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ADELE-Noodles of Neurology > Mental health across the lifespan > Flashcards

Mental health across the lifespan Flashcards

1
Q

What is the average life expectancy reduction in people with drug/alcohol use?

A

9-24 years

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2
Q

What are mental health presentations that may present in childhood/adolescence?

A

Disruptive/behavioural disorders
ADHD, ASD
Separation anxiety (SAD) and school refusal
Trauma and attachment disorders

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3
Q

Autism is equally common in males and females TRUE/FALSE

A

FALSE

M:F ratio is 4:1

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4
Q

What age group is separation anxiety normal in?

A

7 months through preschool years

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5
Q

TRUE/FALSE

Puerperium is a period of increasing risk of new maternal illness and relapsing existing illness

A

TRUE

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6
Q

What are the risk factors for puerperal psychosis?

A 
Thyroid disorder
Previous episode
FH
Unmarried
1st pregnancy
C section 
Perinatal death
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7
Q

What percentage of 65+ have a mental illness?

A

25%

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8
Q

Demyelinating disorders typically affect functionally and anatomically related groups of neurones TRUE/FALSE

A

FALSE

Degenerative disorders affect functionally and anatomically related groups of neuornes

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9
Q

What are degenerative disorders pathologically characterised as?

A

Simple neuronal atrophy and loss with subsequent gliosis

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10
Q

Which degenerative disorders affect the cerebral cortex?

A

Alzheimer’s disease
Picks disease
CJD

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11
Q

Which degenerative disorders affect the brainstem and basal ganglia?

A

Parkinson’s disease, progressive supra nuclear palsy, multiple system atrophy and Huntington’s

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12
Q

Which degenerative disorders affect the spinocerebellar area?

A

Spinocerebellar ataxia (e.g. Friedreich Ataxia)

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13
Q

Which degenerative disorder affects the motor neurones?

A

Motor Neurone disease

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14
Q

What is dementia?

A

Progressive loss of neurones typically affecting functionally related groups, often symmetrical insidious impairment

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15
Q

In dementia consciousness is clouded TRUE/FALSE

A

FALSE

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16
Q

What are the primary dementias?

A

Alzheimers disease
Lewy body dementia
Pick’s disease (frontotemporal dementia)
Huntington’s disease

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17
Q

What are other disorder that give risk to dementia?

A

Multi-infarct (vascular)
Infection (HIV, Syphillis)
Trauma
Metabolic

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18
Q

If cognitive impairment then alongside a full screen what else should you check?

A

B12 and folate

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19
Q

What is the most useful investigation for frontotemporal dementia?

A

SPECT

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20
Q

true/false

dementia must be reported to the DVLA

A

TRUE

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21
Q

With Alzheimers disease the later the onset the more severe and rapid changes TRUE/FALSE

A

TRUE

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22
Q

How does a familial presentation of alzeimers disease differ from that of a regular presentation?

A

Early onset
Unusual presentation
More relatives affected

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23
Q

A family history of which gene mutations would increase the risk of Alzheimers disease?

A

APP
Presenillin (PSEN) 1&2
ApoE4

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24
Q

Which gene variant decreased the risk of alzheimers?

A

ApoE2

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25
Q

Why does Down syndrome increase the risk of Alzheimers disease?

A

As amyloid precursor protein (APP) is on chromosome 21

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26
Q

What 3 things would be found on histology of someone with Alzheimers disease?

A

Excess accumulation of extracellular B-amyloid plaques
Intracellular neurofibrillary tangles
Amyloid angiopathy

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27
Q

What is the central component of neuritic plaques produced by?

A

Cleavage of amyloid precursor protein (APP)

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28
Q

What protein are intracellular neurofibrillary tangles accumulations of?

