Neurocognitive Disorders

Neurocognitive disorders
• Disorders that arise because of changes in brain structure,
function, or chemistry.
• Some brain disorders cause symptoms that look remarkably like
other abnormal psychology disorders.
• Brain damage can cause changes in behavior, mood, and
personality.
• It can also lead to depression and anxiety.
• Affects family members in terms of emotions.
• Disorders in this category are those that involve a loss of
cognitive ability that is presumed to be caused by brain
damage or disease.
 Brain Impairment in Adults
Subsections of this diagnostic category include:
◦ Delirium
◦ Major neurocognitive disorder (formerly dementia)
◦ Mild neurocognitive disorder.
The distinction between major and mild neurocognitive disorder is based
on severity
Within each broad diagnostic category, the specific diagnosis is to be
determined by what is thought to be the cause of the problem.
 Clinical Signs of Brain Damage
•Cell bodies and neural pathways in the brain do not appear to have the power
of regeneration, which means that their destruction is permanent.
•When brain injury occurs in an older child or adult, there is a loss in
established functioning.
•Anosognosia
•The degree of mental impairment is usually related to the degree of damage
to the brain.
•It also depends on the nature and location of the damage as well as the
premorbid (predisorder) competence and personality of the individual.
 Diffuse Versus Focal Damage
Diffuse damage:
◦ Widespread damage
◦ Attention is often impaired by mild to moderate diffuse damage, such as might
occur with moderate oxygen deprivation or the ingestion of toxic substances
such as mercury.
◦ Such a person may complain of memory problems due to an inability to
sustain focused retrieval efforts, while his or her ability to store new
information remains intact.
Focal damage:
◦ lt involve circumscribed areas of abnormal change in brain structure.
◦ This is the kind of damage that might occur with a sharply defined traumatic
injury or an interruption of blood supply (a stroke) to a specific part of the
brain.
•The location and extent of the damage determine what problems the patient
will have. Brain is highly specialized.
•Although the two hemispheres are closely interrelated, they are involved in
somewhat different types of mental processing.
•It is possible to make broad generalizations about the likely effects of damage
to particular parts of the brain.
 Brain damage and impairments
Brain Area Impairments

Frontal areas (1) being unmotivated and passive and with limited
thoughts and ideas
(2) Featuring impulsiveness and distractibility
Right parietal lobe Impairment of visual-motor co-ordination, damage to the
left parietal area may impair certain aspects of language
function, including reading and writing, as well as
arithmetical abilities.
Left parietal lobe Impairment in certain aspects of language function,
including reading and writing, as well as arithmetical
abilities.
Occipital lobe Visual impairments and visual association deficits

Temporal Lobes Disrupts an early stage of memory storage.

Extensive bilateral temporal damage A syndrome in which remote memory remains relatively
intact but nothing new can be stored for later retrieval.

Other areas in temporal lobe Disturbances of eating, sexuality, and emotion

◦
◦
Delirium can occur in a person of any age.
The elderly are at particularly high risk, perhaps because of brain changes caused by
normal aging that lead to reduced “brain reserve.”
Children are also at high risk of delirium, perhaps because their brains are not yet fully
developed.
In addition to advanced age, other risk factors for delirium include dementia,
depression, and tobacco use.
•Somewhere between 10 and 51 percent of patients who have had surgery will experience
delirium; patients who have had cardiac surgery seem to be at especially high risk.
• The presence of delirium is also a bad prognostic sign.
• Delirium is correlated with cognitive decline, longer hospital stays, more health
problems, and increased mortality; 25 percent of elderly patients with delirium die within
the following 6 months
•Delirium may result from several conditions including head injury and infection.
•The most common cause of delirium is drug intoxication or withdrawal.
• Toxicity from medications also causes many cases of delirium. This may explain why
delirium is so common in the elderly after they have had surgery
Treatment and outcome
•Most delirium are reversible, except when it is caused by a terminal illness or by severe
brain trauma.
•Treatment involves medication, environmental manipulations, and family support.
•The medications that are used for most cases are neuroleptics(used for Schizophrenia).
•For delirium caused by alcohol or drug withdrawal, benzodiazepines (such as those used
in the treatment of anxiety disorders) are used.
