Anticipating later botox therapy for migraine, early work by Jancsó "et al." found some success in treatment using denervation or pretreatment with capsaicin to prevent uncomfortable symptoms of neurogenic inflammation.

A recent (2010) study of the treatment of migraine with CGRP blockers shows promise. In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks, but elevated liver enzymes in two participants were found. Other therapies and other links in the neurogenic inflammatory pathway for interruption of disease are under study, including migraine therapies.

Noting that botulinum toxin has been shown to have an effect on inhibiting neurogenic inflammation, and evidence suggesting the role of neurogenic inflammation in the pathogenesis of psoriasis, the University of Minnesota has a pilot clinical trial underway to follow up on the observation that patients treated with botulinum toxin for dystonia had dramatic improvement in psoriasis.

Astelin (Azelastine) "is indicated for symptomatic treatment of vasomotor rhinitis including rhinorrhea, nasal congestion, and post nasal drip in adults and children 12 years of age and older."

Statins appear to "decrease expression of the proinflammatory neuropeptides calcitonin gene-related peptide and substance P in sensory neurons," and so might be of use in treating diseases presenting with predominant neurogenic inflammation.

A number of medications can be used to treat this disorder. Alpha blockers and/or antibiotics appear to be the most effective with NSAIDs such as ibuprofen providing lesser benefit.

- Treatment with antibiotics is controversial. Some have found benefits in symptoms while others have questioned the utility of a trial of antibiotics. Antibiotics are known to have anti-inflammatory properties and this has been suggested as an explanation for their partial efficacy in treating CPPS. Antibiotics such as fluoroquinolones, tetracyclines, and macrolides have direct anti-inflammatory properties in the absence of infection, blocking inflammatory chemical signals (cytokines) such as interleukin-1 (IL-1), interleukin-8 and tumor necrosis factor (TNF), which coincidentally are the same cytokines found to be elevated in the semen and EPS of men with chronic prostatitis.

- The effectiveness of alpha blockers (tamsulosin, alfuzosin) is questionable in men with CPPS. A 2006 meta-analysis found that they are moderately beneficial when the duration of therapy was at least 3 months.

- An estrogen reabsorption inhibitor such as mepartricin improves voiding, reduces urological pain and improves quality of life in patients with chronic non-bacterial prostatitis.

- Therapies that have not been properly evaluated in clinical trials although there is supportive anecdotal evidence include gabapentin, benzodiazepines, and amitriptyline.

Category III prostatitis may have no initial trigger other than anxiety, often with an element of OCD, panic disorder, or other anxiety-spectrum problem. This is theorized to leave the pelvic area in a sensitized condition resulting in a loop of muscle tension and heightened neurological feedback (neural pain wind-up). Current protocols largely focus on stretches to release overtensed muscles in the pelvic or anal area (commonly referred to as trigger points) including digital intrarectal massage, physical therapy to the area, and progressive relaxation therapy to reduce causative stress.

Aerobic exercise can help those sufferers who are not also suffering from chronic fatigue syndrome or whose symptoms are not exacerbated by exercise. Acupuncture has reportedly benefited some patients.

For chronic nonbacterial prostatitis (Cat III), also known as CP/CPPS, which makes up the majority of men diagnosed with "prostatitis", a treatment called the "Wise–Anderson Protocol" (aka the "Stanford Protocol"), has recently been published. This is a combination of:

- Medication (using tricyclic antidepressants and benzodiazepines)

- Psychological therapy (paradoxical relaxation, an advancement and adaptation, specifically for pelvic pain, of a type of progressive relaxation technique developed by Edmund Jacobson during the early 20th century)

- Physical therapy (trigger point release therapy on pelvic floor and abdominal muscles, and also yoga-type exercises with the aim of relaxing pelvic floor and abdominal muscles).

Biofeedback physical therapy to relearn how to control pelvic floor muscles may be useful. Biofeedback is satisfactory for treatment of chronic prostatitis (with mainly voiding problems) during puberty.

Tentative evidence supports the use of bisphosphonates, calcitonin, and ketamine. Doing nerve blocks with guanethidine appears to be harmful. Evidence for sympathetic nerve blocks generally is insufficient to support their use. Intramuscular botulinum injections may benefit people with symptoms localized to one extremity.

Ketamine, a dissociative anesthetic, appears promising as a treatment for complex regional pain syndrome. It may be used in low doses if other treatments have not worked. No benefit on either function or depression, however, has been seen.