A

Tau

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29
Q

Explain amyloid angiopathy

A

Extracellular eosinophilic accumulation in the walls of the arteriole which stiffens and thickens the vessel walls
Disrupts BBB leading to serum leaking, oedema and local hypoxia

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30
Q

In Alzheimers there is narrowing of the gyro and widening of the sulci TRUE/FALSE

A

TRUE

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31
Q

What are the 3 areas first to be affected in alzhimers?

A

Nucleus basalis of meynert
Enthorhinal cortex
Hippocampus

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32
Q

Clinically what does alzhimers look like?

A

Insidious, progressive onset of worsting memory (esp short term), dysphagia, dyspraxia and agnosia

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33
Q

With alzheimers disease all tasks are affected including well practised tasks TRUE/FALSE

A

FALSE- Well practised tasks are not affected

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34
Q

All dementias are associated with behavioural or personality changes in the early stages of the disease?

A

FALSE
AD- not associate din the early stages. however as it progresses these become more prominent
Frontotermporal and vascular dementia are

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35
Q

What do CSF markers in Alzheimers disease show?

A

Increased in phosphorylated tau protein

Decrease in B-amyloid

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36
Q

What drug is used for patients with mild-moderate AD?

A

Acetylcholinesterase (AChE) inhibitors

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37
Q

When would you not used acetylcholinesterase inhibitors?

A

Active peptic ulcer
Severe asthma
COPD

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38
Q

What is used if AchE is contraindicated in the treatment of AD?

A

Memantine

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39
Q

What drugs would be given if someone was having visual hallucinations?

A

Cholinesterase inhibitors

Antipsychotics

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40
Q

Give some examples of BPSD (behavioural and psychological problems of dementia)

A 
Hallucinations
Delusions
Insomnia
Depression
Anxiety
Aggression
Agitation
anxiety
Disinhibition
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41
Q

In Alzheimer’s what is haemorrhage stroke due to?

A

B-amyloid deposits weakening cerebral blood vessels (cerebral amyloid angiopathy)

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42
Q

Frontotemporal dementia presents late in life TRUE/FALSE

A

FALSE

It presents early in life (one of the most common <65)

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43
Q

What is frontotemporal dementia characterised by?

A

Progressive changes in character and social deterioration leading to impairment of intellect, memory and language

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44
Q

What are the 3 variants of frontotemporal dementia?

A

BEHAVIOURAL VARIANT

Primary progressive aphasia (split into SEMANTIC DEMENTIA and PROGRESSIVE NON-FLUENT APHASIA)

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45
Q

What is the most common variant of FTD?

A

Behavioural variant (frontal lobe)

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46
Q

What does the behavioural variant look like?

A

Causes loss on inhibition and social skills

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47
Q

What does semantic dementia look like?

A

Impaired word comprehension and object naming

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48
Q

What does progressive non-fluent aphasia look like?

A

Slow hesitant speech

Word-finding difficulties and agrammatism

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49
Q

What are the histological hallmarks of frontotemporal dementia?

A

Swollen Neurones (Picks cells) and intracytoplasmic filaments (picks bodies)

Picks bodies are enriched in the protein Tau and Tau mutations are one of the causes of this dementia

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50
Q

What should you not use to treat frontotemporal dementia and why?

A

Cholinesterase inhibitors - they make it worse

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51
Q

How do you treat picks disease?

A

SSRIs

Trazodone

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52
Q

What is used to distinguish picks disease from Alzheimers?

A

Lumbar puncture

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53
Q

What is the second most common dementia in the west?

A

Multi-Infarct dementia

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54
Q

What is multi-infarct dementia caused by?

A

Vascular changes secondary to cerebrovascular disease

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55
Q

Why are suffers of multi-infarct dementia prone to depression and anxiety?

A

As they have insight

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56
Q

Name 5 characteristic symptoms of multi-infant dementia?

A 
Executive/attentional difficulties
Cognitive slowing
Behavioural changes (disinhibition)
Focal neurological problems
Difficulty walking/falls
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57
Q

Multi-infarct dementia is difficult to distinguish from alzhimers however it has…

A

Abrupt onset
Stepwise progression
History of hypertension or stroke

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58
Q

What are large vessel infarcts related to?

