Assignment 5-2 1 Walter L Graboski 11/23/08 Cognitive Abilities Biopsychology Professor Kathyrne Mueller
Assignment 5-2 2 Some psychologists attempt to define brain damage as some loss of tissue accompaniedby a noticeable loss of function. However, human beings tend to lose some degree of brain tissueas they age and experience an accompanying loss of function. Brain damage can result from avariety of factors including genetic problems, toxins, infections, physical trauma, anoxia,nutritional deficiencies, tumors, and cerebrovascular accidents. There are six causes of brain damage: brain tumors, cerbrovascular disorders, closed headinjuries, infections of the brain, neurotoxins, and genetic factors, (Pinel, 2008,). Therefore, hisphysician should explain to him that it is not necessary for the skull to be penetrated for the brainto be seriously damaged. In fact, any blow to the head should be treated with extreme caution,particularly when confusion, sensor motor disturbances, or loss of consciousness ensues, (Pinel,2008,). Brain injuries produced by blows that do not penetrate the skull are called close headinjuries, (Pinel, 2008,). So in Gregg’s case, when there is a disturbance of consciousnessfollowing a blow to the head and there is no evidence of a contusion or other structural damage,the diagnosis is a concussion, (Pinel, 2008,). It is commonly assumed that concussions entails atemporary disruption of normal cerebral function with no long term damage, (Pinel, 2008,).However, the punch drunk syndrome is dementia (general intellectual deterioration ) andcerebral scarring that is observed in boxers and other individuals who experience repeatedconcussions. If there were no damage associated with a single concussion, the effects of manyconcussions could not summate to produce damage, (McCrory & Berkovic, 1998, cited Pinel,2008,). Where as contusions are closed head injuries that involve damage to the cerebralcirculatory system. Such damage produces internal hemorrhaging, which results in a hematoma.A hematoma is a localized collection of clotted blood in an organ or tissue- in another words, abruise, (Pinel, 2008,). It is paradoxical that the very hardness of the skull which protects the brain
Assignment 5-2 3from penetrating injuries, is the major factor in the development of contusions. Contusions fromclosed head injuries occur when the brain slams against the inside of the skull. Contusionsfrequently occur on the side of the brain opposite the side struck by blow. The reason for such socalled contrecoup injuries is that the blow causes the brain to strike the inside of the skull on theother side of the head, (Pinel, 2008,). Therefore, this is the reason why Gregg’s recovery ispossible because there was no long term affect, it was a concussion. Ischemia-induced brain damage has three important properties (Krieglestien, 1997,).First, it takes a while to develop. Soon after a temporary cerebral ischemic episodesay, one tenminutes in duration, there usually is little or no evidence of brain damage; however, substantialneuron loss can often be detected a day or two later. Second, ischemia induced brain damagedoes not occur equally in all parts of the brain; particularly susceptible are neurons in certainareas of hippocampus, (Ohtaki etal, 2003,). Third, the mechanisms of ischemia induced damagevary somewhat from structure within the brain, and in at least some areas, astrocytes have beenimplicated, (Pinel, 2008) Gregg’s symptoms may recede or enhance in the following: First, causes of brain damageinclude the following: Toxins: Toxins are substances that can poison healthy tissues. Based onthe circumstances, any substance can be a potential poison. Even substances such as water andoxygen can be harmful if these are absorbed in excessive amounts. Excessive drinking of watercan cause water poisoning — a problem common among distance runners. Physical Trauma: It isobvious that physical trauma to the head can also damage the brain. Such injuries are calledtraumatic brain injuries (TBIs) and are often categorized as either closed head injuries orpenetrating head injuries. If a person is hit on the head and there is no external wound or externalbleeding, but internal damage to the brain, this would be an example of a closed head injury.
