Neurologic signs and symptoms include progressively delayed development, weak muscle tone (hypotonia), seizures, and abnormal movements. The body's network of blood vessels is also affected. Children with this disorder may experience rashes of tiny red spots (petechiae) caused by bleeding under the skin and blue discoloration in the hands and feet due to reduced oxygen in the blood (acrocyanosis). Chronic diarrhea is another common feature of ethylmalonic encephalopathy. EE is often identified by urine organic acid analysis, the excretion of ethylmalonic acid, methylsuccinic acid, isobutyrylglycine and isovalerylglucine. Patients will also often have elevated thiosulphate concentration in their urine.

The signs and symptoms of ethylmalonic encephalopathy are apparent at birth or begin in the first few months of life. Problems with the nervous system typically worsen over time, and most affected individuals survive only into early childhood. A few children with a milder, chronic form of this disorder have been reported, and there can be considerable phenotypic variation, even within families. The life expectancy of individuals with EE is less than ten years.

Ethylmalonic encephalopathy (EE) is a rare autosomal recessive inborn error of metabolism. Patients affected with EE are typically identified shortly after birth, with symptoms including diarrhea, petechiae and seizures. The genetic defect in EE is thought to involve an impairment in the degradation of sulfide intermediates in the body. Hydrogen sulfide then builds up to toxic levels. EE was initially described in 1994. Most cases of EE have been described in individuals of Mediterranean or Arabic origin.

EE is rarely symptomatic and is considered a subclinical condition. However, adults may have mild symptoms or malabsorption such as altered stool consistency, increased stool frequency and weight loss.

Environmental enteropathy is believed to result in chronic malnutrition and subsequent growth stunting (low height-for-age measurement) as well as other child development deficits.

EoE often presents with difficulty swallowing, food impaction, regurgitation or vomiting, and decreased appetite. In addition, young children with EoE may present with feeding difficulties and poor weight gain. It is more common in males, and affects both adults and children.

Many people with EoE have other autoimmune and allergic diseases such as asthma and celiac disease.

The most common symptoms of GERD in adults are an acidic taste in the mouth, regurgitation, and heartburn. Less common symptoms include pain with swallowing/sore throat, increased salivation (also known as water brash), nausea, chest pain, and coughing.

GERD sometimes causes injury of the esophagus. These injuries may include one or more of the following:

- Reflux esophagitis – inflammation of esophageal epithelium which can cause ulcers near the junction of the stomach and esophagus

- Esophageal strictures – the persistent narrowing of the esophagus caused by reflux-induced inflammation

- Barrett's esophagus – intestinal metaplasia (changes of the epithelial cells from squamous to intestinal columnar epithelium) of the distal esophagus

- Esophageal adenocarcinoma – a form of cancer

Some researchers have proposed that recurrent ear infections, and idiopathic pulmonary fibrosis might be tied, in some cases, to GERD; however, a causative role has not been established. GERD does not appear to be linked to chronic sinusitis.

Eosinophilic esophagitis (EoE, also spelled eosinophilic oesophagitis), also known as allergic oesophagitis, is an allergic inflammatory condition of the esophagus that involves eosinophils, a type of white blood cell. Symptoms are swallowing difficulty, food impaction, vomiting, and heartburn.

Eosinophilic esophagitis was first described in children but also occurs in adults. The condition is not well understood, but food allergy may play a significant role. The treatment may consist of removal of known or suspected triggers and medication to suppress the immune response. In severe cases, it may be necessary to stretch the esophagus with an endoscopy procedure.

GERD may be difficult to detect in infants and children, since they cannot describe what they are feeling and indicators must be observed. Symptoms may vary from typical adult symptoms. GERD in children may cause repeated vomiting, effortless spitting up, coughing, and other respiratory problems, such as wheezing. Inconsolable crying, refusing food, crying for food and then pulling off the bottle or breast only to cry for it again, failure to gain adequate weight, bad breath, and burping are also common. Children may have one symptom or many; no single symptom is universal in all children with GERD.

Of the estimated 4 million babies born in the US each year, up to 35% of them may have difficulties with reflux in the first few months of their lives, known as 'spitting up'. One theory for this is the "fourth trimester theory" which notes most animals are born with significant mobility, but humans are relatively helpless at birth, and suggests there may have once been a fourth trimester, but children began to be born earlier, evolutionarily, to accommodate the development of larger heads and brains and allow them to pass through the birth canal and this leaves them with partially undeveloped digestive systems.

Most children will outgrow their reflux by their first birthday. However, a small but significant number of them will not outgrow the condition. This is particularly true when a family history of GERD is present.

Visual looming syndrome is a problem with visual perception that causes people to inaccurately think that a stationary object is moving towards them, and might poke their eyes.

It is a neurological and muscular state, where faulty eye coordination causes the brain to interpret incoming information as a visual looming event (i.e. feeling that an object is approaching and might hit the eye). Because this condition is muscular in nature, anything that causes eye cooperation to fail, such as being tired, under the of narcotics or alcohol, or even minor differences in eye pressure or eyesight (e.g. nearsightedness), may be the cause of an episode. The is usually a narrow or pointy object which is near enough to cause confusion in the eyes, or which is in front of an undetermined or busy background. Some peer to peer studies have indicated that certain conditions, such as nyctalopia or night blindness, may worsen the syndrome.

