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.

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.

Treatment of hypokalemic periodic paralysis focuses on preventing further attacks and relieving acute symptoms. Avoiding carbohydrate-rich meals, strenuous exercise and other identified triggers, and taking acetazolamide (Diamox®) or another carbonic anhydrase inhibitor, may help prevent attacks of weakness. Some patients also take potassium-sparing diuretics such as spironolactone (Aldactone®) to help maintain potassium levels.

Paralysis attacks can be managed by drinking one of various potassium salts dissolved in water (debate exists over which, if any one in particular, is best used, but potassium chloride and bicarbonate are common). Rapidly absorbed boluses of liquid potassium are generally needed to abort an attack, but some patients also find positive maintenance results with time-released potassium tablets. IV potassium is seldom justified unless the patient is unable to swallow. Daily potassium dosage may need to be much higher than for potassium replacement from simple hypokalemia: 100-150 mEqs of potassium is often needed to manage daily fluctuations in muscle strength and function.

When someone presents with an ischemic event, treatment of the underlying cause is critical for prevention of further episodes.

Anticoagulation with warfarin or heparin may be used if the patient has atrial fibrillation.

Operative procedures such as carotid endarterectomy and carotid stenting may be performed if the patient has a significant amount of plaque in the carotid arteries associated with the local ischemic events.

Initial treatment can be medical, involving the use of drugs like isoprenaline (Isuprel) and epinephrine (adrenaline). Definitive treatment is surgical, involving the insertion of a pacemaker – most likely one with sequential pacing such as a DDI mode as opposed to the older VVI mechanisms, and the doctor may arrange the patient to undergo electrocardiography to confirm this type of treatment.

Alteplase (tpa) is an effective medication for acute ischemic stroke. When given within 3 hours, treatment with tpa significantly improves the probability of a favourable outcome versus treatment with placebo.

The outcome of brain ischemia is influenced by the quality of subsequent supportive care. Systemic blood pressure (or slightly above) should be maintained so that cerebral blood flow is restored. Also, hypoxaemia and hypercapnia should be avoided. Seizures can induce more damage; accordingly, anticonvulsants should be prescribed and should a seizure occur, aggressive treatment should be undertaken. Hyperglycaemia should also be avoided during brain ischemia.

If the above treatment is not possible venlafaxine is recommended. Evidence for benefit is not as good.

Previous treatments include tricyclic antidepressants such as imipramine, clomipramine or protriptyline. Monoamine oxidase inhibitors may be used to manage both cataplexy and the REM sleep-onset symptoms of sleep paralysis and hypnagogic hallucinations.

Sodium oxybate and gamma-hydroxybutyrate has been found to be effective at reducing the number of cataplexy episodes. Sodium oxybate is generally safe. Sodium oxybate is typically the recommended treatment.

Patients should discuss with their physician possible causes for their VBI symptoms. As discussed above, postural changes, exercise, and dehydration are some of the likely culprits. Treatment usually involves lifestyle modifications. For example, if VBI is attributed mainly to postural changes, patients are advised to slowly rise to standing position after sitting for a long period of time. An appropriate exercise regimen for each patient can also be designed in order to avoid the excessive pooling of blood in the legs. Dehydrated patients are often advised to increase their water intake, especially in hot, dry climates. Finally, when applicable, patients are often advised to stop smoking and to control their hypertension, diabetes, and cholesterol level.

In the event that a patient suffers a “drop attack,” and especially for the elderly population, the most important action is to be evaluated for associated head or other injuries. To prevent drop attacks, patients are advised to “go to the ground” before the knees buckle and shortly after feeling dizzy or experiencing changes in vision. Patients should not be concerned about the social consequences of suddenly sitting on the floor, whether in the mall or sidewalk, as such actions are important in preventing serious injuries.

Sometimes, to prevent further occlusion of blood vessels, patients are started on an antiplatelet agent (aspirin, clopidogrel, or aspirin/dipyridamole) or sometimes an anticoagulant (warfarin) once hemorrhage has been excluded with imaging.

For treatment of vertebrobasilar stenosis due to atherosclerosis, researchers from Stanford University found that intracranial angioplasty can be performed with an annual stroke rate in the territory of treatment of 3.2% and 4.4% for all strokes, including periprocedural events. Randomized control trials need to be performed.

A drop attack is a sudden fall without loss of consciousness. Drop attacks stem from diverse mechanisms, including orthopedic causes (for example, leg weakness and knee instability), hemodynamic causes (for example, transient vertebrobasilar insufficiency, a type of interruption of blood flow to the brain), and neurologic causes (such as epileptic seizures or unstable vestibular function), among other reasons. Those afflicted typically experience abrupt leg weakness, sometimes after sudden movement of the head. The weakness may persist for hours.

