It is not clear whether the adrenalectomy or reduced cortisol secretion causes aggressive tumor growth. Diagnosis
Common diagnostic techniques include: 
MRIs
CAT scans
blood samples.Blood samples are assessed for the absence or presence of aldosterone and cortisol. Physical examinations are also useful in patients in order to examine vision, skin pigmentation, how the body replaces steroids, and the cranial nerves. Recent advancements in high-resolution MRIs allow for adenomas to be detected during the early stages of Nelson syndrome. Physical examination including height, weight, vital signs, blood pressure, eye examination, thyroid examination, abdominal examination, neurological examination, skin examination and pubertal staging needs to be assessed. Through blood pressure and pulse readings can indicate hypothyroidism and adrenal insufficiency. Hyper-pigmentation, hyporeflexia, and loss of vision can also indicate Nelsons syndrome when assessed together. Specifically for a child who might have Nelsons syndrome, the patient should be questioned about the symptoms of the disease, and well as symptoms of other diseases to narrow down which disease the patient presents with. The patient should be questioned about how often and to what degree headaches, visual disturbances, and symptoms associated with pituitary malfunction occur. Additionally, adrenal steroid replacement should be assessed. Treatment
Common treatments for Nelsons 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.
Subacute combined degeneration of spinal cord, also known as myelosis funiculus, or funicular myelosis, also Lichtheims disease, and Putnam-Dana syndrome, refers to degeneration of the posterior and lateral columns of the spinal cord as a result of vitamin B12 deficiency (most common), vitamin E deficiency, and copper deficiency. It is usually associated with pernicious anemia. Signs and symptoms
The onset is gradual and uniform. The pathological findings of subacute combined degeneration consist of patchy losses of myelin in the dorsal and lateral columns. Patients present with weakness of the legs, arms, and trunk, and tingling and numbness that progressively worsens. Vision changes and change of mental state may also be present. Bilateral spastic paresis may develop and pressure, vibration and touch sense are diminished. A positive Babinski sign may be seen. Prolonged deficiency of vitamin B12 leads to irreversible nervous system damage. HIV-associated vacuolar myelopathy can present with a similar pattern of dorsal column and corticospinal tract demyelination.It has been thought that if someone is deficient in vitamin B12 and folic acid, the vitamin B12 deficiency must be treated first. However, the basis for this has been challenged, although due to ethical considerations it is no longer able to be tested if "neuropathy is made more
severe as a result of giving folic acid to vitamin B12-
deficient individuals".