There have been hypotheses about visual looming syndrome to be linked with several neural and gastroenterology diseases, such as celiac disease, epilepsy and migraines. Also physical differences between the eyes, such as astigmatism may be a factor. There have not been any empirical medical studies about the syndrome, though the consensus is all these may have affect on the muscular function of the eye, but most likely the visual looming syndrome is a separate symptom. There have been studies of a similar neurological situation. Gabbiani Peron has studied the "looming stimulus selectivity in a collision-detecting neuron". Beverley Regan has studied "Binocular and monocular stimuli for motion in depth". Moors P, Huygelier H, Wagemans J, de-Wit L, van Ee R; "Suppressed visual looming stimuli are not integrated with auditory looming signals"

Peer to peer studies have shown many common symptoms, such are "fear of pointy objects hitting the eye", "weird sensation behind the eyes", "difficulty in focusing on objects nearby, which are moving and are not operated by the observer, such as windscreen wipers or a pencil someone else is holding". In these studies visual looming syndrome is often referred as sharp edges eye syndrome (SEES).

Any of the components of the nervous system can be involved. Sarcoidosis affecting the nervous system is known as neurosarcoidosis. Cranial nerves are most commonly affected, accounting for about 5–30% of neurosarcoidosis cases, and peripheral facial nerve palsy, often bilateral, is the most common neurological manifestation of sarcoidosis. It occurs suddenly and is usually transient. The central nervous system involvement is present in 10–25% of sarcoidosis cases. Other common manifestations of neurosarcoidosis include optic nerve dysfunction, papilledema, palate dysfunction, neuroendocrine changes, hearing abnormalities, hypothalamic and pituitary abnormalities, chronic meningitis, and peripheral neuropathy. Myelopathy, that is spinal cord involvement, occurs in about 16–43% of neurosarcoidosis cases and is often associated with the poorest prognosis of the neurosarcoidosis subtypes. Whereas facial nerve palsies and acute meningitis due to sarcoidosis tends to have the most favourable prognosis. Another common finding in sarcoidosis with neurological involvement is autonomic or sensory small fiber neuropathy. Neuroendocrine sarcoidosis accounts for about 5–10% of neurosarcoidosis cases and can lead to diabetes insipidus, changes in menstrual cycle and hypothalamic dysfunction. The latter can lead to changes in body temperature, mood and prolactin (see the endocrine and exocrine section for details).

Abnormal blood tests are frequent, accounting for over 50% of cases, but are not diagnostic. Lymphopenia is the most common blood anomaly in sarcoidosis. Anemia occurs in about 20% of people with sarcoidosis. Leukopenia is less common and occurs in even fewer persons but is rarely severe. Thrombocytopenia and hemolytic anemia are fairly rare. In the absence of splenomegaly, leukopenia may reflect bone marrow involvement, but the most common mechanism is a redistribution of blood T cells to sites of disease. Other nonspecific findings include monocytosis, occurring in the majority of sarcoidosis cases, increased hepatic enzymes or alkaline phosphatase. People with sarcoidosis often have immunologic anomalies like allergies to test antigens such as "Candida" or purified protein derivative (PPD). Polyclonal hypergammaglobulinemia is also a fairly common immunologic anomaly seen in sarcoidosis.

Lymphadenopathy (swollen glands) is common in sarcoidosis and occurs in 15% of cases. Intrathoracic nodes are enlarged in 75 to 90% of all people; usually this involves the hilar nodes, but the paratracheal nodes are commonly involved. Peripheral lymphadenopathy is very common, particularly involving the cervical (the most common head and neck manifestation of the disease), axillary, epitrochlear, and inguinal nodes. Approximately 75% of cases show microscopic involvement of the spleen, although only in about 5–10% of cases does splenomegaly appear.

On average, the ovaries supply a woman with eggs until age 51, the average age of natural menopause.

POF is not the same as a natural menopause, in that the dysfunction of the ovaries, loss of eggs, or removal of the ovaries at a young age is not a normal physiological occurrence.

Infertility is the result of this condition, and is the most discussed problem resulting from it, but there are additional health implications of the problem, and studies are ongoing. For example, osteoporosis or decreased bone density affects almost all women with POF due to an insufficiency of estrogen. There is also an increased risk of heart disease, hypothyroidism in the form of Hashimoto's thyroiditis, Addison's disease, and other auto-immune disorders.

Hormonally, POF is defined by abnormally low levels of estrogen and high levels of FSH, which demonstrate that the ovaries are no longer responding to circulating FSH by producing estrogen and developing fertile eggs. The ovaries will likely appear shriveled.

The age of onset can be as early as the teenage years, or can even exist from birth, but varies widely. If a girl never begins menstruation, it is called primary ovarian failure. The age of 40 was chosen as the cut-off point for a diagnosis of POF. This age was chosen somewhat arbitrarily, as all women's ovaries decline in function over time. However an age needed to be chosen to distinguish usual menopause from the abnormal state of premature menopause. Premature ovarian failure has components to it that distinguish it from normal menopause.

By the age of 40, approximately one percent of women have POF. Women suffering from POF usually experience menopausal symptoms that are more severe than the symptoms found in older menopausal women.

Premature ovarian failure (POF) is the loss of function of the ovaries before age 40. A commonly cited triad for the diagnosis is amenorrhea, hypergonadotropism, and hypoestrogenism. If it has a genetic cause, it may be called gonadal dysgenesis.

The term "primary ovarian insufficiency" was first used in 1942 by Fuller Albright who first described the condition. About 5 to 10% of women with primary ovarian insufficiency conceive subsequent to the diagnosis without medical intervention.