16 year old male with previous diagnoses of autism spectrum disorder and severe anxiety disorder was referred to Child and Adolescent Mental Health Services (CAMHS). His presentation included increasing anxiety, difficulty articulating his thoughts and emotions, difficulty completing tasks, school non-attendance, reduced food intake and possible auditory hallucinations. Risperidone was trialled in the community however refused after 5 days due to “brain fog”. He was seen by CAMHS community team twice weekly for 3 months prior to his emergency detained admission to adolescent psychiatric inpatient unit, due to no oral intake for 72 hours.

Family history included schizophrenia, bipolar disorder, depression and anxiety.

Upon admission, symptoms observed included reduced verbal communication, psychomotor retardation, low mood, agitation, sleep difficulties, ambitendency, echolalia and poor oral intake. He had a Bush-Francis rating score of 8 and given a working diagnosis of catatonia. He responded positively to a lorazepam challenge therefore commenced on 1mg of lorazepam twice daily. Despite increasing doses, the catatonia worsened with severe psychomotor retardation, “psychological pillow” and nil food or fluid intake with Bush Francis score of 18. ECT was arranged as an emergency treatment but put on hold while tolerating all food and fluids requirements via nasogastric tube. Lorazepam dose was titrated to 3mg three times daily but signs seen of benzodiazepine toxicity therefore dose was reduced and ECT arranged for treatment resistance. Improvement seen on reduced dose prior to receiving ECT, therefore ECT put on hold again. His lorazepam dose was titrated up at a slower rate to 4mg three times daily which he was able to tolerate. His catatonia fully resolved at 12mg. Once stable, lorazepam dose was very gradually decreased until stopped. No evidence of catatonia returned.

Medical and psychiatric causes of catatonia were explored.

Two positive blood anti-NMDA receptor tests two months apart; both 1/10 titre. This was discussed with the specialist neurology team in Oxford who advised this was an incidental finding with no clinical implication (1% of healthy population are positive).

Throughout admission, possible fleeting psychotic and depressive symptoms were noted, including not trusting food, hallucinations, worries about contamination and apathetic mood. However, these all improved as the catatonia was treated.

There was no clear underlying psychiatric or medical illness identified as a cause of the patient’s catatonia. Catatonia has a higher prevalence in people with autism. At discharge he was well and reintegrated back to community life without requiring further medication.

A recent Cochrane review published in December 2023 concluded that “no trials found that interventions to reduce anticholinergic burden led to any other improvements in cognition compared to usual care”. We describe the case of a 62-year-old lady who developed significant cognitive decline following the initiation of a low dose of procyclidine, which was rapidly reversed upon stopping the medication.

We present the case of a 62-year-old lady with a diagnosis of schizo-affective disorder, whose symptoms had been stabilized on a regime of lithium carbonate 500mg nocte, sulpiride 400mg BD and fluoxetine 20mg OD. When the patient presented to the outpatient clinic, she was noted to have bilateral coarse tremors and slight cogwheel rigidity. Procyclidine was started at a dose of 5mg OD to manage these extrapyramidal side-effects.

Following this, family members reported that the patient had difficulty initiating and following conversations. Short-term memory was affected and she was observed to have reduced attention span. These problems were reportedly getting worse with time, with a simultaneous decline in functional abilities. She was no longer able to carry out her daily shop, and family members ensured that she was no longer driving as they had concerns about her road safety. She stopped taking procyclidine after 1 month and notably, these problems ceased within one week of stopping the medication.

Cognitive testing confirmed that the patient was cognitively intact after procyclidine was stopped. The patient scored 96 on the ‘Addenbrooke's Cognitive Examination’ scale, which falls within the normal range. The ‘Instrumental Activities of Daily Living’ scale was administered to assess functioning at the time of the cognitive impairment. This returned a score of 1/8, indicating that there was significant functional impairment secondary to cognitive impairment when prescribed procyclidine. The ‘Informant Questionnaire on Cognitive Decline in the Elderly’ was administered to objectively quantify the extent of cognitive decline as noted by family. This returned a score of 4.3, confirming that the patient's cognition had indeed been worse when compared with her baseline.

Our case report highlights the rapid improvement in cognition with the removal of anticholinergic burden in a 62-year-old female. Our report can, therefore, be a harbinger for more robust trials to determine the efficacy of interventions to reduce anticholinergic burden in preserving or improving cognition.

It is important to monitor for any change in cognition when prescribing anticholinergic medication in at-risk individuals.

Ornithine transcarbamylase (OTC) is an enzyme of the urea cycle catalyzing the condensation of carbamyl phosphate and ornithine to form citrulline. OTC deficiency leads to elevated serum ammonia and presents as different neurological or psychiatric symptoms. OTC deficiency is an X-linked inborn error of metabolism and most cases occur in neonatal period with severe presentation. Lesser known is the late-onset form that remains latent from infancy and only presents with intriguing symptoms mimicking psychiatric disease in adulthood.

Case report.

We describe a case of adult-onset OTC deficiency in a 40-year-old man with borderline intellectual functioning and a psychotic episode following a protein rich meal. The case was first diagnosed as undifferentiated schizophrenia, until the genetic study was carried out.

Awareness of the adult onset ornithine transcarbamylase deficiency being a rare but possible differential diagnosis in a patient with acute psychiatric symptoms with hyperammonemia. Organic causes such as cerebral, metabolic, toxic causes of psychosis should be actively sought especially when encountering cases of acute psychosis.

