Dementia Flashcards
What is the frontal lobe responsible for?
Problem-solving, emotions, reasoning, planning, personality. A site of many inhibitory functions.
Primary Motor Cortex: generates voluntary movements of muscles.
Broca’s area: (usually left) postero-inferior part of the frontal cortex, involved with motor aspects of speaking.
What is the function of the temporal lobe?
Perception/recognition of auditory stimuli, memory, speech. Contains Wernicke’s area – helps formulation/understanding of speech.
What is the function of the parietal lobe?
Recognition, movement, orientation, perception.Primary Sensory cortex: processes sensory stimuli.
What is the function of the occipital lobe?
Visual processing
What is the function of the cerebellum?
Posture, balance and co-ordination of movement
What are the different types of dementia?
- Alzheimer’s disease
- Vascular dementia
- Frontotemporal dementia (including Pick’s disease)
- Mixed dementia
- Dementia with Lewy bodies
- Alcohol related brain damage
- Young onset dementia
- Huntington’s disease
- Parkinson’s disease
Define dementia.
Dementia - appreciable deterioration in cognition resulting in behavioural problems and impairment in the ADLs. Decline in cognition is extensive, often affecting multiple domains of intellectual functioning.
(Progressive decline in higher cortical functions across various domains -/+ dterioration in emotional and behavioural regulation. )
Describe the epidemiology of dementia.
The prevalence of dementia is approximately 1% at the age of 60 years, and doubles every 5 years, to reach 30% to 50% by the age of 85 years.
It is important to consider the aetiology of dementia syndrome because an estimated 10% to 20% of cases are caused by potentially reversible conditions.
What are the most common types of dementia? What % affected?
Alzheimer’s disease (60%) - degenerative
Vascular dementia (5-20%)
Other:
Lewy body
Frontotemporal
Other: Dementia in Parkinson’s, dementia in Huntington’s, HIV related, CJD
List some general causes of dementia.
- Mild cognitive impairment (MCI) - amnesia can progress to dementia
- Degenerative
- Vascular - stroke
- Psychiatric - delirium/depression/amnestic syndromes
- Neurological - NPH
- Neoplastic
- Endocronological, metabolic, nutritional deficiency
- Traumatic
- Infectious
- Inflammatory
- Iatrogenic
- Toxic
Name some causes of dementia linked to endocronological, metabolic, nutritional deficiency.
- vitamin B12 or folate deficiency
- Cushing’s disease/ hypopituitarism/ parathyroid disease,
- porphyria
- thyroid disease (hypo- or hyperthyroid state)
- uraemia
- Wilson’s disease
What is Wilson’s disease?
Wilson’s disease, also known as hepatolenticular degeneration and progressive lenticular degeneration, is a rare genetic disorder that causes copper poisoning in the body.
It affects about 1 in 30,000 people worldwide.
In a healthy body, the liver filters out excess copper and releases it through urine.
Name some infectious causes of dementia?
- Lyme disease
- Neurosyphilis
- TB meningitis
- CJD (prions = infectious proteins)
What are the inflammatory causes of dementia?
- dymelinating diseases
- lupus erythematosus
- sarcoidosis
- Sjogren’s syndrome
- limbic encephalitis
What are the iatrogenic causes of dementia?
Antihistaminic and anticholinergic meds
What are the toxic causes of dementia?
- Alcohol
- Heavy metals such as arsenic, lead, mercury,
- Histotoxic anoxia due to CO
- Cyanide
What are the differentials when diagnosing dementia?
- MCI (mild cognitive impairment)
- Delirium
- Depression
- Alzheimer’s
- Vascular dementia
- Lewy body dementia
Define AD
- Insidious onset
- Memory impairment
Early onset - <65yrs and rapid progression
Treatments
- Acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine)
- NMDA antagonists (memantine)
Pathophysiology of AD.
Beta-amyloid plaques(extracellular) and tau neurofibrillary tangles(intracellular)
Acetylcholinergic neuronal loss
Areas where neurones are particularly lost in AD.
Nucleus basalis of Meynert
Temporal lobe
Amygdala
Hippocampus
Risk factors for AD.
- Advanced age (risk doubles eevry 5 years)
- 1st degree relative affected
- Downs syndrome
- Vascular risk factors
- APOE e4 allele (sporadic late onset). ApoE-2 is protective. Other genes: presenelin 1, presenelin 2 and APP
- Poor lifestyle and hyperlipidaemia
What percentage of people with Down’s syndrom develop dementia by 60?
50%
What are the symptoms of AD?
- Memory loss
- Disorientation
- Nominal dysphasia
- Misplacing items/getting lost
- Apathy (sleep more than usual and become passive)
- Decline in ADLs and IADLs
- Personality change and mood changes
- Poor abstract thinking
- Constructional dyspraxia
Uncommon: prosopagnosia, autoprosopagnosia
What is constructional dyspraxia?
Parietal lobe deficits may lead to difficulties completing the clock-drawing test or intersecting pentagons in the Mini-Mental State Examination.
What is prosopagnosia/autoprosopagnosia?
Prosopagnosia - failure to recognise familiar faces
Autoprosopagnosia - mirror sign: failure to recognise oneself in the mirror. More common late in the illness.
