Ultra-rapid cycling bipolar affective disorder (BPAD), defined by mood episodes occurring within weeks rather than months, is associated with significant morbidity and limited evidence-based guidance. Management becomes particularly challenging in women with pre-existing biological vulnerability factors such as hypothyroidism and pronounced sensitivity to antidepressants. This case highlights the complexity of balancing suicide risk, patient preference, and treatment-related mood destabilisation in ultra-rapid cycling BPAD.

We describe the case of a woman with a diagnosis of ultra-rapid cycling BPAD and a history of multiple prior admissions for mood instability. She had pre-existing hypothyroidism, neurodevelopmental comorbidity, and a past history of substance misuse, with no active substance use during admission. The patient experienced severe bipolar depressive episodes associated with high suicide risk, for which duloxetine was prescribed. However, even minor antidepressant dose changes were associated with mood elevation.

Lithium was optimised and maintained within the therapeutic range throughout admission, alongside initiation of clozapine for mood stabilisation. Following an inadvertent antidepressant dose escalation, the patient developed emerging manic symptoms, prompting urgent multidisciplinary medication review. Hypothyroidism management was concurrently reassessed, revealing suboptimal levothyroxine administration due to incorrect timing with food and other medications. Targeted education for the patient and staff was implemented, alongside dose escalation and regular thyroid function monitoring.

This case demonstrates pronounced antidepressant sensitivity in ultra-rapid cycling BPAD, with dose variability precipitating mood destabilisation even at low doses. Hypothyroidism represented a potentially modifiable biological vulnerability factor, with impaired medication absorption contributing to affective instability. A key clinical paradox emerged in which treatment required to mitigate suicide risk simultaneously increased the risk of manic relapse.

Shared decision making was central to management. Despite guideline based concerns regarding antidepressant use in rapid cycling BPAD, a consensus decision which was supported by wider acute consultant discussion and independent second opinion was made to continue antidepressant treatment at a reduced dose for a limited period, with close monitoring. Diagnostic clarity and coordinated multidisciplinary working were essential in maintaining therapeutic alliance and managing risk.

Ultra-rapid cycling BPAD necessitates highly individualised care. Antidepressants may destabilise mood even at low doses in biologically vulnerable patients, particularly women with comorbid hypothyroidism. Optimisation of physical health conditions, including attention to medication administration practices, can be clinically significant. This case underscores the importance of balancing guideline recommendations with patient-centred decision-making in complex, high-risk presentations.

Prescribing stimulant medication for Attention-Deficit/Hyperactivity Disorder in patients with Postural Orthostatic Tachycardia Syndrome presents a recognised clinical dilemma due to the potential for stimulants to exacerbate tachycardia and autonomic instability. There is limited practical guidance on how such prescribing can be undertaken safely within psychiatric inpatient settings. This case aims to demonstrate how structured multidisciplinary collaboration, robust monitoring protocols, and clear system ownership can enable safe initiation of stimulant treatment in a patient with POTS, while highlighting vulnerabilities in protocol implementation within complex care systems.

A woman in her early twenties was admitted to an acute psychiatric ward with complex psychiatric and medical comorbidities, including POTS (stable on Ivabradine), Epilepsy, and Schizoaffective disorder. Following comprehensive assessment, she was diagnosed with ADHD using the DIVA-5 diagnostic interview.

Given the cardiovascular risks associated with stimulant medication, extensive liaison was undertaken with multiple consultant cardiologists at a tertiary NHS trust. Cardiology confirmed stable POTS, a normal recent ECG, and no evidence of structural heart disease, advising that Lisdexamfetamine 20 mg once daily could be initiated with appropriate precautions.

A detailed monitoring protocol was developed and disseminated, including baseline and thrice-daily lying, sitting, and standing heart rate and blood pressure measurements, NEWS2 scoring, predefined red-flag thresholds, and a clear escalation plan. The patient received structured education regarding symptom reporting, and informed written consent was obtained. The plan was shared with nursing staff and on-call medical teams to support safe implementation.

Lisdexamfetamine was initiated without cardiovascular complications. During the initial two-week intensive monitoring period, no tachycardia, blood pressure instability, or worsening of POTS symptoms were observed. The patient reported significant subjective improvement in ADHD symptoms, corroborated by staff observations. Ongoing weekly monitoring continued following dose changes.

A systems-based challenge was identified when elements of the monitoring protocol were not implemented consistently during a period of medical handover, despite prior written communication. This highlighted a critical gap between protocol dissemination and execution, underscoring the importance of clear ownership and active follow-up when implementing high-risk prescribing plans.

This case demonstrates that stimulant medication can be safely initiated in selected patients with POTS when supported by specialist cardiology input, structured monitoring, and robust multidisciplinary collaboration. However, safe prescribing extends beyond clinical decision-making alone; system-level safeguards, clear accountability, and effective handover processes are essential to mitigate risk. Patient education and proactive MDT engagement are pivotal in ensuring both safety and therapeutic benefit in complex psychiatric prescribing.

Congenital insensitivity to pain (CIP) is a rare neurogenetic condition characterised by lifelong absence of nociception, removing a fundamental biological deterrent to injury. Psychiatric risk-assessment frameworks implicitly rely on pain perception, distress cues, and behavioural feedback to signal escalation. We describe a case of severe self-harm escalation in a young adult with genetically confirmed CIP, emotionally unstable personality disorder (EUPD) highlighting critical limitations of standard inpatient risk-management approaches and the need for pain-independent safeguarding strategies.

