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Neurosciences > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

Gross changes seen in Alzheimer’s disease

A

Generalised atrophy
Flattened sulci
Enlarged ventricles

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2
Q

Peptides which make up amyloid plaques in Alzheimer’s disease

A

Amyloid beta

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3
Q

Protein which amyloid beta is a fragment of

A

Amyloid-beta precursor protein

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4
Q

Conformation of amyloid plaques

A

Beta pleated sheets

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5
Q

Enzymes which cause amyloid-beta precursor protein to be cleaved into amyloid plaques in Alzheimer’s disease

A

Beta secretase

Gamma secretase

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6
Q

Enzyme which prevents the formation of amyloid plaques from amyloid-beta precursor protein

A

Alpha secretase

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7
Q

Two main subtypes of amyloid plaques

A

Neuritic plaques

Diffuse plaques

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8
Q

Form of amyloid which is found in neuritic plaques

A

Fibrils

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9
Q

Cell types found in neuritic plaques

A

Dystrophic neurites

Microglia and astrocytes at the periphery

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10
Q

Core of neuritic plaques

A

Dense amyloid core

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11
Q

Stain neurites are best visualised with

A

Silver stain

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12
Q

Stain of neuritic plaques under Congo red

A

Apple green birefringent

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13
Q

Component of diffuse plaques

A

Non-fibrillar extracellular amyloid beta

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14
Q

Main component of neurofibrillary tangles

A

Hyperphosphorylated tau protein

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15
Q

Purpose of tau protein

A

Microtubule assembly

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16
Q

Components required to make abnormally phosphorylated tau

A

Beta amyloid peptide

Cholinergic receptors

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17
Q

Conditions apart from Alzheimer’s disease where neurofibrillary tangles can be seen

A

Down syndrome
Dementia pugilistica (punch drunk syndrome)
Parkinson’s dementia
Normal aging

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18
Q

Appearance of neurofibrillary tangles on staining

A

Basophlic

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19
Q

Position of neurofibrillary tangles vs. beta amyloid plaques

A

Neurofibrillary tangles largely intraneuronal

Amyloid plaques extracellular

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20
Q

Earliest parts of the brain neurofibrillary tangles are seen - not usually associated with clinical symptoms

A

Entorhinal complex

CA1 field of the hippocampus

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21
Q

Parts of the brain affected by neurofibrillary tangles at the point clinical symptoms are first seen - as well as the entorhinal complex and CA1 region of the hippocampus

A

Other parts of the hippocampus
Medial temporal lobe
Then hypothalamus and thalamus

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22
Q

Condition caused by the accumulation of amyloid beta in blood vessel walls in the cerebral cortex

A

Cerebral amyloid angiopathy

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23
Q

Percentage of elderly population without Alzheimer’s disease who have cerebral amyloid angiopathy

A

30%

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24
Q

Percentage of elderly people with Alzheimer’s disease who have cerebral amyloid angiopathy

A

90%

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25
Q

Complication of cerebral amyloid angiopathy

A

Strokes - especially haemorrhagic

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26
Q

Eosinophilic bodies seen in the cytoplasm of neurons in patients with Alzheimer’s disease

A

Hirano bodies

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27
Q

Shape of Hirano bodies

A

Rod shaped

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28
Q

Protein involved in Hirano bodies

A

Actin

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29
Q

Area of the brain where Hirano bodies are often seen

A

Hippocampal pyramidal cells

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30
Q

Best neuropathological correlate for clinical decline in patients with Alzheimer’s

A

Number of synapses

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31
Q

Neuropathological marker used to measure the number of synapses in patients with dementia

A

Antibody to synaptophysin (protein found in presynaptic endings)

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32
Q

Alternative names for Binswanger’s disease

A

Subcortical vascular dementia

Subcortical arteriosclerotic encephalopathy

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33
Q

Cause of Binswanger’s disease

A

Multiple small infarctions to the deep layers of white matter in the brain

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34
Q

Clinical features of Binswanger’s disease

A

Memory issues (not as severe as with Alzheimer’s disease)
Psychomotor retardation
Unsteady, slow gait
Urinary urgency or incontinence

