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NV - Phase 3A > Neuro > Flashcards

Neuro Flashcards

1
Q

What disease causes a rapidly progressive decline and what other features would you see?

A

Creutzfeldt-Jacob disease
prion infection causing spongiform encephaopathy
causes rapidly fata demetia - death within 1 year
myoclonic jerks and extra-pyramidal signs

causes - sporadic, infected hosipital infection, familial, blood transfusions in 1995

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2
Q

What is Huntington’s disease?

A

autosomal dominant disease with 100% peetrance - trinucleotide expansion repeat of CAG.

symptoms - cognitive decline –> progresses to subcortical dementia, personality change, choreinform involuntary movements, dysarthria, psychiatric disturbance.

genetic test - children must wait until old enough to decide

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3
Q

What is the pathophysilogy of HD?

A 
reduced GABA (reduced inhibition)
causing dopamine hypersensitvity and increase in dopamine transmission
increased stimualtion at thalamus and cortex --> involuntary movements
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4
Q

Name 2 medical conditions that can cause psychiatric symptoms?

A

neurosyphilis - grandiosity, euphoria, mania, personality change

Wilson’s disease - copper excess leading to both neuro and psych changes, liver disease and kayser-fleischer rings

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5
Q

Name a potentially reversible cause of dementia?

A

Normal pressure hydrocephalus
triad of - ataxia, dementia and urinary incontinence
causes - idiopathic, SAH, head trauma, meningitis
tx with ventriculoperitoneal shunt

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6
Q

What are the features of an ataxc gait?

A

wide-based
falls
cannot walk heel-to-toe
often worse in the dark or with eyes closed

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7
Q

What are the 2 main causes of an ataxic gait?

A
  1. cerebellar problem

2. issue with proprioception

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8
Q

What are the cerebellar causes of an ataxic gait?

A

MS
posterior fossa tumour
alcohol
phenytoin toxicity

deficits are ipsilateral to cerebellar lesion

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9
Q

What are the features of cerebellar syndrome?

A

ataxia + nystagmus

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10
Q

What are the proprioceptive causes of an ataxic gait?

A

sensory neuropathies - low B12

inner ear problems affecting the vestibular system

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11
Q

How do you distinguish between a cerebellar and proprioceptive cause of ataxic gait?

A

walk normally with eyes open, problems start when eyes closed –> proprioceptive

problems exists all the time –> cerebellar

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12
Q

What are the features and causes of a circumduction (spastic) gait?

A

features - stiff gait, circumduction of the legs +/- scuffing of the toe of the shoes

cause - strone (hemiplegia)

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13
Q

What are the features and causes of a shufflinf (extra-pyramidal) gait?

A

features - flexed posture, shuffling feet, postural instability, slow to start

cause - Parkinson’s diease, PD+ syndromes, other causes of Parkinsonism such as antipsychotic medications

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14
Q

What are the causes of an antalgic gait?

A

AKA limping

MSK cause - painful limb

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15
Q

What are the features and causes of high stepping gait?

A

features - trip over often, struggle with dorsiflexion of the foot, lift ffeet high whilst walking to avoid tripping over

cause - foot srop (common peroneal nerve pasly)

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16
Q

What are the features and causes of Trendelenberg gait?

A

Features - unstable hip, sound side sags on Tredelenberg test

Causes - congenital hip dislocation, DDH, gluteus medius muscle weakness, superior gluteal nerve damage

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17
Q

What are the features and causes of an apraxic gait?

A

features - glued to the floor when attempting to walk, wide based unsteady gait with a tendency to fall (novice on ice)

causes - normal pressure hydrocephalus, multi-infarct states, Alzheimer’s disease

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18
Q

How does the onset of an episode of weakness help you assess the cause of it?

A

Sudden onset - likely to be a vascular event

medium onset - likely to be related to demyelination

insidious onset - slow-growing tumours etc

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19
Q

What are the patterns and distributions of muscle weakness?

A
  1. proximal weakness - muscle problem - hair, chair, stairs - struggle to do things close to their trunk
  2. distal weakness - nerve problem - nueropathy starts distally and works its way up - glove and stocking distribution
  3. symmetrical - genetic or metabolic cause eg. diabetes, muscular dystrophy
  4. asymmetrical - vasculitis or inflammatory
  5. mononeuropathy - entrapment
  6. polyneuropathy - systemic like diabetes
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20
Q

What are the features of peripheral neuropathy?

A

chronic and slowly progressive
length-dependent
sensnory, motor or both
glove and stocking distribution

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21
Q

How does mononeuritis multiplex present and what are some causes?

