Aims: Without a plan to support ongoing abstinence, detoxification (“detox”) could increase, rather than reduce, risks to a patient. Before referring for inpatient detox from alcohol or opioids, community teams are expected to discuss relapse prevention medications (RPMs) with patients, as part of their wider support plan.

This clinical audit examined whether RPMs were mentioned in referrals by community teams to our inpatient detox unit.

Methods: We examined referrals for patients admitted to The Level Nottingham inpatient detox unit between 1 January and 31 August 2024. Of a total of 215 patients that completed opioid or alcohol detox, a random sample of 50 were selected, stratified according to referring team. Referral forms and running notes were used to assess compliance with the following criteria:

1. Referring teams mention RPMs (whether to be considered or not considered).

2. Referring teams provide blood test investigations.

There was no previous literature or audit to specify a standard, so, given the importance of the issues under consideration, this was set as 100% for each criterion. We also extracted: whether patients were planned to go to residential rehabilitation after detox, and, where relevant, which RPMs were mentioned and time from blood test results to referral and to admission.

Results: 68% of referrals were for alcohol, and 24% for opioid, detoxification (2% were for alcohol and opioid, and 6% for other substances).

40% of referrals for alcohol, and 77% of referrals for opioid, detoxification did not mention RPMs.

29% of referrals for alcohol, and 31% of referrals for opioid, detoxification did not mention RPMs and were not planned to go to residential rehabilitation (considered as some of these settings do not accept patients on RPMs, focusing solely on psychosocial support).

48% of referrals for any detoxification did not have blood test results available. Where blood test results were available, median time from test results was 22 days to referral and 85 days to admission.

Conclusion: During the study period, an estimated one-third of referrals for alcohol or opioid detoxification did not mention RPMs (and were not going to residential rehabilitation post inpatient stay).

Approximately half of admissions did not have blood test results available.

The above is likely to delay the prescription of RPMs, and potentially increase the risk of relapse post-detoxification.

Recommendations to increase performance include discussions with referrers, changes to the referral form, and changes to referral screening.

Aims: Panic disorder, also known as paroxysmal episodic anxiety, is a severe, unpredictable, and debilitating form of anxiety that is characterised by sudden onset of palpitations, chest pain, choking sensations, dizziness, and feelings of unreality (depersonalization or derealization). People that suffer from panic attack often have a secondary fear of dying or losing control. Like many other mental illnesses, the causes of panic disorder are unknown, but some predisposing factors have been identified including genetics, neurobiology, medications, psychiatric disorders, psychosocial factors and medical conditions.

Brucellosis is an infective medical condition caused by Brucella. In the UK, it is a very rare notifiable disease and transmission is usually from consumption of unpasteurised milk and cheese or from contact with infected animals. Brucellosis is considered a public health problem by many countries not only because of the economic loss it brings but it also causes chronic pain, anxiety, and depression, affecting the life quality of patients. Treatment for human brucellosis is based on combinations of antibiotics such as doxycycline, streptomycin, gentamicin, ciprofloxacin, and trimethoprim–sulfamethoxazole and rifampicin over a period of about 6 weeks. Rifampicin on the other hand has been implicated in worsening mental health conditions like anxiety and depression in many previous literatures.

The mechanism by which this occurs has been put to the drug-to-drug interaction that rifampicin might have with other medication patients are taking and the effect of rifampicin as cytochrome p450 enzyme inducers. This case report presents another perspective of rifampicin inducing and worsening panic disorder in a patient that has not previously been diagnosed with anxiety disorder.

Methods: This patient was a 70-year-old woman with background of depression, stable on sertraline, who contracted canine brucellosis from her dog. While on isolation ward in physical health hospital, she was commenced on rifampicin intravenously and oral doxycycline. She developed new onset panic attack five days into the treatment. was referred by the General practitioner following reports of new onset panic attacks. She continued to suffer from these panic attacks even when rifampicin was changed to oral after discharge from hospital. This affected her quality of life significantly. She was commenced on short course benzodiazepine after risk and benefit explained to her. Her sertraline was increased from 50 mg to 100 mg daily. Other psychological options were also explored. Patient reported good improvement within two weeks of commencement of treatment.

She reported good improvement during four-week follow up visit. She had not had panic attacks two weeks prior to the review. She had been tapered off the diazepam and she was one week left in completing her antibiotic regimen. Patient was followed up for two more weeks and discharged back to the GP.

Results: This patient presented with new onset panic attacks following commencement on rifampicin in the treatment of brucellosis. There have been reports that anxiety and depression are the commonest mental health conditions associated with brucellosis. It is therefore a possibility that the new severe debilitating form of anxiety is due to the infection with Brucella. On the other hand, there have been reports that patients treated for tuberculosis with rifampicin have increased incidence of anxiety. The mechanism of this has been linked to the inducing effect rifampicin has on liver enzyme cytochrome P450 which plays a crucial role in the metabolism of most medications. In the case of index patient, rifampicin might have had a drug-drug interaction with sertraline this patient was taking for depression. Though the sertraline was intended for treatment of depression, it is obvious that it was also helpful for premorbid anxiety for this patient. Once the beneficial effect of sertraline was reduced by the rifampicin, it led to the onset of severe and debilitating anxiety. Similar reports about interaction between rifampicin and citalopram have been reported.

Conclusion: The follow-up to this report would be to conduct a case series and observe the occurrence of drug-drug interaction between rifampicin and other common psychotropics.

Aims: We present a case of a 36-year-old patient on clozapine who was an inpatient in a mental health rehabilitation service diagnosed with Schizophrenia. During clozapine titration, the patient complained of chest pain and elevated temperature. The patient was subsequently transferred to the emergency department for further evaluation and management. Following the discontinuation of clozapine and the initiation of brief supportive medical therapy, the patient’s symptoms, ECG changes, and troponin levels fully resolved.

