Delirium vs. Dementia Flashcards
(67 cards)
1
Q
What are the differences in delirium vs. dementia in terms of their: Time course?
A
- Delirium = acute
* Dementia = chronic
2
Q
What are the differences in delirium vs. dementia in terms of their: Attention?
A
• Delirium = impaired
Dementia = normal
3
Q
What are the differences in delirium vs. dementia in terms of their: Level of consciousness?
A
- Delirium = fluctuating
* Dementia = normal
4
Q
What are the differences in delirium vs. dementia in terms of their: Memory
A
- Delirium = poor registration
* Dementia = amnesia
5
Q
What are the differences in delirium vs. dementia in terms of their: Reversibility
A
- Delirium = common
* Dementia = uncommon
6
Q
What are the differences in delirium vs. dementia in terms of their: Toxic and metabolic causes
A
- Delirium = typical
* Dementia = unusual
7
Q
What are the differences in delirium vs. dementia in terms of their: Speech and language
A
- Delirium = inchoherent speech
* Dementia = aphasia
8
Q
What is the definition of delirium?
A
- From latin “off the track”
- Rapidly developing disorder of attention characterized by an inability to maintain a coherent line of thought
- Acute confusional state
- Toxic-metabolic encephalopathy
- Incorporates the more rare but visual delirium tremens - to describe the hyperaroused, agitated, hallucinatory state
- MORE COMMON is underaroused, lethargic, somnolent state
9
Q
What is meant by “clouded dementia”?
A
- The phenomenon where demented patients more easily and quickly become delierious
- This can reflect poor outcomes in these older, demented patients and contribute to progression of dementia
10
Q
What are most vulnerable neurons to delirium?
A
- Chonlinergic, dopaminergic, histaminergic, noradrenergic and serotonergic
- Note NOT GABA or glutamate systems
11
Q
What is the pathophysiology of delirium?
A
- Perturbations in the metabolic environment of the brain…and the brain freaks out
- Represents diffuse brain dysfunction related to a disruption of normal brain homeostasis
- The neuronal dysfunction is widespread affecting arousal systems in the brainstem and diencephalon as well as cortical regions
- There is usually an underlying shift in the brain’s environment that causes the delirium, and removal of that cause can often reverse the condition
12
Q
What psychiatric disorders go on the differential for delirium?
A
• Schizoprenia and psychotic diseases
○ Main differentiator here is the fluctuations in level of consciousness
• Mania and depression
○ No fluctuation in level of consciousness like there is in delirium though
○ And also there is change in affect usually (not in delirium)
13
Q
What might cause delirium?
A
• Anything that would mess with the metabolic environment of the brain • Most often drugs and toxins ○ OTC drugs, recreational drugs, illicit substances ○ Intoxication AND withdrawal • Infectious and inflammatory disease ○ Meningitis ○ Encephalitis ○ CNS vasculitis ○ Systemic infection • Structural lesions ○ TBI, stroke • Seizure disorders
14
Q
What are the routine laboratory tests for delirium?
A
• Complete metabolic panel • Complete blood count • Urinalysis • Urinary toxicology screen • Electrocardiogram • Chest radiograph • Image of brain ○ CT or MRI • LP is required if brain infection is suspected • EEG can be helpful for confirmin non-convulsive status epilepticus
15
Q
What always starts your evaluation of the delirium patient?
A
History, physical exam, neurologic exam
*not necessarily the mini mental status exam which is usually unrewarding with the confused state of the patient
16
Q
What is the most important rule of delirium treatment?
A
• Find the cause, and reverse/treat the cause
• You can enhance normal cognitive function during treatment:
○ Clock and calendar (environmental manipulations)
○ Provision of adequate sleep and restore the sleep-wake cycle
○ Calming medications such as the atypical neuroleptics
17
Q
What causes dementia (etiology)?
A
• Reversible (10-20%) and irreversible (80-90%) • Reversible ○ Drugs and toxins ○ Mass lesions ○ Normal pressure hydrocephalus ○ Hypothyroidism ○ Vitamin B12 deficiency ○ Neurosyphilis ○ CNS inflammatory disease (like SLE) ○ Systemic infection/inflammation ○ Severe depression ○ Mild traumatic brain injury • Irreversible ○ Alzheimer ○ Frontotemporal dementia ○ Vascular dementia ○ Huntington ○ Parkinson ○ Lewy body dementia ○ Creutzfeldt-jakob ○ Multiple sclerosis ○ HIV-associated dementia ○ Severe traumatic brain injury
18
Q
What are the reversible causes of dementia we discussed?
