Brain damage is an injury that causes the destruction or deterioration of brain cells. In the U.S., every year, about 2.6 million people have some type of brain injury -- whether as a result of trauma, stroke, tumor, or other illnesses, according to the Brain Injury Association of America.

1. BRAIN DAMAGE
BY
Sidra Akhtar
2/21/2023 1
PRESTON UNIVERSITY, ISLAMABAD

2. CAUSES OF BRAIN DAMAGE
• BRAIN TUMORS
• CEREBROVASCULAR DISORDERS
• CLOSED-HEAD INJURIES
• INFECTIONS OF THE BRAIN
• NEUROTOXINS
• GENETIC FACTORS
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3. BRAIN TUMORS
• A tumor (neoplasm) is a mass of cells that grows
independently of the rest of the body – “A CANCER”
• 20% of brain tumors are meningiomas
– Encapsulated, growing within their own membranes
– Usually benign, surgically removable
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4. BRAIN TUMORS
• Most brain tumors are infiltrating
1. Grow diffusely through surrounding tissue
2. Malignant, difficult to remove or destroy
• About 10% of brain tumors are metastatic – they originate
elsewhere, usually the lungs
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5. BRAIN DAMAGE
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METASTATIC BRAIN TUMORS
BRAIN DAMAGE
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8. CEREBROVASCULAR DISORDERS
1. STROKE – a sudden-onset cerebrovascular event that
causes brain damage.
1. Cerebral hemorrhage – bleeding in the brain
2. Cerebral ischemia – disruption of blood supply
1. 3rd leading cause of death in the US and most common cause
of adult disability
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9. Cerebrovascular Disorders
• Cerebral hemorrhage – blood vessel ruptures
– Aneurysm – a weakened point in a blood vessel that
makes a stroke more likely. May be congenital or
due to poison or infection.
– Congenital – present at birth
Cerebral ischemia – disruption of blood supply
– Thrombosis – plug forms
– Embolism – plug forms elsewhere and moves to the
brain
– Arteriosclerosis – wall of blood vessels thicken, usually
due to fat deposits
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10. BRAIN DAMAGE
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Angiogram showing narrowing of the carotid
artery--the main blood pathway to the brain
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11. Damage due to Cerebral Ischemia
• Does not develop immediately
• Most damage is a consequence of excess
neurotransmitter release – especially glutamate
• Blood-deprived neurons become overactive and release
glutamate
• Glutamate overactivates its receptors, especially NMDA
receptors leading to an influx of Na+ and Ca++
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12. Damage due to Cerebral Ischemia
• lnflux of Na+ and Ca++ triggers:
– the release of still more glutamate
– A sequence of internal reactions that ultimately
kill the neuron
• Ischemia-induced brain damage
takes time
– Does not occur equally in all parts of the brain
– Mechanisms of damage vary with the brain
structure affected
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14. Closed-Head Injuries
• Brain injuries due to blows that do not penetrate the skull – the
brain collides with the skull
– Contrecoup injuries – contusions are often on the side
of the brain opposite to the blow
• Contusions – closed-head injuries that involve damage to the
cerebral circulatory system. A hematoma, a bruise, forms.
• Concussion – when there is a disturbance of consciousness
following a blow to the head and no evidence of structural
damage.
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16. Concussions
• While there is no apparent brain
damage with a single concussion,
multiple concussions may result in a
dementia referred to as “punch-drunk
syndrome”
• When might this occur?
• Can it be prevented?
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18. Brain Infection
• Invasion of the brain by microorganisms
• Encephalitis – the resulting inflammation
• Bacterial infections
– Often leads to abscesses, pockets of pus
– May inflame meninges, creating meningitis
– Treat with penicillin and other antibiotics
• Viral infections
– Some viral infections preferentially attack neural tissues
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PRESTON UNIVERSITY, ISLAMABAD

21. Brain Infections - Some Causes
• Bacterial
• Syphilis – may produce a
syndrome of insanity and
dementia known as general
paresis
• Syphilis bacteria are passed
to the noninfected and
enter a dormant stage for
many years.
