Neuropathology Flashcards
1
Q
Gross changes seen in Alzheimer’s disease
A
Generalised atrophy
Flattened sulci
Enlarged ventricles
2
Q
Peptides which make up amyloid plaques in Alzheimer’s disease
A
Amyloid beta
3
Q
Protein which amyloid beta is a fragment of
A
Amyloid-beta precursor protein
4
Q
Conformation of amyloid plaques
A
Beta pleated sheets
5
Q
Enzymes which cause amyloid-beta precursor protein to be cleaved into amyloid plaques in Alzheimer’s disease
A
Beta secretase
Gamma secretase
6
Q
Enzyme which prevents the formation of amyloid plaques from amyloid-beta precursor protein
A
Alpha secretase
7
Q
Two main subtypes of amyloid plaques
A
Neuritic plaques
Diffuse plaques
8
Q
Form of amyloid which is found in neuritic plaques
A
Fibrils
9
Q
Cell types found in neuritic plaques
A
Dystrophic neurites
Microglia and astrocytes at the periphery
10
Q
Core of neuritic plaques
A
Dense amyloid core
11
Q
Stain neurites are best visualised with
A
Silver stain
12
Q
Stain of neuritic plaques under Congo red
A
Apple green birefringent
13
Q
Component of diffuse plaques
A
Non-fibrillar extracellular amyloid beta
14
Q
Main component of neurofibrillary tangles
A
Hyperphosphorylated tau protein
15
Q
Purpose of tau protein
A
Microtubule assembly
16
Q
Components required to make abnormally phosphorylated tau
A
Beta amyloid peptide
Cholinergic receptors
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
18
Q
Appearance of neurofibrillary tangles on staining
A
Basophlic
19
Q
Position of neurofibrillary tangles vs. beta amyloid plaques
A
Neurofibrillary tangles largely intraneuronal
Amyloid plaques extracellular
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
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
22
Q
Condition caused by the accumulation of amyloid beta in blood vessel walls in the cerebral cortex
A
Cerebral amyloid angiopathy
23
Q
Percentage of elderly population without Alzheimer’s disease who have cerebral amyloid angiopathy
A
30%
24
Q
Percentage of elderly people with Alzheimer’s disease who have cerebral amyloid angiopathy
A
90%
25
Complication of cerebral amyloid angiopathy
Strokes - especially haemorrhagic
26
Eosinophilic bodies seen in the cytoplasm of neurons in patients with Alzheimer's disease
Hirano bodies
27
Shape of Hirano bodies
Rod shaped
28
Protein involved in Hirano bodies
Actin
29
Area of the brain where Hirano bodies are often seen
Hippocampal pyramidal cells
30
Best neuropathological correlate for clinical decline in patients with Alzheimer's
Number of synapses
31
Neuropathological marker used to measure the number of synapses in patients with dementia
Antibody to synaptophysin (protein found in presynaptic endings)
32
Alternative names for Binswanger's disease
Subcortical vascular dementia
| Subcortical arteriosclerotic encephalopathy
33
Cause of Binswanger's disease
Multiple small infarctions to the deep layers of white matter in the brain
34
Clinical features of Binswanger's disease
Memory issues (not as severe as with Alzheimer's disease)
Psychomotor retardation
Unsteady, slow gait
Urinary urgency or incontinence
35
Areas of the brain where neuronal loss is seen the most in Alzheimer's dementia
Subiculum of the hippocampus
| Layers II and IV of the entorhinal cortex
36
Appearance of Lewy bodies
Spherical
| Eosinophilic
37
Part of the cell Lewy bodies are found
Cytoplasm
38
Two main types of Lewy bodies
Classical
| Cortical
39
Area of the brain Lewy bodies are found in Parkinson's disease
Substantia nigra - pars compacta
40
Areas of the brain Lewy bodies are found in dementia with Lewy bodies
Substantia nigra
Temporal lobe
Cingulate gyrus
Frontal lobes
41
Differences in appearance between classical (found in the substantia nigra) and cortical Lewy bodies
Classical Lewy bodies are more conspicuous, more eosinophilic and have a halo
42
Markers which can be used to identify Lewy bodies
Antibody to ubiquitin
| Antibody to alpha-synuclein
43
Protein accumulations found in Lewy bodies
Abnormal alpha-synuclein
| Some ubiquitin