A

Atheroma of large cerebral arteries provoke thromboembolism

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59
Q

What are small vessel infarcts related to?

A

Longstanding hypertension and atherosclerosis of small vessels

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60
Q

MRI scans show the presence of lacunar infarcts TRUE/FALSE

A

TRUE

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61
Q

What is Creutzefeldt-Jacob disease?

A

Transmissible prion neurodegenerative disease, causes cell death (spongiform changes in the cortex) and astrocytosis

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62
Q

How does Creutzfeldt-Jacob disease present?

A

Rapidly progressing dementia, ataxia and myoclonic jerks

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63
Q

What is the difference between explicit and implicit memory?

A

Implicit- performance of task facilitated in absence of conscious recollection
Explicit- Performance of test requires conscious recollection of past experiences

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64
Q

What is Antegrate amnesia?

A

Difficulty in acquiring new material

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65
Q

What is retrograde amnesia?

A

Difficulty in remembering information prior to the onset of the illness/injury

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66
Q

What are classic reports of a memory problem?

A 
Forgetting a message
Inability to remember a familial place
Losing track of a conversation
Increased misplacing of things
Forgetting to do things
Struggling to remember names
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67
Q

How does the onset of dementia, delirium and depression differ?

A

Dementia- insidious
Delirium- Acute
Depression- Gradual

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68
Q

What is 4AT a rapid test for?

A

Delerium

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69
Q

What are the 4 things tested for in 4AT?

A

ALERTNESS
AMT-4
ATTENTION
ACUTE OR FLUCTUATING COURSE

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70
Q

What is MoCA a test for?

A

mild cognitive dysfunction

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71
Q

MMSE is used in the diagnosis of what?

A

Dementia

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72
Q

What are the 6 questions used in GP land in order to test cognitive ability

A

1- More trouble remembering things that happened recently used to?
2-Trouble recalling conversations a few days later?
3-Difficulty in finding the right words or tend to use the wrong words more often?
4- Less able to manage money and financial affairs?
5-Less able to manage medication?
6- Need more assistance with transport?

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73
Q

What does clock drawing test?

A

Fronto-parietal functioning

  • Executive function (planning)
  • Visuospatial ability
  • Abstraction (ability to use symbols)
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74
Q

What is the ICD-10 criteria for dependence?

A 
A strong desire to take the substance
Difficulties in controlling substance use
A physiological withdrawal state
Tolerance
Neglect of alternative pleasures
Persistence despite evidence of harm
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75
Q

What are the CAGE signs of addiction?

A

Cut down
Annoyed
Guilty
Eye-opener

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76
Q

What is incentive salience due to?

A

Dopimanergic activity in the mesolimbic pathway- it is a motivating signal

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77
Q

When someone takes lots of drugs a tolerance develops. Why?

A

Downregulate the dopamine receptors

(OVERSTIMULATION–> DESENSITISATION)

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78
Q

What is addiction driven by?

A

Initial stages- driven by reward (positive reenforcement)

Eventually becomes a thirst (negative reenforcement)

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79
Q

How is the pre-frontal cortex involved in the neurobiology of addiction?

A

Helps intention guide behaviour

Modulates effects of the reward pathway, keeps emotions/impulses under control to achieve long-term goal

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80
Q

When is the pre-frontal cortex fully developed?

A

Not until mid-20s (as cortical maturation is in a back to front direction, vulnerable while developing)

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81
Q

TRUE/FALSE

Frontal lobe areas mature later than limbic (emotional) symptoms

A

TRUE

82
Q

What 3 things does dopamine release effect?

A
  1. Ability to update info in PFC
  2. Goal setting
  3. Ability to avoid compulsive repetition
83
Q

What part of the brain makes the decision about whether to carry out an activity?

