MedEd Neuro Lecture Flashcards
MS- where and what?
Affects braiin and spinal cord
Immunological attack on myelin
Causes oligodendroglial and axonal pathology
Symptoms of MS
optic neuritis
motor weakness
sensory disturbance
fatigue
Optic neuritis
Meylin in optic nerve is being destroyed
DANISH symptoms (not necessarily MS)
dysdiadochokinesis. ataxia (cerebellar) nystagmus. intention tremor. scanning dysarthria. heel-shin test.
Epidemiology of MS
The more vit d you get the less likely you are to get MS - so more common in places like Norway and less common around equator
More common in women
More likely in those already affected by AI conditions
MS MRI
Demyelinated plaques - different people are affected in different ways
Light plaques - recent
Dark plaques - old
MS diagnosis
- absense of alternative diagnosis
- dissemination in time (DIT)*
- dissemination in space (DIS)**
- (2 attacks of MS - if you have one you might be fine. The second increases probability that the pt has MS)
- *(Location of the plaques - i.e. optic neuritis and then something else is affected and not optic neuritis again)
Based on: history and exam Scan - MRI Lab - CSF Electrophysiology - VEPs
Oligoclonal bands
CSF/plasma antibodies
Oligoclonal bands appear in infection - if the infection gets into the brain you get bands as well in CSF
If present in plasma and in CSF then probably
If only in CSF (inflammation confined to brain) then MS probable
VEPs
Visual evoked potentials - helps with MS diagnosis e.g when pt has not noticed visual disturbance?
Myaesthenia gravis
Fatiguable with use - if you look up long enough –> ptosis.
Symptoms of MG
ptosis diplopia dysarthria dysphagia \+/- SOB
Aetiology MG
antibodies against ACh receptors in neuromuscular junction
Associations with MG
Thymic hyperplasia
Thymoma
Investigations MG
bloods - anti-AChR and anti-MuSK
EMG - amplitude of action potentials goes down
AT/MRI
Lambert-Eaton myaesthenic syndrome vs MG
Opposite of MG
The more you use the muscle the better it gets
VGCC Ab - some cancers (esp lung) can release these antibodies
Motor neuron disease
5-8/100,000
Progressive destruction of muscle and motor neurons
MND symptoms (how do you distinguish from stroke)
dysphagia
SOB
progressive muscle weakness
SENSATION NOT AFFECTED
Wasting in MND
thenar muscle
tongue
Is MND upper or lower MN ?
BOTH
Investigations for MND
rule out everything else
MND onset
gradual
What type of gait in Parkinson’s?
Shuffling
Parkinsonism Triad
Bradykinesia
Rigidity
Resting Tremor (pill-rolling)
6Ms
Monotonous
Micrographia
HypomiMesis
…
Rigidity in Parkinson’s
Cog-wheel rigidity - tremor imposed on rigidity
Parkinsonism vs Parkinson’s
Parkinson’s - substantia niagra (dopamine) gets destroyed
Parkinsonism - can result from drugs, Lewy bodies etc, PD, atypical parkinsonism
Aetiology PD
alpha synuclein deposition so neuron doesn’t function properly and neuron dies
Epidemiology of PD
Farmers - pesticide?
Age
PDD
Amnestic, language deficits Visuospatial dysfunction - can't draw clock Hallucinations - little people Fluctuations Aggression/anxiety
Lewy body dementia - later onsent between motor and
hemiplegic
scissoring
choreiform
stroke
cerebral palsy
huntington’s - dance-like/involuntary movements
Dementia definition
severe loss of memory and other cognitive abilities which leads to impaired daily function, regardless of underlying casuse
Effects of dementia
cognition and memory
affect
motivation and attention
personality and behaviour
Alzheimer’s - 5As
amnesia anomia apraxia agnosia aphasia \+/- depression
Aetiology of AD
Hippocampus most affected - encodes memories - short term memory affected first
Amyloid precursor protein (APP) usually helps neurons function - as body ages it can’t process APP well so APP is moved out of cells, deposits and damages neurons
Tau - stabilises microtubules but in AD falls off and forms neurofibrillary tangles (hyperphosphorylated tau)
Down’s syndrome
APP is found on Chr21 - since those with Down’s syndrome have 3 of these there is extra –>
AMTS
Questions in the AMTS (1 point each):
- Age
- Current time (to the nearest hour)
- Recall: Ask the patient to remember an address (e.g. 42 West Register Street) - ensure they are able to say it back to you immediately, then check recall at the end of the test
- Current year
- Current location (e.g. name of hospital or town)
- Recognise two people (e.g. relatives, carers, or if none around, the likely profession of easily identified people such as doctor/nurse)
- Date of birth
- Years of the first (or second) world war
- Name of the current monarch (or prime minister)
- Count sequentially backwards from 20 to 1
A score of less than 8 in the AMTS implies the presence of cognitive impairment
Vascular dementia
Like AD location specific emptional and personality changes focal neurology Older vasculopaths sudden onset stepwise deterioration
VD on MRI
fluffy areas in several parts on MRI
Pick’s disease
Tau + frontal lobe Personality change disinhibition overeating, preference for sweet foods emotional blunting YOUNGER
Wernicke’s encephalopathy - classic ACE
Ataxia
confusion
Eye signs - ophthalmoplegia
(ACE)
Signs Wernicke’s
ataxia
malnourished
Is Wernicke’s damage reversible?
No - MRI later will show little reversibility
Wernicke’s investigation
bloods - B1 especially
others
Korsakoff
Chronic
Alert
Amnesia and confabulation(brain makes stuff up to fill in gaps of what they have forgotten)
Irreversible (?)
(VS Wernicke’s = acute, confusion, cerebellar and eye signs, reversible)
