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.

Aims: Capgras syndrome (CS) is a rare delusional misidentification syndrome characterized by the belief that a close relative has been replaced by an identical impostor. It is commonly associated with schizophrenia and other psychiatric disorders.

A 43-year-old married Asian female presented with a 5-year history of behavioural changes, including social withdrawal, suspiciousness, reduced self-care, and irrelevant speech. Her symptoms began following a familial conflict, leading to social isolation, self-neglect, and delusional misidentification, including Capgras syndrome, where she believed her mother had been replaced by an imposter. She later developed grandiose delusions, claiming to be a significant political figure. Despite initial improvement with antipsychotic treatment, she discontinued medication, resulting in symptom relapse and aggressive behaviour.

Methods: Case report.

Results: Capgras syndrome, first described in 1923, involves the delusional belief that familiar individuals have been replaced by impostors. It is often associated with psychiatric disorders, such as schizophrenia, and neurodegenerative conditions. This case aligns with the dual-route model of face recognition, suggesting impaired implicit-affective processing alongside intact conscious recognition. The patient’s aggressive behaviour underscores the potential for violence in Capgras syndrome, highlighting the need for careful risk assessment and management. Non-adherence to treatment remains a significant challenge in managing such cases.

Conclusion: This case highlights the importance of early recognition and sustained treatment adherence in Capgras syndrome associated with schizophrenia to prevent deterioration and improve outcomes.

Aims: Emotionally unstable personality disorder (EUPD) is a mental disorder that can be one of the most misunderstood diagnoses. It is a controversial and stigmatised condition among healthcare professionals which may lead to sub-standard levels of care and sub-therapeutic patient experience.

Methods: A 47-year-old female was admitted to an inpatient unit four times over five years. She exhibited visual and auditory hallucinations and fixed delusions. This patient had a diagnosis of Paranoid Schizophrenia.

During the fourth admission, she was admitted under Section 2 after she was found walking on the M57 in the middle of the night with suicidal ideation.

The clerking doctor had made note, upon admission, of self-harm behaviours that had occurred five years prior. On the ward, the patient would walk around half-naked and behave bizarrely towards staff and other service users. After discussion, the nursing staff concluded that the patient “knew what she was doing” and must have a diagnosis of EUPD considering her record of self-harm and odd behaviour on the ward. This was then included in the handover sheet, with a query, which was shared amongst ward staff.

The resulting stigma led to staff behaving in a discriminatory manner including avoidance of the patient and unchallenged refusals during medication administration. The negative approach of the ward staff dissipated when the patient’s behaviours settled with an antipsychotic. An informal meeting was conducted with the ward staff to highlight the potential iatrogenic harm that stigma can cause. Staff were evidently remorseful and understood the importance of engaging with all patients with the same standard of care, regardless of diagnosis.

Results: The stigma associated with EUPD is so potent that it may filter through to patients without the diagnosis based on loose associations. Healthcare professionals may distance themselves from patients with EUPD which may perpetuate sensitivities such as rejection and abandonment. This study highlights that this stigma poses a risk to the wider patient cohort should similar risk profiles or symptoms be displayed.

Conclusion: Mitigating the negative impact of an EUPD diagnosis must start with an acceptance and recognition of the dangers that staff narrative can have on patient care. This case study demonstrates the dangerous impact of stigma whereby a place of safety, the hospital, becomes the antithesis of therapeutic intervention. Of course, a more conclusive outcome would be to revisit the use of this diagnostic label and review policies in the management of EUPD in the inpatient setting.

Aims: Ketamine, a dissociative anaesthetic, is used therapeutically to treat mental health disorders like depression, anxiety, and PTSD. However, its recreational misuse can lead to severe physical and psychological consequences. A concerning long-term effect of ketamine misuse is ketamine-induced bladder syndrome (KIBS), which presents with symptoms such as urinary urgency, frequency, and pain. As dependence on ketamine develops, the severity of KIBS increases, potentially leading to significant organ damage. In such cases, ketamine detoxification becomes essential for reducing or eliminating ketamine from the system while managing withdrawal symptoms and psychological distress. While no FDA-approved medication exists for ketamine detoxification, treatment generally focuses on addressing withdrawal symptoms, psychological and physical dependence, and related complications.

Methods: This case involves a 23-year-old woman with a complex mental health history, including ADHD, Borderline Personality Disorder (BPD), anxiety, and previous self-harm attempts, well-documented by community mental health services. Her substance use began at age 18, starting with ketamine use during university. Over time, her ketamine consumption escalated from 0.5 grams every few months to 3.5–5 grams, causing both physical and psychological harm. Her usage pattern varied; sometimes she refrained from use for a day or two, but often she would use it continuously for 3 to 4 days, followed by a break. At times, she alternated days of use, with usage depending on her mood, occasionally taking the entire dose at once.

