ORAL-REV-REVIEWER.pdf

1. ASD
Definition
According to Diagnostic and Statistical Manual of Mental Disorders (5th
ed.; DSM–5; American Psychiatric Association, 2013) Autism Spectrum Disorder
(ASD) is a neurodevelopmental disorder that causes persistent impairment
in reciprocal social communication and social interaction and restricted,
repetitive patterns of behavior, interests, or activities. These symptoms are
typically recognized during the second year of life (12-24 months of age) but may
be seen earlier than 12 months if developmental delays are severe or noted later
than 24 months if symptoms are more subtle which significantly limit or impair
everyday functioning. The stage at which functional impairment becomes obvious
will vary according to the characteristics of the individual and his or her
environment. Manifestations of the disorder also vary greatly depending on the
severity of the autistic condition, developmental level, and chronological age;
hence, the term spectrum.
Etiology
The etiology of ASD is likely to be multifactorial, with both genetic and
non-genetic factors playing a role. ASD can be syndromic or non-syndromic.
Syndromic ASD is often associated with chromosomal abnormalities or
monogenic alterations. Such examples include Rett syndrome, fragile X
syndrome, and MECP2 duplication syndrome. Contrary to syndromic ASD, the
etiology of non-syndromic ASD is still relatively undefined due to its genetic
heterogeneity. A collaboration of de novo mutations and prenatal plus postnatal
environmental factors is likely to play a role.
Epidemiology
• Experts estimate that 3 to 6 children out of every 1000 will have
autism.
• In the Philippines, it is estimated that 1 out of every 500 Filipinos suffers
from autism or approximately 200,000 Filipinos out of two million total
population.
• Recent studies further suggest that some people have a genetic
predisposition to autism.
• In families with one autistic child, the risk of having a second child with
the disorder is approximately 5 percent, or one in 20 (Lima, 2017).
Pathophysiology
• Autism appears to result from developmental factors that affect many or
all functional brain systems, and leads to disruption in the development of
the brain.
• Neuroanatomical studies and study in the area of genetic inheritance
have suggested that autism occurs after conception.
• Environmental factors play an important role in the development of autism
after an anomaly in the brain leads to activation of pathological
pathways.
• Autism also includes structural changes in the brain.
• The cellular and molecular bases of pathological early overgrowth are not
known, nor is it known whether the overgrown neural systems cause
autism’s characteristic signs.
Signs and Symptoms
A. Persistent deficits in social communication and social interaction across
multiple contexts, as manifested by the following, currently or by history (example
are illustrative, not exhaustive; see text):
1. Deficits in social-emotional reciprocity, ranging for example,
from abnormal social approach and failure of normal back and
forth conversation; to reduced sharing of interests, emotions, or
affect; to failure to initiate or respond to social interactions.
2. Deficits in nonverbal communicative behaviors used for
social interaction, ranging, for example, from poorly integrated
verbal and nonverbal communication; to abnormalities in eye
contact and body language or deficits in understanding and use
of gestures: to a total lack of facial expressions and nonverbal
communication.
3. Deficits in developing, maintaining, and understanding
relationships, ranging, for example, from difficulties adjusting
behavior to suit various social contexts; to difficulties in sharing
imaginative play or in making friends; to the absence of interest
in peers
B. Restricted, repetitive patterns of behavior, interests, or activities, as
manifested by at least two of the following, currently or history (examples are
illustrative, not exhaustive; see text):
a. Stereotypes or repetitive motor movements, use of objects, or
speech ( e.g., simple motor stereotypes, lining up toys or flipping
objects, echolalia, idiosyncratic phrases).

b. Insistence on sameness, inflexible adherence to routines, or
ritualized patterns of verbal or nonverbal behavior (e.g extreme
distress at small changes, difficulties with transitions, rigid thinking
patterns, greeting rituals, need to take the same route or eat the
same food every day).
c. Highly restricted, fixated interests that are abnormal in intensity
or focus (e.g., strong attachment to or preoccupation with unusual
objects, excessively circumscribed or perseverative interests).
d. Hyper-or hypo reactivity to sensory input or unusual interest in
sensory aspects of the environment (e.g., apparent indifference to
pain/temperature, adverse response to specific sounds or textures,
excessive smelling or touching of objects, visual fascination with
lights or movement)
Prognosis
• According to the DSM-V, the best-established prognostic factors for
individual outcomes within autism spectrum disorder are the presence or
absence of associated intellectual disability and language impairment,
and additional mental health problems.
OT Managements and Intervention
• Comprehensive intervention, including
o Parental counseling
o Behavioral treatment
o Special education in highly structured environments
o Sensory integrative therapy
o Social skills training
o Speech-language therapy
o Medications
o Family support
• Joint attention
• Expressive and receptive language
• Work behaviors
2. Attention-Deficit Hyperactivity Disorder
Definition
• According to the DSM-5, ADHD is a persistent pattern of inattention
and/or hyperactivity-impulsivity that interferes with functioning or
development.
• Inattention manifests as wandering off task, lacking persistence,
having difficulty sustaining focus, and being disorganized and is not
due to defiance or lack of comprehension.
• Hyperactivity refers to excessive motor activity that is not
appropriate; it may manifest as extreme restlessness or wearing
others out with their activity.
• Impulsivity refers to hasty actions that occur in the moment without
forethought and have high potential for harm to the individual.
Etiology
One theory that persists in popular literature is that ADHD is related to
food allergies or food additives and the amount of sugar in a child’s diet. The
National Institutes of Health (NIH) concluded that there is no evidence that diet
is responsible for the onset of ADHD and that only in a fraction of children with
ADHD is a restricted diet efficacious in reducing symptoms associated with this
disorder. The current etiologic theories, widely supported but still under
investigation, include genetic factors, neurologic factors, and neurochemical
imbalances.
Epidemiology
• Population surveys suggest that ADHD occurs in most cultures in about
5% of children and about 2.5% of adults.
• Boys (13%) are more likely to be diagnosed with ADHD than girls (6%).
• Black, non-Hispanic children and White, non-Hispanic children are
more often diagnosed with ADHD (12% and 10%, respectively), than
Hispanic children (8%) or Asian, non-Hispanic children (3%).
Pathophysiology
• In neuroimaging studies, a significant decrease in brain activity in the
frontal parietal lobes, which inhibit impulsiveness and control attention,
has been demonstrated in adults with ADHD.
• Two theories have been proposed for the cognitive impairments seen in
ADHD.
• Barkley suggests that the symptoms seen in ADHD are a result of
response inhibition, which prevents accurate self-regulation to
environmental stimuli.
• He suggests that the response inhibition stems from underfunctioning
of the orbital frontal cortex and its subsequent connections to the limbic
system.

Signs and Symptoms
A. A persistent pattern of inattention and/or hyperactivity-impulsivity that
interferes with functioning or development, as characterized by (1) and/or
(2):
B. Inattention:
a. Often fails to give close attention to details or makes careless
mistakes in schoolwork, at work, or during other activities
b. Often has difficulty sustaining attention in tasks or play
activities
c. Often does not seem to listen when spoken to directly
d. Often does not follow through on instructions and fails to finish
schoolwork, chores, or duties in the workplace
e. Often has difficulty organizing tasks and activities
f. Often avoids, dislikes, or is reluctant to engage in tasks that
require sustained mental effort
g. Often loses things necessary for tasks or activities
h. Is often easily distracted by extraneous stimuli
i. Is often forgetful in daily activities
C. Hyperactivity and impulsivity
a. Often fidgets with or taps hands or feet or squirms in seat
b. Often leaves seat in situations when remaining seated is
expected
c. Often runs about or climbs in situations where it is inappropriate
d. Often unable to play or engage in leisure activities quietly
e. Is often “on the go,” acting as if “driven by a motor”
f. Often talks excessively
g. Often blurts out an answer before a question has been
completed
h. Often has difficulty waiting his or her turn
i. Often interrupts or intrudes on others
The symptoms must persist for at least 6 months to a degree that is
maladaptive and that subsequently interferes with all occupational activities,
including self-care, academic performance, and peer relationships.
Prognosis
• There is no cure for ADHD.
• Most children with this condition continue with its symptoms into
adulthood.
• If left untreated, ADHD can gravely interfere with the social and
educational performance of an individual and may impair the individual's
self-esteem.
• 25% of ADHD children with conduct disorder problems develop antisocial
personality disorder and become victims of substance abuse, criminal
behavior.
• Being prone to depression and anxiety, they have suicidal tendencies too.
• It is, therefore, imperative that these individuals get medical attention as
early as possible.
• Time management
• Building organizational skills
• Executive function training
• Working on social skills
• Sensory integrative therapy
3. Intellectual Disability
Definition
According to Diagnostic and Statistical Manual of Mental Disorders (5th
ed.; DSM–5; American Psychiatric Association, 2013), Intellectual Disability is a
disorder with onset during the developmental period that includes both
intellectual and adaptive functioning deficits in conceptual, social, and
practical domains.
Etiology
The etiology of ASD is genetic and physiological (DSM-V).
• Prenatal etiologies include genetic syndromes, inborn errors of
metabolism, brain malformations, maternal disease, and
environmental influences such as alcohol, other drugs, and
toxins.
• Perinatal causes include a variety of labor and delivery-related
events leading to neonatal encephalopathy.
• Postnatal causes include hypoxic ischemic injury, traumatic brain
injury, infections, demyelinating disorders, seizure disorders,
severe and chronic social deprivation, and toxic metabolic
syndromes and intoxications.
Epidemiology
• Intellectual disability has an overall general population prevalence of
approximately 1%, and prevalence rates vary by age.
• Prevalence for severe intellectual disability is approximately 6 per 1,000.

