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Introduction – Chronic orchialgia is defined as 3 months of intermittent or constant testicular pain that is significantly bothersome to the patient. It is the cause of about 2.5% to 5% of all urology consultations and currently affects about 100,000 men in the United States each year.

1. When it cannot be directly be attributed to any specific, identifiable source, the condition is called idiopathic chronic orchialgia.
2. Evaluation can be confusing as the underlying cause is often idiopathic and conservative therapy is often unsuccessful making this a challenging condition to diagnose and treat.

Conservative therapy is usually tried first, but more invasive treatments are used when first-line options fail. Surgical options include spermatic cord blocks, varicocelectomy, epididymectomy, vasovasostomy (if the patient has had a vasectomy), microsurgical denervation of the spermatic cord (MDSC), botulinum toxin injections, and orchiectomy.

Can testicular pain last for years?

What is testicular pain? – Testicular pain is a condition that can affect males at any age. The testicles (testes) are small egg-shaped reproductive (sex) organs inside a thin pouch of skin called the scrotum. If you have testicular pain, you may feel it in one or both testicles.

However, the pain may not actually be coming from your testicles themselves. The pain may be coming from another part of your body such as the stomach or groin. This type of pain is called referred pain. Testicular pain can be either acute (sudden and short) or chronic (gradual and long-lasting). Aside from the sharp pain of sudden injury, your first symptom might be a dull ache that increases with time or with activity.

Testicular pain can be severe because the testicles have many sensitive nerves. You should get medical care if your pain lasts longer than an hour or if it’s unusually intense, as this could be a sign of an emergency condition called testicular torsion,

How do you fix chronic testicular pain?

Treatment / Management – A multi-disciplinary approach to patients with chronic orchialgia is recommended. This would ideally include pain management specialists, psychiatry, pelvic floor physical therapists as well as primary care and urology. This type of approach along with conservative therapy should be tried before resorting to invasive and irreversible surgical procedures.

1. There are no clear and established guidelines for treatment.
2. The following are the consensus treatment recommendations for idiopathic chronic orchialgia from the published literature.
3. If an obvious source of the pain is found, begin specific therapy (hernias, spermatoceles, epididymitis).
4. If unsuccessful or if no specific etiology is found, a course of conservative therapy is undertaken.

If the patient is on amiodarone, the drug may have to be discontinued as the orchalgia it sometimes produces is not self limiting. Conservative therapy includes heat, ice, scrotal elevation, antibiotics, analgesics, NSAIDs, antidepressants (doxepin or amitriptyline), anticonvulsants (gabapentin and pregabalin), regional and local nerve blocks, pelvic floor physical therapy, biofeedback, acupuncture, and psychotherapy for at least 3 months.

While conservative therapy has almost always been considered first-line treatment, success is relatively poor ranging from 4.2% to 15.2% in some studies. There are no good, published studies regarding reliable non-surgical interventions. Nevertheless, it is advisable to try conservative therapies first.

Treatment starts with dietary and lifestyle advice usually consisting of eliminating dietary caffeine, citrus, hot spices, and chocolate as well as avoidance of constipation and prolonged sitting. Antibiotics prescribed are usually trimethoprim/sulfamethoxazole or a quinolone because of their lipid solubility.

They are typically prescribed for 2 to 4 weeks. Antibiotic therapy is not recommended for empiric use, only if there are objective signs or a reasonable suspicion of an infection. Initial pharmacological therapy is usually with non-steroidal anti-inflammatory drugs (NSAIDs). They are typically prescribed for at least 30 days.

Preferred agents include 600 mg ibuprofen 3 times daily, naproxen (Naprosyn), celecoxib 200 mg daily or piroxicam (Feldene) 20 mg daily. Recurrence rates after successful NSAID use are as high as 50%. Narcotic analgesics should be avoided except possibly for occasional breakthrough pain.

• There is some evidence than tamsulosin may be of some use in selected patients.
• Tricyclic antidepressants work by blocking the reuptake of norepinephrine and serotonin in the brain.
• Their analgesic effect is thought to be due to inhibition of sodium and L-type calcium channel blockers in the dorsal horn of the spinal cord.

Tertiary amines in this class (amitriptyline and clomipramine) are more effective for neuropathic pain than secondary amines (desipramine and nortriptyline) but are also more sedating and more likely to be associated with postural hypotension. They are usually given as a single dose at bedtime and will typically require at least 2 to 4 weeks for their effectiveness to become apparent although this may take up to 8 weeks.

