The word "hypopnea" uses combining forms of "" + "", from the Greek roots "hypo-" (meaning "low", "under", "beneath", "down", "below normal") and "pnoia" (meaning "breathing"). See pronunciation information at "dyspnea".

In the context of diagnosis and treatment of sleep disorders, a hypopnea is not considered to be clinically significant unless there is a 30% or greater reduction in flow lasting for 10 seconds or longer and an associated 4% or greater desaturation in the person's O levels, or if it results in arousal or fragmentation of sleep.

The direct consequence of hypopnea (as well as apnea) is that the in the blood increases and the oxygen level in the patient's blood decrease is proportionate to the severity of the airway obstruction. This disruptive pattern of breathing generates disruptive sleep patterns, the consequences of which being that those individuals may exhibit increased fatigability, , decreased ability to concentrate, increased irritability, and morning headaches. Basically, those individuals are extremely tired due to their inability to get a good night's sleep.

Hypopneas can be either central i.e., as part of a waxing and waning in breathing effort, or obstructive in origin. During an obstructive hypopnea, in comparison to an obstructive apnea, the airway is only partially closed. However, this closure is still enough to cause a physiological effect i.e., an oxygen desaturation and/or an increase in breathing effort terminating in arousal.

A Hypopnea Index (HI) can be calculated by dividing the number of hypopnea events during the sleep period by the number of hours of sleep. The Apnea-Hyponea Index (AHI) is an index of severity that combines apneas and hypopneas. Combining them both gives an overall severity of sleep apnea including sleep disruptions and desaturations (a low level of oxygen in the blood). The apnea-hypopnea index, like the apnea index and hypopnea index, is calculated by dividing the number of apneas and hypopneas by the number of hours of sleep. Another index that is used to measure sleep apnea is the Respiratory Disturbance Index (RDI). The RDI is similar to the AHI, however, RDI also includes respiratory events that do not technically meet the definitions of apneas or hypopneas, such as a Respiratory Effort Related Arousal (RERA), but do disrupt sleep.

Although central and obstructive sleep apnea have some signs and symptoms in common, others are present in one but absent in another, enabling differential diagnosis as between the two types:

Signs and symptoms of sleep apnea generally

- Signs:

- Symptoms:

Signs and symptoms of central sleep apnea

- Signs:

- Symptoms:

Signs and symptoms of and conditions associated with obstructive sleep apnea

- Signs:

- Symptoms:

- Associated conditions:

A diagnosis of sleep apnea requires determination by a physician. The examination may require a study of an individual in a sleep lab, although the AAST has said a two belt IHT (In Home Test) will replace a PSG for diagnosing obstructive apnea. There, the patient will be monitored while at rest, and the periods when breathing ceases will be measured with respect to length and frequency. During a PSG (polysomnography) (a sleep study), a person with sleep apnea shows breathing interruptions followed by drops/reductions in blood oxygen and increases in blood carbon dioxide level.

- In adults, a pause must last 10 seconds to be scored as an apnea. However, in young children, who normally breathe at a much faster rate than adults, shorter pauses may still be considered apneas.

- Hypopneas in adults are defined as a 30% reduction in air flow for more than ten seconds, followed by oxygen-saturation declines of at least 3% or 4% per the AASM stndards. and/or EEG arousal. The Apnea-Hypopnea Index (AHI) is expressed as the number of apneas or hypopneas per hour of sleep.

As noted above, in central sleep apnea, the cessation of airflow is associated with the absence of physical attempts to breathe; specifically, polysomnograms reveal correlation between absence of rib cage and abdominal movements and cessation of airflow at the nose and lips. By contrast, in obstructive sleep apnea, pauses are not correlated with the absence of attempts to breathe and may even be correlated with more effortful breathing in an instinctive attempt to overcome the pressure on the sufferer's airway. If the majority of a sleep-apnea sufferer's apneas/hypopneas are central, his condition is classified as central; likewise, if the majority are obstructive, his condition is classified as obstructive.

Common symptoms of OSA include unexplained daytime sleepiness, restless sleep, and loud snoring (with periods of silence followed by gasps). Less common symptoms are morning headaches; insomnia; trouble concentrating; mood changes such as irritability, anxiety and depression; forgetfulness; increased heart rate and/or blood pressure; decreased sex drive; unexplained weight gain; increased urination and/or nocturia; frequent heartburn or gastroesophageal reflux disease; and heavy night sweats.

