Week 15 - Neurology
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Week 15 - Neurology
Cranial nerves, stroke, myasthenia gravis, parkinsons
Name to 12 Cranial nerves and breifly sate their function
1 → Olfactory → smell
2 → Optic → Vision
3 → Occulomotor → 4/6, levaetor pelpebrae sup, pupil constrictors
4 → Trochlear → motor to superior oblique, long course
5 → Trigeminal → sensation face [3 segments] muscles of mastication [messeter, pterygoid & temporalis]
6 → Abducens → lateral rectus [abduct eye]
7 → Facial → sensory ant 2/3 tongue [taste], motor = facial muscles
8 → Vestibulocochlear → sensory, balance & hearing
9 → Glossopharyngeal → sensory post 1/3 tongue, motor soft palate, salivary glands
10 → Vagus → longest, chemoceptors in carotid bodies, HR, SV etc
11 → Spinal Accessory → motor to sternocleidomastoid & trapezius
12 → Hypoglossal → motor to tongue [deviate to affected side]
What is Horners syndrome?
Pancoast tumour invasion of cervical/thoracic sympathetic chain
Affects CN 3 & 6
What are teh features of a 3rd nerve palsy?
Eyelid droop [Ptosis]
Eye in down & out position
What are the features of a 4th nerve palsy?
Longest intracranial course → susceptible to tumour/ ^^ICP
Head tilt away from lesion
Hypertropia [one eye higher than other]
when looking down towards nose, other eye moves upwards
What are the components of the brainstem?
Why is it important?
Brainstem = Midbrain, pons & medulla
Origin of all cranial nerves
all spinal tracts pass thru here
What structures comprise the basal Ganglia?
PutamenGlobus pallidus [interna & Externa]
Venterolateral nucleus of thalamus
What is the function(s) of the basal ganglia?
Initiate voluntary movement
Maintain posture/ movement
Executive functions → working memory
What is the Pathology sorrounding Parkinsons Disease?
→ intracytoplasmic inclusion body containing misfolded protein
gradually ascend thru stem
loss of dopaminergic neurones
within substansia nigra [CF >50% loss]
1 → Lewy bodies in lower brain stem
3-4 → midbrain/ substansia nigra ~symptomatic
6 → throughout basal ganglia, severely demented
What are the CF of Parkinsons?
→ slow to initiate voluntary movement, reduction in sped of following movements
Non motor → dementia, poor sleep [restless legs] ^^ANS [constipation, ED, urinary urgency]
What is the role of Imaging in Parkinsons?
CT/ MRI = normal
Abn in vascualr/ parkinson plus disorders
Functional imaging → DAT SPEC → dopaminergic sys
DDx for Parkinsons?
Benign tremor disorder
dementia w lewy bodies
Vascular Parkinsons [Stepwise progression, leg symptoms]
Parkinson plus disorders
Drug induced parkinsonism → dopamine antagonists
Outline the drug Tx of Parkinsons?
1. Replace DA/ DA agonists
MoA → DA precursor, crosses BBB, converted to DA in brain
A/E → abn voluntary movement, confusion & hallucinations
PK/PD → give with decarboxylase inhibitor or will convert in tissues → lethal
MoA → DA-r agonist [D2]
A/E → nausea, headache & vom
2. Prevent DA synapse degredation
MoA → MAO-B inhibitors, prevent DA degredation, ^^acting DA
3. Reduce Action of ACh
MoA → anticholinergic, reduces tremor & rigidity
Outline the CF & complications of Myasthenia Gravis?
Acquired autoimmune disorder
→ muscle weakness & ^^fatigueability on exertion
→ respiratory failure, dysphagia, long term steroid use
What is te underlying pathology in myasthenia gravis?
B cell mediated
Ab against ACh-R
reduced receptors = reduced Na influx
smaller end plate potential → no muscle movement
Outline the drug Tx of Myasthenia Gravis?
MoA → acetyl cholinesterase inhibitors, ^ACh at junction, muscle movement
A/E → Cholinergic crisis [sweating, salivation, miosis]
MoA → immunosuppression, decrease circulating Ab
A/E → cushings
What is multiple sclerosis?
Chronic disease of brain & SC
CF → changes in sensation, visual problems, weakness, poor coordination & speech, impaired mobility →
Outline the pathology underlying MS?
