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Intradural spinal teratoma is a rare tumor that can be associated with dysraphic defects. Although the origin of these tumors is traditionally thought to be secondary to primordial germ cells misplaced early in embryogenesis, the pathogenesis of intraspinal teratoma remains unclear. The authors present a series of patients in whom an intradural teratoma arose at the same site as a developmental spinal cord abnormality, including a split cord malformation, myelomeningocele, and lipomyelomeningocele. It is postulated that these lesions were the result of a dysembryogenic mechanism and were not neoplastic.

In a 25-year-old woman pregnant for the second time after a successful first pregnancy, a locally aggressive, invasive sacrum tumour was diagnosed. The execution of the necessary but potentially mutilating surgical procedures was seriously hampered even during the preparative phase, in spite of the conscious wish of the patient to comply, by her severe psychiatric problems (posttraumatic stress disorder with dissociative symptoms). The Psychiatric Consultation Service took over the case management and an integrated (biopsychosocial) diagnostic investigation was carried out, involving analysis of the problems on four system levels: the biological, the psychological, the social and the health care level. An integrated treatment plan was drafted. By collaboration of the entire multidisciplinary treatment team conditions were secured under which patient would let herself be treated. In this way she was enabled to undergo the necessary procedures, with good results.

Immediate diagnostic clarification is required in patients who develop acute or subacute symptoms suggestive of an intraspinal lesion. In case of symptoms indicating a monoradicular lesion a spinal CT investigation is mostly sufficient. Since polyradicular syndromes are often due to inflammation, examination of the cerebrospinal fluid is the most important diagnostic measure. However, in case of symptoms suggestive of intramedullary lesions, spinal MRT is by far the most effective diagnostic procedure. In patients with symptoms suggestive of a lesion of the cauda equina spinal CT is sufficient in most cases as a first measure, particularly if the lesion can be precisely localized by clinical examination. The decision as to which diagnostic method should be performed first is relevant mainly because of the limited availability of MRT examinations within the daily clinical routine. MRT should thus be used selectively in patients with lesions that cannot be identified by alternative diagnostic methods.

We report a 29-year-old man with diabetes insipidus and cerebellar ataxia who developed spinal cord swelling 15 years after the onset. He was well until 14 years of the age when he noted dizziness. Two years after there was an onset of gait disturbance and slurred speech. He also noted polydipsia and polyuria. He was evaluated at the neurosurgery service of our hospital when he was 17 years of the age. Neurologic examination at that time revealed memory loss, horizontal nystagmus, cerebellar ataxic gait, dysmetria and decomposition more on the left. Cranial CT scan revealed a mass lesion involving the left subthalamic region and the head of the caudate area. Spinal fluid was unremarkable, however, human chorionic gonadotropin was increased to 27 mIU/ml. He was treated by radiation therapy (3,000 rads for total brain area and 5,460 rads for focal region). His CT scan and memory loss improved, however, cerebellar ataxia was unchanged. Three years after the radiation, he started to show choreic movement in his neck and left upper extremity. He was admitted to our service in August 14, 1995 when he was 29 years of the age. On admission, he was alert but disoriented to time; calculation was also poor. Higher cerebral functions were intact. The optic fundi were normal without papilledema. Visual field appeared intact. Gaze nystagmus was observed in all the directions, but more prominent in the horizontal direction. Speech was slurred. Otherwise, cranial nerves were unremarkable. Motor wise, he showed marked truncal and gait ataxia; he was unable to walk because of ataxia. Muscle atrophy and marked weakness was noted in both upper extremities more on the left side. Deep tendon reflexes were diminished in the upper extremities but active in the lower extremities. He was polyuric; urinary specific gravity was low. Spinal fluid contained 6 cells/cmm and 113 mg/ dl of protein; Queckenstedt was positive. MRI revealed swelling of the cervical cord; in addition, the entire cervical region and the medullar oblongata appeared as high signal intensity areas. No mass lesion was noted in the supratentorial structures but the third ventricle was markedly enlarged. Surgical biopsy was performed on the cervical lesion. The patient was discussed in neurologic CPC, and the chief discussant arrived at the conclusion that the patient had germinoma with syncytiotrophoblastic giant cells in the diencephalic region which appeared to have been cured by radiation therapy; he thought that the cervical lesion was the seeding of germinoma. Cerebellar ataxia was ascribed to the remote effect of germinoma. Most of the participants thought that the original tumor was germinoma and the cervical lesion was its spread. Some participants thought that his ataxia was caused by germinoma cells involving the medulla and the inferior cerebellar peduncles. Histologic observation of the biopsied tissue from the spinal cord revealed the typical two cell patterned germinoma. Most of the tumor cells were not stained for an antibody against HCG, but some tumor cells were positively stained. Germinoma is very radio-sensitive; this patient showed T2 high signal lesion involving the medulla oblongata and cervical cord continuously. Probably, tumor cells in the lower brain stem escaped radiation, and gradually spread to the spinal cord over many years. At the time of operation, the surface of the spinal cord was free from tumor cells. Therefore, tumor cells invaded the spinal cord continuously from the medulla oblongata. He was treated with cervical radiation, and his neurologic as well as radiologic findings showed marked improvement.

