Secondary Mania Research Articles

A Comprehensive Review of the Evaluation, Diagnosis, and Treatment of Older Adult Bipolar Disorder

This review summarizes the extant literature on the epidemiology, neuropsychology, clinical assessment, and treatment/management of older adult bipolar disorder (OABD). The primary aim was to provide a contemporary and accessible reference for clinicians involved in the care of OABD patients. Important research into the unique features of OABD has been carried out in recent years, providing a more robust albeit still limited foundation to help guide clinical decision-making. Some of the more consistent findings have highlighted (1) the importance of assessing for potentially reversible sources of secondary mania (i.e., manic symptoms unrelated to a primary mood disorder but with qualitatively similar presentation) in patients with late-onset mania; (2) the need for closer follow-up and more aggressive treatment to help stabilize illness course in OABD patients with earlier symptom onset; (3) the presence of domain-general cognitive dysfunction (but not accelerated cognitive aging) in OABD; and (4) the strong need for more randomized control trials examining the safety and efficacy of various psychopharmacological interventions in OABD samples. Research continues to support lithium as the gold-standard treatment for OABD, but there are other promising therapies. Asenapine, lurasidone, and divalproex have demonstrated efficacy in reducing symptoms, but future research must also categorize their side effect profile and most effective use in treatment (e.g., monotherapy or adjunctive therapy). ECT may be a useful alternative to pharmacotherapy, but very little research has been conducted in the OABD patient population. Compared with mixed age and younger samples, there is a paucity of clinical research specific to OABD. To date, the treatment literature in OABD is limited by small sample sizes, cohorts of mixed-age populations, and non-randomized and uncontrolled study designs. Consequently, making evidence-based treatment decisions often requires extrapolating data from studies of younger adults with BD. Fortunately, international collaborative efforts have recently been established that will include, for the first time, much larger sample sizes to better characterize the natural history, clinical course, comorbidities, and effective therapies for OABD.

New-onset mania in an elderly patient five months after acoustic neuroma resection.

1. Even in cases of acoustic neuroma without psychiatric symptoms before surgical intervention, secondary mania could develop after surgery. 2. It is necessary to be aware of potential mania onset following acoustic neuroma resection for at least several months.

A case report of mania with abnormal cerebral blood flow and cognitive impairment 24\xa0years after head trauma

BackgroundMania usually occurs secondary to organic etiologies such as head trauma within a short time of the primary condition’s onset; however, there have been a few cases reported in the literature of long time spans before the manifestation of mania. The orbitofrontal cortex has been reported to be associated with manic states in bipolar disorder and with mania-inducing lesions. Head trauma commonly disrupts various cognitive functions, including attention and information processing. Traumatic brain injury patients have been shown to have greater posterior cingulate cortex and precuneus functional connectivity to the rest of the default mode network. We describe a case of secondary mania after head trauma 24 years ago with low blood flow in the orbitofrontal cortex, high blood flow in the posterior cingulate cortex, and impaired cognitive functioning, including impaired attention and lowered processing speed.Case presentationWe describe a 30-year-old Japanese man with secondary mania and a medical history of head trauma 24 years ago. After head trauma at 6 years of age, the patient first showed apathy as a sign of frontal lobe impairment. After recovering, he experienced no psychiatric problems during adolescence, although he did show disinhibited behavior. At the onset of mania, low blood flow in the OFC and high blood flow in the PCC were observed as well as impaired cognitive function, including inattention and lowered processing speed. Abnormal cerebral blood flow was less prominent and cognitive dysfunction was partially recovered following recovery from mania, but his processing speed remained low.ConclusionsAlthough functional recovery from head trauma in childhood is better than that in adulthood, the brain may remain vulnerable for a long time. The risk of psychotic symptoms such as mania should be considered, even if sufficient superficial brain functional recovery is shown.

