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What is anxiety?

▪ Anxiety is an affective state characterised by:
- cognitive expectations of a diffuse and certain danger.
- an internal physiological preparedness to deal with the threat (e.g. increased heart rate) and an external
physiological sign of anxiety (e.g. pale skin, trembling)
- an emotional sense of dread, fear, panic or worry.
- behaviours directed at escaping or avoiding the source of anxiety
▪ Anxiety is adaptive if it motivates effective behaviours, but if the behavioural component becomes maladaptive, it is referred to as an anxiety disorder.


Five Classes of Anxiety Disorders to know for neuro
Gp pop (no s ones)

1. Generalised anxiety disorders occur in the absence of any precipitating stimulus.

2. Phobia anxiety disorders are triggered by exposure to particular objects or situations.

3. Panic disorders are rapid-onset attacks of extreme fear and severe stress symptoms (e.g. choking, heart palpitations).***

4. Obsessive-compulsive disorders are characterised by frequently recurring, uncontrollable anxiety producing thoughts (obsessions) and impulses (compulsions). ***

5. Posttraumatic stress disorder is an ongoing emotional reaction to an extreme psychological trauma.


Read PTSD in text



Panic Disorder characteristics/correlates

▪ People with panic disorder suffer from episodes of acute and unremitting terror characterised by recurring panic attacks.
Happens more often in women. Adolescents

▪ Symptoms of panic attacks are universal .
Physical symptoms of panic attacks include shortness of breath, perspiration, irregularities in heartbeat, dizziness and faintness.

The victim of a panic attack thinks he/she is going to die.

▪ Between panic attacks, the person may/will experience anticipatory anxiety: the fear that another panic attack will strike.

➔ Agoraphobia (fear of open spaces) prevents the person venturing outside the house.


What Causes Physical Symptoms of Panic Attacks?

▪ Lactic acid (a by product of muscular activity) and breathing air with elevated levels of CO2, anarobic exercise.
- increase heart and rate of respiration

Yohimbine (an α2 adrenergic receptor antagonist) and
- have direct stim pharmacological effects on the nervous system

- People with panic disorder have a family history of anxiety disorders.


Pharmacological Treatment: Benzodiazepines
For panic disorder

▪ Clinically used benzodiazepines such as diazepam (i.e. valium) are full agonists at the benzodiazepine receptor.
The benzodiazepine receptor forms part of the GABAA receptor complex.
▪too much puts you to sleep.
▪ Benzodiazepine agonists increase sensitivity of the GABA binding
site ➔ anxiolytic effect, reduce anxiety by
▪ Benzodiazepine antagonists occupy the receptor thereby reducing sensitivity of GABA binding site ➔ anxiogenic effect. Increase anx.
▪ Treatment of flumazenil (a benzodiazepine antagonists) produces panic in patients with panic disorder, not controls (Nutt et al., 1990).
Suggests Anx, caused by dismissed benzo emperors in certain ppl.


Benzopdiazepines are ? And this is an issue to ocnsider


▪ Benziodiazepine is a psychoactive drug because it causes a change in perception, mood and consciousness.

▪ Long term use of benziodiazepine causes physical dependence.

Dose dependant too! I'd add


Benzodiazepines are also used to

treat the panic caused by hallucinogen intoxication.

▪ Benzodiazepines can also be prescribed as sleep-inducing, muscle relaxants, and sedatives.


Pharmacological Treatment: Serotonin
▪ Selective Serotonin Reuptake Inhibitors (SSRI’s) are very effective in treating panic attacks.

In anxiety, SSRI efficacy is related to the

5-HT1A receptor!

Demonstrated by a mouse elevated plus maze. Cross open exposes or not arms.

Mice with 4 weeks treatment of SSRI’s are more likely to enter an elevated, open, brightly lit arm to retrieve food (i.e. less anxious).
- the drug has no effect on mice with targeted mutation against 5-HT1A receptor (Santarelli et al., 2003).

