Aims (Background)

Clozapine is associated with severe gastrointestinal hypomotility, constipation, ileus, and bowel obstruction through anticholinergic and antiserotonergic mechanisms. Tirzepatide, a dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist, delays gastric emptying and intestinal transit as part of its pharmacodynamic effect. Both agents independently impair gastrointestinal motility, yet their combined use is increasing as tirzepatide is prescribed to manage clozapine-associated metabolic dysfunction.

We hypothesised that the pharmacological combination of clozapine and tirzepatide may produce additive gastrointestinal hypomotility, increasing the risk of small bowel obstruction (SBO) in vulnerable patients.

Methods (Case Report)

We describe a single case (n=1) of a 54-year-old Black British woman with paranoid schizophrenia treated with clozapine since 2016, type 2 diabetes mellitus, and chronic constipation despite regular laxative therapy. Her medical history included extensive abdominal surgery for sigmoid volvulus with subtotal colectomy and ileostomy in 2012, followed by reversal in 2013.

Tirzepatide was initiated in March 2025 by the diabetes team for poor glycaemic control. Weight, glycaemic indices, clinical presentation, and radiological findings were reviewed using electronic health records.

Results (Discussion)

Following initiation of tirzepatide, significant metabolic improvement occurred, with weight reduction from 71.5 kg to 64 kg and Hbs-782c improvement from 86 mmol/mol to 43 mmol/mol within four months.

In May 2025, approximately two months after starting tirzepatide, the patient was admitted with acute abdominal pain and vomiting. Computed tomography (CT) imaging demonstrated markedly dilated small bowel loops (up to 63 mm) with an abrupt transition point, consistent with SBO. A second SBO occurred in October 2025, again confirmed radiologically with dilated loops and a transition point, without evidence of malignancy, perforation, or ischaemia.

There was no documented history of SBO in the years preceding tirzepatide initiation. Both episodes were managed conservatively. Tirzepatide was discontinued following the second obstruction.

Conclusion

This case highlights a potential pharmacodynamic interaction between clozapine and tirzepatide, resulting in additive gastrointestinal hypomotility and recurrent SBO in a high-risk patient. While tirzepatide provided substantial metabolic benefit, its use alongside clozapine may pose significant gastrointestinal risk. Careful patient selection, baseline bowel assessment, and close monitoring are essential when prescribing GLP-1/GIP agonists to individuals receiving clozapine.

Background

People with severe mental illness experience significantly higher rates of physical morbidity and premature mortality, with diabetes mellitus being a major contributor. When psychotic symptoms impair insight and decision-making, refusal of essential medical treatment can present acute and recurrent risks. In such situations, clinicians must navigate the interface between the Mental Health Act (MHA) and the Mental Capacity Act (MCA), two statutory frameworks that were not designed to address sustained community-based enforcement of physical healthcare in the context of fluctuating mental capacity.

Case Report

We describe the case of a patient with a chronic psychotic disorder and insulin-dependent diabetes mellitus who repeatedly refused insulin during psychotic relapses, leading to recurrent episodes of diabetic ketoacidosis requiring emergency hospital admission. During periods of florid psychosis, the patient lacked capacity to make decisions regarding insulin administration, with refusal directly driven by delusional beliefs. Despite multidisciplinary involvement, optimisation of psychiatric treatment, and repeated capacity assessments, adherence could not be sustained in the community. Each crisis was managed reactively through emergency admission, with no clear mechanism for anticipatory or preventative intervention once the immediate medical emergency resolved.

Discussion

This case highlights a recurrent clinical and ethical dilemma at the MHA–MCA interface. While the MCA permits best-interests’ decisions during acute incapacity, it offers limited scope for proactive intervention when capacity fluctuates, and risk is foreseeable but not immediate. Conversely, the MHA allows compulsory treatment for mental disorder but does not clearly support sustained enforcement of treatment for physical illness, even when refusal is a direct consequence of psychosis. This case does not advocate for routine compulsory treatment of physical illness under the MHA. Rather, it illustrates a structural gap in existing legal frameworks when psychosis-driven refusal leads to repeated, predictable medical crises that are addressed only reactively.

Psychosis-related refusal of life-sustaining medical treatment exposes limitations in current statutory frameworks, particularly for individuals with recurrent incapacity and high physical health risk. Earlier, legally supported escalation: including proactive capacity planning, structured review of statutory options, and consideration of Court of Protection involvement may help reduce preventable harm and improve parity between mental and physical healthcare. This case underscores the need for clearer guidance and integrated approaches to managing sustained physical health risk in the context of severe mental illness.

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist used for anaesthesia and analgesia, with increasing interest in its rapid antidepressant effects. This case evaluates the feasibility, tolerability and clinical response to subcutaneous ketamine in a medically frail older adult with psychotic depression, hypothesising that ketamine would rapidly improve engagement and depressive burden to support nutritional intake and medical recovery.

A 77-year-old man with a prior severe episode of psychotic depression had previously achieved full recovery after eight sessions of electroconvulsive therapy (ECT). In the current episode, he presented similarly with disorientation, nihilistic beliefs, poor engagement, self-neglect and severe weight loss from reduced oral intake, consistent with a depressive relapse with psychotic features.

His case was complicated by medical instability with suspected delirium, as well as limited adherence to and response from conventional antidepressant treatment. Anaesthetic risk in the context of acute physical illness, led to ECT being deferred and subcutaneous ketamine being used as a practical ward-based intervention when urgent treatment was required.