44
Abnormal neurons seen in dementia with Lewy bodies, Parkinson's disease dementia and occasionally Alzheimer's dementia
Lewy neurites
45
Area of the brain where Lewy neurites are most common
CA2/3 region of the hippocampus
| Substantia nigra
46
Diseases associated with alpha-synuclein aggregation
Parkinson's disease
Dementia with Lewy bodies
Multisystem atrophy
47
Diseases associated with tau deposits
Alzheimer's dementia
Frontotemporal dementia
Progressive supranuclear palsy
48
Most common pathological type of frontal lobe dementia
Frontal lobe degeneration type
49
Three clinical types of frontotemporal dementia
Behavioural variant FTD
Semantic variant primary progressive aphasia
Non-fluent variant primary progressive aphasia
50
Features of behavioural variant FTD
Loss of inhibition
Loss of motivation
Repetitive or obsessive behaviours
51
Features of semantic variant primary progressive aphasia
Loss of vocabulary
| Inability to remember what familiar objects are for
52
Features of non-fluent variant primary progressive aphasia
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)
53
Proteins associated with frontotemporal lobar degeneration
Tau
Transactive response DNA binding protein (TDP 43)
Fused in sarcoma protein (FUS)
54
Macroscopic changes seen in frontotemporal lobar degeneration
Atrophy of frontal and temporal lobes
| Focal atrophy with knife-blade appearance
55
Pathological type of frontotemporal lobar degeneration associated with Pick bodies
Tau type
56
Shape of Pick bodies
Sphrerical
57
Protein composing Pick bodies
Tau
58
Proteins seen aggregated in TDP frontotemporal lobar degeneration
Ubiquitin
| TDP-43
59
Macroscopic changes seen in Huntington's disease
Shrunken head of caudate
| Dilatation of the anterior horns of the lateral ventricles
60
Three types of Creutzfeldt-Jakob disease
Sporadic
Familial
Variant
61
Most common type of Creutzfeldt-Jakob disease
Sporadic
62
Lobe generally spared in Alzheimer's disease
Occipital
63
Brain area showing particular depigmentation in Alzheimer's disease
Locus Coeruleus
64
Area of the brain which degenerates in Alzheimer's disease leading to lower levels of acetylcholine
Nucleus of Meynert/nucleus basalis magnocellularis
65
Difference between Lewy bodies and Hirano bodies
Lewy bodies contain ubiquitin
66
General age of presentation of sporadic CJD
55-65
67
General age of presentation of variant CJD
25-30
68
Origin of variant CJD
Infected meat products
69
Origin on sporadic CJD
Genetic mutation
70
Duration of disease between onset and death for sporadic CJD
Few months
71
Duration of disease between onset and death for variant CJD
Year +
72
Earliest clinical features of sporadic CJD
Neurological signs - cerebellar ataxia, myoclonic jerks
| Dementia
73
Earliest clinical features of variant CJD
Psychiatric and behavioural features
74
Inheritance pattern of familial CJD
Autosomal dominant
75
Histological appearance of the grey matter in CJD
Spongiform changes
Round vacuoles in the neuropil
Vacuoles joining to form microcysts
76
Chromosome where the gene which codes for prion protein is found
20
77
Abnormal form of prion protein found in CJD
PrPSc
78
Other parts of the body where PrPSc may be found in CJD
Skeletal muscle
| Spleen
79
Staining used to identify PrPSc in CJD
Immunoperixodase staining
80
MRI sign seen with variant CJD
Pulvinar sign
81
EEG changes classically seen with sporadic CJD
Triphasic sharp waves 1-2 per second
82
Abnormal protein sometimes found in the CSF with CJD
14-3-3
83
Most common type of CJD where protein 14-3-3 is found
Sporadic
84
Percentage of classic CJD which is familial
10-15%
85
Type of lymphocytes which are reduced in HIV infection
CD4+
86
Cells which are activated by HIV infection and which kill HIV-infected cells
CD8+ cells
87
Most common psychiatric presentation in patients with AIDS
HIV-related dementia
88
Second most common psychiatric presentation in patients with AIDS
Depression
89
Most common cerebral lesion in patients with HIV
Toxoplasmosis
90
