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Neuroscience Flashcards

1
Q

what are the different type of apraxia

A

limbic kientic
ideomotor
Oculomotor apraxia
Constructional apraxia
ideation apraxia

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2
Q

what is Ideomotor apraxia

A

ideomotor apraxia: This condition is characterised by a patient’s inability to perform a task on command but may be able to do so automatically. In the scenario described, the patient’s attempt to brush their teeth with a pencil, despite understanding the task, suggests a disconnect between the concept and the performance of the motor action. This is indicative of ideomotor apraxia, where the patient cannot use an object correctly on command due to a disruption in the ability to plan or execute motor functions, despite understanding the use of the object and having the physical ability to perform the action.

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3
Q

define limbic kinetic apraxia

A

Limb kinetic apraxia: This type of apraxia affects fine motor movements and is not typically related to the use of objects inappropriately. It is characterised by clumsiness or loss of dexterity in the limbs, which is not what is described in the scenario.

.

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4
Q

define oculomotor apraxia

A

Oculomotor apraxia: This affects the control of eye movements and would not explain the misuse of an object in a task. It is not relevant to the action described in the scenario

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5
Q

define constructional apraxia

A

Constructional apraxia: This involves difficulty in constructing or drawing objects and is not related to the misuse of objects for a task, as seen in the patient’s behaviour.

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6
Q

define ideational apraxial

A

Ideational apraxia: This form of apraxia involves a breakdown in the knowledge of what is to be done or how to perform a sequence of actions, which is not the case here, as the patient appears to understand the concept of brushing teeth but uses the wrong object.

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7
Q

what is the fissure of rolando

A

the fissure of Rolando, also known as the central sulcus, divides the frontal and parietal lobes

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8
Q

what is the metabolite of serotonin

A

5 hydroxyindolacetic acid
5-HIAA

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9
Q

what IS 5HIAA associated with

A

1/3 of depressed patients had low

also low levels are associated with
poor response to antidepressants aggression and more likely to commit suicide

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10
Q

where do the majority of acoustic neuromas take place

A

90% at the cerebellarpontine angle

5% intracranial tumour

also known as vestibular schwanomma

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11
Q

what is bilateral acoustic neuroma associated with

A

neurofibromatosis 2

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12
Q

what is the investigation choice for acoustic neuroma

A

MRI of cerebellar pontine angle

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13
Q

what is seen with each nerve affected
V (5)
VII (7)
vIII (8)

A

v - Absent corneal reflex
VII facial palsy
VIII– vertigo, hearing difficulities

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14
Q

how does alpha secretase work?

A

it cleaves APP to break it down into non toxic fragnments

beta and gamma secretase break APP into fragments which clump into amyloid plaques which accumulate

new drugs to increase alpha secretase and decrease the beta/gamma are being developeed

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15
Q

what is prosopagnosia

A

inability to recognise faces

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16
Q

which part of brain does propsoagnosia affect

A

fusiform gyri

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17
Q

what is anosognosia

A

inability to recognise own condition

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18
Q

which area does anosognosia affect

A

R hemisphere of brain

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19
Q

what is autopagnosia
what does it affect

A

inability to recognise ones own parts of the body

it affects L parietal region

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20
Q

what is phonagnosia

A

inability to recognise familiar voices

affects R temporal lobe

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21
Q

what is simulatenognosia

A

the inability to recognise two objects in the same visual field
affects bilateral damage to occipital pareital lobe

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22
Q

what is asterognosia

A

aster- touch
affecting somatosensory cortex in Parietal lobe

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23
Q

what is the resting potential

A

-70mV
-55mV influx of Na
+40mV at which depolarisation takes place

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24
Q

what are macroscopic changes seen in alzehimers

A

cerebral atrophy especially of hippocampus

amyloid plaque with tangles

formation
enlarged ventricles

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25
Q

what is a core and corona in dementia plaques

A

Senile (or neuritic) plaques consist of a core and a corona (see below). The core is an extracellular deposit of Aβ, while the corona is made of degenerating neurites, mainly axons.

