Currently, no treatment slows the neurodegeneration in any of the neuroacanthocytosis disorders. Medication may be administered to decrease the involuntary movements produced by these syndromes. Antipsychotics are used to block dopamine, anticonvulsants treat seizures and botulinum toxin injections may control dystonia. Patients usually receive speech, occupational and physical therapies to help with the complications associated with movement. Sometimes, physicians will prescribe antidepressants for the psychological problems that accompany neuroacanthocytosis. Some success has been reported with Deep brain stimulation.

Mouthguards and other physical protective devices may be useful in preventing damage to the lips and tongue due to the orofacial chorea and dystonia typical of chorea acanthocytosis.

The GABA antagonist CGP-35348 (3-amino-propyl-(diethoxymethyl) phosphinic acid) has been used in Aldh5a1-/- mice with strong results. It has shown to reduce the frequency of absence seizures, though there have been some cases in which it worsened convulsive seizures.

Hyporeflexia refers to below normal or absent reflexes (areflexia). It can be detected through the use of a reflex hammer. It is the opposite of hyperreflexia.

Hyporeflexia is generally associated with a lower motor neuron deficit (at the alpha motor neurons from spinal cord to muscle), whereas hyperreflexia is often attributed to upper motor neuron lesions (along the long, motor tracts from the brain). The upper motor neurons are thought to inhibit the reflex arc, which is formed by sensory neurons from intrafusal fibers of muscles, lower motor neurons (including alpha and gamma motor fibers) and appurtenant interneurons. Therefore, damage to lower motor neurons will subsequently result in hyporeflexia and/or areflexia.

Note that, in spinal shock, which is commonly seen in the transection of the spinal cord (Spinal cord injury), areflexia can transiently occur below the level of the lesion and can , after some time, become hyperreflexic. Furthermore, cases of severe muscle atrophy or destruction could render the muscle too weak to show any reflex and should not be confused with a neuronal cause.

Hyporeflexia may have other causes, including hypothyroidism, electrolyte imbalance (e.g. excess magnesium), drug induced (e.g. the symptoms of benzodiazepine intoxication include confusion, slurred speech, ataxia, drowsiness, dyspnea, and hyporeflexia).

Diseases associated with hyporeflexia include

- Centronuclear myopathy

- Guillain–Barré syndrome

- Lambert-Eaton myasthenic syndrome

- Polyneuropathy (Achilles and plantar reflexes)

Sodium valproate has been used for the treatment of generalized and partial seizures in humans for both epilepsy and bipolar disorder. Valproate enhances GABA synthesis and release leading to augmented GABAergic functions in some areas of the brain. Successful interventions with valproate have been noted, but no clinical trials have been conducted thus far.

However, Valproate is usually contraindicated as it may inhibit residual SSADH enzyme activity.

Although there is no cure for NM, it is possible, and common for many people live healthy active lives even with moderate to severe cases. Research continues to seek ways to ameliorate debilitating symptoms and lengthen the life-span in quality ways for those affected. Some people have seen mild improvements in secretion handling, energy level, and physical functioning with supplemental L-tyrosine, an amino acid that is available through health centers. Some symptoms may worsen as the patient ages. Muscle loss increases with age naturally, but it is even more significant with nemaline myopathy.

Most common causes of lower motor neuron injuries are trauma to peripheral nerves that serve the axons – a virus that selectively attacks ventral horn cells.

Disuse atrophy of the muscle occurs i.e., shrinkage of muscle fibre finally replaced by fibrous tissue (fibrous muscle)

Other causes include Guillain–Barré syndrome, "C. botulism", polio, and cauda equina syndrome; another common cause of lower motor neuron degeneration is amyotrophic lateral sclerosis.

At present, Nemaline myopathy does not have a cure. Nemaline myopathy is a very rare disease that only effects 1 out of 50,000 on average, although recent studies show that this number is even smaller. There are a number of treatments to minimize the symptoms of the disease. The treatments and procedures to help patients with nemaline myopathy vary depending on the severity of the disease. A possible accommodation could be the use of a stabilizer, such as a brace. Other means include moderate stretching and moderate exercise to help target muscles maintain maximum health.

As people with NM grow and develop throughout their lives, it is important for them to see a variety of health professionals regularly, including a neurologist, physical therapist, and others, such as speech therapists and psychologists, to help both the patient and family adjust to everyday life.