Approximately four years after initiating ketamine use, she developed significant bladder pain, frequent urinary tract infections (UTIs), and a constant urge to urinate. To manage these symptoms, she began using pregabalin, initially obtained illegally but later prescribed at a dosage of up to 600 mg daily by her GP. Despite this, her bladder pain remained inadequately controlled, and she resorted to using paracetamol and co-codamol, which proved ineffective. She also visited a urologist biweekly. She underwent two private ketamine detoxifications in 2021, although relapse occurred a few days later.

Considering her ketamine addiction and bladder pain, she underwent detoxification treatment. Managing her bladder pain was a key focus of her treatment. Diazepam was prescribed for anxiety, and in addition to pregabalin, baclofen was added to address the bladder pain. During detox, the patient reported significant improvement in bladder pain.

Results: One of the most challenging aspects of ketamine-induced bladder syndrome is the chronic bladder pain. Baclofen, a GABA-B receptor agonist, helped relax smooth muscles, including those in the bladder, reducing spasticity and discomfort. Baclofen also alleviated neuropathic pain, which contributed to ketamine-induced bladder dysfunction. Baclofen’s ability to manage neuropathic pain makes it a valuable option when traditional painkillers fail. By inhibiting pain signal transmission, baclofen provides relief from discomfort and reduces urinary urgency and frequency. In this case, baclofen effectively alleviated bladder pain, reducing reliance on pregabalin during detoxification. Despite the complexities of her treatment plan, baclofen was vital in improving the patient’s quality of life during detox.

Conclusion: Baclofen proves to be an effective alternative for managing ketamine-induced bladder pain, particularly when traditional treatments fail. This case emphasizes the importance of a multidisciplinary approach to address both physical and psychological challenges during ketamine detoxification. By managing bladder pain and other withdrawal symptoms, patients can experience a sustainable detox process, ultimately improving their chances of recovery and decreasing the risk of relapse.

Aims: Clozapine is the cornerstone of treatment for treatment-resistant schizophrenia. It primarily acts by inhibiting dopamine D2 receptors based on the hyperdopaminergic theory of psychosis. Additionally, second-generation antipsychotics (SGAs) interact with serotonin receptors (5-HT2A and 5-HT1A), mitigating extrapyramidal side effects. However, widespread activity on D2 receptors and additional anticholinergic effects can impact gastrointestinal motility, leading to complications such as paralytic ileus. Clozapine has potent anticholinergic activity and is associated with higher risks of paralytic ileus compared with other SGAs.

Methods: A male in his late 40s with treatment-resistant schizophrenia, anxiety and panic attacks underwent an elective inguino-sacrotal hernia repair with mesh reconstruction. Psychiatric history was significant for past suicide attempts, including a self-defenestration leading to traumatic brain injury, aggression towards his elderly father and past clozapine-induced neutropenia. He was an ex-smoker. Medications included clozapine 100 mg twice daily, amisulpride 200 mg twice daily, lithium carbonate 625 mg once daily, and hyoscine hydrobromide 300 mcg twice daily.

Postoperatively, the patient developed constipation and abdominal distension consistent with a paralytic ileus. He was placed nil by mouth and managed with nasogastric decompression. During a three-day lapse in antipsychotic treatment on the surgical ward, his mental health deteriorated, presenting with acute psychotic symptoms. The patient lacked insight into his mental health at this time.

Given the failure of alternative antipsychotics previously, the multidisciplinary team (MDT) faced a complex risk-benefit analysis. The potential dangers of reintroducing clozapine, including worsening ileus, were weighed against its irreplaceable role in managing his psychosis, suicidality, and aggression. Ultimately, clozapine was restarted cautiously with haematological and gastrointestinal response closely monitored. Psychosis subsequently improved with no recurrence of ileus, allowing him to continue clozapine treatment.

Results: This case highlights the complexities of managing antipsychotic treatment in patients with comorbid physical conditions. Clozapine’s advantage of reducing suicidality and violence were balanced with its potent anticholinergic activity, warranting caution in patients at risk of gastrointestinal complications. The decision to restart clozapine was made after evaluating the significant risks of psychotic relapse. Close MDT monitoring facilitated safe reintroduction, demonstrating necessary case-by-case risk assessments when managing antipsychotics in medically vulnerable patients.

Conclusion: Rechallenging clozapine posed significant clinical and ethical challenges, requiring an evidence-based MDT approach. This case underscores the importance of balancing psychiatric needs with medical risks, particularly in treatment-resistant schizophrenia. It also highlights the role of ongoing monitoring and individualised treatment plans in managing complex psychopharmacological decisions. Further studies are warranted to explore safety of clozapine in patients with gastrointestinal-motility disorders.