•Environmental manipulations that help patients stay oriented, such as good lighting,
clear signage, and easily visible calendars and clocks, can be helpful.
• It is also important that staff members introduce themselves when they work with
patients, explain what their role is, and provide reorienting prompts whenever
necessary.
•Some patients, however, especially elderly ones, may still have orientation problems,
sleep problems, and other difficulties even months after an episode of delirium
 Major Neurocognitive Disorder (Dementia)
Major neurocognitive disorders are those that involve marked deficits in cognitive
abilities.
These may be apparent in such areas as attention, executive ability, learning and
memory, language, perception, and social cognition (skills required for
understanding, interpreting, and responding to the behavior of others).
There is a decline from a previously attained level of functioning
In older people the onset of cognitive deficits is typically quite gradual.
Early on, the individual is alert and fairly well attuned to events in the environment.
Even in the early stages, memory is affected, especially memory for recent events.
As time goes on, patients show increasingly marked deficits in abstract thinking, the
acquisition of new knowledge or skills, visuospatial comprehension, motor control,
problem solving, and judgment.
These are often accompanied by impairments in emotional control and in moral and
ethical sensibilities.
Deficits may be progressive (getting worse over time) or static,
Occasionally a major neurocognitive disorder is reversible if it has an underlying cause
that can be removed or treated.
At least 50 different disorders are known to cause the types of cognitive deficits that
are now included in the category of major neurocognitive disorders.
They include:
◦ Degenerative diseases such as Huntington’s disease and Parkinson’s disease.
◦ Strokes, certain infectious diseases such as syphilis, meningitis, and AIDS
◦ Intracranial tumors and abscesses
◦ Certain dietary deficiencies (especially of the B vitamins)
◦ Severe or repeated head injury
◦ Anoxia (oxygen deprivation)
◦ Ingestion or inhalation of toxic substances such as lead or mercury.
 [Link]’S DISEASE
•James Parkinson 1817
•Second most common neurodegenerative disorder
• It is more often found in men than in women. It affects between 0.5 and 1 percent of people
between ages 65 and 69 and 1 to 3 percent of people over 80.
•Characterized by motor symptoms such as resting tremors or rigid movements.
• The underlying cause of this is loss of dopamine neurons in an area of the brain called the substantia
nigra. Dopamine is a neurotransmitter that is involved in the control of movement.
• When dopamine neurons are lost, a person is unable to move in a controlled and fluid manner
•Parkinson’s disease can involve psychological symptoms such as depression, anxiety, apathy,
cognitive problems, and even hallucinations and delusion
•Over time, 25 to 40 percent of patients with Parkinson’s disease will show signs of cognitive
impairment.
•The causes of Parkinson’s disease are not clear, although both genetic and environmental factors are
suspected.
• Genetic factors may be more important in cases where the Parkinson’s disease develop
earlier in life, and environmental factors may be more relevant in later onset cases.
• Interestingly, smoking and drinking coffee may provide some protection against the
development of Parkinson’s disease.
•The symptoms of Parkinson’s disease can be temporarily reduced by medications, such
as Mirapex (pramipexole), that increase the availability of dopamine in the brain.
•However, once the medications wear off, the symptoms return.
•Another treatment approach that is now being tried is deep brain stimulation
• In the future, stem cell research may also offer some hope for patients with this
disease.
 Huntington’s Disease
American neurologist George Huntington in1872
A rare degenerative disorder of the central nervous system that afflicts about 1 in every
10,000 people
Begins in midlife (the mean age of onset is around 40 years)
Affects men and women in equal numbers.
Characterized by a chronic, progressive chorea (involuntary and irregular movements that
flow randomly from one area of the body to another).
Subtle cognitive problems often predate the onset of motor symptoms by many years.
These cognitive problems are no doubt due to the progressive loss of brain that occurs as
much as a decade before the formal onset of the illness
Patients eventually develop dementia, and death usually occurs within 10 to 20 years of first
developing the illness.
There are currently no effective treatments that can restore functioning or slow down the
course of this terrible and relentless disorder.
Huntington’s disease is caused by a single dominant gene (the Huntingtin gene) on
chromosome 4.
