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Open access

Izumi Koyanagi, Yasuhiro Chiba, Hiroyuki Imamura, Masami Yoshino, and Toshimitsu Aida

BACKGROUND

Secondary Chiari malformation can be caused by various disorders associated with cerebrospinal fluid (CSF) leakage at the spinal level. In this report, the authors describe a rare case of secondary Chiari malformation caused by excessive CSF absorption through the enlarged spinal arachnoid villi–like structure.

OBSERVATIONS

A 20-year-old woman presented with progressive severe headache and posterior neck pain. Magnetic resonance imaging showed tonsillar herniation and decreased subarachnoid space around the spinal cord. A hypointense signal area was observed in the ventral spinal canal on a T2-weighted image. An axial image revealed multiple small, arachnoid cyst–like structures at the right T1 nerve root sleeve. Direct surgery revealed that the cyst-like structures were continuous with the arachnoid membrane and protruded into the abnormally large epidural venous sinus. The cyst-like structures were resected, and the dural sleeve was repaired using fascia. The patient showed good improvement of symptoms after surgery.

LESSONS

Excessive CSF absorption through the enlarged spinal arachnoid villi–like structure can cause secondary Chiari malformation. Neurosurgeons should be aware of this unusual mechanism of CSF leakage. Simple posterior fossa decompression will be ineffective or even harmful.

Open access

Izumi Koyanagi, Yasuhiro Chiba, Hiroyuki Imamura, and Toshiya Osanai

BACKGROUND

Intradural radicular arteriovenous malformation (AVM) of the cauda equina is a rare entity of spinal AVMs. Because of the specific arterial supply of the conus medullaris and cauda equina, AVMs in this area sometimes present with confusing radiological features.

OBSERVATIONS

The authors reported a rare case of intradural radicular AVM arising from the lumbar posterior root. The patient presented with urinary symptoms with multiple flow void around the conus medullaris, as shown on magnetic resonance imaging. Digital subtraction angiography demonstrated arteriovenous shunt at the left side of the conus medullaris fed by the anterior spinal artery via anastomotic channel to the posterior spinal artery and rich perimedullary drainers. There was another arteriovenous shunt at the L3 level from the left L4 radicular artery. Preoperative diagnosis was perimedullary AVM with radicular arteriovenous fistula. Direct surgery with indocyanine green angiography revealed that the actual arteriovenous shunt was located at the left L4 posterior root. The AVM was successfully treated by coagulation of feeding branches.

LESSONS

Unilateral arteriovenous shunt fed by either posterior or anterior spinal artery at the conus medullaris may include AVM of the cauda equina despite abundant perimedullary venous drainage. Careful pre- and intraoperative diagnostic imaging is necessary for appropriate treatment.

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Charles H. Tator and Izumi Koyanagi

✓ Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3–5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3–9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

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Charles H. Tator and Izumi Koyanagi

Vascular injury plays an important role in the primary and secondary injury mechanisms that cause damage to the acutely traumatized spinal cord. To understand the pathophysiology of human spinal cord injury, the authors investigated the vascular system in three uninjured human spinal cords using silicone rubber microangiography and analyzed the histological findings related to vascular injury in nine acutely traumatized human spinal cords obtained at autopsy. The interval from spinal cord injury to death ranged from 20 minutes to 9 months. The microangiograms of the uninjured human cervical cords demonstrated new information about the sulcal arterial system and the pial arteries. The centrifugal sulcal arterial system was found to supply all of the anterior gray matter, the anterior half of the posterior gray matter, approximately the inner half of the anterior and lateral white columns, and the anterior half of the posterior white columns. Traumatized spinal cord specimens in the acute stage (3-5 days postinjury) showed severe hemorrhages predominantly in the gray matter, but also in the white matter. The white matter surrounding the hemorrhagic gray matter showed a variety of lesions, including decreased staining, disrupted myelin, and axonal and periaxonal swelling. The white matter lesions extended far from the injury site, especially in the posterior columns. There was no evidence of complete occlusion of any of the larger arteries, including the anterior and posterior spinal arteries and the sulcal arteries. However, occluded intramedullary veins were identified in the degenerated posterior white columns. In the chronic stage (3-9 months postinjury), the injured segments showed major tissue loss with large cavitations, whereas both rostral and caudal remote sites showed well-demarcated necrotic areas indicative of infarction mainly in the posterior white columns. Obstruction of small intramedullary arteries and veins by the initial mechanical stress or secondary injury mechanisms most likely produced these extensive white matter lesions. Our studies implicate damage to the anterior sulcal arteries in causing the hemorrhagic necrosis and subsequent central myelomalacia at the injury site in acute spinal cord injury in humans.

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Kazuhisa Yoshifuji, Nobuhito Morota, Yoshinori Omori, Izumi Koyanagi, and Nobuhiro Mikuni

OBJECTIVE

Spinal lipomas are congenital malformations. They do not express tumorous growth but are found to increase in volume like other normal subcutaneous fat tissue during the early postnatal period. To understand the natural course of volume changes in spinal lipomas, the authors measured the changes in size of spinal lipomas together with the normal subcutaneous fat in relation to BMI.

METHODS

A total of 27 patients with conus spinal lipoma excluding lipomyelomeningocele who underwent MRI twice before surgery (on initial diagnosis and immediately preoperatively) were included. Patients’ ages at the time of the first MRI ranged from 0 to 32 months (mean 2.9 months, median 1 month). Candidates were categorized by age into three groups: < 1 month, 1–2 months, and ≥ 3 months. The growth rate of the spinal lipomas (in three directions), change in thickness of the normal subcutaneous fat, growth rate of the normal spinal canal (dorsoventral direction), and change in BMI were retrospectively analyzed between the three groups.