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26
Q

what are neurofibrillary tangles made of

A

hyperphosphorylated tau

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27
Q

what are the tauopthies

A

Frontotemporal dementia
Progressive supranuclear palsy
Corticobasal syndrome
Chronic traumatic encephalopathy (e.g. dementia pugilistica)

alzehimers

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28
Q

what is glossis

A

is marked by increased activated microglia and reactive astrocytes at the site of amyloid plaques

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29
Q

what is the nucleus basalts of meynert

A

he nucleus basalis, also known as the nucleus basalis of Meynert

in substantia innominata in basal forebrain

somewhat diffuse collection of large cholinergic (produce acetylcholine) neurons

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30
Q

what happens to basalis of meynert in Alzheimer’s

A

degenerates in Alzheimer’s resulting decrease in acetylcholine in the brain. For this reason, most currently available pharmacological treatments for Alzheimer’s focus on compensating for faltering function of the nucleus basalis through artificially increasing acetylcholine levels.

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31
Q

what are hirano bodies

A

hirano bodies are actin-rich, eosinophilic (they stain with the bright pink dye eosin) intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure.

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32
Q

what is the difference between hirano bodies and lewy bodies

A

Lewy bodies are made of ubiqiuin

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33
Q

where are hirano bodies predominantly found

A

in the hippocampi of the elderly

are especially numerous in patients with various dementias or degenerative diseases (amyotrophic lateral sclerosis, Alzheimer’s disease, Pick’s disease, and some forms of Creutzfeldt-Jacob disease) and alcoholism

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34
Q

what is found on neuroimaging in azlehimers

A

hypoperfusion of pastoral and temporal lobes
especially on SPECT imaging

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35
Q

how do u differentiate between LB dementia and Alzheimers on SPECT

A

DLB shows lower perfusion in occipital cortex (long arrows). In contrast, AD showed lower perfusion in medial temporal areas (short arrowheads).

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36
Q

where is the amygdala

A

in the anterior temporal lobe of the limbic system

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37
Q

how many nuclei are there

A

6

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38
Q

name the six nuclei

A

lateral
basolateral
central
media
corticomedial
basomedial

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39
Q

what does the lateral nuclei of amygdala

A

receive sensory information
involved in learning /fear conditioning

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40
Q

basolateral nuclei of amygdala does

A

role in the processing and interpretation of emotional valence from the sensory input.

cognition and attention, particularly regarding the emotional significance of events.

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41
Q

what does the central nuclei or amygdala do?

A

main output

fight or flight

expression of emotional responses and initiation of the fight-or-flight response via connections with various brainstem areas.

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42
Q

what about the
medial, corticomedial and basomedial nuclei of amygdala

A

coritcomedial -> olfactory system,

corticomedial - projects into ventromedial nucleus to hypothalamus re: - hunger and eating

basomedial autonomic -response and memory

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43
Q

where are Broca and wernike situated

A

by the sylvian fissure in the perisylvian language area’.

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44
Q

which is non fluent and fluent language

A

broca
non fluent
comprehension not impaired

wernike
fluent
but comphrension impaired

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45
Q

two main aphasia classifications

A

are the Boston Group classification

and Luria’s aphasia interpretation

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46
Q

which is the most severe form of aphasia

A

global is most severe
non fluent and no comprehension
MCA, ICA and SCA affected usually

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47
Q

what is agraphia
what is it seen in

A

inability to write

with Broca aphasia

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48
Q

what supplies the Broca region and wernikes

A

superior part of MCA

wernike -inferior part of MCA

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49
Q

what is conductive aphasia

A

arcuate fasciculus which connects Wernicke’s to Broca’s area.

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50
Q

there are four perisylvan aphasia what are they

A

broca
wernike
conductive
global

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51
Q

what are extrasylvian aphasias

A

share the clinical characteristic of preserved repetition and the sparing of the core perisylvian language zone. T

less common than perisylvian aphasias.

Many arise from infarcts, but they may also appear in conjunction with tumors, abscesses, hemorrhages, and other lesions.

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52
Q

what is seen in anomic aphasia

A

Naming or word finding problems

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53
Q

Transcortical motor aphasia

transcortical sensory aphasia

A

TSA
like wernikes but with repetition

TMA

Spontaneous output is severely disrupted, non-fluent, and halting. In contrast, the ability to repeat sentences verbatim is preserved, as is reading aloud. Comprehension is undisturbed. Naming may be mildly impaired.

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54
Q

Alexia

A

Alexia without agraphia (pure alexia):

Presents as an acquired loss of reading ability in a literate person, with preserved ability to write spontaneously.

impacts left occipital lobe and the splenium of the corpus callosum

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55
Q

Alexia with agraphia:

A

Patients exhibit loss of literacy (inability to read or write) but relatively well-preserved oral language function. Speech is fluent, although anomia is often present, and auditory comprehension and repetition are intact.