Important aspects of history in suspected dementia.
Timeline of deficits
Particular aspects of deficit e.g. memory
Activities of daily living
Finances
Medication
Other symptoms
What are the signs of dementia on physical examination?
Physical examination is mostly unremarkable in early stages.
In advanced disease, patients tend to appear sloppily dressed, confused, apathetic, and disorientated with a slow, shuffling gait and stooped posture. Terminal disease is marked by rigidity and inability to walk or speak.
What tests should you do to exclude a reversible cause of dementia?
- FBC - to rule out anaemia
- Metabolic panel - to exclude abnormal Na, Ca, glucose causing hypo/hypernatraeamia, calcaemia, glycaemia.
- Serum TSH - rule out hyper/hypothyroid
- Serum vit B12
- Urine drug screen
- MRI/CT - exclude space occupyng lesions/pathology
What does an MRI in AD show?
Generalised atrophy with medial temporal lobe and later parietal predominance. It also has increased sensitivity in identifying lesions when compared with CT findings.
What might CSF analysis show in AD?
May show evidence of infectious aetiology for dementia
Biomarker testing may show patterns of Abeta and p-tau that may be suggestive of AD as the aetiology of the dementia
How do you manage AD?
- Supportive care - written instructions, advising carers. calendars, clocks, lighting.
- Envirvonmental - home safety evaluation
- Cholinesterase inhibitor
- (+Antidepressant)
- (+Antipsychotics)
- (+Manage insomnia)
- (+Manage behavioural/psychological symptoms)
- Antiglutamatergics - switch to or add memantine
Give examples of cholinesterase inhibitors.
- Donepezil
- Rivastigmine
- Galantamine
Transdermal and oral have similar efficacies.
What is memantine? When should memantine be added in the treatment of AD?
Antiglutamatergic - an antagonist of N-methyl-D-aspartate.
In severe disease or cholineterase inhibitors not tolerated/ineffective. Co administration with cholinesterase inhibitor may improve cognition in people with moderate to severe AD.
Features suggesting vascular dementia rather than AD.
Stepwise deterioration
Various vascular risk factors/events
Alzheimer’s dementia tends to progress steadily over time.
What are the main risk factors for vascular dementia?
Hypertension is a major risk factor for diffuse vascular dementia. Other general “vascular” risk factors increase the chances of developing vascular dementia and can increase cognitive decline:
- Age over 60
- Obesity
- Hypertension
- Cigarette smoking
Stroke increases the risk x9
Give 4 causes of vascular dementia.
- Infarction - (many small strokes)
- Haemorrhage
- Leukoaraiosis/subcortical leukoencephalopathy
- Alzheimer’s disease
What are the most commonly affected areas of the brain in vascular dementia?
The most commonly affected areas of the brain are the white matter of both cerebral hemispheres, grey nuclei, thalamus and the striatum.
What are the gender differences in dementias?
Vascular is more common in males
AD is more common in females
What is the pathophysiology of vascular dementia?
Define catatonia.
Abnormality of movement and behaviour arising from a disturbed mental state (typically schizophrenia). It may involve repetitive or purposeless overactivity, or catalepsy, resistance to passive movement, and negativism.
What happens to the brain in normal ageing?
Brain -
- Decrease in brain size (global)
- Neuronal loss in cortex, hippocampus, cerebellum
- Decrease in synaptic connectivity
- Deposits of tau and amyloid protein
Brain function - decline in IQ after age 60; Decline in working memory, problem solving, cognitive flexibility
Psychosocial - fear of death, bereavement, financial problems, illness, social isolation, loss of independence.
Define pseudodementia.
Define vasuclar dementia
- Multi-infarct
- Step-wise
- TIA/stroke/vascular risk factors
No treatment - optimise risk factors
What is LEwy body dementia?
- Onset is within 1 year of onset of Parkinsons
- Fluctualting attention and awareness
- VISUAL halluctinations (characteristic but NB: exclude delirium)
- REM sleep behaviour disorder
If more than 1 year then just dementia with Parkinson’s disease
What is RUDAS?
People of lower educational level or people whose first language is not English
What is the triad of normal pressure hydrocephalus?
Tiad of dementia, ataxia and urinary incontinence = NORMAL PRESSURE HYDROCEPHALUS
Define delirium.
Acute brain failure
- Reduced ability to direct, focus and sustain and shift attention (often tested by subtracting successive 7’s from a large number)
- Disturbance of consciousness (on a continuum from clouding to coma)
- Disturbance of perception, thinking, memory, psychomotor behaviour, emotion and sleep-wake cycle.
Worse at night (partly because it interferes with rhythm of sleep but also because it is dark)
Describe the course of delirium.
At any age, transient, fluctuating
What are the causes of delirium?
PInCHME
- Pain
- Infection
- Constipation
- Hydration (and urinary retention)
- Medication (esp. aticholinergics (boosting acetylcholine in brain helps boost depression but oxybutinin)
- Electrolye (Na, Ca, glucose)
Depends on predisposition.
How do you manage delirium?
When might you not do a pericardiocentesis in trauma case?
When you need to stop the source of bleeding e.g. in stab wound
You would do a thoracostomy instead - opening up he chest across between the sites where you would put a chest drain on both sides
