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Neuropathology Flashcards

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1
Q

Gross changes in Alzheimers?

A

Diffuse atrophy
Flattened cortical sulci
Enlarged cerebral ventricles

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2
Q

Histological changes in Alzheimers?

A 
Neuronal loss in cortex and hippocampus
Synaptic loss
Granulovascular degeneration
Senile plaques
Neurofibrillary tangles
Hirano bodies
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3
Q

What is granulovascular degernation?

A

Small vacuoles with central granules in cytoplasm of neurons - particularly in temporal lobes

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4
Q

Structure of senile plaques

A

Insoluble amyloid peptide deposits

Peptide called Beta A4 peptide

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5
Q

Structure of amyloids

A

Fibrils of multimeric chains of peptides deposited extracellulaly, with beta pleated sheet confirmation

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6
Q

What cleaves beta A4?

A

Cleaved from amyloid-beta precursor protein by beta and gamma-secretases

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7
Q

What prevents cleavage of amyloid beta precursor protein?

A

Alpha secretase

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8
Q

Subtypes of plaques?

A

Neuritic plaque

Diffuse

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9
Q

Structure of neuritic plaque

A

Beta A in form of amyloid fibrils, among which are irregularly swollen dystrophic neuritis (defenerated neuronal processes)

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10
Q

How are neuritic plaques visualised?

A

Neurites visualised with silver stains.

May be seen as an eosinophilic mass on haematoxylin and eosin stains.

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11
Q

Core of neuritic plaques?

A

May contain dense central core of amyloid

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12
Q

Periphery of neuritic plaques?

A

Microglia and astrocyte processes

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13
Q

Diseases in which neuritic plaques are seen?

A

Normal ageing

Downs

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14
Q

What is the ‘apple green’ birefringence of stained stissue with neuritic plaques?

A

Amyloid sensitive stain Congo red under polaroid light leads to ‘apple green’ stain of neuritic plaques due to presence of beta-pleated sheets.

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15
Q

Structure of diffuse plaques?

A

Consist of non-fibrillar extracellular A beta.

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16
Q

Which plaques are not related to cognitive decline?

A

Diffuse

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17
Q

Peptides in diffuse plaques?

A

Same peptides as those responsible for amyloid formation in neuritic plaques but not polymerized to form fibrils and lack of beta-sheet configuration.

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18
Q

What are neurofibrillary tangles composed of?

A

Cytoskeletal elements - primarily abnormally phosphorylated tau protein.

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19
Q

What type of tauopathy is Alzheimers?

A

One of several degenerative tauopathies

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20
Q

What is tau?

A

Peptide required for microtubule assembly.

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21
Q

Function of microtubules?

A

Transport of materials down axons.

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22
Q

What stimulates formation of abnormal tau?

A

Beta A4 peptide interacts with cholinergic receptors, stimulating abnormal hyperphosphorylation of tau.

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23
Q

Where is hyperphosphorylated tau present?

A

Abnormal tau

Degenerated neurites

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24
Q

How can hyperphosphorylated tau be visualised?

A

Staining with antibody to abnormal tau

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25
Q

Which conditions do neurofibrillary tangles occur in?

A 
Alzheimers
Downs
Dementia pugilistica (punch-drunk syndrome)
Parinkson-dementia complex of Guam
Hallervorden-Spatz disease
Normal elderly
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26
Q

Location of tangles?

A

Mainly intraneuronal

Upon neuronal degeneration may appear extracellularly, thus losing their basophilia

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27
Q

How can tangles be visualised?

A

Faintly basophilic

Tau immunostaining and silver impregnation can be used to improve chances of light microscopic detection.

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28
Q

Location of tangles on early Alzheimers?

A

Tangles and neuropil threads are restricted to parts of the entorhinal cortex and CA1 field of hippocampus.

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29
Q

Location of tangles as Alzheimers develops?

A

Tangles and neutrophil threads accumulate in increasing density in other parts of the hippocampus and medical temporal neocortex, then in other cortical regions and in subcortical grey matter structures such as hypothalamus and thalamus.

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30
Q

What staging scheme is used to describe extent of tangle related abnormalities in Alzheimers?

A

Braak and Braak (1995)

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31
Q

Which stages of Braak and Braak’s staging scheme operationally define Alzheimers?

A

Stages V-VI

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32
Q

Structure of C Hirano bodies?

