Neuropsychological disorders and management

NEUROPSYCHOLOGICAL
DISORDERS
MANAGEMENT/ASSESSMENTS
KRISHNA NS
MOT SECOND YEAR-NEURO

CHAPTER OUTLINE-NEURO DISORDER
• Epilepsy
• Parkinson’s disease
• Alzheimer’s Disease: Burning Out with Age?
• Huntington’s Disease: A Genetic Rarity, in Two Senses
• Tourette Syndrome
• Traumatic brain injury
2

CHAPTER OUTLINE-PSYCHIATRIC
• Obsessive-Compulsive Disorder: Neurological or Psychiatric?
• Schizophrenia: A Dementia of the Young
• Bipolar Disorder
3

• Figure 16.17 Some brain disorders are
traditionally considered neurological, while
others are traditionally considered
psychiatric. The distinction is somewhat
arbitrary, since both categories of disorders
involve abnormal functioning of the neural
pathways of the brain. This survey of
scientific articles published in the peer
reviewed journals Neurology and American
Journal of Psychiatry from 1990 to 2011
shows whether the conditions named were
more commonly considered neurological or
psychiatric.

EPILEPSY
• Epilepsy is any disorder in which epileptic seizures recur
spontaneously
• Seizures - sudden rush of electrical activity in the brain
• When convulsions (motor seizures) are present, it is easy to
diagnose; include tremor, rigidity, loss of balance, or loss of
consciousness
• However, many seizures involve subtle changes in thought, mood,
and or behavior with no convulsions whatsoever

EPILEPSY
• The observation of epileptic spikes in the EEG is evidence of epilepsy
• Epileptic auras sometime precede an epileptic seizure
• There are two main classes of seizures:
1. Partial Seizure
2. Generalized Seizure

EPILEPSY
• Partial Seizures: do not involve the entire brain
simple partial seizures produce symptoms in the sensory or
motor areas; start in one part of the body and spread to other
parts of the body as discharges spread through the brain
complex partial seizures are often restricted to the temporal
lobes; epileptics typically have no memory of the event

EPILEPSY
• Generalized seizures: involve the entire brain;
• they may start from a focus and gradually spread or they may
begin simultaneously throughout the entire brain include grand
mal seizures (“big trouble”) with
• symptoms of tremor, rigidity, loss of balance and consciousness,
tongue biting, incontinence, turning blue from hypoxia and petit
mal seizures (“small trouble”)

TREATMENT
• Anti-epileptic (anticonvulsant, antiseizure) drugs
• Vagus nerve stimulator(surgically placed under the skin on the chest and
electrically stimulates the nerve that runs through your neck. This can help
prevent seizures)
• Brain surgery(Very Rarely)

INTRO
• Traumatic Brain Injury (TBI) is a disruption in the normal function of the brain that
can be caused by a blow, bump or jolt to the head, the head suddenly and
violently hitting an object or when an object pierces the skull and enters brain
tissue.
• SIGNS:
• Loss of or decreased consciousness
• Loss of memory for events before or after the event (amnesia)
• Focal neurological deficits such as muscle weakness, loss of vision, change in
speech
• Alteration in mental state such as disorientation, slow thinking or difficulty
concentrating

SYMPTOMS BASED ON SEVEIRITY
• mild,
• moderate, or
• severe,
• (depending on the extent of damage to the brain)

TYPES OF INJURIES
• Below are different types of sequelae developed from TBIs:
• Hematoma: A hematoma is a blood clot within the brain or on its surface.
Hematomas may occur anywhere within the brain. An epidural hematoma is a
collection of blood between the dura mater (the protective covering of the brain) and
the inside of the skull. A subdural hematoma is a collection of blood between the
dura mater and the arachnoid layer, which sits directly on the surface of the brain.
• Contusion: A cerebral contusion is bruising of brain tissue. They consist of areas of
injured or swollen brain mixed with blood that has leaked from arteries, veins, or
capillaries. Most commonly, contusions are at the base of the front parts of the brain,
but may occur anywhere.