Pathophysiology
• Onset of intellectual disability is in the developmental period.
• The age and characteristic features at onset depend on the etiology and
severity of brain dysfunction.
• Delayed motor, language, and social milestones may be identifiable
within the first 2 years of life among those with more severe intellectual
disability, while mild levels may not be identifiable until school age
when difficulty with academic learning becomes apparent.
• All criteria (including Criterion C) must be fulfilled by history or current
presentation.
Signs and Symptoms
The essential features of intellectual disability are:
• Deficits in general mental abilities (Criterion A)
o This refers to intellectual functions that involve
reasoning, problem solving, planning, abstract thinking,
judgment, learning from instruction and experience, and
practical understanding.
o Critical components include verbal comprehension,
working memory, perceptual reasoning, quantitative
reasoning, abstract thought, and cognitive efficacy.
• Impairment in everyday adaptive functioning, in comparison
to an individual's age-, gender-, and socioculturally matched
peers (Criterion B).
o This refers to how well a person meets community
standards of personal independence and social
responsibility, in comparison to others of similar age and
sociocultural background.
o Adaptive functioning involves adaptive reasoning in three
domains: conceptual, social, and practical.
o The conceptual (academic) domain involves
competence in memory, language, reading, writing, math
reasoning, acquisition of practical knowledge, problem
solving, and judgment in novel situations, among others.
o The social domain involves awareness of others'
thoughts, feelings, and experiences; empathy;
interpersonal communication skills; friendship abilities; and
social judgment, among others.
o The practical domain involves learning and self-
management across life settings, including personal care,
job responsibilities, money management, recreation, self-
management of behavior, and school and work task
organization, among others.
• Onset is during the developmental period (Criterion C).
To meet diagnostic criteria for intellectual disability, the deficits in
adaptive functioning must be directly related to the intellectual impairments
described in Criterion A. Criterion C, onset during the developmental period,
refers to recognition that intellectual and adaptive deficits are present during
childhood or adolescence.
Prognosis
• A person with mild ID has a Assistive technology , and health care is
improving long-term health outcomes for people with all types of
intellectual disabilities.
• Many people with ID can support themselves, can live independently,
and can be successfully employed with appropriate support.
• Because intellectual disability sometimes coexists with serious physical
problems, the life expectancy of people with ID may be shortened,
depending on the specific condition.
• People with more severe intellectual disability are more likely to
require support for life. In general, the more severe the cognitive
disability and the more physical problems the person has, the shorter
the life expectancy.
• Reference:
o Sulkes, S. B. (2022, November 19). Intellectual Disability. MSD
Manual Consumer Version.
https://www.msdmanuals.com/home/children-s-health-
issues/learning-and-developmental-disorders/intellectual-disability
• ADL training
• Accessibility and environmental modification
• Assistive technology
• Caregiver education
• Community integration interventions
4. Global Developmental Delay
Definition
This diagnosis is reserved for individuals under the age of 5 years when
the clinical severity level cannot be reliably assessed during early childhood. This
category is diagnosed when an individual fails to meet expected
developmental milestones in several areas of intellectual functioning, and
applies to individuals who are unable to undergo systematic assessments of

intellectual functioning, including children who are too young to participate in
standardized testing. This category requires reassessment after a period of time.
Etiology
The etiology of developmental delay is multifactorial. The etiology for the
vast majority of developmental delay is idiopathic. When known, etiology may
include genetic, environmental, and/or psychosocial factors.
• Genetic: There is no known genetic substrate for developmental delay,
per se. However, developmental patterns are often familial, including late
walking and talking. Nonetheless, these developmental delays can also
represent risks for syndromes or developmental disorders.
• Environmental: A wide number of environmental factors can lead to
developmental delays and subsequent developmental disorders. These
factors can affect development at a single of multiple points in the
developmental process.
• Antenatal: heritable factors, early maternal infections, teen pregnancy
• Perinatal: Poverty, prematurity
• Postnatal: Infections, poverty, malnutrition
Epidemiology
• Although the exact prevalence of developmental delay is unknown,
according to the World Health Organization (WHO), 10% of the
population in each country population has a disability of one or another
kind.
• According to Drakenstein Child Health Study (DCHS) conducted in
Western Cape, South Africa, the risk of low developmental performance
in the high-risk environment was high among boys.
Pathophysiology
• Except for specific syndromes that include developmental delay, the vast
majority of developmental delay is idiopathic.
• Although the exact underlying pathophysiology is unknown, several
mechanisms have been proposed by epidemiologic studies that lead to
some sort of developmental delay and/or disabilities.
• Since some forms of developmental delay may run in families, genes
have been assumed to play a significant role in developmental delay.
Signs and Symptoms
Sometimes you may see signs in infancy, but in other cases they may not be
noticeable until your child reaches school age. Some of the most common
symptoms can include:
• Learning and developing more slowly than other children same age
• Rolling over, sitting up, crawling, or walking much later than
developmentally appropriate
• Difficulty communicating or socializing with others
• Lower than average scores on IQ tests
• Difficulties talking or talking late
• Having problems remembering things
• Inability to connect actions with consequences
• Difficulty with problem-solving or logical thinking
• Trouble learning in school
• Inability to do everyday tasks like getting dressed or using the restroom
without help
Prognosis
• Since most developmental delays resolve spontaneously, the prognosis is
generally good.
• However, developmental delay is a significant and powerful risk for
progression to a neurodevelopmental disorder or syndrome.
• As a result, it is critical that each developmental delay is carefully followed
until it resolves or evolves into a developmental disorder.
• Gross and fine motor skills training
• Emotional regulation interventions
• Social skills training
• Sensory integrated therapy
• Cognitive training
5. Cerebral Palsy
Definition
Cerebral palsy is characterized by nonprogressive abnormalities in the
developing brain that create a cascade of neurologic, motor, and postural deficits
in the developing child.
Etiology
Cerebral palsy is caused by abnormal development of the brain or
damage to the developing brain that affects a child’s ability to control their
muscles. The abnormal development of the brain or damage that leads to CP
can happen before birth, during birth, within a month after birth, or during the first
years of a child’s life, while the brain is still developing. Cerebral palsy related to
abnormal development of the brain or damage that occurred before or during

birth is called congenital CP. The majority of CP (85%–90%) is congenital. A
small percentage of cerebral palsy is caused by abnormal development of the
brain or damage that occurs more than 28 days after birth. This is called acquired
CP, and usually is associated with an infection (such as meningitis) or head
injury.
Epidemiology
• Cerebral palsy (CP) is the most common motor disability in childhood.
• Population-based studies from around the world report that the
prevalence estimates of CP range from 1.5 to more than 4 per 1,000 live
births or children of a defined age range.
• The overall birth prevalence of CP is approximately 2 per 1,000 live
births.
Pathophysiology
• The premature neonatal brain is susceptible to two main pathologies:
intraventricular hemorrhage (IVH) and periventricular leukomalacia (PVL).
o Intraventricular Hemorrhage (IVH)
▪ Refers to bleeding from the subependymal matrix (the
origin of fetal brain cells) into the ventricles of the brain.
▪ The blood vessels around the ventricles develop late in the
third trimester, thus preterm infants have underdeveloped
periventricular blood vessels, predisposing them to
increased risk of IVH.
o Periventricular Leukomalacia (PVL).
▪ Refers to white matter in the periventricular region that is
underdeveloped or damaged (“leukomalacia”)
▪ Pathogenesis of PVL arises from two important factors:
• Ischemia/hypoxia
o The periventricular white matter of the
neonatal brain is supplied by the distal
segments of adjacent cerebral arteries.
o Since preterm and even term neonates
have low cerebral blood flow, the
periventricular white matter is susceptible to
ischemic damage.
o Autoregulation of cerebral blood flow usually
protects the fetal brain from hypoperfusion;
however, it is limited in preterm infants due
to immature vasoregulatory mechanisms
and underdevelopment of arteriolar smooth
muscles.
• Infection/inflammation.
o Infections also activate microglial cells,
which release free radicals.
o Premyelinating oligodendrocytes have
immature defenses against reactive oxygen
species.
o IVH is hypothesized to cause PVL because
iron-rich blood causes iron-mediated
conversion of hydrogen peroxide to hydroxyl
radical, contributing to oxidative damage.
Signs and Symptoms
• Abnormal muscle tone: spasticity, flaccidity
• Dystonia
• Athetosis
• Chorea
• Ataxia
• Muscle spasms or feeling stiff
• Poor muscle control, reflexes and posture
• Delayed development
• Feeding or swallowing difficulties
Prognosis
• Cerebral palsy is a permanent and non-progressive disorder.
• The condition does not get better or worse as time goes on, but the
severity of symptoms can be improved and managed with adequate
treatment.
• The life expectancy of someone with cerebral palsy can vary based on
the severity of their symptoms. Cerebral palsy severity is generally
categorized as mild or severe depending on the extent of the brain
damage and the co-occurring conditions present.
• An individual with mild cerebral palsy will likely have a similar life
expectancy as an individual who does not have the condition
• Patients with severe cerebral palsy tend to have significant mobility
and/or intellectual limitations. For this reason, these individuals have a
40% chance of living to 20 years old.

