Organic Psychiatry Flashcards
What are organic psychiatry disorders
Organic psychiatry disorders are directly caused by demonstrable physical illnesses or structural problems of the brain e.g space occupying lesions. Traditionally and conversely functional illnesses were though to have no organic basis e.g schizophrenia, thought they are now being shown to have underlying physical causes.
Function and symptoms of dysfunction of the fronatl lobe
Function:
- Executive function
- Personality/ social behaviour
- Initiatve/ motivation
- Speech production: Broca’s area= dominant lobe
- Motor cortex: suppression of primitive reflexes
Symptoms of Dysfunction:
- Poor judgment and planning
- Innapropriate behaviour and impulsivity
- Apathy or decline in self-care
- Telegraphic speech: short words and sentances
- Normal comprehension
- Contralateral spastic hemiparesis
- Primitive re-flexes re-emerge e.g sucking or rooting
Function and symptoms of dysfunction of temporal lobe
Function:
- Auditory, olfactory, gustatory perception
- Understanding of speech : Wernicke’s area= dominant lobe
- Memory and emotional regulation
Symptoms of dysfunction:
- Auditory impairment and agnosia
- Auditory, olfactory and gustatory hallucinations (temporal lobe epilepsy)
- Receptive dysphasia- speech is fluent but nonsensical with mistakes and additional words/sounds/neologisms
- Lability
Function and symptoms of dysfunction of parietal lobe
Function:
- Somatosensory perception
- Integration of sensory perception, allowing awareness and movemnt of body
- Communication between Broca’s and Wernicke’s areas
- Calculation
Symptoms of dysfunction:
- Contralateral sensory impairment
- Apraxia
- Agnosia (inability to recognise a sensory stimulus despite normal peripheral sensation)
- Contralateral sensory neglect
- Receptive dysphasia
Function and symptoms of dysfunction of occipital lobe
Function: Visual perception and interpretation
Symptoms of dysfunction: Contralateral visual defects, visual agnosia and cortical blindness
Definition of delirium and who it affects
An acute and transient state of confusion which arises due to an underling physical problem. Patients are often unaware of their surroundings. It affects up to:
- 30% of medical inpatients
- 50% of postoperative patients
- 80% of patients admitted to intensive care
Risk factors for delirium
older age, male sex, pre-existing physical/mental illness (especially dementia), substance misuse, polypharmacy, malnutrition, pain, sensory impairment and immobility.
Causes of delirium
Aetiology: VITTAMIN
- Vascular: stroke or heart attack
- Infections: Urinary tract/ chest infection, encephalitis, sepsis
- Traumatic: Head injury, burns, fractures
- Toxic: drug or alcohol intoxication/ withdrawal, poisoning, overdose
- Autoimmune: SLE, MS
- Metabolic: liver/renal failure, electrolyte imbalance, hypoglycaemia
- Iatrogenic: ‘Deliriogenic’ medications include sedatives, anticholinergics, opiates and steroids
- Neoplastic: Space occupying lesion
Onset and presentation of delirium
The onset is sudden (hours to days) though symptoms may fluctuate throughout the day, with brief lucid moments. Altered consciousness can range from drowsiness or stupor to clouded consciousness to vigilance and hyper-alertness. Symptoms are often worse at night:
- Mood changes are prominent and may resemble depression or mania
- Global cognitive impairment includes inattention, disorientation, and poor memory
- Thinking may be disorganised (illogical/rambling) or impoverished
- People may experience transient, often persecutory delusions, illusions and hallucinations (most commonly visual).
- Behavioural changes
- Hyperactivity, agitation and aggression. Wandering, climbing into other patients’ beds, pulling out catheters, easily identified
- Hypoactivity, lethargy, stupor, drowsiness and withdrawal. ‘Quiet delirium’ which is easily missed
- CAM- delirium bedside testing
Investigations for delirium
Requires a full physical examination and observations (BP, HR, RR, SpO2, temperature.) A DRE must be included if there is a history of constipation. Also must get a collateral history and perform a MSE. It is important to consider a cognitive assessment since delirium is often comorbid with dementia. Essential testing includes: FBC, U&Es, LFTs, TFTs, CBG (both hypos and hypers cause confusion), Vit B + Folate, Bone profile, BBV, septic screen, MSU, CT, UDS.
