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Misc. Notes Year 3 > NeuroSoc Revision doc > Flashcards

NeuroSoc Revision doc Flashcards

1
Q

What is the Parkinsonism triad of symptoms

A

Rigidity
Bradykinesia
Tremor

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2
Q

What kinds of rigidity can be seen in Parkinsonism

A

Cog-wheel

Lead pipe

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3
Q

What kind of tremor is seen in Parkinsonism and how can it be made more apparent

A

Resting pill-rolling tremor

Can be accentuated by asking the patient to perform a task requiring concentration such as counting backwards from 100

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4
Q

Which joints can be flexed to test for rigidity

A

Elbow and wrist joints can be flexed and extended whilst relaxed

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5
Q

What is a Lewy Body

A

Intracytoplasmic, eosinophilic, alpha-synuclein containing inclusion

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6
Q

Where do Lewy Bodies tend to affect in Parkinson’s disease

A

The pars compacta of the substantia nigra

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7
Q

Which neurotransmitter pathway is affected in Parkinson’s

A

Dopaminergic

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8
Q

What is micrographia

A

Decreasing amplitude of handwriting.

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9
Q

What disease is micrographia seen in

A

Parkinson’s

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10
Q

What are 4 non-motor symptoms of Parkinson’s

A

non-REM sleep disorder, dementia, depression, constipation

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11
Q

What is considered the most effective treatment for Parkinson’s

A

Levodopa

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12
Q

What is the mode of action of Levodopa

A

Dopamine precursor that can cross the blood-brain barrier

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13
Q

Name 3 side effects of Levodopa

A

Hypotension
Nausea
Dyskinesia

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14
Q

What drug can Levodopa be given with

A

Can be combined with peripheral dopa- decarboxylase inhibitors (carbidopa) to prevent peripheral metabolism of levodopa

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15
Q

Which class of drug, also used for depression, can be given for Parkinson’s

A

Monoamine oxidase B inhibitors

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16
Q

How do Monoamine oxidase B inhibitors work and give an example

A

Inhibits monoamine oxidase B, an enzyme responsible for catabolising dopamine to homovanillic acid.
Example: rasagiline

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17
Q

What is dopamine catabolised to by MAO-B

A

Homovanillic acid

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18
Q

What is a potentially fatal side effect of MAO-B inhibitors

A

Hypertensive crisis due to tyramine excessive diet

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19
Q

What is a treatment option for those under 70 with Parkinson’s

A

Dopamine agonists

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20
Q

Why might you prefer giving dopamine agonists to a young Parkinson’s patient rather than Levodopa

A

Due to the high risk of dyskinesia in younger patients using levodopa.

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21
Q

Give an example of a dopamine agonist

A

Pramipexole

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22
Q

Name 4 side effects of dopamine agonists

A

Hypotension
Nausea
Ankle swelling
Hallucinations

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23
Q

What kinds of drugs can cause parkinsonism

A

Typical Anti-psychotics (since they block dopamine 2 receptors)

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24
Q

Define Lewy Body dementia

A

Dementia or cognitive symptoms occurring before or at the same time as parkinsonism

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25
Q

Define Parkinson’s disease dementia

A

Dementia starting more than 1 year after the onset of parkinsonism

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26
Q

What are 3 defining features of Lewy Body dementia

A

Features of parkinsonism
Visual hallucinations
Cognitive decline

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27
Q

What is multiple system atrophy

A 
Parkinsonism
Autonomic dysfunction (resulting in postural hypotension, erectile dysfunction or urinary urgency)
± cerebellar dysfunction
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28
Q

A ‘hot cross bun” appearance of the pons on axial MRI suggests what disease

A

Multiple system atrophy

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29
Q

What will an MRI show in multiple system atrophy

A

Putaminal atrophy

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30
Q

MRI showing midbrain atrophy with a ‘hummingbird’ sign on sagittal view should suggest which disease

A

Progressive supranuclear palsy

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31
Q

What are some symptoms of Progressive supranuclear palsy

A 
Axial akinesia and rigidity, 
loss of balance and unexplained falls
Forgetfulness
Dysarthria 
Loss of eye movements (vertical gaze)
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32
Q

