid comes of before L from arch of aorta
name 3 significant causes of embolic stroke
1 heart failure (AF –> stasis –> embolus –> ejected when sinus rhythm returns)
2 blood pressure (stretches artery /longer –> turbulent blood flow –> clot embolus)
3 also kidney/lung/liver failure
what drugs may be given to AF patient for stroke prophylaxis
warfarin - prevent clot formation
where may a clot form with AF
in auricular appendage of atria in heart (Stasis of blood)
where does external carotid supply
dura
skull
face
neck
where does internal carotid supple
circle of willis
which vessels lie extradurally
meningeal arteries
which vessels lie subdurally
bridging veins
which vessels lie subarachnoidly
circle of willis
what symptoms is associated with a subarachnoid haemorrhage
thundeclap headache
what is the main cause of a subarachnoid haemorrhage
berry anerysrm in circle of willis
which haemorrhage type would cause dura to be pushed away from bone
extradural - meningeal
which groups are more suscpetible to subdural haemorrhage
elderly
children
alcoholics
they have brains smaller than their ckulls
epidemioloogy of migraines
common
f>m
<40y. most have 1st in adolescence
epidemiology of tension headaches
very common
f>m
epidemiology of cluster headaches
m>f
<40y
disabling
triggers for migraine
chocolate:
chocolate hangover orgasm cheese oral contraceptuve lie ins alcohol tumult exercise
triggers for tension headache
stress sleep deprivation bad posture hunger eyestrain anxiety noise
red flags for headaches patient
thunderclap headache seizure+ new headache red eye (gllaucoma) immunosuppressed prev malignancy recent trauma fever neck stiffness papilloedema - swollen optic discs
classification of headaches
Primary (migraine, cluster, tension)
Secondary (meningitis, subarachnoid haemorrhage, Giant cell arteritis, idiopathic intracranial HTN, medication overuse headache)
painful cranial neuroptahies, facial pains and othe headaches (trigeminal neuralgia)
pathophysiology of migraines
Changes in brainstem blood flow → unstable trigeminal nerve nucleus and nuclei in the basal thalamus → release of vasoactive peptides (CGRP and substance P)→ inflammation, vasodilation and plasma protein extravasation
migraine
severity
features
uni/bilateral
moderate to severe
aura disrupt daily activity naus/vom photo/phonophobia throbbing
unilateral
tension
severity
features
uni/bilateral
mild-modeate. continue with activities
squeezing/tightening
no naus/vom
none/one of phot/phonophobia
scalp tenderness
bilateral
cluster
severity
features
uni/bilateral
v/ severe
pain around eye/ temporal cranial autonomic features, ipsilateral --red eye --- lactimation --swollen lid -- facial flushing -- blocked nose -rhinnorhea agitated frequent but short may but nocturnal- wake u up
unilateral
rhinnorhea
= blocked nose
trigeminal neuralgia
uni/bilateral
features
unilateral
facial pain
severe
electric shock/shooting/stabbing
triggor= eating, talking
trigeminal neuralgia treatment
carbamazepine
non pharmocological headache management
lifestyle modification
trigger management
psychological and behaviour treatment
surgical treatment (rare)
migraine preventative treatment
B blocker- propanolol
acupuncutre
topiramate - anticonvulsant
botulinum toxin injections
Riboflavin (vit B2)
amitriptyline- tricyclic antidepressant
BAT BRA
migraine relief treatment
triptan (eg sumatriptan) + NSAID
antiemetics (naus/vom)
what should NOT be given to headache patients
opioids/ergots
tension headaches treatment
analgesics - aspirin, NSAIDs tricylci antidepressant (amitryptilline)
cluster headaches treatment for acute attack
triptan
- sumatriptan
- (zolmitriptan)
100% oxygen
cluster headache prevention treatment
verapamil (CCB)
corticosteroids
avoid alcohol
lithium
visual fortification spectra
visual patterns seen withiin aura of migraine
- zig zags
- lines
- flashing lights
non-visual aura experiences do exist – tingling, weakness, dysphasia
meningitis management that is not to do with patient
notify public health
how is neisseria meningitidis spread
droplet
glasgow coma scale
a measure of consciousness
eye/verbal/motor response
neonatal causes of menigitis
e coli
strep b
listeria
infant causes of menigitis
hemophilius influenzae b
neisseria menigitidis
strep pneumonia
adults causes of meningitis
neisseria meningitidis
strep pneumoniae
listeria if immunocompromised
name some complications of meningitis
death amputation scars (from rash) seizures hearing loss (from brain swelling) brain damage, neurological dysfunction
meningitis and encephalitis risk factors
immunosuppression
travel
name 2 causes of chronic meningitis
TB
syphillis
cryptococcal – fungus!
