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Unformatted text preview: Chapter 14
Cognitive Disorders; Brain Impairment & Delirium
Brain Impairment in Adults 0. Prior to the DSMIV, disorders involving some kind of identifiable pathology (e.g., a brain tumor, stroke, drug intoxication) were labeled organic mental disorders
1. Functional mental disorders were considered not to have an organic basis
2. Functional vs organic distinction no longer viable Brain Impairment in Adults 3. This material deals with what were formerly labeled organic mental disorders
4. It is incorrect to assume other disorders (such as schizophrenia) have no organic basis
5. Current view recognizes neuroanatomy and neurochemistry in all psychological disorders Brain Impairment in Adults 6. The DSMIVTR presents the diagnostic coding of various neuropsychological disorders in different and somewhat inconsistent ways
7. Both psychological and biological problems are coded on Axis I
8. Disease is coded on Axis III Brain Impairment in Adults
Brain Impairment in Adults 9. Included because:
10. Are psychopathological conditions
11. Cause symptoms that look like other abnormal psychological disorders
12. Cause changes in behavior, mood and personality
13. They may be preceded or followed by depression
14. They take a toll on others causing depression Brain Impairment in Adults 0. The brain weighs 3 pounds
1. Most complex organ in body
2. Capable of studying itself
3. Involved in every aspect of life
4. Vulnerable to damage – external/internal
5. Protected by skull and thick outer membrane Brain Impairment and Adults 15. Damage or destruction of brain tissue may involve only limited behavioral deficits or a wide range of psychological impairments depending on:
16. The nature, location, and extent of neural damage
17. The premorbid competence and personality of the individual
18. The individual’s life situation
19. The amount of time since the first appearance of the condition Brain Impairment and Adults 6. When damage occurs to brain, damage is 6.
permanent since cell bodies and neural pathways cannot regenerate
7. Thus, permanent loss of function (stem cells may change that) Screening for Cognitive Impairment (I) 20. During the MiniMental State Examination, the clinician will ask the patient questions concerning (points given for correct response)
21. 1. Orientation (e.g., Where are we now?)
22. 2. Registration (Repeat these three words.)
23. 3. Attention and concentration (Count backwards by seven.)
24. 4. Recall (Do you remember those three words?) Screening for Cognitive Impairment (II) 8. During the MiniMental State Examination, the clinician will ask the patient questions concerning (points given for correct response)
9. 5. Language (Name what I’m pointing to.)
10.6. Comprehension (Pick up the paper in front of you.)
11.7. Construction ability (Copy this design.) Brain Structures and Associated Behaviors
25. Left hemisphere: serial processing; language and math
26. Right hemisphere: overall meaning; nonverbal, intuition; spatial 27.
30. Right parietal: visual motor coordination
Left parietal: language function
Temporal lobes: memory
Occipital lobes: visual processing Brain Structures and Associated Behaviors
Diffuse Versus Focal Damage (I) 31. Attention is often impaired by moderate diffuse damage (such as damage from moderate oxygen deprivation) (e.g. general memory loss)
32. Focal damage (such as damage from an injury or stroke) can cause different problems depending on what part of the brain is affected (location and extent) Diffuse versus Focal Damage: (II) 0. Some consequences of brain disorders that have mainly focal origins but commonly appear in the context of progressively diffuse damage are as follows:
1. 1. Impairment of memory (temporal lobes)
2. 2. Impairment of orientation (parietal lobes)
3. 3. Impairment of learning, comprehension, and judgment (frontal lobes) Diffuse versus Focal Damage: (III) 4. Some consequences of brain disorders that have mainly focal origins but commonly appear in the context of progressively diffuse damage are as follows:
5. 4. Impairment of emotional control or modulation (frontal lobes)
6. 5. Apathy or emotional blunting (frontal lobes)
7. 6. Impairment in the initiation of behavior (frontal) Diffuse versus Focal Damage: (IV)
Diffuse versus Focal Damage: (IV) 8. Some consequences of brain disorders that have mainly focal origins but commonly appear in the context of progressively diffuse damage are as follows:
9. 7. Impairment of controls over matters of propriety and ethical conduct (temporal lobes)
10. 8. Impairment of receptive and expressive communication (parietal lobes)
11. 9. Impaired visuospatial ability (occipital lobes) Brain Impairment and Adult Disorder (I) 33. There appears to be a close link between neuropsychological and psychopathological conditions
34. It is erroneous to assume that a psychological disorder is necessarily and completely explained by the patient’s brain damage Brain Impairment and Adult Disorder (II) 35. There is an interaction between neuropsychological functioning and psychopathology:
36. 1. Some develop psychopathological problems (depression, anxiety, dissociation, delusions)
37. 2. Some develop cognitive disorders and deficits (memory, attention, orientation, emotion) Brain Impairment and Adult Disorder (III) 38. There is an interaction between neuropsychological functioning and psychopathology
39. 3. Some with good premorbid condition do better with neuropsychological problems 40. 4. Sufficient damage will eventually produce 40.