• Children with cerebral palsy can increase life expectancy and live
independently with the help of quality health care and proper treatment.
1. Training in use of adaptive feeding equipment (e.g. modified eating
utensils)
2. Intervention for physical problems which restrict a child from bringing food
or liquid to the mouth (e.g. children with upper limb contractures may
have limited ability self-feed or bring food to mouth).
3. Intervention for oral motor and mechanical issues which impact the child’s
ability to chew and manage food or liquid during the oral phase of eating.
Children with CP who have abnormal oral-facial muscle tone may require
special oral motor exercises for hypo or hypertonicity of oral-facial
muscles.
4. Intervention for sensory issues which impact desire to eat (e.g. oral
sensory defensiveness).
5. Behaviorally based feeding disorders (e.g. refusal to eat).
6. Positioning problems which may impact feeding, eating, and swallowing.
For example, poor head control and inability to hold head at midline can
impact functional and safe swallowing.
6. Schizophrenia
Definition
Schizophrenia causes psychosis and is associated with considerable
disability and may affect all areas of life including personal, family, social,
educational, and occupational functioning. Schizophrenia is characterized by
significant impairments in the way reality is perceived and changes in behavior
related to persistent delusions and hallucinations; experiences of influence,
control, or passivity; disorganized thinking; highly disorganized behavior;
negative symptoms; and extreme agitation or slowing of movements,
maintenance of unusual postures
Etiology
Research has not identified one single cause of schizophrenia. It is
thought that an interaction between genes and a range of environmental factors
may cause schizophrenia. Psychosocial factors may also affect the onset and
course of schizophrenia. Heavy use of cannabis is associated with an elevated
risk of the disorder.
Epidemiology
• The lifetime prevalence of schizophrenia appears to be approximately
0.3%-0.7%, although there is reported variation by race/ethnicity, across
countries, and by geographic origin for immigrants and children of
immigrants.
• The sex ratio differs across samples and populations: for example, an
emphasis on negative symptoms and longer duration of disorder
(associated with poorer outcome) shows higher incidence rates for males,
whereas definitions allowing for the inclusion of more mood symptoms
and brief presentations (associated with better outcome) show equivalent
risks for both sexes.
Pathophysiology
• Schizophrenia is a complex disorder involving dysregulation of multiple
pathways in its pathophysiology.
• Dopaminergic, glutamatergic and GABAergic neurotransmitter systems
are affected in schizophrenia and interactions between these receptors
contribute to the pathophysiology of the disease.
• Deficits in acetylcholine muscarinic receptors have been identified in a
sub-group of individuals with schizophrenia. Inflammation has also been
found to play a major role in the development and exacerbation of
psychotic symptoms in schizophrenia.
• Additionally, evidence from genetic, post-mortem and animal studies over
the past decade has identified a number of susceptibility factors for
schizophrenia.
Signs and Symptoms
A. Two (or more) of the following, each present for a significant portion of
time during a 1-month period (or less if successfully treated). At least one
of these must be (1 ), (2), or (3):
1. Delusions.
2. Hallucinations.
3. Disorganized speech (e.g., frequent derailment or incoherence).
4. Grossly disorganized or catatonic behavior.
5. Negative symptoms (i.e., diminished emotional expression or
avolition).
B. For a significant portion of the time since the onset of the disturbance,
level of functioning in one or more major areas, such as work,
interpersonal relations, or self-care, is markedly below the level achieved
prior to the onset
C. Continuous signs of the disturbance persist for at least 6 months. This 6-
month period must include at least 1 month of symptoms and may include
periods of prodromal or residual symptoms. During these prodromal or
residual periods, the signs of the disturbance may be manifested by only

negative symptoms or by two or more symptoms listed in Criterion A
present in an attenuated form
D. Schizoaffective disorder and depressive or bipolar disorder with psychotic
features have been ruled out because either
1. no major depressive or manic episodes have occurred
concurrently with the active-phase symptoms, or
2. if mood episodes have occurred during active-phase symptoms,
they have been present for a minority of the total duration of the
active and residual periods of the illness.
E. The disturbance is not attributable to the physiological effects of a
substance or another medical condition.
F. If there is a history of autism spectrum disorder or a communication
disorder of childhood onset, the additional diagnosis of schizophrenia is
made only if prominent delusions or hallucinations, in addition to the other
required symptoms of schizophrenia, are also present for at least 1
month.
Prognosis
• The effect of age at onset is likely related to gender, with males having
worse premorbid adjustment, lower educational achievement, more
prominent negative symptoms and cognitive impairment, and in general a
worse outcome.
• Focused on occupational engagement and occupational balance.
• Psychosocial ot is concerned with helping persons with schizophrenia
become occupied with experiences that are real.
• Purposeful activity through occupational engagement is central.
• Behavior modify intervention (bmi) can be used in behavior therapy to
change habits which are currently dysfunctional.
7. BIPOLAR DISORDER
BIPOLAR I DISORDER
Definition
According to the DSM-5, the bipolar I disorder criteria represent the
modern understanding of the classic manic-depressive disorder or affective
psychosis described in the nineteenth century, differing from that classic
description only to the extent that neither psychosis nor the lifetime
experience of a major depressive episode is a requirement. However, the
vast majority of individuals whose symptoms meet the criteria for a fully
syndromal manic episode also experience major depressive episodes during the
course of their lives.
Etiology
The exact cause of bipolar disorder is unknown. Experts believe there are a
number of factors that work together to make a person more likely to develop it.
These are thought to be a complex mix of physical, environmental and social
factors.
• Chemical imbalances in the brain
The chemicals responsible for controlling the brain's functions are called
neurotransmitters, and include noradrenaline, serotonin and dopamine. There's
some evidence that if there's an imbalance in the levels of 1 or more
neurotransmitters, a person may develop some symptoms of bipolar disorder.
• Genetics
It is also thought bipolar disorder is linked to genetics, as it seems to run in
families. The family members of a person with bipolar disorder have an increased
risk of developing it themselves.
But no single gene is responsible for bipolar disorder. Instead, a number of
genetic and environmental factors are thought to act as triggers.
• Triggers
o Stressful circumstances or situations often trigger the symptoms
of bipolar disorder. Examples of stressful triggers include the
breakdown of a relationship, physical, sexual or emotional abuse,
or the death of a close family member or loved one. These types
of life-altering events can cause episodes of depression at any
time in a person's life.
o For a diagnosis of bipolar I disorder, it is necessary to meet the
following criteria for a manic episode. The manic episode may
have been preceded by and may be followed by hypomanic or
major depressive episodes.
Epidemiology
• Epidemiological studies have suggested a lifetime prevalence of
around 1% for bipolar type I in the general population.
• A large cross-sectional survey of 11 countries found the overall lifetime
prevalence of bipolar spectrum disorders was 2.4%, with a prevalence of
0.6% for bipolar type I.
• Although findings varied across different countries, this suggested a lower
prevalence of bipolar type I and II than previous studies, while the
prevalence of bipolar type I in the USA was found to be 1%, slightly
higher than the other countries.

Signs and Symptoms
• Manic Episode
A. A distinct period of abnormally and persistently elevated, expansive,
or irritable mood and abnormally and persistently increased goal-
directed activity or energy, lasting at least 1 week and present
most of the day, nearly every day (or any duration if hospitalization
is necessary).
B. During the period of mood disturbance and increased energy or
activity, three (or more) of the following symptoms (four if the mood is
only irritable) are present to a significant degree and represent a
noticeable change from usual behavior:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are
racing.
5. Distractibility
6. Increase in goal-directed activity or psychomotor agitation
7. Excessive involvement in activities that have a high potential for
painful consequences
C. The mood disturbance is sufficiently severe to cause marked
impairment in social or occupational functioning or to necessitate
hospitalization to prevent harm to self or others, or there are psychotic
features.
D. The episode is not attributable to the physiological effects of a
substance (e.g., a drug of abuse, a medication, other treatment) or to
another medical condition.
• Hypomanic Episode
A. A distinct period of abnormally and persistently elevated, expansive,
or irritable mood and abnormally and persistently increased activity
or energy, lasting at least 4 consecutive days and present most
of the day, nearly every day.
B. During the period of mood disturbance and increased energy and
activity, three (or more) of the following symptoms (four if the mood is
only irritable) have persisted, represent a noticeable change from
usual behavior, and have been present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are
racing.
5. Distractibility as reported or observed.
6. Increase in goal-directed activity or psychomotor agitation.
7. Excessive involvement in activities that have a high potential for
painful consequences
• Major Depressive Episode
A. Five (or more) of the following symptoms have been present during
the same 2-week period and represent a change from previous
functioning; at least one of the symptoms is either (1) depressed
mood or (2) loss of interest or pleasure.
1. Depressed mood most of the day, nearly every day, as
indicated by either subjective report
2. Markedly diminished interest or pleasure in all, or almost all,
activities most of the day, nearly every day
3. Significant weight loss when not dieting or weight, or decrease
or increase in appetite nearly every day.
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt
early every day
8. Diminished ability to think or concentrate, or indecisiveness,
nearly every day (
9. Recurrent thoughts of death, recurrent suicidal ideation without
a specific plan, or a suicide attempt or a specific plan for
committing suicide.
C. The symptoms cause clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
D. The episode is not attributable to the physiological effects of a
substance or another medical condition.
Pathophysiology
• Despite major research achievements, the underlying pathophysiology of
bipolar disorders, including molecular causes and mechanisms, is still
unclear.
Prognosis
• Bipolar 1 disorder usually has a poor prognosis. 50% of patients
experience a second episode within two years of the first episode.