Capgras syndrome is the most common of the delusional misidentification syndromes. It is characterised by the delusional belief that a familiar person has been replaced by an identical imposter. Capgras syndrome is associated with functional conditions, like psychosis, but also with a range of organic conditions such as dementia, brain injury and Parkinson's disease.

The COVID-19 pandemic created a unique situation where patients were unable to see their relatives in person, resulting in their only form of contact being via telephone or virtually.

We present a case of a 70 year old lady Mrs W, who was admitted with first episode psychosis. She developed Capgras syndrome during her admission, based purely in the auditory modality of talking to her husband on the telephone. She was firm in her conviction that he was an imposter, mainly based of ‘a different tone’ and using ‘different words’. Showing a photograph of her husband was met with full and appropriate recognition. Given that a significant minority of elderly patients with a Capgras delusion have an organic aetiology, neuroimaging and extended laboratory investigations, including auto-antibodies for limbic encephalitis, were performed which were unremarkable.

With psychotropic medication, the Capgras delusion resolved, and on discharge she recognised her husband when they met again.

The aetiology of Capgras syndrome remains unclear, although a range of causes have been suggested. Early psychodynamic theories related to conflict between love and hate towards the relative, which could be relevant in functional conditions but may have less significance in organic conditions.

Other theories examine Capgras syndrome as a mirror of prosopagnosia, where people have difficulties recognising familiar faces. This would indicate a pathological process affecting visual pathways. However, our case challenges this theory, suggesting that deficits in other sensory modality pathways may also contribute.

Although rare, our case is not entirely unique; several cases of Capgras syndrome in people with blindness have been reported. However, our case differs in that our patient was able to recognise photos of her husband despite misidentification based on auditory cues. As Mrs W did not have visual impairment, it is unclear if she would have presented with the more classical visual misidentification in the absence of the unique circumstances of the COVID-19 pandemic.

Capgras syndrome is classically associated with misidentification based on visual cues, however a growing number of case reports challenge this. Further investigation is required to create theories that encompass other sensory modalities.

Attention Deficit Hyperactivity Disorder (ADHD), is a neurodevelopmental condition affecting both children and adults, with a global prevalence estimated to be around 5% in children and 2.5% in adults, significantly impacting daily functioning, academic performance, and interpersonal relationships.

Glycogen Storage Disease Type 1A (GSD1A) is a rare metabolic disorder that occurs in approximately 1 in 100,000 births. It is characterized by accumulation of excessive glycogen and fat in the liver and kidneys that can result in growth retardation.

The aim is to increase knowledge of pharmacological management of ADHD in patients with GSD1A.

Our patient is a 16-year-old boy with both diagnoses of GSD1A and ADHD.

GSD1A is treated with a special diet of frequent small servings of carbohydrates which must be maintained day and night throughout life, given via PEG tube.

ADHD symptoms cause functional impairment and affecting his school attainment requiring treatment. However, stimulant medication, such as methylphenidate, which are first- and second-line treatments, can cause appetite suppression that would increase the risk of fatal hypoglycaemia in GSD1A.

The literature review of case reviews with similar presentations, aiming to confirm the absence of contraindications for prescribing methylphenidate in patients with GSD1A, showed no identified contraindications, and relevant papers were not found.

Collaboration with the metabolic disorders team at Great Ormond Street Hospital was established to verify the absence of contraindications and facilitate potential adjustments to feeds if necessary.

Short-acting methylphenidate was administered to mitigate appetite suppression and enable prompt reversal of potential side effects, owing to its brief half-life. This approach also aimed to facilitate regular dietary intake.

Gradual bi-weekly dosage increments of 5mg, coupled with vigilant side-effect monitoring, lead to enhanced attention and concentration, ultimately contributing to improved school attainment.

Trial of short acting methylphenidate to ensure limited appetite suppression and allow opportunities for regular dietary intake. Slow dose titrations and weekly monitoring for response and side effects is vital. This young man's ADHD was successfully and safely treated.

This case shows that with careful liaison and planning, methylphenidate can be safely prescribed to patients with GSD1A. Our experiences show that using short-acting preparations of methylphenidate initially allows slow and careful titrations.

Restorative justice (RJ) is the process of bringing together offender and victim in the aftermath of an offence. Handled correctly, there can be substantial benefits for both parties. Communication is typically direct with an RJ facilitator from the criminal justice system, but the Crown Prosecution Service makes reference to the option of “shuttle mediation”, with the RJ facilitator relaying information indirectly between parties.

The use of RJ in forensic psychiatry has been limited, with reasons including concern for the patient offender's vulnerability, impact on their mental state from the stress of facing their victim, and unpredictability of response. Adaptation of the “shuttle mediation” model with use of a trusted mental health professional may help to overcome many such obstacles.

Patient A committed his index offence of murder at age 22. During his mandatory life sentence, he developed schizophrenia and was transferred to a secure hospital. His illness proved treatment resistant and many years passed before he was discharged to the community on life licence following Parole Board release. Although generally stable, he was easily overwhelmed by stressful situations, in which he could struggle to articulate his thoughts.

His victim’s wife and daughter enquired about the possibility of restorative justice. A's probation officer liaised with A's consultant psychiatrist. A was considered unsuitable for direct approach, but following discussion with an RJ facilitator, a proxy model was agreed upon. This was based on shuttle mediation but with the consultant psychiatrist acting as shuttle, or proxy, for A.

The aims of the family were elicited in advance. Capacitous consent to information sharing was obtained from A, with boundaries of what would be shared clearly agreed. Information A wished to share with the family was established, including verbatim quotes.

