More than 200 different symptoms have been associated with PMS. Common emotional and non-specific symptoms include stress, anxiety, difficulty with sleep, headache, feeling tired, mood swings, increased emotional sensitivity, and changes in interest in sex.

Physical symptoms associated with the menstrual cycle include bloating, lower back pain, abdominal cramps, constipation/diarrhea, swelling or tenderness in the breasts, cyclic acne, and joint or muscle pain, and food cravings. The exact symptoms and their intensity vary significantly from woman to woman, and even somewhat from cycle to cycle and over time. Most women with premenstrual syndrome experience only a few of the possible symptoms, in a relatively predictable pattern.

Premenstrual syndrome (PMS) refers to physical and emotional symptoms that occur in the one to two weeks before a woman's period. Symptoms often vary between women and resolve around the start of bleeding. Common symptoms include acne, tender breasts, bloating, feeling tired, irritability, and mood changes. Often symptoms are present for around six days. A woman's pattern of symptoms may change over time. Symptoms do not occur during pregnancy or following menopause.

Diagnosis requires a consistent pattern of emotional and physical symptoms occurring after ovulation and before menstruation to a degree that interferes with normal life. Emotional symptoms must not be present during the initial part of the menstrual cycle. A daily list of symptoms over a few months may help in diagnosis. Other disorders that cause similar symptoms need to be excluded before a diagnosis is made.

The cause of PMS is unknown. Some symptoms may be worsened by a high-salt diet, alcohol, or caffeine. The underlying mechanism is believed to involve changes in hormone levels. Reducing salt, caffeine, and stress along with increasing exercise is typically all that is recommended in those with mild symptoms. Calcium and vitamin D supplementation may be useful in some. Anti-inflammatory drugs such as naproxen may help with physical symptoms. In those with more significant symptoms birth control pills or the diuretic spironolactone may be useful.

Up to 80% women report having some symptoms prior to menstruation. These symptoms qualify as PMS in 20 to 30% of pre-menopausal women. Premenstrual dysphoric disorder (PMDD) is a more severe form of PMS that has greater psychological symptoms. PMDD affects three to eight percent of pre-menopausal women. Antidepressant medication of the selective serotonin reuptake inhibitors class may be used in addition to usual measures for in PMDD.

Premenstrual dysphoric disorder (PMDD) is a severe form of premenstrual syndrome (PMS). Like PMS, premenstrual dysphoric disorder follows a predictable, cyclic pattern. Symptoms begin in the late luteal phase of the menstrual cycle (after ovulation) and end shortly after menstruation begins. On average, the symptoms last six days but can start up to two weeks before menses. The most intense symptoms occur two days before the start of menstrual blood flow through the first day of menstrual blood flow. The symptoms should cease shortly after the start of the menstrual period.

The symptoms in PMDD can be both physical and emotional with mood symptom being dominant. The most debilitating symptoms are emotional and include "irritability, depression, mood lability, anxiety, feelings of ‘loss of control’, difficulty concentrating and fatigue." The physical symptoms include "abdominal bloating, breast tenderness, headache and generalized aches."

Premenstrual dysphoric disorder (PMDD) is a severe and disabling form of premenstrual syndrome affecting 3–8% of menstruating women. The disorder consists of a "cluster of affective, behavioral and somatic symptoms" that recur monthly during the luteal phase of the menstrual cycle. PMDD was added to the list of depressive disorders in the "Diagnostic and Statistical Manual of Mental Disorders" in 2013. The exact pathogenesis of the disorder is still unclear and is an active research topic. Treatment of PMDD relies largely on antidepressants that modulate serotonin levels in the brain via serotonin reuptake inhibitors as well as ovulation suppression using contraception.

Cyclical breast pain (cyclical mastalgia) is often associated with fibrocystic breast changes or duct ectasia and thought to be caused by changes of prolactin response to thyrotropin. Some degree of cyclical breast tenderness is normal in the menstrual cycle, and is usually associated with menstruation and/or premenstrual syndrome (PMS).