Aims: Meditation is widely regarded as a beneficial practice for mental well-being, but intensive forms, such as those practiced during retreats, can pose risks. In vulnerable individuals, prolonged meditation may trigger psychosis. This case explores a psychotic episode in a previously healthy individual during an intensive meditation retreat, with a focus on clinical presentation, management, and implications for practice.

Methods: Case report.

Patient overview: Demographics: Female, 31 years old, with no ongoing mental health treatment. Psychiatric history: Previous drug-induced psychosis 6 years ago, resolved without recurrence. Substance use: Denied drug use since the prior episode. Admission toxicology screening (urine drug screen) was negative.

Retreat context: Attended a 7-day meditation retreat involving intensive mindfulness practices, minimal social interaction, and prolonged sitting meditations. Psychotic symptoms began after 3 days, prompting early withdrawal from the retreat.

Clinical presentation: Visual hallucinations: Reported seeing people’s faces transform into demonic appearances. Auditory hallucinations: Hearing voices reinforcing delusions. Persecutory delusions: Believed she and her family were in grave danger, and that her death was the only way to save them. Behavioural changes: Heightened distress and withdrawal from the retreat.

Management and outcome: Admitted to the psychiatric unit. Started on olanzapine 5 mg daily. Rapid symptom resolution within 6 days. Discharged with no residual psychotic symptoms.

Literature review: Intense meditation practices, especially during retreats, can lead to adverse psychological effects, including psychosis, depersonalisation, and emotional dysregulation. Risk factors identified in literature:

Pre-existing vulnerability (e.g., history of psychosis or trauma).

Retreat conditions (e.g., fasting, sleep deprivation, and isolation).

Lack of individualised guidance or screening.

Meditation-induced psychosis has been noted to present with symptoms such as hallucinations, paranoia, and altered states of consciousness. Recovery is typically rapid with antipsychotic treatment.

Results: Mechanisms: Prolonged meditation may disrupt normal cognitive and emotional regulation, leading to altered reality testing. Psychotic symptoms could result from sensory deprivation, emotional overload, or resurfacing of unresolved trauma.

Case-specific insights: While the patient had a history of drug-induced psychosis, her 6-year symptom-free period and negative toxicology suggest that meditation-induced stress was the primary trigger. The rapid response to low-dose olanzapine highlights the transient nature of the condition.

Implications for practice: Pre-retreat mental health screenings are crucial to identify vulnerable individuals. Retreats should offer tailored practices and provide professional mental health support. Awareness among clinicians is necessary to distinguish between culturally induced altered states and pathological psychosis.

Conclusion: This case underscores the potential for intensive meditation to induce psychosis, even in individuals without active mental illness. Clinicians and meditation facilitators must collaborate to mitigate risks, particularly for individuals with prior psychiatric vulnerabilities.

Aims: This case involves a 32-year-old female with a history of Anorexia Nervosa and Post-Traumatic Stress Disorder (PTSD) admitted for restricted eating. During admission, she reported worsening PTSD symptoms, including nightmares, linked to a reduction in her doxazosin dose. Doxazosin, an alpha-1 adrenergic antagonist, is used off-label to treat PTSD-related nightmares by reducing noradrenergic hyperactivity. This case highlights the challenges of managing complex comorbidities and balancing physical and mental health.

Methods: The patient, a 32-year-old female, was admitted for restricted eating. She had a history of Anorexia Nervosa (restrictive subtype) and PTSD. During admission, she reported increased PTSD symptoms, including frequent nightmares and difficulty distinguishing nightmares from reality.

Initially, her doxazosin dose was reduced from 16 mg to 8 mg due to hypotension concerns. However, this reduction coincided with worsening nightmares and distress. After confirming physical stability (stable blood pressure and no refeeding complications), the dose was increased to 12 mg. This adjustment led to significant improvement: reduced nightmare frequency, decreased distress, and better ability to differentiate nightmares from reality.

Her treatment involved a multidisciplinary approach, including medical monitoring of refeeding syndrome, psychiatric support for PTSD, and nutritional rehabilitation for anorexia nervosa. Regular monitoring of her physical and psychiatric health was maintained throughout her hospital stay.

Results: This case illustrates the complex interplay between physical and psychiatric conditions, particularly in patients with comorbid anorexia nervosa and PTSD. The reduction in doxazosin dose likely disrupted its therapeutic effect on PTSD-related nightmares, leading to symptom exacerbation. Doxazosin alleviates nightmares by blocking noradrenergic hyperactivity, which is implicated in PTSD pathophysiology. Restoring the dose to 12 mg balanced psychiatric symptom management with physical stability.

The case underscores the importance of a multidisciplinary approach in managing complex comorbidities. Collaboration between medical, psychiatric, and nutritional teams was essential to address both her physical health (refeeding syndrome, hypotension risk) and psychiatric needs (PTSD-related nightmares, anorexia nervosa). Regular monitoring and individualized treatment adjustments were key to achieving a positive outcome.