Obstructive sleep apnea (OSA) is the most common type of sleep apnea and is caused by complete or partial obstructions of the upper airway. It is characterized by repetitive episodes of shallow or paused breathing during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation. These episodes of decreased breathing, called "apneas" (literally, "without breath"), typically last 20 to 40 seconds.

Individuals with OSA are rarely aware of difficulty breathing, even upon awakening. It is often recognized as a problem by others who observe the individual during episodes or is suspected because of its effects on the body. OSA is commonly accompanied with snoring. Some use the terms obstructive sleep apnea syndrome or obstructive sleep apnea–hypopnea syndrome to refer to OSA which is associated with symptoms during the daytime. Symptoms may be present for years or even decades without identification, during which time the individual may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. Individuals who generally sleep alone are often unaware of the condition, without a regular bed-partner to notice and make them aware of their symptoms.

As the muscle tone of the body ordinarily relaxes during sleep, and the airway at the throat is composed of walls of soft tissue, which can collapse, it is not surprising that breathing can be obstructed during sleep. Although a minor degree of OSA is considered to be within the bounds of normal sleep, and many individuals experience episodes of OSA at some point in life, a small percentage of people have chronic, severe OSA.

Many people experience episodes of OSA for only a short period. This can be the result of an upper respiratory infection that causes nasal congestion, along with swelling of the throat, or tonsillitis that temporarily produces very enlarged tonsils. The Epstein-Barr virus, for example, is known to be able to dramatically increase the size of lymphoid tissue during acute infection, and OSA is fairly common in acute cases of severe infectious mononucleosis. Temporary spells of OSA syndrome may also occur in individuals who are under the influence of a drug (such as alcohol) that may relax their body tone excessively and interfere with normal arousal from sleep mechanisms.

Some people with sleep apnea have a combination of both types; its prevalence ranges from 0.56% to 18%. The condition is generally detected when obstructive sleep apnea is treated with CPAP and central sleep apnea emerges. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown but is most likely related to incorrect settings of the CPAP treatment and other medical conditions the person has.

Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing. The muscle tone of the body ordinarily relaxes during sleep, and at the level of the throat the human airway is composed of collapsible walls of soft tissue which can obstruct breathing. Mild occasional sleep apnea, such as many people experience during an upper respiratory infection, may not be significant, but chronic severe obstructive sleep apnea requires treatment to prevent low blood oxygen (hypoxemia), sleep deprivation, and other complications.

Individuals with low muscle tone and soft tissue around the airway (e.g., because of obesity) and structural features that give rise to a narrowed airway are at high risk for obstructive sleep apnea. The elderly are more likely to have OSA than young people. Men are more likely to suffer sleep apnea than women and children are, though it is not uncommon in the last two population groups.

The risk of OSA rises with increasing body weight, active smoking and age. In addition, patients with diabetes or "borderline" diabetes have up to three times the risk of having OSA.

Common symptoms include loud snoring, restless sleep, and sleepiness during the daytime. Diagnostic tests include home oximetry or polysomnography in a sleep clinic.

Some treatments involve lifestyle changes, such as avoiding alcohol or muscle relaxants, losing weight, and quitting smoking. Many people benefit from sleeping at a 30-degree elevation of the upper body or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Lateral positions (sleeping on a side), as opposed to supine positions (sleeping on the back), are also recommended as a treatment for sleep apnea, largely because the gravitational component is smaller in the lateral position. Some people benefit from various kinds of oral appliances such as the Mandibular advancement splint to keep the airway open during sleep. Continuous positive airway pressure (CPAP) is the most effective treatment for severe obstructive sleep apnea but oral appliances are considered a first line approach equal to CPAP for mild to moderate sleep apnea according to the AASM parameters of care. There are also surgical procedures to remove and tighten tissue and widen the airway.

Snoring is a common finding in people with this syndrome. Snoring is the turbulent sound of air moving through the back of the mouth, nose, and throat. Although not everyone who snores is experiencing difficulty breathing, snoring in combination with other risk factors has been found to be highly predictive of OSA. The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, there may not be enough air movement to make much sound. Even the loudest snoring does not mean that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs when snoring "stops".

Other indicators include (but are not limited to): hypersomnolence, obesity BMI >30, large neck circumference ( in women, in men), enlarged tonsils and large tongue volume, micrognathia, morning headaches, irritability/mood-swings/depression, learning and/or memory difficulties, and sexual dysfunction.

