CNS Week 2 Anxiety And Depression Flashcards
1
Q
What key behaviours does the limbic system integrate
A
Emotions Reward driven activity: feeding and sex Motivation Social behaviours: friend and foe Memory of environment and experience
2
Q
What Brain regions does the limbic system link
A
Hypothalamus, sensory, motor and frontal regions
3
Q
Function of the parahippocampal gyrus
A
Route which information gets to the hippocampus
4
Q
Function of the dentate gyrus
A
Gatekeeper of information flow into the hippocampus
5
Q
Basic circuit of hippocampus for forming memories
A
Sensory information from multiple cortical areas -> entorhinal cortex -> dentate gyrus -> CA3 -> CA1 -> subiculum -> entorhinal cortex -> cortical areas
6
Q
How is the hippocampus connected to the septal nuclei
A
They have a reciprocal relationship in which the septal nucleus inputs into the hippocampus and the hippocampus outputs to the septal nuclei
7
Q
Summary of hippocampal inputs
A
1) Sensory information from throughout Cortex via entorhinal cortex > performant path to dentate gyrus
2) modulatory inputs from septal nuclei, brainstem nuclei influence the overall functioning
8
Q
Summary of hippocampal outputs
A
1) via subiculum and entorhinal cortex to neocortex
2) via fornix to septal region, mamillary bodies, hypothalamus, median forebrain bundle
9
Q
What is working memory (short term)
A
Limited capacity (7+/-2)
Rapid decay without sustained attention
Prefrontal cortex
Visual and auditory versions of working memory
10
Q
Difference between declarative (explicit) and non declarative (implicit) memories
A
Declarative: events and facts
Non declarative: unconscious knowledge, motor skills and conditioned responses
11
Q
2 different types of declarative memory
A
Semantic: general knowledge
Episodic: personal experience (role of the hippocampus)
12
Q
How do we know that the hippocampus is key to episodic memory
A
Patient HM had a bilateral hippocampal amygdala entorhinal resection to help his epilepsy
Resulted in a profound deficit in episodic memory
He preserved his procedural memory (learning skills) and preserved memory of events before the surgery
This shows that the hippocampi are integral to episodic memory
13
Q
Different types of spatial cells represented in the limbic system
A
Place cells
Head direction cells
Grid cells
Border cells
14
Q
What is temporal lobe epilepsy
A
When one hippocampus is damaged and one is healthy causing seizures and memory problems
15
Q
Summarise the hippocampus as a key memory structure
A
Inputs from multiple sensory cortices via entorhinal cortex
Specialised intra-hippocampal circuits
LTP- synaptic plasticity is the basis of long term memory
Spatial functioning
Disorders of hippocampus involve memory impairment
16
Q
What are emotions
A
CNS response to certain stimuli
Output from:
- autonomic
- hormonal
- behavioural
Innate and learned elements , multiple neural networks involved
17
Q
Describe the anatomy of the amygdala
A
Multiple sub nuclei Multiple sensory and limbic inputs Organise emotional responses to stimuli (hormonal, autonomic, behavioural) Both pleasant and harmful Special role in fear
18
Q
What is kluver-bucy syndrome
A
Large bilateral anterior temporal lobe resections removing amygdala, hippocampus and surrounding temporal lobe
Very docile - no longer aggressive towards keepers
Indiscriminant sexual activity - low visual discrimination
Lost ability to visually discriminate edible from inedible
A breakdown of visual input to channeling drives
19
Q
Describe the reward circuit
A
Midbrain dopaminergic neurons
Ventral tegmental area to nucleus accumbens
Median forebrain bundle
Orbitofrontal and medial frontal cortex, ventral striatum, Amygdala
Reward signals use environmental signals to drive behaviour
20
Q
Location of the nucleus accumbens
A
Medial aspect of the basal ganglia
21
Q
Function of the midbrain dopaminergic neurons
A
Show brief phasic bursts of activity after
- rewarding stimuli like food or sex
- stimuli predicting reward
- causes wanting rather than liking
22
Q
What happens when there is an absence of a reward after stimulus predicting a reward
A
There is a drop in neural firing
23
Q
Describe characteristics of addiction
A
A compulsion to take a substance despite consequences
Loss of control over intake
Negative symptoms when access to substance is prevented
Wanting occurs despite tolerance to liking
Many factors determine whether occasional use becomes addiction including the drug, the person and the context
24
Q
Role of drugs of addiction chemically
A
They acutely boost dopaminergic signalling
Chronically they down regulate reward signals to normal stimuli due to altered gene expression
Repeated use leads to craving, withdrawal and compulsive use
25
Describe the dorsal striato pallidal circuit (motor loop)
Allows coordinated behaviour