Valproic Acid in the Treatment of Secondary Mania Caused by Metastatic Brain Tumors

Valproic Acid in the Treatment of Secondary Mania Caused by Metastatic Brain Tumors

Poststroke Mania: Cardioembolic Multifocal Right Hemispheric Stroke Leading to Secondary Mania

Poststroke Mania: Cardioembolic Multifocal Right Hemispheric Stroke Leading to Secondary Mania

Mood disorder following traumatic brain injury: a case report

Traumatic brain injury is a clinical situation that generally affects young people aged 45 years or younger and causes mortality and critical functional losses. The most common psychiatric disorder following taumatic brain injury is depression. Although the relationship between depression and organic diseases has been studied a lot, there is less data about mania. Secondary mania differs from primary mania with advanced beginning age, absence of family history, more difficult and slower response to treatment; and secondary mania usually has no recurrence. In this report, secondary mania and its clinical features are discussed in light of a mood disorder following a trauma case. The case is still followed with mood stabilizer treatment and the patient is euthymic.

Secondary mania as a possible presentation of a C9orf72 hexanucleotide repeat expansion.

Secondary mania as a possible presentation of a C9orf72 hexanucleotide repeat expansion.

Bipolar affective disorders in senescence

Diagnostic and therapeutic measures in patients with bipolar disorders are significantly different depending on the age of those affected. Given the demographic changes and the fact that approximately one quarter of patients with bipolar disease are in old age, it is important for geriatricians to be aware of the specific aspects of bipolar disease. This review article presents the diagnostics of bipolar disorders in old people. Interactions with somatic comorbidities, which may lead to the occurrence of secondary mania, just to mention one of the characteristics of old age, are elaborated. Furthermore, age-specific differences also necessitate altered or adjusted therapy regimens, which deviate from those of younger patients.

Manic Episodes Due to Medical Illnesses: A Literature Review.

The body of evidence for mania as a secondary syndrome due to organic diseases is small. The clinical diagnosis and management of these patients are mainly based on clinical experience and on some case reports. Treatment should be focused on both the underlying medical illness and the control of acute symptoms. Mania due to a medical condition is relevant in the clinical setting, and thus more research is needed to add evidence-based recommendations to the currently available clinical knowledge. In this review, we summarize the latest information on the etiology, epidemiology, diagnostic aspects, and management of secondary mania.

The late-onset bipolar disorder: A comparative study

IntroductionBipolar disorders (BP) with late onset are underestimated by their frequency, their misleading presentations and therapeutic difficulties due to the high prevalence of somatic comorbidities.AimTo identify sociodemographic, clinical and therapeutic characteristics in subjects with a late-onset BP.Patients and methodsRetrospective and comparative study of 101 patients followed for a BP (12 patients with BP started after 50 years and 89 patients with BP started earlier) from 2009 to 2015, in the department of psychiatry of the University Hospital Farhat Hached, Sousse, Tunisia.ResultsThe mean age of subjects with late-onset TBP was 46.11 ± 12.85 years. Women were in the majority (65.3%). Ten patients had a novo mania, four patients had a late-onset mania and one patient had a secondary mania. Regarding the socio-demographic data, only the regular professional activity was more reported in the elderly (P = 0.017). Regarding clinical data, BP type 1 and secondary mania were more reported in elderly with (P = 0.050 and P = 0.000 respectively). Elderly had significantly fewer depressive episodes (P = 0.026), fewer hypomanic episodes (P = 0.000). The durations of the latest episodes and the last intervals were shorter in elderly (P = 0.045 and P = 0.000). Concerning therapeutic data, elderly had fewer hospitalizations (P = 0.045), required lower mean doses of lithium (P = 0.04) and greater mean doses of tricyclic antidepressants (P = 0.047).ConclusionIt is always necessary to look for an organic cause in manic syndrome in late-onset BP. Doses of lithium should be lower. However, doses of TAD should be higher.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Late onset bipolar disorder: Clinical characterization

IntroductionBipolar disease is a chronic mental illness with a deep personal and social impact. Alongside with the considerable progress in understanding and treating bipolar disorder, and despite the growing interest in geriatric psychiatry, late onset bipolar disorder has been relatively little studied so far.ObjectivesTo review the literature regarding the epidemiology, characteristics and clinical implications of late onset bipolar disorder.MethodologyA literature review was performed by searching articles in Pubmed, using the following search terms: “late onset bipolar disorder” and “elderly bipolar disorder”. All literature in English published in the last 15 years was examined and 11 articles were selected.ResultsAlthough the frequency of bipolar disorder type 1 or 2 decrease with age, approximately 6 to 8% of the new cases of bipolar disorder develop in people over 60 years of age. Clinically, late-onset bipolar disorder appears to be associated with a better level of pre-morbid functioning, a less severe psychopathology as well as a smaller family burden of psychiatric illness. The term “secondary mania” postulated by Krauthmamer Klerman has been used to describe a bipolar disease variant associated with a variety of organic factors that may be responsible for this late-onset disease.ConclusionsLate onset bipolar disorder is probably a different diagnostic than the entity that occurs in younger patients, since it presents with a different clinical presentation. It is a heterogeneous disease with a complex etiology that still needs more research.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Mania secondary to focal brain lesions: implications for understanding the functional neuroanatomy of bipolar disorder.