This genetic mutation was discovered as a result of intense research on people living in
villages around Lake Maracaibo in Venezuela, where this disease is extremely common
(Marsh & Margolis, 2009).
Because the Huntingtin gene is a dominant gene, anyone who has a parent with the
disease has a 50 percent chance of developing the disease himself or herself.
A genetic test can be given to at-risk individuals to determine whether they will eventually
develop the disorder.
 Alzheimer’s Disease
A progressive and fatal neurodegenerative disorder.
Alois Alzheimer (1864–1915), the German neuropathologist 1907
It is the most common cause of dementia
Alzheimer’s disease is associated with a characteristic dementia syndrome that has an
imperceptible onset and a usually slow but progressively deteriorating course,
terminating in delirium and death.
The diagnosis of Alzheimer’s disease is made after a thorough clinical assessment of
the patient.
However, the diagnosis can only be confirmed after the patient’s death.
This is because an autopsy must be performed to see the brain abnormalities that are
such distinctive signs of this disease.
Alzheimer’s disease usually begins after about age 45
It is characterized by multiple cognitive deficits, not just problems with
memory.
There is a gradual declining course that involves slow mental deterioration.
In its earliest stages, Alzheimer’s disease involves minor cognitive impairment.
◦ For example, the person may have difficulty recalling recent events, make
more errors at work, or take longer to complete routine tasks.
In the later stages, there is evidence of dementia; deficits become more severe,
cover multiple domains, and result in an inability to function.
◦ For example, the person may be easily disoriented, have poor judgment, and
neglect his or her personal hygiene. Because they have impaired memory for
recent events, many patients have “empty” speech in which grammar and
syntax remain intact but vague and seemingly pointless expressions replace
meaningful conversational exchange
The temporal lobes of the brain are the first regions to be damaged in the person with
Alzheimer’s disease.
Because the hippocampus is located here, memory impairment is an early symptom of the
disease.
Loss of brain tissue in the temporal lobes may also explain why delusions are found in some
patients.
Although delusions of persecution are predominant, delusional jealousy is sometimes seen.
With appropriate treatment, which may include medication and the maintenance of a calm,
reassuring, and unprovocative social environment, many people with Alzheimer’s disease
show some alleviation of symptoms.
Deterioration continues its downward course over a period of months or years.
Eventually, patients become oblivious to their surroundings, bedridden, and reduced to a
vegetative state.
Resistance to disease is lowered, and death usually results from pneumonia or some other
respiratory or cardiac problem.
The median time to death is 5.7 years from the time of first clinical contact
 Prevalence
It has been estimated that the rate of Alzheimer’s disease doubles about every 5 years
after a person reaches the age of 40
Fewer than 1 percent of 60- to 64-year-olds have the disease, up to 40 percent those
aged 85 and older.
In the United states, more than 5 million people are living with this disease.
Worldwide, the figure is over 35 million
Women seem to have a slightly higher risk of developing Alzheimer’s disease than
men a relevant factor may be loneliness.
The prevalence of Alzheimer’s disease is higher in North America and Western Europe
and lower in such places as Africa, India, and South East Asia.
Such observations have led researchers to suspect that lifestyle factors such as a high-
fat, high-cholesterol diet are implicated in the development of Alzheimer’s disease
Also implicating diet, researchers have found that high levels of an amino
acid called homocysteine (which is a risk factor for heart disease) seem
to increase a person’s risk of developing Alzheimer’s disease later in life.
Levels of homocysteine in the blood can be reduced by taking folic acid
and certain B vitamins.
Taking statin drugs to lower cholesterol also seems to offer some
protection against Alzheimer’s disease
 Causal factors
GENETICS
Cases of early-onset Alzheimer’s disease appear to be caused by rare genetic
mutations.
Three such mutations have been identified.
i. One involves the APP (amyloid precursor protein) gene, which is located on
chromosome 21. Mutations of the APP gene are associated with an onset of Alzheimer’s
disease somewhere between 55 and 60 years of age
ii. Other cases of even earlier onset appear to be associated with mutations of a gene on
chromosome 14 called presenilin 1 (PS1) and with a mutation of the presenilin 2 (PS2)
gene on chromosome 1. These genes are associated with an onset of Alzheimer’s disease
somewhere between 30 and 50 years of age
iii. A gene that plays an important role in cases of late-onset Alzheimer’s disease is the
APOE (apolipoprotein) gene on chromosome 19. This gene codes for a blood protein that
helps carry cholesterol through the bloodstream. We know that differing forms (genetic
alleles) of APOE differentially predict risk for late-onset Alzheimer’s disease.
