Organic Psychiatry Flashcards
(28 cards)
What is the difference between organic psychiatric disorders and functional illnesses?
- Organic Psychiatric Disorders are those caused directly by a demonstrable physical problem (e.g. brain tumour, hypothyroidism)
- Functional Illnesses are traditionally viewed as having NO organic basis (e.g. schizophrenia)
Outline the main functions of the frontal lobe & some main symptoms of dysfunction
Executive funciton
Personality/social behaviour
Speech production (Broca’s area)
Motor cortex
Poor judgement/planning
Inappropriate behaviour/impulsivity
Expressive dysphasia
Contralateral hemiparases
Outline the main functions of the temporal lobe & some main symptoms of dysfunction
Auditory, olfactory, gustatory (taste) perception
Understanding of speech (Wernicke’s area)
Memory
Emotional regulation
Auditory impairment/agnosia Auditory, olfactory and gustatory hallucinations Receptive dysphasia Amnesic syndrome Lability
Outline the main functions of the parietal lobe & some main symptoms of dysfunction
Somatosensory perception
Communication between Broca’s and Wernicke’s
Contralateral sensory impairment
Apraxias and agnosia (inability to recognise sensory stimulus despite normal peripheral sensation)
Outline the main functions of the occipital lobe & some main symptoms of dysfunction
Visual perception and interpretation
Contralateral visual defects
Visual agnosia
What is the definition of delirium?
Acute and transient global brain dysfunction with clouding of consciousness (acute confusional state)
It is a manifestation of a physical problem so always search for an underlying cause
Give some causes for delirium
Trauma (e.g. head injury)
Hypoxia (cardiovascular, respiratory)
Infection (e.g. intracranial infection or systemic (septicaemia))
Metabolic (e.g. liver failure, renal failure, electrolyte imbalance)
Endocrine (e.g. hypoglycaemia)
Nutritional (e.g. Wernicke’s encephalopathy)
CNS pathology (e.g. raised intracranial pressure)
Drugs and alcohol (e.g. intoxication, withdrawal)
Medication (e.g. anticholinergics, opiates)
Give the clinical onset and symptoms of delirium
Onset is sudden (hours to days) and symptoms fluctuate often worsening in the evening/night
- Disorientated: poor attention and short term memory
- Mood changes (can be mistaken for depression or mania)
- Illusions
- Hallucinations
- May have delusions
- Sleep disturbances: insomnia, reversal of sleep-wake cycle
What are the two types of behavioural changes present in delirium?
HYPERactivity
• Agitation and aggression
HYPOactivity
• Lethargy, stupor, drowsiness and withdrawal
What investigations would you do for delirium?
o Physical examination
o Collateral history (what is the baseline?)
o Check the drug chart
Essentials: • FBC • U&Es • Glucose • Calcium • MSU • Oxygen saturation • ECG • CXR • Septic screen o Consider: LFTs, blood cultures, CT head, CSF, EEG
Outline the management for delirium
Treat the cause
• Manage aggravating factors (e.g. pain, dehydration, constipation)
• Stop unnecessary medications
Behavioural Management
• Frequent reorientation (e.g. clocks, calendars, verbal reminders)
• Good lighting (gloomy conditions increase risk of hallucinations/illusions)
• Address sensory problems (e.g. hearing aids, glasses)
Medication
• Small night-time dose of benzodiazepines could promote sleep
• If short-term sedation is needed, low-dose typical antipsychotics (e.g. haloperidol) or benzodiazepines can be used
What are frontotemporal lobar degenerations?
Asymmetrical frontal and/or anterior temporal lobe atrophy
Outline 3 types of frontotemporal lobar degeneratoins
Frontotemporal Dementia
• Causes frontal lobe syndrome with prominent disinhibition and social/personality changes
Semantic Dementia
• Progressive loss of understanding of verbal and visual meaning
Progressive Non-Fluent Aphasia
• Begins with naming difficulties progressing to mutism
Outline the pathophysiology of Huntington’s disease
- Autosomal dominant
- Caused by CAG trinucleotide repeat in the Huntingtin gene on chromosome 4
- Deposits of abnormal Huntingtin protein causes atrophy of the basal ganglia and thalamus as well as some cortical lobe loss (particularly frontal lobe)
Which factors influence the severity and time of onset of Huntington’s?
Severity: more CAG repeats
Earlier onset: lengthening of CAG repeats occurs with each inheritance so onset is younger in subsequent generations (anticipation)
What are the clinical features of Huntington’s?
o Personality and behavioural changes (sometimes aggression)
o Depression, irritability and euphoria are common
o Chorea affects limbs, trunk, face and speech muscles
o Wide-based lurching gait
Outline the causes and clinical features of normal pressure hydrocephalus
Causes: Meningitis, Head injury, Idiopathic
• CSF absorption is impaired with normal communication between ventricles (i.e. not obstructed)
• CSF accumulates in the ventricles (hydrocephalus) but the CSF pressure remains fairly normal as CSF production adjusts to compensate
Clinical features, triad:
o Dementia (subcortical)
o Unsteady gait
o Urinary incontinence
Outline the pathophysiology of prion diseases
Tranmissable spongiform encephalopathies (e.g mad cow disease)
Most common is sporadic CJD (Creutzfeldt-Jakob disease)
• Normal prion protein changes into an insoluble form which appears to act as a template for further transformation of normal to abnormal prion
• Accumulation of abnormal prion proteins leads to spongiform and amyloid changes
Outline the causes and key clinical features of amnesic syndromes
Anterograde memory loss - an inability to lay down new memories from the time of brain damage onwards
Causes: o Hypoxia o Encephalitis o Carbon monoxide poisoning Korsakoff Syndrome is the most common type of amnesic syndrome o Caused by thiamine (B1) deficiency o Usually secondary to alcohol abuse
Outline the key clinical features of transient global amnesia
Acute global memory loss , lasting from 1-24 hours
- May be due to transient ischaemia of memory structures
- Anterograde memory is particularly affected
- Patient does NOT forget their identity
- Consciousness and cognition re normal
- NO signs of neurological disease
Outline the key clinical features of frontal lobe syndrome
Caused by anything that can damage the frontal lobe (e.g trauma, dementia, stroke)
Executive Dysfunction
o Poor judgement
o Poor planning and decision-making
Social Behaviour and Personality Change
o Loss of social awareness: irresponsible/disinhibited, inappropriate behaviour
o Impulsivity
o Euphoric or fatuous mood, lability
Apathy
o Lack of motivation and initiative
o Decline in self-care
Differentiate between open and closed head trauma
- Open: skull is penetrated causing local cerebral damage
* Closed: no penetration but brain damage is caused by acceleration/deceleration and shearing forces
What symptoms are commonly seen with head trauma?
- Post-Traumatic Amnesia: lasts from the time of injury until recovery of normal memory
- Retrograde Amnesia: memory loss before the injury. NOT a good predictor of outcome
- Previous personality traits may be exaggerated
- Depression and anxiety occur in up to 50%
• Post-Concussional Syndrome may follow head injury with loss of consciousness o Mood (e.g. depression, anxiety, irritability) o Cognitive (e.g. poor concentration and memory) o Somatic (e.g. headache, dizziness, fatigue, insomnia, noise sensitivity)
Outline the pathology of Parkinson’s disease and its key clinical features
• Degeneration of dopaminergic neurones in the substantia nigra
TRIAD of extrapyramidal symptoms:
o Tremor (pill-rolling)
o Rigidity (stiffness)
o Bradykinesia
Other features: stooped posture, shuffling gait, hypomimic face, recurrent falls, constipation, urinary problems, sleep disturbance