A

individually erves picked off randomly - wrist drop, leg numbness, foot drop

subacute presentation (months) 
inflammatory/immune-mediated

causes - inflammation of the vasa nervorum can block off the blood supply to the nerve causing sudden deficit
vasculitis (Wegner’s, PAN, RA), sarcoidosis

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22
Q

Give some examples of entrapment mononeuropathies.

A

Median nerve at wrist = carpal tunnel syndrome

ulnar nerve at elbow

radial nerve at axilla

common peroneal nerve in leg

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23
Q

What causes a myasthenic crisis?

A

infection
natural part of the disease
under or overdosing of medication

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24
Q

How should a myasthenic crisis be treated?

A

urgent neuro review
monitor breathing - serial FVC measurements
anaesthetic review

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25
Q

How does muscular dystrophy present and what clinical test can be done to demonstrate it?

A

presents in childhood with proximal muscle weakness

can have bulky muscles at first = pseudohypertrophy

then muscle wasting occurs
scoliosis is prominent later on

Gower test = positive

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26
Q

How is myopathy investigated?

A

creatinine kinase
EMG
ESR, CRP

+/- genetic (DMD, Becker)
+/- biopsy

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27
Q

What is the definition of coma/brain death?

A

unarousal unresponsiveness

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28
Q

What are the 3 domains used in assessing the Glasgow Coma Scale (GCS)?

A
  1. best eye opening response
  2. best verbal response
  3. best pain response
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29
Q

What are the 4 levels of best eye opening response?

A
  1. spontaenously
  2. to speech
  3. to pain
  4. None
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30
Q

What are the 5 levels to best verbal response?

A
  1. orientated in time/place/person
  2. confused
  3. inappropriate words
  4. incomprehensible sounds
  5. none
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31
Q

What are the 6 levels o best pain response?

A
  1. obeys commands
  2. localises pain
  3. normal flexion to pain (aka withdraws from pain)
  4. abnormal flexion to pain (decorticate response)
  5. extends to pain - decerebrate response
  6. none
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32
Q

What causes a fixed dilated pupil?

A

3rd nerve palsy

occulomotor nerve comes out of the brain stem and goes over the apex of the petrous part of the temporal bone as goes through the cavernous sinus to supply the eye. This means it’s susceptible to being damaged when the brain is swollen, bleeding, trauma, etc.
parasympathetic fibres’ job is to constrict the pupil so when they are damaged the pupil is fixed in the dilated position.

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33
Q

What is another differential for fixed dilated pupil?

A

blind eye

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34
Q

What are some metabolic causes of coma?

A

drugs, poisoning - alcohol, tricyclics, carbon monoxide
hypoglycaemia
hyperglycaemia - ketoacidotic or HONK (hyperglycaemic hyperosmotic non-ketotic coma)
hypoxia
CO2 narcosis (COPD) - when people are given too much oxygen, the hypoxic drive to breathe slows down, which means CO2 builds up and can lead to lethal hypercapnia
Septicaemia, hypothermia, myxoedema, Addisonian crisis, hepatic/uraemia encephalopathy due to kidney or liver failure

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35
Q

What are some neurological causes of coma?

A

trauma
infection - meningitis, encephalitis, HSV
vascular - stroke, SAH, hyptertensive encephalopathy
epilepsy - non-convulsive status epilepticus, post-ictal state

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36
Q

How is the unconscious patient managed?

A

ABCDE
IV access
stabilise cervical spine (esp in trauma)
control any seizures - phenytoin
tx potential causes - IV glucose, thiamine, naloxone if pinpoint pupils
brief collateral hx and exam
vital signs and pupils checked often
investigtions - blood, cultures, CXR, CT head
continually re-assess and plan investigations

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37
Q

What is the definition of vertigo?

A

An illusion of movement, often rotary, of the patient or their surroundings
spinning.tilting.veering sideways feeling
as if being pushed or pulled
always worse with movement

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38
Q

What are the causes of vertigo?

A

motion sickness
alcohol intoxication
benign paroxysmal positional vertigo - disturbance of crystals in the ear, worse when turning head or rolling over in bed
acute labyrinthitis - severe vertigo, acute onset, usually viral adn settles down
Meniere’s disease - triad of vertigo, hearing loss and tinnitus - abnormal fluctuations in endolymphatic fluid, attacks that come and go
Ototoxicity - aminglycoside antibiotics (gentamicin), thiazide diuretics, lithium
Acoustic neuroma - unilateral hearing loss and vertigo causes by Scwannoma in the brain
Traumatic damage involving petrous part of temporal boe
herpes zoster around the external acoustic meatus

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39
Q

Which medications are associated with ototoxicity that can present as vertigo?