Methods: A 36-year-old Asian male diagnosed with paranoid schizophrenia, admitted to rehabilitation psychiatry. With no significant past medical history, clozapine was introduced in January 2024 using a slow titration protocol, resulting in minimal mental state improvement and physical deterioration. In February 2024, he developed a severe chest infection requiring a two-week hospitalization, during which clozapine was discontinued.

After discharge, clozapine was reinitiated with a slow titration protocol; however, in March 2024, the patient presented with tachycardia, elevated temperature, and chest discomfort during the titration process. ECG findings revealed sinus tachycardia with a heart rate of 112 bpm, a prolonged QTc interval of 470 ms, frequent premature ventricular complexes (PVCs), and ventricular bigeminy. Blood tests showed an elevated troponin T of 16 ng/L (normal range: 0–14). During an A&E evaluation, the patient was asymptomatic apart from the noted ECG abnormalities and was discharged within 24 hours with recommendations to reassess his medications. Clozapine was subsequently discontinued, and no antipsychotic therapy was initiated immediately.

A follow-up ECG performed one week later showed normalized findings, including a heart rate of 54 bpm and a QTc interval of 443 ms, while troponin T levels returned to normal at 14 ng/L. Clinical resolution of myocarditis-like symptoms was observed.

Results: In this case, the patient developed significant ECG abnormalities and elevated troponin levels within two months of clozapine initiation. These findings, combined with clinical symptoms, necessitated immediate discontinuation of clozapine. Subsequent resolution of cardiac abnormalities within one week strongly indicated clozapine-induced myocarditis or cardiotoxicity. This outcome aligns with existing evidence that supports stopping clozapine in the presence of significant cardiac derangements.

Conclusion: This case emphasizes the critical need for monitoring for any adverse effects from clozapine particularly in the titration phase. Regular monitoring, including ECG and blood tests, is essential to identify early signs of myocarditis or cardiotoxicity. If there are any symptoms indicating cardiac abnormalities, clozapine should be discontinued immediately and referral should be made to medical or cardiology specialist for further evaluation.

Aims: Genital self-mutilation (GSM) is a rare but severe form of self-harm often linked to underlying psychiatric disorders, particularly psychotic conditions. Approximately 54% of GSM cases occur in patients with psychosis, with substance use disorders being the second most common associated condition. Various triggers, including perceived rejection, lack of social support, and acute substance intoxication, have been implicated in GSM. When GSM arises from psychotic symptoms, it is referred to as Klingsor syndrome. Immediate psychiatric intervention is critical for managing such cases and preventing recurrence.

Methods: A 28-year-old divorced male was brought to the nearest hospital by his family following a penile self-amputation with a blade. Immediate surgical repair was performed. Three weeks later, he was admitted to Bethlehem Psychiatric Hospital for further evaluation and treatment. The patient had a history of self-harm that previously necessitated hospitalization. His psychiatric symptoms included commanding auditory hallucinations, delusions of reference, feelings of worthlessness, and psychotic features that emerged after cannabis use. In the weeks leading up to the self-mutilation, the patient exhibited insomnia, social withdrawal, and a growing preoccupation with self-castration. On examination, he appeared distressed, with an irritable affect and poor insight into his actions. He expressed a strong belief that his genitals were “the source of all problems” and reported suicidal ideations, stating he “needed to get rid of his penis or else would commit suicide”. He also exhibited persecutory delusions, delusions of guilt, control, and thought broadcasting. A comprehensive psychiatric assessment confirmed a diagnosis of Schizoaffective Disorder, exacerbated by substance use. He was admitted to the psychiatric ward following medical stabilization and was treated with quetiapine 600 mg/day, titrated as needed, and carbamazepine for mood stabilization. Supportive psychotherapy aimed at improving insight and addressing delusional distress was initiated, alongside family psychoeducation to prevent recurrence.

Results: During his four-week inpatient stay, the patient demonstrated gradual improvement in his psychotic symptoms. His insight improved significantly, and he ceased expressing delusional beliefs about his genitals. Upon discharge, he was referred to the Community Mental Health Centre (CMHC) and enrolled in an outpatient psychiatric programme, which included ongoing medication management and psychotherapy. At the few-months follow-up, he remained adherent to his treatment plan with no recurrence of self-harm behaviours.

Conclusion: This case highlights the interplay of psychosis and substance use in GSM and underscores the necessity for early intervention and psychiatric care. A multidisciplinary treatment approach including pharmacotherapy, psychotherapy, and family support is essential for prevention of future episodes.

Aims: Idiopathic Regression in Down Syndrome (IRDS) is reported to be present in 16% of people with Down syndrome however the clinical presentation is heterogeneous with no universal diagnostic criteria. It often presents in adolescence or early adulthood and there are often no known triggers. Common symptoms include language regression, mood symptoms, psychotic phenomena, motor symptoms and loss of previously acquired cognitive skills.

We present a case series of two patients who presented to the West Norfolk Community Intellectual Disability Service with symptoms suggesting IRDS.

Methods: AB (F; 34 years) has the diagnoses of Mild Learning Disability, Down syndrome, Bipolar Affective Disorder following a manic episode at the age of 18 and obsessive-compulsive disorder with predominantly compulsive acts. She was described by parents as a very sociable, active, and high achieving before she developed acute regression. Around the age of 12 years following an episode of profoundly serious pneumonia, she became catatonic, anorexic, and doubly incontinent. Clearly described episodes of depression and mania, obsessional behaviours and speech deterioration were also noted.

The diagnosis of IRDS was raised by parents in 2023 and AB is currently being assessed for immunotherapy.

XY (M; 46 years). Following a gastrointestinal infection aged 18 years, the family noticed he became more housebound, obsessional about symmetry, and depressed. No specialist investigations were done but he was managed for depression with several antidepressants with no improvement. He was also diagnosed with dementia and started on donepezil but nothing changed. He is currently psychotropics-free and following a retrospective diagnosis of IRDS and discussion with family, they were relieved that the correct diagnosis of XY’s condition has been found.

