- Email: [email protected]
Brown-Sequard syndrome caused by ossification of the ligamentum flavum
Case reports / Journal of Clinical Neuroscience 14 (2007) 887–890
887
Brown-Sequard syndrome caused by ossification of the ligamentum flavum Pin-Yuan Chen a
a,*
, Chin-Yew Lin b, Wen-Ching Tzaan a, Hsien-Chih Chen
a
Department of Neurosurgery, Chang Gung University and Chang Gung Memorial Hospital, 222, Mai-Chin Road, Keelung 204, Taiwan, Republic of China b Department of Pathology, Chang Gung University and Chang Gung Memorial Hospital, Republic of China Received 19 January 2006; accepted 3 July 2006
Abstract Ossification of the ligamentum flavum (OLF) commonly occurs in the thoracic and lumbar regions. We present a patient with OLF at the C4–5 level with presentation as Brown-Sequard syndrome. Symptoms were relieved following a laminectomy and total lesion excision. The relevant literature is reviewed to discuss the racial distribution, unique presentation and pathogenesis of OLF. 2006 Elsevier Ltd. All rights reserved. Keywords: Brown-Sequard syndrome; Ossification of the ligamentum flavum; Cervical spine
1. Introduction Ossification of the ligamentum flavum (OLF) is rare in the cervical region and frequently presents with radiculopathy or myelopathy. The Brown-Sequard syndrome features ipsilateral upper motor neuron paralysis and loss of proprioception and vibratory sensation, combined with contralateral loss of pain and temperature sensation. Traumatic injury to the spinal cord is the most common cause of the condition. This report describes a rare case of OLF at the C4–5 level, resulting in Brown-Sequard syndrome that was relieved dramatically with surgery. 2. Case report A 61-year-old Taiwanese female, a writer, suffered mild left hand numbness for several years for which she had not sought medical treatment. She was admitted to the neurosurgery department at Chang Gung Memorial Hospital due to progressive weakness and clumsiness of her left extremities and numbness with an intermittent burning sensation over the right side of her body for 3 months prior to this admission. No urine or stool incontinence was observed. The patient had no history of neck injury, diabetes mellitus or any other systemic disease. On admission, a neurological physical examination revealed left-sided limb weakness. Deep tendon reflexes were increased in both legs, and she had ankle clonus on the left. Proprioception, touch, and vibratory sensations were impaired on the left, whereas pinprick and temperature sensa*
Corresponding author. Tel.: +886 2 2431 3131x2670; fax: +886 2 2433 2655. E-mail address: [email protected] (P.-Y. Chen).
tions were impaired on the right side of the body below the neck. Pinprick sensation in the left C5 and C6 dermatomes was also diminished. Concentrations of blood glucose, phosphate, calcium and uric acid were within normal limits. A test for human leukocyte antigen B27 (HLA-B27) was negative. A lateral cervical spine roentgenogram demonstrated a round hyperdense lesion at the posterior part of the C4–5 canal (Fig. 1). MRI of the spine indicated a nodular lesion with low signal intensity continuous with the ligamentum flavum at the C4–5 level on the left side with cord compression. Also noted was C4–7 osteophyte formation with spinal canal stenosis (Fig. 2a,b). A laminectomy was performed at C3–7 and the nodular mass was removed en bloc. The lesion was contained within the ligament without connection to the lamina or dura. Dural indentation was seen. Pathologically, the specimen was a firm bony fragment, measuring 1.0 · 0.6 · 0.3 cm, and was attached to the ligamentum flavum. Microscopic examination demonstrated lamellar bone formation within the ligament. Fibrocartilaginous cells with ossified areas, which adjoined the ligament, were observed (Fig. 3). Polarized light microscopy examination revealed no crystal elements. Following surgery, the patient’s neurological deficits recovered dramatically. Sensation returned to normal, and muscle power was regained after 3 months. 3. Discussion Since the first reported case of calcification/ossification of the ligamentum flavum (OLF) by Polgar in 1920, this entity has been implicated in thoracic myelopathy in Japanese
888
Case reports / Journal of Clinical Neuroscience 14 (2007) 887–890
populations.1 Kudo identified asymptomatic OLF in 6.2% of male and 4.8% of female Japanese patients after reviewing 1744 chest radiographs.2 The incidence of OLF in Chinese populations remains unknown; however, it is likely
Fig. 1. A round hyperintense lesion (white arrow) located at the posterior part of the spinal canal at the C4–5 level on plain lateral X-ray.
