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Year 4 > Neurology > Flashcards

Neurology Flashcards

1
Q

Types of increased tone

A

Spasticity and Rigidity

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2
Q

Difference between spasticity and rigidity

A

In spasticity resistance is different in different directions and is velocity dependent
In rigidity resistance isn’t direction dependent

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3
Q

Spasticity associated with

A

Upper Motor Neuron Lesions

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4
Q

Rigidity associated with

A

Basal Ganglia

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5
Q

Grading Power

A

0 - no muscle contraction seen
1 - flicker of contraction seen, not enough to move the joint
2 - muscle can move if gravity is eliminated
3 - muscle can move the joint with full range but without any resistance
4 - muscle can move the joint against partial resistance
5 - the muscle can move the joint against full resistance

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6
Q

Power 2 =

A

Slight movement with gravity eliminated

Usually a movement parallel to the floor

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7
Q

Power 3 =

A

Movement against gravity

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8
Q

Power 4 =

A

Movement against resistance

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9
Q

Management of Trigeminal Neuralgia

A

Carbamazepine

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10
Q

Preventative Medications in MS (3)

A

Natalizumab
Alemtuzumab
Ocrelizumab

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11
Q

Prophylaxis of Cluster Headaches

A

Verapamil

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12
Q

Management of Cluster Headaches (Acute)

A

High flow oxygen

S/C Sumatriptan

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13
Q

Provocation Procedures in EEG (2)

A
  1. Hyperventilation
    = vigorous breathing results in a transient respiratory alkalosis, causes the constriction of small cerebral blood vessels
    Decreases oxygen supply to the brain
  2. Photic Stimulation
    = stimulation with flashes of light to elicit visual responses in the occipital region
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14
Q

Dysphagia from a neurological cause

A

More likely to be dysphagia to liquids then solids

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15
Q

Examination Findings in Motor Neurone Disease

Finding pattern

A

Fasciculation and brisk reflexes
Pout reflex
Weakness of shoulder abduction
See mixed pattern - combination of UMN and LMN signs. See a LACK of sensory symptoms

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16
Q

Bulbar Palsy =

A

= signs/symptoms occurring due to an impairment of CN IX-XII due to lower motor neurone
Affects muscles of mastication, facial muscles and tongue

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17
Q

Pseudobulbar Palsy =

A

= inability to control facial movements, caused by damage to the corticobulbar pathways
= UMN lesion

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18
Q

Corticobulbar Pathways are

A

The UMN course from the cerebral cortex to the nuclei

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19
Q

Investigation of MND

A

Need MRI, neurophysiology and CK

Usually trying to exclude mimics/other differentials

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20
Q

Drug management in MND

A

Riluzole - prolongs survival

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21
Q

Management in MND

A

SALT and OT
Non-invasive ventilatory support e.g. BiPAP
PEG feeding can be used as long as there isn’t significant bulbar dysfunction

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22
Q

Investigation of choice in suspected SAH

A

Non-contrast CT, under 6 hours of first presentation

Contrast isn’t always of benefit

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23
Q

Preventative medications that can be used in migraine

A

Propranolol
Topiramate
Amitriptyline
Candesartan

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24
Q

Medication to ease vomiting in migraine

A

Prochloperazine

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25
Q

Eye Examination Findings in MS (3)

A

Pale optic disc on affected side
Relative afferent pupillary defect on affected side
Reduced visual acuity on affected side

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26
Q

Examination Findings in MS (5)

A 
Pin and temperature loss on side of weakness 
Spasticity 
Weakness of shoulder abduction 
Brisk reflexes
Extensor plantars
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27
Q

Presentation of GBS (2)

A

Distal weakness and sensory disturbance

May see areflexia/diminished reflexes

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28
Q

Monitoring Requirements in GBS

A

Vital signs

FVC - GBS can produce a restrictive lung problem

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29
Q

What antibodies can be seen in GBS?