A

aminogylcoside antibiotics like gentamicin

thiazide diuretics

lithium

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40
Q

What are some features in the history which would point you away from a diagnosis of vertigo?

A

feeling faint
light-headedness
loss of awareness during attacks

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41
Q

How would you investigate vertigo?

A

hx
tilt table test
MRI scan if suspecting acoustic neuroma

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42
Q

How is vertigo managed?

A

symptomatic tx for dizzinessin acute labyrinthitis - prochlorperazine (stemil)

antihistamines can help with dizziness - cinnarizine

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43
Q

How does a headache due to venous sinus thrombosis present?

A

subacute or sudden headache

papilloedema - do fundoscopy!!

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44
Q

What are the symptoms of a sinusitis headache?

A 
dull, constan ache over frontal/maxillary sinuses, may also be felt right in the middle of the nose/forehead
tenderness
post-nasal drip
pain worse when leaning forwards 
common with coryza 
pain lasts 1-2 weeks
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45
Q

How does acute glaucoma present?

A

elderly, long-sighted people
constant aching pain develops rapidly around one eye, radiating to the forehead
symptoms - markedly reduced vision, visual halos, nausea/vomiting
signs - red congested eye, cloudy cornea, dilated non-responsive pupil (may be oval shaped), decreased acuity

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46
Q

What sort of things can precipitate acute glaucoma?

A

dilating eye-drops
emotional upset
sitting in the dark (cinema)

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47
Q

How do you treat acute glaucoma?

A

immediate expert help

IV acetazolamide - a carbonic anhydrase inhibitor

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48
Q

How are migraines treated and prevented?

A

Tx - NSAID + triptan or paracetamol + triptan

Prophylaxis - topiramate or propranolol

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49
Q

How are cluster headaches treated?

A

acute attack - 100% oxygen for 15 mins + sumatriptan SC

prophylaxis - verapamil

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50
Q

How is trigeminal neuralgia treated?

A

Carbamazepine

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51
Q

What are the clinical features and treatment of giant cell arteritis?

A

exclude in all >50 with headache lasting a few weeks

tender, thickened, pulseless temporal arteries
jaw cluadication
ESR>40

tx - stat high dose methylprednisolone

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52
Q

What are the main signs of Parkinson’s disease?

A
  1. bradykinesia (cardinal sign)
  2. rigidity
  3. pill-rolling resting tremor
  4. shuffling gait
  5. loss of postural reflexes
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53
Q

What are some red flag symptoms which may lead you to believe that it’s not PD but instead a PD+ syndrome?

A

Early falls
ealy cognitive decline
early bladder and bowel dysfunction
both sides affected equally

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54
Q

What are the 4 PD+ syndromes?

A
  1. progressive supranuclear palsy (PSP)
  2. cortico-basal degeneration
  3. Multi-system atrophy
  4. Lewy body dementia
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55
Q

What are the features of progressive supranuclear palsy?

A 
early falls
early cognitive impairment 
occurs above the nuclei of C3, 4 and 6
difficulty moving the eyes
ocular cephalic reflex will be present (caused by supranuclear issue) they tilt/turn their head to look at things rather than moving their eyes
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56
Q

What are the features of multi-system atrophy?

A

early bladder and bowel dysfunction

autonomic involvement i.e. casuing postural hypotension and falls

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57
Q

What are the features of Lewy Body dementia?

A

early visual hallucinations
clouding of consciousness
sleep behaviour disorder

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58
Q

What are the extra features of cortico-basal degeneration?

A

early myoclonic jerks
apraxia
agnosia
alien limb

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59
Q

What are the 3 types of tremor and what can cause them?

A
  1. intention - cerebellar issue
  2. resting - PD
  3. Postural - anxiety, increased adrenaline, slabutamol, valproate, lithium, benign essential tremor
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60
Q

What are some neurological causes of altered sensation?

A

MS
peripheral neuropathy due to DM
GBS - ascending paralysis and numbness
Spinal cord compression - legs, saddle anaesthesia

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61
Q

What are some causes of blackouts/LOC?

A 
vasovagal - neruocardiogenic syncope 
situational syncope 
carotid sinus syncope 
epilepsy 
NEA
drop attacks - cataplexy, hydrocephalus 
hypoglycaemia
orthostatic hypertension 
anxiety - hyperventilation
factitious blackouts
choking
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62
Q

What are the vascular causes of unilateral vision loss?