Following multidisciplinary and family discussion, subcutaneous ketamine was initiated as a rapid antidepressant intervention. Three doses were administered over approximately ten days (two at 0.25 mg/kg, followed by escalation to 0.5 mg/kg due to limited initial response). Depressive symptoms were rated using the Cornell Scale for Depression in Dementia (CSDD), alongside serial clinical assessments of mental state, engagement and oral intake.

Treatment was well tolerated, with no dissociative or behavioural adverse effects observed. CSDD scores showed modest change, decreasing from 15 at baseline to 12 after the first dose and to 10 after the third and final dose, with transient improvements in engagement and acceptance of care that were not sustained and did not translate into lasting improvement in overall mental state or nutritional intake.

Subcutaneous ketamine was a feasible and well-tolerated option in this medically frail older adult but did not achieve a clear or sustained antidepressant response in this case. Given the patient’s prior robust response to ECT and the limited benefits observed with ketamine, referral for ECT was re-initiated once anaesthetic risk was acceptable, highlighting the potential role of subcutaneous ketamine as a short-term bridging intervention when ECT is temporarily high-risk and the need for further evidence in older adults with psychotic depression and comorbid physical illness.

This case reports aim to describe the clinical presentation, diagnostic evaluation, and treatment response of an adolescent male with Kleine-Levin Syndrome, thereby increasing clinical awareness and contributing to the limited evidence on effective management strategies for this rare condition.

A 16-year-old adolescent male with a one-year history of recurrent episodes of hyperphagia, excessive sleepiness, hypersexuality, cognitive impairment, and behavioural disturbances was evaluated. Each episode lasted approximately one week and recurred every 2-3 months, with complete inter episodic recovery. Detailed clinical history and comprehensive physical, neurological, and psychiatric examinations were performed. Laboratory investigations, karyotyping, brain magnetic response imaging, and electroencephalography were conducted to exclude alternative neurological, metabolic, and psychiatric diagnoses. The diagnosis of Kleine-Levin syndrome was established based on clinical features and fulfilment of the International Classification of Sleep Disorders, Third Edition (ICSD-3) criteria. Pharmacological treatment with methylphenidate and carbamazepine was initiated, and the patient was followed up at two-month intervals to assess treatment response.

Baseline investigations, including laboratory tests, MRI, and EEG, were unremarkable. Following treatment initiation, the patient demonstrated significant clinical improvement. The duration of hypersomnia episodes decreased from approximately seven days to three to four days, and episode frequency reduced from every 2-3 months to every 4-5 months. The severity of associated hypersexual behaviour, cognitive disturbances, and irritability also diminished. Inter episodic functioning and overall quality of life improved, with no reported adverse effects from treatment.

This case highlights the importance of considering Kleine-Levin syndrome in adolescents presenting with recurrent episodic hypersomnia and behavioural changes. Early diagnosis and appropriate pharmacological intervention may reduce symptom severity and episode frequency. Further research is required to better understand the pathophysiology and establish standardized treatment guidelines for KLS.

A 38-year-old male with an 8-year history of schizophrenia presented with inadequate response to multiple antipsychotics and tardive dyskinesia. Tetrabenazine was initiated for dyskinesia, and Clozapine was started with gradual titration. On day 14, T. Clozapine was increased from 125 mg to 150 mg. Following this, the patient had an episode of sleep disturbances and purposeless motor movements that lasted for half an hour. Afterwards, the patient slept well, and the following day, his mental status examination revealed no new findings. The following night, 3 hours after receiving the second dose of Clozapine 150 mg, the patient developed disorientation, restlessness, and visual hallucinations. He was not cooperative with any instructions. Laboratory investigations, including haematological and metabolic parameters, were performed and were within normal limits. The acute onset of these clinical features supported the diagnosis of Clozapine-Induced Delirium.

Case Report

Management included immediate discontinuation of all medications. Pharmacological sedation with parental Lorazepam and Haloperidol was required. Even after this, the patient had to be retrained to start intravenous Ringer’s lactate for maintenance of hydration. Delirium subsided within 18 hours, and orientation returned without any residual deficits. S. Clozapine levels could not be done due to financial limitations. This adverse drug reaction suggests a probable link between Clozapine and Tetrabenazine, precipitating delirium, possibly through cholinergic-dopaminergic imbalance.

To the best of our knowledge, this is the first known case of its kind where the combination of Tetrabenazine with Clozapine, at relatively low dosage, has led to the life-threatening side effect of delirium. This case highlights the complexities of treating a patient who has become hypersensitive to both first-generation and second-generation antipsychotics, including Clozapine. While further research needs to be done regarding this unusual reaction, clinicians should remain vigilant for delirium during clozapine initiation, particularly when used alongside VMAT2 inhibitors such as tetrabenazine.

This case report reviews a rare presentation of a young male patient presenting with Catatonia, who was later diagnosed with Wilson’s Disease (WD), and explores the diagnostic challenges faced with atypical neuropsychiatric presentations and how this affects long-term outcomes.

A previously healthy Caucasian man in his early-30’s presented with acute-onset catatonia over 48 hours, characterised by social withdrawal, psychomotor retardation, staring spells, and posturing. He was initially diagnosed as having catatonia with depression and psychotic symptoms and treated with Lorazepam, Sertraline, Promethazine, and Olanzapine. Over the proceeding few months he deteriorated, showing signs of tremulousness, muscle rigidity with autonomic features, and hyper-reflexia. MRI Head demonstrated abnormal signal intensity in the corpus striatum, ventrolateral thalami, and brainstem, with basal ganglia and substantia nigra hypointensity on SWI sequences suggestive of iron or mineral deposition. Blood tests revealed low caeruloplasmin (0.1g/L), elevated 24-hour urinary copper excretion (5.37umol/24h), elevated CK (1907 U/L), and elevated ALT (105U/L). Kayser-Fleischer Rings were evident on ophthalmology assessment, Liver Ultrasound revealed a coarse irregular liver, and genetic studies confirmed mutations in the ATP7B gene. He had no family history of liver or movement disorders. He was treated with penicillamine, zinc supplements, muscle relaxants, and anticholinergics with no paradoxical worsening.

