Subacute joint degeneration, also known as vitamin B12 neuropathy, is due to vitamin B12 deficiency. It is most commonly seen in adults over 40 years of age. It can affect both men and women. Slowly progressive degenerative changes occur mainly in the posterior and lateral spinal cords and peripheral nerves. It presents with signs of progressive sensory ataxia, spastic paralysis, profound sensory deficits and peripheral nerve damage, and is often accompanied by pernicious anemia and absence of gastric acid. Recent studies suggest that subacute joint degeneration of the spinal cord has an autoimmune pathogenetic basis. Auto-genetic quality may play an important role. Autoimmune dysfunction may produce antibodies to gastric lining cells or antibodies to internal factors, and infiltration of gastric mucosal lymphocytes, affecting gastric acid secretion and secretion of internal factors. In patients with autoimmune atrophic gastritis, anti-IF immunoglobulin may be closely related to impaired selective absorption of vitamin B12. Digestive tract diseases and post-gastrectomy can directly affect the absorption of vitamin B12 and lead to vitamin B12 deficiency. It has been shown that 15% of partial gastrectomy patients have a significant decrease in serum vitamin B12 levels. Congenital deficiency of endogenous factors or disorders of cobalamin metabolism can affect the metabolic process of vitamin B12. It has also been reported that breastfed infants have been affected by low intake of vitamin B12 by the mother. Clinical manifestations: Both men and women can be affected. The disease usually starts after middle age. The disease gradually worsens. It is mainly a manifestation of damage to the posterior spinal cord, corticospinal tract and peripheral nerves, and may also have damage to the optic nerve. Psychiatric and cerebral symptoms may be present, but are less frequent. The most frequent first symptoms are generalized weakness and symmetric distal limb tingling, burning, chills and other sensory abnormalities, especially in the lower limbs. The sensory abnormalities may extend upward to the trunk and produce fasciculation in the chest and abdomen. In lateral cord degeneration, there is weakness or paralysis of both lower extremities, increased muscle tone, hyperactive tendon reflexes and positive cone bundle signs. In posterior cord degeneration, deep sensory deficits such as vibration and position sensation in the lower extremities are reduced. The lower extremity ataxia, clumsy limb movements, unstable gait, easy to fall, more pronounced when walking with eyes closed or in the dark, hypotonia and tendon reflexes are reduced or absent. In late stages, there are sphincter symptoms. Peripheral nerve degeneration produces hyperalgesia or loss of superficial sensation in glove or sock-like distribution, gastrocnemius pressure pain and extremity weakness. The severity of clinical signs depends on the relative severity of the lesion’s effect on the peripheral nerve, posterior cord and conus fasciculus. Complications The severity of the disease varies with the degree of vitamin B12 deficiency and the patient’s own immunological pathogenesis, so the symptoms and signs are varied. It can also be regarded as a complication of this disease. Differential diagnosis Attention should be paid to differentiate from the following diseases: Spinal cord compression: early symptoms of nerve root irritation can occur and last for a long time, and sensory impairment develops in an upward direction. It usually starts on one side, and the posterior and lateral spinal cords can be involved. It manifests as Brown-Sequard syndrome with later transverse damage with sphincter dysfunction and no brain or optic nerve damage. Elevated cerebrospinal fluid proteins and spinal MRI imaging help confirm the diagnosis. Common causes include intramedullary and extramedullary tumors, cervical osteoarthropathy, and cervical spinal stenosis. Multiple sclerosis: The onset is rapid, with a clear history of alternating remission and relapse. The first symptoms are mostly visual loss or diplopia. Nystagmus, cerebellar signs, pyramidal fasciculus signs, posterior cord dysfunction, no manifestation of symmetric peripheral nerve damage, cerebrospinal fluid examination, evoked potentials, cranial CT and MRI are helpful for diagnosis. Peripheral neuropathy: Peripheral neuropathy caused by poisoning, inflammation, nutritional deficiency, vascular disease, etc. may have distal sensory impairment of the extremities, similar to peripheral nerve damage in subacute joint degeneration of the spinal cord. However, there are generally no posterior or lateral cord changes and no vitamin B12 deficiency, which are not difficult to differentiate when combined with the medical history. Spinal consumption: involvement of the posterior roots and posterior cords of the spinal cord with degenerative atrophy. A-ro pupil is a more typical sign. Combined with the patient’s history of smut and positive syphilis serology can be identified. V. Treatment In severe cases, the neurological symptoms will continue to worsen without treatment, and even death. After adequate treatment, anemia symptoms usually improve significantly within days or weeks, while the improvement of neurological function is slower. An improvement is usually seen in 2 months. Treatment with vitamin B12 500-1000μg daily or every other day intramuscular injection for 2 weeks, later changed to 100-200μg daily intramuscular injection or 2-3 times a week, after 3 months of small dose maintenance, some patients must be lifelong medication. Those who cannot tolerate intramuscular injection can take the medication. In addition, nutritional supplementation with vitamin B1, vitamin C and other neurotrophic drugs is required. In addition to drug treatment, functional exercise, physiotherapy and rehabilitation should be strengthened for the affected limbs, and the susceptibility factors should be eliminated or preventive treatment should be carried out in time for easy patients. Prognosis Most of the neurological symptoms are recovered when treatment is carried out at an early stage. In the late stage of the disease, the effect is very poor, and the effect is worse for those who have been paralyzed for more than two years. Therefore, early diagnosis and early treatment are extremely important for the prognosis of the disease.