Frontal dermoid cyst presenting with urinary incontinence

INTRODUCTION

The bladder stores urine at low pressure and empties it voluntarily when appropriate. Unlike most visceral organs, it is partially under conscious control, which requires full maturation of the central nervous system. Any involuntary loss of urine is defined as urinary incontinence.

Bladder function depends on coordinated interaction between somatic and autonomic systems. The somatic system controls voluntary structures such as the external urethral sphincter, whereas the autonomic nervous system regulates detrusor contraction and relaxation. Parasympathetic fibres originate from cranial and sacral segments, while sympathetic pathways arise from thoracic and lumbar spinal segments.

The pontine micturition centre (Barrington’s nucleus) integrates detrusor contraction with urethral sphincter relaxation. Spinal cord lesions below this level may result in detrusor–sphincter dyssynergia. Cortical regions, particularly the anterior cingulate and prefrontal cortex, modulate bladder sensation and voluntary voiding decisions. Although micturition is fundamentally an autonomic reflex, higher brain centres exert inhibitory control by suppressing the reflex and maintaining sphincter contraction until voiding is initiated.

CASE REPORT

A 79-year-old male with hypertension presented with a one-year history of urinary incontinence. Urodynamic evaluation suggested benign prostatic hyperplasia, and treatment with alpha-adrenergic receptor–modulating agents was initiated. Despite dose escalation and therapeutic modification, no improvement was observed. Due to persistent symptoms and accompanying depressive mood, the patient was referred for neurological and psychiatric evaluation.

Duloxetine was initiated due to depressive mood and urinary incontinence; however, no clinical benefit was observed.

His history included three prior lumbar disc surgeries, and incontinence was initially attributed to possible spinal pathology.

Neurological examination showed an alert, oriented patient with fluent speech. Cranial nerve examination was normal. No lateralised motor deficit, paraparesis or sensory level was detected. Deep tendon reflexes were present, and gait was normal except for inability to perform tandem walking. There were no signs suggestive of active spinal cord pathology. Cerebellar testing of the upper limbs was intact.

In the absence of spinal findings and given treatment resistance, brain magnetic resonance imaging was performed. Imaging revealed a cystic mass in the frontal region compressing the anterior horn of the right lateral ventricle and causing approximately 5 millimetres of leftward midline shift. The patient underwent neurosurgical resection, and histopathological examination confirmed a dermoid cyst.

CONCLUSION

Micturition is modulated by supraspinal centres that integrate autonomic reflex activity with cortical inhibitory control. The pontine micturition centre coordinates detrusor and sphincter function, while frontal cortical regions regulate voluntary suppression. Disruption of these inhibitory pathways may result in urinary dysfunction.

This case illustrates that urinary incontinence resistant to conventional urological therapy may reflect central nervous system pathology. Frontal cortical lesions may impair inhibitory control over bladder function. Persistent or atypical urinary incontinence should prompt neurological evaluation and consideration of neuroimaging, even when urological explanations appear plausible. A multidisciplinary approach is essential to ensure timely diagnosis and appropriate management.

References

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