The underlying lesion classically involves the dominant inferior parietal lobule (angular gyrus).

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56
Q
A

Pure word deafness (auditory verbal agnosia):

Patients resemble Wernicke’s aphasics. Comprehension and repetition of spoken language are impaired, whereas speech is fluent
can recognise sounds like car horn

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57
Q

what produced neuropeptide Y

A

hypothalamus to increase appetite

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58
Q

what produced ghrelin

A

gut to increase appetite

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59
Q

what produced leptin

A

adipose issues to indicate saitety
and reduced appetite

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60
Q

what produces CCK

A

gut to decrease appetite

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61
Q

who is autoimmune encephalitis usually seen in

A

young people
sudden onset

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62
Q

what are the four conditions affecting the basal ganglia
which parts do they affect

A

Huntington’s chorea (caudate nucleus)

Wilson’s disease (copper deposition in basal ganglia)

Parkinson’s disease (substantia nigra)
Hemiballism (subthalamic nucleus)

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63
Q

what is seen in bipolar on neuroimaging

A

increased bilateral ventricular volume
lower hippocampal volime
lower amygdala volume
lower thalamic volume
widespread pattern of thinner cortex

reduced white matter

64
Q

what specficially seen in bipolar compared to healthy controls

A

difference seen in ventrolateral prefrontal coretex

the region involved in emotions and controlling responses

65
Q

what can pass the BBB and what can increase permeability

A

lipid molecules

water molecules not so much

inflammation

66
Q

what are the regions for tumours in adults and children

A

adult;~ supratentorial
childhood : infratentorial

67
Q

what aere gliostoma

A

most common tumour
pleomorphic
tumour cell necrotic area

68
Q

meningoma are what

A

2nd most common primary brain tumour in adults
spindle cells

69
Q

how do meningoma present on CT

A

dura tail

70
Q

what are schwanomma associated with

A

cereballipontine angle
acoustic neuroma
verocay bodies

71
Q

who are pilocystic astrocytoma seen in

A

most common primar in children
presents with rosenthal fibre corkscrew bundle

72
Q

most common type of tumour

A

metastases

73
Q

what are carinopharygoma formed from

A

ratkhke pouch

74
Q

which tumour is made of fourth ventricle

A

ependymoma

75
Q

which tumour is made with foam cells

A

haemganioblastoma
vascular tumour of cerebellum
associated with VHL von hippel lindau

76
Q

what do pituary adenoma produce

A

prolactinoma

77
Q

significant brodmann areas

A

45/45 broca

wernike 22

78
Q

what are catecholamines

A

bezene ring with 2 hydroxyl groups + amine
neuromodulators most common examples are norephierine and dopamine adrenaline

79
Q

which AA make catechoalmines

A

The amino acids phenylalanine and tyrosine are precursors for catecholamines.

80
Q

list the cells of the CNS

A

oliogdendrocytes
schwann cells
astrocytes
microglia
ependymal cells

81
Q

list the cerebellar dysfunction signs

A

ataxia
intentional tremor
disdyskinesia
nystagsmus
intetentional tremor
broad based giat
dysmetiia

82
Q

list the function of each cell

A

oliogdendrocytes = produces myelin in CNS
schwann cells = form myelin sheath and produce myelin in PNS
astrocytes = remove K cells ,bbb, metabolic proceeses
microglia = immune cells by phagocytosis
ependymal cells- lining to ventriclesd

83
Q

what divides the cerellebum into two

A

the medial sulcus

84
Q

what lobes is the cerebellum divided into

A

flucculonodular
anterior posterior

functionally : vestibulo, spino and cerebro

85
Q

what is another name for the atnterior tranverse temporal gyrus

A

heschl gyrus
part of temporal lobe

86
Q

where is heschl situated compared to planium temporal

A

the planum temporale is the cortical area just posterior to the auditory cortex (Heschl’s gyrus) within the Sylvian fissure

87
Q

what is heschl gyrus important for

A

primary auditory cortex for auditory processing
broadman 41
sounds first proceeded here

88
Q

where is planum temporal in relation to heschl gyrus

A

within sylvian fissues
posterior to hesch gyrus
cortical area of superior temporal gyrus