1. Usual dosing is amitriptyline 25 mg at HS.
2. If tricyclic therapy is not successful after 30 days, the next conservative therapy approach would be to add an anticonvulsant such as gabapentin (Neurontin) at 300 mg TID and pregabalin (Lyrica) at 75 to 150 mg daily.
3. Usually, gabapentin is used first as insurance coverage often requires a gabapentin failure before pregabalin will be covered.

These are recommended due to their proven efficacy in neuropathic pain and their relative lack of side effects. They work by modulating the N-type calcium channels which significantly affects pain fibers. Typical dosage of pregabalin for pain control would be 75 mg 3 times daily.

1. If the pain persists beyond 30 days, the treatment would be judged ineffective.
2. In one small study, over 60% of patients with idiopathic chronic orchialgia showed significant pain relief, but large-scale, definitive studies are lacking.
3. Trigger point dry needling was recently found to be effective in 85% of patients with chronic orchialgia.

For those patients who responded, the average number of dry needling treatments was 4.6 while this increased to 6.5 for those who did not respond. Pelvic floor physical therapy is useful for those with pelvic muscle dysfunction or identifiable myofascial trigger points.

In properly selected patients, about 50% have noted improvement in their pain after 12 sessions. It also appears that physical therapy can improve pain and quality of life scores for chronic orchialgia patients even after other treatments. Therefore, a physical therapy evaluation and treatment should be considered an effective, low risk therapeutic option for patients with chronic orchialgia.

The next step is the spermatic cord block which is recommended prior to performing any invasive or irreversible surgical procedures. This is usually done by injection 20 mL of 0.25% bupivacaine without epinephrine using a 27 gauge needle. Steroids may or may not be added.

• The injection is done directly into the spermatic cord at the level of the pubic tubercle.
• Ultrasound can be used to assist if the anatomy is challenging due to body habitus or prior surgery.
• If spermatic cord nerves are involved in the pain signals, the testicular discomfort should be rapidly relieved by the injection.

While this often provides relief, it is rarely long term. Those patients who experience more than 90% pain relief can be offered repeated blocks up to every 2 weeks. If the injection provides no pain relief, it is not repeated. If the spermatic cord block is not at least 50% successful in reducing the orchialgia, consider a possible missed diagnosis.

A re-examination of the patient along with a careful review of his laboratory studies and imaging is suggested. In general, the better the response to the spermatic cord block, the better the outcome with MDSC. The use of “sham blocks,” with normal saline instead of local anesthetic, is discouraged due to ethical considerations.

Surgical intervention is indicated if the spermatic cord block is at least 50% successful in reducing the orchialgia. About 1% to 2% of all men who undergo vasectomies will develop constant or intermittent testicular pain lasting greater than 3 months which is then defined as post-vasectomy pain syndrome,

Post-vasectomy patients who fail conservative therapy should consider a vasectomy reversal. This is especially recommended if scrotal imaging shows evidence of epididymal congestion and there is an association of testicular pain with sexual intercourse. The success rate of vasectomy reversal for chronic orchialgia patients with post-vasectomy pain syndrome has been reported as 69%.

Sperm granulomas should be removed if they appear to be tender or contributing to the scrotal pain. Varicoceles are relatively common findings in men with orchialgia and are found in 2% to 10% of such patients. Partial or complete relief of pain symptoms after varicocele surgery is reported in 72.4% to 94.3% of men in various studies.

1. Epididymectomy is a more aggressive surgical option that is highly successful (greater than 90%) in selected patients when the source of the pain is localized to the epididymis such as from a spermatocele or granuloma.
2. It also demonstrates reasonable success in controlling post-vasectomy pain as an alternative to vasectomy reversals.

Epididymectomy is less successful in patients with chronic epididymitis (43% patient satisfaction). It is probably not an acceptable surgical choice for diffuse pain in the cord or testicle that cannot be well localized to the epididymis. Microsurgical Denervation of the Spermatic Cord (MDSC) has become the de facto surgical standard when a procedure is indicated for idiopathic chronic orchialgia unresponsive to conservative therapies.

Very good outcomes with microsurgical denervation of the spermatic cord (MDSC) are reported (up to 76.5%), especially if patients have had a positive response to a spermatic cord block. Originally described by Devine and Schellhammer in 1978, it is performed with an operating microscope to avoid injury to the testicular arteries which are otherwise very difficult to visualize.