CD4 T cells activate B cells → anti-myelin
Macrophages & Cytotoxic T → demyelination
Failure of conducton & loss of function
Eventual remyelination but never same function
What are the differenct types of MS?
decent recovery from initial attacks, variable freq
70% → secondary progressive MS
Secondary Progressive MS
gets steadily worse, after initial relapsing remitting course of disease
Progressive spinal damage
gets steadily worse with occaisional really bad patches
What are the main symptoms of MS?
Could be anything, most neuro problems
Relapsing remitting → clinically isolated syndromes
optic neuritis [PAIN]
Brainstem syndrome → opthalmoplegia, dyarthria, ataxic
Spinal cord → transverse myelitis
How is MS diagnosed?
2 clinical attacks, >1m apart & O/E evidence of 2 separate lesions
MR brain & Spine
→ T2 & FLAIR weighted
→ paraventricular, corpus callosum, BS/Cerebellum
→ Lumbar puncture
→ IgG heavy chains
Outline the Mx of MS
Prednisalone for first timers
Refer to MS specialist nurses
Later → Natalizumab → anti-TNF alpha
What are the signs of an upper motor neurone lesion?
Pronator Drift [indicates spasticity]
Extensor Plantar Response
UMN lesion → lower half of face = paralysed
What are the features of a Lower motor neurone lesion?
Muscle loss → weakness
LMN → complete facial paralysis
Draw and label the circle of willis?
Outline the pathophysiological mechanism of damage in ischaemic stroke
When BF stops, not instant tissue death
Tissue death via
→ breakdown of Na/K pumps [
K out, Na in
], water in cell swells,
stimulate Glu release
, ^^Ca, Protease activeation →
Infarct core = irreversible dam
Ischaemic Penumbra = potentially salvageable sorrounding tissue
Give 5 RF for Iscaemic Stroke?
Heart Disease [AF]
Previous stroke/ TIA
Give 3 RF for haemorrhagic stroke
Cerebral Amyloid Angiopathy
Illegal drugs → cocaine
Vascular lesions → aneurisms
What is the Oxford Community Stroke classification?
→ Total Anterior Circulation Syndrome
All 3 of; Contra-lateral hemiparesis, contra-lateral hemianopia, higher dysfunction [dysphasia, visuospatial]
→ Partial Anterior Circulation Syndrome
2 of above or higher function dysfunction alone
→ Lacunar Stroke
small lacunae of blood [stroke]
Pure motor or pure sensory or sensorimotor [Ataxic hemiparesis, dyarthria]
Perforating arteries/ small artery disease
→ Posterior Circulation syndrome
Isolated Hemianopia/ brainstem syndrome
Perforating arteries, PCA or cerebella arteries
Give 3 investigations for stroke & why you would use them?
ECG → look for AF
FBC → low PLTs cant give rTPA
BM → hypoglycaemia can mimic stroke
CT/ MRI → distinguish between ischaemic & haemorrhagic
Outline the Acute management of Ischaemic Stroke
Admit Pt to stroke unit
Thrombolysis <4.5hrs → Alteplase [rTPA]
Exclude heamorrhagic on non contrast CT
Antiplatelets after 24hr scan
>4.5hr → antiplatelet therapy [300mg aspirin]
Outline the secondary prevention of stroke?
Aspirin + dipyramidol/ clopidogrel
Cholesterol lowering therapy
Warfarin if in AF
Carotid Endartectomy → remove carotid stenosis
What is status epilepticus?
Sustained synchronised electrical discharge in brain causing symptoms/signs
Series of seizures w/o regaining consciousness [benzos/ anticonvulsants]
A tendency to have recurrant unproveked seizures
Imbalance of excitation & inhibition in brain
How are seizures classified?
Tonic phase → stiff, rigid muscles
Clonic → dysrhythmic shaking **better define
Loss of awareness
What are the Hx & O/E features of a raised pressure headache?
Worse lying flat
Worse in morning
Persistant nausea & Vom
Worse w exertion
Pain on valsalva
What are the Hx features of a low pressure headache?
Worse sitting/ standing up
Eased by lying flat
Due to CSF leakage → traction of meninges → pain
What is the normal ICP?
What causes ^^ICP?
ICP = 7-15mmHg
>25 = shit your pants time [Brain herniation]
Mass effect → space occupying lesion
^ venous pressure → cerebral sinus thrombosis
Idiopathic → obese young women
What are the red flag features of a headache?
lder age onset
revious headaches = different/ absent
cute onset <5min → thunderclap
eurological signs/ Symptoms
riggered headache → valsalva/ postural
What is a thunderclap headache?
Abrupt onset, reaching maximum severity in <5min
Subarachnoid haemorrhage until proven otherwise