A

Rod-shaped eosinophilic bodies n cytoplasm of neurons

Intracellular aggregates of actin and actin-associated proteins

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33
Q

Location of Hirano bodies when neuron dies?

A

Extracellular space

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34
Q

Location of HIrano bodies normally?

A

Hippocampal pyramidal cells

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35
Q

Pathology of cerebral amyloid angiopathy?

A

Accumulation of A beta in walls of blood vessels, particularly arteries and arterioles in cerebral cortex overlying leptomeninges

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36
Q

What % of the elderly have Cerebral amyloid angiopathy?

A

30%

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37
Q

What % of patients with Alzheimers have Cerebral Amyloid Angiopathy?

A

90%

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38
Q

What important disease can Cerebral Amyloid Angiopathy?

A

Haemorrhagic strokes confined to superficial blood vessels.

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39
Q

How does Cerebral Amyloid Angiopathy lead to haemorrhagic stroke?

A

Rupture of amyloid laden blood vessels causes superficial lobar haemorrhages that may extend into subarachnoid space

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40
Q

Relation between tangles and cognitive decline

A

Increase in number and distribution

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41
Q

Link between tangles, neuritic plaque and cognitive decline?

A

If both are present, presence of even a few tangles in a single field in neocortex can suggest significant cognitive decline.

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42
Q

Best neuropathological correlate of decline?

A

Number of synapces

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43
Q

Marker for synapses?

A

Antibody to synaptophysin, a protein fund in presynaptic endings

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44
Q

Where is synaptophysin found?

A

Presynaptic endings

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45
Q

Cellular pattern of neuronal loss in hippocampal pathology?

A

Subiculum of hippocampal formation and layers II and IV of entorhinal cortex.

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46
Q

Affected cells involved in hippocampal pathology?

A

Connect hippocampal formation with association cortices, basal forebrain, thalamus and hypothalamus, structures crucial to memory.

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47
Q

Significance of neuronal loss in hippocampal pathology?

A

Isolates hippocampal formation from its input and output, contributing to memory disorder in Alzheimers

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48
Q

What is Binswanger’s Disease?

A

Subcortical vascular dementia/subcortical arteriosclerotic encephalopathy
Many small infarctions of what matter that spares cortical regions.
Co-exists with Alzheimers-type changes

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49
Q

Which type of dementia co-exists with Alzheimers?

A

Subcortical

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50
Q

Histology of Lewy bodies?

A

Weakly eosinphilic
Spherical
Cytoplasmic inclusions

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51
Q

Where are Lewy bodies in Parkinsons?

A

Confined to substantia nigra

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52
Q

Where are Lewy bodies in Lewy body Dementia?

A

Substantia nigra
Areas of cerebrum including temporal and frontal lobe and cingulate gyrus
Dorsal motor nucleus of vagus

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53
Q

Difference between lewy bodies in substantia nigra and cortex?

A

In cortex they are less conspicuous, eosinophilic and lack clear halo
Take up homeneous eosinophilic staining in cytoplasm along with peripheral displacement of nucleus

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54
Q

Correlation between number of Lewy bodies and cognitive decline?

A

None

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55
Q

What can we use to identify Lewy body?

A

Antibody to protease ubiquitin

Staining with alpha-synuclein antibodies

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56
Q

What do lewy bodies contain?

A

Accumulations of alpha-synuclein

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57
Q

What type of disease is Lewy body dementia?

A

Degenerative synucleopathies

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58
Q

What does alpha-synuclein do?

A

Accelerates reuptake of dopamine in neurons; this dopamine overload may be toxic

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59
Q

What are Lewy neuritis?

A

Nerve cell processes that contain aggregates of alpha-synuclein

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60
Q

Where are Lewy neuritis most numerous?

A

CA2/3 region of hippocampus

Substania nigra

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61
Q

Which diseases do Lewy neurites occur?

A

Lewy body Dementia

Idiopathic Parkinsons

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62
Q

Where does microvacuolation occur in Lewy Body Dementia?

A

Microvacuoalation of cerebral cortex, mainly in medial temporal region.

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63
Q

What are Tauopathies?

A

Diseases with tau deposits

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64
Q

What are synucleopathies?

A

Disease with alpha synuclein deposits

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65
Q

Name some tauopathies?

A 
Alzheimers
Picks
Progressive supranuclear palsy
Corticobasal degenerations
Frontotemporal dementia with Parkinsonism (FTDP-17)
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66
Q

Name some synucleopathies?

