Brief periods of unconsciousness do no harm and are seldom symptoms of disease.

The main danger of vasovagal syncope (or dizzy spells from vertigo) is the risk of injury by falling while unconscious. Medication therapy could possibly prevent future vasovagal responses; however, for some individuals medication is ineffective and they will continue to have fainting episodes.

Treatment for lightheadedness depends on the cause or underlying problem. Treatment may include drinking plenty of water or other fluids (unless the lightheadedness is the result of water intoxication in which case drinking water is quite dangerous). If a sufferer is unable to keep fluids down from nausea or vomiting, they may need intravenous fluid. Sufferers should try eating something sugary and lying down or sitting and reducing the elevation of the head relative to the body (for example, by positioning the head between the knees).

Other simple remedies include avoiding sudden changes in posture when sitting or lying and avoiding bright lights.

Several essential electrolytes are excreted when the body perspires. When people are out in unusual or extreme heat for a long time, sweating excessively can cause a lack of some electrolytes, which in turn can cause lightheadedness.

Adenosine, an ultra-short-acting AV nodal blocking agent, is indicated if vagal maneuvers are not effective. If unsuccessful or the PSVT recurs diltiazem or verapamil are recommended. Adenosine may be safely used during pregnancy.

SVT that does not involve the AV node may respond to other anti-arrhythmic drugs such as sotalol or amiodarone.

If the person is hemodynamically unstable or other treatments have not been effective, synchronized electrical cardioversion may be used. In children this is often done with a dose of 0.5 to 1 J/Kg.

Treatment for reflex syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures that interrupt or prevent the pathophysiologic mechanism described above.

If there is evidence of overdose or it is suspected, the patient should be given gastric lavage, activated charcoal, or both; this could make the difference between life and death in a close situation. It can however aggravate the patient which should be taken into account.

The first line treatments are diazepam and a non-selective beta blocker; other antihypertensive drugs may also be used. It is important to note that not all benzodiazepines and beta blockers are safe to use in an adrenergic storm; for instance, alprazolam and propranolol; alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol mildly promotes some catecholamine release - each worsening the condition.

Adrenergic storms are often idiopathic in nature; however if there is an underlying condition, then that must be addressed after bringing the heart rate and blood pressure down.

Lightheadedness can be simply (and most commonly) an indication of a temporary shortage of blood or oxygen to the brain due to a drop in blood pressure, rapid dehydration from vomiting, diarrhea, or fever. Other causes are: low blood sugar, hyperventilation, Postural Orthostatic Tachycardia Syndrome, panic attacks, and anemia. It can also be a symptom of many other conditions, some of them serious, such as heart problems (including abnormal heart rhythm or heart attack), respiratory problems such as pulmonary embolism, and also stroke, bleeding, and shock. If any of these serious disorders is present, the individual will usually have additional symptoms such as chest pain, a feeling of a racing heart, loss of speech or change in vision.

Many people, especially as they age, experience lightheadedness if they arise too quickly from a lying or seated position. Lightheadedness often accompanies the flu, hypoglycaemia, common cold, or allergies.

Dizziness could be provoked by the use of antihistamine drugs, like levocetirizine or by some antibiotics or SSRIs. Nicotine or tobacco products can cause lightheadedness for inexperienced users. Narcotic drugs, such as codeine can also cause lightheadedness.

Caffeine may cause or exacerbate panic anxiety. Anxiety can temporarily increase during withdrawal from caffeine and various other drugs.

Increased and regimented aerobic exercise such as running have been shown to have a positive effect in combating panic anxiety. There is evidence that suggests that this effect is correlated to the release of exercise-induced endorphins and the subsequent reduction of the stress hormone cortisol.

There remains a chance of panic symptoms becoming triggered or exacerbated due to increased respiration rate that occurs during aerobic exercise. This increased respiration rate can lead to hyperventilation and hyperventilation syndrome, which mimics symptoms of a heart attack, thus inducing a panic attack. Benefits of incorporating an exercise regimen have shown best results when paced accordingly.

Heliophobia can be treated using talk therapy, exposure therapy, self-help techniques, support groups, cognitive-behavioral therapy, and relaxation techniques. For people who are severely heliophobic, anti-anxiety meditation is a recommended mode of treatment.

Individuals can benefit from a variety of physical therapy interventions. Persons with neurological/neuromuscular abnormalities may have breathing difficulties due to weak or paralyzed intercostal, abdominal and/or other muscles needed for ventilation. Some physical therapy interventions for this population include active assisted cough techniques, volume augmentation such as breath stacking, education about body position and ventilation patterns and movement strategies to facilitate breathing.

