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The purpose of this paper is to suggest that student-led case studies are an important way to learn about mental health problems and to highlight this by presenting a case study of the comedic genius Spike Milligan.

Celebrities live their lives in the public eye. In recent years, many have talked about their struggles with mental health. This paper is based on a student-led case study of the celebrity Spike Milligan.

This case study suggests one previously under-emphasised issue and argues that Spike Milligan’s wartime experiences may have led to post-traumatic stress disorder. Second, that he may have developed neuro-inflammation, through contracting sandfly fever during the war. This could have been an additional trigger for bipolar disorder.

While this is a single case study, it draws on a wide variety of research sources to back up the arguments advanced.

Student-led case studies provide a way of engaging students more actively with mental health problems.

Mental illness is complex, if not more complex, than physical health problems. Case studies of celebrities like Spike Milligan can help develop a public understanding of mental illness, as they already have a working knowledge about the person.

The case study illustrates how Bipolar 1 disorder is a complex and unique condition and that every individual’s illness has different predisposing characteristics. It suggests that student-led case studies are a helpful learning tool.

Hypersexuality and gender dysphoria have both been described in the literature as symptoms of mania. Hypersexuality is listed in the Diagnostic and Statistical Manual of Mental Disorders 5 as part of the diagnostic criteria for bipolar disorder. Gender dysphoria is less often described and its relation to mania remains unclear. This case report describes a young homosexual man presenting in a manic episode with co-morbid amphetamine abuse whose mania was marked by hypersexuality and the new onset desire to be a woman. Both of these symptoms resolved with the addition of valproic acid to antipsychotics. This case report presents the existing literature on hypersexuality and gender dysphoria in mania and describes a treatment option that has not been previously reported.

This audit was conducted on acute psychiatric in‐patient wards with the aim of establishing if valproate prescribing in acute mania followed evidence‐based guidelines with particular emphasis on formulations used and whether accelerated valproate dosing was employed.

Case notes from 43 (42 percent male) patients admitted with mania and subsequently discharged on valproate were reviewed. Valproate formulation, weight measurement (necessary for dose‐calculation in accelerated dosing), initial valproate dose and increments, serum valproate monitoring and other prescribed psychotropic agents were noted.

Most (95 percent) patients received sodium valproate (epilim chrono/generic), the remaining received valproate semi‐sodium (depakote). All but one patient received antipsychotic medication in combination. Weight was recorded in only four (9 percent) patients. The mean valproate daily dose after the first week was 1,027 mg (sd=408). It took 29 (sd=42) days to reach the maximum daily dose (1,426 mg sd=467) from valproate initiation. Serum levels were monitored in 34 (79 percent) cases, but the mean period between valproate initiation to the first serum level test was 38 (sd=47) days. A significant positive correlation was found between days taken to reach maximum dose and hospital stay (Spearman's rho=0.41, n=43, p=0.006, two‐tailed).

Accelerated valproate dosing was not common practice, which may have resulted in suboptimal efficacy, probably leading to combination treatment.

This study highlights the need for adequate initial dosing and dose increments when treating manic patients and suggests current practice is not evidence‐based. Local prescribing policy and national guidelines' influence on practice are discussed.

There is evidence to suggest an association between mood disorders, in particular bipolar disorder, and creativity. This paper aims to examine the evidence that the writer Herman Melville suffered from bipolar disorder.

An interdisciplinary approach is adopted, examining the genetic and biographical evidence as well as textual examples that illustrate the argument in his masterpiece Moby Dick.

Taking the genetic, behavioural, and textual evidence together, it is concluded that the likelihood that Melville did have bipolar disorder is high.

Retrospective analysis of the biographies and work of deceased writers has acknowledged limitations. Close examination of all Melville's literary output would be useful to either add credence to this theory or refute it.

Adding to the evidence that revered writers and artists were on the bipolar disorder spectrum helps people with the condition feel more positive and reduces stigma.

Close literary examination of textual examples of hypomanic writing, combined with a psychological approach to Melville's biography provides evidence that Melville's mental illness contributed positively to his creativity as a writer and is therefore evidence that this condition has some benefits to society.

Although first rank symptoms focus on positive symptoms of psychosis they are shared by a number of psychiatric conditions. The difficulty in differentiating bipolar disorder from schizophrenia with affective features has led to a third category of patients often loosely labeled as schizoaffective. Research in schizophrenia has attempted to render the presence or absence of negative symptoms and their relation to etiology and prognosis more explicit. A dichotomous population is a recurring theme in experimental paradigms. Thus, schizophrenia is defined as process or reactive, deficit or non-deficit and by the presence or absence of affective symptoms. Laboratory tests confirm the clinical impression showing conflicting responses to dexamethasone suppression and clearly defined differences in autonomic responsiveness, but their patho-physiological significance eludes mainstream theory. Added to this is the difficulty in agreeing to what exactly constitutes useful clinical features differentiating, for example, negative symptoms of a true deficit syndrome from features of depression. Two recent papers proposed that the general and specific cognitive features of schizophrenia and major depression result from a monoamine-cholinergic imbalance, the former due to a relative muscarinic receptor hypofunction and the latter, in contrast, to a muscarinic hypersensitivity exacerbated by monoamine depletion. Further development of these ideas will provide pharmacological principles for what is currently an incomplete and largely, descriptive nosology of psychosis. It will propose a dimensional view of affective and negative symptoms based on relative muscarinic integrity and is supported by several exciting intracellular signaling and gene expression studies. Bipolar disorder manifests both muscarinic and dopaminergic hypersensitivity. The greater the imbalance between these two receptor signaling systems, the more the clinical picture will resemble schizophrenia with bizarre, incongruent delusions and increasingly disorganized thought. The capacity for affective expression, by definition a non-deficit syndrome, will remain contingent on the degree of preservation of muscarinic signaling, which itself may be unstable and vary between trait and state examinations. At the extreme end of muscarinic impairment, a deficit schizophrenia subpopulation is proposed with a primary and fixed muscarinic receptor hypofunction.

The genomic profile of bipolar disorder and schizophrenia overlap and both have a common dopaminergic intracellular signaling which is hypersensitive to various stressors. It is proposed that the concomitant muscarinic receptor upregulation differentiates the syndromes, being marked in bipolar disorder and rather less so in schizophrenia. From a behavioral point of view non-deficit syndromes and bipolar disorder appear most proximate and could be reclassified as a spectrum of affective psychosis or schizoaffective disorders. Because of a profound malfunction of the muscarinic receptor, the deficit subgroup cannot express a comparable stress response. None -theless, a convergent principle of psychotic features across psychiatric disorders is a relative monoaminergic-muscarinic imbalance in signal transduction.

The prevalence of diabetes among 915 sexual, violent, and non‐violent non‐sex offenders was found to be more than twice the prevalence in the general population. Diabetes was most common among violent offenders and among sex offenders who victimized children. The older diabetics presented significantly more often with cognitive impairment and younger diabetics more often with manic and psychotic symptoms. Younger diabetics were significantly more likely to use force and a weapon in their offenses and were most likely to injure their victims when compared to older diabetics and younger and older non‐diabetic offenders. In more than one in four cases, the diabetes was undiagnosed at the time of their offenses prior to clinical assessment, suggesting that undiagnosed diabetes may be a possible mitigating factor in some sexual and violent offenses. Results indicate that a routine endocrine evaluation with blood tests would be a valuable addition to the assessment of violent and sexual offenders.