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35
Q

Areas of the brain where neuronal loss is seen the most in Alzheimer’s dementia

A

Subiculum of the hippocampus

Layers II and IV of the entorhinal cortex

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36
Q

Appearance of Lewy bodies

A

Spherical

Eosinophilic

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37
Q

Part of the cell Lewy bodies are found

A

Cytoplasm

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38
Q

Two main types of Lewy bodies

A

Classical

Cortical

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39
Q

Area of the brain Lewy bodies are found in Parkinson’s disease

A

Substantia nigra - pars compacta

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40
Q

Areas of the brain Lewy bodies are found in dementia with Lewy bodies

A

Substantia nigra
Temporal lobe
Cingulate gyrus
Frontal lobes

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41
Q

Differences in appearance between classical (found in the substantia nigra) and cortical Lewy bodies

A

Classical Lewy bodies are more conspicuous, more eosinophilic and have a halo

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42
Q

Markers which can be used to identify Lewy bodies

A

Antibody to ubiquitin

Antibody to alpha-synuclein

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43
Q

Protein accumulations found in Lewy bodies

A

Abnormal alpha-synuclein

Some ubiquitin

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44
Q

Abnormal neurons seen in dementia with Lewy bodies, Parkinson’s disease dementia and occasionally Alzheimer’s dementia

A

Lewy neurites

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45
Q

Area of the brain where Lewy neurites are most common

A

CA2/3 region of the hippocampus

Substantia nigra

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46
Q

Diseases associated with alpha-synuclein aggregation

A

Parkinson’s disease
Dementia with Lewy bodies
Multisystem atrophy

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47
Q

Diseases associated with tau deposits

A

Alzheimer’s dementia
Frontotemporal dementia
Progressive supranuclear palsy

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48
Q

Most common pathological type of frontal lobe dementia

A

Frontal lobe degeneration type

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49
Q

Three clinical types of frontotemporal dementia

A

Behavioural variant FTD
Semantic variant primary progressive aphasia
Non-fluent variant primary progressive aphasia

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50
Q

Features of behavioural variant FTD

A

Loss of inhibition
Loss of motivation
Repetitive or obsessive behaviours

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51
Q

Features of semantic variant primary progressive aphasia

A

Loss of vocabulary

Inability to remember what familiar objects are for

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52
Q

Features of non-fluent variant primary progressive aphasia

A

Different speech - changing grammar, words in the wrong order
Use of shorter sentences
Saying the opposite of what is meant
Retention of ability to know what words mean (in contrast to semantic variant primary progressive aphasia)

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53
Q

Proteins associated with frontotemporal lobar degeneration

A

Tau
Transactive response DNA binding protein (TDP 43)
Fused in sarcoma protein (FUS)

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54
Q

Macroscopic changes seen in frontotemporal lobar degeneration

A

Atrophy of frontal and temporal lobes

Focal atrophy with knife-blade appearance

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55
Q

Pathological type of frontotemporal lobar degeneration associated with Pick bodies

A

Tau type

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56
Q

Shape of Pick bodies

A

Sphrerical

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57
Q

Protein composing Pick bodies

A

Tau

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58
Q

Proteins seen aggregated in TDP frontotemporal lobar degeneration

A

Ubiquitin

TDP-43

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59
Q

Macroscopic changes seen in Huntington’s disease

A

Shrunken head of caudate

Dilatation of the anterior horns of the lateral ventricles

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60
Q

Three types of Creutzfeldt-Jakob disease

A

Sporadic
Familial
Variant

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61
Q

Most common type of Creutzfeldt-Jakob disease

A

Sporadic

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62
Q

Lobe generally spared in Alzheimer’s disease

A

Occipital

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63
Q

Brain area showing particular depigmentation in Alzheimer’s disease

A

Locus Coeruleus

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64
Q

Area of the brain which degenerates in Alzheimer’s disease leading to lower levels of acetylcholine