Results: A physical illness appears to have triggered the regression in both cases. Personality and mood changes especially a manic presentation which is uncommon in people with Down syndrome were also reported. Psychotropic medications were not beneficial in at least the second case. In both cases, the diagnosis of Idiopathic Regression in Down Syndrome was an acceptable explanatory model for the family.

Conclusion: We hope clinicians will make the diagnosis more promptly thus facilitating quick access to adequate treatment.

Aims: Presented is a 33-year-old gentleman with a diagnosis of emotionally unstable personality disorder (EUPD) well-known to mental health services, including inpatient, community, liaison, and psychological care teams, with a long-standing history of self-harm and suicide attempts, which included deliberately placing himself in high-risk public areas which have at times resulted in detention under mental health legislation.

Methods: Over the past several years, this gentleman has fabricated claims of a cancer diagnosis, terminal prognosis, and multiple surgical procedures – assertions refuted by his medical records – while leveraging these falsehoods on social media and through a crowd sourcing campaign to raise funds by misrepresenting his physical health. Furthermore, he has strategically leveraged medical admissions to access medications, including strong analgesics and for a self-reported diagnosis that remains unverified.

During conducted assessments, he has expressed a desire for psychological therapy and enhanced crisis support yet consistently avoids engaging with the planned, regular support offered by teams who are familiar with his history, including appointments scheduled after episodes of self-harm.

While services have considered a factitious component in his presentation others contest it aligns more strongly with malingering. Consensus with professionals is that given his presentation there are difficulties in developing and maintaining a safe therapeutic relationship due to his disingenuity, threats of complaints, and his active avoidance of any meaningful, structured, recovery-focused work.

Results: Factitious disorder is driven by an internal need to assume the sick role and receive attention or care, with patients intentionally producing symptoms rooted in psychological need rather than for external rewards where the behaviour is characterized by a willingness to undergo invasive tests and treatments, reinforcing their patient identity. Factitious disorder is recognised as a psychiatric diagnosis warranting treatment, whereas malingering is motivated by external incentives and is not considered a mental illness but rather a behavioural strategy. Individuals who malinger tend to avoid procedures that might expose their deception and selectively engage in behaviours that yield tangible benefits.

Conclusion: This case underscores the importance of comprehensive, multidisciplinary assessments in achieving accurate diagnoses by clarifying key differences in motivation, behaviour, and clinical classification. Enhanced diagnostic clarity not only improves patient care, but also safeguards healthcare resources. Despite evident secondary gains in this case, the long-standing emotional instability and interpersonal dysfunction associated with EUPD still necessitate a balanced, empathetic therapeutic approach.

Aims: Dissociative Identity Disorder (DID) is a complex psychiatric condition that is often misdiagnosed due to its overlapping symptoms with other disorders such as mood and psychotic disorders. The presence of psychotic features, including auditory and visual hallucinations, disorganized behaviour, and memory gaps, can make the diagnosis of DID particularly challenging. This case study highlights a 27-year-old female whose DID diagnosis was delayed due to misinterpretation of her psychotic symptoms, which were initially attributed to other psychiatric disorders.

Methods: A 27-year-old female with a 15-year history of psychiatric care began experiencing symptoms at the age of 13, initially presenting with anxiety and panic attacks. Over time, her symptoms escalated to include episodes of auditory and visual hallucinations, disorganized speech, and erratic behaviour, leading to multiple hospitalizations. During one hospitalization, she displayed regressive behaviours, mutism, aggressive outbursts, hypomania, and dissociative amnesia. Despite extensive workups, including MRI scans and lab tests, no organic causes were found. Her diagnosis fluctuated between psychotic disorders, mood disorders, anxiety disorder, and dissociative disorder. Her mood and psychotic symptoms were initially treated as schizoaffective disorder, but the patient experienced adverse reactions to antipsychotic medications, including galactorrhoea from risperidone and weight gain from amisulpride. These medications were ineffective, prompting a reassessment of her diagnosis. A thorough review of her clinical history, including reports of memory gaps, identity disturbances, and dissociative episodes, led to the reconsideration of DID as the primary diagnosis.

Results: The psychotic features in this patient, such as hallucinations and disorganized behaviour, were secondary to her dissociative episodes, occurring during times of identity disturbance. This case underscores that psychotic symptoms in DID can easily be misinterpreted as part of a mood or psychotic disorder, especially when dissociative episodes are not initially recognized. The prolonged misdiagnosis delayed appropriate treatment, but a more comprehensive understanding of her symptoms led to the correct diagnosis and tailored management.

Conclusion: This case highlights the diagnostic challenges in identifying DID, particularly when psychotic features overlap with other psychiatric conditions. Early recognition of DID, with a thorough longitudinal assessment of both dissociative and psychotic symptoms, is crucial for accurate diagnosis and improving patient outcomes. A more targeted approach, including trauma-informed care and psychotherapy, would have been beneficial and should be considered in similar cases.

Aims: Miss X, a 39-year-old postpartum mother with a strong family history and previous diagnosis of Huntington’s disease, was admitted to mother and baby unit three months after delivery due to psychotic symptoms and delusional disorder. Initially admitted informally, her deteriorating mental state necessitated detention under Section 2 of the Mental Health Act. Her symptoms significantly impaired her ability to care for herself and her children.

Methods: Her psychiatric history included past depression and anxiety, previously managed with counselling, but no prior inpatient admissions. Family history was significant for Huntington’s disease in her mother, maternal aunt, and grandfather, as well as schizophrenia in her paternal aunt.

Miss X presented with persistent paranoid delusions, believing she was being stalked by both a male and female figure whom she could see and hear throughout the day. These hallucinations interfered with her sleep, appetite, and self-care. Additionally, she reported intrusive thoughts of accidentally harming her baby, further affecting her ability to meet the needs of her children. She lacked insight into her condition and was treated with risperidone for her psychotic symptoms and mirtazapine for depressive symptoms, given the history of Huntington’s disease and the distress following the loss of custody of her baby.

