Bell's mania

The majority of Bell's mania cases studied are triggered by psychostimulant drug usage or preexisting medical or neurological conditions, which impedes the apprehension of this syndrome.  Hence at present, there is still no scientific consensus on the clinical features of Bell's mania. Researchers are currently working on varying case studies to derive common clinical characteristics. Some frequent signs and symptoms include acute onset of delirium, mania or psychosis. They tend to be excited, agitated, paranoid, delusional and alarmed. Impaired concentration, memory loss, disorientation, insomnia, auditory and visual hallucinations are additional symptoms that follow. == Diagnosis ==

This condition is currently not recognized as a diagnosable issue by psychiatric journals such as the Diagnostic and Statistical Manual of Mental Disorders-IV Additionally, mental status examination using questionnaires the face-hand test and hidden figures tests. Patients with Bell's mania tend to make obvious mistakes in these tests, for instance drawing a clock-face with incorrect numbering or missing clock hands. Differential diagnosis Upon acute onset of the symptoms, an instant investigation for a toxic or systemic cause is undertaken. Prominence of thought disorder, grandiosity and delusional ideation, and catatonic signs indicates the diagnosis of acute schizophrenia, bipolar disorder and catatonia respectively. Diagnostic complications arise as these signs are also often the notable feature of Bell's mania. With the cause undetermined, Bell's mania diagnosis is usually justified with the presence of both mania and delirium regardless of the catatonic symptoms. Distinguishing from catatonia Bell's mania and catatonia are regarded as "overlapping syndromes", making differential diagnosis essential when catatonic signs are observed. Thus, researchers must distinguish between excited catatonia and Bell's mania, and among malignant catatonia, excited catatonia, and neuroleptic malignant syndrome (NMS). When catatonic features are prominent, it is diagnosed as excited catatonia and when absent or subtle, it is identified as Bell's mania. Alternatively, the presence of delirium is recognized as the discerning factor. A difference between the two is that catatonia is viewed from a movement aspect, whereas delirium from consciousness. Nevertheless, a formal set of diagnostic criteria is required to distinguish between Bell's mania and catatonia. Failure to diagnose Bell's mania appearing as catatonia could lead to deleterious consequences and, in worse cases, death. == Pathophysiology ==

Dopamine is the primary neurotransmitter involved in the pathophysiology of Bell's mania. Increased extracellular dopamine levels can be caused by low levels of dopaminergic transporters, sensitization of postsynaptic dopaminergic receptors, and dopamine transporters dysfunction. Genetic studies have hypothesized a relationship between low transporter protein levels and the gene for dopamine transporter in bipolar affective patients. In chronic users, drug sensitization occurs which induces increased neurotransmission and modified protein expression within the mesolimbic dopamine neurons. Adaptations in dopamine transporters is further triggered causing behavioral sensitization. This phenomenon is not distinct to drug abuse but also other psychomotor stimulants such as stress. Dopamine imbalance can hence result in hyperthermia, tachycardia, hyperventilation, hypertension and sleep disturbance symptoms. == Risk factors ==

Given that hyperdopaminergic state is postulated to be the underlying mechanism of Bell's mania, people prone to dopamine imbalance, sensitization and low levels of dopamine transporters are susceptible. • People with severe manic episodes • Sleep deprivation which can trigger and even worsen acute manic episodes • People with medical history of neurological and physiological conditions == Treatment and management ==

Whilst the scope of Bell's mania is extensively studied, there remain some significant challenges that need to be solved with respect to treatment and management. resulting in autonomic hyperactivity and increase in dopamine levels in the victims. can help. Several studies also point at the increased effectiveness of combination of two or more sedatives in the treatment of hyper-agitated patients. Intramuscular ketamine injections Patients with Bell's mania may not have optimum time for the sedatives to start showing effect. Due to this fact, electroconvulsive therapy Although adult data on the use of ketamine on patients is not readily available, a study by Strayer et al. concluded that the use of ketamine for controlling the hyperactivity was reliable and can further facilitate other management techniques with fewer side effects. Other preventative measures Along with sedation techniques, a few other prevention and protection measures can decrease fatal outcomes, some of which are: • management of catecholamine cascade, • basic medical monitoring of bodily functions, • blood tests, • physical examination and • rapid cooling of the body temperature. and neuroleptic malignant syndrome (NMS), dantrolene is also a probable treatment route owing to its swift acidosis correction. Although more research is needed in correspondence to the cause and consequences of this disease, the significance of the behavioral and physical symptoms need to be given importance to provide medical institutions as well the constabulary the necessary information to respond to Bell's mania appropriately. == Epidemiology ==

The first case of Bell's mania was observed by medical examiners during the cocaine epidemic The term Bell's mania was first coined to describe the clinical condition with a 75% mortality rate. The prevalence of this condition ranges from 15% to 25% in Bipolar 1 patients, and is not an infrequent occurrence. == History ==

First mention Bell's mania is a syndrome with unexplained etiology which was first explained by American psychiatrist Luther Bell in the 1850s after observing institutionalized psychiatric patients. The first clinical reports and descriptions of people with acute exhaustive mania and delirium were provided by a few psychiatrists in the United States of America, France and the United Kingdom. He termed this description as lethal catatonia. Other reasons for the manifestation of Bell's mania, points at the use of stimulant drugs in excessive amounts and also psychiatric diseases like depression or schizophrenia. In 1985, Bell's mania was first mentioned in a definitive manner using the term excited delirium (EXD). Prior to that year, most cases of death by cocaine intoxication during the cocaine epidemic that happened in a sudden manner. This involved the exposure to highly toxic amounts of the drug due to the bursting of cocaine packets being carried within the body by "body stuffers". In the same year a series of observations were made by Welti and Fishbain regarding psychosis, cardiorespiratory arrest and sudden death in individuals with cocaine addiction. Since the law enforcement were often called to contain violent behavior exhibited by these individuals, it was speculated that police brutality might be the underlying cause of the deaths. Upon medical review of the cases related to the use of batons, pepper sprays and restraint methods did not disclose any autonomic cause behind the death, albeit problems like cardiac diseases and trauma was excluded from the extensive evaluation. == See also ==