What is an essential tremor

A

A movement disorder characterized by a postural or action tremor, rather than a resting tremor seen in Parkinson’s

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33
Q

What are intention tremors caused by

A

Caused by lesions in the cerebellum or its pathways, most commonly seen in multiple sclerosis

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34
Q

What is dystonia

A

Dystonia is a common movement disorder characterised by involuntary muscle spasms leading to abnormal postures of the affected body part

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35
Q

What is chorea

A

Chorea consists of continuous spontaneous jerky movements, irregularly timed and randomly distributed.

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36
Q

Which triplet is repeated in Huntington’s

A

CAG

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37
Q

How many CAG repeats are needed to cause Huntington’s

A

> 35

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38
Q

How is Huntington’s inherited

A

Autosomal dominant

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39
Q

Name 3 early signs of Huntington’s

A

Depression
Apathy
Clumsiness

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40
Q

Huntington’s progresses to cause which 3 symptoms

A

CHorea
Dementia
Rigidity

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41
Q

Which drug can be given for symptomatic relief in Huntington’s

A

Tetrabenazine (Anti-Choreic)

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42
Q

How does Tetrabenazine work

A

Inhibits vesicular monoamine transporter (VMAT)

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43
Q

Rheumatic fever can manifest into which chorea

A

Sydenham’s chorea

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44
Q

What are tics

A

Tics are typically relatively brief rapid intermittent stereotyped involuntary movements or sounds

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45
Q

What is the most common syndrome characterised by tics

A

Gilles de la Tourette syndrome

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46
Q

What is myoclonus

A

Defined as a sudden brief shock(like involuntary movement caused by muscular contraction or inhibition

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47
Q

What is Hemiballism

A

Wild flinging/throwing movements of one arm or leg

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48
Q

Why does hemiballism occur

A

cerebrovascular lesion to the subthalamic nucleus

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49
Q

What is a seizure

A

A short episode of symptoms caused by a burst of abnormal electrical activity in the brain

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50
Q

What is epilepsy

A

The ongoing liability to recurrent seizures

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51
Q

What should you always ask patients about in an OSCE if they have presented with a seizure

A

Preceding Aura

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52
Q

How would a focal seizure in the occipital lobe present

A

Visual phenomena such as flashing lights, colours or hallucinations

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53
Q

How would a focal seizure in the parietal lobe present

A

Sensory manifestations can take the form of tingling or numbness or pain.

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54
Q

How would a focal seizure in the frontal lobe present

A

Motor signs such as stiffness, twitching or spasm

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55
Q

How would a focal seizure in the temporal lobe present

A

Changes in mood or behaviour

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56
Q

A rising epigastric sensation is a common manifestation in which type of focal seizure

A

Temporal lobe focal seizure

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57
Q

What is the difference between a simple and a complex focal seizure

A

Simple = no loss of consciousness

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58
Q

What is an Absence seizure and how long do they typically last

A

An abrupt sudden loss of consciousness (“the absence”) and of all motor activity rapidly stopped
Usually lasts 10 seconds

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59
Q

Do people fall during an absence seizure

A

Not usually since muscle tone is preserved

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60
Q

What is a characteristic sign of an absence seizure on EEG

A

3Hz generalised spike-wave

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61
Q

What is a clonic seizure

A

During a clonic seizure, the individual’s muscles begin to spasm and jerk. The elbows, legs and head will flex and relax rapidly

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62
Q

What is a tonic seizure

A

A tonic seizure causes a brief loss of consciousness, the patient falls to the ground and often there is extension of the neck; with upturning of the eyes and arching of the back