parasitic
what are non-infective causes of meningitis and encephalitis
cancer
drug side effects
autoimmune - vasculitis, SLE
what is different about the presentation of chronic menigitis (compared to acute)
triad = absent/ late
anorexia
menigitis triad
other symptoms
headache
stiff neck
fever
photophobia rash malaise, vomitting irritable wants to lie still papilloedema -- due to increased ICP -- usuaully bilateral
encephalitis symptoms
preceding
- flu like illness (headache, sore throat, myalgia, malaise, runny nose)
then: - fever altered GCS - seizures - memory loss - headache
+/- meningism
kernigs sign
resistnace to extension of the leg while hip flexed (thigh at 90 degrees and calf straightened)
sign of menigism
- specific but not sensitive
brudzinki’s sign
neck in lifted (flexion) and there is reflex flexion of hips and knees in response (in order to relieve meninges discomfort)
sign of menigism
- specific but not sensitive
CSF biochemistry results for menigitis
bacteru, TB, cryptococcus (fungus):
- HIGH in protein and LOW in glucose
virus:
- HIGH in protein and NORMAL in glucose
(virus does not use glucose in order to replicate whereas the others do)
antibiotic treatment for bacterial meningitis
most = cefotaxime and ceftriaxone (3rd gen cephlosporin)
listeria = amoxycillin
non antibiotic treatment for menigitis
steroids - IV dexamethosone –> reduces brain swelling
call public health
treatment for encephalitis
mainly supportive
- fluid/nutrients
- protect, keep on wards
- painkillers
- physio and neuro rehab
antiobiotics for potential menigitis
if herpes simplex virus or varicella zoster virus –> ACICLOVIR
when is aciclovir given to encephalitis
if the cause is herpes simplex virus or varicella-zoster virus
which prophylactic antibiotics are given to close contacts of meningitis
ciprofloxacin
rifampicin
what might GP have to get meningitis started on treatment asap
IM benzylpenicillin (long shelf life)
varicella zoster virus – shingles
- cause
- preeruptive
- eruptive phase
- investigation
- treatment
varicella zoster virus reactivated after lying dormant in the sensory nervous system. when flares up, travels down affected nerve
no skin lesion. but burning and itching in one dermatome
eruption 2 days later: skin lesions appear
- red, swellen plaques. rash within dermatome. these lesions are infectious
sample fluid –> culture. + history and symptoms
oral aciclovir
watershed stroke
due to low BP -low cerebral blood flow
vulnerable areas of brain at the water shed area between arterial territories are the first to be deficient in perfusion lead to infarcts
what is obstructive hydrocephalus
complication…
Blood (haemorrhagic stroke), pus (meningitis) or mass (tumour) around the brainstem/cerebellum - squashes /covers 4th ventricle and exiting foramen
…. raise ICP!!!
long term stroke treatment
clopidogrel (antiplatelet)
secondary prevention –
statin,
warfarin (if AF)
antihypertensives
haemorrhagic stroke treatment
monitor GCS
reverse any anticoagulants (vit k for warfarin)
control hypertesnion
manual and medical decompression of high ICP (diuretics, raise head etc)
how do you reverse warfarin
vitamin K)
contraindication for thrombolysis for ischaemic stroke. name 5
1 Recent surgery (3m) 2 Recent arterial puncture 3 History of active malignancy 4 Brain ansyursm 5 Patient is on anticoagulation 6 Severe liver disease 7. Acute pancreatitis 8 Clotting disorder 9 If time of onset not unknown. Don't give thrombolysis -- give aspirin for 2w than clopidogrel after
ischaemic stroke treatment
thrombolysis tissues plasminogen activator = ALTEPLASE antiplatelet therapy = CLOPIDOGREL/ASPIRIN
general stroke supportice treatment
oxygen
hydration inc glucose
CHADVASC=
calculates risk of stroke for patients with AF
ABCD score
calculates risk of stroke for TIA patients
age diabetes high BP clinical features (of TIA/stroke) duration (longer than 1h = 2 points, less =1)
calculates risk of stroke for TIA patients
ABCD score
calculates risk of stroke for patients with AF
CHADVASC=
stroke investigation
** CT/MRI head – see if haemorrhagic or ischemic (ischaemi = less dense)
look for AF - pulse, BP, ECG
look for thrombocytopenia/polycythaemia (highrbc) – FBC
look for hypoglycaemia – serum glucose
can also do doppler ultrasound of carotid
lenticulostriate artery haemorrhagic stroke
- these are small vessels off the anterior cerebral artery that supply mid brain, and cross internal capsule
- theyre prone to rupture due to thin adventitia
- this disturbs all motor and sensory axons - cant transmit (internal capsule)
- but the cellbodies are not affected so there is no necrosis. this means there is the possibility of recovery as pressure on axons decreases
amaurosis fugax
transient visual distubrance - sudden temporary sight loss in one or both eyes. painless (stroke/TIA)
Due to atherosclerosis / thromboembolism in Internal carotid artery Ophthalmic artery Retinal artery -leading to temporary retinal hypoxia
symptoms of PCA stroke
Visual issues - peripheral vision, face recognition, colour naming, can’t interpret what they can see, cortical blindness
Headache
–Rare in ischaemic stroke! Think PCA!
