A 12-Year-Old With Urinary Retention Who Can't Grasp Objects

Liana Meffert; Daniel Miller, MD


April 18, 2022

Central cord syndrome (CCS) is most frequently associated with traumatic hyperextension of the cervical spinal cord in patients with chronic cervical spondylosis; however, it can also be caused by slow-growing intramedullary tumors, as seen in this patient. CCS is defined as a symptomatic central cord lesion involving either the corticospinal tract (CST) or the anterior horn. As in this patient's presentation, weakness is more evident in the upper extremities than in the lower ones. CCS usually presents without bladder symptoms, although urinary retention can occur. Classically, pain and temperature sensation are impaired, whereas vibration and proprioception are typically uninvolved.

The potential differential diagnoses for myelopathy include classic spinal cord syndromes. Brown-Séquard syndrome (BSS), also known as lateral hemisection syndrome, results in ipsilateral weakness via disruption of the CST. Of note, both upper motor neuron (UMN) and lower motor neuron (LMN) lesion signs are evident, with LMN signs at the level of the lesion and UMN signs below the level of the lesion. UMN-positive features include hyperreflexia and spasticity, whereas LMN syndrome is typified by weakness, hyporeflexia, fasciculations, and atrophy.[2]

BSS also presents with the loss of proprioception and the contralateral loss of pain, temperature, and fine touch sensation. Proprioception and vibration loss are due to interruption of the posterior dorsal columns (consisting of the fasciculus gracilis, which is responsible for the lower half of the body, and the fasciculus cuneatus, which is responsible for the upper half). Contralateral loss of pain, temperature, and fine touch sensation several levels below the lesion results from interruption of the spinothalamic tract. This finding occurs because the spinothalamic tract crosses to the contralateral side several levels below the lesion.[3]

The most common cause of BSS is a traumatic injury, such as a knife or bullet wound, a motor vehicle accident, or blunt trauma. Nontraumatic causes include multiple sclerosis, radiation, and vertebral disc herniation.[4]

Dorsal, or posterior, cord syndrome results from the loss of the posterior columns and the lateral CST, as well as the descending central autonomic tracts involved in bladder function. Dorsal column interruption typically causes gait ataxia, whereas CST interruption produces muscle weakness and ultimately hyperreflexia and hypertonia when chronic. Although many possible etiologies exist, some of the better-known ones include multiple sclerosis, tabes dorsalis (secondary to tertiary neurosyphilis), and Friedreich ataxia, a hereditary trinucleotide repeat expansion.

In contrast, anterior cord syndrome typically spares the dorsal columns and affects only the anterior two thirds of the spinal cord, which includes the CST and spinothalamic tracts as well as the autonomic tracts involved in bladder control. The most common causes of anterior cord syndrome are spinal cord infarction (of the anterior spinal artery), intervertebral disc herniation, and radiation myelopathy (a complication of radiation therapy).

The conus medullaris typically terminates around the L1 vertebra[5]; thus, lesions near L1 can result in conus medullaris syndrome, which presents with distinct sphincter dysfunction, urinary and/or anal incontinence or constipation, impotence, and the oft-cited saddle sensory loss.[6] In contrast to cauda equina syndrome, the deficits are usually symmetric, and lower-extremity weakness may not be present. Typical causes include disc herniation, spinal fracture and, less commonly, tumors that compress the spinal cord.[6]

Another possible initial presentation for patients with neurologic symptoms induced by neoplasms is neoplastic epidural spinal cord compression (ESCC), which is the first sign of cancer in approximately 20% of patients.[7] In children, the tumors that are most commonly responsible for ESCC include sarcomas, neuroblastomas, germ cell neoplasms, and Hodgkin lymphoma.[8] ESCC usually occurs in the thoracic spine (60%-70%) and presents with pain that is often worse at night and predates neurologic dysfunction by an average of 7 weeks.[9] Motor findings indicate more advanced stages of ESCC, whereas the degree of weakness coincides with the degree of severity.[10] Urinary retention is considered the most common autonomic dysfunction finding yet is rarely the only presenting symptom in ESCC.[11]

MRI is considered the criterion standard for the diagnosis of ESCC. A retrospective study evaluating the diagnostic accuracy of MRI in the detection of neoplastic spinal cord compression and cauda equina syndrome in patients presenting with myelopathy found a high sensitivity of 93% and specificity of 97%.[12] CT is considered a second-line option when MRI is contraindicated.


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