We describe a female in her early twenties admitted to an acute psychiatric ward under the Mental Health Act following overdose and repeated self-harm. She has a childhood diagnosis of genetically confirmed congenital insensitivity to pain due to a homozygous SCN9A mutation, with lifelong absence of pain perception and a history of significant injuries without reported pain. She also has longstanding neurodevelopmental and personality vulnerabilities, including autism spectrum traits and emotionally unstable personality disorder, with self-harm beginning in early life. During admission, she described persistent internal voices and intrusive phenomena consistent with pseudo-hallucinations associated with EUPD and autism, rather than primary psychotic illness. Despite prior minor self-harm episodes, environmental access to hazards such as sharps and boiling water continued. This culminated in a severe self-inflicted scald injury requiring admission to a specialist burns unit and intravenous antibiotics, with minimal behavioural or verbal pain response observed during injury assessment and wound care.

This case demonstrates how self-harm can escalate rapidly and silently when nociceptive feedback is absent. The absence of pain and distress cues rendered conventional observation levels and harm-minimisation strategies ineffective, delaying recognition of injury severity. Risk could not be reliably inferred from reported experience, expressed intent, or diagnostic category. Even in the absence of primary psychosis, self-harm associated with EUPD and autism progressed to life-threatening physical injury without typical warning signals, exposing a critical blind spot in inpatient psychiatric risk frameworks that rely on pain-dependent deterrence and behavioural escalation markers.

In patients with congenital insensitivity to pain, self-harm risk must be assessed independently of pain perception and expressed distress. Psychiatry services should implement pain-independent safeguards, including early and sustained environmental restriction, routine body mapping, scheduled wound and physical observations, and prioritisation of psychotic symptom control. This case highlights the need for integrated neuropsychiatric approaches and revised inpatient risk frameworks when biological pain deterrents are absent.

Delusional misidentification syndromes are rare but clinically disruptive phenomena. Fregoli syndrome, characterised by the belief that a familiar individual is disguising themselves as others, is particularly uncommon in general adult psychiatry. This case describes a unique presentation in which Fregoli-type delusional misidentification was directed towards the treating clinician, resulting in a profound therapeutic rupture and requiring a deliberate and counter-intuitive reconfiguration of care.

A middle-aged woman was admitted following police detention under Section 136 of the Mental Health Act and managed under Section 2. She presented with acute catatonia, including mutism, rigidity, marked psychomotor retardation, and self-neglect. Lorazepam was commenced following clinical diagnosis, leading to rapid resolution of catatonic features within 24 hours. As catatonia resolved, florid psychotic symptoms emerged. The patient developed a fixed delusional belief that the treating specialty doctor was her first husband’s first wife’s daughter, disguising herself as a clinician and orchestrating her detention with police involvement. Reassurance was ineffective, and the patient persistently refused to recognise the clinician as a doctor, while engaging appropriately with other medical staff.

The delusional misidentification was consistent with Fregoli-type syndrome and had immediate, observable consequences for care. Direct contact with the identified clinician precipitated marked distress, verbal aggression, refusal to engage, and escalation of paranoia, repeatedly disrupting treatment. A consultant-supported multidisciplinary decision was made for the clinician to withdraw from direct patient contact while continuing to coordinate care indirectly. This decision led to immediate improvement in engagement with the wider team. Persistent psychotic symptoms following catatonia resolution necessitated antipsychotic treatment under Section 3 of the Mental Health Act. Over the course of admission, psychotic symptoms resolved fully, insight returned, and the patient was discharged informally with community follow-up. At discharge, the delusional misidentification had resolved completely, with no recollection of its content.

This case demonstrates that Fregoli-type delusional misidentification can directly undermine therapeutic relationships and compromise treatment delivery. It highlights the importance of recognising clinician-directed delusions and reframing clinician withdrawal, when appropriately supported by the multidisciplinary team, as an active therapeutic intervention rather than a failure of engagement. Awareness of delusional misidentification syndromes is essential to guide flexible, patient-centred care in complex psychosis.

Dissociative fugue is a rare dissociative disorder characterised by sudden, reversible loss of autobiographical memory, identity disturbance, and purposeful wandering, often precipitated by acute psychological stress. Due to its infrequency and overlapping presentation with psychosis, delirium, and substance-induced amnesia, dissociative fugue is frequently misdiagnosed. We present a case of dissociative fugue in a previously high-functioning adult, highlighting diagnostic clarity, multidisciplinary management, and the critical role of family involvement in recovery.

A man in his late thirties with no known psychiatric or medical history was brought to hospital by police after being found wandering outdoors inadequately dressed during winter. He was unable to identify himself, his personal history, or recognise family and friends, although he adopted an alternative name. He appeared emotionally neutral about his identity loss and demonstrated preserved ability to follow ward routines independently. Orientation to time was impaired, with reduced awareness of seasonality, while orientation to place was intact. There were no hallucinations, delusions, thought disorder, or features of delirium. Physical observations remained stable throughout admission.

Extensive investigations, including neuroimaging and blood tests (including infection and metabolic screening), were normal. Urine toxicology was negative, with no evidence of intoxication or withdrawal. Organic, psychotic, neurological, and substance-induced causes were excluded, and a working diagnosis of dissociative fugue was formally established. Psychosocial assessment revealed a sudden relationship breakdown preceding symptom onset alongside occupational stress. Psychological formulation conceptualised the presentation as trauma-related dissociation with identity fragmentation.

Management focused on psychological and systemic interventions rather than pharmacological treatment. Input included trauma-informed psychological therapy, occupational therapy with graded re-exposure, and structured family involvement. Identity reintegration was facilitated through in-person family visits, video calls, photographs, familiar language cues, and supported visits to the patient’s home. A marked emotional breakthrough occurred during the third week of admission, when the patient became tearful upon seeing his brother, coinciding with gradual restoration of autobiographical memory. Retrospective consent was obtained once capacity returned.