A

Nucleus of Meynert/nucleus basalis magnocellularis

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65
Q

Difference between Lewy bodies and Hirano bodies

A

Lewy bodies contain ubiquitin

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66
Q

General age of presentation of sporadic CJD

A

55-65

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67
Q

General age of presentation of variant CJD

A

25-30

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68
Q

Origin of variant CJD

A

Infected meat products

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69
Q

Origin on sporadic CJD

A

Genetic mutation

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70
Q

Duration of disease between onset and death for sporadic CJD

A

Few months

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71
Q

Duration of disease between onset and death for variant CJD

A

Year +

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72
Q

Earliest clinical features of sporadic CJD

A

Neurological signs - cerebellar ataxia, myoclonic jerks

Dementia

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73
Q

Earliest clinical features of variant CJD

A

Psychiatric and behavioural features

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74
Q

Inheritance pattern of familial CJD

A

Autosomal dominant

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75
Q

Histological appearance of the grey matter in CJD

A

Spongiform changes
Round vacuoles in the neuropil
Vacuoles joining to form microcysts

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76
Q

Chromosome where the gene which codes for prion protein is found

A

20

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77
Q

Abnormal form of prion protein found in CJD

A

PrPSc

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78
Q

Other parts of the body where PrPSc may be found in CJD

A

Skeletal muscle

Spleen

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79
Q

Staining used to identify PrPSc in CJD

A

Immunoperixodase staining

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80
Q

MRI sign seen with variant CJD

A

Pulvinar sign

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81
Q

EEG changes classically seen with sporadic CJD

A

Triphasic sharp waves 1-2 per second

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82
Q

Abnormal protein sometimes found in the CSF with CJD

A

14-3-3

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83
Q

Most common type of CJD where protein 14-3-3 is found

A

Sporadic

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84
Q

Percentage of classic CJD which is familial

A

10-15%

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85
Q

Type of lymphocytes which are reduced in HIV infection

A

CD4+

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86
Q

Cells which are activated by HIV infection and which kill HIV-infected cells

A

CD8+ cells

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87
Q

Most common psychiatric presentation in patients with AIDS

A

HIV-related dementia

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88
Q

Second most common psychiatric presentation in patients with AIDS

A

Depression

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89
Q

Most common cerebral lesion in patients with HIV

A

Toxoplasmosis

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90
Q

Ventricles enlarged in schizophrenia

A

Lateral

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91
Q

Part of the lateral ventricle enlarged in schizophrenia

A

Temporal horn

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92
Q

CT appearance of toxoplasmosis

A

Ring enhancing lesions +/- mass effect

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93
Q

CT appearance of primary CNS lymphoma associated with HIV

A

Single (or sometimes multiple) homogenous enhancing lesion

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94
Q

Area of the brain which sees reduced asymmetry in schizophrenia

A

Planum temporale

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95
Q

Impact of schizophrenia on brain volume

A

Reduced by up to 5%

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96
Q

Areas of the brain which see reduced cell numbers in schizophrenia

A

Hippocampus
Dorsolateral prefrontal cortex
Superior temporal gyrus

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97
Q

Most common functional imaging appearances in schizophrenia

A

Reduced activation of frontal regions during cognitive tasks

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98
Q

Functional imaging appearances seen during hallucinations in schizophrenia

A

Increased activation of temporal regions

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99
Q

Common imaging finding in mood disorders seen on T2 weighted images, especially in older people

A

White matter hyperintensities particularly in the deep subcortical white matter

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100
Q

Areas of the brain where hypoplasia is seen in autism

A

Cerebellar vermis

Cerebellar hemispheres

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101
Q

Areas of the brain which see degenerative changes in Wernicke’s encephalopathy

A 
Mamillary bodies
Hypothalamus
Mediodorsal thalamus
Colliculi
Midbrain tegmentum
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102
Q

Area of the brain which shows depigmentation in Parkinson’s disease

A

Substantia nigra

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103
Q

Abnormal protein seen in Alzheimer’s disease which correlates best to clinical severity

A

Neurofibrillary tangles

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104
Q

CSF finding which can indicate worse prognosis in those with mild cognitive impairment

A

Increased tau to amyloid ratio

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105
Q

Age of patients with mood disorders where white matter hyperintensities are more often seen

A

Elderly patients

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106
Q

Physical disease which white matter hyperintensities can be associated with

A

Vascular disease

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107
Q

Type of dysarthria characterised by explosive and forceful, but slow speech

A

Spastic dysrathria

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108
Q

Type of dysarthria characterised by a breathy, nasal voice

A

Flaccid dysarthria

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109
Q

Type of dysarthria characterised by slow, quiet, tremulous speech

A

Hypokinetic dysarthria

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110
Q

Type of dysarthria characterised by a variable rate and inappropriate stoppages, and a strained quality

