Histological evidence of benign prostatic hyperplasia (BPH) exceeded 50% in men over 50 years of age and rose to 75% as men entered the eighth decade. Therapeutic options for BPH generally fall into one of the three categories: watchful waiting, medical treatment and surgery. Excluding watchful waiting, the other forms of intervention directed at modifying the physiologic effects of BPH with or without directly altering the prostatic mass or its configuration come with varying effectiveness and risk. Botulinum toxin (BTX–A) produce inhibition of acethylcholine release at the neuromuscular junction causes paralyzing effects and atrophy of striated as well as the smooth muscle fiber. BTX–A also causes inhibitory effects on the ganglionic and post– ganglionic fibres of autonomic nervous system inducing diffuse atrophy and apoptosis of nasal and prostate glands.

Clinical series demonstrates efficacy of BTX–A in alleviating symptoms induced by BPH. Larger randomized clinical trials studies are necessary in order to identify the mechanisms by which BTX–A affects the prostate, the ideal dose and the duration of effect. BTX–A injected into prostate appears safe and effective