For the human body, vitamins are crucial elements. In all functions and systems of our body, they influence various processes, such as the development of the central nervous system in the child. And vitamin B12 is one of the essential nutrients that people need. It is prevalent in a variety of animal protein foods [1],[2].

Low serum B vitamin levels are potentially causally related to these prevalent mental symptoms. Because of this, vitamin B12 is crucial for producing myelin and neurotransmitters. Enteral malabsorption is the main reason for low serum levels of vitamin B12, particularly in older people due to gastric atrophy [3],[4].

Additionally, subacute combined degeneration (SCD) is one of the consequences of B12 deficiency. The dorsal columns and lateral corticospinal tracts exhibit myelinolytic lesions in SCD caused by severe vitamin B12 deficiency [5],[6].

Symptomatology often is paraplegia, spasticity, and contractures are typically progressive. In addition, as the disease advances, they experience a distal sensorimotor loss that ascends proximally and causes spastic quadriparesis and generalized hypoesthesia [7].

In more severe cases, it has been reported that other central nervous system structures like the cerebellum and cerebrum are involved. On T2-weighted images, magnetic resonance imaging (MRI) in patients with clinically suspected SCD may reveal increased signal intensity involving the posterior and lateral spinal cord white matter columns. Most frequently and severely affected are the cervical and upper thoracic cords [3],[8].

Time to diagnosis was also considered an important factor because delays in diagnosis of more than six months were linked to permanent neurological deficits [5].

A recent systematic review that compared the length of the B12 replacement intervention and the severity of the pathology produced intriguing findings regarding the prognosis of these patients. 89% of people who can walk unaided fully recover, compared to 50% who can walk with assistance, and 6% who require a wheelchair. This suggests that individuals with less severe spinal cord myelinolysis may have a better prognosis after beginning B12 replacement [4].

Male, 33 years old, with a history of a fall in December 2015, when pain and discomfort started in the left lower limb. A year ago, he evolved with paraparesis, loss of sphincterial control, sensitive alteration in limb extremities, and sensitive level in T10, as well as the report of visual disturbance in the left eye. At this time, the laboratory dosage of vitamin B12 was significantly reduced.

On physical examination: extrapyramidal syndrome with hypoesthesia distal level. Sensitive in T10. Bilateral Hoffmann sign, spastic paraparesis, hyperreflexia in the lower limbs, clonus in the feet, and loss of sphincterial control.

Magnetic resonance imaging of cervical spine with hypersignal focus in the lateral (corticospinal tracts) and posterior columns (Figure 1 and Figure 2).

Cranial MRI focuses on hypersignal in the topography of the corticospinal tracts, suggesting subacute combined degeneration (Figure 3 and Figure 4).

Visual evoked potential with alteration of amplitude and latency in the left eye-suggestive of initial injury in optical pathways cerebrospinal fluid (CSF) study with slight hyperproteinorachia and signal increase in lactate levels.

Electroneuromyography (ENMG) preganglionic impairment suggests polyradiculoneuritis, with no signs of current denervation.

After correlating the clinical with neuroimaging, cyanocobalamin supplementation 5000 mcg intramuscularly 1×/week for eight weeks was started, with substantial improvement already at the beginning of treatment. Subsequently, continued therapy with a dosage of 5000 mcg intramuscularly 1×/month.

Subacute combined medullary degeneration should be part of the radiological differential diagnosis of demyelinating central nervous system lesions. Even so, as there are few case reports, it needs to be included in the register of differential diagnoses of demyelinating lesions. As we can observe in the case report, in the magnetic resonance of the skull, we have a hypersignal in T2 and FLAIR, showing involvement of the periventricular white matter, which corresponds to a decrease, an impairment of the myelin sheath [9],[10],[11],[12].

The symptomatology presented by the patient clearly demonstrated an extrapyramidal syndrome with a sensitive level. Due to her history of falls, there was a diagnostic hypothesis relating the patient’s clinic to the trauma suffered. There are no reports in the literature dealing with any correlation between subacute combined medullary degeneration after traumatic injuries; therefore, there is great importance on a thorough neurological examination and targeted complementary exams. As in this case, the dosage of vitamin B12 and the neuroimaging findings confirmed the diagnostic hypothesis [10],[13].

Clinical aspects and MRI findings in patients with SCD showed a predominance of involvement of the cervical spinal cord, followed by involvement of the thoracic spinal cord with simultaneous involvement of both segments. Cranial MRI allows the observation of radiological alterations in the pyramidal tract, probably caused by hypovitaminosis B12. In the anatomopathological study, edema of the myelin sheath is observed at the onset of hypovitaminosis; on microscopy, destruction of myelin and axons in the white matter ensues, segmentally at the mid-thoracic level, causing vacuoles. The most affected region is the posterior cervical and thoracic spinal cord. The morphological study of the medulla showed involvement of the lateral and anterior corticospinal tracts and the spinothalamic tract. With increasing vitamin deficiency, axons decline in ascending lots of the posterior bundle and the descending pyramidal tracts. The most common clinical picture is spastic paraparesis, usually with no identified sensory level, hypoesthesia or reduced vibration sensitivity, loss of segmental position sensation, and possibly related bilateral symmetrical distal sensory polyneuropathy. The isolated involvement of one or the other tract can occur in different clinical situations (multiple sclerosis, neoplasms); the combined degeneration of both is characteristic of vitamin B12 deficiency, leading to the designation of this condition as subacute combined degeneration of the spinal cord [11],[12].

Interestingly, a recent study grouped 68 patients with subacute combined degeneration and followed them for six months. This study concluded that anemia, vitamin B12 deficit, and spinal cord MRI abnormalities are associated with worse clinical manifestations [14].

Magnetic resonance imaging can reveal areas of demyelination in the brain or spinal cord, representing areas of hyperintensity on T2-weighted sequences. This finding is most often found in the posterior medulla of the spinal cord. Radiological changes may take up to 12 months to disappear [12].

Therefore, although the clinic and the B12 dosage suggest the diagnosis, it was through neuroimaging that this hypothesis was confirmed, ruling out any differential diagnosis related to the trauma reported by the patient. Furthermore, a recent retrospective study reported cases in which the serum B12 level was normal or even elevated, and the altered neuroimaging, together with the patient’s clinical condition, confirmed the diagnosis [15].

Vitamin B12 deficiency and other pathologies are also found in subacute combined degeneration due to the injury in the myelin sheath, which becomes reversible with early diagnosis and treatment. In the magnetic resonance, we can observe the involvement of the cervical, thoracic, and brain spinal cord, corresponding to a decrease in the myelin sheath. These alterations found in the imaging exam, when treated early, can be resolved without signs of atrophy. Thus, neuroimaging plays a relevant role in the diagnosis, complementing the clinic.

A case study should be carried out, with an in-depth follow-up should also be carried out, as it is a problem that is sometimes asymptomatic and has irreversible conditions for the patient. Any sign or symptom that the patient presents related to hypovitaminosis B12 must be treated to reach desirable levels without causing problems for the patient’s health.