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Phase 2 > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the treatment for TIA

A
  • Stroke prevention
    • Aspirin
    • Statins
    • ACE inhibitors
    • Lifestyle changes
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2
Q

Describe the Aetiology of Stroke (3)

A
  • Ischaemic (80%)

- Haemorrhagic (17%)

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3
Q

How might someone with an anterior cerebral artery stroke present (5)

A
  • Contralateral leg weakness/numbness
  • Difficulty speaking
  • Decreased consciousness
  • Ataxia
  • Incontinence
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4
Q

How might someone with a middle cerebral artery stroke present (4)

A
  • Contralateral leg AND arm weakness/numbness
  • Visual loss in ONE eye
  • Difficulty understanding words
  • Facial drooping
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5
Q

How might someone with a posterior cerebral artery stroke present (4)

A
  • Vision loss
  • Difficulty interpreting vision
  • Generalised weakness
  • Headache
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6
Q

What tests would you run for stroke

A
  • URGENT HEAD CT
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7
Q

How would you treat a stroke acutely (3)

A
  • Oxygen and fluids
  • If ischaemic
    - Thrombolysis within 4.5 hours
    - iv alteplase followed by clopidogrel 24 hours after
  • If Haemorrhagic
    - iv Mannitol (decrease ICP)
    - Surgery
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8
Q

How might someone with SAH present (5)

A
  • Thunderclap headache
  • Nausea, vomiting, seizure, coma
  • Decreased consciousness
  • Vision loss/double vision
  • Neck stiffness
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9
Q

What tests would you do for SAH

A

Head CT

- Diagnostic

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10
Q

How would you treat SAH

A
  • iv mannitol
  • Stabilise patients
  • Neurosurgery
  • Endovascular stent
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11
Q

How might someone with a SDH present (6)

A
  • Decreasing cognition
  • Personality change
  • Headache
  • Nausea and Vomiting
  • Decreasing conscouisness
  • Focal Neurology (late)
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12
Q

What tests would you do for SDH

A
  • Head CT

- Sickle shaped bleed

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13
Q

How do you treat SDH (3)

A
  • Stabilise patient
  • Iv Mannitol
  • Neurosurgery- drain
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14
Q

How might someone with an EDH present (5)

A
  • Head trauma then unconsciousness
  • Often followed by lucid period
  • Severe headache
  • Nausea, vomiting, seizure, coma
  • Decreased consciousness
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15
Q

What tests would you do for EDH

A
  • Head CT

- Lemon shaped bleed

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16
Q

What are the partial triggers of migraine

A 
Chocolate
Hangover
Orgasm
Cheese
Oral contraception
Lie in
Alcohol
Tunus (loud noise)
Exercise
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17
Q

How does migraine present (4)

A
  • With/without aura
  • 30 mins - 72 hours
  • At least 3/4
    1) Unilateral
    2) Pulsing
    3) Moderate/severe pain
    4) Worse with movement
  • At least 1/2
    1) Nausea/vomiting
    2) Photophobia/phonophobia
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18
Q

How do you treat Migraine

A 
Acute
- Sumatriptan
- NSAIDs (Naproxen) avoid ibuprofen/paracetamol
- Anti-emetics
Prevention  
- Avoid triggers (headache diary)
- Beta blockers
- Amitriptyline 
- Topiramate
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19
Q

How might someone with Tension Headache present (5)

A
  • Mins to days
  • Bilateral
  • Pressing
  • Mild/moderate
  • Scalp tenderness
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20
Q

How do you treat tension headache (4)

A
  • Paracetamol/Aspirin/Ibuprofen
  • Use sparingly to avoid medication overuse headache
  • Avoid opiates
  • Amitriptyline if severe
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21
Q

How might someone with cluster headache present (5)

A
  • Sudden onset debilitating unilateral pain
  • Localised to one eye or temple or forehead
  • Crescendo pattern
  • Clusters of attacks followed by remission
  • Can be chronic
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22
Q

How do you treat cluster headache (3)

A 
Acute attack
- Sumatriptan
- Oxygen
Prevention
- CCB (verapamil) 1st line prevention
- Prednisolone + alcohol avoidance during cluster
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23
Q

What is the aetiology of trigeminal neuralgia (2)

