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FINALS REVISION > Neurology/Neurosurgery > Flashcards

Neurology/Neurosurgery Flashcards

1
Q

What are the two types of brain injury?

A

Focal

Diffuse

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2
Q

Give examples of focal brain injuries

A

Contusion

Haematoma

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3
Q

Give an example of a diffuse brain injury

A

Diffuse axonal injury

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4
Q

What is the mechanism behind diffuse axonal injury?

A

Physical shearing forces following deceleration cause disruption and tearing of axons

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5
Q

What are contusions?

A

Micro-haemorrhages into brain parenchyma?

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6
Q

What are coup and contra-coup contusions?

A

Coup - adjacent to side of impact

Contra-coup - contralateral to impact

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7
Q

Give examples of secondary brain injury?

A 
Cerebral oedema
Ischaemia
Infection
Tonsillar herniation
Tentorial herniation
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8
Q

How does the disruption of normal cerebral auto-regulatory processes following trauma affect the brain?

A

Renders the brain more susceptible to blood flow changes and hypoxia

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9
Q

What is the Cushing’s reflex?

A

Bradycardia and Hypertension

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10
Q

What is Cushing’s triad?

A
  1. Bradycardia
  2. Cheyne-Stokes respirations
  3. Widened pulse pressure
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11
Q

How does increased ICP activate Cushing reflex?

A
  1. As ICP increases, it becomes greater than Mean Arterial Pressure. (ICP must be less than MAP for adequate cerebral perfusion)
  2. This causes decreases Cerebral Perfusion Pressure
  3. Decreased cerebral perfusion pressure activates sympathetic system
  4. HTN and initially tachycardia
  5. HTN triggers carotid and aortic baroceptors to activate parasympathetic nervous system
  6. Parasympathetic leads to bradycardia
  7. Continually increasing ICP causes brainstem dysfunction -> Cheyne-Stokes breathing
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12
Q

How do you treat raised ICP?

A

IV Mannitol

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13
Q

How does mannitol work?

A

osmotic diuretic

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14
Q

What is normal ICP?

A

7-15mmHg in supine position

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15
Q

How do you calculate Cerebral perfusion pressure?

A

MAP - ICP

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16
Q

What are the symptoms of raised ICP?

A 
Headaches
Vomiting
Reduced consciousness
Papilloedema
Cushing's reflex:
- Bradycardia
- Cheyne-Stokes breathing
- Widened pulse pressure
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17
Q

How do you monitor ICP?

A

Invasive monitoring:

  • Catheter placed into the lateral ventricles
  • Catheter may also be used to collect CSF samples/drain CSF to reduce pressure
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18
Q

What is the cut-off used to determine if further treatment is required to reduce ICP?

A

> 20mmHg

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19
Q

How is raised ICP treated?

A
  • Treat underlying cause
  • Head elevation to 30º
  • IV mannitol
  • Controlled hyperventilation
  • CSF removal
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20
Q

How does controlled hyperventilation aid in reducing CSF pressure?

A

Reduces PCO2 -> vasoconstriction of cerebral arteries -> reduced ICP

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21
Q

Why is caution needed when using controlled hyperventilation to reduce ICP?

A

May reduce blood flow to parts of brain which are already ischaemic

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22
Q

List 3 ways of removing CSF

A
  1. Drain from intraventricular monitor
  2. Repeated lumbar puncture (used in idiopathic intracranial hypertension)
  3. Ventriculoperitoneal shunt (hydrocephalus)
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23
Q

Where is the falx cerebri?

A

Fold of dura between cerebral hemispheres of brain

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24
Q

What structures are involved in subfalcine herniation?

A

Cingulate gyrus displaced beneath the falx cerebri

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25
Q

What is central herniation?

A

Downwards displacement of brain

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26
Q

What is transtentorial/uncal herniation?

A

Uncus of the temporal lobe is displaced beneath the tentorium cerebelli (tent above cerebellum)

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27
Q

What are the clinical consequences of transtentorial herniation?

A

Third nerve parasympathetic compression - ipsilateral fixed dilated pupil, looking down and out

Compression of cerebral peduncle - contralateral paralysis

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28
Q

What is tonsillar herniation?

A

Displacement of cerebellar tonsils through foramen magnum (aka coning - brainstem compression)

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29
Q

What are the two main causes of tonsillar herniation?

