Brain related causes are less commonly associated with isolated vertigo and nystagmus but can still produce signs and symptoms, which mimic peripheral causes. Disequilibrium is often a prominent feature.

- Degenerative: age related decline in balance function

- Infectious: meningitis, encephalitis, epidural abscess, syphilis

- Circulatory: cerebral or cerebellar ischemia or hypoperfusion, stroke, lateral medullary syndrome (Wallenberg's syndrome)

- Autoimmune: Cogan syndrome

- Structural: Arnold-Chiari malformation, hydrocephalus

- Systemic: multiple sclerosis, Parkinson's disease

- Vitamin deficiency: Vitamin B12 deficiency

- CNS or posterior neoplasms, benign or malignant

- Neurological: Vertiginous epilepsy, abasia

- Other – There are a host of other causes of dizziness not related to the ear.

- Mal de debarquement is rare disorder of imbalance caused by being on board a ship. Patients suffering from this condition experience disequilibrium even when they get off the ship. Typically treatments for seasickness are ineffective for this syndrome.

- Motion sickness – a conflict between the input from the various systems involved in balance causes an unpleasant sensation. For this reason, looking out of the window of a moving car is much more pleasant than looking inside the vehicle.

- Migraine-associated vertigo

- Toxins, drugs, medications; it is also a known symptom of carbon monoxide poisoning.

Local damage and inflammation that interferes with the taste buds or local nervous system such as that stemming from radiation therapy, glossitis, tobacco use, and denture use also cause ageusia. Other known causes include loss of taste sensitivity from aging (causing a difficulty detecting salty or bitter taste), anxiety disorder, cancer, renal failure and liver failure.

Deficiency of vitamin B (niacin) and zinc can cause problems with the endocrine system, which may cause taste loss or alteration. Disorders of the endocrine system, such as Cushing's syndrome, hypothyroidism and diabetes mellitus, can cause similar problems. Ageusia can also be caused by medicinal side-effects from antirheumatic drugs such as penicillamine, antiproliferative drugs such as cisplatin, ACE inhibitors, and other drugs including azelastine, clarithromycin, terbinafine, and zopiclone.

A somatosensory disorder is an impairment of the somatosensory system.

The disease is an inherited autosomal dominant disease, but the physiological cause of the dysfunction is still unclear. An acidophyllic mucopolysaccharide-containing substance was discovered, especially in cochleas, maculas, and crista ampullaris of patients with DFNA9 (a chromosome locus), as well as severe degeneration of vestibular and cochlear sensory axons and dendrites. It is suggested that the mucopolysaccharide deposit could cause strangulation of nerve endings.

The maculas and crista ampullaris are what allow for non-visual sensation of head movements. The crista ampullaris resides in the semicircular canals of the inner ear and detects angular acceleration, while the maculas are housed within the vestibule of the inner ear and detect linear acceleration. When affected, these organs can lead to vertigo and nausea because the body would always feel off-balance.

About 20–30% of the population report to have experienced dizziness at some point in the previous year.

Causes of dizziness related to the ear are often characterized by vertigo (spinning) and nausea. Nystagmus (flickering of the eye, related to the Vestibulo-ocular reflex [VOR]) is often seen in patients with an acute peripheral cause of dizziness.

- Benign Paroxysmal Positional Vertigo (BPPV) – The most common cause of vertigo. It is typically described as a brief, intense sensation of spinning that occurs when there are changes in the position of the head with respect to gravity. An individual may experience BPPV when rolling over to the left or right, upon getting out of bed in the morning, or when looking up for an object on a high shelf. The cause of BPPV is the presence of normal but misplaced calcium crystals called otoconia, which are normally found in the utricle and saccule (the otolith organs) and are used to sense movement. If they fall from the utricle and become loose in the semicircular canals, they can distort the sense of movement and cause a mismatch between actual head movement and the information sent to the brain by the inner ear, causing a spinning sensation.

- Labyrinthitis - An inner ear infection or inflammation causing both dizziness (vertigo) and hearing loss.

- Vestibular neuronitis - an infection of the vestibular nerve, generally viral, causing vertigo

- Cochlear Neuronitis – an infection of the Cochlear nerve, generally viral, causing sudden deafness but no vertigo

- Trauma – Injury to the skull may cause either a fracture or a concussion to the organ of balance. In either case an acute head injury will often result in dizziness and a sudden loss of vestibular function.

- Surgical trauma to the lateral semicircular canal (LSC) is a rare complication which does not always result in cochlear damage. Vestibular symptoms are pronounced. Dizziness and instability usually persist for several months and sometimes for a year or more.

- Ménière's disease - an inner ear fluid balance disorder that causes lasting episodes of vertigo, fluctuating hearing loss, tinnitus (a ringing or roaring in the ears), and the sensation of fullness in the ear. The cause of Ménière's disease is unknown.

- Perilymph fistula – a leakage of inner ear fluid from the inner ear. It can occur after head injury, surgery, physical exertion or without a known cause.