A
  • Usually trigeminal compression due to loop of artery or vein
  • May be caused by a tumour or aneurysm
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24
Q

How might someone with trigeminal neuralgia present (2)

A
  • At least 3/4
    1) Attacks last 1 sec to 2 mins
    2) Severe
    3) electric shock/stabbing like pain
    4) Brought on by innocuous stimuli eg. shaving
  • At least 3 attacks for diagnosis
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25
Q

How do you treat trigeminal neuralgia (3)

A
  • Anti-convulsant (carbamazepine)
  • Surgery to relieve compression
  • Surgery to remove tumour/clip aneurysm if present
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26
Q

What can cause epilepsy (5)

A
  • Idiopathic (2/3)
  • Tumour
  • Stroke
  • Dementia
  • Cortical scarring
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27
Q

What are the 2 general categories of epileptic seizure

A
  • Primary Generalised (40%)
    - Electrical activity throughout entire cortex
    - Simultaneous, bilateral motor onset
    - Associated with loss of awareness/consciousness
  • Partial/Focal (57%)
    - Focal onset, may later become generalised
    - Often seen with underlying structural disease
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28
Q

What are the types of Primary generalised seizure (5)

A
  • Generalised tonic clonic seizure
    • Loss of consciousness (eyes remain open)
    • Rigidity (fall) followed by jerking (may be
      incontince)
    • Post-ictal confusion/drowsiness
  • Absence seizure
    • Stop activity and pale/stare, then resume
    • Unaware they have had seizure
  • Myoclonic seizure
    • Sudden jerking of limb
  • Tonic seizure
    • Sudden onset rigidity plus associated grunt
  • Atonic seizure
    • Sudden loss of muscle tone/movement
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29
Q

How might Partial/Focal seizure present (4)

A
  • Temporal
    - Aura and out of body experience or anxiety
  • Frontal
    - Motor movements eg. peddling legs
  • Parietal
    - Tingling/numbness
  • Occipital
    - Spots/lines/flashes
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30
Q

How would you diagnose epilepsy

A
  • 2 seizures more than 24 hours apart

- EEG (supports diagnosis)

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31
Q

How do you treat epilepsy (4)

A
  • Diazepam (rectally during seizure)
  • Carbamezapine (Not in abscence)
  • Sodium Volproate
  • Educate patients eg. don’t swim alone
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32
Q

How might frontotemporal (picks) dementia present

A
  • Middle aged onset
  • Personality change - decreased inhibitions, inappropriate behaviour
  • Picks - Pricks
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33
Q

How might someone with alzheimers present (4)

A
  • Slow progressive onset
  • Usually short term memory loss first noticed
  • Progressive decline in cognition/motor skills
  • Personality change
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34
Q

How might someone with Vascular dementia present (2)

A
  • Stepwise deterioration

- Signs of vascular disease eg. high B.P or stroke

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35
Q

How might someone with Lewy-bodies dementia present (4)

A
  • Fluctuation in cognition/skills
  • Hallucinations
  • Often associated with Parkinsons
  • Lowered inhibitions
36
Q

How might you diagnose dementia (2)

A
  • History and assess cognitive function
  • Mini metal state examination
    • > 25 = normal
    • 18-24 = mild/moderate impairment
    • <17 = severe impairment
37
Q

How do you treat dementia (5)

A
  • Encourage healthy lifestyle
  • Inform/educate friends and family
  • Nurse at home/care home
  • Acetylcholinerase inhibitors (rivastigimine)
  • B.P control in vascular dementia
38
Q

Define parkinsons disease

A
  • A degenerative movement disorder caused by a lack of dopamine in the substantia nigra
  • Triad of
    • Bradykinesia
    • Rigidity
    • Resting tremor
39
Q

Describe the pathophysiology of parkinsons

A
  • Destruction of dopaminergic neurones in substantia nigra

- Decreased dopamine to striatum so decreased stimulation of thalamus leading to decreased movemnet

40
Q

How might someone with parkinsons present (4)

A
  • Asymmetrical and progressive
  • Bradykinesia
    • Shuffling walk/narrow stance
    • Decreased arm swing
    • Drags one leg
  • Resting tremor (vs active in BET, asymmetrical)
    • Difficulty with fine motor skills eg. doing
      buttons/writing
  • Rigidity
    • Pain rolling over in bed
41
Q

