Treatment of people believed to have ATN or TN is usually begun with medication. The long-time first drug of choice for facial neuralgia has been carbamazepine, an anti-seizure agent. Due to the significant side-effects and hazards of this drug, others have recently come into common use as alternatives. These include oxcarbazepine, lamotrigine, and gabapentin. A positive patient response to one of these medications might be considered as supporting evidence for the diagnosis, which is otherwise made from medical history and pain presentation. There are no present medical tests to conclusively confirm TN or ATN.

If the anti-seizure drugs are found ineffective, one of the tricyclic antidepressant medications such as amitriptyline or nortriptyline, may be used. The tricyclic antidepressants are known to have dual action against both depression and neuropathic pain. Other drugs which may also be tried, either individually or in combination with an anti-seizure agent, include baclofen, pregabalin, anti-seizure drugs (to calm nerve endings), muscle relaxants, and opioid drugs such as oxycodone or an oxycodone/paracetamol combination.

For some people with ATN opioids may represent the only viable medical option which preserves quality of life and personal functioning. Although there is considerable controversy in public policy and practice in this branch of medicine, practice guidelines have long been available and published.

Both forms of facial neuralgia are relatively rare, with an incidence recently estimated between 12 and 24 new cases per hundred thousand population per year.

ATN often goes undiagnosed or misdiagnosed for extended periods, leading to a great deal of unexplained pain and anxiety. A National Patient Survey conducted by the US Trigeminal Neuralgia Association in the late 1990s indicated that the average facial neuralgia patient may see six different physicians before receiving a first definitive diagnosis. The first practitioner to see facial neuralgia patients is often a dentist who may lack deep training in facial neurology. Thus ATN may be misdiagnosed as Tempormandibular Joint Disorder.

This disorder is regarded by many medical professionals to comprise the most severe form of chronic pain known in medical practice. In some patients, pain may be unresponsive even to opioid drugs at any dose level that leaves the patient conscious. The disorder has thus acquired the unfortunate and possibly inflammatory nickname, "the suicide disease".

Symptoms of ATN may overlap with a pain disorder occurring in teeth called atypical odontalgia (literal meaning "unusual tooth pain"), with aching, burning, or stabs of pain localized to one or more teeth and adjacent jaw. The pain may seem to shift from one tooth to the next, after root canals or extractions. In desperate efforts to alleviate pain, some patients undergo multiple (but unneeded) root canals or extractions, even in the absence of suggestive X-ray evidence of dental abscess.

ATN symptoms may also be similar to those of post-herpetic neuralgia, which causes nerve inflammation when the latent herpes zoster virus of a previous case of chicken pox re-emerges in shingles. Fortunately, post-herpetic neuralgia is generally treated with medications that are also the first medications tried for ATN, which reduces the negative impact of misdiagnosis.

The subject of atypical trigeminal neuralgia is considered problematic even among experts. The term atypical TN is broad and due to the complexity of the condition, there are considerable issues with defining the condition further. Some medical practitioners no longer make a distinction between facial neuralgia (a nominal condition of inflammation) versus facial neuropathy (direct physical damage to a nerve).

Due to the variability and imprecision of their pain symptoms, ATN or atypical odontalgia patients may be misdiagnosed with atypical facial pain (AFP) or "hypochondriasis", both of which are considered problematic by many practitioners. The term "atypical facial pain" is sometimes assigned to pain which crosses the mid-line of the face or otherwise does not conform to expected boundaries of nerve distributions or characteristics of validated medical entities. As such, AFP is seen to comprise a diagnosis by reduction.

