Role of degenerated neuron density of dorsal root ganglion on anterior spinal artery vasospasm in subarachnoid hemorrhage: experimental study.

BACKGROUND: The spinal arteries are innervated by several systems that contribute to the control of spinal cord blood flow. The sensory fibers of upper cervical nerves have vasodilatatory effect on the anterior spinal arteries (ASA). Subarachnoid hemorrhage (SAH) causes severe vasospasm by various neurochemical mechanisms. We examined whether there is a relationship between the neuron density of the C3 dorsal root ganglion and the severity of ASA vasospasm in SAH. METHODS: This study was conducted on 20 rabbits. Four of them were used as baseline group. Experimental SAH has been applied to all of 16 animals by injecting homologous blood into cisterna magna. After 20 days of injection, ASA and C3 dorsal root ganglia (C3DRG) were examined histopathologically. ASA volume values and normal and degenerated neuron densities of C3DRG were estimated stereologically and the results were analyzed statistically. RESULTS: The mean ASA volume was 1.050±0.450 mm³, [corrected] and the mean neuronal density of C3DRG was 10,500 ± 850 in all animals. The mean volume value of ASA was 0.970±0.150 [corrected] mm³, and the normal neuron density of C3DRG fell to 8,600 ± 400/mm³ in slight vasospasm group. In severe vasospasm-developed animals, mean volume value of ASA was 0.540±0.90 [corrected]mm³ and the normal neuron density of C3DRG fell to 5,500 ± 360/mm³. An inverse relationship between the degenerated neuronal density of the C3DRG and ASA volume values may indicate the severity of ASA vasospasm. CONCLUSION: The neuron density of C3DRG may be an important factor on the regulation of ASA volume values and the continuation of spinal cord blood flow. Low neuron density of C3DRG may be considered as an important factor in the pathogenesis of severe ASA vasospasm in SAH.

Anterior spinal artery syndrome in a girl with Down syndrome: case report and literature review.

BACKGROUND/OBJECTIVE: Anterior spinal artery syndrome is an extremely rare cause of acute ischemic cord infarction in children. It is caused by hypoperfusion of the anterior spinal artery, leading to ischemia in the anterior two thirds of the spinal cord. The presentation is usually with an acute and painful myelopathy with impaired bladder and bowel control. Pain and temperature sensation below the lesion are lost, whereas vibration and position sense is intact because of the preservation of the posterior columns. METHODS: Case report. RESULTS: A 16-year-old girl with Down syndrome presented with urinary retention and acute complete flaccid paralysis of the legs with absent deep tendon and abdominal reflexes. Magnetic resonance imaging showed a signal abnormality in the anterior half of the thoracic cord from T5 to T12, consistent with anterior spinal artery infarction. CONCLUSIONS: Pediatricians should consider anterior spinal artery syndrome in the child who presents with acute, painful myelopathy. We summarize the etiology, neurological findings and outcomes of 19 children found in the literature with anterior spinal artery syndrome.

Time course of diffusion weighted image and apparent diffusion coefficient in acute spinal cord infarction: A case report and review of the literature.

An 80-year-old woman was admitted to our hospital with acute onset of flaccid paraplegia and sensory and urinary disturbances that developed soon after acute pain in her lower back and leg. Neurological examination revealed, severe flaccid paraplegia, bladder and rectal disturbances and dissociated sensory loss below the level of L1 spinal cord segment. MR imaging with T2 weighted imaging (T2WI) and diffusion weighted imaging (DWI) on day 2 showed hyper signal intensity in the spinal cord at the vertebral level of L1 while initial apparent diffusion coefficient (ADC) showed decreased signal intensity in the lesion. We diagnosed spinal cord infarction, and anticoagulant and neuroprotective agents were administrated. Serial MRI findings revealed that the DWI signal of the lesion attenuated with time, and pseudo-normalization of the ADC occurred approximately 1 month after onset. These findings were similar to those seen in brain infarction. Our patient demonstrated serial MRI changes of spinal cord infarction showing anterior spinal cord syndrome.

Anterior spinal artery syndrome after aortic surgery in a child.

Anterior spinal artery syndrome is rare in children. In adults, where it is observed most frequently after resection of thoracoabdominal aortic aneurysms, spinal magnetic resonance imaging is considered the first-line investigation to confirm the clinical diagnosis. A 3-year-old male who presented with this syndrome after palliative cardiac surgery for a complex cardiac malformation associated with aortic coarctation is presented. Clinical diagnosis of anterior horn cell impairment below the L2 level was confirmed by electromyography and F-wave studies. Sparing of dorsal sensory tracts was documented by normal somatosensory-evoked potentials, which confirmed the anterior localization of the lesion. Spinal magnetic resonance imaging performed on day 15 and day 105 after surgery was normal. Neurologic deficits, including flaccid paraplegia, remained stable except for the reappearance of patellar reflexes on day 83. Neurophysiologic conduction studies were consistent with lower motoneuron loss. In this patient, magnetic resonance imaging was less sensitive in demonstrating spinal cord lesion than clinical neurophysiology. Somatosensory-evoked potentials failed to detect the insult. Prevention may therefore require other neurophysiologic monitoring techniques.

The crossing of the spinothalamic tract.

The question whether the spinothalamic and spinoreticular fibres cross the cord transversely or diagonally was investigated in cases of anterolateral cordotomy and in a case of thrombosis of the anterior spinal artery. The pattern of sensory loss following transection of the anterolateral quadrant of the cord consists of a narrow area of decreased nociception and thermanalgesia at the level of the incision; it extends for 1-2 segments cranial and cordal to the incision. This area is immediately cranial to the area of total loss of these modalities. This pattern of sensory loss is explained as follows. The cordotomy incision transects two groups of fibres: those that are already within the anterior and anterolateral funiculi and those that are crossing the cord. The area of total thermanaesthesia and analgesia is due to transection of fibres that are already within this region. The area of partial sensory loss is due to transection of the fibres that are crossing the cord at that level. Owing to the craniocaudal extent of the branches of the dorsal roots, there is an overlap of their collaterals that results in every spinothalamic neurone receiving an input from several dorsal roots. The narrow cordotomy incision thus divides the few fibres crossing at that level, causing diminished noxious and thermal sensibility over a few segments above and below the incision. These facts can be accounted for only on the assumption that these spinothalamic fibres are crossing the cord transversely. This evidence of transverse crossing was found in the cervical, thoracic and lumbar segments. There were three of 63 cordotomies for which this explanation of the partial sensory loss could not be maintained. Although no explanation has been suggested, this is unlikely to be due to the fibres crossing the cord diagonally.