A

Hyperkinetic dysarthria

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111
Q

Type of dysarthria characterised by rapid, monotone, slurred speech

A

Ataxic dysarthria

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112
Q

Type of dysarthria associated with pseudobulbar palsy

A

Spastic dysarthria

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113
Q

Type of dysarthria associated with spastic hemiplegia

A

Spastic dysarthria

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114
Q

Type of dysarthria associated with myasthenia gravis

A

Flaccid dysarthria

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115
Q

Type of dysarthria associated with Parkinson’s disease

A

Hypokinetic dysarthria

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116
Q

Type of dysarthria associated with Huntington’s disease

A

Hyperkinetic dysarthria

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117
Q

Type of dysarthria associated with Syndenham’s chorea

A

Hyperkinetic dysarthria

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118
Q

Type of dysarthria associated with tardive dyskinesia

A

Hyperkinetic dysarthria

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119
Q

Type of dysarthria associated with Friedreich’s ataxia

A

Ataxic dysarthria

120
Q

Type of dysarthria associated with alcohol abuse

A

Ataxic dysarthria

121
Q

Lesion area associated with spastic dysarthria

A

Upper motor neuron

122
Q

Lesion area associated with flaccid dysarthria

A

Lower motor neuron

123
Q

Lesion area associated with hypokinetic dysarthria

A

Extrapyramidal

124
Q

Lesion area associated with hyperkinetic dysarthria

A

Extrapyramidal

125
Q

Lesion area associated with ataxic dysarthria

A

Cerebellar

126
Q

Structure where degeneration is found in Huntington’s disease

A

Striatum

127
Q

Lobe associated with aura in epilepsy

A

Temporal

128
Q

Lobe associated with dysphoric, euphoric, or other strong emotional feelings

A

Temporal

129
Q

Structures involved in OCD

A 
Lentiform nucleus (putamen and globus pallidus)
Caudate nucleus
130
Q

Structure where lesions are associated with hemiballismus

A

Subthalamus

131
Q

Structure where lesions are associated with dystonia, athetosis and chorea

A

Corpus striatum

132
Q

Structure where lesions are associated with Parkinsonism

A

Substantia nigra

133
Q

Symptom caused by damage to the lingual gyrus

A

Visual snow

134
Q

Structure where lesions are associated with nominal aphasia

A

Angular gyrus

135
Q

Structure most severely damaged in early Alzheimer’s dementia

A

Entorhinal cortex

136
Q

Lobe initially affected in Alzheimer’s disease

A

Temporal lobe

137
Q

Hemispheric lesion associated with aphasia

A

Left

138
Q

Hemispheric lesion associated with right-left disorientation

A

Left

139
Q

Hemispheric lesion associated with finger agnosia

A

Left

140
Q

Hemispheric lesion associated with aphasic dysgraphia

A

Left

141
Q

Hemispheric lesion associated with number dyscalculia

A

Left

142
Q

Hemispheric lesion associated with visuospatial defects

A

Right

143
Q

Hemispheric lesion associated with anosognosia

A

Right

144
Q

Hemispheric lesion associated with neglect

A

Right

145
Q

Hemispheric lesion associated with constructional apraxia

A

Right

146
Q

Hemispheric lesion associated with dysgraphia or dyscalculia associated with spatial issues

A

Right

147
Q

Hemispheric lesion associated with dressing apraxia

A

Right

148
Q

Hemispheric lesion associated with aprosodia (inability to convey or interpret emotional elements of speech)

A

Right

149
Q

Hemispheric lesion associated with alexia (inability to read)

