Treatment Grinker's myelinopathy is still in the experimental stages and is very individualized. Some suggested treatments are early supportive care, rehabilitation therapies, oxygen treatments, and bed rest. Some episodes of Grinker's myelinopathy that progress to comas have no known treatment to reverse the course.

Early supportive care is the anchor of treatment during the first two weeks. Rehabilitation is an important part of the care process and it is important to start the rehabilitation as soon as the patient is able to participate in therapy. Types of therapy include: physical therapy, occupational therapy, speech therapy, and respiratory therapy. This therapies are used to assess the patient's functional status and to develop treatment goals. Each goal is individualized to target the specific neurological impairments to improve the patient's functional abilities.

One way to prevent the likelihood of Grinker's myelinopathy occurring is standard or hyperbaric oxygen after carbon monoxide poisoning. The hyperbaric oxygen treatment eliminates carbon dioxide from the brain, while the standard oxygen treatment normalizes carboxyhemoglobin levels. Another preventative measure one can take is to be on bed rest and abstain from stressful and strenuous procedures for the first 10 days after an extended hypoxic event. Expectation and recognition will also lead to an earlier and more accurate and appropriate use of health care services.

Those patients who survive initial hospitalization are likely to recover from Grinker's Myelinopathy, but may take up to a year or longer. Age seems to be a factor in the time for recovery, as one study indicated that the mean age of patients who recovered within one year was 10 years younger than that of patients who did not. For most patients, a recovery time of 3–6 months is typical. Even after recovering, however, some symptoms may persist, including cognitive deficits or Parkinsonian symptoms that can be treated separately.

Initial treatment for carbon monoxide poisoning is to immediately remove the person from the exposure without endangering further people. Those who are unconscious may require CPR on site. Administering oxygen via non-rebreather mask shortens the half-life of carbon monoxide from 320 minutes, when breathing normal air, to only 80 minutes. Oxygen hastens the dissociation of carbon monoxide from carboxyhemoglobin, thus turning it back into hemoglobin. Due to the possible severe effects in the fetus, pregnant women are treated with oxygen for longer periods of time than non-pregnant people.

Hyperbaric oxygen is also used in the treatment of carbon monoxide poisoning, as it may hasten dissociation of CO from carboxyhemoglobin and cytochrome oxidase to a greater extent than normal oxygen. Hyperbaric oxygen at three times atmospheric pressure reduces the half life of carbon monoxide to 23 (~80/3 minutes) minutes, compared to 80 minutes for oxygen at regular atmospheric pressure. It may also enhance oxygen transport to the tissues by plasma, partially bypassing the normal transfer through hemoglobin. However, it is controversial whether hyperbaric oxygen actually offers any extra benefits over normal high flow oxygen, in terms of increased survival or improved long-term outcomes. There have been randomized controlled trials in which the two treatment options have been compared; of the six performed, four found hyperbaric oxygen improved outcome and two found no benefit for hyperbaric oxygen. Some of these trials have been criticized for apparent flaws in their implementation. A review of all the literature on carbon monoxide poisoning treatment concluded that the role of hyperbaric oxygen is unclear and the available evidence neither confirms nor denies a medically meaningful benefit. The authors suggested a large, well designed, externally audited, multicentre trial to compare normal oxygen with hyperbaric oxygen.

In the treatment of polyneuropathies one must ascertain and manage the cause, among management activities are: weight decrease, use of a walking aid, and occupational therapist assistance. Additionally BP control in those with diabetes is helpful, while intravenous immunoglobulin is used for multifocal motor neuropathy.

According to Lopate, et al., methylprednisolone is a viable treatment for chronic inflammatory demyelinative polyneuropathy (which can also be treated with intravenous immunoglobulin) The author(s) also indicate that prednisone has greater adverse effects in such treatment, as opposed to intermittent (high-doses) of the aforementioned medication.

According to Wu, et al., in critical illness polyneuropathy supportive and preventive therapy are important for the affected individual, as well as, avoiding (or limiting) corticosteroids.

The causes of polyneuropathy can be divided into hereditary and acquired and are therefore as follows:

- "Inherited" -are hereditary motor neuropathies, Charcot–Marie–Tooth disease, and hereditary neuropathy with liability to pressure palsy

- "Acquired" -are diabetes mellitus, vascular neuropathy, alcohol abuse, and Vitamin B12 deficiency