Recommended initial treatment for those with mild to moderate symptoms are simple analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) or the combination of paracetamol, aspirin, and caffeine. Several NSAIDs, including diclofenac and ibuprofen have evidence to support their use. Aspirin can relieve moderate to severe migraine pain, with an effectiveness similar to sumatriptan. Ketorolac is available in an intravenous formulation.

Paracetamol (also known as acetaminophen), either alone or in combination with metoclopramide, is another effective treatment with a low risk of adverse effects. Metoclopramide is also effective by itself. In pregnancy, paracetamol and metoclopramide are deemed safe as are NSAIDs until the third trimester.

Triptans such as sumatriptan are effective for both pain and nausea in up to 75% of people. When sumatriptan is taken with naproxen it works better. They are the initially recommended treatments for those with moderate to severe pain or those with milder symptoms who do not respond to simple analgesics. The different forms available include oral, injectable, nasal spray, and oral dissolving tablets. In general, all the triptans appear equally effective, with similar side effects. However, individuals may respond better to specific ones. Most side effects are mild, such as flushing; however, rare cases of myocardial ischemia have occurred. They are thus not recommended for people with cardiovascular disease, who have had a stroke, or have migraines that are accompanied by neurological problems. In addition, triptans should be prescribed with caution for those with risk factors for vascular disease. While historically not recommended in those with basilar migraines there is no specific evidence of harm from their use in this population to support this caution. They are not addictive, but may cause medication-overuse headaches if used more than 10 days per month.

The other primarily recommended treatment of acute attacks is subcutaneous or intranasal sumatriptan. Sumatriptan and zolmitriptan have both been shown to improve symptoms during an attack with sumatriptan being superior. Because of the vasoconstrictive side-effect of triptans, they may be contraindicated in people with ischemic heart disease.

Lithium, methysergide, and topiramate are recommended alternative treatments, although there is little evidence supporting the use of topiramate or methysergide. This is also true for tianeptine, melatonin and ergotamine. Valproate, sumatriptan and oxygen are not recommended as preventative measures. Botulinum toxin injections have shown limited success. Evidence for baclofen, botulinum toxin, and capsaicin is unclear.

Tension-type headaches can usually be managed with NSAIDs (ibuprofen, naproxen), acetaminophen or aspirin. Triptans are not helpful in tension-type headaches unless the person also has migraines. For chronic tension type headaches, amitriptyline is the only medication proven to help. Amitriptyline is a medication which treats depression and also independently treats pain. It works by blocking the reuptake of serotonin and norepinephrine, and also reduces muscle tenderness by a separate mechanism. Studies evaluating acupuncture for tension-type headaches have been mixed. Overall, they show that acupuncture is probably not helpful for tension-type headaches.

Abortive therapy for cluster headaches includes subcutaneous sumatriptan (injected under the skin) and triptan nasal sprays. High flow oxygen therapy also helps with relief.

For people with extended periods of cluster headaches, preventive therapy can be necessary. Verapamil is recommended as first line treatment. Lithium can also be useful. For people with shorter bouts, a short course of prednisone (10 days) can be helpful. Ergotamine is useful if given 1–2 hours before an attack. See cluster headaches for more detailed information.

Over-the-counter drugs, like acetaminophen, aspirin, or ibuprofen, can be effective but tend to only be helpful as a treatment for a few times in a week at most. Analgesic/sedative combinations are widely used (e.g., analgesic/antihistamine combinations like Syndol, Mersyndol and Percogesic, analgesic/barbiturate combinations such as Fiorinal). Frequent use of analgesics may, however, lead to medication overuse headache.

Botulinum toxin does not appear to be helpful.

People who have 15 or more headaches in a month may be treated with certain types of daily antidepressants which act to prevent continued tension headaches from occurring. In those who are predisposed to tension type headaches the first-line preventative treatment is amitriptyline, whereas mirtazapine and venlafaxine are second-line treatment options. Tricyclic antidepressants appear to be useful for prevention. Tricyclic antidepressants have been found to be more effective than SSRIs but have greater side effects. Evidence is poor for the use of SSRIs, propranolol, and muscle relaxants for prevention of tension headaches.

In general, any patient who has frequent headaches or migraine attacks should be considered as a potential candidate for preventive medications instead of being encouraged to take more and more painkillers or other rebound-causing medications. Preventive medications are taken on a daily basis. Some patients may require preventive medications for many years; others may require them for only a relatively short period of time such as six months. Effective preventive medications have been found to come from many classes of medications including neuronal stabilizing agents (aka anticonvulsants), antidepressants, antihypertensives, and antihistamines. Some effective preventive medications include Elavil (amitriptyline), Depakote (valproate), Topamax (topiramate), and Inderal (propranolol).