Wilson’s Disease (WD) is a rare inherited autosomal recessive disorder of copper metabolism resulting mainly in neurological and hepatic pathology. However, in 10-25% it can present with progressive neuropsychiatric symptoms, often resulting in delayed diagnosis for up to 65-months. Notable psychiatric manifestations include personality and mood disorders, sleep disturbance, cognitive impairment, and occasionally psychosis. Rarely, WD can present with Catatonia – a neuropsychiatric syndrome characterised by mutism, stupor, posturing and catalepsy, echolalia and staring. Research suggests that up to 65.6% of patients with WD are initially misdiagnosed, prolonging commencement of treatment and potentially worsening patient outcome. Copper chelation therapy with D-Penicillamine and Zinc can in some cases reverse neuropsychiatric manifestations in WD, and if these are not tolerated Trientine Dihydrochloride is a possible second line agent.

Wilson’s Disease (WD) is a rare condition with a vast range of clinical manifestations, and prompt diagnosis can improve patient outcomes. This case highlights the importance of having a high index of suspicion for WD, particularly during refractory acute-onset psychiatric presentations, and notably for those with no personal or familial psychiatric history. Diagnostic tools include testing for caeruloplasmin levels, 24-hour urinary copper excretion, ophthalmology assessment, MRI Head scanning, and ATP7B genetic testing for diagnostic confirmation.

No pharmacological stabilising treatments are currently approved for stimulant use disorder, despite its rapidly increasing global prevalence. Stimulants–including methamphetamine, amphetamine, and cocaine–continue to rise in production and availability worldwide. Methamphetamine remains one of the most misused Class A drugs. In Singapore, Methamphetamine–commonly known as “ICE”–is the leading drug implicated in arrests. In the absence of effective treatments, patients’ lived experiences may provide insights into potential therapeutic strategies.

We describe two cases illustrating non-prescription use of Armodafinil among individuals with methamphetamine use disorder.

Mr M, a 40-year-old Indian man with methamphetamine use disorder with three prior incarcerations for methamphetamine-related offences, presented to the emergency department with methamphetamine withdrawal symptoms and poor sleep. He reported intermittent use of ICE over the preceding three months. He disclosed substituting with armodafinil when unable to obtain ICE from his usual supplier. He described armodafinil as improving focus and mood, enabling him to function in daily activities, including his work as a cleaner, without producing the euphoric “high” associated with methamphetamine.

Mr N, a 54-year-old Malay man with methamphetamine use disorder, sedative–hypnotic use disorder, and prior drug-induced psychotic episodes, was brought to clinic by his cousin. He presented with acute psychotic symptoms, including auditory and visual hallucinations and grandiose delusions, along with insomnia of two days. After stabilisation with antipsychotic treatment, he denied recent ICE use but disclosed regular armodafinil use over several months. He reported ingesting approximately 500 mg of daily dose, purchased illicitly, to maintain alertness and daily functioning. He described armodafinil as more effective and longer-lasting than caffeinated beverages and denied cravings comparable to ICE.

Chronic stimulant exposure dysregulates dopaminergic and noradrenergic neurotransmission, resulting in blunted reward processing, and compulsive drug-seeking. Modafinil and armodafinil, approved for sleep–wake disorders, act via atypical dopamine transporter inhibition. Modafinil has been explored as a substitution agent in stimulant use disorder, though randomised controlled trials have not demonstrated clear relapse-prevention efficacy. There has been no trials of armodafinil yet. Mechanistically, armodafinil is more potent and longer-acting than modafinil. This case study shows its risks, including psychosis and insomnia, particularly at high or unsupervised doses.

These cases highlight an emergent, patient-driven harm-reduction pattern in which Armodafinil is used as a functional substitute for methamphetamine to preserve wakefulness and daily functioning. This behaviour underscores the unmet need for stabilising pharmacological options in stimulant use disorder and warrants further systematic investigations.

Autism Spectrum Disorder (ASD) is associated with social communication deficits, atypical social cognition, and behavioural regulation difficulties, which can complicate forensic evaluations of criminal responsibility. This case study aims to illustrate the assessment process and clinical reasoning used to determine criminal responsibility in a young offender with ASD and below-average intellectual functioning.

A 17-year-old male was referred for forensic psychiatric assessment following an alleged vehicle theft and reckless driving. A multidisciplinary evaluation was undertaken including psychiatric assessment (developmental, behavioural, substance use history and mental state examination) and clinical psychological testing. ASD assessment used ADI-R and ADOS; cognitive functioning was assessed using the Stanford-Binet Intelligence Scales (Fifth Edition).

Assessment findings supported a diagnosis of ASD with moderate symptom severity and significant social communication deficits. Cognitive testing showed below-average intellectual functioning (Full-Scale IQ 82) with relative strengths in visual-spatial processing and weaknesses in quantitative reasoning and knowledge domains. Clinically, the patient demonstrated limited insight into broader social consequences and reduced emotional reciprocity, without evidence of psychosis. Despite neurodevelopmental vulnerabilities and contextual risk factors (including alcohol use), the forensic conclusion was that the capacity to distinguish right from wrong at the time of the alleged offence was preserved, and criminal responsibility was not negated. The case highlights how ASD-related impairments may affect judgement and impulsivity while still allowing intact understanding of wrongfulness, underscoring the need for structured, ASD-informed forensic formulation.

