No abstract

Charles Bonnet Syndrome (CBS) is diagnosed when a patient who is psychiatrically intact experiences visual hallucinations in the setting of significant visual acuity or field loss. The exact pathophysiology of the CBS hallucinations remains largely unknown. The main theories include the deafferentation theory and perceptual release theory. There are suspected neurotransmitters involved, including acetylcholine and dopamine. There is no defined treatment protocol with medication for CBS, but various psychotropic medications have been used with varying degrees of remission of symptoms.This case report describes a 64-year-old male with Charles Bonnet Syndrome in the setting of superimposed delirium. We note the different medications that were trialed to reduce his CBS symptoms and decrease episodes of behavioral disturbances. Clinical features of this rare syndrome with superimposed delirium are summarized in hopes of providing directions for management and future study.

A 64-year-old female patient presented to the emergency department with a 3-week history of persistent nausea and vomiting. Her serum creatine prior to admission was 118 µmol/L and on presentation was elevated to 420 µmol/L. On clinical history, she indicated that 3 weeks prior, she had been initiated on a cyclooygenase-2 (COX-2) inhibitor, celecoxib, for her osteoarthritis of her knees. Renal biopsy confirmed the diagnosis of acute interstitial nephritis (AIN). Celecoxib was discontinued and the patient's renal function improved to a discharge creatine of 205-220 µmol/L. Nine months later, her creatine had decreased to 195 µmol/L and she was initiated on tapering doses of prednisone therapy for 4 months, after which time her creatine had improved further to 143 µmol/L. She was later transitioned to mycophenolatemofetil for 9 months and her creatine improved to 110 µmol/L. This report provides further evidence that COX-2 inhibitors are associated with AIN.

We summarize the case of an 81-year-old Caucasian female who presented to her family physician with signs and symptoms of nephrotic syndrome following a brief exposure to quinine. Prior to that visit, she was clinically well with no chronic medical ailments and met with her family physician for annual physical assessments. She had taken 11 tablets of quinine for nocturnal leg cramps over the course of 28 days before starting to notice mild peripheral edema, which subsequently progressed, leading to a family physician review. Her initial serum albumin level was 12 g/L, and a 24-hour urine protein output was quantified at 8.14 g/day; she was diagnosed as having nephrotic syndrome. A kidney biopsy confirmed the diagnosis of minimal change disease (MCD). Quinine therapy was stopped, and she was initiated on a tapering regime of prednisone with concurrent cyclosporine therapy. Within a fortnight of starting therapy, she went into remission and her immunosuppressive medications were rapidly tapered and discontinued. This paper reports an association between the use of quinine and subsequent MCD. This case report proposes that the use of quinine has an association with, and may be causal for, the development of minimal change disease. As this is yet an unreported adverse effect, this paper seeks to increase the knowledge of the varied and numerous effects of quinine.