The term "drop attack" is used to categorize otherwise unexplained falls from a wide variety of causes and is considered ambiguous medical terminology; drop attacks are currently reported much less often than in the past, possibly as a result of better diagnostic precision. By definition, drop attacks exclude syncopal falls (fainting), which involve short loss of consciousness. In neurology, the term "drop attack" is used to describe certain types of seizure which occur in epilepsy. Drop attacks that have a vestibular origin within the inner ear may be experienced by some people in the later stages of Ménière's disease (these may be referred to as Tumarkin [drop] attacks, or as Tumarkin's otolithic crisis).

Drop attacks often occur in elderly people. Falls in older adults happen for many reasons, and the goals of health care include preventing any preventable falls and correctly diagnosing any falls that do happen.

Early treatment is essential to keep the affected limb viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularisation, or amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. Continuous IV unfractionated heparin has been the traditional agent of choice.

If the condition of the ischemic limb is stabilized with anticoagulation, recently formed emboli may be treated with catheter-directed thrombolysis using intraarterial infusion of a thrombolytic agent (e.g., recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase). A percutaneous catheter inserted into the femoral artery and threaded to the site of the clot is used to infuse the drug. Unlike anticoagulants, thrombolytic agents work directly to resolve the clot over a period of 24 to 48 hours.

Direct arteriotomy may be necessary to remove the clot. Surgical revascularization may be used in the setting of trauma (e.g., laceration of the artery). Amputation is reserved for cases where limb salvage is not possible. If the patient continues to have a risk of further embolization from some persistent source, such as chronic atrial fibrillation, treatment includes long-term oral anticoagulation to prevent further acute arterial ischemic episodes.

Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects of hypoxia. Reduction of body temperature also reduces the inflammation response and reperfusion injury. For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reduce reperfusion injury.

There is no general treatment for patients with a seizure disorder. Each treatment plan is specifically tailored to the individual patient based on their diagnosis and symptoms. Treatment options may include medical therapy, nerve stimulation, dietary therapy, or surgery, as appropriate. Clinical trials may also be a valuable treatment alternative.

Usually, anticonvulsants are given based on other symptoms and / or associated problems.

Because the areas of the cerebellum which determine increases and decreases in muscular tonus are close together, people experiencing atonic seizures are most likely experiencing myoclonic ones too, at some point. This may play a role in therapy and diagnostic.

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 undiagnosed (or untreated), Stokes–Adams attacks have a 50% mortality within a year of the first episode. The prognosis following treatment is very good.

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.

Treatment of the primary gastroenterological distress is the first concern, mitigation of gastric symptoms will also alleviate cardiac distress.

- Anticholinergics, magnesium, or sodium (to raise blood pressure) supplements

- Anticonvulsants have eliminated all symptoms in some RS sufferers; Lorazepam, Oxcarbazepine increase GI motility, reduce vagus "noise" (sodium channel blocking believed to contribute to positive effects)

- Alpha blockers may increase gi motility if that is an issue, also 5 mg to 10 mg amitriptyline if motility is an issue that can't be solved by other methods

- antigas - simethicone, beano, omnimax reduces epigastric pressure

- Antacids - nexium, tums, Pepcid AC, rolaids, etc. reduces acid reflux in the case of hiatal hernia or other esophageal type RS.

- Vagusectomy

- Beta blockers - reduces contractility and automaticity of the heart which reduces irregular rhythms but also lowers blood pressure when symptoms occur, and further reduces perfusion ex: Atenolol, this will control disarrhythmia, but can precipitate Prinzmetal Angina and Heart block substantially.

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.

Medium-term (and less well-demonstrated) treatments of hypotension include:

- Blood sugar control (80–150 by one study)

- Early nutrition (by mouth or by tube to prevent ileus)

- Steroid support

To relieve reactive hypoglycemia, the NIH recommends taking the following steps:

- Avoiding or limiting sugar intake;

- Exercising regularly; exercise increases sugar uptake which decreases excessive insulin release

- Eating a variety of foods, including meat, poultry, fish, or nonmeat sources of protein, foods such as whole-grains, fruits, nuts, vegetables, and dairy products;

- Choosing high-fiber foods.

Other tips to prevent sugar crashes include:

- Avoiding eating meals or snacks composed entirely of carbohydrates; simultaneously ingest fats and proteins, which have slower rates of absorption.

- Consistently choosing longer lasting, complex carbohydrates to prevent rapid blood-sugar dips in the event that one does consume a disproportionately large amount of carbohydrates with a meal

- Monitoring any effects medication may have on symptoms.

Low-carbohydrate diet and/or frequent small split meals is the first treatment of this condition. The first important point is to add small meals at the middle of the morning and of the afternoon, when glycemia would start to decrease. If adequate composition of the meal is found, the fall in blood glucose is thus prevented. Patients should avoid rapidly absorbable sugars and thus avoid popular soft drinks rich in glucose or sucrose. They should also be cautious with drinks associating sugar and alcohol, mainly in the fasting state.

As it is a short-term ailment, a sugar crash does not usually require medical intervention in most people. The most important factors to consider when addressing this issue are the composition and timing of foods.

