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Chapter 15

B64 - Chapter 15.docx

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Janelle Leboutillier

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Chapter 15 PSYB64 Chapter 15 Neurological Disorders Brain Damage  Soccer players perform worse on tests for attention, memory, and planning compared to swimmers and track athletes o Sortland and Tysvaer (1989) using CT found that 1/3 of former Norwegian national soccer members had cerebral atrophy. o Most likely the source of injury is from “heading” the ball. o It is reported that the greatest cognitive deficits occurred among players who headed the ball frequently.  Brain is protected by skull bones/meninges, cerebrospinal fluid (CSF), and blood-brain barrier. Damage can occur due to interruptions in the blood supply and head injuries. Stroke  Cells in nervous system (NS) rely on oxygen which is supplied by rich network of blood vessels o Circulation of blood to neural tissue can be ruptured/blocked and that can cause serious damage to brain  Stroke – type of brain damage caused by an interruption of blood supply to the brain by bleeding or blockage of blood vessel. o Risk factors of stroke – age, hypertension, smoking, diabetes, high cholesterol, obesity, alcohol use, cocaine, amphetamines, heroin, and other drugs o Atherosclerosis also increases risk of stroke when arteries are narrowed/hardened  Cerebral hemorrhage (Bleeding in the brain)– Condition caused by bleeding in the brain. o Generally results from hypertension (high blood pressure) or structural defects in arteries serving brain o Sometimes occur due to rupture of aneurysms –balloon-like bulge in walls of arteries o Can occur due to blood diseases such as leukemia or exposure to toxic chemicals. o Usually fatal because of brain damage produced by blocking blood supply to neurons and flooding areas of brain with salty blood that dehydrates and kills nearby neurons  Ischemia (low oxygen level) – Blockage of blood vessels result in ischemia. It is condition where inadequate blood flow results in insufficient quantities of oxygen being delivered to tissue. o Cases of Ischemia account for 80% of all strokes. o Can result in neural tissue death in an area called infarct – can causes changes in consciousness, sensation, ability to move (depends on their size and location) o Transient ischemic attacks (TIAs) – produces brief (less than 24 hours) episode of stroke symptoms that doesn’t cause permanent damage. They are strong predictors of subsequent strokes.  When an area of the brain is deprived of oxygen for a sufficient amount of time, cells begin to die. The area of dead tissue is referred to as an infarct.  Material causing blockage of a blood vessel can be classified as either a thrombosis or an embolism.  Thrombosis –A plug of blood or other material that blocks a blood vessel without from its point of origin.  Embolism – A plug that passes into smaller and smaller blood vessels until it forms a blockage. o Blockages in small blood vessels are less damaging than in large arteries serving the brain but multiple small strokes can cause significant damage.  Cells in middle layers of cortex and hippocampus are most vulnerable to ischemia. It isn’t only lack of oxygen that caused cell dead, there are other processes involved in brain damage caused by ischemia.  Excitotoxicity – coined by John Olney to describe ability of excess glutamate to kill neurons o Now believe that cell death after a stroke is caused by excess glutamate activity triggered by lack of oxygen o Excess glutamate in neuron initiates cascade of events leading to cell death o In response to unusual amounts of glutamate, abnormal calcium activity in the cell stimulates 4 ‘executioner’ enzymes that damage cell’s energy stores, membranes, cytostructure, and DNA Chapter 15 PSYB64  To reduce risk of stroke = surgery, reduce formation of thrombosis and emboli, as well as reducing blood pressure  Penumbra = areas of tissue surrounding an infarct. Although some cells die immediately following a stroke, medical attention can save many other neurons and glia in ischemic penumbra. Head Injuries  Traumatic brain injuries – result of physical damage to the brain o Usually caused by traffic accidents, gunshot wounds, falls  Divided into 2 categories: o Open head injuries – penetration of skull  Usually because of gunshot wound or fractures of skull where bone fragments can enter the brain  Most fatal when damage is caused in ventricles, both hemispheres, or multiple lobes in brain o Concussions/closed head injuries – occurs because of blows to the head or to the body that causes “impulsive” force transmitted to brain  Can be mild – no loss of consciousness or for only a brief time  Can be severe – coma  Can cause physical, behavioural, and cognitive problems that lasts for