Approximately 3.5 million Americans will experience a manic episode during their lifetimes. The most common causes are psychiatric illnesses such as bipolar I disorder and schizoaffective disorder, but mania can also occur secondary to neurological illnesses, brain injury, or neurosurgical procedures. For this narrative review, we searched Medline for articles on the association of mania with stroke, brain tumors, traumatic brain injury, multiple sclerosis, neurodegenerative disorders, epilepsy, and neurosurgical interventions. We discuss the epidemiology, features, and treatment of these cases. We also review the anatomy of the lesions, in light of what is known about the neurobiology of bipolar disorder. The prevalence of mania in patients with brain lesions varies widely by condition, from <2% in stroke to 31% in basal ganglia calcification. Mania occurs most commonly with lesions affecting frontal, temporal, and subcortical limbic brain areas. Right-sided lesions causing hypo-functionality or disconnection (e.g., stroke; neoplasms) and left-sided excitatory lesions (e.g., epileptogenic foci) are frequently observed. Secondary mania should be suspected in patients with neurological deficits, histories atypical for classic bipolar disorder, and first manic episodes after the age of 40 years. Treatment with antimanic medications, along with specific treatment for the underlying neurologic condition, is typically required. Typical lesion locations fit with current models of bipolar disorder, which implicate hyperactivity of left-hemisphere reward-processing brain areas and hypoactivity of bilateral prefrontal emotion-modulating regions. Lesion studies complement these models by suggesting that right-hemisphere limbic-brain hypoactivity, or a left/right imbalance, may be relevant to the pathophysiology of mania.

AIDS mania – is it a potential indicator to initiate HAART?

IntroductionMania occurs in higher rates among individuals with HIV/AIDS, especially with the progression of HIV infection, and constitutes an additional risk factor for facilitate the HIV spread.ObjectiveTo provide an overview of secondary mania in HIV-infected patients.MethodsLiterature review based on PubMed/Medline, using the keywords “HIV”, “AIDS” and “mania”.ResultsSecondary mania or AIDS mania may be due to illicit or prescribed drugs, CNS infection with HIV, medical illness, including opportunistic infections. Of these, HIV neurotoxicity has been proposed to be the most important factor in its pathogenesis. Mania AIDS differs from primary mania with regard to clinical presentation, course, management and prognosis. The authors will analyze them. Besides decrease to treatment adherence, maniac symptoms also predispose to HIV risk behaviors, which may lead to further HIV transmission. Importantly, the occurrence of HIV mania may announce the transition from HIV infection to AIDS perhaps before other clinical signs are evident. Early recognition and treatment of manic symptoms with mood stabilisers, antipsychotics and HAART improve quality of life, protect from further cognitive deterioration and decrease mortality. In these patients, medication side-effects toxicity, drug interactions, and adherence require special attention.ConclusionsMania has been associated with HIV/AIDS and in many instances acts as a barrier to achieving best treatment outcomes. Thus, psychiatrists need to be aware of the complexities involved in the emergence of manic episodes in HIV-infected patients in order to deal with them in the most appropriate and effective manner.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Bipolar Disorders and Valproate: Pharmacokinetics,Pharmacodynamics, Therapeutic Effects and Indications of Valproate: Review of Articles

