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Biological Bases of Behaviour.
Lecture 11: Brain Damage.
Kalat (2001) p133
Learning Outcomes.
• By the end of this lecture you should be able to:
• 1. Describe the major causes of brain damage.
• 2. Explain the processes involved in recovery from neural
damage.
1. Vascular Disorders.
• CNS cells are easily damaged,
especially when their blood
supply is impaired.
• Disruption of neural blood
supply by disease or accident
is called a stroke.
• These are very common with
an incidence of around 2 per
1000.
• 35% of stroke sufferers die
within a year, the remainder
experience varying degrees
of impairment depending
upon
the brain
regions
affected.
Kolb & Whishaw (1990) p 132
Strokes (continued).
• The most common cause of strokes is blockage of the
artery (ischemia) caused by the build up of fat, less
common is the rupture of an artery (haemorrhage).
• Both types produce the same effect.
• A stroke produces an area of dead tissue (infarct), the size
of which depends on where the damage occurred.
• The behavioural symptoms depends upon the exact
location of the damage, e.g. a lesion in the visual cortex can
produce an area of blindness, one affecting the
hippocampus can affect memory.
Migraine.
• A migraine headache is a transient ischemia, and they
affect around 5-20% of the population.
• They consist of visual disturbances, headache, movement
difficulties, and aphasia, the precise symptoms depending
on the areas affected. There are 2 main types:
• i) Classic migraine: Experienced by 12% of sufferers and
includes a visual aura due to constriction of one or more
cerebral arteries. This may be followed by a severe
headache, which may last hours or days.
• ii) Common migraine: Occurs in 80% of sufferers, with no
visual aura but feelings of nausea. This is followed by a
cluster headache in the head or face lasting about 2 hours.
• These are more common in younger people and can be
triggered by anxiety, fatigue, bright lights, food allergies,
and hormonal changes during the menstrual cycle.
2. Traumatic Head Injuries.
• Cerebral trauma is the commonest form of brain damage in
young people (vehicle/horse-riding/industrial accidents,
warfare). Such trauma can affect the brain in several ways:
• Direct damage to the brain in which neurons are damaged
directly.
• Disruption of blood supply resulting in ischemia and
possibly infarction.
• Bleeding within the skull, leading to increased intracranial
pressure.
• Bruising of the brain leading to swelling.
• A compound fracture of the skull can open the brain to
infection.
• Scarring of brain tissue can later become a focus for
epileptic seizures.
Types of Head Injury
• i) Open-Head Injuries.
• The skull is penetrated, or
fragments of bone penetrate
the brain.
• Victims remain conscious and
have distinctive symptoms that
may
undergo
rapid
and
spontaneous recovery.
• The specificity of neurological
symptoms following open-head
injuries makes these patients
especially
good
research
subjects. E.g. Phineas Gage
described by Macmillan (1984).
ii) Closed Head Injuries.
• These result from a blow to the head :
• The damage at the site of the blow is called a coup as the
brain is compacted by the bone being forced inward.
• The pressure on the brain at the time of the coup forces the
brain against the opposite side of the skull, producing a
countercoup.
• Movement of the brain causes twisting and shearing of
nerve fibres, producing tiny lesions in frontal and temporal
lobes. Such damage also affects fibres in the corpus
callosum
and
anterior
commissure
producing
a
disconnection syndrome.
• The bruises and strains may produce bleeding within the
skull which forms a growing mass (haematoma) exerting
pressure on surrounding structures.
Impairments Following A
Closed-Head Injury.
• CHI’s are accompanied by loss of consciousness (coma)
resulting from strain on fibres in the reticular formation.
• Coma duration serves as a predictive measure of the
severity of the damage, it correlates directly with
subsequent mortality, intellectual impairment, and deficits
in social skills.
• Two kinds of impairments are seen following closed-head
injuries.
• Discrete impairments: Specific impairment of functions at
the site of the coup or countercoup. Personality changes,
aggression, and the inability to plan and organise are
commonly seen.