Where an underlying neoplasm is the cause, treatment of this condition is indicated in order to reduce progression of symptoms. For cases without a known cause, treatment involves suppression of the immune system with corticosteroid treatment, intravenous immunoglobulin, immunosuppressive agents like Rituximab, Cellcept, or Imuran or plasmapheresis.

Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including IL-1, Interleukin 6 (IL-6), and TNF-alpha (TNFα), which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation. In a later study, researchers provided rats dietary levels of magnesium that were reduced but still within the range of dietary intake found in the human population, and observed an increase in substance P, TNF alpha (TNFα) and Interleukin-1 beta (IL-1β), followed by exacerbated bone loss. These and other data suggest that deficient dietary magnesium intake, even at levels not uncommon in humans, may trigger neurogenic inflammation and lead to an increased risk of osteoporosis.

Exercise is a promising mechanism of prevention and treatment for various diseases characterized by neuroinflammation. Aerobic exercise is used widely to reduce inflammation in the periphery. Exercise has been shown to decreases proliferation of microglia in the brain, decrease hippocampal expression of immune-related genes, and reduce expression of inflammatory cytokines such as TNF-α.

Costochondritis may be treated with physical therapy (including ultrasonic, TENS, with or without nerve stimulation) or with medication. Treatment may involve the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or other pain relief medications (analgesics) such as acetaminophen. Severe cases of costochondritis may call for the use of opioid medications such as hydrocodone or oxycodone, tricyclic antidepressant medications such as amitriptyline for pain from chronic costochondritis, or anti-epileptic drugs such as gabapentin may be used. Oral or injected corticosteroids may be used for cases of costochondritis unresponsive to treatment by NSAIDs; however, this treatment has not been the subject of study by rigorous randomized controlled trials and its practice is currently based on clinical experience. Rest from stressful physical activity is often advised during the recovery period.

There is evidence for a link between inflammation and depression. Inflammatory processes can be triggered by negative cognitions or their consequences, such as stress, violence, or deprivation. Thus, negative cognitions can cause inflammation that can, in turn, lead to depression.

In addition there is increasing evidence that inflammation can cause depression because of the increase of cytokines, setting the brain into a "sickness mode". Classical symptoms of being physically sick like lethargy show a large overlap in behaviors that characterize depression. Levels of cytokines tend to increase sharply during depressive episodes in manics and drop off during remission. Furthermore, it has been shown in clinical trials that anti-inflammatory medicines taken in addition to antidepressants not only significantly improves symptoms but also increases the proportion of subjects positively responding to treatment.

Inflammations that lead to serious depression could be caused by common infections such as those caused by a virus, bacteria or even parasites.

H-wave therapy (HWT) is a form of electrical stimulation that produces a direct, localized effect on the conduction of underlying nerves. The electrical stimulation used in HWT differs from other forms of electrical stimulation such as TENS in terms of its waveform; it is intended to emulate the H waveform found in nerve signals, thus permitting the machine to use less power while attaining greater and deeper penetration of its low-frequency current. The waves used in HWT are distinct from the H-waves that are part of electromyography. It has been used in the treatment of pain related to diabetic neuropathy, muscle sprains, temporomandibular joint disorders, type I complex regional pain syndrome as well as the healing of wounds such as diabetic ulcers. This electroanalgesic modality was originally recommended as an alternative to TENS for dental analgesia. In a 1999 randomized controlled trial involving a mechanical pain model, the analgesic effects of HWT were found to be short-lasting and identical to those provided by TENS therapy. HWT has not been shown effective in reducing pain in cases other than diabetic neuropathy, nor has it been shown effective in reducing edema or swelling, and it has specifically not been shown effective in treating chronic pain due to ischemia.

Given that localized acute inflammation is a necessary component for muscle growth, and that chronic low-grade inflammation is associated with a disruption of anabolic signals initiating muscle growth, it has been theorized that a signal-to-noise model may best describe the relationship between inflammation and muscle growth. By keeping the "noise" of chronic inflammation to a minimum, the localized acute inflammatory response signals a stronger anabolic response than could be achieved with higher levels of chronic inflammation.