A

Raised ICP

Chiari malformation

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30
Q

What happens as a result of tonsillar herniation due to raised ICP?

A

Respiratory depression. Does not occur with chiari malformation

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31
Q

What is the calvaria?

A

Top part of skull

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32
Q

What is transcalvarial herniation?

A

Brain is displaced through defect in skull (eg fracture or craniotomy site)

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33
Q

What are the cerebral peduncles?

A

connect the cerebrum with spinal cord (compression causes contralateral paralysis)

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34
Q

Binocular vision post-facial trauma is suggestive of fracture of what? (+pain on opening mouth)

A

Depressed fracture of the zygomatic bone

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35
Q

What is the most sensitive investigation for diffuse axonal injury?

A

MRI brain

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36
Q

What are the layers of the dura?

A

Periosteal layer

Meningeal layer

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37
Q

Where does the haematoma form in a subdural haematoma?

A

In the potential space between the dura and the arachnoid

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38
Q

How do you test for each nerve root?

A

C5,6 pick up sticks (biceps reflex)

C7,8 lay them straight (triceps reflex)

S1,S2 buckle my shoe (ankle reflex)

L3/L4 kick the door (patellar reflex)

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39
Q

What nerve is at risk in a Smith’s fracture?

A

Median nerve

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40
Q

How can you test for median nerve damage following a Smiths fracture?

A

Thumb opposition (loss of function of the thenar eminence

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41
Q

Which nerves are at risk during axillary dissection (eg in mastectomy and lymph node clearance)?

A

Intercostobrachial - if damaged, loss of cutaneous axillary sensation

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42
Q

What nerve is responsible for fore-arm pronation?

A

Median nerve - also responsible for thumb opposition and thenar eminence muscles

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43
Q

What is pituitary apoplexy?

A

Haemorrhage in the pituitary gland - usually due to a pituitary adenoma

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44
Q

How does pit. apoplexy present?

A

Sudden onset headache, similar to SAH
Visual field defects
Evidence of pituitary insufficiency - hypoadrenalism

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45
Q

How are prolactinomas treated?

A

Cabergoline

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46
Q

How would hypoadrenalism present?

A

Caused by pituitary tumour
hyponatraemia
hypotension

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47
Q

How can neuroleptic malignant syndrome affect the kidneys?

A

Can cause AKI

- abnormal U&Es

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48
Q

What is the most common complication following meningitis?

A

Sensorineural hearing loss

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49
Q

When are triptans contra-indicated?

A

Coronary artery disease

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50
Q

Why are triptans contra-indicated in coronary artery disease?

A

Can cause vasospasm

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51
Q

Which vitamin in pabrinex can prevent Wernicke’s encephalopathy

A

B1

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52
Q

Which sign, if positive, points to a diagnosis other than Carpal tunnel syndrome?

A

Hoffmann’s sign

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53
Q

Which anaesthetic agents are likely to be ineffective in patients with myasthenia gravis?

A

Suxamethonium (Sucks in MG)

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54
Q

Which anaesthetic agent would you need to reduce the dose for for a patient with myasthenia gravis?

A

Rocuronium (Rocks in MG)

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55
Q

What is the best initial treatment for MG (if no myasthenic crisis)

A

Pyridostigmine

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56
Q

What happens in a myasthenic crisis?

A

Respiratory muscles affected - treat with IVIg and plasmapheresis

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57
Q

How to differentiate between chronic and acute subdural haematoma?

A 
Acute = HYPERdense
Chronic = HYPOdense
58
Q

How is Bell’s palsy treated

A

If presented within 3 days of onset - prednisolone + artificial tears + advise eye taping at night

If not, artificial tears +advise eye taping at night

59
Q

What is Lambert-Eaton syndrome?

A

Paraneoplastic syndrome associated with SCLC

60
Q

What are the features of lambert eaton syndrome?

A

autonomic symptoms = dry mouth, impotence, difficulty micturating

limb-girdle weakness - waddle gait (lower limbs affected first)

hyporeflexia

61
Q

How is LEMS managed?

A

treat cancer
immunosuppression with pred/azathioprine
3,4 diaminopyridine is trialled
IVIg and plasmapheresis may be beneficial

62
Q

How to check if fluid draining from nose is CSF in basal skull fracture?

A

Check for glucose

63
Q

What happens in Lhermitte’s sign?