Following the RJ meeting, feedback from the victim's family and A was strongly positive. The victim's family reported a sense of peace and closure from the experience. A's longstanding anxiety, with feelings of guilt and self-blame reduced. Both parties expressed gratitude for the meeting and did not find the use of a proxy negated the benefits of the experience.

This case report demonstrates that a proxy model of restorative justice is feasible and can be successful for patient offenders with severe and enduring mental disorder. The potential benefits to patient and victim suggest that it could be considered more widely as an option in forensic psychiatry settings.

The scandal of sub-postmasters wrongly accused by the post office of offences relating to the faulty IT Horizon system is of ongoing media prominence.

Since May 2021 I have undertaken personal injury medico legal assessments at the request of a solicitor representing those falsely accused and convicted of offences by the post office. Their convictions had been quashed in the court of appeal.

I interviewed fourteen individuals, age range 35 to 70 years, five women and nine men. Ten had brought claims for Malicious Prosecution. The remaining four sub-postmasters were part of the historical financial shortfalls scheme set up for those who had not been prosecuted but were applying for compensation.

Of the ten convicted sub-postmasters, four spent periods in prison and the remaining six were given suspended or community sentences. Those in prison were often separated from young children by distance or withholding family members.

I assessed to what extent and in what way their mental health and that of their families had been adversely affected as a result of their experiences.

Assessments were undertaken remotely, including speaking with a family member.

ICD 10 diagnostic criteria were used.

All of the cases revealed evidence of psychopathology at the time of the allegations or convictions and continued to varying degrees subsequently.

A diagnosis of PTSD was made in five cases, Adjustment Disorder in 2 cases, Dysthymia in one case and depressive illness in eight cases. In only four cases had the disorders resolved.

Four of the five cases of PTSD had evidence of a past psychiatric history prior to becoming sub-postmasters. Past history included depression, impulsive overdose, eating disorder, problems related to gambling and abuse of alcohol and cocaine.

Both sub-postmasters who had been accused of taking money due to faulty software and those who had been wrongly convicted had high rates of psychopathology.

These findings are consistent with the only other study of the psychological effects on sub-postmasters which found high rates of psychopathology in both accused and convicted individuals.

Existing diagnostic criteria were limited in capturing the suffering of individuals who had endured such complex trauma so a narrative description including the effects on family members was also used.

This study of the mental health of falsely accused sub-postmasters demonstrates a high degree of psychopathology which may require therapeutic intervention.

Self-harm affects around 20% of all young people in the UK. Treatment options for self-harm remain limited and those available are either non-specific or long and costly and may not suit all young people. There is an urgent need to develop new scalable interventions to address this gap.

Imaginator is a novel imagery-based intervention targeting self-harm initially developed for 16–25-year-olds. It is a blended digital intervention delivering Functional Imagery Training (FIT) via therapist sessions and a smartphone app. In this study we piloted a new version of Imaginator extended to adolescents from age 12 after co-producing a new app with a diverse group of young people experts-by-experience.

We aimed to assess feasibility of delivering Imaginator in Children and Adolescent Mental Health Services (CAMHS) and adult secondary mental health services and gather young people's feedback on the intervention

Participants were recruited from West London NHS Trust Tier 2 CAMHS and adult Mental health Integrated Network Teams (MINT) teams. They underwent a baseline screening and were allocated to a therapist for three face-to-face FIT sessions in which the app was introduced followed by five phone support sessions. Outcome assessments were conducted after completing therapy, approximately 3-months post-baseline, including questionnaire measures and a qualitative feedback interview.

Qualitative data were analysed using a co-produced thematic analysis method with lived experience co-researchers.

Thirty-four participants were referred (31 female, 2 male, 1 transgender; mean age = 18.4), of which 30 met inclusion criteria and completed screening. Out of 25 who started therapy 16 completed the intervention. Only 15 completed the quantitative outcome assessment, and 10 the interviews. There was an overall reduction in number of self-harm episodes over 3-months from pre- to post-intervention

Five main themes were identified: Imaginator therapy impact, mental imagery acceptability and efficacy, usefulness and usability of the app, integration of the app in therapy and need for improvements. Young people found Imaginator helpful at improving their mental health, in particular the use of mental imagery techniques. The app was overall well received but improvements were suggested.

Our study suggests that Imaginator can be extended to adolescents, is acceptable and has potential as a brief intervention reducing self-harm in young people under mental health services. A future RCT is needed to robustly test the intervention efficacy, after considering issues around high attrition in outcome measures.

The aim of this study is to explore the off-label use of atropine, administered sublingually, for the management of clozapine-induced sialorrhea in a patient who showed inadequate response to commonly used agents. The investigation stems from a clinical scenario where traditional approaches failed, prompting an exploration of alternative and cost-effective options to alleviate sialorrhea associated with clozapine therapy in a patient of lower socio-economic status.

Mr. A, a 29-year-old with bipolar affective disorder, experienced persistent sialorrhea during clozapine treatment, resistant to trials with trihexyphenidyl and glycopyrrolate. Following a brief discontinuation of clozapine, the patient relapsed into a manic episode, leading to hospitalization. Despite the re-initiation of clozapine, sialorrhea reoccurred. Various doses and combinations of trihexyphenidyl and glycopyrrolate were ineffective, with affordability issues limiting the latter. As sialorrhea persisted, clozapine dose reduction was necessary. Attempts with different antipsychotics were made, and valproate sodium was increased, but sialorrhea remained problematic.