Acute low blood sugar symptoms are best treated by consuming small amounts of sweet foods, so as to regain balance in the body’s carbohydrate metabolism. Suggestions include sugary foods that are quickly digested, such as:

- Dried fruit

- Soft drinks

- Juice

- Sugar as sweets, tablets or cubes.

Aggressive risk factor modification is required for effective treatment of microvascular angina where exercise plays a major role. Several other treatment strategies including b-blockers, angiotensin-converting enzyme inhibitors, ranolazine, l-arginine, statin drugs and potentially estrogen replacement therapy have been shown to relieve anginal symptoms as well as improve vascular function. Nitrates may be effective for symptom relief. Further studies are required to determine whether specific treatments are associated with improved survival as well as decreased symptoms.

The prognosis for periodic paralysis varies. Overactivity, a diet that is not low in sodium and carbohydrates, or simply an unfortunate gene mutation can lead to a type of chronic, low level weakness called an "abortive attack," or to permanent muscle damage. Abortive attacks often respond to extra potassium, cutting carbohydrates, getting plenty of rest, increasing doses of medication and gentle daily exercise such as short walks. Permanent muscle weakness is just what it sounds like: Permanent, irreparable damage to the muscles and associated weakness. Vacuoles and tubular aggregates form in and destroy healthy muscle tissue. This type of damage can typically be observed via a muscle biopsy. Not even anabolic steroids can repair this type of muscular damage.

Life span is expected to be normal, but attacks can drop potassium to levels low enough to cause life-threatening breathing problems or heart arrhythmia. Patients often report muscle pain and cognitive problems during attacks. Migraines occur in up to 50% of all hypokalemic periodic paralysis patients and may include less common symptoms like phantom smells, sensitivity to light and sound or loss of words. Medical literatures states that muscle strength is normal between attacks, but patients often report that their baseline strength is in fact lower than that of healthy individuals.

Because there are dozens of possible gene mutations, some drugs and treatments that work fine for one patient will not work for another. For example, most patients do well on acetazolamide, but some don't. Some patients will do well with extra magnesium (the body's natural ion channel blocker) or fish oil, while these same nutrients will make other patients worse. Patients and caregivers should take extreme caution with all new drugs and treatment plans.

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

The treatment for hypotension depends on its cause. Chronic hypotension rarely exists as more than a symptom. Asymptomatic hypotension in healthy people usually does not require treatment. Adding electrolytes to a diet can relieve symptoms of mild hypotension. A morning dose of caffeine can also be effective. In mild cases, where the patient is still responsive, laying the person in dorsal decubitus (lying on the back) position and lifting the legs increases venous return, thus making more blood available to critical organs in the chest and head. The Trendelenburg position, though used historically, is no longer recommended.

Hypotensive shock treatment always follows the first four following steps. Outcomes, in terms of mortality, are directly linked to the speed that hypotension is corrected. Still-debated methods are in parentheses, as are benchmarks for evaluating progress in correcting hypotension. A study on septic shock provided the delineation of these general principles. However, since it focuses on hypotension due to infection, it is not applicable to all forms of severe hypotension.

1. Volume resuscitation (usually with crystalloid)

2. Blood pressure support with a vasopressor (all seem equivalent with respect to risk of death, with norepinephrine possibly better than dopamine). Trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

3. Ensure adequate tissue perfusion (maintain SvO2 >70 with use of blood or dobutamine)

4. Address the underlying problem (i.e., antibiotic for infection, stent or CABG (coronary artery bypass graft surgery) for infarction, steroids for adrenal insufficiency, etc...)

The best way to determine if a person will benefit from fluids is by doing a passive leg raise followed by measuring the output from the heart.

Medications, while included in guidelines, have not been shown to improve survival to hospital discharge following out-of-hospital cardiac arrest. This includes the use of epinephrine, atropine, lidocaine, and amiodarone. Epinephrine is generally recommended every five minutes. Vasopressin overall does not improve or worsen outcomes compared to epinephrine.

Epinephrine does appear to improve short-term outcomes such as return of spontaneous circulation. Some of the lack of long-term benefit may be related to delays in epinephrine use. While evidence does not support its use in children guidelines state its use is reasonable. Lidocaine and amiodarone are also deemed reasonable in children with cardiac arrest who have a shockable rhythm. The general use of sodium bicarbonate or calcium is not recommended.

The 2010 guidelines from the American Heart Association no longer contain the recommendation for using atropine in pulseless electrical activity and asystole due to the lack of evidence for its use. Neither lidocaine nor amiodarone, in those who continue in ventricular tachycardia or ventricular fibrillation despite defibrillation, improves survival to hospital discharge but both equally improve survival to hospital admission.

Thrombolytics when used generally may cause harm but may be of benefit in those with a confirmed pulmonary embolism as the cause of arrest. Evidence for use of naloxone in those with cardiac arrest due to opioids is unclear but it may still be used. In those with cardiac arrest due to local anesthetic lipid emulsion may be used.