A
• Reversible (10-20%) and irreversible (80-90%) • Reversible ○ Drugs and toxins ○ Mass lesions ○ Normal pressure hydrocephalus ○ Hypothyroidism ○ Vitamin B12 deficiency ○ Neurosyphilis ○ CNS inflammatory disease (like SLE) ○ Systemic infection/inflammation ○ Severe depression ○ Mild traumatic brain injury
19
Q
what are the irreversible causes of dementia we discussed?
A
• Reversible (10-20%) and irreversible (80-90%) • Irreversible ○ Alzheimer ○ Frontotemporal dementia ○ Vascular dementia ○ Huntington ○ Parkinson ○ Lewy body dementia ○ Creutzfeldt-jakob ○ Multiple sclerosis ○ HIV-associated dementia ○ Severe traumatic brain injury
20
Q
What is the definition of dementia?
A
• “down from the mind” - latin
• Acquired and persistent impairment in intellectual function with deficits in at least three:
○ Memory
○ Language
○ Visuospatial skills
○ Emotion and personality
○ Complex cognition
• Must interfere with usual social and occupational activities (be actual pathology)
• Need not be either progressive or irreversible by definition, though it largely is
21
Q
What is the most important objective of the demential work-up?
A
- Find, if possible, a reversible cause and treat it
* Rare-ish to find, but you need to look for it
22
Q
What tests/procedures are considered in the dementia work up?
A
• History and physical exam (neuro, mental status, physical)
• CMP
• CBC
• TSH
• B12
• RPR - rapid plasma reagin - screen for syphilis
• MRI/CT scan
• Only in select cases:
○ HIV, EEG, ESR, antibody for autoimmune dementia, heavy metal screen, angiography and biopsy
23
Q
What are the two most common cortical dementias?
A
- These are neurodegenerative dementias
- Alzheimer
- FTD or frontotemporal dementia
24
Q
What are the clinical features of alzheimer’s disease?
A
• Know that AD has a defined clinical profile that helps make this dx
• Stage I - amnesia is notable
• Stage II - dementia is obvious
• Stage III - mental and physical incapacity
• MCI - mild cognitive impairment - is associated with age but can convert to true AD (10-15% per year)
○ 1-2% of non-MCI elderly convert
• Most common in older individuals with 5-10% prevalence after 65 and near 40% over 85
25
What must be present on neuropathology to confirm the AD dx?
* AD is characterized by cerebral atrophy and amyloid plaques and neurofibrillary tangles
* Sufficient plaques and tangles either on brain biopsy or at autopsy
* Brain biopsy is rarely done, the clinical features are pretty telling
* 90% accuracy with probable AD dx (clinical)
26
What causes AD?
• Largely unknown, but it is a mix of environmental and genetic factors
27
What are the genetic factors in AD?
* Not tested for much b/c can't do much if you get a positive result
* Trisomy 21 - overexpression of APP or amyloid precursor protein
* Early-onset - APP, presenilin-1 (chromosome 14) and presenilin-2 (chromosome 1)
* Late-onset - APOE gene, epsilon-4 allele presence
28
What is the cholinergic hypothesis of AD?
* Ach is relatively deficient in AD
* Loss of cholinergic cells in basal forebrain is correlated with cognitive impairments in AD
* Donepezil, rivastigmine and glantamine are ache inhibitors approved for AD
* The other drug is memantine, an NMDA antagonist
29
What is the standard drug treatment for AD?
* Ache inhibitor and memantine
| * Memantine = NMDA antagonist
30
What's up with frontotemporal dementia?
* FTD = frontotemporal dementia
* Most salient features are changes in behavior and comportment
* NOT changes in memory
* Once was "pick's disease"
* Disinhibition, apathy, executive dysfunction while memory is still normal
31
In addition to dementia, what do the subcortical dementias share?
* Some variety of abnormal movement in additinon to dementia
| * Disease in which subcortical gray matter structures are affected
32
What is LBD?