Ventricles enlarged in schizophrenia
Lateral
91
Part of the lateral ventricle enlarged in schizophrenia
Temporal horn
92
CT appearance of toxoplasmosis
Ring enhancing lesions +/- mass effect
93
CT appearance of primary CNS lymphoma associated with HIV
Single (or sometimes multiple) homogenous enhancing lesion
94
Area of the brain which sees reduced asymmetry in schizophrenia
Planum temporale
95
Impact of schizophrenia on brain volume
Reduced by up to 5%
96
Areas of the brain which see reduced cell numbers in schizophrenia
Hippocampus
Dorsolateral prefrontal cortex
Superior temporal gyrus
97
Most common functional imaging appearances in schizophrenia
Reduced activation of frontal regions during cognitive tasks
98
Functional imaging appearances seen during hallucinations in schizophrenia
Increased activation of temporal regions
99
Common imaging finding in mood disorders seen on T2 weighted images, especially in older people
White matter hyperintensities particularly in the deep subcortical white matter
100
Areas of the brain where hypoplasia is seen in autism
Cerebellar vermis
| Cerebellar hemispheres
101
Areas of the brain which see degenerative changes in Wernicke's encephalopathy
```
Mamillary bodies
Hypothalamus
Mediodorsal thalamus
Colliculi
Midbrain tegmentum
```
102
Area of the brain which shows depigmentation in Parkinson's disease
Substantia nigra
103
Abnormal protein seen in Alzheimer's disease which correlates best to clinical severity
Neurofibrillary tangles
104
CSF finding which can indicate worse prognosis in those with mild cognitive impairment
Increased tau to amyloid ratio
105
Age of patients with mood disorders where white matter hyperintensities are more often seen
Elderly patients
106
Physical disease which white matter hyperintensities can be associated with
Vascular disease
107
Type of dysarthria characterised by explosive and forceful, but slow speech
Spastic dysrathria
108
Type of dysarthria characterised by a breathy, nasal voice
Flaccid dysarthria
109
Type of dysarthria characterised by slow, quiet, tremulous speech
Hypokinetic dysarthria
110
Type of dysarthria characterised by a variable rate and inappropriate stoppages, and a strained quality
Hyperkinetic dysarthria
111
Type of dysarthria characterised by rapid, monotone, slurred speech
Ataxic dysarthria
112
Type of dysarthria associated with pseudobulbar palsy
Spastic dysarthria
113
Type of dysarthria associated with spastic hemiplegia
Spastic dysarthria
114
Type of dysarthria associated with myasthenia gravis
Flaccid dysarthria
115
Type of dysarthria associated with Parkinson's disease
Hypokinetic dysarthria
116
Type of dysarthria associated with Huntington's disease
Hyperkinetic dysarthria
117
Type of dysarthria associated with Syndenham's chorea
Hyperkinetic dysarthria
118
Type of dysarthria associated with tardive dyskinesia
Hyperkinetic dysarthria
119
Type of dysarthria associated with Friedreich's ataxia
Ataxic dysarthria
120
Type of dysarthria associated with alcohol abuse
Ataxic dysarthria
121
Lesion area associated with spastic dysarthria
Upper motor neuron
122
Lesion area associated with flaccid dysarthria
Lower motor neuron
123
Lesion area associated with hypokinetic dysarthria
Extrapyramidal
124
Lesion area associated with hyperkinetic dysarthria
Extrapyramidal
125
Lesion area associated with ataxic dysarthria
Cerebellar
126
Structure where degeneration is found in Huntington's disease
Striatum
127
Lobe associated with aura in epilepsy
Temporal
128
Lobe associated with dysphoric, euphoric, or other strong emotional feelings
Temporal
129
Structures involved in OCD
```
Lentiform nucleus (putamen and globus pallidus)
Caudate nucleus
```
130
Structure where lesions are associated with hemiballismus
Subthalamus
131
Structure where lesions are associated with dystonia, athetosis and chorea
Corpus striatum
132
Structure where lesions are associated with Parkinsonism
Substantia nigra
133
Symptom caused by damage to the lingual gyrus
Visual snow
134
Structure where lesions are associated with nominal aphasia
