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The cortical representation of micturition is speculated to reside in the medial frontal lobes.1,2 Lesion pathology, however, varies from acute stroke to a neoplasm, and there is not necessarily a small, distinct lesion.2 We report a case of urinary retention in which the main presenting symptom is thought to have been caused by a small cortical infarction.
One morning, a 66 year old, right handed man had difficulty urinating. He had no history of voiding difficulty, diabetes mellitus, injury to the lower urinary tract, or neurological disease. Digital rectal examination and ultrasonography of the prostate detected no enlargement. Urinalysis showed no haematuria or pyuria. He was not taking any medications that cause voiding dysfunction. There was no urinary incontinence, but he had difficulty in voiding even though he felt the bladder was full. At that time, he also had difficulty in lifting his left arm and leg and so was brought to our hospital. Neurological examination in the emergency room found no weakness, and he was sent home. Later, he experienced urinary retention and visited the emergency room again. His post void residual urine volume was 350 ml, and an urinary catheter was inserted. At that time the patient was alert, and his cranial nerves were intact. Limb muscle strength was normal. Sensory examination was unremarkable. Tendon reflexes were normal in all four limbs. Tandem gait and standing on one foot were difficult. He had normal bladder sensation but difficulty in urinating. Drip infusion pyelography revealed no abnormality in the upper urinary tract or the form of the bladder. Filling cystometry showed stable detrusor with normal bladder sensation, whereas acontractile detrusor was noted in the voiding phase. He could void only with strain, having a peak flow rate of 5.0 ml/s and a voided volume of 135 ml. Diffusion weighted MRI, performed on the day of onset, showed a small, distinct, high intensity signal, and T1 weighted imaging showed a low signal in the right caudal part of the anterior cingulate gyrus, indicative of an infarct in the acute stage (fig 1A and C). No definitive infarct was observed elsewhere. MR angiography showed no occlusion or stenosis of the intracranial vessels. An electrocardiogram was normal. Transthoracic echocardiograms showed no abnormal findings. The urinary catheter was withdrawn 3 days after admission, and he had no subsequent difficulty with urination. His gait returned to normal about the same time.
In the acute stage of a cerebral vascular accident, the presenting symptom often is urinary retention due to detrusor areflexia,3 but patients who have this problem usually have a major stroke with severe neurological deficits.
To the best of our knowledge, this is the first report in the English literature of urinary retention, although temporary, caused by a small cortical infarct as shown by diffusion weighted MRI.
Various cortical areas are activated during voiding because a network of brain regions is necessary for voiding modulation.4 The locations of the primary cerebrum cortical areas for voiding and storage are speculated to be separate, the former being at the para-central lobule.2 A PET study found normal micturition to be associated with activation of the middle frontal gyrus, superior frontal gyrus, superior precentral gyrus, thalamus, and the caudal part of the anterior cingulate gyrus in the left hemisphere.5 Another recent PET study showed that increased brain activity related to increasing bladder volume was located in the bilaterally mid-cingulate cortex, while that related to decreased urge to void was bilaterally in a different portion of the mid-cingulate gyrus.4
Although the infarct in our patient was located in the caudal part of the anterior cingulate gyrus, it was on the right side, nearby the region activated in the PET study.4 SPECT showed increased blood flow in the right medial frontal area, indicative that urinary retention was due to “decreased urge to void”, and decreased flow in the right medial parietal lobe, which might explain the gait disturbance, in light of the essentially normal sensory examination. Unfortunately, a PET scan was not available in our hospital (Kameda Medical Center). Because there has been no report of an isolated lesion of the cingulate gyrus causing hemiparesis, these brain imaging studies indicate that the left hemiparesis, which disappeared within a half day of onset, could have been due to a transient ischaemic attack.
Urinary symptoms disappeared 3 days after admission, probably because the cortical neuron network compensated by providing a functional alternative to the lesion damaged by the infarct. This is similar to the condition of urinary incontinence after cerebral infarction, as is well documented. The laterality of the lesion in this patient differs from that in a previous PET study4 which showed bilateral activation in the cingulate gyrus. Because this report cites only a single case, its applicability is limited. Additional lesion studies of patients with micturition disturbance due to small cortical infarcts should help to identify the anatomical cerebral structures involved in voiding.
Competing interests: none declared
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