Fig. 3. Photomicrograph shows ossification (O) and fibrocartilaginous (FC) areas in the ligamentum flavum (Hematoxylin and eosin staining, ·40).
Fig. 2. A hypointense spindle-shaped lesion (white arrow) at the left-posterior part of the spinal canal at the C4–5 level is seen on the T2-weighted image, axial view (a). Multiple levels of stenosis with significant cord compression (white arrow) are seen on the sagittal view (b).
Case reports / Journal of Clinical Neuroscience 14 (2007) 887–890
not common. Li et al. described seven cases and Mak et al. reported one case.3,4 Genetic differences in different races or a lack of focus on this entity may be responsible for the racial differences in these reports. Sporadic reports for this lesion have come from other countries, including Arab, black, caucasian, Indian and Tunisian patients.1,5–8 Ossification of the ligamentum flavum (OLF) is found predominantly in the thoracic and lumbar spine and seldom in the cervical spine. Kobayashi et al. described one male patient with OLF in the cervical spine and reviewed seven additional Japanese cases in 1991.9 In that report, average age was 53.5 years, and the male:female ratio was 5:3. Most lesions in that study occurred at the C5–6 and C6–7 levels. Four patients had multiple-level lesions, and two had laterality. Kruse et al. described one patient with cervical OLF. 7 In Chinese patients, Li et al. described two men with low cervical spine involvement without laterality, and Mak et al. reported a 71-year-old man with a lesion on the right side of the cervicothoracic junction.3,4 All reported cases presented with cervical radiculopathy or myelopathy; thus, the clinical picture of Brown-Sequard syndrome in this patient is unique. In our patient, the presentation may have been due to the OLF lesion superimposed on pre-existing spinal canal stenosis on one side. Compression of the left posterior column and lateral corticospinal tract produced ipsilateral impairment of proprioception, vibratory sensation and motor function. Compression of the left posterior gray horn caused impaired pinprick sensation of the ipsilateral C5 and C6 dermatomes. Compression of left spinothalamic tract resulted in contralateral impairment of pain and temperature sensation. Histologically, OLF results from metaplastic endochondral ossification. Various stages in the metaplastic process can be identified in adjacent areas. Hypertrophy of the ligamentum flavum, with an increase in the number and size of collagen fibers and a decrease in elastic fibers is commonly seen. Fibrocartilaginous cells usually produce cartilaginous matrices, and osteoblasts generate lamellar bone with abundant osteous and Haversian canals.4,8 Bone marrow can develop in rare cases.9 Calcification of the ligamentum flavum, which is another entity defined by many authors8–12 occurs most frequently in the cervical spine and is diagnosed via detection of crystals of calcium pyrophosphate dihydrate or calcium hydroxyapatite within the ligamentum flavum without mature bone formation. In our patient, endochondral ossification was identified without any crystal formation; thus, diagnosis of OLF was straightforward. The etiology of OLF remains unknown. Maigne et al. determined that OLF may be a normal feature of an aging spine. This process initiates with ligament hypertrophy, then proceeds through calcification to ossification.13 Miyamoto et al. described elevation of plasma fibronectin concentrations in OLF patients, which may enhance differentiation of fibroblasts into chondrocytes.14 Bone morphogenic protein-2 (BMP) has also been identified, and can induce differentiation of fibroblasts into chondrocytes. Notably, BMP
889
