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302 review > Neuro > Flashcards

Neuro Flashcards

1
Q

what is MS

A

autoimmune disease causing CNS demyleination
CD4 mediated oligodendrocyte destruction + humoral response to myelin binding protein

mainly affects female 20-40yr
associated with HLA-DRB1 gene (+ absence of HLA-A)

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2
Q

what is radio + histological hallmark feature of MS

A

demyelination plaques in CNS - radiological
eventual axonal loss - pathological

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3
Q

what are the classifications of MS

A

primary progressive

relapsing-remitting -> secondary progressive
mostly relapsing remitting

progressive-relapsing

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4
Q

what is diagnostic criteria for MS

A

McDonalds criteria to diagnose

2+ relapses disseminated in time (by a month) and space (2+ hyper intense T2-weighted lesions on MRI)

if 1 ep of demyelination + clinical signs = clinically isolated syndrome
not diagnosed as MS as not disseminated in time+space

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5
Q

what are 2 phases of MS

A

early active phase neuroinflammation (disease activity):
macrophage myelin destruction, T cell infiltration, axonal damage, reactive astrocytes
new T2 lesions on MRI +/- clinical relapse (may be asymptomatic)

late chronic phase neurodegeneration:
myelin debris, axonal loss, activated microglia
more clinical markers (MRI, atrophy) but independent of relapse activity (occurs but symptoms don’t worsen)

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6
Q

what is pathophysiology of MS + effects on white/grey matter

A

only affects oligodendrocytes in CNS

causes multifocal neuroinflammation plaques within:
white matter - more apparent
grey matter (subcortical/cortical) - fewer T/B cells, causes cognitive impairment (late disease)

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7
Q

what immune cells cause MS

A

auto-CNS-reactive T cells (mostly CD8>CD4)
infiltrates CNS via endothelial adhesion molecules
APC reactive T cell so they release MMP that breakdown BBB
causes oligodendrocyte demyelination, axonopathy, gliosis

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8
Q

what occurs in first attack

A

MS usually presents with optic neuritis (first attack)

inflammatory processes occur long before
causes optic neuritis - loss of central vision, painful eye movements

MS is disseminated in time and space - so affects different nerves, causing different symptoms

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9
Q

how does early + late MS disease differ

A

early - re-myelination can resolve symptoms
late - re-myelination is incomplete, so symptoms don’t resolve

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10
Q

how does MS present

A

optic neuritis (first attack) - loss of central vision (central scotoma), painful eye movements, impaired colour vision
CN6 lesion - double vision, conjugate lateral gaze disorder
lesion in medial longitudinal fasciculus - internuclear opthalmoplegia

Horner syndrome, limb paralysis, incontinence

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11
Q

what are MS RF

A

20-40yr female, scandanavian
symptoms improve in pregnancy + postpartum

low VitD, UVB exposure, past EBV infection
obese, diabetes, smoker

genes: present HLA-DRB1, absent HLA-A
sarcoidosis, SLE

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12
Q

how is MS investigated

A

CSF shows oligoclonal bands, indicating ongoing inflammation

gold standard - MRI (shows hyper intense T2-weighted lesions disseminated in time + space)
lesions = inflammation, demyelination, axon damage, oedema
location: periventricular, juxtacortical, infratentorial, medullar

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13
Q

how does MS look micro + macroscopically

A

micro - initial perivascular/myelin swelling with BBB breakdown
early active phase (neuroinflammation) - T cell infiltration, macrophage myelin destruction, reactive astrocytes
late chronic phase (neurodegenration) - myelin debris, axonal loss, activated microglia

macro - global atrophy, hydrocephalus ex vacuo, thinned corpus callosum, periventricular/juxtacortical demyelination

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14
Q

how is acute MS attack managed

A

glucocorticoids = IV methylprednisolone 1g OD for 3/7

if not responding to steroids, give plasma exchange

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15
Q

how is relapsing-remitting MS chronically managed

A

DMART + symptom relief

DMART - reduce disease activity to induce long term remission (3months to reach full effectiveness)

symptom relief - physiotherapy, baclofen (for muscle spasm), anticholinergic (for incontinence), sildenafil (for erectile dysfunction)

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16
Q

what DMART are given for MS

A

injectable: B-interferon, glatiramer
oral: dimethyl fumarate, teriflunamide, fingolimod
biologic: natalizumab, alemtuzumab

