ch 10 cont'd.
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Date Created: 11/15/15
Antipsychotics 11/18/2015 ▯ Before antipsychotics existed The history of schizophrenia treatment was dismal Patients lived in huge mental hospitals, often permanently Treatments included o Isolation o Restraint o Shock treatment Inducing seizures via administration of insulin or using electrical current o Surgeries such as frontal lobotomies ▯ Introduction of antipsychotic drugs Before the advent of psychopharmacological agents, schizophrenia and affective disorders accounted for more than half of all hospital admissions in the US In the 1950s, the serendipitous discovery of the antipsychotic effects of chlorpromazine (thorazine) revolutionized the treatment of schizophrenia This drug was initially used before surgeries to calm the patient and reduce awareness of external stimuli When tried in schizophrenic patients, it was shown to calm excited ones and activate withdrawn ones ▯ Efficacy of schizophrenia treatment The law of thirds o One third of patients treated with antipsychotics will have significant symptom reduction as a result of the drugs May not need later hospitalization Few residual signs of schizophrenia Are able to be employed, have a family, have a social life, etc. o Another third show improvements in symptoms but may have relapses from time to time May need re-hospitalization Can hold a job but at a reduced occupational level May be socially isolated o The other third do not respond well to antipsychotic drugs and will be hospitalized more Often unemployed Have few social relationships About 30% of the homeless population in the US suffer from un-or-poorly-treated psychosis ▯ Drugs used to treat schizophrenia These drugs are known as antipsychotics An older term is neuroleptics o Traditional neuroleptics These are typically effective in reducing the positive symptoms of schizophrenia, but not the negative or cognitive ones Many of these have significant side effects relating to problems in movement E.g. thorazine, Haldol o Second generation (atypical) antipsychotics These are defined as drugs that reduce the positive symptoms of schizophrenia but do not have the movement related side effects of the traditional neuroleptics E.g. clorazil, risperidal, abilify None of these types of drugs are consistently more effective than the others and their desired and side effects differ by person ▯ Effects of antipsychotic drugs A few doses will reduce hyperactive and manic symptoms A few weeks of treatment will reduce positive symptoms of schizophrenia including delusions, hallucinations, and disordered thinking Most antipsychotic drugs are less successful in treating the negative and cognitive symptoms of schizophrenia After a patient’s initial recovery, antipsychotic drugs are typically prescribed as maintenance therapy (usually indefinitely) to prevent relapse However, side effects can be severe, so many people stop taking the antipsychotic drugs and this frequently leads to relapse ▯ How do antipsychotic drugs work? Antipsychotic drugs can modify multiple neurotransmitter systems o Their clinical effectiveness is best correlated with their ability to reduce dopamine signaling o This can occur in 2 ways Blocking dopamine receptors Inhibiting dopamine release Older and second generation antipsychotics block D2 dopamine receptors o They also block other neurotransmitter receptors (e.g. serotonin, histamine, noradrenergic, D1 dopamine) but the blocking of these other receptors is not correlated with drug efficacy D2 dopamine receptors are inhibitory ▯ Two locations for D2 dopamine receptors The D2 autoreceptor reduces the amount of dopamine produced Presynaptic D2 autoreceptors o Because these receptors are on the same cell (a dopaminergic cell) that is releasing the neurotransmitter (dopamine) that activates them, they are known as autoreceptors o When dopamine binds to D2 autoreceptors on a presynaptic dopamine neuron, decreases the excitability of the neuron and decreases its release of dopamine Postsynaptic D2 receptors (in the synaptic cleft) o Reduce the excitability of the neuron ▯ Tolerance, dependence, addiction, overdose Antipsychotic drugs rarely lead to/have o Tolerance for antipsychotic effects (but there can be tolerance for some side effects such as sedation) o Physical dependence o Abuse potential (do not produce euphoria and have unpleasant side effects) o Overdose Antipsychotics have a very high therapeutic index so do not typically cause overdose ▯ Side effects of antipsychotics Older and second generation antipsychotics all have significant side effects Often patients will stop taking the drug(s) they have been prescribed and suffer relapses Many antipsychotics can cause sedation but this can be good for some patients and bad for others Three categories of side effects o Parkinsonism (also known as extrapyramidal side effects: the pyramids contain