• Intracerebral Hemorrhage: An intracerebral hemorrhage (ICH) describes
bleeding within the brain tissue, may be related to other brain injuries, especially
contusions. Can be removed surgically.
• Subarachnoid Hemorrhage: Subarachnoid hemorrhage (SAH) is caused by
bleeding into the subarachnoid space.
Most cases of SAH associated with head trauma are mild. Hydrocephalus may
from severe traumatic SAH.

• Diffuse Injuries: TBIs can produce microscopic changes that do not appear on
CT scans and are scattered throughout the brain. This category of injuries, called
diffuse brain injury, may occur with or without an associated mass lesion.
• Diffuse Axonal Injury: Axonal injury refers to impaired function and gradual loss
of axons.These long extensions of nerve cells enable them to communicate with
each other. If enough axons are harmed in this way, the ability of nerve cells to
communicate with each other and to integrate their function may be lost or
greatly impaired, possibly leaving a patient with severe disabilities.

• Ischemia: Another type of diffuse injury is ischemia or insufficient blood supply
to certain parts of the brain. A decrease in blood supply to very low levels may
occur commonly in a significant number of TBI patients. This is crucial since a
brain that has just undergone a traumatic injury is especially sensitive to slight
reductions in blood flow. Changes in blood pressure during the first few days
after head injury can also have an adverse effect.
• Skull Fractures: Linear skull fractures or simple breaks or “cracks” in the skull may
accompany TBIs.

3 TYPES OF SYMPTOMS
Physical Symptoms
Head ache,Nausea,Fatigue etc
Sensory Symptoms Sensitivity to light
Cognitive/Behavioural Symptoms
Loss of consciousness, Mood changes,Behaviour changes,Difficulty sleeping,Memory problems

TREATMENT
Inpatient Rehab tools:
1. Functional independence measure
2. Functional assessment measure
3. LOTCA and KTA (Kitchen Task Assessment)
Post acute Rehabilitation:
1. COPM
2. SAFER(Safety Assessment of function and environment for rehabilitation)
3. Interest checklist

PARKINSON’S DISEASE
• Parkinson's disease is a brain disorder that leads to shaking, stiffness, and
difficulty with walking, balance, and coordination
• Parkinson's symptoms usually begin gradually and get worse over time.
• As the disease progresses, people may have difficulty walking and talking.
• Attacks 0.5% of the population; usually 50-60 yr olds, males
• The first symptom is often a tremor or stiffness of the fingers
• Symptoms of the full-blown disorder are tremor at rest, muscular rigidity,
slowness of movement, and a masklike face

PARKINSON’S DISEASE
• There is no intellectual deterioration
• Its cause is unknown but it is associated with degeneration of dopamine neurons
in the substantia nigra in basal ganglia; this neurons project to the striatum
• Treated with L-DOPA, the metabolic precursor of dopamine

CONTIN
• INVESTIGATIONS: MRI, PET Scan, SPECT Scan
• TREATMENT:
1. Deep brain stimulation
2. L-Dopa
3. Supportive therapies like OT,PT and ST

HUNTINGTON’S DISEASE
• Huntington's disease (HD), also known as Huntington's chorea, is a
neurodegenerative disease that is mostly inherited.
• The earliest symptoms are often subtle problems with mood or mental abilities.
• A general lack of coordination and an unsteady gait often follow.
• It is also a motor disorder; it is inherited but rare, its cause is understood and is
always associated with dementia
• Its main symptoms are complex jerky movements of entire limbs,dementia
occurs later in the disease, which is always fatal

HUNTINGTON’S DISEASE
• Caused by a single dominant gene;
• 50% chance for offspring to get it, the reason it has not disappeared is that the
first symptoms do not appear until after the age of reproduction (40-50 yrs)