BIPOLAR II DISORDER
Definition
Bipolar II disorder, requiring the lifetime experience of at least one episode
of major depression and at least one hypomanic episode, is no longer
thought to be a "milder" condition than bipolar I disorder, largely because of the
amount of time individuals with this condition spend in depression and because
the instability of mood experienced by individuals with bipolar II disorder is
typically accompanied by serious impairment in work and social functioning.
Epidemiology
• While in DSM-IV, BP-II is reported to have a lifetime community
prevalence of 0.5%, epidemiological studies have instead found that it
has a lifetime community prevalence (including the bipolar spectrum) of
around 5%.
• The 12-month prevalence of bipolar II disorder, internationally, is 0.3%.
Signs and Symptoms
• For a diagnosis of bipolar II disorder, it is necessary to meet the following
criteria for a current or past hypomanic episode AND the following
criteria for a current or past major depressive episode.
Bipolar II Disorder
A. Criteria have been met for at least one hypomanic episode and at least
one major depressive episode
B. There has never been a manic episode.
C. The occurrence of the hypomanic episode(s) and major depressive
episode(s) is not better explained by schizoaffective disorder,
schizophrenia, schizophreniform disorder, delusional disorder, or other
specified or unspecified schizophrenia spectrum and other psychotic
disorder. D. The symptoms of depression or the unpredictability caused
by frequent alternation between periods of depression and hypomania
causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning.
Prognosis
• Bipolar II disorder has a more chronic course of illness than bipolar I
disorder.
• If untreated, bipolar II disorder results in patients spending most of their
lives suffering from depression and related disability.
• Psychosocial impairment is usually worse than in bipolar II disorder.
• To improve prognosis, long-term therapy is recommended. With
treatment, suicide risks usually decrease (especially when lithium is
used), and the episodes are reduced in frequency and severity.
OT Management and Intervention
• ADL training
• Leisure and social exploration and participation
8. MAJOR DEPRESSIVE DISORDER
Definition
Major depressive disorder (MDD) has been ranked as the third cause of the
burden of disease worldwide in 2008 by WHO, which has projected that this
disease will rank first by 2030. It is diagnosed when an individual has a
persistently low or depressed mood, anhedonia or decreased interest in
pleasurable activities, feelings of guilt or worthlessness, lack of energy,
poor concentration, appetite changes, psychomotor retardation or
agitation, sleep disturbances, or suicidal thoughts. Per the Diagnostic and
Statistical Manual of Mental Disorders, 5th Edition (DSM-5), an individual must
have five of the above-mentioned symptoms, of which one must be a depressed
mood or anhedonia causing social or occupational impairment, to be diagnosed
with MDD.
Etiology
The etiology of major depressive disorder is believed to be multifactorial,
including biological, genetic, environmental, and psychosocial factors. MDD
was earlier considered to be mainly due to abnormalities in
neurotransmitters, especially serotonin, norepinephrine, and dopamine.
This has been evidenced by the use of different antidepressants such as
selective serotonin receptor inhibitors, serotonin-norepinephrine receptor
inhibitors, dopamine-norepinephrine receptor inhibitors in the treatment of
depression. People with suicidal ideations have been found to have low levels of
serotonin metabolites. However, recent theories indicate that it is associated
primarily with more complex neuroregulatory systems and neural circuits,
causing secondary disturbances of neurotransmitter systems.
Severe early stress can result in drastic alterations in neuroendocrine and
behavioral responses, which can cause structural changes in the cerebral cortex,
leading to severe depression later in life. Structural and functional brain
imaging of depressed individuals has shown increased hyperintensities in
the subcortical regions, and reduced anterior brain metabolism on the left
side, respectively. Family, adoption, and twin studies have indicated the role of

genes in the susceptibility of depression. Genetic studies show a very high
concordance rate for twins to have MDD, particularly monozygotic twins. Life
events and personality traits have shown to play an important role, as well. The
learned helplessness theory has associated the occurrence of depression with
the experience of uncontrollable events. Per cognitive theory, depression occurs
as a result of cognitive distortions in persons who are susceptible to depression.
Epidemiology
• Major depressive disorder is a highly prevalent psychiatric disorder.
• It has a lifetime prevalence of about 5 to 17 percent, with the average
being 12 percent.
• The prevalence rate is almost double in women than in men.
• Mean age of onset is about 40 years
• MDD is more common in people without close interpersonal relationships,
and who are divorced or separated, or widowed.
• Depression is found to be more prevalent in rural areas than in urban
areas.
Pathophysiology
• GABA, an inhibitory neurotransmitter, and glutamate and glycine, both of
which are major excitatory neurotransmitters, are found to play a role in
the etiology of depression as well.
• Depressed patients have been found to have lower plasma, CSF,
and brain GABA levels.
• GABA is considered to exert its antidepressant effect by inhibiting the
ascending monoamine pathways, including mesocortical and mesolimbic
systems.
Signs and Symptoms
A. Five (or more) of the following symptoms have been present during the
same 2-week period and represent a change from previous functioning; at
least one of the symptoms is either (1) depressed mood or (2) loss of
interest or pleasure.
1. Depressed mood most of the day, nearly every day, as indicated by
either subjective report or observation made by others
2. Markedly diminished interest or pleasure in all, or almost all, activities
most of the day, nearly every day
3. Significant weight loss when not dieting or weight gain, or decrease
or increase in appetite nearly every day.
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate nearly every
day
8. Diminished ability to think or concentrate, or indecisiveness, nearly
every day
9. Recurrent thoughts of death, recurrent suicidal ideation without a
specific plan, or a suicide attempt or a specific plan for committing
suicide.
B. The symptoms cause clinically significant distress or impairment in social,
occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance
or to another medical condition.
D. The occurrence of the major depressive episode is not better explained
by schizoaffective disorder, schizophrenia, schizophreniform disorder,
delusional disorder, or other specified and unspecified schizophrenia
spectrum and other psychotic disorders.
E. There has never been a manic episode or a hypomanic episode.
Prognosis
• The prognosis of MDD is good in patients with mild episodes, the
absence of psychotic symptoms, better treatment compliance, a strong
support system, and good premorbid functioning.
• The prognosis is poor in the presence of a comorbid psychiatric disorder,
personality disorder, multiple hospitalizations, and advanced age of
onset.
• Teaching strategies to help with the fatigue that can accompany
depression. This may include relaxation, pacing and prioritization
• ADL training
• Establishing routines
• Self-esteem management techniques
• Work hardening
• Role exploration
• Improving self-esteem
9. Personality disorders
Definition
• An enduring pattern of inner experience and behavior that deviates
markedly from the expectations of the individual’s culture, is pervasive
and inflexible, has an onset in adolescence or early adulthood, is stable
over time, and leads to distress or impairment.

• A collection of traits that have become rigid and work to a person’s
disadvantage, to the point that it may impair functioning or cause
distress.
• These patterns of behavior and thinking have been present since early
adult life and have been recognizable in the patient for a long time.
• In the DSM-5, these personality disorders are grouped into three clusters
based on descriptive similarities.
Cluster A:
• Paranoid, schizoid, and schizotypal personality disorders.
• People with Cluster A PD can be described as
• Individuals with these disorders often appear odd or eccentric.
Cluster B:
• Antisocial, borderline, histrionic, and narcissistic personality disorders.
• Those with Cluster B PDs tend to be theatrical, emotional, and attention-
seeking; their moods are labile and often shallow. They often have
intense interpersonal conflicts.
• Individuals with these disorders often appear dramatic, emotional,
or erratic.
Cluster C:
• Avoidant, dependent, and obsessive-compulsive personality disorders.
• Someone with a Cluster C PD will tend to be anxious and tense, often
overcontrolled.
• Individuals with these disorders often appear anxious or fearful.
Etiology
• The cause of Paranoid Personality Disorder is unknown.
• Schizotypal personality disorder is genetically linked with
schizophrenia. Evidence for dysregulation of dopaminergic pathways in
these patients exists.
• a combination of genetic and environmental factors, particularly in early
childhood, may play a role in developing schizoid personality disorder.
• A genetic contribution to antisocial behaviors is strongly supported.
• There may also be developmental or acquired abnormalities in the
prefrontal brain systems and reduced autonomic activity in antisocial
personality disorder.
• Psychosocial formulations point to the high prevalence of early abuse in
these patients, and the borderline syndrome is often formulated as a
variant of posttraumatic stress disorder.
Epidemiology
• The prevalence for paranoid personality disorder is estimated to be
between 2.3 to 4.4%.
• Schizoid personality disorder is slightly more common in males than in
females
• Reported prevalence of schizotypal personality disorder varies, but
estimated prevalence is about 3.9% of the general US population.
This disorder may be slightly more common among men.
• Antisocial personality disorder is 3 times more prevalent in men than in
women.
• Borderline personality disorder is 3 times more common in women than in
men.
• Histrionic Personality Disorder has a prevalence of 2.1% in a general
population
• patients with narcissistic personality disorder, 50-75% are male.
• In the general adult population, the prevalence of avoidant personality
disorder is estimated to be 2.1–2.6%.
• Less than 1% of adults meet the criteria for DPD. More women than men
tend to have Dependent Personality Disorder
• Obsessive-compulsive personality disorder is diagnosed twice as often in
men as in women
Pathophysiology
• In patients with personality disorders, abnormalities may be seen in the
frontal, temporal, and parietal lobes.
• These abnormalities may be caused by perinatal injury, encephalitis,
trauma, or genetics.
• Personality disorders are also seen with diminished monoamine
oxidase (MAO) and serotonin levels.
Signs and Symptoms
• Cluster A: Paranoid, schizoid, and schizotypal personality
disorders.
o Withdrawn, cold, suspicious, or irrational.
o Individuals with these disorders often appear odd or
eccentric.
o Paranoid Personality Disorder
▪ The essential feature of paranoid personality disorder is
a pattern of pervasive distrust and suspiciousness of
others such that their motives are interpreted as
malevolent.
o Schizoid Personality Disorder
▪ The essential feature of schizoid personality disorder is
a pervasive pattern of detachment from social relationships