Forensic assessments of adolescents with ASD should integrate developmental history, structured ASD measures, cognitive profiling, and careful analysis of moral/legal understanding at the material time. This case supports a nuanced approach that balances legal accountability with neurodevelopmental formulation and recommends tailored interventions (e.g., behavioural therapy, social skills work and family psychoeducation) to reduce future risk.

This case presentation explores an extreme form of self-harm by M, a woman in her late fifties, with historical diagnosis of schizophrenia, later revised to mixed personality disorder with anxious-avoidant, impulsive and antisocial traits. She experienced significant trauma in childhood in the form of physical abuse by father, needing hospital admission. Additionally, she has multiple medical comorbidities including Multiple Sclerosis and multiple transient ischaemic attacks, and two previous incidents of self-harm, including an intentional overdose requiring intensive care and tracheostomy. She has received trazodone and flupentixol depot intermittently since the 1980s, stopped in November 2025 by a covering consultant, against M’s wishes, due to absence of psychotic symptoms and worsening of physical health comorbidities.

M was admitted to the ward informally after presenting to the Emergency Department with suicidal ideation and thoughts of jumping in front of a lorry if not admitted. She quickly became comfortable in the ward setting but was noted to have personality changes compared to the community, including selective engagement with staff members. She became dependent on staff for Activities of Daily Living (ADLs), despite Occupational Therapy deeming her able of independent ADLs. Her behaviour became disruptive and challenging, including stripping naked, spreading faeces, and pulling her hair. This escalated to M attempting to remove her left eye from the orbit with her fingers, requiring an emergency lateral canthotomy and emergency repair of her ruptured globe in theatre, and resulted in loss of vision from that eye. M appeared to enjoy the attention she received during this incident. She has since attempted to remove her right eye, requiring close observation and frequent interventions by staff to prevent this.

M’s complex, lengthy psychiatric presentation and physical health comorbidities resulted in challenges in her management. Her presentation appears to be on the neurotic rather than psychotic spectrum, with antipsychotics prescribed for agitation. She has periods of lucidity before dissociation, with bizarre, disinhibited behaviour. Her distressed family queried the possibility of Munchausen Syndrome. Early severe trauma can present with challenging behavioural traits, emotional dysregulation and fight-flight response, leading to fluctuating withdrawal and aggression depending on context and perceived unmet needs.

This case is an example of a complex patient with multiple diagnostic and management challenges which culminated in rare and extreme self-harm resulting in loss of sight. It highlights the importance of collateral history and multi-disciplinary approach regarding diagnosis and management, contributing to the literature on mixed personality disorder.

Psychiatric inpatient units are often geographically, organisationally and culturally distinct from tertiary care hospitals, creating separation. When these two worlds inevitably collide, challenges often arise. Evidently, there is a limited understanding of each team’s challenges and, in this game of tug-of-war, patients bear the ultimate price.

Case Presentation

A 67-year-old man with dementia was admitted to a psychiatric inpatient unit for management of behavioural and psychological symptoms. During admission, he developed an acute change in mental state, consistent with delirium. He was therefore referred to tertiary care, where investigations revealed urinary retention, with an estimated three litres in the bladder.

Despite discussions between the emergency department (ED) and Psychiatry, the patient was discharged back to the psychiatry unit, with advice for catheterisation and intravenous (IV) antibiotics. Unfortunately, mental health wards could not perform these tasks due to a lack of experience, staff and equipment. Hence, the patient was transferred back to ED. On re-presentation, twenty-four hours after initial escalation, the patient became unconscious, was intubated and admitted to intensive care.

This case illustrates the systemic challenges posed by the mental-physical health interface. From a psychiatric perspective, there was a sense of frustration and helplessness, whilst ED was similarly challenged due to the complexity of the patient’s confusion. Pressures on services to remain efficient and meet targets, coupled with the disconnect between psychiatry and acute care, led to poor understanding of each party’s limitations, meaning the underlying cause of the patient’s life-threatening distress remained untreated. Limitations include a psychiatric unit’s inability to administer IV medications, lack of medically trained psychiatry staff and the increasing demands placed on services. Inadequate awareness of these challenges, along with the patient’s dementia, legal status, and psychiatric admission, may have subtly influenced how their needs were prioritised.

The structural separation between mental health services and acute medical care within the UK healthcare system continues to widen, despite ongoing efforts from psychiatry liaison services. This case underscores the need for a shared understanding of resources, capabilities and clinical responsibility across services. Fragmentation between teams can lead to ambiguity, with acute medical services overestimating the capabilities of psychiatric units due to their designation as tertiary hospitals, while mental health services lack the infrastructure to deliver routine medical care.

Improved education, cross-service exposure and enhanced ward provisions may strengthen communication, clarify escalation pathways and, ultimately, improve patient outcomes.

Rapid cognitive decline in later life often prompts urgent assessment for neurodegenerative dementia. However, severe depression and anxiety can produce profound but potentially reversible cognitive impairment, frequently described as depressive pseudodementia. Presentations characterised by abrupt onset, marked functional impairment, prominent subjective memory complaints, preserved insight, and disproportionate distress should raise suspicion for affective pathology. Failure to recognise reversible causes can lead to misdiagnosis, unnecessary investigations, and distress for patients and families.

Mr X is a 71-year-old White British retired man who presented with a two-week history of rapidly progressive cognitive and functional decline. He reported severe memory impairment, including inability to recall his date of birth or home address. He became unable to perform basic activities of daily living, forgetting how to make a cup of tea, operate household appliances, manage finances or shop independently. He frequently lost track of tasks midway and described episodes of intending to shower but later realising he had not done so.