A

parasthesiae in limbs on neck flexion

64
Q

What are the most common cause of brain mets?

A

Lung Ca

65
Q

how does acoustic neuroma present?

A
  • sensorineural hearing loss
  • vertigo
  • tinnitus
  • absent corneal reflex
  • sense of fullness in ear
66
Q

what investigations for acoustic neuroma

A

audiogram

MRI cerebellopontine angle

67
Q

what treatment for acoustic neuroma

A

conservative
radiotherapy
surgery

68
Q

what risks associated with treatment in acoustic neuroma

A
  • facial nerve or vestibulocochlear nerve damage
69
Q

what symptoms in bells palsy

A
  • unilateral facial nerve paralysis (forehead affected)
  • hyperacusis
  • altered taste
  • postauricular pain
  • dry eyes
70
Q

when should referral be considered in bell’s palsy

A

if no sign of improvement in 3 weeks ENT referral

if months - plastic surgery referral

71
Q

what causes of brain abscess

A
  • emboli from infective endocarditis
  • extension of infection from middle ear/sinuses
  • penetrating head injury
  • trauma/injury to scalp
  • neurotoxoplasmosis infection
72
Q

what symptoms of brain abscess

A
  • headache
  • fever
  • pressure effects - focal neuro: oculomotor/abducens nerve palsy

raised ICP features:
seizures
nausea
papilloedema

73
Q

how are brain abscess managed

A
  1. surgical drainage
  2. IV cefotaxime and metronidazole
  3. dexamethasone for raised ICP
74
Q

what cancers met to brain

A 
breast 
skin
kidney
pancreas
lung
75
Q

what types of diabetic neuropathy

A
  • sensory peripheral polyneuropathy
  • autonomic neuropathy
  • mononeuritis multiplex
  • diabetic amyotrophy
76
Q

what symptoms/signs of diabetic peripheral neuropathy

A
  • glove and stocking, burning pain, pins and needles
  • worse at night
  • no ankle reflex
  • no vibration sense
77
Q

what features of ischaemic diabetic foot

A
  • claudication and pain at rest
  • trophic changes - pale pulseless hairless cold paraesthesia paralysis
  • painful ulcers on heels/toes
78
Q

what features of neuropathic diabetic foot

A
  • usually painless
  • high arched foot, clawed toes
  • warm, bounding pulses
  • painless ulcers at soles where shoes rub
79
Q

what is autonomic neuropathy in diabetes

A
  • gastroparesis - bloating, vomiting, erratic BM control
  • chronic diarrhoea worse at night
  • GORD (decreased LOS pressure)
  • postural hypotension
  • erectile dysfunction
  • urinary retention/incontinence
  • gustatory sweating
80
Q

how can gastroparesis be treated in diabetic neuropathy

A

metoclopramide, domperidone or erythromycin

81
Q

how can hypotension be treated in diabetic neuropathy

A

fludrocortisone or midodrine

82
Q

what are the main side effects of valproate

A 
teratogenic
liver damage
tremor
weight gain
curly hair
drug interactions (CYP450)
83
Q

what are the main side effects of carbamazepine

A

agranulocytosis
aplastic anaemia
CYP450 inducer

84
Q

what are the main side effects of lamotrigine?

A

steven johnson syndrome

leukopaenia

85
Q

what are the main side effects of phenytoin

A

folate deficiency - megaloblastic anaemia

vit D deficiency - osteopaenia

86
Q

define status epilepticus

A

seizure lasting more than 5 minutes

more than 3 seizures in an hour

87
Q

how is status treated

A

IV lorazepam
buccal midazolam
rectal diazepam

if established, refractory - IV phenytoin/phenobarbital
if unable to control seizure activity, induce general anaesthesia.