This case highlights the need for careful medication adjustments in patients with comorbid conditions. The decision to increase the doxazosin dose was guided by clinical response and physical stability, demonstrating the importance of personalized care.

Conclusion: This case demonstrates the challenges of managing comorbid anorexia nervosa and PTSD, particularly when physical and psychiatric symptoms interact. The careful adjustment of doxazosin dose, combined with a multidisciplinary approach, led to significant symptom improvement. It emphasizes the importance of individualized treatment plans, close monitoring, and collaboration between medical and psychiatric teams in achieving optimal outcomes.

Aims: Each person is born with an unique personality/mental nature, determined by the genetic predisposition from biological parents. Starting from intrauterine period till the last date of life human beings are subjected to innumerable stressful factors, for which we are neither prepared or trained to face. Some of these stressors may have detrimental effects on our behavioural patterns by influencing the levels of neurotransmitters mainly platelet serotonin and dopamine (which has an inverse relationship with serotonin).

Methods: Here we present a case of ‘SS’, a Muslim lady 33 years married to a staunch Hindu male after having an affair for 6 years presenting in the OPD with recurrent suicidal thoughts for last 4 months with one failed attempt. She comes from a broken family. From her childhood she had seen her father regularly abusing her mother verbally and physically. Her mother separated when she was just 15 years and remarried. After one year of separation SS lost her biological father in a train accident which had affected her greatly.

After that loss, she ran away from her mom and stepfather and was staying alone when she met her present husband. After marriage her husband was also found to be very abusive verbally and physically and did not allow her to eat non-veg, neither was she allowed to do her regular namaz prayers. Recently she found her husband having an extra-marital affair that triggered the suicidal attempt. Her platelet serotonin was found to be very low and she was prescribed SSRI and antipsychotics.

Results: Leaving aside the natural calamities, aberrant/unsocial behaviours in the society mostly go unnoticed or not given the due importance until a grave crime is committed or the victims who are subjected to these sort of behaviours, by some reason or rather, themselves develop mental health issues.

Thus the preventable cause and effect factors are usually overlooked and treatment is targeted only to the affected patients. This causes a huge gap in the management of mental health issues in the society at large which seems to be increasing day by day.

Conclusion: Routine platelet serotonin test may help to unearth the hidden players with no insight causing unsocial and maleficent behaviours and thus affecting unwary family members or anyone outside coming in contact with them. Until and unless we cater to these predisposing and/or precipitating factors leading to mental stress, good mental health of the global society remains a myth.

*No financial sponsorship was taken in this case study.

Aims: Some language which is now used day-to-day appears to be built upon the foundations of mental illness, such as “I am going to kill myself” or “I’m so OCD about things”. However, these phrases seem to be brushed past in so many social situations. Two years ago, I attempted suicide during a particularly difficult period of my life. My experiences have made me more perceptive of this language heard in everyday conversations. This case study aims to spark early discussions around why this language has become so common and the impact that this has on the identity and spiritual well-being of individuals affected by mental illness.

Methods: This is an individual self-reflective case study of my own lived experiences. It embraces reflexivity as a method to understand one’s own thoughts both past and present. During the depths of my depression, hearing others use this language made me believe that suicidal thoughts were a normal part of being human, delaying my pursuit of any mental health support. Conversely, after my suicide attempt, such language left me feeling isolated, triggering vivid flashbacks. My journey to recovery has frequently been overtaken by thoughts that my past mental health is what solely defines me as a person.

Results: This case study proposes that the increasing use of statements like ‘I am going to kill myself’ reflects a deeper societal need for connection to others, yet it also diminishes autonomy over when and how individuals process their own mental and spiritual experiences. Overcoming mental illness is a difficult battle, often shaking one’s sense of purpose in life. Reflecting on these experiences is essential for growth, but our society must help create a mindful and respectful space for this to happen.

Conclusion: A single case study goes a long way in proving that at least one individual has been affected by the use of mental health phrases by others. Whether that is the case for every person who has been mentally unwell at some point in their life or not, it is important to raise awareness of the negative setbacks it can have for vulnerable individuals. Further research should aim to recruit more participants affected by mental illness, gathering more evidence to either support or challenge the findings of this case study.

Aims: Catatonia is a neuropsychiatric syndrome characterized by a paucity of movement and speech. Benzodiazepines are the mainstay of treatment for catatonia, but a subset of patients do not respond. While electroconvulsive therapy is another treatment option for catatonia, access can be limited. This case report discusses the use of zolpidem, a hypnotic non-benzodiazepine GABA-A receptor modulator, in a patient with benzodiazepine-resistant catatonia.

Methods: A 19-year-old male presented to a hospital in the United States from jail custody with altered mental status. His medical history was notable for psychosis with paranoid delusions and severe catatonia.