A

Anti-ganglioside antibodies

Seen in up to 60% of GBS cases

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30
Q

Management of severe GBS

A

IV immunoglobulin

Plasma exchange

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31
Q

What is CADASIL?
Presentation?
Genetics?

A

Hereditary stroke disorder
Presentation = migraine with aura, subcortical TIA, progresses to vascular dementia
Genetics: mutation of Notch 3 on Ch 19

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32
Q

Stiff Person Syndrome
Presentation
Investigation

A

= stiffness of axial muscles and superimposed painful spasms

Ix: EMG evidence of continuous motor unit activity, anti-GAD antibodies (tens of thousands)

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33
Q

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

A

= neurological disorder characterised by progressive weakness and impaired sensory function
Often seeen as the chronic progression of GBS

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34
Q

CIDP
Pathophysiology
Management

A

Path: damage to the myelin sheath via an unknown autoimmune mechanism
Mx: corticosteroids and IV immunoglobulin
Physiotherapy may improve muscle strength

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35
Q

What are the Parkinson Plus Syndromes?

A

Multiple System Atrophy
Dementia with Lewy Bodies
Progressive Supranuclear Palsy
Corticobasal Degeneration

36
Q

What areas of the brain are affected in PSP?

A

Basal ganglia
Brainstem (especially the midbrain)
Cortex (frontal lobes, limbic system)

37
Q

Presentation of PSP (5)

A 
Loss of balance 
Slowing of movement 
Impairment of vertical gaze 
Dementia 
Pseudobulbar palsy
Procerus Sign = characteristic furrowing of the forehead with frowning expression and wide eyed stare
38
Q

Presentation of Pseudobulbar Palsy

A 
= UMN lesion of CN IX-XII
Slow indistinct speech 
Dysphagia 
Brisk jaw jerk 
UMN signs in the limbs
39
Q

MRI findings in PSP

A

Atrophy in the midbrain

40
Q

Differentiating between Parkinson’s and PSP

A

Both have slowed movements and gait difficulty
Tremor common in Parkinsons, rare in PSP
Abnormal eye movements in PSP, normal in Parkinsons
PSP also has a poor response to levodopa

41
Q

Presentation of Multiple System Atrophy (4)

A

Autonomic Dysfunction e.g. orthostatic hypotension, impotence, dry mouth, urinary retention/incontinence
Tremors
Slow Movement
Muscle Rigidity

42
Q

Types of MSA

A

MSA-P - parkinsonian features dominate

MSA-C - cerebellar features dominate

43
Q

Neurons degenerated in MSA (3)

A

Basal ganglia
Inferior olivary nucleus
Cerebellum

44
Q

Management of MSA

A

Little levodopa response

Fludrocortisone is useful to prevent orthostatic hypotension

45
Q

Definitive way to diagnose corticobasal degeneration

A

Neuropathology Examination

46
Q

Presentation of corticobasal degeneration (4)

A

Parkinsonism
Alien Hand Syndrome = unable to control hand movements, feel that the hand is foreign
Apraxia
Aphasia

47
Q

What are Lewy Bodies?

A

A-synuclein cytoplasmic inclusions, eosinophillic

48
Q

Presentation of Dementia with Lewy Bodies (4)

A

Fluctuating cognition
Impairments in attention + executive funciton
REM sleep disorder
Visual hallucinations

49
Q

Investigation of Dementia with Lewy Bodies

A

SPECT imaging is best

50
Q

Need to avoid using haloperidol in

A

Dementia with Lewy Bodies

Can cause irreversible Parkinsonism

51
Q

Management of Dementia with Lewy Bodies

A

Acetylcholinesterase inhibitors

e.g. donsepil, rivastigmine

52
Q

Features of Parkinsonism (4)

A

Tremor
Bradykinesia
Rigidity
Postural Instability

53
Q

Gait seen in PD

A

Stooping, shuffling gait

54
Q

Non-Motor Features of PD (3)

A

Anosmia
Depression
REM sleep disorder

55
Q

Investigation of PD

A

Usually clinical diagnosis
MRI often normal
SPECT imaging can be helpful

56
Q

Management of PD

A

Levodopa

May use MAO-B inhibitor or dopamine agonist

57
Q

Complication of PD/not taking PD medication

A

Neuroleptic Malignant Syndrome
= high fever, confusion, rigidity, sweating, increased heart rate
Can lead to rhabdomyolysis, high K+ and seizures

58
Q

Which drugs block sodium channel influxes in the presynaptic neuron?

