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Neurocognitive Disorders DSM 5
Colleen Kirsch Hiltz Whiteon 15 November 2012
Transcript of Neurocognitive Disorders DSM 5
by: Colleen M. Kirsch Hiltz White Rationale Mild Neurocognitive Disorder Subtypes
A. Evidence of modest cognitive decline from a previous level of performance in one or more of the domains outlined above based on:
1. Concerns of the individual, a knowledgeable informant, or the clinician that there has been a modest decline in cognitive function; and
2. A decline in neurocognitive performance, typically involving test performance in the range of 1 and 2 standard deviations below appropriate norms (i.e., between the 3rd and 16th percentile) on formal testing or equivalent clinical evaluation.
B. The cognitive deficits are insufficient to interfere with independence (i.e., instrumental activities of daily living [more complex tasks such as paying bills or managing medications] are preserved), but greater effort, compensatory strategies, or accommodation may be required to maintain independence.
C. The cognitive deficits do not occur exclusively in the context of a Delirium.
D. The cognitive deficits are not primarily attributable to another mental disorder (e.g., Major Depressive Disorder, Schizophrenia). S XX.01 Neurocognitive Disorder due to Alzheimer's Disease
S XX.02 Vascular Neurocognitive Disorder
S XX.03 Frontotemporal Neurocognitive Disorder
S XX.04 Neurocogntive Disorder due to Traumatic Brain Injury
S XX.05 Neurocognitive Disorder due to Lewy Body Dementia
S XX.06 Neurocognitive Disorder due to Parkinson's Disease S XX.07 Neurocognitive Disorder due to HIV Infection
S XX.08 Substance-Induced Neurocognitive Disorder
S XX.09 Neurocognitive Disorder due to Huntington's Disease
S XX.10 Neurocognitive Disorder due to Prion Disease
S XX.11 Neurocognitive Disorder due to Another Medical Condition
S XX.12 Neurocognitive Disorder Not Elsewhere Classified Subtypes B. Documented infection with Human Immunodeficiency Virus (HIV)
C. Impaired performance in at least two of the following cognitive domains: Complex Attention, Learning and Memory, Language, Executive function, Visual constructual-perceptual function
D. The Neurocognitive Disorder cannot be explained better by non-HIV conditions. B. The Neurocognitive Disorder presents in the context of current or past use of a substance capable of causing the neurocognitive deficit.
C. There is strong presumptive evidence of an etiological relationship between the substance use and the Neurocognitive Disorder as suggested by one or more of the following:
1. the duration and extent of substance use are judged to be sufficient to induce neurocognitive deficits;
2. the temporal course of the neurocognitive deficits is consistent with this etiological relationship (e.g. there is no progression of neurocognitive deficits if the individual is demonstrably abstinent from continuing substance use for an extended period of time); and
3. the cognitive domains involved are consistent with the particular substance misused (e.g. memory and frontal-executive deficits in Alcohol Use Disorder).
D. The Neurocognitive Disorder cannot be explained better by substance intoxication, substance withdrawal, or other non-Substance Use Disorder conditions. B. There is insidious onset and gradual progression of impairment in one or more cognitive domains (for Major Neurocognitive Disorder, two domains must be impaired).
C. Memory impairment is an early and prominent feature (see text for other presentations)
D. The syndrome as a whole is not better attributed to:
1. Cerebrovascular disease (i.e., there is no history of stroke temporally related to the onset of cognitive impairment; and any infarcts or white matter hyperintensities are judged insufficient to account for the clinical picture)
2. Lewy body disease (i.e., core features of Lewy body disease are absent)
3. Parkinson’s disease (i.e., spontaneous parkinsonism with onset well before the cognitive decline)
4. Fronto-temporal lobar degeneration (i.e., core features of fronto-temporal lobar degeneration are absent)
5. Other concurrent, active neurologic or systemic illness (i.e., there is no other condition with an appropriate temporal relationship and severity to account for the clinical picture). DSM 5 Criteria
A. Evidence of substantial cognitive decline from a previous level of performance in one or more of the domains outlined above based on:
1. Concerns of the individual, a knowledgeable informant, or the clinician that there has been a substantial decline in cognitive function; and
2. A decline in neurocognitive performance, typically involving test performance in the range of 2 or more standard deviations below appropriate norms (i.e., below the 3rd percentile) on formal testing or equivalent clinical evaluation.