Investigations revealed no acute intracranial abnormality on CT Head, but there was mild diffuse cerebral and hippocampal atrophy disproportionate for her age. Cognitive assessments included a Frontal Assessment Battery score of 16/18 and an ACE-III score of 78/100. Urine dip on admission was negative. Blood investigations and ECG were largely unremarkable. Differential diagnoses considered included Post-partum psychosis, Schizophrenia, Schizophreniform disorder.

Results: Miss X’s lack of insight into her Huntington’s disease has contributed to a significant breakdown in her caregiving ability. The persistence of her paranoid delusions, particularly the belief of being stalked, suggests a deeply entrenched belief system that may have been reinforced over time, making it more resistant to treatment. The overlap between neurodegenerative and psychiatric symptoms presents a challenge in management, requiring a tailored, multidisciplinary approach.

Conclusion: This case highlights the complex interplay between Huntington’s disease and severe psychiatric manifestations, particularly delusional disorder. Her enduring psychotic symptoms, compounded by cognitive impairment, significantly impact her functionality and caregiving capacity. Early intervention, close psychiatric monitoring, and integrated neurological care are essential to improve patient outcomes.

Aims: Individuals with learning disabilities (LD) have a higher rate of mental health disorders and behavioural difficulties.

Conventional interventions may be limited in addressing non-verbal emotional expression.

Art therapy offers a creative, structured medium for self-expression, emotional regulation and social skill development.

Methods: Case Report

A 42-year-old lady, Ms X, with moderate LD with challenging behaviour, paranoid schizophrenia and past history of mixed anxiety and depressive disorder and impact of art therapy in her treatment and quality of life.

Ms X has gone through a series of unfortunate events, for example, her brother committed suicide by jumping off a bridge. She lost her mother and her father had been diagnosed with Alzheimer’s dementia. Considering her level of LD and the trauma that she has gone through and the past history of risky behaviours including verbal and physical aggression, requiring inpatient admission and intensive support, she has been doing well.

There are times she tends to become increasingly anxious needing reassurance, however, these are more infrequent now. In general, she has been compliant with the prescribed medications, Depakote and olanzapine. She goes out for swimming quite frequently and also she enjoys walking along the beach with staff. She keeps herself active.

A significant improvement in her presentation is attributed to the art therapy she has been having regularly since September 2024–January 2025. She has completed 12 sessions and a remarkable positive change has been noted by staff supporting her.

Results: Discussion.

1. Improvement in Psychosocial Functioning.

A systematic review (37 studies) indicated that art therapy interventions significantly enhanced psychosocial well-being.

Key therapeutic factors included varied artistic mediums and therapist-guided sessions.

2. Reduction of Aggression.

Ms X had reduced episodes of aggression which is also supported by a quasi-experimental study (Egypt) that found 85% of participants exhibited reduced aggression.

3. Alleviation of Mental Health Symptoms.

Art therapy provides a non-verbal mode of expression, effective in treating patients with learning disabilities and comorbid anxiety/depression. Shown to improve emotional processing and engagement in therapy.

4. Enhancement of Social Skills.

Studies indicate that art therapy significantly improves social interactions, particularly in patients with learning disabilities.

Conclusion: Art therapy is a valuable adjunct that provides alternative communication channel, especially for non-verbal or emotionally withdrawn individuals.

Clinical Implications and Future Directions:

Incorporate art therapy into multidisciplinary-treatment plans for patients with learning disabilities.

Investigating neurobiological mechanisms underpinning art therapy’s impact could optimise therapeutic approaches.

Aims: Dissociative Neurological Symptom Disorder (DNSD), also known as Conversion Disorder, is a common diagnosis among mental health patients in Pakistan. Despite its prevalence, research on DNSD, especially regarding patient experiences, is limited. Family-related stressors are significant contributing factors in its development, with familial discord playing a key role in triggering symptoms.

Methods: A 24-year-old female was referred by a neurologist after presenting to the outpatient department in a wheelchair due to a fear of falling. She reported symptoms including jerky body movements, episodes of apparent loss of consciousness, diarrhoea, weakness, visual disturbances, headaches, and palpitations, which had persisted for over two years. Despite multiple consultations, no organic cause was identified. She had been prescribed various medications with no improvement. Upon evaluation, a diagnosis of DNSD was made, compounded by significant emotional stress, particularly familial discord. A multidisciplinary approach, involving specialists in neurology, ophthalmology, ENT, and gastroenterology, helped rule out underlying physical conditions. Her pre-morbid history indicated high academic achievement but chronic familial stress.

Results: This case emphasizes the importance of recognizing psychosomatic presentations in patients with unexplained neurological and physical symptoms. Despite extensive negative investigations, the patient’s psychological stressors, such as familial discord and fear of stigma, were key contributors to the onset of her symptoms. The patient’s fear of walking further exacerbated her physical disability. Treatment included sertraline, mirtazapine, and short-term benzodiazepines for anxiety and depression. Psychological therapies such as Cognitive Behavioural Therapy (CBT), deep breathing, safe-place visualization, imaginal exposure, systematic desensitization, and gratitude journalling were used to address emotional issues and reduce disability. This comprehensive approach resulted in symptom resolution, and the patient was symptom-free within 18 months, now pursuing an MPhil degree.

Conclusion: This case highlights the value of a multidisciplinary approach in diagnosing and treating complex physical symptoms with unclear aetiology. Addressing underlying psychological stressors and utilizing appropriate psychosocial interventions significantly improved the patient’s condition. Early identification and holistic management combining medical, psychological, and emotional support are crucial for effective treatment of DNSD.

Aims: Sodium amytal is a barbiturate medication, first synthesised in Germany in the 1920s to treat anxiety and sleep disorders; as well as being used as an anaesthetic. This case report discusses sodium amytal prescription and subsequent dependence in an 82-year-old female with a history of anxiety and agoraphobia. It aims to highlight historical indications, mechanism of action of and potential dangers of cessation. As such, clinical management of withdrawal is discussed including the initial use of a more commonly prescribed barbiturate in place of amobarbital; with the ultimate aim being to cease such dangerous medication and to consider safer alternatives – pharmacological and psychological.

