organic disorders Flashcards
what is an organic mental disorder
mental disorders that are due to common, demonstratable aetiology in cerebral disease, brain injury or other insult leading to cerebral dysfunction
they are acquired and are different from functional mental illnesses
can be:
1y - direct effect on the brain
2y - systemic diseases that affect the brain in addition to other systems/organs
problems when defining organic mental illnesses
many (if not all) psychiatric disorders have an organic basis - sz, BPAD, melancholia
many mental disorders present w/ a mixture of mental and physical features
physical disorders also have an effect on psychological functioning
common features to organic mental disorders
cognitive - memory, intellect, learning
sensorium - consciousness, attention
mood - depression, elation, anxiety
psychotic - hallucinations, delusions
personality and behaviour disturbance
onset of organic mental disorders
any age
most tend to start in adult or later life
prognosis for organic mental disorders
some irreversible and progressive
some transient/respond to treatment
acute/sub-acute organic mental disorders - 3 examples
delirium
organic mood disorder
organic psychotic disorder
- recently appearing state of mental impairment as a result of intoxication, drug OD, infection, pain etc
- often temporary
3 examples of chronic organic mental disorders
dementia
amnesic syndrome
organic personality change
-
what can cause chronic organic mental disorders
chronic drug/alcohol dependence - due to their long lasting toxic efffects
vascular problems - strokes
management of organic mental disorders
varies depending on cause
key points:
- correct diagnosis
- medication not usually that useful (except acute)
- MDT approach
- management of environment
triad of symptoms in Wernicke’s encephalopathy
acute confusional state
ataxia
opthalmoplegia
nystagmus
what causes wenicke’s encephalopathy
relataed to acute thiamine deficiency (B1)
what is wernicke’s encephalopathy often confused with
delirium tremens
prognosis of wernicke’s encephalopathy
untreated acute phase lasts ~ 2wks
84% develop korsakoff psychosis
- 15% mortality in untreated pts
w/ treatment: confusional state and opthalmoplegia can resolve within days
nystagmus, neuropathy and ataxia may be prolonged or permanent
treatment of wernicke’s encephaloptahy
high potency parenteral B1 replacement
- 3-7 days, oral thiamine
avoid carb load until thiamine replacement completed
all pts w/ WE symptoms or at high risk: parenteral thiamine
other undergoing detox/under investigation should be commenced on oral thiamine
concurrent treatment for alcohol withdrawal
what characterises alcohol amnesic syndrome (Korsakoff’s psychosis)
marked impairment of anterograde memory (ability to learn new info)
disturbance of time sense
features of korsakoff’s psychosis
no clouding of consciousness, absence of defect in immediate recall or global impairment
variable degrees of cognitive impairment
personality changes, apathy, loss of initiative
confabulation in the early stage
can improve w/ prolonged abstinence
differential diagnosis for wernicke’s encephalopathy
hepatic encephalopathy
where is hepatic encephalopathy usually seen
advanced alcoholic liver disease
features of hepatic encephalopathy
general psychomotor retardation, drowsiness
flucutating levels of confusion
related to build up of toxic products e.g. ammonia
when does hepatic encephalopathy improve
if and as liver function improves§
what type of illness is alcohol related brain damage
part of a spectrum of alcohol relate medical disorders
not a specific diagnosis
what causes alcohol related brain damage
neurotoxic effects of alcohol
head injury
vitamin deficiencies
cerebrovascular disease
hypoxia
hypoglycaemia
seizures
how common is alcohol related brain damage
35% of alcohol dependent persons will exhibit post-mortem evidence
prevalence is increasing - increased awareness/increased prevalence
when does alcohol related brain damage present
women tend to present 40-50y/o
- usually a decade younger than men
trend towards people presenting earlier than in the past
features of alcohol related brain damage
50-80% of heavy drinkers display cognitive impairment when sober
impairment in short term memory, long term recall, new skill application, set-shifting ability
visuospatial ability decline > language ability decline
features of alcohol related brain damage on imaging
cortical atrophy (mainly white matter loss)
ventricular enlargement
when can alcohol related brain damage improve
may recover spontaneously w/ abstinence/greatly reduced drinking
adults w/ incapacity act
when is a person unable to make a decision
a person is unable to make a decision for themselves if, due to mental disorder or inability to communicate because of physical disability, they are incapable of:
acting or making decisions or communicating decisions or understanding decisions or retaining the memory of decisions
what is dementia
syndrome characterised by global cognitive impairment which is chronic in nature
underlying pathology in dementia
variable
usually, but not always progressive
what are the different types of dementia
alzheimer vascular mixed Lewy body frontotemporal due to other brain disorders - huntington's, head injury, parkinson's
difference between dementia and depressive pseudodementia
how common is steroid induced psychosis
mild-moderate psychiatric symptoms in 28% pts treated w/ steroids
~6% severe reaction
factors affecting severity of steroid induced psychosis
dosage related to incidence but not timing, duration or severity
subsequent events not predicted by previous (or lack of previous) reaction
management of steroid induced psychosis
consider tapering steroids - might not be possible due to medical condition being treated
consider antipsychotic/mood stabiliser
endocrine and metabolic disorders - presentation
