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1.
J Opioid Manag ; 15(4): 342-344, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31637686

RESUMO

A 49-year-old male with major depressive disorder well-managed with venlafaxine [serotonin and norepinephrine reuptake inhibitor (SNRI)] and no history of manic episodes developed his first manic episode following use of tramadol. Tramadol-induced mania has been described with selective serotonin reuptake inhibitors but not SNRIs. In addition, mania is not listed as a potential clinical side effect-further illustrating this relative rarity. Due to tramadol's SNRI activity, there is definitive risk for mood lability in individuals managed with tramadol and other serotonergic medications as seen in this patient. The authors findings suggest the need for greater risk consideration when prescribing tramadol with other related agents such as venlafaxine.


Assuntos
Transtorno Bipolar , Transtorno Depressivo Maior , Tramadol , Cloridrato de Venlafaxina , Analgésicos Opioides , Transtorno Bipolar/induzido quimicamente , Transtorno Depressivo Maior/tratamento farmacológico , Humanos , Masculino , Pessoa de Meia-Idade , Inibidores de Captação de Serotonina/efeitos adversos , Tramadol/efeitos adversos , Tramadol/uso terapêutico , Cloridrato de Venlafaxina/efeitos adversos , Cloridrato de Venlafaxina/uso terapêutico
3.
Braz J Psychiatry ; 41(5): 419-427, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30843957

RESUMO

OBJECTIVE: To evaluate whether an animal model of mania induced by lisdexamfetamine dimesylate (LDX) has an inflammatory profile and whether immune activation by lipopolysaccharides (LPS) has a cumulative effect on subsequent stimuli in this model. We also evaluated the action of lithium (Li) on inflammatory and neurotrophic factors. METHODS: Adult male Wistar rats were subjected to an animal model of mania. After the open-field test, they were given LPS to induce systemic immune activation. Subsequently, the animals' blood was collected, and their serum levels of brain-derived neurotrophic factor and inflammatory markers (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-1ß, IL-10, and inducible nitric oxide synthase [iNOS]) were measured. RESULTS: LDX induced hyperactivity in the animals, but no inflammatory marker levels increased except brain-derived neurotrophic factor (BDNF). Li had no effect on serum BDNF levels but prevented iNOS levels from increasing in animals subjected to immune activation. CONCLUSION: Although Li prevented an LPS-induced increase in serum iNOS levels, its potential anti-inflammatory effects in this animal model of mania were conflicting.


Assuntos
Anti-Inflamatórios/farmacologia , Transtorno Bipolar/imunologia , Modelos Animais de Doenças , Dimesilato de Lisdexanfetamina , Lítio/farmacologia , Fatores de Crescimento Neural/efeitos dos fármacos , Animais , Transtorno Bipolar/induzido quimicamente , Transtorno Bipolar/fisiopatologia , Fator Neurotrófico Derivado do Encéfalo/sangue , Citocinas/sangue , Ensaio de Imunoadsorção Enzimática , Lipopolissacarídeos/farmacologia , Locomoção/efeitos dos fármacos , Masculino , Óxido Nítrico Sintase Tipo II/sangue , Ratos Wistar , Reprodutibilidade dos Testes , Fatores de Tempo , Resultado do Tratamento
4.
Clin Neuropharmacol ; 42(3): 97-98, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30829883

RESUMO

Levetiracetam is an antiepileptic agent that is used for partial and generalized epilepsy. Although it is well tolerated in most cases, behavioral and nonbehavioral adverse effects may be observed. Among behavioral symptoms, depression, hostility, and agitation have been frequently reported. However, mania or mania-like symptoms are relatively rare, especially in children and adolescents. Hereby, we report mania-like symptoms with levetiracetam use in a 15-year-old boy. Mania-like symptoms emerged 3 weeks after starting levetiracetam and disappeared after adding risperidone to ongoing levetiracetam treatment.