A

amaurosis fugax
central retinal artery occlusion
central retinal vein occlusion
anterior ischaemic optic neuropathy (think GCA)
stroke affecting the occipital lobe
GCA
vitreous haemorrhage - diabetic retinopathy, CRVO, macular degeneration

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63
Q

What are the non-vascular causes of unilateral vision loss?

A 
optic neuritis (MS)
retinal detachment - flashes/floaters with decreased vision
acute angle closure glaucoma - painul red eye, N&V
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64
Q

What investigations would you do in someone presenting with unilateral vision loss?

A

full eye exam - movements, acuity, fundoscopy
MRI
VEP - visual evoked potentials - helps dx optic neuritis
Fluorescecin angiography - central retinal vein occlusion
tonometry - measures intra-ocular pressure (glaucoma)
USS - ocular USS to look for vitreous haemorrhage/retinal detachment
LP - shows oligoclonal bands in MS

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65
Q

What can cause spinal cord compression?

A 
malignancy or benign mass
infection (epidural abscess)
disc prolapse 
haematoma (esp if on warfarin)
myeloma - rule out in anyone >50 with back pain
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66
Q

Secondary malignancy is the most common cause of cord compression. What are the 5 cancers which spread to the bone?

A 
Breast
Thyroid
Prostate 
Kidney
Lung
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67
Q

What is the ddx for cord compression?

A 
transverse myelitis 
MS
trauma 
dissecting aneurysm 
GBS
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68
Q

What causes dyarthria?

A

cerebellar disease
extrapyramidal disease i.e. stroke
pseudobulbar palsy - MND, severe MS
bulbar palsy - facial nerve palsy, GBS, MND

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69
Q

What is the difference between bulbar and pseudobulbar palsy?

A

pseudo - affects upper motor neurones
bulbar - affects te lower motor neurone (of C9, 10, 11, 12)

pseudobulbar dysarthria - slow, nasal, effortful “hot potato” voice

bulbar dysarthria - nasal speech due to paralysis of the palate

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70
Q

What causes dysphonia (reduced volume of speech due to weakness of respiratory muscles)?

A

Myasthenia gravis
Gullain Barre Syndrome
Parkinson’s disease (dysphonia + dysarthria)

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71
Q

How does Broca’s dysphasia differ from Wernicke’s dysphasia?

A

Broca’s - expressive - non-fluent speech produced with effort and frustration, malformed words, reading and writing are impaired but comprehension is intact.

Wernicke’s - receptive - empty, fluent speech, cannot respond to requests. Reading, writing and comprehension are impaired, replies are inappropriate

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72
Q

What are some neurological disorders that can cause difficulty swallowing?

A 
myasthenia gravis 
bulbar palsy 
pseudobulbar palsy 
syringobulbia (fluid filled cavities in the brain stem)
bulbar poliomyelitis 
wilson's disease
Parkinson's disease
stroke
73
Q

What are some non-neurological conditions which cause swallowing difficulty?

A 
cancer
benign strictures
pharyngeal pouch 
achalasia 
oesophageal spasm 
systemic sclerosis - scleroderma
74
Q

What drug can help in the management of urinary retention?

A

Tamsulosin - alpha-blocker - relaxes muscle in the bladder neck

75
Q

What are the causes of optic neuritis?

A

MS
infection - lyme, syphilis, HIV
B12 deficiency
arteritis (GCA)

76
Q

How does optic neuritis present?

A

reduced visual acuity over a few days
pain on moving eye
exacerbated by heat or on exercise
relative afferent pupillary defect
dyschromatopsia - abnormal perception of colours
recovery of vision usually occurs within 6 weeks

77
Q

What are the diagnostic criteria for MS?

A

2 CNS lesions
with symptoms lasting >24 hours
disseminated in time (>1 month apart)
and space (clinically or on MRI)

MCDONALD CRITERIA

78
Q

What are the 4 subtypes of MS?

A
  1. relapsing remitting
  2. primary progressive
  3. secondary progressive
  4. benign
79
Q

What are the typical symptoms of MS?

A
  • visual loss (optic neuritis)
  • pyramidal weakness, spastic paraparesis
  • sensory disturbance
  • cerebellar symptoms - nystagmus, vertigo, tremor, ataxia, dysarthria
  • bladder involvement
  • sexual dysfunction
  • fatigue
  • cognitive impairment
80
Q

What are the 2 named signs seen in MS?

A
  • Lhermitte’s sign - electric shock sensation down trunk and limbs when they flex their neck
  • Uhtoff’s phenomenon - symptoms worse in hot bath/hot environment
81
Q

What is internuclear ophthalmoplegia?