wide variety of clinical presentations
likely to 1st present to GP/general medicine but some conditions (hypothyroidism, addison’s) may present 1st to psychiatry - risk of mistaken diagnosis
link between CNS and endocrine/metabolic issues
CNS requires stable biochemical and metabolic environment for proper functioning
how reversible are endocrine/metabolic presentations
psychiatric presentations may be reversible if detected
what is anti-NMDA receptor encephalities
AI disease that targets NMDA receptors
- ionotropic glutamate receptor involved in synaptic plasticity and memory function
presentation of anti-NMDA receptor encephalitis
~1/2 associated w/ malignancy - typically ovarian teratoma in women
often presents initially w/ psychiatric symptoms
management of anti-NMDA receptor encephalitis
prognosis
immunotherapy and tumour resection if indicated
- IVIg, plasmapheresis, rituximab
prognosis w/ treatment generally good
- can be longer lasting cognitive and neuropsychiatric symptoms in a minority
what is delirium
aetiologically non-specific syndrome
characterised by concurrent disturbances of: consciousness and attention perception thinking memory psychomotor behaviour emotion sleep-wake cycle
presenting features of delirium
impairment of consciousness and attention global disturbance of cognition psychomotor disturbances disturbance of sleep-wake cycle emotional disturbance
timing of presentation of delirium
rapid onset
diurnally fluctuating
duration <6mths
physical signs of delirium
due to underlying cause
autonomic activation: tachycardia, hypertension, diaphoresis, dilated pupils, fever
dysgraphia often evident
causes of delirium
medication
druga buse
withdrawal syndromes
metabolic
vitamin deficiencies
endocrinopathies
infections
neurological
toxins and industrial exposures
other
medication causes of derlirum
anticholinergic drugs - atropine, TCAs, antipsychotics, anti-histamines, OTC hypnotics, anti-vertigo, anti-spasmodics
sedative hypnotics - esp w/ long 1/2 life e.g. flurazepam
decongestants
anti-asthmatics
other sympathomimetics
cimetidine, digitalis, L-dopa, meperidine, methyldopa, glucocorticoids
drug abuse causes of delirium
amphetamines
cocaine
PCP
hallucinogens
inhaled drugs - glue, NO
withdrawal syndrome causes of delirium
alcohol
benzodiazepines - esp alprazolam
barbiturates
other sedative hypnotics
metabolic causes of delirium
hepatic encephalopathy
uraemia
hypoglycaemia
hypercalcaemia
hypo/hypermagnesaemia
porphyria
vitamin deficiency causes of delirium
thiamine - wernicke-korsakoff syndrome
vit B12
nicotinic acid - pellagra
endocrinopathy causes of delirium
hypo/hyperthyroidism
hypo/hyperparathyroidism
cushings
addisons
hypopituitarism
infectious causes of delirium
any systemic infection in the elderly
esp w/ co-existing dementing process
meningitis, encephalitis, brain abscess, neurosyphilis
AIDS encephalopathy
neurological causes of delirium
head injury - post-concussive syndromes, bleeds
stroke
hypertensive encephalopathy
intracranial neoplasm - esp frontal and temporal
complex partial status epilepticus
post-ictal states
toxins and industrial exposure causes of delirium
CO
carbon disulphide
organic solvents
heavy metals
other causes of delirium
SLE - lupus cerebritis
cerebral vasculitis - temporal arteritis, periarteritis nodosa
paraneoplastic syndromes - limbic encephalitis
hyperviscosity syndromes
mechanism of delirium
pathophysiology unclear
- GABAergic and cholinergic NT systems?
- central cholinergic deficiency? - increased risk associated w/ GABA agonists and anticholinergic drugs
- increased dopaminergic activity?
- direct neurotoxic effect of inflammatory cytokines?
delirium vs dementia
delirium vs functional psychosis
implications of delirium
disruption of other pts and anxiety of clinical staff
prolonged hospital stays
increased risk of institutionalisation
~£13000 per admission
prognosis for delirium
fluctuating course
gradual resolution of symptoms w/ effective treatment of underlying cause - may improve more quickly at home
slower symptom resolution in the elderly
often patchy amnesia for delirious period following recovery
mortality
may be a marker for subsequent dementia
mortality rates for delirium
20% die during this admission
up to 50% at 1yr
management of delirium
correct contributing factors (disorientation, dehydration, constipation, hypoxia, immobility/limited, infection, polypharmacy, pain, poor nutrition, sensory impairment, sleep disturbance)
enviornmental and supportive measures - education of relatives and healthcare staff, safe environment, optimise stimulation, orientation
medications
medications for management of delirium - things to remember
avoid sedation unless required to maintain safety (severely agitated or required to facilitate investigation/treatment)
evidence base and guidelines don’t support use of medications in delirium
medications sometimes have to be used for acute distress and to maintain safety: antipsychotics, benzodiazepines, promethazine
use single medication, start low and assess response - slow doses in frail elderly
cautions to take with medications in delirium
antipsychotics - lower seizure threshold, be cautious if suspected withdrawal case
benzodiazepines - safer first choice (interact w/ fewer things), can prolong delirious episode
promethazinde - can ultimately worsen delirium
drugs to use when managing delirium
ANTIPSYCHOTICS:
- risperidone 0.5-1mg
- quetiapine 25-50mg
if IM required - consider olanzapine/aripiprazole
avoid in withdrawal state unless pt well covered w/ benzodiazepines - lower seizure threshold
BENZODIAZEPINES:
can prolong delirium
- lorazepam 0.5-1mg
use in withdrawal states - diazepam/chlordiazepoxide, caution in liver failure
PROMETHAZINE:
- oral/IM 10-25mg
- off licence use
- caution: in elderly (anticholinergic effect), prolonged QTc, lower seizure threshold
