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Finals Club (Dundee Medicine Master Summary Deck) > Year 3: Neurology > Flashcards

Year 3: Neurology Flashcards

Everything you need to know to pass for Neurology in Dundee Medical School

1
Q

Prosencephalon becomes

A

Telencephalon > Cerebrum Diencephalon > Thalamus and Hypothalamus

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2
Q

Mesencephalon becomes

A

Midbrain

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3
Q

Rhombencephalon

A

Metencephalon > Pons and Cerebellum

Myelencephalon > Medulla

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4
Q

Ascending Pathways are

A

Somatosensory

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5
Q

2 Ascending pathways

A
  • Spinothalamic Tract
  • Dorsal Column Medial Leminiscus (DCML)
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6
Q

Spinothalamic Tract is responsible for

A

Pain and Temperature

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7
Q

Spinothalamic fibres decussate at

A

Spinal cord

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8
Q

A lesion in the spinothalamic tract would cause

A

Contralateral loss of pain and temperature

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9
Q

Spinothalamic tract is

A

Anterior

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10
Q

DCML Pathway is responsible for

A

Fine touch, pressure and vibration

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11
Q

DCML fibres decussate in

A

the medulla

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12
Q

A lesion in the DCML pathway would cause

A

ipsilateral loss of fine touch, pressure and vibration sensations

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13
Q

DCML pathway is

A

Posterior

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14
Q

DCML is split into

A
  • Fasciculus cuneatus: Upper limbs and trunk
  • Fasciculus gracilis: Lower limbs and trunk

“You stand with grace”

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15
Q

Fasiculus Cuneatus ends at

A

T6

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16
Q

Descending pathways are

A

Somatomotor

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17
Q

2 main descending pathways

A
  • Pyrimidal (Corticospinal, Corticobulbar)
  • Extrapyrimidal (Reticulospinal, Rubrospinal)
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18
Q

Pyramidal Tracts are

A

Anterior

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19
Q

Extrapyramidal tracts are

A

Anterior

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20
Q

Corticospinal tract is split into

A
  • Lateral corticopsinal tract
  • Anterior corticospinal tract
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21
Q

Lateral Corticospinal tract is responsible for

A

Voluntary motor control of the limbs and digits

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22
Q

Lateral corticospinal fibres decussate in the

A

Medulla (pyramidal decussation)

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23
Q

A lesion in the lateral corticospinal tract would cause

A

Weakness in ipsilateral limbs and digits

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24
Q

Anterior corticospinal tract is responsible for

A

Voluntary motor control of the trunk (maintains posture)

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25
Q

Corticobulbar tract is responsible for

A

Motor control of the muscles of the face, head and neck

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26
Q

Corticobulbar tract is associated with

A

Cranial Nerves

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27
Q

Rubrospinal tract

A

controls flexion in the upper limbs

“RuBROspinal as they are bicep curling”

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28
Q

Origin of rubrospinal tract is in the

A

red nucleus (in the midbrain)

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29
Q

Reticulospinal tract

A

excites extensor muscles

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30
Q

Decerebrate posture

A
  • Extension of all upper and lower limbs
  • Pronation of the wrist
  • Damage to brain, including midbrain

“You De-celebrate because they are dead, or look like it”

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31
Q

Decorticate

A
  • Flexion of upper limbs
  • Extension of the lower limbs
  • Damage to brain, excluding midbrain (rubrospinal is intact)

“Your arms are flexed to your deCOREticate”

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32
Q
  • Ipsilateral loss of touch, pressure, vibration
  • Ipsilateral loss of motor strength
  • Contralateral loss of pain and temperature
A

Brown Sequards Syndrome

“Hemi-section of the cord”

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33
Q

Bilateral loss of touch, pressure and vibration

A

Posterior Cord Syndrome

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34
Q
  • Bilateral loss of pain and temperature in a cape-like pattern
  • Bilateral weakness in proximal upper limbs
A

Central Cord Syndrome

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35
Q
  • Bilateral loss of motor strength
  • Bilateral loss of pain and temperature sensation
A

Anterior Cord Syndrome

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36
Q
  • Bilateral loss of touch, pressure and vibration
  • Bilateral loss of pain and temperature
  • Bilateral loss of motor strength
A

Complete Cord Sydnrome

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37
Q

Muscle weakness is a sign of

A

Upper and lower motor neuron lesion

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38
Q

Muscle atrophy is

A

LMN lesion

“Loss of muscle = Lower”

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39
Q

Hyperreflexia is

A

UMN lesion

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40
Q

Hyporeflexia is

A

LMN lesion

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41
Q

Increased tone

A

UMN lesion

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42
Q

Decreased tone

A

LMN lesion

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43
Q

Fasciculations

A

LMN lesion

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44
Q

Babinski sign is positive

A

UMN lesion

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45
Q

Types of Motor Neurone Disease (MND)

A
  • Amyotrophic Lateral Sclerosis (ALS)
  • Primary Lateral Sclerosis (PLS)
  • Progressive Muscular Atrophy (PMS)
  • Spinal Muscular Atrophy (SMA)
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46
Q

ALS

A

UMN and LMN lesions

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47
Q

At the beginning ALS involves

A

upper limbs (starts distally)

