neuro vol 2 Flashcards

1
Q

discuss extra dural haematoma

A

an acute haemorrhage between the dura mater and the inner surface of the skull.

most commonly affects males in 20s-30s- being struck in the temple

caused by skull trauma in the temporoparietal region, typically following a fall, assault or sporting injury.

symptoms = headache, nausea/vomiting, confusion and reduced level of consciousness.

signs= confusion, cranial nerve deficits, motor or sensory deficits

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2
Q

disease cause of extra dural haematoma + Ix appearances + Rx of disease

A

associated with skull fracture in 75% of cases.

Middle meningeal artery damaged from trauma on pterion

loss of consciousness–> then lucid phase where feel fine. –> then drop off a cliff

Cushing’s syndrome is present- HTN, bradycardia,

Ix:
as with any head trauma with loss of consiousness - CT non contrast.
looks like a lemon- stays within suture lines.

ECG, FBC + coag etc.

Rx:
reversal of anticoagulation
anticonvulsants to prevent seizures
trauma/ burr hole craniectomy

generally a good prognosis but better if treated early.

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3
Q

discuss head trauma and management of this including coma

A

manage ABC

if GCS less than 8 then contact anesthetics and intubate.
once stabilised get CT <1 hr if:
gcs <13 or 15 2 hrs later
focal neuro deficit
suspected skull # (panda eyes etc)
csf leak
vom >1 x
seziure

ct < 8 hr if
LOC/ amnesia
over 65, coagulopathy, high impact fall >1m or 5 stairs.. retrograde amnesia >30 mins.

don’t consider alcohol incapacitation if blood conc less than 44mmol/L.

many people will live for a long time even if consciousness loss is greater than 1 month.

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4
Q

discuss multiple sclerosis diagnostic criteria

A

Mcdonald diagnostic criteria:
defined by at least 2 separate episodes of / clinical evidence of 2 lesions OR clinical evidence of 1 lesion + reasonable history of another.

Or two or more attacks + evidence of 1 lesion

Or one attack + evidence of 2 or more lesions

peripheral nerves are not affected
can be relapsing remitting or progressive, or combination. (preg is protective against relapses)

one episode does not count

onset after puberty or before 65

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5
Q

risk factors for MS + epidemiology

A

Older age
EBV contracted at later age
Smoking
Vit D deficiency
Family Hx
Northern latitude

epidemiology:
3x more common in women
20-40 years old.
distance from the equator during pre adult years.

some genetic factors- HLA-DRB1
some environmental factors

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6
Q

pathophysiology of MS

A

an autoimmune reaction against myelin and oligodendrocites.

normally macrophages don’t cross blood brain barrier- but in MS they express a4b1 which enables adherence and movement through.

myelin is broken down- conduction slowing/ block

more commonly seen in:
Optic nerves
Periventricular region
Corpus callosum
Brainstem and cerebellar connections
Cervical spinal cord => posterior and corticospinal tracts
Ventricles/ fluid filled spaces => called Dawson’s finger

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7
Q

investigations and management of MS

A

Ix; full history
neuro exam- inc RAPD/ pupillary reflexes
MRI is imaging of choice brain + spine
LP for CSF evaluation (normal in 20-30%)

Mx;
acute flare- rule out any co cominant infection
high dose methylprednisolone with oral taper

chronic Rx:
interferon beta e.g glatiramer- supress T cell actions leading to reduce flares.

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8
Q

classification of headaches and the red flags for these

A

primary- occurring without physiological cause - usually not serious.
2’- s a consequence of some other pathology- usually serious

Red flags:
new onset in over 50
hx cancer or immuno def
thunderclap features or sudden onset
history of aneurysm.
Raised ICP features (inc on lying down, worse in morning)
GCS/ any neuro signs
meningism
fever

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9
Q

discuss migraines

A

an episodic neuro disorder- strong genetic components. 4-72 hour duration usually.

S- unilateral
O- slow onset
C- pulse/ throbbing
R- back of head retro orbital
A- photophobia, phonophobia N + V
T- hours- days
E- fatigue, hangover, travel
S- severe 8-9/10

Mx- avoid triggers + healthy lifestyle
high dose NSAIDS 1st, then - tryptans.
high flow o2 in emergency dept.

Generally a clinical diagnosis but can rule out other things. painful dilation of arteries in the brain.

should not take the combines oral contraceptive pill if have migraines with aura.

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10
Q

discuss cluster headaches

A

S- unilateral centered around one eye
O- fast and repeated - 1 hour
C- intense stabbing pain
R- no
A- red eye, lacrimation, blocked nose.
T- 1 hour duration but up to 8 a day. can last weeks with months gaps.
E- alcohol
S- really very bad.

