CASC Knowledge Essentials13 · Liaison psychiatry and neuropsychiatry
13 · Liaison psychiatry and neuropsychiatry
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Written by Resident Doctor Committee · Published
13.1 Depression during physical illness
Depression or an adjustment response?
A depressive episode depends on symptoms, duration and impairment, even when the circumstances are understandable. ICD-11 requires low mood or reduced interest plus sufficient associated symptoms, usually for at least two weeks. Bereavement, infarction, cancer or disability can precipitate a full episode.
Fatigue, poor sleep, appetite loss and slowing overlap with physical disease. Interpret them in context. Anhedonia, hopelessness, excessive guilt, worthlessness and suicidal thinking are particularly informative when somatic symptoms overlap.
Explanation | Distinguishing feature |
|---|---|
Depressive episode with physical illness | Full depressive syndrome; illness may be the precipitant |
Adjustment disorder | Stressor preoccupation and failure to adapt, with impairment, not better explained by another disorder |
Secondary mood syndrome | Direct physiological effect of a medical disorder, such as endocrine/neurological disease |
Medication/substance-related syndrome | Plausible relationship to a drug/substance and its effects |
Delirium | Acute, fluctuating attention/awareness change; hypoactive delirium may look depressed |
Post-infarction depression affects suffering, functioning, adherence and rehabilitation. Its association with worse cardiac outcomes does not prove that treating depression reduces later infarction or mortality. Established benefits concern mood, function and engagement.
Antidepressants and cardiac disease
Drug/group | Main cardiac consideration |
|---|---|
Sertraline | Preferred first-line antidepressant in coronary heart disease |
Mirtazapine | Another option; still consider QT risk, sedation, weight and interactions |
Citalopram/escitalopram | Dose-related QT concerns |
Tricyclics | Conduction problems, arrhythmia and postural hypotension |
Venlafaxine | Can increase BP |
SSRIs with antiplatelets/anticoagulants | Increased bleeding risk; review the combination and gastroprotection needs, rather than imposing a blanket ban |
Interactions: fluoxetine/paroxetine inhibit CYP2D6 and can affect cardiovascular medicines. Omeprazole/esomeprazole impair clopidogrel activation, so PPI selection matters.
ACE inhibitors, some diuretics and NSAIDs can raise lithium levels; dehydration and renal deterioration add risk.
ECT may be appropriate for severe or life-threatening depression. Recent myocardial infarction requires individual cardiology/anaesthetic assessment; a universal waiting period is inadequate.
Advanced neurological disease and a wish to die
A wish for death or treatment withdrawal may reflect depression, fear, uncontrolled symptoms, lost autonomy, demoralisation or personal values. These are different explanations. Inability to speak is not incapacity: writing, eye movements, switches or other reliable methods may establish reasoning.
Suicidal intent, treatment preferences and assisted-dying law are separate issues. A capacitous treatment refusal does not itself authorise assistance to end life.
13.2 Traumatic brain injury: the syndromes that follow
Severity and amnesia
Severity depends on the original GCS, unconsciousness, post-traumatic amnesia (PTA), imaging and subsequent course. PTA is the period when continuous new memories are not reliably established, often with confusion. Retrograde amnesia concerns memories before injury. Someone can converse while still in PTA.
Initial GCS | Usual TBI category |
|---|---|
13–15 | Mild |
9–12 | Moderate |
8 or less | Severe |
Timing, sedation, intoxication and other injuries affect interpretation; GCS alone does not predict outcome.
A normal early CT does not exclude concussion, microscopic injury or persistent symptoms. New deterioration needs reassessment, rather than automatic attribution to post-concussion symptoms.
Frontal and executive dysfunction
Dysfunction | Everyday effect |
|---|---|
Reduced inhibition/social judgment | Impulsivity, tactless/sexual remarks, unsafe spending |
Reduced initiation | Apathy, inactivity, prompting needed for self-care |
Executive difficulty | Poor planning, sequencing, working memory, flexibility and error correction |
Emotional dysregulation | Irritability, lability, frustration intolerance, disproportionate outbursts |
Reduced self-awareness | Underestimates disability or impact on others |
Vocabulary or brief memory-test performance may remain good despite substantial daily disability. Apathy does not establish depression; disinhibition does not establish mania.
Persistent personality change requires an acquired difference from the premorbid pattern related to the injury. Behaviour during delirium, intoxication or withdrawal is insufficient. Diffuse injury affects networks, so behaviour does not provide a precise anatomical map.
A worsening course
Stable or improving residual deficits differ from progressive decline months later. Consider subdural haematoma, seizures, drug toxicity, substances, depression, sleep disorder or neurodegeneration. Symptoms predating a fall may mean disease caused the injury.