Given the patient's unique case and previous medication failures, an off-label use of atropine via a sublingual route was done after obtaining informed consent. Quantitative measurement of sialorrhea was conducted using a sialometry machine. The patient underwent a trial with sublingual atropine drops, and the salivary rate significantly decreased, indicating a potential efficacy in managing clozapine-induced sialorrhea.

The discussion encompasses the challenges faced in managing clozapine-induced sialorrhea in the presented case. Traditional agents, including glycopyrrolate and trihexyphenidyl, proved ineffective or were hindered by affordability issues. The subsequent reduction of clozapine dose compromised overall treatment efficacy. The introduction of atropine eye drops via sublingual administration emerged as a novel approach, demonstrating a reduction in salivary rate without notable adverse effects except elevated heart rate 2 hours after administration of atropine. The unique pharmacological properties of atropine, despite being an off-label use, provided a potential avenue for addressing persistent sialorrhea.

In conclusion, the off-label use of atropine via the sublingual route showed promise in alleviating clozapine-induced sialorrhea in this particular case. Despite demonstrable efficacy in pre and post-sialometry, the clinical challenges and practical considerations associated with atropine's use in this context raise concerns. The case underscores the need for alternative strategies in managing medication-induced side effects, especially when standard interventions fail. Further research is warranted to explore the broader applicability and safety of this approach in a larger cohort.

Anxiety disorders are common in Autistic Spectrum Disorder (ASD) patients. There are limited resources dedicated to ASD and mental health services are not equipped to adapt assessment and treatment protocols to address their needs. Adaptations to diagnosis and treatment are discussed in a single case study of an autistic patient with anxiety disorders. In addition, effectiveness of providing adapted versus standard treatment is evaluated.

This study describes a 45-year-old, single, employed male diagnosed as autistic at age 37. He was referred for a second course of Cognitive Behavioural Therapy (CBT) for anxiety disorders consisting of agoraphobia with panic; blood injury phobia; needle phobia; dental phobia; claustrophobia. The duration of symptoms was 35 years. The main impairments to functioning were inability to use public transport; attending healthcare appointments; going to public places; returning to office-based working.

Questionnaires routinely completed at assessment and end of treatment: Montgomery–Åsberg Depression Rating Scale (MADRS); Beck's Anxiety Inventory (BAI); Beck's Depression Inventory (BDI). Adapted treatment with CBT included an extended assessment which helped differentiate anxiety symptoms from ASD. Main CBT adaptations included development of skills for the patient to identify and express emotional experiences and thoughts with the focus on physical sensations and behaviour. Graded exposure items were linked to concrete aims or interests and structured to fit around the patient's routine daily activities. Clinical data was analysed and compared outcomes from the initial standard and subsequent adapted treatment.

The patient's response to the initial course of standard CBT showed a 14% increase in anxiety and 14% increase in symptoms of depression on self-rated measures. The subsequent adapted CBT showed a 31% improvement in anxiety and a 16% improvement in symptoms of depression on self-rated measures.

This case report supports literature describing the need to adapt standard assessment and treatment to differentiate experiences related to ASD from discrete anxiety disorders, although there may be some overlap. The promising results support using adapted CBT to ensure appropriate treatment of anxiety disorders in autistic people.

Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder characterised by a pathologically prolonged CAG nucleotide sequence in the huntingtin gene (HTT). Neuropsychiatric symptoms such as aggression, depression, impulsivity and psychosis are non-motor signs of HD. The association between HD and criminal behaviour is debated, and evidence lacking. This is particularly relevant in forensic psychiatry, which focusses on the risk assessment of mentally disordered offenders. This manuscript examines the antecedents of offending behaviour in a male diagnosed with HD during admission to a high secure unit, and the evolution of his risk profile from childhood to post-diagnosis. Additionally, through exploration of psychopharmacological management of psychiatric symptoms in HD, this study aims to further our understanding as to how we can best support people with HD in a forensic mental health setting.

Following review of relevant literature on criminal behaviour in the context of HD, we report the case of a 41-year-old man with a background of dissocial personality traits admitted to a high security unit with symptoms of a delusional disorder; manifesting as paranoia, delusional beliefs and aggression. These were believed to be organically induced within the context of HD, a diagnosis confirmed through genetic testing six months following admission. The patient's symptoms were only partially responsive to first-line antipsychotics; however, good symptomatic control was achieved with clozapine and sodium valproate, enabling step-down to medium secure specialist services.

In HD patients, there may be a challenge of discerning whether offending behaviour relates to prodromal presentation or whether there are pre-existing antisocial attitudes or behaviour; an uncertainty which was present in this case and within the literature. The age of HD onset is inversely correlated with CAG repeat length, and a longer repeat length has been associated with criminal behaviour. This has the potential for use as a marker to determine the time point in which presenting features are attributable to HD. In this case study it was possible to determine through analysis of the CAG repeat length that the delusional disorder was likely linked to the onset of HD; however, dissocial personality traits were not.

A patient's background relating to the life-course persistence of violence, suicidality and psychiatric symptoms in patients with HD informs the process of formulating their risk profile. Changes to the risk profile also reflect the progressing stages of HD. This highlights the need for awareness of how HD may contribute or predispose to criminal behaviour and how interventions could be targeted during critical periods where they benefit most.

Huntington’s disease (HD) is a rare inherited disease in an autosomal dominant pattern, that is most prevalent among Caucasians.

Juvenile onset Huntington disease (JHD) is a rare subtype of the disease, defined by presence of the disease by the age of 20 or younger.

We report a case of a 28-year-old woman with JHD and discuss the challenges we faced in her diagnosis and management.