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 Viral
 Rabies – high affinity for
the nervous system
 Mumps and herpes –
typically attack tissues
other than the brain
 Viruses may lie dormant for
years
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22. Neurotoxins
• May enter general circulation from the GI
tract, lungs, or through the skin
• Toxic psychosis – chronic insanity produced by
a neurotoxin.
• The Mad Hatter – may have had toxic
psychosis due to mercury exposure
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23. Neurotoxins
• Some antipyschotic drugs produce a motor
disorder caused tardive dyskinesia
• Recreational drugs, such as alcohol, may cause
brain damage
– Neurotoxic effects of alcohol
– Thiamine deficiency
• Some neurotoxins are endogenous – produced
by the body
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24. Genetic Factors
• Most neuropsychological diseases of genetic
origin are associated with recessive genes.
Why?
• Down syndrome
– 0.15% of births, probability increases with
advancing maternal age
– Extra chromosome 21
– Characteristic disfigurement, mental retardation,
other health problems
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26. Neuropsychological Diseases
• Epilepsy
• Parkinson’s disease
• Huntington’s disease
• Multiple sclerosis
• Alzheimer’s disease
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27. Epilepsy
• Primary symptom is seizures, but not all who
have seizures have epilepsy
• Epileptics have seizures generated by their own
brain dysfunction
• Affects about 1% of the population
• Difficult to diagnose due to the diversity and
complexity of epileptic seizures
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28. Epilepsy
• Types of seizures
– Convulsions – motor seizures
– Some are merely subtle changes of thought, mood, or
behavior
• Causes
– Brain damage
– Genes – over 70 known so far
• Diagnosis
– EEG – Electroencephalogram
– Seizures associated with high amplitude spikes
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30. Epilepsy
• Seizures often preceded by an aura, such as a
smell, hallucination, or feeling
– Aura’s nature suggests the epileptic focus
– Warns epileptic of an impending seizure
• Partial epilepsy – does not involve the whole
brain
• Generalized epilepsy – involve the entire brain
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The bursting of an epileptic neuron, recorded by extracellular unit
recording.
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32. Partial Seizures
• Simple
– symptoms are primarily sensory or motor or both
(Jacksonian seizures)
– symptoms spread as epileptic discharge spreads
• Complex – often restricted to the temporal lobes
(temporal lobe epilepsy)
– patient engages in compulsive and repetitive simple
behaviors – automatisms
– more complex behaviors seem normal
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34. Generalized Seizures
• Grand mal
– Loss of consciousness and equilibrium
– Tonic-clonic convulsions
-rigidity (tonus) and tremors (clonus)
– Resulting hypoxia may cause brain damage
• Petit mal
– not associated with convulsions
– A disruption of consciousness associated with a
cessation of ongoing behavior
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36. Parkinson’s Disease
• A movement disorder of middle and old age
affecting ~ .5%of the population
• Pain and depression commonly seen before the
full disorder develops
• Tremor at rest is the most common symptom of
the full-blown disorder
• Dementia is not typically seen
• No single cause
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37. Parkinson’s Disease
• Associated with degeneration of the substantia
nigra whose neurons use dopamine and project
to the striatum of the basal ganglia
• Almost no dopamine in the substantia nigra of
Parkinson’s patients
• Treated temporarily with L-dopa
• Linked to ~10 different gene mutations
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38. Huntington’s Disease
• Also a progressive motor disorder of middle and old
age – but rare, with a strong genetic basis, and
associated with dementia.