HUNTINGTON’S DISEASE: A GENETIC RARITY, IN
TWO SENSES
• Patients perform restless involuntary movements of the face, trunk, and limbs.
• It commonly also includes psychiatric symptoms such as depression, apathy,
anxiety, delusions, and hallucinations.
• The biological cause is degeneration of the anterior caudate nucleus of the
striatum.
27

HUNTINGTON’S DISEASE: A GENETIC RARITY, IN
TWO SENSES
28
Enlargement of
Caudate Nucleus

CONTIN
• Investigations: Brain imaging -MRI ,CT scan and others like Genetic counselling
and Testing and Pre natal testing
• Management: OT (Behaviour issues, PT- Gait issues)
• Medications: Antiparkinsonian drugs

OVERVIEW
• A disease in which the immune system eats away at the protective covering of
nerves
• In MS, resulting nerve damage disrupts communication between the brain and
the body.
• SYMPTOMS:
1. vision loss,
2. pain,
3. fatigue and impaired coordination.
4. The symptoms, severity and duration can vary from person to person.

MULTIPLE SCLEROSIS
• A disease of the CNS myelin; breakdown of myelin leads
to breakdown of associated axons; development of areas
of hard scar tissue throughout the CNS
• Common symptoms are ataxia (loss of motor
coordination), weakness, numbness, tremor, and poor
vision
• Generally worsening progression of the disorder

• TREATMENT: Chemotherapy, Anti inflammatory drugs,Immuno suppressive drug
and steroids
• Therapies include :PT,
• OT,
• Counselling services and
• ST

ALZHEIMER’S DISEASE
• A progressive disease that destroys memory and other important mental
functions.
• Brain cell connections and the cells themselves degenerate and die, eventually
destroying memory and other important mental functions.
• Memory loss and confusion are the main symptoms.
• No cure exists, but medication and management strategies may temporarily
improve symptoms.
• 15% of people over 65 and 35% over 85 suffer

ALZHEIMER’S DISEASE: BURNING OUT WITH AGE?
• First sign is forgetfulness and emotional instability (depression); eventually there
is total dementia and an inability to perform even the most simple responses
(e.g., swallowing); it is terminal
• Dementias are neurologic disorders characterized by slow deterioration of higher
cognitive functions.
• Such functions include language, memory, judgement, and emotion.
• Alzheimer’s disease or Alzheimer’s dementia is thought to affect about 24 million
people world-wide.
36

37

• The major deficit of Alzheimer’s is the loss of episodic memory.
• Executive functions decline throughout Alzheimer’s disease.
• Biological markers of Alzheimer’s disease include amyloid-beta plaques and
neurofibrillary tau tangles.
38

• Most cases of Alzheimer’s disease occur in individuals over age 60.
• The epsilon 4 variant of the apolipoprotein E (ApoE4) gene seems to increase the
risk of developing the disease.
• Genetic forms of Alzheimer’s disease account for only a small percentage of
cases.
39

40

• A potential treatment uses the immune system to remove plaques, but this has
not resulted in any clinical improvement.
• Social, mental, and physical activity can decrease the risk and severity of
Alzheimer’s disease.
41

• Caused by amyloid plaques (clumps of degenerating
neurons and an abnormal protein called amyloid) and
tangles of neurofibrils within neurons
• Loss of neurons is common; plaques, tangles, and neuron
loss are often most common in areas involved in memory
such as the hippocampus, amygdala, and entorhinal
cortex

• Clear genetic component; 50% chance of suffering if have immediate family
member with AD
• Cholinergic neurons often die early in the course of AD; cholinergic agonists are
effective at reducing symptoms early in disease

• Treatment of Alzheimer’s disease
• There are currently no cures for Alzheimer’s disease.
• No medications significantly slow down or reverse the progression of the disease.
• Acetylcholinesterase inhibitors and NMDA glutamate receptor antagonists sometimes
slow the progression of the disease.
44

OBSESSIVE-COMPULSIVE DISORDER:
NEUROLOGICAL OF PSYCHIATRIC?
• Obsessive-compulsive disorder is a psychiatric disorder that affects about 2 – 3%
of the population.
• Symptoms include
obsessions (intrusive, disturbing thoughts) and
compulsions (stereotyped, ritualized behaviors).
46