This case demonstrates that dissociative fugue is not merely a theoretical diagnosis but a real and reversible clinical presentation in contemporary psychiatric practice. Preserved executive functioning, emotional neutrality towards identity loss, and absence of psychotic features were key diagnostic clues. Without early diagnostic clarity, the patient was at significant risk of misdiagnosis as dementia, psychosis, or substance-induced amnesia, potentially leading to unnecessary pharmacological treatment or prolonged institutionalisation. Coordinated multidisciplinary care, early collaboration with police and community services, and family involvement were central to recovery.

Weight-loss medications such as tirzepatide are increasingly prescribed, yet their potential psychiatric effects remain under-recognised. This case explores diagnostic uncertainty between personality pathology and hypomania following significant weight loss and exposure to tirzepatide in an individual with pre-existing narcissistic personality traits. The aim was to examine whether behavioural escalation represented an exacerbation of personality traits alone or a superimposed affective episode temporally associated with medication use.

A man in his late 40s with established Narcissistic Personality traits and no prior history of mood disorder was assessed following escalating behavioural concerns in the workplace. Prior to medication exposure, occupational functioning was stable, though interpersonal behaviour was characterised by inconsistency, criticality, and sensitivity to perceived errors in others.

Tirzepatide was initiated for weight loss at a starting dose of 2.5 mg and gradually escalated to 10 mg. Over approximately six months, the patient experienced rapid weight loss of 20 kg. Over the last three months of the treatment, marked behavioural changes were observed, including reduced need for sleep, increased energy, heightened grandiosity beyond baseline, impulsive decision-making, disinhibition, and poor insight into the impact of his actions on colleagues.

He demonstrated abrupt rule-breaking behaviour, including suspending colleagues without completing appropriate investigations or following established procedures, causing significant distress within the workplace. Symptoms were escalating rather than static. There were no psychotic symptoms, substance misuse, or alternative medical explanations identified.

The primary diagnostic considerations included exacerbation of narcissistic personality traits, hypomania, and medication-associated affective destabilisation. Several features supported hypomania over personality traits alone, including a clear change from baseline functioning, reduced sleep, increased goal-directed activity, behavioural disinhibition, and a marked reduction in insight. The temporal association with tirzepatide initiation and rapid weight loss raised the possibility of medication-related affective change in a psychologically vulnerable individual, despite no prior bipolar diagnosis.

This case highlights the diagnostic complexity of distinguishing personality pathology from emergent mood disorder in the context of metabolic pharmacotherapy. Clinicians should remain vigilant for affective destabilisation in patients prescribed GLP-1–based weight-loss agents, particularly those with underlying personality vulnerabilities. Careful longitudinal assessment is essential before attributing behavioural change solely to personality traits.

Schizophrenia affects an estimated 24 million people worldwide, with around one third experiencing inadequate response to first-line antipsychotics. Clozapine is the most effective treatment for this group but is reserved as a last-line option due to serious adverse effects and intensive monitoring requirements. Its metabolism varies widely due to age, smoking, genetics and ethnicity. Significant risks include neutropenia, myocarditis, metabolic syndrome. We present the case of a patient with clozapine-induced dysarthria, an uncommon but debilitating side effect. The associated reduced speech intelligibility and difficulties in communication can cause considerable distress for patients who are already coping with the challenges of a psychiatric disorder, and increases the chances of poor adherence to the medication.

Patient A is a male in his 40s who developed schizophrenia during early adulthood. He was diagnosed with treatment-resistant schizophrenia; Clozapine trials were complicated by dose-related adverse effects, most notably that of sudden onset dysarthria for which no other cause was identified. Rechallenge was further complicated by adverse cardiovascular effects. Clozapine plasma levels were found to be consistently raised despite relatively low doses of Clozapine, suggesting that the patient was a poor metaboliser of the drug. Progressive dose reductions improved speech while maintaining psychiatric stability. The dysarthria subsequently improved on low-dose clozapine with adjunctive sodium valproate.

The presented case demonstrates a clear chronology of the development of dysarthria at sub-therapeutic doses of Clozapine, and its subsequent resolution with reduction of the dose. Existing literature describes similar clozapine-associated speech dysfluency, more commonly stuttering, often showing a dose-response relationship. Some cases link symptoms to orofacial dyskinesia, prior neurological vulnerability, or possible micro-seizure activity, even with normal EEG findings. Proposed mechanisms include reduced seizure threshold via dopaminergic selectivity, GABAergic inhibition, glutamatergic enhancement, and anticholinergic effects. Prophylactic sodium valproate may improve the dysarthria, and allow continuation of clozapine in selected high-risk patients.

This case emphasises dysarthria as a dose-related adverse effect of clozapine, particularly in patients with unexpectedly high plasma levels. It highlights the importance of close therapeutic drug monitoring during titration and consideration of individual metabolic factors such as ethnicity and comorbidities. When speech dysfluency emerges, clinicians should assess potential risk of clozapine-associated seizures and consider EEG investigation. Anecdotal evidence suggests sodium valproate may alleviate speech disturbance even without overt seizure activity. Further research is needed to clarify the mechanisms underlying clozapine-related speech dysfluency and to inform strategies that balance efficacy and tolerability in treatment-resistant schizophrenia.

Memantine is an NMDA receptor antagonist used as pro-cognitive medication across the world. In the UK, it is licensed for moderate-to-severe stages of Alzheimer’s dementia. Memantine, like other medications, is associated with side effects that could be life-threatening in certain occasions. While clinicians mainly focus on medication initiation, titration and switch-over, deprescribing remains a critical step to uphold patients’ care especially in older adults and those who are more vulnerable to side effects.

