Other olfactory disorders such as hyposmia and anosmia have been found to be a symptom of mood disorders (depression). However, it is not known what olfactory disorders occur and if they are indeed a symptom of a depressive disorder.

It has been found that phantosmia may be an early sign of the neurodegenerative disease Parkinson's disease. It may also be a sign of an intracranial hemorrhage (brain tumours or epilepsy).

Other studies have also found that the symptoms of phantosmia have been alleviated after the patient has been treated for depression.

Another case of a 70-year-old male reported that his first abnormal symptoms were irregular bowel movements. After this the patient developed irregular eye movements and had developed a sleep and behavior disorder after this he developed phantosmia; which was described to be as "stinky and unpleasant". The patient did not display the following symptoms: loss of awareness, confusion, automatisms, convulsive seizures, auditory/visual hallucinations.

Hyperosmia is an increased olfactory acuity (heightened sense of smell), usually caused by a lower threshold for odor. This perceptual disorder arises when there is an abnormally increased signal at any point between the olfactory receptors and the olfactory cortex. The causes of hyperosmia may be genetic, environmental or the result of benzodiazepine withdrawal syndrome.

When odorants enter the nasal cavity, they bind to odorant receptors at the base of the olfactory epithelium. These receptors are bipolar neurons that connect to the glomerular layer of the olfactory bulb, traveling through the cribriform plate. At the glomerular layer, axons from the olfactory receptor neurons intermingle with dendrites from intrinsic olfactory bulb neurons: mitrial/tufted cells and dopaminergic periglomerular cells. From the olfactory bulb, mitral/tufted cells send axons via the lateral olfactory tract (the cranial nerve I) to the olfactory cortex, which includes the piriform cortex, entorhinal cortex, and parts of the amygdala. From the entorhinal cortex, axons extend to the medial dorsal nucleus of the thalamus, which then proceed to the orbitofrontal cortex.

Phantosmia (phantom smell), also called an olfactory hallucination, is smelling an odor that is not actually there. It can occur in one nostril or both. Unpleasant phantosmia, cacosmia, is more common and is often described as smelling something that is burned, foul, spoiled, or rotten. Experiencing occasional phantom smells is normal and usually goes away on its own in time. When hallucinations of this type do not seem to go away or when they keep coming back, it can be very upsetting and can disrupt an individual's quality of life.

Olfactory hallucinations can be caused by common medical conditions such as nasal infections, nasal polyps, or dental problems. It can result from neurological conditions such as migraines, head injuries, strokes, Parkinson's disease, seizures, or brain tumors. It can also be a symptom of certain mental disorders such as depression, bipolar disorder, intoxication or withdrawal from drugs and alcohol, or psychotic disorders. Environmental exposures are sometimes the cause as well, such as smoking, exposure to certain types of chemicals (e.g., insecticides or solvents), or radiation treatment for head or neck cancer.

A physician can determine if the problem is with the sense of smell (olfactory system) or taste (gustatory system), or if it is caused by a neurological or psychiatric disorder. Phantosmia usually goes away on its own, though this can sometimes be gradual and occur over several years. When caused by an illness (e.g., sinusitis), it should go away when the illness resolves. If the problem persists or causes significant discomfort, a doctor might recommend nasal saline drops, antidepressant or anticonvulsant medications, anesthesia to parts of the nose, or in very rare circumstances, surgical procedures to remove the olfactory nerves or bulbs.

There has not been extensive research into environmental causes of hyperosmia, but there are some theories of some possible causes.

In a study by Atianjoh et al., it has been found that amphetamines decrease levels of dopamine in the olfactory bulbs of rodents. On this basis, it has been hypothesized that amphetamine use may cause hyperosmia in rodents and humans, but further research is still needed. Anecdotal support for the belief that amphetamines may cause hyperosmia comes from Oliver Sacks's account of a patient with a heightened sense of smell after taking amphetamines.