- Superior canal dehiscence syndrome – a balance and hearing disorder caused by a gap in the temporal bone, leading to the dysfunction of the superior canal.

- Bilateral vestibulopathy – a condition involving loss of inner ear balance function in both ears. This may be caused by certain antibiotics, anti-cancer, and other drugs or by chemicals such as solvents, heavy metals, etc., which are ototoxic; or by diseases such as syphilis or autoimmune disease; or other causes. In addition, the function of the semicircular canal can be temporarily affected by a number of medications or combinations of medications.

Patients may experience numbness, prickling or tingling sensations (paresthesias), or the feeling a limb has "fallen asleep" (an indicator of nerve compression), burning, cutting or other sensations.

Vestibulocochlear dysfunction progressive familial, known also as familial progressive vestibulocochlear dysfunction is an autosomal dominant disease that results in sensorineural hearing loss and vestibular areflexia. Patients report feelings of vague dissiness, blurred vision, dysequilibrium in the dark, and progressive hearing impairment.

Mirror-touch synesthesia is a rare condition which causes individuals to experience the same sensation (such as touch) that another person feels. For example, if someone with this condition were to observe someone touching their cheek, they would feel the same sensation on their own cheek. Synesthesia, in general, is described as a condition in which a stimulus causes an individual to experience an additional sensation. Synesthesia is usually a developmental condition; however, recent research has shown that mirror touch synesthesia can be acquired after sensory loss following amputation.

Of the millions experiencing strokes worldwide, over 30,000 in the United States alone have developed some form of Dejerine–Roussy syndrome. 8% of all stroke patients will experience central pain syndrome, with 5% experiencing moderate to severe pain. The risk of developing Dejerine–Roussy syndrome is higher in older stroke patients, about 11% of stroke patients over the age of 80.

Hypoesthesia (or hypesthesia) refer to a reduced sense of touch or sensation, or a partial loss of sensitivity to sensory stimuli. In everyday speech this is sometimes referred to as "numbness".

Hypoesthesia is one of the negative sensory symptoms associated with cutaneous sensory disorder (CSD). In this condition, patients have abnormal disagreeable skin sensations that can be increased (stinging, itching or burning) or decreased (numbness or hypoesthesia). There are no other apparent medical diagnoses to explain these symptoms.

Cutaneous hyperesthesia has been associated with diagnosis of appendicitis in children but this symptom was not supported by the evidence.

Hypoesthesia originating in (and extending centrally from) the feet, fingers, navel, and/or lips is one of the common symptoms of beriberi, which is a set of symptoms caused by thiamine deficiency.

Hypoesthesia is also one of the more common manifestations of decompression sickness (DCS), along with joint pain, rash and generalized fatigue.

The imbalance in sensation characterized by Dejerine–Roussy syndrome can be argued through a model addressing a system of inputs and outputs that the brain must constantly process throughout life, suggesting latent plasticity. The right and left hemispheres of the brain both play important roles in the sensory input and output. When a stroke damages one hemisphere, it is proposed that the other hemisphere will cope with the discrepancies in a specific manner. The left hemisphere tends to "gloss over" discrepancies from inputs, eliciting either denial or rationalization defense mechanisms in order to stabilize said discrepancy. In contrast, the right hemisphere does the opposite, and will focus on the discrepancy, and motivate action to be taken to restore equilibrium. Therefore, damage to the left hemisphere can cause both an indifference to pain and hypersensitivity to pain (dysaesthesia or allodynia), while damage to the right hemisphere can cause denial as a defense mechanism (anosognosia and somatoparaphrenia).

The insular cortex, part of the cerebral cortex, is responsible for self-sensation, including the degree of pain perceived by the body, and for self-awareness and defense mechanisms. The insular cortex is often lesioned by a stroke. Particularly, the posterior insula has been mapped to correlate to pain experienced by an individual. In addition, it has been proven that the posterior insula receives a substantial amount of the inputs of the brain, and can be treated with visual, kinesthetic, and auditory inputs.

Left untreated, tabes dorsalis can lead to paralysis, dementia, and blindness. Existing nerve damage cannot be reversed.

Ramsay Hunt syndrome type 2 refers to shingles of the geniculate ganglion. After initial infection, varicella zoster virus lies dormant in nerve cells in the body, where it is kept in check by the immune system. Given the opportunity, for example during an illness that suppresses the immune system, the virus travels to the end of the nerve cell, where it causes the symptoms described above.

The affected ganglion is responsible for the movements of facial muscles, the touch sensation of a part of ear and ear canal, the taste function of the frontal two-thirds of the tongue, and the moisturization of the eyes and the mouth. The syndrome specifically refers to the combination of this entity with weakness of the muscles activated by the facial nerve. In isolation, the latter is called Bell's Palsy.

However, as with shingles, the lack of lesions does not definitely exclude the existence of a herpes infection. Even before the eruption of vesicles, varicella zoster virus can be detected from the skin of the ear.