and its receptor have been shown to be expressed at the ossified site.15,16 Associations of OLF with ossification of the posterior longitudinal ligament (OPLL), diffuse idiopathic skeletal hyperostosis, Paget’s disease, X-linked hyperphosphatemia, hyperthyroidism, diabetes mellitus and obesity have all been reported.5,4,17 In our patient, neither OPLL, metabolic diseases nor abnormal electrolyte levels were observed. Cervical OLF occurs much less frequently than thoracic and lumbar OLF, likely as a result of two factors: the capsular portion of the ligamentum flavum above the C6 level does not adhere to bone tissue and ossification always starts at the ligament-osseous junction (enthesis); and, dynamic tension affects the cervical ligamentum flavum, which maintains an increased number of elastic fibers.18 The process of ossification is therefore uncommon. In this patient, a lack of neck motion during long periods of work may have caused formation of cervical OLF. Ossification of the ligamentum flavum can be detected on lateral plain radiography. Computed tomography is standard for documenting OLF. An MRI provides additional important information. Typically, OLF presents as a triangular or hemispheric area of either central hyperintensity surrounded by a hypointense margin or hypointensity on T1- and T2-weighted images in the posterior margin of the canal. MRI facilitates extensive longitudinal visualization of the spinal canal and can detect multilevel lesions. Study by MRI also demonstrates the degree of medullary compression.1,19 In this patient, nodular OLF involved only one level, and did not adhere to the dura. Consequently, en bloc removal of the lesion was possible and surgical outcome was satisfactory. Dural adhesions were noted in 62% of cases in the series reported by Miyakoshi et al.20 Dural adhesions are a preoperative deleterious factor for short-term postoperative neurological status, but not for the long-term prognosis of OLF of the thoracic spine. The incidence of OLF of the cervical spine with dural adhesions and its prognosis remain to be determined. 4. Conclusion Ossification of the ligamentum flavum in the cervical spine is rare and must be differentiated from calcification or hypertrophy of the ligamentum flavum. Clinically, Brown-Sequard syndrome caused by OLF is extremely rare. Neurosurgeons should be aware of OLF as a possible cause of cervical spinal cord compression and carefully dissect lesions during surgery to avoid tearing the dura.
References 1. Trivedi P, Behari S, Paul L, et al. Thoracic myelopathy secondary to ossified ligamentum flavum. Acta Neurochir(wien) 2001;143:775–82. 2. Kudo S, Ono M, Russel W, et al. Ossification of thoracic ligamenta flava. Am J Roentgenol 1983;141:117–21.
890
Case reports / Journal of Clinical Neuroscience 14 (2007) 890–895
3. Li KK, Chung OM, Chang YP, et al. Myelopathy caused by ossification of ligamentum flavum. Spine 2002;27:E308–12. 4. Mak KH, Mak KL, Gwi-Mak E. Ossification of the ligamentum flavum in the cervicothoracic junction. Spine 2002;27:E11–4. 5. Al-Orainy IA, Kolawole T. Ossification of the ligament flavum. Euro J Radiolog 1998;29:76–82. 6. Wiseman DB, Stokes JK, Toselli RM. Paraparesis in a black man brought on by ossification of the ligamentum flavum: case report and review of the literature. J Spinal Disord Tech 2002;15:542–5. 7. Kruse JJ, Awasthi D, Harris M, et al. Ossification of ligamentum flavum as a cause of myelopathy in North America: Report of three cases. J Spinal Disord Tech 2000;13:22–5. 8. Ben Hamouda K, Jemel H, Haouet S, et al. Thoracic myelopathy caused by ossification of the ligamentum flavum : a report of 18 cases. J Neurosurg (Spine 2) 2003;99:157–61. 9. Kobayashi S, Okada K, Onoda K, et al. Ossification of the cervical ligamentum flavum. Surg Neurol 1991;35:234–48. 10. Iwasaki Y, Akino M, Abe H, et al. Calcification of the ligamentum flavum of the cervical spine: report of four cases. J Neurosurg 1983;59:531–4. 11. Kawano N, Maesuno T, Miyazawa S, et al. Calcium pyrophosphate dihydrate crystal deposition disease in the cervical ligamentum flavum. J Neurosurg 1988;68:613–20. 12. Muthukumar N, Karuppaswamy U, Sankarasubbu B. Calcium pyrophosphate dihydrate deposition disease causing thoracic cord compression: case report. J Neurosurg 2000;46:222–5.