and a restricted range of expression of emotions in
interpersonal settings. This pattern begins by early
adulthood and is present in a variety of contexts.
o Schizotypal Personality Disorder
▪ The essential feature of schizotypal personality disorder
is a pervasive pattern of social and interpersonal deficits
marked by acute discomfort with, and reduced capacity for,
close relationships as well as by cognitive or perceptual
distortions and eccentricities of behavior.
• Cluster B: Antisocial, borderline, histrionic, and narcissistic
personality disorders.
o Theatrical, emotional, and attention-seeking; their moods are
labile and often shallow.
o They often have intense interpersonal conflicts.
o Individuals with these disorders often appear dramatic, emotional,
or erratic.
o Antisocial personality disorder
▪ A pervasive pattern of disregard for and violation of the
rights of others
o Borderline Personality Disorder
▪ The essential feature of borderline personality disorder
is a pervasive pattern of instability of interpersonal
relationships, self-image, and affects, and marked
impulsivity that begins by early adulthood and is present in
a variety of contexts.
o Histrionic Personality Disorder
▪ Essential feature: pervasive and excessive emotionality
and attention-seeking behavior
o Narcissistic Personality Disorder
▪ The essential feature of narcissistic personality disorder is
a pervasive pattern of grandiosity, need for admiration, and
lack of empathy that begins by early adulthood and is
present in a variety of contexts.
• Cluster C: Avoidant, dependent, and obsessive-compulsive
personality disorders
o Tend to be anxious and tense, often overcontrolled.
o Individuals with these disorders often appear anxious or fearful
o Avoidant Personality Disorder
▪ The essential feature of avoidant personality disorder ís a
pervasive pattern of:
▪ Social inhibition
▪ Feelings of inadequacy
▪ Hypersensitivity to negative evaluation that begins
by early adulthood and is present in a variety of
contexts
o Dependent Personality Disorder
▪ a pervasive and excessive need to be taken care of that
leads to:
▪ Submissive and clinging behavior
▪ Fears of separation.
o Obsessive- Compulsive Personality Disorder
o The essential feature of obsessive-compulsive personality
disorder is a preoccupation with orderliness, perfectionism, and
mental and interpersonal control, at the expense of flexibility,
openness, and efficiency.
Prognosis
• Personality disorders are lifelong conditions, although attributes of cluster
A and B disorders tend to become less severe and intense in middle age
and late life.
• Patients with a cluster B personality disorder are particularly susceptible
to problems of substance abuse, impulse control, and suicidal behavior,
which may shorten their lives.
• ADL retraining
• Cognitive behavioral therapy
• Psychodynamic psychotherapy
• Trauma-informed care
• Dialectical behavioral therapy (DBT
• Sensory stimulation
• Realistic self-appraisal
• Relaxation training
10. OBSESSIVE-COMPULSIVE DISORDER
Definition
OCD is characterized by the presence of obsessions and/or compulsions.
Obsessions are recurrent and persistent thoughts, urges, or images that are
experienced as intrusive and unwanted, whereas compulsions are repetitive
behaviors or mental acts that an individual feels driven to perform in response to
an obsession or according to rules that must be applied rigidly.

Etiology
The exact cause of obsessive-compulsive disorder (OCD) remains
unknown, but it is likely multifactorial. There is a genetic predisposition, as 45 to
65% of the variance of OCD is attributable to genetic factors. Other factors
include:
Temperamental. Greater internalizing symptoms, higher negative
emotionality, and behavioral inhibition in childhood are possible temperamental
risk factors.
Environmental. Physical and sexual abuse in childhood and other
stressful or traumatic events have been associated with an increased risk for
developing OCD.
Epidemiology
• The 12-month prevalence of OCD in the United States is 1.2%, with a
similar prevalence internationally (1.1%–1.8%).
• Females are affected at a slightly higher rate than males in adulthood,
although males are more commonly affected in childhood.
Pathophysiology
• By evaluating individuals who develop OCD after developing a brain
lesion or stroke, OCD symptoms were localized to certain areas of the
brain through fMRIs, DTI, and SPECT imaging.
• OCD has been observed to be linked to the cortico-striato-thalamo-
cortical circuits, particularly the orbitofrontal cortex, the caudate, anterior
cingulate cortex, and thalamus.
Signs & Symptoms
• Cleaning (contamination obsessions and cleaning compulsions)
• Symmetry (symmetry obsessions and repeating, ordering, and counting
compulsions)
• Forbidden or taboo thoughts (e.g., aggressive, sexual, and religious
obsessions and related compulsions)
• Harm (e.g., fears of harm to oneself or others and related checking
compulsions)
• Repetitive behaviors (e.g., mirror checking, excessive grooming, skin
picking, or reassurance seeking)
• Mental acts (e.g., comparing one’s appearance with that of other people)
Prognosis
• Obsessive-compulsive disorder (OCD) typically is a lifelong illness,
though some experience a waxing and waning course.
• Even with CBT and/or SSRIs, seldom do the symptoms ever resolve.
• Of those who have successful treatment, about 50% have residual
symptoms.
• If OCD does not get treated, the course is typically chronic, and it may be
an episodic course, with a minority having a deteriorating course.
OT management and intervention
• Cognitive-behavioral therapy is a treatment for OCD that uses two
scientifically based techniques to change a person’s behavior and
thoughts: exposure and response prevention (ERP) and cognitive
therapy.
• Imaginal Exposure. Referred to as visualization, can be a helpful way to
alleviate enough anxiety to move willingly to ERP
• Habit Reversal Training. This intervention includes awareness training,
introduction of a competing response, social support, positive
reinforcement, and often relaxation techniques.
11. CEREBROVASCULAR ACCIDENT (CVA)
Definition
It is a complex dysfunction caused by a lesion in the brain. According to
WHO, stroke is defined as an “acute neurological dysfunction of vascular origin
with symptoms and signs corresponding to the involvement of focal areas of the
brain.”
Etiology
There are two main causes of stroke: a blocked artery (ischemic stroke)
or leaking or bursting of a blood vessel (hemorrhagic stroke). Some people may
have only a temporary disruption of blood flow to the brain, known as a transient
ischemic attack (TIA), that doesn't cause lasting symptoms.
Ischemic stroke
This is the most common type of stroke. It happens when the brain's blood
vessels become narrowed or blocked, causing severely reduced blood flow
(ischemia). Blocked or narrowed blood vessels are caused by fatty deposits that
build up in blood vessels or by blood clots or other debris that travel through the
bloodstream, most often from the heart, and lodge in the blood vessels in the
brain.
Hemorrhagic stroke
Hemorrhagic stroke occurs when a blood vessel in the brain leaks or ruptures.
Brain hemorrhages can result from many conditions that affect the blood vessels.
Factors related to hemorrhagic stroke include:
• Uncontrolled high blood pressure