Transcutaneous acupoint electrical stimulation, or TAES, is a variant of TENS therapy that involves applying cutaneous electrodes at classical Chinese acupoints and stimulating with alternating high- and low-frequency electric current ("dense-disperse"). Acupoint stimulation is as effective as dermatomal stimulation in producing an analgesic-sparing effect after lower abdominal surgery

Because neuroinflammation has been associated with a variety of neurodegenerative diseases, there is increasing interest to determine whether reducing inflammation will reverse neurodegeneration. Inhibiting inflammatory cytokines, such as IL-1β, decreases neuronal loss seen in neurodegenerative diseases. Current treatments for multiple sclerosis include interferon-B, Glatiramer actetate, and Mitoxantrone, which function by reducing or inhibiting T Cell activation, but have the side effect of systemic immunosuppression In Alzheimer's disease, the use of non-steroidal anti-inflammatory drugs decreases the risk of developing the disease. Current treatments for Alzheimer's disease include NSAIDs and glucocorticoids. NSAIDs function by blocking conversion of prostaglandin H2 into other prostaglandins (PGs) and thromboxane (TX). Prostoglandins and thromboxane act as inflammatory mediators and increase microvascular permeability.

Trochleitis is diagnosed based on three criteria: 1) demonstration of inflammation of superior oblique tendon/ trochlea region, 2) periorbital pain and tenderness to palpation in the area of the sore trochlea, and 3) worsening of pain on attempted vertical eye movement, particularly with adduction of the eye. It is important to identify trochleitis because it is a treatable condition and the patient can benefit much from pain relief. Treatment consists of a single injection of corticosteroids to the affected peritrochlear region. A specific "cocktail" consisting of 0.5 ml of depomedrol (80 mg/ml) and 0.5 ml of 2% lidocaine can be injected into the trochlea; immediate relief due to the effects of the local anesthetic indicates successful placement. However, great care must be taken as the injection is in the region of several arteries, veins and nerves. The needle should not be too small (so as not to penetrate tiny structures), the surgeon should draw back on the syringe (to ensure not have pierced a vessel), the lidocaine should not contain epinephrine (which could cause vasospasm), and the pressure of the injection must always be controlled. Only a limited number of injections can be made as they would otherwise lead to muscle atrophy. Diagnosis can be confirmed by response to this treatment; pain and swelling are expected to disappear in 48–72 hours. Some patients experience recurrence of trochleitis.

Treatment of aortitis depends on the underlying cause. Infectious causes commonly require antibiotic treatment, while those associated with autoimmune vasculitides are generally treated with steroids.

Management includes the following treatment priorities: stop the inflammation, treat complications, prevent and monitor for re-occurrence.

Antibiotic therapy has to overcome the blood/prostate barrier that prevents many antibiotics from reaching levels that are higher than minimum inhibitory concentration. A blood-prostate barrier restricts cell and molecular movement across the rat ventral prostate epithelium. Treatment requires prolonged courses (4–8 weeks) of antibiotics that penetrate the prostate well. The fluoroquinolones, tetracyclines and macrolides have the best penetration. There have been contradictory findings regarding the penetrability of nitrofurantoin , quinolones (ciprofloxacin, levofloxacin), sulfas (Bactrim, Septra), doxycycline and macrolides (erythromycin, clarithromycin). This is particularly true for gram-positive infections.

In a review of multiple studies, Levofloxacin (Levaquin) was found to reach prostatic fluid concentrations 5.5 times higher than Ciprofloxacin, indicating a greater ability to penetrate the prostate.

Persistent infections may be helped in 80% of patients by the use of alpha blockers (tamsulosin (Flomax), alfuzosin), or long term low dose antibiotic therapy. Recurrent infections may be caused by inefficient urination (benign prostatic hypertrophy, neurogenic bladder), prostatic stones or a structural abnormality that acts as a reservoir for infection.

In theory, the ability of some strains of bacteria to form biofilms might be one factor amongst others to facilitate development of chronic bacterial prostatitis.

Escherichia coli extract and cranberry have a potentially preventive effect on the development of chronic bacterial prostatitis, while combining antibiotics with saw palmetto, lactobacillus sporogens and arbutin may lead to better treatment outcomes.

Bacteriophages hold promise as another potential treatment for chronic bacterial prostatatis.

The addition of prostate massage to courses of antibiotics was previously proposed as being beneficial and prostate massage may mechanically break up the biofilm and enhance the drainage of the prostate gland. However, in more recent trials, this was not shown to improve outcome compared to antibiotics alone.

The management of rhinitis depends on the underlying cause.

For allergic rhinitis, intranasal corticosteroids are recommended. For severe symptoms intranasal antihistamines may be added.

Exercise can improve symptoms, as can revascularization. Both together may be better than one intervention of its own.

