The symptoms include many of the symptoms associated with milder degrees of hypoglycemia, especially the adrenergic symptoms, but do not progress to objective impairment of brain function, seizures, coma, or brain damage.

- Shakiness

- Sense of weakness

- Altered or depressed mood

- Confusion

- Fatigue

- Anxiety

- Paleness

- Perspiration

- Increased pulse or respiratory rate

- Hunger

Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration.

A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:

- double vision or blurry vision

- unclear thinking

- insomnia

- heart palpitation or fibrillation

- fatigue

- dizziness

- light-headedness

- sweating

- headaches

- depression

- nervousness

- muscle twitches

- irritability

- tremors

- flushing

- craving sweets

- increased appetite

- rhinitis

- nausea, vomiting

- panic attack

- numbness/coldness in the extremities

- confusion

- irrationality

- bad temper

- paleness

- cold hands

- disorientation

- the need to sleep or 'crash'

- coma can be a result in severe untreated episodes

The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body’s response to low blood sugar levels following periods of glucose deficiency.

Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.

People with this condition suffer from recurrent episodes of altered mood and cognitive efficiency, often accompanied by weakness and adrenergic symptoms such as shakiness. The episodes typically occur a few hours after a meal, rather than after many hours of fasting. The principal treatments recommended are extra small meals or snacks and avoidance of excessive simple sugars.

Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

- Shakiness, anxiety, nervousness

- Palpitations, tachycardia

- Sweating, feeling of warmth (sympathetic muscarinic rather than adrenergic)

- Pallor, coldness, clamminess

- Dilated pupils (mydriasis)

- Hunger, borborygmus

- Nausea, vomiting, abdominal discomfort

- Headache

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may also vary by age, by severity of the hypoglycemia and the speed of the decline. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, as well as previous incidents.

In newborns, hypoglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or "spells." Hypoglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed "hypoglycemia unawareness" and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Hypoglycemic symptoms can also occur when one is sleeping. Examples of symptoms during sleep can include damp bed sheets or clothes from perspiration. Having nightmares or the act of crying out can be a sign of hypoglycemia. Once the individual is awake they may feel tired, irritable, or confused and these may be signs of hypoglycemia as well.

In nearly all cases, hypoglycemia that is severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.

Research in healthy adults shows that mental efficiency declines slightly but measurably as blood glucose falls below 3.6 mM (65 mg/dL). Hormonal defense mechanisms (adrenaline and glucagon) are normally activated as it drops below a threshold level (about 55 mg/dL (3.0 mM) for most people), producing the typical hypoglycemic symptoms of shakiness and dysphoria. Obvious impairment may not occur until the glucose falls below 40 mg/dL (2.2 mM), and many healthy people may occasionally have glucose levels below 65 in the morning without apparent effects. Since the brain effects of hypoglycemia, termed neuroglycopenia, determine whether a given low glucose is a "problem" for that person, most doctors use the term "hypoglycemia" only when a moderately low glucose level is accompanied by symptoms or brain effects.

Determining the presence of both parts of this definition is not always straightforward, as hypoglycemic symptoms and effects are vague and can be produced by other conditions; people with recurrently low glucose levels can lose their threshold symptoms so that severe neuroglycopenic impairment can occur without much warning, and many measurement methods (especially glucose meters) are imprecise at low levels.

It may take longer to recover from severe hypoglycemia with unconsciousness or seizure even after restoration of normal blood glucose. When a person has not been unconscious, failure of carbohydrate to reverse the symptoms in 10–15 minutes increases the likelihood that hypoglycemia was not the cause of the symptoms. When severe hypoglycemia has persisted in a hospitalized person, the amount of glucose required to maintain satisfactory blood glucose levels becomes an important clue to the underlying etiology. Glucose requirements above 10 mg/kg/minute in infants, or 6 mg/kg/minute in children and adults are strong evidence for hyperinsulinism. In this context this is referred to as the "glucose infusion rate" (GIR). Finally, the blood glucose response to glucagon given when the glucose is low can also help distinguish among various types of hypoglycemia. A rise of blood glucose by more than 30 mg/dl (1.70 mmol/l) suggests insulin excess as the probable cause of the hypoglycemia.

Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within 4 hours after a high carbohydrate meal in people who do not have diabetes.

The condition is related to homeostatic systems utilised by the body to control blood sugar levels. It is variously described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be less if one has undertaken a lot of physical activity within the next few hours after consumption.