problems in everyone Congresswoman Gabriel Giffords
Brain Impairment in Adults 12.Three types of cognitive disorders that result from damage
Amnesic syndrome 13.Type of disorder depends on nature and site of damage Delirium: Description 44. Delirium:
45. Is a commonly occurring syndrome
46. Is an acute confusional state that lies between normal wakefulness and stupor or coma
47. Has a sudden onset and involves a fluctuating state of reduced awareness
48. Reflects a major change in the way the brain is working
49. Generally unable to carry out purposeful mental activities Delirium: Description 50. When information processing is impaired it effects attention, perception, memory, thinking: 51. Hallucinations, delusions are common 51.
52. Also abnormal psychomotor activity results Delirium: Prevalence 53. Can occur in a person of any age, though the elderly are at particularly high risk due to reduced brain reserve
54. Up to 40% of hospitalized patients Delirium: Causes 55. Delirium:
56. May result from several conditions, including head injury and infection
57. Is most commonly caused by drug intoxication or withdrawal Delirium: Treatment 58. Delirium
59. Is a true medical emergency
60. Is often reversible (except when caused by trauma or illness)
61. Is most often treated by medications, environmental manipulations, and family support
62. Medications: neuroleptics; benzodiazepines Cognitive Disorders: Dementia &Traumatic Head Injury
63. Dementia: 64. Is not a rapidly fluctuating condition (unlike delirium) 64.
implies permanent loss
65. Is characterized by a decline from a previously attained level of functioning
66. Has a slow onset and a deteriorating course
67. Early on person is alert and attuned; memory first to be effected; increasing deficits over time in thinking, learning, comprehension, problem solving Dementia: Causes
Can be caused by over 50 different disorders
Is most commonly caused by Alzheimer’s disease Dementia: Causes 71. Dementia: possible causes
72. Degenerative diseases: Huntington’s, Parkinson’s, Alzheimer’s
73. Infectious diseases: AIDS
74. Strokes (Vascular Dementia)
75. Also: Head injury; Deficiencies (vitamin B), Oxygen deprivation, Toxins Alzheimer’s Disease: Description 76. Alzheimer’s disease (AD) is associated with a characteristic dementia syndrome that has
77. An imperceptible onset
78. Early on, alert and attentive
79. Memory first to be effected
80. As time goes on, increasingly marked deficits 81. A usually slow but progressively deteriorating 81.
course terminating in delirium and death (within 10 years after diagnosis) Alzheimer’s Disease: Description 14.Clinical picture varies from person to person 82. Depends on nature and extent of degeneration, premorbid status, present stressors
83. 1. Narrowing of social activities & interests
84. 2. Lessening of alertness & adaptability
85. 3. Lowering of tolerance for change
86. 4. Activities selfcentered & childlike Alzheimer’s Disease: Description 15.Clinical picture varies from person to person
91. 5. Impaired memory and judgment
6. ‘Empty' speech
7. Agitation and confusion
9. Delusions of persecution Alzheimer’s Disease: Diagnosis
16.Diagnosis of Alzheimer’s disease 92. Based on clinical assessment
93. Can’t be absolutely confirmed until after death
94. Autopsy indicates formation of amyloid plaques and neurofibrillary tangles
95. Must first rule out other causes
96. Even MRI not absolute in assessment Alzheimer’s Disease: Prevalence
17.Prevalence: 18.Major health problem
19.Largest proportion of dementia cases
20.Rate of AD doubles every five years of age after age 40 (6574 12%; Over 85 25%)
21.4 million in US with AD Alzheimer’s Disease: Prevalence 22.Prevalence
23.Women are at higher risk than men
24.Fewer in nonwestern & less industrialized
25.Diet may be factor: high fat, cholesterol
26.Early onset (4050) – rapid deterioration Alzheimer’s Disease: Causes 27.Genes play a major role in susceptibility to and risk for Alzheimer’s disease
28.Genetic mutations of the APP (presenilin 1 and presenilin 2) genes are implicated
97. However, these are rare – under 5% of AD
98. APP gene involved in Down's syndrome Alzheimer’s Disease: Causes 29.Genes play a major role in susceptibility to and risk for Alzheimer’s disease
30.The APOE4 allele of the APOE gene is also a risk factor (about 35% AD cases)
99. Plays a larger role in late onset 100.
On chromosome 19 (involved in cholesterol)
Lower risk with antiinflammatory drug Alzheimer’s Disease: Neuropathology
Alzheimer 31.The characteristic neuropathology of Alzheimer’s disease involves 102.
