delirium and dementia Flashcards
Delirium vs dementia (time course, conciousness, attention, memory, speech/language, toxic and metabolic causes, reversibility
Delirium: acute, fluctuating levels of conciousness, impaired attention, poor registration of memory, incoherent speech, toxic and metabolic causes typical, commonly reversible. Dementia: chronic, normal levels of conciousness, normal attention, amnesia, aphasia, toxic and metabolic causes unusual, reversibility is uncommon.
- Define the syndrome of delirium.
rapidly developing disorder of attention characterized by an inability to maintain a coherent line of thought. Usually hypoaroused, but can be hyperaroused
Alternate names for delirium
acute confusional state, favored by many because it emphasizes the acute nature of the syndrome and the prominence of the attentional disorder, and toxic-metabolic encephalopathy, which highlights the most common etiologies.
Delirium pathophys
disruption of normal brain homeostasis. Neuronal dysfunction is widespread, affecting arousal systems in the brainstem and diencephalon as well as cortical regions, but the most vulnerable neurons are thought to be those involved in cholinergic, dopaminergic, histaminergic, noradrenergic, and serotonergic neurotransmission. If the insult causing delirium is corrected within a few days, normal brain function can usually be restored, but a prolonged insult may damage neurons irreversibly and limit recoverability.
Delirium differential diagnosis
Aphasia/Wernicke’s aphasia (resembles delirum b/c impaired speech and language, but aphasia usually follows a stroke). Schizophrenia and other psychotic diseases can mimic delirium, but there is typically no fluctuation in level of consciousness. In both mania and depression, prominent affective features are typical, but no fluctuation in level of consciousness.
Etiology of delirium
Drugs/toxins (prescription meds, OTC, recreational), intoxication and withdrawal, Metabolic disorders, infectious/inflammatory disease ( meningitis, encephalitis, vasculitis, systemic infection), TBI, stroke, seizure disorders,
evaluation of delirium
History/PE, MSE is NOT necessary b/c patient is too confused, CMP, urinalysis, urine toxicology, EKG, chest radiograph, CT/MRI of brain, lumbar puncture if infection is suspected, EEG (for status epilepticus)
Treatment of delirium
Treat the cause, manipulations such as providing a clock and calendar, provision of adequate sleep and restoration of the sleep-wake cycle, and judicious use of calming medications such as the atypical neuroleptics.
- Define the syndrome of dementia.
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 is neither progressive nor irreversible.
- Discuss the reversible etiologies of dementia.
Reversible (10-20%): drugs/toxins, mass lesions, normal pressure hydrocephalus, hypothyroidism, Vitamin B12 deficiency, neurosyphilis, CNS inflammatory dz, mild TBI.
- Discuss the irreversible etiologies of dementia.
Irreversible (80-90%): Alzheimers, frontotemporal dementia, vascular dementia, huntingtons, parkinsons, lewy body dementia, Creutzfeldt-jakobs, MS, HIV, Severe TBI
Evaluation of dementia
Detect reversible causes! CBC, CMP, TSH, B12, RPR, MRI/CT, lumbar puncture, EEG, HIV, ESR, Abs for autoimmune
Types of cortical dementia
Alzheimers dz and frontotemporal dementia
Survival after onset of Alzheimers
6-12 yrs
Alzheimers clinical stages
stage I (1-2 years), when amnesia is most notable; stage II (2-10 years), when dementia is obvious; and stage III (8-12 years), when the patient has severe mental and physical incapacity
Mild cognitive impairment and relationship to Alzheimers
Mild cognitive impairment (MCI) is a transitional stage between normal aging and AD; memory complaints, normal general cognitive function and intact daily living activities. No dementia yet. in a person over 65 with MCI, the conversion rate to AD is 10-15% per year as opposed to 1-2% without MCI.
Alzheimers neuropath
Cerebral atrophy (loss of cortical neurons/synapses), damage to limbic and association cortices, neuritic (amyloid) plaques and neurofibrillary tangles in neocortex and hippocampus (occur in normal aging, but less dramatically)
Alzheimers etiology
Amyloid precursor protein mutations on chrom 21 (or overexpression in down syndrome), Presenilin-1 mutations on chrom 14 or presenilin-2 mutation on chrom 1 are linked to early onset AD (these mutations only account for 1% of all cases). Late onset cases often have epsilon-4 allele of apolipoprotein E gene
Cholinergic hypothesis for AD
acetylcholine is relatively deficient in AD, and loss of cholinergic cells in the basal forebrain is correlated with cognitive impairments in AD
Treatment of Alzheimers
Donepezil, rivastigmine, and galantamine are cholinesterase inhibitors approved for AD. memantine is an NMDA antagonist that is available as a neuroprotective agent. Standard drug treatment for AD now includes a cholinesterase inhibitor and memantine.