Valproate is a mood stabilizer which is approved for use in acute and maintenance mania. It is the first line drug for bipolar patients with presence rapid cycling, irritable mania, bipolar disorder with comorbid substance use disorders, severe mania with psychosis, mixed mania and secondary mania. The specific mechanism of action of valproate in stabilizing mood is unknown. It exerts effects by enhancement of brain γ-aminobutyric acid (GABA) levels via multiple actions of synthesis and degradation, and modulation of other neurotransmitters, voltage sensitive Na+ channels, extra hypothalamic neuropeptides, secondary messenger systems, and neuro protection. Common side effects include gastrointestinal (GI) distress, tremor, sedation, hair loss, increased appetite and weight gain. Hepatic failure, pancreatitis, and hyperammonemic encephalopathy are rare serious side effects associated with use of valproate. Routine blood level monitoring is not necessary. There is an increased risk of fetal abnormalities if valproateis taken in pregnancy. Valpraote concentrations are known to be increased with concurrent use of benzodiazepines, non-steroidal antiinflammatory drugs (NSAIDS) such as spirin, cemitidine and erythrpmycin. Its level decrease when administrated with phenobarbitone, phenytoin and carbamazepine.

Secondary psychotic mania following traumatic brain injury: a case report

Secondary psychotic mania following traumatic brain injury: a case report

Changes in Painting Style by Poststroke Mania.

Changes in Painting Style by Poststroke Mania.

Secondary Mania and Tapentadol

Introduction Tapentadol is a centrally-acting synthetic analgesic which acts as a mu-opioid receptor agonist as well as a norepinephrine re-uptake inhibitor. It is use to treat cronic pain. Most prevalence adverse effects are gastrointestinal and nervous symptoms. Furthermore, it has objectified, with less frequency, psychiatric disturbances. Objetives To analyse the relationship between a maniac episode and tapentadol. Methods Forty-nine-year-old female, with personal history of dyslipidemia and lumbar herniated discs in L4-L5, L5-S1, in treatment with tapentadol 200 mg/day for 20 days and no past psychiatric history. She was admitted to the Psychiatry Department due to a maniac episode, with desinhibition, pressure and loud speech, euphoria, megalomaniac delusion and sleep disturbance for the last 10 days. Young Mania Rating Scale (YMRS) was 36 points. Olanzapina 15 mg/day was introduced and tapentadol was removed. Symptoms remitted quickly and 6 days later, at discharge, YMRS was 4 points. One year later, the patient continued to be asymptomatic. Results Opioids can produce psychiatric disorders like hallucination, sleep disorders, depressed mood, disorientation, agitation, nervousness, restlessness, euphoric mood. Secondary mania to tapentadol mechanism is unknown, but having opiate cases described, it is possible to attribute this episode to tapentadol. Conclusions – Secondary mania is associated with various medical conditions, including vitamin B12 deficiency, brain injury, HIV infection and drugs such as alcohol, caffeine, sympathomimetics, steroids, bupropion, isoniazid, clarithromycin and opioids. – Further research is required to determine if the maniac episode was only isolated by the tapentadol or it is the beginning of a bipolar disorder.

Can a Manic Be Organic?

Introduction Secondary mania is still an under-recognized pathology even if nowadays psychiatrist benefit from a wide range of imagistic and laboratory tools. The following case study illustrates bipolar affective disorder, manic episode with psychotic symptoms in a 36 years old female which had an abrupt beginning. At the moment of examination in the office at the medical centre she presented tachypsychia, grandiosity and interpretative delusions, positive hyperthymia, sterile hyperactivity, elevated appetency, hyperbulia, low sleep need. Objective The importance of having in mind the 5 most frequent causes of mania caused by generalized medical condition when presented with an atypical manic episode. Aim Our aim is to increase the acknowledgement of a more elaborate paraclinic approach for psychiatrists whom find themselves in front of bipolar disease case that also have somatic issues attached. Methods For this type of cases the laboratory and imagistic exploration are the key to an accurate diagnosis and therefore for an aimed treatment. In our case the imagistic exploration and blood tests revealed a well defined tumor in the left suprarenal gland. Results The psychiatric diagnosis was bipolar affective mood disorder due to a general medical condition and the patient was transferred to the Endocrinology Clinic. Conclusions After the surgery of the tumor both the psychiatric symptoms and the secondary Cushing syndrome disappeared completely.