A

Orbitofrontal cortex (provides internal representation of the saliency of events and assigns value to them)

84
Q

Addicted brains shows increased activation of OFC TRUE/FALSE

A

TRUE

85
Q

Which three parts of the brain are critical in acquisition, consolidation and expression of drug stimulus learning?

A

Hippocampal
Striatum
Amygdala

86
Q

What is the most heritable psychiatric condition?

A

Addiction

87
Q

How does stress motivate drug seeking in dependent individuals?

A

Triggers release of dopamine in neural reward pathway

88
Q

What does chronic stress lead to?

A

Dampening of dopaminergic activity through down regulation fo D receptors (reduces sensitivity to normal receptors)

89
Q

How do you make heroin?

A

Opium–> Morphine –> Diamorphine (Heroin)

90
Q

What are the two most common ways of taking heroin?

A

IV & Smoking (fastest way to enter bloodstream)

91
Q

How can opiate misuse lead to poor dentition?

A

The analgesic effect means that they don’t realise when pain

92
Q

How long does it take for withdrawal symptoms to appear?

A

within 6-8h (therefore tend to use 3x a day to avoid)

93
Q

What are the withdrawal symptoms of opiates?

A

Dysphoria and craving, agitation, tachycardia and hypertension, piloerection
Diarrhoea, N&V
Dilated pupils
Joint pains
Yawning, Running nose (rhinorrhoea) and watery eyes (lacrimation)
Insomnia
BP + HR^

94
Q

Opiate withdrawal may cause psychosis or harm TRUE/FALSE

A

BIG LIFE

Opiate withdrawal does not cause psychosis or harm

95
Q

What it opiate substitution therapy (OST)

A

Replace short acting opiod with long acting opiod

Either Buprenorphine or Methadone

96
Q

What is opiate detoxify?

A

Achieve complete abstinence from ALL opiates

97
Q

Why is there a huge risk of death with opiate detoxification?

A

As when detoxify decrease tolerance

BUT 70-80% relapse within 1y as although physically not dependent, psychologically dependent

98
Q

What is the definition of an alcoholic?

A

Someone whose repeated drinking leads to harm in work or social life. Lifetime prevalence ~10%

99
Q

How much is 1 unit?

A

10ml of alcohol

100
Q

How do you calculate the number of units?

A

%*volume/ 10

101
Q

What is used to identify someone with a harmful use of alcohol?

A

AUDIT (FAST is the quicker version)

CAGE

102
Q

What channels does alcohol affect?

A

Inhibits the action of excitatory NMDA- gutamate controlled ion channels
ALSO
Potentiate the actions of GABA type A controlled ion channels

103
Q

What does alcohol withdrawal lead to

A

Excess glutamate activity (toxic to nerve cell)

Reduced GABA activity

104
Q

When does withdrawal syndrome start to appear?

A

10h after the last drink

105
Q

What is the weekly allowance of alcohol?

A

14u/ week spread over 3 days with alcohol free days

106
Q

The first symptoms of withdrawal syndrome start to occur within hours and peak at 24-48h. When do they resolve?

A

5-7 days

107
Q

When does Delirium tremens peak?

A

within 2 days of abstinence

108
Q

What is the mortality of delirium tremens?

A

Mortality 2-5%

109
Q

What does delirium tremens look like?

A 
Night time confusion
disorientation
Agitation
Hypertension
Fever
Visual/auditory hallucination
Paranoid ideation
Epileptic seizures can occur
110
Q

How do you treat withdrawal syndrome?

A

Chlordiazepoxide

111
Q

Lab tests are useful for screening and monitoring response for alcohol related problems TRUE/FALSE

A

FALSE

Useful for monitoring but not useful for screening

112
Q

What treatment can be used in alcoholics to detox?