A

decreased adduction of the ipsilateral eye
nystagmus on abduction of contralateral eye

lesion is in medial longitudinal geniculus

82
Q

What will you see in the results of a lumbar puncture from someone with MS?

A

oligoclonal bands

83
Q

How is MS treated?

A

methylprednisolone to tx relapses

interferons - IFN-1beta and IFN-1alpha - used to maintain remissions

monoclonal antibodies

84
Q

What are some side effects of interferons?

A
  • depression
  • flu symptoms
  • miscarriage
85
Q

What is the definition of epilepsy?

A

continuing tendency to have seizures

86
Q

What is a seizure?

A

A paroxysmal event in which changes of behaviour, sensation, cognition and consciousness are caused by excessive, hypersynchronous neurological discharges in the brain.

87
Q

How long does a seizure normally last?

A

30-120 seconds

88
Q

What is the ddx for epileptic seizures?

A 
postural syncope, cardiogenic syncope
TIA
Migraine
Hypoglycaemia
NEAD
Dystonia
Vertigo
89
Q

How is status epilepticus managed?

A

Benzos followed by AEDs:

  • 2 doses of benzo e.g. 2 x lorazepam
  • then IV valproate or phenytoin or phenobarbitol

can be stopped with anaesthesia if all else fails but high risk procedure

90
Q

When should someone be seen by a specialist after a TIA?

A

within 24 hours

91
Q

What are the features of a total anterior circulation infarct and which blood vessels does this involve?

A

problem with internal carotid artery and therefore MCA, ACA and PCA

causes cognitive imapirment, speech torubles, unilateral weakness/incooridnation, unilateral numbness or loss of sensation, dysarthra, unilateral visual loss or loss in 1 visual field.

92
Q

What are the features of a lacunar stroke?

A 
weakness or paralysis of the face, arm, leg, foot or toes  - hemiplegia or hemiparesis 
sudden numbness
difficulty walking 
difficulty speaking 
clumsiness of hand or arm
weakness or paralysis of eye muscles
93
Q

What are the clinical features of a posterior circulation infarct and which vessels are involved?

A 
vertigo
nausea and vomiting
imbalance
unilateral limb weakness
slurred speech 
doubl vision
headache
gait ataxia, limb ataxia, nystagmus

basilar or vertebral arteries

94
Q

What is the most important investigation to do if stroke is suspected?

A

CT head

95
Q

What are some early CT signs of stroke?

A

hyperdense MCA
loss of grey white matter differentiation and sulcal effacement - cortical infarction
hypodense basal ganglia (deep vessel infarct)

96
Q

What are some primary prevention methods for stroke?

A

smoking cessation
control hypertension
control hypercholesterolaemia
control diabetes
encourage active lifestyle and weight loss
reduce alcohol intake
in pts with AF - CHADSVASc to assess need for anticoagulation vs HASBLED for risk of bleeding.

97
Q

What are some secondary prevention measures for stroke after TIA?

A

investigations - 72 hours ECG to look for paroxysmal AF, carotid doppler to look for carotid stenosis, BP, echo to look for endocarditis or patent foramen ovale, if neck pain investigate for dissection with CTA/MRA

drugs - aspirin, clopidogrel, antihypertensives, statins, diatary control and diabetes mgmt

physiotherapy and MDT approach to rehab

98
Q

How is an acute ischaemic stroke managed?

A
  • aspirin 300mg for 2 weeks
  • potential for thrombolysis within 4.5 hours of onset
  • seen by specialist within 24 hours
  • control BP
  • swallow assessment and supportive care
  • FBC, LFT, U&E
99
Q

What is the time cut-off for thrombolysis in ischaemic strokes?

A

4.5 hours from onset of symptoms

100
Q

What medication is given for thrombolysis?

A

alteplase

streptokinase

101
Q

What needs to be done within 24 hours of thrombolysis therapy?

A

second CT scan to check if they’ve had a bleed

102
Q

What are some contraindications of thrombolysis?

A
  • on anticoagulants (can if on warfarin and below 1.7)
  • haemorrhagic stroke
  • > 6 hours after onset of symptoms
  • recent surgery or GI bleed
  • if active cancer
  • hypertension cut off 185/110
103
Q

What are some risks for thrombolysis?

A

haemorrhage - 1 in 20

reaction to rTPA

104
Q

What are some complications of stroke?

A

raised ICP - cerebral oedema, haemorrhage (signs = hypertension, new neuro signs, reduced GCS)

aspiration 
pneumonia 
VTE due to immobility 
pressure sores
depression
cognitive impairment 
long-term disability
105
Q

What causes SAH?