89
Q

what is the function of the planum temporal region

A

music memory
language processing
detection of sound location

90
Q

what is found about R handed people

A

70% have 10x larger Left hemisphere
seen even in gestation

91
Q

which conditions is reduced planum temporal assyemtry seen in

A

dyslexia
schizophrenia

92
Q

what are the layers of the outerlayer of ceberal hemispjere

A

neocortex
paelocortex
archicortex

93
Q

which one makes most of the cerebral hemisphere

A

95% neocortex

94
Q

how many layers is each layer

A

neocortex - 6
paelocortex -3
archicortex -2 to 4 layers

95
Q

name layers of the neocortex
where is it located

A

Molecular (plexiform) layer *
External granular layer
External pyramidal layer
Internal granular layer
Internal pyramidal layer
Multiform (fusiform) layer

under pia mater*

96
Q

what cells are in the neocortex

A

pyramidal and non pyramidal

what does the non pyramidal make up of stellate and granular

97
Q

what are archicortex
and plaeocortex involved in

A

archi -learning and memory limbic system
palecortex - olfactory system broadman 34

98
Q

what do stellate cells do

A

excitatory -glutmate production
gaba inhibitory

99
Q

normal intracranial pressure

A

5-15 mmhg

100
Q

which cells makes CSF

A

ependymal cells in chorid plexus
of lateral /3/4th ventricle

101
Q

how does csf pass through brain

A

lateral ventricle –> foramen munro –> 3rd ventricle —> aqudaduct to fourth ventricle –> formen magendie and luskha foramen –> subachrdoid space –> spinal cord

102
Q

what does raised ICP do to CSF

A

increase absorption but not production

103
Q

what is the difference between CSF and aplasma

A

same sodium content
raised mag and chloride
reduced ph, calcium, ph, cholesterol, glucose and protein

104
Q

what are the meninges

A

lympahtic vessels

105
Q

what is the cingulate gyrus

A

fold in the cortex of medial cerebral hemisphere next to corpus callosum

106
Q

function on cingulate gyrus

A

process emotion
connects action, sensation and emotion
reward

107
Q

what is seen oN PET imaging in depression

A

elevated amygdala activity
increased amygdala activity with negative stimuli
increased activity with subgunseal anterior cingulate cortex
reduced activity in dorsolateral prefontal cortex

108
Q

layers of mater in brain

A

DURA
ARAChnoid
pia

109
Q

which one is folded and where

A

dura is folded at:

The tentorium cerebelli - cerebellum and brainstem from the occipital lobes of the cerebrum.

The falx cerebri, which separates the two hemispheres of the brain, is located in the longitudinal cerebral fissure

The cerebellar falx (falx cerebelli) is a vertical dural infolding that lies inferior to the cerebellar tentorium in the posterior part of the posterior cranial fossa. It partially separates the cerebellar hemispheres.

sellar diaphragm covers pituary gland

110
Q

what is dysarthria

A

defect in production of speech
affecting volume, rate, pitch, quantity, tone

commonly seen as first sign in stroke

111
Q

name the types of dysarthria

A

spastic
flaccid
hypokinetic
hyperkinetic
ataxia

112
Q

where does spastic affect and how does it present

A

forceful slow rate UMN
pseudobublar palsy
drooling
hyperreflex

113
Q

what is flaccid dysarthria

A

LMN bulbary palsy
nasally breathy voice
mono pitch
short phrases
no gag reflex
e.g. myanethis gravis

114
Q

ataxia dyarthria

A

cerebellum damage
slow speech
prolonged vowels/letters
drunk speech

alcoholic
fdererichs

115
Q

hypokinetic dysartharia

A

basal ganglia- parkinson
e.g. slow quiet with tremor
inappropriate silences
low pitch

116
Q

how does it differ from hyperinetic dysarthria

A

excess doapmine
also basal ganglia

e.g. huntingdons , Tardive dyskinesia
strained and variable

117
Q

what is inheritance patternof ssential tremors

A

bengin or autosomal dominant

118
Q

when are essential tremors worse

A

with hands out spread

improved with alcohol or rest

mx with propanolol

119
Q

what are difference between fissure and sulci

A

The surface is folded to increase surface area. Grooves are called sulci and ridges are called gyri.

