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.

In patients with cognitive impairment, it is important to assess the possible impact of medications on cognition. Levetiracetam is an antiepileptic medication used in the management of epilepsy. Its effect on cognition is unclear.

We present a case study of a 57-year-old female who developed cognitive impairment associated with levetiracetam.

She was referred to Memory Services from her GP due to cognitive impairment. Her past medical history included an optic nerve glioma which was surgically removed followed by radiotherapy, and meningiomas which were managed with stereotactic radiosurgery. She had no previous psychiatric history.

Following a first seizure, she was started on levetiracetam 250 mg BD. Over the following months, she developed worsening symptoms of poor memory, fatigue and lethargy, sleeping excessively, headaches, and subsequently, low mood and occasional suicidal thoughts. Levetiracetam dose was halved. When seen in Memory Services 3 months later, it was reported that there had been a gradual but partial improvement in her symptoms since the dose reduction. Addenbrooke's Cognitive Examination (ACE-III) score was 67/100. Short form mood scale was 3/15, below the threshold for depression. Blood tests were normal. MRI Head showed meningiomas and diffuse white matter hyperintensities, both unchanged from previous imaging.

The patient then started lamotrigine and stopped levetiracetam. On follow up (2 months after initial memory assessment), ACE-III score improved to 80/100 and it was reported that her symptoms had completely resolved.

In this case, there is evidence to support a causal link between levetiracetam and the patient's cognitive impairment – there was a temporal relationship, dose response relationship, and reversibility, which are all in the Bradford Hill criteria for causation. Other causes were considered and deemed less likely, including depression; the mood symptoms were not the predominant symptoms and developed after the other symptoms, and the patient scored below the threshold score for depression on short form mood scale.

Regarding the aetiology in this case, one hypothesis is that there may have been risk factors that made this patient more susceptible to cognitive side effects from the biological effects of levetiracetam, such as previous neurosurgery and radiosurgery. Another hypothesis is that the levetiracetam may have triggered an atypical depressive episode which manifested predominantly with memory symptoms and tiredness.

This case study highlights the importance of reviewing medications when assessing cognitive impairment, and of obtaining a clear timeline of symptoms. There is a need for further research looking at the effect of levetiracetam on cognition.

This report describes the treatment of a patient with ketamine induced uropathy. This condition can be significantly debilitating due to its severe effect on the urinary system. This report outlines an interdisciplinary approach to the care of the patient involving addictions services, urology and primary care.

The patient presented with a history of inhalation of ketamine intermittently for four years and daily for three years. His highest daily use was 14 grams per day.

He developed multiple urinary symptoms including dysuria, urgency, incontinence, haematuria and abdominal and urethral pain. He had significant weight loss and suicidal thoughts. After six years of use, he was reviewed by urology, however was discharged within a year, after missing appointments. Investigations included ultrasound which showed kidneys of normal appearance; flexible cystoscopy which showed a small bladder with acute bleeding and posterior wall ulcer; urodynamic studies showed overactive bladder.

He attended a private, inpatient detoxification programme, however relapsed after this admission and self-referred to local addictions services. When assessed there, a detailed history and physical examination were completed. Baseline electrocardiogram and blood investigations were completed and were broadly normal.

It was felt that a collaborative approach between addictions services, primary care, urology, and a regional addictions detoxification centre could help him manage his symptoms and achieve more sustained abstinence. Following interdisciplinary discussions, he was commenced on solifenacine to treat his urinary frequency, mirtazapine for his mood and buscopan for pain. Motivation interviewing approaches were used to help him reduce his ketamine use.

Ketamine is a synthetic drug with marked dissociative, stimulant and hallucinogenic properties. There has been a rising trend in adults entering treatment with harmful ketamine use in recent years. In 2023, 2,211 people entered treatment for harmful ketamine use in England, a fivefold increase from 2014. Ketamine induced uropathy would be expected to occur in a high proportion of these people. A survey of adolescents demonstrated that 60% of ketamine users had lower urinary tract symptoms. There are a range of medical and surgical options to treat ketamine induced uropathy but no clear agreed approach for its holistic management in the UK.

This case report highlights the consequences of prolonged ketamine use on the urinary tract system. It highlights an example of effective interdisciplinary working between addictions services, primary care and urology. The authors recommend the development of nationally agreed guidelines on ketamine induced uropathy with emphasis on collaborative, inter-service working.