Information from substantia nigra -> dorsal striatum -> pallidum -> thalamus -> motor cortex
26
Describe the ventral striato palllidal circuit
Loop involved with motivational behaviour
| VTA -> ventral striatum -> ventral pallidum-> thalamus -> limbic and prefrontal cortex
27
Describe the neurobiology of depression
Involves dysfunction of a complex network of limbic - striatum - frontal cortex
Amygdala - anxiety
Hippocampus - memory deficits (sometimes shows as a smaller hippocampus on MRI)
Reward circuits - anhedonia and motivation
Frontal lobe - motivation and decision making
Striatum - motor slowing
28
Summarise the pre frontal cortex
Inputs to and from key limbic structures
Important in decisions about reward and appetite behaviour
Motivation and regulation of behaviour
Disorders can include psychiatric and personality disorders
29
Top 7 leading causes of disability in ages 10-24 in 2019
1. Road injuries
2. Headache disorders
3. Self harm
4. Depressive disorder
5. Interpersonal violence
6. Anxiety disorders
7. Lower back pain
30
What are DALYs
Disability adjusted life years
| Overall disease burden expressed as a number of years lost to ill health
31
What is the commonest complication of pregnancy
Post natal depression
32
Effect of depression and anxiety disorders on GDP
1% loss of UK GDP
| Leading reason people retire early from work
33
Describe the course of depression and anxiety disorders
50% long term condition with a relapsing and remitting course
50% in response to an adverse life event only eg loss of job / relationship
34
Risk of depression and anxiety disorders
Suicide
Self harm (often without suicidal intent)
Self neglect
Neglect of vulnerable others
Exploitation by others
Addiction
Homicide (often intended as an act of kindness in a perceived awful world)
35
Associated symptoms of depression
```
Fatigue / loss of energy
Weight gain
Change in sleep
Low libido
Change in appetite
Decline in hygiene
Agitated / slow movement
Poor concentration
Feeling worthless / excessive guilt
Suicidal thoughts / acts
```
36
What is the mental state examination steps (ASEPTIC)
Appearance: clothing, self care, eye contact, poor nutrition, agitation
Speech: slow, monotone, short answers
Emotion: mood
Perception: hallucinations, derogatory voices talking to them in 2nd person
Thought: worthless, hopeless, helpless, low self confidence, suicidal ideation
Insight: undeserving of help
Cognition: poor concentration and attention
37
What is adjustment disorder
Subthreshold response to specific life event (behaviour or emotional reaction)
38
What is dysthymia
Subthreshold depressive symptoms most days for 2+ years
39
What is seasonal affective disorder
Recurrent depression at the same time each year
40
What is grief
A normal reaction to significant loss
41
What is bipolar depression
Separate episodes of mania, >4 days of elation or irritability, increased energy and activity
But treating as normal depression can trigger a manic episode
42
What is atypical depression
Sleep more, eat more, worse in evening
43
What is melancholic depression
Most severe, slowed down / agitated, worse in morning, early morning waking , weight loss
44
Factors to determining a patients suicide risk
Intention: has a plan to end their life: when, how, what they will do, planning for end of life eg putting affairs in order
Thinking: hopeless, helpless, painfulness of living
Behaviour: suicide can occur with very little planning - evidence of recklessness with life, recent self har, (x 10 risk), substance misuse, past violence
Medical risk: likelihood of death of injury eg hanging, asphyxia, fall
Protective factors: responsibilities eg to children, beliefs eg suicide is wrong, events to look forward to
45
What do blood tests look for as a cause of depression
FBC (anaemia, chronic disease)
U+ E/ LFT (renal or hepatic disease, hyponatraemia)
Bone profile (calcium, vit D)
Haematinics (ferritin, B12, folate, blood glucose)
46
Substances and physical health conditions as organic causes of depression
Alcohol and benzodiazepines are depressants, substance withdrawal
Prescribed interferon alpha (some cancers) , steroids, anti HIV, isotretinoin (acne), hormonal treatment eg contraception, Parkinson’s drugs (block dopamine), beta blockers
Endocrine, viral infections, head injury, neurological disease
47
Define fear
An emotional reaction to a specific, present, danger
48
Define panic
Intense fear accompanied by physical symptoms of autonomic arousal
49
Define phobia
Repeated fear associated with a non typical, specific, source of threat eg spiders, flying, public speaking
50
How are anxiety and depression different
Anxiety is psychological symptoms about the future- fear of what might happen versus in depression about loss that has already happened
51
How does a person with anxiety process thoughts about fear and panic