Post-traumatic hypopituitarism is a treatable contributor: fatigue, low mood, sexual dysfunction and unexplained electrolyte disturbance may have an endocrine basis.
Timing | Additional possibilities |
|---|---|
Hours–days | Intracranial injury, delirium, hypoxia, intoxication/withdrawal, metabolic disturbance |
Days–weeks | Evolving subdural collection, infection, drug effects, continuing PTA, emerging mood disorder |
Months onward | Residual cognitive/behavioural effects, depression/PTSD, epilepsy, substances; investigate new progression separately |
Headache, photophobia, dizziness, fatigue, poor concentration and disturbed sleep can persist after concussion. “Mild” initial injury does not imply fabricated symptoms. Persistent problems may need neuropsychological or brain-injury assessment.
Rehabilitation targets function, compensatory strategies, fatigue, relationships and mood. Recovery varies; there is no fixed completion date. Alcohol worsens cognition, inhibition and seizures; sedatives may obscure assessment.
13.3 Seizures and episodic altered awareness
Definitions and terminology
An epileptic seizure is a transient event caused by abnormal excessive or synchronous neuronal activity. An acutely provoked seizure, for example during metabolic disturbance, differs from an enduring predisposition to unprovoked seizures.
Epilepsy can be diagnosed through:
Two unprovoked or reflex seizures more than 24 hours apart.
One such seizure with at least 60% estimated recurrence probability over ten years.
A diagnosed epilepsy syndrome.
One seizure does not always mean epilepsy, but two are not always required.
The 2025 ILAE classification describes focal seizures with preserved/impaired consciousness, assessing awareness and responsiveness. Older records use 2017 “focal aware/impaired awareness” or earlier “simple/complex partial”. Focal seizures can become bilateral tonic–clonic.
Temporal lobe features
An aura may involve a rising epigastric sensation, sudden fear, déjà vu, jamais vu, unusual smell/taste or altered reality. The aura is itself seizure activity.
The event may progress to behavioural arrest, reduced responsiveness and lip-smacking, chewing or fumbling automatisms. Confusion, headache, sleepiness or dysphasia may follow. A stereotyped sequence carries more weight than an isolated unusual experience.
Event | Typical pattern | Limitation |
|---|---|---|
Temporal focal seizure | Aura, altered response, automatisms, postictal confusion; often one–two minutes | Every phase need not occur |
Typical absence | Abrupt interruption lasting seconds, rapid recovery, little postictal confusion | Usually childhood/adolescence; new adult blank spells need a broader differential |
Syncope | Warmth, nausea, visual dimming or postural trigger, then brief unconsciousness | Brief jerks can occur |
Functional seizure | Combinations of prolonged, fluctuating or inconsistent seizure-like features | No individual movement/eye sign establishes diagnosis |
Panic | Sudden fear/autonomic symptoms, usually retained awareness | Fear can also be a seizure aura |
Tongue injury, incontinence, falls and exhaustion help interpret an event but are not individually diagnostic. Their absence does not exclude epilepsy.
ECG, EEG and imaging
Witness accounts, event sequence, medication/substance history, examination and metabolic causes guide assessment. A 12-lead ECG after a first suspected seizure helps identify cardiac mimics. Normal EEG does not exclude epilepsy. Sleep-deprived/ambulatory EEG may clarify uncertainty; MRI assesses structural causes where indicated.
A new antidepressant is not automatically the cause. Consider sleep deprivation, alcohol/benzodiazepine withdrawal, missed antiseizure treatment, metabolic disturbance and new neurological disease alongside medication timing.
Psychiatric complications and medicines
Depression/anxiety substantially affect quality of life. Postictal confusion follows the seizure directly; postictal psychosis may follow a lucid interval, particularly after seizure clusters. Interictal psychosis is not confined to this immediate relationship. Interpret hallucinations by timing, cognition, mood, drugs and the broader syndrome.
Lamotrigine or levetiracetam are NICE first-line monotherapy options for focal seizures. Remember serious rash with lamotrigine and irritability/mood/behavioural effects with levetiracetam. Choice is seizure-specific; a drug appropriate for one syndrome may be unsuitable for another.
Valproate: initiation below 55 generally requires the prescribed two-specialist process. Pregnancy-prevention requirements and advice for male patients also matter; “use contraception” is insufficient. Do not abruptly stop established treatment because of a general warning.
SSRIs are generally preferred for depression in epilepsy, but no SSRI is universally first choice. Seizure control, interactions, sodium, cardiac risk and previous response determine selection. Clomipramine and amitriptyline carry greater seizure concerns; no antidepressant is “seizure-proof”.