Angular gyrus
135
Structure most severely damaged in early Alzheimer's dementia
Entorhinal cortex
136
Lobe initially affected in Alzheimer's disease
Temporal lobe
137
Hemispheric lesion associated with aphasia
Left
138
Hemispheric lesion associated with right-left disorientation
Left
139
Hemispheric lesion associated with finger agnosia
Left
140
Hemispheric lesion associated with aphasic dysgraphia
Left
141
Hemispheric lesion associated with number dyscalculia
Left
142
Hemispheric lesion associated with visuospatial defects
Right
143
Hemispheric lesion associated with anosognosia
Right
144
Hemispheric lesion associated with neglect
Right
145
Hemispheric lesion associated with constructional apraxia
Right
146
Hemispheric lesion associated with dysgraphia or dyscalculia associated with spatial issues
Right
147
Hemispheric lesion associated with dressing apraxia
Right
148
Hemispheric lesion associated with aprosodia (inability to convey or interpret emotional elements of speech)
Right
149
Hemispheric lesion associated with alexia (inability to read)
Left
150
Hemispheric lesion associated with colour anomia
Left
151
Hemispheric lesion associated with Broca's aphasia
Left
152
Hemispheric lesion associated with Wernicke's aphasia
Left
153
Symptoms seen in Gerstmann syndrome
Dysgraphia
Dyscalculia
Finger agnosia
Right left disorientation
154
Hemispheric lesion seen in Gerstmann syndrome
Left
155
Hemispheric lesion seen in prosopagnosia
Right
156
Receptor changes seen after ECT in patients with depression
Reduced beta receptors
Increased noradrenaline turnover
Reduced 5HT2 receptors
157
Features associated with Klüver-Bucy syndrome
```
Hyperorality
Hypersexuality
Docility
Visual agnosia
Dietary changes
```
158
Area of brain affected in Klüver-Bucy syndrome
Bilateral medial temporal lobes
| Amygdala
159
Common causes of Klüver-Bucy syndrome
```
Herpes
Late stage Alzheimer's disease
Frontotemporal dementia
Trauma
Bilateral temporal lobe infarction
```
160
Description of pulvinar sign
Bilateral high signal of the medial thalamus
161
Abnormal structure in dementia pugilistica
Septum pellucidum
162
Abnormality seen in the septum pellucidum in dementia pugilistica
Fenestrated cavum septum pellucidum
163
Distribution of tau accumulation seen in dementia pugilistica
Irregular, focal perivascular distribution
| At the depths of cortical sulci
164
Macroscopic features of schizophrenia
Enlarged ventricles
Reduction in grey matter volume and total brain volume
Reduced asymmetry of the planum temporale
165
Macroscopic feature associated with first generation antipsychotic exposure
Enlargement of the caudate
166
Movement disorder associated with damage to the subthalamic nucleus in the basal ganglia
Hemiballismus
167
Features of hemiballismus
Involuntary violent movements of the arms and legs
168
Macroscopic features of multisystem atrophy
Pale substantia nigra
Greenish putamen
Atrophied putamen
Cerebellar atrophy
169
Microscopic features of multisystem atrophy
Papp-Lantos bodies
170
Areas of the brain which show increased glucose metabolism in OCD
```
Orbitofrontal area
Caudate
Thalamus
Prefrontal cortex
Anterior cingulate
```
171
Three categories the Boston Classification uses to divide aphasias
Fluency
Repetition
Comprehension
172
Most severe type of aphasia where there is non-fluent speech, lack of comprehension, and lack of repetition
Global aphasia
173
Non-speech features usually present with global aphasia
Inability to read and write
Hemiplegia
Hemisensory loss and hemianopia
174
Area of damage for global aphasia
Entire L perisylvian region - often MCA occlusion
175
Type of aphasia where speech is not fluent and repetition is impaired, but comprehension is intact
Broca's aphasia
176
Broca's area in Brodmann areas
44 and 45
177
Area Broca's area is found in
L Frontal lobe
178
Blood vessel which supplies Broca's area
Superior division of MCA
179
Type of aphasia where the speech is fluent but comprehension and repetition are impaired