neurons that cause movement) Movement disorders that resemble symptoms of parkinson’s disease Includes tremors, slowing or loss of voluntary movement, muscle rigidity, discomfort in legs, inability to sit Due to blockade of dopamine receptors in the basal ganglia Reducing acetylcholine with anticholinergic drugs can help Less common with second generation drugs o Tardive dyskinesia A movement disorder that is associated with prolonged use of antipsychotic drugs Causes repeated involuntary movements, especially in the face and jaw, but can also be in the limbs Occurs in 10-20% of patients treated with neuroleptics These movements can be permanent Less common with second generation drugs o Neuroendocrine effects The endocrine system releases hormones in the body Neuroendocrine refers to interactions between the endocrine and nervous systems Blocking dopamine receptors can alter function of the neuroendocrine system Side effects include Breast enlargement Decreased sex drive Lack of menstruation Weight gain Also, reduced growth hormones which is an issue when children and adolescents are given these drugs ▯ Off label use of antipsychotic drugs Risperdal o “Johnson and Johnson has agreed to pay more than $2.2 billion in criminal and civil fines to settle accusations that it improperly promoted the antipsychotic drug Risperdal to older adults, children, and people with developmental disabilities” – NY Times, November 4 2013 ▯ How might antipsychotic drugs be improved? Selective D2 dopamine receptor antagonists o Three strategies for developing improved antipsychotic drugs Creation of Selective D2 dopamine receptor antagonists Dopamine system stabilizers Broad spectrum antipsychotics o Strategy 1: selective D2 dopamine receptor antagonists Bind mostly to D2 receptors Effects on the autonomic nervous system are minimal Sedation is mild Hormonal side effects are common Dopamine system stabilizers o Strategy 2: dopamine system stabilizers These are fairly new and include abilify Abilify is a partial agonist of dopamine receptors This means it binds readily to dopamine receptors but does not cause as much of an effect as dopamine itself would This reduces positive symptoms of schizophrenia Additionally, abilify can also activate dopamine receptors in areas of the brain where there is too little dopamine, which may reduce the negative symptoms of schizophrenia Very few side effects Borad spectrum antipsychotics o These drugs block multiple types of receptors in addition to the D2 dopamine receptors o The most well known of this type is clozapine which affects D1, D2, D4, serotonin, muscarinic, and histaminergic receptors Clozapine is not more effective than other antipsychotics It is useful in some treatment resistant patients (patients who have not had symptom reduction with other antipsychotics) It can reduce negative and cognitive symptoms of schizophrenia It causes few motor side effects (parkinsonism and tardive dyskinesia) It has many serious side effects so it is rarely used ▯ ▯ Social Cognitive cont’d. 12/01/2015 ▯ Motives Self enhancement motive: biased toward positive view of the self o Based on liking to see ourselves the same day to day o Establish and maintain a positive self image People tend to prefer positive feedback o Tend to overestimate our own positive attributes o There is evidence that we enhance our own self image by comparing ourselves to others that aren’t doing as well as we are Self verification motive: experience self as consistent and predictable o Bias toward seeing ourselves the same day to say o Would rather get negative feedback when we have negative self views o Seek out relationships with other people based on how we see ourselves ▯ Goals Organized in a system and hierarchically Vary by o Challenge People who have higher levels of self efficacy choose more challenging goals o Proximity: proximal and distal Hoe close are they vs how far away Ability to envision the future enables us to be able to set goals Directs our behavior Subjective meaning What meaning do they have to us Social cognitive theorists: learning goals/performance goals ▯ Goals are central to motivation Learning goals: think about the task and all you can learn from it (choosing these goals because we want to do them; what can it do for me) Performance goals: aim to o Show people how smart you are o Avoid embarrassment when you don’t know something o Make a good impression ▯ Evaluative standards Personal standards: fundamental to motivation and performance o Self evaluative reactions (emotional) o Subjective standards vary from person to person ▯ Higgins (1987, 1996) Ideal and ought standards (ought- should, ideal-most beneficial) Actual and ideal self o Discrepancies lead to sadness o We are not how we would ideally like to be Actual and ought self o Discrepancies lead to anxiety o We are not doing what we think we should be doing ▯ Bandura Reciprocal determinism o Person