120
Q

what is the role of glycine

A

binds to receptor on post synamic membrane
makes it more perameable to chloride ions

121
Q

what is an antagonist of glycine

A

strychnine

122
Q

what is a trigger for gullian barre syndrome

A

camyplobacter jejuni

123
Q

which inflammatory cytokines are increased in depression

A

IL6
INF alpha
CRP

124
Q

What is a intracranial venous thrombosis

A

cerebral infaraction
50% are isolated from sigital sinus

125
Q

how does an Intracranial venous thrombosis present

A

hyeadache
nausea vomiting

sagitial sinus thormbosis - seizure, hemiplegia

126
Q

cushing triad

A

regular, decreased respirations (caused by impaired brainstem function) · Bradycardia · Systolic hypertension (widening pulse pressure

127
Q

which head injury shows with a cresent

A

subdural

128
Q

What is kluver bucy syndrome

A

bilateral damage to medial temporal lobe

129
Q

how does kluver bucy syndrome present

A

docility
dietary changes -eating inedible objects
hyperorality - puttings things in mouth licking chewing
visual agnosia unable to recognise objects- can see but not register

130
Q

what are the causes of kluver bucy syndrome

A

herpes (children)
FTD
late alzheimers
trauma /stroke
infarct

131
Q

another name for lateral medullary syndrome

A

wallenberg syndrome

132
Q

what is LMS

A

due to ischemia in the lateral part of the medulla oblongata in the brainstem. The ischemia is a result of a blockage most commonly in the vertebral artery or the posterior inferior cerebellar artery.[1

133
Q

LOCKED in syndrome affects which part of brain

A

pons or medulla
basilar artery emboli

134
Q

what secretes melatonin

A

pineal gland

135
Q

which part of brain is involved in lying

A

dorsolateral frontalcortex

136
Q

what is motor neuron disease

A

fasciculations
wasting of muscles
Motor Upper and lower neuron signs
no cerebellum signs

it is a clinical diagnosis
progressive
exclusion

137
Q

what is seen in amytrophic lateral sclerosis

A

U/L neuron
limb weakness

138
Q

progressive bulbar palsy

A

U+L Neuron
swallowing
speech

139
Q

progressive bulbar palsy

A

LMN

140
Q

primary lateral sclerosis

A

UMN

141
Q

when does myelin production start

A

week 14 gestation

frontal lobes last to myelinate

142
Q

what are autonomic disturbances

A

atonic bladder
postural hypotension

143
Q

shy drager syndrome

A

revised name, multiple system atrophy

T half of the people with this condition become wheelchair-bound due to a progressive lack of motor skills within 5 to 6 years of diagnosis.

parkinsonism cerebaellar signs

Some of the symptoms reported with MSA include:

fatigue
weakness
blurred vision
problems with bowel or bladder control
incontinence
erectile dysfunction
constipation
dry skin

144
Q

what causes the signs in shy drager syndrome

A

striangiral degeneration parkinsonism
oliopontocerebellar atrophy - cerebellum feature

macroscopic features - pallor of s.nigra, greenish putamen, cerebral atrophy
microscopy - Papp lantos bodies, alpha inclusions in SN, cerebellum, basal ganglia

145
Q

UMN

A

increase reflex
weakness
increase tone
mild atrophy
bakinski reflex
pronator drift
clonus

146
Q

LMN

A

reduced reflex
reduced tone
atrophy
weakness

147
Q

What neuroimaging techniques are there classified by

A

structural and functional

148
Q

what do structural neuroimaging techniques look at

A

size structure shape location
whereas functional is more neural firing and metabolic profile

149
Q

summarise CT

A

uses radiational XR
2d picture
dense tissue appears as as white 9bone)
air black

150
Q

how does MRI work

A

capitalises on magnetic properities of tissue
specifically hydrogen nuclei (proteins in water molecular)
and align based on their magnetic moment

151
Q

what is DTI

A

a type of MRI
anisotropic diffusion to estimate the axonal (white matter) organisation of the brain.

Diffusion tensor imaging (DTI)
in cerebral white matter, water molecules tend to diffuse more freely along the direction of axonal fascicles

assessment of the deformation of white matter by tumours - deviation, infiltration, destruction of white matter

delineation of the anatomy of immature brains

presurgical planning

Alzheimer disease - detection of early disease

schizophrenia

focal cortical dysplasia

multiple sclerosis - plaque assessment

152
Q

what are functional MRis

A

PET and SPECT
looks at blood flow and o2 consumption
injection of radioactive substance required

153
Q

an example of a dye used in PET scan

A

raclopride d2/d3 antagonist

154
Q

what does spect use

A

SPECT gamma ray as substance decays, poorer quality but longer half life

PET
collision of positions and electrons
higher resolution but limited half life

155
Q

Magnetic resonance spectroscopy (MRS)

A

Magnetic resonance spectroscopy (MRS) and the related technique of magnetic resonance
looks at metabolites from chemical breakdown

LS MRPSYCH (17 decks)

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