• A more modern criteria based on the symptoms.
• Psychiatric conditions impact emotion, motivation, social behaviors, personality, or
reality testing.
• Neurological conditions impact strength, movement, sensory perception, memory,
attention, or level of consciousness.
47

• Obsessions include contamination,
• fear of committing inappropriate acts,
• symmetry and repeated checking
• number, and hoarding.
• The most common age of onset for symptoms of obsessive-compulsive disorder
is either about age 11 or 23.
48

49

• Management:
• Cognitive behavioral therapy addresses cognitive distortions and decreases
anxiety.
• Medications than increase serotonin reduce the obsessions, compulsions, and
anxiety.
• Neuroleptics are sometime prescribed for severe cases.
50

SCHIZOPHRENIA: A DEMENTIA OF THE YOUNG
• A disorder that affects a person's ability to think, feel and behave clearly.
• Schizophrenia is characterized by loss of contact with reality.
• The exact cause of schizophrenia isn't known, but a combination of genetics,
environment and altered brain chemistry
• The age of onset is typically around early adulthood.
• Schizophrenia affects about 1% of the world’s population.
52

• Positive symptoms include hallucinations and delusions.
• Delusions include paranoid delusions, delusions of reference, delusions of passivity,
and somatic delusions.
• Negative symptoms include poverty of speech, apathy, social withdrawal, and loss
of emotion.
53

54

55

• Neurodevelopmental factors
• Abnormal pruning of neurons
• Smaller cell bodies of neurons
• Decreased functioning of inhibitory GABA interneurons in the cortex
56

• Dopamine hypothesis
• There is too much dopamine signaling or the dopamine receptors are oversensitive.
• The first-generation antipsychotic drugs were dopamine D2 receptor antagonists.
• Drugs that increase dopamine, such as amphetamines and cocaine, can mimic the
positive symptoms of schizophrenia.
57

• Glutamate hypothesis(deficiency in activity of glutamate at the glutamate
synapse)
• Schizophrenia is caused by too little glutamate neurotransmission.
• NMDA receptor antagonists, like ketamine, can mimic both the positive and negative
symptoms of schizophrenia.
• Many of the genes associated with schizophrenia affect NMDA glutamate receptors.
58

• Management:
• Antipsychotic medications treat the positive symptoms, but do not treat the
negative symptoms.
• Such medications often cause unwanted side effects.
• Second-generation antipsychotic medications are no better at treating the
negative symptoms.
• OT:cognitive therapy (cognitive behavioral and cognitive remediation therapy),
psychoeducation, family intervention, social skills training, and assertive
community treatment
59

BIPOLAR DISORDER
• A disorder associated with episodes of mood swings ranging from depressive
lows to manic highs.
• Normal mood alternates with periods of depression and mania.
• This affects 1% of the population and a milder form may affect as much as 4-5%
of the population.
• The age of onset is about 20 years of age.
• There is a genetic basis to the condition, but no specific genes have been
identified.
61

BIPOLAR DISORDER
• Individuals with bipolar disorder show thinner gray matter in the
• Bilateral ventrolateral frontal cortex
• Bilateral anterior insula
Dorsomedial prefrontal cortex
• Subgenual cingulate cortex
• Some of these regions are also affected in unipolar depression.
63

BIPOLAR DISORDER
64
Grey matter in the
brains of people
with bipolar disorder is
destroyed with each
manic or depressive
episode. This was the
finding of an MRI study
of 21 patients
with bipolar disorder, a
mental illness marked
by successive episodes
of mania followed by
deep depression.

BIPOLAR DISORDER
• Common treatments include
• Mood-stabilizing drugs, such as lithium
• Anti-dpileptic drugs
• OT: Cognitive Behavior Therapy
65

NEURAL DAMAGE
ANATOMY AND PHYSIOLOGY

DEFINITION
• NEUROPSYCHOLOGICAL DISORDER:
• A disturbance of mental function due to brain trauma, associated with one or
more of the following: neurocognitive, psychotic, neurotic, behavioral, or
psychophysiologic manifestations, or mental impairment.