The alleged mechanism for the feeling of a crash is correlated with an abnormally rapid rise in blood glucose after eating. This normally leads to insulin secretion (known as an "insulin spike"), which in turn initiates rapid glucose uptake by tissues either accumulating it as glycogen or utilizing it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash".. A deeper cause might be hysteresis effect of insulin action, i.e., the effect of insulin is still prominent even if both plasma glucose and insulin levels were already low, causing a plasma glucose level eventually much lower than the baseline level.

Sugar crashes are not to be confused with the after-effects of consuming large amounts of "protein", which produces fatigue akin to a sugar crash, but are instead the result of the body prioritising the digestion of ingested food.

The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.

To assist diagnosis, a doctor can order an HbA1c test, which measures the blood sugar average over the two or three months before the test. The more specific 6-hour glucose tolerance test can be used to chart changes in the patient's blood sugar levels before ingestion of a special glucose drink and at regular intervals during the six hours following to see if an unusual rise or drop in blood glucose levels occurs.

According to the U.S. National Institute of Health (NIH), a blood glucose level below 70 mg/dL (3.9 mmol/L) at the time of symptoms followed by relief after eating confirms a diagnosis for reactive hypoglycemia.

Oxyhyperglycemia is a special type of impaired glucose tolerance characterized by a rapid and transient hyperglycemia (i.e. rise in blood glucose) spike after an oral intake of glucose, the peak of this spike being high enough to cause transient, symptom free glycosuria (i.e. detectable glucose in urine), but this hyperglycemia reverses rapidly and may even go to hypoglycemia in the later phase. This sharp downstroke overshooting towards hypoglycemia distinguishes this pathologic phenomenon from the artificial hyperglycemia inducible by an intravenous bolus dose of a large amount of glucose solution. Early dumping syndrome patients usually have oxyhyperglycemia associated with any meal or OGTT.

The Greek root "oxy" means "sharp" or "pointy". The OGTT curve in this condition appears sharp and somewhat pointy (at least relative to the other forms of hyperglycemia)- hence this name.

Dorlands dictionary defines oxyhyperglycemia as:

A blood level of approximately 180 mg/dL is the renal glucose threshold below which all glucose is reabsorbed from glomerular filtrate. But at blood concentrations above the renal threshold sugar starts appearing in the urine.

Oxyhyperglycemia, like other forms of Impaired glucose tolerance has also been suggested to be a prediabetic condition

Idiopathic hypoglycemia is, literally, a medical condition in which the glucose level in the blood (blood glucose) is abnormally low due to an undeterminable cause. This is considered an incomplete and unsatisfactory diagnosis by physicians and is rarely used by endocrinologists, as it implies an unfinished diagnostic evaluation. In general, the more severe the hypoglycemia and the more clearly it is proven, the less likely it is to remain "idiopathic".

"Idiopathic hypoglycemia" can also be a synonym for reactive hypoglycemia or for hypoglycemia that is not diagnosed by a physician and does not fulfill the Whipple triad criteria. A more precise term for that condition is idiopathic postprandial syndrome.

Manifestations of hyperinsulinemic hypoglycemia vary by age and severity of the hypoglycemia. In general, most signs and symptoms can be attributed to (1) the effects on the brain of insufficient glucose (neuroglycopenia) or (2) to the adrenergic response of the autonomic nervous system to hypoglycemia. A few miscellaneous symptoms are harder to attribute to either of these causes. In most cases, all effects are reversed when normal glucose levels are restored.

There are uncommon cases of more persistent harm, and rarely even death due to severe hypoglycemia of this type. One reason hypoglycemia due to excessive insulin can be more dangerous is that insulin lowers the available amounts of most alternate brain fuels, such as ketones. Brain damage of various types ranging from stroke-like focal effects to impaired memory and thinking can occur. Children who have prolonged or recurrent hyperinsulinemic hypoglycemia in infancy can suffer harm to their brains and may be developmentally delayed.

There are several genetic forms of hyperinsulinemic hypoglycemia:

Oxyhyperglycemia is most commonly caused by early dumping syndrome, but it can rarely caused by other conditions like Graves' disease. It was first described by Lawrence et al. in 1936 as often happening after gastroenterostomy. It is seen in most forms of gastrectomy, gastric bypass and gastrostomy procedures, all of which are surgical causes of dumping syndrome.

These depend on poorly understood variations in individual biology and consequently may not be found with all people diagnosed with insulin resistance.