RESULTS

The mean interval between MRI studies was 83.1 days. During this time, the mean lipoma growth rates were 199%, 149%, and 133% in the dorsoventral, lateral, and craniocaudal directions, respectively (with 100% representing the first measurement). The mean change in the thickness of the normal subcutaneous fat was 183%. The mean growth of the normal spinal canal was 111%. The mean increase in BMI was 124%. These rates were all significantly higher in the younger groups. There was no significant difference in the growth rates between the lipoma and the subcutaneous fat in every age group. In contrast, the growth rate of the lipoma significantly exceeded that of the spinal canal in patients younger than 3 months. The subarachnoid space around the lipoma became obstructed in 35.3%, and spinal cord distortion occurred in 48.1% of the patients younger than 3 months.

CONCLUSIONS

Spinal lipomas rapidly increase in volume before the age of 3 months and especially in infants younger than 1 month. Their features closely correlate with the physiological growth of the normal subcutaneous fat and the increase in BMI. The rapid growth of lipomas suggests the importance of close observation in this period, keeping in mind the typical anatomical changes of lipomas and their surrounding structures.

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Takeo Baba, Yoshihiro Minamida, Takeshi Mikami, Izumi Koyanagi, and Kiyohiro Houkin

✓ The authors report on the case of a 14-year-old boy who presented with bilateral visual impairment due to optic canal stenosis caused by hyperplasia of the bone marrow arising from anemia. The patient had hereditary hemolytic anemia with unstable hemoglobin of the Christchurch type. This congenital form of anemia caused hyperplasia of the bone marrow as well as hyperostosis of the entire calvarial bone, which in turn led to optic canal stenosis. The patient underwent surgical decompression of the optic canal, resulting in significant improvement in visual acuity. Pathological findings in the calvarial bone indicated hypertrophic bone marrow with no other specific features such as neoplastic pattern or fibrous dysplasia. With the exception of objective hearing impairment, no other significant cranial neuropathy has been detected thus far.

On reviewing the published literature, this case was found to be the first in which hyperostosis due to congenital anemia resulted in symptomatic entrapment neuropathy of the optic nerve. The authors concluded that surgical decompression effectively improves visual acuity.

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Izumi Koyanagi, Yoshinobu Iwasaki, Kazutoshi Hida, Hiroyuki Imamura, and Hiroshi Abe

Object. Because of the lack of magnetic resonance (MR) signal from cortical bones, MR imaging is inadequate for diagnosing ossified lesions in the spinal canal. However, MR imaging provides important information on spinal cord morphology and associated soft-tissue abnormality. The purpose of this study is to determine the role of MR imaging in the diagnosis and treatment of patients with ossification of the posterior longitudinal ligament (OPLL) of the cervical spine.

Methods. The authors reviewed MR imaging findings in 42 patients with cervical OPLL who were examined with a superconducting MR imaging system. The types of OPLL reviewed included eight cases of continuous, 21 cases of segmental, and 13 cases of the mixed type. All patients were treated surgically either by anterior (26 cases) or posterior decompression (16 cases).

Conclusions. The T1-weighted images clearly demonstrated the spinal cord deformity caused by OPLL. Associated disc protrusion was found to be present at the maximum compression level in 60% of the patients in this series. The highest incidence of disc protrusion (81%) was found in patients with segmental OPLL. Intramedullary hyperintensity on T2*-weighted imaging was noted in 18 patients (43%). The neurological deficits observed in these 18 patients were significantly more severe than those observed in the other 24 patients. Postoperative MR imaging revealed improvement in the spinal cord deformity, although the intramedullary hyperintensity was still observed in most cases. The present study demonstrates the importance of associated disc protrusion in the development of myelopathy in patients with cervical OPLL. Magnetic resonance imaging findings may be used to help determine the actual levels of spinal cord compression and to suggest the method of surgical treatment.

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Jangbo Lee, Izumi Koyanagi, Kazutoshi Hida, Toshitaka Seki, Yoshinobu Iwasaki, and Kenji Mitsumori

Object

Spinal cord edema is a rare radiological finding in chronic degenerative disorders of the spine. Between 1997 and 2001, the authors treated six patients with cervical spondylotic myelopathy in whom postoperative spinal cord edema was demonstrated. The authors describe the radiological and clinical features of this unusual condition.

Methods

The six patients were all men, and ranged in age from 44 to 72 years. All patients presented with mild quadriparesis and underwent laminoplasty or anterior fusion. Preoperative magnetic resonance (MR) imaging revealed marked spinal cord compression with intramedullary hyperintensity on T2-weighted sequences and spinal cord enhancement at the compression level after administration of Gd.

After surgery, spinal cord edema was observed in all patients; the spinal cord appeared swollen on the postoperative MR images. Preoperative and postoperative Gd-enhanced MR imaging demonstrated clear enhancement of the white matter at the compressed segment. Neurologically, five of six patients experienced good improvement of symptoms; however, the spinal cord edema as documented on follow-up MR imaging persisted for several months after surgery.

Conclusions

The radiological characterization of spinal cord edema was based on the reversible white matter lesion most likely caused by disturbed local venous circulation induced by chronic spinal cord compression. Such unusual MR findings in cervical spondylotic myelopathy should be differentiated from intramedullary spinal cord tumors, demyelinating disorders, or inflammatory processes.