The patient reportedly had severely reduced oral intake for the past month, with almost no intake at all in the prior eight days. His presentation, which included psychomotor retardation, mutism, and posturing, raised a high clinical suspicion for catatonia.

Initial treatment with 1 mg of lorazepam every 6 hours was ineffective, and the patient developed tachycardia, raising concern for malignant catatonia. At this time, his differential diagnosis included schizophrenia. His treatment regimen was adjusted to include olanzapine for suspected schizophrenia, memantine for catatonia treatment augmentation, and metoprolol for tachycardia. Despite this regimen, along with escalating lorazepam doses up to 7 mg three times daily, the patient remained severely catatonic. A trial of clozapine also failed to yield significant improvement.

Given the patient’s limited response to benzodiazepines, zolpidem was introduced. He showed rapid improvement in his catatonic symptoms, including markedly improved speech, oral intake, and overall participation. Zolpidem was dosed throughout the day to limit drowsiness. By day 30, the patient demonstrated substantial recovery, with minimal catatonic symptoms and improved engagement in daily activities. He was discharged home on a regimen of zolpidem, clozapine, and memantine.

Results: A subset of patients with catatonia fail to respond to benzodiazepines, necessitating alternative treatments. Prompt intervention is crucial due to the life-threatening nature of catatonia and its numerous complications. While electroconvulsive therapy is often effective, its availability can be limited. Zolpidem, acting through a distinct mechanism of GABA-A receptor subunit binding, may offer an effective alternative for benzodiazepine-resistant cases.

Conclusion: Further research into zolpidem and other alternative therapies for catatonia is warranted, especially in settings where electroconvulsive therapy is not accessible. Zolpidem’s potential as a treatment for benzodiazepine-refractory catatonia deserves further investigation.

Aims: ECT is a well-evidenced, cost-effective intervention for treatment-resistant depression. In Ireland acute (twice-weekly) outpatient ECT for depression has not been reported, though common elsewhere. Ireland has among the lowest number of inpatient psychiatry beds per person in Europe. We observed a clinical need for acute outpatient ECT for people who could not access elective inpatient care.

Methods: All cases provided written informed consent. A multidisciplinary (psychiatry, anaesthesiology, nursing) protocol for assessment and delivery of acute outpatient ECT was developed and implemented, cases described and feedback from stakeholders sought in an acceptability forum.

Results: Four medically stable patients (ASA Grades 2) completed acute outpatient ECT, receiving between n=6 and n=14 ECT treatments, attending from home. N=140 inpatient psychiatry bed days were saved, and n=45 community psychiatry reviews were required. No adverse events or medical interventions occurred. Three people had CGI outcome of “very much improved” and one person halted their treatment course when “minimally improved”, citing lack of response. Stakeholder feedback in an acceptability forum highlighted the increased resource intensity of twice weekly community review for outpatient ECT, and the positive outcomes for treatment-resistant depression.

Conclusion: Acute outpatient ECT was safe and effective in this case series and resulted in n=140 psychiatry inpatient bed days being saved. There was an increased need for reviews from the community team during the treatment protocol. Medically stable patients with substantial social support were eligible for this pilot phase, thus a priority for future development must be equity of access to this effective intervention.

Aims: Creutzfeldt–Jakob Disease (CJD) is a rare, fatal neurodegenerative disorder caused by prion proteins, leading to progressive brain damage. CJD has sporadic, variant, genetic, and iatrogenic forms, with sporadic being the most common, affecting 1–2 people per million annually. It typically presents with rapid cognitive decline, motor dysfunction, and personality changes, with no effective treatment available.

Methods: A 59-year-old physically fit, male with no past medical history presented to A&E with a two-week history of behavioural changes, aggression, left facial droop, disorientation, poor coordination, and mild dysarthria. He had repetitive speech and his GCS on admission was 14/15.

Stroke was suspected and CT scan showed hypoattenuation of the right frontal lobe. Contrast MRI showed multifocal areas of gyriform diffusion restriction affecting bilateral cerebral hemispheres. Initial differential diagnoses were stroke, vasogenic oedema, old brain injury, post-ictal changes, encephalitis.

EEG and initial blood tests were normal. CSF analysis revealed elevated proteins, normal glucose and lactate and no oligoclonal bands. CSF virology and cultures were negative. A protein assay from specialist services in Edinburgh confirmed a diagnosis of sporadic CJD.

The patient was discharged to a care home with clonazepam and a plan to introduce low-dose quetiapine if needed. Upon transfer, he became increasingly agitated, displaying verbal and physical aggression towards staff and residents, wandering and damaging property. His sleep was poor, and his aggression unpredictable, escalating late in the evening.

The care home implemented a low-stimulus environment with one-to-one care and covert medication administration. Initially treated with quetiapine and benzodiazepines, his aggression persisted, prompting introduction of haloperidol, which resulted in some reduction in aggression. He was later transferred to an inpatient ward.

