The patient complains of nervousness or irritability and appears to be restless and fidgety, with rapid speech.  The reaction to all sorts of stimuli is distinctly excessive. Often emotional instability is combined with this pattern, perhaps to the point of a significant change in personality. The patient may have frequent crying spells, but may have sufficient insight to realize that the crying is not normal. Some patients become hyper-irritable and combative, and this can lead to accidents or even assaultive behavior.

Thyroid hormone has been recognized as an important factor in brain function, so either too much or too little causes malfunction.  In a few patients, the emotional pattern is that of mild euphoria. In others, profound fatigue or weakness may be the most noticeable symptom. The mind is often very active, and the patient may have insomnia.  Rarely, patients develop visual or auditory hallucinations or a frank psychosis. The latter may not completely clear up after thyrotoxicosis has been treated, but may result from an underlying condition existing before the Graves' disease.

Impairment of intellectual function has been found in patients with untreated hyperthyroidism. It is usually assumed that such abnormalities return to normal with therapy to normalize thyroid levels. However, Perild et al. report that ten years after successful therapy of thyrotoxicosis, a group of patients manifested abnormal neuropsychological tests, and half had significant intellectual impairment which was apparently permanent. Other studies have produced similar findings, and work continues in this area, mainly in the field of neuropsychiatry.

The disease typically begins gradually in adult women and may be progressive unless treated. Muscle weakness and excess calcium in the urine are common, and kidney stones rarely occur. Thyrotoxicosis can cause congestive heart failure. Mitral valve prolapse occurs with increased frequency in toxic patients. Atrial tachycardia and fibrillation are commonly caused by thyrotoxicosis. Patients are often anemic. Diarrhea occurs, but malabsorption is unusual. Minimal liver damage may occur. Amenorrhea (lack of menstruation) or anovulatory cycling is common in women, and fertility is reduced. 

When pregnancy occurs, it can result in increased risk of miscarriage.  When the mother has a high number of antibodies, they sometimes affect the infant, which  may be born with temporary  hyperthyroidism that persists until maternal antibodies are depleted, which may take a few months.

Oxygen consumption is greatly increased, lipid production and turnover are accelerated, and plasma total lipid and cholesterol levels tend to be low.

Thyrotoxicosis in untreated cases leads to cardiovascular damage, bone loss and fractures, or exhaustion from lack of nourishment, and can be fatal. The long-term history also includes the possibility of spontaneous remission in some cases, and eventual development of hypothyroidism, if autoimmune thyroiditis coexists and destroys the thyroid gland.

Thyrotoxicosis itself (regardless of cause) is associated with pathologic changes including damage to muscles and sometimes mild damage to the liver, and occasionally neuropathy (nerve pain). Graves' disease is associated with enlargement of and lymphoid infiltrates in the thyroid, generalized lymphoid enlargement, infiltrative ophthalmopathy (eye disease) and pretibial myxedema (swelling and painless nodules on the shins and tops of the feet).

Graves' disease is caused by "autoimmunity", but the cause of the autoimmunity remains unclear. A strong hereditary tendency for autoimmune thyroid disease exists.  Psychic or physical trauma, strenuous weight reduction,  excess iodine, and viral illness have been associated with the onset of Graves' disease in people with the hereditary predisposition, but have not been proven to play a causative role. The family history may not include known cases of Graves' disease, but possibly Hashimoto's thyroiditis, which causes destruction of thyroid cells and low thyroid function. The two conditions have similar causes, which sometimes overlap.  In some cases, patients have fairly rapid changes between the two conditions, until one eventually predominates.

At the present time, there is no "cure" for the autoimmunity, so all treatments are aimed at stopping the production of excess thyroid hormone, either by blocking its production (antithyroid drugs) or by removing part (or most) of the thyroid gland--either surgically or by radioactive destruction, using radioactive iodine (I131).

The incidence of Graves' disease is reported in recent studies to be 1 to 2 cases per 1,000 population per year.  The frequency in women is much greater than it is in men.