Along with the measure above, systemic immediate release opioids are beneficial in emergently reducing the symptom of shortness of breath due to both cancer and non cancer causes; long-acting/sustained-release opioids are also used to prevent/continue treatment of dyspnea in palliative setting. Pulmonary rehabilitation may alleviate symptoms in some people, such as those with COPD, but will not cure the underlying disease. There is a lack of evidence to recommend midazolam, nebulised opioids, the use of gas mixtures, or cognitive-behavioral therapy.

Sedative drugs are often prescribed for vertigo and dizziness, but these usually treat the symptoms rather than the underlying cause. Lorazepam (Ativan) is often used and is a sedative which has no effect on the disease process, but rather helps patients cope with the sensation.

Anti-nauseants, like those prescribed for motion sickness, are also often prescribed but do not affect the prognosis of the disorder.

Specifically for Meniere's disease a medication called Serc (Beta-histine) is available. There is some evidence to support its effectiveness in reducing the frequency of attacks. Also Diuretics, like Diazide (HCTZ/triamterene), are effective in many patients. Finally, ototoxic medications delivered either systemically or through the eardrum can eliminate the vertigo associated with Meniere's in many cases, although there is about a 10% risk of further hearing loss when using ototoxic medications.

Treatment is specific for underlying disorder of balance disorder:

- anticholinergics

- antihistamines

- benzodiazepines

- calcium channel antagonists, specifically Verapamil and Nimodipine

- GABA modulators, specifically gabapentin and baclofen

- Neurotransmitter reuptake inhibitors such as SSRIs, SNRIs and Tricyclics

Case reports and small randomized studies suggest benzodiazepines, propranolol, and anticholinergics may help treat acute akathisia, but are much less effective in treating chronic akathisia. Taylor et al. found success in lowering the dose of antipsychotic medication as an initial response to drug-induced akathisia, which should be done gradually, if possible. To minimize the risk of akathisia from antipsychotics, the clinician is advised to be conservative when increasing dosages.

One study showed vitamin B to be effective for the treatment of neuroleptic-induced akathisia.

Additional pharmacologic interventions found to have antiakathisia effects (especially for neuroleptic-induced akathisia) include ß-adrenergic antagonists (e.g., propranolol), benzodiazepines (e.g., lorazepam), anticholinergics (e.g., benztropine), and serotonin antagonists (e.g., cyproheptadine) as an alternative.

Meditation-relaxation (MR) therapy is a published direct treatment for sleep paralysis. The treatment was partly derived from the neuroscientific hypothesis suggesting that attempting movement during sleep paralysis (e.g., due to panic-like reactions) can lead to neurological distortions of one's "body image", possibly triggering hallucinations of shadowy human-like figures. The therapy is based on four steps applied during sleep paralysis: (1) reappraisal of the meaning of the attack (cognitive reappraisal); which entails closing one's eyes, avoid panicking and re-appraising the meaning of the attack as benign. (2) psychological and emotional distancing (emotion regulation); the sleeper reminds him- or herself that catastrophizing the event (i.e., fear and worry) will worsen and possibly prolong it; (3) inward focused-attention meditation; focusing attention inward on an emotionally salient positive object; 4) muscle relaxation; relaxing one's muscles, avoid controlling breathing and avoid attempting to move.There are preliminary case reports supporting this treatment, although no randomized clinical trials yet to show its effectiveness.

Some of the earliest work in treating sleep paralysis was done using a culturally sensitive cognitive-behavior therapy called CA-CBT. The work focuses on psycho-education and modifying catastrophic cognitions about the sleep paralysis attack. This approach has previously been used to treat sleep paralysis in Egypt, although clinical trials are lacking.

The first published psychosocial treatment for recurrent isolated sleep paralysis was cognitive-behavior therapy for isolated sleep paralysis (CBT-ISP). CBT-ISP is manualized, has an adherence manual for research purposes, and is intended to both prevent and disrupt ISP episodes. It begins with self-monitoring of symptoms, cognitive restructuring of maladaptive thoughts relevant to ISP (e.g., "the paralysis will be permanent"), and psychoeducation about the nature of sleep paralysis. Prevention techniques include ISP-specific sleep hygiene and the preparatory use of various relaxation techniques (e.g. diaphragmatic breathing, mindfulness, progressive muscle relaxation, meditation). Episode disruption techniques are first practiced in session and then applied during actual attacks. No controlled trial of CBT-ISP has yet been conducted to prove its effectiveness.