The procedure is usually done through an inguinal incision, and the spermatic cord is exposed and delivered out of the wound. A sub-inguinal incision is an acceptable alternative approach. The testicle is usually left in place in the scrotum. The spermatic cord is then stabilized and supported by a Penrose drain or tongue depressor placed underneath.

• The cord is carefully dissected using a microscope to locate the cremasteric and testicular arteries which are identified and isolated with small vessel loops.
• These arteries are spared along with the artery of the vas deferens if present.
• The peri-vasal fascia is stripped as this tissue is full of afferent nerves.

A vasectomy is typically done if it was not previously performed. Leaving the vas for fertility reasons tends to reduce the success of the procedure. However, a few experts recommend leaving the vas after stripping the perivasal fascia for about 2 cm, to avoid epididymal congestion and possible post-vasectomy pain syndrome.

The vasal artery is preserved if not previously sacrificed. Cremasteric muscle fibers are cut, with care taken to avoid injury to the cremasteric artery. The goal of the procedure is to transect all of the nerves in the spermatic cord while preserving the arterial supply (testicular artery, cremasteric artery, and the artery of the vas deferens) and a few lymphatics which are left to reduce the likelihood of developing a post-operative hydrocele.

Testicular veins and the ilioinguinal nerve are also sacrificed. (Despite this, patient complaints of sensory loss in the ilioinguinal nerve distribution area are uncommon.) The proximal end of the ilioinguinal nerve is buried to minimize neuroma formation.

• Roughly 70% to 80% of men have complete relief of symptoms and another 10% to 20% have partial pain relief after MDSC.
• Even in patients who have previously undergone a prior surgical intervention, MDSC provided 50% of them with complete relief of pain.
• Complete resolution of the pain after this surgery may take up to 3 months, but 40% noted complete pain relief immediately after the MDSC.

The procedure has been done with the da Vinci robot with similar results. Possible complications include hydrocele formation (less than 1% risk), wound infections, incisional hematomas and testicular atrophy (1% risk). Vasectomy reversal may be effective in relieving post-vasectomy pain syndrome not responding to conservative measures.

Only relatively small studies are available, but they consistently show high rates of pain relief from vasovasostomy, with 50% to 69% of patients getting complete pain relief. The negatives with this procedure include negating the purpose of the original vasectomy and the cost which may not be covered by insurance.

Failure of the procedure to provide substantial pain relief include neuropathic causes, nerve entrapment, post-operative scarring and continuing vasal obstruction. In one series of 6 men who had persistent pain after their initial vasectomy reversal, a second reversal was performed, and 50% of those men noted pain relief.

Can testicular pain be psychological?

History and Physical – A detailed history and physical with particular attention to the sexual and surgical history is essential. Any association of the pain with voiding, bowel movements, strenuous physical activities, sexual intercourse, or prolonged sitting should be explored and documented.

The history should include very specific details of the pain including exact location, quality, timing, aggravating factors, acuity of onset, and radiation to other organs or areas. For example, prolonged sitting and constipation often worsen pain in patients with idiopathic chronic orchialgia while interstitial cystitis patients would tend to have suprapubic pain associated with bladder function.

The physical examination should focus on the scrotum and genitals. Examining the patient in both the standing and sitting position is helpful. Always begin by examining the non-painful side. Each portion of the testicle (testis, epididymis, and vas) should be carefully examined for pain on palpation, swelling, and abnormal nodules.

A digital rectal examination should be performed to evaluate for possible prostatitis and abnormal pelvic floor muscle tension. An attempt should be made to try and identify the specific anatomical source of the pain, if possible. Pelvic floor pain or muscular weakness may play a role in chronic orchialgia in some men.

In one study, 93% of 41 men with chronic idiopathic orchialgia had at least one symptom of pelvic floor dysfunction and 88% of these demonstrated increased pelvic floor muscle tension on electromyographic testing. Men with pelvic floor pain or tightness on DRE are likely to demonstrate improvement with pelvic floor physical therapy.

1. Psychological factors appear to play an important role in chronic testicular pain, especially when no organic cause can be identified.
2. Psychological issues that may affect chronic genital pain include sexual dysfunction, anxiety, history of sexual abuse, major depression, and somatization disorder.
3. Types of Pain: Nociceptive versus Neuropathic Nociceptive pain is usually described as dull or aching.

It is usually elicited by gentle compression of the testis and may be associated with anatomical testicular changes such as enlargement or shrinkage and atrophy. Nociceptive pain is the typical type which would be expected from a common pain stimulus.

