Although most patients with only optic nerve involvement lead normally productive lives, those with accompanying endocrine dysfunction or other midline cerebral abnormalities are more at risk for on-going intellectual and other disabilities. Epidemiology
Optic nerve hypoplasia (ONH) is a congenital condition in which the optic nerve is underdeveloped (small). Many times, de Morsier’s Syndrome or septo-optic dysplasia (SOD) is associated with ONH, however, it is possible to have ONH without any additional issues like SOD. SOD is a condition that can involve multiple  problems in the midline structures of the brain, stemming from miswiring of the brain and central nervous system. Besides having small optic nerves, persons with ONH can have agenesis of the corpus callosum, absence of the septum pellucidum, maldevelopment of the anterior and posterior pituitary gland, and anomalies of the hypothalamus. Because of this, all children with ONH are at risk for developmental delays and hormonal deficiencies, regardless of severity of ONH, or whether abnormalities are visible by MRI. ONH is the single leading cause of permanent legal blindness in children in the western world. The incidence of ONH is increasing, although it is difficult to estimate the true prevalence. Between 1980 and 1999, the occurrences of ONH in Sweden increased four-fold to 7.2 per 100,000, while all other causes of childhood blindness had declined. In 1997, ONH overtook retinopathy of prematurity as the single leading cause of infant blindness in Sweden, with 6.3 in every 100,000 births diagnosed with ONH.
Toxic multinodular goiter (TMNG), also known as multinodular toxic goiter (MNTG), is an active multinodular goiter associated with hyperthyroidism. It is a common cause of hyperthyroidism in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).Toxic multinodular goiter is the second most common cause of hyperthyroidism (after Graves disease) in the developed world, whereas iodine deficiency is the most common cause of hypothyroidism in developing-world countries where the population is iodine-deficient. (Decreased iodine leads to decreased thyroid hormone.) However, iodine deficiency can cause goiter (thyroid enlargement); within a goitre, nodules can develop. Risk factors for toxic multinodular goiter include individuals over 60 years of age and being female. Signs and symptoms
Symptoms of toxic multinodular goitre are similar to that of hyperthyroidism, including:
heat intolerance
muscle weakness/wasting
hyperactivity
fatigue
tremor
irritability
weight loss
osteoporosis
increased appetite
non-painful goitre (swelling of the thyroid gland)
tachycardia (high heart rate - above 100 beats per minute at rest in adults)
tracheal compression
exophthalmos

Causes
Sequence of events:
Iodine deficiency leading to decreased T4 production. Induction of thyroid cell hyperplasia due to low levels of T4. This accounts for the multinodular goitre appearance. Increased replication predisposes to a risk of mutation in the TSH receptor. If the mutated TSH receptor is constitutively active, it would then become toxic and produces excess T3/T4 leading to hyperthyroidism. Diagnosis
Treatments
Toxic multinodular goiter can be treated with antithyroid medications such as propylthiouracil or methimazole, radioactive iodine, or with surgery. Another treatment option is injection of ethanol into the nodules.