There is no known treatment for FTS, as the cause is not yet known. There are conflicting reports on whether the paralysis is reversible; some sources claim that moving an elephant away from the area in which it contracted the condition will allow it to recover, while others claim that damage to the trunk is irreversible.

In some extreme cases, wildlife managers have killed affected elephants for humane reasons.

Although no treatment has been found it has been shown that affected individuals benefit considerably from rehabilitation and use of adequate walking aids. In the Central African Republic some children have been operated with an elongation of the Achilles tendon which improved the position of the foot but the long term consequence remains uncertain.

With rest, the tail returns to normal within a few days. Pain relief, such as a nonsteroidal anti-inflammatory drug may be administered. The symptoms may reoccur.

Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Konzo can be prevented by use of the “wetting method,” which is used to remove residual cyanogens from cassava flour, as an additional processing method. Cassava flour is placed in a bowl and the level marked on the inside of the bowl. Water is added with mixing until the height of the wet flour comes up to the mark. The wet flour is placed in a thin layer on a mat for 2 hours in the sun or 5 hours in the shade to allow the escape of hydrogen cyanide produced by the breakdown of linamarin by the enzyme linamarase. The damp flour is then cooked in boiling water in the traditional way to produce a thick porridge called “fufu” or “ugali”, which is flavoured by some means such as a sauce. The wetting method is accepted by rural women because it requires little extra work or equipment and produces fufu which is not bitter, because the bitter tasting linamarin has gone.

In 2010 the wetting method was taught to the women in Kay Kalenge village, Popokabaka Health Zone, Bandundu Province, DRC, where there were 34 konzo cases. The women used the method and during the intervention there were no new konzo cases and the urinary thiocyanate content of the school children fell to safe levels. Konzo had been prevented for the first time ever in the same health zone in which it had first been discovered by Dr Trolli in 1938. Fourteen months after the intervention ceased the village was visited again. It was found that there were no new cases of konzo, the school children had low urinary thiocyanate levels, the wetting method was still being used and it had spread by word of mouth to three nearby villages. It is important to teach the women that konzo is due to a poison present in their food, to get them to regularly use the wetting method and posters are available in 13 different languages as a teaching aid as an additional method to remove residual cyanogens.

The wetting method has now been used in 13 villages in DRC with nearly 10000 people. The time of the intervention has been reduced from 18 months in the first intervention, to 12 months in the second intervention, to 9 months in the third and fourth interventions. This has reduced the cost per person of the intervention to prevent konzo by removing cyanogens from cassava flour, to $16 per person. This targeted method to reduce cyanide intake is much cheaper and more effective in preventing konzo than broad based interventions.

The underlying disorder must be treated. For example, if a spinal disc herniation in the low back is impinging on the nerve that goes to the leg and causing symptoms of foot drop, then the herniated disc should be treated. If the foot drop is the result of a peripheral nerve injury, a window for recovery of 18 months to 2 years is often advised. If it is apparent that no recovery of nerve function takes place, surgical intervention to repair or graft the nerve can be considered, although results from this type of intervention are mixed.

Non-surgical treatments for spinal stenosis include a suitable exercise program developed by a physical therapist, activity modification (avoiding activities that cause advanced symptoms of spinal stenosis), epidural injections, and anti-inflammatory medications like ibuprofen or aspirin. If necessary, a decompression surgery that is minimally destructive of normal structures may be used to treat spinal stenosis.

Non-surgical treatments for this condition are very similar to the non-surgical methods described above for spinal stenosis. Spinal fusion surgery may be required to treat this condition, with many patients improving their function and experiencing less pain.

Nearly half of all vertebral fractures occur without any significant back pain. If pain medication, progressive activity, or a brace or support does not help with the fracture, two minimally invasive procedures - vertebroplasty or kyphoplasty - may be options.

Ankles can be stabilized by lightweight orthoses, available in molded plastics as well as softer materials that use elastic properties to prevent foot drop. Additionally, shoes can be fitted with traditional spring-loaded braces to prevent foot drop while walking. Regular exercise is usually prescribed.