Methods: Mrs F was referred to Older Persons Psychiatric Services in 2024. At this time, her GP reported that she was ‘one of only 30 patients in the UK’ to be prescribed sodium amytal, and that it was ‘no longer being produced’. At the time of referral, Mrs F had just a 7-day supply of medication left.

Guidance from the local Medicines Information team had been sought prior to admission. They recommended a phenobarbital taper for seizure prophylaxis when discontinuing other barbiturates, where 100 mg amobarbital was roughly equivalent to 30 mg phenobarbital. Phenobarbital is a long-acting barbiturate which would be more commonly found in practice, given its use in management of epilepsy.

As such, an attempt was made at the safe withdrawal of sodium amytal in the inpatient setting. This was due to the significant risks associated with abrupt withdrawal, including seizure, hallucinations and cardiovascular collapse tending to occur after 16 hours of cessation with such risk remaining up until approximately 5 days.

Mrs F had run out of medication on the day that she was admitted, and given the aforementioned risks, a thorough plan was developed to ensure close monitoring. She was commenced on 1:1 special observations initially due to the risk of seizures. Her clinical observations were performed on a regular basis and a CIWA (Clinical Institute Withdrawal Assessment for Alcohol) score was also performed hourly to monitor withdrawal severity. To this end, lorazepam was prescribed at a dose of 1 mg every 6 hours, as well as an ‘as required’ dose of 1 mg prescribed for when CIWA score was >8.

At consultant review the following day, Mrs F was commenced on phenobarbital at a dose of 30 mg QDS + 30 mg PRN to a maximum of 150 mg/day, continuing on regular lorazepam at 1 mg QDS. Of note, this is slightly lower than the aforementioned recommendation which would equate to 162 mg/day. Subsequently, owing to increasing agitation and anxiety, Mrs F’s dose was increased to 60 mg mane, 30 mg TDS plus 30 mg PRN and her dose of lorazepam was reduced to 1 mg TDS. She was discharged on both medications, 9 days after admission.

Results: The treating team discussed the preferred option to follow on from the withdrawal of amobarbital with subsequent tapering of phenobarbital, given that it shares many of the same risks as the former. Mrs F however was not keen to change medications again at present, owing to her age and ongoing anxiety. In fact, at a subsequent outpatient review, Mrs F reported that she felt that she would require more lorazepam to cope with ongoing anxiety, however this was not facilitated. In terms of patient safety, it should be highlighted that the patient was discharged on 2 addictive, sedative medications (even if the lorazepam was a short-term measure), which could prove challenging to rationalise moving forward and perhaps gives an insight into the ongoing difficulties faced by outpatient teams in terms of cessation of addictive medicines. Importantly, the patient would not however experience the same supply issues currently with phenobarbital. It should also be noted that she had declined psychological therapy with the Community Mental Health Team for Older Persons.

Conclusion: The aims of this report were to highlight the use and action of the barbiturate class of medications, whilst also discussing difficulties with supply issues, dependence and the associated potential for withdrawal. Ensuring patient safety is paramount, and in many cases patients who are prescribed this class of medications for a prolonged period of time require inpatient management to allow for a safe transition to an alternative medication.

Aims: Ketamine is a novel and exciting putative antidepressant medication for patients with treatment-resistant depression. A complication commonly seen in frequent and heavy recreational use of ketamine is ulcerative cystitis, which presents with lower urinary tract symptoms (LUTS) and upper renal tract damage and can be seen in over 25% of regular users.

Although ketamine-induced cystitis (KIC) is a recognised complication in recreational use of ketamine, its occurrence in therapeutic use of ketamine in depression has so far not been reported. The exact pathogenesis of KIC is currently unknown, making treatment and prevention advice much more difficult. Early diagnosis of KIC and immediate cessation of ketamine has been shown to improve adverse urinary tract symptoms and prevent further damage.

Methods: We present a case of a 28-year-old female who was started on ketamine treatment for depression, and who then developed symptoms of KIC, which was confirmed by urine microscopy, culture and analysis.

Results: Ketamine-induced cystitis (KIC) typically starts with urinary symptoms that include dysuria, urgency, nocturia and urinary frequency. With continued use, symptoms can progress to incontinence, haematuria, bladder wall fibrosis and ulcerative cystitis. Ongoing use of the drug can lead to involvement of the upper renal tract, including hydronephrosis and chronic kidney failure. Physical examination and investigations may demonstration suprapubic pain, sterile pyuria and increased eosinophils within the bladder wall. The pathophysiological mechanisms of LUTS are not yet fully understood and further research to define therapeutic options would be useful.

Imaging of the bladder in severe cases may demonstrate a grossly constricted bladder with thickened walls. Cystoscopy often demonstrates a friable bladder mucosa that is prone to bleeding. Microscopically, the urothelium may appear denuded, ulcerated and infiltrated by inflammatory cells, such as mast cells and eosinophils. Other findings include submucosal fibrosis, muscle hypertrophy and collagen deposition.

Although the exact pathogenesis of KIC is not yet fully understood, various mechanisms have been postulated and it is likely that several pathways are involved simultaneously.

One theory is that the ketamine and its metabolites (which are largely excreted by the urinary tract), cause direct toxicity to the bladder. These disrupt the urothelial integrity of the bladder epithelium and initiate interstitial fibrosis. This has been demonstrated in animal models and the level of damage directly correlates with the dose of ketamine used.

Another theory is an IgE-mediated response. Bladder samples in ketamine users frequently show raised inflammatory cells and messengers, including mast cells, eosinophils, COX-2 (cyclo-oxygynase-2), NOS (nitric oxide synthase) and IgE. These levels fall once the patient is in remission from ketamine use and rise again once ketamine is restarted. This suggests an inflammatory response or a hypersensitivity reaction leading to bladder damage.