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48
Q

Frontotemporal Dementia is seen in

A

ALS

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49
Q

The gene that links FTD and ALS is

A

C9ORF gene

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50
Q

Treatment to improve survival in ALS

A

Riluzole

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51
Q

Treatment to improve spasticity in ALS

A

Baclofen

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52
Q

Treatment to reduce the viscosity of sputum in ALS

A

Carbocisteine

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53
Q

Primary Lateral Sclerosis presents with

A

UMN symptoms

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54
Q

Progressive Muscular Atrophy presents with

A

LMN symptoms

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55
Q

Spinal Muscular Atrophy presents with

A

LMN symptoms

“Floppy Baby Syndrome” - hypotonia

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56
Q

Gene for SMA

A

SMN 1 gene

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57
Q

Cyst in spinal cord

A

Syringomyelia

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58
Q
  • Sensory loss (pain and temperature) in the upper limps and “cape” area
  • Paralysis
  • Muscle weakness
  • Neck pain
  • Bladder problems
A

Syringomyelia

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59
Q
  • Sciatica
  • Lower back pain
  • Lower Limb/buttocks loss of sensation/ tingling
A

Lumbar stenosis

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60
Q

Compression of the spinal cord

A

Spinal Stenosis

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61
Q

Pain relieved on sitting forward or walking uphill

A

Lumbar stenosis

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62
Q

Spinal cord stops at

A

L1/2

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63
Q

Lumbar punctures are taken at

A

L3/4

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64
Q

Intervertebral disc prolapse causing Cauda Equina Syndrome usually happens at

A

L4/5

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65
Q
  • Lower limb weakness/ pain/ loss in sensation
  • Saddle area anaesthesia
  • Bladder/bowel incontinence
A

Cauda Equina Syndrome

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66
Q
  • Unliateral mydriasis (dilated pupil)
  • Down and out eye
  • Ptosis (drooping eye lid)
A

Third Nerve Palsy

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67
Q
  • Facial drooping
  • Loss of forehead wrinkles
  • Inability to close eye
  • Inability to produce tear film (dry eyes)
  • Hyperacusis (stapedius)
A

Bell’s Palsy (Facial Nerve palsy)

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68
Q

Treatment for Bell’s Palsy

A

Steroids

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69
Q
  • Miosis (constricted pupil)
  • Partial ptosis
  • Enophthalmos (sinking of the eyeball in socket)
  • Ipsilateral anhidrosis
A

Horner’s Syndrome

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70
Q

Horner’s Syndrome is due to

A

Sympathetic nerve problem/damage

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71
Q
  • Damage to C5/C6
A

Erb’s Palsy

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72
Q
  • Internally rotated arm
  • Pronated forearm
  • Flexed wrist

“Waiters tip posture”

A

Erb’s Palsy

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73
Q

Damage to C8 and T1

A

Klumpke’s Palsy

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74
Q

“Claw hand”

A

Klumpke’s Palsy

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75
Q
  • Muscle fatigue at the end of the day
  • Diplopia, ptosis, heavy head
A

Myasthenia Gravis

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76
Q

Myasthenia Gravis pathophysiology

A
  • Autoimmune neuromuscular junction disorder (B-cell mediated)
  • Auto-antibodies attack post-synaptic Acetylcholine receptors
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77
Q

Myasthenia Gravis Antobodies

A

Anti Acetylcholine receptor antibodies (AChR)

(Produced in thymus)

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78
Q

1st line Treatment for Myasthenia Gravis

A

Pyridostigmine (Acetylcholinesterase inhibitor)

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79
Q

2nd line for myasthenia gravis

A

Thymectomy

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80
Q

Side effect of Pyridostigmine

A

Can cause a cholinergic crisis

Tx: Plasmapheresis and Ig

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81
Q
  • Distal proximal weakness in arms and legs
  • Pins and needles in hands and feet
  • Recent GI campylobacter infection
A

Guillain-Barré Syndrome

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82
Q

Guillain-Barré Syndrome

A

Autoimmune destruction of peripheral nerves and their myelin insulation

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83
Q

Guillain-Barré Syndrome Antibodies

A

Anti-ganglioside antibodies

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84
Q

Treatment for Guillain-Barré Syndrome

A

Immunoglobins

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85
Q
  • “Wine bottle legs/stork like legs”- like a saber tooth
  • “Claw hand”
  • “Hammer toe”
  • Foot drop
A

Charcot-Marie-Tooth Disease

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86
Q

Pathophysiology of Charcot-Marie-Tooth disease

A

Motor and sensory neuropathies of the peripheral nervous system with associated muscle loss

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87
Q

Lambert-Eaton Myasthenis Syndrome

A

Muscle weakness to the limbs due to autoimmune antibodies attacking presynaptic Ca2+ channels, interfering with cell signals from nerve cells

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88
Q

Voltage gate calcium channel antibodies (VGCC)

A

Lambert-Eaton Myasthenic Syndrome

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89
Q

Lambert-Eaton Myasthenic Syndrome is associated with

A

Small cell carcinoma (lung cancer)

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90
Q

Treatment for Lambert Eaton Syndrome

A
  • 3,4-Diaminopyridine +Steroids
  • Pyridostigmine
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91
Q
  • Optic neuritis
  • Incontinence
  • Ataxia
  • Weakness
  • Spasticity
  • Pyramidal Dysfunction (Weakness in UL extensors, weakness in LL flexors)