symptoms of MCA stroke
upper limb and face
face droop
hemianopia
if L stroke:
brocas (expressive dysphasia)
wernickes (receptive dysphasia + cant understand others)
symptoms of ACA
lower limb -- gait incontinence drowsiness decrease in spontaneous speech and movement
why is necrosis of cell bodies in stroke so bad?
no regeneration of these – non-recoverable
internal and external carotid supply where?
internal –> brain
external –> head and neck except for brain (neck, dura, skull, face)
causes of hemorrhagic stroke
Trauma
Aneurysm rupture
Thrombolysis, Anticoagulation
Carotid artery dissection
how does high blood pressure contribute to stroke
Blood pressure → stretches artery → longer → turbulent blood flow → clot → emboli
causes of ischaemic stroke
thromboembolism:
AF (stasis) infective endocarditis valve disease mural thrombosis from the damaged ventricle hypoperfusion fat emboli after a long bone fracture
venous sinus thrombosis
liver/lung/kidney failure
where is clot likely to go after leaving the heart
arch of aorta –> brachiocephalic –> R common carotid (R brain)
risk factors for stroke, name 5
1 Age ---Increases with age --Uncommon under 40 2 Race --Asian --Black African 3 Hypertension 4 Past TIA 5 Family history 6 Smoking 7 obesity 8 Diabetes 9 Alcohol 10 Heart disease (AF, valvular, infective endocarditis) 11 Blood clotting disorders (thrombophilia, polycythemia (high RBC)) --Combined pill 12 Hypercholesterolemia
are embolic or hemorrhagic strokes more common
85% embolic
15% hemorrhagic
male or female more likely for strokes
and what age group
and what ethnicities
male
older
Asian, black African
what blood vessels are between: skull and dura dura and arachnoid arachnoid and pia pia and brain
skull and dura – meningeal vessels
dura and arachnoid – bridging veins
arachnoid and pia – the circle of Willis
pia and brain – no veins. pia forms part of the blood-brain barrier, cannot separate
complication of TIA
stroke!