Ketamine can also directly stimulate various chemicals, including adenosine triphosphate, antiproliferative factor and oxidative stressors, which subsequently lead to changes in the bladder wall. It has been reported that the NMDA receptor (NMDAR) and angiogenic factors can also cause microvascular injury within the bladder.

Other proposed theories include aberrant neurotrophic factors, protein kinase B, mTOR pathways, metadherin and MAPK pathways, leading to downstream fibrosis of the bladder.

Early diagnosis of KIC and immediate cessation of ketamine use has been shown to improve symptoms, reverse early disease and prevent further damage.

Conclusion: To our knowledge, this is the first reported case of KIC in a patient receiving treatment-dose ketamine as part of their antidepressant therapy.

Aims: Anorexia nervosa (AN) is a severe eating disorder, with a lifetime prevalence estimated to be 0.3–0.9%. Transaminase elevations are common in patients during hospital admission, reaching a prevalence of 43%. Although usually caused by refeeding, prolonged starvation can also cause an exacerbation of liver enzyme levels. It is important to differentiate between the two, as the treatment plans are quite different. We herein present a report of a 34-year-old lady with anorexia nervosa, who presented with extreme worsening of liver functions due to starvation hepatitis, while on admission for refeeding and her gradual recovery.

Methods: ‘A’ is a 34 year-old lady, who is known to specialist eating disorders team with long-standing history of anorexia nervosa, restrictive sub-type, in the background of coeliac disease. Body mass index (BMI) on admission was 11.4, and reported food intake till that point was less than 300 calories/day. Ward dietician started her on stage 2 refeeding menu – 750 calories, 25 g protein, 1350 ml fluid with appropriate thiamine, multivitamin and mineral cover. Liver function was mildly deranged (Alanine transaminase ALT 256 U/L, Gamma-glutamyl transferase activity GGT 38). ‘A’ struggled to eat on the ward, and over the next week deteriorated with LFT as follows – ALT 2362 U/L, AST 2288 U/L, GGT 88 U/L. Upon shifting to medical bed and failure of less restrictive options, ‘A’ was treated under the Mental Health Act with full nasogastric feeding with 1:1 supervision. Liver appeared normal on Ultrasound abdomen and serum electrolytes were mostly normal, ruling out refeeding hepatitis. Over the course of several weeks, as slowly BMI increased with improvement in nutrition, liver parameters improved with ALT dropping down to 346 U/L on day of transfer out of medical bed for psychological treatment.

Results: Starvation hepatitis, as in this case, appears when weight is at lowest with markedly elevated transaminases, normal liver appearance on radiological investigations. In this patient, BMI went to as low as 10 kg/m2 and expectedly, LFT derangements worsened, and improved on gaining weight.

Conclusion: Though anorexia nervosa has a plethora of medical complications, it is important to anticipate hepatitis as an important complication, and be aware of potential differential diagnoses including starvation hepatitis and refeeding hepatitis, which needs to be analysed carefully to delineate, and treat appropriately.

Aims: Abnormalities of vision have long been documented in psychosis. One syndrome of interest is Inverse Anton’s syndrome. This is a rare manifestation of visual abnormality where a person describes being blind despite objective evidence against this. In this case report, we discuss a patient who presents with a complaint of blindness despite evidence to the contrary.

Methods: Case Report.

A 46-year-old male part-time worker, with a childhood history of photosensitive myoclonic seizures which were treated with anti-epileptic medications. At 21 years, he required mental health services as he complained of episodic blindness. He was diagnosed with a delusional disorder. His symptoms resolved drastically after he was treated on olanzapine which he discontinued and remained well for over 2 decades.

He returned to services following a recurrence. His reported blindness is associated with emotional distress and self-harming. He is able to independently mobilise, complete forms and questionnaires but would insist that he is blind despite doing these. He reported mood changes which were treated with sertraline but with no benefits. He was unsuccessfully treated on olanzapine and then switched to quetiapine.

Cognitive Behavioural Therapy based Initial Interventions were unsuccessfully attempted. He was reviewed by neuropsychiatry and complex psychosis service. He is engaged to Occupational Therapy interventions aimed at maximising practical skills. He was assessed by the ophthalmologist and opticians with no significant findings. He was referred to the neurologist. He had a brain Magnetic Resonance Imaging scan which found no abnormality.

Results: Discussion.

Inverse Anton’s syndrome is scantily described. There are few case reports with similar presentations. In a 2019 case report, the presentation was similar to this. The exact cause of this syndrome is unclear. It is thought to result from a structural disconnection of the parietal lobe attentional systems from visual perception. In the absence of radiological evidence, this leads to a suggestion of a functional illness or a neuropsychological syndrome in which visual perception and cognitive awareness are dissociated. In the absence of known secondary gain, it continues to present a diagnostic dilemma. This puzzle requires multidisciplinary efforts to solve. Management is focussed on secondary prevention and rehabilitation to improve quality of life.

Conclusion: Inverse Anton’s syndrome continues to present with unclear aetiology and diagnostic dilemma. It is hoped that multidisciplinary efforts together with advances in neuroimaging would help understand this syndrome better. We hope that our case report contributes to the body of knowledge and adds more perspective to this.

Aims: Language variant frontotemporal dementia (lvFTD) is a neurodegenerative disorder primarily affecting language, often presenting with speech and comprehension difficulties, commonly in people aged 45–65 years. LvFTD presents a perplexing diagnostic challenge, often masquerading as primary progressive aphasia (PPA) while progressively dismantling communication and cognition. Despite growing recognition of lvFTD, a critical gap remains in distinguishing its early presentation with overlapping neurodegenerative syndromes, delaying accurate diagnosis and intervention.

Methods: This case report highlights the challenges of diagnosing lvFTD in a patient with atypical early symptoms and the implications of late diagnosis on patient care and outcomes.

Patient in her late 50s, with background of anaemia and hypothyroidism presented with memory issues, word-finding difficulties, and trouble understanding conversations which began in early 50s, initially attributed to menopause. Symptoms worsened over time, revealing frontal lobe atrophy on brain imaging and a psychotic episode, including auditory hallucinations and paranoid delusions.