Symptoms separated in space and time

Increasing frequency of symptoms

Relapsing and remitting disease

A

Multiple Sclerosis (MS)

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92
Q

Pathophysiology of MS

A
  • Inflammatory process of demyelination of CNS
  • Deposition of plaques around lateral ventricles “dawson’s fingers”
  • Acute: Pink
  • Chronic: Pearl grey
    *
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93
Q

Lhermitte’s Sign

A

Movement of neck sends electric shock pain down spine

Present in MS

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94
Q

Investigations for MS

A
  • MRI: lesions will be seen
  • LP: Oligoclonal Bands seen in CSF
    Raised Lymphocytes in CSF
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95
Q

Acute treatment of MS

A

High dose steroids (methylprednisolone)

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96
Q

1st line Treatment for MS

A
  • Beta-interferon (Avonex, Extavia)
  • or sometimes Copaxone
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97
Q

2nd line for MS

A
  • Natalizomab (Monoclonal antibody)
  • or sometimes Fingolimod
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98
Q

MS treatment for fatigue

A

Amantidine

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99
Q

MS treatment for increased sleepiness

A

Modafinil

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100
Q

MS treatment for spasticity

A

Baclofen, botox

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101
Q

Type types of Seizure

A
  • General (all of the brain)
  • Focal (partial bits of the brain)
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102
Q

Types of generalised seizures

A
  • Tonic-clonic
  • Myoclonic
  • Myotonic
  • Atonic
  • Absence
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103
Q

Tonic-Clonic Seizure

A
  • Tonic: Muscles tense up
  • Clonic: Convulsions and shaky movements

Often bite tongue

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104
Q

Myotonic seizure

A

Muscles tense up

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105
Q

Myoclonic Seizure

A

Clonic jerks: Shaky movements

Common in kids, often happen in the morning

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106
Q

Atonic seizure

A

All muscles lose tone

They fall to the floor like in Toy Story

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107
Q

Absence seizure

A

Motionless stare for 15-30s

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108
Q

Types of Focal/Partial Seizures

A
  • Simple: Remains consciousness
  • Complex: Loss of consciousness + Aura
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109
Q

Classifications of Focal/Partial Seizures

A
  • Frontal
  • Temporal
  • Parietal
  • Occipital
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110
Q

Frontal Seizure

A

Motor signs: Twitching movements, stiffness

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111
Q

Temporal Seizure

A
  • Deja Vu feeling
  • Weird smell / taste
  • Lip smacking
  • Feeling of impending doom
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112
Q

Parietal Seizure

A

Loss of sensation in distal limbs

Burning / tingling sensation

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113
Q

Occipital Seizure

A

Visual problems

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114
Q

Todd’s Paralysis

A

A period of temporary paralysis following a seizure

Can last up to 24hrs

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115
Q

Investigation for someone having a seizure

A

ECG

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116
Q

1st line treatment of Generalised Seizures

A

Sodium Valproate

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117
Q

2nd line treatment for Generalised Seizures

A

Lamotrigine

Myoclonic: Levetiracetam

Absence: Ethosuximide

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118
Q

1st line treatment for Focal/Partial Seizures

A

Carbamazepine

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119
Q

2nd line treatment for Focal/Partial Seizures

A

Lamotrigine

or sometimes Levetiracetam

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120
Q

Contraindications for sodium valproate

A
  • Teratogenic (don’t use in pregnancy), but can use in breastfeeding
  • Weight gain
  • Hair loss
  • Fatigue
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121
Q

Contraindications of carbamazepine

A

Makes general seizures worse

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122
Q

Side effects of Lamotrigine

A

Dizziness and a rash

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123
Q

Contraceptive contraindications of Epileptic medications

A
  • POP won’t work
  • Increase dosage of COC
  • Take 5mg Folic Acid for pregnancy
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124
Q

Status Epilepticus

A
  • Single epileptic seizure lasting more than five minutes
  • Two or more seizures within a five-minute period without the person returning to normal between them
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125
Q

Acute treatment of Status Epilepticus

A

1st: Rectal Diazepam, IV Lorazepam
2nd: Phenytoin

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126
Q

Single seizure patient can’t drive for

A

6 months

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127
Q

Single Seizure patient who drives heavy goods vehicles can’t drive for

A

5 years

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128
Q

Epilepsy patient without seizures has to wait

A

1 year of being seizure free to drive again

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129
Q

Epilepsy patient who drives a heavy goods vehicle has to wait

A

10 years seizure free while off of their medication

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130
Q

4 main types of Dementia

A
  • Alzheimer’s
  • Frontotemporal “Picks disease”
  • Vascular
  • Lewy Body’s
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131
Q

Criteria for dementia

A

2 or more of:

  • Forgetfulness
  • Memory loss
  • Confusion
  • Poor reason
  • Personality changes
  • Decreased concentration
  • Visual perceptions
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132
Q

Tools for diagnosing Dementia

A
  • 4AT
  • MMSE
  • MOCA
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133
Q

Frontal lobe is responsible for

A

Sequencing, fluency and behaviour

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134
Q

Parietal lobe is responsible for

A
  • Language- Left side
  • Spacial awareness- Right side
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135
Q