On the ward, his dysphasia worsened, but he had no further behavioural challenges. He received regular physiotherapy, occupational therapy and specialised nursing care. Parkinsonism symptoms prompted the discontinuation of haloperidol, which was later reinstated at a lower dose due to return of restlessness. Quetiapine was gradually tapered off. At discharge, he was compliant with medication, required assistance with feeding and personal care, had severe dysphasia and some ataxia.

Results: This case demonstrates the atypical presentation of CJD with neuropsychiatric symptoms at onset, rather than the usual neurological signs. The patient’s agitation and aggression required careful pharmacological adjustments and highlighted challenges in managing CJD’s neuropsychiatric symptoms.

Conclusion: This case highlights the importance of considering CJD in the differential diagnosis for patients with rapid-onset neuropsychiatric disturbances. Early recognition and symptomatic management, although not curative, can improve the patient’s quality of life during the disease’s progression.

Aims: A 45-year-old Afro-Caribbean male with a history of paranoid schizophrenia, hypertension, Gilbert syndrome, epilepsy, vitamin D deficiency, mitral regurgitation, and penicillin allergy was admitted in March 2024 for clozapine titration following mental state deterioration. This was his first clozapine re-challenge since suspected clozapine-induced rhabdomyolysis in October 2022, during which CK levels had risen to 7442 IU/L, necessitating discontinuation.

Methods: Clinical findings: During titration in March 2024, CK levels rose to 7096 IU/L. The patient, engaging in vigorous exercise, reported mild myalgia but no severe symptoms or NMS.

Diagnostic focus: Clozapine-induced rhabdomyolysis was suspected. IV hydration was initiated, and CK levels decreased to 1500 IU/L after two days but later rose to 4500 IU/L. Clozapine was discontinued, and haloperidol was started, leading to CK normalization.

Second Re-challenge (August 2024): Re-challenged with clozapine, CK levels fluctuated but remained within acceptable limits (1016–833 IU/L), with no symptoms. The patient was encouraged to hydrate and avoid vigorous exercise.

Results: Clozapine is effective for treatment-resistant schizophrenia but risks rhabdomyolysis. The mechanism remains unclear but may involve direct myotoxicity or indirect factors like seizures. This case highlights the need for CK monitoring, especially during titration. Elevated CK levels exceeding 5000 IU/L necessitate clozapine discontinuation, IV hydration, and reassessment.

Re-challenging clozapine requires careful evaluation. This patient was successfully re-challenged under close monitoring with tailored CK testing, hydration, and activity recommendations. Vigilance and individualized care minimized risks while maintaining therapeutic benefits.

Conclusion: This case underscores the importance of routine CK monitoring, patient education, and interdisciplinary care during clozapine therapy, particularly in those with prior rhabdomyolysis. Personalized treatment strategies and adherence to evidence-based protocols ensure safety and optimize outcomes. Ethnicity- and sex-specific CK reference values should be developed to enhance clinical decision-making. Despite challenges, clozapine re-challenge is feasible with vigilant monitoring and risk mitigation strategies.

Aims: Background: Attention deficit hyperactivity disorder (ADHD) can present differently in adults and often goes misdiagnosed due to overlapping symptoms. Maladaptive daydreaming may also be misdiagnosed, as it shares similarities with dissociative symptoms, depersonalization, derealization, and temporal lobe epilepsy. Jasper has identified pseudohallucinations as akin to normal perception and occurring in the inner subjective space. Adults with ADHD often experience zoning out, daydreaming, and cognitive hyperactivity, which may resemble psychosis.

Methods: Case Report.

This case study highlights the relationship between pseudohallucinations, maladaptive daydreaming, and ADHD in adults. A 19-year-old patient with a childhood history of trauma and isolation presented with hallucinations that began at age eight and progressed over time. She reported hearing up to 50 voices, described as “good and friendly”.

The voices were connected to multiple families and included visual, tactile, and auditory modalities. She claimed she could touch, feel, and see them, identifying them as her friends. She sought guidance from these voices and communicated with most of them. The patient had good insight and understanding of her condition. She referred to these entities as imaginary beings that served as a coping mechanism for stress and loneliness. She experienced episodes of persistent zoning out, living in an imaginary world, and actively engaging in conversations with multiple internal voices. Depersonalization, derealization, and dissociation led to her isolation, adversely affecting her interactions with her real family and academic performance. She had been prescribed antidepressants to manage her anxiety and insomnia, but these were discontinued due to no response previously.

To rule out organic causes for her hallucinations, an MRI brain, EEG, and comprehensive tests were performed, which excluded epilepsy. An ADHD assessment was conducted using standardized tools and DSM–5 diagnostic criteria, leading to a diagnosis of ADHD combined type.

