Progressive Myelopathy After Neck Pain

A 36-year-old woman with a history of hypothyroidism, gout, fibromyalgia, depression, substance use disorder, and nephrolithiasis had development of neck pain. Three months later, she noted numbness in the left leg, which slowly worsened over the course of several months, spreading to involve the right leg and eventually forming a sensory level across the trunk at T8. At that time she also noted numbness in both hands. She had stiffness and weakness in both legs and had trouble emptying her bladder. Neurologic examination showed mild weakness restricted to the bilateral iliopsoas and hyperreflexia in the upper and lower extremities. Hoffmann and Babinski signs were positive bilaterally. There was moderate spasticity in both lower extremities and mild distal vibratory sensation loss, with a sensory level across the trunk at T8. Her gait examination indicated a spastic gait, and she had a mildly positive Romberg sign. On re-evaluation of her previous magnetic resonance image, a transverse band or pancakelike enhancement pattern was noted at the center of a moderate to severely stenotic region of the cervical spine sparing gray matter on axial sequences. The magnetic resonance imaging findings were highly suggestive of cervical spondylotic myelopathy. A neurosurgical referral was made, and the patient underwent anterior cervical discectomy with decompression and fusion from C4-C7. At her follow-up visit 4 months after surgery, the patient reported improvement in her strength and walking. Her neurologic examination showed normal lower extremity strength, resolution of spasticity, and negative Babinski sign bilaterally but persistent sensory deficits. Magnetic resonance imaging of the cervical spine at that time showed a decrease in the degree of T2 hyperintensity and enhancement, consistent with interval response to surgery. The presence of a progressive myelopathy over many months in this case patient argued against a diagnosis of transverse myelitis. Furthermore, the cerebrospinal fluid was noninflammatory, which also favored cervical spondylosis over idiopathic transverse myelitis. However, the gadolinium enhancement pattern was the key diagnostic feature that strongly suggested cervical spondylotic myelopathy as the diagnosis and ultimately led to neurosurgical referral for decompression.

Progressive Myelopathy After Spine Surgery

A 69-year-old man with a progressive myelopathy for 2 years was referred for evaluation of suspected transverse myelitis. His medical history included discectomies, a severe episode of herpes simplex virus type 1 meningoencephalitis, and development of insidiously progressive numbness and weakness of his hands. Cervical spine magnetic resonance imaging showed 2 small, dural-based, gadolinium-enhancing lesions. Biopsy of these lesions showed only normal neural tissue. Subsequently, the dura was stripped away surgically from the lower cervical region, in an effort to remove these lesions. During the next year, a sensory level developed at about the level of the nipples (T4), along with a squeezing sensation on his trunk below. Imbalance and bilateral lower extremity weakness and numbness then developed. Magnetic resonance imaging showed a longitudinally extensive cord signal abnormality. The cause of the patient’s initial subjective hand numbness and weakness was indeterminate. The onset of severely progressive symptoms after surgical removal of those lesions and the reported stripping of dura made it likely that the progressive cord edema was due to chronic adhesive arachnoiditis. His prior meningoencephalitis was a potential additional risk factor for arachnoiditis. Computed tomography myelography showed a markedly abnormal spinal canal with scalloping of the cord contour, with delayed flow of contrast above C6-C7, consistent with arachnoid adhesions causing obstruction of normal cerebrospinal fluid flow. The patient was diagnosed with chronic adhesive arachnoiditis. A C4-C7 laminectomy and surgical lysis of the cord meningeal adhesions was performed, with subsequent intensive neurorehabilitation. Follow-up spinal cord magnetic resonance imaging 6 months after surgery showed improvement of the T2-signal abnormality but persistent myelomalacia and spinal cord atrophy. Adhesive arachnoiditis is an uncommon cause of progressive myelopathy resulting from an insult to the arachnoid meningeal layer, followed by inflammation and fibrosis. This process renders the arachnoid abnormally thick and adherent to the pia and dura mater. Abnormal adhesion of nerve roots or spinal cord to the dura produces neurologic impairment. Typical symptoms include back pain, paresthesias, lower limb weakness, and sensory loss. It is diagnosed clinically with supportive magnetic resonance imaging and computed tomography myelography findings.

Intracranial Subarachnoid Haemorrhage Caused by Cervical Spinal Dural Arteriovenous Fistulas: Case Report

Cervical spinal vascular abnormalities commonly present with progressive myelopathy as a result of venous congestion. They are not very prone to bleed and tend to be underdiagnosed due to their subtle clinical presentation. We came across a rare case of intracranial subarachnoid haemorrhage caused by cervical spinal dural fistula in the Imperial College Healthcare NHS Trust Hospitals/UK in June 2020. We diagnosed the patient under strict evidence base medicine guidance, which otherwise would have been missed. We discussed the case in several multidisciplinary team (MDT) meetings, and patient was treated under the joint care of the neurology and neurosurgical teams. Patient made a full recovery and discharged home with no neurological defects or complications. Here, we reported this case with all the evidence we gathered from our MDT discussion. We hope our experience would help improve the diagnosis and management protocol for future patients with a similar condition.