We report a case of a radiation-induced spinal cord glioma. A 20-year-old girl presented with neck pain and new significant neurological deficits 17 years after resection of a posterior fossa medullomyoblastoma and subsequent craniospinal irradiation. She was found to have a cervical intramedullary tumor that was resected using a standard microsurgical technique. The permanent histopathological diagnosis was anaplastic astrocytoma. Her neurological status was worse immediately following the operation. She improved to her pre-operative status, but then had a relentless neurological decline resulting in death 16 weeks following surgery. Because of the high incidence of malignancy in the few radiation-induced spinal cord gliomas reported in the literature, and the poor outcome independent of therapy in patients with malignant spinal cord gliomas, an initial strategy of biopsy only may be more appropriate than attempted resection for the patient with a suspected radiation-induced intramedullary spinal cord tumor.

A histopathological study was carried out on the spinal cord of rats after boron neutron capture (BNC) irradiation. Rats were irradiated with thermal neutrons alone or in combination with borocaptate sodium (BSH) or p-boronophenylalanine (BPA). Spinal cords were examined 1 year after irradiation, or at earlier times in rats developing myelopathy. Considered overall, the pathology of the spinal cord after BNC irradiation was comparable with that reported previously after X irradiation of the spinal cord in the identical strain of rat. When BSH was used as the neutron capture agent, the biologically effective dose of radiation delivered to the CNS parenchyma was a factor of -2.7 lower than that delivered to the vascular endothelium. In effect, the blood vessels were selectively irradiated using this BNC modality. The resultant pathology was similar to that observed after irradiation with thermal neutrons alone or in the presence of BPA, situations in which the CNS vasculature was not selectively irradiated. This points to the vascular endothelium as being the critical target cell population, damage to which results in the development of the lesions seen in the spinal cord after BNC irradiation and, by inference, after irradiation with more conventional modalities.

An adult female rhesus monkey that had received 44.0 Gy of cobalt 60 radiation to 8 cm of the cervical and upper thoracic spinal cord approximately 2.8 years postirradiation developed a sudden onset of self-mutilation and loss of function of the right arm followed progressively by loss of function of the left arm and terminally bilateral paresis of the legs. Histopathologic examination of the cervical spinal cord revealed a glioblastoma multiforme that extended from the cervical medullary junction to the sixth cervical vertebrae. Because of the infrequent occurrence of spontaneous neoplasia in rhesus monkeys and the location in the radiation field, the glioblastoma is believed to be radiation induced.

Eighteen cases of vertebral and spinal cord tumors associated with spine deformity are included in this study. Thoracic spine was involved most frequently. Neurological deficits were found in 14 patients. Surgical management was carried out in 14 cases. In 4 patients with complete transversal spine lesion percutaneous needle biopsy was done to establish the diagnosis. Surgery was supplemented by radiotherapy or radiotherapy and chemotherapy in 10 cases. Neurological improvement was found in 15 cases.