B. The cognitive deficits are sufficient to interfere with independence (i.e., requiring assistance at a minimum with instrumental activities of daily living [more complex tasks such as paying bills or managing medications]).
C. The cognitive deficits do not occur exclusively in the context of a Delirium.
D. The cognitive deficits are not primarily attributable to another mental disorder (e.g., Major Depressive Disorder, Schizophrenia). DSM IV Criteria There is no DSM-IV criteria for just neurocognitive disorder listed at DSM5.org
Basic DSM-IV criteria for Dementia is:
A. The development of multiple cognitive deficits manifested by both:
1.Memory impairment (impaired ability to learn new information or to recall previously learned information)
2.One or more of the following cognitive disturbances:
(a) aphasia (language disturbance)
(b) apraxia (impaired ability to carry out motor activities depite intact motor function)
(c) agnosia (failure to recognize or identify objects despite intact sensory function)
(d) disturbance in executive functioning (i.e., planning, organizing, sequencing, abstracting)
B. The cognitive deficits in criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning.
C. The course is characterized by gradual onset and continuing cognitive decline. B. The clinical features are consistent with a vascular etiology as suggested by one of the following:
1. The onset of the cognitive deficits is temporally related to one or more vascular events
2. Evidence for decline is prominent in speed of information processing, complex attention and/or frontal-executive functioning
C. There is evidence of the presence of cerebrovascular disease from history, physical examination and/or neuroimaging considered to be sufficient to account for the neurocognitive deficits (see details in text)
D. The symptoms are not better accounted for by another brain disease or systemic disorder as evidenced by any of the following:
1. Early onset of memory deficit and progressive worsening of memory and other cognitive functions such as language (transcortical sensory aphasia), motor skills (apraxia), and perception (agnosia), in the absence of corresponding focal lesions on brain imaging or history of vascular events (suggestive of consistent with Alzheimer’s disease).
2. Early and prominent Parkinsonian features suggestive of Lewy body disease
3. Absent or minimal cerebrovascular lesions on brain CT or MRI
4. Other medical disorders severe enough to account for cognitive impairment, e.g. brain tumour, multiple sclerosis, encephalitis, toxic and metabolic abnormalities, etc.
5. Major depression, with a temporal association between cognitive impairment and the time of onset of depression.
1. Probable: Vascular Neurocognitive Disorder is considered probable if:
a) Clinical criteria are supported by neuroimaging evidence of significant parenchymal injury due to cerebrovascular disease (neuroimaging-supported)
b) The neurocognitive syndrome is temporally related to one or more cerebrovascular events and there is documented evidence of these events
c) If both clinical and genetic (e.g. cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, CADASIL) evidence of cerebrovascular disease are present. B. The clinical features are indicative of frontotemporal degeneration, either as a behavioral or a language variant. Individuals must meet criteria for one of the following variants, although they may have features from within both
1. For Behavioral Variant Frontotemporal Neurocognitive Disorder, there is evidence of decline from a previous level of performance or behavior, based on the following:
i. Report of, or observation by the examiner, of at least three of the following behavioral/cognitive symptoms
a) Behavioral disinhibition: Socially inappropriate behavior; or loss of manners or decorum; or impulsive, rash, or careless actions
b) apathy or inertia
c) loss of sympathy or empathy (e.g., diminished response to other people’s needs and feelings; diminished social interest, interrelatedness, or personal warmth)
d) perseverative, stereotyped, or compulsive/ritualistic behavior
e) Hyperorality and dietary changes (e.g., altered food preferences, binge eating, increased consumption of alcohol or cigarettes, or oral exploration or consumption of inedible objects)
ii. Clear evidence of impairment in frontal-executive functioning, involving two or more of the following:
a) mental flexibility impairments (e.g., Trail Making Test Part B)
b) decrease in generation tasks (e.g., letter fluency/design fluency)
c) presence of errors (e.g., perseverations or rule violations) deficits in planning
d) deficits in reversal learning
e) relative sparing of visuospatial skills (e.g., ability to copy simple line drawings)
iii. The change in behavior is of gradual onset and progressive in nature
2. For Language Variant Frontotemporal Neurocognitive Disorder, both of the following must be present:
i. Gradual worsening of language ability, in the form of speech production, word finding, object naming, grammar, or word comprehension; and evidence that language function was normal premorbidly
ii. Memory function and visuospatial skills ((e.g., ability to copy simple line drawings) are comparatively less impaired or not impaired relative to the language impairment which must be at least moderate.