Wernicke's aphasia
180
Area of the brain Wernicke's area is found
L superior temporal gyrus
181
Brodmann area which is Wernicke's area
22
182
Blood vessel which supplies Wernicke's area
Inferior division of MCA
183
Type of aphasia where the speech is fluent and comprehension is intact but there is specific deficit in repetition
Conduction aphasia
184
Area of the brain damaged in conduction aphasia
Arcuate fasciculus which connects Wernicke's area and Broca's area
185
Blood vessel which supplies the arcuate fasciculus
Inferior or superior division of the MCA
186
Type of aphasia where fluency, repetition and comprehension are all largely intact and the biggest issue is word finding
Anomic aphasia
187
Areas of the brain often damaged in anomic aphasia
Less well localised than most aphasias
| Often temporal-parietal area, sometimes angular gyrus
188
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
Transcortical aphasia
189
Subtype of transcortical aphasia with fluent speech, impaired comprehension and intact repetition
Sensory transcortical aphasia
190
Subtype of transcortical aphasia with non-fluent speech, impaired comprehension and intact repetition
Motor transcortical aphasia
191
Loss of reading ability with preserved writing ability - but inability to read words they have written after a break
Alexia without agraphia
192
Most common brain areas affected in alexia without agraphia
Angular gyrus - often by simultaneous lesions of the L occipital lobe and the splenium of corpus callosum
193
Medical causes of alexia without agraphia
L PCA stroke
Tumour
MS
194
Loss of reading and writing ability but intact speech and oral language understanding - sometimes with word finding difficulty
Alexia with agraphia
195
Most common area of lesion causing alexia with agraphia
Angular gyrus - L inferior parietal lobe
196
Type of aphasia which is similar to Wernicke's aphasia but reading comprehension is intact
Auditory verbal agnosia/pure word deafness
197
Dopamine abnormality causing positive symptoms in schizophrenia
Increased dopaminergic activity in the striatum
198
Dopamine activity causing negative symptoms in schizophrenia
Decreased dopaminergic activity in the frontal lobe
199
Disease classically associated with an abnormal tonsillar biopsy
Variant CJD
200
Alternative name for dementia pugilistica
Chronic traumatic encephalopathy
201
Type of neurodegenerative condition which can occur immediately after a single traumatic brain injury
Dementia pugilistica
202
Conditions in which kuru plaques are seen
Kuru
Gerstmann-Sträussler–Scheinker syndrome
CJD
203
Condition in which Verocay bodies are seen
Schwannoma
204
Disease in which haematoxylin bodies are seen
SLE
205
Conditions in which zebra bodies are seen
Niemann-Pick disease
Tay-Sachs disease
Mucopolysaccharides
206
Conditions in which Schaumann bodies are seen
Sarcoidosis
| Berylliosis
207
Diseases in which Mallory bodies are seen
Alcoholic hepatitis and cirrhosis
Wilson's disease
PBC
208
Diseases in which asteroid bodies are seen
Sarcoidosis
| Berylliosis
209
Areas of the brain which have been shown to be hyperactive in depression
Amygdala
| Anterior cingulate cortex
210
Area of the brain which has been shown to be underactive in depression in some studies, and overactive in others
Dorsolateral prefrontal cortex
211
Important prion diseases
CJD
Kuru
Gerstman-Sträussler–Scheinker syndrome
Fatal familial insomnia
212
Disease balloon cells are associated with
Pick's disease
213
Macroscopic features of Parkinson's disease
Pallor of the substantia nigra in the midbrain
| Pallor of the locus coeruleus in the pons
214
Condition associated with reductions in interneurons in cortical layer II of the prefrontal cortex
Schizophrenia
215
Area of low perfusion seen in SPECT scan of Alzheimer's dementia
Medial temporal areas
| Parietal areas
216
Cellular distribution of Lewy bodies - extracellular vs. intracellular
Intracellular
217
Response of Parkinsonian features of multisystem atrophy to levodopa
Poor response
218