He had recently commenced tirzepatide (Mounjaro) for weight loss, raising family concern about potential cognitive effects. Six-CIT score was 24/28. Blood investigations, including thyroid function, vitamin levels, and routine metabolic screening, as well as CT brain imaging, were unremarkable. He was referred to memory services for assessment.

During further reviews with the secondary care team, it was evident that affective symptoms were prominent. He was intensely anxious, preoccupied with fears of dementia, and distressed about becoming dependent or forgetting his family. He described low mood, anhedonia, early morning waking, appetite disturbance, and longstanding passive suicidal ideation. DASS-21 scores indicated severe depression, anxiety, and stress. Cognitive symptoms fluctuated in parallel with anxiety. Treatment with sertraline, alongside biopsychosocial support, led to early improvement in mood, confidence, and cognitive clarity.

The abrupt onset, fluctuating deficits, preserved insight, and overwhelming affective distress were inconsistent with neurodegenerative dementia. Anxiety-driven hypervigilance likely perpetuated impairment. Memory assessments conducted during severe mood and anxiety disturbance may be misleading. Treating underlying mood and anxiety through pharmacological and non-pharmacological interventions can substantially improve cognitive function.

This case highlights the importance of recognising late-life depression and anxiety as reversible mimics of dementia. Clinicians should routinely screen for reversible causes of cognitive impairment, including depression, nutritional deficiencies, hypothyroidism, medication effects, infection, alcohol misuse, and electrolyte disturbances, to avoid misdiagnosis and support recovery.

Suicidal and homicidal behaviors are typically assessed as distinct risk domains, despite overlapping psychopathology in psychosis and severe mood disorder. We introduce the new concept Suicide by Proxy as a psychodynamic formulation in which homicide (or attempted homicide) represents a displaced enactment of suicidal intent when direct self-destruction is inhibited. Drawing on Freudian models of internalized aggression, persecutory superego dynamics, and object-related conflict (Oedipal/Electra configurations), we aim to illustrate how self-directed destructive drive may be externalized toward a symbolic other.

Three retrospective forensic psychiatric case reports were analyzed using a psychodynamic framework. All cases involved severe mental disorder (schizophrenia-spectrum or major depressive episode with psychotic features), documented suicidal ideation and/or attempts, and a homicide or attempted homicide. Data sources included clinical interviews, collateral histories, medical/legal records, and psychological testing (including MMPI and SIMS). Identifying details were removed or altered to preserve confidentiality without changing clinical meaning.

Case 1:A 26-year-old man with paranoid schizophrenia and persecutory delusions purchased a firearm intending suicide but reported inability to act. He subsequently killed an unknown man in a mosque, then left the weapon beside the body. The act is conceptualized as displacement of self-destruction onto an authority-linked symbolic target, enabling rebellion against a persecutory superego without direct suicide or parricide.

Case 2:A 39-year-old woman with psychotic depression and intense suicidal communications stabbed her sleeping father after planning to kill herself in his presence, then attempted self-stabbing. This is formulated as a negative Electra configuration: ambivalent attachment and rage toward a passive betrayer father, with psychosis collapsing boundaries between self-attack and object-attack.

Case 3:A 36-year-old woman with schizophrenia, shaming maternal criticism, and relapsed hallucinations broke a mirror and attempted to attack her mother with glass while concealing suicidal intent. The mother is conceptualized as a proxy self-representing the rejected, humiliated part of the patient targeted for annihilation.

Across cases, homicidal acts functioned as symbolic self-attacks emerging from internalized aggression, persecutory superego pressures, and unresolved parental-object conflict. Suicide by Proxy may help forensic clinicians integrate suicidality into violence formulations, prompting dual-screening for suicidal and displaced homicidal risk in severe mental disorder. Further empirical work is needed to test the model beyond case-series evidence.

Catatonia is a neuropsychiatric condition that is frequently under-recognised in children and adolescents and may co-occur with a range of psychiatric and neurodevelopmental disorders, including autism spectrum disorder (ASD). Diagnosis is often challenging due to symptom overlap with neurological and psychotic conditions. In individuals with ASD, catatonia may be precipitated or exacerbated by environmental stressors and disruption to established routines. This case report aims to describe the presentation, diagnostic process, treatment, and longer-term management of catatonia in an adolescent with ASD, with particular emphasis on pharmacological treatment, electroconvulsive therapy (ECT), and psycho-ecological interventions.

We report the case of a 16-year-old female who presented with a five-month history of mutism, immobility, unsteady gait, and markedly reduced oral intake, resulting in significant weight loss, nasogastric feeding, and hospital admission. Extensive investigations, including CT and MRI brain imaging, EEG, autoimmune encephalitis screening, metabolic testing, chromosomal microarray, and whole genome sequencing, were unremarkable. A lorazepam challenge produced a marginally positive reaction, thus supporting the catatonia diagnosis. The lorazepam dosage was escalated to 12 mg per day, which yielded partial improvement, though this was limited by sedation. Due to the inadequate response, electroconvulsive therapy (ECT) was commenced.

The first six ECT sessions did not produce any improvement; however, from the seventh session onwards, a substantial and sustained recovery was noted, marked by the resumption of speech, mobility, and functional autonomy. Rehabilitation strategies incorporated structured physical activity and social engagement. Despite the initial progress, symptoms later recurred, including psychomotor retardation and confusion. Fluoxetine and quetiapine were subsequently introduced based on collateral history, resulting in partial improvement. A subsequent neurodevelopmental assessment confirmed a diagnosis of ASD, along with learning difficulties.