C. A diagnosis of Frontotemporal Neurocognitive Disorder is not made if one of the following is present:
1. The symptoms are better accounted for by a non-neurodegenerative medical condition
2. Behavioral symptoms are better accounted for by a psychiatric disorder (e.g., Schizophrenia or Depressive or Bipolar Disorder)
3. Change occurs exclusively in the course of a Delirium
4. Clinical assessment and/or biomarkers indicate that Alzheimer’s disease or other neurodegenerative disorder is present. B. The disorder is caused by a traumatic brain injury (TBI), that is, an impact to the head or other mechanisms of rapid movement or displacement of the brain within the skull, with one or more of the following:
1. loss of consciousness
2. posttraumatic amnesia
3. disorientation and confusion
4. neurological signs (e.g., positive neuroimaging demonstrating injury, a new onset of seizures or a marked worsening of a preexisting seizure disorder, visual field cuts, anosmia, hemiparesis)
C. The Neurocognitive Disorder presents immediately after the occurrence of a TBI or immediately after recovery of consciousness, and persists for at least one week.
D. While cognitive presentation is variable, difficulties with the domains of Complex Attention, Executive Ability, and Learning and Memory are common, particularly at the Mild Neurocognitive level. Disturbances in Social Cognition are often present. B. Insidious onset and gradual progression.
C. The symptoms are not better attributed to cerebrovascular disease, as evident on focal neurologic signs or on brain imaging
D. The symptoms are not better attributed to another physical illness or brain disorder.
1. Major or Mild Neurocognitive Disorder due to Probable Lewy Body Disease. Probable requires two core features, or one suggestive feature with one or more core features
2. Major or Mild Neurocognitive Disorder due to Possible Lewy Body Disease. Possible requires one core feature, or one or more suggestive features
Core Diagnostic Features of Lewy Body Disease include the following:
a) Fluctuating cognition with pronounced variations in attention and alertness.
b) Recurrent visual hallucinations that are typically well-formed and detailed.
c) Spontaneous features of parkinsonism with onset at least 1 year later than the cognitive impairment. B. The disorder occurs in the setting of established Parkinson’s disease with motor symptoms for at least one year before the onset of cognitive decline.
C. There is insidious onset and gradual progression of impairment in one or more cognitive domains (for Major Neurocognitive disorder, at least two domains must be impaired).
D. The symptoms are not better attributed to cerebrovascular disease, or another systemic illness or brain disorder.
Probable: Most likely attributable to Parkinson’s Disease
Possible: Possibly attributable to Parkinson’s Disease B. There is insidious onset and gradual progression.
C. There is evidence of the risk of Huntington Disease either from family history or from genetic testing of the CAG expansion > 36 in gene IT-15 on chromosome four.
D. The Neurocognitive Disorder cannot be better explained by other conditions. B. There is evidence from the history, physical examination, or laboratory findings that the neurocognitive disorder is attributable to prion disease (e.g., Creutzfeldt-Jakob Disease, bovine spongiform encephalopathy).
C. The cognitive deficits do not occur exclusively in the context of a Delirium. B. There is evidence from the history, physical examination, or laboratory findings that the Neurocognitive disorder is attributable to medical condition other than a DSM disorder
C. The cognitive deficits do not occur exclusively in the context of a Delirium.
Neurocognitive Disorders may be diagnosed as Not Elsewhere Classified under the following circumstances.
1. Subthreshold Disorder. In cases of Delirium where the severity of cognitive impairment falls short of that required to diagnose Delirium, or where some but not all the diagnostic criteria for Delirium are met, the diagnosis of Delirium Not Elsewhere Classified may be given. This condition corresponds to what is known as “subsyndromal delirium” in the delirium literature.
2. Atypical Disorder. If an individual does not meet all criteria for Major or Mild Neurocognitive disorder but the clinical picture more closely resembles these disorders than any other disorder in DSM-5, a diagnosis of Major or Mild Neurocognitive Disorder may be made.
3. Uncertain Etiology. If a Major or Mild Neurocognitive disorder is diagnosed, but the etiological subtype is uncertain, the Not Elsewhere Classified diagnosis can be made. This includes situations where the subtype will eventually be known but the assessments and investigations have not been concluded.