A now 28-year-old Arab woman, presented to the psychiatric hospital when she was an 18-year-old, complaining of restlessness and low mood. She was diagnosed to be having social phobia and panic attacks, and was given escitalopram. About 6 months after her first presentation, the patient's mother showed up reporting that the patient is doing well without the medication and that she is not going to take them anymore. However, the patient started developing anxiety symptoms two years later and started taking the same medication. Moreover, three years after her first presentation, the patient started developing movement symptoms and mentioned that her father passed away by Huntington's disease. The patient was immediately referred to a genetic lab and a Huntington disease diagnosis was given along with tetrabenazine and risperidone. Moreover, the patient attempted suicide multiple times after worsening of symptoms over the years. A brain magnetic resonance imaging of the patient showed bilateral caudate nuclei atrophy with similar changes affecting the putamen as well but to a lesser extent, changes that are associated with Huntington's disease.

Juvenile onset Huntington disease is rare, especially among people who are not of European ancestry. Therefore, clinicians are not likely to suspect the illness at an early stage. Late diagnosis not only can prevent patients from receiving the symptomatic treatments that they need, but it can also lead to misdiagnosis. Early referral to genetic testing is required among patients presenting with symptoms and a positive family history. However, risk of suicide is high among patients of Huntington's disease.

Juvenile onset Huntington disease is extremely rare. Initial symptoms of the disease could vary and can be misdiagnosed as epilepsy, mood or behavioral disorders, or schizophrenia. Genetic testing is controversial for patients below 18 years old. Having a low suspicion threshold in diagnosing patients with positive family history of HD who are presenting with such symptoms is recommended. There is no cure and treatment is symptomatic.

Electroconvulsive therapy (ECT) stands as a crucial intervention for severe and treatment-resistant schizophrenia. Despite being recognized as the most effective acute treatment for severe mood and psychotic disorders, its controversial nature persists due to misconceptions and a lack of familiarity among healthcare professionals regarding modern ECT techniques. This case explores the effectiveness of maintenance ECT in preventing relapse among individuals with schizophrenia, a dimension with scarce existing data.

A 28-year-old unemployed Caucasian male with treatment-resistant schizophrenia underwent multiple trials of atypical, typical, and depot antipsychotics, yielding no significant improvement in the Positive and Negative Syndrome Scale (PANSS) score. Two attempts with clozapine were hindered by neutropenia. With a baseline PANSS symptom score of 110, the patient struggled with severe auditory and visual hallucinations, preventing coherent conversations. Following 26 sessions of bilateral ECT, the PANSS scale score decreased to 65, prompting transfer to a Transitional Living Facility. After an additional 14 sessions, the patient exhibited significant symptomatic improvement, leading to discharge. The PANSS scale score, after 40 sessions, reached 50. Monthly bilateral ECT sessions and one antipsychotic medication now maintain the patient's reasonably functional lifestyle, encompassing employment, social outings, and assistance in farming with his father. ECT proved highly successful in alleviating both positive and negative symptoms, transforming the patient from severe conversational impairment to independent living and employment.

Empirical data validates clozapine's efficacy for treatment-resistant schizophrenia, yet its clinical use is limited by the substantial risks of agranulocytosis and neutropenia, relegating it to a third-line option. Neutropenia's onset in our case during clozapine trials prompted a therapeutic shift to electroconvulsive therapy (ECT). Aligned with American Psychiatric Association guidelines, our case underscored ECT's superior efficacy compared with traditional antipsychotics. Acknowledging a 40% non-response rate to clozapine across diverse studies emphasizes ECT's significance as a viable alternative. Despite challenges, contemporary ECT methods promise to overcome traditional constraints, reduce stigma, and improve treatment accessibility.

This case underscores the potential benefits of ECT as a valuable treatment modality for individuals with treatment-resistant schizophrenia, effectively managing both positive and negative symptoms and significantly improving daily functioning. The success observed in this case suggests that monthly bilateral ECT and one antipsychotic medication can play a crucial role in enhancing the quality of life for patients with treatment-resistant schizophrenia.

Gliomas, encompassing astrocytomas, oligodendrogliomas, and ependymomas, constitute the majority (40–55%) of primary brain tumors. Diagnosis can be challenging due to their uncommon nature, subtle symptoms, and diverse clinical manifestations. While neurological signs are typical, psychiatric symptoms may occasionally precede them. This case report explores a 59-year-old man whose initial psychiatric symptoms, resistant to treatment, evolved into memory impairment, ultimately revealing a high-grade glioma in the thalamus.

A 59-year-old male patient presented to the psychiatric service, expressing concerns about excessive anger and aggression. His family observed his behavior as abnormal, noting uncharacteristic personality changes, particularly increased irritability. Following an outpatient psychiatric evaluation, he was diagnosed with excessive irritability. Over time, the patient's aggressive behaviors intensified, accompanied by feelings of being ignored and devalued by his family, heightened emotional sensitivity, and episodes of muteness. Despite two trials of medication (i.e., sertraline and alprazolam), there was a deterioration in adaptive functioning. Two years after the first onset, the patient experienced unfamiliarity with surroundings, forgetting place names, memories, and people's names. The patient had no family history of neurological or psychiatric illness, and there was no evidence of substance use in his past. To rule out organic causes, an MRI revealed a 17×21 mm lesion in the right thalamus and a calcified focus in the superior part of the left tentorium. Subsequent biopsy confirmed a high-grade glial tumor: anaplastic astrocytoma Grade III, with a Ki-67 index of 10%.