Amyloid precursor protein (APP)
•People with Down syndrome (which is caused by a tripling, or trisomy, of chromosome 21)
who survive beyond about age 40 develop an Alzheimer’s-like dementia.
•Cases of Down syndrome tend to occur more frequently in the families of patients with
Alzheimer’s disease.
• One study has found that mothers who gave birth to a child with Down syndrome before
age 35 had a 4.8 times greater risk of developing Alzheimer’s disease when they were older
compared to mothers of children with other types of mental retardation.
Presenilin 1
•One carrier of the PS1 mutation is even known to have developed the disorder at age 24.
•However, these mutant genes, which are autosomal dominant genes and so nearly always
cause disease in anyone who carries them, are extremely rare.
• The APP, PS1, and PS2 genetic mutations probably account, together, for no more than
about 5 percent of cases of Alzheimer’s disease.
APOE (apolipoprotein):
•Differing forms (genetic alleles) of APOE differentially predict risk for late-onset
Alzheimer’s disease.
•Three such alleles have been identified, and everyone inherits two of them, one from each
parent.
• One of these alleles, the APOE-E4 allele, significantly enhances risk for late-onset disease.
•Thus a person may inherit zero, one, or two of the APOE-E4 alleles, and his or her risk for
Alzheimer’s disease increases correspondingly.
•APOE-E4 has been shown to be a significant predictor of memory deterioration in older
individuals with or without clinical dementia.
•The APOE-E4 allele (which can be detected by a blood test) is overrepresented in all types
of Alzheimer’s disease including the early-onset and late-onset forms.
• Approximately 65 percent of patients have at least one copy of the APOE-E4 allele
ENVIRONMENTAL FACTORS:
Diet
Being overweight, having Type 2 diabetes, or not being physically active have also been implicated
as risk factors.
The association with diabetes is interesting because researchers have found that insulin levels are
abnormally low in some of the brain areas that are most affected by Alzheimer’s disease.
Other environmental factors under consideration include exposure to metals such as aluminum
and experiencing head trauma.
Exposure to nonsteroidal anti-inflammatory drugs such as ibuprofen may be protective and lead
to a lower risk of Alzheimer’s disease
People with more cognitive reserve (a concept combining education, occupation, and mental
engagement) also seem to be at reduced risk.
Recent research with mice further suggests that exposure to a more stimulating and novel
environment slows down the development of Alzheimer-related changes in the brain.
In other words, it may be possible to reduce or delay the occurrence of Alzheimer’s disease by
deliberately limiting exposure to risks, living a more interesting life, and taking other preventive
measures
Neuropathology
First autopsy identified:
(1) Amyloid plaques
(2) Neurofibrillary tangles
(3) Atrophy (shrinkage) of the brain.
Although plaques and tangles are also found in normal brains, they are present in much
greater numbers in patients with Alzheimer’s disease, particularly in the temporal lobes.
Amyloid Plaque:
Neurons in the brain secrete a sticky protein substance called beta amyloid much faster than it can be
broken down and cleared away.
This beta amyloid then accumulates into amyloid plaques.
These are thought to interfere with synaptic functioning and to set off a cascade of events that leads to the
death of brain cells.
Beta amyloid has been shown to be neurotoxic (meaning it causes cell death).
Amyloid plaques also trigger local chronic inflammation in the brain and release cytokines that may further
exacerbate this process.
Having the APOE-E4 form of the APOE gene is associated with the more rapid buildup of amyloid in the
brain.
Insulin may also play a role in regulating amyloid.
Although some scientists believe that the accumulation of beta amyloid plays a primary role in the
development of Alzheimer’s disease, others suspect that it may be a defensive response rather than a
causal factor.