Results: After starting methylphenidate (Concerta 54 mg OD), the patient experienced significant resolution of symptoms, including improved focus and no daydreaming episodes resulting in the loss of internal voices. This sudden quietness caused distress and adjustment difficulties, triggering identity disruption due to her long-term reliance on these voices for emotional regulation. Dissociation and pseudohallucinations were reinterpreted as manifestations of cognitive inattention, emotional dysregulation, and an overactive inner monologue.

Conclusion: The internal voices were recognized as non-psychotic self-dialogue, a phenomenon observed in ADHD. Zoning out, daydreaming, and depersonalization were linked to severe attention deficit disorder. ADHD overlaps with dissociative symptoms, depersonalization, and pseudohallucinations. Understanding the diverse manifestations of ADHD is crucial for accurate diagnosis and effective management.

Aims: Background: Standard depression treatments often provide partial relief but fail to address the underlying cognitive and motivational deficits associated with undiagnosed comorbid Attention Deficit Hyperactivity Disorder (ADHD), leaving patients feeling stuck in an endless cycle of procrastination, fatigue, and low mood. This case study explores how a missed diagnosis can lead to years of failed depression treatment and how crucial the diagnosis of comorbid conditions in both depression and ADHD is.

Methods: Case report.

A 36-year-old health professional presented with chronic insomnia, severe anxiety, low motivation, and persistent depressive symptoms that significantly impacted his professional and academic performance. Despite multiple trials of SSRIs, SNRIs, and antipsychotic augmentation, he continued to struggle with procrastination, difficulty initiating tasks, and performance anxiety, leading to numerous exam failures resulting in low self-esteem, self-doubt, emotional exhaustion, and thoughts of self-harm.

He developed a dependence on clonazepam (4 mg daily) to manage his chronic insomnia, leading to anxiety. This led to cognitive clouding and emotional instability, which exacerbated his struggle with low motivation, attention, and memory difficulties. Insomnia, mind-wandering, forgetfulness, and irritability continued with poor response to medications. An ADHD assessment was conducted using DSM–5 diagnostic criteria, and diagnosis of Adult ADHD Combined Type was confirmed.

The patient was given a trial of Vyvanse (lisdexamfetamine) 30 mg initially and increased to 50 mg once daily, along with venlafaxine 150 mg OD. The introduction of the stimulant brought about a near-immediate improvement in the patient’s condition. He reported increased focus, motivation, and productivity. Procrastination decreased, leading to better academic performance, cognitive clarity, improved sleep, and emotional engagement, resulting in better treatment outcomes. The patient could gradually taper clonazepam and pass his post-graduate clinical exams. The patient responded to a combination of stimulant and antidepressant immediately and described the diagnosis as life-changing. This emphasised further the importance of looking for comorbid conditions while assessing any patient with treatment-resistant depression.

Results: Standard antidepressants alone can fail in addressing underlying causes like executive dysfunction and emotional dysregulation associated with undiagnosed Adult ADHD. Robust treatment plans should address both ADHD and any comorbid conditions. Conventional antidepressant treatment proved ineffective until the introduction of Vyvanse and venlafaxine, which highlights the need for ADHD screening in individuals with persistent depression.

Conclusion: Comorbid conditions such as depression and anxiety in Adult ADHD can further complicate recognition and proper management, leading to symptom masking and misdiagnosis. The negative impact of undiagnosed and untreated adult ADHD is multifaceted, affecting education, employment, career, and financial stability.

Aims: Delusional parasitosis, first described by Karl Ekbom in the 1930s, is a rare psychiatric disorder characterised by a persistent, false belief of parasitic infestation. The condition is typically classified into three categories: primary, secondary and organic. Primary delusional parasitosis arises in the absence of any other psychiatric or medical condition, while secondary and organic forms are associated with underlying psychiatric disorders or organic diseases. Here, we present the case of a 50-year-old male with a history of crack cocaine use, previously unknown to mental health services, presenting to our drug treatment centre with delusions of infestation.

Methods: Mr A, a 50-year-old male with a 20-year history of crack cocaine use, was referred for psychiatric review by his keyworker after expressing unusual beliefs. He had been engaged in treatment for his substance use for the past year. During this period, he disclosed a persistent belief that he had contracted a parasitic infection in his gastrointestinal tract, which he attributed to consuming sashimi during a trip to Cambodia a decade ago. He described feeling worms moving within his abdomen, with heightened nocturnal activity that disrupted his sleep. His appetite was affected by fear of worsening the infestation, though no significant weight loss was noted. His mental state exam revealed no signs of thought disorder, additional delusions or perceptual disturbances. His cognitive function, social interactions, and self-care remained intact. Despite reassurance that repeated blood tests and abdominal ultrasound scans showed no abnormalities, his delusions persisted.