The extended onset of memory impairment in our patient, following a 3-year history of aggressive attacks and irritation, prompts an exploration of the intricate interplay between psychiatric and neurological manifestations. Unlike typical associations of personality changes with frontal lobe tumors, our case challenges this by implicating a thalamic tumor, highlighting the complexity of symptom correlation with precise brain lesion locations. Psychiatric symptoms, though not exclusive, may indicate underlying brain tumors. New-onset psychosis, mood or memory symptoms, atypical occurrences, personality changes, and anorexia in individuals over 40 warrant a thorough diagnostic workup, including neuroimaging, to investigate potential intracranial lesions.

This case emphasizes the significance of identifying psychiatric symptoms as potential indicators of underlying brain tumors. The diverse manifestations, such as sudden psychosis, mood or memory changes, or unusual symptoms, should prompt further investigation, including neuroimaging. Early detection is crucial for improving overall quality of life, and understanding these psychiatric signs aids in unraveling the broader narrative of potential brain tumor involvement.

Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infection (PANDAS) is an inflammatory brain disorder characterised by a new onset of obsessive-compulsive disorder, triggered by streptococcal infection likely inducing molecular mimicry of antistreptococcal antibody action within brain tissue. PANDAS is perhaps considered controversial in the field of psychiatry due to debates over the validity of the diagnosis, controversy surrounding aggressive antibiotic and immunomodulatory treatment and limited well-controlled case studies.

A 13-year-old boy, X, presented with new onset worsening confusion, on a background of autism, to a child psychiatric clinic in the Lake District. During the summer, he developed a fixation with Harry Potter and began to act on confabulating beliefs that his mother is (and always has been) Lord Voldemort. X's behaviour became increasingly violent and aggressive and he now only spoke in ‘parseltongue’, refusing to communicate with anyone in any other way. A new personality change was identified as his usual routine behaviours and fixations had dissipated, such as a decrease in his ritualistic behaviours, a loss of his usual inquisitive nature, and an increased fascination with wearing sunglasses due to beliefs that the sun was poisoned by his mother, ‘Lord Voldemort’. Additionally, X's eating habits had markedly changed and now refused all forms of food. Clinically, X also developed a new and sustained tic and was tremulous in clinics, despite no evidence of focal neurological signs. Due to the relatively acute onset of symptoms, an organic cause was queried, which eventually led to the presumed diagnosis of PANDAS.

Extensive investigations, such as an MRI of the brain, autoantibody testing for anti-AQP4, MOG-Ab, and other serological testing, showed no specific cause could be identified other than evident inflammatory changes in the brain. A ‘three-pronged’ treatment approach was adopted: increased psychotherapeutic intervention, antibiotic treatment and IV immunoglobulin therapy.

This case illustrates the importance of recognition of PANDAS and, more pertinently, an appreciation of the biological aspect of the biopsychosocial approach to psychiatry. From the minimal evidence available, there is a suggestion of a relatively good prognosis for patients with suspected PANDAS when intervened timely; however, repeated infections or a chronic course of illness is more difficult to treat. PANDAS remains a diagnostic challenge and perhaps a mystery, with complicated impacts on not only the patient and their families but also the psychiatrist and wider teams involved in the management of care.

In patients presenting with acute mania & psychosis, it is important to rule out organic cause of their symptoms. Neuropsychiatric problems include affective disorders, disturbances in cognition and psychosis. Mania is commonly associated with hyperthyroidism, But hypothyroidism is a medical condition commonly encountered in a variety of the clinical settings. Patients with severe hypothyroidism may present with psychosis and less commonly with symptoms of mania. We report a case of 37 year old male presenting with acute mania & psychosis, in context of severe hypothyroidism.

Thyroid dysfunction is known to have a significant impact on mental health. Hypothyroidism, in particular, has been linked to mood disorders and acute psychosis. Though most commonly associated with depression, hypothyroidism has been linked to psychosis since the late 1800s, in reports of delusions and hallucinations in patients with myxedema. More recent literature highlights the incidence and coexistence of hypothyroidism and psychiatric disorders, describing possible mechanisms contributing to the pathophysiology of these disorders. The link between hypothyroidism and mania, however, is less clear, with few reports in the literature. We present a case report of a 37 year old male presenting with acute onset mania with psychosis and previously undiagnosed severe hypothyroidism.

AB, a 37-year-old married male from a Telugu-speaking rural background, was brought to the psychiatric outpatient department with his family. The patient's attendants reported concerns about inappropriate talk, bizarre behavior, hyperactivity, sleeplessness, decreased appetite, and suspiciousness lasting for 10 days, indicative of acute psychosis. AB, with no previous psychiatric history, attributed his symptoms to stress related to business and property issues. Family members described him screaming in his apartment, displaying grandiose delusions of a divine presence within him, and exhibiting restlessness and aggression.

Further exploration revealed a history of sleepless nights preceding these symptoms, during which AB initiated a fast, abstaining from eating or drinking to establish himself as a ‘spiritual advisor.’ He expressed paranoia, believing neighbors and family members were conspiring against him due to fictitious landownership claims. Upon examination, AB appeared conscious but restless, agitated, and inattentive for the past 15 days.

Blood work unveiled thyroid abnormalities, with elevated thyroid-stimulating hormone (TSH) (>100 mIU/L) and decreased free triiodothyronine (T3). AB denied prior hypothyroidism diagnoses, though his mother had a history managed with levothyroxine. Notably, no apparent physical symptoms of hypothyroidism were observed.

AB's social history included occasional alcohol (30ml once in a blue moon) and tobacco use (3–4 cigarettes/day). Three days before admission, he ceased smoking, and his last social drink occurred a month earlier.

