Learn — Organic, childhood & personality disorders

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Delirium

Delirium is an acute, fluctuating disturbance of attention and awareness accompanied by a change in cognition such as disorientation, memory impairment, disorganised thinking or perceptual disturbance, developing over hours to days as the direct physiological consequence of a medical condition, a drug or withdrawal. It is a medical emergency and a marker of serious underlying illness, carrying high in-hospital mortality, yet it is potentially reversible when the cause is found and treated.

The diagnostic core is inattention plus an acute onset with a fluctuating course, typically worse at night, a pattern described as sundowning; consciousness is clouded and the sleep-wake cycle is disrupted.
Three motor subtypes: hyperactive with agitation and hallucinations, hypoactive with drowsiness and withdrawal, which is the commonest and the most often missed, and mixed; the quiet patient is the one who gets overlooked.
The Confusion Assessment Method is the bedside screen and is positive when there is acute onset with a fluctuating course and inattention, plus either disorganised thinking or an altered level of consciousness.
Common precipitants can be worked through as a list: infection (urinary and chest above all), drugs with anticholinergic or sedative effects, opioids and benzodiazepines, alcohol or benzodiazepine withdrawal, electrolyte and glucose disturbance, hypoxia, uncontrolled pain, urinary retention and constipation, dehydration, and sensory deprivation from missing spectacles or hearing aids.
Investigate for the cause rather than treating the behaviour: full blood count, urea, electrolytes, glucose, calcium, renal and liver function, urinalysis and culture, chest radiograph, oxygen saturation, electrocardiogram, and a drug review; add neuroimaging when there are focal signs, a fall or head injury.
Non-pharmacological management is first line and works: reorientation with a clock and calendar, familiar objects and family presence, daylight by day and a quiet dark ward by night, spectacles and hearing aids in place, early mobilisation, adequate hydration and pain relief, and avoidance of physical restraint and of an unnecessary urinary catheter.
Medication is only for severe agitation that threatens the patient's or others' safety when non-drug measures have failed: low-dose haloperidol for the shortest possible time, avoided in Parkinson's disease and Lewy body dementia, where quetiapine is preferred; benzodiazepines are first line only in alcohol or sedative withdrawal and otherwise worsen delirium.
Under the Mental Healthcare Act 2017 any restraint is a last resort, must be authorised and recorded by the psychiatrist or the treating medical officer, must be for the shortest period, and requires that the nominated representative be informed; seclusion is prohibited outright.

Delirium vs dementia

Delirium and dementia are the two great causes of confusion in an older person, and separating them decides whether the nurse looks for a reversible cause tonight or plans long-term care. Delirium is an acute, fluctuating disturbance of attention and awareness caused by a physical illness, a drug or withdrawal and is potentially reversible, whereas dementia, called major neurocognitive disorder in DSM-5-TR, is a chronic, usually progressive decline in memory and other cognitive domains with a clear sensorium until the late stages.

Onset and course: delirium begins over hours to days and fluctuates through the day, typically worsening at night, while dementia begins insidiously over months to years and is steadily present from hour to hour.
Attention and consciousness: inattention with a clouded, fluctuating level of consciousness is the hallmark of delirium; in dementia attention and consciousness stay intact until very late, and memory, especially recent memory, is the leading deficit.
Duration and reversibility: delirium lasts days to weeks and is reversible when the cause is treated; dementia lasts years and is generally irreversible, though hypothyroidism, vitamin B12 deficiency, neurosyphilis, normal-pressure hydrocephalus and subdural haematoma are the reversible mimics worth excluding.
Perception and psychomotor activity: vivid visual hallucinations, illusions, transient persecutory ideas and marked psychomotor swings between agitation and stupor belong to delirium; hallucinations in dementia appear later and are less prominent, except in Lewy body dementia where detailed visual hallucinations occur early.
Sleep and speech: delirium reverses the sleep-wake cycle and produces incoherent, rambling speech; dementia fragments sleep more gradually and produces word-finding difficulty, empty speech and eventually aphasia.
The two coexist: dementia is the single biggest risk factor for delirium, and about two-thirds of delirium episodes in hospital occur in people who already have dementia, so any sudden worsening in a person with dementia is treated as delirium superimposed on dementia.
The practical test is a collateral history: ask a relative or the care home what the person was like a week ago, because a documented baseline turns an unanswerable question into an easy one; a Mini-Mental State Examination score alone cannot separate the two.
Assessment tools differ in purpose: the Confusion Assessment Method detects delirium, while the Mini-Mental State Examination, the Montreal Cognitive Assessment and the Clock Drawing Test measure cognitive impairment and are only interpretable once delirium is excluded.