13. Maigne JY, Ayral X, Guerin-Surville H. Frequency and size of ossification in the caudal attachments of the ligamentum flavum of the thoracic spine : role of rotatory strains in their development: An anatomic study of 121 spines. Surg Radiol Anat 1992;14:119–24. 14. Miyakoshi N, Shimada Y, Suzuki T, et al. Factors related to longterm outcome after decompressive surgery for ossification of the ligamentum flavum of the thoracic spine. J Neurosurg(3 Suppl) 2003;99:251–6. 15. Hayashi K, Ishidou Y, Yonemori K, et al. Expression and localization of bone morphogenic proteins (BMPs) and BMP receptors in the ossification of the ligamentum flavum. Spine 1997;22:710–5. 16. Hoshi K, Amizuka N, Sakou T, et al. Fibroblasts of spinal ligaments pathologically differentiate into chondrocytes induced by recombinant human bone morphogenetic protein-2: morphological examinations for ossification of spinal ligaments. Bone 1997;21:23–30. 17. Sugimura H, Kakitisubata Y, Suzuki Y, et al. MRI of ossification of ligamentum flavum. J Comput Assist Tomogr 1992;16:73–6. 18. Hotta Y. Anatomical study of the yellow ligament of spine with special reference to its ossification. J Jpn Orthop Assoc 1985;59:311–25. 19. Hanakita J, Suwa H, Ohta F, et al. Neuroradiological examination of thoracic radiculomyopathy due to ossification of the ligamentum flavum. Neuroradiology 1990;32:38–42. 20. Miyamoto S, Yonenbu K, Ono K. Elevated plasma fibronectin concentrations in patients with ossification of posterior longitudinal ligament and ossification of ligamentum flavum. Spine 1993;18: 2267–70.
doi:10.1016/j.jocn.2006.07.002
Spontaneous superior sagittal sinus thrombosis secondary to type II heparin-induced thrombocytopenia presenting as an acute subarachnoid hemorrhage Kostas N. Fountas a
a,*
, Laurie R. Faircloth a, Tom Hope b, Arthur A. Grigorian
a
Department of Neurosurgery, Medical Center of Central Georgia, School of Medicine, Mercer University, Macon, GA, USA Department of Neurology, Medical Center of Central Georgia, School of Medicine, Mercer University, Macon, GA, USA
b
Received 10 March 2006; accepted 13 June 2006
Abstract Cerebral sinus thrombosis is a rare cause of spontaneous subarachnoid hemorrhage. The development of cerebral sinus thrombosis as a complication of heparin-induced thrombocytopenia is even rarer. In this paper, we present a 59-year-old patient admitted to our service with cerebral sinus thrombosis secondary to type II heparin-induced thrombocytopenia. We also review the literature in regard to the incidence, pathophysiology and management of this rare clinicopathological entity. 2006 Published by Elsevier Ltd. Keywords: Heparin; Subarachnoid hemorrhage; Superior sagittal sinus; Thrombocytopenia; Thrombosis
1. Introduction *
Corresponding author. Present address: 840 Pine St. Suite 880, Macon, GA 31201, USA. Tel.: +1 478 743 7092x213; fax: +1 478 743 0523. E-mail address: [email protected] (K.N. Fountas).