• Neuropathic testicular pain is characterized by a burning sensation, hyperesthesia or hypoesthesia, and radiation to the scrotal skin.
• It is typically caused by a lesion in the nervous system away from the area affected by the pain, usually the central or peripheral nervous system.
• Symptoms may be triggered by walking, stooping or hyperextending the hip.

Relief may be noted by lying down and thigh flexion. Allodynia refers to an exaggerated perception of pain to the point where a typically non-painful stimulus is perceived as painful.

Is testicular pain ever normal?

What is testicular pain? – The testicles are a sensitive part of a man’s body. Causes of testicular pain may be trauma, testicular torsion, epididimytis and other conditions. The testicles are a sensitive part of the male body. Even relatively minor injuries to them cause great pain, and many conditions can affect them.

Testicles hang from the body in a pouch of skin called the scrotum. They play a necessary role in the male reproductive system, producing sperm and testosterone, the male sex hormone. Given their sensitivity, occasional testicular pain or discomfort is normal and usually resolves itself. However, sharp, sudden, or especially severe pains are signs of an underlying condition and possibly a medical emergency.

Left untreated, severe testicular pain can lead to:

Infertility Loss of one or both testiclesInfectionAbscesses

Can anxiety cause sore testicle?

Anxiety and Sexual Function & Genital Issues

Anxiety affects every part of the body, including the genitals. On men, this may result in conditions such as testicular pain and a smaller penis. In women, this could result in yeast infections, dryness, and other health conditions. Anxiety may also lead to issues with libido and sexual desire. There are several strategies that can be implemented now to reduce anxiety, though long-term anxiety treatment will be needed.

While anxiety can cause a number of different chances in your body, the reality is that none can cause as much anxiety as problems with your genitals. No matter if you are a man or woman, young or old, married or single, no one likes the idea that something is affecting them in their most private of areas.

Is it normal for testicle pain to come and go?

Testicular Pain | Tennessee | Urology Associates P.C. Thousands of men suffer from a serious, disabling condition called Chronic Testicular Pain (CTP). CTP can be intermittent or constant. Most testicular pain is considered chronic if the patient has suffered from it for at least three months.

Approximately 25 percent of testicular pain has no known cause and may be CTP. In some patients, the pain originates in the epididymis, a crescent-shaped organ around the testicle, responsible for sperm transport and storage. This condition can mimic chronic testicular pain. CTP can interfere with normal, daily living and the ability to work.

Anyone who has suffered CTP knows the frustration of going from doctor to doctor trying to find a treatment. Our urologists offer state-of-the-art treatments and are dedicated to helping patients who suffer from CTP so that they can regain their quality of life. Chronic Testicular Pain (CTP) pain can vary from person to person. Some men with CTP have constant pain, while others have pain that goes away and comes back periodically. Some men only have pain during activities, while others only have pain when the testicle is touched or examined.

The pain may be in one testicle, in both, or change from side to side. In some men, pain in the epididymis is mistaken for chronic testicular pain. Men describe the sensations of CTP in many ways. It can feel like burning, aching, pressure, throbbing, heaviness, pulling, or a combination. It can also feel like a groin pull.

Some men report that their CTP occurs in combination with lower back pain or pain in their upper thighs or legs. Sexual activity can aggravate the pain. CTP may also worsen when sitting for long periods of time, such as at a desk job or driving a truck.

Swelling and redness of the testicles and scrotum Nausea or vomiting Fever Painful or burning urination or penile discharge Pain with intercourse or ejaculation Blood in semen or urine

Many conditions can cause or result in chronic testicular pain. They range from trauma to infections of the testicle (called orchitis) or epididymis, where sperm is stored (called epididymitis), to post-surgical pain, hernia, torsion (twisting of the testicle), tumor, kidney stones, blockage, varicoceles, spermatoceles, hydroceles, benign cysts and more.

Sometimes, even after testicular pain with a known cause is treated properly, it does not go away, or it comes back and becomes chronic. Occasionally CTP will occur following surgery. For example, a condition known as nerve entrapment can sometimes occur from scar tissue following a hernia repair, resulting in CTP.

Most conditions that cause testicular pain are easily diagnosed and can be treated effectively through medication, surgery, and other therapies. : Testicular Pain | Tennessee | Urology Associates P.C.

How long does chronic testicular pain last?

What is the initial evaluation for a patient presenting with CSCP? – Evaluation for a patient presenting with CSCP The first step is a thorough history and physical exam. Pain location, radiation to surrounding areas, severity, and exacerbating and relieving factors are all important to understand. A thorough examination of the genitalia is mandatory, with careful inspection of the testicle, epididymis and spermatic cord, along with evaluation of the pelvic floor (digital rectal exam).