Noncyclical breast pain has various causes and is harder to diagnose. Noncyclical pain has frequently its root cause outside the breast. Some degree of non-cyclical breast tenderness can normally be present due to hormonal changes in puberty (both in girls and boys), in menopause and during pregnancy. After pregnancy, breast pain can be caused by breastfeeding. Other causes of non-cyclical breast pain include alcoholism with liver damage (likely due to abnormal steroid metabolism), mastitis and medications such as digitalis, methyldopa (an antihypertensive), spironolactone, certain diuretics, oxymetholone (an anabolic steroid), and chlorpromazine (a typical antipsychotic). Also, shingles can cause a painful blistering rash on the skin of the breasts.

Ruling out the other possible causes of the pain is one way to differentiate the source of the pain. Breast pain can be due to:

- angina pectoris

- anxiety and depression

- bra

- blocked milk duct

- breastfeeding

- chest wall muscle pain

- consensual, rough sex

- costal chondritis (sore ribs)

- cutaneous candida infection

- duct ectasia (often with nipple discharge)

- engorgement

- fibroadenoma

- fibrocystic breast changes

- fibromyalgia

- gastroesophageal reflux disease

- herpes infection

- hormone replacement therapy

- mastalgia

- mastitis or breast infection

- menopause

- menstruation and Premenstrual syndrome

- perimenopause

- neuralgia

- pregnancy

- physical abuse

- pituitary tumor (often with nipple discharge)

- puberty in both girls and boys

- sexual abuse

- shingles

- sore nipples and cracked nipples

- surgery or biopsy

- trauma (including falls)

Medications can be associated with breast pain and include:

- Oxymetholone

- Chlorpromazine

- Water pills (diuretics)

- Digitalis preparations

- Methyldopa

- Spironolactone

Diagnostic testing can be useful. Typical tests used are mammogram, excisional biopsy for solid lumps, fine-needle aspiration and biopsy, pregnancy test, ultrasonography, and magnetic resonance imaging (MRI).

Wilson's (temperature) syndrome, also called Wilson's thyroid syndrome or WTS, is an alternative medicine concept which is not recognized as a medical condition by evidence-based medicine. Its supporters describe Wilson's syndrome as a mix of various common and non-specific symptoms which they attribute to low body temperature and impaired conversion of thyroxine (T4) to triiodothyronine (T3), despite normal thyroid function tests. E. Denis Wilson, a physician who named the syndrome after himself, advocates treating these symptoms with sustained-release triiodothyronine.

The American Thyroid Association (ATA) describes Wilson's syndrome as at odds with established knowledge of thyroid function. The ATA described the diagnostic criteria for Wilson's syndrome as imprecise and non-specific, and found a lack of any scientific evidence supporting Wilson's claims. The ATA further raised concern that the proposed treatments were potentially harmful. Florida State Medical Board members described Wilson's syndrome as a "phony syndrome" and a scam during disciplinary action against Wilson.

Affected individuals present with a broad array of medical and behavioral manifestations (tables 1 and 2). Patients are consistently characterized by global developmental delay, intellectual disability, speech abnormalities, ASD-like behaviors, hypotonia and mild dysmorphic features. Table 1 summarizes the dysmorphic and medical conditions that have been reported in individuals with PMS. Table 2 summarize the psychiatric and neurological associated with PMS. Most of the studies include small samples or relied on parental report or medical record review to collect information, which can account in part for the variability in the presentation of some of the presenting features. Larger prospective studies are needed to further characterize the phenotype.

Table 1: Dysmorphic features and medical comorbid conditions that have been reported in individuals with Phelan McDermid Syndrome.