A

Left

150
Q

Hemispheric lesion associated with colour anomia

A

Left

151
Q

Hemispheric lesion associated with Broca’s aphasia

A

Left

152
Q

Hemispheric lesion associated with Wernicke’s aphasia

A

Left

153
Q

Symptoms seen in Gerstmann syndrome

A

Dysgraphia
Dyscalculia
Finger agnosia
Right left disorientation

154
Q

Hemispheric lesion seen in Gerstmann syndrome

A

Left

155
Q

Hemispheric lesion seen in prosopagnosia

A

Right

156
Q

Receptor changes seen after ECT in patients with depression

A

Reduced beta receptors
Increased noradrenaline turnover
Reduced 5HT2 receptors

157
Q

Features associated with Klüver-Bucy syndrome

A 
Hyperorality
Hypersexuality
Docility
Visual agnosia
Dietary changes
158
Q

Area of brain affected in Klüver-Bucy syndrome

A

Bilateral medial temporal lobes

Amygdala

159
Q

Common causes of Klüver-Bucy syndrome

A 
Herpes
Late stage Alzheimer's disease
Frontotemporal dementia
Trauma
Bilateral temporal lobe infarction
160
Q

Description of pulvinar sign

A

Bilateral high signal of the medial thalamus

161
Q

Abnormal structure in dementia pugilistica

A

Septum pellucidum

162
Q

Abnormality seen in the septum pellucidum in dementia pugilistica

A

Fenestrated cavum septum pellucidum

163
Q

Distribution of tau accumulation seen in dementia pugilistica

A

Irregular, focal perivascular distribution

At the depths of cortical sulci

164
Q

Macroscopic features of schizophrenia

A

Enlarged ventricles
Reduction in grey matter volume and total brain volume
Reduced asymmetry of the planum temporale

165
Q

Macroscopic feature associated with first generation antipsychotic exposure

A

Enlargement of the caudate

166
Q

Movement disorder associated with damage to the subthalamic nucleus in the basal ganglia

A

Hemiballismus

167
Q

Features of hemiballismus

A

Involuntary violent movements of the arms and legs

168
Q

Macroscopic features of multisystem atrophy

A

Pale substantia nigra
Greenish putamen
Atrophied putamen
Cerebellar atrophy

169
Q

Microscopic features of multisystem atrophy

A

Papp-Lantos bodies

170
Q

Areas of the brain which show increased glucose metabolism in OCD

A 
Orbitofrontal area
Caudate
Thalamus
Prefrontal cortex
Anterior cingulate
171
Q

Three categories the Boston Classification uses to divide aphasias

A

Fluency
Repetition
Comprehension

172
Q

Most severe type of aphasia where there is non-fluent speech, lack of comprehension, and lack of repetition

A

Global aphasia

173
Q

Non-speech features usually present with global aphasia

A

Inability to read and write
Hemiplegia
Hemisensory loss and hemianopia

174
Q

Area of damage for global aphasia

A

Entire L perisylvian region - often MCA occlusion

175
Q

Type of aphasia where speech is not fluent and repetition is impaired, but comprehension is intact

A

Broca’s aphasia

176
Q

Broca’s area in Brodmann areas

A

44 and 45

177
Q

Area Broca’s area is found in

A

L Frontal lobe

178
Q

Blood vessel which supplies Broca’s area

A

Superior division of MCA

179
Q

Type of aphasia where the speech is fluent but comprehension and repetition are impaired

A

Wernicke’s aphasia

180
Q

Area of the brain Wernicke’s area is found

A

L superior temporal gyrus

181
Q

Brodmann area which is Wernicke’s area

A

22

182
Q

Blood vessel which supplies Wernicke’s area

A

Inferior division of MCA

183
Q

Type of aphasia where the speech is fluent and comprehension is intact but there is specific deficit in repetition

A

Conduction aphasia

184
Q

Area of the brain damaged in conduction aphasia

A

Arcuate fasciculus which connects Wernicke’s area and Broca’s area

185
Q

Blood vessel which supplies the arcuate fasciculus

A

Inferior or superior division of the MCA

186
Q

Type of aphasia where fluency, repetition and comprehension are all largely intact and the biggest issue is word finding

A

Anomic aphasia

187
Q

Areas of the brain often damaged in anomic aphasia

A

Less well localised than most aphasias

Often temporal-parietal area, sometimes angular gyrus

188
Q

Type of aphasia where comprehension is impaired but sentences can be repeated verbatim or read aloud. May be fluent or non-fluent depending on if it is sensory or motor subtype

A

Transcortical aphasia

189
Q

Subtype of transcortical aphasia with fluent speech, impaired comprehension and intact repetition

