Neuro Flashcards

1
Q

what is a migraine?

A

complex neurological condition causing episodes or attacks of headache and associated symptoms due to hypothesised inflammation, vasodilation etc

*triggers - stress, dehydration, menstruation, disrupted sleep, missed meals, bright lights

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2
Q

what is a hemiplegic migraine?

A

unilateral limb weakness, ataxia, impaired consciousness

  • familial can be autosomal dominant can mimic stroke or TIA
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3
Q

what is the management of a migraine?

A

acute: NSAIDs, triptan, antiemetics
prophylaxis: propranolol, amitriptyline etc
other: CBT, meditation, acupunture etc

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4
Q

what is the mechanism of action of triptans in the management of migraines?

A

abort migraines when they start to develop - 5-HT receptor agonists which cause cranial vasoconstriction, inhibiting transmission of pain signals and release of inflammatory neuropeptides

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5
Q

what is the significance of migraines and the complications it may cause?

A

Migraines are associated with a slightly increased risk of stroke, particularly when associated with aura

  • The risk of stroke is further increased with the combined contraceptive pill, making them a contraindication to the combined pill
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6
Q

what is Bell’s palsy?

A

idiopathic, unilateral lower motor neurone facial palsy

  • most recover within several weeks-12m
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7
Q

how do you differentiate between a stroke and Bell’s palsy?

A
  • forehead has only ipsilateral, unilateral innervation from LMN
  • forehead NOT spared
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8
Q

what are some other features of Bell’s palsy?

A
  • unilateral facial weakness
  • post-auricular pain
  • difficulty chewing
  • incomplete eye closure
  • drooling
  • tingling
  • hyperacusis
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9
Q

what are some differentials for bell’s presentation?

A
  • Ramsay hunt
  • infections: otitis media+externa+HIV+lyme
  • systemic: DM, sarcoid, leukaemia, MS, GBS
  • tumours: acoustic neuroma
  • trauma
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10
Q

how is Bell’s palsy managed?

A
  • prednisolone in those 72h from onset
    • 50mg 10 days
    • antivirals
  • prognosis good - reassure patient
  • eye care - lubricating drops, tape when sleeping etc
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11
Q

What is an essential tremor?

A

most common type of action tremor (during voluntary contraction) that typically involves the hands and is brought out by anti-gravity positions (out-stretched)

  • associated with family history in autosomal dominant pattern
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12
Q

how does essential tremor present?

A
  • b/L voluntary tremor seen when performing task
  • typical nodding
  • tremor in voice when holding note
    *rarely affects legs
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13
Q

what differentials would you consider in essential tremor?

A
  • parkinsonism
  • anxiety
  • thyrotoxicosis
  • hepatic encephalopathy
  • CO2 retention
  • cerebellar disease
  • alcohol or drug withdrawal
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14
Q

how is essential tremor managed?

A
  • propranolol
  • other: primidone, gabapentin
  • neuromodulation, botulinum toxin, deep brain stimulation
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15
Q

what is Horner’s syndrome?

A

IPSILATERAL ptosis, anhidrosis, miosis

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16
Q

how do you differentiate the levels of lesions in Horner’s?

A

*location of anhidrosis
- face, arm and trunk: first order, spinal
- face only: post spinal cord exit, on decent down towards lung
- none: postganglionic lesions

17
Q

how would you investigate horners?

A
  • systemic
  • CXR
  • apraclonidine to rever pupillary constriction
  • hydroxyamphetamine: dilated pupil if underlying preganglionic lesion
18
Q

how is Horner’s managed?

A
  • treat underlying - may restore nerve function
  • neuro-imaging, discussion with hyperacute stroke unit
  • thrombolysis
  • anti-platelets or anticoag
19
Q

what is the pathophysiology of Subacute combined degeneration of the spinal cord?

A
  • classical metabolic disorder of the spinal cord - due to vitamin B12 or folate deficiency - over 40y/o
  • posterior columns and cortico-spinal tracts are specifically damaged
  • symmetrical dorsal column loss - joint position sense and vibration affected
20
Q

how does subacute spinal degeneration present?

A

*impaired proprioception, vibration sensation, muscle weakness and hyperreflexia

  • peripheral and CNS sings
  • visual loss
  • incontinence
  • numbness
21
Q

how is subacute degeneration investigated?

A
  • FBC - Hb low high MCV
  • serum B12
  • methylmalonic acid and homocysteine levels
  • blood film - megaloblasts, hypersegmented polymorphs
  • pernicious anaemia - intrinsic factor antibodies, parietal cell antibodies, schilling test
  • MRI
22
Q

how is subacute degeneration managed?

A
  • B12 replacement key! and treat cause
  • most improve
    • peripheral neuropathy improved within first 3-6m
    • cord signs shows little improvement to treatment
  • not using nitrous oxide in anaesthetising those with malnutrition or gastrectomy
23
Q

what is the pathophysiology of wernicke’s encephalopathy?

A
  • disorder that occurs as a result of inadequate levels of vitamin B1 (thiamine)
  • degradation of thalamic nuclei, brainstem nuclei and cerebellum and other structures around 3rd and 4th ventricles and the aqueduct
  • associated with eating disorders, GI malignant, alcoholics
24
Q

What is the triad of wernickes?

A
  • ataxia
  • opthalmoplegia
    • nystagmus - horizontal and vertical
    • conjugate gaze problems
  • confusion
25
Q

how is Wernicke’s managed?

A

*to prevent Korsakoff’s

  • high dose IV thiamine (500mg thiamine TDS, pabrinex)
    • continue with oral thiamine
      *be weary of hypoglycaemia
26
Q

How does Korsakoff’s present?

A

antero and retrograde amnesia, loss of orientation in time and space, apathy to that around him, confabulation

*thiamine and adequate hydration

27
Q
A