In mice, turning off the 5-HT1A receptor gene in the
hippocampus and cerebral cortex during embryological development leads to anxious behaviour during adulthood.
- If the gene is turned off during adulthood, there is no effect on anxious behaviour.

Presence of serotonin could have different effects at different times during an animals life.


Obsessive-compulsive Disorder (OCD)

▪ OCD patients suffer from obsessive distressing, intrusive thoughts which they are eager to remove or neutralise with compulsive acts or rituals.

▪ Obsessions:
- Disgust with bodily waste
- fear that something terrible might happen
- need for symmetry, order and exactness
- perverse sexual thoughts, images, impulses

▪ Compulsions:
- excessive, ritualised hand washing, showering, bathing
- ordering, arranging, counting, hoarding
- checking stoves, burners, locks, windows
- miscellaneous rituals (licking, spitting, special dress


Possible aetiology of OCD

▪ Patients with OCD have tics and patients with Tourette’s syndrome show obsessions and compulsions. Perhaps same underlying genotype?

▪ OCD can occur after brain damage; symptoms are associated with damage/dysfunction of basal ganglia and prefrontal cortex.

▪ OCD is associated with increased activity in orbitofrontal cortex and caudate nucleus of the basal ganglia.

Group A β-hemolytic streptococcal infection can attack the tissue of the basal ganglia. Cause ocd


Cingulotomy as a treatment for OCD

▪ A cingulotomy is the surgical destruction of the cingulum bundle of fibres which connect limbic structures of the temporal lobe with the frontal lobe. Limits transmission presumably.

▪ Cingulotomy is considered the last resort in patients and used when conventional treatments fail to work. Used to be first.

▪ Adverse effects of surgery include problems in planning, behavioural inhibition and apathy.


Drug Therapy for OCD?

▪ Leonard et al (1989) compared the effects of chlomipramine (SSRI) with desipramine (SNRI).
▪ All patients received placebo for three weeks.
▪ For five weeks, half were treated with chlomipramine and the other half with desipramine (phase A).
▪ Treatments were then switched for another 5 weeks (phase B).

▪ Chlomipramine is more effective, overall the ssri


Serotonergic Activity Inhibits Compulsive Behaviours,
Control compulsions.

▪ Chlomipramine can successfully treat?

- Trichotillomania, compulsive hair pulling (and
sometimes eat them).

- Onychophagia, compulsive nail biting

- Acral lick dermitius in dogs is a compulsive tendency to lick parts of their body which which eventually erodes away the skin.


Symptoms of Autistic Disorder (I) social

▪ Failure to develop normal social relationships
▪ Self-absorbed
▪ Avoid eye contact; do not look at others, or smile
▪ Don’t want to be held or touched.
▪ Abnormal language development; they may echo what is said to them and refer to themselves in second or third person. E.g. “you want some milk” means I want some milk.
▪ May interpret others speech literally. E.g. when asked “Can you pass the salt?” ➔ “Yes.”


Reciew parental bonding Nd nesting in text, ch 13? Sex I think.

Aside history though parents to blame for autism, turns out child, as is biological.


Symptoms of Autistic Disorder (II) behavioural apart from social

▪ Show stereotyped movements, e,g., flapping hands or rocking back and forth.
▪ Become obsessed with investigating objects, sniffing, touching, moving them.
▪ Preoccupied with arranging objects or items in a pattern formation.
▪ Insist on following particular routines and become violently upset when prevented from doing so.
▪ Lack of imaginative ability
▪ Some have isolated skills (e.g. mathematical skills)savant/gifted

Lack of theory of mind


Theory of Mind (ToM) related to autism, and affective, cognitive and behaviours syndrome disorder.

▪ Theory of Mind (ToM) refers to the ability to attribute mental states, beliefs, intents, desires to oneself AND to understand that others have beliefs, desires and intentions that are different from one’s own.