months or can be permanent  Concussions produce damage in several ways *Figure 15.4* o Coup – damage to brain where blow to the head occurs  Can cause damage by compression of the skull against neural tissue o Countercoup – damage to brain on the opposite side of blow because force of the blow pushes brain against the skull opposite the coup  Severe coup/countercoup can be have subdural hematoma = mass of clotted blood (like bruise) that forms between dura mater and arachnoid after head injury  White matter damage can occur due to twisting of the brain within the skull in response to blow  Pressure exerted on brain because of welling of injured tissues can cause damages or interruptions in normal function  Post-concussion syndrome (PCS) – set of symptoms that follow concussion for period of days to years – headaches, cognitive deficits, emotional changes, etc. It can occur in some but not all cases of concussions. o Cognitive deficits = lack of concentration, reduction in processing speed, deficits in higher-order cognitive functions (memory, attention) o Physical symptoms = headache o Emotional changes = depression, irritability, etc. o Persistence of PCS correlated with damage in brain structures such as white matter (corpus callosum and fornix) and gray matter = upper brainstem, base of frontal lobes, medial temporal lobes  Repeated mild head injuries like in athletes can still be damaging  Dementia pugilistica (Boxer’s syndrome)= severe form of chronic traumatic brain injury often seen in boxers due to repeated blows to the head over the course of their careers.  Chronic traumatic brain injury (CTBI) –type of brain damage caused by repeated concussions. o Associated with slurred speech, memory impairment, personality changes, lack of coordination, Parkinson’s-like syndrome o Shows similar patterns of degeneration like in Alzheimer’s o Boxer George Foreman is an example of a person who escaped CTBI. Boxers who carry the E4 variant of APOE are more likely to develop CTBI because it makes them more vulnerable to negative effects of brain injury. They found that boxers who had E4 variant and had participated in more than 12 professional bouts had greater neurological damage than those who didn’t carry E4. Chapter 15 PSYB64 Athletes and Post-Concussive Syndrome: When Is It Safe To Play?  American Academy of Neurology has provided a grading system coupled with recommendations for returning to play.  Grade 1 concussion – No loss of consciousness, concussion symptoms lasting less than 15 minutes – may return to play after 15 minutes without any symptoms.  Grade 2 concussion – No loss of consciousness, concussion symptoms lasting more than 15 minutes – the athlete should have one week without any symptoms prior to returning to play.  Grade 3 concussion – Loss of consciousness for any duration – if it lasts seconds then athlete may return to play after one week without symptoms. If loss of consciousness lasts minutes or more than two weeks must pass before the athlete returns to play  Colorado Medical Society and others do recommend termination of a season following Grade 3 concussion.  Brain Tumors  Tumours – independent growth of tissues that lacks purpose. Tumors are seen mostly in uterus (1) and brain (2). o Usually don’t grow from mature neurons because these cells don’t replicate o Most brain tumours arise from glial cells and cells from the meninges o Can form in cells lining ventricles  Malignant tumours – type of abnormal cell growth, lacking boundaries, that invades surrounding tissue and is very likely to recur after surgical removal  Metastasis – migration of cancerous cells from one part of the body to another o Malignant tumours shed cells that travel to other areas of body and form new tumours  Tumours that originate in brain rarely metastasize and when they do, the shed cells travel through CSF to other parts of NS (not through blood stream)  Benign tumours – abnormal cell growth that develops within their own membrane and is unlikely to recur after surgical removal (because they’re contained within own membrane) o Don’t metastasize but can still be harmful o If benign tumor is located in areas where it can’t be removed – it can be as life threatening as malignant tumours Symptoms of tumours:  Symptoms arise due to increased pressure within the skull once the tumors have attained sufficient size. o Symptoms are headache, vomiting, double vision, reduced heart rate, reduced alertness, seizures o Specific disruptions can also occur depending on tumor’s location (e.g. tumors in frontal lobe causes changes in emotionality and ability to plan or tumor of occipital lobe would affect vision) Types of tumours:  Identified according to tissue they arise from o Gliomas – tumours that arise from glial cells and account for 45% of brain tumours
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