• Generalised Impairments: Less specific impairments
resulting from diffuse cortical damage. Loss of mental
speed and concentration problems are common.
3. Epilepsy.
• This is characterised by recurrent excessive synchronised
production of action potentials from many neurons, mainly
due to decreased release of the inhibitory neurotransmitter
GABA (During et al., 1995).
• Such seizures are very common with 1 in 20 experiencing
at least one fit in their lifetime, but multiple seizures are
much rarer at 1 in 200.
• The cause of epilepsy remained unknown until the
invention of the electroencephalograph (EEG), which
demonstrated that different types of epilepsy were
associated with different abnormal electrical rhythms in the
brain.
Characteristics of Epilepsy.
• Sometimes epileptic seizures are symptomatic i.e. they can
be linked with specific factors such as trauma, infection,
drugs, or fever.
• Other seizures are idiopathic, they arise spontaneously in
the absence of other neurological disorders. Three common
symptoms are often reported:
• i) An aura, or warning of the impending seizure in the form
of as odours or noises.
• ii) Loss of consciousness which may consist of a complete
collapse, or simply a 'staring into space', there is often
amnesia of the seizure.
• iii) Uncontrolled movements such as shaking and vocal
utterances.
Classifications of Epilepsy.
• a) Focal seizures: Begin locally and spread, they generally
affect cortical motor areas so that an attack begins with
jerks in the fingers, and then spreads so that the whole
hand, and arm becomes affected.
• b) Complex partial seizures: Originate in the medial
temporal lobe and are characterised by the intrusion of
repetitive thoughts, hallucinations, déjà vu, repetitive
movements such as lip smacking, and a frozen posture.
• c) Generalised seizures: In a Petit Mal seizure there is a loss
of awareness during which there is motor activity such as
blinking or rolling the eyes but the episodes are brief and
seldom exceed 10 seconds.
Generalised Seizures continued.
•
In a Grand Mal seizure, the individual experiences an aura followed
by loss of consciousness in which they stiffen, shake, and perhaps
make noises, this is followed by post-seizure confusion and
amnesia.
Before the
seizure
Seizure onset
Clonic phase
Coma phase
Kolb & Whishaw (1990) p 140
4. Tumours.
• A tumour (neoplasm) is a mass of new tissue that persists
and grows independently of its surrounding structures.
• Some are unlikely to reoccur after removal (benign) but
others are likely to regrow again (malignant), they are
equally dangerous depending on their location.
• There are several types distinguished on the basis of where
they originate:
• a) Glioma's: These arise from glial cells and infiltrate brain
tissue. 45% of all brain tumours are of this type and they
can be benign or malignant, there are three types:
• i) Astrocytomas: Develop from the astrocytes, they are slow
growing and commonest in adults over the age of 30. They
are not often malignant, and can be easily treated.
Glioma’s continued.
• iii) Glioblastomas:
• These are highly
malignant, rapidly
growing, and are common
in men over 35. They are
difficult to treat and have
poor life expectancy.
• iii) Medulloblastomas:
These are highly malignant
and are found exclusively
in the cerebellum of
children, prognosis is very
poor.
glioblastoma
Kolb & Whishaw (1990) p 145
b) Meningiomas
• These are growths
attached to the meninges
and so grow outside the
brain.
• They exert pressure on
brain tissue.
• As they do not enter the
brain they can be removed
easily.
• They are generally benign.
Meningioma
Kolb & Whishaw (1990) p 144
Recovery After Brain Damage.
• Neurons cannot be replaced once destroyed or damaged.
• However, some recovery often occurs following brain
damage. How does this recovery take place?
• It was assumed that another region of the brain took over
the impaired functioning of a damaged region, but this only
occurs in a limited manner.
• E.g if motor cortex in the left hemisphere is damaged, the
corresponding area of the right hemisphere takes over
some function of the ipsilateral limbs but only by
strengthening already existing ipsilateral pathways.