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63
Q

What is a tonic-clonic seizure

A

Tonic phase - muscles become stiff

Clonic phase - muscles will start to contract and relax rapidly

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64
Q

How is epilepsy typically diagnosed

A

Generally by clinical history

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65
Q

Why is EEG useful in epilepsy

A

To help support a diagnosis of epilepsy and determine a seizure type

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66
Q

Name 2 first-line drugs for focal seizures

A

Carbamazepine

Lamotrigine

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67
Q

Name 2 first-line drugs for generalised tonic-clonic seizures

A

Sodium Valproate

Lamotrigine

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68
Q

Name 2 first-line drugs for generalised absence seizures

A

Sodium Valproate

Ethosuximide

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69
Q

Name a drug used first-line for myoclonic generalised seizures

A

Sodium Valproate

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70
Q

If someone has an unclassified type of epilepsy, which drugs would be used first-line and second-line

A

1st line- Sodium Valproate

2nd line - Lamotrigine

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71
Q

2nd line drug for generalised myoclonic seizures

A

Levetiracetam

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72
Q

Name 2 second-line drugs for generalised tonic-clonic seizures

A

Lamotrigine

Levetiracetam

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73
Q

Which drug should you never give for generalised seizures and why

A

Carbamazepine

Can make them worse

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74
Q

How does Carbamazepine work

A

Na+ channel inactivation

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75
Q

Which anti-convulsants work by inactivating Na+ channels

A

Carbamazepine

Phenytoin

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76
Q

How does Lamotrigine work

A

Blocks voltage-gated Na+ channels

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77
Q

How does Ethosuximide work and when can it be used

A

Blocks thalamic T- type Ca2+ channels

Used 1st line for absence seizures

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78
Q

Which anticonvulsant is teratogenic

A

Sodium Valproate

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79
Q

How does Sodium Valproate work

A

Na+ channel inactivation with increase GABA concentration

80
Q

Which anti-convulsant can cause Steven-Johnson’s syndrome

A

Lamotrigine

81
Q

What is status epilepticus

A

Status epilepticus is defined as a convulsive seizure which continues for a prolonged period (longer than five minutes)

82
Q

How would you manage status epilepticus

A

community - rectal diazepam

hospital - IV lorazepam

83
Q

What is Motor Neurone Disease

A

A group of neurodegenerative conditions which affect only the upper and/or lower motor neurones

84
Q

What is the most common MND type

A

Amyotrophic Lateral Sclerosis (ALS)

85
Q

Which chromosome has genes which have been linked to MND

A

Chromosome 21

86
Q

Which type of dementia is MND often linked to

A

Frontotemporal dementia (FTD)

87
Q

What is the only drug given to those with MND and how does it affect prognosis

A

Riluzole

Extends life expectancy by 3 months

88
Q

How does Riluzole work

A

Blocks glutaminergic neurotransmission in the CNS

89
Q

Name 3 complications of MND

A

Depression
Weight loss + malnutrition (2ndary to dysphagia)
Respiratory depression

90
Q

Name an autosomal recessive muscle disease

A

McArdle’s disease

91
Q

What is deficient in McArdle’s disease

A

Myophosphorylase

92
Q

What is the mode of inheritance of myotonic dystrophy

A

Autosomal dominant

93
Q

What is split hand syndrome and which disease is it linked to

A

Thenar muscles atrophy but hypothenar muscles are spared

Seen in ALS

94
Q

A tri-nucleotide repeat on chromosome 19 should suggest which disease

A

Myotonic Dystrophy

95
Q

Name 3 characteristic signs of myotonic dystrophy

A

‘Christmas tree-like’ bilateral cataracts
Early frontal balding
Sternocleidomastoid and distal muscle wasting

96
Q

In Lambert-Eaton Myasthenic syndrome, what structure are autoantibodies created against

A

Ca2+ voltage-gated channels at the pre-synaptic terminal

97
Q

How is LEMS diagnosed

A

Presence of anti(VGCC antibodies and by characteristic electrophysiological findings using a 20–50 Hz repetitive stimulation