What is testicular stress?

Causes, effects and molecular mechanisms of testicular heat stress , January 2015, Pages 14-27 The lack of thermoregulation of scrotal temperature causes testicular hyperthermia, which leads to genital heat stress. This is detrimental to spermatogenesis and results in spermatozoa of inferior quality. Both the epididymal sperm and testicular germ cells are sensitive to damage by heat stress (Zhu et al., 2004).

• Spermatozoa resulting from sperm cells exposed to hyperthermia in mice undergo apoptosis (Yin et al., 1997b) and contain damaged DNA (Perez-Crespo et al., 2008), leading to poor fertilizing capacity in vivo and in vitro (Yaeram et al., 2006).
• Significant apoptotic loss of germ cells after testicular heat stress may occur either through intrinsic or extrinsic pathways.

The molecular events that arise in germ cells exposed to heat stress include the pro-apoptotic Bax and anti-apoptotic Bcl-2, cytochrome C, caspases and other heat-induced factors (Kim et al., 2013). The germ cell apoptosis response that follows heat stress takes place in a developmental stage-specific manner, with the spermatocytes (diplotene and pachytene) and spermatids being most prone to heat-induced changes (Lue et al, 1999, Setchell, 1998).

1. The reason for this vulnerability, however, has not been elucidated.
2. The severity of damage to sperm cells subjected to heat stress varies with the intensity, frequency and duration of heat exposure (Collins, Lacy, 1969, Paul et al, 2008).
3. When germ cell apoptosis occurs it is also influenced by the severity and duration of heat stress (Kim et al., 2013).

In this review, the following are discussed: the effects of hyperthermia on spermatogenesis, the measurement methods of scrotal temperatures, the various modifiable and non-modifiable factors that could cause increased testicular temperatures, the molecular mechanism of apoptosis, DNA damage and autophagy, changes in gene expression and the pathways of germ cell apoptosis in response to testicular heat stress.

For optimal spermatogenesis to occur, testicular temperatures are maintained 2–4°C lower than core body temperature (Mieusset and Bujan, 1995). The temperature within the testes is reflected by the temperature of the surrounding scrotal sac. Thermoregulation of the testis is aided by several characteristics of the scrotal sac, such as thin skin with minimal subcutaneous fat, dense sweat glands and scant hair distribution.

The musculature and vasculature in the genitals play a role in regulating The testis and epididymis represent the major thermal mass in the hemiscrotum, and intrascrotal skin surface temperatures reflect the temperature of the underlying testis (Zorgniotti, 1991, Zorgniotti, Macleod, 1973).

When measuring testicular and intra-scrotal temperatures, accuracy and reproducibility is essential as temperature differences in a euthermic and hyperthermic testis may be as little as 0.6–1.4°C (Zorgniotti and Macleod, 1973). Ideally, instruments used must be well-calibrated, Maintaining a temperature difference between the body and testes is crucial to ensure the production of normal spermatozoa.

In daily life, however, a multitude of external and internal factors could narrow this temperature difference, thereby increasing the risk of abnormal spermatogenesis and the changes associated with increased testicular heat exposure. These thermogenic factors can be broadly grouped into lifestyle and behavioural factors, occupational and environmental factors (external Several studies (mainly using the cryptorchid model) have investigated the molecular aspects of male germ cell apoptosis after heat stress, and these findings are elaborated upon in this section.

1. The aforementioned responses occur through various diverse pathways, and there may be some degree of crosstalk among them too (Paul et al., 2009).
2. The pathways that will be explained in detail in this section are that of gene expression changes, stress response, impaired DNA repair as well as apoptosis (both intrinsic and extrinsic).

Spermatogenesis involves a complex series of stages that involve the development of spermatogonia into specialized spermatozoa. The developmental processes of the male gamete may be influenced by various factors, including heat stress, causing the production of sperm with lower quality and thus affecting fertility.

The factors that contribute to increased scrotal temperatures range from lifestyle, occupational, environmental to pathophysiological. Many of these factors can hardly be avoided Damayanthi Durairajanayagam, PhD is a Senior Lecturer in Physiology at the Faculty of Medicine, MARA University of Technology (UiTM), Malaysia.