85-year-old lady with advanced mixed dementia on a psychiatric ward had a fall and a pelvic fracture. Following surgery, there was evident decline in her physical and mental health. She was nursed in bed all time and could not engage with post-operative rehabilitation. She became agitated on personal care interventions then started to present with impaired consciousness for extended periods during the day. The presentation continued to get worse to the extent that her impaired consciousness affected her diet and fluid intake and she lost significant amount of weight. Prolonged postoperative delirium was evident but there was no clear culprit to why her presentation is getting worse. Interestingly, her medication concordance was not affected for the majority of that period. It was felt that the patient could be slowly dying so we discussed the situation with palliative care team; they noticed some choreo-athetotic movements in the patient’s limbs which prompted reviewing her psychotropic medications which included Memantine 20mg. Once Memantine was discontinued, all the patient’s symptoms improved including her impaired conscious level and the abnormal limb movements.

Literature review highlighted rare associations between Memantine, such abnormal movements and impaired consciousness. This patient’s recovery from this post-operative state was lengthy and was eventually achieved after addressing “a blind spot” which was the prescribed medication Memantine. The main reason to stop Memantine was the patient’s abnormal movements but it was also responsible for the impaired conscious level. Once Memantine was discontinued, the patient’s mental and physical states changed dramatically. She became more responsive and her conscious level was back to normal. The choreo-athetotic movements were no longer visible as well.

Deprescribing is a valuable yet missed tool for improving patient outcomes. It is commonly undertaken when a medication is clearly linked to adverse effects and is often paired with prescribing alternatives. However, deprescribing is frequently overlooked when symptoms are not evidently medication-related. Implementing a proactive deprescribing process can help reduce iatrogenic harm and improve overall clinical outcomes.

Delusional Misidentification Syndromes represent disorders that are neuropsychiatric in nature. They include four main disorders: Capgras Syndrome, Frégoli Syndrome, Intermetamorphosis and Syndrome of Subjective Doubles. These syndromes are more noted in context of Schizophrenia but they can be encountered in other psychiatric disorders. Strokes and head traumas have also been implicated as contributing factors/causes for the development of these syndromes. Mainstay of treatment is antipsychotic medications.

75-year-old gentleman with no past psychiatric history, had a stroke that affected “posterior left insula and left temporal operculum”.A “right frontal and right parietal infarcts” were established on his head scan at the time. The right frontal infarct was present on an MRI three months prior but the right parietal one was not. Following the stroke, he presented with receptive and expressive dysphasia but no motor symptoms. There were elements of mild cognitive impairment but the main symptoms align with Delusional Misidentification Syndrome, subtype Syndrome of Subjective Doubles. He became convinced that there are people that look exactly like him, including “a brother who had facial surgery” to look like him. Of note, the patient does not have brothers. Another “double” is “someone who lives in a care home and is in a vegetative state”. Interestingly, the patient was residing in a care home for few months.

Timeline of events reflects that the patient lived alone independently in his home till he had a stroke and was admitted to hospital. Post-stroke rehabilitation efforts were not successful and he was discharged to a care home. After a while, the care home struggled to meet his needs due to emergence of frequent suspiciousness that led to aggressive episodes. He was later detained to a psychiatric ward for a period of assessment and treatment. The patient’s function and quality of life was clearly affected as a consequence of the stroke. Due to the patient’s dysphasia, it was difficult to understand his psychiatric symptoms. It took some time until his symptoms were pieced together indicating Delusional Misidentification Syndrome. Improvement noted once Olanzapine was started and dose increased up to 10mg.

Delusional Misidentification Syndromes are rare neuropsychiatric disorders that require treatment with antipsychotic medications. They also have some organic basis and some links to strokes and traumatic brain injuries. This case is vital in understanding the link between neurology and psychiatry and offers further notions to clinicians to reflect more on the organic nature of mental disorders.

First-episode psychosis with treatment resistance can present with diagnostic uncertainty and often necessitate complex psychopharmacological decisions alongside multidisciplinary interventions. Selecting effective antipsychotic treatment while minimising adverse effects is critical, particularly when initial monotherapy is unsuccessful. This case report reviews clinical management and functional improvements in a young woman admitted to an acute psychiatric ward following combination treatment with Cariprazine and Olanzapine, supported by multidisciplinary team interventions.

X is a young adult female with no prior secondary-care mental health involvement, a family history of schizophrenia. She presented following a 2.5 year deterioration marked by aggression, social decline, and psychotic symptoms. On admission, she was presenting with behavioural disturbance, exhibited prominent paranoia, persecutory delusions, and auditory hallucinations. Initial treatment with oral Olanzapine was limited by non-compliance.

Zuclopenthixol depot was initiated but discontinued due to extrapyramidal side effects. Subsequent treatment with Amisulpride resulted in limited symptom control and cognitive slowing. Clozapine was deferred due to abnormal inflammatory and cardiac markers. A switch and gradual increase to Cariprazine 4.5 mg/d led to an improvement in insight and behaviour, with low-dose Olanzapine 5 mg/d later added to address residual positive symptoms (auditory hallucinations).

MDT input included extensive collateral history, family involvement, and structured Occupational Therapy and Psychology interventions.

This case suggests that Cariprazine augmented with low-dose Olanzapine may be an effective and tolerable strategy in treatment-resistant psychosis when Clozapine is contraindicated. Improvements in functional and psychological outcome measures underscored gradual symptomatic recovery.Symptom severity, measured using the Brief Psychiatric Rating Scale (BPRS), reduced from 38 to 29, representing 23.7 % improvement with the most marked improvement observed in unusual thought content and hallucinations.

The Occupational Therapy Task Observation Scale (OTTOS) - total score improved from 121/200 (08/10/25) to 182/200 (09/01/26), representing a 50.4% increase. Task Behaviour improved by 39.7%, and General Behaviour by 62.1%, with marked gains in engagement, independence, and socialisation.

Autism Spectrum Quotient (AQ-50) score reduced from 22 to 15, a 31.8% reduction in self-reported autistic-type traits. The greatest improvements were observed in Social Skills (90% of items) and Communication (70%), indicating improved interpersonal functioning and cognitive flexibility.