13.4 Functional neurological symptoms and functional seizures
Positive diagnosis
FND produces real, involuntary neurological symptoms associated with altered nervous-system functioning: weakness, tremor, sensory change or seizures. Functional does not mean fabricated.
Positive signs include internally inconsistent movement, tremor entrainment and Hoover sign. In Hoover sign, weak voluntary hip extension improves during resisted flexion of the opposite hip. This demonstrates preserved automatic movement; it does not establish motive or conscious control. Interpretation requires appropriate clinical expertise.
Trauma/stress may contribute but is not required. FND can coexist with structural neurological illness, including epilepsy. Neither stress nor a normal scan establishes the diagnosis.
Functional seizures
Specialist assessment of a typical recorded event, sometimes using video-EEG, can establish the diagnosis. Normal interictal EEG differs from a typical event assessed on video-EEG; scalp EEG can also miss some epileptic events.
Antiseizure drugs do not treat functional seizures themselves, though coexisting epilepsy or another indication may require them. Withdrawal needs an individual neurological plan where uncertainty or dual diagnosis exists.
Treatment combines a positive explanation, rehabilitation, psychological work and treatment of depression, anxiety, pain or trauma-related symptoms. In CODES, seizure-specific CBT plus standardised care did not significantly improve monthly seizure frequency at twelve months, the primary outcome. Several secondary outcomes, including psychosocial function and quality of life, improved. Goals should include functioning and distress, without promising seizure elimination.
Driving
Relevant epileptic and functional seizure conditions require stopping driving and DVLA notification. Rules depend on diagnosis, licence group and circumstances. Established epilepsy commonly requires one seizure-free year for Group 1, with defined exceptions. Group 2 is substantially stricter; “five years” is not an adequate summary. Functional seizures have separate criteria; a brief event-free period does not establish fitness.
13.5 Metabolic illness presenting as cognitive decline
Encephalopathy means disturbed brain function; delirium is a clinical syndrome that may result. Metabolic illness often impairs attention and causes slowing/fluctuation. Dementia or an old stroke can coexist with a new reversible contributor.
Cause | Clues |
|---|---|
Uraemia/renal failure | Anorexia, nausea, pruritus, altered taste, fatigue, cramps/restless legs; severe disease may cause encephalopathy |
Hepatic dysfunction | Altered sleep/attention, asterixis; drugs, infection or bleeding may precipitate deterioration |
Sodium, calcium or glucose disturbance | Confusion, reduced consciousness or seizures, depending on severity/speed |
Thyroid disease | Hypothyroid slowing/depression-like symptoms; thyrotoxic anxiety/activation |
Hypoxia/hypercapnia | Respiratory disease, drowsiness, confusion, physiological instability |
Drug toxicity | Renal accumulation, interactions, anticholinergic effects, sedation |
Hiccups or unusual breath odour are uraemic clues, not diagnostic tests. Systemic symptoms, functional decline and abnormal medication/monitoring history require medical investigation.
ACE inhibitors reduce intraglomerular pressure and may raise creatinine/potassium, especially with hypovolaemia, renal artery disease or interacting drugs. Check renal function/electrolytes at baseline and after initiation/dose changes, usually one–two weeks, sooner when risk is higher. A concerning change requires assessment of volume status, other drugs and underlying illness, not simple attribution to the prescription.
13.6 Capacity: the clinical distinctions behind the law
Assess this decision at this time, after making information accessible. In England/Wales, the abilities are understanding, retention, use/weighing of relevant information, and communication. Inability must be caused by an impairment or disturbance of mind or brain.
Presentation | Relevant distinction |
|---|---|
Schizophrenia and refusal | A delusion matters if it prevents relevant understanding/weighing; diagnosis alone is insufficient |
Depression after self-injury | Hopelessness/psychotic guilt may affect reasoning; self-harm does not automatically remove capacity |
Dementia and refused carers | A risky choice may remain capacitous; assess the actual proposal/consequences |
Financial disorganisation | Poverty, executive difficulty and psychosis differ; inability to pay is not inability to decide |
Limited speech after neurological illness | Alternative communication may reveal intact decision-making |
Capacity differs from insight, agreement and screening-test performance. Someone may reject advice for personal reasons or retain capacity despite unrelated poor insight. Accurate repetition of treatment information does not prove ability to weigh consequences.
Physical treatment needs its own lawful basis. Psychiatric detention does not automatically authorise unrelated physical treatment, and a relative cannot automatically consent for an adult. Capacity may improve with resolution of acute illness, making support and reassessment important.