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Neurodevelopmental disease Flashcards

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1
Q

What is DSM-5 used for

A

To categorise different conditions in abnormal mental state such as depression and bipolar disorder

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2
Q

Depression categories

A

Minor depression includes 2-4 symptoms
Major depression includes 5 or more symptoms

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3
Q

What is dysthymia

A

Milder form of depression but is long lasting(must last for at least 2 years)

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4
Q

Parts of the brain involved in depression

A

HPA axis- Reduced energy
Attention/Cognitive impairment-prefrontal cortex

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5
Q

Hypothalamic pituitary adrenal axis(HPA)

A

Part of the brain responsible for adjusting the balance of hormones especially to stress affecting the immune system(inhibiting metabolism)

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6
Q

Monoamine hypothesis

A

Modulation problems can cause depression

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7
Q

Reserpine

A

A drug that controlled blood pressure caused depression in 20% of patients(affected serotonin and catecholamines)

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8
Q

Treatment for depression

A

Anti depressants block the re-uptake of neuropenepherine and serotonin transporters

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9
Q

SSRI drugs

A

Block serotonin transporters in depression

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10
Q

MAO inhibitors

A

Reduce degradation of serotonin in depression patients

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11
Q

Target for newer antidepressants

A

work on the CRH receptor which affects HPA axis

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12
Q

Stress on depression

A

Stress usually comes from cortisol and effects 5ht receptors and NA
The cortisol will change the structure of receptors of 5HT

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13
Q

CHR in depression

A

Stimulates secretion of ATCH increasing cortisol levels

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14
Q

Theureptic effects on depression

A

delayed 3-4 weeks but increase throughout the plasma

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15
Q

Moamine inhibitors for depression

A

Can cause seizures due to allergic reaction Cheese reaction is when foods like cheese increase NA and goes straight into the blood stream

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16
Q

Psychotherapy

A

Best at treating mild depression uses neurocortical control over activity patterns
CBT is most commonly used

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17
Q

Tricyclic antidepressants

A

enhance NE and 5HT by blocking uptake and are unselective compared to SSRI’s

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18
Q

What is bipolar disorder

A

The main symptoms of bipolar disorder are episodes of extreme highs and lows

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19
Q

treatment of bipolar disorder

A

Cannot be treated alone by anti depressant usually needs anti psychotic and is used to stabilise moods instead of going into mania and depression

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20
Q

What is mania in bipolar disorder

A

a state of mind characterized by high energy

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21
Q

Stress on bipolar disorder

A

Stress increases mania as it activates the hippocampal system

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22
Q

co morbility involved with bipolar

A

Anxiety- hyperactivation of fear in hippocampus and amygdala
OCD- inefficient CTSC for regulating behaviour

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23
Q

alcohol and anxiety

A

co mobility between alcohol and anxiety

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24
Q

Co mobility with depression

A

co mobility between anxiety, Major deppresion and panic disorder

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25
Q

PTSD

A

diagnosed after a person experiences symptoms for at least one month following a traumatic event.
Re-experiencing the trauma through intrusive distressing recollections of the event, flashbacks, and nightmares

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26
Q

OCD

A

An obsession is an unwanted and unpleasant thought, image or urge that repeatedly enters your mind, causing feelings of anxiety, disgust or unease

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27
Q

Anxiety on rats experiment

A

Conditioned to responed to stressful event via a shock and causes acrivity in the amygala

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28
Q

ADHD

A

ADHD is being more difficult to pay attention resulting in behavioural problems and peer rejection

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29
Q

Categories of ADHD

A

Inattentiveness (difficulty concentrating and focusing)
Hyperactivity and Impulsiveness
Combined

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30
Q

Diagnosis of ADHD

A

Takes a while to diagnosis it is done over 10 weeks and the use of schools

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31
Q

Nueroinflamation in ADHD

A

Nueroinflamation occurs maybe from neurotransmission imbalance

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32
Q

Genes in ADHD

A

A lot of genes affect DA transporters and serotonin are impaired-DAT1 gene

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33
Q

Brain structure in ADHD

A

Frontal lobe function is affected linked to attention
Smaller brain volume
Pre frontal cortex reduced and pre motor cortex reduced
Reduction in grey matter and cortical thinning

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34
Q

co mobility with ADHD

A

75% of ADHD have 1 or more psychiatric disorders and is more likely to miss other disorders(depression or anxiety)

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35
Q

Dopamine transporters in ADHD

A

Higher dopamine transporter in ADHD - May mean there is not enough dopamine that is why there is more transporters