• Overtreatment with blood thinners (anticoagulants)
• Bulges at weak spots in your blood vessel walls (aneurysms)
• Trauma (such as a car accident)
• Protein deposits in blood vessel walls that lead to weakness in the
vessel wall (cerebral amyloid angiopathy)
• Ischemic stroke leading to hemorrhage
A less common cause of bleeding in the brain is the rupture of an irregular tangle
of thin-walled blood vessels (arteriovenous malformation).
Transient ischemic attack (TIA)
A transient ischemic attack (TIA) — sometimes known as a ministroke — is a
temporary period of symptoms similar to those in a stroke. A TIA doesn't cause
permanent damage. A TIA is caused by a temporary decrease in blood supply to
part of the brain, which may last as little as five minutes.
Like an ischemic stroke, a TIA occurs when a clot or debris reduces or blocks
blood flow to part of the nervous system.
Epidemiology
• Stroke is the second leading cause of death globally.
• It affects roughly 13.7 million people and kills around 5.5 million
annually.
• Approximately 87% of strokes are ischemic infarctions, a prevalence that
increased substantially between 1990 and 2016, attributed to decreased
mortality and improved clinical interventions. Primary (first-time)
hemorrhages comprise the majority of strokes, with secondary (second-
time) hemorrhages constituting an estimated 10–25%
• The incidence of stroke increases with age, doubling after the age of
55 years.
• The occurrence of stroke in men and women also depends on age. It
is higher at younger ages in women, whereas incidence increases slightly
with older age in men.
Pathophysiology
• Stroke is defined as an abrupt neurological outburst caused by impaired
perfusion through the blood vessels to the brain.
• Ischemic stroke is caused by deficient blood and oxygen supply to the
brain; hemorrhagic stroke is caused by bleeding or leaky blood vessels.
Signs and Symptoms
• Contralateral hemiplegia
• Sensory loss / proprioceptive loss
• Discoordination/ataxia
• Spasticity / altered muscle tone
• Pain - leads to contractures and learned non-use difficulty with weight
shifts balancing and stepping resulting in the risk of falls and injury
• Balance
• Communication
o Aphasia
o Dysarthria
• Cognition
• Difficulty with attention, memory, problem-solving, safety awareness, and
planning - executive processing skills
• Cognitive endurance affected
Prognosis
• The patient prognosis after an ischemic stroke is much more positive than
after a hemorrhagic stroke.
• Hemorrhagic stroke increases the risk of dangerous complications such
as increased intracranial pressure or spasms in the brain vasculature.
• Many people who survive a stroke recover their independence, although
around one quarter are left living with minor disabilities and around 40%
have more severe disabilities
• Transfers
• Bed mobility
• Wheelchair techniques
• Sling use
• Bed level activities
• Splints
• Edema management
• Pain management
12. Traumatic Brain Injury (TBI)
Definition
TBI is defined as an alteration in brain function, or other evidence of
brain pathology, caused by an external force.
Etiology
TBI is usually caused by a blow or other traumatic injury to the head
or body. The degree of damage can depend on several factors, including the
nature of the injury and the force of impact.

• Falls
• Motor vehicular accidents
• Violence (gunshot wounds, domestic violence, child abuse, assault)
• Sports injuries
• Explosive blasts and other combat injuries
Epidemiology
• Each year, approximately 1.7 million civilians in the United States
sustain a TBI
• Approximately 80,000–90,000 Americans experience a new onset of
disability resulting from TBI each year with an estimated 3.1 million
children and adults in the United States living with a lifelong TBI-
related disability.
• Adolescents aged 15-19 years have the highest rate of TBI-related
emergency visits in the U.S., where adults aged 75 years and older have
the highest rates of TBI-related hospitalization and death.
• Regardless of age, the rates for TBI are higher for males than for
females.
Pathophysiology
• Traumatic brain injury of any sort can cause cerebral edema and
decreased brain blood flow.
• Any swelling from edema or an intracranial hematoma can lead to
increase of intracranial pressure which makes cerebral perfusion
pressure decrease.
• When the cerebral perfusion pressure falls below 50 mmHG, the brain
may become ischemic.
• Ischemia and edema may trigger various secondary mechanisms of
injury, causing further cell damage, edema, and increase of ICP.
• If excessive ICP is unrelieved, it can cause brain herniation.
Signs and Symptoms
• Loss of consciousness (moderate or severe)
• Confusion or amnesia (minor injuries)
• Emotional lability
• Behavioral changes (agitation, impulsivity, lack of motivation, etc)
• Sleep disturbances
• Decrease intellectual function
• Seizures (within first hour or day)
• Coma
• Headache
• Hemiparesis
• Hypertension
Prognosis
• Children overall do better than adults with a comparable injury.
• The vast majority of patients with mild TBI retain good neurologic
function.
• With moderate or severe TBI, the prognosis is not as good but is
much better than is generally believed.
• Posttraumatic anosmia and acute traumatic blindness seldom resolve
after 3 to 4 months. Hemiparesis and aphasia usually resolve at least
partially, except in older patients.
• Home management
• Social skills
• Improve cognitive function
• Regain functional independent living skills
• Community reintegration
13. SPINAL CORD INJURY (SCI)
Definition
According to World Health Organization, this refers to damage to the
spinal cord resulting from trauma or from disease or degeneration
Etiology
Spinal cord injuries can be grossly divided into two broad etiological
categories: traumatic and nontraumatic.
• Traumatic injury results from damage caused by events such as
motor vehicle accidents (38%), falls (30.5%), violence (13.5%),
and sports-related injuries (9%).
• Nontraumatic damage in adult populations generally results from
disease or pathological influence.
o Conditions that may damage the spinal cord are
▪ Vascular dysfunction
▪ Spinal stenosis
▪ Spinal neoplasms
▪ Syringomyelia
▪ Infection
▪ Neurological diseases

Epidemiology
• Every year, around the world, between 250 000 and 500 000 people
suffer a spinal cord injury (SCI).
• Estimated annual global incidence is 40 to 80 cases per million population
• Males are most at risk in young adulthood (20-29 years) and older age
(70+).
• Females are most at risk in adolescence (15-19) and older age (60+).
Pathophysiology
1. Primary Injury: acute compression, impact, missile, distraction, laceration
and shear
2. Secondary injury begins:
1. Acute Phase:
1. Spinal ischemia
2. Vasogenic edema
3. Glutamate excitotoxicity
2. Sub-acute Phase:
1. Mitochondrial phosphorylation
2. Production of reactive oxygen species and reactive
nitrogen species
3. Neuroinflammation
3. Chronic Phase
1. Apoptosis and necrosis
2. Acute axonal degeneration, axonal remodeling and
demyelination
3. Glilal scar formation
Signs and Symptoms
• Partial or complete loss of sensory function or motor control of arms, legs
and/or body.
• Spinal Shock
• Autonomic Dysreflexia
• Spastic Hypertonia
• Cardiovascular Impairment
• Impaired Temperature Control
• Pulmonary Impairment
• Bladder and Bowel Impairment
• Sexual Dysfunction
Prognosis
• Life expectancy for people with SCI has not significantly improved since
the 1980s and is lower than people without SCI.
• Factors that influence life expectancy are age at onset and level and
extent of neurological injury.
• Individuals with an incomplete neurological SCI have a longer life
expectancy than those with a complete injury, and individuals with more
caudal injuries also have a greater life expectancy
• ADL training
• Restorative rehabilitation
• Skin management
• Home modification
• Assistive devices
• Adaptive equipment
• Work rehabilitation
• Leisure participation
14. BURNS
Definition
“A burn is an injury to the skin or other organic tissue primarily caused by heat or
due to radiation, radioactivity, electricity, friction or contact with
chemicals.” (WHO, 2018)
Etiology
• Fire and flames (43%), Scald injuries (34%), Contact burns (9%),
Electrical injury (4%), Chemical burns (3%), Others (7%)
• Home (73%), Occupational sites (8%), Motor vehicles (5%),
Recreation/sport activities (5%), Others (9%)
• The chances of dying of fire or smoke inhalation is about 1 in 1,442.
Epidemiology
• Burns are a global public health problem, accounting for an estimated 180
000 deaths annually.
• The majority of these occur in low- and middle-income countries and
almost two thirds occur in the WHO African and South-East Asia regions.
• Burns are among the leading causes of disability-adjusted life-years
(DALYs) lost in low- and middle-income countries.
• Men are twice likely as women to suffer a burn injury
Pathophysiology
• Characterized by an inflammatory reaction leading to rapid edema
formation, due to increased microvascular permeability, vasodilation and
increased extravascular osmotic activity.

• These reactions are due to the direct heat effect on the
microvasculature and to chemical mediators of inflammation.
Signs and Symptoms and Prognosis
BURN WOUND CHARACTERISTICS
Burn Depth Common
Causes
Tissue
Depth
Clinical
Findings
Healing Time Healing
Time
Superficial
(1st degree
burn)
Sunburn, brief
flash burns,
brief exposure
to hot liquids
or chemical
Superficial
epidermis
Erythema,
dry, no
blisters, short-
term
moderate
pain
3–7 days No potential
scars or
contractures
Superficial
partial
thickness and
donor sites
(2nd degree
burn)
Severe
sunburn or
radiation burn,
prolonged
exposure to
hot liquids,
contact with
hot metal
objects
Epidermis,
upper
dermis
Erythema,
wet, blisters;
significant pai
Less than 2
weeks
Minimal
potential for
scars or
contractures
if healing is
delayed
Deep partial
thickness
(3rd degree
burn)
Flames or
contact of hot
surfaces
Epidermis
and much
of the
dermis
Erythema;
larger, usually
broken
blisters on
skin with hair
Longer than 2
weeks
High potential
for
hypertrophic
scarring and
contractures
across joints,
web spaces,
and facial
contours
Boutonniere
deformities in
fingers
Full thickness
(4th degree
burn)
Extreme heat
or prolonged
exposure to
heat, hot
objects, or
chemicals
Epidermis
and
dermis
Pale, non
blanching,
dry,
coagulated
capillaries
possible; no
sensation to
light touch
Surgical
intervention
required for
wound closure
in larger areas;
Extremely
high potential
for
hypertrophic
scarring or
contractures
Full thickness
with
complications
(5th degree
burn)
with
complications
Electrical
burns and
severe long
duration burns
Full-
thickness
burn with
damage to
underlying
tissue
Possible
charring of
nonviable
surface or,
with exposed
fat, possible
presence of
small external
wounds on
tendons,
muscles; with
electrical
injuries
Requires
surgical
intervention for
wound closure;
may require
amputation or
significant
reconstruction
Similar to full-
thickness
burns except
when
amputation
removes the
burn site
• Edema (swelling) management
• Scar management
• Functional upper limb therapy
• Occupational therapy may also address:
• Burn skin hypersensitivity
• Cognition/thinking ability
• Assistive equipment for safety and independence
• Home environment assessment and modifications
• Corrective cosmetics
• Return to work or school and driving
• Referral to other specialist services as required.
• Movement, exercise, strengthening, stretching
15. CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Definition
Chronic obstructive pulmonary disease (COPD) is a combination of
emphysema and bronchitis (MedicineNet, 2005). Emphysema is the progressive
and irreversible destruction of the alveoli walls (Etkin, Lenker, & Mills, 2005). The
walls of the alveoli have elastic fibers, and when these are destroyed, the lung
loses some of its elasticity, resulting in air trapping. This air trapping reduces the
ability of the lung to shrink during exhalation; the lung then inhales less air with
the next breath (MedicineNet, 2005). Chronic bronchitis is defined as excessive
sputum production and cough of at least 3 months in duration occurring 2 years
in a row (MedicineNet, 2005). This inflammation also causes the bronchial tubes
to increase their production of mucus. The result of these processes is that the
patient experiences sudden shortness of breath and may wheeze or cough.