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17
Q

what are neurological + cardiological causes of collapse

A

neuro - sieuzures, non-epileptic attack disorders
cardio - syncope

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18
Q

how do seizure + syncope differ

A

seizure = post-ictal confusion, syncope = no confusion

seizure:
sudden onset, with limb jerk/tongue bite/incontinence
usually last <5min
pt is confused after (post-ictal confusion) and may have Todd paresis (residual focal neurological deficit)

syncope:
there is no confusion after fall
vasovagal (neurocardiogenic) - sweating, light-headed, narrowing of vision, lower themself to floor
arrhythmogenic syncope (stokes adams attack) - abrupt onset, no warning

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19
Q

what is status epileptics

A

seizure lasting 30min+, or multiple seizures over 30min with incomplete resolution

assume status epileptics at 5min

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20
Q

what are 4 stages of status epileptics management

A

premonitory 0-10min
early status 0-30min
established status 0-60min
refractory 30-90min

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21
Q

how is status epileptics immediately managed

A

premonitory 0-10min

rectal diazepam 10-20mg
repeat (or buccal midazolam 10mg) once 15min later if status continues

if seizures continue (in hospital), IV lorazepam and if needed repeat once 15min after

22
Q

what is monitored during status epileptics

A

O2 sats + glucose (as they are common and rapidly reversible causes of seizures)

if history of alcohol abuse, give parbinex before glucose - to prevent wernicke encephalopathy

23
Q

how are epileptic syndromes categorised

A

focal + generalised

focal - usually temporal lobe:
simple
complex - consciousness impaired, loose consciousness after an aura/seizure onset
secondary generalised - initially focal, then become bilateral seizure (usually tonic clonic - convulsive seizure)

generalised:
absence - common in children, lasting <10sec
tonic-clonic - pt looses consciousness with post-ictal confusion, limbs stiffen (tonic) then jerks (clonic)
myoclonic - sudden jerking of limb/trunk/face
atonic seizure - pt falls due to sudden loss of muscle tone, pt retains consciousness

24
Q

what are features of specific focal seizures

A

temporal lobe - most common:
hallucinations - auditory/olfactatory/gustatory, automatism (lip smacking)

frontal lobe:
motor features = dysphasia, Todd paresis (residual focal neurological deficit),
Jacksonian (only on 1 side, progressing from 1 muscle group to nearby ones quickly)

parietal lobe: sensory symptoms (tingling/numbness)

occipital lobe: visual symptoms (spots/lines in field)

25
Q

how are focal seizures treated

A

1 - lamotrigine or levetiracetam

then consider carbamazepine, orxcabenzapine
lacosamide

26
Q

how are general seizures treated

A

absence = sodium valproate (avoid carbamazepine as worsens seizure)

tonic-clonic = sodium valproate or lamotrigine

myoclonic = sodium valproate, unless women of child-bearing age then use levetiracetam/topiramate (avoid carbamazepine as worsens seizure)

atonic = sodium valproate or lamotrigine

27
Q

what triggers seizures + what are complications

A

triggers: poor sleep, alcohol/drug (+ withdrawal), stroke, SOL, intracranial haemorrhage

complications:
status epilepticus (5+min of continuous seizures - 30min of seizure or incomplete resolution of multiple seizures) = rectal/IV lorazepam -> repeat/buccal midazolam -> IV phenytoin
depression, suicide, sudden death

28
Q

what is an ideal AED (anti-epileptic drug) for women of child bearing age

A

lamotrigine
as sodium valproate is highly teratogenic so risks neural tube defects

29
Q

what are the guidelines for epilepsy+driving if:
one off seizure
multiple seizures
seizure after changing medication

A

one-off seizure = reapply in 6 months
multiple = reapply in 1yr
after changing medication = reapply if seizure more than 6 months ago, OR back on previous med for 6+ months

30
Q

what are RF for subarachnoid haemorrhage (SAH)

A

SAH due to ruptured berry aneurysm

HTN, APCKD - autosomal dominant inheritance
alcohol excess, smoking

31
Q

how does SAH present

A

sudden onset occipital headache ‘thunderclap’
worst headache of their life
physical exertion before onset

on exam - reduced GCS, meningism (neck stiffness), focal neurological signs

32
Q

how is SAH investigated

A

CT head - berry aneurysm in circle of willis (base of skull)

if CT head doesn’t confirm diagnosis, LP done (ideally 12hr after symptom onset)
shows xanthochromia

33
Q

how is SAH managed

A

medical - nimodipine (CCB to prevent vasospasm to prevent subsequent ischaemic damage), don’t treat HTN

surgical - EVAR for coiling/stenting SAH bleed, surgical clipping of vessel

34
Q

what is main neuromodulator + neuropeptide in pain

A

modulator - 5HT
peptide - CGRP calcitonin gene related peptide

35
Q

what brainstem nuclei are involved in pain processing

A

trigeminocervical complex
superior salivary nucleus - ANS
locus coreulus - NA
dorsal raphe nucleus - 5HT
hypothalamus - orexin

