The treatment for vestibular neuronitis depends on the cause. However, symptoms of vertigo can be treated in the same way as other vestibular dysfunctions with vestibular rehabilitation.

In most cases, the condition tends to be self-limiting. In 95% or greater, vestibular neuritis is a one-time experience with most people fully recovering.

Recovery from acute labyrinthine inflammation generally takes from one to six weeks, but it is not uncommon for residual symptoms (dysequilibrium and/or dizziness) to last for a couple of months.

Recovery from a temporary damaged inner ear typically follows two phases:

1. An acute period, which may include severe vertigo and vomiting

2. approximately two weeks of sub-acute symptoms and rapid recovery

When diagnosing, PLF should be differentiated from Ménière's disease. Tympanostomy has been reported to be a way to diagnose and cure PLF.

Patients are advised to treat with bed rest and avoiding activities that increase intracranial pressure (i.e. weightlifting, valsalva, scuba diving, flying in airplanes) with the hopes of the membrane healing on their own. Appropriate Physical therapy / vestibular rehabilitation techniques can be helpful in managing symptoms of movement sensitivity.

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.

It was found that based on sensitized measures of auditory dysfunction and on psychological assessment, Subjects could be subdivided into seven subcategories:

1. middle ear dysfunction

2. mild cochlear pathology

3. central/medial olivocochlear efferent system (MOCS) auditory dysfunction

4. purely psychological problems

5. multiple auditory pathologies

6. combined auditory dysfunction and psychological problems

7. unknown

Different subgroups may represent different pathogenic and aetiological factors. Thus, subcategorization provides further understanding of the basis of King–Kopetzky syndrome, and hence may guide the rehabilitative management of these patients.This was suggested by Professor Dafydd Stephens and F Zhao at the Welsh Hearing Institute, Cardiff University.

It seems that somatic anxiety and situations of stress may be determinants of speech-hearing disability.

Some studies indicated an increased prevalence of a family history of hearing impairment in these patients. The pattern of results is suggestive that King-Kopetzky patients may be related to conditions of autosomal dominant inheritance.

As of 2014, no clinical trials had been conducted to determine what treatments are safe and effective; a few case reports had been published describing treatment of small numbers of people (two to twelve per report) with clomipramine, flunarizine, nifedipine, topiramate, carbamazepine, methylphenidate. Studies suggest that education and reassurance can reduce the frequency of EHS episodes. There is some evidence that individuals with EHS rarely report episodes to medical professionals.

Diagnosis is based on clinical findings.

'Clinical findings'

- Profound congenital sensorineural deafness is present

- CT scan or MRI of the inner ear shows no recognizable structure in the inner ear.

- As michel's aplasia is associated with LAMM syndrome there will be Microtia and microdontia present(small sized teeth).

Molecular genetic Testing

1. "FGF3" is the only gene, whose mutation can cause congenital deafness with Michel's aplasia, microdontia and microtia

Carrier testing for at-risk relatives requires identification of mutations which are responsible for occurrence of disease in the family.

There have not been sufficient studies conducted to make conclusive statements about prevalence nor who tends to suffer EHS. One study found that 13.5% of a sample of undergrads reported at least one episode over the course of their lives, with higher rates in those also suffering from sleep paralysis.

Reported symptoms include:

- Sensorineural hearing loss

- Vestibular areflexia

- Hearing impairment

- Vertigo

- Nausea and vomiting

- Head movement-dependent oscillopsia

Diagnostic methods vary, and are based on specific possible etiologies; however, an X-ray computed tomography scan of the face (or magnetic resonance imaging, or both) may be helpful.

Presence of inner ear abnormalities lead to Delayed gross development of child because of balance impairment and profound deafness which increases the risk of trauma and accidents.

- Incidence of accidents can be decreased by using visual or vibrotactile alarm systems in homes as well as in schools.

- Anticipatory education of parents, health providers and educational programs about hazards can help.

Currently there are no official tests or treatments for ROHHAD. Each child has the symptoms above at different ages, yet most symptoms are eventually present. Many children are misdiagnosed or are never diagnosed until alveolar hypoventilation occurs.