They overestimate threat / danger / vulnerability
Underestimate their own ability to cope
Underestimate rescue factors / resources eg chance and help from others
They have painful recurrent thoughts as if trying to solve an unsolvable problem
52
What is social anxiety disorder
Fear of being judged negatively by others
53
What is panic disorder
Panic attacks with avoidance of source or place of panic
| Often with agoraphobia or other phobias - recurrent panic attacks to the point of fearing having a panic attack
54
Describe the panic cycle in a panic attack
Internal / external trigger eg crowded place, caffeine
Perceived threat
Anxiety eg intense fear
Avoidance and safety behaviour or physical / cognitive symptoms eg palpitations
Misinterpretation eg i am having a heart attack
Panic attacks stop because the body runs out of adrenaline
55
What is PTSD
Witnessed a terrifying life event eg assault, reliving nightmares and flashbacks, hypervigilance, avoidance of reminders
56
What is OCD
Obsessive thoughts around a threatening outcome + compulsions to try to neutralise this threat -> can sometimes forget what the obsessions were
57
What is health anxiety
Fear of having a serious illness, misinterpreting the symptoms
58
What is generalised anxiety disorder
Worry for >6 months out of proportion to stress with insomnia, muscle tension with headaches, backaches, autonomic physical symptoms
59
Describe electroconvulsive therapy for severe or treatment resistant depression
General anaesthetic and muscle relaxant, electricity given to produce a controlled generalised epileptic seizure
Course of up to 12 treatments
Vagal nerve stimulation and deep brain stimulation. Rarely used for very treatment resistant depression. Requires an operation to implant transcranial direct current stimulation
60
Describe transcranial magnetic stimulation for depression
Course of up to 20 treatments. No anaesthetic. No seizures. Can be focused but does not penetrate far into the brain so usually targeted at fronto-limbic circuits implicated in depression
61
Purpose of cognitive behaviour therapy
Tackles reasons why depression or anxiety are still present, not what caused them
Generally the strongest evidence base of all psychotherapies
62
Describe the type of thinking in depression
Negative automatic thoughts eg I didn’t get a promotion but john did so all my colleagues think john is better than me
Cognitive distortions:
- all or nothing thinking: i do things perfectly or I’m useless
- emotional reasoning - i feel like a bad friend therefore i must be a bad friend
- personalisation: my friend looked sad when I spoke to her earlier, it must be my fault
- mental filtering: focusing on a small negative thing or ignoring positives
63
What is becks cognitive triad - negative thoughts about the self, world and future
I am a bad person
The world is a bad place
Nothing will ever get better
64
What is mindfulness based CBT
Identify unhelpful negative thoughts of depression, use meditation to disinvest these thoughts as being unimportant
65
What is behaviour therapy
Exposure to fear in real life, virtual reality or imagination
66
What is eye movement desensitisation and reprocessing (EMDR)
Trauma, eye movements during recollection intended to allow processing of raw memories
67
What is problem solving counsellling
Depression due to specific life events or difficulties
68
What is interpersonal therapy
Relationships, isolation - looking at recurring patterns
69
What is family and martial therapy
Working on how people relate to each other at the same time
70
What is psychodynamic psychotherapy
Subconscious, predisposing / precipitating factors
71
What is supportive listening
Non judgemental support, helping the person to reframe their situation by listening, asking questions and repeating back to person in more natural ways
72
What is emotion
An emotion is a positive or negative reaction to an appropriately evocative stimulus which involves: cognitve appraisal, physiological arousal, subjective experience, expressive beahvaiour and goal directed actiivty
Complex systems that prepare us to act in response to a stimulus
73
How is emotion different to mood
Mood is a frame of mind or emotional state that is defined by ones internal state rather than external behaviour; moods are more long lasting and less spontaneous than emotions
74
What did plutchik suggest
That there are 8 basic emotions grouped in 4 pairs of opposites
1) joy / sadness
2) affection / disgust
3) anger / fear
4) expectation / surprise
All other emotiuons are derived from combinations of this array
75
Factor 1 of the process of emotion
Cognitive apprasial: evaluation of relevance of current situation to personal wellbeing : am i in trouble or am i ok
Then evaluation of capacity for dealing wirh the situation; what can be done about it?