Diagnosed with acute mania per ICD-10, AB commenced treatment with Tab. diazepam 5mg HS and levothyroxine 100 mcg daily. With this regimen, he showed improved goal-directed behavior and reduced grandiosity, although mild restlessness persisted. Continuing the treatment, the endocrinology team increased levothyroxine to 300 mcg daily, leading to stabilized restlessness. Remarkably, psychosis and mania resolved after two weeks without antipsychotics or mood stabilizers, accompanied by a downward trend in TSH (83.10 mIU/L) and an upward trend in free T3 (0.70 ng/mL) and free T4 (5.03 mg/dL). At discharge, AB showed no residual psychotic or manic symptoms, and levothyroxine was maintained at 300 mcg daily, with diazepam discontinued after a few days.

In the above case rare effect of hypothyroidism was observed. The coexistence of hypothyroidism with depression, bipolar disorder and psychosis has been reported, dating back to the late 1800s. In 1949, Asher reported 14 cases of psychosis with hypothyroidism, 9 of which recovered with thyroid hormone treatment alone. Numerous cases have since linked psychosis to hypothyroidism. The majority of these cases were managed with a combination of antipsychotic medication and thyroid replacement, however in some cases maintenance therapy included thyroid replacement alone. There was no correlation between the degree of hypothyroidism and the severity of psychiatric symptoms. Psychosis usually remits after 1 week of thyroid replacement, with earlier resolution with the addition of antipsychotic medications. Although psychosis is less commonly associated with hypothyroidism than depression, it is a possible manifestation of the disorder.

Hypothyroidism is a common co-morbidity in bipolar disorder. The association between hypothyroidism and mania is less clear. Mania with concomitant hypothyroidism has been reported in patients previously undiagnosed with psychiatric illness. Patients presenting with acute manic episodes and hypothyroidism have improved clinically with a combination of psychotropic medications and thyroid hormone. But in this case patient’s manic condition improved with levothyroxine alone.

Delineating aetiology of psychiatric symptoms in our patient is not difficult. AB's description of manic & psychotic symptoms with no past or family history of bipolar illness would suggest the diagnosis of acute mania. It is possible that hypothyroidism aggravated an underlying psychiatric illness or induced a manic episode with psychotic features. Treatment with levothyroxine & diazepam was considered for this patient to see whether the patient improves with levothyroxine alone & to prove mania is secondary to hypothyroidism. It is possible that levothyroxine contributed to improvement of ABs psychotic and manic symptoms. It is surmised psychotic symptoms completely resolved when the TSH, T3, T4 levels returned to normal.

Thyroid function should be investigated in all patients presenting with mania or psychotic symptoms. Without an underlying psychiatric illness, thyroid hormone replacement may suffice in the treatment of acute onset psychosis in the context of severe hypothyroidism. However, during an acute manic episode, treatment with thyroid hormone therapy alone may not suffice in some cases, and likely requires concomitant therapy with an antipsychotic or mood stabilizer.

Usher syndrome (USH) is the leading genetic aetiology of congenital hearing loss and progressive vision loss. It is linked with a high prevalence of mental health issues, including depression. Previous literature attribute this to communication barriers, constraints in mobility, and general feelings of dependency and uncertainty. However, there is little literature considering poor mental health in USH patients as a consequence of gaps in service provision on a national level.

The present report is the case of a 54 year old woman, who was born with USH Type IIa, and was previously diagnosed with depression and retinitis pigmentosa. The patient was recruited via the RareBeacons charity through volunteer sampling. A semi-structured interview was conducted, with 3 main categories: the impact of diagnosis, interpersonal relationships, and challenges in day-to-day life. A common theme of self-isolation was found, largely due to inefficient communication between healthcare providers, including but not limited to years of waiting for hearing aid treatment exacerbating symptoms of social withdrawal. The patient also reported inadequacies in physician knowledge regarding USH and their general unwillingness to be educated further. Unprofessional physician attitudes and lack of sensitivity towards the patient's deafblindness over time led the patient to feel distrust towards the system, which further compromises care.

Areas of improvement on a systemic scale were identified, including increasing awareness of deafblindness in both the medical community and the general public through patient advocacy, as well as streamlining dedicated support pathways. The patient found formal support to be unhelpful, conversely emphasising the impact of informal support, namely web-based support group platforms. Support groups can provide a sense of community and belonging, alongside sharing valuable resources – often overlooked yet vital in USH, a rare condition with little official support. Subsequent research may include expansion of this case report to yield quantitative data, alongside investigating further factors increasing depression in USH patients (e.g. psychosocial, genetic and biological factors).

This report concludes that the gaping inadequacies of the current medical system poses a significant psychological, emotional and social burden on USH patients.

Integral to Bleuler's concept of schizophrenia, anomalous beliefs regarding the self are crucial to maladaptive social functioning. In schizophrenia, a predisposition to unusual bodily experiences, coupled with reduced awareness and increased social isolation, leads to hallucinations and delusions. Proprioceptive hallucinations, a subset of bodily hallucinations, present a challenging diagnosis due to their subjective nature, often resembling genuine bodily perceptions. We present the case of a 42-year-old man with untreated psychotic illness, manifesting perceptual abnormalities in the modality of proprioception.

