A Case of Oligospermia
NATIONAL JOURNAL OF HOMOEOPATHY 2003 Mar / Apr VOL V NO 2.
Dr Girish Gupta
'Nat-m / Ph-ac

INTRODUCTION:
Oligospermia or Oligozoospermia means a condition of reduced number of sperm cells (spermatozoa) while Azoospermia, means no sperm in the ejaculate of the male. The normal range of sperm count is between 20 millions/ml to 200 millions/ml. The sperm count below 20 millions/ml indicates Oligospermia.

Sterility in male is responsible for the infertility of approximately one half of all childless marriages. The cause is usually defective development of the germinal epithelium in the seminiferous tubules, with Oligospermia or Azoospermia but may follow hypogonadism due to antibodies to sperms. Klinefelter’s syndrome is almost invariably associated with Azoospermia. The additional X chromosome may be recognized by examination of buccal smear for Barr bodies, but confirmation requires a full karyotype analysis. (3)

In most Azoospermia patients where there is defective spermatogenesis due to primary testicular dysfunction FSH level will be high. If FSH level is normal it suggests possibility of obstruction. If semen has decreased fructose concentration, it suggests obstruction to fluid coming from seminal vesicles.

AETIOLOGY, PATHOGENESIS AND EVALUATION OF AZOOSPEREMIA

Constitutional weakness, irregular sexual life, chronic illness, malnourishment and anaemia may cause slow liquefaction of semen, dead sperms with or without nocturnal seminal emission, impotency and premature ejaculation. (1)

There are four major causes for lack of sperm production viz. Hormonal problems, Testicular failure, Varicocele and Sperm delivery problems:-(2)

1. Hormonal problems: Spermatogenesis may be severely reduced or absent in absence of pituitary hormones required to stimulate testicles for it. Androgens (steroids) taken by men (oral or injectable) for bodybuilding suppresses the production of pituitary hormones required for spermatogenesis. If Follicle stimulating hormone (FSH) level is normal, it suggests obstruction while elevated FSH indicates decreased Spermatogenesis. Testosterone, Prolactin, Luteinizing hormone (LH) and Thyroid stimulating hormone (TSH) also indicate a man’s hormonal status.

2. Testicular failure: This is inability of germinal epithelium of seminiferous tubules epithelium of the testicle to make adequate numbers of mature sperm. It may occur at any stage in sperm production due to genetic abnormality.
a. Sertoli Cell Syndrome-Testicle may lack the cells that divide to form sperm.
b. Maturation arrest-Inability of the sperm to complete their development.
Testicular biopsy can be performed if a primary testicular problem is suspected. Genetic testing is essential for specific genetic abnormalities on the male chromosomes.

3. Varicocele: Dilated veins in the scrotum due to inadequate drainage of blood leads to pooling of extra blood in scrotum resulting in reduced spermatogenesis. Varicocele can be directly visualized on physical examination, but Ultrasonography is confirmatory. Physical examination can also reveal a dilated epididymis indicating blockade, severely diminished size of the testicles indicating defective germinal epithelium of seminiferous tubules and congenital bilateral absence of the vas deferens (CBAVD).

4. Neurological damage: Surgery, diabetes, or spinal cord injury may prevent emission process in which sperms are deposited in urethra before real ejaculation. Urinalysis can rule out backward ejaculation of the sperm into the bladder that can be washed out during micturition after ejaculation.

5. Sperm delivery problems: Sperm delivery complications are due to problem with ductal system that carries the sperm or with ejaculation or congenital bilateral absence of the vas deferens (CBAVD). Physical examination can reveal a dilated epididymis indicating block or blockade may be in muscular vas deferens. Severely diminished size of the testicles indicating defective germinal epithelium of seminiferous tubules. Mechanical blockade during hernia or hydrocele repairs are also likely. A transrectal ultrasound can rule out blockade of the ejaculatory duct. Dilated seminal vesicles indicate non–emptying of semen.