Importantly, amyloid deposits can be present as many as 10 years before clinical signs of Alzheimer’s
disease first show themselves
Neurofibrillary tangles:
Webs of abnormal filaments within a nerve cell.
These filaments are made up of another protein called tau.
In a normal, healthy brain, tau acts like a scaffolding, supporting a tube inside neurons
and allowing them to conduct nerve impulses.
In Alzheimer’s disease the tau is misshaped and tangled. This causes the neuron tube to
collapse.
Although Abnormal tau aggregation can occur independently, there is reason to believe
that buildup of tau protein is accelerated by an increasing burden of amyloid in the brain.
It may suggests that the most promising drug treatments for Alzheimer’s disease may be
those that can target and prevent amyloid buildup.
Acetyl Choline:
This neurotransmitter is known to be important in the mediation of memory. Although there is
widespread destruction of neurons in Alzheimer’s disease, particularly in the area of the
hippocampus
The reduction in brain ACh activity in patients with Alzheimer’s disease is correlated with the
extent of neuronal damage (i.e., plaques, tangles) that they have sustained
The loss of cells that produce ACh makes a bad situation much worse. Because ACh is so
important in memory, its depletion contributes greatly to the cognitive and behavioral deficits
that are characteristic of Alzheimer’s disease.
For this reason, drugs (called cholinesterase inhibitors) that inhibit the breakdown of ACh (and
so increase the availability of this neurotransmitter) can be clinically beneficial for patients.
 Treatment and Outcome
Current treatments, targeting both patients and family members, aim to diminish
agitation and aggression in patients and reduce distress in caregivers as much as possible
Some common problematic behaviors associated with dementia are wandering off,
incontinence, inappropriate sexual behavior, and inadequate self-care skills. These can be
somewhat controlled via behavioral approaches
Behavioral treatments need not be dependent on complex cognitive and communication
abilities (which tend to be lacking in patients with dementia).
Because of this, they may be particularly well suited for therapeutic intervention with
Alzheimer’s disease.
In general, reports of results are moderately encouraging in terms of reducing
unnecessary frustration and embarrassment for the patient and difficulty for the care
giver.
Some patients with Alzheimer’s disease develop psychotic symptoms and are very agitated. Antipsychotic
medications (like those used in the treatment of schizophrenia) are sometimes given to alleviate these
symptoms.
The Food and Drug Administration has issued a warning that patients with dementia who receive atypical
antipsychotic medications are at increased risk of death (Schultz, 2008).
There is no good evidence that they are better than placebo when it comes to patients’ overall daily
functioning and cognition
Treatment efforts to improve cognitive functioning have focused on the consistent findings of acetylcholine
depletion in Alzheimer’s disease.
The reasoning here is that it might be possible to improve functioning by administering drugs that enhance
the availability of brain ACh.
Currently, the most effective way of doing so is by inhibiting the production of acetylcholinesterase, the
principal enzyme involved in the metabolic breakdown of acetylcholine.
The newest medication that has been approved to treat Alzheimer’s disease is memantine, which is
marketed as Namenda.
It appears to regulate the activity of the neurotransmitter glutamate, perhaps by protecting cells against
excess glutamate by partially blocking NMDA receptors.
Memantine, which can be used alone or in combination with donepezil, appears to provide patients
with some cognitive benefits .
However, when it comes to day-to-day functioning, the improvements that come from taking
medications are still very small.
Yet another line of treatment research is focused on developing vaccines that might help clear away
any accumulated amyloid plaques.
Human clinical trials of a vaccine were terminated prematurely because of dangerous side effects.
Unfortunately, once most types of neuronal cells have died they are permanently lost.
This means that even if some new treatment could halt a patient’s progressive loss of brain tissue, he
or she would still be left seriously impaired. This makes the research effort to detect Alzheimer’s
disease in its earliest stages all the more important.
 Neurocognitive Disorder Associated with HIV-1 Infection
•In addition to devastating the body, the HIV virus is also capable of inducing neurological
disease that can result in neurocognitive problems.
• First, because the immune system is weakened, people with HIV are more susceptible to
rare infections caused by parasites and fungi.
• However, the virus also appears capable of damaging the brain directly, resulting in
neuronal injury and destruction of brain cells more.
