Use of Bupropion in the Management of Negative Symptom Schizophrenia: A Case Series.

Antipsychotic treatment has been documented as the mainstay for the management of schizophrenia. Evidence in literature has suggested that the management of negative symptoms of schizophrenia continues to be a treatment challenge. Therefore, residual negative symptoms can become more pervasive and visible after the treatment of positive symptoms, leading to an impaired marked deficit in the vital daily functions of patients. We present a case series of three patients with a past psychiatric history of schizophrenia who presented to the psychiatric emergency with acute symptoms of schizophrenia. Following antipsychotic treatment, all these patients showed improvement of positive symptoms, however, profound negative symptoms of schizophrenia became visible. The negative symptoms include anhedonia, amotivation, alogia, affective flattening, and passive social withdrawal. We added bupropion to manage the negative symptoms, and all three patients achieved a good treatment response. This case series suggests that the anti-depressive effects of bupropion might be a valuable treatment option in the treatment of negative symptoms of schizophrenia.

Traumatic brain Injury related schizophrenia in individuals without family history: A case series.

Traumatic brain injury (TBI) related mental disorder has been hypothesized in the literature before 1969 as the etiology of schizophrenia. TBI has been described as a complex of multiple genetic factors and interacting non-genetic factor influence. Most research on non-genetic factors has focused on the period from conception through childhood. Thus far, there is no evidence suggestive of schizophrenic features for individuals without family history of mental health disorder following TBI in adulthood. Hence, we present these case series of three different TBI related schizophrenia with no past psychiatric history nor positive family psychiatric background. Though there are scientific reports suggesting association between TBI and schizophrenia, most of the links are either based on pre-teen exposure to TBI or positive family history of mental illness. Discussed in line of current literature, this case series adds to the body of evidence on adult TBI related schizophrenia in individuals with no family history of mental health disorder.

Opioid-Induced Psychosis in a Patient With Sickle Cell Disease.

Sickle cell disease (SCD) is a common inherited hemoglobin disorder in which people have atypical hemoglobin, known as hemoglobin S. It is highly prevalent in non-Hispanic Blacks and people of Arab descent. It causes a distortion of the shape of red blood cells, leading to occlusion of blood vessels and thus tissue hypoxia and injury. The resultant infarction/reperfusion, in turn, causes fatigue and pain. Patients with SCD require constant analgesic medications for pain management. In the general population, opioids are amongst the most prescribed medications for pain management and the trend has been gradually growing during the past two decades. Side effects commonly associated with opioids are gastrointestinal and central nervous system-related, with up to 80% of patients experiencing at least one adverse effect. We report the case of a 36-year-old male patient who has a history of cannabis use and no prior psychiatric history, who developed acute psychosis while receiving a high dose of hydromorphone for sickle cell pain crisis. This case contributes to the growing literature about opioid-induced psychosis and also explores psychosis in sickle cell disease. Understanding the pharmacology and potential side effects of opioids is critical given the increasing number of patients using prescribed and illicit opioids.

Granulocyte-colony stimulating factor activates JAK2/PI3K/PDE3B pathway to inhibit corticosterone synthesis in a neonatal hypoxic-ischemic brain injury rat model.

OBJECTIVE: Our previous study demonstrated that granulocyte-colony stimulating factor (G-CSF)-induced neuroprotection is accompanied by an inhibition of corticosterone production in a neonatal hypoxic-ischemic (HI) rat model. The present study investigates how G-CSF inhibits corticosterone production, using adrenal cortical cells and HI rat pups. METHODS: Cholera toxin was used to induce corticosterone synthesis in a rodent Y1 adrenal cortical cell line by increasing cyclic adenosine monophosphate (cAMP). Both corticosterone and cAMP were quantitatively measured using a commercial enzyme-linked immunosorbent assay (ELISA). The downstream signaling components of the G-CSF receptor, including Janus Kinase 2 (JAK2)/Phosphatidylinositol-3-kinase (PI3K)/Protein kinase B (Akt) and Phosphodiesterase 3B (PDE3B), were detected by western blot. Sprague-Dawley rat pups at the age of 10days (P10) were subjected to unilateral carotid artery ligation followed by hypoxia for 2.5hours. Brain infarction volumes were determined using 2,3,5-triphenyltetrazolium chloride monohydrate (TTC) staining. RESULTS: G-CSF at 30ng/ml inhibited corticosterone synthesis but lost its inhibitory effect at higher doses. The inhibitory effect of G-CSF was conferred by interfering with cAMP signaling via the activation of the JAK2/PI3K/PDE3B signaling pathway. The degradation of cAMP by G-CSF signaling reduced corticosterone production. This mechanism was further verified in the neonatal HI brain injury rat model, in which inhibition of PDE3B reversed the protective effects of G-CSF. CONCLUSION: Our data suggest that the neuroprotective G-CSF reduces corticosterone synthesis at the adrenal level by degrading intracellular cAMP via activation of the JAK2/PI3K/PDE3B pathway.

Delayed remote ischemic postconditioning improves long term sensory motor deficits in a neonatal hypoxic ischemic rat model.

OBJECTIVE: Remote Ischemic Postconditioning (RIPC) is a promising therapeutic intervention wherein a sub-lethal ischemic insult induced in one organ (limb) improves ischemia in an organ distant to it (brain). The main objective of this study was to investigate the long-term functional effects of delayed RIPC in a neonatal hypoxia-ischemia (HI) rat model. METHOD: 10 day old rat pups were subjected to delayed RIPC treatment and randomized into four groups: 1) Sham, 2) HI induced, 3) HI +24 hr delayed RIPC, and 4) HI +24 hr delayed RIPC with three consecutive daily treatments. Neurobehavioral tests, brain weights, gross and microscopic brain tissue morphologies, and systemic organ weights were evaluated at five weeks post surgery. RESULTS: HI induced rats performed significantly worse than sham but both groups of delayed RIPC treatment showed improvement of sensory motor functions. Furthermore, compared to the HI induced group, the delayed RIPC treatment groups showed no further detrimental changes on brain tissue, both grossly and morphologically, and no changes on the systemic organ weights. CONCLUSION: Delayed RIPC significantly improves long term sensory motor deficits in a neonatal HI rat model. A 24 hr delayed treatment does not significantly attenuate morphological brain injury but does attenuate sensory motor deficits. Sensory motor deficits improve with both a single treatment and with three consecutive daily treatments, and the consecutive treatments are possibly being more beneficial.