As noted in material published by the [US] National Pain Foundation: "atypical facial pain is a confusing term and should never be used to describe patients with trigeminal neuralgia or trigeminal neuropathic pain. Strictly speaking, AFP is classified as a "somatiform pain disorder"; this is a psychological diagnosis that should be confirmed by a skilled pain psychologist. Patients with the diagnosis of AFP have no identifiable underlying physical cause for the pain. The pain is usually constant, described as aching or burning, and often affects both sides of the face (this is almost never the case in patients with trigeminal neuralgia). The pain frequently involves areas of the head, face, and neck that are outside the sensory territories that are supplied by the trigeminal nerve. It is important to correctly identify patients with AFP since the treatment for this is strictly medical. Surgical procedures are not indicated for atypical facial pain."

The term "hypochondriasis" is closely related to "somatoform pain disorder" and "conversion disorder" in the Diagnostic and Statistical Manual (DSM-IV) of the American Psychiatric Association. As of July 2011, this axis of the DSM-IV is undergoing major revision for the DSM-V, with introduction of a new designation "Complex Somatic Symptom Disorder". However, it remains to be demonstrated that any of these "disorders" can reliably be diagnosed as a medical entity with a discrete and reliable course of therapy.

It is possible that there are triggers or aggravating factors that patients need to learn to recognize to help manage their health. Bright lights, sounds, stress, and poor diet are examples of additional stimuli that can contribute to the condition. The pain can cause nausea, so beyond the obvious need to treat the pain, it is important to be sure to try to get adequate rest and nutrition.

Depression is frequently co-morbid with neuralgia and neuropathic pain of all sorts, as a result of the negative effects that pain has on one's life. Depression and chronic pain may interact, with chronic pain often predisposing patients to depression, and depression operating to sap energy, disrupt sleep and heighten sensitivity and the sense of suffering. Dealing with depression should thus be considered equally important as finding direct relief from the pain.

External Compression Headache is caused by any type of headwear. This includes headwear that places pressure on the head — including tight hats, helmets, headbands, headphones and goggles. It is not known why some people are more sensitive than others to this type of pressure. External compression headaches can affect anyone who uses headwear. The headaches are more common among people who have migraines. It is believed to affect about four percent of the population. It is also referred to as "swim goggle headache".

These headaches can be brought on by such innocuous sources as wearing a halter top (presses against the neck), earplugs (presses against the jaw and inner ear), or wearing even a tiny hair clip (compresses the scalp). There is no known preventative treatment except to avoid the offending trigger. However, once symptoms arise and the trigger is removed, "Triptan"-type migraine treatment is effective.

The diagnostic criteria for SCSFLS is based on the 2004 International Classification of Headache Disorders, 2nd edn (ICHD-II) (Table 1) (50) criteria. However, the presentation of patients with confirmed diagnosis may be very different from that of the clinical diagnostic criteria and cannot be considered authoritative.

The symptoms and signs depend on which nerve is affected, where along its length the nerve is affected, and how severely the nerve is affected. Positive sensory symptoms are usually the earliest to occur, particularly tingling and neuropathic pain, followed or accompanied by reduced sensation or complete numbness. Muscle weakness is usually noticed later, and is often associated with muscle atrophy.

A compression neuropathy can usually be diagnosed confidently on the basis of the symptoms and signs alone. However, nerve conduction studies are helpful in confirming the diagnosis, quantifying the severity, and ruling out involvement of other nerves (suggesting a mononeuritis multiplex or polyneuropathy). A scan is not usually necessary, but may be helpful if a tumour or other local compressive lesion is suspected.Nerve injury, as a mononeuropathy, may cause similar symptoms to compression neuropathy. This may occasionally cause diagnostic confusion, particularly if the patient does not remember the injury and there are no obvious physical signs to suggest it.The symptoms and signs of each particular syndrome are discussed on the relevant pages, listed below.

When cranial CSF leak is suspected because of discharge from the nose or ear that is potentially CSF, the fluid can be collected and tested with a beta-2 transferrin assay. This test can positively identify if the fluid is cerebrospinal fluid.

