LECTURE_16_SLIDES

LECTURE_16_SLIDES - NPB12 Lecture 16 Bill Murray as Carl,...

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Unformatted text preview: NPB12 Lecture 16 Bill Murray as Carl, the assistant groundskeeper Conscious vs. Unconscious Right now we are fully conscious (sleep is different that either conscious or unconscious). You can become unconscious for a short time (e.g. during an epileptic seizure or after a blow to the head) and then you recover. You can become unconscious for a longer time, and that is when it gets tricky. The problem is that there is conscious, unconscious, and everything in between. Coma / Comatose State: A lack of arousal or purposeful motor response and reflects overwhelming functional impairment of brainstem arousal mechanisms. This can happen due to an injury, etc., and then potentially progress to either full recovery or one of the following: (Permanent) Vegetative state: This has periods of where your eyes are open, and you may have orienting responses. The person shows no signs of awareness of themselves or others. This can be particularly troubling and confusing to family members. After 30 days it is considered permanent , although there have been cases where the person comes out of it after much longer than that. Minimally conscious state: There are fluctuating periods when the person is clearly aware of themselves or others. Often this is a verbal or physical response to a question that shows that they understood what was asked. Cognitive disability: This is more commonly referred to as brain damage , where the person does not have the same cognitive abilities that they had before. paramedian mesodiencephalic structures (PMD) A small lesion here will result in a permanent vegetative state. These structures are near the brainstem areas that control pupil size. The basilar artery feeds the brainstem if you get a clot your brainstem will be paralyzed large-scale degeneration of the cerebral cortex will lead to a vegetative state / coma (Permanent) Vegetative state: T his is when the patient will have alternating eyes-open “awake” periods with eyesclosed “sleeping” periods. However, patients show no signs of an awareness of self or others or their environment. Where is the conscious part of the brain? Is it all conscious? Medial pre-frontal cortex (MPFC) Are you happy? vs Is happy the same as optimistic? You remember that happy was a word in the question better if it is about you, and your MPFC is activated. Girls develop this sooner than boys. Theory of Mind: Empathy and introspection. MPFC is activated when you think about how others are feeling. Do other animals have it as well? Mental Illness Historically, mental illness was not well understood. The inherent problem is in most cases a dysfunction of one or more neuromodulator systems. We know this because psychoactive drugs work by manipulating these neuromodulators. T he reason that we suspect the neuromodulators as the culprits in mental illnesses is that the most effective drug treatments in some way alter the patient's neuromodulator levels. You can bind to the dopamine receptor and make it think that dopamine bound to it. You can bind to the dopamine receptor and prevent dopamine from binding to it. You can block the reuptake mechanism. You can alter the action of monoamine oxydase. You can alter the activity of COMT. MAO and COMT are used in a number of different neuromodulator systems, so it is difficult to target only one (the one that is broken). nausea, diarrhea, and low blood pressure dizziness, drowsiness, dry mouth, rash, constipation, vision changes, difficulty urinating, involuntary movements, sore throat, pounding heart beat, unusual bruising or bleeding, mood changes, anxiety, panic attacks, trouble sleeping, irritability, agitation, aggressiveness, severe restlessness, mania thoughts of suicide or hurting yourself. Abdominal cramps, blurred vision, dry mouth, racing heartbeat / palpitations, shaking / slurred speech, urination problems, convulsions, hallucinations, memory loss, trouble breathing, staggering / trembling, headache, clumsiness, sleepiness or confusion. Schizophrenia ( Shattered Mind ) Clara Bow Peter Green Syd Barrett 1% of Americans Age of onset of symptoms usually late adolescence or early adulthood. Some genetic component, but no single schizophrenia gene . Incidence increases over the past few decades. Why? Schizophrenia Positive Symptoms: Hallucinations (usually auditory) Delusions (Grandeur and/or Persecution) Disorganized Speech Bizarre Behavior Schizophrenia: Means literally (in latin), "shattered mind". T here is no single set of symptoms, or apparent etiology, for schizophrenia, and thus it is considered a "disorder" rather than a "disease". Schizophrenia Negative Symptoms: Alogia: Poverty of speech (muteness) or speech that is empty of content. Affective flattening: The patient is unable to feel emotions that a normal person would, whether it be sadness, happiness, anger, etc. Avolition: The inability to initiate or persist in goal-directed behavior. Attentional Impairment Attentional impairment: The inability to focus and maintain attention on a particular task. T hese individuals are easily distracted, and in fact complain about all the "noise" that is around them that prevents them from accomplishing a particular goal. T his problem is closely associated with avolition. Dopamine Hypothesis Schizophrenics have too much dopamine in their cerebral cortex (temporal and frontal lobes). Treatments are usually drugs that block the dopamine receptor, decrease the release, or increase the re-uptake. Cocaine and amphetamines cause an increase in dopamine action, and lead to a similar (but different) problem: amphetamine induced psychosis. The NMDA receptor has also recently been implicated in schizophrenia, so perhaps it is the influence of both of these neurotransmitter systems that are at the root of the problem. Chronic treatment can lead to serous side effects. Tardive Dyskinesia Clozapine T hese are characterized by repeated, and usually bizarre, movements of the face and mouth that the patient cannot control. This is due, presumably, by a compensation of the dopamine neurons in the substantia nigra, and the dopamine- receiving neurons in the basal ganglion to make up for the reduction in dopamine. T his can be done by either an increase in the dopamine release, increase in the dopamine receptors, and/or increase in the intracellular response to the dopamine synapses in the basal ganglion cells 5% more likely to successfully commit suicide. 45-55% of schizophrenics attempt suicide at some point in their life. ...
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This note was uploaded on 12/01/2011 for the course NPB 72965 taught by Professor Recanzone during the Fall '11 term at UC Davis.

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