Etiology
• The cause of COPD is usually long-term exposure to irritants that
damage your lungs and airways.
• In the United States, cigarette smoke is the main cause.
• Pipe, cigar, and other types of tobacco smoke can also cause COPD,
especially if you inhale them.
• Exposure to other inhaled irritants can contribute to COPD.
Epidemiology
• Chronic Obstructive Pulmonary Disease (COPD) is the fourth leading
killer of Americans (American Lung Association, 2004).
• Lung disease is not only a killer; it is also chronic and significantly alters
the lives of those who have it.
• 70% of persons with COPD say it limits their ability to do normal exertion
(American Lung Association, 2004).
Pathophysiology
Damage to the lung results in a flattening of the diaphragm due to
hyperinflation. This flattening takes away the ability of the diaphragm to act
effectively in assisting with expansion of the lungs during inspiration. To
compensate for the lack of inspiratory pressure, patients with COPD tend to use
their shoulder girdle muscles to expand their lungs, making it difficult to use those
muscles in unsupported upper extremity activities (Coppola & Wood, 2000).
Signs and Symptoms
• COPD symptoms often don't appear until significant lung damage has
occurred, and they usually worsen over time, particularly if smoking
exposure continues.
• Signs and symptoms of COPD may include:
o Shortness of breath, especially during physical activities
o Wheezing
o Chest tightness
o A chronic cough that may produce mucus (sputum) that may be
clear, white, yellow or greenish
o Frequent respiratory infections
o Lack of energy
o Unintended weight loss (in later stages)
o Swelling in ankles, feet or legs
• People with COPD are also likely to experience episodes called
exacerbations, during which their symptoms become worse than the
usual day-to-day variation and persist for at least several days.
Prognosis
• The prognosis of COPD is variable based on adherence to treatment
including smoking cessation and avoidance of other harmful gases.
• Patients with other comorbidities typically have a poorer prognosis.
• The airflow limitation and dyspnea are usually progressive.
• The goals of the occupational therapist in pulmonary rehabilitation are
(AACVPR, 2004b; O’Dell-Rossi et al., 1999):
1. ADL evaluation and training to increase functional endurance
2. Instruction and training in appropriate breathing techniques with
ADLs
3. Evaluation and strengthening of the upper extremity
4. Work simplification and energy conservation
5. Evaluation of the need for adaptive equipment
6. Assistance in adapting leisure activities
7. Education in stress management and relaxation techniques
16. MULTIPLE SCLEROSIS (MS)
Definition
Multiple sclerosis is a progressive autoimmune disease characterized by
inflammation, selective demyelination, and gliosis. It causes both acute and
chronic symptoms and can result in significant disability and impaired quality of
life.
Etiology
• The cause of multiple sclerosis is unknown
• A combination of genetics and environmental factors appears to be
responsible.
Epidemiology
• MS affects approximately 400,000 persons in the United States;
worldwide,
• MS affects approximately 2.1 million people.
• The disease is more common in women than in men by a ratio of 2:1 to
3:1, but men display a more progressive disease course and more rapid
disability.

Pathophysiology
In MS, the immune system attacks the protective sheath (myelin) that
covers nerve fibers and causes communication problems between your brain and
the rest of your body. Eventually, the disease can cause permanent damage or
deterioration of the nerves.
Relapsing-remitting MS (RRMS) is the most common course, affecting
approximately 85% of patients with MS. It is characterized by discrete attacks or
relapses followed by remissions and can also be further characterized as active
or not active. Most people diagnosed with RRMS will eventually transition to
secondary-progressive MS (SPMS). SPMS begins with a relapsing-remitting
course followed by progression to steady and irreversible worsening of
neurologic function and accumulation of disability. Primary-progressive MS
(PPMS) is a less common form occurring in about 15% of cases. It is
characterized by a nearly continuous worsening of the disease from the onset
without distinct attacks and is further characterized as active or not active and as
with progression or without progression. The 1996 category of progressive-
relapsing MS is eliminated since these patients are now classified as PPMS with
disease activity.
Signs and Symptoms
Symptoms often affect movement, such as:
• Numbness or weakness in one or more limbs that typically occurs on one
side of your body at a time, or your legs and trunk
• Electric-shock sensations that occur with certain neck movements,
especially bending the neck forward (Lhermitte sign)
• Tremor, lack of coordination or unsteady gait
Vision problems are also common, including:
• Partial or complete loss of vision, usually in one eye at a time, often with
pain during eye movement
• Prolonged double vision
• Blurry vision
Multiple sclerosis symptoms may also include:
• Slurred speech
• Fatigue
• Dizziness
• Tingling or pain in parts of your body
• Problems with sexual, bowel and bladder function
Prognosis
• It's a lifelong condition that can sometimes cause serious disability,
although it can occasionally be mild.
• Average life expectancy is slightly reduced for people with MS.
In most programs, occupational therapists focus on three specific domains:
• Self-care activities, such as bathing and using the bathroom
• Productive activities, which may include cooking, paid work, caring for
children, or volunteering
• Leisure activities, such as gardening, exercise, or other activities a person
enjoys
17. GUILLAIN BARRE SYNDROME (GBS)
Definition
Guillain-Barré (ghee-YAN bah-RAY) syndrome (also known as acute idiopathic
neuropathy, infectious polyneuritis, and Landry’s syndrome) is an acute
inflammatory disorder in which the body’s own immune system attacks
part of the peripheral nervous system. The immune system destroys the
myelin sheath that surrounds the axons of many peripheral nerves or even the
axons themselves, damaging the nerves’ ability to transmit signals to the
muscles.
Etiology
• Many infections have been linked with GBS.
• The most common are gastrointestinal or respiratory illnesses.
• Case reports detail many other possible etiologies linked to GBS
including medications and surgeries.
Epidemiology
• Although rare, with an incidence of 0.4 to 2 per 100,000, Guillain-
Barre syndrome (GBS) has major effects on the healthcare system.
• Males are affected at a slightly higher incidence than females.
• Each year, it is estimated 100,000 patients worldwide would contract
GBS.
Pathophysiology
Antecedent infections are reported in up to 70% of patients with Guillain-
Barre Syndrome (GBS). Therefore, molecular mimicry plays a substantial role in
our understanding of GBS, particularly the axonal variant. The
lipooligosaccharide of Campylobacter jejuni is similar to the gangliosides of
peripheral nerve membranes. Ganglioside antibodies have been shown to have
different peripheral nerve targets. Anti-GD1a antibodies bind to paranadol myelin,
nodes of Ranvier, and neuromuscular junction. GM1 and GQ1B antibodies bind
to a peripheral nerve or neuromuscular junction. These different peripheral nerve

targets may play a role in the heterogeneity of the clinical presentation of GBS.
Additionally, complement cascade is activated and plays a key role in the
disease’s pathogenesis.
Certain gangliosides are more likely to be associated with specific presentations.
For example, Miller-Fisher syndrome is associated with the anti-GQ1B antibody.
The axonal motor neuropathy form may be associated with anti-GM1 antibodies.
The pharyngeal-cervical-brachial variant of GBS may be associated with anti-
GT1A antibodies. However, besides Miller-Fisher syndrome’s association with
anti-GQ1B antibodies, sensitivity and specificity of all antibodies for specific
subtypes are low-to-moderate yield for clinical utility.
Given that not all patients test positive for anti-ganglioside antibodies, further
research is needed to elucidate the roles of anti-ganglioside antibodies in GBS,
as causal or epiphenomenon. Less is known about the pathophysiology behind
the acute inflammatory demyelinating polyneuropathy variant (AIDP) of GBS,
despite the fact that it is considered the most common variant in the United
States.
Signs and Symptoms
• Varying degrees of weakness and sensory changes in the legs.
• Rapidly progressive ascending symmetric weakness of bilateral
extremities, usually proceeding from distal to proximal (feet to trunk).
• Descending paralysis with predominant proximal muscle weakness rarely
appears.
• Tingling or painful sensations.
• Weakness and abnormal sensations first noticed in the legs progress to
the arms and upper body, and some muscles are almost totally
paralyzed.
• Problems with breathing, speaking, swallowing, blood pressure, or heart
rate
Prognosis
• Passive ROM should begin with gentle movement of the joints and should
not exceed the point of pain.
• Positioning
• Splinting
• Electronic Aids for Daily Living (EADLs) increase the level of
independence in the client’s control of the environment through the use of
technology
• Education about energy conservation, work simplification, avoidance of
overstretching, and overuse of muscles is critical to recovery
18. AMYOTROPHIC LATERAL SCLEROSIS (ALS)
Definition
**also known as Lou Gehrig’s DSE.
• a group of progressive, degenerative neuromuscular diseases.
• affected individuals exhibit a combination of both upper motor neuron
(UMN) and lower motor neuron (LMN) deficits at some point in the
progression of the disease.
Two primary forms of ALS are recognized: sporadic and familial. Sporadic ALS
makes up about 90% to 95% of ALS cases. Between 5% and 10% of individuals