A

Parkinsons
Lewy Body Dementia
Multisystem atrophy

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67
Q

Which types of pathology is frontotemporal dementia associated with?

A

Frontal lobe degeneration type
Picks type
Motor neurone disease type

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68
Q

Most common type of frontotemporal dementia?

A

Frontal lobe degeneration

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69
Q

Underlying pathology of Frontal lobe degeneration?

A

Spongiform degeneration or microvacuolation of superficial neuropil seen chiefly in layers III and V of cortex
Loss of large cortical nerve cells with minimal gliosis

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70
Q

Which cells are mainly lost in Frontal lobe degeneration?

A

Large cortical nerve cells

71
Q

Characteristics of Picks disease?

A

Prepronderance of atrophy in frontotemporal regions

72
Q

What are Pick cells?

A

Abnormal swollen oval-shaped neuronal cells with loss of Nissl’s substance and peripherally displaced nucleus

73
Q

What are Picks bodies seen in post-mortem?

A

Argentophilic, tau and ubiquitin reactive filamentous inclusions

74
Q

Are Hirano bodies seen in Picks disease?

A

Yes but less than in Alzheimers

75
Q

Characteristics of motor neurone disease type frontotemporal disease?

A

Cerebral atrophy is less marked
Limbic areas are largely preserved
Ubiquitinated inclusions in frontal cortex and hippocampus

76
Q

Cell loss in motor neurone disease type frontotemporal disease?

A

Large cortical nerve cells
Microvacuolation
Mild gliosis

77
Q

MND pathology in motor neurone disease type frontotemporal disease?

A

MND pathology in anterior horn cells

78
Q

Pathology in Huntington’s dementia?

A

Severe loss of small neurons in caudate and putamen with subsequent astrocytosis
Head of caudate shrinks and there is ‘ex vacuo’ dilatation of anterior horns of lateral ventricles

79
Q

Characteristics of Huntington’s dementia?

A

Protein deposits form nuclear inclusions in neurons

80
Q

Forms of CJD?

A

Sporadic
Familial
Variant

81
Q

Most common form of CJD?

A

Sporadic

82
Q

What is variant CJD related to?

A

Bovine spongiform encephalopathy

83
Q

Characteristic pathological features of CJD?

A

None due to short course of disease

84
Q

Pathological features of CJD >6 months?

A

Degree of generalized cerebral atrophy

85
Q

Microscopic changes in CJD?

A

Spongiform encephalopathy secondary to neutrophil variation
Round to oval vacuoles in neuropil of cortical gray matter - vacuoles are single or multiloculated.
Vacuoles may coalesce to microcysts.

86
Q

Cell loss in CJD?

A

Neuronal loss

Gliosis

87
Q

What is Prion protein?

A

Normal neuronal cell surface protein

88
Q

Which gene encodes prion protein?

A

On chromosome 20

89
Q

What happens to prion protein in CJD?

A

Chromosome 20 is converted via conformational change to abnormal form - PrPSc.

90
Q

What does PrPSc do?

A

Protease-resistant
Accumulates in CNS
Triggers conversion of normal PrPc to PrPSc.

91
Q

What causes degenerative changes in cerebral cortex in CJD?

A

PrPSc.

92
Q

How can PrPSc be identified?

A

Immunoperoxidase staining

93
Q

How can PrPSc be transmitted between people?

A

If person has spongiform encephalopathy, via:
pituitary extracts
cornal transplants
dural grafts
contaminated electrodes from neurosurgical procedures

94
Q

Pathology in vCJD?

A

Marked accumulation of prion protein

Plaques are florid

95
Q

What protein is found in CSF in CJD?

A

14-3-3

96
Q

What is protein 14-3-3 associated with?

A

CJD
Viral encephalitis
Stroke

97
Q

Which type of CJD is protein 14-3-3 least frequent in?

A

Variant CJD

98
Q

In which type of CJD are the EEG changes lacking?

A

Familial

99
Q

In which type of CJD are 14-3-3 proteins absent?

A

Familial - <50%

100
Q

What may have an influence on susceptibility of disease?

A

Presence of polymorphisms at codon 129 of PrP

101
Q

Which aa may be present at codon 129 of PrP?

A

Methionine

Valine

102
Q

Which phenotype of codon 129 at PrP is present in CJD?

A

M/M phenotype

103
Q

What % of people with sporadic CJD have M/M phenotype?

A

73%

104
Q

What % of people with variant CJD have M/M phenotype?