- Increased hunger

- Lethargy (tiredness)

- Brain fogginess and inability to focus

- High blood sugar

- Weight gain, fat storage, difficulty losing weight – for most people, excess weight is from high subcutaneous fat storage; the fat in IR is generally stored in and around abdominal organs in both males and females; it is currently suspected that hormones produced in that fat are a precipitating cause of insulin resistance

- Increased blood cholesterol levels

- Increased blood pressure; many people with hypertension are either diabetic or pre-diabetic and have elevated insulin levels due to insulin resistance; one of insulin's effects is to control arterial wall tension throughout the body

The most common clinical history in patients with glycogen-storage disease type 0 (GSD-0) is that of an infant or child with symptomatic hypoglycemia or seizures that occur before breakfast or after an inadvertent fast. In affected infants, this event typically begins after they outgrow their nighttime feeds. In children, this event may occur during acute GI illness or periods of poor enteral intake.

Mild hypoglycemic episodes may be clinically unrecognized, or they may cause symptoms such as drowsiness, sweating, lack of attention, or pallor. Uncoordinated eye movements, disorientation, seizures, and coma may accompany severe episodes.

Glycogen-storage disease type 0 affects only the liver. Growth delay may be evident with height and weight percentiles below average. Abdominal examination findings may be normal or reveal only mild hepatomegaly.Signs of acute hypoglycemia may be present, including the following:

Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin. The body produces insulin when glucose starts to be released into the bloodstream from the digestion of carbohydrates in the diet. Normally this insulin response triggers glucose being taken into body cells, to be used for energy, and inhibits the body from using fat for energy. The concentration of glucose in the blood decreases as a result, staying within the normal range even when a large amount of carbohydrates is consumed. When the body produces insulin under conditions of insulin resistance, the cells are resistant to the insulin and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level. This often remains undetected and can contribute to the development of type 2 diabetes or latent autoimmune diabetes of adults. Although this type of chronic insulin resistance is harmful, during acute illness it is actually a well-evolved protective mechanism. Recent investigations have revealed that insulin resistance helps to conserve the brain's glucose supply by preventing muscles from taking up excessive glucose. In theory, insulin resistance should even be strengthened under harsh metabolic conditions such as pregnancy, during which the expanding fetal brain demands more glucose.

People who develop type 2 diabetes usually pass through earlier stages of insulin resistance and prediabetes, although those often go undiagnosed. Insulin resistance is a syndrome (a set of signs and symptoms) resulting from reduced insulin activity; it is also part of a larger constellation of symptoms called the metabolic syndrome.

Insulin resistance may also develop in patients who have recently experienced abdominal or bariatric procedures. This acute form of insulin resistance that may result post-operatively tends to increase over the short term, with sensitivity to insulin typically returning to patients after about five days.

In medicine and specifically endocrinology, postprandial dip is a term used to refer to mild hypoglycemia occurring after ingestion of a heavy meal.

The dip is thought to be caused by a drop in blood glucose resulting from the body's own normal insulin secretion, which in turn is a response to the glucose load represented by the meal.

While postprandial dip is usually physiological after a generous meal, a very sharp or sustained drop in blood glucose may be associated with a disorder of glucose metabolism.

Glycogen storage disease type 0 is a disease characterized by a deficiency in the glycogen synthase enzyme (GYS). Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is often classified as a glycogen storage disease because it is another defect of glycogen storage and can cause similar problems. There are two isoforms (types) of glycogen synthase enzyme; GYS1 in muscle and GSY2 in liver, each with a corresponding form of the disease. Mutations in the liver isoform (GYS2), causes fasting hypoglycemia, high blood ketones, increased free fatty acids and low levels of alanine and lactate. Conversely, feeding in these patients results in hyperglycemia and hyperlactatemia.

Hyperlipoproteinemia type II, by far the most common form, is further classified into types IIa and IIb, depending mainly on whether elevation in the triglyceride level occurs in addition to LDL cholesterol.

The primary symptoms of hypotension are lightheadedness or dizziness.

If the blood pressure is sufficiently low, fainting may occur.

Low blood pressure is sometimes associated with certain symptoms, many of which are related to causes rather than effects of hypotension:

- chest pain

- shortness of breath

- irregular heartbeat

- fever higher than 38.3 °C (101 °F)

- headache

- stiff neck

- severe upper back pain

- cough with sputum

- Prolonged diarrhea or vomiting

- dyspepsia (indigestion)

- dysuria (painful urination)

- adverse effect of medications

- acute, life-threatening allergic reaction

- seizures

- loss of consciousness

- profound fatigue

- temporary blurring or loss of vision

- Black tarry stools

Type I hyperlipoproteinemia exists in several forms:

- Lipoprotein lipase deficiency (type Ia), due to a deficiency of lipoprotein lipase (LPL) or altered apolipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver

- Familial apoprotein CII deficiency (type Ib), a condition caused by a lack of lipoprotein lipase activator.