assess with ABCD score
what in your liefstyle is adjusted after TIA
no driving for 4w smoking weight activity alcohol
pharm treatment for TIA
antiplatelet -ASPIRIN (or clopidogrel) statins long term anticoagulant if AF (warfarin0 control diabetes control CV with antihypertensives
TIA investigations
hisotyr can be diagnostic Bloods --FBC - polycythemia --ESR- raised in vasculitis --Glucose - hypoglycaemia --Creatinine --Electrolytes --Cholesterol Doppler US/MRI/CT angiography - look for stenosis + determine extent ECG/ echo/ Cardiac monitoring - AF, MI , other heart problems
TIA symptoms sudden or gradual
sudden
are more TIAs anterior or posterior circulation
and what vessels do each refer to
90% anterior circ
– carotid artery
10% posterior circ
– vertebrobasilar artery
anterior circ TIA symptoms
- amauris fugax
- aphasia (production /comprehension of speech- brocas/wernickes)
- hemiparesis (unilateral weakenss)
- hemisensory loss
posterior circ TIA symptoms
- diplopia (double vision)
- vertigo
- vomitting
- choking, dysarthia (speech -muscular)
- ataxia
- hemisensory loss
- hemianopia
- tetraparesis (muscle weakness in all 4 extremeties)
- transient confusion
what is pathophysiological diff between stroke and TIA
TIA ischaemia is short lived WITHOUT infarction so it resolves before irreversible cell death
TIA- small vessel occlusion
TIA causes
Microemboli
- From carotid
- Cardiac embolus (IE, AF, valve issue)
Hyperviscosity
- Polycythaemia
- Sickle cell anaemia
- V raised wbc
- Meyloma
Hypoperfusion
- Esp young people
- Postural hypertension
- Atherosclerosis - reduced flow
- Cardiac dysrhythmia
risk factors of TIA. name 5
1. age 2 gender - m>f 3 race: black = :/ 4 CV - hypertension, heart disease, PAD 5 past TIA 6 combined pill 7 alcohol 8 hyperlipidaemia 9 diabetes 10 blood - raised packed cell volume, clotting disorder, polycythaemia
2 complications of epilepsy
status epilepticus = continuous seizure without recoevery of conciousness
- emergency!! risk CV/resp failure
- causes : alcohol abuse, anti-epileptic therapy poor compliance inc abrupt cessation
sudden unexpected death
- more common if nocturnal and if uncontrolled epilepsy
treatment of epilepsy - pharmacological
anti-epileptics
- carbamazepine
- lamotrigine
- sodium valproate (not if preggers)
surgical epilepsy treatment
remove part of brain
implant electrical device to control seizure - vagus nerve/ deep brain stimulation
epilepsy investigations
Diagnosis = 2 or more seizures, 24h+ apart
–Video telemetry
EEG
- -Electrical impulses in brian measured to detect unusual activity (even when not having stroke)
- -Not diagnostic, supports diagnosis
- -May help determine type of seizure
Image brain - CT/MRI/PET
- -Check for bleeds/ underlying cause/ lesions (tumour) / rule out differentials
- -Image hippocampus
Neural examination(behaviours, skills, functionS)
Bloods
- FBC, electrolytes, renal/liver function
- -Discover comorbidities
- -Rule out infection/metabolic causes
- -Genetic conditions associated with epilepsy
ECG
what does prodrome mean
change in modd/behavious
hour/days before epileptic seizure
how long does epileptic seizure last
30s - 2min
what does postictally mean? give charactheristics too
this is the state after a epileptic seizure
- headache, sore tongue, myalgia, confusion, weakness, dysphasia
Generalised tonic-clonic seizure (grand mal)
No aura
Loss of consciousness
Tonic phase = rigid, stiff (may fall)
Clonic phase = generalised bilateral rhythmic muscle jerking
Second-minutes
Maybe incontinence
Followed by drowsiness, confusion, coma (postically)
this is a primarily generalised type
Typical absence seizure (petit mal)
Usually childhood
Cease activity and stare pale (eg stop talking mid sentence)
Few seconds
Unaware of attack
May go on to develop generalised tonic-clonic seizures as an adult
this is a primarily generalised type
myoclonic seizure
sudden isolated jerk (limb, face trunk) (inc fall)
this is a primarily generalised type
tonic seizure
sudden body stiff (tonic) but not followed by jerking
atonic seizure
sudden loss of tone (floppy ) –> fall
Simple partial seizure
Not affecting consciousness / memory. With awareness
Temporal lobe - deja vu, fear, olfactory, auditory and gustatory hallucinations
Occipital lobe - auras
Frontal lobe - conjugate gaze (eyes not working together), jacksonian march (spread of seizure along motor homunculus starting in face / thumb)
partial/focal type
Complex partial seizure
inc features, where
Impaired awareness (before, during or after)
Commonly temporal lobe - automatisms eg rubbing hands, smacking lips, chewing, fiddling
Less commonly frontal lobe - peddling legs
Often preceded by auras
Postictal confusion
partial/focal type
Partial seizure with secondary generlisation
Often, electrical disturbance starts focally spreads wider, causing secondary generalised seizure - typically convulsive
primarily generalised vs partial/focal seizures
generliased= electrical discharge throughout whole cortex, both sides –> bilateral manifestations
associated with loss of conciousness/awareness
focal = electrical discharge limited to one part of one hemisphere so focal onset with features referable to one part of one hemisphere
how does syncope differ from epilepsy
Hypoperfusion to brain
Lasts shorter - typically <30s
Rarely occurs in sleep. much more likely when standing
Pre-syncope symptoms = nausea, sweating, seeing stars, noises distorted, dizzy, light-headed
May also have limb jerks, eye closed
how does non epileptic seizure NES differ from epilepsy
Gradual onset Longer duration - 1-20min Associated with Trigger. Protective Eyes closed Crying + speaking History of psychiatric illness
name 5 epilepsy risk facotrs
1 family history 2 premature babies + small for age 3 childhood febreile convulsion 4 abnormal brain blood vessels 5 alzeimers/dementia 6 trauma 7stroke /TIA 8 drugs- cocaine 9 alcohol withdrawal
epilepsy age for onset=
most = before 20 or after 60
complications of PD
- psychiatric – depression, anxiety, phobias
- dementia
- -autonomic problems - constipation, increased urinary frequency
- drugs wear off - painful dystonic posturing + loss of mobility
surgical treatment of PD
ablation of overactive basal ganglia
non pharmacological PD treatment
physiotherpay
- balance and speech and gait disturbance do not respons to medication !