Superior sagittal sinus (SSS) thrombosis is a rare but well-described disease. Several factors have been associated with SSS thrombosis such as bacterial fulminant
887
Brown-Sequard syndrome caused by ossification of the ligamentum flavum Pin-Yuan Chen a
a,*
, Chin-Yew Lin b, Wen-Ching Tzaan a, Hsien-Chih Chen
a
Department of Neurosurgery, Chang Gung University and Chang Gung Memorial Hospital, 222, Mai-Chin Road, Keelung 204, Taiwan, Republic of China b Department of Pathology, Chang Gung University and Chang Gung Memorial Hospital, Republic of China Received 19 January 2006; accepted 3 July 2006
Abstract Ossification of the ligamentum flavum (OLF) commonly occurs in the thoracic and lumbar regions. We present a patient with OLF at the C4–5 level with presentation as Brown-Sequard syndrome. Symptoms were relieved following a laminectomy and total lesion excision. The relevant literature is reviewed to discuss the racial distribution, unique presentation and pathogenesis of OLF. 2006 Elsevier Ltd. All rights reserved. Keywords: Brown-Sequard syndrome; Ossification of the ligamentum flavum; Cervical spine
1. Introduction Ossification of the ligamentum flavum (OLF) is rare in the cervical region and frequently presents with radiculopathy or myelopathy. The Brown-Sequard syndrome features ipsilateral upper motor neuron paralysis and loss of proprioception and vibratory sensation, combined with contralateral loss of pain and temperature sensation. Traumatic injury to the spinal cord is the most common cause of the condition. This report describes a rare case of OLF at the C4–5 level, resulting in Brown-Sequard syndrome that was relieved dramatically with surgery. 2. Case report A 61-year-old Taiwanese female, a writer, suffered mild left hand numbness for several years for which she had not sought medical treatment. She was admitted to the neurosurgery department at Chang Gung Memorial Hospital due to progressive weakness and clumsiness of her left extremities and numbness with an intermittent burning sensation over the right side of her body for 3 months prior to this admission. No urine or stool incontinence was observed. The patient had no history of neck injury, diabetes mellitus or any other systemic disease. On admission, a neurological physical examination revealed left-sided limb weakness. Deep tendon reflexes were increased in both legs, and she had ankle clonus on the left. Proprioception, touch, and vibratory sensations were impaired on the left, whereas pinprick and temperature sensa*
Corresponding author. Tel.: +886 2 2431 3131x2670; fax: +886 2 2433 2655. E-mail address: [email protected] (P.-Y. Chen).
tions were impaired on the right side of the body below the neck. Pinprick sensation in the left C5 and C6 dermatomes was also diminished. Concentrations of blood glucose, phosphate, calcium and uric acid were within normal limits. A test for human leukocyte antigen B27 (HLA-B27) was negative. A lateral cervical spine roentgenogram demonstrated a round hyperdense lesion at the posterior part of the C4–5 canal (Fig. 1). MRI of the spine indicated a nodular lesion with low signal intensity continuous with the ligamentum flavum at the C4–5 level on the left side with cord compression. Also noted was C4–7 osteophyte formation with spinal canal stenosis (Fig. 2a,b). A laminectomy was performed at C3–7 and the nodular mass was removed en bloc. The lesion was contained within the ligament without connection to the lamina or dura. Dural indentation was seen. Pathologically, the specimen was a firm bony fragment, measuring 1.0 · 0.6 · 0.3 cm, and was attached to the ligamentum flavum. Microscopic examination demonstrated lamellar bone formation within the ligament. Fibrocartilaginous cells with ossified areas, which adjoined the ligament, were observed (Fig. 3). Polarized light microscopy examination revealed no crystal elements. Following surgery, the patient’s neurological deficits recovered dramatically. Sensation returned to normal, and muscle power was regained after 3 months. 3. Discussion Since the first reported case of calcification/ossification of the ligamentum flavum (OLF) by Polgar in 1920, this entity has been implicated in thoracic myelopathy in Japanese
888
Case reports / Journal of Clinical Neuroscience 14 (2007) 887–890
populations.1 Kudo identified asymptomatic OLF in 6.2% of male and 4.8% of female Japanese patients after reviewing 1744 chest radiographs.2 The incidence of OLF in Chinese populations remains unknown; however, it is likely
Fig. 1. A round hyperintense lesion (white arrow) located at the posterior part of the spinal canal at the C4–5 level on plain lateral X-ray.