Assuntos
Anticonvulsivantes/efeitos adversos , Transtorno Bipolar/induzido quimicamente , Epilepsias Parciais/tratamento farmacológico , Levetiracetam/efeitos adversos , Adolescente , Humanos , Masculino , Risperidona/uso terapêutico
5.
J Affect Disord ; 245: 1106-1113, 2019 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-30699853

RESUMO

BACKGROUND: Bipolar disorder (BD) and substance use disorders share common symptoms, such as behavioral sensitization. Amphetamine-induced behavioral sensitization can serve as an animal model of BD. Neurotrophic factors have an important role in BD pathophysiology. This study evaluated the effects of amphetamine sensitization on behavior and neurotrophic factor levels in the brains of rats. METHODS: Wistar rats received daily intraperitoneal (i.p) injections of dextroamphetamine (d-AMPH) 2 mg/kg or saline for 14 days. After seven days of withdrawal, the animals were challenged with d-AMPH (0.5 mg/kg, i.p) and locomotor behavior was assessed. In a second protocol, rats were similarly treated with d-AMPH (2 mg/kg, i.p) for 14 days. After withdrawal, without d-AMPH challenge, depressive- and anxiety-like behaviors were evaluated through forced swimming test and elevated plus maze. Levels of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin 3 (NT-3), neurotrophin 4/5 (NT-4/5) and glial-derived neurotrophic factor (GDNF) were evaluated in the frontal cortex, hippocampus, and striatum. RESULTS: D-AMPH for 14 days augmented locomotor sensitization to a lower dose of d-AMPH (0.5 mg/kg) after the withdrawal. d-AMPH withdrawal induced depressive- and anxious-like behaviors. BDNF, NGF, and GDNF levels were decreased, while NT-3 and NT-4 levels were increased in brains after d-AMPH sensitization. LIMITATIONS: Although d-AMPH induces manic-like behavior, the mechanisms underlying these effects can also be related to phenotypes of drug abuse. CONCLUSIONS: Together, vulnerability to mania-like behavior following d-AMPH challenge and extensive neurotrophic alterations, suggest amphetamine-induced behavioral sensitization is a good model of BD pathophysiology.


Assuntos
Ansiedade/metabolismo , Transtorno Bipolar/metabolismo , Encéfalo/metabolismo , Depressão/metabolismo , Dextroanfetamina/farmacologia , Fatores de Crescimento Neural/metabolismo , Animais , Ansiedade/induzido quimicamente , Comportamento Animal/efeitos dos fármacos , Transtorno Bipolar/induzido quimicamente , Encéfalo/efeitos dos fármacos , Fator Neurotrófico Derivado do Encéfalo/efeitos dos fármacos , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Corpo Estriado/efeitos dos fármacos , Corpo Estriado/metabolismo , Depressão/induzido quimicamente , Modelos Animais de Doenças , Lobo Frontal/efeitos dos fármacos , Lobo Frontal/metabolismo , Fator Neurotrófico Derivado de Linhagem de Célula Glial/efeitos dos fármacos , Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Locomoção/efeitos dos fármacos , Masculino , Fator de Crescimento Neural/efeitos dos fármacos , Fator de Crescimento Neural/metabolismo , Fatores de Crescimento Neural/efeitos dos fármacos , Neurotrofina 3/efeitos dos fármacos , Neurotrofina 3/metabolismo , Ratos , Ratos Wistar
7.
Artigo em Inglês | MEDLINE | ID: mdl-30677265

RESUMO

Traumatic brain injury (TBI) has had increased notoriety in light of chronic traumatic encephalopathy in professional sports. However, despite the increased rate at which mood disorders affect this population, there remains little information on management of these disorders. TBI has also been implicated in the development of Parkinson disease, increasing the likelihood that patients may be treated with dopaminergic agents. Management of coexisting pathologies can become challenging, especially when confounded by medication side effects. A case is presented of a 58-year-old man who was admitted to the hospital in a manic state 15 years after having suffered a closed head injury. Several psychiatric admissions during the past 2 years were noted, with various diagnoses including different iterations of bipolar disorder. Among his medications, levodopa-carbidopa was present for an unsubstantiated Parkinson disease diagnosis. His mania resolved after discontinuation of the agent. This case is presented with a review of the relevant literature pertaining to the use of levodopa-carbidopa in this context, the use of other dopaminergic agents, and a biological hypothesis for the potential increased likelihood of manic symptoms in TBI patients who receive levodopa-carbidopa. Currently, there is a lack of research in this area, which emphasizes a need to review treatment guidelines for Parkinson disease patients with TBI.


