NROSCI 1030Exam # 3 Study Guide Lectures: 15 - 21Lecture 15 (3/4): Attention Deficit/Hyperactivity Disorder (ADHD)General Characteristics- Inattention: kids don’t stick to tasks; problems organizing or completing tasks- Impulsiveness – not thinking before acting; often engaging in dangerous activities without concern for consequences- Hyperactivity – can’t remain seated; fidgeting even when sitting still- Age of onset – 50% of children have an onset before age 4, but they don’t recognize it as ADHD until they are in the classroom- The course of ADHD persists through childhood and even into adulthood- In adults, 57% often have other disorders, primary among them being drug use- Prevalence: like OCD, ADHD is a sliding scale, from mild to severe ADHD- 2-3 times more common in males than females- Concordance: monozygotic – 85%; dizygotic – 40%- Classic test for impulsivity: Continuous Performance Test (AX-CPT)Biology- ADHD is a deficit in inhibitory control – problems inhibiting a prepotent response- Patients having problems stopping an ongoing response – hyperactivity- Problems preventing interference by external stimuli – distractability- Prefrontal cortex is involved in developing executive control through inhibitory activity and in working memory; prefrontal cortex is involved in telling you to stop- It is also important to have subcortical system control on arousal and affect- In ADHD, you see normal prefrontal cortical activation despite of seeing deficits that looklike prefrontal in nature (unlike in schizophrenia, where you see deficits in prefrontal cortex)- You also see deficits in reward systems: kids with ADHD need larger, more frequent rewards- You also see an increase in CSF HVA, which is the primary DA metabolite – this increase is proportional to the Sx.; more the DA turnover, the worse the Sx- Systems thought to be involved: nucleus accumbens, prefrontal cortex, and hippocampus; all form a triangular circuit, working together to help you stay focused on a task and conduct goal-directed behavior- The prefrontal cortex is also important for suppressing inappropriate responses; it has a projection to the amygdala through inhibitory interneurons; sensory neurons alsoactivate the amygdala; the prefrontal cortex can suppress the sensory response onto theamygdala- In ADHD, the prefrontal cortex seems to be working normally- DA can act on presynaptic prefrontal input onto amygdala inhibitory interneurons, inhibiting prefrontal input onto amygdala and lack of prevention of sensory effects, thus causing susceptibility to hyperresponsiveness to sensory stimuliTreatments- Amphetamine: releases DA, NE, and 5-HT, both releasing and blocking reuptake- Methylphenidate-ritalin: pure uptake blocker; it is selective for NE and DA; when given intravenously, it causes worsening of ADHD Sx by amphetamine-induced hyperactivity due to increased DA turnover; thus, it is given orally at a rather low dose – it slowly increases extracellular DA, which hits autoreceptors and decreases DA responsivity; Ritalin blocks reuptake and directs DA to attach to autoreceptors, causing a decrease in DA effects, thus improving ADHD Sx; you don’t develop tolerance, as it is due to changes in autoreceptor regulation rather than effects on postsynaptic receptors, which can cause tolerance- Drug effects: Decreased interrupting, forgetfulness, fidgeting, CPT scores normalize- Side effects: difficulty taking in food; Ritalin has high potential for abuse- Ritalin has effects on rate dependency: it normalizes everybody; it brings hypoactivity to normal activity and hyperactivity back down to normal activity; it normalizes even the borderline cases- New Tx: atomoxetine (Strattera) – selective NE uptake inhibitor; unlike Ritalin, one dose of this drug works for the whole day rather than having to take repeated doses of Ritalin;it increases NE and DA in prefrontal cortex; when DA is released in prefrontal cortex, instead of being taken back up into the DA terminals, it diffuses and is taken up into NE terminals; the system is fixed by boosting the prefrontal cortex rather than decreasing DA transmission (this is just a hypothesis of how this drug works)Lecture 16 (3/6): AnxietyGeneral Characteristics- Anxiety is fearful anticipation; it is an adaptive response to stress and motivation to prevent reckless behavior- Hysteria: somatic complaint without a biological basis; this has also been called conversion symptoms, where one converts a psychological stressor to a body function- Psychosomatic – this is where the psyche changes the body- Usually, it is not the stressor itself, but like the control of the excitability caused by the stressor- State anxiety – you feel anxious right now (like panic disorder)- Trait anxiety – always anxious (like the generalized anxiety disorder)DSM Categories of Anxiety- Generalized anxiety disorder: people that are hyperresponsive to stressors all the time; phobias- Simple phobias: irrational fear of a normally non-threatening object; ex. arachnophobia- Social phobias: people avoid groups or social situations- Agoraphobia – fear of being alone in public places- Post Traumatic Stress Disorder (PTSD) - described first in the civil war as a soldiers disease, where repeated exposure to environments with guns and such leads to a situation where patients are hyperresponsive to stressors; with extreme stress, you havea build up of CRF, which causes LC to be hyperresponsive to stressors, causing a larger response- Panic disorder – people have this fear of losing control and behaving in a weird manner; associated with somatic displacement – SOB, palpitations, etc.Panic Disorder- Serious anxiety disorder; also known as “Anxiety Neurosis”; chronic illness; you have recurrent, acute, anxiety attacks that have a definite onset and spontaneous termination- Autonomic signs – palpitations, rapid/shallow breathing, dizziness, tremor; between the attacks, people are pretty much normal; this is different from ordinary fear as it does notinvolve a precipitating factor – it is thus often called “free-floating anxiety”- People with panic disorder also show more responsiveness to pain and low exercise tolerance; strong buildup of lactic acid with low levels of exercise – exercise can lead to apanic attack- Epidemiology: most common of the serious anxiety disorders;