* lewy body dementia
* Related disorder to PD
* Dementia, parkinsonism, visual hallucinations and fluctuating confusion
* Hard to treat as PD drugs worsen psychosis while neuroleptics worsen parkinsonism
33
What's up with Parkinson's Disease?
* PD resting tremor, bradykinesia, rigidity, postural instability are CLASSIC signs
* Lewy bodies in substantia nigra are characteristic histopatholoic finding
* Dopamine deficiency is the movement disorder cause
* Subset is LBD or lewy body dementia
34
What are the two subcortical dementias we talked about?
* Parkinson's Disease (PD)
| * Huntington's Disease (HD)
35
What structures are affected in subcortical dementia?
• Basal ganglia
• Thalamus
• Brainstem nuclei
○ Subcortical gray matter
36
What are the manifestations and cause of Huntington Disease?
* HD - huntington's disease
* Autosomal dominant disease that involves dementia and chorea, with either presenting
* Many have premonitory (like a premonition, or a warning sign) personality changes
* Also present are a variety of neuropsychiatric features
* Caudate atrophy is commonly seen on neuroimaging reflecting a major site of neuronal loss
* CAG triplet repeat disease (basis of genetic test)
* Chorea = a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and face.
37
Tetrabenazine is used in what disease?
* HD-related chorea Can be treated with neuroleptic drugs and tetrabenazine
* Chorea = a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and face.
* This is one of the presenting signs of HD
38
What is chorea and what should it make you think?
* Chorea = a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and face.
* This is one of the presenting signs of HD
* Can be treated with neuroleptic drugs and tetrabenazine
39
What are the given examples of white matter dementia?
* Binswanger's Disease (BD)
| * Normal Pressure Hydrocephalus (NPH)
40
What's up with BD?
* BD - binswanger's disease
* Form of vascular dementia in which long-standing hypertension leads to the development of ischemia an dlacunar infarction that falls heavily on the cerebral white matter
* White matter dementia
* Often underdiagnosed
* Course is typical of widespread white matter problems
41
What's up with NPH?
* NPH - normal pressure hydrocephalus
* Reversible dementia
* Present with dementia, gait disorder and urinary incontinence and have enlarged ventricles with normal sulci on neuorimaging indicating hydrocephalus and neuopatholgy affecting the periventricular white matter
* If patients respond well to large volume spinal tap they may be candidates for a ventricular or lumbar shunt to divert CSF
* NPH is rare, and shunting even more so
* Large tap is 30-55cc of CSF
42
What are the given examples of mixed dementia?
* Multi-infarct dementia
| * CJD or creutzfeldt-Jakob
43
What's up with multi-infarct dementia?
* Vascular dementia, contrast with BD
* Repeated strokes erode cognitive function so that eventually enough brain tissue is destroyed to cause dementia
* Can be large vessel ischemic infarcts affecting cerebral cortex
* Can be small vessel lacunar infarcts involving subcortical gray and white matter
* Some patients have both
* Only treatment is stroke prevention
44
While CJD is potentially transmissible, what percentage of cases are sporadic in origin?
```
• 85-90%
• Remainder are familial. SUPER uncommon is a case of transmissibility
○ Dura mater grafts
○ Neurosurgical instruments
○ Corneal transplantation
○ Cadaveric pituitary growth hormone
○ EEG depth electrodes
• Present with dementia that progresses over weeks to months
• Ofen confusion or spychotic features
• Myoclous
• Cortical or subcortcial hyperintenstities on diffusion weighted MRI
• Death in 4-12 months
```
45
What drugs should be avoided in dementia?
* These drugs can make things worse
* Benzodiazepines
* Anticholinergic drugs
46
What conditions warrant use of atypical antipsychotics in AD patients?
```
• Neuropsychiatric syndromes:
○ Delusions,
○ Hallucinations
○ Paranoia
○ agitation
```
47
What are the pharm treatments for AD?
• Ache inhibitors
• Tacrine was first but superseded by donepezil
○ Standard of care with efficacy and well tolerated)
• Rivastigmine
• Galantamine
• Rivastigmine can be given transdermally to reduce GI side effects
• Memantine is an NMDA antagoinst with similar efficacy to ache
• With psychiatric syndromes use atypical antipsychotics
48
What drugs can you use in dementia?