Pharmacological options exist, as well. Medicines that control lipid profile, diabetes, and hypertension may increase blood flow to the affected muscles and allow for increased activity levels. Angiotensin converting enzyme inhibitors, beta-blockers, antiplatelet agents (aspirin and clopidogrel), naftidrofuryl, pentoxifylline, and cilostazol (selective PDE3 inhibitor) are used for the treatment of intermittent claudication. However, medications will not remove the blockages from the body. Instead, they simply improve blood flow to the affected area.

Catheter-based intervention is also an option. Atherectomy, stenting, and angioplasty to remove or push aside the arterial blockages are the most common procedures for catheter-based intervention. These procedures can be performed by interventional radiologists, interventional cardiologists, vascular surgeons, and thoracic surgeons, among others.

Surgery is the last resort; vascular surgeons can perform either endarterectomies on arterial blockages or perform an arterial bypass. However, open surgery poses a host of risks not present with catheter-based interventions.

Over time, the relapse rate is high, exceeding 50%. However, recent research indicates that combination therapies offer a better prognosis than antibiotics alone.

A 2007 study showed that repeated combination pharmacological therapy with antibacterial agents (ciprofloxacin/azithromycin), alpha-blockers (alfuzosin) and Serenoa repens extracts may eradicate infection in 83.9% of patients with clinical remission extending throughout a follow-up period of 30 months for 94% of these patients.

A 2014 study of 210 patients randomized into two treatment groups found that recurrence occurred within 2 months in 27.6% of the group using antibiotics alone (prulifloxacin 600 mg), but in only 7.8% of the group taking prulifloxacin in combination with Serenoa repens extract, Lactobacillus Sporogens and Arbutin.

While conservative approaches for rehabilitation are ideal, some patients will not improve and surgery is still an option. Patients with large cervical disk bulges may be recommended for surgery, however most often conservative management will help the herniation regress naturally. Procedures such as foraminotomy, laminotomy, or discectomy may be considered by neurosurgeons and orthopedic surgeons.

Catheterization methods range from intermittent catheterization, which involves no surgery or permanently attached appliances, to the creation of a stoma, which bypasses the urethra to empty the bladder directly.

Intermittent catheterization is the use, several times a day, of straight catheters (which are usually disposable or single-use products) to empty the bladder. This can be done independently by the patient, or with help, in the case that the patient lacks the dexterity to manage the catheter. For patients who are unable to tolerate disposable straight catheters, a Foley catheter allows continuous drainage of urine into a sterile drainage bag that is worn by the patient.

Other treatments involve creation of a stoma that is continent and readily accepts a catheter. These are known as Mitrofanoff mechanisms. An example of this treatment is the creation of an Indiana pouch. Additionally, a muscarinic agonist like Bethanechol may also be used, particularly in the postpartum or postoperative period. Function of the stoma may be augmented by periodic injections of botulinum toxin to relax one of the two sphincters involved in normal urination. The effect is longer-lasting with botulinum toxin type A than with type B. This use of botulinum toxin is discussed at length in the French medical literature.

Blocking agents of the adrenoceptors alpha 1/alpha 2 are typically used to treat the effects of the vasoconstriction associated with vascular claudication. Cilostazol (trade name: Pletal) is FDA approved for intermittent claudication. It is contraindicated in patients with heart failure, and improvement of symptoms may not be evident for two to three weeks.

Neurogenic claudication can be treated surgically with spinal decompression.

Ideally, effective treatment aims to resolve the underlying cause and restores the nerve root to normal function. Common conservative treatment approaches include physical therapy and chiropractic. A systematic review found moderate quality evidence that spinal manipulation is effective for the treatment of acute lumbar radiculopathy and cervical radiculopathy. Only low level evidence was found to support spinal manipulation for the treatment of chronic lumbar radiculopathies, and no evidence was found to exist for treatment of thoracic radiculopathy.

Treatment for acquired noninflammatory myopathy is directed towards resolution of the underlying condition, pain management, and muscle rehabilitation.

Drug induced ANIMs can be reversed or improved by tapering off of the drugs and finding alternative care. Hyperthyroidism induced ANIM can be treated through anti-thyroid drugs, surgery and not eating foods high in Iodine such as kelp. Treatment of the hyperthyroidism results in complete recovery of the myopathy. ANIM caused by vitamin D deficiency can easily be resolved by taking vitamin supplements and increasing one's exposure to direct sunlight.

Pain can be managed through massaging affected areas and the use of nonsteroidal anti-inflammatory drugs (NSAIDs).

Exercise, physical therapy, and occupational therapy can be used to rehabilitate affected muscle areas and resist the atrophy process.

As with all myopathies, the use of walkers, canes, and braces can assist with the mobility of the afflicted individual.