Eating disorders often present as a significant challenge in adolescents; especially with regards to early diagnosis and intervention. This case report explores the complex presentation of a 15-year-old female initially suspected of having an eating disorder. The complexity in this case lies in the differentiation between a formal eating disorder and disordered eating, emphasising the importance of thorough assessment and understanding of the underlying psychological factors.

This patient presented to the CAMHS eating disorders team having lost 14 kg in 6 weeks. Such an alarming weight loss had triggered the urgent referral and review. These symptoms initially suggested a classic eating disorder. However as the patient spent more time on the physical health ward a comprehensive evaluation revealed underlying issues related to body image, self-esteem, and emotional wellbeing as well as complex family dynamics leading to a diagnosis of disordered eating rather than a specific eating disorder. The multidimensional approach involved collaboration between mental health professionals, paediatricians and dieticians, to address the multifaceted nature of the condition whilst the patient was admitted to a physical health ward.

The case highlights the intricate interplay between physical and psychological factors contributing to disordered eating behaviours in adolescence. Factors such as societal pressures, peer influences, personal expectations as well as dynamics within a family home may all contribute to a distorted relationship with food and body image. Recognising these complexities is crucial for tailored interventions that address the root causes rather than merely focusing on symptomatic relief. We also established in this case the difference in efficacy between utilising aripiprazole vs olanzapine in terms of treatment of anorexic cognitions.

This case study underscores the necessity of a thorough and holistic approach in assessment, diagnosis and management of eating-related concerns in adolescents. By differentiating between eating disorders and disordered eating, healthcare professionals may better accommodate interventions to address the specific needs of the individual. Early identification and comprehensive care, involving medical, nutritional, and psychological components, are essential for promoting healthy relationships with food and preventing the escalation of disordered eating into more severe conditions.

This case presentation is on a 54 year old female patient. Prior to 2023, she had never had an inpatient admission for her mental health. She was referred to her local community mental health team in May 2023 as they were concerned that she was suffering from panic disorder. The GP referral stated that this lady was suffering from anxiety and panic attacks. At the time of the GP referral, she was on maximum doses of escitalopram, propranolol and zolpidem (and she had been on these maximum doses for three years prior to the referral). This lady has significant caring responsibilities (she has a brother who is severely disabled and she lives with him and she is his main carer). She sustained an injury to the tip of her left index finger in April 2023 and this injury seemed to cause an acute deterioration in her mental health.

This lady had her first inpatient admission in June 2023 and at that time she was treated for the following: mixed anxiety and depressive disorder. She was discharged to the care of her Community Mental Health Team at that time. Post-discharge, her mental state started to deteriorate and she waded into a river and she also made a serious hanging attempt. After this hanging attempt, she sustained multiple rib fractures, a pleural effusion and atelectasis. She also ended up in ICU following this suicide attempt. She was re-admitted to Holywell Hospital in November 2023.

During her second inpatient admission, it became clear that this lady is very medication-seeking. She was treated for the following mental health conditions on her second inpatient admission in 2023: Generalised Anxiety Disorder and Recurrent Depressive Disorder, Unspecified. Help was also sought from an Addictions Specialist on the second inpatient admission. This lady was given five ECT sessions on her second inpatient admission but it was felt that this was making her more agitated so it was stopped.

This patient is currently still an inpatient and she is hoping to attend a specialist addictions unit when she is discharged from hospital. I will follow her progress with interest. I found this case to be an interesting one as it forced me to consider how to best manage a patient who is very medication-seeking.

The Capgras syndrome is one of the four disorders defined under Delusional Misidentification. In the Capgras syndrome the patient believes that someone close to them has been replaced by an imposter pretending to be that person; the abnormality is delusional and not hallucinatory. It is a specific delusion of a person with whom the subject has close emotional ties and towards whom there is a feeling of ambivalence at the time of the onset.

37 year old Caucasian female presented to the local emergency department 4 months after delivery of her baby. She presented with a suicidal attempt in which she cut her neck and drank bleach. She was convinced that her parents and daughters were replaced by a network and her ex-partner was part of this network. She also believed that the network was out to harm her. She showed other psychotic symptoms along with low mood and hopelessness. Despite being offered high doses of antidepressants and antipsychotics she did not show any improvement hence she was given 12 sessions of ECT. Though this treatment was seen to bring in some benefits, her beliefs were still observed to persist. As her delusions were resistant to treatment and lasted more than 3 months, she was diagnosed to have a Persistent Delusional Disorder.

