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D TO REVISE - PHASE 3A > TO REVISE NEURO > Flashcards

TO REVISE NEURO Flashcards

1
Q

STROKE
What are the causes of ischaemic strokes?

A

small vessel occlusion by thrombus
atherothromboembolism (e.g. from carotid artery)
cardioembolism (post MI, valve disease, IE)
hyper viscosity
hypoperfusion
vasculitis
fat emboli from a long bone fracture
venous sinus thrombosis

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2
Q

STROKE
What are the causes of haemorrhagic stroke?

A

Bleeding from the brain vasculature

  1. Hypertension - stiff and brittle vessels, prone to rupture
  2. Secondary to ischaemic stroke - bleeding after reperfusion
  3. Head trauma
  4. Arteriovenous malformations
  5. Vasculitis
  6. Vascular tumours
  7. Carotid artery dissection
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3
Q

SAH
What is the pathophysiology of a subarachnoid haemorrhage (SAH)?

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
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4
Q

EDH
What are some differentials for EDH?

A
  • Epilepsy,
  • CO poisoning,
  • carotid dissection
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5
Q

EPILEPSY
Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

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6
Q

PARKINSON’S DISEASE
What is the management of Parkinson’s disease?

A
  • Lifestyle: education, exercise, physio, MDT

young onset + fit
- Dopamine agonist (ropinirole)
- MAO-B inhibitor (rasagiline)
- L-DOPA (co-careldopa)

frail + co-morbidities
- L-DOPA (co-careldopa)
- MAO-B inhibitor (rasagiline)

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7
Q

HUNTINGTON’S DISEASE
What is the pathophysiology of Huntington’s disease?

A
  • Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
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8
Q

MND
What is the general clinical presentation of MND?

A
  • Insidious + progressive muscle weakness affecting limbs, trunk, face + speech
  • Often first noticed in upper limbs, may be fatigue when exercising
  • May have stumbling spastic gait, weak grip + clumsiness
  • Dysarthria, dysphagia, emotional lability in pseudobulbar palsy
  • NO SENSORY SYMPTOMS
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9
Q

MND
What medication may be given in MND?

A
  • RILUZOLE – Na+ blocker inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
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10
Q

MULTIPLE SCLEROSIS
What are the symptoms of MS?

A

DEMYELINATION –
- Diplopia (CN VI)
- Eye movement pain (optic neuritis, v common)
- Motor weakness
- nYstagmus
- Elevated temp worsens
- Lhermitte’s sign
- Intention tremor
- Neuropathic pain
- Ataxia
- Talking slurred (dysarthria)
- Impotence
- Overactive bladder
- Numbness

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11
Q

MULTIPLE SCLEROSIS
What are some signs of MS?

A
  • UMN = spastic paraparesis, brisk reflexes, hypertonia
  • Sensory = loss of sensation, cerebellar signs
  • Relative afferent pupillary defect
  • Internuclear ophthalmoplegia
  • Optic atrophy (pale optic disc) in chronic MS
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12
Q

MULTIPLE SCLEROSIS
What is the general symptomatic management for MS?

A

Spasticity
- BACLOFEN (GABA analogue, reduces Ca2+ influx)
- TIZANIDINE (alpha-2 agonist)
- BOTOX INJECTION (reduces ACh in neuromuscular junction)

urinary incontinence = catheterisation

incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs

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13
Q

MENINGITIS
What is the management of bacterial meningitis

A
  • IV cefotaxime
    • amoxicillin to cover listeria (potential contraction in birth) in <3m
  • Dexamethasone to reduce frequency + severity of neurological sequelae
  • Adjust treatment according to sensitivities
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14
Q

ENCEPHALITIS
What investigations would you do for encephalitis?

A
  • Blood culture + CSF serology for viral PCR
    MRI - shows areas of inflammation, may be midline shifting
    EEG - periodic sharp and slow wave complexes
    lumbar puncture
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15
Q

BRAIN ABSCESS
What are the most common causative organisms?

A
  • Staph. aureus + strep. pnuemoniae
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16
Q

BRAIN ABSCESS
What is the management of brain abscess?

A
  • CT guided aspiration via burr hole or craniotomy + abscess cavity debridement
  • Craniotomy usually if no response to aspiration or if reoccurs
  • Abx with IV ceftriaxone + metronidazole, ICP Mx with dexamethasone
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17
Q

BRAIN DEATH + COMA
What are the components of ‘motor’ in GCS?

A

M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = flexion to pain
M2 = extension to pain
M1 = no response

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18
Q

MYASTHENIA GRAVIS
What investigations would you do for myasthenia gravis?

A

mostly clinical examination
positive tensilon test
anti-AChR antibodies
TFTs
EMG
CT of thymus
crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis

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19
Q

GUILLAIN-BARRE
What are the investigations for GBS?

A

Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
bloods - FBC, U&E, LFT, TFT
Spirometry = respiratory involvement
ECG

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20
Q

NEUROPATHY
What are the causes of peripheral neuropathy?

A

ABCDE –
- Alcohol
- B12 deficiency
- Cancer + CKD
- Diabetes + drugs (isoniazid, amiodarone)
- Every vasculitis

21
Q

NEUROPATHY
What is Charcot-Marie-Tooth disease?