Temporal lobe is responsible for

A

Memory and speech

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136
Q

Alzheimer’s criteria

A

a decline in function in 2+ areas

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137
Q

Pathophysiology of Alzheimer’s Dementia

A
  • Deposition of amyloid plaques (alphabeta) that are neurotoxic and cause an inflammatory response when broken down
  • Deposition of Tau protein which is also neurotoxic
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138
Q

Alzheimer’s effects

A

Frontal, temporal and parietal lobes first

Starts in nucleus basalis of meynert

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139
Q

Amyloid plaques and Tau Protein cause

A
  • Decrease in ACh which leads to less serotonin
  • Decrease in GABA which leads to less NorA
140
Q

Pathological changes to the brain in Alzheimer’s

A
  • Huge sulci
  • Narrowed gyri
  • Cortical atrophy
  • Thin brain
  • Dilated ventricles
141
Q

Genes associated with Alzheimer’s

A
  • PSE1/2 is found in early onset dementia
  • APP is found in Trisomy 21
142
Q

Treatment for Alzheimer’s Dementia

A
  • ACh inhibitor (Donepezil, Rivastigmine, Galantamine)
  • Memantine (NMDA receptor antagonist)
143
Q

Pathophysiology of Frontotemporal Dementia

A
  • Deposition of Tau proteins- silver staining “Pick Bodies”
  • Frontal lobe atrophy
  • Gyral atrophy with knife-blade appearance
144
Q

Do not offer

A

ACh receptor antagonists or memantine in Frontotemporal dementia

145
Q

Presentation of Frontal temporal dementia

A
  • Early insidious onset
  • Personality changes
  • Preserved memory
146
Q

Lewy Body Dementia is caused by

A
  • Deposition of Lewy bodies (alpha-synuclein)
147
Q

Ubiquitin detects

A

Lewy bodies when stained

148
Q

Lewy Body Dementia is associated with

A

Parkinson’s Disease

149
Q

To have DWLB (Dementia with Lewy Bodies) and not Parkinson’s you must have

A

Onset of dementia symptoms within 1 year of onset of Parkinson’s symptoms

150
Q

Presentation of DWLB

A
  • Parkinson’s symptoms
  • Visual Hallucinations
  • REM Sleep disorder
151
Q

Investigations for DWLB

A

Positive DAT (Dopamine active transporter) scan

152
Q

Treatment for DWLB

A

ACh inhibitor (Donepezil, Rivastigmine, Galantamine)

153
Q

Vascular Dementia pathology

A
  • Multiple lacunar infarcts in small vessels in brain
154
Q

Vascular Disease is found in

A

CHD/stroke patients

155
Q

Vascular Dementia has a

A

Step wize progression

156
Q

Dementia Pugilistica is found in

A

Boxers

Due to repeated trauma

157
Q

Pathophysiology of Parkinson’s Disease

A
  • Lewy bodies also aggregate in the brain and destroy the substantia nigra (produces dopamine)
  • Decrease in dopamine leads to the inhibition of the thalamus (motor cortex) which in turn inhibits motor movement
158
Q

Core features of Parkinson’s Disease

A
  • Bradykinesia (causes shuffling gait)
  • Resting Tremor
  • Rigidity (cogwheeling limbs)
159
Q

Other associated features with Parkinsonism

A
  • Quiet speech
  • Decreased facial expressions
  • Decreased sense of smell
  • Bladder dysfunction
160
Q

Genes associated with Parkinson’s

A
  • LRRK2 gene
  • PRKN gene
161
Q

Investigations for Parkinson’s

A
  • Positive DAT scan
  • Treatment with Levodopa will work- diagnostic
162
Q

1st line treatment for Parkinson’s

A

Levodopa

(Carbidopa is prescribed alongside to prevent Levodopa from being broken down before it reaches the brain)

163
Q

2nd line treatment for Parkinson’s

A
  • Monoamine Oxidase Inhibitors (MAOIs): Selegiline, rasagiline
  • Dopamine agonist (D2 receptor agonists): Pramipexole, Ropinirole, Bromocriptine
  • COMT inhibitor: Entacapone
164
Q

1st line treatment for Parkinson’s tremor

A

Anticholinergics

165
Q

Parkinsons Plus

A

Parkinson’s plus additional neurodegenerative features

166
Q

Parkinson’s Plus features

A
  • Multi-system atrophy: Decreased BP, Ataxia
  • Progressive supranuclear palsy: Vertical gaze, Hummingbird sign
  • Cortical Basil Degeneration: Alien hand syndrome
167
Q

Huntington’s disease

A

Progressive degeneration of striatium, basal ganglia, and cerebral cortex due

168
Q

Huntington’s Genetics

A

Autosomal dominant

>38 glutamine (CAG repeats)

Chromosome 4

  • The more repeats, the earlier the onset
  • CAG repeats get longer in men, shorter in women
169
Q

Huntington’s Presentation

A
  • Middle aged
  • Chorea
  • Progressive dementia
170
Q

Treatment for Huntington’s

A

Tetrabenazine (monoamine depletor) to help with chorea

171
Q

Wilson’s Disease

A

Autosomal recessive disease that causes deposition of copper in your brain and other organs

172
Q

Symptoms of Wilson’s Disease

A
  • “Wing beating” tremor
  • Keiser-fleischer rings
173
Q

Tourette’s Syndrome

A

Autosomal dominant neurodevelopmental disorder with onset in childhood, characterized by multiple motor tics and at least one vocal (phonic) tic