A

rupture of berry aneurysms
AVM
unknown

106
Q

What are some medical conditions associated with berry aneurysms?

A

polycystic kidneys
coarctation of the aorta
Ehlers-Danlos syndrome - hypermobile joints and skin elasticity

107
Q

What are some risk factors for SAH?

A 
smoking
alcohol misuse
hypertension
bleeding disorders
infected aneurysm
family hx
108
Q

What are the symptoms of SAH?

A 
sudden onset thunderclap headache 
vomiting 
collapse
seizures
coma 
may have experienced a warning sentinel headache earlier on
109
Q

What signs are associated with SAH?

A

neck stiffness
photophobia
Kernig’s sign (takes 6 hrs to develop) - painful extension of knee on flexion of hip

retinal haemorrhages

110
Q

What investigations should be done for suspected SAH?

A

CT head - white star shaped sign on CT - ventricles look white instead of black

LP if CT negative and no contraindications >12 hrs after headache onset

CT angiogram to locate aneurysms before surgical procedure

111
Q

What would be seen on an LP for SAH?

A

Xanthochromia (yellow CSF) - confirms SAH

112
Q

How is SAH treated?

A

immediate neurosurgery referral
nimodipine - calcium channel blocker - for 3 weeks to reduce vasospasm and cerebral ischaemia
endovascular coiling
surgical clipping

113
Q

What are some complications of SAH?

A

re-bleeding
cerebral ischaemia due to vasospasm
hydrocephalus
hyponatraemia

114
Q

How does an extradural bleed look on CT?

A

convex shape

lentiform lesion that does not cross the suture lines as the periosteum crosses through the suture continuous with the outer periosteal layer.

115
Q

How does a subdural bleed look on CT?

A

concave shape - from front to back

crescentic lesion with internal margin paralleling the cortical margin of the adjacent brain.

116
Q

What is a subdural haemorrhage?

A

bleed in between dura and arachnoid mater

venous bleeds from the dural venous sinuses

consider in all whose conscious level fluctuates

117
Q

What is the most common cause of subdural haemorrhage?

A

truama - often forgotten/minor trauma from up to 9 months ago

result of acceleration-deceleration injury

particularly in elderly people, alcoholics and shaken babies due to smaller brain size

118
Q

What are the symptoms of a subdural haemorrhage?

A

gradually reducing levels of consciousness
insidious onset of physical/intellectual slowing
sleepiness
headache
personality change
unsteadiness

119
Q

What are some signs of subdural haemorrhage?

A

raised ICP
seizures
localising neuro symptoms - unequal pupils, hemiparesis

120
Q

How is a subdural haemorrhage investigated?

A

CT scan showing concave bleed

half-moon/crescent shape

121
Q

How is a subdural haemorrhage treated?

A

evacuate the bleed - Burr holes, craniotomy

122
Q

Where does an extra-dural haemorrhage occur?

A

happens in the space between the dura and the skull

usually arterial - middle meningeal artery

can be venous bleed if fractures disrupt venous sinuses

123
Q

What is a big red-flag symptom of extradural haemorrhage?

A

lucid interval after head injury before becoming drowsy

then conscious levels fall and are slow to improve

124
Q

What is often the cause of an extradural haemorrhage?

A

fractured temporal or parietal bone at a place caled the pterion causing laceration of the middle meningeal artery and vein

typically after trauma to the temple

125
Q

How do extradural haemorrhages present?

A

deteriorating consciousness after a head innjury that initially produced no LOC
lucid interval
headache, vomiting, confusion, fits, hemiparesis with brisk reflexes and up-going plantars
if bleeding continues - ipsilateral pupil dilates, coma, bilateral limb weakness, breathing becomes deep and irregular due to brainstem compression

126
Q

What is the ddx for extradural haemorrhage?

A

epilepsy
carotid artery dissection
carbon monoxide poisoning

127
Q

What investigations should be done for a suspected extradural haemorrhage?

A

CT head - convex shape
X-ray skull

LP CONTRAINDICATED

128
Q

What are some signs seen in meningitis?

A

neck stiffness
photophobia
positive Kernig’s sign
positive Brudzinski’s sign

non-blanching petechial rash - later sign of meningococcal septicaemia

129
Q

What investigations would you do for suspected meningitis?

A

blood cultures
blood glucose
LP - MC&S, glucose, virology
thorat swab looking for meningococcus

130
Q

What LP findings would you see in someone with a bacterial meningitis?