When an underlying medical condition is causing the neuropathy, treatment should first be directed at this condition. For example, if weight gain is the underlying cause, then a weight loss program is the most appropriate treatment. Compression neuropathy occurring in pregnancy often resolves after delivery, so no specific treatment is usually required. Some compression neuropathies are amenable to surgery: carpal tunnel syndrome and cubital tunnel syndrome are two common examples. Whether or not it is appropriate to offer surgery in any particular case depends on the severity of the symptoms, the risks of the proposed operation, and the prognosis if untreated. After surgery, the symptoms may resolve completely, but if the compression was sufficiently severe or prolonged then the nerve may not recover fully and some symptoms may persist. Drug treatment may be useful for an underlying condition (including peripheral oedema), or for ameliorating neuropathic pain.

Diagnosis is principally by MRI. Frequently, arachnoid cysts are incidental findings on MRI scans performed for other clinical reasons. In practice, diagnosis of symptomatic arachnoid cysts requires symptoms to be present, and many with the disorder never develop symptoms.

Additional clinical assessment tools that can be useful in evaluating a patient with arachnoid cysts include the mini-mental state examination (MMSE), a brief questionnaire-based test used to assess cognition.

Diagnosis is by X-rays but preferably magnetic resonance imaging (MRI) of the whole spine. The most common causes of cord compression are tumors, but abscesses and granulomas (e.g. in tuberculosis) are equally capable of producing the syndrome. Tumors that commonly cause cord compression are lung cancer (non-small cell type), breast cancer, prostate cancer, renal cell carcinoma, thyroid cancer, lymphoma and multiple myeloma.

The diagnosis is typically made clinically with magnetic resonance imaging of the brain often revealing hyperintensities on "T"-weighed imaging. Three patterns have been described: superior frontal sulcus, dominant parieto-occipital, and holohemispheric watershed.

Adson's sign and the costoclavicular maneuver lack specificity and sensitivity and should comprise only a small part of the mandatory comprehensive history and physical examination undertaken with a patient suspected of having TOS. There is currently no single clinical sign that makes the diagnosis of TOS with any degree of certainty.

Additional maneuvers that may be abnormal in TOS include Wright's Test, which involves hyperabducting the arms over the head with some extension and evaluating for loss of radial pulses or signs of blanching of the skin in the hands indicating a decrease in blood flow with the maneuver. The "compression test" is also used, exerting pressure between the clavicle and medial humeral head causes radiation of pain and/or numbness into the affected arm.

Doppler arteriography, with probes at the fingertips and arms, tests the force and "smoothness" of the blood flow through the radial arteries, with and without having the patient perform various arm maneuvers (which causes compression of the subclavian artery at the thoracic outlet). The movements can elicit symptoms of pain and numbness and produce graphs with diminished arterial blood flow to the fingertips, providing strong evidence of impingement of the subclavian artery at the thoracic outlet. Doppler arteriography does not utilize probes at the fingertips and arms, and in this case is likely being confused with plethysmography, which is a different method that utilizes ultrasound without direct visualization of the affected vessels. It should also be noted that Doppler ultrasound (not really 'arteriography') would not be used at the radial artery in order to make the diagnosis of TOS. Finally, even if a Doppler study of the appropriate artery were to be positive, it would not diagnose neurogenic TOS, by far the most common subtype of TOS. There is plenty of evidence in the medical literature to show that arterial compression does not equate to brachial plexus compression, although they may occur together, in varying degrees. Additionally, arterial compression by itself does not make the diagnosis of arterial TOS (the rarest form of TOS). Lesser degrees of arterial compression have been shown in normal individuals in various arm positions and are thought to be of little significance without the other criteria for arterial TOS.

In cases of neurapraxia, the function of the nerves are temporarily impaired. However, the prognosis for recovery from neurapraxia is efficient and quick. Recovery begins within two to three weeks after the injury occurs, and it is complete within six to eight weeks. There are instances when function is not completely restored until four months after the instance of injury. The recovery period of neurapraxia is not an entirely ordered process, but the recovery is always complete and fast.