Following discharge, a relapse occurred several months later, which was linked to stopping lorazepam and less social interaction. When the patient was readmitted, a psycho-ecological approach was emphasised. This approach focused on organising the environment, managing sensory input, establishing predictable schedules, and helping the patient reintegrate socially. All psychotropic medications were stopped due to low efficacy, except lorazepam. Gradual improvement was seen, along with increased involvement in psychosocial activities.

This case highlights the importance of catatonia as a significant but treatable condition in adolescents with ASD. Although lorazepam and ECT were effective for quickly controlling symptoms, lasting recovery depended on psycho-ecological approach with consistent environment, structured routines, family involvement, and ongoing social interaction.

Autism Spectrum Disorder (ASD)-related catatonia presents a significant diagnostic and management challenge, due to the overlap between catatonic features and core autistic traits. Adolescents with ASD appear to be at increased risk of catatonic deterioration often triggered by psychosocial stressors and underlying neurobiological factors. This case describes a 16-year-old female adolescent whose catatonia was primarily driven by underlying autism, illustrating the crucial role of ASD-related mechanisms in both her deterioration and recurrence. Current literature review reveals a small number of documented adolescent catatonia cases indicating limited clinical and research consideration to this population.

A multidisciplinary treatment approach integrating pharmacological, psychological, and environmental strategies was implemented. Pharmacological management included Lorazepam (1 mg BD) targeting motor symptoms, alongside Olanzapine (5 mg ON) and Sertraline (150mg OD) to address comorbid anxiety, emotional dysregulation, and behavioural rigidity. Regular physical health monitoring remained unremarkable throughout. Additionally, the adapted for children version of the Bush Francis catatonia scaled was utilised to measure symptoms. Psychological interventions focused on anxiety reduction, restoration of independence, and development of structured daily routines. Environmentally, a low-arousal setting was prioritised with consistent 1:1 support as part of Level 3 observations. This provided containment, predictability, relational stability and reduced sensory overload. Collaborative multidisciplinary working and graded Section 17 leave facilitated a smooth transition back to the community.

A clinical decline was observed when Lorazepam was tapered and observation levels reduced to Level 2 (15-minute checks). Catatonic features including behavioural “stuckness,” delayed motor initiation, increased ritualistic behaviour, and reduced self-care re-emerged. Marked improvement was observed following the reintroduction of 1:1 support as part of Level 3 observations and an increased Lorazepam dose. This clear temporal association emphasises that environmental structure and sustained relational support are as critical as pharmacological treatment.

This case highlights the importance of recognising catatonia as a treatable manifestation of ASD. The clinical course established how ASD specific neurobiological vulnerabilities impacted to the initial deterioration and subsequent relapse. Recovery was dependent not only on benzodiazepine responsiveness but also on maintaining consistency, predictability, and therapeutic connection. A formulation driven, multidisciplinary approach balancing pharmacological, psychological, and environmental interventions is essential for sustaining improvement and preventing relapse in autistic adolescents with catatonia.

Behavioural and psychological symptoms of dementia(BPSD) are very common in people with dementia, including Alzheimer’s disease.The prevalence is very varied,ranging from 25%-75%.There are many treatment options available including pharmacological and non-pharmacological methods.We present a patient with Alzheimer’s disease whose BPSD were successfully managed with the synthetic cannabinoid,Nabilone.

Mr. KS,a 73-year-old gentleman with multiple physical comorbidities and a family history of dementia,was admitted to the ward with complaints of worsening memory and functioning since a few months.He had severe irritability,agitation,verbal and physical aggression along with suspiciousness towards his family.On assessment, his mood was irritable with delusion of persecution;he was disoriented to time and place and had poor recent memory along with word-finding difficulties.Delirium was ruled out.Cognitive assessment was done using Standardised Mini-Mental State Examination and he scored 13/30.Brain imaging(MRI) showed mild vascular changes and medial temporal lobe atrophy score of 3.A diagnosis of Dementia in Alzheimer’s disease with late onset was made.Clinical Dementia Rating(CDR) Global Score showed 2 which meant moderate dementia and he was started on Memantine.BPSD symptoms continued to be severe in nature.Various non-pharmacological techniques(redirection,ABC method,activity engagement) were tried with minimal effect.Following this,medications such as lorazepam,melatonin,and trazodone were tried.Though there was partial improvement with trazodone,he continued to be severely agitated and aggressive.Hence,following discussion with the team including senior pharmacists,nabilone 500mcg daily was initiated.

Nabilone is a synthetic cannabinoid of delta-9 tetrahydrocannabinol(THC) which has weak partial agonist activity at Cannabinoid-1 and Cannabinoid-2 receptors.The use of nabilone in dementia for BPSD management is an off-licence indication.For this patient,NPI(neuropsychiatric inventory) was done and he scored 51 in frequency and severity score and 21 in distress score,with high scores in the domains of delusions,agitation/aggression,disinhibition,irritability/lability,and sleep and nightmare behaviour disorders.Following introduction of nabilone,his agitation and aggression improved significantly within 2 weeks.After 3 weeks,NPI was repeated and he scored 9 in frequency and severity score and 5 in distress score with improvement in all domains including care-giver distress.There was a trial to decrease his Nabilone to 250 mcg–however his behavioural symptoms worsened so he was put back on 500mcg.He is maintaining well on this dose.

There have been many trials looking into the effectiveness of nabilone in managing non-cognitive symptoms of dementia.In patients who have been tried on conventional treatment regimens and have had poor response,it is an effective option and can be considered in managing BPSD.We have successfully managed this patient with a low dose of nabilone with no significant long-lasting side-effects.