The extensor Babinski reflex is usually absent. Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are usually seen immediately following an insult. Muscle wasting, fasciculations and fibrillations are typically signs of end-stage muscle denervation and are seen over a longer time period. Another feature is the segmentation of symptoms – only muscles innervated by the damaged nerves will be symptomatic.

Spinal shock was first defined by Whytt in 1750 as a loss of accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening

Research is underway worldwide to increase scientific understanding of these disorders as well to identify prevention and treatment methods. Known genetic mutations provide a basis for studying some of the conditions.

Treatment including addressing the cause, such as improving the diet, treating diarrhea, or stopping an offending medication. People without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment.

Mild hypokalemia (>3.0 meq/l) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, avocados, tomatoes, coconut water, citrus fruits, oranges, or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications.

Severe hypokalemia (<3.0 meq/l) may require intravenous supplementation. Typically, a saline solution is used, with 20–40 meq/l KCl per liter over 3–4 hours. Giving IV potassium at faster rates (20–25 meq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 meq/hr. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained-release formulations should be avoided in acute settings.

Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.

When replacing potassium intravenously, infusion by a central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral infusion, or the rare occurrence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of KCl per 50 ml of fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors.

The treatment and prognosis of myelopathy depends on the underlying cause: myelopathy caused by infection requires medical treatment with pathogen specific antibiotics. Similarly, specific treatments exist for multiple sclerosis, which may also present with myelopathy. As outlined above, the most common form of myelopathy is secondary to degeneration of the cervical spine. Newer findings have challenged the existing controversy with respect to surgery for cervical spondylotic myelopathy by demonstrating that patients benefit from surgery.

In spinal cord injuries above T6, neurogenic shock may occur, from the loss of autonomic innervation from the brain. Parasympathetic is preserved but the synergy between sympathetic and parasympathetic system is lost in cervical and high thoracic SCI lesions. Sacral parasympathetic loss may be encountered in lesions below T6 or T7. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrhythmias – which resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It is characterized by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder or bowel control, sweating, headaches, and other sympathetic effects.

The goal of therapy is to treat the hypercalcaemia first and subsequently effort is directed to treat the underlying cause.

Through multiple advancements within the medical field, care-givers have been able to stray away from utilizing bilateral adrenalectomy as the treatment for Cushing's disease. This has decreased the risk of patients presenting with Nelson's syndrome. Alternative treatments for Nelson's syndrome have been discovered. The most utilized technique for Nelson's syndrome has been transsphenoidal surgery. In addition, pharmacotherapy, radiotherapy, and radiosurgery have been utilized accompanying a surgical procedure. Pharmalogical drugs can also be given accompanying a transsphenoidal surgery including the following: pasireotide, temozolomide and octreotide. Within rats/mice, rosiglitazone has been an effective measure, however this has not been discovered in humans yet.

Additional therapy:

- bisphosphonates are pyrophosphate analogues with high affinity for bone, especially areas of high bone-turnover.

- they are taken up by osteoclasts and inhibit osteoclastic bone resorption

- current available drugs include (in order of potency): (1st gen) etidronate, (2nd gen) tiludronate, IV pamidronate, alendronate (3rd gen) zoledronate and risedronate

- all people with cancer-associated hypercalcaemia should receive treatment with bisphosphonates since the 'first line' therapy (above) cannot be continued indefinitely nor is it without risk. Further, even if the 'first line' therapy has been effective, it is a virtual certainty that the hypercalcaemia will recur in the person with hypercalcaemia of malignancy. Use of bisphosphonates in such circumstances, then, becomes both therapeutic and preventative

- people in kidney failure and hypercalcaemia should have a risk-benefit analysis before being given bisphosphonates, since they are relatively contraindicated in kidney failure.

- Calcitonin blocks bone resorption and also increases urinary calcium excretion by inhibiting calcium reabsorption by the kidney

- Usually used in life-threatening hypercalcaemia along with rehydration, diuresis, and bisphosphonates

- Helps prevent recurrence of hypercalcaemia

- Dose is 4 international units per kilogram via subcutaneous or intramuscular route every 12 hours, usually not continued indefinitely due to quick onset of decreased response to calcitonin

Myelopathy describes any neurologic deficit related to the spinal cord. When due to trauma, it is known as (acute) spinal cord injury. When inflammatory, it is known as myelitis. Disease that is vascular in nature is known as vascular myelopathy. The most common form of myelopathy in human, "cervical spondylotic myelopathy (CSM)", is caused by arthritic changes (spondylosis) of the cervical spine, which result in narrowing of the spinal canal (spinal stenosis) ultimately causing compression of the spinal cord. In Asian populations, spinal cord compression often occurs due to a different, inflammatory process affecting the posterior longitudinal ligament.