A

100%

105
Q

Most supportive diagnostic test for CJD?

A

MRI

106
Q

Abnormality seen in MRI in CJD?

A

Posterior thalamic region (pulvinar sign)

107
Q

Which type of MRI most shows pulvinar sign?

A

FLAIR sequences of MRI

108
Q

Age of onset of classic CJD?

A

7th or 8th decade of life

109
Q

Age of onset of vCJD?

A

3rd/4th decade of life

110
Q

Course of classic CJD?

A

5 months

111
Q

Course of vCJD?

A

1 year

112
Q

Symptoms of classic CJD?

A

Early neurological signs

Dementia

113
Q

Symptoms of vCJD?

A

Early psychiatric/behavioural signs with delayed neurological features

114
Q

EEG signs in classic CJD?

A

Triphasic, sharp waves

115
Q

EEG signs in vCJD?

A

Triphasic waves rare

Changes often non-specific

116
Q

In which type of CJD are trophasic waves seen?

A

Classic CJD

117
Q

In which type of CJD is pulvinar sign not seen?

A

CLassic

118
Q

In which type of CJD are large number of plaques noted in biopsy?

A

Variant

119
Q

Tonsils in classic CJD?

A

Prion protein cannot be isolated from lymphoid tissue

120
Q

Tonsils in vCJD?

A

Tonsillar tissue carries prion agent

121
Q

Major HIV receptors?

A

CD4

CD8

122
Q

Chemokine receptors associated with HIV?

A

CXCR4 and CCR5 considered HIV-1 co-receptors

123
Q

Main method of replication in HIV?

A

CD4+ helper T lymphocytes main route of multiplication and entry apart from monocytes

124
Q

Source of CNS infection in HIV?

A

Infected CD4+ T cells and monocytes

125
Q

Characteristic of stains of HIV in brain?

A

Infecting macrophages rather than lymphocytes

126
Q

What is Macrophage-tropism?

A

Related to mutation in region of gp120 which is the external glycoprotein of HIV

127
Q

Which mutation is related to the external glycoprotein of HIV?

A

Macrophage-tropism of a specific region of gp120

128
Q

How does HIV-1 cross blood brain barrier?

A

Trojan Horse hypothesis:

Enters CNS as passenger in cells to the brain via CD4 T cells or monocytes.

129
Q

What confirms the Trojan Horse hypothesis in HIV?

A

Virus accumulation in perivascular region

130
Q

What is the alternative hypothesis of how HIV enters CNS?

A

Entry of free HIV-1 by migration between or transcytosis of endothelial cells.

131
Q

Most commonly infected neurocells of HIV-1?

A

Perivascular macrophage and microglia

132
Q

Which CNS cells contain receptors/co-receptors for HIV-1 entry?

A

Astrocytes
Oligodendrocytes
Neurons
Perivascular macrophages and microglia

133
Q

Components of mechanism of HIV

A

Direct effect of HIV-1 infection

Indirect consequences of infection comprising secretion of cytokines and neurotoxins

134
Q

How do infected macrophages and microglia lead to neurodegeneration in HIV?

A
  1. Shedding viral proteins
  2. Releasing significant amount of cytokines and neurotoxins into CNS
  3. Tat and TNF-alpha contribute to disruption of blood brain barrier which becomes more permeable to infected monocytes and cytokines in periphery
135
Q

What do pro-inflammatory cytokines secreted by infected macrophages and microglia in HIV do?

A

Activate microglia and astrocytes which in turn secrete neurotoxins

136
Q

What secretes neurotoxins in HIV?

A

Microglia and astrocytes activated by pro-inflammatory cytokines stimulated by infected macrophages and microglia

137
Q

What type of neuronal injury occurs in HIV?

A

Apoptosis

138
Q

How does apoptosis occur in HIV to neuronal cells?

A

By toxic products released by HIV-infected macrophages and microglia or by activated astrocytes

139
Q

Which factors cause demyelination of oligodendrocytes?

A

Tumour necrosis factor

140
Q

Which factors are neurotoxic and cause apoptosis of neuronal cells?

A

Platelet activating factor
Quinolinic acid
Nitric oxide
Some metabolites of arachidonic acid

141
Q

Findings in biopsy of HIV in CNS

A

Infiltration of macrophages in CNS
Formation of microglial nodules
Astrocyte activation and damage
Myelin damage

142
Q

Cells in white and grey matter in biopsy of HIV?