Parkinson disease — psych features

Parkinson's disease is a degenerative disorder of the dopaminergic neurons of the substantia nigra that presents with resting tremor, rigidity, bradykinesia and postural instability, but its non-motor and neuropsychiatric features cause as much disability as the movement disorder. Depression, anxiety, apathy, cognitive impairment progressing to dementia, psychosis with visual hallucinations, REM sleep behaviour disorder and drug-induced impulse control disorders are all part of the illness, and several of them appear years before the tremor.

Depression affects roughly two in five people with Parkinson's disease and is intrinsic to the illness rather than only a reaction to it; it is under-recognised because the flat facial expression, slowness and soft voice of parkinsonism mimic depressive signs.
Anxiety, often as generalised anxiety or panic, is common and frequently fluctuates with the drug cycle, worsening during off periods when levodopa levels fall.
Apathy is distinct from depression: the person has lost drive and initiative but not mood or the capacity for pleasure, and treating it as depression with an antidepressant alone usually fails.
Psychosis in Parkinson's disease typically begins with a sense of presence or passage, then well-formed visual hallucinations of people or animals with insight retained, and later loses insight and adds persecutory delusions; it is provoked by dopaminergic drugs, by infection and by dehydration.
Management of psychosis starts by treating the physical trigger and simplifying the drug regimen, withdrawing anticholinergics, amantadine and dopamine agonists before reducing levodopa; if an antipsychotic is still needed, quetiapine or clozapine are the ones used, and clozapine requires the full white cell and absolute neutrophil count monitoring.
Typical antipsychotics such as haloperidol and chlorpromazine, and the more D2-blocking atypicals such as risperidone, must be avoided because they block the very receptors the treatment is replacing and can precipitate severe rigidity and immobility; metoclopramide and prochlorperazine are avoided for the same reason and domperidone or ondansetron used instead.
Parkinson's disease dementia is diagnosed when cognitive decline follows the motor disorder by at least a year, is dominated by executive, attentional and visuospatial deficits rather than early amnesia, and is treated with rivastigmine; when the cognitive and motor features begin within a year of each other the diagnosis is dementia with Lewy bodies.
REM sleep behaviour disorder, in which the person acts out dreams and may injure a bed partner, can precede the motor disease by years; impulse control disorders such as pathological gambling, hypersexuality and compulsive shopping are a recognised effect of dopamine agonists and must be asked about directly, because families rarely volunteer them.

Vascular dementia

Vascular dementia, called vascular neurocognitive disorder in DSM-5-TR, is cognitive decline caused by cerebrovascular disease, whether from multiple large-vessel infarcts, a single strategically placed infarct, small-vessel disease with lacunes and white matter change, or haemorrhage. It is the second commonest cause of dementia after Alzheimer's disease and is distinguished by a stepwise or fluctuating course with early executive dysfunction and focal neurological signs, while memory is relatively better preserved in the early stages.

The course is classically stepwise, with abrupt declines that follow each vascular event and plateaus in between, in contrast with the smooth gradual decline of Alzheimer's disease; small-vessel disease can, however, produce a slower and more continuous decline.
The cognitive profile is frontal and subcortical: slowed processing, poor planning, sequencing and judgement, reduced attention, apathy and emotional lability, with retrieval-type memory failure that improves with cueing, whereas Alzheimer's disease shows early episodic amnesia that cueing does not help.
Focal neurological signs are the physical clue: hemiparesis, exaggerated reflexes, an extensor plantar response, pseudobulbar palsy with emotional incontinence, dysarthria, small-stepped gait and early urinary incontinence.
Risk factors are the vascular ones and are modifiable: hypertension above all, diabetes, dyslipidaemia, smoking, atrial fibrillation, previous stroke or transient ischaemic attack, obesity and physical inactivity.
Imaging is required for the diagnosis: computed tomography or magnetic resonance imaging shows multiple infarcts, lacunes or confluent white matter change, and the Hachinski Ischaemic Score is the traditional bedside tool, with a higher score favouring a vascular cause and a low score favouring Alzheimer's disease.
There is no drug that reverses the disease, so treatment is prevention of the next event: control blood pressure, diabetes and lipids, give antiplatelet therapy or anticoagulation for atrial fibrillation as prescribed, stop smoking, and encourage exercise and a healthy diet. Cholinesterase inhibitors and memantine are not routinely recommended for pure vascular dementia.
Depression is far commoner in vascular dementia than in Alzheimer's disease and is treatable; screen for it, because apathy and slowness are otherwise written off as the dementia itself.
Antipsychotics for behavioural symptoms in any dementia carry an increased risk of stroke and death and are used only for severe distress or risk, at the lowest dose, for the shortest time, and after non-drug approaches; benzodiazepines worsen confusion and falls and are avoided.