Dysequilibrium arising from bilateral loss of vestibular function – such as can occur from ototoxic drugs such as gentamicin – can also be treated with balance retraining exercises (vestibular rehabilitation) although the improvement is not likely to be full recovery.

Pharmacological techniques are often continued in conjunction with other treatment options. Doses of pain medications needed often drop substantially when combined with other techniques, but rarely are discontinued completely. Tricyclic antidepressants, such as amitriptyline, and sodium channel blockers, mainly carbamazepine, are often used to relieve chronic pain, and recently have been used in an attempt to reduce phantom pains. Pain relief may also be achieved through use of opioids, ketamine, calcitonin, and lidocaine.

Like many other phobias, lilapsophobia can often be treated using cognitive-behavioral therapy, but if it stems from post-traumatic stress disorder, then alternative therapy may be more recommended.

Cognitive behavioral therapy is the mainstay of treatment. At other times counseling, anti-anxiety and antidepressant medications have been shown to be of use.

In general, atrial flutter should be managed the same as atrial fibrillation. Because both rhythms can lead to the formation of a blood clot in the atrium, individuals with atrial flutter usually require some form of anticoagulation or antiplatelet agent. Both rhythms can be associated with dangerously fast heart rates and thus require medication to control the heart rate (such as beta blockers or calcium channel blockers) and/or rhythm control with class III antiarrhythmics (such as ibutilide or dofetilide). However, atrial flutter is more resistant to correction with such medications than atrial fibrillation. For example, although the class III antiarrhythmic agent ibutilide is an effective treatment for atrial flutter, rates of recurrence after treatment are quite high (70-90%). Additionally, there are some specific considerations particular to treatment of atrial flutter.

Atrial flutter is considerably more sensitive to electrical direct current cardioversion than atrial fibrillation, with a shock of only (20 to 50) J commonly being enough to cause a return to a normal heart rhythm (sinus rhythm). Exact placement of the pads does not appear important.

Various methods have been used to treat phantom limb pain. Doctors may prescribe medications to reduce the pain. Some antidepressants or antiepileptics have been shown to have a beneficial effect on reducing phantom limb pain. Often physical methods such as light massage, electrical stimulation, and hot and cold therapy have been used with variable results.

There are many different treatment options for phantom limb pain that are actively being researched. Most treatments do not take into account the mechanisms underlying phantom pains, and are therefore ineffective. However, there are a few treatment options that have been shown to alleviate pain in some patients, but these treatment options usually have a success rate less than 30%. It is important to note that this rate of success does not exceed the placebo effect. It is also important to note that because the degree of cortical reorganization is proportional to phantom limb pains, any perturbations to the amputated regions may increase pain perception.

Daily oral muscle physical therapy, or the administration of antidepressants have been reported as effective therapy for occlusal dysesthesia patients. Tooth grinding, and the replacement or removal of all dental work should be avoided in patients with occlusal dysesthesia, despite the frequent requests for further surgery often made by these patients.

Antidepressants are also often prescribed for scalp dysesthesia.

Prakash et al. found that many patients suffering from burning mouth syndrome (BMS), one variant of occlusal dysesthesia, also report painful sensations in other parts of the body. Many of the patients suffering from BMS met the classification of restless leg syndrome (RLS). About half of these patients also had a family history of RLS. These results suggest that some BMS symptoms may be caused by the same pathway as RLS in some patients, indicating that dopaminergic drugs regularly used to treat RLS may be effective in treating BMS as well.

Various devices (Urgent PC Neuromodulation System) may also be used. Botulinum toxin A (Botox) is approved by the Food and Drug Administration in adults with neurological conditions, including multiple sclerosis and spinal cord injury. Botulinum Toxin A injections into the bladder wall can suppress involuntary bladder contractions by blocking nerve signals and may be effective for up to 9 months. The growing knowledge of pathophysiology of overactive bladder fuelled a huge amount of basic and clinical research in this field of pharmacotherapy. A surgical intervention involves the enlargement of the bladder using bowel tissues, although generally used as a last resort. This procedure can greatly enlarge urine volume in the bladder.

OAB may be treated with electrical stimulation, which aims to reduce the contractions of the muscle that tenses around the bladder and causes urine to pass out of it. There are invasive and non-invasive electrical stimulation options. Non-invasive options include the introduction of a probe into the vagina or anus, or the insertion of an electrical probe into a nerve near the ankle with a fine needle. These non-invasive options appear to reduce symptoms while they are in use, and are better than no treatment, or treatment with drugs, or pelvic floor muscle treatment, but the quality of evidence is low. It is unknown which electrical stimulation option works best. Also, it is unknown whether the benefits last after treatment stops.