1. Assignment 5-2 1
Walter L Graboski
11/23/08
Cognitive Abilities
Biopsychology
Professor Kathyrne Mueller

2. Assignment 5-2 2
Some psychologists attempt to define brain damage as some loss of tissue accompanied
by a noticeable loss of function. However, human beings tend to lose some degree of brain tissue
as they age and experience an accompanying loss of function. Brain damage can result from a
variety 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 head
injuries, infections of the brain, neurotoxins, and genetic factors, (Pinel, 2008,). Therefore, his
physician should explain to him that it is not necessary for the skull to be penetrated for the brain
to 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 head
injuries, (Pinel, 2008,). So in Gregg’s case, when there is a disturbance of consciousness
following 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 a
temporary disruption of normal cerebral function with no long term damage, (Pinel, 2008,).
However, the punch drunk syndrome is dementia (general intellectual deterioration ) and
cerebral scarring that is observed in boxers and other individuals who experience repeated
concussions. If there were no damage associated with a single concussion, the effects of many
concussions could not summate to produce damage, (McCrory & Berkovic, 1998, cited Pinel,
2008,). Where as contusions are closed head injuries that involve damage to the cerebral
circulatory 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, a
bruise, (Pinel, 2008,). It is paradoxical that the very hardness of the skull which protects the brain

3. Assignment 5-2 3
from penetrating injuries, is the major factor in the development of contusions. Contusions from
closed head injuries occur when the brain slams against the inside of the skull. Contusions
frequently occur on the side of the brain opposite the side struck by blow. The reason for such so
called contrecoup injuries is that the blow causes the brain to strike the inside of the skull on the
other side of the head, (Pinel, 2008,). Therefore, this is the reason why Gregg’s recovery is
possible 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 ten
minutes in duration, there usually is little or no evidence of brain damage; however, substantial
neuron loss can often be detected a day or two later. Second, ischemia induced brain damage
does not occur equally in all parts of the brain; particularly susceptible are neurons in certain
areas of hippocampus, (Ohtaki etal, 2003,). Third, the mechanisms of ischemia induced damage
vary somewhat from structure within the brain, and in at least some areas, astrocytes have been
implicated, (Pinel, 2008)
Gregg’s symptoms may recede or enhance in the following: First, causes of brain damage
include the following: Toxins: Toxins are substances that can poison healthy tissues. Based on
the circumstances, any substance can be a potential poison. Even substances such as water and
oxygen can be harmful if these are absorbed in excessive amounts. Excessive drinking of water
can cause water poisoning — a problem common among distance runners. Physical Trauma: It is
obvious that physical trauma to the head can also damage the brain. Such injuries are called
traumatic brain injuries (TBIs) and are often categorized as either closed head injuries or
penetrating head injuries. If a person is hit on the head and there is no external wound or external
bleeding, but internal damage to the brain, this would be an example of a closed head injury.

4. Assignment 5-2 4
Closed head injuries cause damage at the moment of impact and may later result in further
damage if the brain develops a swelling, as is common after head injuries. Penetrating head
injuries 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 was
discussed earlier, is a result of poor nutrition. It is observed in individuals who have a long
history of heavy drinking. However, Korsakoff’s syndrome is not directly caused by alcohol
abuse but by the depletion of thiamine or vitamin B1 from the body. This vitamin is deficient
among chronic alcohol abusers. Tumors: Another cause of brain damage could be tumors.
Tumors are growths that result when cells divide uncontrollably. Life-threatening brain tumors
are 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 and
hemorrhagic. Ischemic strokes may be caused by the narrowing of an artery or by a piece of
plaque from a different location getting lodged in the artery, cutting off the blood supply to that
location. 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 the
oxygen 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 and
disease, ( Coleman, 2005, Low & Cheng, 2005, cited Pinel, 2008,). A widely used method for
the controlled study of neural degeneration is to cut the axons of neurons. Two kinds of neural
degeneration ensue: anterograde degeneration and retrograde degeneration, (Coleman & Perry,
2002, cited Pinel, 2008,). Anterograde degeneration is the degeneration of the distal segment, the

5. Assignment 5-2 5
segment of a cut axon between the cut and the synaptic terminals. Retrograde degeneration is the
degeneration of the proximal segment, the segment of a cut axon between the cut and the cell
body, (Pinel, 2008,). Anterograde degeneration occurs quickly following axotomy, because the
cut separates the distal segment of the axon from the cell body, which is the metabolic center of
the neuron. The entire distal segment becomes badly swollen within a few hours, and it breaks
into fragments with in a few days, (Pinel, 2008,). The course of retrograde degeneration is
different; 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 cell
body changes are either degenerative or regenerative in nature, (Pinel, 2008,). Early degenerative
changes to the cell body suggest that the neuron will ultimately die usually by apoptosis but
sometimes by necrosis or a combination of both, ( Syntichaki & Tavernarakis, 2003, ). Early
regenerative changes (an increase in size) indicate that the cell body is involved in a massive
synthesis of the proteins that will be used to replace the degenerated axon. But early regenerative
changes in the cell body do not guarantee the long term survival of the neuron; if the
regenerating axon does not manage to make synaptic contact with an appropriate target, the
neuron eventually dies, (Pinel, 2008,). Sometimes, degeneration spreads from damaged neurons
to neurons that are linked to them by synapses; this is called transneuronal degeneration. In some
cases, transneuronal degeneration spreads from damaged neurons to the neurons on which they
synapse; this is called anterograde transneuronal degeneration, (Pinel, 2008,). And in some
cases, it spreads from damaged neurons to the neurons that synapse on them; this is called
retrograde transneuronal degeneration, (Pinel, 2008,). Neural regeneration the growth of
damaged neurons, does not proceed as successfully in mammals and other higher vertebrates as
it does in most invertebrates and lower vertebrates, (Pinel, 2008,). For example, as discussed in

6. Assignment 5-2 6
chapter 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 early
development, is lost once they reach maturity, (Pinel, 2008,). In the mammalian PNS, re growth
from the proximal stump of a damaged nerve usually begins two or three days after axonal
damage, (Pinel, 2008,). There are three possibilities on what happens next, first, if the original
Schwann cell myelin sheaths remain intact, the regenerating peripheral axons grow through them
to their original targets at a rate of a few millimeters per day. Second, if the peripheral nerve is
severed and the cut ends become separated by a few millimeters, regenerating axon tips often
grow into incorrect sheaths and are guided by them to incorrect destinations; that is why it is
often difficult to regain the coordinated use of limb affected by nerve damage even if there has
been substantial regeneration, (Pinel, 2008,). And third, if the cut ends of a severed mammalian
peripheral nerve become widely separated or if a lengthy section of the nerve is damaged, there
may be no meaningful regeneration at all; regeneration axon tips grow in a tangled mass around
the proximal stump, and the neurons ultimately die, (Pinel, 2008,).

7. Assignment 5-2 7
References:
Pinel, J. P.J. (2009). Biopsychology (7th Ed.). Boston, MA: Pearson Education, Inc
Argosy University Online