A herniated disc is a condition in which the nucleus pulposus is displaced from the intervertebral space. It usually leads to back pain, thus being the most common reason for it. Patients often describe the first symptoms of a herniated disc as extreme and decisive pain. Unlike the usual mechanical back pain, a herniated disc is often related to a stinging or burning sensation that often spreads to the lower extremities and proves to be continuous at lower temperatures. We present a case of a 58-year-old male patient who visited the Acibadem City Clinic with complaints of pain initially starting from his hip, which in time extended to his left leg (L5 radiculopathy) and a few days later to his right leg (L5 radiculopathy). Before visiting the clinic, he had been treated in Germany with physiotherapy and supplements, which had proved ineffective. After an MRI, which revealed an L4-L5 herniated disc, he underwent conservative treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and proton pump inhibitors (PPIs) for 14 days in addition to Medrol 4mg tablets (3x1 per day for 10 days). On the third day of the treatment, 60% of the symptoms had subsided. Seven months later, he came in for a scheduled checkup, and 95% of the symptoms were gone. A controlled MRI was done, and the herniated disc had completely vanished. We hope that this type of research will benefit medical professionals, patients, researchers, doctors, and students, among others. Such cases also contribute to the quality of care for such patients and help set regulated factual guidelines regarding their treatment as a whole.

Subacute combined degeneration (SCD) from vitamin B12 deficiency and spinal stenosis from degenerative changes may present similarly with weakness, sensory disturbances, and ataxia but require different treatments. This case report describes a 74-year-old male with suspected SCD who was discharged to an inpatient rehabilitation facility (IRF), did not improve with B12 supplementation, and later developed signs of myelopathy and diffuse joint pain. He ultimately was found to have severe cervical stenosis and pseudogout that were treated with a laminectomy and colchicine, respectively. Following surgical intervention, he returned to the IRF, where he had considerable functional improvement and was safely discharged home. This report shows the importance of recognizing the two conditions, their overlap, and the contrast between Occam\'s razor and Hickam\'s dictum.

OBJECTIVE: Neuromyelitis optica is an autoimmune disease characterized mainly by the involvement of the spinal cord and optic nerve. Clinical studies have identified the disease progression as the most important red flag. Previous researches showed that only 2% of patients with neuromyelitis optica experience a progressive course. On the other hand, neuromyelitis optica is rarely occurred in children. In the present study a case of neuromyelitis optica was reported in a female who suffered from progressive myelopathy in the course of the disease.
METHODS: The patient was a 30-year-old woman who has been affected to the disease at the age of 10 manifesting the quadriparesis. The patient also manifested optic neuritis twice. The disease became progressive at the age of 27. According to the results of the magnetic resonance imaging on spinal cord, severe atrophy was observed in the cervical and thoracic spine cord. The patient\'s antiaquaporin 4 antibody was positive.
CONCLUSIONS: Neuromyelitis optica is an astrocytopathy disease characterized by debilitating attacks. A very small percentage of patients may suffer a progressive course. According to the reported cases, this progressive course may be completely variable symptomatically, including progressive myelopathy, progressive vision impairments, and progressive cognitive impairment.

Posterior cervical laminectomies and laminoplasties are common treatments for cervical spondylotic myelopathy. However, recent studies demonstrated that positional spinal cord compression occurred after cervical laminectomies and caused postoperative progressive myelopathy. Although there were no such reports after laminoplasties, we report two cases in which symptomatic extraordinary positional spinal cord compression occurred after laminoplasties in this paper.
This study included two patients who showed progressive myelopathy: one case after a laminectomy following failure of a single-door laminoplasty and one case after a double-door laminoplasty without interlaminar spacers.
The MRIs showed mild cord compression in the neutral position in both cases. However, the patients could not extend their necks, because it triggered severe neck pain and numbness. Therefore, the positional CT myelography (CTM) was taken in the flexion and extension positions, and it showed severe spinal cord compression only in the extension position. Posterior instrumented fusions were performed for both patients, which improved their symptoms.
This paper demonstrates that postoperative positional spinal cord compression during neck extension caused a progressive myelopathy even after laminoplasty. When myelopathy symptoms worsen after laminoplasties, we recommend positional CTM/MRI evaluation, even though there is no apparent cord compression in the neutral MRI.