Mr. X was referred to Early Intervention in Psychosis (EIP), believing that all his joints were dislocated despite a normal neurological examination, Magnetic Resonance Imaging (MRI), and blood tests. Pertinently, childhood adversities and a seven-year history of prodromal and schizophrenia symptoms, chronic marijuana usage, potentially triggered by separating from his ex-partner, were present. At assessment, Mr. X recalled a delusional memory from age 5, seemingly heralding the onset of his illness. He displayed thought disorder, poor sleep and lacked insight. Olanzapine titrated to 15mg omni nocte (ON) improved sleep, but insight remained poor.

This case of rare proprioceptive hallucinations presenting in middle-age underscores the impact of positive schizophrenia symptoms on social impairment, suggesting a link between unusual bodily experiences and social isolation. Proprioception, encompassing joint perceptions, muscle force, and effort, contributes to body image by combining with exteroception. Interactions with others, influenced by our bodily sense, are crucial for adaptive social functioning. The social deafferentation hypothesis posits that loneliness in schizophrenia may heighten susceptibility to bodily aberrations. The psychological formulation and the chronic use of marijuana on Mr. X's psychopathology, although not thoroughly explored, cannot be overstated.

Proprioception, vital for body image and social interactions, contributes to maladaptive functioning. The potent link between positive schizophrenia symptoms and social impairment needs exploring.

Catatonia is a rare neuropsychiatric syndrome in children. It is characterised by mutism, stupor, posturing, negativism, and rigidity. Historically, catatonia was associated only with psychosis, however catatonic symptoms are being recognised as more prevalent in people with Autism Spectrum Disorder (ASD). Our case report highlights the importance of investigating the potential underlying psychopathology and/or neurodevelopmental condition as this may guide management.

We present a case of a boy in early adolescence who was admitted to the Emergency Department for abnormal slowing of movement and stuttered speech. He described losing all interest in his hobbies, lying down for long periods of time, sometimes being unresponsive and ‘freezing’ in place. On examination, his symptoms were consistent with catatonia: mutism, grimacing, abnormal gait, and ambitendency were all present. He was investigated extensively to rule out medical and neurological causes, all of which were normal. He was assessed and managed by the Centre for Interventional Paediatric Psychopharmacology and Rare Diseases (CIPPRD). After appropriate treatment, he was discharged from the hospital and was managed jointly by CIPPRD and the local Child and Adolescent Mental Health Service (CAMHS). This assessment revealed that the presentation of catatonia occurred during a depressive episode on a background of ASD and underlying Intellectual Disability. He was prescribed fluoxetine as opposed to benzodiazepines or antipsychotics, which led to the catatonic symptoms receding. The neurodevelopmental review revealed that his pattern of social communication and speech after catatonia improvement was consistent with ASD, which was then formally diagnosed.

Untreated catatonia can be fatal. Early diagnosis and management are crucial to avoiding complications. Our case report highlights the challenge of treating paediatric catatonia and the diagnostic and therapeutic importance of understanding underlying psychopathology to decide treatment. Studies have shown that in this population, assessing and treating the underlying psychopathology as opposed to sole use of the lorazepam is essential.

Catatonia in paediatric and adolescent populations may be a first presentation of emotional and behavioural problems underlying autism spectrum disorder (ASD). When treating catatonia, consideration of the underlying psychopathology may warrant alternative pharmacological treatments to the traditional lorazepam challenge test and antipsychotics. The course of catatonia and associated comorbid affective and/or psychotic disorders may fluctuate with environment and therefore a biopsychosocial therapeutic model is warranted.

The use of Clozapine treatment requires rigorous and mandatory monitoring due to the side effects profile of Clozapine. Certain clinical situations may pose a dilemma for clinicians such as concomitant use of clozapine during myelosuppressive chemotherapy. There is limited evidence-based data regarding Clozapine and chemotherapy. We report on a case of a clozapine-stabilized, Schizophrenia patient with Mild ID who was diagnosed with High Grade B-cell Non-Hodgkin's Lymphoma (NHL) requiring chemotherapy. The challenges of this complex case are detailed in this paper.

A 56-year old man with a diagnosis of Mild ID, Schizophrenia and OCD. The patient has been taking Clozapine since 2001 daily dose of 600-400 mg for the past 20 years. Unfortunately, he was diagnosed with High Grade NHL in 2023. The decision was reached to continue Clozapine while undergoing chemotherapy sessions with frequent blood monitoring. Towards the end of his chemotherapy his bloods showed dangerously low (Clozapine red alert) requiring stopping Clozapine. The patient started showing signs of relapse in his mental state and subsequently commenced on Olanzapine. He continued to show signs of relapse and didn't recover to his previous baseline; the treatment plan is adding another antipsychotic or considering re challenging Clozapine.

This report contributes to a very limited literature on the concurrent use of clozapine with chemotherapy and the use of Clozapine “outside license”. The main treatment options facing clinician is stopping or continuing clozapine during chemotherapy. The dilemma of taking the path of withdrawing a medication on which a patient is stabilized may compromise psychiatric stability, yet there is a valid argument that such inconvenience would present more favourable outcome than facing the serious haematological risks of neutropenia. There is a need for robust and close liaison between psychiatrists, oncologist, and haematologist on the various clinical considerations.

In summary, both clozapine and chemotherapy are known to cause neutropenia and agranulocytosis. The clinical decision to continue clozapine during chemotherapy could be challenging. Clinicians should be aware that psychotic decompensation in such patients would inevitably increase morbidity and perhaps mortality due to nonadherence to all proposed treatment, including chemotherapy. In the absence of guidelines and given the nature of treatment-resistant symptoms, clinicians should work in a multidisciplinary approach and carefully weigh the risks and benefits of continuing clozapine during chemotherapy.