If situation is appraised as unfavourable and coping potential is appraised as low then the emotional state experienced is likely to be sadness or anxiety
76
Factor 2 of the process of emotion
Arousal: emotions are based on feedback of bodily changes: we feel sorry because we cry, angry bevause we strike, afraid becuase we tremble
Emotions are a directl result of the different patterns of physiologicla response associated with them; they are cognitive responses to information from the periphery
77
How do lie detectors work
Beta blockers reduce anxiety / fear eg blood pressure or tightening of muscles
So when someome experiences anxeity or guilt when they lie specific patterns of physiological arousal accompanying these emotions should be detectable
78
Describe the process of emotion
The sympathetic and parasympathetic parts of the nervous system act in balance in non excited states; when the balance has been upset the sympathetic nervous system prepares the body for specific actions and mobilises emergency and stress responses
79
Voluntary facial movements
Controlled by the pyramidal motor system, a brain system that includes the motor cortex
80
Involuntary facial movements
Controlled by the extrapyramidal motor system, which depends on subcortical areas; brain damage can disrupt either system
81
What is the facial feedback hypothesis
The pattern of muscles during facial expression feeds back to the brain, providing it with information for subjective feel of an emotion
Darwin argues that the facial expression of an emotion will intesnfiy it while the suppression of an expression will reduce the meoiton
82
Factor 4 of the process of emotion
Action readiness: the tendency to serve as an impulse for an action specific to the emotion being experienced
83
Advantages of xray
Assess for fracture or radio opaque foregin body
Quick imag acquisition and inexpensive
84
Disadvanatges of xray
Difficult to interpret due to overlying structures
No assessment of the brain
Non displaced fractures may be missed
85
Advantages of CT scan
Imaging for most acute neurological presentations
Allows anatomical assessment in multiple planes
Excellent assessment in cases of trauma and most vascular abnormalities
86
Disadvantages of CT
Prone to artefact
Evaluation of the brain is limited
Subtle abnormalities may be missed
87
Advantages of MRI
Exquisite details of the cerebrum and cerebellum
Multiple planes and sequences allow detailed evaluation
Radiation sparing investigation
88
Disadvantages of MRI
Time consuming and expensove
Cannot be used in all patients
Limited bone assesment
89
Describe the bones of the skull
Formed of 28 bones
- calvarium (6)
- facial bones (16)
- middle ear ossicles (6)
Mostly articulate via strong fibrous joints at suture lines
Temporomandibular joint and middle ear ossicles articulate via synovial joints
90
What are the 6 calvarium bones
Single frontal bone
Paired parietal bones
Paired temporal bones
Single occipital bones
91
What bones make up the facial bones
Midline single: vomer, sphenoid, ethmoid, mandible
Paired bilateral: lacrimal, nasal, inferior nasal concha, maxillary, palatine, zygoma
92
Describe the paediatric skull
Unfused sutures allow for growth of the brain (metopic suture is most common - appearance of 2 frontal bones)
Metopic suture dividing the frontal bone can persist into adulthood
93
What is the difference between sutures and fractures
Sutures are more jagged in appearance and symmetrical
Fractures more linear and unilateral
Abnormal suture widening is also indicative of fracture
Wormian bones and metopic suture can be mistaken for fracture in paediatric patients
94
What are the sinuses of the sjull
Air filled spaces lines with mucous membrane
- frontal
- ethmoid
- maxillary
- sphenoid
Variation in normal anatomy is common
95
Functions of the sinuses of the skull
Reducing the weight of the skull, air humidifcation and aiding in sound resonance
96
What does asymmetry of the sinuses indicate
Indicates injury even if a fracture cannot be seen
If in doubt, a CT scan will allow for further assesment
An opacified sinus could also be due to obstruction or infective or inflammatory sinus disease
97
Where is CSF produced
By the epithelium of the choroid plexus and then flows freely within the ventricles and subarachnoid space
98
Usual volume of CSF
150-250ml with approx 700ml produced daily
