Pituitary Apoplexy in Macroadenoma After Minor Surgery: An Unusual Case and Literature Review.

Pituitary apoplexy is a rare and severe complication of pituitary adenoma that may present with new-onset headache, ocular palsy, visual disturbances, life-threatening electrolyte imbalance, and endocrinological disturbances due to pituitary hemorrhage and/or infarction. We report the case of a 58-year-old previously healthy patient who developed isolated mild oculomotor nerve palsy of the left eye following osteosynthesis of a traumatic right distal radius fracture. Initial cerebral magnetic resonance imaging showed a pituitary macroadenoma without characteristic signs of pituitary infarction or hemorrhage. The patient presented to the neurology department on the fifth postoperative day with malaise and fatigue due to pituitary insufficiency, deteriorated rapidly and required intensive care monitoring. Clinical stabilization was achieved through the administration of hydrocortisone, and transsphenoidal resection of the pituitary lesion was performed on the 10th day after acute symptom onset. Histological examination revealed a necrotic pituitary adenoma. Pituitary apoplexy may occur after minor surgery in patients with pituitary adenoma. Clinicians should pay particular attention to laboratory signs of pituitary insufficiency in new-onset oculomotor nerve palsy associated with sellar lesions, as cerebral imaging may miss pituitary apoplexy and therefore delay diagnosis and treatment. In our case, delayed decompressive transsphenoidal resection resulted in the normalization of the oculomotor nerve palsy while the pituitary insufficiency persisted. The potential impact of an earlier surgical intervention on the outcome of pituitary function remains uncertain.

Resilience Predicts Self-Stigma and Stigma Resistance in Stabilized Patients With Bipolar I Disorder.

The identification of factors that prevent self-stigma and on the other hand promote stigma resistance are of importance in the long-term management of bipolar disorder. Accordingly, the aim of the current study was to investigate the association of factors deemed relevant in this context, i.e., resilience, premorbid functioning, and residual mood symptoms, with self-stigma/stigma resistance. Sixty patients diagnosed with bipolar I disorder were recruited from a specialized outpatient clinic. Self-stigma and stigma resistance were measured by the Internalized Stigma of Mental Illness (ISMI) Scale. The presence and severity of symptoms were assessed by the Montgomery-Asberg Depression Rating Scale (MADRS) and the Young Mania Rating Scale (YMRS). Resilience and premorbid functioning were measured by the Resilience Scale (RS-25) and the Premorbid Adjustment Scale (PAS), respectively. Resilience correlated negatively with self-stigma and positively with stigma resistance and was a predictor for self-stigma/stigma resistance in multiple linear regression analysis. Residual depressive symptoms correlated positively with self-stigma and negatively with stigma resistance. There were no significant correlations between sociodemographic variables, premorbid functioning as well as residual manic symptoms and self-stigma/stigma resistance. The findings of this study implicate that resilience may be considered as an important component of self-stigma reduction interventions.

Adenosine A1 receptor activates background potassium channels and modulates information processing in olfactory bulb mitral cells.

KEY POINTS: Adenosine is a widespread neuromodulator in the mammalian brain, but whether it affects information processing in sensory system(s) remains largely unknown. Here we show that adenosine A1 receptors hyperpolarize mitral cells, one class of principal neurons that propagate odour information from the olfactory bulb to higher brain areas, by activation of background K+ channels. The adenosine-modulated background K+ channels belong to the family of two-pore domain K+ channels. Adenosine reduces spontaneous activity of mitral cells, whereas action potential firing evoked by synaptic input upon stimulation of sensory neurons is not affected, resulting in a higher ratio of evoked firing (signal) over spontaneous firing (noise) and hence an improved signal-to-noise ratio. The study shows for the first time that adenosine influences fine-tuning of the input-output relationship in sensory systems. ABSTRACT: Neuromodulation by adenosine is of critical importance in many brain regions, but the role of adenosine in olfactory information processing has not been studied so far. We investigated the effects of adenosine on mitral cells, which are projection neurons of the olfactory bulb. Significant expression of A1 and A2A receptors was found in mitral cells, as demonstrated by in situ hybridization. Application of adenosine in acute olfactory bulb slices hyperpolarized mitral cells in wild-type but not in adenosine A1 receptor knockout mice. Adenosine-induced hyperpolarization was mediated by background K+ currents that were reduced by halothane and bupivacaine, which are known to inhibit two-pore domain K+ (K2P) channels. In mitral cells, electrical stimulation of axons of olfactory sensory neurons evoked synaptic currents, which can be considered as input signals, while spontaneous firing independent of sensory input can be considered as noise. Synaptic currents were not affected by adenosine, while adenosine reduced spontaneous firing, leading to an increase in the signal-to-noise ratio of mitral cell firing. Our findings demonstrate that A1 adenosine receptors activate two-pore domain K+ channels, which increases the signal-to-noise ratio of the input-output relationship in mitral cells and thereby modulates information processing in the olfactory bulb.