98
Q

Which imaging scan must be carried out in suspected LEMS and why

A

CT scan to rule out small cell lung cancer

99
Q

How is LEMS usually treated

A

3- 4 diaminopyridine (Amifampridine)

blocks presynaptic Ca2+ channels

100
Q

Which part of the NMJ does Myasthenia gravis affect

A

post-synaptic nicotinic acetylcholine receptors

101
Q

What is a common presentation of myasthenia gravis

A

Muscle fatiguability

usually of extra-ocular muscles

102
Q

Are proximal or distal muscles usually affected in myasthenia gravis

A

Proximal

103
Q

What is a Myasthenia crisis

A

weakness of the muscles of respiration causes ventilator failure

104
Q

What is the treatment for myasthenia crisis

A

plasmapheresis
IV immunoglobulins
systemic steroids

105
Q

What is a cholinergic crisis and what kind of people is it common in

A

common in patient receiving high dose anticholinesterase medication

106
Q

What kind of hyperplasia is Myasthenia Gravis

A

Thymus hyperplasia

thymoma

107
Q

Which connective tissue disease is associated with Myasthenia Gravis

A

SLE

108
Q

Name 4 drugs that can exacerbate myasthenia gravis

A

Gentamicin
Lithium
Beta-blockers
Verapamil

109
Q

Which antibody can be tested for in Myasthenia Gravis

A

IgG antibodies against acetylcholine receptor (anti-AChR)

110
Q

How is myasthenia gravis usually treated

A

Acetylcholinesterase inhibition using Pyridostigmine

111
Q

Which bacteria infection can precede Guillan-Barre syndrome

A

Campylobacter

112
Q

How is polio spread

A

Facael-oral transmission

113
Q

What does a poliomyelitis infection cause destruction of

A

Destruction of cells in anterior horn of spinal cord (LMN death)

114
Q

What are the 2 broad categories of pain

A

Nociceptive pain

Neuropathic pain

115
Q

What is allodynia

A

pain produced in response to a stimulus that is normally not painful

116
Q

What is hyperalgesia

A

increase in pain response, with lowering of the pain threshold, to a
stimulus that is normally painful

117
Q

What is the leading cause of dementia

A

Alzheimer’s disease

118
Q

Which syndrome increases your risk of developing Alzheimer’s

A

Down syndrome

119
Q

Which version of the ApoE gene increases and decreases risk for Alzheimer’s

A

ApoE4 - increases

ApoE2 - decreases

120
Q

What happens to the gyri and sulci in Alzheimer’s

A

Narrowing of gyri

Widening of sulci

121
Q

What are the plaques and neurofibrillary tangles made up of in Alzheimer’s

A

B-amyloid plaques

Tau tangles

122
Q

Which source of cholinergic projections to the brain is often first affected in Alzheimer’s

A

nucleus basalis of Meynert

123
Q

What change is seen in CSF biomarkers in Alzheimer’s disease

A

increase in phosphorylated tau protein and decrease in β-amyloid

124
Q

What class of drugs can be given for Alzheimer’s disease

A

Acetylcholinesterase inhibitors

rivastigmine or galantamine

125
Q

Which drug apart from cholinesterase inhibitors can be given for Alzheimer’s and how does it work

A

Memantine is a voltage-dependent, non-competitive

(NMDA) receptor antagonist

126
Q

How could a haemorrhagic stroke occur in Alzheimer’s

A

due to β-amyloid deposits in cerebral blood vessels that can weaken them (cerebral amyloid angiopathy)

127
Q

What are the 3 broad variants of frontotemporal dementia

A

Behavioural
Primary progressive aphasia
(semantic and progressive non-fluent aphasia)

128
Q

Which scan is particularly useful for showing the changes of Frontotemporal dementia

A

SPECT scan

129
Q

What is the second most common form of dementia

A

Vascular dementia

130
Q

What will an MRI or SPECT scan show in vascular dementia

A

Infarcts and white matter changes

131
Q

What is Creutzfeldt–Jakob disease

A

A transmissible prion neurodegenerative disease which causes cell death (spongiform changes in the cortex) and astrocytosis