NEURO ANATOMY
ANATOMY
SUBCORTICAL STRUCTURES ie. Hippocampus,
Cerebellum, Basal ganglia
CORTICAL STRUCTURES
ie. Frontal lobe, Temporal Lobe, Parietal lobe and
Occipital lobe

DEGENERATION
• Two types of deterioration of the neuron following
damage:
• Anterograde deterioration involves distal segments of the
axon and occurs rapidly;
• Retrograde deterioration involves changes in the proximal
segments of the axon from damaged site

REORGANIZATION
• Reorganization of neural connections is believed to occur via 2 types of changes:
• Rapid reorganization of neural connections usually results from experience; this is
believed to reflect the strengthening of existing connections; and
• Gradual reorganization usually results from neural damage; this is believed to reflect
the establishment of new connections via collateral sprouting

REORGANIZATION
• The actual extent of neural reorganization and recovery of function after brain
damage remains unclear;
• it is difficult to conduct well-controlled studies on populations of brain-damaged
patients, and the nervous system can compensate for brain damage in a way that
looks like true recovery of function

REORGANIZATION
• Cognitive reserve is important in the apparent recovery of cognitive function
that is often observed; this seems to be due to the adoption of alternative
strategies to solve a problem, rather than true recovery of function
• 2 general conclusions have emerged:
• Small lesions are more likely to be associated with recovery of function than large
lesions
• Recovery is more likely in young patients

TREATMENT IN NEUROPSYCHOLOGICAL
• Define neuropsychological assessment
• Identify advantages of neuropsych testing vs. neuroimaging
• Discuss value of neuropsych assessment in differentiating and/or establishing
severity of injury
• Review various neuropsychological evaluation processes

NEUROPSYCHOLOGICAL ASSESSMENT
• Neuropsychological assessment was traditionally carried out to assess the extent
of impairment to a particular skill and to attempt to determine the area of the
brain which may have been damaged following brain injury or neurological
illness
• administration of neuropsychological tests for the formal assessment of
cognitive function, though neuropsychological testing is more than the
administration and scoring of tests and screening tools. It is essential that
neuropsychological assessment also include an evaluation of the
person's mental status. This is especially true in assessment of Alzheimer's
disease and other forms of dementia.

Diagnosis of a
neuropsychological disorder
History taking Interviewing Test-taking
Intelligence
testing
Testing other
areas
PROCESS OF
ASSESMENT

NEUROPSYCHOLOGICAL REHABILITATION
• Enabling people with cognitive, emotional or behavioral deficits arising from
neurological conditions to achieve their maximum potential in the domains of
psychological, social, leisure, vocational and everyday functioning

TEAM MEMBERS
• Neuropsychological rehabilitation requires an interdisciplinary team
• (e.g. doctors, speech and language therapists,
• occupational therapists,
• physiotherapists,
• psychologists,
• and others

DEFINITION OF NEUROPSYCHOLOGICAL
ASSESSMENT
• A branch of clinical psychology that studies how the brain and nervous system
affect how we function on a daily basis
• Uses various assessment methods to ascertain function and dysfunction and
applies this knowledge to evaluate, treat and rehabilitate individuals with
suspected or demonstrated neurological or psychological problems.
• In essence, goal is to identify cognitive strengths and weaknesses

• Unlike the use of neuroimaging techniques such as MRI, CT scans and EEG where
the focus is on nervous system structures, neuropsychology seeks to understand
how various components of the brain are able to do their jobs (FUNCTIONING)
• Entails a detailed knowledge of brain anatomy, the role that different brain areas
serve and how these functions are likely to be impacted by various disorders
• AB include point about assessing across biopsychosocial domains