•The neuropathology of HIV-associated neurocognitive impairment involves various changes
in the brain- generalized atrophy, edema (swelling), inflammation, and patches of
demyelination.
•No brain area may be entirely spared, but the damage appears to be concentrated in
subcortical regions, notably the central white matter, the tissue surrounding the ventricles,
and deeper gray matter structures such as the basal ganglia and thalamus.
• Ninety percent of patients with AIDS show evidence of such changes on autopsy
The neuropsychological features of AIDS tend to appear as a late phase of HIV infection,
although they often appear before the full development of AIDS itself.
They begin with mild memory difficulties, psychomotor slowing, and diminished
attention and concentration.
Progression is typically rapid after this point, with clear-cut dementia appearing in
many cases within 1 year, although considerably longer periods have been reported.
The later phases also include behavioral regression, confusion, psychotic thinking,
apathy, and marked withdrawal.
Treatment with antiretroviral therapy does not fully prevent the HIV virus from
damaging the brain.
This may be because HIV penetrates into the nervous system soon after a person
becomes infected.
Even though the new therapies have made HIV/AIDS a chronic but manageable
condition, prevention of infection remains the only certain strategy for avoiding the
cognitive impairments associated with this disease.
 Neurocognitive Disorder Associated with Vascular Disease
•Frequently confused with Alzheimer’s disease because of its similar clinical picture of progressive
dementia and its increasing incidence and prevalence rates with advancing age.
•A series of circumscribed cerebral infarcts—interruptions of the blood supply to minute areas of the
brain because of arterial disease, commonly known as “small strokes”—cumulatively destroy neurons
over expanding brain regions.
• The affected regions become soft and may degenerate over time, leaving only cavities.
•Although vascular cognitive impairment tends to have a more varied early clinical picture than
Alzheimer’s disease, the progressive loss of cells leads to brain atrophy and behavioral impairments
that ultimately mimic those of Alzheimer’s disease.
•Vascular cognitive impairment tends to occur after the age of 50 and affects more men than women.
• Abnormalities of gait (e.g., being unsteady on one’s feet) may be an early predictor of this condition.
•Vascular cognitive impairment is less common than Alzheimer’s disease, accounting for only 19 percent
of dementia cases in a community sample aged 65 years or older.
One reason for this is that these patients have a much shorter course of illness because
they are vulnerable to sudden death from stroke or cardiovascular disease.
Accompanying mood disorders are also more common in vascular dementia than in
Alzheimer’s disease, because subcortical areas of the brain are more affected.
The medical treatment of vascular dementia, though complicated, offers slightly more
hope than that of Alzheimer’s disease.
Unlike Alzheimer’s disease, the basic problem of cerebral arteriosclerosis (decreased
elasticity of brain arteries) can be medically managed to some extent decreasing the
likelihood of further strokes.
The daunting problems that caregivers face, however, are much the same in the two
conditions, indicating the appropriateness of support groups, stress reduction
techniques, and the like.
 Amnestic Disorder
•Strikingly disturbed memory.
•Memory for remote past events is also usually relatively preserved.
• However, short-term memory is so impaired that the person is unable to recall events that
took place only a few minutes previously.
•To compensate, patients sometimes confabulate, making up events to fill in the void that they
have in their memories.
•Overall cognitive functioning in an amnestic disorder patient is often quite good.
• The affected person may be able to execute a complex task if it provides its own distinctive
cues for each stage of the sequence.
•Brain damage is the root cause of amnestic disorder. This damage might be caused by strokes,
injury, tumors, or infections
•Not all brain damage is permanent. Eg:- Korsakoff’s Syndrome
•Another common cause is head trauma.
•Stroke, surgery in the temporal lobe area of the brain, hypoxia (oxygen deprivation), and
some forms of brain infections (such as encephalitis) can also lead to amnestic disorder.
•In these cases, depending on the nature and extent of damage to the affected neural
structures and on the treatment undertaken, the disorder may remit with time.
• A wide range of techniques have been developed to assist the good-prognosis amnestic
patient in remembering recent events.
•Moreover, because procedural memory (i.e., the ability to learn routines, skills, and actions)
is often preserved in patients with amnesia, even patients without memory for specific
personal experiences can still be taught to perform tasks that might help them reenter the
workforce.