| Excess CSF is drained into dural venoous sinuses via arachnoid granulations
99
Location of the circle of willis
In the sub arachnoid space
100
course of the middle meningeal artery
Arises from the external carotid artery via the maxilary artery
Courses aling the inner table of the skull and supplies the cranial meninges
Enters the cranial vault via the foramen spinosum
Clinically relevant in cases of head trauma
101
What are the dural venous sinuses
Venous channels located between the 2 layers of dura mater
Differ from systemic veins as they are valveless and run independent of the arteries
Form major venous drainage pathway predominantly to the internal jugular veins
102
What are bridging veins
Perforate through the meninges allowing venous drainage of the superficial cerebrum
Prone to shearing in elderly patients leading to a subdural haemorrhage
Usually secondary to trauma but can be spontaneous
103
What is a extradural haemorrhage
Usually a sign of fracture
| Damage to the middle meningeal artery
104
What is the behaviour therapy theory
An action based approach; relies on experimentally tested principles tested of learning theory
Modern approaches have been developed guided by learning theory and applied through innovative techniques in clinical intervention
105
What is the aim of behaviour modification
- increase frequency of existing adaptive behavior
- decrease frequency of existing maladaptive behaviours
- teach new appropriate behaviours
106
Describe the ABC model of operant conditioning
A= antecedent stimulus (condition / situation in which the behaviour occurs)
B= behaviours - behavioural response (rat presses lever)
C = consequence - what happens as a result of the operant behaviour (food is given = reinforcement
Shock is given = punishment)
107
Most widely used techniques for behaviour therapy
- graded exposure eg systematic desensitisation
- exposure and response prevention
- social skills training
- modelling ; behaviour rehearsal
- reinforcement, punishenment and aversion therapy
108
Describe the process of systematic desensitisation
A type of graded exposure
Construct a hierarchy of events related to original stimulus which elicits the maladaptive response for each patient
1) driving to clinic
2) entering treatment room
3) seeing clinic nurse
Train the patient to associate alternative response eg deep muscle relaxation with these events
109
What is virtual reality therapy
Uses specially programmed computer software, visual immersion devices and artifically created environments to give the patient a stimulated experience
Graded exposure and habituation to a vivid experience, without the associated cots of an in vivo experience
Particularly effective in anxiety related disorders
110
Describe cognitive therapy
Emphasises role of negative beliefs in the cause and maintenance of depression; magnification, minimisation and over generalisation
Involved identifying and replacing distorted thoughts and ultimately changing the associated habitual behaviour towards them
111
What is becks negative triad
Negative thoughts about
- oneself
- the world
- the future
112
What is the diathesis stress model
The greater the vulnerability an individual has, the less stress is required for that individual to become ill
A) presence of a diathesis
B) level of stress
Determine the degree of risk for the onset or reoccurrence of an illness
113
What is the differential activation hypothesis (cognitive reactivity)
Important factors determining whether ones initial depression or anxious state becomes more severe or persistent are the degree of activation and content of maladaptive thinking patterns that become accessible in the depressed state
114
What is cognitive behavioural therapy (CBT)
Behavioural and cognitive therapies joined forces to create CBT
Based on the principle that behaviour is learnt, and can therefore be relearnt or reconditioned; focuses on the ‘here and now’
115
Integrative methods of CBT
- Disrupting irrational thoughts and beliefs
- doing cognitive homework
- changing ones language
- using humour, emotive imagery, role play
- desensitisation
- skills training eg assertiveness
116
Cognition of CBT
Recognising that emotional problems stem from maladaptive beliefs and recognising the importance of disrupting self defeating beliefs
Accepting we have the ability to change maladaptive thoughts and behaviours by counteracting them