She is a past recipient of the Fulbright Research Exchange Scholar Award and recently completed her Research Fellowship at the Center for Reproductive Medicine, Cleveland Clinic, USA. Her research interests include oxidative stress, antioxidants and male infertility, and the use of proteomics and bioinformatics in studying the molecular markers of

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Potential adverse effects of non-optimum temperatures on human semen quality have drawn much concern worldwide; however, the exposure–response relationship remains less understood. To quantitatively assess the association between exposure to ambient temperature and semen quality in South China, and to identify potential critical exposure windows. We conducted a longitudinal study to investigate 11,050 volunteers who lived in Guangdong province, China and intended to donate sperm in the Guangdong provincial human sperm bank during 2016–2021. Exposure to ambient temperature during 0–90 days before semen collection was assessed by extracting daily temperatures from a validated grid dataset at each subject’s residential address. Linear mixed models and linear regression models were used to perform exposure–response analyses. During the study period, the 11,050 subjects underwent 44,564 semen analyses. Each 5 °C increase of lag 0–90 day exposure to ambient temperature was approximately linearly associated with a 3.11 (95 % confidence interval : 2.08, 4.14) × 10 6 /ml, 9.31 (4.83, 13.80) × 10 6, 1.27 % (0.91 %, 1.62 %), 8.20 (5.33, 11.08) × 10 6, 1.37 % (1.01 %, 1.74 %), 8.29 (5.52, 11.06) × 10 6, 0.67 % (0.28 %, 1.05 %), and 4.50 (2.20, 6.80) × 10 6 reduction in sperm concentration, total sperm number, total motility, total motile sperm number, progressive motility, total progressive sperm number, normal forms, and total normal form sperm number, respectively (all p < 0.001), which was not significantly modified by age (all p for effect modification > 0.05). We identified a critical exposure period of 10–14 days before semen collection for sperm motility, and 70–90 days before semen collection for sperm count and morphology. Our study provides consistent evidence that higher ambient temperature was significantly associated with a reduction in semen quality in South China. The findings highlight the needs to reduce high temperature exposures during 3 months before ejaculation to maintain better semen quality. Abnormal sperm quality in men is one of the common causes of infertility. Both ambient temperature and extreme heat exposure have been shown to be associated with sperm quality, but there is no epidemiological evidence for the effect of ambient temperature variability. Our aim was to investigate the association between ambient temperature variability exposure and a decline in sperm quality at different stages of sperm development. A total of 4912 semen samples collected from the Guangdong Human Sperm Bank between 1 January 2019 and 31 December 2019 were analyzed. We selected three exposure periods: the full-stage (0–90 lag days), early-stage (34–77 lag days) and late-stage (0–37 lag days) of sperm development, and then calculated the standard deviation of daily temperature (TVSD), the maximum day-to-day temperature difference (TVD max ) and the mean day-to-day temperature difference (TVD mean ) for the three exposure periods. A linear mixed model was used to explore the exposure response relationship between temperature variability exposure and sperm quality indicators (including sperm concentration, sperm count and sperm motility). There was a significant negative association of decreased sperm count with the exposure to temperature variability during 0–90 days prior to sperm collection. (TVD max : −0.041; −0.063, −0.019; TVD mean : −0.237; −0.386, −0.088; TVSD: −0.103; −0.196, −0.011). We observed a significant association between the decline in sperm concentration, sperm count and per 1 °C increase in TVD mean during early spermatogenesis. No significant association of temperature variability with sperm motility was found. The results indicate that exposure to temperature variability during the entire period of sperm development is significantly associated with a decline in sperm counts. We found that mean day-to-day temperature differences had a detrimental effect on sperm counts in the early-stage. Our findings provide a scientific basis for public health policy and further mechanistic studies.