gold standard PD treatment
- what is it
- what else is given
- effect
- over time?
L dopa = levodopa = dopamine precursor (dopamine cannot cross blood brain barrier)
given alongside decarboxylase inhibitor(co- beneldopa, co-careldopa, carbidopa) – to stop peripheral conversion of L dopa to dopamine (maximise amount that enters brain)
symptom releif. no help with disease progression
effect decreases over time (5-10y)
why is dopamine not given for PD
dopamine cannot cross blood brain barrier)
what is given instead of L dopa and why
L dopa saved for late on as effect decreases. instead…
dopamine agonist (ropinrole)
MAO-B (-giline) / COMT (-capone) inhibitors - enzyme inhibiterer prevent dopamine breakdown so active for longer
anticholinergics (amantadine)- treat tremor
L dopa s/e
name 3
dyskinesia, painful dystonia, psychosis, hallucinations, nausea, vom, a rrhythmias
PD investigation
observe cardinal signs
imaging (cT/MRI/PET) - see substantia nigra atrophy and rule out other things eg tumour
confirm with levodopa response
3 cardinal PD signs
BRADYKINESIA/ AKENISA Slow movement Low amplitude on repetition Deteriorated walking- foot drag, slower hands, smaller writing, expressionless face, soft indistinct speech, reduced blink rate, reduced gait arm swing Difficulty with buttons Difficulty swallowing is a late feature
RESTING TREMOR At rest. Improved by voluntary movements Unilateral/asymmetrical ‘Pill-rolling’- thumb over fingers Made worse by anxiety Made worse by repetitive hand movements
RIGIDITY (HYPERTONIA) Pain Reduced mobility Resists movement throughout the movement (unlike UMN lesion where resistance falls away as the movement continues (clasp knife) - spasticity) Characteristic stoop
before motor symtpoms develop for PD …
Anosmia (smell) Depression /anxiety Aches, pains REM sleep disorders Urinary urgency Hypotension Constipation
HOW do the triad of PD signs present
gradual onset
unilateral -worse on one side
often mild presentation at beginning (reduced dexterity- difficulty with buttons/ unilateral foot drop / depression)
pathophysiology of PD
Neurodegenerative loss of dopamine-secreting cells (dopaminergic neurons) from the substantia nigra (substantia nigra produces dopamine)
- -So less striatal dopamine levels
- -So thalamus inhibited
- -So decreased of movement
Causes oF PD
enviromental (pesticides, MPTP in illegal opiates) and genetic (parkin gene, alpha synuclein gene)
results from oxidative stress and mitochondrial dysfunction
accumulation of what in PD
There is an Abnormal accumulation of lewy bodies (contains protein aggregates. alpha-synuclein bound to ubiquitin) in cytoplasm
These become more widespread as the condition progresses (lower brainstem → midbrain → cortex)
cerebellar ataxia (cerebellar atrophy)
Clumsy
Intention tremor
Broad based gait
generalised dystonia
=sustained muscle contraction
Onset in childhood, family history
No cell death
Twisting, repetitive movement, abnormal posture
essential tremor
- pathology
- commonness
- features
- treatment
No pathology – benign
Common
Action tremor- worse on movement, rare at rest
treatment
- B blockers (Unless asthmatic/diabetes)
- Antiepileptic treatment
name 5 risk factors for PD
1 Age 2 Male 3 Family history - Parkin gene - Alpha synuclein gene 4 NON smoker 5 Environmental factors - Pesticides - MPTP , in illegal opiates
how long does it take kernig sign to develop in sub arach haemor
6h
diplopia =
double vision
hydrocephalus
=?