Thoracic ventral spinal cord herniation with progressive myelopathy – A case report and review of the literature

Background: Idiopathic spinal cord herniation (ISCH) is a rare, underrecognized, and often misdiagnosed entity of unclear pathogenesis that typically presents as a slowly progressive thoracic myelopathy. There are less than 200 such cases reported in the literature. ISCH diagnosis and treatment are often delayed contributing to greater fixed neurological deficits, often leading to costly, unnecessary imaging studies, and inappropriate surgery. Case Description: Here, a 48-year-old female presented with trauma-induced ISCH characterized by gradually worsening lower extremity myelopathy. Conclusion: Idiopathic spinal cord herniation (ISCH) is rare, often underdiagnosed posttraumatic myelopathy that, when accurately diagnosed and treated, can result in good outcomes.

NMOSD-like and longitudinal extensive HTLV1-associated myelitis are extremes that flank an overlooked continuum

Background HTLV1-associated myelitis (HAM) is a slowly progressive myelopathy in which spinal cord MRI demonstrates no lesion or atrophy. Objective We examined the overlap between NMOSD features and HTLV1 infection. Methods We included all HTLV1-infected patients recruited in French West Indies (FWI) or referred from different centers, and suffering from at least one NMOSD feature. Literature connecting HTLV1-infection and NMOSD was reviewed. Results We included six NMOSD-like HAM with acute onset, seronegative against AQP4 and MOG-Abs. All displayed extensive longitudinal myelitis, and the optic nerve was involved in three. We gathered 39 cases of NMOSD-like HAM patients from the literature. Atypical signs of HAM were relapses (15.4%), sensory level (50%), upper limb symptoms (35.9%), optic neuritis (10.2%). Typical lesions involved lateral funiculi and featured a double rope sign (56.3%). Conclusion We propose that acute onset of NMOSD-like HAM could be more frequent than expected and should be evoked in high-risk patients. Extensive but often transient cord lesions could be the hallmark of an excessive inflammation of the funiculi targeted by HTLV1 infection. Although usually minor, a few HAM cases demonstrate specific MRI lesions, and the most severe cases may mimic NMOSD attacks.

A Rare T2-T3 Synovial Facet Cyst Causing Progressive Myelopathy

Intraspinal extradural synovial cysts are a rare occurrence at the spinal cord level and thus a rare cause of myelopathy. Synovial cysts usually present in the more mobile lumbar and cervical parts of the spine; however, they may also arise in the thoracic spine. We present a case of a 59-year-old male with a left upper thoracic synovial cyst at T2-3 causing disabling, progressive myelopathy, and an incomplete spinal cord injury syndrome with inability to ambulate. An urgent decompressive laminectomy with bilateral facetectomies, cyst excision, and posterior fusion was performed. Subsequently, the patient recovered full function. Synovial cysts should be considered in the differential diagnosis of progressive thoracic myelopathy. This is only the sixth reported case of a synovial cyst of this kind occurring between the levels of T1 and T7. Urgent surgical decompression is the recommended treatment.

Fatal Case of COVID-19 Pneumonia Associated with Acute Myelopathy

In December 2019, a novel coronavirus outbreak with multiple system involvement started initially in Wuhan City, Hubei Province of China. Coronavirus disease 2019 (COVID-19) infection is a systemic disorder typically presenting with fever, fatigue, and upper and lower respiratory symptoms, although neurological manifestations are increasingly reported, but pathological mechanisms have yet to be established. The symptoms of infection with COVID-19 are dependent on the patient’s age and underlying medical illness, and on the condition of the immune system. Neurotropic and neuroinvasive capabilities of coronaviruses have been described in humans. We herein report a patient infected with COVID-19 who developed pneumonia associated with acute progressive myelopathy. Neurological examination revealed progressive flaccid areflexic paralysis of lower limbs over 3 days with retention of urine and sensory level at 10th spinal thoracic segment (T10). The patient had a positive nasopharyngeal swab for COVID-19 at the onset of the neurological symptoms. This case of acute progressive myelopathy adds further evidence of the complications of severe COVID-19 infection, and we are dealing with a virus of unpredictable behavior. Since this virus neurotropism is not clear yet, further investigations should be conducted on the mechanism of possible neurological infection in patients with COVID-19.

Thoracolumbar intraosseous spinal epidural arteriovenous fistulas after vertebral compression fracture: A case report and literature review

Background: The pathophysiology of spinal epidural arteriovenous fistulas (SEAVFs) with perimedullary venous drainage remains to be elucidated. This report describes a case of intraosseous SEAVF in a patient with a history of a thoracolumbar vertebral fracture at the same level 10 years before presenting with progressive myelopathy secondary to retrograde venous reflux into the perimedullary vein. Case Description: A 71-year-old man presenting with progressive paraparesis was diagnosed with a SEAVF involving a previous Th12 and L1 vertebral compression fracture on which feeders from multiple segmental arteries converged. The interesting feature of this case was that the fistula was located in the fractured vertebral body. The fistula was totally obliterated by transarterial embolization of the segmental arteries followed by symptom improvement. Conclusion: We presented a rare case of an intraosseous SEAVF secondary to a thoracolumbar compression fracture with perimedullary venous reflux causing progressive myelopathy. The fistula was located in the fractured vertebral body.