The term "sleep-disordered breathing" is commonly used in the U.S. to describe the full range of breathing problems during sleep in which not enough air reaches the lungs (hypopnea and apnea). Sleep-disordered breathing is associated with an increased risk of cardiovascular disease, stroke, high blood pressure, arrhythmias, diabetes, and sleep deprived driving accidents. When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do "not" drop significantly when the individual is sleeping. Stroke is associated with obstructive sleep apnea.

It has been revealed that people with OSA show tissue loss in brain regions that help store memory, thus linking OSA with memory loss. Using magnetic resonance imaging (MRI), the scientists discovered that people with sleep apnea have mammillary bodies that are about 20 percent smaller, particularly on the left side. One of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury.

Obesity hypoventilation syndrome is a form of sleep disordered breathing. Two subtypes are recognized, depending on the nature of disordered breathing detected on further investigations. The first is OHS in the context of obstructive sleep apnea; this is confirmed by the occurrence of 5 or more episodes of apnea, hypopnea or respiratory-related arousals per hour (high apnea-hypopnea index) during sleep. The second is OHS primarily due to "sleep hypoventilation syndrome"; this requires a rise of CO levels by 10 mmHg (1.3 kPa) after sleep compared to awake measurements and overnight drops in oxygen levels without simultaneous apnea or hypopnea. Overall, 90% of all people with OHS fall into the first category, and 10% in the second.

Most people with obesity hypoventilation syndrome have concurrent obstructive sleep apnea, a condition characterized by snoring, brief episodes of apnea (cessation of breathing) during the night, interrupted sleep and excessive daytime sleepiness. In OHS, sleepiness may be worsened by elevated blood levels of carbon dioxide, which causes drowsiness ("CO narcosis"). Other symptoms present in both conditions are depression, and hypertension (high blood pressure) that is difficult to control with medication. The high carbon dioxide can also cause headaches, which tend to be worsening in the morning.

The low oxygen level leads to physiologic constriction of the pulmonary arteries to correct ventilation-perfusion mismatching, which puts excessive strain on the right side of the heart. When this leads to right sided heart failure, it is known as "cor pulmonale". Symptoms of this disorder occur because the heart has difficulty pumping blood from the body through the lungs. Fluid may, therefore, accumulate in the skin of the legs in the form of edema (swelling), and in the abdominal cavity in the form of ascites; decreased exercise tolerance and exertional chest pain may occur. On physical examination, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to blood leaking through the tricuspid valve, hepatomegaly (an enlarged liver), ascites and leg edema. Cor pulmonale occurs in about a third of all people with OHS.

The most common sleep disorders include:

- Bruxism, involuntarily grinding or clenching of the teeth while sleeping.

- Catathrenia, nocturnal groaning during prolonged exhalation.

- Delayed sleep phase disorder (DSPD), inability to awaken and fall asleep at socially acceptable times but no problem with sleep maintenance, a disorder of circadian rhythms. Other such disorders are advanced sleep phase disorder (ASPD), non-24-hour sleep–wake disorder (non-24) in the sighted or in the blind, and irregular sleep wake rhythm, all much less common than DSPD, as well as the situational shift work sleep disorder.

- Hypopnea syndrome, abnormally shallow breathing or slow respiratory rate while sleeping.

- Idiopathic hypersomnia, a primary, neurologic cause of long-sleeping, sharing many similarities with narcolepsy.

- Insomnia disorder (primary insomnia), chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for these symptoms. Insomnia can also be comorbid with or secondary to other disorders.

- Kleine–Levin syndrome, a rare disorder characterized by persistent episodic hypersomnia and cognitive or mood changes.

- Narcolepsy, including excessive daytime sleepiness (EDS), often culminating in falling asleep spontaneously but unwillingly at inappropriate times. About 70% of those who have narcolepsy also have cataplexy, a sudden weakness in the motor muscles that can result in collapse to the floor while retaining full conscious awareness.

- Night terror, "Pavor nocturnus", sleep terror disorder, an abrupt awakening from sleep with behavior consistent with terror.

- Nocturia, a frequent need to get up and urinate at night. It differs from enuresis, or bed-wetting, in which the person does not arouse from sleep, but the bladder nevertheless empties.