PURPOSES OF NEUROPSYCH TESTING
• Lesion Location
• Diagnosis
• Level of Functioning
• Strengths
• Weaknesses
• Conditions
• Rehab Recommendations
• Prognosis

NEUROPSYCH EVALUATION VS. NEUROIMAGING
• MRI/CT
• Examiner bases clinical opinion on visual representation of brain anatomy/metabolic
processes
• Neuropsych assess. based on functional status of patient and norm-based, providing
more accurate depiction of patient’s abilities
• While imaging typically more clearly observable for acute ABI, as brain heals, images
change, but deficits remain
• Neurologist's expertise is diagnosing and treating the structural and physiological
consequences of brain injuries and neurological illnesses.
• Neuropsychologists assess the effects of brain injuries and illnesses on cognition and
behavior; they are experts in assessing functional capacities

VALUE OF NEUROPSYCHOLOGICAL TESTING
• Specific profiles obtained on testing reveal more detailed data on location and
severity of injury
• Injury can cause inflammatory response affecting whole brain
• Pressure-related affects on other areas
• Coup-Contrecoup
• Frontal- “everything” connection (i.e., frontal-cerebellar)
• Helps differentiate co-morbid conditions

TYPES OF NEUROPSYCHOLOGICAL ASSESSMENTS
• Low-level evaluation
• Glasgow Coma Scale
• Brief Cognitive Examinations
• Montreal Cognitive Assessment (MOCA)
• Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)
• Neurobehavioral Cognitive Status Examination (Cognistat)

NEUROPSYCHOLOGICAL TEST
CATEGORIES
Intelligence Memory Language
Executive
function
Visuo Spatial
Batteries
assessing
normal
functions

• INTELLIGENCE
• Wechsler Adult Intelligence Scale
(WAIS) Wechsler Intelligence Scale
for Children (WISC)
• Wechsler Preschool and Primary
Scale of Intelligence (WPPSI)
• MEMORY
• Memory Assessment Scales (MAS)
• Rey Auditory Verbal Learning Test
• Wechsler Memory Scale (WMS)

• LANGUAGE
• Boston Naming Test
• Comprehensive Aphasia Test (CAT)
• Multilingual Aphasia Examination
• VISUOSPATIAL
• Clock Test
• Hooper Visual Organisation Task
(VOT)
• Rey-Osterrieth Complex Figure

COMMON
ASSESSMENTS
AND BATTERIES

MINI-MENTAL STATE EXAMINATION (MMSE)
• The Mini-Mental State Examination (MMSE) was originally designed to
differentiate organic from functional disorders in psychiatric practice, and as a
quantitative measure of cognitive impairment useful in monitoring change, but
not primarily as a diagnostic tool
• The MMSE has good intra- and inter-rater reliability and internal consistency
• 30-point questionnaire
• Administration of the test takes between 5 and 10 minutes

ADDENBROOKE'S COGNITIVE EXAMINATION
• Neuropsychological tests used to identify cognitive impairment in conditions
such as dementia.
• This consists of 19 activities which test five cognitive
domains: attention, memory, fluency, language and visuospatial processing.
• Total score out of 100 (18 points for attention, 26 for memory, 14 for fluency, 26
for language, 16 for visuospatial processing
• (score of 88 and above is considered normal; below 83 is abnormal; and between
83 and 87 is inconclusive)

MOCA-MONTREAL COGNITIVE ASSESSMENT
• screening assessment for
detecting cognitive impairment
• Mo-CA test is a one-page 30-point test
administered in approximately 10 minutes
• It assess:
1. Orientation
2. Short-term memory/delayed recall
3. Executive function/visuospatial ability
4. Language abilities
5. Abstraction
6. Animal naming
7. Attention
8. Clock drawing

• MoCA scores range between 0 and
30. A score of 26 or over is
considered to be normal.
• In a study, people
without cognitive impairment score
d an average of 27; people with
mild cognitive impairment
(MCI) scored an average of 22;
people with Alzheimer's
disease scored an average of 16

LOTCA- LOEWENSTEIN OCCUPATIONAL THERAPY
COGNITIVE ASSESSMENT
• (LOTCA) is a cognitive battery that measures basic cognitive skills required for
everyday function including orientation, visual perceptual and psychomotor
abilities, problem-solving skills and thinking operations
Can be used with individuals below the age of 70 years with neurological dysfunction
and consisted of a total of 20 items within 4 areas:
Orientation (2 items);
Perception (6 items);
Visuomotor Organization (7 items); and
Thinking Operations (5 items).