There is no specific treatment for NDPH. Often they are treated similar to migraines.

A number of medications have been used including amitriptyline, gabapentin, pregabalin, propranolol, and topiramate. There are no prospective placebo controlled trials of preventive treatment. In those with migrainous features treatment may be similar to migraines.

Opiates, or narcotics, tend to be avoided because of their side effects, including the development of medication overuse headaches and potential for dependency. NDPH is often associated with medication overuse. To avoid the development of medication overuse headaches, it is advised not to use pain relievers for more than nine days a month.

NDPH, like other primary headaches, has been linked to comorbid psychiatric conditions, mainly mood and anxiety and panic disorders. The spectrum of anxiety disorders, particularly panic disorder, should be considered in NDPH patients presenting with psychiatric symptoms. Simultaneous treatment of both disorders may lead to good outcomes.

Medications within the tetracycline family, mexiletine, corticosteroids and nerve blocks are being studied. Occipital nerve block have been reported to be helpful for some people. 23/71 people had undergone a nerve block for their severe headache. The NDPH-ICHD group responded to the nerve block much more often (88.9%) than the NDPH with migraine features (42.9% responded to nerve block).

Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.

MOH is common and can be treated. The overused medications must be stopped for the patient's headache to resolve. Clinical data shows that the treatment of election is abrupt drugs withdrawal, followed by starting prophylactic therapy. However, the discontinuation of overused drugs usually leads to the worsening of headache and the appearance of drug withdrawal symptoms (that greatly depend on the previously overused drugs and typically last from two to ten days and that are relieved by the further intake of the overused medication), which might reinforce the continuation of overuse. Where physical dependence or a rebound effect such as rebound headache is possible, gradual reduction of medication may be necessary. It is important that the patient's physician be consulted before abruptly discontinuing certain medications as such a course of action has the potential to induce medically significant physical withdrawal symptoms. Abruptly discontinuing butalbital, for example, can actually induce seizures in some patients, although simple over the counter analgesics can safely be stopped by the patient without medical supervision. A long-acting analgesic/anti-inflammatory, such as naproxen (500 mg twice a day), can be used to ease headache during the withdrawal period. Two months after the completion of a medication withdrawal, patients suffering from MOH typically notice a marked reduction in headache frequency and intensity.

Drug withdrawal is performed very differently within and across countries. Most physicians prefer inpatients programmes, however effective drug withdrawal may also be achieved in an outpatient setting in uncomplicated MOH patients (i.e. subjects without important co-morbidities, not overusing opioids or ergotaminics and who are at their first detoxification attempt). In the absence of evidence-based indications, in MOH patients the choice of preventive agent should be based on the primary headache type (migraine or TTH), on the drug side-effect profile, on the presence of co-morbid and co-existent conditions, on patient’s preferences, and on previous therapeutic experiences.

Following an initial improvement of headache with the return to an episodic pattern, a relevant proportion (up to 45%) of patients relapse, reverting to the overuse of symptomatic drugs.

Predictors of the relapse, and that could influence treatment strategies, are considered the type of primary headache, from which MOH has evolved, and the type of drug abused (analgesics, and mostly combination of analgesics, but also drugs containing barbiturates or tranquillisers cause significantly higher relapse rates), while gender, age, duration of disease and previous intake of preventative treatment do not seem to predict relapse rate.

MOH is clearly a cause of disability and, if not adequately treated, it represents a condition of risk of possible co-morbidities associated to the excessive intake of drugs that are not devoid of side-effect. MOH can be treated through withdrawal of the overused drug(s) and by means of specific approaches that focus on the development of a close doctor-patient relationship in the post-withdrawal period.

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.

Treatment depends on identifying behavior that triggers migraine such as stress, sleep deprivation, skipped meals, food sensitivities, or specific activities. Medicines used to treat retinal migraines include aspirin, other NSAIDS, and medicines that reduce high blood pressure.

Since migralepsy is, for all intents and purposes, a combination of migraines and epilepsy, the medication for the conditions supplied individually can be combined jointly in order to lessen the effects of both. It is also helpful that many antiepileptic drugs also work as antimigraines, lessening the number of medications that must be taken. Thus, while neither can be cured, they can be treated so that they occur less frequently and allow a patient to live a relatively normal life.