Frontotemporal Dementia presentation, brain regions affected, differential diagnosis
Aka Picks disease. Presents as changes in behavior and comportment, not memory. disinhibition, apathy, and executive dysfunction. Degenerative dz of frontal and temporal lobes, sparing hippocampus until later in dz. Many are misdiagnosed with psychiatric dz (ie. bipolar)
What are subcortical dementias and give examples
diseases in which subcortical gray matter structures (basal ganglia, thalamus, brainstem nuclei) bear the major burden of neuropathology. All of these disorders feature some variety of abnormal movement in addition to dementia. Parkinsons and huntingtons are examples
Parkinsons presentation, histology, treatment
resting tremor, bradykinesia, rigidity, and postural instability. Dementia develops in up to 80%. Lewy bodies in the substantia nigra and dopamine deficiency due to loss of dopaminergic cells in midbrain substantia nigra. Standard PD drugs may have a modest effect on cognition, and cholinesterase inhibitors may also help
Lewy Body Dementia symptoms, treatment
characterized by dementia, parkinsonism, visual hallucinations, and fluctuating confusion. Cholinesterase inhibitors can help the dementia of LBD, but this disease is difficult to treat because PD drugs may worsen psychosis while neuroleptics may worsen parkinsonism
Huntingtons gnetics, symptoms, physiology, diagnosis, treatment
Autosomal dominant. Dementia or chorea may be presenting, plus premonitory personality changes, and many neuropsychiatric features. Caudate atrophy. Diagnosed by genetic testing for CAG repeat. Treated with neuroleptic drugs and tetrabenzine for chorea, but no drugs available for dementia
Examples of white matter dementia
genetic, demyelinative, infectious, inflammatory, toxic, metabolic, traumatic, Binswangers disease and normal pressure hydrocephalus
Binswangers disease description/cause, clinical profile
vascular dementia in which long-standing hypertension leads to the development of ischemia and lacunar infarction that falls heavily on the cerebral white matter. Seen as slowly progressive dementia, apathy, confusion, depression, gait disorder, rigidity, incontinenc
Binswangers disease pathology
White matter volume loss, especially in periventricular regions > hydrocephalus ex vacuo, Thickened and hyalinized penetrating arterioles (“small vessels”), Ischemic demyelination, mainly of association fibers, sparing U fibers, “Incomplete infarction” of white matter, Cerebral cortex is essentially normal
Normal pressure hydrocephalus presentation
present with reversible dementia, gait disorder, and urinary incontinence, and have enlarged ventricles with normal sulci on neuroimaging indicating hydrocephalus and neuropathology affecting the periventricular white matter
What procedure improves gait and sometimes cognition in normal pressure hydrocephalus
high volume lumbar tap test (30-50cc) then ventriculo-peritoneal, ventriculo-atrial, and lumboperitoneal shunts show some improvement
high volume lumbar tap test (30-50cc) then ventriculo-peritoneal, ventriculo-atrial, and lumboperitoneal shunts show some improvement
Multi-infarct dementia cause, symptoms, treatment
A series of sequential strokes erodes cognitive function so that eventually, when enough brain tissue is destroyed, dementia appears. These strokes can be large vessel ischemic infarcts affecting the cerebral cortex or small vessel lacunar infarcts involving subcortical gray and white matter. The classic course is that of step-wise deterioration of function, with progressively more cognitive loss evident after each new stroke. The obvious treatment is to prevent strokes from occurring at all.
Creutzfeldt-Jakob Disease cause, presentation, prognosis,
rapidly progressive, always fatal, and potentially transmissible. Human prion disase (most are sporadic, some are familial). Infectious causes are rare but have been found with transplants. Present with dementia progressing over weeks-months, with confusion or psychotic features, myoclonus, cortical or subcortical hyperintensities on diffusion weighted MRI. Death usually within 4-12months.
Variant Creutzfeldt-Jakob Disease
human bovine spongiform encephalopathy or “mad cow disease” is a very rare prion disease acquired by consuming infected English beef, and recently a few cases have occurred after blood transfusion. vCJD has an earlier age of onset and a slightly longer course than CJD
Treatment of irreversible dementia
Avoid benzodiazepines and anticholinergic drugs which make mental status worse, use lose dose atypical antipsychotic drugs (e.g. quetiapine or risperidone) for disruptive neuropsychiatric syndromes, a trial of an antidepressant (SSRI) treatment if depression is significant
Treatment of Alzheimers
Cholinesterase inhibitors: Tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl, Razadyne); all these drugs have been shown to have similar efficacy, but donepezil is often better tolerated, and is easier to use because of once daily dosing. Rivastigmine can now be given transdermally to reduce GI side effects. Memantine (Namenda) is an NMDA antagonist with similar efficacy that can be used in conjunction with a cholinesterase inhibiton