complication of?
blockage of arachnoid granulations (where CSF drains into venous system)
Need drainage
SAH
name 5 SAH complications
CVA cerebrovascular accident = stroke Raised ICP Rebleed Cerebral ischemia may results in permanent deficit (common morbidity) Seizures Hyponatraemia Hydrocephalus
SAH surgical treatments
endovascular coiling = best (promotes thrombosis and ablation of aneurysm)
clipping (leaving collapsed sac)
stenting
SAH medical treatmebts
maintain cerebral perfusion (BP, IV fluids- replace salt)
CCB (nimodipine) - reduce vasospasm so reduce risk of cerebral ischaemia
corticosteroid (dexamethasone) to reduce inflammation if cerebral oedema
what do you do when there is cerebral oedema
corticosteroid (dexamethasone) - reduces inflammation and presh
SAH investigation
CT - gold standard
- star shaped lesion
- CT angiography to see extent of anyeursm if confirmed
ABG- exclude hypoxia
Lumbar puncture (if cT normal) - bloody early on then yellow (xanthochromia - degradation products) later on
SAH symptoms
often asymptomatic until rupture. may have ‘warning headaches’ (sentinel headaches) days before due to small leak from aneurism - sudden intense, persistent
thunderclap headache
- sudden
- severe
- ussualy at back- occipital
nausea seizure collapse coma, drowsy, lower level of conciousness vision loss/diplopia
SAH signs
neck stiffness - kernig and brudsinkis signs
papiloedema (swollen /dilated optic disc)
marked increase in bP (reflex)
retinal/subhyaloid/vitresou bleeds (eye ) - terson’s syndrome - increased mortality
how to differentiate migraine from SAH
SAH has neck stiffness usually
causes of SAH
spontaneous bleeding - no trauma
mainly due to berry aneurism(s) (at branching point of circle of willis)
congential arteriovenous malformation rupture
encephalitis vasculitis tumour bleeding disorder acute meningitis
risk factors of SAH
Smoking Alcohol misuse Increased BP Bleeding disorders Family history known anyerusm .. .... increased risk of anyeyrsm if - ehlers danlos syndrome - aortic coactation - kidney disease
what proportion of strokes are SAH
5%
age most common for SAH
35-65
complication of subdural haem
coning/hernia of cerbrum
- this then compresses brainstem –> coma
subdrual haem management
stabilise patient
surgery – burr hole craniotomy (irrigation, draingage, decompress)
mannitol IV - reduced ICP
addresss cause of trauma
subdural haem inv
CT
- crescent shaped blood over 1 hemisphere
- midline features are shifter
- MRI good for subacute/smaller hematomas
symtpoms/signs of subdural haem
name 6
May have large interval between injury and symptoms
- Headache
- Drowsy, sleepy
- Confusion
- Loss of consciousness
- Naus, vom
- Raised ICP
- Seizures
- Personality change
- Unsteadiness
- Focal sensory loss
- Unequal pupils
where is the rupture in subdural haem
then what
bridging veins
– these run subdurally from hemisphere to feed into saggital sinus (in dura)
bleed–> hematoma
increase in oncotic/osmotic pressure so water is sucked out of blood vessels into the hematoma
ICP rises gradually
risk factors/causes for subdural haem
when brain smaller than skull, bridging veins are more vulnerable
- children
- elderly
- alcholics
- dementia
trauma
– minor : falls
may be months after the incident!
anticoagulation
dural metastases
DM
extradural management
stabilise - ventilation
surgical drainage, decompression, ligation, clot removal
mannitol IV- reduces ICP
extradural inv
CT
- convex lens (lemon)
hyperdense
midline shift away from bleed
Xray
- fracture lines crossing meningeal artery course
extradural presentation
Unconscious
Lucid recovery for few days = typical of extradural
Rapid deterioration-- Loss of consciousness (GCS) Focal neurological signs Severe headaches vomiting Confusion Seizures hemiparesis
most common age for extradural haemor
young adults
causes of extradural haemor
trauma - fractured skull - temporal /parietal bone
due to any tear in dural venous sinus
what does the term positive ictal symptoms mean?
feeling things that are not there
eg hallucination, feeling things etc
spastic =
continual contraction of muscles
MS age?