Macroscopic features of progressive supranuclear palsy
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
Normal form of prion protein
PrPC
220
Enzyme which can break down PrPC but nor PrPSc
Protease
221
Main structure of PrPSc
Beta sheet
222
Method PrPSc has of spreading
It can change nearby PrPC into PrPSc
223
Structure of PrPC
Alpha helix
224
Frontal lobe hemisphere more associated with depression when damaged
Left
225
Frontal lobe hemisphere more associated with disinhibition, aggression and impulsivity if damaged
Right
226
Cells affected in Guillain Barré syndrome
Schwann cells
227
Cell type that makes up an acoustic neuroma
Schwann cells
228
Artery usually affected in a stroke causing amaurosis fugax
Retinal/opthalmic artery
229
Areas of brain damage associated with Wernicke and Korsakoff syndrome
Medial thalamus
| Mamillary bodies of hypothalamus
230
Area of lesion to cause an ipsilateral monocular visual loss
Optic nerve
231
Area of lesion to cause a bitemporal hemianopia
Optic chiasm
232
Area of lesion to cause a contralateral homonymous hemianopia without macular sparing
Optic tract
233
Area of lesion to cause a contralateral homonymous inferior quadrantanopia
Parietal (upper) optic radiation
234
Area of lesion to cause a contralateral homonymous superior quadrantanopia
Temporal (lower) optic radiation
235
Area of lesion to cause a contralateral homonymous hemianopia with macular sparing
Occipital visual cortex
236
Target sites for deep brain stimulation in Parkinson's disease
Subthalamic nucleus
| Globus pallidus interna
237
Number of dopamine transporters in patients with ADHD compared to healthy controls
Fewer
238
Effect of psychostimulant treatment on dopamine transporter numbers in patients with ADHD
Increased
239
Neuropathological features of presymptomatic HIV infection
```
Lymphocytic leptomeningitis
Perivascular lymphocytic cuffing
Parenchymal T and B lymphocyte infilatration
Gliosis
Microglial activation
Axonal damage
```
240
Neuropathological feature of presymptomatic HIV infection which is also found in HIV negative IV drug users as well as in trauma, inflammation and hypoxia
Axonal damage
241
Most common organic cause of anxiety
Hypoglycaemia
242
Lobe associated with Jacksonian seizures
Left frontal lobe
243
Structure which when divided leads to a 'split brain'
Corpus callosum
244
Most common opportunistic CNS infection in patients with AIDS
Toxoplasma gondii (toxoplasmic encephalitis)
245
Area of the brain which shows the pulvinar sign in variant CJD
Thalamus
246
Subtype of opioid receptors associated with depression
Sigma
247
Changes in neurotransmitters seen in Alzheimer's disease
Decreased acetylcholine
| Increased glutamate
248
Main mechanism of spread of HIV to the brain
Infected macrophages
249
Structures involved in Wernicke's encephalopathy
Mamillary bodies
Thalamic nuclei
Walls of the third ventricle
250
fMRI appearances in keeping with a patient experiencing auditory hallucinations
Increased activity at the temporal cortex
251
Mamillary body abnormality seen in Wernicke Korsakoff syndrome
Decreased mamillary body transketolase activity
252
Area of the brain showing increased dopamine release in patients with schizophrenia on the amphetamine challenge test
Striatum
253
Neural process where deficiency is seen in delusions of control
Sensory prediction
254
Area of the brain which shows hypoplasia in autism
Cerebellar vermis
255
Impact of Parkinson's disease on D2 receptor sensitivity
Increased D2 receptor sensitivity at the basal ganglia
256
Part of the brain most associated with prion disease
Cerebellum
257
Area of the brain targeted in transcranial magnetic stimulation treatment for treatment resistant depression
Left frontal lobe
258
Earliest histological change seen in Alzheimer's disease
Amyloid-mediated damage
259
Area of the brain showing hypoperfusion in Lewy body dementia
Occipito-parietal
260
Disease associated with the hummingbird sign on sagittal imaging - midbrain atrophy
Progressive supranuclear palsy
261