A
  • Autosomal dominant condition.
  • Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
22
Q

NEUROPATHY
What are the investigations used in neuropathy?

A
  • Neuropathy screen (symmetrical) = FBC, CRP/ESR, U+E, glucose, TFT, B12 + folate
  • Vasculitis screen (asymmetrical) = first 3 + ANA, ANCA, anti-dsDNA, RhF, complement
  • EMG + nerve conduction studies
23
Q

SPINAL CORD INJURY
What is Brown-Sequard syndrome?

A
  • Lateral hemisection of spinal cord
  • Ipsilateral weakness below the lesion (lateral corticospinal)
  • Ipsilateral loss of fine touch, proprioception + vibration (DCML)
  • Contralateral loss of pain + temp (lateral spinothalamic)
24
Q

MYOPATHY
What are the investigations for myopathies?

A
  • CRP/ESR, creatinine kinase elevated
  • Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy
25
Q

NEURO PHARMACOLOGY
What are the side effects of Levodopa?

A
  • Postural hypotension
  • Confusion
  • Dyskinesias (abnormal movements)
  • Effectiveness decreases with time (even with dose increase)
  • On-off effect
  • Psychosis
26
Q

NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?

A
  • Catechol-o-methyltransferase (COMT) inhibitor = entacapone
  • Monoamine oxidase-B (MAO-B) inhibitor = selegiline
  • Inhibit enzymatic breakdown of dopamine
27
Q

NEURO PHARMACOLOGY
What are some SEs + C/Is of triptans?

A
  • Dizziness, dry mouth, sleepy, nausea
  • C/I in CVD
28
Q

EPILEPSY
Define seizure

A

Paroxysmal event in which changes of behaviour, sensation, cognition + consciousness caused by excessive, hypersynchronous neurological discharges in the brain

29
Q

ENCEPHALITIS
What are the non-viral causes of encephalitis?

A

Bacterial meningitis
TB
Malaria
Lyme’s disease

30
Q

MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?

A

Abx, CCBs, beta-blockers, lithium + statins

31
Q

EDH
what is the appearance of EDH on non-contrast head CT?

A

lens shaped haematoma = LEMON SHAPE
doesn’t cross suture lines
shows midline shift

32
Q

SDH
what is the appearance of SDH on non-contrast head CT?

A

crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time)
unilateral
shows midline shift

33
Q

HUNTINGTON’S DISEASE
what are the signs of Huntington’s disease?

A

Abnormal eye movements
Dysarthria
Dysphagia
Rigidity
Ataxia

34
Q

MND
What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes

35
Q

MYASTHENIA GRAVIS
What can weakness due to myasthenia gravis be worsened by?

A

Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs

36
Q

HORNER’S SYNDROME
what are the clinical features of horner’s syndrome?

A

MAPLE

Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)

37
Q

HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?

A

excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue

  • injury
  • bleeding
  • infection
  • brain tumour
  • brain surgery
38
Q

CHRONIC FATIGUE SYNDROME
what are the differentials?

A

mononucleosis
lyme disease
MS
SLE
hypothyroidism
fibromyalgia
depression
sleep disorders

39
Q

MENIERE’S DISEASE
what is the classical triad of symptoms?

A

vertigo
hearing loss - worse during attacks
tinnitus

40
Q

SAH
give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
41
Q

PARKINSONS DISEASE
what is the pathway for dopamine production?

A

Tyrosine –> L-dopa –> Dopamine

42
Q

STROKE
How would lateral medullary/Wallenberg’s syndrome present?
What vessel is implicated?

A
  • Cerebellar: ataxia, nystagmus
  • Ipsi: dysphagia, facial numbness + CN palsy
  • Contra: limb sensory loss
  • Posterior inferior cerebellar artery
43
Q

STROKE
How would lateral pontine syndrome present?
What vessel is implicated?

A
  • Similar to Wallenberg’s but ipsilateral facial paralysis + deafness
  • Anterior inferior cerebellar artery
44
Q

STROKE
What criteria must be met for a posterior circulation syndrome (POCS)?

A

One of the following –
- Cranial nerve palsy + contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder (e.g. gaze palsy)
- Cerebellar dysfunction (ataxia, nystagmus, vertigo)
- Isolated homonymous hemianopia + cortical blindness

45
Q

STROKE
What areas can be affected in lacunar syndrome (LACS)?

A
  • Thalamus, basal ganglia, internal capsule
46
Q

NEUROPATHY
What are the motor signs of ulnar neuropathy?

A

Weakness/wasting of –
- Interossei (can’t do good luck sign)
- Medial lumbricals (claw hand)
- Hypothenar eminence
- +ve Froment’s sign when grip paper between thumb + index finger

47
Q

NEUROPATHY
Roots of sciatic nerve?
Causes of neuropathy?
Presentation?

A
  • L4–S3
  • Pelvic tumours or pelvic/femoral #
  • M = foot drop, S = loss below the knee laterally
48
Q

NEUROPATHY
Roots of common peroneal nerve?
Causes of neuropathy?
Presentation?

A
  • L4–S1
  • Damaged as winds round fibular head by trauma or sitting cross-legged (classic after night out)
  • M = foot drop, weak ankle dorsiflexion + eversion with high steppage gait, S = loss over dorsal foot

D TO REVISE - PHASE 3A (9 decks)

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