• Much of the recovery seen following brain damage is
achieved by the person making better use of unimpaired
abilities or by learning to use abilities that appeared to be
lost but were actually just impaired.
• There are several factors in recovery:
1. Role of Stimulants.
• Impairment following brain damage does not just reflect
localised damage but also the 'knock-on' effects of that
damage.
• When a neuron dies, other neurons that depended upon
that neuron for input also become impaired - this is called
diaschisis.
• Sutton et al., (1989) showed that injecting the stimulant
amphetamine led to a significant improvement in
undamaged neuron functioning following brain damage to
adjacent regions.
• Injections of antagonists such as haloperidol impaired
behavioural recovery.
2. Axon Regrowth.
• Damaged axons can regrow to
a limited extent. For example
damaged neurons in the
peripheral nervous system
grow back at around 1mm per
day.
• If a myelinated axon is
severed
the
regenerating
axons follows the myelin path
back to its original target.
• Sensory nerves find their way
back to sensory receptors,
and motor nerves to motor
receptors, however they can
sometimes re-connect to the
wrong receptor.
Kalat (2001) p138
3. Sprouting.
• After axons have been damaged, cells that formerly
received their synaptic input begin to secrete neurotrophins
which induce nearby axons to form new branches (sprouts)
that connect to the vacant synapses.
Normal
Loss of axon
Sprouting
Kalat (2001) p138
4. Heightened Sensitivity.
• If a postsynaptic cell is deprived of input for a long time it
becomes more sensitive to its neurotransmitter by creating
additional receptors or by increasing their sensitivity.
• This is known as denervation supersensitivity.
5. Cortical Reorganisation.
• Following amputation, cortical reorganisation can occur; if a
cortical area no longer receives input, other regions 'spread'.
• Merzenich et al., (1984) showed that following amputation of
a single finger, the area of somatosensory cortex previously
sensitive to input from that finger became responsive to the
other fingers and parts of the palm.
Kalat (2001) p141
Phantom Limbs.
• Many people who have lost a limb still perceive it vividly,
these phantom limbs are very real to amputees even to the
extent that they feel pain in their missing fingers.
• Cortical areas representing the arms and face lie close
together, if an arm is missing then the area of cortex
previously responsive to the limb becomes responsive to
the face.
• Stroking the face will trigger sensations in the missing
limb.
• As the areas representing the feet and genitals also lie
close together people, with amputated feet can feel their
missing appendages during sexual stimulation as the
representation of the genitals has spread into the now
unused area representing the feet (Ramachandran &
Herstein, 1998).
Influence of Age.
• Neurons are gradually lost throughout life so that by age 60
dendrites have shrunk, many cells have been lost, and the
sprouting process has slowed down.
• These natural processes can exacerbate the effects of brain
damage, such that recovery from brain damage in the
elderly is always much less than in the young.
• Recovery in the very young may be dramatic, for example if
a child under the age of 2 loses their entire left hemisphere
they may develop near-normal speech.
• However the young brain is more sensitive, and damage to
certain developing neurons may lead to severe problems in
later life (autism, perhaps schizophrenia).
References and Bibliography.
 Kalat, J.W. (1995). Biological Psychology.
 Kolb, B., & Whishaw, I.Q. (1990). Fundamentals of Human
Neuropsychology.
 Macmillan, M.B. (1986). A wonderful journey through skull and
brains: the travels of Mr. Gage's tamping iron. Brain and
Cognition, 5: 67-107.
 Merzenich, M.M., Nelson, R.J., Stryker, M.P., Cynader, M.S.,
Schoppman, A., Zook, J.M. (1984). Somatosensory cortical map
changes following digit amputation in adult monkeys. Journal of
Comparative Neurology, 224: 591-605.
 Sutton, R.L., Hovda, D.A., & Feeney, D.M. (1989). Amphetamine
accelerates recovery of locomotor function following bilateral
frontal cortex ablation in rats. Behavioural Neuroscience, 103:
837-841.