influences behavior and environment o Behavior influences person and environment o Environment influences person and behavior o Cause is a 2 way street ▯ Mischel and Shoda Cognitive affective processing system (CAPS) o Cognitive and emotional linked Personalities should be thought of as a system Thoughts influence feelings and feelings influence thoughts o Situational features Acknowledge situation in the environment Different personality aspects are activated Behave differently in different situations o Situational features lead to variable behaviors ▯ If… then… profiles Mischel: o Behavioral signatures Stable profiles of engaging in specific behaviors Ties into CAPS because of cognitive and affective linkage o Cognitive affective processing system (CAPS) o We haven’t developed a profile for a situation we haven’t been in before ▯ Modeling (Bandura) Desired activities demonstrated by models who experience positive consequences Complex behaviors broken down Effect of modeling can be affected by how good the outcome is You don’t need consequences to learn from modeling but they have an effect if put into effect ▯ Observational learning Model and modeling o Internal mental representation made by observer o Should I do this behavior? Acquisition (learning a behavior in the absence of a reward) Performance (we can take in how to do something but that does not mean that we are going to do it) ▯ Bandura, Ross, and Ross 1963 Bobo doll experiment: aggressive behavior by model in 3 conditions o 1. No consequences o 2. Reward o 3. Punishment Then the conditions are further divided to no incentive or positive incentive conditions Adult model beats up Bobo doll, would children copy the model? Yes Adult beats up Bobo and either gets punished, rewarded, or nothing happens o Children who watched punishment did not act aggressively ▯ Vicarious conditioning Observing a model with an emotional component to it Process of learning emotional reactions through observing others Tend to generalize ▯ Self regulation Capacity to motivate oneself o Set goals o Plan strategies o Evaluate and modify behavior ▯ Cervone and Bandura 1983 Subjects performed strenuous activity 4 groups and 4 different conditions o Goals and feedback Highest percent increase in effortful performance o Goals o Feedback o Control Lowest percent increase in effortful performance ▯ Mischel’s paradigm: the marshmallow test Self regulation can be getting yourself to do something, getting yourself to stop doing something, or not doing something at all Had toddlers in a lab setting and put a plate of marshmallows in front o If you can wait 10 minutes without eating one, you can have them all o If you can’t wait any longer, ring the bell and I will come back o The kids that could wait mostly distracted themselves ▯ Stress When one views circumstances as taxing or exceeding resources and endangering well being ▯ Lazarus and Folkman Primary appraisal: is something at stake? Is there a threat or danger? o Acknowledge something is wrong Secondary appraisal: what, if anything, can be done? o Figure out what to do about the problem Stress and coping o Problem focused coping: attempts to cope by altering features of a stressful situation o Emotion focused coping: attempts to improve internal emotional state Some coping methods are influenced by personality factors o Many coping methods are strongly influenced by situational context The greater level of stress and efforts to cope, the poorer the physical health and greater the likelihood and psychological symptoms The greater the sense of mastery, the better physical and psychological health Planful problem solving more adaptive than escape avoidance or confrontative coping ▯ Stress inoculation Meichenbaum 1995 o Relaxation training o Cognitive restructuring strategies o Problem solving strategies ▯ ▯ Huntington’s disease and neurotoxicants 12/02/2015 ▯ HD A neurodegenerative disease that affects movement and cognitive function Unlike other nervous system diseases, there is a clear genetic cause for HD o Called a trinucleotide repeat o This is a mutation in the Huntingtin gene that makes it interfere with how neurons work o The Huntingtin gene is normally involved in a number of intracellular functions so, because it does not work well, these functions don’t happen o If someone has the huntingtin, they are highly likely to develop huntington’s disease o Age of onset varies from 4 to 65 years but is typically in middle age o Lethal in 10-15 years due to pneumonia, falls, inability to swallow ▯ Prevalence In 2012 o Europe, north America, Australia 5.7 cases per 100,000 people o Asia .4 cases per 100,000 people ▯ Symptoms Movement related symptoms o Inability to suppress unwanted movement (somewhat opposite to Parkinson’s disease) o Movements are jerky or writhing o Speed and coordination of fine movements are also compromised o Rigid muscles o Problems with gait Cognitive functions