Dexamethasone (a potent glucocorticoid) in doses of 16 mg/day may reduce edema around the lesion and protect the cord from injury. It may be given orally or intravenously for this indication.

Surgery is indicated in localised compression as long as there is some hope of regaining function. It is also occasionally indicated in patients with little hope of regaining function but with uncontrolled pain. Postoperative radiation is delivered within 2–3 weeks of surgical decompression. Emergency radiation therapy (usually 20 Gray in 5 fractions, 30 Gray in 10 fractions or 8 Gray in 1 fraction) is the mainstay of treatment for malignant spinal cord compression. It is very effective as pain control and local disease control. Some tumours are highly sensitive to chemotherapy (e.g. lymphomas, small-cell lung cancer) and may be treated with chemotherapy alone.

Once complete paralysis has been present for more than about 24 hours before treatment, the chances of useful recovery are greatly diminished, although slow recovery, sometimes months after radiotherapy, is well recognised.

The median survival of patients with metastatic spinal cord compression is about 12 weeks, reflecting the generally advanced nature of the underlying malignant disease.

The treatment of PRES dependent on its cause. Anti-epileptic medication may also be appropriate.

According to medical professionals with the Cleveland Clinic, once an athlete suffers from an episode of cervical spinal cord, team physician or athletic trainer first stabilize the head and neck followed by a thorough neurologic inspection. If the injury is deemed severe, injured parties should be taken to a hospital for evaluation. Athletes that suffer from severe episodes of neurapraxia are urged to consult orthopaedic or spinal medical specialists. In mild cases of neurapraxia, the athlete is able to remove themselves from the field of play. However, the athlete is still advised to seek medical consultation.

This is based on MRI scan, magnetic resonance angiography and CT scan. A cerebral digital subtraction angiography (DSA) enhances visualization of the fistula.

- CT scans classically show an enlarged superior ophthalmic vein, cavernous sinus enlargement ipsilateral (same side) as the abnormality and possibly diffuse enlargement of all the extraocular muscles resulting from venous engorgement.

- Selective arteriography is used to evaluate arteriovenous fistulas.

- High resolution digital subtraction angiography may help in classifying CCF into dural and direct type and thus formulate a strategy to treat it either by a balloon or coil or both with or without preservation of parent ipsilateral carotid artery.

Median arcuate ligament syndrome is a diagnosis of exclusion. That is, the diagnosis of MALS is generally considered only after patients have undergone an extensive evaluation of their gastrointestinal tract including upper endoscopy, colonoscopy, and evaluation for gallbladder disease and gastroesophageal reflux disease (GERD).

The diagnosis of MALS relies on a combination of clinical features and findings on medical imaging. Clinical features include those signs and symptoms mentioned above; classically, MALS involves a triad of abdominal pain after eating, weight loss, and an abdominal bruit, although the classic triad is found in only a minority of individuals that carry a MALS diagnosis.

Diagnostic imaging for MALS is divided into screening and confirmatory tests. A reasonable screening test for patients with suspected MALS is duplex ultrasonography to measure blood flow through the celiac artery. Peak systolic velocities greater than 200 cm/s are suggestive of celiac artery stenosis associated with MALS.

Further evaluation and confirmation can be obtained via angiography to investigate the anatomy of the celiac artery. Historically, conventional angiography was used, although this has been largely replaced by less invasive techniques such as computed tomography (CT) and magnetic resonance (MR) angiography. Because it provides better visualization of intraabdominal structures, CT angiography is preferred to MR angiography in this setting. The findings of focal narrowing of the proximal celiac artery with poststenotic dilatation, indentation on the superior aspect of the celiac artery, and a hook-shaped contour of the celiac artery support a diagnosis of MALS. These imaging features are exaggerated on expiration, even in normal asymptomatic individuals without the syndrome.