A literature search showed that Capgras delusions rarely occur in postpartum psychosis. It generally poses a risk to baby's care and wellbeing since in most cases mother either refuses to care for baby or attempts to harm them. Interestingly in this case, mother met her daughter's physical needs but struggled with baby's emotional needs most of the time and was rarely observed to smile and play with her.

In this case report, we present the occurrence of different psychopathologies during postpartum psychosis including Capgras delusion. We underline that this case is different from other cases reported in the literature due to unusual nature of the bond between the mother and baby and the onset of the symptoms.

This case report focuses on a 68-year-old Caucasian female, with long-standing symptoms of executive and cerebellar dysfunction, which responded well to rTMS targeting the prefrontal cortex and cerebellum.

This patient was seen in the private sector for long-standing symptoms of low mood, mental fog, unsteady gait, along with slurred speech and poor vision. History indicated the possibility of multiple mini strokes several years earlier, which may have contributed to her current presentation, and MRI Brain confirmed diffuse small vessel disease in periventricular areas and deep white matter, with no atrophy of brainstem or cerebellum. Her medications at the time included venlafaxine 75 mg OD, atorvastatin 20 mg OD, amlodipine 5 mg OD, thiamine HCL 100 mg OD and aspirin 75 mg. She then had a course of standard rTMS (F3 and F4), to which she had no real response. The team then performed a Quantitative Electroencephalography which revealed bilateral prefrontal and cerebellar disconnection, with normal connectivity in the rest of the brain and cortex, which enabled a diagnosis of Organic mood (affective) disorder, F06.3.

Based on the above findings, she was then prescribed a course of rTMS as follows:

1. 1. Bifrontal excitatory Theta burst, at 50–60%, daily for 20 treatments.

2. 2. CB1 and CB2 Cerebellar iTBS (10min) at 50–60%, daily for 20 treatments.

Although long known for its function in fine tuning motor function, emerging research indicates the growing importance of the cerebellum and its neural connections in neuropsychiatric disorders.

Recent studies have shown that those with cerebellar damage show impairments in executive function, and emotional regulation, in addition to language deficits and problems with sensory processing. It is bidirectionally connected with areas associated with processing social salience, including the posterior parietal and prefrontal cortex. With its connections to the prefrontal cortex, limbic structures and monoamine producing brainstem areas, it is likely the cerebellum also plays a key role in fine tuning emotional output, which appears to be corroborated by functional neuroimaging.

This case further supports the emerging evidence base that the cerebellum plays a key role in emotional experience, along with the prospect of using targeted rTMS for therapeutic benefit.

Studies estimate that 90% of people with a diagnosis of autism experience sensory abnormalities. The majority of those affected will not have a psychotic illness, however young people with autism are three to six times more likely to develop schizophrenia than their neurotypical equivalents.

This report considers the diagnostic complexities, potential risks and challenges of navigating concurrent referral and treatment pathways for an adolescent awaiting an autism assessment, who has psychotic-like experiences.

An adolescent female was referred to our Tier 3 service for an autism assessment. Whilst on the waiting list, our service was contacted on three occasions by adults who knew the patient, expressing concerns that she had psychotic-like experiences, namely perceptual abnormalities which had not been included in the original referral.

On the third occasion, approximately six months after the initial referral was accepted, a decision was made to review the patient face-to-face to explore these symptoms further.

During this review she appeared to have positive and negative symptoms of schizophrenia, including perceptual abnormalities in all sensory modalities, thought block, paranoid ideation and a mood incongruent affect. Her sleep cycle was reversed and she had not attended school for several years.

She was subsequently referred to the Early Intervention Psychosis Service, underwent an eight week assessment and was discharged back to the autism service.

Young people in the UK are on average waiting nine months for an autism assessment, although some are waiting up to seven years for treatment. NICE recommends that young people referred due to first episodes of psychosis are seen within two weeks, as delays in treatment can negatively impact on the patient's response to treatment.

Diagnostic uncertainty can arise due to overlapping symptoms, clinician inexperience and difficulties with eliciting a thorough history. With waiting times for autism assessments growing, young people who may have psychotic symptoms are waiting longer to see a clinician. The referral pathways for neurodevelopmental and psychiatric disorders typically exist independently, but inclusion on one pathway can create barriers in accessing the other.

It is good practice for comorbid psychiatric disorders to be considered by the referrer, when referring a young person for an autism assessment.