Fig. 3. Photomicrograph shows ossification (O) and fibrocartilaginous (FC) areas in the ligamentum flavum (Hematoxylin and eosin staining, ·40).
Fig. 2. A hypointense spindle-shaped lesion (white arrow) at the left-posterior part of the spinal canal at the C4–5 level is seen on the T2-weighted image, axial view (a). Multiple levels of stenosis with significant cord compression (white arrow) are seen on the sagittal view (b).
Case reports / Journal of Clinical Neuroscience 14 (2007) 887–890
not common. Li et al. described seven cases and Mak et al. reported one case.3,4 Genetic differences in different races or a lack of focus on this entity may be responsible for the racial differences in these reports. Sporadic reports for this lesion have come from other countries, including Arab, black, caucasian, Indian and Tunisian patients.1,5–8 Ossification of the ligamentum flavum (OLF) is found predominantly in the thoracic and lumbar spine and seldom in the cervical spine. Kobayashi et al. described one male patient with OLF in the cervical spine and reviewed seven additional Japanese cases in 1991.9 In that report, average age was 53.5 years, and the male:female ratio was 5:3. Most lesions in that study occurred at the C5–6 and C6–7 levels. Four patients had multiple-level lesions, and two had laterality. Kruse et al. described one patient with cervical OLF. 7 In Chinese patients, Li et al. described two men with low cervical spine involvement without laterality, and Mak et al. reported a 71-year-old man with a lesion on the right side of the cervicothoracic junction.3,4 All reported cases presented with cervical radiculopathy or myelopathy; thus, the clinical picture of Brown-Sequard syndrome in this patient is unique. In our patient, the presentation may have been due to the OLF lesion superimposed on pre-existing spinal canal stenosis on one side. Compression of the left posterior column and lateral corticospinal tract produced ipsilateral impairment of proprioception, vibratory sensation and motor function. Compression of the left posterior gray horn caused impaired pinprick sensation of the ipsilateral C5 and C6 dermatomes. Compression of left spinothalamic tract resulted in contralateral impairment of pain and temperature sensation. Histologically, OLF results from metaplastic endochondral ossification. Various stages in the metaplastic process can be identified in adjacent areas. Hypertrophy of the ligamentum flavum, with an increase in the number and size of collagen fibers and a decrease in elastic fibers is commonly seen. Fibrocartilaginous cells usually produce cartilaginous matrices, and osteoblasts generate lamellar bone with abundant osteous and Haversian canals.4,8 Bone marrow can develop in rare cases.9 Calcification of the ligamentum flavum, which is another entity defined by many authors8–12 occurs most frequently in the cervical spine and is diagnosed via detection of crystals of calcium pyrophosphate dihydrate or calcium hydroxyapatite within the ligamentum flavum without mature bone formation. In our patient, endochondral ossification was identified without any crystal formation; thus, diagnosis of OLF was straightforward. The etiology of OLF remains unknown. Maigne et al. determined that OLF may be a normal feature of an aging spine. This process initiates with ligament hypertrophy, then proceeds through calcification to ossification.13 Miyamoto et al. described elevation of plasma fibronectin concentrations in OLF patients, which may enhance differentiation of fibroblasts into chondrocytes.14 Bone morphogenic protein-2 (BMP) has also been identified, and can induce differentiation of fibroblasts into chondrocytes. Notably, BMP
889