young
20-40y
MS gender?
f>m (as other autoimmune)
- and hits f sooner
except primary progressive MS is m>f
MS pathophysiology
T cell mediated (autoimmune) :T cells activate B cells to produce antibody against myelin. So demyelination at multiple sites (+ loss of oligodendrocytes)
Affects white matter (axons). This disrupts conduction. Sclerosis along neurones → slowed/blocked conduction → impaired movement / sensation
Myelin sheath regenerates but new myelin is less efficient and is much worse in high heat
- -This healing is what is observed with remissions
- -This is why heat exacerbates it (Uhthoff’s phenomenon)
Especially at : perivenular sites (around vein /ventricle )
- -Optic nerves (optic neuritis)
- -Corpus callosum
- -Brainstem
- -Spinal cord
types of MS
Benign
- Few relapses
- Little disability
Relapsing and remitting
- -Most common
- -Onset = days (sudden). Recovery (partial/fully) = weeks
Secondary progressive MS
- -Follows on from relapsing and remitting, normally after 35 years - late stage MS
- -Gradually worsening symptoms with fewer remissions
Primary progressive MS
- -Gradually worsening disability without relapses or remission
- -Typically presents later
- -Associated with fewer inflammatory changes on MRI
Lhermitte’s sign
tingling (electric shock) down back into limb on the flex of the neck (head forward)
seen in MS
Uhthoff’s sign
symptoms worse after heat
seen in MS
in what way do MS symptoms present
Initially monosymptomatic
Progressive disability
Symptoms worsen with
- Heat (= Uhthoff’s phenomenon)
- Exercise
Symptoms relapse and remit
3 broad presentations of MS
SPINAL CORD (weak, spastic, stiff, reduced movement, tingly/numb/painful, tremor)
OPTIC NEURITIS (pain on eye movement and reduced central vision blurred)
BRAINSTEM DEMYELINATION (diplopia, vertigo, facial numbness/weakness, dysarthria, dysphagia, nystagmus, clumsy)
spinal cord MS symptoms
weakness (motor)
- -Often leg
- -Spasticity (continual contraction) → stiffness/tightness
- -Movement / function impaired eg speech slurred, gait
- Intention tremor
numbness/ tingling (Sensory) / pain
–Often limbs
optic neuritis
Plaques collect around optic nerve in MS
- -Pain in eye on movement
- -Reduced central vision- blurred
brainstem demyelination in MS (symptoms)
Diplopia Vertigo Facial numbness/weakness Dysarthria Dysphasia Nystagmus Brainstem or spinal tract plaque -- Clumsy / poor proprioception
other MS symptoms (other than spinal cord, optic or brainstem)
- cerebellar – ataxia
- constipation
- amnesia
- cognitive decline
- brown sequard
- sexual dysfunction (erectile dysfunction)
- bladder dysfunction (LUTS)
diagnosis of MS critera
requires 2 or more attack affecting different parts of CNS
MS investigations (4)
bloods to exclude differentials
MRI brain +spinal cord
- looking for periventricular plaques /lesions /white matter abnormalities
- exclude other things eg spinal compression
lumbar puncture = raised cell count and oligoclonal IgG bands on electrophoresis (not in serum) suggesting CNS inflammation (but this is not specific)
electrophysiology - delayed nerve conduction
MS lifestyle management
Reduce stress Stop smoking Vit D/ sun exposure Avoid triggers Avoid infections Regular exercise Physiotherapy inc speech and language Occupational therapy education
MS treatment for acute relapse
IV methylprednisolone
Used during relapse. Shortens relapse
Try to use infrequently
MS treatment: disease modifying therapies for aggressive MS
SC inferon IB/IA (anti-inflammatory cytokines)
Monoclonal antibodies
- Alemtuzumab (targets T cells)
- Natalizumab (reduces number of immune cells that cross the blood brain barrier so less damage in CNS. and increases the activity of T regulator/suppressor cells)
- Dimethyl fumarate
these reduce number of relapses so are good for frequent relapse patients
stem cell transplant
symptoms relief for MS
Antispasticity = Baclofen (GABA analogue) or gabapentin or tizanidine
Neuropathic pain = Gabapentin (blocks GABA breakdown)
Tremor = Botox (botulinum injections (reduce ACh in neuromuscular junction)
– Transient effect
LUTS
urgency/frequency
—Self catheterisation
—-Tolterodine (anticholinergic)
Incontinence
Doxazosin (Alpha blocker)