o Problems with planning and organizing o Thoughts and behaviors are repeated over and over o Problems with learning, memory, attention, language o Eventually will lead to dementia Personality changes o Can have irritability, impulsivity, and anxiety ▯ HD involves damage to the basal ganglia The basal ganglia are involved in initiating movement and initiating cognitive and emotional processes o Damage is due to proteins, including the huntingtin gene, accumulating in neurons, primarily in the basal ganglia and the neocortex o This leads to death of these neurons Cerebral cortex also is affected in HD ▯ Treatments Only symptomatic treatments are available o No treatments slow or stop the disease o The only FDA approved drug available is xenazine which decreases monoamine vesicle packaging o Side effects include psychiatric symptoms (frequently depression), parkinsonism, and sedation Other drugs that can be used include o Dopamine antagonists (e.g. those used to treat schizophrenia) will suppress movements o Anti seizure drugs and anxiolytic drugs reduce movements and muscle rigidity o Antidepressants and/or antipsychotics and/or mood stabilizers are used to treat the psychiatric symptoms of HD ▯ Neurotoxicity Neurotoxicant: an element or compound that damages the central or peripheral nervous system Categories of neurotoxicants o Organic pollutants o Insecticides o Toxic metals Neurotoxic effects can be transient or permanent and can occur as soon as exposure to a neurotoxicant occurs or up to years afterward In what ways is toxicity to the brain different from that in other organs? o The nervous system is incompletely developed in children and before birth o Other than in a few specific brain areas, no new neurons can grow after birth so neurons that die cannot be replaced ▯ Persistent organic pollutants Synthetic organic compounds that are resistant to environmental degradation Characteristics o Low water solubility o High lipid solubility o Large molecule sizes o There molecules accumulate in fatty tissues in the body and become higher in concentration higher on the food chain o They are highly concentrated in larger animals o E.g. DDT, PCBs ▯ PCBs Polychlorinated biphenyls: synthetic molecules containing the element chlorine that were used in industrial and consumer products PCB production was banned in the late 1970s but they still exist as contaminants Methods of exposure in general population o Ingestion of contaminated foods (including across the placenta) o Measurable levels are found in low concentrations in a majority of the US population o Longest half lives: about 10-15 years Acute effects in adults may include o Movement and sensory related problems o Can occur 2-4 years after exposure Long term exposure in adults o Impaired learning and memory Neurotoxic effects o In utero exposure to PCBs can cause Delayed cognitive development Behavioral problems Slow growth o PCBs can lead to death of neurons via Alteration of cell membranes Changes in calcium dependent systems (including neurotransmitter release) Alterations in dopamine signaling (including reduced production of dopamine, inhibition of the dopamine transporter) ▯ PBDEs Polybrominated diphenyl ethers o Organic molecules containing the element bromine o Used as flame retardants (e.g. in plastics, electronics, polyurethane foams) o Some PBDEs have been banned in the US and EU Methods of exposure in general population o Ingestion through food and house dust o Found in high levels in breast milk o Half lives in humans: days to years Neurotoxic effects of PBDEs o Adults: little information is available In the developing nervous system, it is not clear what the specific effects are but there is concern because o PBDEs can cross the placenta o Animal studies suggest PBDEs cause impairments in movement, learning, memory, and hyperactivity How do PBDEs cause neuronal damage? o PBDEs affect the endocrine (hormone) system o PBDEs can lead to death of neurons via Alterations in chemical processes within neurons Changes in enzyme function ▯ BPA Bisphenyl A o Synthetic molecule used mainly in the production of plastics (e.g. those found in toys, CDs, paints, food and beverage containers, dental sealants, flooring) Methods of exposure in general population o Ingestion from food and water o About 92% of the US population has a detectable level of BPA Neurotoxic effects of BPA o Animal studies show Increased anxiety Cognitive deficits Changes in dopaminergic and NMDA systems How does BPA cause neuronal damage? o BPA affects the endocrine system, especially in that it mimics estrogen and otherwise affects estrogen levels ▯ Insecticides Methods of exposure in general population o Food, water, home and garden products Two categories o Organophosphates (OPs) o Pyrethrins/pyrethroids ▯ Ops Organophosphate insecticides o Contain the element phosphorus bound to other atoms o Can be absorbed through the skin, mouth, or