Eating disorders — anorexia vs bulimia

Anorexia nervosa and bulimia nervosa are both driven by a self-worth that has become tied to body shape and weight, and they are separated by weight and by behaviour. In anorexia nervosa the person restricts intake so that body weight is significantly low for age and height, fears weight gain intensely, and experiences the body as fat despite all evidence; in bulimia nervosa the weight is usually normal or above, and recurrent binges are followed by compensatory vomiting, laxatives, fasting or exercise, on average at least weekly for three months.

Amenorrhoea was removed as a diagnostic criterion for anorexia nervosa in DSM-5 and is not required in DSM-5-TR, because periods may continue and because the old criterion excluded men and girls before menarche.
DSM-5-TR grades adult anorexia by body mass index: mild at 17 and above, moderate 16 to 16.99, severe 15 to 15.99 and extreme below 15, while ICD-11 sets significantly low weight in adults at a body mass index under 18.5.
Anorexia nervosa has two subtypes, restricting and binge-eating or purging, so purging by itself does not make the diagnosis bulimia — the weight decides the name.
Physical signs of anorexia are bradycardia, hypotension, hypothermia, dry skin, lanugo hair, carotenaemia, hair loss, constipation, osteoporosis and a prolonged QT interval; signs of purging are Russell's sign, a callus over the knuckles, erosion of dental enamel on the inner surfaces of the teeth, parotid swelling, and a hypokalaemic hypochloraemic metabolic alkalosis.
Binge-eating disorder, with binges at least weekly for three months and no compensatory behaviour, and avoidant or restrictive food intake disorder are the other diagnoses in this DSM-5-TR group.
Refeeding syndrome is the great danger of treatment: as carbohydrate returns, insulin drives phosphate, potassium and magnesium into the cells, and falling phosphate is the hallmark, with arrhythmia, heart failure, seizures and death. Feeding starts low and increases slowly, thiamine is given before or with the first feed, and phosphate, potassium and magnesium are measured daily through the first week.
Fluoxetine 60 mg a day is the antidepressant dose used in bulimia nervosa to reduce bingeing and purging; no drug is first-line in anorexia nervosa, where weight restoration and psychotherapy come first, and bupropion is contraindicated in eating disorders because it lowers the seizure threshold in purging patients.
Family-based treatment, the Maudsley approach, is first-line for adolescents with anorexia nervosa, and enhanced cognitive behavioural therapy is used for adults and for bulimia nervosa, with care shared between psychiatrist, physician, dietitian and nurse.
Anorexia nervosa carries the highest mortality of any psychiatric disorder, from cardiac and metabolic complications and from suicide, so asking about suicidal ideation belongs in every review.
When a person with anorexia nervosa refuses food to the point of danger, the Mental Healthcare Act 2017 provides for supported admission and for emergency treatment to prevent death, applied as the least restrictive option and with the nominated representative involved.

Autism spectrum disorder

Autism spectrum disorder is a neurodevelopmental condition defined by two things together: persistent difficulty with social communication and social interaction across settings, and restricted, repetitive patterns of behaviour, interests or activities. The features are present from early development, although they may only become obvious once social demands exceed the child's capacity, and DSM-5 merged autistic disorder, Asperger's disorder, childhood disintegrative disorder and pervasive developmental disorder not otherwise specified into this single spectrum, graded by the level of support required.