A

Sensory transcortical aphasia

190
Q

Subtype of transcortical aphasia with non-fluent speech, impaired comprehension and intact repetition

A

Motor transcortical aphasia

191
Q

Loss of reading ability with preserved writing ability - but inability to read words they have written after a break

A

Alexia without agraphia

192
Q

Most common brain areas affected in alexia without agraphia

A

Angular gyrus - often by simultaneous lesions of the L occipital lobe and the splenium of corpus callosum

193
Q

Medical causes of alexia without agraphia

A

L PCA stroke
Tumour
MS

194
Q

Loss of reading and writing ability but intact speech and oral language understanding - sometimes with word finding difficulty

A

Alexia with agraphia

195
Q

Most common area of lesion causing alexia with agraphia

A

Angular gyrus - L inferior parietal lobe

196
Q

Type of aphasia which is similar to Wernicke’s aphasia but reading comprehension is intact

A

Auditory verbal agnosia/pure word deafness

197
Q

Dopamine abnormality causing positive symptoms in schizophrenia

A

Increased dopaminergic activity in the striatum

198
Q

Dopamine activity causing negative symptoms in schizophrenia

A

Decreased dopaminergic activity in the frontal lobe

199
Q

Disease classically associated with an abnormal tonsillar biopsy

A

Variant CJD

200
Q

Alternative name for dementia pugilistica

A

Chronic traumatic encephalopathy

201
Q

Type of neurodegenerative condition which can occur immediately after a single traumatic brain injury

A

Dementia pugilistica

202
Q

Conditions in which kuru plaques are seen

A

Kuru
Gerstmann-Sträussler–Scheinker syndrome
CJD

203
Q

Condition in which Verocay bodies are seen

A

Schwannoma

204
Q

Disease in which haematoxylin bodies are seen

A

SLE

205
Q

Conditions in which zebra bodies are seen

A

Niemann-Pick disease
Tay-Sachs disease
Mucopolysaccharides

206
Q

Conditions in which Schaumann bodies are seen

A

Sarcoidosis

Berylliosis

207
Q

Diseases in which Mallory bodies are seen

A

Alcoholic hepatitis and cirrhosis
Wilson’s disease
PBC

208
Q

Diseases in which asteroid bodies are seen

A

Sarcoidosis

Berylliosis

209
Q

Areas of the brain which have been shown to be hyperactive in depression

A

Amygdala

Anterior cingulate cortex

210
Q

Area of the brain which has been shown to be underactive in depression in some studies, and overactive in others

A

Dorsolateral prefrontal cortex

211
Q

Important prion diseases

A

CJD
Kuru
Gerstman-Sträussler–Scheinker syndrome
Fatal familial insomnia

212
Q

Disease balloon cells are associated with

A

Pick’s disease

213
Q

Macroscopic features of Parkinson’s disease

A

Pallor of the substantia nigra in the midbrain

Pallor of the locus coeruleus in the pons

214
Q

Condition associated with reductions in interneurons in cortical layer II of the prefrontal cortex

A

Schizophrenia

215
Q

Area of low perfusion seen in SPECT scan of Alzheimer’s dementia

A

Medial temporal areas

Parietal areas

216
Q

Cellular distribution of Lewy bodies - extracellular vs. intracellular

A

Intracellular

217
Q

Response of Parkinsonian features of multisystem atrophy to levodopa

A

Poor response

218
Q

Macroscopic features of progressive supranuclear palsy

A

Pallor of the substantia nigra with sparing of the locus coeruleus - pallor of both seen in Parkinson’s
Mild midbrain atrophy
Superior cerebellar peduncle atrophy
Discolouration of the dentate nucleus

219
Q

Normal form of prion protein

A

PrPC

220
Q

Enzyme which can break down PrPC but nor PrPSc

A

Protease

221
Q

Main structure of PrPSc

A

Beta sheet

222
Q

Method PrPSc has of spreading

A

It can change nearby PrPC into PrPSc

223
Q

Structure of PrPC

A

Alpha helix

224
Q

Frontal lobe hemisphere more associated with depression when damaged

A

Left

225
Q

Frontal lobe hemisphere more associated with disinhibition, aggression and impulsivity if damaged