A combination of lifestyle modifications and medications can be used for the treatment of dolichoectasias.

- Antihypertensive medications such as Thiazides, Beta Blocker, ACE Inhibitor

- Trental or other Pentoxifylline drugs

- Dietary changes

- Weight loss

- Regular exercise

Traditional autonomic testing is used to aid in the diagnosis of AAG. These tests can include a Tilt Table Test (TTT), thermoregulatory sweat test (TST), quantitative sudomotor autonomic reflex testing (QSART) and various blood panels. Additionally, a blood test showing high levels of the antibody ganglionic nicotenic acetylcholine receptor (gAChr) occur in about 50% of patients with AAG (seropositive AAG). The seronegative patients (those without detectable gAChR levels) are theorized to have one or more different antibodies responsible for the autonomic dysfunction. However, both seropositive and seronegative patients have been seen to respond to the same treatments. A paraneoplastic panel may also be ordered to rule out paraneoplastic syndrome.

MRI will help with the diagnosis of structural abnormality of the brain. Genetic testing may also be pursued.

Jacod Syndrome is commonly associated with a tumor of the middle cranial fossa (near the apex of the orbit); but it can have several other causes.

The diagnosis of dysautonomia depends on the overall function of three autonomic functions – cardiovagal, adrenergic, and sudomotor. A diagnosis should, at a bare minimum, include measurements of blood pressure and heart rate while lying flat, and after at least 3 minutes of standing. The best way to achieve a diagnosis includes a range of testing, notably an autonomic reflex screen, tilt table test, and testing of the sudomotor response (QSART or thermoregulatory sweat test).

Additional tests and examinations to determine a diagnosis of dysautonomia include

Penile color duplex doppler ultrasound can help with preoperative planning to minimize bulbar necrosis.

Criteria for CSF abnormalities:

- Increased opening pressure (> 200mm of H2O)

- Increased Leukocytes (>4/mm3)

- Elevated protein (>50 mg/dL)

- Decreased glucose (<60 mg/dL)

Tumor Markers:

- Carcinoembryonic antigin (CEA)

- alpha-fetoprotein

- beta-human chorionic gonadotropin

- carbohydrate antigen19-9

- creatine-kinase BB

- isoenzyme

- tissue polypeptide antigen

- beta2-microglobulin,

- beta-glucoronidase

- lactate dehydrogenase isoenzyme-5

- vascular endothelial growth factor

These markers can be good indirect indicator of NM but most are not sensitive enough to improve cytogical diagnosis.

Avoiding false-negative

- Draw CSF from symptomatic or radiographically demonstrated disease.

- Draw large amount of CSF (>10.5mL).

- Don't delay processing of specimen.

- Obtain at least 2 samples. The first sample has diagnostic sensitivity of 54% but with repeated sampling, diagnostic sensitivity is increased to 91%.

Ideal procedure for diagnosis:

Lumbar puntures --> cranial MRI --> spinal MRI --> radioisotope CSF flow --> ventricular or lateral cervical spine CSF analysis (if previous step yields no definitive answer)

Particularly in the Russian literature, a subtype of dysautonomia which particularly affects the vascular system has been called vegetative-vascular dystonia. The term "vegetative" reflects an older name for the autonomic nervous system: the vegetative nervous system.

The diagnosis of NM is based on the detection of malignant cells in the CSF, the demonstration of leptomeningeal tumor cell deposits on neuroimaging, or both. CSF examination is the most useful diagnostic tool for NM. Patients with suspected NM should undergo one or two lumbar punctures, cranial magnetic resonance imaging (MRI), spinal MRI, and a radioisotope CSF flow study to rule out sites of CSF block. If the cytology remains negative and radiological studies are not definitive, consideration may be given to ventricular or lateral cervical spine CSF analysis based on the suspected site of predominant disease. Consideration of signs, symptoms, and neuroimaging can help with the placement to where CSF is drawn. Median time of diagnosis from initial primary cancer diagnosis is between 76 days and 17 months. NM diagnosis has been increasing and will continue to increase due to better primary care and longer survival time of cancer patients.

