Cystocerebral Syndrome: A Case Report and Review of Literature and Mechanisms

To the Editor: Elderly men are at risk of bladder outlet obstruction secondary to benign prostatic enlargement. Acute urinary retention (AUR) mechanisms include neurogenic (e.g., diabetes mellitus), obstructive (e.g., constipation), or detrusor muscle underactivity (e.g., itself secondary to immobility).1 Symptoms include abdominal pain, urinary retention, and dysuria. Encephalopathy may also occur, ranging from altered mental status (AMS) to agitation.2-5 Cystocerebral syndrome was first described in three elderly men presenting with AUR and AMS who rapidly responded to decompression.2 A case of cystocerebral syndrome is presented, pathomechanistic models offered, and future investigational directions proposed. A 79-year-old man with severe benign prostatic hypertrophy (BPH) and hypertension was admitted with AMS. According to his family, he lacked any psychiatric history. A urologist was actively considering him for transurethral resection of the prostate (TURP) after a computed tomography (CT) urogram 2 weeks before had revealed bilateral hydronephrosis and an enlarged prostate. His wife reported that, over the preceding days, he had complained of dysuria and cloudy urine; she had also observed increasingly agitated and paranoid behavior over the previous weeks. When she contacted an on-call nurse, her husband began yelling, prompting a police call out of concern for the wife's safety. He fled the house, stating that his wife wanted to commit him to the “drunk tank.” He was found and brought to the emergency department (ED) in an agitated state. Vital signs were unremarkable, although serological studies revealed acute kidney injury (AKI), with creatinine levels approximately five times above baseline without uremia. Urinalysis suggested urinary tract infection (UTI); culture later confirmed growth of Enterobacter aerogenes. He was treated empirically in the ED with ceftriaxone 1 g intramuscularly followed by piperacillin-tazobactam 3.375 g intravenously twice daily for 5 days. Abdominal CT revealed constipation, and Foley catheterization yielded 1,100 mL of output. Within hours, he was observed to be calm, requiring no behavioral interventions. He was monitored for renal recovery for 1 week; psychiatry was consulted during discharge planning for a safety assessment after his wife expressed concerns for her own safety because of his behavior before admission. On interview, he was calm, cooperative, and without focal neuropsychiatric signs or symptoms. He denied any prior psychiatric history and reported a “normal childhood” lacking trauma or abuse. In describing the days leading to his admission, he felt his wife had exaggerated events and that he had been upset that she was going to put him in a psychiatric hospital. He revealed guarded and hypervigilant behaviors, including barring of doors and fearing someone might break into his home and acknowledged feeling afraid yet aware and oriented throughout this. His Montreal Cognitive Assessment score was 21 out of 30, with deficits in delayed recall and visuospatial functioning, suggesting an underlying cognitive impairment. He was diagnosed with resolved delirium secondary to urinary retention. Cystocerebral syndrome is described as encephalopathy resulting from bladder distension and responding rapidly to bladder decompression.2-4 The current case is one such example in which a variety of factors contributed to paranoid psychosis and agitation. BPH-mediated urinary retention and constipation work in confluence to cause bladder outlet obstruction. UTI developed in the setting of such retention, probably contributing to encephalopathy. Last, underlying cognitive impairment elevates the risk of AMS significantly. Although UTI is conventionally considered a sufficient cause of AMS, a recent systematic review seriously questions the mechanistic role of UTI in encephalopathy.6 A complementary brain–bladder interaction is through increased sympathetic tone secondary to bladder wall distention.7 Bladder wall beta receptors are activated during bladder wall relaxation and filling; in the event of severe obstruction, central and peripheral adrenergic responses lead to catecholamine release, contributing to confusion and agitation, particularly in individuals with underlying cognitive deficits.7 Lack of peripheral sympathetic response (tachycardia, hypertension) may be due to a blunted beta-adrenergic response, as observed in senescence.3 In addition, an increase in locus coeruleus norepinephrine release and related hyperarousal has been seen in rats with bladder distention.8, 9 A case of cystocerebral syndrome with rapid, temporal response to mechanical decompression within the context of various other risk factors is described (Figure 1). It is doubtful a single antibiotic dose promptly resolved agitation, and the alleviation of bladder-mediated sympathetic activation is proposed as the mechanism of rapid recovery. This case is reported to raise awareness of the dynamic interaction between bladder and brain. Clinically, this scenario may be easily managed with rapid decompression, avoiding psychiatric interventions. Bladder-mediated sympathetic activation and associated neuropsychiatric phenomena warrant investigational attention, including serum catecholamine and symptom correlation studies or evaluation of behavioral responses to bladder decompression. Conflict of Interest: The authors disclosed no proprietary or commercial interest in any product mentioned or concept discussed in this article. Author Contributions: Both authors contributed equally to the writing of this letter. Sponsor's Role: No sponsor.

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