Functional electrical stimulation (FES) is a technique that uses electrical currents to activate nerves innervating extremities affected by paralysis resulting from spinal cord injury (SCI), head injury, stroke and other neurological disorders. FES is primarily used to restore function in people with disabilities. It is sometimes referred to as Neuromuscular electrical stimulation (NMES)

The latest treatments include stimulation of the peroneal nerve, which lifts the foot when you step. Many stroke and multiple sclerosis patients with foot drop have had success with it. Often, individuals with foot drop prefer to use a compensatory technique like steppage gait or hip hiking as opposed to a brace or splint.

Treatment for some can be as easy as an underside "L" shaped foot-up ankle support (ankle-foot orthoses). Another method uses a cuff placed around the patient's ankle, and a topside spring and hook installed under the shoelaces. The hook connects to the ankle cuff and lifts the shoe up when the patient walks.

Mild cases are managed by limiting activity, keeping a healthy body weight, and avoiding exposure to high ambient temperatures. Mild sedatives can be used to decrease anxiety and panting and therefore improve respiration. Corticosteroids may also be administered in acute cases to decrease inflammation and edema of the larynx.

Severe acute symptoms, such as difficulty breathing, hyperthermia, or aspiration pneumonia, must be stabilized with sedatives and oxygen therapy and may require steroid or antibiotic medications. Sometimes a tracheotomy is required to allow delivery of oxygen. Once the patient is stabilized, surgical treatment may be beneficial especially when paralysis occurs in both aretynoid cartilages (bilateral paralysis). The surgery (aretynoid lateralization, or a "laryngeal tieback") consists of suturing one of the aretynoid cartilages in a maximally abducted (open) position. This reduces the signs associated with inadequate ventilation (such as exercise intolerance or overheating) but may exacerbate the risk of aspiration and consequent pneumonia. Tying back only one of the aretynoid cartilages instead of both helps reduce the risk of aspiration. Afterwards the dog will still sound hoarse, and will need to be managed in the same way as those with mild cases of LP.

Recent studies have found that many dogs with laryngeal paralysis have decreased motility of their esophagus. Animals with a history of regurgitation or vomiting should be fully evaluated for esophageal or other gastrointestinal disorders. Dogs with megaesophagus or other conditions causing frequent vomiting or regurgitation are at high risk for aspiration pneumonia after laryngeal tie-back. Permanent tracheostomy is an alternative surgical option for these dogs to palliate their clincical signs.

Floppy trunk syndrome (abbreviated FTS, also known as flaccid trunk paralysis) is a condition that causes trunk paralysis in African bush elephants. Initially observed in 1989, the syndrome primarily affected bull elephants in several select regions in Zimbabwe. Afflicted elephants exhibit paralysis in their trunk, often having to adapt to feed. The loss of their trunks' prehensile abilities results in malnutrition and possibly death. The condition is a result of degeneration of nerves in the trunk, and is suggested to be a result of either heavy metals or toxins. There is debate over whether the condition is reversible.

Treatment of the periodic paralyses may include carbonic anhydrase inhibitors (such as acetazolamide, methazolamide or dichlorphenamide), taking supplemental oral potassium chloride and a potassium-sparing diuretic (for hypos) or avoiding potassium (for hypers), thiazide diuretics to increase the amount of potassium excreted by the kidneys (for hypers), and significant lifestyle changes including tightly controlled levels of exercise or activity. However, treatment should be tailored to the particular type of periodic paralysis.

Treatment of periodic paralysis in Andersen-Tawil syndrome is similar to that for other types. However, pacemaker insertion or an implantable cardioverter-defibrillator may be required to control cardiac symptoms.

Physiotherapy

To increase strength of muscle

To improve muscle functions

Electrical modalities =Electric stimulation.etc.