Difficulties in Diagonsis:

NM is multifocal and CSF at a particular site may show no abnormalities if the pathological site is far away. Only 50% of those suspected with NM are actually diagnosed with NM and only the presence of malignant cells in the CSF is diagnosis conclusive.

Techniques:

- MRI: Meningeal findings are described with the following characteristics: Nodular meningeal tumor, meningeal thickening >3 mm and a subjectively strong contrast enhancement. A smooth contrast enhancement of the meninges was judged to be typical for inflammatory, nonneoplastic meningitis.

- CSF cytology: is performed after drawing the CSF by lumbar puncture.

- Cytogenetic: measures chromosomal content of cells and fluorescence in situ hybridization which detects numerical and structural genetic aberrations as a sign of malignancy. This is especially useful for liquid tumors such as leukemia and lymphoma. Some of the techniques that achieve this are flow cytometry and DNA single-cell cytometry. However, cytogenetic only assist in diagnosis and is less preferred.

- Meningeal Biopsy: may be performed when all of the above criteria is inconclusive. Biopsy is only effective when performed at the region where there's enhancement on the MRI.

There is no known prevention of spinocerebellar ataxia. Those who are believed to be at risk can have genetic sequencing of known SCA loci performed to confirm inheritance of the disorder.

It is analyzed in several ways:

- Obtaining full erections at some times, such as nocturnal penile tumescence when asleep (when the mind and psychological issues, if any, are less present), tends to suggest that the physical structures are functionally working.

- Other factors leading to erectile dysfunction are diabetes mellitus (causing neuropathy).

There are no formal tests to diagnose erectile dysfunction. Some blood tests are generally done to exclude underlying disease, such as hypogonadism and prolactinoma. Impotence is also related to generally poor physical health, poor dietary habits, obesity, and most specifically cardiovascular disease such as coronary artery disease and peripheral vascular disease. Therefore, a thorough physical examination is helpful, in particular the simple search for a previously undetected groin hernia since it can affect sexual functions in men and is easily curable.

A useful and simple way to distinguish between physiological and psychological impotence is to determine whether the patient "ever" has an erection. If "never", the problem is likely to be physiological; if "sometimes" (however rarely), it could be physiological or psychological. The current diagnostic and statistical manual of mental diseases (DSM-IV) has included a listing for impotence.

- Duplex ultrasound:Duplex ultrasound is used to evaluate blood flow, venous leak, signs of atherosclerosis, and scarring or calcification of erectile tissue. Injecting prostaglandin, a hormone-like stimulator produced in the body, induces the erection. Ultrasound is then used to see vascular dilation and measure penile blood pressure.

- Penile nerves function:Tests such as the bulbocavernosus reflex test are used to determine if there is sufficient nerve sensation in the penis. The physician squeezes the glans (head) of the penis, which immediately causes the anus to contract if nerve function is normal. A physician measures the latency between squeeze and contraction by observing the anal sphincter or by feeling it with a gloved finger inserted past the anus.

- Nocturnal penile tumescence (NPT):It is normal for a man to have five to six erections during sleep, especially during rapid eye movement (REM). Their absence may indicate a problem with nerve function or blood supply in the penis. There are two methods for measuring changes in penile rigidity and circumference during nocturnal erection: snap gauge and strain gauge. A significant proportion of men who have no sexual dysfunction nonetheless do not have regular nocturnal erections.

- Penile biothesiometry:This test uses electromagnetic vibration to evaluate sensitivity and nerve function in the glans and shaft of the penis.

- Dynamic infusion cavernosometry (DICC): technique in which fluid is pumped into the penis at a known rate and pressure. It gives a measurement of the vascular pressure in the corpus cavernosum during an erection.

- Corpus cavernosometry:Cavernosography measurement of the vascular pressure in the corpus cavernosum. Saline is infused under pressure into the corpus cavernosum with a butterfly needle, and the flow rate needed to maintain an erection indicates the degree of venous leakage. The leaking veins responsible may be visualized by infusing a mixture of saline and x-ray contrast medium and performing a cavernosogram. In Digital Subtraction Angiography (DSA), the images are acquired digitally.

- Magnetic resonance angiography (MRA): This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the patient's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.