174
Q

Treatment for Tourette’s

A
  • 1st: CBT
  • 2nd: Clonidine (alpha agonist)
  • 3rd: Tetrabenazine (monoamine depletor)
175
Q

Dystonia

A

Neurological movement disorder syndrome in which sustained or repetitive muscle contractions result in twisting and repetitive movements or abnormal fixed postures

176
Q

Treatment for Dystonia

A
  • Levodopa
  • Botox
177
Q

Narcolepsy

A
  • Patient goes from being awake to being straight into REM sleep
  • Often have daytime sleepiness
  • Can be triggered by emotion: Cataplexy
178
Q

Investigations for Narcolepsy

A
  • Overnight polysomnography
  • Multiple Sleep Latency Test
179
Q

Treatment for Narcolepsy

A
  • Modafinil- stimulant
  • SSRIs for cataplexy
180
Q

Two classifications of strokes

A
  • Ischaemic (85%)
  • Haemorrhagic (15%)
181
Q

Ischaemic strokes

A
  • Artheroembolic: Arterial (white thrombus)
  • Cardioembolic: Venous (red thrombus)
182
Q

Haemorrhagic strokes

A

Due to:

  • HTN
  • Abnormalities (e.g. aneurysm)
  • Cerebral amyloid angiopathy
  • Warfarin etc
183
Q

Which score do you use on A&E admission to distinguish between a stroke and a stroke mimic

A

Rosier score

>0 = Stroke

184
Q

4 types of strokes

A
  • Total Anterior Circulation Stroke (TACS)
  • Partial Anterior Circulation Stroke (PACS)
  • Lacunar Anterior Circulation Stroke (LACS)
  • Posterior Circulation Stroke (POCS)
185
Q

Oxford Stroke Classification has 3 criteria

A
  1. Unilateral motor loss and/or sensory loss of face/ arm/ leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction (e.g. dysphagia)
186
Q

TACS affects

A

Anterior and middle cerebral arteries

187
Q

TACS presents with

A

3/3 from Oxford’s Stroke Classification (OSC)

188
Q

PACS involves

A

Smaller arteries of anterior and middle cerebral circulation

189
Q

PACS presents with

A

2/3 features of OSC

190
Q

LACS involves

A

Arteries around the internal capsule, thalamus and basal ganglia

191
Q

LACS presents with

A
  • Unilateral weakness/sensory loss in face/arms/legs
  • Pure sensory stroke
  • Ataxic hemiparesis
192
Q

POCS involves

A

Vertebrobasilar arteries

193
Q

POCs presents with

A
  • Isolated homonymous hemianopia
  • Cerebellar/Brainstem syndromes (CNs)
  • Loss of consciousness
194
Q
  • Decrease in consciousness
  • Vomiting/Nausea
  • Headaches
  • Seizures
A

are more common in haemorrhagic strokes

195
Q

Treatment for Ischaemic Stroke

A

<4.5 hours since onset of symptoms and haemorrhage is excluded:

  • Thrombolysis: Alteplase + Aspirin (300mg)

>4.5 hours since onset of symptoms

  • Surgical removal of clot
196
Q

Alteplase is a

A

Tissue plasminogen activator

197
Q

Prophylaxis treatment commenced post ischaemic stroke

A

A: Antiplatelets (Aspirin)

B: Blood pressure control (amlodipine if >65, ACE i if <65)

C: Cholesterol management (Statins) if >3.5

D: Diabetes management (if needed)

198
Q

Treatment for haemorrhagic stroke

A
  • Opiates and antiemetics for nausea and pain
  • Increase fluids (IV drip) and blood (transfusion) to support brain
  • Calcium channel blockers to cause vasodilation to maintain cerebral perfusion
  • Neurosurgery
199
Q

3 types of brain haemorrhages

A
  • Subarachnoid
  • Extradural (Epidural) Haematoma
  • Subdural Haematoma
200
Q

Subarachnoid Headache effects

A

Arteries in the circle of Willis

Often caused by a berry aneurysm

201
Q

Subarachnoid haemorrhage bleeds into

A

the subarachnoid space and so can be seen in the eyes as a vitreous haemorrhage

202
Q

Subarachnoid haemorrhage presents with

A
  • Acute loss of consciousness
  • “Thunderclap” occipital headache (extremely painful)
  • Meningism: (Neck pain, Brudzinski’s sign positive)
203
Q

Brudzinski’s Sign

A

Flexion of the knees/hips on flexion of the neck in meningism

204
Q

Treatment for Subarachnoid Haemorrhage

A

Nimodipine (Calcium channel blocker)

205
Q

Extradural (Epidural) Haematoma effects

A
  • Middle meningeal artery (often due to pterion fracture in head trauma)
  • Tear in the dura

“MMA fighters get head trauma”

206
Q

Extradural (Epidural) Haematoma can cause a

A

Contra-coup injury

(Injury on the contralateral side of primary injury)

207
Q

Extradural Haematoma appear as

A

Unilateral hyperdense biconvex lesions on CT

208
Q

Extradural Haematoma Present with

A
  • Trauma (e.g. sports head injury”
  • Lucid interval followed by loss in consciousness
209
Q

Subdural Haematoma effects

A

Bridging veins (tear)