A

Reassurance
Advice (adequate hydration, analgesia, antiemetics, treat infections and environment)
Benzodiazepines
Vitamin supplementation

113
Q

Name 3 symptoms of Wernickes encephalopathy?

A

Ataxia
Nystagmus
Ophthalmoplegia

114
Q

NO BENZODIAZEPINES BEYOND THE DETOXIFICATION PERIOD

A

tis a fact of life

115
Q

What percentage of people will relapse?

A

50%

116
Q

Name 3 drugs used to prevent relapses

A

Disulfiram (deterrent)
Acamprosate (reduce craving)
Naltrexone (reduces the reward)

117
Q

What are some of the CNS effects of alcohol?

A 
Self-neglect
Decrease memory/cognition
Cortical atrophy
Retrobulbar neuropathy
Fits
Falls
Wide-based gait
Wericke-Korsakoff's encephalopathy
118
Q

What are alcohol contraindications?

A 
Driving
Hepatitis, Cirrhosis
Peptic Ulcer
Drugs (e.g. antihistamines, metronidazole)
Carcinoid
Pregnancy
119
Q

What is the treatment for alcoholic hepatitis?

A

Supportive + prednisolone

120
Q

What is the criteria for diagnosing anorexia nervosa?

A 
BMI <17.5
Self-induced wt loss
Body image disturbance
Fear of fatness
Amenorrhoea
121
Q

What are some of the physical signs of anorexia nervosa?

A 
Muscle wasting 
Hair loss
Cold dry peripheries, dry skin
Hypercartenaemia
Bradycardia, hypotension
Bruising
Osteopenia/Osteoporosis
122
Q

What is referring syndrome?

A

Caused by depletion of already inadequate stores of nutrients (Use marsipan guidelines)

123
Q

What are the criteria for bulimia?

A 
Persistent preoccupation with eating
Irresistible craving for food 
Binges
Attempts to counter the effects of binges
Morbid dread of fatness
124
Q

Physical signs of bulimia?

A

Calluses on knuckles (Russels sign)
Parotid Hypertrophy
Dental caries
U+Es

125
Q

What can be some medical complications of bulimia?

A 
Hypokalaemia (common and problematic)
Oesophageal reflux
Oesophageal tears/rupture
Subconjunctival haemorrhage
Dehydration
Seizures
126
Q

What is psychosis?

A

A loss of contact with reality

127
Q

What does psychosis look like?

A

Hallucinations
Delusions
Disorder of the form of thought
Agitation/aggression

128
Q

What is a hallucination?

A

A perception that occurs in the absence of visual stimulus

129
Q

What is a delusion?

A

Fixed, falsely held belief with unshakable conviction (misinterpretation of real sensory stimuli w/o evidence to support)

130
Q

You can be swayed from an overvalued idea TRUE/FALSE

A

true

131
Q

What are functional hallucinations?

A

Hallucinations triggered by a stimulus in the same modality, can co-occur with it

132
Q

What is paranoia?

A

Belief that external events are related to ones self (vary in intensity, be aware of colloquialism)

133
Q

What are ideas of reference?

A

Innoculus or coincidental events ascribed meaning by the person e.g. thinking the TV is talking to them directly

134
Q

Is primary or secondary delusions more common?

A

Secondary (trying to explain why weird stuff is happening)

135
Q

A formal thought disorder cannot be directly observesd therefore has to be inferred from patterns of speech TRUE/FALSE

A

TRUE

136
Q

What is neologisms?

A

Coining of a new word or expression

137
Q

What are the 5 types of thought interference?

A 
Thought insertion
Thought withdrawl
Thought broadcasting
Thought blocking
Thought echo
138
Q

What is passive phenomena?

A

Not having control of your body, emotions changed by others

139
Q

What increased the risk of schizophrenia by 50%?

A

Childhood viral CNS infection

140
Q

What is heritability?

A

Proportion of observable differences in a trait between individuals in a population

141
Q

What drugs are most and least likely to cause a drug induced psychosis?