and its receptor have been shown to be expressed at the ossified site.15,16 Associations of OLF with ossification of the posterior longitudinal ligament (OPLL), diffuse idiopathic skeletal hyperostosis, Paget’s disease, X-linked hyperphosphatemia, hyperthyroidism, diabetes mellitus and obesity have all been reported.5,4,17 In our patient, neither OPLL, metabolic diseases nor abnormal electrolyte levels were observed. Cervical OLF occurs much less frequently than thoracic and lumbar OLF, likely as a result of two factors: the capsular portion of the ligamentum flavum above the C6 level does not adhere to bone tissue and ossification always starts at the ligament-osseous junction (enthesis); and, dynamic tension affects the cervical ligamentum flavum, which maintains an increased number of elastic fibers.18 The process of ossification is therefore uncommon. In this patient, a lack of neck motion during long periods of work may have caused formation of cervical OLF. Ossification of the ligamentum flavum can be detected on lateral plain radiography. Computed tomography is standard for documenting OLF. An MRI provides additional important information. Typically, OLF presents as a triangular or hemispheric area of either central hyperintensity surrounded by a hypointense margin or hypointensity on T1- and T2-weighted images in the posterior margin of the canal. MRI facilitates extensive longitudinal visualization of the spinal canal and can detect multilevel lesions. Study by MRI also demonstrates the degree of medullary compression.1,19 In this patient, nodular OLF involved only one level, and did not adhere to the dura. Consequently, en bloc removal of the lesion was possible and surgical outcome was satisfactory. Dural adhesions were noted in 62% of cases in the series reported by Miyakoshi et al.20 Dural adhesions are a preoperative deleterious factor for short-term postoperative neurological status, but not for the long-term prognosis of OLF of the thoracic spine. The incidence of OLF of the cervical spine with dural adhesions and its prognosis remain to be determined. 4. Conclusion Ossification of the ligamentum flavum in the cervical spine is rare and must be differentiated from calcification or hypertrophy of the ligamentum flavum. Clinically, Brown-Sequard syndrome caused by OLF is extremely rare. Neurosurgeons should be aware of OLF as a possible cause of cervical spinal cord compression and carefully dissect lesions during surgery to avoid tearing the dura.
References 1. Trivedi P, Behari S, Paul L, et al. Thoracic myelopathy secondary to ossified ligamentum flavum. Acta Neurochir(wien) 2001;143:775–82. 2. Kudo S, Ono M, Russel W, et al. Ossification of thoracic ligamenta flava. Am J Roentgenol 1983;141:117–21.
890
Case reports / Journal of Clinical Neuroscience 14 (2007) 890–895
3. Li KK, Chung OM, Chang YP, et al. Myelopathy caused by ossification of ligamentum flavum. Spine 2002;27:E308–12. 4. Mak KH, Mak KL, Gwi-Mak E. Ossification of the ligamentum flavum in the cervicothoracic junction. Spine 2002;27:E11–4. 5. Al-Orainy IA, Kolawole T. Ossification of the ligament flavum. Euro J Radiolog 1998;29:76–82. 6. Wiseman DB, Stokes JK, Toselli RM. Paraparesis in a black man brought on by ossification of the ligamentum flavum: case report and review of the literature. J Spinal Disord Tech 2002;15:542–5. 7. Kruse JJ, Awasthi D, Harris M, et al. Ossification of ligamentum flavum as a cause of myelopathy in North America: Report of three cases. J Spinal Disord Tech 2000;13:22–5. 8. Ben Hamouda K, Jemel H, Haouet S, et al. Thoracic myelopathy caused by ossification of the ligamentum flavum : a report of 18 cases. J Neurosurg (Spine 2) 2003;99:157–61. 9. Kobayashi S, Okada K, Onoda K, et al. Ossification of the cervical ligamentum flavum. Surg Neurol 1991;35:234–48. 10. Iwasaki Y, Akino M, Abe H, et al. Calcification of the ligamentum flavum of the cervical spine: report of four cases. J Neurosurg 1983;59:531–4. 11. Kawano N, Maesuno T, Miyazawa S, et al. Calcium pyrophosphate dihydrate crystal deposition disease in the cervical ligamentum flavum. J Neurosurg 1988;68:613–20. 12. Muthukumar N, Karuppaswamy U, Sankarasubbu B. Calcium pyrophosphate dihydrate deposition disease causing thoracic cord compression: case report. J Neurosurg 2000;46:222–5.
