To address the consistent finding of asthenospermia in spinal cord injured men we compared the biochemical constituents of antegrade fractions of electroejaculates of 6 such patients with the manual ejaculates of 6 volunteers. Semen samples in each group were analyzed for 19 biochemical parameters, pH and osmolality. Organic components included triglycerides, glucose, fructose, uric acid, creatinine, urea, total protein, albumin and cholesterol. Metabolic enzymes, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase, lactate dehydrogenase and alkaline phosphatase, were measured. Inorganic constituents included chloride, sodium, potassium, zinc and phosphorous. Although not significant, higher levels of blood urea nitrogen and creatinine were demonstrated in most electroejaculates suggesting urinary contamination of the antegrade specimens. In electroejaculates significantly lower levels (p less than 0.05) of fructose, albumin, GOT and alkaline phosphatase as well as significantly higher levels (p less than 0.05) of chloride were noted. No significant difference in osmolality or pH was found. Moreover, in the electroejaculates the levels of glucose, uric acid and all inorganic constituents approached their corresponding levels in serum. We conclude that biochemical abnormalities of the seminal plasma may contribute to seminal dysfunction of spinal cord injured men and may result from neurological injury to the accessory sex glands or from the electroejaculation procedure itself.
Lyme disease, which is caused by the spirochete Borrelia burgdorferi, is associated with a variety of neurological sequelae. We describe 7 patients with neuro-borreliosis who also had lower urinary tract dysfunction. Urodynamic evaluation revealed detrusor hyperreflexia in 5 patients and detrusor areflexia in 2. Detrusor external sphincter dyssynergia was not noted on electromyography in any patient. We observed that the urinary tract may be involved in 2 respects in the course of Lyme disease: 1) voiding dysfunction may be part of neuro-borreliosis and 2) the spirochete may directly invade the urinary tract. In 1 patient bladder infection by the Lyme spirochete was documented on biopsy. Neurological and urological symptoms in all patients were slow to resolve and convalescence was protracted. Relapses of active Lyme disease and residual neurological deficits were common. Urologists practicing in areas endemic for Lyme disease need to be aware of B. burgdorferi infection in the differential diagnosis of neurogenic bladder dysfunction. Conservative bladder management including clean intermittent catheterization guided by urodynamic evaluation is recommended.
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