Table 2: Psychiatric and Neurologic Manifestations associated with Phelan McDermid Syndrome

The term "Wilson’s syndrome" was coined in 1990 by E. Denis Wilson, a physician practicing in Longwood, Florida. Wilson said that the syndrome's manifestations included fatigue, headaches, PMS, hair loss, irritability, fluid retention, depression, decreased memory, low sex drive, unhealthy nails, easy weight gain, and about 60 other symptoms. Wilson wrote that the syndrome can manifest itself as "virtually every symptom known to man." He also says that it is "the most common of all chronic ailments and probably takes a greater toll on society than any other medical condition."

Wilson says that low thyroid symptoms and low temperatures in the presence of normal thyroid function tests are not due to hypothyroidism, and might be reversed with a few months of treatment. To distinguish this condition from hypothyroidism, he named it Wilson's (temperature) syndrome. He states that it is "especially brought on by stress" and can persist after the stress has passed. He says that the main diagnostic sign is a body temperature that averages below (oral), and that the diagnosis is confirmed if the patient responds to treatment with a "special thyroid hormone treatment". He says that certain herbs can also help support normal body temperatures.

22q13 deletion syndrome (spoken as "twenty-two q one three", see Locus (genetics)) is a genetic disorder caused by deletions or rearrangements on the q terminal end (long arm) of chromosome 22. Any abnormal genetic variation in the q13 region that presents with significant manifestations (phenotype) typical of a terminal deletion may be diagnosed as 22q13 deletion syndrome. 22q13 deletion syndrome is often called Phelan-McDermid syndrome (abbreviated PMS). There is disagreement among researchers as to the exact definition of 22q13 deletion syndrome. The Developmental Synaptopathies Consortium defines PMS as being caused by "SHANK3" mutations, a definition that appears to exclude terminal deletions. The requirement to include "SHANK3" in the definition is supported by many, but not by those who first described 22q13 deletion syndrome.

A prototypical terminal deletion of 22q13 can be uncovered by karyotype analysis, but many terminal and interstitial deletions are too small. The availability of DNA microarray technology for revealing multiple genetic problems simultaneously has been the diagnostic tool of choice. The falling cost for whole exome sequencing and, eventually, whole genome sequencing, may replace DNA microarray technology for candidate evaluation. However, fluorescence in situ hybridization (FISH) tests remain valuable for diagnosing cases of mosaicism (mosaic genetics) and chromosomal rearrangements (e.g., ring chromosome, unbalanced chromosomal translocation). Although early researchers sought a monogenic (single gene genetic disorder) explanation, recent studies have not supported that hypothesis (see Etiology, below).

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. Early on there may be no symptoms. Over time the thyroid may enlarge forming a painless goiter. Some people eventually develop hypothyroidism with its accompanying weight gain, feeling tired, constipation, depression, and general pains. After many years the thyroid typically shrinks in size. Potential complications include thyroid lymphoma.

Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors. Risk factors include a family history of the condition and having another autoimmune disease. Diagnosis is confirmed with blood tests for TSH, T4, and antithyroid antibodies. Other conditions that can produce similar symptoms include Graves’ disease and nontoxic nodular goiter.

Hashimoto's thyroiditis is typically treated with levothyroxine. If hypothyroidism is not present some may recommend no treatment while others may treat to try to reduce the size of the goiter. Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. Surgery is rarely required to treat the goiter.

Hashimoto's thyroiditis affects about 5% of the population at some point in their life. It typically begins between the ages of 30 and 50 and is much more common in women than men. Rates of disease appear to be increasing. It was first described by the Japanese physician Hakaru Hashimoto in 1912. In 1957 it was recognized as an autoimmune disorder.

There are many symptoms that are attributed to Hashimoto's thyroiditis or Hashimoto's disease. The most common symptoms include the following: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and maintaining pregnancy.

Hashimoto’s disease is about seven times more common in women than in men. It can occur in teens and young women, but more commonly shows up in middle age, particularly for men. People who develop Hashimoto’s disease often have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves.

The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) (also called TPOAb) and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. A rare but serious complication is thyroid lymphoma, generally the B-cell type, non-Hodgkin lymphoma.