MS complications
disease progresses - more areas of disease with reduced function
reduced life expectancy 5-10y (dysphagia, pneumonia)
GU - overactive bladder, incomplete emptying
race relation to MS
more common in white
more risk if further from equator (Esp if higher eg uk, usa)
how is MS related to virus
If CNS share epitope to virus then , T lymphocytes attack (and B cells –> antibodies)
what is MND prognosis
very poor. most die within 3 y from respiratory failure
treatment for MND symptoms
palliative care
Drooling - amitriptyline (tricyclic antidepressant) or propantheline (anti-muscarinic)
Spasticity - baclofen (GABA agonist)
Joint pain - analgesia
respiratory failure - non-invasive ventilator and feeding tube
Dysphasia - blend food/ NG feeding tube
Speech : physiotherapy
Occupational therapy
MND disease-altering treatment
Riluzole
Sodium channel blocker → Inhibits glutamate release (anti-glutaminergic)
Prolongs life by a few months
MND investigations
clinical mainly -UMN/LMN signs
EMG- electromyography : denervation of muscles due to degeneration of LMN
NCS - nerve conduction studies
Exclude other diagnoses
- – Lumbar puncture - excludes inflammatory causes
- –MRI - excludes structural causes
umn/lmn signs
UMN -- everything upped increased muscle tone --> spasticity hyper-reflexes increased plantar (minimal muscle atrophy ) positive babinksi sign(big toe goes up rather than down when sole is stroked)
LMN - everything lowered! muscle atrophy (wasting) hypo- reflexia reduced muscle tone --> flaccid fasciculation (brief spontaneous contraction) negative babinski sign
what is definite / probable/ possible/suspected MND
Definite = LMN+UMN in 3 regions
Probable = LMN +UMN in 2 regions
Possible = LMN + UMN in 1 region
Suspected = LMN or UMN in 1 region
UMN presentation
No sensory loss
No sphincter disturbance
No eye movements affected
muscular atrophy (weakness and wasting) and spasticity (increased tone, stiffness)
- reduced dexterity
- stumbling spastic gait
- foot/wrist drop
- speech (slurred, hoarse, nasal) /swallowing disturbed (choking) (bulbar palsy)
- fasciculation
- dementia
what distinguishes MND from differential diagnosis
No sensory loss
No sphincter disturbance
No eye movements affected
—These distinguish from MS and polyneuropathies. Myasthenia gravis : eye movements are affected
MRI to rule out structural causes
lumbar puncture to rule out infective causes
types of MND
- which is most common and most rare
- do they affect LMN/UMN
- particular features of the type
amyotophic lateral sclerosis (ALS)
- most common
- UMN and LMN (loss of motor neurones in motor cortex and anterior horn)
progressive bulbar and pseudobulbar palsy
- LMN
- affects CN9-12 only so involved in dysarthria, dysphagia (inc choking), nasal regurgitation of fluids and fasciculating tongue, jaw
progressive muscular atrophy
- LMN only (anterior horn lesion)
- affects distal groups before proximal
- starts in one place and gradually affects more
primary lateral sclerosis
- rare
- UMN only (loss of Betz cells in motor cortex)
- affects groups of muscles rather than individual muscles
- no cognitive decline
- Upper limb - flexors > extensors
- Lower limb - extensors> flexors
UMN pathophysiology
Destruction of upper motor neurons (namely motor cortex) and anterior horn cells (this is where LMN are) in the CNS and motor cranial nerve nuclei (also LMN)
Causes LMN and UMN dysfunction → mixed picture of muscular paralysis
motor only!!
MND epidemiology
- gender?
- common?
- age?
- genetic?
m>f
uncommon
60 - middle aged
there is a familial link
pyramidal pattern of weakness
characteristic pattern of
limb muscle weakness in UMN pathology
Upper limb
- flexors > extensors
- proximal > distal
Lower limb
- extensors> flexors
- distal >proximal
parkinsons disease vs parkinsonism
parkinsonism = drug induced movement disorder, non-progressive
parkinsons disease = neurodegenerative disease (not drug induced)
what is co-careldopa?
carbidopa (prevent premature breakdown of levodopa) and levodopa (dopamine precursor)
PD first line treatment
What score of CHADVASC is significant and what does this mean
risk of stroke if AF
2 + —> anticoagulant
MND speed of onset
gradual
