OPMH Flashcards
(28 cards)
AD
Chronic, neurodegenerative disorder characterised by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain
Leads to deterioration of cognitive function, memory loss & various behavioural and psychological symptoms
AD risk factors
Increasing age
FHx of Alzheimer’s disease
Genetic predisposition
- mutations in the amyloid precursor protein, presenilin 1 & presenilin 2
Apoprotein E allele E4
Caucasian ethnicity
Down’s syndrome
AD pathological changes
Macroscopic: widespread cerebral atrophy, particularly involving the cortex & hippocampus
Microscopic: cortical plaques due to deposition of type A-beta-amyloid protein & intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
Biochemical: deficit of acetylcholine from damage to an ascending forebrain projection
AD clinical features
Memory impairment - early in the disease → difficulties in recalling recent events & conversations
Language impairment - difficultly finding words, struggling to express oneself & aphasia
Executive dysfunction - impaired ability to plan, organize & carry out tasks → difficulties in activities of daily living
Behavioural changes - agitation, aggression or apathy
Psychological symptoms - hallucinations, delusions & paranoia can occur
Disorientation - unable to recognize places or people
Loss of motor skills - motor skills decline, leading to difficulties with mobility and self-care
AD ix
History - Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) / Functional Activities Questionnaire (FAQ)
- assess cognitive decline using an approved scoring tool eg. MMSE, MOCA
Examination - neuro
Bloods - confusion screen → FBC, U&E, LFT, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV
Neuroimaging
Cerebrospinal fluid analysis
AD general management principles
Non-pharmacological approaches - psychological interventions, cognitive stimulation therapy & OT
Support for carers
Patient-centred care
AD pharmacological mx
Acetylcholinesterase inhibitors (donepezil, galantamine & rivastigmine) options for managing mild to moderate AD
- donepezil is relatively contraindicated in patients with bradycardia
- adverse effects include insomnia
Memantine = 2nd line
- moderate AD for those who have contraindication to first line
- add-on drug
- monotherapy in severe AD
Antipsychotics should only be used for patients at risk/agitation causing severe distress
FTD
Heterogenous group of neurodegenerative disorders characterised by progressive atrophy of the frontal and/or temporal lobes of the brain → impairments in behaviour, personality, language & motor functions
FTD clinical features
Personality changes - disinhibited behaviour and apathy early on
Language impairments - early language difficulties to severe aphasia
Cognitive decline - executive function is frequently impaired
Motor abnormalities - features of MND
FTD ix
Neuroimaging - atrophy of frontal and/or temporal lobes, focal gyral atrophy & knife-blade appearance
Genetic testing - if inherited form is suspected
FTD mx
Focused on alleviating symptoms and providing support
Behavioural interventions - counselling, behaviour modification strategies
Pharmacotherapy - SSRIs & antipsychotics
Supportive care - SALT, physio & OT to help manage the impacts of the disease on daily functioning
Vascular dementia
Umbrella term denoting a collection of cognitive impairment syndromes caused by cerebrovascular disease
Vascular dementia subtypes
Stroke-related VD - multi-infarct or single-infarct dementia
Subcortical VD - caused by small vessel disease
Mixed dementia - presence of both VD & Alzheimer’s disease
Vascular dementia risk factors
Hx of stroke or TIA
AF
HTN
DM
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
FHx of stroke or cardiovascular
Vascular dementia clinical features
Progressive, stepwise deterioration in cognition (over a span of several months to years)
Focal neurological abnormalities eg. visual disturbance, sensory or motor symptoms
Difficulty with attention & concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance
Vascular dementia ix
Comprehensive H&E
Formal cognition screening - MMSE or MoCA
Medication r/w to exclude medication-induced cognitive impairment
Exclusion of reversible organic causes
Neuroimaging (MRI head) - extensive white matter change & infarcts evident
Vascular dementia mx
Detection of and addressing cardiovascular risk factors
Cognitive stimulation programmes - music & art therapy
Symptomatic treatment - cholinesterase inhibitors/memantine if co-morbid AD, PD, dwLD
Advanced care planning to prepare for progressive cognitive and physical decline
DLB
Dementia with Lewy bodies (DLB) is a type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, forming cytoplasmic inclusions known as Lewy bodies within brain cells
Aggregates disrupt normal cell functioning & eventually lead to neuronal death
DLB clinical features
Progressive cognitive impairment
- typically occurs before parkinsonism, but both features usually occur within a year of each other
- in contrast to Parkinson’s disease → motor symptoms typically present at least one year before cognitive symptoms
- cognition may be fluctuating
- early impairments in attention & executive function
Parkinsonism
Visual hallucinations
DLB ix
Diagnosis primarily clinical
DaT scan: can help distinguish DLB from other types of dementia
Neuropsychological testing: assess cognitive functioning and fluctuations
EEG: not diagnostic but a slowing background rhythm
DLB mx
Cognitive stimulation, physical therapy & occupational therapy
Supportive care: palliative & EoL care considerations are essential
Medications: cholinesterase inhibitors can help manage cognitive symptoms
- caution required with antipsychotic meds due to neuroleptic sensitivity
DLB complications
Rapid disease progression
Severe neuroleptic activity
Delirium
Acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness
Typically reversible & frequently seen in the elderly
Delirium types
Hyperactive - marked by increased psychomotor activity, restlessness, agitation & hallucinations
Hypoactive - characterised by lethargy, reduced responsiveness & withdrawal
Mixed delirium - combines features of both hyperactive and hypoactive
