Genetic - female - HLA-DR2 Environment - Infection - vit D deficiency

Charcots Dysarthria - difficult / unclear speech -plaques in brain stem Nystagmus - plaques on optic nerve -> loss of vision Eg blurring / dark spot - may have pain / double vision Intention tremor - plaques on motor pathways of spinal cord - muscle weakness, spasms, ataxia as well

Osmosis Neuro Flashcards by Hamish Reed-Embleton

Level of vertebrae for LP?

L3/4

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Main excitatory neurotransmitter? Receptor?

Glutamate

NMDA

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Focal seizure that starts in one muscle group and then spreads is called? Type of seizure?

Jacksonian march

Focal without impaired awareness (likely to remember it)

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Tonic seizure?

Muscles become stiff and flexed

-> tend to fall backwards

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Atomic seizure?

Muscles become relaxed

-> tend to fall forwards

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Myoclonic?

Short muscle twitches

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Post vital Sx?

Confusion
Paralysis (Todd’s paresis - around 15 hours -2 days)
-due to supression of area of brain affect

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What happens in MS?

Demyelination of brain and spinal cord
T cell mediated autoimmune

Type IV hypersensitivity reaction

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What produces myelin

Oligodendrocytes

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Which cytokines are made by T cells?

IL-1, IL6

TNF-a, INF-y

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Rf for MS?

Genetic

female
HLA-DR2

Environment

Infection
vit D deficiency

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4 main types of MS?

Relapsing remitting (most common) 
-may be months-years between bouts with residual disability

Secondary progressive
Initially similar to RRMS -> progressive

Primary progressive
Steady progression of disability

Progressive relapsing
Progression with additional bouts

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Usual age of MS

Usually aged 20-40

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What Sx triad in MS?

Charcots

Dysarthria - difficult / unclear speech
-plaques in brain stem

Nystagmus

plaques on optic nerve -> loss of vision Eg blurring / dark spot
may have pain / double vision

Intention tremor

plaques on motor pathways of spinal cord
muscle weakness, spasms, ataxia as well

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Can you get sensory sx in MS?

Yes

Numbness, parathesia …

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Key sign in MS?

Lhermittes
-electric shock runs down back and radiates to limbs when bending neck forward

Uhthoffs
-Exacerbation of Sx in heat Eg bath / exercise

What happens if ms plaques in autonomic nervous system?

Bowel/bladder - eg incontinence

Sex - eg dysfunction

Ix of MS

Sx with spread over space and time

MRI - multiple white matter plaques

LP - presence of oligoclonal bands on gel electrophoresis

Visual evoked potential - Measure response to visual stimuli

Bloods
Anti-MOG, AQP-4
Metabolic causes of neuropathy
-FBC, inflammatory markers, B12/folate, HIV, Ca, Glucose

Tx of MS? Which type are these useful for?

Relapse

Corticosteroids - high dose methyprednisolone
Plasmapheresis - removes autoantibodies

1st line Prevention

immunosuppressants - Eg B-INF
Dimethyl fumarate
alentuzumab

2nd line

Natalizumab
fingolimod
cyclophosphamide (cell cycle inhibitor)
IVIg

RRMS

What is treatment for progressive MS?

Mainly to manage Sx
Eg. Depression, bladder dysfunction

Cognitive rehabilitation therapy / Physio
?Vit D

Diagnosis of RRMS?

Mc Donald criteria

Evidence of 2 events, disseminated by space and time (at least 30 days apart)

Time
-evidence of new lesions on follow-up MRI with reference to baseline

Space

At least 1 lesion in 2+ out of 4 areas of CNS
Periventricular, juxtacortical, infrateriotoral, spinal cord

Mechanism of tissue damage in wilsons?

Free copper -> free radicals

How does the copper get into blood ?

Absorbed in gut 
-> liver 
If ATP7B is defective -> free copper in hepatocyte 
-> damage 
-> copper into extra cellular space 
-> blood

2 functions of ATP7B?

Bind copper to apoceruloplasmin

Package copper into vesicles -> bile

Bar liver what other organs are affected in Wilson’s disease ?

Brain Basal ganglia -> movement disorder similar to Parkinson’s Cortex -> neuronal cells death and dementia Cornea Kayser fleischer rings Hepatosplenomegaly Renal disease Haemolytic anaemia (from free Cu in blood)

Ix? WD

Blood - Decreased ceruloplasmin - Increased copper Urine -Increased copper

Penicillamine - copper chelation Zinc -> reduce copper reabsorption -> more excreted in urine If liver cirrhosis / failure -> transplant

Gene in Huntington’s? Chromosome? How many repeats to be called hungtingtons ?

Huntingtin - Chromosome 4 36

Which part of brain is affected by HD

Basal ganglia (putamen + caudate)

What is anticipation

Earlier Sx onset. With each generation

Neurotransmitter changes in HD? How this reflects class of drugs for chorea Mx?

Decreased GABA + Ach Increased Dopamine Chorea -> Dopamine receptor antagonists (Antipsychotics) -Tetrabenazine (depletes dopamine)

Injury to receptors in Myasthenia gratis is by?

Type II hypersensitivity Cytotoxic injury -> Damaged receptors -> lack of contraction Also triggers classical complement pathway -> muscle cell destruction

MX of myasthenia gravis

Acetylcholinesterase inhibitors (Neostigmine) -> Increase Ach Immunosuppression - prednisolone Surgical removal of thymus -> reduces muscle weakness

What factors can worsen fibromyalgia?

Depression Anxiety Negative beliefs

Neurotransmitter changes in polymyalgia?

Decreased serotonin -> less pain inhibition Increased Nerve growth factor + substance p

Diagnosis of fibromyalgia

Pain in 7+ areas Symptom severity score 5+ /12 -Eg headache, poor sleep, fatigue, ‘fibro fog’ Duration >3months OR Pain in 5 locations and a score of 9/12

Mx of polymyalgia

Exercise Relaxation and good sleep hygiene Pharma Amitriptyline SNRIs Anticonvulsants (pregabalin and gabapentin) -> help with sleep problems

General sx of polymyalgia

``` Long lasting Widespread muscle pain Low threshold to pain Excessive tenderness Sleep disturbance ```