GAP (Global Assessment of Progress) score improved from 29/70 on admission to 63/70, representing an absolute increase of 34 points and reflecting a 48.6% improvement across the different domains.

Combination treatment with Cariprazine and Olanzapine was associated with meaningful symptomatic, functional, and psychological improvement, demonstrating its potential role in complex treatment resistant psychosis.

Patients with severe mental illness frequently present with complex physical health comorbidities, creating significant challenges for safe inpatient management on acute psychiatric wards. Patient’s impaired capacity and behavioural disturbance can further complicate engagement with essential medical care. This case highlights the importance of integrated physical and mental health management and multidisciplinary team collaboration in achieving positive outcomes.

X is a 46-year-old female with a diagnosis of Schizoaffective disorder and poorly controlled Type I Diabetes. She presented with a progressive deterioration in mental state following discontinuation of Clozapine and Lithium. Intermittent refusal of BG monitoring, erratic and unhealthy dietary habits, and variable cooperation with insulin administration led to significant glycaemic instability, requiring coordinated Multidisciplinary team (MDT) input to ensure patient safety. Patient was transitioned to Paliperidone depot injection due to the favourable metabolic profile.

A coordinated MDT approach was implemented. Nursing staff adhered to a structured rapid-acting insulin management plan, administering additional doses in response to BG readings. A Freestyle Libre continuous glucose monitoring sensor was introduced, with staff educating the patient, helping to set up alerts for hypo- and hyperglycaemia. Dietitian’s input was provided, alongside liaison with hospital catering services to facilitate healthier food substitutions.

As a result the patient’s glycaemic control improved markedly, with reduced BG fluctuations and decreased need for additional rapid-acting insulin. This improvement was reflected in a significant reduction in HbA1c from 92 mmol/mol (21/11/25) to 69 mmol/mol (14/01/26) within less than 3 months. The patient demonstrated sustained behavioural change, discontinuing takeaway food and adopting healthier eating habits.

Symptom severity, measured using the Brief Psychiatric Rating Scale (BPRS), reduced from 52 to 29, representing 44 % demonstrating a substantial reduction in psychotic, affective, and behavioural symptoms.

Occupational therapy task observation scale (OTTOS) total score increased from 61/200 to 190/200, representing 64.5% increase, indicating a substantial improvement in both task performance and overall functional behaviour.

GAP (global assessment of progress) score improved from 40/70 on admission to 59/70, representing an absolute increase of 19 points and reflecting a 27% improvement across the different domains, highlighting a marked improvement in clinical stability and functional engagement.

Integrated physical and mental health care is essential for patients with severe mental illness and complex comorbidities. This case demonstrates that even during acute psychiatric deterioration, effective management of complex physical health conditions is achievable through structured care plans, consistent nursing input, and strong multidisciplinary team collaboration.

Seizures can manifest with different symptoms including motor, autonomic, behavioural, cognitive, emotional, or sensory dysfunction. Non motor seizures can therefore be referred to a psychiatrist or missed. This study looks at a similar case where seizure disorder was mistaken for a cognitive disorder and sun downing in dementia.

An 81-year-old gentleman was referred to the memory clinic due to concerns about his memory and behavioural changes occurring mostly at night. At initial review he reported having episodes of disorientation, with associated behavioural changes like wandering, attending to chores e.g. cleaning, hoovering, with confusion and scored score 85/100 on ACE III. Further history revealed a previous episode of collapse, preceded by patient doing household chores at 3 am, lip smacking, urinary incontinence and retrograde amnesia of events. Diagnosis of cardiac syncope was made at the hospital, following ECG with dynamic changes but no rise in troponin. EEG showed no positive findings and He was then asked to inform Neurology if there are further episodes . Unfortunately, he had several episodes with similar behavioural symptoms but not motor manifestation which delayed treatment as family did not report them to neurology. He was then seen in psychiatry clinic for MCI review where a diagnosis of likely seizure disorder, with behavioural manifestation was made and was referred to the neurologist who prescribed lamotrigine with significant reduction in the frequency of these episodes.

The case highlights again, epilepsy as watershed between neurology and psychiatry. Seizure episodes may present with behavioural symptoms which can be referred to mental health specialists.

Mental health specialists should take detailed history, consider various differential diagnosis and complete a holistic review including medical history to avoid missing focal and complex partial seizures without motor manifestation.

Background:

Foetal Alcohol Spectrum Disorder (FASD) is under-recognised in Children in Care (CiC), Adopted Children (AC) and those on Special Guardianship Order (SGO) known to Child and Adolescent Mental Health Services (CAMHS. While neurodivergent conditions such as Attention Deficit Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD), or behavioural problems are recognised, underlying neurocognitive impairments associated with Prenatal Alcohol Exposure (PAE) remain rarely explored. This case series aims to describe the neurocognitive profiles of children diagnosed with FASD identified via local diagnostic pathways, in the CiC specialist CAMHS ‘Symbol’ team.

Case Report:

Of the four children reviewed on the neurodevelopmental care pathway, three received a multidisciplinary diagnosis of FASD. Assessments included detailed mental health assessment, developmental and family histories, school reports and information collated from CiC medical records, OT (Occupational Therapy), SALT (Speech and Language Therapy), EP (Educational Psychology) reports and social care records. Standardised cognitive assessments (WISC-V -including full-scale IQ and domain-level profiles) and Adaptive Behaviour Assessment System (ABAS) were completed. Particular attention was given to variability across cognitive domains, adaptive functioning, and discrepancies between verbal ability, working memory, processing speed and fluid reasoning. The Scottish SIGN guidance was used to guide diagnostic process.