88
Q

what differential diagnoses of essential tremor

A 
WILSON'S DISEASE
parkinson's
MS
Huntington's chorea
hyperthyroidism
fever
drug induced - antipsychotics
89
Q

what are the symptoms of essential tremor

A

symmetrical tremor affecting mainly upper limbs, head voice, worse when arms outstretched/in attempt to carry out voluntary movements
exacerbated by stress, caffeine
better with rest/alcohol

90
Q

what mode of inheritance in essential tremor

A

autosomal dominant

91
Q

what mgmt of essential tremor

A
  • propranolol

- primidone

92
Q

what happens in a third nerve palsy

A

eye down and out
ptosis
pupil FIXED AND DILATED

93
Q

what causes lyme disease

A

Borrelia burgdorferi a spirochaete spread by ticks

94
Q

what symptoms of lyme disease

A
  • erythema migrans (bullseye rash)
  • headache, fever, lethargy, arthralgia
  • myocarditis, pericarditis, heart block
  • facial nerve palsy, radiculopathy, meningitis
95
Q

what investigations for lyme disease

A

elisa

immunoblot

96
Q

what management of early lyme disease

A

doxycycline

97
Q

what management of disseminated lyme disease

A

ceftriaxone

98
Q

what reaction can occur after Abx treatment in lyme disease and syphilis

A

jarisch-herxhaimer reaction - fever, rash, tachy

99
Q

what are the main umn and lmn signs

A

umn signs:
hypertonia, spasticity
hyperreflexia
upgoing plantars

lmn
fasciculations
muscle wasting
hypotonia
hyporeflexia
downgoing plantars
100
Q

how can mnd present

A
  • mixture of umn and lmn signs
  • muscle wasting (tibialis anterior, small muscles of hand)
  • weakness, fatigue when exercising
  • clumsiness, tripping over, dropping things
  • fasciculations
  • dysarthria
  • no cerebellar signs
  • no sensory signs
  • external ocular muscles not affected
101
Q

what investigations can be done for MND and what would they show?

A

nerve conduction - normal motor conduction
EMG - reduced number of action potentials, but higher amplitude
MRI - exclude DCM/cervical cord compression

102
Q

what symptoms of MS

A

lethargy, uhthoff’s phenomenon

  • optic neuritis
  • abducens lesions:
    • internuclear ophthalmoplegia
    • conjugate lateral gaze disorder
  • focal weakness:
    • bell’s palsy
    • Horner’s syndrome
    • Limb paralysis
    • Incontinence
  • focal sensory signs
    • Lhermitte’s sign - shooting pain down spine limbs on neck flexion
    • trigeminal neuralgia
    • numbness, paraesthesia
  • ataxia: cerebellar or proprioceptive (positive Romberg)
103
Q

what investigations for MS

A
  • Contrast-enhanced MRI brain and spine
  • LP for CSF - oligoclonal bands
  • visual evoked potentials - delayed, but well-preserved waveform
104
Q

what MRI changes in MS

A
  • high signal hyperintense T2 lesions
  • periventricular lesions
  • Dawson’s fingers projecting from near the corpus callosum
105
Q

how are MS relapses treated

A

steroids - high dose methylpred

orally or IV

106
Q

what treatments for MS

A

beta-interferon
galatiramer acetate
natalizumab
fingolimod

107
Q

what treatment for MS fatigue

A

amantadine

108
Q

what treatment for MS spasticity

A

baclofen

gabapentin

109
Q

what treatment for MS incontinence

A
  • if significant residual post-void volume, intermittent self-catheterisation
  • if urge incontinence - oxybutynin/tolterodine. (anticholinergics can worsen cognitive impairment)
110
Q

what is oscillopsia in MS and how is it treated

A

visual fields appear to oscillate

treat with gabapentin

111
Q

what is uhthoff’s phenomenon?

A

worsening of symptoms following rise in body temp (when taking a hot bath)

112
Q

what is internuclear ophthalmoplegia and how does it present

A

lesion in the median longitudinal fasciculus (3rd, 4th, 6th CNs)
causes:
- impaired adduction of eye on same side of lesion
- horizontal nystagmus of abducting eye on contrallateral side

113
Q

what is conjugated lateral gaze disorder

A

eye on same side of lesion unable to abduct. double vision.

114
Q

explain pathophys of myasthenia gravis

A
  • auto-antibodies against post-synaptic Ach receptors at neuromuscular junction
115
Q

what symptoms of myasthenia gravis

A
  • fatigability following repetitive movements, slow improvement with rest
  • ptosis
  • diplopia
  • slurred speech
  • weakness in chewing
  • dysphagia
  • proximal limb girdle, head, shoulder and neck muscles
116
Q

what investigations for myasthenia gravis

A
  • single fibre EMG
  • anti-AChR antibodies
  • anti-Muscle-specific tyrosine kinase antibodies
  • CT thorax to exclude thymoma
  • Creatinine Kinase - normal

tensilon no longer used (edrophonium) as risk arrhythmias

117
Q

how is myasthenia gravis treated

A
  • pyrodostigmine (long acting acetylcholinesterase inhibitor)
  • can add immunosuppressants (pred, aza, mycophenolate mofetil)
    In myasthenic crisis, plasmapharesis, IVIg
118
Q

what is a myasthenic crisis?