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36
Q

Phasic phase

A

Phasic phase happens where there is more dopamine usually due to a reward

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37
Q

Treatment for ADHD

A

Parent training and attention training is first line then medication and CBT is last result

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38
Q

prefrontal cortex in ADHD treatment

A

extremely sensitive to its neurochemical environment, particularly dopaminergic and noradrenergic signalling

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39
Q

Side effects of ADHD drug treatment

A

Loss of appetite
Sleep disturbance
Increased blood pressure
Headache
Motor activity is reduced

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40
Q

Functional epilepsy

A

When you are so stressed it causes a seizure

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41
Q

Primary Motor stereotype

A

Seen in neurotypical children
Stabilise or regress as children age

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42
Q

Secondary Motor stereotype

A

Appears along with neurological disorder
Rett syndrome, ASD or metabolic disorders often primary cause

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43
Q

Kinesiogenic in Motor disorders

A
  • Kinesiogenic (induced by movement or startle)
  • Non-kinesiogenic dyskinesias are triggered by other factors (stress, fatigue, alcohol/caffeine)
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44
Q

Motor tics

A

can be simple (single area, eye blinking etc) or complex (repetitive and/or compulsive sequences)

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45
Q

Phonic/vocal tics:

A

grunting, throat clearing, whooping, sniffing etc. up to words and repetition.

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46
Q

Rat experiment for Tics

A

In between test a sequence of behaviour will occur where they were not sure which behaviour was giving them reward so sterotypies occur in the brain because if they don’t do it they wont get a reward

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47
Q

Echopraxia in tics

A

mimicking the actions or gestures of others(often happens in children)

48
Q

Akathisia in tics

A

Restlessness – the compulsion to move or walk around to alleviate a perceived feeling of discomfort

49
Q

Hyperekplexia

A

Excessive startle resulting from hypertonicity

50
Q

Sociogenic illness

A

When people pick up other peoples behaviour but it is not tourette’s

51
Q

The cortico-striato-thalamo-cortical circuit (CTSC) in tics

A

A lot of the sensory information occurs in the thalamus and other parts of the brain including the basal ganglia communicate with each other in a circuit to the cortex and is said goes wrong in the brain

52
Q

HPA in tics

A

When external stressors activate the hypothalamic-pituitary-adrenal (HPA) axis, more dopamine is produced, furthering the excitation of tic-producing pathways.

53
Q

CTSC Dysfunction in Tics

A

Small shifts causes massive changes even in animals
Striatum: In individuals with tic disorders, there is evidence of abnormal activity within the striatum, a component of the CSTC circuit.
Imbalance in cortex, striatum, and thalamus can cause ticks

54
Q

What Is a rare disease

A

A rare disease in the Uk is a condition that affects less than 1 in 2000 people
80% of rare diseases are genetic
75% of rare diseases affect children

55
Q

Why rare disease in neuroscience

A

A majority of rare diseases are affect the brain
Many of rare diseases are incurable
Neurological aspect of the disease affects the mortality of the individual

56
Q

Stages of rare disease

A

Helping patients get a diagnoses faster
Increasing awareness of rare disease among health care professionals
Better coordination of care
Improving access to specialist care, treatment and drugs

57
Q

Common identifiers in rare disease(epilepsy)

A

600 genes identified to cause metabolic epilepsy
37% of metabolic epileptics are inherited
100+ genes identified as rare form causing at least 700 distinct rare epilepsy syndromes
Rare epilepsy are more resistant to drugs

58
Q

Mitochondrial dysfunction in rare disease

A

Primary mitochondrial disease is caused by mutation in mtDNA(Used to distribute genetic variation)
Secondary mitochondrial disease is where mitochondrial dysfunction is a driver in the diseases progression causes epilepsy and neuro degradation

59
Q

Lysosomal dysfunction

A

Lysosomal storage disorder are inborn errors of metabolism leading to accumulation of substances in the cells
2/3 exhibit neurological impairment

60
Q

Tuberous sclerosis complex in rare disease

A

Genetic disease caused by mutation in TSC1 and TSC2 genes associated with brain lesions(tubers)

61
Q

Link between TBS and epilepsy

A

80-90% of TSC experience epilepsy

62
Q

How brain sessions occur is TSC

A

Gillal and ballon cells expand in the brain
Small accumulation of calcium occurs leading to benign brain tumours

63
Q

TSC affected levels

A

Behavioural
Psychiatric
intellectual
Academic
physioscocial
Neuropsychological

64
Q

Tsc in the lungs

A

Lung cancer occurs in smooth muscle cells which form cyst making it harder to breath

65
Q

AML in TSC

A

Another tumour that occurs in the kidney

66
Q

TSC1&2 Gene

A

TSC1 gene encodes the protein hamartin. TSC2 gene encodes the protein tuberin.
Together, the TSC1 and TSC2 protein form a complex which functions as inhibitor of the mammalian target of rapamycin (mTOR) pathway.