Prion disease which does not show spongiform change
Fatal familial insomnia
262
CNS cell type most susceptible to HIV infection
Microglia
263
Characteristics of medial prefrontal syndrome
Poverty of speech
| Lack of spontaneous behaviour
264
Characteristics of orbitofrontal syndrome
Explosive outbursts
| Poor impulse control
265
Characteristics of dorsolateral prefrontal syndrome
Executive dysfunction
| Diminished planning
266
Alternative name for medial prefrontal syndrome
Apathetic type/pseudo depressive type prefrontal syndrome
267
Alternative name for orbitofrontal syndrome
Disinhibited type/pseudopsychopathic type frontal syndrome
268
Alternative name for dorsolateral prefrontal syndrome
Dysexecutive/disorganised type prefrontal syndrome
269
Structural changes associated with normal pressure hydrocephalus
Enlarged lateral and third ventricles out of proportion to rest of the brain
270
Characteristic structural change seen in autism
Hypoplasia cerebellar vermis
271
Neurotransmitter deficient in Lewy Body dementia and Parkinson's disease dementia
Acetylcholine
272
Areas of the brain which see hypoperfusion in schizophrenia
Frontal lobe and prefrontal cortex
Anterior and medial cingulate gyri
Parietal lobes
273
Areas of the brain which see hyperperfusion in schizophrenia
Cerebellum
Brainstem
Thalamus
274
Hyperintensities seen on imaging in patients with depression
Periventricular
Deep white matter
Thalamic
Striatal
275
Areas of decreased volume seen on imaging of patients with depression
Frontal
| Basal ganglia
276
Areas of decreased metabolism seen on imaging of patients with depression
Prefrontal cortex
Anterior cingulate
Amygdala
277
Finding seen on imaging of patients with depression which suggests psychomotor retardation
Elevated D2 binding
278
Areas of loss of grey matter seen on imaging of patients with schizophrenia
Insular cortex
Anterior cingulate
Medial temporal lobe
279
Area of poor activation seen on fMRI imaging of patients with schizophrenia
Dorsolateral prefrontal cortex
280
Area of brain with low DAA seen on MR spectroscopy of patients with schizophrenia
Prefrontal cortex
281
Diffusion tensor imaging findings seen on imaging of patients with schizophrenia
Widespread reduction
282
Area where there is loss of volume seen on imaging of patients with Alzheimer's
Temporal lobe especially the hippocampus
283
Area of decreased activation on fMRI imaging of patients with Alzheimer's
Parieto-temporal
284
Neuropathological changes seen in patients with depression
```
Enlarged lateral ventricles
Enlarged amygdala
Reduced hippocampal volume
Reduced basal ganglia volume
Reduced grey matter in the prefrontal cortex
```
285
Areas shown to have altered blood flow on SPECT scan among patients with depression
Dorsolateral prefrontal cortex
Basal ganglia
Anterior cingulate
Amygdala
286
Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to the cognitive dysfunction seen
Prefrontal cortex
287
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
Anterior cingulate
288
Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to abnormal emotional processing
Amygdala
289
Area of abnormal blood flow seen in SPECT scans of patients with depression which is likely to relate to psychomotor retardation
Basal ganglia
290
Altered metabolism seen in OCD
Increased metabolism in the orbitofrontal area, caudate, thalamus, prefrontal cortex, and anterior cingulate
291
Site of brain lesion causing alexia without agraphia, colour agnosia, and visual object agnosia
Dominant occipital lobe
292
Site of brain lesion causing profound amnesia
Bilateral temporal lobe
293
Site of brain lesion causing visuospatial agnosia, prosopagnosia, and complex visual hallucinations
Non-dominant occipital lobe
294
Site of brain lesion causing apraxias, prosopagnosia, and neglect of one side of the body (hemisomatognosia)
Non-dominant parietal lobe
295
Part of the brain which sees increased blood flow when a patient is experiencing hallucinations and delusions
Left medial temporal cortex