It has been observed that the inhalation of hydrocarbons can cause hyperosmia, most likely due to the destruction of dopaminergic neurons in the olfactory bulb.

Methotrexate, administered in the treatment of psoriasis, has been known to cause hyperosmia, and may be more likely to do so in patients with a history of migraines. However, this is only an observation and not part of a study, therefore it is yet to be verified.

Anosmia can have a number of harmful effects. Patients with sudden onset anosmia may find food less appetizing, though congenital anosmics rarely complain about this, and none report a loss in weight. Loss of smell can also be dangerous because it hinders the detection of gas leaks, fire, and spoiled food. The common view of anosmia as trivial can make it more difficult for a patient to receive the same types of medical aid as someone who has lost other senses, such as hearing or sight.

Losing an established and sentimental smell memory (e.g. the smell of grass, of the grandparents' attic, of a particular book, of loved ones, or of oneself) has been known to cause feelings of depression.

Loss of olfaction may lead to the loss of libido, though this usually does not apply to congenital anosmics.

Often people who have congenital anosmia report that they pretended to be able to smell as children because they thought that smelling was something that older/mature people could do, or did not understand the concept of smelling but did not want to appear different from others. When children get older, they often realize and report to their parents that they do not actually possess a sense of smell, often to the surprise of their parents.

A study done on patients suffering from anosmia found that when testing both nostrils, there was no anosmia revealed; however, when testing each nostril individually, tests showed that the sense of smell was usually affected in only one of the nostrils as opposed to both. This demonstrated that unilateral anosmia is not uncommon in anosmia patients.

Anosmia is the inability to perceive odor or a lack of functioning olfaction—the loss of the sense of smell. Anosmia may be temporary, but some forms such as from an accident, can be permanent. Anosmia is due to a number of factors, including an inflammation of the nasal mucosa, blockage of nasal passages or a destruction of one temporal lobe. Inflammation is due to chronic mucosa changes in the paranasal sinus lining and the middle and superior turbinates.

When anosmia is caused by inflammatory changes in the nasal passageways, it is treated simply by reducing inflammation. It can be caused by chronic meningitis and neurosyphilis that would increase intracranial pressure over a long period of time, and in some cases by ciliopathy including ciliopathy due to primary ciliary dyskinesia (Kartagener syndrome, Afzelius' syndrome or Siewert's syndrome).

Many patients may experience unilateral anosmia, often as a result of minor head trauma. This type of anosmia is normally only detected if both of the nostrils are tested separately. Using this method of testing each nostril separately will often show a reduced or even completely absent sense of smell in either one nostril or both, something which is often not revealed if both nostrils are simultaneously tested.

A related term, hyposmia, refers to a decreased ability to smell, while hyperosmia refers to an increased ability to smell. Some people may be anosmic for one particular odor. This is known as "specific anosmia". The absence of the sense of smell from birth is called congenital anosmia.

Symptoms range in severity from mild to disabling.

Symptoms are common, but vague and non-specific for the condition. The most common are feeling tired, "brain fog" (short-term memory problems, difficulty concentrating), gastrointestinal problems, headaches, and muscle pain.

A partial list of other symptoms patients have attributed to MCS include: difficulty breathing, pains in the throat, chest, or abdominal region, skin irritation, headaches, neurological symptoms (nerve pain, pins and needles feelings, weakness, trembling, restless leg syndrome), tendonitis, seizures, visual disturbances (blurring, halo effect, inability to focus), anxiety, panic and/or anger, sleep disturbance, suppression of immune system, digestive difficulties, nausea, indigestion/heartburn, vomiting, diarrhea, joint pains, vertigo/dizziness, abnormally acute sense of smell (hyperosmia), sensitivity to natural plant fragrance or natural pine terpenes, dry mouth, dry eyes, and an overactive bladder.

People who suffer from MCS may have a neurological dysfunction in the odor-processing areas of the brain or otherwise have an exaggerated response to scents.