CMV polyradiculomyelopathy (PRAM) is one of the five distinct neurological syndromes caused by CMV in HIV/AIDS. It causes subacute ascending lower extremity weakness with paresthesias and radicular pain, hyporeflexia or areflexia, and urinary retention. It has been suggested that CMV polyradiculomyelopathy should be treated with both ganciclovir and foscarnet in patients who develop the disease while taking either of these drugs.

Common treatments for Nelson's syndrome include radiation or surgical procedure. Radiation allows for the limitation of the growth of the pituitary gland and the adenomas. If the adenomas start to affect the surrounding structures of the brain, then a micro-surgical technique can be adapted in order to remove the adenomas in a transsphenoidal (bone at base of the skull) process. Death may result with development of a locally aggressive pituitary tumor. However, does not commonly occur with pituitary diseases. In the rare case, ACTH-secreting tumors can become malignant. Morbidity from the disease can occur due to pituitary tissue compression or replacement, and compression of structures that surround the pituitary fossa. The tumor can also compress the optic apparatus, disturb cerebrospinal fluid flow, meningitis, and testicular enlargement in rare cases.

The amount of potassium deficit can be calculated using the following formula:

Meanwhile, the daily body requirement of potassium is calculated by multiplying 1 mmol to body weight in kilogrammes. Adding potassium deficit and daily potassium requirement would give the total amount of potassium need to be corrected in mmol. Dividing mmol by 13.4 will give the potassium in grams.

Chylomicron retention disease is a disorder of fat absorption. It is associated with SAR1B. Mutations in SAR1B prevent the release of chylomicrons in the circulation which leads to nutritional and developmental problems. It is a rare autosomal recessive disorder with around 40 cases reported worldwide. Since the disease allele is recessive, parents usually do not show symptoms.

Without functional chylomicrons certain fat-soluble vitamins such as vitamin D and vitamin E cannot be absorbed. Chylomicrons have a crucial role in fat absorption and transport, thus deficiency in chylomicron functioning reduces available levels of dietary fats and fat-soluble vitamins.

In the months following birth, signs and symptoms will appear. Some symptoms will manifest gradually during childhood.

- Failure to gain weight

- Failure to thrive

- Diarrhea

- Foul-smelling feces, steatorrhea

- Impaired nervous system functions

- Decreased reflexes, hyporeflexia

Vascular myelopathy (vascular disease of the spinal cord) refers to an abnormality of the spinal cord in regard to its blood supply. The blood supply is complicated and supplied by two major vessel groups: the posterior spinal arteries and the anterior spinal arteries—of which the Artery of Adamkiewicz is the largest. Both the posterior and anterior spinal arteries run the entire length of the spinal cord and receive anastomotic (conjoined) vessels in many places. The anterior spinal artery has a less efficient supply of blood and is therefore more susceptible to vascular disease. Whilst atherosclerosis of spinal arteries is rare, necrosis (death of tissue) in the anterior artery can be caused by disease in vessels originating from the segmental arteries such as atheroma (arterial wall swelling) or aortic dissection (a tear in the aorta).

Most people recover from West Nile virus without treatment. No specific treatment is available for WNV infection. In mild cases over the counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases treatment consists of supportive care that often involves hospitalization, intravenous fluids, pain medication, respiratory support, and prevention of secondary infections.

Anterior spinal artery syndrome is necrosis of tissue in the anterior spinal artery or its branches. It is characterised by pain which radiates at onset and sudden quadraplegia (paralysis of all four limbs) or paraplegia (paralysis of the lower body). Within days, flaccid limbs become spastic and hyporeflexia (underactive nerve responses) turns into hyperreflexia (overactive nerve responses) and extensor plantar nerve responses. Sensory loss to pain and temperature also occurs up to the level of damage on the spinal cord, as damage to different areas will affect different parts of the body.

In diagnosis, other causes of abrupt paralysis should be excluded such as cord compression, transverse myelitis (inflammation of the spinal cord) and Guillain–Barré syndrome. A specific cause of the infarction should be looked for, such as diabetes, polyarteritis nodosa (inflammatory damage of vessels) or systemic lupus erythematosus. Neurosyphilis is also a known cause. Other causes include:

Treatment is supportive and aims to relieve symptoms. The prognosis is dependent upon individual circumstances and factors.