Note: if a Major or Mild Neurocognitive disorder is of mixed etiology (e.g., Alzheimer’s and Vascular), and the multiple underlying diseases are known, the Not Elsewhere Classified label should not be used; rather, the multiple etiological subtypes should all be diagnosed.
Note: A Major or Mild Neurocognitive Disorder occurring as the result of a known disease that is not specifically listed should be coded as a Neurocognitive Disorder Associated with Another Medical Condition.
Note: Neurocognitive Disorders due to Frontotemporal Lobar Degeneration, and Dementia with Lewy Bodies, which were classified as Dementia Not Otherwise Specified in DSM-IV, are distinct Neurocognitive Disorders with their own criteria in DSM-5 Rationale DSM-5 changes in subtypes of due to General Medical Condition:
This was changed into the Prion type. Prion is a protien that can cause Creutzfeldt-Jakob Disease, Gerstmann-Straussler-Scheinker
disease, and fatal familial insomnia. Prion protein causes degenerative neurological functioning and death.
Diagnosis for other Prion Disease Dementia in DSM-IV was catergorized under General Medical Condition. DSM 5 places diagnoses based on cause of Demetia, instead of relation to a specific disorder. Added:
Lewy Bodies type
According to Fujishiro et al, Lewy Bodies is the second most common cause of Dementia, after Alzhemier.
Lewy Bodies is another medical condition that can cause degenerative neurological functioning. Like many of the subtypes of Dementia there needs to be evidence of the disease, though diseases like Lewy Bodies can only be classified as possible of probable causes of Demetia. Rationale References:
Fujishiro, H., Ferman, T. J., Boeve, B. F., Smith, G. E., Graff-Radford, N. R.,
Uitti, R. J., Wszolek, Z. K., & Knopman, D. S. (2008). Validation of the neuropathologic criteria of the third consortium for dementia with lewy bodies for prospectively diagnosed cases. Journal of Neurolopathology, 67, 649-656.
Jonker, C., Geerlings, M. I., & Schmand, B. (2000). Are memory complaints
predictive for dementia? . International Journal of Geriatric Psychiatry, 15, 983-991.
Kennedy, G. J. (2010). Proposed revisions for the diagnostic categories of
dementia in the dsm-5. Primary Psychiatry, 17, 26-28. Retrieved from http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=2623
Kertesz, A., & Munoz, D. (1998). Pick's disease, frontotemporal dementia, and
pick complex. Neurological Review, 55, 302-304.
Spudich, S., Mastrianni, J. A., Wrensch, M., Gabizon, R., Meiner, Z., Kahana, I.
Rosenmann, H., Kahana, E.& Prusiner, S. B. (1995). Complete penetrance of creutzfeldt- jakob disease in libyan jews carrying the e200k mutation in the prion protein gene. Molecular Medicine, 1, 607-613.
Visser, P. J., Scheltens, P., Verhey, F. R. J., Schmand, B., Launer, L. J., Jolles, J., &
Jonker, C. (1999). Medial temporal lobe atrophy and memory dysfunction as predictors for dementia in subjects with mild cognitive impairment. Journal of Neurology, 246, 477-485. The name change to Neurocognitive Disorder to separate Alzhemier's Dementia and other forms of Dementia.
The DSM wants to focus diagnoses on performance of the individual, instead of the disabilities of the individual.
Dementia is not only loss of memory, that many lay people assume.
Though memory can help predict Neurocognitive Disorders (Jonker et al, 2000), medical exams such as Medial Temporal Lobe Atrophy (Visser et al, 1999).
HIV related Dementia and Lewy Bodies related dementia to not show memory loss in the earlier stages.
Like many of the DSM changes, name change was also to reduce stigma, especially is younger adults who have Dementia, because of the previous association of Dementia only with the eldery (Kennedy, 2010). Rationale Dementia due to Pick's Disease has been removed
Instead Frontotemporal subtype has been added
Rationale is again that the subtype is focusing on whether the cause of the impairment is coming from, and not the particular subtype (Kertesz et al, 1998).
Like Prion and Lewy Bodies, Frontotemporal subtype is difficult to diagnose without an autopys after the fact. Studies focusing of autopyses of Dementia patients has lead to the understanding of including Medical Cause Subtypes, instead relate to a disease subtype (Spudich et al, 1995).