Spinal cord tumors (SCT) are a diverse group of uncommon neoplasms that develop from tissues in and around the spinal canal. They often have an indolent onset and progression of signs and symptoms, which may include back pain, extremity weakness, sensory alterations, and bowel or bladder incontinence. The most common SCTs are located in the extramedullary space and include meningiomas and neurofibromas. Intramedullary SCTs, for example ependymomas and astrocytomas, occur less frequently. The most useful screening test for diagnosis of a SCT is enhanced magnetic resonance imaging; myelography and computed tomography also can be helpful. The majority of SCTs are amenable to surgical therapy and can be partially or completely resected. Radiation therapy is reserved for incompletely resected low-grade tumors, malignant tumors, and recurrent tumors. The rehabilitative process should be initiated early on following diagnosis, if possible, in patients with neurologic deficits to minimize long-term disability.

A series of 3 studies explored the hypothesis that the preponderance of spinal meningiomas among postmenopausal women relates to their higher prevalence of spinal osteoporosis: (a) medical records showed that meningiomas in women, unlike other spinal tumors, usually arise in the mid thoracic spine where osteoporotic vertebral fractures predominate; (b) radiographic evidence of osteoporosis was seen commonly with meningiomas but not with other spinal tumors; and (c) age-adjusted multivariate analysis of data from an interview study of 81 women with spinal meningioma and 155 random digit dial controls showed 6 factors related to risk. Four factors were protective: (a) current use (at diagnosis) of estrogen replacement therapy [odds ratio (OR) = 0.2; 95% confidence interval (CI) = 0.1-0.6]; (b) past use of oral contraceptives (P trend < 0.01); (c) past participation in sports (OR = 0.5; CI = 0.2-0.9); and (d) premenopausal status (OR = 0.2; CI = 0.1-0.7). Risk increased among women who had ever smoked cigarettes (OR = 1.7; CI = 0.9-3.1) or had a history of high dose radiography (> 500 mrad exposure to active marrow/examination; includes upper or lower gastrointestinal series and/or cardiac angiography; OR = 2.9, and CI = 1.6-5.3), although no association was seen with prior radiotherapy. Other results that did not support the hypothesis include findings that cases and controls were similar in mean body weight and in the proportion who had postmenopausal fractures or height loss. In conclusion, these studies lend some support to our hypothesis, but other known meningioma risk factors such as ionizing radiation also appear important.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: Myelopathy in Klippel-Trenaunay-Weber syndrome is uncommon but has been reported secondary to spinal vascular malformations., Report: A patient with Klippel-Trenaunay-Weber syndrome who presented with spinal cord compression from a spinal extradural mass lesion (angiomyolipoma) is described., Discussion: This association has not been reported previously but is consistent with the segmental vascular abnormalities observed in Klippel-Trenaunay-Weber syndrome.

MR findings in two patients with intradural spinal epidermoid tumors without spinal anomalies are reported. In one case this tumor was congenital, the other one was considered iatrogenic. Origin and MR characteristics of this lesion are discussed.

A review of 262 histologically verified spinal cord tumours in Black Zimbabweans who were operated on in Harare Central and Parirenyatwa Hospitals, Harare, Zimbabwe during the period 1st January 1972 to 31st December 1991 is presented. Fifty one pc of the neoplasms were found in the thoracic region, 53.4 pc were found extradurally, and of these the majority were metastatic (52 pc) and malignant tumours (85 pc). Most (96 pc) intradural-extramedullary tumours were benign with Schwannomas as the largest group (54 pc). Malignant astrocytomas presented as 71.4 pc of all intramedullary tumours. Metastatic tumours represented 28.6 pc of all spinal cord tumours. The most common sites of metastasis were from liver, thyroid and prostate.

Leptomeningeal relapse is a common finding in acute lymphoblastic leukemia (ALL), but a solid intraspinal mass with cord compression as the sole site of extramedullary relapse is unusual. We report an adult patient with ALL, after 2 years of complete remission, who developed a spinal cord compression due to an intraspinal mass as a first manifestation of extramedullary relapse. Manifestation of first relapse in ALL presenting as an intraspinal mass is rare and may be added to other unusual extramedullary sites of relapse.