Discussion:

There was variability in overall cognitive functioning across the children assessed, ranging from Mild Learning Disability to Low Average cognitive ranges. Across cognitive domains, there was great variability, with the majority showing relative strengths in Verbal Comprehension. There was variability in the Working Memory domain across assessments, and all children showed significant relative impairments in Processing Speed, Fluid Reasoning and Visuo-Spatial domains. This “spiky profile” contributed to diagnostic overshadowing, as average/ low average full-scale IQ scores sometimes masked clinically significant cognitive impairments at domain level. The ABAS often revealed gaps between cognitive abilities and real-world functioning.

Conclusion:

FASD may be under-diagnosed in CAMHS populations, particularly where children present with complex needs and uneven cognitive profiles. Awareness of “spiky” neurocognitive patterns and systematic multidisciplinary assessment can improve diagnostic accuracy and inform educational and therapeutic support. The ABAS, alongside cognitive assessments are important in identifying domains of difficulty in the real world. Early identification has significant implications for care-planning, family understanding and psychological support in receiving a diagnosis of FASD.

The patient is a 76 years old female without any past psychiatric history. She was married for 50 years and her husband died a year ago. Since then she became withdrawn and stopped eating, drinking. She was admitted to general hospital with hyponatremia.

The patient was reviewed by Liaison psychiatry, she had symptoms of anhedonia, self-neglect, guilt, paranoia and psychomotor retardation. She was diagnosed with severe depressive episode with psychotic features and treated with Mirtazapine 45mg and Quetiapine 100mg.

There was no improvement on medication. She continued to decline food, water and had frequent hypoglycaemic attacks. Her BMI was 12.9. Bifrontal Electroconvulsive therapy (ECT) treatment was decided. During pre-ECT check-up her CRP was 38.

During the first episode, she didn’t have seizure on 10% stimulus. On 15% stimulus she had 109 seconds seizure on EEG. Post-ictal suppression was poor.

During the second episode, on 15% stimulus she had 77 seconds seizure on EEG.Post-ictal suppression was fair. Etomidate 10 mg was used as anaesthetic for both episodes.

While in recovery the patient was nonresponsive. Her blood sugar level was 4.6 mmol/L and she was given Dextrose. It rose to 9.9 mmol/L and she started to have seizure.

She had two observed seizures lasting 42 and 20 seconds. Her third seizure lasted 94 seconds while connected to EEG. She was given Propofol 20mg to stop the seizure.

She had a CT head without any acute findings. Chest X-ray showed shadow on the right base. Her CRP was 43 and sodium was 131.

Tardive seizure is a rare complication of ECT. It is a spontaneous seizure after ECT, there should be full recovery of consciousness before the onset.

Lansari et el (2025) found several factors associated with tardive seizure such as treatment that lowers the epileptogenic threshold, anaesthesia with Etomidate, prolonged seizure, and poor post-ictal suppression.

Another differential is that the seizure didn’t fully terminate after ECT, it became focal and later manifested as general tonic-clonic seizure. It is unclear if the patient fully recovered consciousness after ECT.

The patient was started on Lamotrigine and remained seizure free. Due to her deteriorating physical health, she didn’t receive further ECT. There were some improvement to her mood and appetite with Mirtazapine and Venlafaxine.

Repeated ECT has been safe for many patients even after tardive seizure. Only 15% of patients developed further tardive seizure after restarting ECT (Warren et el 2022).

BACKGROUND

Neurological deterioration during alcohol detoxification is commonly attributed to alcohol-related complications, particularly Wernicke’s encephalopathy, withdrawal syndromes or side effect of detox treatment.While such diagnostic pathways are clinically appropriate, they may predispose to premature diagnostic closure. This case highlights the risk of diagnostic overshadowing when alternative neurovascular pathology presents with overlapping features.

AIMS

1. To examine diagnostic challenges associated with recurrent falls and neurological symptoms during inpatient alcohol detoxification

2. Highlight the clinical overlap between Wernicke’s encephalopathy and thalamic stroke, necessitating early neuroimaging

3. Emphasise the importance of structured reassessment and vigilance during week-two detox complications.

A retrospective single-case clinical analysis was undertaken within an inpatient addiction detoxification unit. Clinical records, nursing observations, withdrawal monitoring tools, medical reviews, and neuroimaging reports were examined to reconstruct the diagnostic trajectory, differential formulation, and escalation decisions.

Case Presentation:

A 60-year-old man was admitted for planned alcohol detoxification, reporting daily consumption of approximately 14 units of lager with a Severity of Alcohol Dependence Questionnaire (SADQ) score of 28. He had no prior detoxifications, no history of delirium tremens, and no active psychiatric comorbidity. Past medical history included thrombocytopenia and abnormal liver function tests attributed to non-alcoholic fatty liver disease. Baseline physical examination was unremarkable.

During week two of detoxification, he developed recurrent falls preceded by dizziness and a “funny head” sensation. One episode occurred after rising from bed; another followed standing from the toilet. There was no loss of consciousness, seizure activity, or incontinence. Subsequent review identified a new broad-based gait,nystagmus, left upper limb hypertonia, and subtle postural weakness, although other cranial nerve examination and speech remained intact. Cognitive biases (anchoring to withdrawal, premature closure, and diagnostic overshadowing) were identified as potential contributors to delayed escalation. Initial differentials included Wernicke’s encephalopathy, hypotensive episodes related to antihypertensive use, high dose in detox reducing regime and transient ischaemic attack. The patient initially declined emergency transfer due to lack of confidence in emergency department waiting times, but was urgently escalated for acute hospital assessment and a brain scan following clinical concern.

Emergency department evaluation noted nystagmus, gait ataxia, and memory impairment. MRI revealed anacute right thalamic infarct, with additional cerebellar microhaemorrhages and chronic small-vessel disease. The thalamic lesion explained the patient’s gait disturbance, postural instability, and subtle motor changes, which had initially mimicked Wernicke’s encephalopathy.