- Chylomicronemia due to circulating inhibitor of lipoprotein lipase (type Ic)

Type I hyperlipoproteinemia usually presents in childhood with eruptive xanthomata and abdominal colic. Complications include retinal vein occlusion, acute pancreatitis, steatosis, and organomegaly, and lipemia retinalis.

The symptoms of Rabson–Mendenhall syndrome vary from case to case. Major symptoms of Rabson–Mendenhall syndrome include abnormalities of the teeth and nails, such as dental dysplasia, and deformities of the head and face, which include a coarse prematurely-aged facial appearance with a prominent jaw. A skin abnormality known as acanthosis nigricans, which involves a discoloration (hyperpigmentation) and “velvety” thickening (hyperkeratosis) of the skin around skin fold regions of the neck, groin and under arms is also a common symptom. Symptoms will negatively impact the daily life of the patient, and will persist until treated.

Minor symptoms may include an enlargement of the genitalia and precocious puberty and a deficiency or absence of fat tissue. Because individuals with Rabson–Mendenhall syndrome fail to use insulin properly, they may experience abnormally high blood sugar levels (hyperglycemia) after eating a meal, and abnormally low blood sugar levels (hypoglycemia) when not eating.

Orthostatic hypotension, also called "postural hypotension", is a common form of low blood pressure. It occurs after a change in body position, typically when a person stands up from either a seated or lying position. It is usually transient and represents a delay in the normal compensatory ability of the autonomic nervous system. It is commonly seen in hypovolemia and as a result of various medications. In addition to blood pressure-lowering medications, many psychiatric medications, in particular antidepressants, can have this side effect. Simple blood pressure and heart rate measurements while lying, seated, and standing (with a two-minute delay in between each position change) can confirm the presence of orthostatic hypotension. Orthostatic hypotension is indicated if there is a drop in 20 mmHg of systolic pressure (and a 10 mmHg drop in diastolic pressure in some facilities) and a 20 beats per minute increase in heart rate.

Vasovagal syncope is a form of dysautonomia characterized by an inappropriate drop in blood pressure while in the upright position. Vasovagal syncope occurs as a result of increased activity of the vagus nerve, the mainstay of the parasympathetic nervous system .

Another, but rarer form, is postprandial hypotension, a drastic decline in blood pressure that occurs 30 to 75 minutes after eating substantial meals. When a great deal of blood is diverted to the intestines (a kind of "splanchnic blood pooling") to facilitate digestion and absorption, the body must increase cardiac output and peripheral vasoconstriction to maintain enough blood pressure to perfuse vital organs, such as the brain. Postprandial hypotension is believed to be caused by the autonomic nervous system not compensating appropriately, because of aging or a specific disorder.

Hypotension is a feature of Flammer syndrome which is characterized by cold hands and feet and predisposes to normal tension glaucoma.

Rabson–Mendenhall syndrome is a rare autosomal recessive disorder characterized by severe insulin resistance. The disorder is caused by mutations in the insulin receptor gene. Symptoms include growth abnormalities of the head, face and nails, along with the development of acanthosis nigricans. Treatment involves controlling blood glucose levels by using insulin and incorporating a strategically planned, controlled diet. Also, direct actions against other symptoms may be taken (e.g. surgery for facial abnormalities) This syndrome usually affects children and has a prognosis of 1–2 years.

Terms such as "functional colonic disease" (or "functional bowel disorder") refer in medicine to a group of bowel disorders which are characterised by chronic abdominal complaints without a structural or biochemical cause that could explain symptoms. Other "functional" disorders relate to other aspects of the process of digestion.

The consensus review process of meetings and publications organised by the Rome Foundation, known as the Rome process, has helped to define the functional gastrointestinal disorders. Successively, the Rome I, Rome II, Rome III and Rome IV proposed consensual classification system and terminology, as recommended by the Rome Coordinating Committee. These now include classifications appropriate for adults, children and neonates / toddlers.

The current Rome IV classification, published in 2016, is as follows:

A. Esophageal Disorders

- A1. Functional chest pain

- A2. Functional heartburn

- A3. Reflux hypersensitivity

- A4. Globus

- A5. Functional dysphagia

B. Gastroduodenal Disorders

- B1. Functional dyspepsia

- B1a. Postprandial distress syndrome (PDS)

- B1b. Epigastric pain syndrome (EPS)

- B2. Belching disorders

- B2a. Excessive supragastric belching

- B2b. Excessive gastric belching

- B3. Nausea and vomiting disorders

- B3a. Chronic nausea vomiting syndrome (CNVS}

- B3b. Cyclic vomiting syndrome (CVS)