```
• Low-dose atypical antipsychotic drugs
○ Quetiapine
○ Risperidone
• For disruptive neuropsychiatric syndromes
• SSRI's for depression is helpful
```
49
Should you use the term confused when discussing a patient's care?
• No, this term is used in too many places and therefore has very little clinical meaning
50
What's the "pyramid" of basic cognition?
* Base = arousal
* Attention
* Language
* Memory
* Praxis
* gnosia
* Tip = executive function
51
Where can you expect to see delirium?
* 10-40% of hospitalized elderly
* 80% of terminally ill
* 51% post-op cases
* Presenting feature in 30% of bacteremia in elderly
* Indicator of increased morbidity and mortality, as well as worse outcome
* Consider this a vital organ failure and sign of underlying serious disease
52
What are the DSM-5 criteria for the diagnosis of delirium?
* Disturbance in attention and awareness (to environment)
* Develops over a short period of time (hours to days), fluctuates and is a change from baseline
* Additional disturbance in cognition (memory, language, visuospatial)
* The disturbances are not due to another preexisting or established neurocognitive disorder
* Evidence exists that there is an underlying cause (drugs, withdrawal, toxin, etc)
53
What is gnosia?
• 1. The perceptive faculty enabling one to recognize the form and the nature of people and things; the faculty of perceiving and recognizing.
54
What is praxis?
• Learned skills and the performance of skills learned through practice
55
What are the two ends of the spectrum that is delirium?
```
• Hyperactive and hypoactive
• Hyperactive is more "classic"
○ Irritable, angry, laughing, euphoric (emotional lability)
○ Wandering
○ Distractible, tangential
• Hypoactive
○ Can easily be missed as the patients are quiet
○ Apathetic, lethargic
○ Slow of speech and movement,
○ staring off
```
56
What are the clinical characteristics of delirium?
* Fluctuating arousal
* Attention deficits
* Alterations in memory, language, construction, perception and mood
* Spontaneous speech may be incoherent, rambling, shifting topics
57
How can you use a patient's writing as diagnostic help for delirium?
* There is a marked impairment in writing and constructional abilities
* "agraphia"
* Illegible, abnormal spacing, agrammatical, spelling errors, omissions, substitutions, and duplication errors
* Distorted or unrecognizable drawing of shapes or figures
58
What is meant by "patient is perseverative"?
• Some initial stimulus will get a patient started on something, but they will continue to repeat themselves, even after the stimulus is gone
59
What are the psychosis manifestations of delirium?
* If they do hallucinate, they tend to be silent fully formed visual hallucinations
* Auditory is less common
* Range from simple and transient to complex and rigid
* Frequent affective alterations with lability
60
What neurological motor disturbances would be something to look for in delirium?
* Asterixis
* Altered tone
* Myoclonus
* hyperrreflexia
61
What is asterixis?
* Extended wrists, push back on them and notice an unconscoious/uncontrolled flapping movement
* Can be synchronous or not
* Indicative of encephalopathy or altered mental status
62
What are some other neurological things you should look for in the delirium patient?
* Autonomic disturbances
| * Neurological motor disturbances
63
What autonomic disturbances might surface in the delirium patient?
* (sympathetic drive)
* Tachycardia
* Diaphoresis
* Pupillary dilation
64
A pitfall to remember in the delirium patient (pharm)…?
* Unless alcohol withdrawal, avoid the pitfall of giving a patient benzos
* Results in paradoxical agitation
* Physical restraints are dangerous. Only use during the acute agitation episode and remove them as soon as they calm down
65
What does the state of delirium do to a patient's long-term outcomes?
* In non-demented patients up to 8x increased risk of future dementia after delirium
* In AD patients, decline 2x faster for up to 5 years after delirium
66
What are the DSM-5 criteria for dementia?
* Evidence of significant cognitive decline from a prior level of performance in one or more cognitive domains
* Deficits interfere with independence in everyday activities
* Do not occur in the context of delirium alone
* Not better explained by another disorder
67
Delirium is a "bottom up" impairment while dementia…?
* Dementia is a top-down impairment
* Executive function is first
* Gnosia, praxis, memory, language, attention, arousal
* In that descending order
* Think of the pyramid of cognitive function