A stroke (either ischemic or hemorrhagic) involving the posterior fossa is a cause of central vertigo. Risk factors for a stroke as a cause of vertigo include increasing age and known vascular risk factors. Presentation may more often involve headache or neck pain, additionally, those who have had multiple episodes of dizziness in the months leading up to presentation are suggestive of stroke with prodromal TIAs. The HINTS exam as well as imaging studies of the brain (CT, CT angiogram, and/or MRI) are helpful in diagnosis of posterior fossa stroke.

The disease is more frequent in males than in females. Onset is commonly during mid-life. The incidence of tabes dorsalis is rising, in part due to co-associated HIV infection .

Treatment with the steroid "prednisone" and the antiviral drug "acyclovir 800mg 5 times a day" is controversial, with some studies showing to achieve complete recovery in patients if started within the first three days of facial paralysis, with chances of recovery decreasing as treatment was delayed. Delay of treatment may result in permanent facial nerve paralysis. However, some studies demonstrate that even when steroids are started promptly, only 22% of all patient achieve full recovery of facial paralysis.

Treatment apparently has no effect on the recovery of hearing loss. Diazepam is sometimes used to treat the vertigo.

Vertigo is recorded as a symptom of decompression sickness in 5.3% of cases by the US Navy as reported by Powell, 2008 It including isobaric decompression sickness.

Decompression sickness can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium, but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect.

Three conditions must be met in order to confirm the presence of mirror touch synesthesia. The first condition is that the synaesthetic response, which is defined as the sensation synesthetes feel after observing someone else being touched, should feel like conscious experiences. The second condition is that synesthetic responses are induced by a stimulus that normally does not induce that response. The third condition is that the synesthetic experiences must occur automatically, without conscious thought. In order to examine the prevalence of this condition, a study was conducted at the University College London and University of Sussex. 567 undergraduate participants were recruited and given a questionnaire. From the questionnaire, it was determined that approximately 2.5% of the population experienced mirror-touch synesthesia symptoms. Further studies have shown the prevalence to be 1.6%, meaning that this condition is one of the more common types of synesthesia, along with grapheme-color synesthesia (1.4%) and day-color synesthesia (2.8%). At the moment it is believed that there are two subtypes of the condition. The first type causes a person to feel sensations on the part of their body that mirrors the observed touch. The second type causes a person to feel sensations on the same side of their body as the observed touch.

Studies have attempted to more explicitly define the of synesthetic responses. In most studies, participants are asked to observe someone else being touched and report what kind of synesthetic response they experience. In one particular instance, video clips were used to show different types of observed touch. The of the synesthetic touch is not affected by the location of the observed touch (arm, leg, hand, etc.); however, it is sometimes affected by the spatial orientation of the observed touch. When crossed hands are touched, the hands become uncrossed in the perception of synesthetes. However when the observed hand is upside down, the observed touch does not get rotated. Intensity is also not affected if the observed act consists of someone touching themselves, versus someone touching them. Additionally, the type of object doing the touching has a significant effect on the intensity of the response. If a finger or knife tip is used, a much higher intensity is experienced than if a feather is used. Finally, watching a dummy being touched decreases the intensity of the observed touch significantly. For this reason, it is suspected that in order to experience a synesthetic touch, synesthetes must observe somebody who is capable of feeling sensations.

Mirror touch responses are not limited to feeling touch. Mirror touch synesthetes have a higher ability to feel empathy than non-synesthetes, and can therefore feel the same emotions that someone else may be observed to feel. Additionally, some individuals experience pain when observing someone else in pain, and this is a condition usually developed from birth. Approximately 30% of the normal population experience some form of this condition and around 16% of amputees report synesthetic pain after an amputation. This condition can either be acquired or developed. In the congenital condition, synesthetes experience pain in the same location as the observed pain; however, in the acquired condition, high intensity pain is felt at the same location as the trauma.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

Hereditary sensory and autonomic neuropathy (HSAN) or hereditary sensory neuropathy (HSN) is a condition used to describe any of the types of this disease which inhibit sensation.

They are less common than Charcot-Marie-Tooth disease.

In terms of prognosis radial neuropathy is not necessarily permanent, though sometimes there could be partial loss of movement/sensation.Complications may be possible deformity of the hand in some individuals.

If the injury is axonal (the underlying nerve fiber itself is damaged) then full recovery may take months or years ( or could be permanent). EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

Hyperpathia is a clinical symptom of certain neurological disorders wherein nociceptive stimuli evoke exaggerated levels of pain. This should not be confused with allodynia, where normally non-painful stimuli evoke pain.

Initial line of treatment is with anti-inflammatory drugs or cortisone injections. There have been trials with gloves which help protect the ulnar nerve from compression. The most radical treatment option is surgery to relieve tension in the volar carpal ligament which forms the roof of Guyon's canal, thereby reducing compression on the ulnar nerve.

The place of chiropractic-, physical-, occupational-, massage- and osteopathic therapy was not confirmed in scientific studies. These treatments can be both expensive as well as dangerous (causing permanent damage when performed wrongly).

It is advised to consult a physician beforehand starting any therapy, albeit an alternative approach, to avoid any permanent nerve damage.