- Parasomnias, disruptive sleep-related events involving inappropriate actions during sleep, for example sleep walking, night-terrors and catathrenia.

- Periodic limb movement disorder (PLMD), sudden involuntary movement of arms and/or legs during sleep, for example kicking the legs. Also known as nocturnal myoclonus. See also Hypnic jerk, which is not a disorder.

- Rapid eye movement sleep behavior disorder (RBD), acting out violent or dramatic dreams while in REM sleep, sometimes injuring bed partner or self (REM sleep disorder or RSD).

- Restless legs syndrome (RLS), an irresistible urge to move legs. RLS sufferers often also have PLMD.

- Shift work sleep disorder (SWSD), a situational circadian rhythm sleep disorder. (Jet lag was previously included as a situational circadian rhythm sleep disorder, but it doesn't appear in DSM-5 (see Diagnostic and Statistical Manual of Mental Disorders)).

- Sleep apnea, obstructive sleep apnea, obstruction of the airway during sleep, causing lack of sufficient deep sleep, often accompanied by snoring. Other forms of sleep apnea are less common. When air is blocked from entering into the lungs, the individual unconsciously gasps for air and sleep is disturbed. Stops of breathing of at least ten seconds, 30 times within seven hours of sleep, classifies as apnea. Other forms of sleep apnea include central sleep apnea and sleep-related hypoventilation.

- Sleep paralysis, characterized by temporary paralysis of the body shortly before or after sleep. Sleep paralysis may be accompanied by visual, auditory or tactile hallucinations. Not a disorder unless severe. Often seen as part of narcolepsy.

- Sleepwalking or "somnambulism", engaging in activities normally associated with wakefulness (such as eating or dressing), which may include walking, without the conscious knowledge of the subject.

- Somniphobia, one cause of sleep deprivation, a dread/ fear of falling asleep or going to bed. Signs of the illness include anxiety and panic attacks before and during attempts to sleep.

Parasomnia disorders are classified into the following categories:

- arousal disorders

- sleep-wake transition disorders

- parasomnias associated with REM sleep

A sleep disorder, or somnipathy, is a medical disorder of the sleep patterns of a person or animal. Some sleep disorders are serious enough to interfere with normal physical, mental, social and emotional functioning. Polysomnography and actigraphy are tests commonly ordered for some sleep disorders.

Disruptions in sleep can be caused by a variety of issues, from teeth grinding (bruxism) to night terrors. When a person suffers from difficulty falling asleep and/or staying asleep with no obvious cause, it is referred to as insomnia.

Sleep disorders are broadly classified into dyssomnias, parasomnias, circadian rhythm sleep disorders involving the timing of sleep, and other disorders including ones caused by medical or psychological conditions and sleeping sickness.

Some common sleep disorders include sleep apnea (stops in breathing during sleep), narcolepsy and hypersomnia (excessive sleepiness at inappropriate times), cataplexy (sudden and transient loss of muscle tone while awake), and sleeping sickness (disruption of sleep cycle due to infection). Other disorders include sleepwalking, night terrors and bed wetting. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.

Under DSM-5 criteria, there are 11 diagnostic groups that comprise sleep-wake disorders. These include, Insomnia disorder, Hypersomnolence disorder, Narcolepsy, Obstructive sleep apnea hypopnea, Central sleep apnea, Sleep-related hypoventilation, Circadian rhythm sleep-wake disorders, Non–rapid eye movement (NREM) sleep arousal disorders, Nightmare disorder, Rapid eye movement (REM) sleep behavior disorder, Restless legs syndrome, and substance-medication-induced sleep disorder. Sexsomnia is classified under NREM arousal parasomnia.

The Great Imitator (also The Great Masquerader) is a phrase used for medical conditions that feature nonspecific symptoms and may be confused with a number of other diseases. Most great imitators are systemic in nature. Diseases sometimes referred to with this name include:

- Various cancers

- Intravascular large B-cell lymphoma

- Various rheumatic conditions, including:

- Fibromyalgia

- Psoriatic arthritis

- Lupus erythematosus

- Systemic lupus erythematosus

- Sarcoidosis

- Multiple sclerosis

- Celiac disease

- Addison's Disease

- Pulmonary embolism

- Various infectious diseases, including:

- Syphilis

- Lyme disease

- Nocardiosis

- Tuberculosis

- Brucellosis

- Malaria

- Breathing-related sleep disorders (chiefly sleep apnea/hypopnea and upper-airway resistance syndrome).