Venous

210
Q

Subdural Haematoma appear as

A

Hypodense crescent-shaped haemorrhage

211
Q

Subdural Haematoma present as

A
  • Low impact trauma (e.g. elderly, alcoholic fall- due to decreased clotting factors)
  • Progressive headache and confusion since trauma
212
Q

Treatment for Subdural Haematoma

A

Burr hold drainage

213
Q

Racoon Eyes (peri-ocular) bruising

A

Anterior Cranial Fossa Fracture

214
Q

“Battle sign” mastoid bruising

A

Middle cranial fossa fracture

215
Q
  • Trouble opening jaw
  • Diplopia
A

Zygoma fracture

216
Q
  • Ophthalmoplegia (weakness in eye muscles)
  • Ataxia
  • Confusion
A

Wernicke Encephalopathy

217
Q

Korsakoff’s Syndrome

A
  • Impaired memory
  • Confabulation
  • Confusion
  • Personality changes
218
Q

Wernicke Encephalopathy and Korsakoff’s Syndrome are seen in

A

Alcoholics (and sometimes other malnourished people)

Due to deficiency of thiamine (B1)

219
Q

Broca’s area is responsible for

A

Production of speech

220
Q

Patient’s with Broca’s aphasia

A
  • Can’t find words to say (non-fluent)
  • Have trouble producing speech
  • Are aware of disability
221
Q

Broca’s area is found

A
  • Left side of brain
  • More anterior than Wernicke’s area
  • Inferior frontal lobe
222
Q

Wernicke’s area is responsible for

A

Speech comprehension

223
Q

Patients with Wernicke’s aphasia

A
  • Cannot comprehend their own speech
  • Cannot comprehend other people’s speech
  • Are not aware of their disability

Can produce fluent sentences, however, they do not make sense

224
Q

Types and causes of Headaches

A
  • Migraine
  • Trigeminal Autonomic Cephalopathies
  • Cluster
  • Paroxysmal Hemicrania
  • SUNCTs
  • Tension
  • Sinusitis
  • Idiopathic Intracranial Hypertension (IIH)
  • Temporal Arteritis
  • Trigeminal Neuralgia
  • Acute Glaucoma
225
Q

Headache Red Flags

A
  • New onset >55
  • Previous Malignancy
  • Immunosuppressed
  • Early morning (wakes them up)
  • Exacerbation by valsalva maneouvre
226
Q

IHS Criteria for a Migraine

A

2/3 of:

  • Debilitating
  • Unilateral
  • Throbbing

+ nausea/ photophobia/ phonophobia

+ aura

227
Q

Migraine’s usually last for

228
Q

You only treat migraines if they are happening

A

3 times per month

229
Q

Acute Migraine treatment

A
  • During aura (pre-pain): Triptan
  • During pain: NSAID and antiemetic
230
Q

Migraine prophylaxis

A
  • Propranolol
  • Topiramate
  • Amitriptyline
231
Q

Trigeminal Autonomic Cepholopathies (TACs) consist of

A
  • Cluster
  • Paroxysmal Hemicrania
  • SUNCTs
232
Q

Cluster headaches last for

233
Q

Cluster headaches presentation

A
  • 30 year old
  • Unilateral supraorbital pain
  • 1-8 headaches per day for many weeks
234
Q

Acute treatment of cluster headache

A
  • High flow O2
  • Steroids
  • Triptans
235
Q

Prophylaxis for Cluster headaches

A

Verapamil (Calcium channel blocker)

236
Q

Paroxysmal Hemicranias last for

237
Q

Presentation of Paroxysmal Hemicrania

A
  • Elderly patient
  • Severe unilateral pain
  • 1-40 headaches per day
  • Horner’s Syndrome
238
Q

Treatment for Paroxysmal Hemicrania

A

Indomethacin

239
Q

SUNCT stands for

A
  • Short-lived
  • Unilateral
  • Neuralgiform
  • Conjunctival infection
  • Tearing
240
Q

Treatment for SUNCTs

A

Antiepileptics

  • Lamotrigine
  • Gabapentin
241
Q

Tension headaches last for

A

30mins - 7 days

242
Q

Presentation of a tension headache

A
  • Tight band
  • Non-pulsatile
  • Stressed patient
243
Q

Treatment for Tension headache

A
  • Antidepressant for 3 months
  • Stress relief
244
Q

Presentation of a sinus headache

A
  • Recent viral infection
  • Worse when leaning forward
245
Q

Presentation of Idiopathic Intracranial Hypertension

A
  • Young and overweight patients
  • Increased CSF (papilloedema)
  • Morning vomiting/ nausea
246
Q

Treatment for Idiopathic Intracranial Hypertension

A
  • Lose weight
  • Acetazolamide
  • Ventricular shunt
247
Q

Side effects of ventricular shunts

A

Can cause infection

Can cause low-pressure headache

248
Q

Trigeminal Neuralgia Presentation

A
  • Female patient in 60s
  • V2/V3 pain on touching
  • Gone in seconds
249
Q

Treatment for Trigeminal neuralgia

A
  • Gabapentin
  • Carbamazepine
  • Pregabalin
250
Q

Temporal arteritis presentation

A
  • Temple pain
  • Scalp tenderness
  • Associated with jaw claudication
251
Q