A

Right

226
Q

Cells affected in Guillain Barré syndrome

A

Schwann cells

227
Q

Cell type that makes up an acoustic neuroma

A

Schwann cells

228
Q

Artery usually affected in a stroke causing amaurosis fugax

A

Retinal/opthalmic artery

229
Q

Areas of brain damage associated with Wernicke and Korsakoff syndrome

A

Medial thalamus

Mamillary bodies of hypothalamus

230
Q

Area of lesion to cause an ipsilateral monocular visual loss

A

Optic nerve

231
Q

Area of lesion to cause a bitemporal hemianopia

A

Optic chiasm

232
Q

Area of lesion to cause a contralateral homonymous hemianopia without macular sparing

A

Optic tract

233
Q

Area of lesion to cause a contralateral homonymous inferior quadrantanopia

A

Parietal (upper) optic radiation

234
Q

Area of lesion to cause a contralateral homonymous superior quadrantanopia

A

Temporal (lower) optic radiation

235
Q

Area of lesion to cause a contralateral homonymous hemianopia with macular sparing

A

Occipital visual cortex

236
Q

Target sites for deep brain stimulation in Parkinson’s disease

A

Subthalamic nucleus

Globus pallidus interna

237
Q

Number of dopamine transporters in patients with ADHD compared to healthy controls

A

Fewer

238
Q

Effect of psychostimulant treatment on dopamine transporter numbers in patients with ADHD

A

Increased

239
Q

Neuropathological features of presymptomatic HIV infection

A 
Lymphocytic leptomeningitis
Perivascular lymphocytic cuffing
Parenchymal T and B lymphocyte infilatration
Gliosis
Microglial activation
Axonal damage
240
Q

Neuropathological feature of presymptomatic HIV infection which is also found in HIV negative IV drug users as well as in trauma, inflammation and hypoxia

A

Axonal damage

241
Q

Most common organic cause of anxiety

A

Hypoglycaemia

242
Q

Lobe associated with Jacksonian seizures

A

Left frontal lobe

243
Q

Structure which when divided leads to a ‘split brain’

A

Corpus callosum

244
Q

Most common opportunistic CNS infection in patients with AIDS

A

Toxoplasma gondii (toxoplasmic encephalitis)

245
Q

Area of the brain which shows the pulvinar sign in variant CJD

A

Thalamus

246
Q

Subtype of opioid receptors associated with depression

A

Sigma

247
Q

Changes in neurotransmitters seen in Alzheimer’s disease

A

Decreased acetylcholine

Increased glutamate

248
Q

Main mechanism of spread of HIV to the brain

A

Infected macrophages

249
Q

Structures involved in Wernicke’s encephalopathy

A

Mamillary bodies
Thalamic nuclei
Walls of the third ventricle

250
Q

fMRI appearances in keeping with a patient experiencing auditory hallucinations

A

Increased activity at the temporal cortex

251
Q

Mamillary body abnormality seen in Wernicke Korsakoff syndrome

A

Decreased mamillary body transketolase activity

252
Q

Area of the brain showing increased dopamine release in patients with schizophrenia on the amphetamine challenge test

A

Striatum

253
Q

Neural process where deficiency is seen in delusions of control

A

Sensory prediction

254
Q

Area of the brain which shows hypoplasia in autism

A

Cerebellar vermis

255
Q

Impact of Parkinson’s disease on D2 receptor sensitivity

A

Increased D2 receptor sensitivity at the basal ganglia

256
Q

Part of the brain most associated with prion disease

A

Cerebellum

257
Q

Area of the brain targeted in transcranial magnetic stimulation treatment for treatment resistant depression

A

Left frontal lobe

258
Q

Earliest histological change seen in Alzheimer’s disease

A

Amyloid-mediated damage

259
Q

Area of the brain showing hypoperfusion in Lewy body dementia

A

Occipito-parietal

260
Q

Disease associated with the hummingbird sign on sagittal imaging - midbrain atrophy