 Traumatic Brain Injury (TBI)
•The most common cause of TBI is falls, followed by motor vehicle accidents. Other causes
include assaults and sports injuries.
•Children aged 0 to 4, adolescents aged 15 to 19, and adults aged 65 years and older are
most likely to experience a TBI.
• In every age group rates of TBI are higher for males than they are for females.
•TBI can be closed or penetrating.
•In closed-head injury, the damage to the brain is indirect—caused by inertial forces that
cause the brain to come into violent contact with the interior skull wall or by rotational
forces that twist the brain mass relative to the brain stem.
•Closed-head injury also causes diffuse neuron damage because of the inertial force.
•The rapid movement of the rigid cranium is stopped on contact with an unyielding object.
•However, the softer brain tissue within keeps moving, and this has a shearing effect on nerve
fibers and their synaptic interconnections.
•Severe head injuries usually cause unconsciousness and disruption of circulatory, metabolic,
and neurotransmitter regulation.
•Anterograde and retrograde amnesia
•A person rendered unconscious by a head injury usually passes through stages of stupor and
confusion on the way to recovering clear consciousness.
•This recovery of consciousness may be complete in the course of minutes, or it may take hours
or days.
•In rare cases, an individual may live for extended periods of time without regaining
consciousness, a condition known as coma.
• The duration of the coma is generally related to the severity of the injury.
• If the patient survives, coma may be followed by delirium, marked by acute excitement and
disorientation and hallucinations. Gradually the confusion may clear up and the individual may
regain contact with reality.
•Concussions and Contusions
 Signs of concussion
•Temporary loss of consciousness
• Confusion or foggy feeling in the brain
• Amnesia for the period surrounding the event/injury
•Headache that gets worse and doesn’t go away
•Nausea or vomiting
• Excessive drowsiness
•Slurred or incoherent speech
• Difficulty remembering new information
•Dizziness
These symptoms may not be immediately apparent. Some symptoms may develop several days
after the injury.
Presence of APOE- E4 allele can be a risk factor in developing serious problems after head injury.
 Treatments and Outcomes
•Immediate medical treatment may also have to be supplemented by a long-range program of
reeducation and rehabilitation involving many different professionals.
•Common symptoms of minor TBI include headaches, memory problems, sensitivity to light and
sound, dizziness, anxiety, irritability, fatigue, and impaired concentration.
•When the brain damage is extensive, a patient’s general intellectual level may be considerably
reduced, especially if the temporal lobe or parietal lobes are damaged.
• Most people have significant delays in returning to their occupations, and many are unable to
return at all.
•Other losses of adult social role functioning are also common and are related to the severity of
the injury.
• Some 24 percent of TBI cases, overall, develop posttraumatic epilepsy, presumably because of
the growth of scar tissue in the brain. Seizures usually develop within 2 years of the head injury.
• For decades after a head injury, there is also an elevated risk of depression as well as other
disorders such as substance abuse, anxiety disorders, and personality disorders.
•Brain injury can also result in changes in personality. A relatively common change is
that the person becomes more easily emotionally dysregulated. This emotional
lability is frequently accompanied by irritability or disinhibition.
•Less commonly, apathy and paranoia may also be apparent.
• Children who undergo significant TBI are more likely to be adversely affected the
younger they are at the time of injury and the less language, fine motor, and other
competencies they have.
•This is because brain damage makes it harder to learn new skills and because young
children have fewer developed skills to begin with.
•Intellectual capacity, processing speed, attention, and memory are all affected.
Social competence is also compromised.
•The severity of their injury, limited socioeconomic resources, and family
dysfunction play a role in how well children recover.
•Treatment of TBI beyond the purely medical phase is often long, difficult, and
expensive.
• It requires careful and continuing assessment of neuropsychological functioning and
the design of interventions intended to overcome the deficits that remain.
•Many different treatment approaches are used including medication, rehabilitative
interventions (such as occupational, physical, and speech/language therapy,
cognitive therapy, behavior therapy, social skills training, vocational and recreational
therapy), and individual, group, and family therapy.
• Often, a treatment goal is to provide patients with new techniques to compensate
for losses that may be permanent.