Outcome:

The patient was transferred to neurology, commenced on stroke-appropriate management, and referred for physiotherapy. He continued relapse-prevention work with our community alcohol services and was started on acamprosate. This case demonstrates how acute stroke can present with symptoms easily misattributed to alcohol withdrawal syndromes, underscoring the need for repeated assessment and a low threshold for neuroimaging when the clinical picture evolves.

This case underscores the potential for neurovascular events to mimic alcohol-related neurological syndromes during detoxification. Thalamic infarcts may present with gait disturbance, cognitive change, and ocular signs that overlap with Wernicke’s encephalopathy. Clinicians should maintain a broad differential when new focal signs, persistent/new ataxia, or incomplete response to thiamine therapy emerge. Early neuroimaging is essential to avoid diagnostic delay and optimise neurological outcomes.

Regardless of comorbid personality disorder there is value in use of ECT for treatment resistant depression. We present a case of a patient with treatment resistant depression and dependent personality disorder.

There is evidence that ECT used to treat depression with a comorbid personality disorder has poorer outcomes. Ferrea et al., 2023, found poor response rates in comorbid personality disorder as opposed to depression alone, with increased risk of relapse, but still showed a remission rate of 1 in 3 and 50% response rate. However, most of the studies included didn’t differentiate the type of personality disorder, leaving us without clear evidence around the impact of dependent personality disorder specifically.

We present a case of a 78-year-old female patient with diagnoses of recurrent depressive disorder and generalised anxiety disorder. The patient had two admissions in two years under the mental health act with similar presentations in keeping with severe depression. In the community she was being investigated for autism, underlying cognitive impairment, dependent personality disorder and being treated for recurrent depression and generalised anxiety disorder which didn’t fully remit in the 2 years she was open to the service.

She is followed through admission and investigations to a course of treatment with Bilateral ECT lasting for 12 sessions.

On Montgomery-Åsberg Depression Rating Scale the patient scored 34 before starting ECT treatment, and after completing the course scored 20. Clinical global impression rating rose from 6- severely ill, before course of ECT to 4- moderately ill, following.

Despite the potential multiple contributing diagnoses, the patient’s mental state and presentation improved in response to treatment with ECT.

There is evidence of benefit in switching and augmenting antidepressants in older adults where there is treatment resistance (Lenze et al. 2023). This case supports the hypothesis that in treatment resistance in the elderly population we should persevere up to and including the use of ECT, until remission is achieved.

There’s a lack of research looking specifically at the impact of comorbid dependent personality disorder on efficacy of ECT for depression. Most of the existing evidence focusses on Emotionally unstable personality disorder.

This case study supports the hypothesis that there is evidence of treatment response with the use of ECT for treatment resistant depression regardless of comorbid dependent personality disorder.

Frontotemporal dementia (FTD) is the second most common cause of early-onset dementia accounting for approximately 10–20% of all dementia cases. The behavioural variant (bvFTD) is the most common presentation, comprising 50–57% of autopsy-confirmed FTD cases. bvFTD is highly heritable, and most implicated genes are MAPT, GRN (progranulin), and C9orf72.

We report a case of two brothers, the first brother, aged 62, was assessed in the memory service in 2022 following a five-year history of behavioural change including inappropriate behaviour, overeating, apathy, and memory impairment. His Addenbrooke’s Cognitive Examination (ACEIII) score was 56/100. CT brain imaging showed generalised atrophy, more pronounced on the right. PET CT demonstrated hypometabolism particularly in the right frontotemporal region. Amyloid PET imaging showed no abnormal amyloid binding.

The second brother, aged 64, was assessed in 2024 with a two-year history of progressive cognitive decline and pronounced frontal lobesymptoms including apathy, irritability, lack of insight, impaired executive function, and poor financial management leading to debt. He required family support for most activities of daily living and scored 24/100 on the ACE. CT brain imaging showed pronounced frontal and medial temporal lobe atrophy. FDG-PET demonstrated reduced uptake in the frontal, temporal, and parietal lobes.

Both brothers underwent whole genome sequencing and were found to be heterozygous for a GRN mutation. Predictive genetic testing was recommended to their children, and two of four tested positive for the mutation.

GRN mutations account for 35% of genetic FTD and around 10% of all FTD cases. GRN-FTD follows an autosomal dominant inheritance pattern. In our patients, there was no family history of FTD, although their father had possible undiagnosed dementia while their mother had Parkinson’s disease and Alzheimer’s disease. Notably, up to 13% of bvFTD cases carry a genetic variant despite no family history.

Genetic testing is a crucial diagnostic tool for defining the molecular pathology of the disease particularly in psychiatric settings where early bvFTD is often misdiagnosed as a primary psychiatric disorder. Furthermore, Identification of a GRN mutation is also essential for determining eligibility for clinical trials.

Predictive genetic testing for at-risk relatives enables them to make informed decisions regarding life and future care.

This case highlights the importance of whole genome sequencing and predictive genetic testing even in the absence of a convincing family history. This could improve both patient care and our overall understanding of the disease.

Distinguishing primary functional disorders from psychiatric illness arising secondary to chronic physical symptoms remains a significant clinical challenge, particularly when structural pathology is absent. Failure to make this distinction risks premature psychological attribution, diagnostic overshadowing, and invalidation of patient experience. Although ICD-11 offers updated frameworks for understanding disorders at the brain–body interface, their application to complex presentations requires careful clinical judgement to avoid misinterpretation of psychiatric risk.

Case Report

We present a case that illustrates this diagnostic tension. A 48-year-old woman with high premorbid functioning and no prior psychiatric history developed a progressive multisystem physical illness following international travel. Symptoms included gastrointestinal dysmotility, bladder dysfunction, autonomic instability, and sleep disruption. Despite extensive investigation, no unifying structural or neurodegenerative diagnosis was identified.