Management of delirium
Need to treat the cause and any exacerbating factors. Stop any unnecessary medications. Optimise nutrition and ensure dentures fit etc. Behavioural management includes:
- Frequent reorientation: clocks, calendars
- Good lighting and addressing sensory problems e.g. hearing aids. Avoiding over or understimulation (e.g silencing any unnecessary noises)
- Minimise change
- Remove things that can be thrown or tripped over
- Allow safe wandering
- If agitated behaviour is risky (e.g aggression), or if there is extreme distress, consider short-term, low-dose medication e.g antipsychotic (haloperidol or olanzapine) or a benzodiazepine if antipsychotics are contraindicated
Complications of delirium
Delirium is associated with increased mortality, longer and repeated admissions and subsequent nursing home placements. There is also an increased risk of developing subsequent dementia
Classification of dementia
Dementia may be cortical (Alzheimers) which affects cortical functions such as memory and language, or subcortical (Huntington’s) which affects subcortical structures (thamaus, basal ganglia) and causes problems including bradyphrenia (mental slowing), bradykinesia, depression, movement disorders and executive dysfunction.
Patients most commonly affected by frontotemporal dementia + pattern of inheritance
Most commonly diagnosed in 45–65 year-olds. Most cases are ‘sporadic’ but around 1/3 of cases are familial, with autosomal dominant inheritance.
Hallmarks of frontotemporal dementia
The hallmarks include asymmetrical anterior temporal and/or frontal lobe atrophy, cortical atrophy, neuronal loss and gliosis.
FTD includes Pick disease, which involves collection of hyperphosphorylated tau protein (pick bodies) and ballooned neurones (pick cells) on biopsy
Variants of frontotemporal dementia
Initially there are TWO main variants:
- Behavioural variant FTD: prominent disinhibition and personality change (‘frontal lobe syndrome’)
- Primary progressive aphasia: worsening speech and language problems which progresses to aphasia
Eventually, particularly later, these syndromes overlap and present with memory problems
Cause and onset of Huntington’s disease
- An autosomal dominant disease which causes dementia and chorea.
- Caused by the CAG repeat in the huntingtin gene on chromosome 4
- Get deposit of abnormal huntingtin protein cause atrophy of the basal ganglia, thalamus and some cortical neurone loss (mostly frontal).
- Onset is usually in middle age, however each inheritance lengthens the repeat causing earlier onset.
CT/ MRI and EEG changes in Huntington’s disease
CT/MRI may show caudate nucleus atrophy and the EEG may be flat
Clinical presentation of Huntington’s disease
- Personality and behavioural changes such as depression, euphoria, irritability and aggression. Subcortical dementia may develop later on.
- Chorea affectsthe limbs, trunk, face and speech muscles. It produces a wide-based, lurching gait.
- Causes death within 15 years
Causes and presentation of HIV encephalopathy
- HIV associated neurocognitive disorder (HAND)
- The risk of developing HAND increases with age, CVD factors and substance misuse
- HIV encephalopathy may occur after progression from HIV to AIDS
- Causes early apathy and withdrawal progressing to subcortical dementia (get ataxia, tremor, seizures, myoclonus.)
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Normal pressure hydrocephalus causes and presentation. What is the definitive treatment
- Rare but potentially reversible cause of dementia affecting older adults which may be caused by
- meningitis
- head injury
- haemorrhage
- idiopathic (50%)
- Caused by impaired CSF absorption in subarachnoid space leading to ventricular CSF accumulation without raised ICP
- Produces a TRIAD of symptoms treated by placing a ventriculo-atrial shunt:
- Dementia (subcortical)
- Unsteady gait
- Urinary incontinence
What is a prion disease. What is the most common prion diseaes seen in humans. What are the causes of prion disease in humans?
- A rare condition causing rapidly progressive neurological and psychiatric symptoms
- Normal human prion protein changes into abnormal insoluble form, which appears to act as a template for further transformation of normal to abnormal prion
- The main form in humans is Creutzfeldt-Jakob Disease (CJD)
- Accumulations of abnormal prion protein are linked to spongiform and amyloid changes in the cerebrum, basal ganglia and cerebellum. The main type is sporadic CJD which occurs due to spontaneous prion misfolding. But may also be variant CJD, from eating BSE-infected meat.
What is amnestic disorder (what is the characteristic defecit)
Amnestic disorder is characterised by relatively circumscribed and profound anterograde amnesia- the inability to lay down new memories after a brain insult
Can also get some retrograde loss, though procedural memory will be intact and they can often learn new skills. Patients will confabulate. However, all other brain functions will be relatively intact.
What are the causes of amnestic disorder
Damage affects limbic structures dealing with explicit memory – hippocampus, mammillary bodies, parts of the thalamus and surrounding cortex. Causes include:
- Hypoxia
- Encephalitis
- CO poisoning
- Korsakoff’s syndrome = most common type of amnesic syndrome. Due to thiamine (B1) deficiency secondary to alcohol misuse or anorexia nervosa