• Begins with fidgetiness and progresses to jerky
movements of entire limbs and severe dementia
• Death usually occurs within 15 years
• Caused by a single dominant gene
• 1st symptoms usually not seen until age 40
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39. Multiple Sclerosis
• A progressive disease that attacks CNS myelin, leaving
areas of hard scar tissue (sclerosis)
• Nature and severity of deficits vary with the nature,
size, and position of sclerotic lesions
• Periods of remission are common
• Symptoms include visual disturbances, muscle
weakness, numbness, tremor, and loss of motor
coordination (ataxia)
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41. Multiple Sclerosis
• Epidemiological studies find that incidence of MS is
increased in those who spend childhood in a cool
climate
• MS is rare amongst Africans and Asians
• Strong genetic predisposition and many genes involved
• An autoimmune disorder – immune system attacks
myelin
• Drugs may retard progression or block some symptoms
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42. Alzheimer’s Disease
• Most common cause of dementia – likelihood
of developing it increases with age
• Progressive, with early stages characterized by
confusion and a selective decline in memory
• Definitive diagnosis only at autopsy – must
observe neurofibrillary tangles and amyloid
plaques
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Amyloid Plaques in an Alzheimer Patient’s Brain
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44. Familial Forms of Alzheimer’s Disease
• Several genes identified as involved in early onset AD
• All affected genes are involved in synthesis of amyloid
or tau, a protein found in the tangles
• Not clear what comes 1st – amyloid plaques or
neurofibrillary tangles
• Declined acetylcholine levels is among one of the
earliest changes seen
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46. Neuroplastic Responses to Nervous
System Damage
• Degeneration - deterioration
• Regeneration – regrowth of damaged neurons
• Reorganization
• Recovery
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47. Degeneration
• Cutting axons is a common way to study responses to
neuronal damage
• Anterograde - degeneration of the distal segment – between
the cut and synaptic terminal
– cut off from cell’s metabolic center
– swells and breaks off within a few days
• Retrograde – degeneration of the proximal segment –
between the cut and cell body
– progresses slowly
– if regenerating axon makes a new synaptic contact, the neuron may
survive
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48. Neural Regeneration
• Does not proceed successfully in mammals
and other higher vertebrates - capacity for
accurate axonal growth is lost in maturity
• Regeneration is virtually nonexistent in the
CNS of adult mammals and unlikely.
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49. Recovery of Function after Brain
Damage Poorly Understood
• Difficult to conduct controlled experiments on
populations of brain-damaged patients
• Can’t distinguish between true recovery and
compensatory changes
• Cognitive reserve – education and intelligence –
thought to play an important role in recovery of
function – may permit cognitive tasks to be
accomplished new ways
• Adult neurogenesis may play a role in recovery
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50. Treating Nervous System Damage
• Reducing brain damage by blocking
neurodegeneration
• Promoting recovery by promoting
regeneration
• Promoting recovery by transplantation
• Promoting recovery by rehabilitative training
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51. Reducing brain damage by blocking
neurodegeneration
• Various neurochemicals can block or limit
neurodegeneration
• Apoptosis inhibitor protein – introduced in rats via a
virus
• Nerve growth factor – blocks degeneration of damaged
neurons
• Estrogens – limit or delay neuron death
• Neuroprotective molecules tend to also promote
regeneration
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52. Promoting Recovery by Promoting
Regeneration
• While regeneration does not normally occur
in the CNS, experimentally it can be induced
• Eliminate inhibition of oligodendroglia and
regeneration can occur
• Provide Schwann cells to direct growth
• Transplanting of olfactory sheathing cells
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53. Promoting Recovery by
Neurotransplantation
• Fetal tissue
– Fetal substantia nigra cells used to treat MPTP-
treated monkeys (PD model)
– Treatment was successful
– Limited success with humans
• Stem cells
– Rats with spinal damage “cured”, but much more
research is needed
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55. Promoting Recovery by
Rehabilitative Training
• Constraint-induced therapy – down
functioning limb while training the impaired
one – create a competitive situation to foster
recovery
• Facilitated walking as an approach to treating
spinal injury
• ROLE OF PSYCHOLOGIST
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59. Can the brain recover
from brain damage?
• Consider what you now know about the
brain’s ability to adapt following brain
damage, can it “recover”?
• If so, what conditions promote recovery?
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