A
  • acute worsening of symptoms often triggered by other illness e.g. respiratory tract infection
  • respiratory muscle weakness
119
Q

how is myasthenic crisis treated

A

plasmapharesis, IVIg

needs ventilatory support, either NIV (bipap) or full intubation and ventilation

120
Q

explain briefly pathophys of parkinsons

A

alpha synuclein deposits

loss of dopaminergic neurons in substantia nigra

121
Q

what features of parkinson’s disease

A

asymmetrical: TRAP: tremor rigidity akinesia postural instability
- impaired olfaction
- mask like face
- flexed posture
- reduced arm swinging
- depression, dementia, psychosis, sleep disorders
- micrographia
- autonomic instability - postural hypotension

122
Q

what drug classes can be used to treat parkinson’s

A
  • levodopa (co-careldopa carbidopa (decarboxilase inhibitor) to prevent peripheral breakdown of levodopa before it reaches the brain)
  • dopamine agonists
  • COMT inhibitors
  • MAOB inhibitors
  • amantadine
123
Q

list some dopamine agonists

A

cabergoline
bromocriptine
pergolide
ropinirole

124
Q

give an example of a comt inhibitor

A

entacapone

125
Q

list some maob inhibitors

A

silegiline

rasagiline

126
Q

what is amantadine and how does it work in parkinsons

A

works against dyskinesia and rigidity

127
Q

what side effects of dopamine agonists?

A
  • cabergoline, bromocriptine
  • impulse control disorders
  • hallucinations
  • excessive daytime sleepiness
  • pulmonary/cardiac fibrosis
128
Q

why must parkinsons medication not be missed?

A

prevent akinesia, acute dystonia, neuroleptic malignant syndrome

129
Q

how should orthostatic hypotension in parkinsons be treated

A

midodrine

130
Q

how should drooling in parkinsons be treated

A

glycopyrrhonium

131
Q

what investigations for raised icp

A
  • MRI/CT to find underlying cause

- invasive ICP monitor with catheter in ventricles

132
Q

what treatment for raised ICP

A
  • treat underlying cause
  • raise head to 30degrees
  • controlled hyperventilation
  • drain CSF
    • via ICP monitor
    • repeated LP (idiopathic intracranial hypertension)
    • ventriculoperitoneal shunt (NPH)
  • IV mannitol/dexamethasone
133
Q

how does controlled hyperventilation decrease ICP

A

decreased CO2 causes vasoconstriction of cerebral arteries therefore reduced ICP

134
Q

what is LEMS

A

antibodies against voltage gated calcium channels in presynaptic terminal at neuromuscular junction

135
Q

what symptoms of lems

A
  • muscle weakness (improves after repetitive contractions) but then weakens again
  • hyporeflexia
  • hyporeflexia improves after sustained muscle contraction (post-tetanic potentiation)
  • autonomic symptoms - dry mouth, difficulty micturating, impotence, blurred vision, dizziness
136
Q

what investigation for LEMS

A

EMG - incremental response to repeated electrical stimulaiton

137
Q

what treatment for LEMS

A

treat underlying ca (SCLC, brca, ovarian ca)
amifampridine
immunosuppressants (steroids etc.)
plasmapharesis and IVIg

138
Q

which medications can exacerbate myasthenia gravis

A
  • lithium
  • suxamethonium
  • penicillamine
  • beta blockers
  • phenytoin
  • procainamide, quinidine
  • Abx: gentamicin, quinolones, macrolides, tetracyclines
139
Q

what treatment for neuroleptic malignant syndrome

A

dantrolene or bromocriptine (dopamine agonist)

140
Q

what are some side effects of levodopa

A 
dyskinesia
psychosis
on-off effect
worsening effectiveness with time
postural hypotension
cardiac arrhythmias
reddish discolouration of urine when standing
nausea and vomiting
141
Q

what staining for cryptococcus in HIV neuroinfection

A

india ink

FINALS REVISION (17 decks)

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