The signs and symptoms of autonomic neuropathy include the following:

- Urinary bladder conditions: bladder incontinence or urinary retention

- Gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhoea, constipation

- Cardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertion

- Respiratory system: impairments in the signals associated with regulation of breathing and gas exchange (central sleep apnea, hypopnea, bradypnea).

- Nervous system: pupillary defect, exaggerated hippus, dizziness or lightheadedness.

- Other areas: hypoglycemia unawareness, genital impotence, sweat disturbances, sicca (dryness).

Children who have suffered silent strokes often have a variety of neuropsychological deficits. These deficits may include lowered I.Q., learning disabilities, and an inability to focus.

Silent strokes are the most common form of neurologic injury in children with sickle cell anemia, who may develop subtle neurocognitive deficits in the areas of attention and concentration, executive function, and visual-motor speed and coordination due to silent strokes which may not have been detected on physical examination.

A silent stroke is a stroke that does not have any outward symptoms associated with stroke, and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being amongst the predisposing factors.

These types of strokes include lacunar and other ischemic strokes and minor hemorrhages. They may also include leukoaraiosis (changes in the white matter of the brain): the white matter is more susceptible to vascular blockage due to reduced amount of blood vessels as compared to the cerebral cortex. These strokes are termed "silent" because they typically affect "silent" regions of the brain that do not cause a noticeable change in an afflicted person’s motor functions such as contralateral paralysis, slurred speech, pain, or an alteration in the sense of touch. A silent stroke typically affects regions of the brain associated with various thought processes, mood regulation and cognitive functions and is a leading cause of vascular cognitive impairment and may also lead to a loss of urinary bladder control.

In the Cardiovascular Health Study, a population study conducted among 3,660 adults over the age of 65. 31% showed evidence of silent stroke in neuroimaging studies utilizing MRI. These individuals were unaware they had suffered a stroke. It is estimated that silent strokes are five times more common than symptomatic stroke.

A silent stroke differs from a transient ischemic attack (TIA). In TIA symptoms of stroke are exhibited which may last from a few minutes to 24 hours before resolving. A TIA is a risk factor for having a major stroke and subsequent silent strokes in the future.

Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include:

- Diabetes, which is the most common cause of autonomic neuropathy, can gradually cause nerve damage throughout the body.

- Injury to nerves caused by surgery or radiation to the neck.

- Treatment with certain medications, including some drugs used in cancer chemotherapy.

- Abnormal protein buildup in organs (amyloidosis), which affects the organs and the nervous system.

- Other chronic illnesses, such as Parkinson's disease, multiple sclerosis and some types of dementia.

- Autonomic neuropathy may also be caused by an abnormal attack by the immune system that occurs as a result of some cancers (paraneoplastic syndrome).

- Certain infectious diseases. Some viruses and bacteria, such as botulism, Lyme disease and HIV, can cause autonomic neuropathy.

- Inherited disorders. Certain hereditary disorders can cause autonomic neuropathy.

- Autoimmune diseases, in which the immune system attacks and damages parts of the body, including the nerves. Examples include Sjogren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain-Barre syndrome is an autoimmune disease that happens rapidly and can affect autonomic nerves.

Neuritis is a general term for inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Causes of neuritis include:

Those with diseases or dysfunctions of their nerves may present with problems in any of the normal nerve functions. Symptoms vary depending on the types of nerve fiber involved.In terms of sensory function, symptoms commonly include loss of function ("negative") symptoms, including , tremor, impairment of balance, and gait abnormality. Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins-and-needles.

Motor symptoms include loss of function ("negative") symptoms of weakness, tiredness, muscle atrophy, and gait abnormalities; and gain of function ("positive") symptoms of cramps, and muscle twitch (fasciculations).

In the most common form, length-dependent peripheral neuropathy, pain and parasthesia appears symmetrically and generally at the terminals of the longest nerves, which are in the lower legs and feet. Sensory symptoms generally develop before motor symptoms such as weakness. Length-dependent peripheral neuropathy symptoms make a slow ascent of leg, while symptoms may never appear in the upper limbs; if they do, it will be around the time that leg symptoms reach the knee. When the nerves of the autonomic nervous system are affected, symptoms may include constipation, dry mouth, difficulty urinating, and dizziness when standing.