13. Maigne JY, Ayral X, Guerin-Surville H. Frequency and size of ossification in the caudal attachments of the ligamentum flavum of the thoracic spine : role of rotatory strains in their development: An anatomic study of 121 spines. Surg Radiol Anat 1992;14:119–24. 14. Miyakoshi N, Shimada Y, Suzuki T, et al. Factors related to longterm outcome after decompressive surgery for ossification of the ligamentum flavum of the thoracic spine. J Neurosurg(3 Suppl) 2003;99:251–6. 15. Hayashi K, Ishidou Y, Yonemori K, et al. Expression and localization of bone morphogenic proteins (BMPs) and BMP receptors in the ossification of the ligamentum flavum. Spine 1997;22:710–5. 16. Hoshi K, Amizuka N, Sakou T, et al. Fibroblasts of spinal ligaments pathologically differentiate into chondrocytes induced by recombinant human bone morphogenetic protein-2: morphological examinations for ossification of spinal ligaments. Bone 1997;21:23–30. 17. Sugimura H, Kakitisubata Y, Suzuki Y, et al. MRI of ossification of ligamentum flavum. J Comput Assist Tomogr 1992;16:73–6. 18. Hotta Y. Anatomical study of the yellow ligament of spine with special reference to its ossification. J Jpn Orthop Assoc 1985;59:311–25. 19. Hanakita J, Suwa H, Ohta F, et al. Neuroradiological examination of thoracic radiculomyopathy due to ossification of the ligamentum flavum. Neuroradiology 1990;32:38–42. 20. Miyamoto S, Yonenbu K, Ono K. Elevated plasma fibronectin concentrations in patients with ossification of posterior longitudinal ligament and ossification of ligamentum flavum. Spine 1993;18: 2267–70.
doi:10.1016/j.jocn.2006.07.002
Spontaneous superior sagittal sinus thrombosis secondary to type II heparin-induced thrombocytopenia presenting as an acute subarachnoid hemorrhage Kostas N. Fountas a
a,*
, Laurie R. Faircloth a, Tom Hope b, Arthur A. Grigorian
a
Department of Neurosurgery, Medical Center of Central Georgia, School of Medicine, Mercer University, Macon, GA, USA Department of Neurology, Medical Center of Central Georgia, School of Medicine, Mercer University, Macon, GA, USA
b
Received 10 March 2006; accepted 13 June 2006
Abstract Cerebral sinus thrombosis is a rare cause of spontaneous subarachnoid hemorrhage. The development of cerebral sinus thrombosis as a complication of heparin-induced thrombocytopenia is even rarer. In this paper, we present a 59-year-old patient admitted to our service with cerebral sinus thrombosis secondary to type II heparin-induced thrombocytopenia. We also review the literature in regard to the incidence, pathophysiology and management of this rare clinicopathological entity. 2006 Published by Elsevier Ltd. Keywords: Heparin; Subarachnoid hemorrhage; Superior sagittal sinus; Thrombocytopenia; Thrombosis
1. Introduction *
Corresponding author. Present address: 840 Pine St. Suite 880, Macon, GA 31201, USA. Tel.: +1 478 743 7092x213; fax: +1 478 743 0523. E-mail address: [email protected] (K.N. Fountas).
Superior sagittal sinus (SSS) thrombosis is a rare but well-described disease. Several factors have been associated with SSS thrombosis such as bacterial fulminant