• 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
1. Vascular Disorders.
• CNS cells are easily
damaged, especially when
their blood supply is
• 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
Kolb & Whishaw (1990) p 132
• 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.
• 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
• 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
• These are more common in younger people and can be
triggered by anxiety, fatigue, bright lights, food allergies,
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
• Direct damage to the brain in which neurons are
• Disruption of blood supply resulting in ischemia and
• Bleeding within the skull, leading to increased
• Bruising of the brain leading to swelling.
• A compound fracture of the skull can open the brain to
• Scarring of brain tissue can later become a focus for
Types of Head Injury
• i) Open-Head Injuries.
• The skull is penetrated, or
fragments of bone penetrate
• Victims remain conscious and
have distinctive symptoms that
may undergo rapid and
• The specificity of neurological
symptoms following open-head
injuries makes these patients
especially good research
subjects. E.g. Phineas Gage
described by Macmillan
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
• The bruises and strains may produce bleeding within the
skull which forms a growing mass (haematoma) exerting
pressure on surrounding structures.
Impairments Following A
• 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
• 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
• Generalised Impairments: Less specific impairments
resulting from diffuse cortical damage. Loss of mental
speed and concentration problems are common.
• 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
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
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.
Clonic phase Coma phase
• 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.
Kolb & Whishaw (1990) p 140
• A tumour (neoplasm) is a mass of new tissue that
persists and grows independently of its surrounding
• 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
• 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
• iii) Glioblastomas:
• These are highly
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.
Kolb & Whishaw (1990) p 145
• These are growths
attached to the meninges
and so grow outside the
• They exert pressure on
• As they do not enter the
brain they can be
• They are generally
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
• When a neuron dies, other neurons that depended upon
that neuron for input also become impaired - this is
• Sutton et al., (1989) showed that injecting the stimulant
amphetamine led to a significant improvement in
undamaged neuron functioning following brain damage to
• Injections of antagonists such as haloperidol impaired
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
• Sensory nerves find their
way back to sensory
receptors, and motor nerves
to motor receptors, however
they can sometimes re-
connect to the wrong Kalat (2001) p138
• 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 SproutingLoss of axon
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
• 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
• 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
• 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
• Stroking the face will trigger sensations in the missing
• 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 &
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
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.