Clinicians should avoid making assumptions regarding the aetiology of symptoms based on the original reason for referral, explore symptoms thoroughly and refer to alternative services if needed.

Catatonia is a neuropsychiatric syndrome that affects motor, speech, and behavioural functions. The link between catatonia and cannabis use is complex and poorly understood, with limited evidence from case reports about the neuropsychiatric manifestations. This paper aims to describe an unusual presentation of catatonia precipitated by a drink made from cannabis leaves (a.k.a. ‘Bhang’).

Mr JP, a 22-year-old college student, was admitted to an acute medical ward in North India. The medical team sought psychiatry opinion following the unusual presentation: sudden onset of mutism, staring, and rigidity. Physical examination revealed tachycardia and redness of the eyes. Routine blood investigations, EEG and MRI-Brain were unremarkable. Urine drug screen was positive for cannabis. Initially reluctant due to fear of legal troubles, the accompanying friends later revealed a history of ingestion of cannabis leaves (Bhang) for recreational purposes twelve hours ago. Following the clinical diagnosis of catatonia, the lorazepam challenge test led to improvement in rigidity and verbal responsiveness. No overt psychotic symptoms, such as delusions or hallucinations, were noted at the time or during follow-up. JP had previously experimented with smoked cannabis without any diagnosed psychiatric or medical complications requiring inpatient management. He was abstinent from all forms of cannabis use over the past three months due to college exams and denied any illicit substance use. Over the next two days, as the effects of the ingested cannabis wore off and oral lorazepam (6 mg/day) was continued, JP was back to his previous self with stable vital signs. He was discharged from the hospital with a plan to taper and stop lorazepam on an outpatient basis.

‘Bhang' has been a culturally acceptable cannabis form in the Indian subcontinent for centuries, providing an interesting cultural aspect to the case. This case highlights an unusual clinical instance of cannabis use; Oral ingestion led to a drastic presentation requiring hospitalisation, while the smoked form did not result in any similar sequelae. The study's limitations include the inability to test for synthetic cannabinoids and the lack of objective catatonia scoring scale(s).

With the surging popularity of cannabis use in recent years, it is essential to be aware of its various forms and exercise a high degree of suspicion towards unusual presentations. Further research is needed to understand the link between cannabis use and catatonia at the neurotransmitter level, mediated by individual risk factors.

Neuroleptic malignant syndrome (NMS) is a rare, life-threatening idiosyncratic reaction to medications, specifically dopamine receptor antagonists. We report a case of a patient who initially developed extrapyramidal side effects (EPSE) and subsequently developed NMS after being treated with flupentixol depot.

A 64-year-old woman with an underlying recurrent depressive disorder with psychotic symptoms presented to a psychiatric hospital in June 2023. She exhibited self-neglect, low mood, paranoid delusions, and non-concordance to oral psychiatric medications.

In the first week, she declined all oral medications and was subsequently started on flupentixol decanoate (Depixol) depot injection at 40 mg once every 2 weeks. While showing good improvements in her mental state, she began complaining of akathisia and dystonia since July 2023, consistent with extrapyramidal side effects secondary to flupentixol.

The symptoms improved by lowering flupentixol to 30 mg every 2 weeks and adding procyclidine 5 mg twice daily and propranolol 20 mg three times daily.

In early September 2023, she experienced severe restlessness, stiffness, muscle weakness and felt hot and clammy over 36 hours. Physical observations showed fever, tachycardia, and hypertension. Examination revealed diaphoresis, rigidity in both upper and lower limbs, lower limb weakness, and normal reflexes. Blood tests indicated acute kidney injury (AKI) stage 1, deranged liver function tests, and a creatinine kinase (CK) level of 9405.

She was promptly admitted to the medical hospital for NMS and received extensive intravenous fluid rehydration along with oral Dantrolene. She made a complete recovery, and Depixol was discontinued. Two weeks later, she was started on quetiapine and gradually titrated to 50 mg once daily.

EPSE and NMS are associated with dopamine receptor blockade and commonly occur during the initiation or dosage increment of neuroleptic medications.

NMS is rare but life-threatening, presenting with manifestations of muscle rigidity, pyrexia, altered mental status, sympathetic nervous system lability and elevated CK.

In our case, our patient, who recently started taking neuroleptic medication, experienced EPSE and later deteriorated acutely, raising a high suspicion of NMS. It is essential to consider other possible diagnoses, including serotonin syndrome, malignant hyperthermia, malignant catatonia and electrolyte disturbances.