Proximal celiac artery stenosis with poststenotic dilatation can be seen in other conditions affecting the celiac artery. The hook-shaped contour of the celiac artery is characteristic of the anatomy in MALS and helps distinguish it from other causes of celiac artery stenosis such as atherosclerosis. This hooked contour is not entirely specific for MALS however, given that 10-24% of normal asymptomatic individuals have this anatomy.

Individuals with a history of high blood pressure, diabetes, and smoking are most susceptible to PION as they have a compromised system of blood vessel autoregulation. Hence, extra efforts may need to be taken for them in the form of careful or staged surgery or the controlling the anemia from blood loss (by administration of blood transfusions), and the careful maintenance of their blood pressure.

Palinopsia necessitates a full ophthalmologic and neurologic history and physical exam. There are no clear guidelines on the work-up for illusory palinopsia, but it is not unreasonable to order automated visual field testing and neuroimaging since migraine aura can sometimes mimic seizures or cortical lesions. However, in a young patient without risk factors or other worrisome symptoms or signs (vasculopathy, history of cancer, etc.), neuroimaging for illusory palinopsia is low-yield but may grant the patient peace of mind.

The physical exam and work-up are usually non-contributory in illusory palinopsia. Diagnosing the etiology of illusory palinopsia is often based on the clinical history. Palinopsia is attributed to a prescription drug if symptoms begin after drug initiation or dose increase. Palinopsia is attributed to head trauma if symptoms begin shortly after the incident. Continuous illusory palinopsia in a migraineur is usually from persistent visual aura. HPPD can occur any time after hallucinogen ingestion and is a diagnosis of exclusion in patients with previous hallucinogen use. Migraines and HPPD are probably the most common causes of palinopsia. Idiopathic palinopsia may be analogous to the cerebral state in persistent visual aura with non-migraine headache or persistent visual aura without headache.

Due to the subjective nature of the symptoms and the lack of organic findings, clinicians may be dismissive of illusory palinopsia, sometimes causing the patient distress. There is considerable evidence in the literature confirming the symptom legitimacy, so validating the patient’s symptoms can help ease anxiety. Unidirectional visual trails or illusory symptoms confined to part of a visual field suggest cortical pathology and necessitate further work-up.

A 2014 meta-analysis of three small trials evaluating probiotics showed a slight improvement in management of chronic idiopathic constipation, but well-designed studies are necessary to know the true efficacy of probiotics in treating this condition.

Children with functional constipation often claim to lack the sensation of the urge to defecate, and may be conditioned to avoid doing so due to a previous painful experience. One retrospective study showed that these children did indeed have the urge to defecate using colonic manometry, and suggested behavioral modification as a treatment for functional constipation.

Most arachnoid cysts are asymptomatic, and do not require treatment. Where complications are present, leaving arachnoid cysts untreated, may cause permanent severe neurological damage due to the progressive expansion of the cyst(s) or hemorrhage (bleeding). However, with treatment most individuals with symptomatic arachnoid cysts do well.

More specific prognoses are listed below:

- Patients with impaired preoperative cognition had postoperative improvement after surgical decompression of the cyst.

- Surgery can resolve psychiatric manifestations in selected cases.

Cerebral angiography is the diagnostic standard. MRIs are usually normal.

There are few studies of the long-term outcomes of patients treated for MALS. According to Duncan, the largest and more relevant late outcomes data come from a study of 51 patients who underwent open surgical treatment for MALS, 44 of whom were available for long-term follow-up at an average of nine years following therapy. The investigators reported that among patients who underwent celiac artery decompression and revascularization, 75% remained asymptomatic at follow-up. In this study, predictors of favorable outcome included:

- Age from 40 to 60 years

- Lack of psychiatric condition or alcohol use

- Abdominal pain that was worse after meals

- Weight loss greater than 20 lb (9.1 kg)

Evidence for the treatment of thoracic outlet syndrome as of 2014 is poor.

Once visual loss has occurred, it becomes more problematic, but there are reports of recovered vision if blood transfusions and agents that raise blood pressure are administered within hours.