Paediatric encephalitis is a medical emergency, and empirical treatment is used, given risk of neurological sequelae and death. Catatonia and first-episode psychosis can mimic encephalitis clinically, especially in medically complex children. This case describes an adolescent initially treated for suspected encephalitis.

A neuro-vulnerable 13-year-old refugee girl from Kenya presented to hospital with acute behavioural and mental state change with functional decline preceded by flu infection and major psychosocial stress due to deportation threat. Her medical history includes bilateral glaucoma, cataracts, basal ganglia calcifications, and left temporal arachnoid cyst. The initial working diagnosis was encephalitis and first-episode psychosis. IV methylprednisolone, cefotaxime, aciclovir, and immunoglobulin were commenced, followed by an oral prednisolone taper. Amlodipine 5mg once daily achieved good blood pressure control. Negative results from medical work-up (including neuro-inflammatory process and neuronal antibodies) led to immunotherapy being discontinued. During this time, catatonia developed (Bush-Francis Score of 14), 6kg was lost due to reduced intake, and psychotic symptoms continued. A lorazepam challenge showed substantial improvement in catatonia, engagement, and eating. Aripiprazole showed progressive reduction in psychotic symptoms. The patient was transferred to an adolescent mental health unit. Formulation: catatonia and psychosis in a highly neuro-vulnerable adolescent, triggered by acute psychosocial stress around asylum rejection and fear of return to an abusive environment. Lorazepam and aripiprazole were continued.

Since encephalitis is such a serious condition and takes several days of waiting on tests for diagnosis confirmation, treatment is initiated once encephalitis is suspected. Although it presents non-specifically, suggestive signs include fever, personality change, and reduced consciousness, which fit the case presentation. Subsequent treatment of IV steroids and anti-virals is in line with past literature although use of steroids (often initiated to control raised intracranial pressure) is under further research. Once encephalitis was ruled out, appropriate treatment for psychosis and catatonia was commenced. Due to complex medical history, a genetics test was ordered and results were suggestive of oculodentodigital syndrome (GJA1-related). Two variants of uncertain significance have been found in GJA1 and parental samples are being analysed.

Catatonia and first-episode psychosis can mimic encephalitis. Clinicians should treat suspected encephalitis urgently and maintain a low threshold to re-evaluate diagnosis, integrating psychosocial context (in this case, refugee status) and catatonic signs to guide psychiatric intervention. Constellations of symptoms can be indicative of syndrome diagnosis. Genetic testing should be initiated as required.

Catatonia is a syndrome characterised by decreased, increased, or abnormal psychomotor activity and is seen in conditions such as schizophrenia, and depression. Global meta-analysis carried out in 2017 found mean catatonia prevalence to be 9.0%. This case involves an adolescent patient treated for catatonia.

A 15-year-old boy with a background of severe dyspraxia but otherwise normal development and no prior health problems was admitted to an adolescent mental health unit due to rapid cognitive, motor, functional, and psychological decline, suggestive of catatonia. A paediatric immunology work up found no organic or autoimmune cause. An MRI head was unremarkable. A lorazepam challenge produced transient improvement. Due to persistent severe catatonia with emerging psychotic symptoms, an eight-session course of ECT was initiated under an STDC, later converted to a hospital CTO. Gradual recovery was observed, with Bush–Francis Catatonia Rating Scale scores reducing from 16 to 0. The patient regained normal motor coordination and speech, with improved emotional regulation and social interaction. Residual psychotic symptoms were mild, with preserved insight. Discharge plans included medication review, movement from inpatient to community, phased return to school, and gradual home passes. The patient was discharged from inpatient care after a 2.5 month stay.

Adolescent catatonia is frequently under-recognised and misattributed to neurological or functional disorders, leading to delays in effective treatment. This case is notable due to the rapid progression and severity of symptoms, with prominent motor, cognitive, and autonomic features closely mimicking organic pathology. Although benzodiazepines are recommended as first-line treatment, response in paediatric populations is often incomplete. This patient demonstrated partial improvement which necessitated escalation, illustrating the importance of early consideration of ECT, which is supported by growing evidence as safe and highly effective intervention for severe, or treatment-resistant paediatric catatonia, with reported response rates exceeding 70%. Additionally, the case highlights the ethical and legal complexities of compulsory treatment in young people, demonstrating how proportionate use of legislation can facilitate recovery and restoration of autonomy.

Catatonia in adolescents is serious but highly treatable. Early recognition and escalation of treatment reduce morbidity and risk. Benzodiazepines are first-line, but clinicians should maintain a low threshold for ECT in cases of partial response or high clinical risk, given its safety and efficacy in young people. Treatment guided by clinical presentation can result in full functional recovery and improved outcomes.

Pineal cysts are frequently identified as incidental findings on neuroimaging and are generally considered benign. However, the pineal gland plays a central role in melatonin secretion and circadian rhythm regulation, processes closely linked to mood stability, sleep, and affective vulnerability. Neuropsychiatric presentations occurring alongside pineal cysts, particularly during hormonally and circadian-sensitive periods such as the perinatal phase, remain poorly understood.

This case report describes a 37-year-old woman, employed as a nurse, who experienced recurrent affective episodes over a ten-year period. A comprehensive psychiatric assessment was conducted. Neuroimaging findings were reviewed alongside neurological and psychiatric management. The patient’s clinical course across four episodes was documented, with particular focus on the most recent episode occurring in the postpartum period and managed using a multidisciplinary team approach.