Certain Chinese herbal medicines have antipyretic effects in both animal and human clinical practice. However, no report indicates their antipyretic effects on heat-stressed cells. The present study aimed to identify the protective effects of baicalin on the apoptosis of primary cultured bovine sertoli cells (SCs) subjected to heat stress (HS). The results demonstrated that HS induced apoptosis in the SCs exposed to 43 °C for 1 h as Fas/FasL was activated and caspase-3 was cleaved, the cells apoptotic rate was decreased. Moreover, the mRNA and protein levels of Hsp72 increased, whereas the cells apoptotic rate and expression of Fas, FasL, caspases 8 and 3 decreased in the SCs pretreated with various concentrations (0.1, 1, 10, 20 μg/mL) of baicalin prior to HS. In conclusion, baicalin ameliorates heat stress-induced cell apoptosis via the modulation of the cell survival rate through Fas/FasL pathway activation and the upregulation of Hsp72 expression in bovine SCs. The aim of the study was to investigate the response of the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant system to elevated scrotal temperature in mouse testes. Eight-week-old mice were exposed to a single scrotal heat treatment (42 °C for 25 min). The testes displayed severe damage, with multinucleated giant cells, nuclear condensation and germ cell loss in the seminiferous epithelium. Increased malondialdehyde levels and reduced antioxidant enzyme activities were consistent with an acute oxidative stress response. The number of cleaved caspase 3-positive germ cells per tubule was markedly increased. In addition, scrotal heat caused increased expression of Nrf2 mRNA and translocation of Nrf2 protein into interstitial cell nuclei accompanied by elevated mRNA levels for Nrf2-regulated genes. In conclusion, our data demonstrated the time dependent response of the Nrf2-antioxidant system to a single treatment of scrotal heat in the mouse testes, making this pathway a potential target for new drugs designed to prevent oxidative stress-induced male infertility. Improvements in the estimation of male fertility indicators require advances in laboratory tests for sperm assessment. The aims of the present work were (1) to apply a multivariate analysis to examine sperm set of alterations and interactions and (2) to evaluate the importance of sperm parameters on the outcome of standard IVF and embryonic development. Bulls (n = 3) were subjected to scrotal insulation, and ejaculates were collected before (preinsulation = Day 0) and through 56 days (Days 7, 14, 21, 28, 35, 42, 49, and 56) of the experimental period. Sperm head morphometry and chromatin variables were assessed by a computational image analysis, and IVF was performed. Scrotal heat stress induced alterations in all evaluated sperm head features, as well as cleavage and blastocyst rates. A principal component analysis revealed three main components (factors) that represented almost 89% of the cumulative variance. In addition, an association of factor scores with cleavage (factor 1) and blastocyst (factor 3) rates was observed. In conclusion, several sperm traits were simultaneously altered as a result of a thermal insult. These sperm traits likely play specific roles in IVF and embryonic development. Melatonin is a potent free-radical scavenger, with anti-inflammatory, anti-oxidative, and anti-apoptotic effects. The objective was to determine whether melatonin promoted testicular blood flow and protected sperm quality in rams after mild heat stress (HS; scrotal neck insulation). Twelve yearling Dorset rams with good semen quality were housed indoors (∼18–20 °C). Once weekly for 2 wk, Doppler indices (resistive index and pulsatility index ) were measured in the supratesticular artery and semen collected by electroejaculation. Then, rams were randomly allocated into two equal groups, and given either 36 mg melatonin in 1 ml corn oil SQ under the ear (MEL), or only corn oil (CONT). At 15 d after treatment, all rams were subjected to mild HS for 96 h, with blood flow measurements and semen collection done once weekly for 7 wk. There were group, week and group∗week interaction effects (P < 0.005) for total and progressive sperm motility (CASA); total sperm abnormalities and acrosome integrity had effects of group, week and group∗week interaction effects (P < 0.00); and there were group and week effects for RI and PI (P < 0.005), with no significant differences before treatment. Changes in total and progressive motility and sperm abnormalities were evident at Week 1 post-HS in CONT rams, but MEL mitigated ( P ˂ 0.05) these effects from Weeks 2–7. Furthermore, both PI and RI were reduced ( P ˂ 0.05; i.e., significant increase in blood flow) in MEL versus CONT rams most weeks after HS. In MEL rams, sperm motility and total abnormalities had recovered at Weeks 5 and 6, respectively, whereas CONT rams had not completely recovered by Week 7. There was no difference (P < 0.05) between MEL and CONT groups in scrotal subcutaneous temperatures in the 4-d intervals before, during and after HS. In conclusion, melatonin significantly improved testicular blood flow and protected sperm motility and morphology in rams exposed to testicular HS. Therefore, melatonin has potential for mitigating effects of testicular HS under field conditions. The two gonadal steroid hormones, testosterone and estrogen, regulate spermatogenesis by proliferation, differentiation, and apoptosis of testicular cells. It has been reported that heat stress or increased scrotal temperature impairs spermatogenesis in many mammals. Moreover, testicular heat stress has also been shown to suppress testosterone and estrogen biosynthesis. Furthermore, it is well known that testosterone and estrogen are important for testicular activity. Therefore, we hypothesised that exogenous testosterone and estrogen, alone or in combination, might alleviate the testicular activity in a heat-stressed rat model. To the best of our knowledge, this will be the first report of the exogenous treatment of both testosterone and estrogen in the heat-stressed rat. Our results showed that a combined testosterone and estrogen treatment significantly increased sperm concentration. The histopathological analysis also exhibited a normal histoarchitecture in the combined treatment group along with decreased oxidative stress. The improved spermatogenesis in the combined treatment group was also supported by the increase in PCNA, GCNA, tubule diameter, germinal epithelium height, and Johnsen score in the combined treatment group. Furthermore, the combined treatment also increased the expression of Bcl2, pStat3, and active caspase-3 and decreased expression of Bax. Thus, increased proliferation, apoptotic and anti-apoptotic markers, along with improved histology in the combined treatment group suggest that estrogen and testosterone synergistically act to stimulate spermatogenesis by increasing proliferation and differentiation of germ cells and may also remove the heat-induced damaged germ cells by apoptosis. Overall, the final mechanism of testosterone- and estrogen-mediated improvement of testicular activity could be attributed to amelioration of oxidative stress. We tested the hypothesis that hypoxia replicates effects of hyperthermia on reducing number and quality of sperm produced, whereas hyperoxia mitigates effects of hyperthermia. Forty-eight CD-1 mice (∼50 d old), inspired air with 13, 21, or 95% O 2 and were exposed to ambient temperatures of 20 or 36 °C (3 × 2 factorial, six groups) twice for 12 h (separated by 12 h at 20 °C and 21% O 2 ), with euthanasia 14 or 20 d after first exposure. Combined for both post-exposure intervals, there were primarily main effects of temperature; mice exposed to 20 vs 36 °C had differences in testis weight (110.2 vs 96.9 mg, respectively; P < 0.0001), daily sperm production (24.7 vs 21.1 × 10 6 sperm/g testes, P < 0.03), motile sperm (54.5 vs 41.5%, P < 0.002), morphologically normal sperm (59.9 vs 45.4%, P < 0.002), morphologically abnormal heads (7.3 vs 22.0%, P < 0.0001), seminiferous tubule diameter (183.4 vs 176.3 μm, P < 0.004) and altered elongated spermatids (2.2 vs 15.9, P < 0.001). Increasing O 2 (from 13 to 95%) affected morphologically abnormal heads (15.4, 10.8 and 17.6%, respectively; P < 0.03), seminiferous tubule diameter (175.7, 185.6 and 178.4 μm, P < 0.003) and total altered spermatids (8.3, 3.3 and 15.2, P < 0.05). Our hypothesis was not supported; hypoxia did not replicate effects of hyperthermia with regards to reducing number and quality of sperm produced and hyperoxia did not mitigate effects of hyperthermia. We concluded that hyperthermia per se and not secondary hypoxia was the fundamental cause of heat-induced effects on spermatogenesis and sperm. These findings are of interest to develop evidence-based efforts to mitigate effects of testicular hyperthermia, as efforts should be focused on hyperthermia per se and not on hyperthermia-induced hypoxia.