A

Heroin least likely

Cannabis most likely

142
Q

3rd person auditory hallucinations are most likely…

A

Schizophrenia

143
Q

Self-referential delusions are most likely…

A

tbh not specific

delirium?

144
Q

What is depressive psychosis typified by?

A

Mood congruent of psychotic symtpoms

145
Q

What is this describing?
Delusions of grandeur/special ability/persecutory/religiosity
2nd person hallucinations/auditory
Symptoms of 1st rank present in 20% manic episode

A

Mania with psychosis

146
Q

What is an indictor of poor outcome in brain structural abnormalities?

A

Decreased frontotemporal volume/ frontal lobe grey matter

Enlarged lateral ventricle

147
Q

In schizophrenics what are the grey matter reductions due to?

A

Arborisations, not neuron loss

148
Q

With psychosis there is progressive ventricle enlargement TRUE/FALSE

A

FALSE

There is ventricle enlargement but it is not progressive

149
Q

What is the neurobiology of schizophrenia?

A

Overactivity of dopamine pathways in the brain

150
Q

Dopamine is inhibitory to what?

A

Prolactin

151
Q

Of the dopamine receptor subtypes which is most abundant and which is most important?

A

D1- Most abundant (stimulate cAMP)

D2-Most important

152
Q

How do typical antipsychotics work?

A

Work by D2 inhibition

153
Q

TRUE/FALSE
With typical antipsychotics there is a strong correlation between average antipsychotic dose required to improve clinical symptoms and D2 receptor binding activity

A

true

154
Q

How do atypical (2nd generation work)?

A

Many are 5-HT2A antagonists

155
Q

Typicals often have extrapyramidal side effects TRUE/FALSE

A

true

156
Q

name 4 of the anticholinergic side effects of typical antipsychotics

A

Acute dystonic reaction
Parkinsonism
Akathisia
Tardive dyskinesia

157
Q

How long does tar dive dyskinesia take to develop?

A

years

158
Q

What are side effects of atypicals?

A

Wt gain, sedation & metabolic syndrome

159
Q

Why are never atypical not sedating?

A

They do not cross the BBB

160
Q

Why is clozapine 3rd line in treatment of psychosis?

A

Response is great (50%)
BUT
small risk of agranulocytosis

161
Q

What is a functional disorder?

A

Symtpoms where one cannot easily associate the symptoms with classically identifiable organic disease processes

162
Q

What are common symptoms of functional disorders?

A 
pain
altered sensation
dizziness
movement disorders
weakness
seizures- v common to have functional background
cognitive symptoms
163
Q

define dissociation

A

detachment from reality

164
Q

Define depersonalisation

A

Feeling that your body does not quite belong to you or is disproportionate from you

165
Q

What is derealisation?

A

A feeling that you are disconnected from the world around you or “spaced out”

166
Q

What percentage of functional symptoms have a good response to treatment?

A

60%

167
Q

What is the standard treatment of choice for functional problems?

A

CBT

168
Q

Define personality

A

Cluster of relatively predictable patterns of thinking, feeling and behaving, generally consistent across time, space and context

169
Q

What are the 5 things that the structure of personality consists of?

A

Openess, neuroticism, agreeableness, extraversion and conscientiousness

170
Q

What is a personality disorder?

A

Enduring pattern of inner experiences and behaviour that deviate markedly from the expectations of the individuals culture. The pattern is inflexible and pervasive.

171
Q

The first access of people with personality disorder to the services tends to be around age…

A

14

172
Q

Personality disorder is more common than asthma TRUE/FALSE

A

true

173
Q

What is in cluster A personality disorder?

A

Paranoid

Schizoid

174
Q

What is in cluster B personality disorder?

A

Antisocial
Bordeline
Histrionic

175
Q

What is in cluster C personality disorder?

A

Avoidant
Dependent
Obcessive-Compulsive

176
Q

What are some of the traits of antisocial personality disorder?