As the physical illness persisted, the patient developed a severe depressive syndrome with suicidality. Notably, affective symptoms emerged only after the onset of physical decline and fluctuated in parallel with physiological distress, rather than following an autonomous psychiatric course.

This case highlights the importance of distinguishing primary functional disorders from psychiatric illness that is reactive to chronic physical dysfunction. Contemporary models conceptualise functional conditions as disorders of brain–body interaction, characterised by altered interoceptive processing and maladaptive predictive mechanisms. In such cases, these processes are central to symptom generation and represent appropriate targets for psychiatric intervention.

By contrast, secondary psychiatric illness arises in response to prolonged physical uncertainty, loss of bodily predictability, and erosion of trust in physiological functioning. In this context, the depressive syndrome does not account for the physical symptoms but develops as a consequence of them. Temporal sequencing is therefore a key diagnostic marker. Failure to recognise this distinction risks premature psychological attribution, erosion of the therapeutic alliance, and misinterpretation of suicide risk. In such cases, suicidality is often driven by existential distress related to persistent physical suffering and fear of irreversible decline, rather than affective pathology alone.

Not all distress associated with unexplained physical symptoms is somatoform. Psychiatry’s role is not to resolve medical uncertainty through psychological explanation, but to locate distress accurately within the patient’s causal narrative. Careful formulation, grounded in phenomenology and temporal sequencing, is essential for ethical practice and effective risk management - and in cases such as these can prove to be life saving

This is a comparative study between two unusual and distinct cases of catatonia, managed by the Liaison psychiatry team that helped us to broaden our thinking and explore variable differential diagnoses for patients’ management.

Case1: Mr.P is a 74-year-old male who was admitted following unusual behaviour, including shouting with slurred speech outside his house. During his admission, he was non-verbal, non-compliant with oral intake including medication and demonstrated bradykinesia and stiff joints. His initial investigations were unremarkable.

Mr. P has a background history of Paranoid Schizophrenia and been treated with Aripiprazole 30mg. Four months prior, he had a lengthy hospital admission with a similar presentation, and he was conservatively managed for hypoactive delirium.

Our differential diagnoses included hypoactive delirium, catatonia, CNS infection and NMS. When the physical health issues were ruled out, a Lorazepam challenge test was initiated; this was effective and made a significant change in his presentation. Thus, we diagnosed him with Catatonia and treated him with high dose of Lorazepam according to the policy. At discharge he had returned to his baseline.

Case2: Mrs.Q is a 78-year-old female who was admitted to hospital after concerns of self-neglect and confusion. Her initial investigations showed an AKI and raised inflammatory markers. Thus, she was treated with IV fluid and antibiotics. Collateral from daughter suggested that Mrs. Q had a rapid decline in her presentation prior to the hospital admission.

Mrs.Q has a background history of depression and been treated with Mirtazapine 15mg.

Despite optimisation in her physical health, Mrs. Q did not show significant improvements. She had minimal engagement, minimal oral intake, very slow movements, and significant thought block. Initially, it was presumed that Mrs.Q had a slowly resolving delirium, however as she was not improving as expected so a Lorazepam challenge test was trialled. Mrs Q responded well to the lorazepam challenge, thus, she was diagnosed with catatonia and treated accordingly.

Catatonia is a neuro-psychiatric condition characterised by marked changes in muscle tone or activity that may alternate between extremes of movement deficits (stupor) and excessive movement (excitement). According to DSM-5 and ICD-11, a diagnosis requires the presence of three or more of the 12 clinical features.It can be validated through BFCRS or KCRS. Catatonia is not a disease, but a syndrome associated with various conditions.Its management includes Benzodiazepams, and/or ECT and supportive care.

The co-occurrence of delusional parasitosis (primary Ekbom syndrome) with idiopathic Parkinson’s disease is considered rare. Most literature consists of individual case reports or small series, indicating it is an uncommon but recognised clinical phenomenon. The rarity is compounded by the therapeutic challenge it presents.

A 74-year-old gentleman of Caribbean origin, with a longstanding diagnosis of persistent delusional disorder (delusional parasitosis, F22.0), was admitted under Section 3 of the Mental Health Act. He had a history of non-concordance with olanzapine for three years, resulting in significant clinical deterioration. Comorbidities included idiopathic Parkinson’s disease (also non-concordant with medication) and prostate cancer in remission.

On presentation, he exhibited classic Ekbom syndrome: believing bugs infested his body, he applied yoghurt to his skin and stored debris. Profound self-neglect, hoarding of soiled items and out-of-date food, and environmental squalor were noted. Significant weight loss, worsening mobility, and cognitive decline were reported.

Management was complicated by the contraindication of many antipsychotics in Parkinsonism, where they exacerbate motor symptoms. Olanzapine was briefly restarted but poorly tolerated. Aripiprazole was initiated cautiously at a low dose (max 25mg daily) with monitoring for akathisia. Procyclidine effectively managed resultant hypersalivation. His Parkinson’s medications were recommenced.

Pharmacological guidance, per Maudsley’s guidelines, restricts options. Risperidone and typical antipsychotics like flupentixol are contraindicated due to high extra-pyramidal side effect risk. While quetiapine has marginal efficacy, it is often trialled before clozapine. In this case, aripiprazole was selected as a potentially safer atypical agent.

This case illustrates the complex interplay between psychotic illness and neurodegenerative disease, highlighting the severely limited and high-risk antipsychotic options available. Multidisciplinary management, including SALT input (showing dietary improvement), remains essential for this vulnerable patient with concurrent severe mental illness, physical comorbidity, and challenging medication non-adherence.