Occupational Therapy

Positioning, ROM, Sensory, Splinting

The most effective treatment of astasia seems to be a removal of stress inducing stimuli and allowing the patient to rest and regain strength. Despite the lack of a direct prescribable cure for the effect of astasia on the motor system of the legs, in almost all documented cases physical rehabilitation and relief from mental stressors have led to a full recovery. Although astasia is not expressly associated with any neurological disorders, there is a strong correlation between general mental hysteria and the symptoms of astasia. Therefore, isolation of the patient from the situation causing them hysteria is the most efficient way to rid them of disabling motor symptoms. Another method for treatment that patients who experience astasia is to have therapy for the triceps surae muscle. This therapy can help strengthen these muscles to help maintain an upright posture. It has also been suggested that ankle-foot orthoses be prescribed for these patients. This would help patients with astasia maintain balance by preventing ankle dorsiflexion.

Currently, physical therapy and rehabilitation are widely accepted as the best treatments for the symptoms of astasia. There is, however, evidence to suggest that regulation of a patient's social situation and behavioral influences can influence the effectiveness of rehabilitation. A 1975 study shows that when a patient is given direct encouragement and social distractions their physical recovery proceeds much faster than when only basic instructions are provided to them.

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.

The most common drug used to treat AHC is flunarizine. Flunarizine functions by acting as a calcium channel blocker. Other drugs, in order of frequency of use are benzodiazepines, carbamazapine, barbiturates, and valproic acid. Flunarizine is prescribed for the purpose of reducing the severity of AHC attacks and the number of episodes, though it rarely stops attacks altogether. Minimizing the attacks may help reduce damage to the body from hemiplegic attacks and improve long-term outcomes as far as mental and physical disabilities are concerned.

Experts differ in their confidence in flunarizine's effectiveness. Some studies have found it to be very effective in reducing the duration, severity, and frequency of hemiplegic attacks. It is generally considered the best treatment available, but this drug is thought by some to be of little benefit to AHC patients. Many patients suffer adverse effects without seeing any improvement. Flunarizine also causes problems because it is difficult for patients to obtain, as it is not readily available in the United States.

Sleep is also used as a management technique. An early indication of an episode is tiredness so medication such as melatonin or Buccal midazolam can be administered to induce sleep and avoid the episode.

Those suffering from alternating hemiplegia are often underweight and with the help of dietitians, a meal plan should be developed for times of attack when consumption of food may be difficult.

The first line of treatment is often to treat the patients pain with neuropathic drugs such as tricyclic antidepressants, serotonin reuptake inhibitors, and anticonvulsants. The second lines of drugs to treat pain are non-steroidal anti-inflammatories, tramadol, and opioids. Other techniques used to facilitate healing of the nerve and pain are either static or dynamic splinting that can both help protect the injured part as well as improve function. Sometimes surgery is an option, although the prognosis is still very poor of regaining function of the affected nerve. The goal of surgery is to join healthy nerve to unhealthy nerve. The most common surgical techniques include external neurolysis, end-to-end repair, nerve grafting, and nerve transfer from somewhere else in the body.

While the disability can range from minor, occasional weakness to permanent muscle damage, inability to hold a normal job and use of a powerchair, most people function fairly well with drugs and lifestyle changes.

Current research at the University of Utah is investigating whether sodium oxybate, also known as Gamma-Hydroxybutyric acid is an effective treatment for AHC. Thus far, only a small number of patients have been sampled, and no conclusive results are yet available. While some success has been had thus far with the drug, AHC patients have been known to respond well initially to other drugs, but then the effectiveness will decline over time. Currently, sodium oxybate is used as a narcolepsy-cataplexy treatment, though in the past it has been used controversially in nutritional supplements. This drug was chosen to test because of a possible link between the causes of narcolepsy-cataplexy and AHC.

It has been said by many dog owners that limber tail had been caused shortly (24 hours) after swimming in water that is too cold or on rare occasions too warm and indeed this has certainly produced this very condition. The actual cause is unknown but it may be caused by the narrowing of the space through which the spinal cord passes, typically due to degenerative change to the intervertebral disk spaces. These underlying changes may not lead to visible change until the problem is suddenly exacerbated, such as during physical activity, after trauma, etc. Occasionally other changes are seen prior to or in conjunction with limber tail disease, such as urinary or fecal incontinence, postural abnormalities in the pelvic limb, or pain in response to touching the lower back.

