Overview Dementia is a disorder that is characterized by impairment of cognition, typically involving memory and at least one other cognitive deficit, such as aphasia, apraxia, agnosia, or disturbance in executive functioning. These must represent a decline from previous level of function and be severe enough to interfere with daily function and independence. Decrease in intellectual function without an effect on the level of consciousness.
| Definition Dementia: Cognitive impairment typically caused by anatomic changes in the brain, has slower onset, and is generally irreversible. Dementia mainly affects memory. Delirium: Cognitive impairment typically caused by acute illness or drug toxicity (sometimes life threatening) and is often reversible. Delirium mainly affects attention. Agnosia: Failure to recognize or identify objects despite intact sensory function. Aphasia: Language impairment. Apraxia: Impaired ability to carry out motor activities despite intact motor function. Executive Functioning: Planning, organizing, sequencing, abstracting. |
Major dementia syndromes
| Remember It is important to diagnose the type of dementia as treatment differs |
| AETIOLOGY | |
| Irreversible Causes | Reversible Causes |
| Alzheimer's disease | Hypothyroidism |
| Lewy body dementia | Depression |
| Huntington's disease | Vitamin B12 deficiency |
| Pick's disease | Normal pressure hydrocephalus |
| Cerebral infarct | Neurosyphilis |
| Creutzfeldt-Jakob disease | Chronic Alcohol use |
| Chronic substance abuse | Opiates |
Cardiometabolic factors
Other weaker factors
Clinical Presentation A reasonably healthy elderly person who is experiencing an insidious onset of problems with memory and organizational ability, which worsened markedly over the past few months.
Clinical Examination
| Aetiology |
| Reversible Causes of Dementia |
| Hypothyroidism |
| Depression |
| Vitamin B12 deficiency |
| Normal pressure hydrocephalus |
| Neurosyphilis |
| Chronic Alcohol use |
| Opiates |
Differential Diagnosis (4D's of cognitive decline)
| Remember the reversible causes of dementia such as hypothyroidism, chronic alcohol use and vitamin B12 deficiency |
| Side note Both depression and dementia are relatively common and often coexist. Over 20% of people with an early degenerative dementia may be depressed or apathetic. This sometimes reflects a depressive reaction to the onset of dementia. |
| Definition Dementia: Cognitive impairment typically caused by anatomic changes in the brain, has slower onset, and is generally irreversible. Dementia mainly affects memory. Delirium: Cognitive impairment typically caused by acute illness or drug toxicity (sometimes life threatening) and is often reversible. Delirium mainly affects attention. |
| Difference between Dementia and Delirium | ||
| Dementia | Delirium | |
| Onset | Sub-acute | Acute |
| Conscious level | Normal | Fluctuates |
| Hallucinations | Late event | Common |
| Agitation/agression | Uncommon until late | Common |
| Thought form | Poverty of thought late | Flight of ideas |
| Memory | Slow decline | Poor |
Cases of reversible dementia are uncommon, but their identification is important. Effective treatment may reverse the impairment and prevent its progression.
Assessment of Cognition
Bloods
Other
| Indications for Neuroimaging |
| Early onset (<65 years old) |
| Sudden onset or brisk decline |
| Focal CNS signs or symptoms |
| High risk of structural pathology (e.g., infarct, subdural hematoma, normal-pressure hydrocephalus, or tumor) |
DSM-V Criteria of Dementia
Significant cognitive impairment in at least one of the following cognitive decline:
With the following:
| AETIOLOGY | |
| Irreversible Causes | Reversible Causes |
| Alzheimer's disease | Hypothyroidism |
| Lewy body dementia | Depression |
| Huntington's disease | Vitamin B12 deficiency |
| Pick's disease | Normal pressure hydrocephalus |
| Cerebral infarct | Neurosyphilis |
| Creutzfeldt-Jakob disease | Chronic Alcohol use |
| Chronic substance abuse | Opiates |
The pathophysiology section will focus on the most common irreversible causes of dementia:
Alzheimer’s Disease (50-70%) 15% are familial with two main groups
Pathogenesis
Vascular Dementia (10-20%) Accumulation of small (lacunar) or large infarctions
Pathogenesis
| Side note One way of differentiating between Alzheimer's disease and vascular dementia is with a trial of cholinesterase inhibitors which is effective in Alzheimer's but much weaker in vascular. |
Lewy-Body Dementia (10%) Clinically characterised by dementia and signs of Parkinson’s disease. Often inherited – mutations in alpha-synuclein and beta-synuclein
Pathogenesis
Frontaltemporal Lobe Dementia (Pick's Disease)
Pathogenesis
| Remember Involve the patient in her own therapy |
Non-Pharmacological Management
Pharmacological Management
Treatment of Dementia
| Pharmacology Cholinesterase Inhibitors or ChEIs (donepezil, rivastigmine and galantamine) work by inhibiting cholinesterase, an enzyme responsible for the break down of acetylcholine. ChEIs result in ↑acetylcholine molecules that are available to interact with the postsynaptic acetylcholine receptors, which results in an increase in central nervous system acetylcholine activity. ChEIs offer symptomatic benefit through stabilization of cognition (NOT A CURE). The underlying disease continues to progress at the same rate. Side effects: nausea, vomiting, diarrhea, anorexia, weight loss, dizziness, bradycardia, myalgias, and insomnia. |
| Side note In Alzheimer disease, atrophy of the nuclei in the cells in key areas of the brain, such as the basal forebrain, leads to a demonstrable decrease in cholinergic function. |
Treatment of behavioural and psychological symptoms
Treatment of Agitation
| Pharmacology The GABA-A receptor is a ligand-gated chloride-selective ion channel. The GABA molecule is inhibitory in nature and thus reduces the excitability of neurons. GABA produces a calming effect on the brain. Benzodiazepines also known as Benzo's, are GABA-A agonists. They work by binding to GABA-A receptors in the brain increasing the affinity of GABA and its receptor (benzodiazepines potentiate GABAergic neurotransmission). Side effects: drowsiness, lethargy, and fatigue. At higher dosages, impaired motor coordination, dizziness, vertigo, slurred speech, blurry vision, mood swings, and euphoria can occur, as well as hostile or erratic behavior in some instances. Tolerance, dependence, and withdrawal are adverse effects associated with long-term use |
Complications many with continuing management and abuse. This also encompasses problems towards the careers.