A

LOW glucose
raised polymorphs - neutrophils, basophils and eosinophils
raised protein
cloudy appearance of fluid

131
Q

What LP findings would you in a viral meningitis?

A

raised lymphocytes
normal/slightly low glucose
normal protein
clear appearance

132
Q

How is meningitis treated?

A

as soon as suspected - stat dose of IM benzylpenicillin before admitting to hospital
in hospital - take cultures and treat BEFORE cultures come back with IV cefotaxime
if viral - IV acyclovir
adjust tx based on sensitivities from culture result
prophylaxis for close contacts with rifampicin

133
Q

What type of presentation shoudl always raise suspicion of encephalitis?

A

whenever odd behaviour, decreased consciousness, focal neurology or a seizure
is preceded by an infectious prodrome - pyrexia, rash, lymphadenopathy, sores, conjunctivitis, meningeal signs

134
Q

What are the viral causes of encephalitis?

A 
HSV
CMV
EBV 
VZV
HIV
mealses 
mumps
rabies
West Nile virus 
Tick-borne encephalitis
135
Q

How is suspected encephalitis investigated?

A

blood cultures ans serology for viral PCR
CT
LP
EEG

136
Q

How should encephalitis be treated?

A

start acyclovir within 30 mins of pt arriving if suspected encephalitis
suppotive therapy in HDU or ICU if needed
symptomatic treatment - phenytoin for seizures

137
Q

What is the most common cell type seen in primary brain tumours?

A

glial cell origin - 90% astrocytomas, 5% oligodendrocytoma

138
Q

Which types of cancer can spread to the brain?

A 
Lung
breast
melanoma 
GI tract
kidney
139
Q

What is the triad of presenting symptoms for brain tumours?

A

symptoms of raised ICP
loss of function/focal neurological deficit
seizures/epilepsy

140
Q

What are the symptoms of raised ICP?

A 
headache worse in the morning 
worse when laying down/leaning forwards, coughing
drowsiness
confusion
comiting 
papilloedema on fundoscopy
141
Q

What is the gold standard investigation for a suspected brain tumour?

A

MRI brain

142
Q

What is an important side effect of giving dexamethasone to reduce brain swelling in mgmt of tumours?

A

insomnia so give in the morning

143
Q

What are some medications that can cause Parkinson’s disease-like symptoms and how are they managed?

A

Haloperidol (dopamine blockade) and metoclopramide/domperidone (anti-emetics)

manged with anticholinergics like oxybutinin

144
Q

How is PD managed?

A

education, exercise, physio
dopaine replacement - L-dopa (plus carbidopa - stops levodopa breaking down into dopamine outisde the brain to reduce side effects)

dopamine agonists - bromocriptine
MAO-B inhibitors - rasigiline, selegiline - inhibit dopamine breakdown
DBS

145
Q

What are some side effects of L-dopa?

A

nausea
dyskinesia - chorea-like movements
effectiveness decreases over time

146
Q

Which PD medication is most associated with gambling addiction?

A

dopamine agonists - cabergoline, bromocriptine

147
Q

What are the main causes of GBS?

A

usually triggered by infection esp campylobacter jejuni, EBV and CMV

148
Q

How does GBS present?

A

progressive onset of limb weakness/paralysis and peripheral neuropathy
stats distally and works its way up
usually symmetrical
reflexes lost early in illness
often sensory symptoms
can involve facial muscles –> bulbar palsy
respiratory failure

149
Q

What is Miller-Fisher syndrome?

A

related varaint to GBS that affects CNS and eye muscles

characterised by ophthalmoplegia (eye muscle paralysis) and ataxia

150
Q

Ddx for GBS?

A

other causes of neuromuscular paralysis - hypokalaemia, polymyositis, botulism, poliomyelitis

MRI spineto exclude transverse myelitis or cord compression

151
Q

What investigations need to be done for GBS?

A

LP - CSF - protein elevated, normal glucose, normal cell count

NCS - show slowing of motor conduction

monitor serial FVC

152
Q

How is GBS treated?

A

supportive therapy

IVIG (CI - IgA deficiency –> allergic reaction)

plasmapheresis

DVT prophylaxis

153
Q

What are the 2 main complications of GBS?

A

resp failure

prolonged disability

154
Q

What is motor neurone disease?

A

UMN + LMN lesions

relentless and unexplained destruction of upper motor neurones and anterior horn cells in the brain and spinal cord

155
Q

What are the symptoms of MND?

A

weakness - progressive
dysarthria
dysphagia

NO SENSORY SYMPTOMS

156
Q

What are the signs associated with MND?