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

If drug treatment is found to be ineffective or causes disabling side effects, one of several neurosurgical procedures may be considered. The available procedures are believed to be less effective with type II (atypical) trigeminal neuralgia than with type I (typical or "classic") TN. Among present procedures, the most effective and long lasting has been found to be microvascular decompression (MVD), which seeks to relieve direct compression of the trigeminal nerve by separating and padding blood vessels in the vicinity of the emergence of this nerve from the brain stem, below the cranium.

Choice of a surgical procedure is made by the doctor and patient in consultation, based on the patient's pain presentation and health and the doctor's medical experience. Some neurosurgeons resist the application of MVD or other surgeries to atypical trigeminal neuralgia, in light of a widespread perception that ATN pain is less responsive to these procedures. However, recent papers suggest that in cases where pain initially presents as type I TN, surgery may be effective even after the pain has evolved into type II.

There is limited data on treating the visual disturbances associated with HPPD, persistent visual aura, or post-head trauma visual disturbances, and pharmaceutical treatment is empirically-based. It is not clear if the etiology or type of illusory symptom influences treatment efficacy. Since the symptoms are usually benign, treatment is based on the patient’s zeal and willingness to try many different drugs. There are cases which report successful treatment with clonidine, clonazepam, lamotrigine, nimodipine, topiramate, verapamil, divalproex sodium, gabapentin, furosemide, and acetazolamide, as these drugs have mechanisms that decrease neuronal excitability. However, other patients report treatment failure from the same drugs. Based on the available evidence and side-effect profile, clonidine might be an attractive treatment option. Many patients report improvement from sunglasses. FL-41 tinted lenses may provide additional relief, as they have shown some efficacy in providing relief to visually-sensitive migraineurs.

The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine, but the symptoms are usually less severe than those of classic migraine, so treatment is less likely to be required.

Most patients have persistent headaches, although about 15% will remit, and 8% will have a relapsing-remitting type. It is not infrequent for NDPH to be an intractable headache disorder that is unresponsive to standard headache therapies.

There is no known cure for CVS, but there are medications that can be used for treatment, intervention, and prevention. There is a growing body of publications on both individual cases and the experiences of the CVS cohort. Treatment is usually on an individual basis, based on trial and error.

The most common therapeutic strategies for those already in an attack are maintenance of salt balance by appropriate intravenous fluids and, in some cases, sedation. Having vomited for a long period prior to attending a hospital, patients are typically severely dehydrated. For a number of patients, potent anti-emetic drugs such as ondansetron (Zofran) or granisetron (Kytril), and dronabinol (Marinol) may be helpful in either preventing an attack, aborting an attack, or reducing the severity of an attack. Lifestyle changes may be recommended, such as extended rest and reduction of stress. Because the symptoms of CVS are similar (or perhaps identical) to those of the disease well-identified as "abdominal migraine", treatment of CVS with a regimen of anti-migraine drugs, such as topiramate and amitriptyline, is showing promise in preventing recurrent attacks.

Definitive treatment depends on the underlying cause of vertigo. Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet and intratympanic injections of the antibiotic gentamicin or surgical measures such as a shunt or ablation of the labyrinth in refractory cases.

Common drug treatment options for vertigo may include the following:

- Anticholinergics such as hyoscine hydrobromide (scopolamine)

- Anticonvulsants such as topiramate or valproic acid for vestibular migraines

- Antihistamines such as betahistine, dimenhydrinate, or meclizine, which may have antiemetic properties

- Beta blockers such as metoprolol for vestibular migraine

- Corticosteroids such as methylprednisolone for inflammatory conditions such as vestibular neuritis or dexamethasone as a second-line agent for Ménière's disease

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided. Several treatments may be necessary, and treatment will generally be repeated until either all symptoms resolve, or no further improvement is apparent.

There is no established treatment for visual snow. It is difficult to resolve visual snow with treatment, but it is possible to reduce symptoms and improve quality of life through treatment.

Medications that may be used include lamotrigine, acetazolamide, or verapamil. But these do not always result in benefits.

There is no cure for Ménière's disease but medications, diet, physical therapy and counseling, and some surgical approaches can be used to manage it.

For most balance and gait disorders, some form of displacement exercise is thought helpful (for example walking, jogging, or bicycling but not on a treadmill or stationary bicycle). This has not been well-studied in MdDS. Medications that suppress the nerves and brain circuits involved in balance (for example, the benzodiazepine clonazepam) have been noted to help and can lower symptoms, but it is not a cure. It is not known whether medication that suppress symptoms prolongs symptom duration or not. Vestibular therapy has not proved to be effective in treating MdDS.

Additional research is being undertaken into the neurological nature of this syndrome through imaging studies. The disorder remains incurable and permanent if the symptoms do not remit in a short period of time.