Neuropsychological disorders and management

NEUROPSYCHOLOGICAL DISORDER which includes
neuropsychological assessment and standardized scales.

1. NEUROPSYCHOLOGICAL DISORDERS management/assessments KRISHNA NS MOT SECOND YEAR-NEURO

2. 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

3. Chapter Outline-psychiatric Obsessive-Compulsive Disorder: Neurological or Psychiatric? Schizophrenia: A Dementia of the Young Bipolar Disorder 3

4. 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.

5. EPILEPSY

6. 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

7. 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 : Partial Seizure Generalized Seizure

8. 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

9. 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”)

10. 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)

11. TBI-Traumatic brain injury

12. 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

13. Symptoms based on seveirity

14. TYPES OF INJURIES B elow 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.

15. Intracerebral Hemorrhage:  An intracerebral hemorrhage (ICH) describes bleeding within the brain tissue, may be related to other brain injuries, especially contusions. C an 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 result from severe traumatic SAH.

16. 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.

17. 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.

18. 3 types of symptoms

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

20. Parkinson’s Disease

21. 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

22. 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

23. contin INVESTIGATIONS: MRI, PET Scan, SPECT Scan TREATMENT: Deep brain stimulation L-Dopa Supportive therapies like OT,PT and ST

24. Huntington’s Disease/CHOREA

25. 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

26. 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 )

27. 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

28. Huntington’s Disease: A Genetic Rarity, in Two Senses 28 Enlargement of Caudate Nucleus

29. 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

30. Multiple Sclerosis

31. 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: vision loss, pain , fatigue and impaired coordination. The symptoms, severity and duration can vary from person to person.

32. 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

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

34. Alzheimer’s Disease

35. 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

36. 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. Alzheimer’s Disease: Burning Out with Age? 37

38. Alzheimer’s Disease: Burning Out with Age? 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

39. Alzheimer’s Disease: Burning Out with Age? 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. Alzheimer’s Disease: Burning Out with Age? 40

41. Alzheimer’s Disease: Burning Out with Age? 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

42. Alzheimer’s Disease 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

43. Alzheimer’s Disease 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

44. Alzheimer’s Disease: Burning Out with Age? 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

45. Obsessive-Compulsive Disorder

46. 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

47. Obsessive-Compulsive Disorder: Neurological of Psychiatric? A more modern criteria based on the symptoms. P sychiatric conditions impact emotion, motivation, social behaviors, personality, or reality testing. Neurological conditions impact strength, movement, sensory perception, memory, attention, or level of consciousness . 47

48. Obsessive-Compulsive Disorder: Neurological of Psychiatric? 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. Obsessive-Compulsive Disorder: Neurological of Psychiatric? 49

50. Obsessive-Compulsive Disorder: Neurological of Psychiatric? Management: Cognitive behavioral therapy addresses cognitive distortions and decreases anxiety. Medications than increase serotonin reduce the obsessions, compulsions, and anxiety. N euroleptics are sometime prescribed for severe cases. 50

51. Schizophrenia

52. 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

53. Schizophrenia: A Dementia of the Young 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. Schizophrenia: A Dementia of the Young 54

55. Schizophrenia: A Dementia of the Young 55

56. Schizophrenia: A Dementia of the Young Neurodevelopmental factors Abnormal pruning of neurons S maller cell bodies of neurons D ecreased functioning of inhibitory GABA interneurons in the cortex 56

57. Schizophrenia: A Dementia of the Young 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

58. Schizophrenia: A Dementia of the Young 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. M any of the genes associated with schizophrenia affect NMDA glutamate receptors . 58

59. Schizophrenia: A Dementia of the Young 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

60. Bipolar Disorder

61. 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

62. Bipolar Disorder 62

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

64. 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.

65. Bipolar Disorder Common treatments include Mood-stabilizing drugs, such as lithium Anti- dpileptic drugs OT: Cognitive Behavior Therapy 65

66. NEURAL DAMAGE ANATOMY AND PHYSIOLOGY

67. 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.

68. NEURO ANATOMY

69. 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

70. 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

71. 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

72. 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

73. ASSESSMENTS

74. 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

75. 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 .

76. PROCESS OF ASSESMENT

77. 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

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

79. 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

80. 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

81. Purposes of Neuropsych Testing Lesion Location Diagnosis Level of Functioning Strengths Weaknesses Conditions Rehab Recommendations Prognosis

82. 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

83. 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

84. 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)

85. Neuropsychological test

86. 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)

87. LANGUAGE Boston Naming Test Comprehensive Aphasia Test (CAT) Multilingual Aphasia Examination VISUOSPATIA L Clock Test Hooper Visual Organisation Task (VOT) Rey- Osterrieth Complex Figure

88. COMMON ASSESSMENTS AND BATTERIES

89. 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

90. Addenbrooke's Cognitive Examination  N europsychological  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 . T otal 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)

91. 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: Orientation Short-term memory/delayed recall Executive function/visuospatial ability Language abilities Abstraction Animal naming Attention Clock drawing

92. 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  scored  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

93. 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).

94. 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

95. 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)

96. 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

97. Neuropsych subtest examples Rey-O Complex Figure Copy Alzheimer’s patient copy

98. Trailmaking B subtest

99. Stroop subtest

100. Picture Naming subtest

101. List Learning subtest

102. Processing Speed Measure

103. 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

104. 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

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

106. 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

107. 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

108. INTERVENTIONS

109. 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)

110. Thank you