A

Carbamazepine
Lamotrigine
Phenytoin

59
Q

Which drugs block calcium channel influxes in the presynaptic neuron?

A

Gabapentin

Pregabalin

60
Q

Which anti-epileptic blocks neurotransmitter release?

A

Levetiracetam

61
Q

Todd’s Paralysis

A

Post-ictal temporary paralysis

62
Q

Types of Posturing

A

Decerebrate

Decorticate

63
Q

Management of Partial Seizures

A

Lamotrigine

Carbamazepine

64
Q

Presentation of Partial Seizures (Motor Fx)

A

Jerking, posturing, vocalisations

65
Q

Difference between simple and complex partial seizures

A 
Simple = no impairment of consciousness, no post-ictal symptoms 
Complex = impairment of consciousness, may see post-ictal confusion
66
Q

Where do complex partial seizures most often originate from?

A

Temporal lobe

67
Q

Presentation and Investigation of Absence Seizure

A

< 10 second pauses

See generalised spike wave abnormalities

68
Q

Management of Absence Seizures

A

Ethosuximide or Sodium Valproate

69
Q

Presentation of Tonic Clonic Seizures (3)

A

Loss of consciousness
Limb stiffening then limb jerking (tonic-clonic)
Post-ictal confusion (15 mins - 1 hour)

70
Q

Management of Tonic Clonic Seizures

A

Sodium valproate

Can offer lamotrigine if SV inappropriate

71
Q

Carbamazepine can make what types of seizure worse?

A

Myoclonic

Atonic

72
Q

Presentation of Myoclonic Seizures (2)

A

Sudden jerk of limbs, face and trunk

May see violently disobedient limb

73
Q

Management of Myoclonic Seizures

A

Sodium Valproate

OR Levetiracetam OR Topiramate

74
Q

Presentation of Atonic Seizures (2)

A

Sudden loss of muscle tone results in fall

No loss of consciousness

75
Q

Precipitants of Atonic Seizures (4)

A

Hyponatraemia
Infection
Head trauma
Withdrawal of anti-convulsants

76
Q

Initial drug of choice for Status Epilepticus

A

Lorazepam 4mg IV

77
Q

Difference between epileptic seizures and functional seizures

A

Epileptic - eyes are open: won’t be able to resist

Functional - eyes shut

78
Q

Management of Spasticity in MS (2)

A

Baclofen

Gabapentin

79
Q

Investigation of GBS

A

Use LP

Normal except high protein

80
Q

Extradural bleed VS subdural bleed difference on CT

A 
Extradural = limited by the sutures 
Subdural = not limited
81
Q

Acute VS chronic subdural bleed

A 
Acute = bright 
Chronic = hypodense/dark
82
Q

Management of MS

A

Pyridostigmine

The -stigmines are ACh-esterase inhibitors

83
Q

Investigation of choice in MS or demyelinating neuropathy

A

MRI with contrast

Contrast helps to identify areas of inflammation

84
Q

Meralgia parasthetica =

A

= entrapment of the lateral femoral cutaneous nerve, results in sensory changes

85
Q

Blood Tests Findings in Neuroleptic Malignant Syndrome (2)

A

Raised CK
Raised WBCs
= acute phase response

86
Q

Lacunar infarct =

A

= can be a pure motor stroke, if so affecting the INTERNAL CAPSULE
Arteries e.g. lenticulostriate

87
Q

Bulbar VS Pseudobulbar Palsy

A 
Bulbar = LMN lesion of CN IX-XII 
Pseudobulbar = UMN lesion of CN IX-XII: more common

Year 4 (27 decks)

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