Assignment 5-2 4Closed head injuries cause damage at the moment of impact and may later result in furtherdamage if the brain develops a swelling, as is common after head injuries. Penetrating headinjuries not only harm the part of the brain that is wounded but also create a risk of infection.Poor Nutrition: nutrition can affect the brain. Korsakoff’s syndrome, a brain disorder that wasdiscussed earlier, is a result of poor nutrition. It is observed in individuals who have a longhistory of heavy drinking. However, Korsakoff’s syndrome is not directly caused by alcoholabuse but by the depletion of thiamine or vitamin B1 from the body. This vitamin is deficientamong chronic alcohol abusers. Tumors: Another cause of brain damage could be tumors.Tumors are growths that result when cells divide uncontrollably. Life-threatening brain tumorsare called malignant, and less dangerous tumors are called benign. Cerebrovascular Accidents:Cerebrovascular accidents are also known as strokes. The two kinds of strokes are ischemic andhemorrhagic. Ischemic strokes may be caused by the narrowing of an artery or by a piece ofplaque from a different location getting lodged in the artery, cutting off the blood supply to thatlocation. Hemorrhagic strokes involve a rupture in the artery wall with bleeding into the tissue.Both these strokes can cause death of the brain tissue or infarction due to interruption in theoxygen supply to brain cells, ( Argosy University Online,) Damage to the nervous system may trigger four neuroplastic responses: regeneration,reorganization, degeneration, and recovery of function, (Pinel, 2008,). Neural degeneration (deterioration) is a common component of brain development anddisease, ( Coleman, 2005, Low & Cheng, 2005, cited Pinel, 2008,). A widely used method forthe controlled study of neural degeneration is to cut the axons of neurons. Two kinds of neuraldegeneration ensue: anterograde degeneration and retrograde degeneration, (Coleman & Perry,2002, cited Pinel, 2008,). Anterograde degeneration is the degeneration of the distal segment, the
Assignment 5-2 5segment of a cut axon between the cut and the synaptic terminals. Retrograde degeneration is thedegeneration of the proximal segment, the segment of a cut axon between the cut and the cellbody, (Pinel, 2008,). Anterograde degeneration occurs quickly following axotomy, because thecut separates the distal segment of the axon from the cell body, which is the metabolic center ofthe neuron. The entire distal segment becomes badly swollen within a few hours, and it breaksinto fragments with in a few days, (Pinel, 2008,). The course of retrograde degeneration isdifferent; it progresses gradually back from the cut to the cell body. In about two or three days,major changes become apparent in the cell bodies of most axotomized neurons. These early cellbody changes are either degenerative or regenerative in nature, (Pinel, 2008,). Early degenerativechanges to the cell body suggest that the neuron will ultimately die usually by apoptosis butsometimes by necrosis or a combination of both, ( Syntichaki & Tavernarakis, 2003, ). Earlyregenerative changes (an increase in size) indicate that the cell body is involved in a massivesynthesis of the proteins that will be used to replace the degenerated axon. But early regenerativechanges in the cell body do not guarantee the long term survival of the neuron; if theregenerating axon does not manage to make synaptic contact with an appropriate target, theneuron eventually dies, (Pinel, 2008,). Sometimes, degeneration spreads from damaged neuronsto neurons that are linked to them by synapses; this is called transneuronal degeneration. In somecases, transneuronal degeneration spreads from damaged neurons to the neurons on which theysynapse; this is called anterograde transneuronal degeneration, (Pinel, 2008,). And in somecases, it spreads from damaged neurons to the neurons that synapse on them; this is calledretrograde transneuronal degeneration, (Pinel, 2008,). Neural regeneration the growth ofdamaged neurons, does not proceed as successfully in mammals and other higher vertebrates asit does in most invertebrates and lower vertebrates, (Pinel, 2008,). For example, as discussed in
Assignment 5-2 6chapter nine accurate regeneration in the frog visual system in Sperry’s eye rotation experiment.The capacity for accurate axonal growth, which higher vertebrates posses during earlydevelopment, is lost once they reach maturity, (Pinel, 2008,). In the mammalian PNS, re growthfrom the proximal stump of a damaged nerve usually begins two or three days after axonaldamage, (Pinel, 2008,). There are three possibilities on what happens next, first, if the originalSchwann cell myelin sheaths remain intact, the regenerating peripheral axons grow through themto their original targets at a rate of a few millimeters per day. Second, if the peripheral nerve issevered and the cut ends become separated by a few millimeters, regenerating axon tips oftengrow into incorrect sheaths and are guided by them to incorrect destinations; that is why it isoften difficult to regain the coordinated use of limb affected by nerve damage even if there hasbeen substantial regeneration, (Pinel, 2008,). And third, if the cut ends of a severed mammalianperipheral nerve become widely separated or if a lengthy section of the nerve is damaged, theremay be no meaningful regeneration at all; regeneration axon tips grow in a tangled mass aroundthe proximal stump, and the neurons ultimately die, (Pinel, 2008,).
Assignment 5-2 7References:Pinel, J. P.J. (2009). Biopsychology (7th Ed.). Boston, MA: Pearson Education, IncArgosy University Online