A 
Disregard for and violation of the rights of others
Impulsive
Deceitfully charming
Fearless
Bad at reading emotional Qs
Tend not to learn from punishement
Blame the victim
177
Q

What are the three subtypes of schizophrenia?

A

Paranoid
Hebephrenic
Catatonic

178
Q

What is the peak onset of schizophrenia in men?

A

15-25

179
Q

What is schizophrenia?

A

A group of brain disorders characterised by disorders of thought, behaviour, perception and emotion

180
Q

What are the main symptoms of schizophrenia?

A

Delusions
Disorders of the form of thought
3rd person auditory hallucinations

181
Q

RF for schizophrenia?

A 
Genes
Birth complications
Winter/spring birth
Drug use
Urban dwelling
Social adversity/deprivation
Neurodevelopmental changes
Neurochemical changes
182
Q

What are 4 good prognostic indicators for schizophrenia

A

Older age of onset
Female gender
Marked mood disturbance especially elation
Fix of mood disorders

183
Q

What is there an increased risk of suicide in schizophrenic patients?

A

In the 1st week post discharge

184
Q

What medication does post schizophrenic depression respond well to?

A

SSRIs

185
Q

What are the 3 main parts of ADHD?

A

Inattention
Hyperactivity
Impulsivity

186
Q

What is the most common neurobehavioral disorder of childhood?

A

ADHD

187
Q

Cause of ADHD

A

Genetic-80% genetically inherited
Perinatal factors-Tobacco/drug/alcohol use in pregnancy, prem, hypoxia, short/long labour, viral infections, forceps
Psychosocial adversity-Parenting styles, marital discord, maltreatment, trauma, criminality, low SES

188
Q

What is the neurobiology of those with ADHD

A

Underactive frontal lobe function
Excessively efficient dopamine-removal system
Reduction in norepinephrine

189
Q

Why is the diagnosis of ADHD delayed until school entry/later?

A

Most children will have hyperactivity as a toddler but this will abate with time

190
Q

What are the non-pharmacological treatment options for those with ADHD?

A 
Parent training
social skill training
sleep 
diet
behavioural classroom management strategies
specific educational interventions
191
Q

What are the pharmacological treatment for those with ADHD?

A 
1st line (stimulants)- Methylphenidate
2nd line (SNRI)- Atomoxetine
192
Q

How long does it take Atomoxetine to reach its full efficacy?

A

6 weeks

193
Q

What is autism?

A

Persistent deficits in social communication and interaction across multiple contexts with restrictive repetitive pattern of behaviour, interests and activities

194
Q

How is social communication I someone with autism impaired?

A

Hard to understand underlying meaning of conversation
Difficulties understanding jokes
Monotonous voice
Pedantic and idiosyncratic language
Narrow interests
Difficulties sharing thoughts and feelings

195
Q

How is social imagination impaired in those with autism?

A

Difficulties thinking flexibly
Takes things literally
Difficulty goal planning

196
Q

How is social interaction more difficult for someone with autism?

A

Difficulties with non-verbal clues

Struggle to make/sustain personal and social relationships

197
Q

What are the repetitive behaviours of someone with autism?

A

Stereotyped/repetitive motor movements

Ritualised patterns of behaviour

198
Q

What is the 3 criteria for autism diagnosis?

A

Present in early developmental period
Cause significant impairment in functioning
Not explained by mental health, intellectual disability or global developmental delay

199
Q

What is a larger amygdala associated with?

A

More severe anxiety and worse social and communication skills

200
Q

What is the aim of non-pharmacological treatment for someone with autism?

A

Lessen associated deficits/ family distress
Increases QOL
Functional independence

201
Q

What pharmacological management can be used for those with autism?

A

Risperidone- aggression
Metatonin- Sleep
SSRIs-Repetative behaviour

ADELE-Noodles of Neurology (38 decks)

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