A

Progressive supranuclear palsy

261
Q

Prion disease which does not show spongiform change

A

Fatal familial insomnia

262
Q

CNS cell type most susceptible to HIV infection

A

Microglia

263
Q

Characteristics of medial prefrontal syndrome

A

Poverty of speech

Lack of spontaneous behaviour

264
Q

Characteristics of orbitofrontal syndrome

A

Explosive outbursts

Poor impulse control

265
Q

Characteristics of dorsolateral prefrontal syndrome

A

Executive dysfunction

Diminished planning

266
Q

Alternative name for medial prefrontal syndrome

A

Apathetic type/pseudo depressive type prefrontal syndrome

267
Q

Alternative name for orbitofrontal syndrome

A

Disinhibited type/pseudopsychopathic type frontal syndrome

268
Q

Alternative name for dorsolateral prefrontal syndrome

A

Dysexecutive/disorganised type prefrontal syndrome

269
Q

Structural changes associated with normal pressure hydrocephalus

A

Enlarged lateral and third ventricles out of proportion to rest of the brain

270
Q

Characteristic structural change seen in autism

A

Hypoplasia cerebellar vermis

271
Q

Neurotransmitter deficient in Lewy Body dementia and Parkinson’s disease dementia

A

Acetylcholine

272
Q

Areas of the brain which see hypoperfusion in schizophrenia

A

Frontal lobe and prefrontal cortex
Anterior and medial cingulate gyri
Parietal lobes

273
Q

Areas of the brain which see hyperperfusion in schizophrenia

A

Cerebellum
Brainstem
Thalamus

274
Q

Hyperintensities seen on imaging in patients with depression

A

Periventricular
Deep white matter
Thalamic
Striatal

275
Q

Areas of decreased volume seen on imaging of patients with depression

A

Frontal

Basal ganglia

276
Q

Areas of decreased metabolism seen on imaging of patients with depression

A

Prefrontal cortex
Anterior cingulate
Amygdala

277
Q

Finding seen on imaging of patients with depression which suggests psychomotor retardation

A

Elevated D2 binding

278
Q

Areas of loss of grey matter seen on imaging of patients with schizophrenia

A

Insular cortex
Anterior cingulate
Medial temporal lobe

279
Q

Area of poor activation seen on fMRI imaging of patients with schizophrenia

A

Dorsolateral prefrontal cortex

280
Q

Area of brain with low DAA seen on MR spectroscopy of patients with schizophrenia

A

Prefrontal cortex

281
Q

Diffusion tensor imaging findings seen on imaging of patients with schizophrenia

A

Widespread reduction

282
Q

Area where there is loss of volume seen on imaging of patients with Alzheimer’s

A

Temporal lobe especially the hippocampus

283
Q

Area of decreased activation on fMRI imaging of patients with Alzheimer’s

A

Parieto-temporal

284
Q

Neuropathological changes seen in patients with depression

A 
Enlarged lateral ventricles
Enlarged amygdala
Reduced hippocampal volume
Reduced basal ganglia volume
Reduced grey matter in the prefrontal cortex
285
Q

Areas shown to have altered blood flow on SPECT scan among patients with depression

A

Dorsolateral prefrontal cortex
Basal ganglia
Anterior cingulate
Amygdala

286
Q

Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to the cognitive dysfunction seen

A

Prefrontal cortex

287
Q

Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to impaired attention and abnormal emotional processing

A

Anterior cingulate

288
Q

Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to abnormal emotional processing

A

Amygdala

289
Q

Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to psychomotor retardation

A

Basal ganglia

290
Q

Altered metabolism seen in OCD

A

Increased metabolism in the orbitofrontal area, caudate, thalamus, prefrontal cortex, and anterior cingulate

291
Q

Site of brain lesion causing alexia without agraphia, colour agnosia, and visual object agnosia

A

Dominant occipital lobe

292
Q

Site of brain lesion causing profound amnesia

A

Bilateral temporal lobe

293
Q

Site of brain lesion causing visuospatial agnosia, prosopagnosia, and complex visual hallucinations

A

Non-dominant occipital lobe

294
Q

Site of brain lesion causing apraxias, prosopagnosia, and neglect of one side of the body (hemisomatognosia)

A

Non-dominant parietal lobe

295
Q

Part of the brain which sees increased blood flow when a patient is experiencing hallucinations and delusions

A

Left medial temporal cortex

Neurosciences (16 decks)

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