lungs How do Ops cause neuronal damage? o Ops inactive the enzyme acetylcholinesterase (AChE) o The normal function of AChE is to degrade the neurotransmitter acetylcholine o When AChE is blocked by Ops, this causes over stimulation of central and peripheral Ach receptors leading to “cholinergic syndrome” Neurotoxic effects in adults o Acute OP poisoning occurs within minutes to hours after exposure o If the inhibition of ACE is irreversible, prolonged effects can occur including Partial respiratory paralysis Muscle weakness Death o Delayed effects can include Degeneration of axons which mainly causes muscle weakness, numbness/pins and needles feelings, paralysis of limbs o The neurotoxic effects in the developing nervous system have been difficult to determine but animal studies suggest that they cause problems with synaptic development and reductions in numbers of brain cells ▯ Pyrethrin/pyrethroid Derived from chrysanthemum plants Are readily degraded in the atmosphere, soil, and water so do not persist in the environment for more than days to weeks Can accumulate in aquatic organisms and are toxic to fish Do not accumulate in humans because they are readily metabolized Methods of exposure in general population o Food, especially fruits and vegetables o Household insecticides, pet shampoos, lice treatments o Exposure can occur via ingestion or through the skin Neurotoxic effects in adults o Dizziness, headache, fatigue o If severe, can be life threatening (coma and convulsions) o These effects are most commonly seen with occupational exposure o The neurotoxic effects in the developing nervous system have been difficult to determine How do they cause neuronal damage? o Disruption of voltage gated Na+ channels The net result is that more Na+ enters the neurons and depolarizes them This can either cause more action potentials (rapidly repeated) or so much depolarization that the neurons can’t generate action potentials o Blockade of GABA receptors ▯ Toxic metals These include lead, mercury, arsenic (also called heavy metals) Lead toxicity o Lead is a naturally occurring element (chemical symbol: Pb) o Used in paints, gasoline, pipes, solders, batteries, cosmetics, ammunition o Methods of exposure in general population In the US, most lead exposure is though old lead paint, lead crystal, contaminated soil or drinking water o Lead absorption through the gut In adults: 3-10% In children: 30-50% Lead will then be contained in red blood cells and in bone Half life in blood: 1 month Half life in bone: 20-30 years o Acute, high dose exposure causes Altered mental state, seizures, coma, problems with movement o Chronic exposure causes Forgetfulness, irritability, muscle weakness, hyperactivity, aggression, loss of neurons in the periphery o How does lead cause neuronal damage? Main effect Substitution for calcium and disruption in calcium homeostasis Lead does not cross the blood brain barrier in adults but may do so in children o In the developing nervous system Effects of acute exposure are similar to those of adults but at lower doses Long term exposure causes Impaired cognitive function Attention deficits Hyperactivity Violence Increased risk of ADHD Reduced IQ o Changes in neurons and neuroanatomy caused by lead Cell death Myelination Reduced brain volume in the prefrontal region Neurotransmitter release/synaptic transmission Levels of neurotransmitters Neurotransmitter receptors ▯ Mercury Naturally occurring element (chemical symbol: Hg) Also known as quick silver because it is a shiny silver colored metal and is liquid at room temperature Mercury enters the environment as a vapor via o Volcanoes o Mining ore deposits o Incineration of waste o Coal burning power plants Mercury is used in o Fluorescent light bulbs o Laptop monitors o Cell phones o Printed circuit boards Methods of exposure in general population o Consumption of fish and shellfish o Mercury accumulates in biological tissues because it is lipid soluble o It then accumulates through the food chain and is found in fish and shellfish humans eat o Does not cross the placenta o Gets into infants via breast milk and infants are unable to eliminate it Acute poisoning in adults causes o Uncoordinated movements o Blindness o Impaired gait o Tremors o Symptoms may not be present for weeks to months after exposure Chronic poisoning in adults causes o Pins and needles feelings of hands and feet o Uncoordinated movements o Muscle weakness o Mood swings o Memory loss o Impairment of speech, seeing, and hearing Effects on the brain o Damage and death of neurons in the cerebral cortex (particularly the visual system) and the cerebellum How does mercury damage the brain? o Affects neurotransmitter receptors o Neurons are highly susceptible, especially motor neurons o Mercury accumulates in the brain and, in some chemical forms, the half life can be years ▯ ▯
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