Assuntos
Transtorno Bipolar/induzido quimicamente , Lesões Encefálicas Traumáticas/tratamento farmacológico , Carbidopa/efeitos adversos , Agonistas de Dopamina/efeitos adversos , Levodopa/efeitos adversos , Carbidopa/uso terapêutico , Agonistas de Dopamina/uso terapêutico , Combinação de Medicamentos , Humanos , Levodopa/uso terapêutico , Masculino , Pessoa de Meia-Idade
8.
Neurochem Int ; 124: 162-170, 2019 03.
Artigo em Inglês | MEDLINE | ID: mdl-30654115

RESUMO

The abuse of methamphetamine (MA), an amphetamine (AMPH)-type stimulant, has been demonstrated to be associated with various neuropsychotoxicity, including memory impairment, psychiatric morbidity, and dopaminergic toxicity. Compelling evidence from preclinical studies has indicated that protein kinase C (PKC), a large family of serine/threonine protein kinases, plays an important role in MA-induced neuropsychotoxicity. PKC-mediated N-terminal phosphorylation of dopamine transporter has been identified as one of the prerequisites for MA-induced synaptic dopamine release. Consistently, it has been shown that PKC is involved in MA (or AMPH)-induced memory impairment and mania-like behaviors as well as MA drug dependence. Direct or indirect regulation of factors related to neuronal plasticity seemed to be critical for these actions of PKC. In addition, PKC-mediated mitochondrial dysfunction, oxidative stress or impaired antioxidant defense system has been suggested to play a role in psychiatric and cognitive disturbance induced by MA (or AMPH). In MA-induced dopaminergic toxicity, particularly PKCδ has been shown to trigger oxidative stress, mitochondrial dysfunction, pro-apoptotic changes, and neuroinflammation. Importantly, PKCδ may be a key mediator in the positive feedback loop composed of these detrimental events to potentiate MA-induced dopaminergic toxicity. This review outlines the role of PKC and its individual isozymes in MA-induced neuropsychotoxicity. Better understanding on the molecular mechanism of PKCs might provide a great insight for the development of potential therapeutic or preventive candidates for MA (or AMPH)-associated neuropsychotoxicity.


Assuntos
Estimulantes do Sistema Nervoso Central/toxicidade , Metanfetamina/toxicidade , Proteína Quinase C-delta/metabolismo , Transtornos Relacionados ao Uso de Substâncias/metabolismo , Animais , Transtorno Bipolar/induzido quimicamente , Transtorno Bipolar/metabolismo , Transtorno Bipolar/psicologia , Dopamina/metabolismo , Humanos , Transtornos da Memória/induzido quimicamente , Transtornos da Memória/metabolismo , Transtornos da Memória/psicologia , Transtornos Relacionados ao Uso de Substâncias/psicologia
10.
Eur J Endocrinol ; 180(1): 31-40, 2019 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-30400048

RESUMO

Background Dopamine agonists (DAs) are the main treatment for patients with hyperprolactinemia and prolactinomas. Recently, an increasing number of reports emphasized DAs' psychological side effects, either de novo or as exacerbations of prior psychiatric disease. Methods Review of prospective and retrospective studies (PubMed 1976, September 2018) evaluating the psychological profile of DA-treated patients with hyperprolactinemia and prolactinomas. Case series and case reports of psychiatric complications were also reviewed. Results Most studies were cross-sectional and had a control group of healthy volunteers or patients with nonfunctioning pituitary adenomas. There were few prospective studies, with/without control group, that included small numbers of patients. Compared with controls, patients with hyperprolactinemia generally had worse quality of life, anxiety, depression and certain personality traits. Patients receiving DAs had higher impulsivity scores than normoprolactinemic controls. Impulse control disorders (ICDs) were reported in both genders, with hypersexuality mostly in men. Multiple ICDs were sometimes reported in the same patient, usually reversible after DA discontinuation. In case reports, DA therapy was temporally associated with severe depression, manic episodes or psychosis, which improved after discontinuation and administration of psychiatric medications. Gender type of DA, dose and duration of therapy did not correlate with occurrence of psychiatric pathology. Conclusion Patients with hyperprolactinemia receiving DAs may develop changes in mood and behavior regardless of prior psychiatric history. Increased awareness for ICDs, depression, mania and other types of psychosis is needed by all physicians who prescribe DAs. Larger prospective controlled clinical studies are needed to delineate prevalence, risk stratification and management.