Damayanthi Durairajanayagam, PhD is a Senior Lecturer in Physiology at the Faculty of Medicine, MARA University of Technology (UiTM), Malaysia. She is a past recipient of the Fulbright Research Exchange Scholar Award and recently completed her Research Fellowship at the Center for Reproductive Medicine, Cleveland Clinic, USA.

Is testicular pain ever normal?

What is testicular pain? – The testicles are a sensitive part of a man’s body. Causes of testicular pain may be trauma, testicular torsion, epididimytis and other conditions. The testicles are a sensitive part of the male body. Even relatively minor injuries to them cause great pain, and many conditions can affect them.

• Testicles hang from the body in a pouch of skin called the scrotum.
• They play a necessary role in the male reproductive system, producing sperm and testosterone, the male sex hormone.
• Given their sensitivity, occasional testicular pain or discomfort is normal and usually resolves itself.
• However, sharp, sudden, or especially severe pains are signs of an underlying condition and possibly a medical emergency.

Left untreated, severe testicular pain can lead to:

Infertility Loss of one or both testiclesInfectionAbscesses

Can stress cause chronic testicular pain?

Testicular hypersensitivity is a relatively common reaction to stress in males and can be highly uncomfortable (it may flare up in either just one of the testicles or in both).

Can not ejaculating for a long time cause testicle pain?

What is blue balls? – Blue balls or epididymal hypertension refer to scrotal pain or a feeling of heaviness after sustained sexual arousal without orgasm and ejaculation. The symptoms of blue balls include mild pain, discomfort, aching, heaviness, and sometimes — as the name suggests — a faint bluish colour in your testes (also known as testicles).