- B3c. Cannabinoid hyperemesis syndrome (CHS)

- B4. Rumination syndrome

C. Bowel Disorders

- C1. Irritable bowel syndrome (IBS)

- IBS with predominant constipation (IBS-C)

- IBS with predominant diarrhea (IBS-D)

- IBS with mixed bowel habits (IBS-M)

- IBS unclassified (IBS-U)

- C2. Functional constipation

- C3. Functional diarrhea

- C4. Functional abdominal bloating/distension

- C5. Unspecified functional bowel disorder

- C6. Opioid-induced constipation

D. Centrally Mediated Disorders of Gastrointestinal Pain

- D1. Centrally mediated abdominal pain syndrome (CAPS)

- D2. Narcotic bowel syndrome (NBS)/ Opioid-induced GI hyperalgesia

E. Gallbladder and Sphincter of Oddi disorders

- E1. Biliary pain

- E1a. Functional gallbladder disorder

- E1b. Functional biliary sphincter of Oddi disorder

- E2. Functional pancreatic sphincter of Oddi disorder

F. Anorectal Disorders

- F1. Fecal incontinence

- F2. Functional anorectal pain

- F2a. Levator ani syndrome

- F2b. Unspecified functional anorectal pain

- F2c. Proctalgia fugax

- F3. Functional defecation disorders

- F3a. Inadequate defecatory propulsion

- F3b. Dyssynergic defecation

G. Childhood Functional GI Disorders: Neonate/Toddler

- G1. Infant regurgitation

- G2. Rumination syndrome

- G3. Cyclic vomiting syndrome (CVS)

- G4. Infant colic

- G5. Functional diarrhea

- G6. Infant dyschezia

- G7. Functional constipation

H. Childhood Functional GI Disorders: Child/Adolescent

- H1. Functional nausea and vomiting disorders

- H1a. Cyclic vomiting syndrome (CVS)

- H1b. Functional nausea and functional vomiting

- H1b1. Functional nausea

- H1b2. Functional vomiting

- H1c. Rumination syndrome

- H1d. Aerophagia

- H2. Functional abdominal pain disorders

- H2a. Functional dyspepsia

- H2a1. Postprandial distress syndrome

- H2a2. Epigastric pain syndrome

- H2b. Irritable bowel syndrome (IBS)

- H2c. Abdominal migraine

- H2d. Functional abdominal pain ‒ NOS

- H3. Functional defecation disorders

- H3a. Functional constipation

- H3b. Nonretentive fecal incontinence

Functional gastrointestinal disorders are very common. Globally, irritable bowel syndrome and functional dyspepsia alone may affect 16–26% of the population.

Those who suffer from idiopathic hypersomnia have recurring episodes of excessive daytime sleepiness (EDS). These occur in spite of "adequate, or more typically, extraordinary sleep amounts (e.g., greater than 10 hours per night)." Sleep is usually deep, with significant difficulty arousing from sleep, even with use of several alarm clocks. In fact, patients with IH often must develop elaborate rituals to wake, as alarm clocks and even physical attempts by friends/family to wake them may fail. Despite getting more hours of sleep than typically required by the human body, patients awake unrefreshed and may also suffer sleep inertia, known more descriptively in its severe form as sleep drunkenness (significant disorientation upon awakening). Daytime naps are generally very long (up to several hours) and are also unrefreshing, as opposed to the short refreshing naps associated with narcolepsy. Sleep paralysis and hypnagogic hallucinations may also occur, as well as motor hyper-reactivity.

Several studies have shown increased frequencies of other symptoms in patients with idiopathic hypersomnia, although it is not clear whether these symptoms are caused by the idiopathic hypersomnia. These symptoms include palpitations, digestive problems, difficulty with body temperature regulation, and cognitive problems, especially deficits in memory, attention, and concentration. Anxiety and depression are often increased in idiopathic hypersomnia, most likely as a response to chronic illness. A large case series in 2010 found that peripheral vascular symptoms, such as cold hands and feet (Raynaud’s-type phenomena) were significantly more common in people with idiopathic hypersomnia than in controls. In addition to difficulty with temperature regulation and Raynaud’s type symptoms, other symptoms associated with autonomic dysfunction were noted to occur in idiopathic hypersomnia. These included: fainting episodes (syncope); dizziness upon arising (orthostatic hypotension); and headaches (possibly migrainous in quality). Food cravings and impotence have also been reported.

Symptom intensity often varies between weeks, months, or years, and symptoms can worsen just prior to menses in women. Many patients are chronically tardy to work, school or social engagements and, over time, may lose the ability to function in family, social, occupational or other settings altogether. (See Prognosis section below).