Investigation for Temporal arteritis

A

Temporal artery biopsy

252
Q

Treatment for Temporal arteritis

253
Q

Acute Primary Angle Closure Glaucoma Presentation

A
  • Severe eye pain
  • Vomiting and nausea
  • Blurred vision
  • See’s lights around halos
  • Tearing
254
Q

Treatment for Acute angle closure glaucoma

A
  • Admit to hospital
  • Pilocarpine eye drops
  • Acetazolamide
  • Pain relief
255
Q

3 Types of Meningitis

A
  • Bacterial
  • Viral
  • Fungal
256
Q

Most common type of meningitis

257
Q

Presentation of Meningitis

A
  • Meningism
  • Fever
  • Rash (non-blanching purpuric)
  • Headache
  • Photophobia
  • Decreased GCS
258
Q

Organisms that affect Neonates

A
  • Listeria
  • Group B Strep
  • E. coli
259
Q

Organism that affect children

A

H. Influenzae

260
Q

Organism that affect teens (10-21)

A
  • Neisseria Meningitidis
261
Q

Organisms that affect adult population (21+)

A
  • Strep pneumoniae
  • Neisseria meningitidis
262
Q

Organisms that affect elderly >65

A
  • Listeria
  • Strep pneumoniae
263
Q

Gram-positive bacillus found in deli foods

264
Q

Gram-negative bacillus

A

H Influenzae

265
Q

Gram-positive cocci found in nasopharynx

A

Strep pneumoniae

Most common cause of bacterial meningitis (51%)

266
Q

Gram-negative cocci, found intracellularly

A

Neisseria Meningitidis

Second most common cause of bacterial meningitis (37%)

267
Q

Most likely organisms to cause meningitis due to a head fracture

A
  • Staph aureus (gram-positive cocci)
  • H influenza
268
Q

Most likely organisms to cause bacterial meningitis due to a cribriform plate fracture

A
  • Strep pneumoniae
  • H influenza
269
Q

Most likely organism to cause bacterial meningitis from a CSF shunt

A

Staph epidermidis

270
Q

Viral meningitis is usually caused by

A

Enterovirus (Echovirus)

Common in Autumn

271
Q

Fungal meningitis is most usually caused by

A

Cryptococcal neoformans

Common in immunosuppressed people

272
Q

Investigations for Meningitis

A

LP

(Don’t do if increased CSF pressure)

273
Q

Bacterial meningitis will show

A
  • High WBC (neutrophils)
  • High protein
  • Low glucose
  • High opening pressure
  • Cloudy CSF
274
Q

Viral meningitis will show

A
  • High WBC (lymphocytes)
  • Normal protein
  • Normal glucose
  • Clear CSF
275
Q

TB meningitis will show

A
  • High WBC (lymphocytes)
  • High protein
  • Low glucose
  • Yellow CSF
276
Q

If someone has meningitis then

A

notify public health within 24hrs

277
Q

1st line treatment in bacterial meningitis (adults)

A

Dexamethasone + Ceftriaxone

“Adults do triathlons”

Give steroids to reduce inflammation from damaging bacterial debris.

278
Q

Treatment for bacterial meningitis for children

A

Dexamethasone + Cefotaxime

“Because kids don’t pay taxes”

279
Q

Treatment for listeria infection in adult/children meningitis

A

Normal 1st line treatment + amoxicillin

If resistant to amoxicillin: Vancomycin + rifampicin

280
Q

Treatment for Penicillin Allergy Bacterial Meningitis

A

Dexamethasone + Chloramphenicol + Vancomycin

281
Q

Treatment for Listeria Penicillin Allergy Meningitis

A

Normal treatment + Co-trimoxazole

282
Q

Do not give steroids in meningitis in

A

Cases that involve

  • Immunocompromised patients
  • Post-surgical patients
  • Septic patients

As they will make them more immunosuppressed

283
Q

Treatment for Viral meningitis

284
Q

Treatment for Fungal Meningitis

A

IV Amphotericin B + Fluconazole

285
Q

Normal CSF production

A
  • 0.35ml/min
  • 500ml per day
286
Q

CSF is produced in

A

Choroid plexus

and 25% in the interstitial fluid

287
Q

CSF if absorbed in

A

arachnoid granulations

288
Q

Hydrocephalus presents with

A
  • In neonates: Bulging fontanelle
  • Nausea/vomiting (especially in morning)
  • Bilateral Headache (wakes you up)
  • Sunsetting of the eyes (fixed downward eyes)
  • Seizure
  • No aura
289
Q

Treatment of Hydrocephalus

A
  • Ventricular shunt
  • Acetazolamide
290
Q

Argyl-Robertson pupils

“Prostitutes sign” - as they accommodate but don’t react

A

Neurosyphilis

291
Q

Sunsetting sign and vertical gaze palsy

A

Perinaud’s Syndrome

292
Q

Cranial nerves that come out above the pons

A

CN I, II, III, IV

293
Q

Cranial nerves that come out of the pons

A

CN V, VI, VII, VIII

294
Q

Cranial nerves that come out below the pons

A

CN IX, X, XI, XII

295
Q

3 types of brain herniation

A
  • Subfalcine
  • Transtentorial
  • Tonsilar
296
Q

Subfalcine Herniation

A

Cingulate gyrus us pushed under the falx cerebri

297
Q

Transtentorial “Uncal” Herniation

A

Temporal lobe herniates under the edge of the tentorium cerebelli

298
Q

Transtentorial herniation will cause

A

Blown pupil “dilated” due to CN III compression

299
Q

Tonsillar Herniation

A

Cerebellar tonsils are forced through the foramen magnum

this is known as “coning”