67
Q

mTORC1 in TSC

A

TSC is associated with mTORC1 hyperactivity; and less so dysfunction in mTORC2.

68
Q

protein S6 is TSC

A

Phosphorylation of protein S6 is often used as indicator of mTORC1 activity.

69
Q

Everolimus in TSC

A

Everolimus is a drug similar structure to Rampamycin and leads to the reduction of mTOR pathway
Use of Everolimus reduces the size of tumours in the brain but when taken off Everolimus tumour grows again

70
Q

Cerebral palsy

A

broad collection of neurological diseases involving difficulty in movement, muscle tone and balance

71
Q

Cause of CP

A

No one cause of cerebral palsy but caused by damage or hypoxia(lack of oxygen) in the brain either pre or peri natal
It can be genetic

72
Q

Pre natal causes of CP

A

Polyhydraminos too much fluid in the womb causes issue during pregnancy
Ritodrine = Beta2 Adrenoceptor agonist used to prevent premature labour
Physical trauma near birth

73
Q

Oxygen debt in CP

A

causes less ATP prduction and cannot cause channels to work properly .The gradient becomes less between the membrane and causes more excitability.
When oxygen debt comes back it causes much more reactants
Cause loss of grey matter

74
Q

Types of CP

A

Spastic- Muscle are too stiffMotor cortex is usually damaged
Dyskinetic- Fluctuating muscle tone caused by damage to basil ganglia
Ataxic- Motor function deficits including speech usually damaged cerebellum
Mixed-More than one of the above

75
Q

Spastic CP type

A

Can be uni lateral or affect the whole body
Most common type
Skeleton will lean to one side due to change of muscle tone

76
Q

Ataxic CP

A

causes walking with a wider stance to have a better base
Eye co ordination and hearing are secondary symptoms

77
Q

Treatment of CP

A

Occupational therapy can improve motor functions and hand eye coordination as well as adapting equipment for use

78
Q

Botox in CP

A

lp with ataxia
Botox is used to relax muscle and casts also used to eventually improve stretching

79
Q

Selective Dorsal Rhizotomy in CP

A

erves are identified and use of a computer can identify which nerves can be striped

80
Q

CP and epilepsy

A

There is a correlation between CP patients and epilepsy the main type being focal seizure

81
Q

Rett syndrome

A

Rett syndrome is impairment in hand skills, verbal, verbal communication and progression motor
More likely in girls because it is x linked

82
Q

MECP2 in Retts syndrome

A

MECP2 is usually the reason for Rett syndrome

83
Q

Receptors in Retts syndrome

A

Rett is regressive because receptors are put in the wrong place(receptor expression) and regulates mRNA production so less proteins are made for AMPAR receptors

84
Q

Expression in Retts syndrome

A

MECP2 regulates expression of certain genes at synapses
Under an over expression leads to changes in the synapse but LTP is always low if not modulated

85
Q

Drug treatment for Retts syndrome

A

Drug treatment is the use of specific proteins to trigger MECP2 activation

86
Q

fragile X syndrome

A

disease occur due to altercation of chromosomes Described as a genetic disease
Chromatin gets condensed to a point where it is fragile

87
Q

fragile X syndrome genes

A

FMR1 gene that codes for FMRP
FRMP provides protein synthesis for neurones in dendrites
FRMP leads to an increase in inotropic glutamate

88
Q

Down syndrome and intellectual disability

A

DS is the most frequent chromosomal cause of mild to moderate intellectual disability

89
Q

Testing for Down syndrome

A

Chorionic villus sampling: A sampling of the placental tissue between 10-13 weeks after conception
Amniocentesis: Needle is inserted through abdominal wall and a syringe is used to extract amniotic fluid performed 16-20 weeks into pregnancy

90
Q

Characteristics of Down syndrome

A

Flattened appearance to face
Small ears
Shorter height due to hypothyroidism(under-active thyroid)
Poor muscle tone
Early onset for Alzheimer’s, memory loss and Dementia