How do you diagnose parkinsons

A
  • Clinical diagnosis based on examination

- Confirmed by medication response

42
Q

How do you treat parkinsons (2)

A
  • Dopamine agonist used initially to delay use of L-Dopa due to side effects (ropinirole)
  • Levo-Dopa combined with decarboxylase inhibitor to reduce peripheral conversion to dopamine
    • Careldopa
43
Q

What is huntingtons chorea

A
  • A progressive neurodegenerative disorder caused by lack of GABA (inhibitory NT) that causes chorea
  • Chorea is involuntary jerking movements that cease during sleep
44
Q

Describe the pathophysiology of huntingtons

A
  • CAG repeat mutation on huntingtin gene on chromsome 4
  • Leads to progressive cerebral atrophy especially in the striatum
  • This leads to decreased GABA synthesis causing decreased inhibition of the thalamus causing increased movement
45
Q

How might someone with huntingtons present (6)

A
  • Progressive involuntary, jerky, explosive movements
  • Ceases when alseep
  • Can’t sit still
  • Increased aggression
  • Depression
  • Unclear speech
46
Q

How do you diagnose huntingtons (3)

A
  • Mostly clinical diagnosis
  • Genetic testing (CAG repeats)
  • Head CT
47
Q

How do you treat huntingtons (3)

A
  • Diazepam (increases GABA binding)
  • Antidepressants eg. SSRI
  • Tertrabenazine (dopamine deleting agent)
48
Q

How might someone with MS present (8)

A
  • Usually monosymptomatic to start
  • Usually relapsing and remitting
  • Trigeminal neuralgia
  • Limb parasthesiae
  • Worse on exercise and heat
  • Optic neuritis (unilateral)
  • Ataxia
  • Leg weakness
49
Q

How do you diagnose MS (2)

A
  • At least 2 attacks in different CNS areas

- MRI is diagnostic if supported by clinical history

50
Q

What is the treatment for MS (3)

A
  • Acute attack give iv Methylprednisolone
  • Disease modifying agents
    • iv alemtuzumab
    • iv natalizumab
  • Stem cell transplant
51
Q

Describe the pathophysiology of myasthenia gravis

A
  • Anti-AchR antibodies block and destroy nicotinic Ach receptors on neuromuscular post-synaptic junction
  • This leads to decreased muscle excitation
52
Q

How might myasthenia gravis present (6)

A
  • Progressive muscle weakness
  • Uusally affects facial/eye, limb and speech muscles
  • Ptosis (upper eyelid droop)
  • Double vision
  • Ask patient to count to 50, voice becomes less audible
  • Ask patient to watch raised finger without moving head, they cannot for more than a few seconds
53
Q

How would you diagnose myasthenia gravis (2)

A
  • Serum anti-AchR

- EMG and NCS

54
Q

How do you treat myasthenia gravis

A
  • Acetylcholinerase inhibitors (Rivastigimine)

- Immunosuppression (prednisolone +/- Azathioprine)

55
Q

How might MND present (5)

A
  • UMN and LMN signs with NO SENSORY LOSS
  • Weakness, hyper-reflexia, wasting and fasciculations
  • Wrist and foot drop
  • Over 40
  • Dementia in 25%
56
Q

How do you diagnose MND (5)

A
  • LMN + UMN in 3+ sites is definite
  • LMN + UMN in 2 sites is probable
  • LMN + UMN in 1 site is possible
  • UMN or LMN in 1+ site is suspected
  • Confirmed by EMG
57
Q

How do you treat MND (4)

A
  • Antiglutaminergic drugs (riluzole)
  • Nasogastric tube
  • Mechanical ventilation
  • Analgesia (NSAIDs and opiates)
58
Q

Describe the pathophysiology of Guillan-Barre syndrome

A
  • Mostly post infection
  • Thought that the pathogens share antigens with schwann cells
  • This leads to autoimmune mediated demyelination of PNS neurones causing polyneuropathy
59
Q

How might Guillan-Barre present (4)

A
  • 1-3 weeks post infection acute ascending muscle weakness that may result in paralysis
  • Proximal muscles affected the most
  • May be paraesthesiae/pain or no sensory signs
  • May be autonomic signs eg. raised B.P or sweating
60
Q