The commonly used diagnostic criteria include Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (DSM-5) and Levenson's criteria but diagnosis of NMS remains clinical.

The crucial step after identifying NMS is to immediately stop the neuroleptic agent, followed by supportive medical treatment.

Early recognition and prompt treatment of NMS in our patient led to a full recovery.

Background

This case study describes the use of fluoxetine for reduction of pre-menstrual dysphoric disorder (PMDD) and bulimia nervosa symptoms. The case report also describes an increase in binge purge symptoms in the pre-menstrual period, along with other mood and cognitive symptoms. This supports a hormonal basis to the exacerbation of eating disorders. Patient consent was obtained prior to the publication of this report.

Case report

A 41-year-old lady with significant binge purge behaviours and mood disturbance was referred to our eating disorder service. She met the diagnostic criteria for bulimia nervosa after a thorough assessment, along with a component of mood dysregulation. She was prescribed sertraline for depressive symptoms in primary care. The patient described a worsening of mood symptoms, along with cognitive difficulties before the start of her menstrual cycle. After a medical review, we agreed on tracking these symptoms along with the binge-purge frequency for a period of two cycles. This was done using a PMDD tracker. The tracker reflected a clear diagnosis of PMDD along with an exacerbation of bingeing and purging symptoms before the start of a menstrual cycle. Following this, sertraline was switched to fluoxetine, and titrated up to its maximum dose of 60 mg a day.

Discussion

Following the commencement of fluoxetine, purging frequency dramatically reduced and subsequently stopped. Although mood symptoms still persisted, the specific mood symptoms along with cognitive symptoms in the pre-menstrual period reduced.

There is some evidence for the use of fluoxetine use for binge purge symptoms in bulimia nervosa. Fluoxetine has also been used either continuously or in the luteal phase for PMDD. This case report reflects the possible correlation between binge-purge symptoms and PMDD symptoms, and the potential use of fluoxetine for dual symptom reduction. PMDD still remains to be a significantly under-diagnosed condition in women. This case report also signifies the importance of exploring PMDD symptoms in eating disorders.

Obsessive-Compulsive or Related Disorders (OCRDs) comprise a group of disorders characterized by repetitive thoughts and behaviours and are fairly less prevalent among children. The recommended treatment for OCRDs involves high doses of antidepressants, specifically selective serotonin reuptake inhibitors (SSRIs), along with non-pharmacological management. However, evidence suggests that the risk of inducing mania with antidepressants may be especially high in children and adolescents aged 14 years and younger.

Here, we present a case of a nine-year girl, studying in fifth standard, with normal birth and development history, with no past/family history of psychiatric illness, presented with psychiatric illness of one-year duration and was diagnosed with Trichotillomania, Obsessive-Compulsive Disorder, Skin picking and Onychophagia as per the 11th revision of International Classification of Diseases (ICD-11). After initiating tab. escitalopram 5 mg for 10 days, child developed a manic episode, which leads to a diagnostic dilemma as well as difficulties in her further management. In view of the bipolarity, escitalopram was stopped and the child was started on tab. aripiprazole 2.5 mg which was gradually up-titrated to 7.5 mg/day, following which the manic episode completely resolved and there was also improvement in OCD, hair pulling and skin picking behaviour. Later for the remaining symptoms few sessions of Habit reversal therapy were held. Currently the patient is maintaining well on aripiprazole 7.5 mg for the last six months.

The uniqueness of this case is demonstrated through current limited literature on comorbid OCRDs and antidepressant coincident manic episode, especially in children in whom diagnosing manic episode possess a great challenge owing to various differential diagnosis. While deciding pharmacological therapy in children with OCRDs or Mania the efficacy as well as their safety profile should be considered. Currently there are no medications approved by FDA for treatment of acute manic episode in patients below 10 years of age and use of SSRI which are considered first line for treatment of some OCRDs may exaggerate the manic episode. In literature, second generation antipsychotics such as aripiprazole is found to be useful for the management of both manic episode (as monotherapy) as well as OCD (as an adjuvant). In this case aripiprazole monotherapy led to significant improvement in both groups of symptoms.

Thus, SSRIs should be used cautiously in children with OCRDs and aripiprazole along with other approved non-pharmacological management strategies can be considered as a good treatment option in children with OCRDs and anti-depressant coincident manic episode.