Following two self-harm attempts, detention under the Mental Health Act led to first mental health admission. Neurological investigations, including PET CT Brain, suggested a diagnosis of potential Logopenic Primary Progressive Aphasia (lvPPA) with mixed dementia and Lewy Body dementia (LBD). Neurologist review confirmed diagnosis of lvFTD. Antipsychotic trial undertaken with aripiprazole, only to stop as led to worsening behavioural symptoms. Subsequently started on mirtazapine, quetiapine, lorazepam and rivastigmine. Improvement noticed in symptomatology. Currently awaiting DAT scan for further evaluation and on waitlist of Young Onset Dementia Psychology.

Results: This case underscores the complex diagnostic challenges in patients with overlapping neurodegenerative and psychiatric symptoms. The patient, in her late 50s, presented with progressive language impairment, memory issues, and psychotic features including auditory hallucinations and paranoid delusions. Neuroimaging revealed frontal lobe atrophy and significant asymmetrical hypometabolism in the left frontal, temporal and parietal lobes, findings suggestive of lvPPA. However, reduced tracer activity in the occipital cortices raised the possibility of mixed dementia, potentially co-existing with LBD. These overlapping features highlight the need for a comprehensive, multidisciplinary approach to refine diagnosis and optimize management strategies.

Conclusion: Breaking through the diagnostic fog, this case exposes the intricate challenge of untangling overlapping neurodegenerative and psychiatric disorders. The patient’s progression from language deficits to memory loss and psychotic symptoms along with neuroimaging showing left hemispheric hypometabolism and frontal lobe atrophy, suggested lvPPA, potentially complicated by mixed dementia and probable LBD. She was diagnosed as lvFTD. This complexity calls for early multidisciplinary evaluation for prompt diagnosis and tailored intervention for improved patient outcomes.

Aims: Catatonia is a complex neuropsychiatric syndrome of disturbed psychomotor function, abnormal behaviours and withdrawal. It remains under-recognised and under-diagnosed, especially within the acute hospital setting.

While often associated with primary mental illness, it can also occur secondary to systemic medical conditions such as systemic lupus erythematosus (SLE), an autoimmune disease in which neuropsychiatric manifestations are commonly described.

We present a case which highlights the diagnostic challenge and importance of recognising catatonia in the context of lupus.

Methods: A 34-year-old female with a three-year history of SLE presented with decline in functioning accompanied by malar rash, joint pains, paucity of speech and altered mental state. She had previously experienced command hallucinations in the context of lupus flares and though the psychotic component resolved between episodes, she was prescribed a daily maintenance dose of olanzapine 2.5 mg.

Assessment revealed an agitated, distracted patient with suspected auditory and visual hallucinations, profound paucity of speech and incoherent mumbling. She required assistance with personal care, displayed rigid posturing, and had stopped eating and drinking. Laboratory results were consistent with an acute SLE flare, and it was proposed that her presentation was SLE-related psychosis, initially addressed by increasing olanzapine dose with minimal effect.

Further clinical deterioration prompted a lumbar puncture after which the patient began to talk and regain some normal functioning. Thorough examination of notes revealed midazolam had been administered so it was proposed that this was catatonia and therefore partially resolved with a benzodiazepine. Further examination revealed waxy flexibility, catalepsy, stupor and mutism. Regular lorazepam was added to the schedule of cyclophosphamide and high-dose prednisolone and led to prompt substantial clinical improvement.

Results: Data suggests neuropsychiatric symptoms are common in SLE and though there are some reports in literature of lupus-associated catatonia, its precise prevalence is uncertain.

It is proposed that the diversity of symptoms can arise due to various pathophysiological mechanisms in lupus, which include autoimmune inflammation of the central nervous system, metabolic disturbances or adverse effects of medication. While treatment of the underlying cause is key, timely recognition of catatonia and pharmacological therapy can result in rapid clinical improvement.

Conclusion: Catatonia is associated with significant morbidity and mortality if untreated. It should be considered as a differential in patients with lupus, particularly those with concurrent neuropsychiatric symptoms, thus resulting in improved patient outcomes.

Aims: Delusional parasitosis (DP), or Ekbom syndrome, is a rare psychiatric disorder in which individuals falsely believe they are infested with parasites. When shared by another person, it is classified as folie à deux (shared psychotic disorder). This case study explores a unique DP case within a close relationship, examining clinical presentation, potential causes, and treatment outcomes.

Methods: A 64-year-old woman sought mental health services, convinced she had fatally infested her 26-year-old neurodivergent son with scabies and transferred her heart disease to him. She had believed for years that she had a scabies infestation, a delusion shared by her mother, who had recently passed away at 89. Multiple dermatology consultations ruled out any infestation, yet she continued self-treating with bleach, essential oils, borax, and horse skin infection chemicals. She also took excessive baths, scrubbing herself vigorously.

Additionally, she was convinced she had heart disease and past cancers, though no medical evidence supported these claims. She exhibited significant anxiety and distress but denied perceptual disturbances and lacked insight into her condition. Treatment was initiated with a combination of an antipsychotic and an antidepressant, leading to a gradual reduction in delusional intensity and increased engagement with mental health services. Psychological support was also provided.

Results: DP is challenging to treat, particularly when reinforced by family members, as seen in this case. The patient’s condition worsened following her mother’s death. However, a multidisciplinary approach is essential to enhance engagement and compliance, which are crucial for a positive prognosis.

Conclusion: Understanding such cases is vital for accurate diagnosis and effective intervention, especially given the reinforcing nature of shared delusions and the persistent nature of DP.

Aims: Evidence is emerging regarding the association between Bipolar Affective Disorder (BPAD) and Parkinson’s disease (PD). Studies have shown patients with BPAD have a higher risk of developing PD. This case series explores the complexities encountered in the management of patients with PD and BPAD.