A

Multinucleated giant cells from virus-induced fusion of microglia and/or macrophages

143
Q

Where is neuronal loss found in biopsies in HIV?

A

Hippocampus
Basal ganglia
Caudate nucleus

144
Q

Findings in biopsy of severe cases of HIV?

A

Lipid macrophages

145
Q

Most common psychiatric presentation in AIDs?

A

HIV-related dementia

Depression

146
Q

What % of HIV-infected patients present with psychosis?

A

10%

147
Q

What is viral load used for in clinical practice?

A

To predict stage of disease
Monitor disease progression
Formulate treatment strategies

148
Q

Definition of viral load?

A

Actual number of viral particles in cubic millimetre of blood

149
Q

Can CSF viral load be used in HIV?

A

No - not accurate indicator of CNS disease

150
Q

Weight, length and volume changes in schizophrenia re brain?

A

Decreased weight
Decreased length and volume of cerebral hemispheres
Enlargement of lateral ventricles - particularly temporal horns

151
Q

Which tissue volume is reduced in schizophrenia?

A

Thalamus

Temporolimbic structures including hippocampus, amygdala and parahyppocampal gyrus

152
Q

White matter reductions in schizophrenia?

A

Parahippocampal gyrus or hippocampus

153
Q

What happens to septum pellucidi in schizophrenia?

A

Increased incidence of cavum septi pellucidi

154
Q

What happens to basal ganglia in schizophrenia?

A

Reduced volume, particularly in preneuroleptic area in catatonic patients.
Enlargement due to classic neuroleptics - reversed by atypicals

155
Q

In which type of epilepsy is schizophrenia-like psychosis more common in?

A

Temporal lobe epilepsy when focus is on left hemisphere

156
Q

Where is the planum temporale?

A

Posterior superior surface of superior temporal gyrus

157
Q

What is planum temporale?

A

Lateralized brain structure involved with language

158
Q

What happens to planum temporale in schizophrenia?

A

Consistent reversal of normal left-larger-than-right asymmetry of planum temporale surface area

159
Q

What is Heschl’s gyrus?

A

Primary auditory cortex

160
Q

Is astrogliosis evident in schizophrenia?

A

No

161
Q

Any cell number or size change in schizophrenia?

A

Reduced numbers and size in affecting neurons in hippocampus and DLPFC

162
Q

Neuronal density in schizophrenia?

A

Increased, may relate o observed decrease in neuronal size, with decreased dendritic arborisation and decreased neuropil compartment.

163
Q

Changes in brain archeticture in schizophrenia?

A

Subtle cytoarchitectural anomalies in hippocampal function, frontal cortex - significant cellular disarray in CA3-CA4 interace

164
Q

What do synaptic studies in schizophrenia show?

A

Decrements in presynaptic markers in hippocampus and DLPFC.

Reflect reduction in synaptic contacts formed

165
Q

What does decrements in presynaptic markers in hippocampus and DLPFC in schizophrenia support?

A

Hypothesis of excessive synaptic pruning in schizophrenia.

166
Q

Which synapses are vulnerable in schizophrenia?

A

Glutamatergic synapses in hippocampus and DLPFC, with predominantly GABAergic involvement in cingulate gyrus.

167
Q

Affect of antipsychotics in histology of schizophrenia?

A

Alter synaptic and neuronal morphology, particularly caudate-putamen and may increase glial density in prefrontal cortex

168
Q

Pathological changes of Wernickes?

A

Degenerative changes including gliosis, small haemorrhages in third ventricle and aqueduct and cerebellar atrophy

169
Q

Where is small haemorrhage seen in Wernickes?

A 
Third ventricle
Mamillary bodies
Hypothalamus
Mediodorsal thalamic nucleus
Colliculi
Midbrain tegmentum
170
Q

Brain damage in uncomplicated alcoholism?

A

Brain shrinkage likely due to white matter loss - reversible

171
Q

Where is alcohol-related neuronal loss found?

A

Superior frontal association cortex
Hypothalamus - supraoptic and paraventricular nuclei
Cerebellum

172
Q

Cell count changes in autism?

A

Lower Purkinje cell count

173
Q

Neocortex changes in Autism?

A

Inconsistent changes - increased cortical volume possibly related to reduced pruning

174
Q

Pathological changes in Autism?

A

Hypoplasia of cerebellar vemis and cerebellar hemispheres

► Med - MRC Psych (21 decks)

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