132
Q

How does Creutzfeldt–Jakob disease present and progress

A

Rapidly progressing dementia, ataxia and myoclonic jerks

133
Q

What would CSF analysis show in a patient with Creutzfeldt–Jakob disease

A

Elevated 14-3-3 protein

134
Q

What is multiple sclerosis characterised by

A

Demyelination of white matter areas in the brain

135
Q

What is the most common phenotype of MS

A

Relapsing-Remitting

136
Q

Areas of demyelination are referred to as what in MS

A

Plaques

137
Q

Name 3 common areas of demyelination

A

Optic nerve
Corpus callosum
Periventricular white matter

138
Q

Name 3 risk factors for MS

A

Those living in a higher latitude
Female
Previous EBV infection

139
Q

Which HLA gene is linked to MS

A

HLA DRB1

140
Q

What is the most ocular symptom of MS

A

Optic Neuritis

141
Q

What is Lhermitte’s sign

A

Electric shock-like sensation down the upper limbs and

trunk on neck flexion

142
Q

WHat is Uhthoff’s phenomenon and which disease is it seen in

A

Exacerbation of current symptoms in hot
environments
seen in MS

143
Q

What does the mneumonic DANISH stand for and what does it indicate

A

Indicates Cerebellar dysfunction
Dysdiadochokinesia, Ataxia, Nystagmus,
Intention tremor, Slurred speech and Hypotonia/Heel-shin test

144
Q

What will an MRI of a brain affected by MS show

A

Multiple white matter plaques

145
Q

What will CSF analysis of a patient with MS show

A

Presence of IgG Oligoclonal bands

146
Q

What are 3 options for 1st line therapy in terms of disease-modifying therapy for MS

A

Interferon-beta
Tecfidera
Glatiramer acetate

147
Q

How is spasticity managed in MS

A

Baclofen

148
Q

How is neuropathic pain managed in MS

A

Gabapentin

149
Q

How is fatigue managed in MS

A

Amantadine + modafinil

150
Q

How is bladder dysfunction managed in MS

A

Anti-Cholinergic drugs (Oxybutynin)

151
Q

Name 5 red flags for a headache

A 
Age >55
Immunosuppressed
Previous/current malignancy 
Early morning headache 
Exacerbated by Valsalva manoeuvre
152
Q

What does aura refer to in regards to a headache

A

Aura refers to reversible visual, auditory, motor or language symptoms
including zigzag lines, central or hemianopic scotoma, aphasia and muscle weakness

153
Q

What are the Trigeminal autonomic cephalgias (TAC)

A

A group of headache disorders categorised by common features of unilateral pain (often severe) in the distribution of the trigeminal nerve

154
Q

Name 4 trigeminal autonomic cephalgias

A

Cluster
Paroxysmal hemicrania
SUNCT
Trigeminal Neuralgia

155
Q

Which of the trigeminal autonomic cephalgias has an absolute response to Indomethacin

A

Paroxysmal Hemicrania

156
Q

What does SUNCT stand for

A 
Short 
Unilateral 
Neuralgiform headache with
Conjunctival injection 
Tearing
157
Q

Name 2 treatments for SUNCT

A

Lamotrigine

Gabapentin

158
Q

How is trigeminal neuralgia treated

A

Carbamazepine

159
Q

Name 3 vascular disorders which can present as a headache

A

Subarachnoid haemorrhage
Carotid dissection
Giant cell arteritis

160
Q

What is Pseudotumor cerebri

A

idiopathic intracranial hypertension

161
Q

What is the treatment for idiopathic intracranial hypertension

A

Weight loss is first line management of IIH and usually is sufficient to reduce ICP.
Acetazolamide (decreases CSF production) can be used as a medical treatment for
IIH
Shunt in refractory cases

162
Q

What are clinical presenting features of idiopathic intracranial hypertension

A

A throbbing headache worse in the morning
Bilateral papilloedema.
Nausea and vomiting.