Cell loss (holes in neural tissue) and cell degeneration
Plaques (which contain a sticky protein called beta amyloid) (neurotoxin) (probably facilitated by APOE4 allele)
Neurofibrillary tangles (which contain an abnormal tau protein) (secondary to presence of beta amyloid) Alzheimer’s Disease: Neuropathology 32.Alzheimer’s disease causes the destruction of cells that make acetylcholine (Ach) , a neurotransmitter important for memory
33.Accounts for cognitive and behavioral deficits Alzheimer’s Disease: Treatment 34.Drug treatments for Alzheimer’s disease include cholinesterase inhibitors such as donepezil (Ariecept) 105.
These drugs help stop ACh from being broken down, making more of it available to the brain 35.Best strategy for dealing with AD is to identify early and develop drugs to prevent Alzheimer’s Disease: Treatment
36.Treatment of AD 106.
Currently no treatment of AD
Only palliative to reduce patient and caregiver distress and reduce complications (incontinence, inappropriate social behavior, inadequate selfcare)
Behavioral approaches helpful Alzheimer’s Disease: Treatment 37.Any comprehensive approach to therapeutic intervention must consider the situation of caregivers
110. 3040% nursing home patients have AD
Those at home put stress on caregivers Tom Rush – I forgot
Dementia from HIV1 Infection
0. HIV associated dementia 111.
Caused by changes in the brain atrophy, swelling, inflammation occurs in limbic system 38.The HIV1 virus (or a mutant form of it) can itself result in the destruction of brain cells Dementia from HIV1 Infection 12. Neuropsychological features include:
13. Mild memory difficulties; psychomotor slowing
14. Diminished attention and concentration
15. Progression is rapid; dementia within one year
16. Between 30% and 60% of untreated patients with HIV/AIDS will develop AIDSrelated dementia 0. Less problems with antiretroviral therapy Vascular Dementia 39.In vascular dementia, a series of circumscribed 39.
cerebral infarcts cumulatively destroy neurons over expanding brain regions
Often confused with AD
Similar clinical picture
Interruption of blood supply to minute areas of brain because of arterial disease
Small (mini) strokes with cumulative effects
Less common than AD Other Cognitive Disorders: Amnestic Syndrome 40.The characteristic feature of amnestic syndrome is strikingly disturbed memory
118. Particularly shortterm memory
Overall cognitive functioning may be normal 119.
122. Chronic alcohol use and vitamin deficiency
Surgery to temporal lobe 41.Causes of amnestic syndrome include Other Cognitive Disorders: Amnestic Syndrome 17. A wide range of techniques have been developed to assist the goodprognosis amnestic patient in remembering recent events Disorders Involving Head Injuries: Types
42.Three types of traumatic brain injury (TBI): 123.
1. Closed head injury (soft tissue of brain 123.
comes in contact with interior skull wall)
2. Penetrating head injury (e.g. bullet) (Congresswoman Gifford)
3. Skull fracture Disorders Involving Head Injuries: Effects
43.Damage produces diffuse neural damage 126.
Often temporary loss of consciousness and post impact confusion 44.Note connection between traumatic head injury and risk for AD if APOE4 present Disorders Involving Head Injuries: Prevalence 45.Prevalence: 2 million injuries per year 127.
Motor vehicle and bicycle accidents, falls, assaults, sports injuries
Men aged 1524
Most common neurological disease except for headaches
Notable longstanding effects on adaptive functioning
Sequence: unconscious, then stupor and confusion when conscious Disorders Involving Head Injuries: Amnesia
46.Head (TBI) injuries can cause 132.
Retrograde amnesia (inability to recall events immediately preceding event) 133.
Anterograde amnesia (unable to store events 133.
after event) Disorders Involving Head Injuries: Personality Changes 47.Head (TBI) injuries can cause personality changes
E.g. Phineas Gage survived a massive head injury but suffered from personality changes
Regarding Henry (Harrison Ford)
Impulsiveness, loss of emotional control, loss of selfreflection
Effects depend on structural areas involved Disorders Involving Head Injuries: Treatment 48.Prompt treatment of brain injury may prevent further damage:
141. E.g. from pooling of blood under skull
Post traumatic epilepsy occurs in 24%
Elevated risk of depression
Interacts with premorbid personality and age 142. Process is difficult and expensive 49.Recovery and rehabilitation can take a long time Unresolved Issues 50.Can dietary supplements enhance brain functioning? End of Chapter 14
End of Chapter 14 ...
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This note was uploaded on 09/06/2011 for the course PSYC 3230 taught by Professor Hoyt during the Spring '08 term at UGA.
- Spring '08
- Abnormal Psychology