Assuntos
Transtorno Bipolar/induzido quimicamente , Depressão/induzido quimicamente , Agonistas de Dopamina/efeitos adversos , Hiperprolactinemia/tratamento farmacológico , Neoplasias Hipofisárias/tratamento farmacológico , Prolactinoma/tratamento farmacológico , Psicoses Induzidas por Substâncias/etiologia , Agonistas de Dopamina/uso terapêutico , Humanos
13.
Eur Arch Psychiatry Clin Neurosci ; 269(1): 107-120, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30564886

RESUMO

With the increasing push to legalize cannabis in Western nations, there is a need to gage the potential impact of this policy change on vulnerable populations, such as those with mental illness, including schizophrenia, mood, and anxiety disorders. This is particularly important as there are strong motives in these individuals to seek short-term reward (e.g., "getting high"). Nonetheless, data to support the beneficial effects of cannabis use in psychiatric populations are limited, and potential harms in patients with psychotic and mood disorders have been increasingly documented. This article reviews the effects of cannabis in people with mental illness. Then, we provide a reconciliation of the addiction vulnerability and allostatic hypotheses to explain co-morbidity addiction in mentally ill cannabis users, as well as to further aid in developing a rational framework for the assessment and treatment of problematic cannabis use in these patients.


Assuntos
Transtornos de Ansiedade/tratamento farmacológico , Transtorno Bipolar/tratamento farmacológico , Canabinoides/farmacologia , Transtorno Depressivo Maior/tratamento farmacológico , Uso da Maconha/efeitos adversos , Esquizofrenia/tratamento farmacológico , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Transtornos de Ansiedade/induzido quimicamente , Transtorno Bipolar/induzido quimicamente , Canabinoides/efeitos adversos , Transtorno Depressivo Maior/induzido quimicamente , Humanos , Esquizofrenia/induzido quimicamente , Transtornos de Estresse Pós-Traumáticos/induzido quimicamente
15.
Br J Pharmacol ; 175(24): 4450-4463, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-30221753

RESUMO

BACKGROUND AND PURPOSE: Children and adolescents are the top consumers of high-fructose corn syrup (HFCS) sweetened beverages. Even though the cardiometabolic consequences of HFCS consumption in adolescents are well known, the neuropsychiatric consequences have yet to be determined. EXPERIMENTAL APPROACH: Adolescent rats were fed for a month with 11% weight/volume carbohydrate containing HFCS solution, which is similar to the sugar-sweetened beverages of human consumption. The metabolic, behavioural and electrophysiological characteristics of HFCS-fed rats were determined. Furthermore, the effects of TDZD-8, a highly specific GSK-3B inhibitor, on the HFCS-induced alterations were further explored. KEY RESULTS: HFCS-fed adolescent rats displayed bipolar-like behavioural phenotype with hyperexcitability in hippocampal CA3-CA1 synapses. This hyperexcitability was associated with increased presynaptic release probability and increased readily available pool of AMPA receptors to be incorporated into the postsynaptic membrane, due to decreased expression of the neuron-specific α3-subunit of Na+ /K+ -ATPase and an increased ser845 -phosphorylation of GluA1 subunits (AMPA receptor subunit) respectively. TDZD-8 treatment was found to restore behavioural and electrophysiological disturbances associated with HFCS consumption by inhibition of GSK-3B, the most probable mechanism of action of lithium for its mood-stabilizing effects. CONCLUSION AND IMPLICATIONS: This study shows that HFCS consumption in adolescent rats led to a bipolar-like behavioural phenotype with neuronal hyperexcitability, which is known to be one of the earliest endophenotypic manifestations of bipolar disorder. Inhibition of GSK-3B with TDZD-8 attenuated hyperexcitability and restored HFCS-induced behavioural alterations.


Assuntos
Transtorno Bipolar/induzido quimicamente , Transtorno Bipolar/tratamento farmacológico , Xarope de Milho Rico em Frutose/efeitos adversos , Hipocampo/efeitos dos fármacos , Sinapses/efeitos dos fármacos , Animais , Transtorno Bipolar/genética , Xarope de Milho Rico em Frutose/administração & dosagem , Hipocampo/metabolismo , Masculino , Fenótipo , Ratos , Ratos Wistar , Sinapses/metabolismo , Tiadiazóis/farmacologia
16.
Turk Psikiyatri Derg ; 29(3): 209-215, 2018.
Artigo em Turco | MEDLINE | ID: mdl-30260467

RESUMO

Bortezomib, an antineoplastic agent used in Multiple Myeloma, is a modified dipeptidyl boronic acid that is selectively and reversibly attached to the 26S proteasome. Bortezomib may be combined with corticosteroids in treatment-resistant multiple myeloma patients. Corticosteroids can cause many psychiatric disorders ncluding mania, depression, psychosis, delirium, suicide and aggression. To date only one case of mania associated with the use of bortezomib was reported in which the patient responded to the treatment with olanzapine and valproic acid. In this article, we present a 57-year-old female with multiple myeloma in whom mania developed after the use of bortezomib combined with dexamethasone.Psychiatric symptoms such as sleep deprivation, increased self-esteem and excessive speech appeared within the first week of bortezomib and dexamethasone treatment. Quetiapine was administered for the treatment of psychiatric symptoms. A gradual improvement was noted in manic symptoms after treatment. Bortezomib is a relatively new drug and there are only a few reports with respect to its psychiatric side effects. While using antineoplastic drugs such as bortezomib, caution should be exercised with regards to the psychiatric symptoms.