163
Q

Which nerve palsy can be a presentation of idiopathic intracranial hypertension

A

Sixth nerve palsy

164
Q

Which investigations can be carried out for idiopathic intracranial hypertension

A

MRI or CT

165
Q

What will be seen upon execution of a lumbar puncture in a patient with idiopathic intracranial hypertension

A

High opening pressure

166
Q

What will idiopathic intracranial hypertension show on MRI/CT

A

Slit-like ventricles

167
Q

What does meningism refer to

A

Triad of symptoms:
Photophobia
Neck stiffness
A headache

168
Q

Where does infection usually spread from to cause meningitis

A

Sinuses
Nasopharynx
Ear

169
Q

Which organism affects mainly neonates and elderly, with regards to meningitis

A

Listeria Monocytogenes

170
Q

Which organism is most commonly the cause of Meningitis in infants + children/adolescents

A

N.Meningitidis

171
Q

Which organism is most commonly the cause of Meningitis in Adults

A

Strep. Pneumoniae

172
Q

Which organism is most commonly the cause of Meningitis in those with recent neurosurgery or head trauma

A

Staph Aureus

173
Q

What is Waterhouse–Friderichsen syndrome

A

Waterhouse–Friderichsen syndrome (WFS) is defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically it is caused by Neisseria meningitidis

174
Q

What is Kernig’s sign and what pathology does it suggest

A 
A patient will resist Knee extension when the hip is flexed
Suggests meningitis (or at least meningeal irritation)
175
Q

What is Brudzinksi’s sign and what pathology does it suggest

A 
Neck flexion will cause flexion at the hip and the knee joints
Suggests meningitis (or at least meningeal irritation)
176
Q

What is the name of the test which involves pushing a glass into a purpuric rash to prove it is non-blanching

A

Tumbler’s test

177
Q

In a patient with suspected meningitis, which investigation must always be carried out before a lumbar puncture and why

A

CT scan-
To rule out increased intracranial pressure
must be done before LP so coning does not occur

178
Q 
What will a lumbar puncture show in meningitis with respect to 
Cells
Colour of CSF
Protein 
Glucose
A

Cloudy turbid CSF
Polymorphs present
Increased protein
Decreased glucose

179
Q

What is the empirical treatment for community-acquired meningitis

A

IV Ceftriaxone + Dexamethasone

180
Q

When would amoxicillin be given alongside Ceftriaxone for meningitis treatment

A

If Listeria is suspected

181
Q

When should you suspect Listeria to be the causative organism in meningitis

A

Neonate or >55 or Immunosuppressed

182
Q

What is the prophylactic treatment given to those who have been in contact with someone with meningitis

A

Ciprofloxacin

Rifampicin if refractory to treatment

183
Q 
What will a lumbar puncture show in viral meningitis with regards to: 
CSF colour 
Glucose 
Cells 
Protein
A

Clear fluid
Low/normal glucose
Lymphocytes
Normal protein

184
Q

Name 3 characteristic CSF findings in Tuberculosis meningitis

A

Clear and culture negative
Lymphocytosis
Fibrin webs

185
Q

What is Inflammation of the brain parenchyma known as

A

Encephalitis

186
Q

What is the most common cause of encephalitis

A

Herpes simplex

187
Q

A patient with seizures with focal neurological deficits (aphasia) should make you think of what

A

Herpes simplex encephalitis

188
Q

Parotitis in an unvaccinated patient should make you think of which type of encephalitis

A

Mumps encephalitis

189
Q

Skin lesions\vesicles in a dermatomal pattern should make you think of which type of encephalitis

A

Varicella-zoster encephalitis

190
Q

MRI in HSV encephalitis will show what

A

Characteristic oedema in temporal lobes

191
Q

What is the treatment for encephalitis

A

IV acyclovir

192
Q

What is a serious consequence of the measles virus involving the brain parenchyma

A

Subacute sclerosing panencephalitis

193
Q

Describe CSF findings in a Subarachnoid haemorrhage

A

Xanthochromia

194
Q

Describe CSF findings in Narcolepsy

A

Low or undetectable levels of CSF orexin/hypocretin

195
Q

Describe CSF findings in Alzheimer’s

A

High hyper-phosphorylated Tau protein

Low B-amyloid

196
Q

Describe CSF findings in Multiple sclerosis

A

IgG oligoclonal bands

Misc. Notes Year 3 (25 decks)

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