The patient experienced four episodes characterised by manic symptoms such as elevated and labile mood, marked anxiety, reduced need for sleep, and transient psychotic features. No depressive episodes were reported. The most recent episode occurred approximately four months postpartum, following a stressful Caesarean section and significant sleep disruption related to infant care. There was a family history of depression but no history of neurological symptoms. Magnetic resonance imaging during the first episode identified a pineal cyst measuring 8 mm with a well-defined rim which remained stable on subsequent imaging and demonstrated no mass effect on adjacent structures. Neurological assessment concluded that no surgical or disease-specific intervention was indicated. Psychiatric management consisted of low-dose olanzapine, short-term sedative medication, and supportive interventions targeting sleep restoration, resulting in good symptomatic recovery after each episode. Prominent sleep–wake cycle disruption was a consistent feature across all presentations. Melatonin was not prescribed, though its potential role in sleep regulation and relapse prevention was considered.

This case illustrates the diagnostic complexity that arises when recurrent affective symptoms coexist with incidental neuroimaging findings. Although a causal relationship between pineal cysts and affective episodes cannot be established, the pineal gland’s role in circadian regulation suggests a possible indirect neuroendocrine contribution, particularly during the perinatal period. The case highlights the importance of integrating neurobiological, circadian, and phenomenological perspectives in psychiatric assessment and management.

The intersection of open justice principles and medical ethics in forensic psychiatry presents complex challenges when courts must decide whether to anonymise judgments involving individuals with mental health conditions. Open justice ensures public accountability, maintains confidence in professional standards, and provides educational precedents. However, this must be balanced against the medical ethical principle of “primum non nocere” (first, do no harm), particularly where psychiatrists owe duties both to individual patients and to the court system.

PDS, a 29-year-old law graduate, was denied admission to the Singapore Bar following findings of collaboration during her Part A Bar examination and non-disclosure of previous academic misconduct in university. PDS sought anonymisation of her court judgment, supported by a private psychiatric assessment diagnosing Major Depressive Disorder (MDD) and Post-Traumatic Stress Disorder (PTSD) symptoms following sexual assault during university. A comprehensive forensic psychiatric assessment by the Institute of Mental Health diagnosed her with MDD of mild severity, directly precipitated by her interactions with legal authorities. Whilst acknowledging her history as a sexual assault survivor, the assessment found insufficient evidence for PTSD. The evaluation revealed that publication of her name would likely constitute a major stressor potentially causing deterioration in her mental health condition, suggesting psychiatric treatment and monitoring before any publication whilst recommending against revealing details about the sexual assault.

The case exemplifies the challenging position of forensic psychiatrists who must balance competing ethical obligations between individual patient welfare and duties to the court. The forensic assessment demonstrates a nuanced approach, distinguishing between different types of potential disclosure. Whilst recommending against publication of details regarding PDS’s sexual trauma, which appears peripheral to the core professional misconduct and would serve no legitimate public purpose, the assessment acknowledges the court’s legitimate interest in transparency about plagiarism and non-disclosure issues directly relevant to professional fitness. The psychiatrist’s recommendations represent a harm-reduction approach that would provide required mental health support whilst maintaining judicial transparency.

Ethical resolution in cases involving mental health and professional accountability may require graduated approaches rather than absolute positions. Courts can balance open justice principles with harm minimisation through careful distinction between relevant professional misconduct requiring transparency and peripheral personal information warranting protection. Forensic psychiatric assessments provide valuable frameworks for achieving proportionate outcomes that acknowledge both public interest in professional standards and individual rights to protection from disproportionate harm.

Functional neurological disorder (FND) frequently co-occurs with psychiatric conditions, most commonly anxiety, depression, and trauma-related disorders. The coexistence of FND and psychotic illness remains less well characterised, particularly in general hospital settings. The emergence of fixed persecutory beliefs in individuals with FND presents significant diagnostic, ethical, and management challenges, especially when such beliefs interfere with essential medical care. This case illustrates the complexity of assessing risk, decision-making capacity, and the role of compulsory psychiatric treatment when physical health deterioration arises from treatment refusal rather than suicidality

We describe a middle-aged man admitted to a general hospital with acute onset functional neurological symptoms, including rapidly evolving limb weakness, sensory disturbance, and functional paralysis, following significant occupational stress. During admission, he developed persistent persecutory delusions characterised by profound mistrust of healthcare professionals, beliefs of deliberate harm and surveillance, and accusations of abuse. These beliefs led to sustained refusal of nutrition, investigations, and treatment, resulting in significant weight loss, electrolyte disturbances, and functional decline. Extensive medical and neurological investigations supported a functional diagnosis, with no evidence of delirium or organic pathology to account for the psychiatric presentation. Multidisciplinary management was complicated by impaired engagement and contested use of mental health legislation.

This case highlights diagnostic uncertainty at the interface between FND and psychotic disorder, emphasising the importance of distinguishing illness-related beliefs from fixed delusions associated with behavioural consequences. Risk arose predominantly from malnutrition, immobility, and impaired decision-making rather than deliberate self-harm. While compulsory psychiatric treatment mitigated immediate physical health risks and resulted in partial behavioural stabilisation, it also appeared to intensify feelings of injustice and mistrust. Prolonged hospitalisation and adversarial dynamics may have reinforced persecutory beliefs, underscoring the need for early integrated neuropsychiatric formulation, consistent communication, and relational safety.

This case demonstrates that FND may coexist with psychotic illness, with significant implications for risk assessment, capacity evaluation, and treatment planning. Clinicians should remain alert to risks arising from treatment refusal and physical deterioration in the absence of suicidality. Early multidisciplinary collaboration and proportionate use of mental health legislation are essential to minimise iatrogenic harm and support recovery in medically complex patients.