The social criterion requires all three of deficits in social and emotional reciprocity, in non-verbal communication such as eye contact and gesture, and in developing, maintaining and understanding relationships.
The restricted and repetitive criterion requires at least two of stereotyped movements or speech, insistence on sameness with distress at small changes of routine, highly restricted fixated interests, and unusual reactivity to sensory input such as covering the ears at ordinary noise.
Asperger's disorder is no longer a separate diagnosis in DSM-5-TR or in ICD-11; severity is described instead by the level of support needed, with specifiers for accompanying intellectual and language impairment.
Referral signs that must not be waited out are no babbling, pointing or gesture by 12 months, no single words by 16 months, no two-word phrases by 24 months, and any loss of language or social skill at any age, which needs referral the same week.
M-CHAT-R is the standard screening tool at 18 and 24 months; in India the Indian Scale for Assessment of Autism and the INCLEN diagnostic tool are used, and the Indian Scale score is the basis for disability certification.
Autism spectrum disorder is a specified disability under the Rights of Persons with Disabilities Act 2016 and is covered by the National Trust Act 1999, which is where entitlements and guardianship sit; the Mental Healthcare Act 2017 defines mental illness so as to exclude intellectual disability, so developmental disability is not managed under that Act.
No medicine treats the core features. Risperidone and aripiprazole are used for severe irritability, aggression and self-injury at the cost of weight gain, sedation, extrapyramidal effects and raised prolactin; melatonin helps sleep; and comorbid epilepsy, attention deficit hyperactivity disorder and anxiety are treated in their own right.
The interventions with evidence are early, intensive and behavioural — applied behaviour analysis, structured teaching, speech and language therapy, occupational therapy including sensory strategies, and parent-mediated training — and the earlier they begin, the better the outcome.
There is no association between autism and vaccines; the study that claimed one was retracted, and saying so plainly to parents is part of the nurse's job.
Always test hearing before concluding that a child who does not respond to their name has autism.

REM and NREM sleep stages

Sleep is not one state but two alternating ones: non-rapid eye movement sleep, staged N1, N2 and N3 on the electroencephalogram, and rapid eye movement sleep, cycling about every 90 minutes, four to six times a night. NREM deepens from the drowsy N1 through N2 with its sleep spindles and K complexes to the slow-wave N3 that restores the body, while REM is the paradoxical stage in which the brain tracing looks awake, the eyes move, vivid dreaming occurs and the skeletal muscles are completely atonic.

Proportions across a healthy adult night are roughly N1 5%, N2 45 to 55%, N3 15 to 20% and REM 20 to 25%.
Electroencephalogram signatures are the examination currency: alpha waves in relaxed wakefulness with the eyes closed, theta with slow rolling eye movements in N1, sleep spindles and K complexes in N2, high-amplitude delta waves in N3, and a low-voltage mixed-frequency pattern resembling wakefulness in REM.
N3 dominates the first third of the night and REM periods lengthen towards morning, which is why the long vivid dream comes just before waking and why deep sleep is what is lost first when the night is cut short.
REM is when dreaming, irregular pulse and respiration, and complete loss of skeletal muscle tone occur, and the atonia spares only the diaphragm and the extraocular muscles.
Growth hormone is secreted mainly during slow-wave N3 sleep, and N3 is the stage from which a sleeper is hardest to rouse and from which they wake confused.
Depression shortens REM latency to under about 60 minutes from the usual 90, increases REM density and reduces slow-wave sleep, with early-morning wakening — a favourite examination item.
Parasomnias sort by stage: sleepwalking, night terrors, confusional arousals and sleep enuresis arise from N3 in the first third of the night and are not remembered, whereas nightmares and REM sleep behaviour disorder arise from REM in the second half of the night and the dream is recalled clearly.
REM sleep behaviour disorder, in which the atonia fails and the person acts out dreams, strongly predicts later Parkinson's disease and related conditions, so it is referred rather than reassured.
Drugs change the architecture: benzodiazepines and Z-drugs increase N2 while suppressing N3 and REM, alcohol suppresses REM early in the night and causes REM rebound with nightmares later, and antidepressants suppress REM, which is why stopping them abruptly brings vivid dreaming.
A newborn spends about half of sleep in REM and enters sleep directly through it, and both REM proportion and slow-wave sleep decline with age, which is part of why older people wake more often.

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