Results: Substance misuse, particularly with stimulants such as cocaine and amphetamine, is a well-established risk factor for delusional parasitosis. Chronic stimulant use can result in a dysregulated dopamine system, contributing to psychotic symptoms. In Mr A’s case, his long history of crack cocaine use is considered the primary contributing factor to his condition. While delusional parasitosis is typically associated with delusions of skin infestation, this case is notable for its gastrointestinal presentation, which is considerably rarer. Importantly, there was no indication that there were other contributory psychiatric or organic factors.

Conclusion: The management of delusional parasitosis requires a holistic, multidisciplinary approach. It is important for health professionals to address the patient’s beliefs with empathy to promote trust and encourage engagement. Addiction services continue to support Mr A’s efforts to reduce cocaine use, while mental health services have initiated antipsychotic treatment and are providing psychological therapy. Early indications suggest a positive response to this integrated treatment plan.

Aims: Thyrotoxicosis is caused by an overactive thyroid gland, leading to excessive production and release of thyroid hormones into the bloodstream. The most common cause is Grave’s disease. Presentation of Grave’s disease with neurological and psychiatric symptoms as first line is rare; however it can lead to mis-diagnosis of a primary psychiatric condition, especially in younger patients. This report illustrates the case of a 24-year-old female presenting with psychotic symptoms on a background of undiagnosed Grave’s disease.

Methods: Case report.

A 24-year-old lady was brought to A&E due to an abrupt change in behaviour, with confusion, bizarre speech, attempts to run on the street, aggression and insomnia. At assessment, she presented with thought disorder, thought block and derealisation phenomena. She was physically well, with only some mild diarrhoea. Routine blood tests were done at initial presentation, but this did not include thyroid function tests. She was detained under the Mental Health Act and transferred to a psychiatric ward. Thyroid function tests revealed an extremely high thyroid hormone level and presence of thyroid receptor antibodies. She was started on carbimazole and propranolol and her psychotic symptoms improved markedly without antipsychotic medication. In the next few months, however, her psychiatric symptoms returned and she required further treatment in hospital as well as commencement of risperidone, an antipsychotic. There was much debate between psychiatry and endocrine teams about the appropriate place of her care and the legal framework for a young woman who lacked capacity to consent to treatment due to an organic psychosis.

Results: Albeit rarely, hyperthyroidism can present with acute onset disorientation which can be misdiagnosed as a primary psychiatric disorder. Prompt treatment of hyperthyroidism with antithyroid medications is crucial for mitigating psychiatric symptoms, but it may take several weeks to months for thyroid hormones to return to baseline. The use of antipsychotics should be considered for symptom management; the dose and duration of treatment will depend on the time needed for return to euthyroid state, severity of symptoms and persistence of psychotic symptoms after correction of thyroid balance. Close collaboration between psychiatrists and endocrinologists is essential for the patient to receive the best quality care. Involving the patient and their family in care is equally important to support recovery in the longer term.

Conclusion: This case highlights the importance of considering organic causes in patients presenting with psychiatric symptoms.

Aims: Bruxism is a stereotyped movement disorder of tooth grinding or clenching. Unlike sleep bruxism, awake bruxism is not a sleep disorder, but is secondary to disorders of the central nervous system, such as Parkinson’s disease, stroke and advanced dementia. We report a case of debilitating awake bruxism that developed during the course of Alzheimer’s dementia, unrelated to neuroleptic use.

Methods: A 63-year-old man presented to our outpatient clinic of a tertiary care hospital in India, with a 4-year history of progressive short-term memory loss, increasing apathy and a constant audible teeth grinding in the day, which distracted him from social interaction. He was not taking any medications. Examination demonstrated phasic teeth grinding and extensive teeth wearing, but no extrapyramidal features or transient hypertonicity induced by distraction. Mini-Mental State Examination (MMSE) score was 15 out of 30. The psychometric testing was consistent with moderate dementia of Alzheimer’s type. Computed tomography revealed age-related cerebral atrophy.

Results: Donepezil 5 mg was initiated and subsequently increased to 10 mg for Alzheimer’s dementia improved MMSE to 20 three months after commencement. Quetiapine was prescribed for the bruxism. The patient reported a complete disappearance of awake bruxism at a daily dose of quetiapine 100 mg, with no occlusal appliances.

The biochemical origin of bruxism involves complicated interactions of various neurotransmitters. A central role of the dopaminergic system in awake bruxism was suggested from clinical observations in patients with Parkinson’s disease and attenuation of symptoms with dopaminergic medications. A favourable response to quetiapine in the present patient suggests that bruxism in dementia might also involve the dopaminergic pathway.

Conclusion: A 63-year-old male treated with 100 mg daily doses of quetiapine for Alzheimer’s dementia experienced a significant reduction of awake bruxism. More studies are needed to determine whether quetiapine has a long-term effect against awake bruxism.