CASE REPORT
Mr NPS, a 28 years old male patient reported for treatment of incomplete erection, premature ejaculation, nocturnal seminal emissions and decreased sexual desire. Patient was married for 4 years and the couple wanted an issue. Past history revealed disappointment in love and habit of masturbation. He was advised semen analysis after proper abstinence. Semen examination report dated April 27, 1996 revealed very low sperm count-9.2 millions/ml out of which about 20 % sperms were sluggishly motile while 80 % were non-motile. 10 % sperms were abnormal. Smear showed 2-3 pus cells/HPF (Report 1). The case was repertorised manually using Kent’s repertory. Symptoms considered for repertorisation were ailments from disappointed love, ailments from anxiety, ailments from masturbation, dreams of falling, dreams of feasting, dreams of being pursued, dreams of unsuccessful efforts (Phosphoric-acid), incomplete erection, premature ejaculation, nocturnal emissions, decreased sexual desire, fear of impending disease, aversion to company, aggravation from consolation, anxiety about future, aversion to mental work, oversensitive to noise, homesickness, difficulty in concentration and desire for salty things. Natrum muriaticum and Phosphoric acid were selected from various drugs of choice.

FOLLOW-UP:
Ist prescription: May 02, 1996: Natrum muriaticum 1000 single dose was prescribed followed by Phosphoric acid 30 for four weeks.
June 03, 1996: Dreams of falling, of feasting, of being pursued, of unsuccessful efforts and nocturnal emissions reduced in frequency. Only Phosphoric acid 30 was repeated for eight weeks.
August 01, 1996: No dream of falling, of feasting, of being pursued, of unsuccessful efforts. Nocturnal emissions much reduced and erection improved considerably. Only Placebo was repeated for three weeks.
August 26, 1996: No dreams of falling. Nocturnal emissions much reduced, erection improved considerably and concentration much better. Semen examination report dated August 19, 1996 revealed increased sperm count of 16.3 millions/ml, out of which about 52% sperms were actively motile, 13 % sluggishly motile while 35 % were non-motile. 8 % sperms were abnormal. Smear showed 2-4 pus cells /HPF (Report 2). Only Placebo was repeated for twelve weeks on different visits.
December 05, 1996: Dreams of falling, of feasting, of being pursued, of unsuccessful efforts recurred. However, erection improved considerably, but no change in nocturnal emissions. Natrum-muriaticum 1000 single dose was repeated followed by Phosphoric-acid 30 for four weeks.

January 01, 1997: Dreams of falling, of feasting, of being pursued, of unsuccessful efforts and nocturnal emissions continued. Erection as such, no further improvement in concentration.Natrum-muriaticum 10 M single dose was prescribed followed byPhosphoric-acid 30 for three weeks.
January 27, 1997: No dream recurred. No nocturnal emissions, erection much better. Semen examination report dated January 22, 1997 revealed increased sperm count of 60.8 millions/ml, out of which about 32% sperms were actively motile, 17 % sluggishly motile while 51 % were non-motile. 4 % sperms were abnormal. Smear showed 4-6 pus cells /HPF (Report 3). Only Placebo was repeated for sixteen weeks on different visits.
June 02, 1997: No dream. No nocturnal emissions, erection much better. Placebo was again repeated for three weeks.
June 30, 1997: No dream. No nocturnal emissions, premature ejaculation. Sexual desire increased and erection much better. Semen examination report dated June 25, 1997 revealed further increase in sperm count to 71.3 millions / ml (within normal limits) out of which about 30 % sperms were actively motile, 10 % sluggishly motile while 60 % were non-motile. 3-6 % sperms were abnormal. Smear showed stray pus cells/HPF (Report 4). Placebo was again repeated for four weeks.

The patient was almost relieved of all the symptoms and his sperm count also reached normal limit. He left the treatment assuming that he was completely cured. The outcome of the treatment could not be known whether the couple had any issue or not.

REFERENCES
1. Internet: http://www.aaaom.org OLIGOSPERMIA.html.
2. Internet: http://www.maleinfertilitymds.com/faq5.html.
3. Davidson’s Principles and Practice of medicine, edited by John Macleod: Endocrine and Metabolic Diseases - Sexual disorders in Male (Infertility in the Male); J. F. Smyth, pp. 456, Fourteenth edition, 1984.