LOTCA – 11 AND SCORING
• The LOTCA-II consists of a total of 26 subtests within 6 areas: Orientation (2 items);
Visual Perception (4 items); Spatial Perception (3 items); Motor Praxis (3 items);
Visuomotor Organization (7 items); and Thinking Operations (7 items).
• Most subtests of the LOTCA are scored from 1 to 4, where:
• 1 = Patient fails to perform the task
• 2 = Patient is able to perform part of the task
• 3 = Patient is able to perform most of the task
• 4 = Patient demonstrates good performance of the task

• TIME: The LOTCA and LOTCA-II take approximately 45 minutes to administer
• EQUIPMENT : The LOTCA kit contains testing materials
(card decks, coloured blocks, pegboard set and other materials)

CLOCK DRAWING
• Clock drawing has a long history as a test for cognitive impairment and remains
popular
• It has the advantage of being quick and simple, and tests a wide range of
cognitive domains (a ‘diffuse’ screening test) including auditory comprehension,
memory, executive control (planning), and visuospatial abilities, as well as motor
skills

NEUROPSYCH SUBTEST EXAMPLES
REY-O COMPLEX FIGURE COPY ALZHEIMER’S PATIENT COPY

COMPREHENSIVE NEUROPSYCHOLOGICAL
BATTERY
• The Neuropsychological Assessment Battery (NAB; Stern & White, 2003) is a
comprehensive test battery that assesses five cognitive domains
(Attention, Language, Memory, Spatial, and Executive Functions).
• The purpose of the current descriptive study was to present data on the index
and primary test scores from the five main NAB cognitive modules in a sample of
patients with moderate-to-severe traumatic brain injury (TBI) admitted to a
residential post acute rehabilitation program

• Purpose :
• Assesses a wide range of cognitive skills and functions
• Age 18–97 years
• Format Paper and pencil; scoring software available
• Time 3 hours and 40 minutes to administer all five modules;
• 75 minutes to score
• Qual C

APPROACHES
• RFOR
• TASK ORIENTED APPROACH
• ACQUISITIONAL FOR
• AFFOLTERS APPROACH
• TOGLIA
• COGNITIVE DISABILITY FOR
• COGNITIVE REMEDIATION THERAPY
• CBT (COGNITIVE BEHAVIOUR
THERAPY)

JOURNAL UPDATE
• Name of the Journal: Occupational Therapy In Health Care
• Date of Publication:08 Jan 2019.
• Authors: Áine Coe, Mary Martin & Tadhg Stapleton
• Title: Effects of An Occupational Therapy Memory Strategy Education Group
Intervention on Irish Older Adults’ Self-Management of Everyday Memory
Difficulties

• memory strategy education group (MSEG) was developed to assist clients with
varying levels of memory impairment to adopt strategies
• Cognitive patients with memory distortions peoples are engaged in this study
• Total n=47
• The program encouraged an increased use of memory strategies among the
client groups
• Results of this study indicate that this type of program may be suitable and
appropriate for clients with SMC who continued to show improved scores in the
longer term follow up and the study says effective foe patient with milder
cognitive impairments

REFERENCES
• Neuropsychology for Occupational Therapists Cognition in Occupational
Performance by June GrieveLinda Gnanasekaran (Text book)
• Neuropsychological Neurology The Neurocognitive Impairments of Neurological
Disorders by A. J. Larner (Text book)
• Principles of Neuropsychology by Eric A Zilmer (Text book)

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