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Carleton (18,205)
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PSYC 2800 (18)
Lecture

Lecture 3b.docx

10 Pages
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Department
Psychology
Course Code
PSYC 2800
Professor
Amanda Helleman

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Description
Lecture 3b *final+ Stroke • Risk factors: Age • Stroke: An interruption of blood flow either from the blockage of a blood vessel or from bleeding of a vessel • Ischemia – Lack of blood to the brain as a result of stroke. Blood important to nourish brain. – Sets off a cascade of cellular events that cause the real damage to the initial site (where blood vessels feeding onto) and surrounding areas – Change gene expression, protein expression, inflammation, lot of recovery early on • Diaschisis – Neural shock that follows brain damage in which areas connected to the site of damage show temporary arrest of function – Not initial stroke region but associated regions? – Stroke - Treatment • Administer anti-clot drugs – E.g., t-PA (tissue plasminogen activator) – Prevent further incidents of stroke – Must be administered within 3 h of stroke! So need to get to hospital right away. • Neuroprotectants – Drug used to try to block the cascade of post stroke neural events – No good ones available yet • Behavioral therapies (e.g., speech or physical) are often used to facilitate plastic changes in the brain following a stroke • Force bad side of body into use Epilepsy • Recurrent seizures accompanied by loss of consciousness • Symptomatic Seizure – Identified with a specific cause, such as infection, trauma, tumor, vascular formation, toxic chemicals, very high fever, or other neurological disorders • Idiopathic Seizure – Appears spontaneously and in the absence of other diseases of the central nervous system – A variety of factors may precipitate a seizure: Stress, fatigue, alcohol – Epilepsy • Three common symptoms of seizures – An aura, or warning of impending seizure – a sensation (odor – “burnt toast” or noise) or a “feeling”. Feel like something is off. – Dogs trained to detect these aura’s, even before person does and guides person to safe place – Loss of consciousness often followed by a period of amnesia that can include the seizure itself – A motor component that can vary in severity from shaking to automatic movements such as hand-rubbing or chewing Two Types of Epileptic Seizures 1. Focal Seizure – Category of seizure that begins locally (at a focus) and then spreads out to adjacent areas – Start focused area of brain (somatosensory motor areas) – “Jacksonian march”: Seizure is neuron firing randomly without input. Start one part then spreads out • Complex Partial Seizure – Type of focal seizure – Originate mostly in the temporal lobe – Not necessarily accompanied by loss of consciousness – Characterized by: • Subjective experiences that presage the attack (e.g., hallucinations so visual cortex firing to produce image not thee) • Automatisms or repetitive stereotyped movements (e.g., lip smacking • Postural changes (e.g., catatonic or frozen posture) 2. Generalized Seizures • Lack focal onset; occur on both sides of the body. Focal start on one hemisphere. – Grand mal Seizure (big bad) • Characterized by loss of consciousness and stereotyped motor activity; 3 stages: – tonic stage: body stiffens and breathing stops – clonic stage: rhythmic shaking – Postictal depression: post seizure state of confusion, can see brain wave activity changed on a EEG – Petit mal Seizure • Of brief duration, characterized by loss of awareness with no motor activity except for blinking, turning the head, or rolling the eyes • Common in children • Past interpreted in possession by devil Epilepsy: Treatment • Anticonvulsant medications – Examples: diphenylhydantoin or phenobarbital. Lower activity of CNS (seizure thought to be over excitation of CNS). GABA is main inhibitor. – Work by stabilizing the neuronal membrane, especially inhibitory neurons • Surgical removal of the abnormal tissue that is the focus of the seizures is sometimes performed in severe cases, can affect circuitry of brain (ex: HM) Multiple Sclerosis • Disease characterized by a loss of myelin, largely in the motor tracts but also sensory nerves • Relapses and remissions (not symptomatic) are common, can also have chronic MS • Brain imaging reveals discrete lesions, showing areas of damage • Cause is unknown, but proposed causes include: bacterial infection, a virus, environmental factors (e.g., pesticides), and an immune response of the central nervous system (most accepted, auto immune disorder) • Body sees myelin as invader and breaks it down. Drugs targeted to slow down immune system to slow down this breakdown. Dementia • Acquired and persistent syndrome of intellectual impairment • Diagnostic features (according to DSM): – Memory and other cognitive deficits and – Impairment in social and occupational functioning • Two broad categories: – Non-degenerative dementias are a heterogeneous group of disorders with diverse etiologies. Not caused by degenerative causes • E.g., vascular dementia (some blood vessels/ arteries not working), Korsakoffs – Degenerative dementias are presumed to have a degree of genetic transmission • E.g., Parkinson's, Alzheimer's, Huntington's . Usually don’t show symptoms until 70% of neurons have dies off. Parkinson’s Disease • Related to the degeneration of the substantia nigra (pathway involved in motor control) and to the loss of the neurotransmitter dopamine • Despite a common site of damage, symptoms vary enormously among people • More than 1 way to get Parkinsons • Many symptoms resemble the changes in motor activity that take place as a normal consequence of aging • Positive (increased incidence, symptoms that appear) Symptoms – Tremor at rest – Muscular rigidity (increased muscle tone) – Involuntary movements • Akathesia : Small, involuntary movements or changes in posture; motor restlessness • Occulogyric crisis: involuntary turns of the head and eyes to one side. Problems with vision. – Negative Symptoms (loss of behaviors) – Disorders of postures(fixation and equilibrium) – Disorders of righting(e.g., standing up) – Disorders of locomotion • Festination : tendency to engage in a behavior, such as walking, at faster and faster speeds – Speech disturbances (e.g., prosity 9tone of voice)) – Akinesia (poverty or slowness of movement Parkinson’s Disease: Causes • Loss of cells in the substantia nigra, which may be caused by diseases such as encephalitis, syphillis, drugs (e.g., MPTP), or unknown causes – Environmental pollutants? Insecticides? – Increasing incidence among individuals <40…suggests environmental toxins Parkinson’s Disease: Treatment • Behavioral therapy – Example: physical therapy is often helpful but limited success • Pharmacological – Increase levels of dopamine (e.g., dopamine agonists such as L-dopa drug) – Suppress the activity of structures that show heightened activity in the absence of adequate dopamine action (e.g., anticholinergic drugs). • Surgical – Electrical stimulation or lesioning of the internal global pallidus reduces rigidity and tremor – Basal ganglia important in movement • Transplantation – Transplant embryonic dopamine-producing cells or multipotential stem cells into the basal ganglia – Highly experimental, limited success Alzheimer’s Disease • Approximately
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