Dementia & Memory Flashcards
Why is memory described as plastic?
Able to change and strengthen neuronal connections in order to form new memories
How does short-term memory become long-term memory?
Consolidation
- emotion
- rehearsal
- association
- automatic
Long-term potentiation:
- glutamate (NMDA receptors)
- hippocampus
Long-term depression: weakening of infrequently used synapses
Outline the formation, interpretation, and storage of memory.
Senses —> cortical sensory areas
FORMATION:
Cortical sensory areas —> amygdala and hippocampus
INTERPRETATION:
Amygdala and hippocampus —> diencephalon, basal forebrain, and pre-frontal cortex
STORAGE:
- diencephalon, basal forebrain, and pre-frontal cortex —> cortical sensory areas
Contrast retrograde and anteretrograde amnesia.
Retrograde amnesia e.g. Alzheimer’s disease
= failure to retrieve old memories
Anteretrograde amnesia e.g. lesion in hippocampus
= failure to form new memories
Give some examples of causes of amnesia. How does the onset time vary?
Alzheimer’s disease
Vascular interruption
Tumours
Trauma
Infection
Wernicke-Korsakoff syndrome —> confabulate to fill gaps in memory
ECT —> lose sense of identity
TIA —> transient global amnesia
What is the definition of dementia?
Chronic and progressive deterioration of behaviour and executive functions due to organic brain disease
Acquired loss of cognitive ability sufficiently severe to interfere with normal functions and quality of life
What are the diagnostic criteria for dementia?
Cognitive/behavioural symptoms which:
- affect ability to function in normal activities
- represent a decline from a previous level of function
- cannot be explained by delirium or other major psychiatric disease
- has been established by history-taking from patient and informant, and formal cognitive assessment
Involves impairment of at least two of:
- ability to acquire and remember new information
- judgement
- ability to reason or handle complex tasks
- visuospatial ability
- language functions
- personality
- behaviour
Rate of progression depends on primary cause of tissue degeneration
Describe the pathophysiology of vascular dementia.
e.g. stroke
Stepwise progression of cortical damage
Subcortical damage to connecting neurones
S&S:
- rigidity of thinking
- apathy
- personality changes
Describe the epidemiology, pathophysiology, and symptoms of Alzheimer’s disease.
EPIDEMIOLOGY:
- 47% over 85yrs
- 2:1 female:male
- prognosis of 5yrs
Insidious onset (affects memory - hippocampus - first)
S&S:
- unsure of things
- repeating questions
- apathy
- short-term memory problems (hippocampus; can usually remember events from childhood clearly)
- difficulty recognising objects and faces (temporal lobe)
- become lost; dressing dyspraxia (parietal lobe)
- passivity; inability to initiate, carry on, and sequence tasks; loss of social functions, incontinence (frontal lobe)
PATHOPHYSIOLOGY:
- beta-amyloid deposits in brain
- global cortical atrophy
Describe the epidemiology, pathophysiology, and symptoms of Lewy body dementia.
EPIDEMIOLOGY:
- ~4%-10%
- 1:1 male:female
- 8yr prognosis after initial symptoms
S&S:
- Parkinsonism
- prominent visual hallucinations
- delusions
- paranoia
- REM sleep behaviour disorder (no muscle atonia —> act out dreams which are freq. frightening/violent)
- haloperidol sensitivity —> worsening movement difficulties, speech/swallowing problems
note: fluctuates in severity from day to day (differentiates from delirium)
PATHOPHYSIOLOGY: alpha-synuclein deposits
Describe the epidemiology, pathophysiology, and symptoms of fronto-temporal dementia.
Includes Pick’s disease, primary progressive aphasia)
EPIDEMIOLOGY:
- 1:1 male:female
- family history in ~10%-15%
- may be associated with movement disorders e.g. motor neurone disease, progressive supranuclear palsy
S&S: BEHAVIOURAL VARIANT: - loss of inhibition - inappropriate social behaviour - loss of motivation without depression - loss of empathy/sympathy - change in preferences - repetitive/compulsive/ritualistic behaviours - loss of control over eating/drinking - difficulties with planning, organisation, and decision making - lack of insight - incontinence - loss of awareness of personal hygiene - perseveration - mutism - echolalia SEMANTIC: - loss of vocabulary with fluency of speech - asking meaning of familiar words - loss of recognition of familiar faces/objects PROGRESSIVE NON-FLUENT: - slow, hesitant, difficult speech - grammatical errors in speech - impaired understanding of complex sentences - loss of literacy skills
+ memory preserved in early stages
+ crave sweet/fatty food
+ lose table etiquette
PATHOPHYSIOLOGY: tau inclusion bodies
Give some examples of causes of dementia.
ACUTE e.g viral encephalitis SUBACUTE e.g. sporadic CJD MEDIUM e.g. normal pressure hydrocephalus CHRONIC - Alzheimer's - Lewy body dementia - fronto-temporal dementia - vascular dementia
INFECTION: CJD, HIV, viral encephalitis, progressive multifocal leucoencephalopathy (JC virus)
METABOLIC: hepatic disease, (para)thyroid disease, Cushing’s
NUTRITIONAL: Wernicke-Korsakoff syndrome (thiamine deficiency), B12/folate deficiency
TUMOUR: e.g. subfrontal meningioma
CHRONIC INFLAMMATION: collagen vascular disease, vasculitis, MS
TRAUMA: heady injury, punch drunk syndrome
DRUGS/POISONS
Normal pressure hydrocephalus
What is punch drunk syndrome?
Seen in boxers and alcoholics
Caused by repeated cerebral contusions
Characterised by:
- weakness in lower limbs
- unsteadiness of gait
- slowness of muscular movements
- hand tremors
- hesitancy of speech
- mental dullness
- dementia
What is normal pressure hydrocephalus?
Abnormal build-up of CSF in ventricles (usually due to global cortical atrophy) causing ventriculomegaly
CSF pressure remains normal (communicating hydrocephalus)
Causes dementia, dyspraxic gait, urinary incontinence
What are some important investigations in dementia?
FBC
Electrolytes, Ca2+, glucose, renal function, liver function
Thyroid function
Serum vitamin B12 and folate
Midstream urine (?delirium caused by UTI)
CXR or ECG if indicated
MRI/CT to detect subcortical vascular changes and focal atrophy