Late Mania: Case Report

Introduction : Bipolar disorders are frequent troubles touching 1 to 2% of the general population. The average age of disease onset is between 20 and 25 years. While the early onset is predictive of a more severe disorder, the late start, with elderly people, raises the problem of the frequency of secondary mania. Methodology Presentation of a clinical case and use of a bibliography from the following search engines: PubMed, Science direct, Medscape. Key words Bipolar disorder, mania, elderly person. Case report This case is about a 62-year-old woman, hypertensive and obese, who had a gastric by-pass complicated by deficiency neuropathy and Gayet Wernicke’s encephalopathy. While neurological symptoms were improved by treatment with B1 and B12 vitamins, carbamazepine and clomipramine, a state of psychomotor excitation persisted and prompted a psychiatric consultation. The diagnosis of a maniac episode was retained and the patient was put under mood stabilizer treatment. Discussion Etiological research discussed three cases: A mania induced by Vitamin B12 deficiency, associated to neurological symptoms with impaired memory, paresthesia, and ataxia. A mania induced by treatment with clomipramine. A primary mania in an obese woman. This possibility is not uncommon. Indeed, several studies have confirmed the frequency of comorbidity of mood disorders and obesity.

Mania induced by clarithromycin in a geriatric patient taking low-dose prednisone.

To the Editor: Bipolar disorder is a chronic mood disorder characterized by episodes of mania, hypomania, and major depression. Bipolar disorder affects roughly 1% of the general population and 0.1% of the geriatric population. In certain clinical settings such as care homes and hospitals, however, the prevalence of geriatric bipolar disorder can be as high as 10%. Bipolar disorder may be divided into early onset bipolar and late-onset bipolar. Vasudev and Thomas1 state that patients in the late-onset group are associated with higher medical and neurologic burden and often have a secondary cause of their presentation. Case report. Mr A, a 78-year-old man with no previous history of mood disorders, presented to the emergency department in June 2013 with a 3-week history of progressive mental decline characterized by disorganized thoughts, aggressive behavior, reduced sleep, impulsive spending, and grandiose religious delusions. Mr A’s past medical history is significant for a remote pituitary adenoma surgery, for which he takes levothyroxine 100 μg per day and prednisone 5 mg per day. Three days prior to hospital admission, Mr A finished a 14-day course of clarithromycin 1 g per day. Mr A denied any use of alcohol or illicit drugs. On examination, Mr A was appropriately dressed and maintained good eye contact. He was found to have elevated mood, pressured speech, disorganized thoughts, and delusions of grandiosity and reference. He demonstrated poor insight and judgment. He denied homicidal and suicidal ideation. A complete hematologic and metabolic blood screen was negative except for a low thyroid-stimulating hormone level, with normal free T3 and T4 levels. Computed tomography and magnetic resonance imaging head scans showed nonaggressive-appearing enlargement of the sella with no significant mass effect or extension into the surrounding tissue, which is consistent with prior sella surgery. Mr A was hospitalized for 9 days and showed rapid clinical improvement within 1 week. He remained on his prior dose of levothyroxine and prednisone and was prescribed oral olanzapine, first at 2.5 mg per day for 6 days then at 7.5 mg per day for 2 days to manage his agitated behavior. Per DSM-IV criteria, Mr A was diagnosed with secondary mania possibly caused by the combination of prednisone and clarithromycin. Prednisone is a corticosteroid that has been widely used in a variety of medical conditions and is associated with well-documented dose-dependent psychiatric side effects. Kenna et al2 state that the prednisone-equivalent mean ± SD dose associated with psychiatric side effects is 63.6 ± 46.2 mg per day; however, in our case, Mr A’s manic episode was associated with a prednisone dosage of as low as 5 mg per day. Clarithromycin is a macrolide antibiotic commonly used in the treatment of community-acquired pneumonia. Prednisone3 and clarithromycin are both metabolized by cytochrome P450 (CYP) 3A isozyme. Quinney et al4 found that clarithromycin can reduce activity of CYP3A by 75%. This reduction in metabolism could theoretically increase the circulating level of prednisone to a level high enough to cause psychiatric symptoms. The only published case of mania induced by prednisone and clarithromycin was described in 1998 by Finkenbine and Frye5 in a 30-year-old woman taking 20–60 mg of prednisone a day. Similar to our case, the patient recovered quickly after discontinuing clarithromycin. Our case is unique, however, because it is the first described case of mania induced by clarithromycin in a geriatric patient on a low dose of prednisone of 5 mg a day. Our study findings caution prescribers to be alert to the possibility of prednisone-induced mania, even at very low doses of prednisone, in the elderly who have received a CYP3A inhibitor like clarithromycin.