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Tomohiro Murakami, Izumi Koyanagi, Takahisa Kaneko, Akihiro Yoneta, Yoshiko Keira, Masahiko Wanibuchi, Tadashi Hasegawa and Nobuhiro Mikuni

Hyperhidrosis is caused by a sympathetic dysfunction of the central or peripheral nervous system. Intramedullary spinal cord lesions can be a cause of hyperhidrosis. The authors report a rare case of intramedullary thoracic spinal cord ganglioglioma presenting as hyperhidrosis. This 16-year-old boy presented with abnormal sweating on the right side of the neck, chest, and the right arm that had been occurring for 6 years. Neurological examination revealed mild motor weakness of the right lower extremity and slightly decreased sensation in the left lower extremity. Hyperhidrosis was observed in the right C3–T8 dermatomes. Magnetic resonance imaging showed an intramedullary tumor at the right side of the spinal cord at the T2–3 level. The tumor showed partial enhancement after Gd administration. The patient underwent removal of the tumor via hemilaminectomy of T2–3. Only subtotal resection was achieved because the margins of the tumor were unclear. Histopathological examination revealed ganglioglioma. Hyperhidrosis gradually improved after surgery. Hyperhidrosis is a rare clinical manifestation of intramedullary spinal cord tumors, and only a few cases have been reported in the literature. The location of the tumor origin, around the right gray matter of the lateral spinal cord, may account for the hyperhidrosis as the initial symptom in this patient. Physicians should examine the spinal cord using MRI studies when a patient has hyperhidrosis with some motor or sensory symptoms of the extremities.

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

Object

An anterior clinoidectomy can provide enormous benefits, facilitating the management of paraclinoid and upper basilar artery lesions, but it also carries the potential risk of cerebrospinal fluid leaks. The aim of this study was to assess the variation in the pneumatization of the anterior clinoid process (ACP) in an attempt to reduce the complications associated with an anterior clinoidectomy.

Methods

The authors analyzed the anatomical variations in the pneumatization of the ACP and optical strut (OS) in 600 sides of 300 consecutive patients by using multidetector-row computed tomography (CT). Computed tomography scans with a 0.5-mm thickness were obtained, and coronal and sagittal reconstructions of the images were displayed in all cases. Pneumatization of the ACP was found in 9.2% of all sides. The origin of pneumatization was the sphenoid sinus in 81.8% of all the sides, the ethmoid sinus in 10.9%, and both of these sinuses in 7.3%. Pneumatized patterns were divided into three groups according to the route: 74.5% were Type I, in which pneumatization occurred via the OS; 14.5% were Type II, pneumatization via the anterior root (AR); and 10.9% were Type III, pneumatization via both the OS and the AR. The origin of pneumatization and the pneumatization pattern showed statistical dependence (p < 0.001). Pneumatization of the OS beyond its narrowest point was found in 6.8% of all sides.

Conclusions

An awareness of the different variations in pneumatization can prevent destruction of the mucous membrane and facilitate orientation during reconstruction with cranialization. During an anterior clinoidectomy, preoperative CT assessments are necessary to evaluate pneumatization of the ACP.

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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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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.

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

Object. It is known that the spinal cord can sustain traumatic injury without associated injury of the spinal column in some conditions, such as a flexible spinal column or preexisting narrowed spinal canal. The purpose of this study was to characterize the clinical features and to understand the mechanisms in cases of acute cervical cord injury in which fracture or dislocation of the cervical spine has not occurred.

Methods. Eighty-nine patients who sustained an acute cervical cord injury were treated in our hospitals between 1990 and 1998. In 42 patients (47%) no bone injuries of the cervical spine were demonstrated, and this group was retrospectively analyzed. There were 35 men and seven women, aged 19 to 81 years (mean 58.9 years). The initial neurological examination indicated complete injury in five patients, whereas incomplete injury was demonstrated in 37.

In the majority of the patients (90%) the authors found degenerative changes of the cervical spine such as spondylosis (22 cases) or ossification of the posterior longitudinal ligament (16 cases). The mean sagittal diameter of the cervical spinal canal, as measured on computerized tomography scans, was significantly narrower than that obtained in the control patients. Magnetic resonance (MR) imaging revealed spinal cord compression in 93% and paravertebral soft-tissue injuries in 58% of the patients.

Conclusions. Degenerative changes of the cervical spine and developmental narrowing of the spinal canal are important preexisting factors. In the acute stage MR imaging is useful to understand the level and mechanisms of spinal cord injury. The fact that a significant number of the patients were found to have spinal cord compression despite the absence of bone injuries of the spinal column indicates that future investigations into surgical treatment of this type of injury are necessary.

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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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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.