117
Advantages of CBT
‘Here and now’ approach
Therapeutic attention is focused on the present situation rather than historical or childhood facts; emphasis on current cognitive factors which can be accessed in order to change thinking, emotion and behaviour
- short term structure
- collaborative approach
118
Disadvantages of CBT
Due to structured nature may not be suitable for people with more complex health problems
Due to its focus on current problems, possible underlying causes of mental health condiitons rooted in the past are not adequately addressed; but in recent years psychotherapeutic elements have also been adopted
119
What conditions has CBT been effective in
Depression; amongst other disorders such as anxiety disorders, bipolar disorder, psychotic disorders, somatoform disorders, personality disorder, eating disorders
Also hypocondriasis, rheumatoid arthritis, chronic pain
120
What is mindfulness based therapy
A process that leads to a mental state of non judgemental awareness and acceptacne of the present
The present moment experience includes ones sensations, thoughts, bodily states, consciousness and environment
121
What is mindfulness based cognitive therapy
Combines mindfulness techniques with CBT components and is empirically beneficial in depressive disorders
Neuroimaging evidence that it is effective in the brain
122
What is the monoamine hypothesis of depression
The underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine and or dopamine in the CNS
123
Why is the monoamine hypothesis of depression seen as inadequate
Doesnt provide a full explanation for the therapeutic action of antidepressants
Doesnt clarify the pathophysiology of depression
Doesnt explain why antidepressants take 2-3 weeks to work
Doesnt explain why antidepressants are effective in other disorders eg phobias
124
What is the hypothalamic pituitary adrenal axis in depression
Depressed patients displayed HPA hyperactivation
Increased cortisol in saliva, plasma and urine
Increase CRH in CSF and in limbic brain region (region associated with processing emotion)
Increased size and activity of the pituitaty and adrenal glands
Impaired negative feedback
125
How do antidepressants work in relation to the HPA axis
Antidepressants enhance the negative feedback and decrease the HPA axis hyperactivity
126
How to treat mild depression in children and young people <18
Psychological therapy eg CBT
127
How to treat moderate to severe depression in children and young people <18
Psychological therapy
Combined therapy ie psychological + fluoxetine (SSRI)
If unresponsive to combined therapy consider alternative psycholoigcal therapy
If side effects switch fluoxetine - sertraline - citalopram
128
How to treat mild depression in adults
Appropriate psychological intervention
NICE does not recommend drug treatment unless under certain circumstances eg previous history of moderate / severe depression
129
How to treat moderate/ severe depression in adulys
Combined therapy ie psychological + antidepressant
130
3 main modes of action of antidepressants
1) reuptake inhibition (at the synaptic cleft)
2) receptor blockade - autoreceptor doesnt release neurotransmitter when activated
3) MAO enzyme inhibition (at the presynaptic neurone)
131
Describe mode of action of tricyclic (TCA) antidepressants
Inhibit serotonin and noradrenaline reuptake
```
Sedative properties (H1 receptor antagonism)
Anticholinergic effects eg dry mouth, blurred vision etc
Cardiovascular effects can be fatal in overdose
```
132
Examples of TCA antidepressants
Amitriptyline
| Imipramide
133
Describe mode of action of MAO inhibitors (monoamine oxidase)
Cheese reaction - tyramine displaces noradrenaline from vesical storage
134
Examples of monoamine oxidase inhibitors
Phenelzine and tranylcypromine
135
Describe selective serotonin reuptake inhibitors
First line option
Favourable side effect profile and less toxic in overdose
Eg citalopram, fluoxetine, paroxetine, sertraline
136
Describe serotonin noradrenaline reuptake inhibitors
Similar to SSRIs
| Eg venlafaxine and duloxetine
137
Describe mirtazapine mode of action
Enhances NA and 5HT transmission
Presynaptic a2 adrenoceptors responsible for inhibiting noradrenaline release are blocked
Presynaptic 5HT2 responsible for inhibiting 5HT release are also blocked
138
Symptoms of generalised anxiety