Many children affected by alternating hemiplegia also suffer from epilepsy. Seizures may occur during an attack but more often occur between attacks. Anti-epilepsy drugs are given to prevent or lessen the seizures, but the drugs often don’t work and have severe side effects that require the patient to discontinue use. Flunarizine, which blocks calcium channels, is an antiepilepsy drugs used in 50% of patients, and has been shown to shorten the duration of attacks as well as reducing the severity of the attacks. While Flunarizine does not stop the attacks, it is most common drug prescribed to treat those suffering from alternating hemiplegia.

Besides complications of surgery and anesthesia in general, there may be drainage, swelling, or redness of the incision, gagging or coughing during eating or drinking, or pneumonia due to aspiration of food or liquids. Undesirable complications are estimated to occur in 10-30% of cases. If medical therapy is unsuccessful and surgery cannot be performed due to concurrent disease (such as heart or lung problems) or cost, euthanasia may be necessary if the animal's quality of life is considered unacceptable due to the disease.

Some babies recover on their own; however, some may require specialist intervention.

Neonatal/pediatric neurosurgery is often required for avulsion fracture repair. Lesions may heal over time and function return. Physiotherapeutic care is often required to regain muscle usage.

Although range of motion is recovered in many children under one year in age, individuals who have not yet healed after this point will rarely gain full function in their arm and may develop arthritis.

The three most common treatments for Erb's Palsy are: Nerve transfers (usually from the opposite arm or limb), Sub Scapularis releases and Latissimus Dorsi Tendon Transfers.

Nerve transfers are usually performed on babies under the age of 9 months since the fast development of younger babies increases the effectiveness of the procedure. They are not usually carried out on patients older than this because when the procedure is done on older infants, more harm than good is done and can result in nerve damage in the area where the nerves were taken from. Scarring can vary from faint scars along the lines of the neck to full "T" shapes across the whole shoulder depending on the training of the surgeon and the nature of the transplant.

Subscapularis releases, however, are not time limited. Since it is merely cutting a "Z" shape into the subscapularis muscle to provide stretch within the arm, it can be carried out at almost any age and can be carried out repeatedly on the same arm; however, this will compromise the integrity of the muscle.

Latissimus Dorsi Tendon Transfers involve cutting the Latissimus Dorsi in half horizontally in order to 'pull' part of the muscle around and attach it to the outside of the biceps. This procedure provides external rotation with varying degrees of success. A side effect may be increased sensitivity of the part of the biceps where the muscle will now lie, since the Latissimus Dorsi has roughly twice the number of nerve endings per square inch of other muscles.

In the acute phase of an attack, administration of potassium will quickly restore muscle strength and prevent complications. However, caution is advised as the total amount of potassium in the body is not decreased, and it is possible for potassium levels to overshoot ("rebound hyperkalemia"); slow infusions of potassium chloride are therefore recommended while other treatment is commenced.

The effects of excess thyroid hormone typically respond to the administration of a non-selective beta blocker, such as propranolol (as most of the symptoms are driven by increased levels of adrenaline and its effect on the β-adrenergic receptors). Subsequent attacks may be prevented by avoiding known precipitants, such as high salt or carbohydrate intake, until the thyroid disease has been adequately treated.

Treatment of the thyroid disease usually leads to resolution of the paralytic attacks. Depending on the nature of the disease, the treatment may consist of thyrostatics (drugs that reduce production of thyroid hormone), radioiodine, or occasionally thyroid surgery.

Some elements of cholinergic crisis can be treated with antimuscarinic drugs like atropine, but the most important element, respiratory arrest, cannot. The neuromuscular junction, where the brain communicates with muscles (like the diaphragm, the main breathing muscle), works by acetylcholine activating nicotinic acetylcholine receptors and leading to muscle contraction. Atropine blocks muscarinic acetylcholine receptors (a different subtype than the nicotinic receptors at the neuromuscular junction), so atropine will not improve the muscle strength and ability to breathe in someone with cholinergic crisis. Such a patient will require mechanical ventilation support via endotracheal intubation until the crisis resolves on its own. The respiratory compromise from cholinergic crisis unfortunately has no pharmacologic solution or therapy.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.