What is the treatment for Guillan-Barre syndrome (3)

A
  • Ventilation if respiratory arrest
  • IV immunoglobulins for 5 days
  • LMW heparin (enoxaparin)/stockings
61
Q

What is the epidemiology of brain tumours (5)

A
  • Secondary more common
  • 16th most common in adults
  • 2nd most common in children
  • Most common are gliomas
  • Astrocytomas most common overall
62
Q

How might someone with a brain tumour present (4)

A
  • 4 Cardinal signs
    1) Signs of raised ICP
    • Progressive headache
    • Drowsiness
    • Vomiting
    • Papilloedema
      2) Seizures
      3) Progressive neurology
      4) Lethargy and tiredness
63
Q

How might you diagnose a brain tumour (2)

A
  • CT/MRI

- Biopsy

64
Q

What is the epidemiology of encephalitis (3)

A
  • Mostly viral cause
  • Mostly seen in elderly and infants
  • More common in imunocompromised
65
Q

How might encephalitis present (5)

A
  • Triad of headache, fever and altered mental state
  • Starts with headache/fever/myalgia
  • Progresses to Dec. consciousness/confusion
  • Focal neurology
  • Seizure
66
Q

How do you diagnose encephalitis (3)

A
  • MRI
    • Inflammation of brain tissue
  • EEG
  • Lumbar puncture
67
Q

How do you treat encephalitis

A
  • Anti-virals (aciclovir)
68
Q

What is the epidemiology of shingles (herpes zoster) (3)

A
  • Re-activation of chicken pox virus
  • Can occur at all ages but mostly seen in elderly
  • Incidence and severity increases with age
69
Q

How might someone with shingles present

A
  • Pain and paraesthesiae in one dermatome
  • Painful red rash on one dermatome
  • May be headache/malaise/myalgia
70
Q

How do you treat shingles

A
  • Anti-virals (aciclovir) x5 daily

- Analgesia for pain eg. NSAIDs

71
Q

How might a median nerve palsy present

A
  • Numbness/parasthesiae of palm, thumb and first two fingers + 1/2 of third
  • Weakness of thumb (thenar wasting)
72
Q

How might an ulnar nerve palsy present

A
  • Loss of wrist flexion
  • Can’t cross fingers
  • Loss of sensation on back of hand
73
Q

How might a radial nerve palsy present

A
  • Wrist and finger drop (extension of wrist)

- Loss of sensation of anatomical snuff box

74
Q

How might a CN 3 palsy present

A
  • Ptosis
  • Down and out eye
  • Pupil dilation
75
Q

How might a CN 4 palsy present

A
  • Diplopia when looking down (eg. stairs)

- Head tilted to correct

76
Q

How might a CN 5 palsy present

A
  • Sensory loss of face
  • Jaw deviation to side of lesion
  • Loss of mastication muscles
77
Q

How might a CN 6 palsy present

A
  • Adducted eye/weakness of abduction
78
Q

How might a CN 7 palsy present

A
  • Facial droop/weakness

- Associated with Bells palsy- caused by HSV, treat with prednisolone

79
Q

How might a CN 8 palsy present

A
  • Vertigo/balance difficulty

- Hearing loss

80
Q

How might a CN 9 palsy present

A
  • Dysphagia

- Palate and tongue sensation impairment

81
Q

How might a CN 10 palsy present

A
  • Uvula deviation away from lesion
  • Dysphagia
  • Hoarse/nasal voice
82
Q

How might a CN 11 palsy present

A
  • Diminished SCM/weakness
83
Q

How might a CN 12 palsy present

A
  • Tongue weakness/paralysis

- Deviation towards lesion

84
Q

What is neurofibromatosis

A 
Type 1 
- Causes tumours to grow on nerves
- Cafe au lait spots
- Abnormal clusters of freckles
Type 2 
- Associated with acoustic neuromas
85
Q

What is tubular sclerosis

A
  • Predisposes to tumours most often affect the brain, skin, kidneys, heart, eyes and lungs.
  • epilepsy
  • learning disabilities
  • behavioural problems – such as hyperactivity or an autistic spectrum disorder
  • skin abnormalities – such as patches of light-coloured or thickened skin or red acne-like spots on the face

Phase 2 (10 decks)

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