Worry for >6 months out of proportion to stress with insomnia, muscle tesnion with headaches, backaches, autonomic physical symptoms
139
Interventions for generalised anxiety disorder
Autonomic symptoms:
- B adrenoceptor antagonists (propranolol)
Reduces autonomic effect
Do not withdraw abruptly to prevent rebound effects
Anxiety symptoms: psychological interventions
Offer SSRI- sertraline as 1st option
Do not offer benzodiazepine except for short term use during a crisis
140
How do benzodiazepines work
They are positive allosteric modulators on GABA A receptor complex (ligand gated chloride selective channel)
BDZ occupy site on GABA a complex between a and y
Conformation change
Allows greater flow of Cl- ions into the neurone
Hyperpolarisation = inhibition
141
What is bipolar disorder
A cycle between depressed mood and mania
Depressed mood - period of at least 2 weeks with core symptoms accompanied by at least 4 other symptoms
Mania - elevated mood; increased energy, incomprehensible speech, racing thoughts, poor concentration
142
Pharmacological interventions of bipolar disorder
Mania: antipsychotics
Longer term: lithium, valporate, olanzapine
```
Managing bipolar depression:
SSRI fluoxetine with olanzapine
Quetiapine alone
Olanzapine alone
Lamotrigine alone
```
143
Symptoms of lithium toxicity level >1.0 mmol /L
```
Severe diarrhoea
Vomiting or anorexia
Coarse hand tremor
Muscle twitching
Dehydration
Drowsiness
Confusion
Muscle weakness
Slurred speech
```
144
Symptoms of lithium toxicity level >2.0mmol/L
```
Convulsions
Renal failure
Electrolyte imbalance
Hypotension
Clouding of consciousness
Coma and death
```
145
What does a routine assessment of cognitive funciton look at
History of cognitive deficit, premorbid level of functioning: educational and occupational history
146
What does the mini mental state examination ask
1) what is the year, season, month, date, day and where are we (country, county, town, hospital)
2) name 3 objects, repeat, repeat unitl correct
3) begin at 100 and count backwards by 7s or spell world backwards
4) ask for names of previous 3 objects
5) show pencil and watch and ask them to name,
Ask to repeat ‘no ifs ands or buts’
Take paper in right hand, fold in half and put on floor
Read and obey this message
Write a sentence
Copy a design
147
Scores for MMSE
```
Max= 30
Mean for normal young = 30
Mean for normal elderly = 27.6
Elderly depressed pts = 25
Elderly with depression, cognitive impairment = 19
Dementia = 9.7
```
Mild cognitive impairment = 23-26
148
What do neuropsychological tests do
Cover the range of mental processes from simple motor performance to complex reasoning and problem solving
149
What is a developmental brain syndrome
Generalised low cognitive functioning as a child
150
What is acquired brain syndrome
Acute organic brain syndrome eg delirium is common as a symptom of infection and will clear up with the infection
History of sudden onset (often in association with physical illness)
Impaired level of consciouness
151
Order of cognitive impairment in alzheimers disease
```
Prominenet impairment of episodic memory: early
Visuospatial impairment: early
Dysphasia: later
Dyspraxia: later
Dysexecutive syndrome: later
```
Well preserved personality and social behaviour
152
Order of cognitive impairment in frontotemporal lobar degeneration
(Frontotemporal dementia, semantic dementia, progressive aphasias)
Prominent dysexecutive syndrome : early
Coarsening of personality: early
Expressive dysphasia: early
Memory impairment: later
153
Times when neuropsychology is not likely to be helpful or appropriate
```
Recently bereaved
Florid psychosis
Patient severely or terminally ill
Patient has systemic infection
Severe behavioural disorders
Assessed less than 6 months ago
```
154
What is immediate (working) memory
```
Digit span (increasing from 2: at 1/sec)
Immediate recall of name and address
```
155
What is recent memory
5 min delayed recall of name and address
| Recall events of the day
156
What is remote memory
Autobiographical data
157
What is sudden onset dysfunction
Check for retrograde amnesia and post traumatic amnesia
158
Examples of visuoconstructional tasks
Copy drawings of cube, flower and house
Place numbers and hands on clockface
159
What is visuospatial neglect
When copying a drawing leaving out one side of the features eg only drawing half a clock