Assuntos
Anti-Inflamatórios/efeitos adversos , Antineoplásicos/efeitos adversos , Transtorno Bipolar/diagnóstico , Bortezomib/efeitos adversos , Dexametasona/efeitos adversos , Mieloma Múltiplo/tratamento farmacológico , Transtorno Bipolar/induzido quimicamente , Diagnóstico Diferencial , Quimioterapia Combinada , Feminino , Humanos , Pessoa de Meia-Idade
18.
BMJ Case Rep ; 20182018 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-30076163

RESUMO

Hypogonadotropic hypogonadism is a rare congenital disorder characterised by the deficiency and the absence of puberty and infertility. It is caused by the deficient production, secretion or action of gonadotropin-releasing hormone, which is the master hormone regulating the reproductive axis. Gonadotropin-releasing hormone or gonadotropin injections and testosterone replacement therapy are required in the treatment of this disorder. Psychiatric symptoms and disorders may be seen with the use of anabolic androgenic steroids. In this case report, we present a case report in which a patient had behavioural symptoms in childhood and develops bipolar disorder after testosterone replacement therapy. This patient was reached to the remission by increasing the doses of psychiatric drugs without interfering with hormonal therapy. It should be considered that patients receiving testosterone replacement therapy may develop bipolar disorder or trigger mood changes in bipolar mood disease, so behavioural and mood state changes should be closely followed in patients who have bipolar mood disease.


Assuntos
Transtorno Bipolar/induzido quimicamente , Gonadotropina Coriônica/uso terapêutico , Terapia de Reposição Hormonal/métodos , Hipogonadismo/tratamento farmacológico , Testosterona/uso terapêutico , Adulto , Antimaníacos/uso terapêutico , Antipsicóticos/uso terapêutico , Transtorno Bipolar/tratamento farmacológico , Terapia de Reposição Hormonal/efeitos adversos , Humanos , Masculino , Risperidona/uso terapêutico , Ácido Valproico/uso terapêutico
20.
Psychiatry Res ; 268: 508-513, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-30165326

RESUMO

In a clinical setting, anxiety disorder is highly correlated with bipolar I disorder in humans. However, the comorbidity of anxiety behavior and bipolar disorder still remains unclear in an animal model. This study utilized an ouabain-induced animal mode to examine anxiety and mania in an open field test. In the present study, 5 µl of artificial cerebrospinal fluid (aCSF) or ouabain (10-5, 10-4, and 10-3 M) were administered into the left ventricle. The animals' motor functions and anxiety behaviors were measured for 15 min. The results showed that 10-3 M ouabain significantly increased the animal's total distance traveled, average speed, and maximum speed compared to the control group. The time spent inside (i.e., how much time rats spent in the center of the square) and the inside-outside times of the central square (i.e., how many times rats ran across the center square) of the higher-concentration groups (10-4 M and 10-3 M) were significantly decreased. Therefore, a high concentration of ouabain may induce hyperactivity. The 10-4 M and 10-3 M ouabain groups exhibited more anxiety behaviors. The study is the first model to examine comorbid anxiety behaviors and bipolar disorder in an animal model. The study provides some insights for comorbid anxiety and bipolar disorder in clinics.


Assuntos
Ansiedade/fisiopatologia , Transtorno Bipolar/fisiopatologia , Desempenho Psicomotor/efeitos dos fármacos , Acatisia Induzida por Medicamentos/fisiopatologia , Acatisia Induzida por Medicamentos/psicologia , Animais , Ansiedade/induzido quimicamente , Ansiedade/psicologia , Comportamento Animal/efeitos dos fármacos , Transtorno Bipolar/induzido quimicamente , Transtorno Bipolar/psicologia , Comorbidade , Modelos Animais de Doenças , Masculino , Ouabaína , Ratos , Ratos Wistar
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