91
Q

Robertsonian translocation down syndrome theory

A

s when some one has 45 chromosomes instead of 46 lost of this chromosome happens between 13,14,15,21,22

92
Q

Roboerstonian person

A

Roboerstonian person is healthy but problems occur when having a child
When having a baby trisomy can happen where the baby will have crossing over of 3 of the same chromosome can cause serious complication

93
Q

Chromosome 21 knockdown in mice

A

Gene FRM1 was knocked out in mouse and house flies to identify brain function
Knockout mice is deleting a gene to figure out its purpose and can later be used to genetically engineer

94
Q

TS65DN gene in Down syndrome

A

Causes an effect on the GIRK2 channel that in increases GABA responsible for inhibiting neuronal inhibition
Affects heart and sodium channels in hippocampus

95
Q

Trisomy and APP gene

A

APP(Amyloid Precursor Protein) is s G protein cell signalling and causes cell adhesion. Amyloid-B peptide is the main component in amyloid plaques that cause Alzheimer’s

96
Q

Autism

A

is a developmental disorder characterised by stereotyped social interaction impairment.

97
Q

Autistic children

A

usually have accelerated growth in the brain and too many axons formed

98
Q

5 types of autism

A

Autistic Disorder
Asperger’s Disorder
PDD-NOS (not otherwise specified)
Childhood Disintegrative Disorder
Rett’s Syndrome
Rett syndrome is more aggressive and causes decline in health

99
Q

Echolalia in Autism

A

Is the repeating of what someone said

100
Q

Primary behaviour in Autism

A

Lack of eye contact
Minimal face expression
Lack of attention
Egocentric social interactions

101
Q

Autism development

A

Autism is usually pre natal and affects happen during neurogenesis, synaptogenesis and programmed apoptosis(cell death)

102
Q

Proliferation in Autism

A

Switching on and off of genes manage proliferation around 20,000 genes in a human
Master gene controller affects the switching on and off of genes that effect neurodevelopment disease

103
Q

Productive and subtractive neurodevelopment in autism

A

roductve:
Neurogenesis and differentation
Migration and synptogensis
Myelination

Subtractive:
Apostosis
Synaptic re-organisation
Synaptic pruning

104
Q

What phase autism starts

A

Autism begins in the G1 phase
Overgrowth of neurones(proliferation) occurs especially in the cortex of cells
G1 cells over produce
Epoch are the master regulators and Epoch 1 and 2 levels are different in autistic people

105
Q

Von Economo Neurones in Autism

A

Von Economo Neurones are important in social interactions
Lots of VEN means more emotions

106
Q

Neuroligins and neurexins

A

Without Neurexins they are fewer GABA cells
Without neuroligins reduced brain volume

107
Q

Shank3 in Autism

A

show greater dendritic complexity
interacts with a variety of ionotropic and metabotropic glutamate receptors
Restoration of Shank3 can lead to reverse in some autism

108
Q

Valproic acid in autism

A

Valproic acid causes a higher risk factor for autism
VPA inhibits histone H3 and H4 deacetylation
In VPA it allows for transcription of all genes for ones that should not be expressed

109
Q

Epilepsy

A

imbalance between inhibition and excitation is what epilepsy
30,000 synapses on a typical cell, a mix of Glu and GABA

110
Q

GABA in epilepsy

A

GABA inhibition means spikes are synchronised so it inhibits making gaps in between signals

111
Q

Phases in seizures

A

Tonic phase is first stiffening of the muscle
Clonic Phase is repeated stiffening of muscles
post ictal phase person is confused and is when the episode if over
Partial seizure occurs when a person doesn’t know they have a seizure

112
Q

AMPA in Epilepsy

A

AMPA causes glutamate response which is inhibitory
NMDA receptors have a slower onset

113
Q

GABA in epilepsy

A

GABAa reduces transmission in neurones
GABAb excites neurones
Work together to cause balance

114
Q

Intrinsic inhibition in epilepsy

A

Excitation and inhibition must be managed
Loss of inhibition and cell becomes more excitable causing multiple spikes
Glutamate causes more excitation and GABA causes more inhibition

115
Q

Ions in epilepsy

A

sodium and calcium ions into the cell cause increase in excitability and potassium in and chlorine ions out causes repolarisation

116
Q

Drug treatment for epilepsy

A

Drug treatment uses gaba and release Na-channel blockers and calcium channel blockers

117
Q

Epilepsy surgery

A

Intervention to remove an identified ‘focus’
70% success rate, now used earlier
But later on seizure arises again

brain disease (4 decks)

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