with ALS are found to have a family history of the disease. There is no difference
in the symptoms or course of the disease for clients with the familial and sporadic
types.
Etiology
• The etiology of ALS has not been established.
• Multiple theories have been proposed as the cause of the motor neuron
destruction, including gene mutation, metabolic disorders of glutamate
insufficiency, metal toxicity, autoimmune factors, and viral infection.
Epidemiology
• ALS incidence increases after age 40, with cases peaking among those in
their 60s and 70s. There is a higher incidence in males than females.
Pathophysiology
The underlying neurologic process involves destruction of motor neurons within
the spinal cord, brainstem, and motor cortex.
Signs and Symptoms
• focal weakness beginning in the arm, leg, or bulbar muscles.
• slurred speech, abnormal fatigue, shortness of breath, and emotional
lability,
• marked muscle atrophy
• weight loss
• spasticity
• muscle cramping
• Specific cognitive deficits have been identified, such as frontal temporal
lobe dysfunction and disorders of executive function.
• Executive function impairment includes reasoning, judgment, sequencing,
ordering, inferring, regulating emotions, planning, retrieval inefficiency,
and a person’s ability to have insight into his or her behaviors.
Prognosis
• Generally, individuals with early bulbar involvement have a poorer
prognosis.
• A more positive prognosis is usually associated with the following factors:
o younger age at onset
o onset involving LMNs located in the spinal cord
o deficits in either UMNs or LMNs, not a combination of both areas;
o absent or slow changes in respiratory function;
o fewer fasciculations; and
o a longer time from the onset of symptoms to diagnosis.
• Environmental modifications
• Assistive devices
• Adaptive equipment
• Home modifications
• Caregiver training and adaptation to ADLs with assistance
19. PARKINSON’S DISEASE
Definition
• aka Primary Parkinson’s disease, Paralysis agitans or “shaking palsy”
• it refers to those cases where the etiology is idiopathic or genetically
determined
• There is a progressive loss of dopaminergic cells (neuromelanin) that
produces dopamine in the substantia nigra
• slowly progressive disorder of CNS with motor and nonmotor symptoms
• (2) Clinical Subgroups:
o (1) Dominant symptoms include postural instability and gait
disturbances (Postural Instability Gait disturbed [PIGD])
o (2) Tremor as the main feature (tremor predominant)
• Genetic forms of PD: PINK1, PARK1, LRRK2, DJ-1
• Genes grouped into (2) categories:
1. Causal genes – produces the disease
2. Associated genes – do not cause PD but increase the risk of
developing it.
Etiology
• Etiology for PD has not been definitively established
• Positive family history has been established as a risk factor for PD
• Environmental factors were considered as a possible cause of PD
Epidemiology
• One of the most common adult onsets, degenerative neurologic disorders
• The incidence rate for PD varies greatly, from 10 to more than 400 per
100,000
• Prevalence increases with age, and the disease affects 1.4% of the
population over the age of 55, but approximately 3% of all PD cases are
initially recognized in individuals younger than 50 years of age
• Prevalence of PD in men between the ages of 55 and 74 is slightly higher
than in women of the same age. After the age of 74, women show a
slightly greater prevalence of pd than do men

• Diagnosis is most often made after the age of 60
Pathophysiology
• The neurologic structure associated with PD is the substantia nigra,
specifically the pars compacta portion. The pars compacta receives input
from other basal ganglia nuclei and appears to serve as a modulator of
striatal activity. The substantia nigra nuclei undergo significant
deterioration as the disease progresses. The significant reduction in the
dopaminergic neurons in the substantia nigra pars compacta produces a
decrease in activity within the basal ganglia and an overall “reduction in
spontaneous movement.” The substantia nigra serves as one of the major
output nuclei for the basal ganglia to other structures. In addition to the
loss of dopaminergic neurons, intracytoplasmic inclusions are found on
postmortem examination within the substantia nigra. These
intracytoplasmic inclusions are also known as Lewy bodies. Although the
greatest amount of neurodegeneration is found in the pars compacta
substantia nigra, destruction of other neurologic structures has been
reported. Deterioration is also seen in the remainder of the substantia
nigra, locus ceruleus, nucleus basalis, and hypothalamus
Signs and Symptoms
• Three classic symptoms are associated with PD:
o Tremor: resting tremor with a rate between 4 and 5 Hz is a
disturbance of involuntary movement – tremor often diminishes
with activity, but in some clients the tremor persists during
performance of functional activities
o Rigidity: the stiffness within a muscle that impedes smooth
movement – this stiffness occurs in both directions for each plane
of motion at a specific joint
o Bradykinesia: disturbances in voluntary movement are identified
as difficulty initiating movement (akinesia) and slowness in
maintaining movement (bradykinesia); bradykinesia and akinesia
are often the most disabling motor symptoms for the client with PD
– the delay in initiating movement patterns and the slowness in
executing the motion compromise functional tasks such as driving,
dressing, and eating
• Additional symptoms of PD
o Disturbances in gait and postural reactions; deterioration in gait is
seen throughout the course of the disease – festinating gait is
often seen; other motor disturbance associated with gait is the
phenomenon of “freezing” to which it occurs when the person
ceases to move, often after attempting to initiate, maintain, or alter
a movement pattern
o Masked face with decreased facial expressions
o Emotional disturbances including depression and psychosis
Prognosis
• Parkinson’s disease itself is not fatal.
• However, although people do not die from Parkinson’s disease, they may
die from complications of the condition.
• The American Parkinson Disease Association also cite falls as a common
cause of death. Those with Parkinson’s are more likely than others to fall
and injure themselves. Serious falls and complications arising from
surgery to treat the injuries can both be fatal.

20. MYOCARDIAL INFARCTION
Definition
Myocardial infarction, also known as a heart attack, is a life-threatening
condition that occurs when blood flow to the heart muscle is abruptly cut off,
causing tissue damage. This is usually the result of a blockage in one or more of
the coronary arteries. A blockage can develop due to a buildup of plaque, a
substance mostly made of fat, cholesterol, and cellular waste products or due to
a sudden blood clot that forms on the blockage.
Etiology
• The coronary arteries take oxygen-rich blood specifically to your heart
muscle.
• When these arteries become blocked or narrowed due to a buildup of
plaque, the blood flow to your heart can decrease significantly or stop
completely.
• This can cause a heart attack.
Epidemiology
• An estimated 16.5 million Americans older than 20 years of age have
coronary artery disease
• The prevalence was higher in males than females for all ages.
Pathophysiology
The acute occlusion of one or multiple large epicardial coronary arteries
for more than 20 to 40 minutes can lead to acute myocardial infarction. The
occlusion is usually thrombotic and due to the rupture of a plaque formed in the
coronary arteries. The occlusion leads to a lack of oxygen in the myocardium,
which results in sarcolemmal disruption and myofibril relaxation. These changes
are one of the first ultrastructural changes in the process of MI, which are
followed by mitochondrial alterations. The prolonged ischemia ultimately results
in liquefactive necrosis of myocardial tissue. The necrosis spreads from sub-
endocardium to sub-epicardium. The subepicardium is believed to have
increased collateral circulation, which delays its death. Depending on the territory
affected by the infarction, the cardiac function is compromised. Due to the
negligible regeneration capacity of the myocardium, the infarcted area heals by
scar formation, and often, the heart is remodeled characterized by dilation,
segmental hypertrophy of remaining viable tissue, and cardiac dysfunction.
Signs and Symptoms
• Pressure or tightness in the chest
• Pain in the chest, back, jaw, and other areas of the upper body that lasts
more than a few minutes or that goes away and comes back
• Shortness of breath
• Sweating
• Nausea
• Vomiting
• Anxiety
• Increased heart rate
“Atypical” Symptoms, such as:
• Shortness of breath
• Jaw pain
• Upper back pain
• Lightheadedness
• Nausea
• Vomiting
Prognosis
• The overall prognosis depends on the extent of heart muscle damage and
ejection fraction.
• Patients with preserved left ventricular function tend to have good
outcomes. Factors that worsen prognosis include:
• Diabetes
• Advanced age
• Delayed reperfusion
• Low ejection fraction
• Presence of congestive heart failure
• Elevations in C-reactive protein and B-type natriuretic peptide
(BNP) levels
• Depression
• Relaxation techniques
• Energy conservation and fatigue management
• Vocational support
• Home adaptations or equipment

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