▪ The impaired socialisation, communicative ability and imagination that characterise autistic behaviour may stem from brain abnormalities that prevent ToM (Frith et al., 1991).


Activation of specific brain regions of autistic adults viewing a ToM animation (Castelli et al., 2002).

▪ Autistics show normal activation of visual association cortex.
▪ Relative to controls, autistics show
significantly reduced activation of the right superior temporal sulcus and the right medial prefrontal cortex.


Ppl with autism Show No Activation of Fusiform Gyrus bc

▪ Fusiform face area of autistics fail to respond to human faces because autistics spend little time studying other people’s faces, not because of abnormalities in the the fusiform face area (Pierce et al., 2001). Lack of stim.


Eye Movements by Autistic People show us?

Subjects asked to identify emotions in faces.
Autistic people failed to look at the eyes, the region of the face that is most informative when making


Aetiology of Autism

Remem, no animal model of asd

- concordance rate for MZ twins in 70% but 5% for
DZ twins.
- non-autistic members of discordant MZ twins
exhibit deficient language development and show signs of social withdrawal.

▪ Brain pathology
- 20% of all cases of autism have definable biological causes(e.g.rubella,prenatal thalidomide, (sold pregnant women morning sickness) encephalitus).

- Abnormal development of prefrontal cortex, temporal lobe and cerebellum.


Attention-Deficit Hyperactivity Disorder (ADHD) (I)
▪ Symptoms of inattention, hyperactivity and impulsivity:

difficulty sustaining attention in tasks of play activities.
- easily distracted by extraneous stimuli.
- often run out or climb excessively when inappropriate.
- often interrupts or intrudes on others.


ADHD is associated with: correlates and epidemiology,

- aggression
- conduct disorder
- learning disabilities
- depression
- anxiety
- low self-esteem

▪ 60% of of ADHD children continue to display symptoms into adulthood.

▪ The most common drug therapy is methylphenidate (Ritalin) which inhibits the reuptake of dopamine.


Heritability of adhd? As demonstrated by

▪ There is strong evidence from family and twin studies that heritability factors play an important role.

▪ The stop signal task is a test that measures one’s ability to inhibit an action that has already been initiated.
- subjects are required to respond as quickly as possible when they see an “X” on the screen, but if they hear a tone they must withhold their response.
- people with ADHD are impaired in their ability to
inhibit an already initiated response.
- unaffected siblings show intermediate
performance between adhd children and controls

Therefore inhibitory response may have genetic basis.

Children with ADHD show a steep delay of reinforcement gradient
▪ In ADHD, immediate reinforcement is effective but even a slight delay effects its potency.


Credit card and adhd connection?

Children with ADHD show a steep delay of reinforcement gradient
▪ In ADHD, immediate reinforcement is effective but even a slight delay effects its potency.
tempo discounting.
Delay in gratification.


So they are instant gratifiers.


Delay of Reinforcement effects in ADHD children

▪ Normal and ADHD boys were trained on an instrumental conditioning task.

▪ When a signal was present, responses would be reinforced after 30 seconds with coins or trinkets.

▪ When a signal was not present responses were never reinforced.
➔ Normal boys waited patiently when a signal was not present.

➔ ADHD boys showed intermittent, burst of rapid responses whether the signal was present or not.


Stimulants as drug therapy for ADHD?

Methylphenidate, a dopamine agonist, alleviates symptoms of ADHD.
- Thus, ADHD related to reduced under activity of dopaminergic transmission.
BUT, mice with a reduction in dopamine transporters show abnormally high extracellular levels of dopamine in the brain leading to hyperactivity in novel environments (i.e., ADHD symptoms), which can be inhibited by amphetamine

Dopamine has a modulatory effect on behaviour.
So Ritalin does not work for all!

Baseline levels of dopa differ between ppl!
Inverted U
Like anx

But still wired to tread stim adhd with stim.