36
Q

what are 3 main primary headaches

A

migraine
tension type
trigeminal autonomic cephalgia

37
Q

how is migraine diagnosed

A

recurrent headaches 5+
lasting 4-72hr

at least 2 of:
unilateral
pulsating
moderate severity
worse with activity

additional:
photo + phono-phobia
nausea/vomit

aura (may or may not occur) - zigzag lines, visual fortification, dysphasia, sensory disturbance (+ve and -ve symptoms)

38
Q

what are the different types of migraine

A

migraine
migraine w aura
silent migraine (migraine w aura but no headache)
hemiplegic migraine - stroke mimic

39
Q

what is pathophysiology of migraine

A

interaction between hypothalamus, thalamus, brainstem nuclei (involves 5HT dorsal raphe, NA from LC)

causes large amounts of extracellular K + glutamate secretion
triggers CSD release (cortical spreading depression - suppresses brain activity)

40
Q

what is given for migraine prophylaxis

A

topiramate, amitriptyline, propranolol

stops CSD release
by interrupting interaction between hypo/thalamus, brainstem nuclei

41
Q

what are the 5HT + DA pathways and how do they contribute

A

5HT = pain, DA = bothersome symptoms

low 5HT causes migraine
high 5HT1AA (5HT metabolite) seen in CSF/urine suggesting high 5HT turnover

DA hypersensitivity causes additional symptoms of nausea/vomit, yawning

42
Q

what is role of CRGP in different nerve fibres + vessels

A

C fibre - release CRGP
A delta - contain CRGP receptors

CRGP is released from C fibre and acts on A-delta
modulating pain transmission

blood vessel - CRGP receptors

CRGP is released from C fibre, causing vasodilation
causes protein release, leading to neurogenic inflammation
this activates A-delta
which transmits signal to brainstem

43
Q

how to manage an acute migraine attack

A

PO sumatriptan - decrease CRGP release (contraindicated in asthma)

+ NSAID - decrease prostaglandin
+ metclopramide - decrease DA (anti-emetic)

conservative - avoid trigger
hydration, good sleep hygiene
reduce alcohol/coffee

44
Q

what is MOA of triptan

A

5HT agonist, decrease CRGP release

vasconstricts arteries smooth muscle
reduces CNS activity, inhibits peripheral pain receptors

45
Q

why does photophobia occur during migraine

A

thalamocortical pathway is modulated by inputs from retina

46
Q

what are RF for migraine

A

20-55yr female
on COCP

alcohol, caffeine, chocolate, cheese
dehydration

trigger - stress, bright lights
around menstruation or menopause as low oestrogen (as E2 increases 5HT)

47
Q

what hormone is linked to E2

A

5HT
as E2 increases, more 5HT released

48
Q

how do migraine differ to headaches

A

migraine - lasts 4-74hr
unilateral
pulsating
moderate severity
worse with activity
additional: photo+phono phobia, nausea/vomit
treat = prophylaxis - topiramate, propranolol, amitryptilline
acute - sumatriptan + paracetamol, NSAID

tension headache - female:
gradual onset
bilateral - tight band around forehead, mild ache
treat = analgesia according to WHO step ladder

cluster headache - 20-40yr male smoker:
sudden onset, pain <4hr
unilateral, around eye (red, swollen, ptosis/meiosis, sweating)
severe group of attacks then pain-free
treat = prophylaxis - verapamil
acute - O2, sumatriptan

trigeminal neuralgia (compressed CN5):
unilateral
short, stabbing pain in V2 + V3 distribution
triggered by cold wind, touching, brushing teeth
treat = medical - carbamazepine (phenytoin, lamotrigine, gabapentin)
surgical - microvascular decompression

49
Q

what are red-flag symptoms in headache

A

meningitis = fever, neck stiffness, photophobia

stroke = new neurological symptoms

SAH = sudden onset occipital, thunderclap

glaucoma/GCA = temporary monocular blindness (treat with high dose steroids)

raised ICP (hydrocephalus, SOL - tumour/haemorrhage) = better after vomiting
worse when bending down, in morning

medication over-use = check DH

50
Q

what are RF for idiopathic intracranial HTN

A

female, obese, PCOS

excess 11B-HSD1 causes:
cytokines (chronic inflammation), adipokines, excess androgen

treat with weight loss

51
Q

what investigations done for headache

A

CT scan to diagnose SOL for raised ICP

MRI to exclude secondary causes

fundoscopy for papilloedema - IIH, raised ICP

302 review (14 decks)

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