100% 02 15L. sub cut sumatriptan, pred at start of cluster to stop.
vermapil to prevent.

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11
Q

trigeminal neuralgia

A

S- unilateral V2-3 distribution
O- sudden
C- stabbing
R- V2-3 dist
A- N/A
T- many times a day for weeks / months then stops
E- touching face (wash, shave)
S- short but painful.

Ix:
MRI usually identifies vascular loop touching V5

more common in women than men. rare in under 40s.

Rx; carbamazepine + referral to neuro if not working.

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12
Q

tension headache

A

most common type of primary headache
occurs repetitively.

aetiology not fully understood- stress, muscle tension, vitamin (D, B12),

last 30 mins to 7 days, 6 hours average.

bilateral with band like quality across forehead.

does not worsen with activity, photophobia usually not present. no N+V. can usually go about most duties.

need 10 episodes for diagnosis- clinical so imaging not needed.

chronic if >15 a month for >3 month.
infrequent if <12 days a year
frequent if between.

NSAIDs mainstay of treatment. ibuprofen + aceaminophen.
can use amytriptaline
Physio!

usually a good prognosis 50% remission, 15% progression to chronic.

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13
Q

discuss syncope inc S+S

A

temporary loss of consciousness due to blood flow disruption (vasovagal)
excessive vagal nerve stimulation –> parasympathetic symptoms –> Vasodilation + BP drop –> floor.

S+S= hot/ clammy
sweats
dizzy
blur vision
headache
convulsions

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14
Q

aetiology of syncope

A

primary- dehydration, excessive warm standing, vasovagal response to blood, surprise, pain etc.

2’ - hypoglycaemia
anaemia
infection
anaphylaxis
arrhythmias
valvular heart disease
obstructive cardiomyopathy.

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15
Q

Ix + Rx of syncope

A

Ix: ECG (look for arrythmia or long QT syndrome)
24 hour ECG
Echo
Bloods, electrolites, BM, viral screens (e.g COVID)

Mx: Rx underlying cause
avoid dehydration, standing for long periods, sit when experancing prodromal features.

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16
Q

definition of status epilepticus + management

A

a seziure or group of seziures without recovery, that is persisting to the point;

where you know it is unlikely to self-terminate (T1)

the point where you know it is associated with a risk of damage (T2)

for tonic clonic status epilepticus - T1 = 5 mins, T2= 30 mins.

management:
ABC- O2 with mask.
1st line is benzos- 10mg diaz, midaz or 4mg loraz

2nd line- 40mg/kg valporate Or 60mg/kg levetiracetam.
if at 30 mins they are still going- need intubation + ICU.

17
Q

investigation of seziures

A

there is no test to find out if someone has had a seziure. clnical doagnosis relying on history- witnessed is better!

in epilepsy- try and determine the type, cause and risk of reocurrance

you would however rule out anything sinister / any causes of acute symptomatic seziures.

EEG will tell you what type or seizure but NOT if you had one or not.
MRI brain if not acute, CT to r/o bleed if acute.

18
Q

what is epilepsy

A

a common clustering of electrical and clinical features (age, type, assoc features) + an enduring predisposition to generate epileptic seziures.

a lowering of the threshold of spontaneous electrical activation.

neeed 2 seziures for diagnosis mroe than 24 hrs apart

19
Q

epidaemiology + aetiology of epilepsy

A

most common neruo condition. 1/25 will develop during thier lifetime.

diagnosis is by a specialist only.

many different causes- neuro damage, tumor, 30-40% are unknown cause. - unprovked may still have some seziures but beningn (hot water, booze, reading, light)

20
Q

generalised vs focal epilepsy + prognosis of epilepsy

A

generalised (idiopathic) - genetic, spike wave EEG, MRI normal,

focal- very varied- multiple causes with abnormal imaging

lots of different types, all vary in prog.
benign focal- good
childhood abscence / juvinile myoclinic – with Rx they will remiss
tumor assoc- will get worse.
encephalic epilepsy- always seziuing

21
Q

types of seziure one can have

A

generalised:
bilateral onset + spreads. loss of awareness at onset. can be asymmetric but both sides will be involved. no warning or aura.
normal on imaging.

subtype: tonic clonic- tonic- stiff clonic- jerky —> loss of consciousness- tounge biting, incontinence, posterior dislocation. –. has a post ictal period where sleepy, irritable. manage with sodium valproate or carbamazepine.

clonic
tonic
clonic- tonic- clonic.
atonic
myoclonic- very jerky but for second/2 only.

absence: sudden loss of awareness without other features. common in children.