Delirium and dementia Flashcards
Define the syndrome of delirium
Disorder of attention characterized by an inability to maintain a coherent line of thought.
Delirium is widely interpreted to mean the hyperaroused, agitated, hallucinatory state of the classic delirium tremens, but in fact an underaroused, lethargic, somnolent state is far more common.
Discuss the common etiologies of delirium
Drugs and toxins most common, including the withdrawl of such substances. The other causing include metabolic disorders, with cardiac, pulmonary, renal, hepatic, endocrine, and nutritional disorders.
Infectious and inflammatory disease can be responsible, including meningitis, encephalitis, CNS vasculitis, and systemic infection. Structural lesions such as traumatic brain injury and stroke often cause delirium along with other clinical signs. Seizure disorders may also be culpable
Define the syndrome of dementia
An acquired and persistent impairment in intellectual function with deficits in at least three of the following areas - memory, language, visuospatial skills, emotion and personality, and complex cognition - that is sufficient to interfere with usual social and occupational activities. By definition, dementia need not be either progressive or irreversible.
Understand the principles guiding treatment of delirium and dementia
Identification and possible correction of offending cause(s).
If not reversible, enhance function of the patient.
Reversible causes of dementia
Reversible cases are (10-20%)
Drugs and toxins Mass lesions Normal pressure hydrocephalus Hypothyroidism Vitamin B12 deficiency Neurosyphilis CNS inflammatory disease (i.e. SLE) Systemic infection/inflammation Severe depression Mild traumatic brain injury
Irreversible causes of dementia
Irreversible cases are (80-90%)
Alzheimer’s Disease Frontotemporal dementia Vascular dementia Huntington’s Disease Parkinson’s Disease Lewy Body Dementia Creutzfeldt-Jakob Disease Multiple sclerosis HIV-associated dementia Severe traumatic brain injury
Evaluation of delirium
Thorough history, physical exam, and neurologic examination. A complete mental status exam is not usually needed because pt is too confused.
Lab tests including metabolic panel, CBC, UA, urinary toxicology screen,
ECG, Lumbar puncture, and brain imagining
Evaluation of dementia
Most important objective is to detect reversible etiologies if present.
History and Physical exam (general, neurologic, mental status), CMP, CBC, TSH, B12, RPR, and MRI/CT
Treatment of Delirium
- Environmental manipulations (clocks, calendar, etc)
- Provision of adequate sleep (avoid daytime sedation and naps, use Trazadone or zolpidem QHS)
- Drugs for attention
Be cautious about alternative therapy
Avoid nihilism!
Mild Cognitive Impairment
- Memory complaint
- Largely normal general cognitive function
- Essential intact daily activities
- NO dementia
- May consider MCI as an intermediate between normal aging and Alzheimer’s
Frontotemporal Dementia (FTD)
- Selectively affects the frontal and/or temporal lobes
- Hippocampus is largely spared until late in disease
- Thus, behavior disorders occur early, before memory loss
- Many patients are first seen psychiatrically and often diagnosed with bipolar disorder
- CT and MRI often show frontal and/or temporal atrophy
Parkinson’s Disease
- Loss of dopaminertic cells in the midbrain substantia nigra (SN)
- 80% develop dementia within 15 years
White Matter Demenia
*Genetic (e.g. metachromatic leukodystrophy, adrenoleukodystrophy)
*Demyelinative (e.g. MS)
Infectious (e.g. HIV-associated dementia)
*Inflammatory (e.g. systemic lupus erythematosus)
*Toxic (e.g. cranial irrad
iation, toluene abuse)
- Metabolic (e.g. vitamin B12 deficiency)
- Vascular (e.g. Binswanger’s Disease)
- Traumatic (e.g. traumatic brain injury)
- Neoplastic (e.g. gliomatosis cerebri)
- Hydrocephalic (e.g. normal pressure hydrocephalus)
Binswanger’s Disease
- Vascular dementia featuring sever cerebral white matter ischemia
- Insidious behavioral and cognitive decline
- Apathy, confusion, memory loss, depression, anxiety, visuospatial dysfunction, pseudobulbar signs, gait disorder, focal corticospinal signs, spasticity, frontal release signs, rigidity, incontinence
TREAT HYPERTENSION = FIX BINSWANGERS
Creutzfeldt-Jakob Disease (CJD)
- A rapidly progressive dementia, often with acute confusion, hallucinations, and delusions
- CJD evolves over weeks to months, and typically ends in death within one year
- Myoclonus is a most helpful sign, present in virtually all patients at some point
- Etiology is a novel agent known as a prion (proteinaceous infectious agent)
- No treatment can reverse or arrest the disease
Multi-Infarct Dementia
- Another of the vascular dementias
- A combination of strokes, cortical or subcortical, produce dementia because of the cumulative destruction of brain tissue
- Clinical course is classically step-wise, indicating the occurrence of new strokes
- Prevention and treatment of stroke are most crucial; aspirin, heparin, warfarin, tPA, carotid surgery, etc.
Clinical Features of Alzheimer’s Disease
Survival after onset is ~ 6-12 years Stage I (1-3 years) – initial amnesia, mild anomia, apathy Stage II (2-10 years) – marked amnesia, fluent aphasia, visuospatial dysfunction, anosognosia, neuropsychiatric features Stage III (8-12 years) – severe dementia, global aphasia or mutism, incontinence
Impacts of Alzheimer’s Disease
AD is the most common cause of dementia in the elderly
50-70% of the total cases of dementia
Prevalence at least 5-10% after age 65
Will be more common as the population ages
Higher prevalence in women
Most common reason for nursing home admission
Gross and Microscopic Neuropathology of AD
Cerebral atrophy
Cortical neuronal and synaptic loss
The major damage is in limbic and association cortices, so that higher functions are most affected
Microscopically see Amyloid plaques and neurofibrillary tables seen in neocortex and hippocampus
Etiology of AD
- Both genetic and environmental factors are important
- Higher education and occupational engagement are protective
- Toxic (aluminium, silicon) and infections (virus, prion) etiologies have not been identified
- Increasing evidence supposts the importance of hypertension, diabetes, and TBI
- Down Syndrome link (extra copy of amyloid precursor protein (APP) leading to overexertion of amyloid and early neuritic plaque formation
