Aim To investigate development of refeeding hypophosphatemia during the refeeding period and the extent of the decrease in the serum phosphorus level among anorexia nervosa patients with severe malnutrition. Objective The accurate prediction of the severity of refeeding hypophosphatemia in patients with anorexia nervosa during acute treatment is of great importance. Although some predictors were found in previous reports, these studies used binominal data—the presence or absence of hypophosphatemia—as an outcome indicator but not the extent of serum phosphorus level decrease. It is crucial in clinical settings to predict the extent of the serum phosphorus level decrease as well as development of refeeding hypophosphatemia, in particular, for patients with severe malnutrition, who has a higher risk of death. Methods We investigated 63 admissions from 37 patients with anorexia nervosa who had severe malnutrition (admission body mass index 11.5 ± 1.6) and carried out a linear discriminant regression analysis for the development of refeeding hypophosphatemia. The extent of the decrease in the serum phosphorus level were investigated using multiple linear regression analysis. Explanatory variables included data upon admission (age, sex, body mass index, blood urea nitrogen to creatinine ratio, albumin, initial serum phosphorus level, anorexia nervosa type, i.e., restrictive or binge-purge) as well as treatment-related indicators (calorie intake, amount of phosphate administered, and rate of weight gain). Results Development of refeeding hypophosphatemia and a change in serum phosphorus levels were predicted by body mass index and elevated blood urea nitrogen to creatinine ratio. Conclusions Our study found that refeeding hypophosphatemia among patients with severe malnutrition was predicted by a lower body mass index and elevated blood urea nitrogen to creatinine ratio.

ObjectiveAlthough catatonia can occur secondary to a general medical condition, catatonia itself has been known to lead to various medical compolications. Although case reports on the association of catatonia with subsequent medical complications have been documented, no comprehensive large-scale study has been performed. To investigate specific medical complications after catatonia, we conducted a retrospective cohort study of specific medical complications of schizophrenia patients with catatonia.MethodsThe 1719 schizophrenia inpatients in our study were categorized into two groups: the catatonia group, i.e., those who exhibited catatonic stupor while they were hospitalized, and the noncatatonia group, i.e., those who never exhibited catatonic stupor. Differences between the two groups in the occurrence of subsequent medical complications were examined using linear and logistic regression analyses, and models were adjusted for potentially confounding factors.ResultsThe catatonia group had an increased risk for mortality (odds ratio = 4.8, 95% confidence interval = 2.0–10.6, p < .01) and certain specific medical complications, i.e., pneumonia, urinary tract infection, sepsis, disseminated intravascular coagulation, rhabdomyolysis, dehydration, deep venous thrombosis, pulmonary embolism, urinary retention, decubitus, arrhythmia, renal failure, neuroleptic malignant syndrome, hypernatremia, and liver dysfunction (all p values < .01, except for deep venous thrombosis, p = .04 in the multiple linear regression analysis).ConclusionsCatatonic stupor in schizophrenia substantially raises the risk for specific medical complications and mortality. Hyperactivity of the sympathetic nervous system, dehydration, and immobility, which are frequently involved in catatonia, might contribute to these specific medical complications. In catatonia, meticulous care for both mental and medical conditions should be taken to reduce the risk of adverse medical consequences.