A

fasciculations (esp in tongue) - LMN
UMN - hypotonia, brisk reflexes
muscle wasting

157
Q

Ddx for MND?

A

cervical spine lesion

158
Q

What is the diagnostic tool used for MND?

A

El-Escorial diagnostic criteria

159
Q

How is MND treated?

A

no curative tx

riluzole - neuroprotective glutamate antagonist

supportive - ventilation, NG feeding, antidepressants
palliative care

160
Q

What are some complications of MND?

A

UTI
pneumonia
constipation
pressure sores

161
Q

What type of dementia is associated with MND?

A

frontotemporal dementia - Pick’s disease

162
Q

What is myasthenia gravis?

A

autoimmune condition

anti-ACH receptor antibodies

associated with thymic hyperplasia

163
Q

How does MG present?

A

Eey dropping (ptosis)
weakness and fatiguability - ocular, bulbar and proximal limb muslces
struggle with - hair, stairs chair, speech, face and neck weakness, mastication and swallowing, breathing
eventual muscle atrophy

164
Q

How do you investigate MG?

A

anti-AChR antibodies
anti-MuSK antibodies
mediastinal CT or MRI to look for thymoma and lung cancer (Lambert-Eaton syndrome - small cell lung cancer)
repetitive nerve stimulation shows reduction

serial monitoring of resp function

165
Q

What medications can worsen symptoms of MG?

A 
antibiotics
CCBs
beta blockers
lithium
statins
166
Q

How do you treat MG?

A

anti-cholinesterases - pyridostigmine or rivastigmine
immune suppress - steroids, azathioprine
thymectomy - in pts with thymoma or anti-AChR +ve disease
plasmapheresis for severe relapsing cases

167
Q

What is a myasthenic criris and what can trigger it?

A

difficulty breathing or speaking, increased WOB with intercostal recessions, tiredness, trouble swallowing

triggers - infection, thyroid disease, monthyl periods/pregnancy, trauma/srugery, change in meds

tx - ventilation anticholinesterases, immunosuppressives, IVIG, IV fluids, plasmapheresis

168
Q

What type of inheritance pattern is seen in Duchenne muscular dystrophy?

A

X-linked recessive
no male-to-male transmission
females are carriers but not affected

169
Q

How does Duchenne’s present?

A

proximal muscle weakness - Gower’s sign
delayed milestones

suspect in all boys not walking by 18 months

170
Q

Who is the typical patient you’d expect to see presenting with idiopathic intracranial hypertension?

A 
obese woman 
narrowed visual fields 
blurred vision +/- diplopia 
6th nerve palsy 
enlarged blind spot if papilloedema present 
consciousness and cognition preserved
171
Q

What causes idiopathic intracranial hypertension?

A

unkonw
secondary to venous sinus thrombosis
drugs - tetracycline, nitrofurantoin, vitamin A, isoreinoin (roccutane), danazol, somatropin

172
Q

What investigations can be done for IIH?

A

CT head - show sno SOL

LP - increased opening pressure

173
Q

How can IIH be treated?

A

weight loss - firstline
acetozolamide (also used for glaucoma)

topiramate can als be used + helps with wt loss
therapeutic LP
surgery - optic nerve sheath decompression and fenestration to prevent optic nerve damage
lumboperitoneal or ventriculoperitoneal shunt

174
Q

What is hydrocephalus and what are the different subtypes?

A

hydrocephalus - abnormal build-up of CSF around the brain

Subtypes -

  1. congenital hydrocephalus - born with excess fluid on the brain
  2. acquired - after birth, due to injury or illness
  3. normla pressure hydrocephalus - develops in >60 yr olds
175
Q

What causes congenital hydrocephalus?

A

spina bifida

infection during pregnanct - mumps, rubella

176
Q

What are the symptoms of normal pressure hydrocephalus?

A

abnormal gait
urinary incontinence
dementia

177
Q

What are the general symptoms of hydrocephalus?

A

headache
vomiting
blurred vision
difficulty walking

178
Q

How is hydrocephalus investigated?

A

CT and MRI scans to diagnose congenital and acquired hydrocephalus
NPH diagnostic criteria = walking, mental ability and bladder control

179
Q

How is hydrocephalus managed?

A

ventriculoperitoneal shunt - sugically implanted into the brain to drain away excess fluid

endoscopic third ventriculotomy - alternative to shunt surgery - home made in the floor of the third ventricle to allow trapped CSF to escape to the surface where it can be re-absorbed

complications - shunt can become blocked or infected

NV - Phase 3A (7 decks)

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