300
Q

Tonsilar herniation will cause

A
  • HTN
  • Bradycardia
  • Respiratory arrest
  • Eventually death
301
Q

A primary cause for tonsillar herniation

A

Chiari Malformation

302
Q

A secondary cause for tonsillar herniation

A
  • SOL in brain
  • Doing a LP in a patient with increased CSF
303
Q

Brain pathology often presents with

A

Hydrocephalus symptoms

Mostly in Non-gliomas types as they are not in the brain tissue and cause mass effect

304
Q

Most common brain cancer is

A

Metastatic (Secondary)

305
Q

Metastatic brain cancer is most commons spread from the

A
  • Lung
  • Breast
  • Melanoma (skin)
  • Colon
  • Kidneys
306
Q

2 classifications of primary brain cancer

A
  • Glioma
  • Astrocytoma
  • Ologodendroglioma
  • Non-Glioma
  • Meningiomas
  • Pituitary
  • Schwannomas
  • Pineal gland tumours
307
Q

Gliomas in kids occur

A

Infratentorial

308
Q

Gliomas in adults occur

A

Supratentorial

309
Q

Astrocytomas occur

A

at any age

310
Q

Astrocytoma grade I

A

Local benign lesion

Vomiting and reduced appetite

  • Pilocytic in kids (optic gliomas)
  • Pleomorphic xanthoastroma in children-teens

Tx: Surgical removal

311
Q

Optic gliomas are associated with

A

Neurofibromatosis Type 1

312
Q

Astrocytoma grade II

A

Low grade, pre-malignant

Frontal, temporal and parietal

  • Fibrillary (firm consistency)

Tx: Chemo/radiation + surgery

313
Q

Astrocytoma Grade III

A

Anaplastic astrocytoma

2 years prognosis

314
Q

Astrocytoma Type IV

A

Glioblastoma Multiforme

“Patchy enhancement”

1 year prognosis

Tx: Surgery + radiotherapy + temozolomide (MGMT+)

315
Q

Oligodendroglial tumours occur in

A

Middle-aged adults

316
Q
  • Calcifications on MRI “toothpaste like”
  • Frontal lobe involvement
  • Seizures
A

Oligodendroglial

317
Q

Treatment for Oligodendroglial tumours

A
  • Radio
  • Chemo
318
Q

Meningiomas occur in

319
Q

Types of Meningiomas

A

CCRAP

C: Clear cell
C: Choroid
R: Rhabdoid
A: Atypical
P: Pupillary

320
Q

Meningiomas

A
  • Dural tail
  • Often due to previous radiation
  • Blush effect on angiography
  • Increased bone lesions around the area

In subtypes can be :

  • Meningioma en plaque (Carpet sheet-like lesion, infiltration of dura and bone)

Tx: Surgery

321
Q

Pituitary Tumours

A

Cause:

  • Cushing’s syndrome
  • Bitemporal hemianopia

Prolactinoma: increased prolactin

322
Q

Schwannoma

A

Acoustic neuroma:

  • Hearing loss
  • Vertigo
  • Tinnitus

others affect: CN V, VII, VIII

323
Q

3 main types of pineal gland tumour

A
  • Choriocarcinoma
  • Yolk sac
  • Germinoma
324
Q

Increased B-hCG pineal gland tumour

A

Choriocarcinoma

325
Q

Increased AFP Pineal tumour

A

Yolk sac (massively raised)

Teratoma

326
Q

Increased PLAP Pineal tumour

Placental Alkaline Phosphotase

327
Q

Symptoms of Pineal tumours

A
  • Commonly obstruct CSF flow and cause non-communicating hydrocephalus
  • Vertical gaze palsy (CN IV)
328
Q

Chemo treatment for Brain tumours

A

“PCV”

Procarbazine, CCNU (Lomustine), Vincristine

329
Q

Schwann cells produce myelin in

330
Q

Oligodendrocytes produce myelin in the

331
Q

Astrocytes make up the

A

Blood brain barrier

332
Q

Ependymal cells are responsible for

A

CSF regulation

333
Q

Microglia are

A

Phagocytes

334
Q

Alpha/Beta/Delta receptors are

A
  • Thinly myelinated
  • Sharp pain= first response
335
Q

C fibres are

A
  • Not myelinated
  • Throbbing pain= secondary response
336
Q

A-Alpha receptors

A

Proprioception

337
Q

A-beta

A

Mechanoreceptors

338
Q

A-delta

A

Pain (nociceptors) and temperature

339
Q

Types of mechanoreceptors

A
  • Meissner’s corpuscles
  • Merkel discs
  • Ruffini endings
  • Pacinian corpuscles
340
Q

Meissner’s corpuscles

A

Light touch

341
Q

Merkel discs

342
Q

Ruffini endings

A

Stretch sensation

343
Q

Pacinian corpuscle

344
Q

Lateral geniculate nucleus

A

Optic fields

345
Q

Medial geniculate nucleus

Finals Club (Dundee Medicine Master Summary Deck) (8 decks)

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