Background Hypokalemia is frequently found in patients with anorexia nervosa and sometimes leads to life-threatening conditions. Although their serum potassium levels are considered to further decrease during refeeding, no previous studies have addressed actual changes in the serum potassium levels and potential mechanisms underlying hypokalemia during the refeeding period of patients with anorexia nervosa. In this study, we investigated factors associated with hypokalemia during refeeding of patients with anorexia nervosa. Methods We recruited 52 independent patients from 89 admissions with anorexia nervosa (body mass index, 13.0 ± 3.3) from the psychiatry unit in Ashikaga Red Cross Hospital during the period from April 2003 to March 2018 and analyzed serum potassium levels at admission. Of the 89 admissions, 66 admissions with > 1-week hospitalization were recruited to determine the lowest potassium levels during the refeeding period. We analyzed these levels with multiple linear regression analysis with explanatory variables, including data upon admission and treatment-related indicators. Results The initial serum potassium level of 3.6 ± 0.9 mg/dl decreased to 3.1 ± 0.7 mg/dl at nadir hypophosphatemia, which was observed an average of 2.5 days after admission. A lower serum potassium level at admission and a lower nadir potassium level during refeeding were associated with a lower body mass index, hypoalbuminemia, and binge–purge behavior. Similar results were obtained when the analysis included restrictive or binge–purge types as well as the independent patient group. Conclusions Lower body mass index, hypoalbuminemia, and binge–purge behavior might be used as indicators to guide clinical approaches for controlling serum potassium levels in patients with anorexia nervosa during refeeding. Plain English summary Hypokalemia, low levels of serum potassium, in patients with anorexia nervosa sometimes leads to life-threatening conditions. Thus, it is of great importance to predict the risk of hypokalemia in patients with anorexia nervosa during the refeeding period. Our study found that hypokalemia in patients with anorexia nervosa during refeeding is associated with a lower body mass index and hypoalbuminemia (low levels of serum albumin), in addition to binge–purge behavior.

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Background: Pisa syndrome (PS) is characterized by an abnormally sustained posture, with flexion of the body and head to one side and slight rotation of the trunk. Although PS most commonly arises as an adverse effect of antipsychotic drugs, choline-esterase inhibitors (ChEIs) are also sometimes known to induce PS. Despite the fact that the precise mechanism remains unclear, cholinergic-dopaminergic imbalance has been considered as a possible pathophysiologic mechanism underlying the genesis of PS. Case presentation: We hereby report the case of a 60-year-old woman with Alzheimer's disease who presented with the signs of PS after her treatment was switched to galantamine, a type of ChEI, even though she had received donepezil, another type of ChEI, for 5 years without any complications. To the best of our knowledge, this is the first report of PS associated with treatment switch from one to another type of ChEI. Galantamine, but not other ChEIs, can enhance striatal dopamine release through allosteric modulation of the nicotinic acetylcholine receptor, and has weaker muscarinic effects than donepezil. Therefore, we propose two novel hypotheses to explain the development of PS, as follows; galantamine, which enhances dopamine release, can induce imbalance of dopamine levels in the striatum of patients with dementia, resulting in PS, and the weaker muscarinic effects of the drug could be one of the factors predisposing to the development of PS. Conclusion: The present case suggests that treatment with galantamine is associated with a higher risk of development of PS than that with other ChEIs, such as donepezil, despite the pharmacological profile of galantamine as a dopamine modulator. Also, this report provides novel insight into another plausible mechanism underlying the development of PS, besides cholinergic-dopaminergic imbalance, namely, dopamine imbalance in the striatum with muscarinic-nicotinic imbalance.

Adult‐onset leucoencephalopathy with axonal spheroids and pigmented glia (ALSP), also known as hereditary diffuse leucoencephalopathy with spheroids (HDLS), is a progressive neurocognitive disorder that predominantly affects the cerebral white matter, mainly the frontal subcortical areas and the corpus callosum. Patients with ALSP are clinically characterized by a gradual onset of cognitive and behavioural dysfunction and personality changes, followed by motor impairments such as gait disturbance and bradykinesia. Given the disease‐related degenerative changes of the frontal white matter, it is no wonder that patients with ALSP present with behavioural symptoms and non‐fluent aphasia, which are found in patients with frontotemporal lobar degeneration. However, behavioural symptoms and non‐fluent aphasia in a patient with ALSP have rarely reported in detail. Here, we describe a patient with ALSP who initially presented with remarkable behavioural signs and non‐fluent primary progressive aphasia, which resembled symptoms of frontotemporal lobar degeneration. The present case suggests that ALSP should be included in the differential diagnosis for frontotemporal lobar degeneration.

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