Delirium vs. Dementia Flashcards
What are the differences in delirium vs. dementia in terms of their: Time course?
- Delirium = acute
* Dementia = chronic
What are the differences in delirium vs. dementia in terms of their: Attention?
• Delirium = impaired
Dementia = normal
What are the differences in delirium vs. dementia in terms of their: Level of consciousness?
- Delirium = fluctuating
* Dementia = normal
What are the differences in delirium vs. dementia in terms of their: Memory
- Delirium = poor registration
* Dementia = amnesia
What are the differences in delirium vs. dementia in terms of their: Reversibility
- Delirium = common
* Dementia = uncommon
What are the differences in delirium vs. dementia in terms of their: Toxic and metabolic causes
- Delirium = typical
* Dementia = unusual
What are the differences in delirium vs. dementia in terms of their: Speech and language
- Delirium = inchoherent speech
* Dementia = aphasia
What is the definition of delirium?
- 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
What is meant by “clouded dementia”?
- 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
What are most vulnerable neurons to delirium?
- Chonlinergic, dopaminergic, histaminergic, noradrenergic and serotonergic
- Note NOT GABA or glutamate systems
What is the pathophysiology of delirium?
- 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
What psychiatric disorders go on the differential for delirium?
• 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)
What might cause delirium?
• 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
What are the routine laboratory tests for delirium?
• 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
What always starts your evaluation of the delirium patient?
History, physical exam, neurologic exam
*not necessarily the mini mental status exam which is usually unrewarding with the confused state of the patient
What is the most important rule of delirium treatment?
• 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
What causes dementia (etiology)?
• 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
What are the reversible causes of dementia we discussed?
• 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
what are the irreversible causes of dementia we discussed?
• 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
What is the definition of dementia?
• “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
What is the most important objective of the demential work-up?
- Find, if possible, a reversible cause and treat it
* Rare-ish to find, but you need to look for it
What tests/procedures are considered in the dementia work up?
• 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
What are the two most common cortical dementias?
- These are neurodegenerative dementias
- Alzheimer
- FTD or frontotemporal dementia
What are the clinical features of alzheimer’s disease?
• 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
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)
What causes AD?
• Largely unknown, but it is a mix of environmental and genetic factors
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
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
What is the standard drug treatment for AD?
- Ache inhibitor and memantine
* Memantine = NMDA antagonist
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
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
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
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
What are the two subcortical dementias we talked about?
- Parkinson’s Disease (PD)
* Huntington’s Disease (HD)
What structures are affected in subcortical dementia?
• Basal ganglia
• Thalamus
• Brainstem nuclei
○ Subcortical gray matter
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.
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
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
What are the given examples of white matter dementia?
- Binswanger’s Disease (BD)
* Normal Pressure Hydrocephalus (NPH)
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
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
What are the given examples of mixed dementia?
- Multi-infarct dementia
* CJD or creutzfeldt-Jakob
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
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
What drugs should be avoided in dementia?
- These drugs can make things worse
- Benzodiazepines
- Anticholinergic drugs
What conditions warrant use of atypical antipsychotics in AD patients?
• Neuropsychiatric syndromes: ○ Delusions, ○ Hallucinations ○ Paranoia ○ agitation
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
What drugs can you use in dementia?
• Low-dose atypical antipsychotic drugs ○ Quetiapine ○ Risperidone • For disruptive neuropsychiatric syndromes • SSRI's for depression is helpful
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
What’s the “pyramid” of basic cognition?
- Base = arousal
- Attention
- Language
- Memory
- Praxis
- gnosia
- Tip = executive function
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
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)
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.
What is praxis?
• Learned skills and the performance of skills learned through practice
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
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
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
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
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
What neurological motor disturbances would be something to look for in delirium?
- Asterixis
- Altered tone
- Myoclonus
- hyperrreflexia
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
What are some other neurological things you should look for in the delirium patient?
- Autonomic disturbances
* Neurological motor disturbances
What autonomic disturbances might surface in the delirium patient?
- (sympathetic drive)
- Tachycardia
- Diaphoresis
- Pupillary dilation
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
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
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
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