Methods: ‘A’ is a woman in her 70s with BPAD. Parkinsonian symptoms were noted for several years, suspected to be medication-induced. She was diagnosed with Parkinson’s disease, after a positive DaT scan, treated with co-beneldopa, which induced a manic episode, requiring hospitalization. Co-beneldopa was stopped, she improved with lamotrigine and clonazepam.

‘B’ is a woman in her 70s with BPAD with a family history of Parkinson’s disease. She was hospitalized after relapse of BPAD. She was noted to have a unilateral tremor, stooped posture and a shuffling gait. She is now being assessed for Parkinson’s disease.

‘C’ is a woman in her 60s with BPAD, on sodium valproate and aripiprazole. She was reviewed by neurology due to bilateral tremor, rigidity and unsteady gait, and subsequently diagnosed with drug-induced parkinsonism. Due to miscommunication, GP started her on co-beneldopa, for Parkinson’s disease. Subsequently, she developed mania warranting hospitalization. The ward team was unaware of the misdiagnosis. Co-beneldopa was subsequently stopped. She continued having poor oral intake, intractable mania, treated with ECT.

Results: Literature review shows BPAD is associated with Parkinson’s disease (PD). Evidence indicates, a diagnosis of BPAD, increases the risk of developing PD. With no established intervention for patients with co-morbid BPAD and PD, treatment becomes complex. Proposed pathology suggests BPAD is exacerbated by heightened dopamine levels, while PD from reduced dopamine. This makes it challenging to treat one without impacting the other. Mood stabilizers and antipsychotics can contribute to drug-induced parkinsonism (DIP), which may clinically be indistinguishable from PD. Antiparkinsonian medications like dopamine agonist and pramipexole can cause manic symptoms.

Conclusion: Historically, heterogeneity in psychiatric disorders, both in presentation and response, remains the norm. In this case series, we try to highlight the complex relationship between BPAD and PD. To establish a direct causal relationship is challenging due to the various confounders. This being a niche topic with limited research, emphasizes the need for large sample studies, which could shed more light on the longitudinal course and relationship between the two disorders and help establish future treatment guidelines.

Aims: Paediatric Autoimmune Neuropsychiatry Syndrome is a rare condition with exact prevalence not known due to dearth of large-scale population studies. Its diagnostic as well as treatment guidelines are not yet validated. There are a few international guidelines but none available in the UK yet.

Methods: The referral of a 15-year-girl presenting with symptoms suggestive of PANS to our team prompted us to write this case report. The patient was brought in to the A&E by her parent after an episode of bizarre and chaotic behaviour at school, which included her throwing belongings at the staff while being emotionally labile. On assessment she reported symptoms suggestive of paranoid delusions, delusional perception, auditory and gustatory hallucinations, thought broadcasting and delusional memory. She was also taking more frequent showers, with clothes on. Her sleep was disrupted.

Extensive blood and radiological investigations initially didn’t yield any positive findings. Antipsychotic (olanzapine) was initiated and the patient’s mental state quickly improved. Two days later blood investigations showed raised antistreptolysin O titres (200–400 U/Ml). Hence, antibiotic (phenoxymethypenicillin) was initiated. The patient was discharged and followed by our team in the community.

The patient continued to present with residual psychotic symptoms which fluctuated in the community setting. But the overall functioning significantly improved.

Results: The acute onset of psychosis, characterized by behavioural disturbances, anxiety, sleep disruption, irritability, and emotional lability, along with elevated antistreptolysin O titres, suggested a diagnostic formulation aligning with PANS.

Conclusion: The case underscores the importance of considering PANS as a differential diagnosis in school-aged children presenting with symptoms of OCD, first episode of psychoses or unexplained emotional lability.

Aims: A 46-year-old female with a 30-year history of bipolar disorder presented with muscle stiffness, slurred speech, and altered sensorium, following fever, vomiting, and diarrhoea. She had been on lithium (400 mg daily) without regular monitoring. Examination showed confusion, hyperreflexia, tachycardia, and dehydration. Laboratory results revealed elevated serum lithium (3.4 mEq/L), renal dysfunction, hypernatremia, and echogenic kidneys. The diagnosis of lithium toxicity with acute kidney injury and dehydration-induced impaired excretion was confirmed. After discontinuing lithium, she underwent haemodialysis, and her condition improved. She developed lithium-induced diabetes insipidus, and long-term monitoring is required.

Methods: Case report.

Results: This case highlights the complexities of chronic lithium toxicity, presenting with neurological, systemic, and renal symptoms. Lithium accumulation exceeds renal clearance, particularly in the presence of factors like dehydration and acute kidney injury (AKI), leading to elevated serum lithium levels (3.4 mEq/L). The patient, with a history of bipolar disorder and long-term lithium use, developed classic neurological signs, including altered sensorium, tremors, hyperreflexia, and hypertonia, along with systemic manifestations such as anaemia, elevated AST, and abdominal symptoms. Lithium-induced nephrogenic diabetes insipidus (NDI) was confirmed, with persistent hypernatremia and polyuria despite normalized lithium levels.

Management included immediate discontinuation of lithium, hydration with intravenous Ringer’s lactate, and two sessions of haemodialysis, which effectively reduced lithium levels. Empirical ceftriaxone addressed a suspected infection, and quetiapine was initiated for mood stabilization. Long-term monitoring, including regular serum lithium and renal function checks, is crucial for patients on chronic lithium therapy, especially those with risk factors.

The case emphasizes the need for therapeutic drug monitoring, patient education on hydration, and early toxicity recognition. Despite clinical improvement, the patient’s prognosis remains guarded due to chronic damage from prolonged lithium exposure, including persistent NDI and hypernatremia.

Conclusion: Chronic lithium toxicity remains a preventable yet potentially life-threatening condition. Early recognition, regular monitoring, and timely intervention are paramount in mitigating its systemic, neurological, and renal effects. This case serves as a reminder of the importance of patient education, family involvement, and coordinated care to improve outcomes in bipolar affective disorder patients on lithium therapy.