Experience of treatment of 36 patients with extramedullary spinal cord tumors is summarized. Pigmented macules, papillomas or the spinous processes painfulness while irritation were determined on skin in accordance to tumor localization in the innervation zone of one or two segments.

In a 62-year-old patient 8 month after radiotherapy for right pulmonary hilus carcinoma signs of thoracis cord involvement with ascending course from Th10 to Th7. Cerebrospinal fluid and myelogram were normal. The patient died after about 12 months. Radiation myelopathy was confirmed by neurohistological examination. The results of experimental studies are quoted which could predict the possibility of early diagnosis of radiation myelopathy by rising level of basic myelin protein in cerebrospinal fluid.

An extremely rare case of intramedullary spinal cord metastasis (Carcinoma solidum metastaticum) is presented. No primary tumour was found. The authors discuss diagnostic and therapeutic problems of treatment in such cases.

Primary malignant neoplasms of the brain and spinal cord occurred in 20/718 male (2.8%) and in 13/717 female (1.8%) Crl:CD Br strain Sprague-Dawley rats. Of 33 neoplasms, 30 were found in brain while 3 were in the spinal cord. In males and females, the most common brain neoplasm was astrocytoma (13 males, 9 females). Other neoplasms, granular cell tumor (1 male), mixed glioma (2 males, 1 female), reticulosis (1 male, 2 females), and oligodendroglioma (2 males), were especially uncommon. Spinal cord neoplasms included 2 schwannomas (1 male, 1 female) and an astrocytoma (1 male). The overall brain neoplasm incidence was similar for males (2.8%) compared to data compiled for this strain, and there was a 2-fold increase for females (1.8% vs 0.9%) compared to available incidence data.

A 61-year-old man had an extramedullary subdural meningioma occurring close to the site of an old vertebral traumatic fracture and spinal cord injury. The tumor was discovered 3 years after the spinal trauma. This finding supports the existence of a causal relationship between trauma and subsequent tumor development. A review of the literature disclosed only one other case of intraspinal meningioma after the traumatic fracture of the spine with spinal cord compression.

The cervical region of the rat, including the spinal cord (cervical 5-thoracic 2) was irradiated with single doses of 15-32 Gy 250 kV X-rays. Hyperthermia, at temperatures of 42-, 43- and 44 +/- 0.1 degrees C for 30 min was applied to the cervical vertebral column and immediate adjacent tissues for 5-10 min or 7 h after X-irradiation. Over a period of 18-21 months, animals were followed up to monitor neurological complications occurring as a result of damage to the spinal cord (Sminia et al. 1991). We also noted the development of neoplasms either inside or outside the cervical region. The data on tumour incidence were analysed retrospectively using the actuarial method. Although hyperthermia alone was not carcinogenic, it led to a significant increase of radiation-induced tumours. This increase of radiation carcinogenesis was observed both with hyperthermia applied 5-10 min after X-rays and with an interval of 7 h between X-rays and heat. Cancer induction was highest after the lower radiation doses (16 Gy) combined with high heat doses (30 min 44 degrees C). The latent period for induction of tumours by X-rays was 472 +/- 19 days (mean +/- SEM; n = 24). Latency was significantly shortened by hyperthermia to 404 +/- 34 days (n = 22) if applied 5-10 min after X-rays and to 348 +/- 6 days (n = 33) with an interval of 7 h. Histology revealed that 86% (38/44) of the examined tumours found inside the volume treated with hyperthermia and irradiation were sarcomas. The percentage of animals with a tumour outside the treated volume was almost the same for all treatment groups. Most of these tumours were of the mammary gland type.

We report an extremely unusual case of von Hippel-Lindau disease, characterized by almost total replacement of the spinal cord and most of the medulla by capillary hemangioblastoma (CHB). A 34-year-old female presented 20 years earlier with signs of lower limb weakness. She developed progressive quadriplegia despite multiple surgical attempts to remove separate CHBs from the midthoracic and cervical spinal cord. Spinal cord lesions continued to develop as did multiple cerebellar CHBs. She eventually became respirator-dependent and died following severe upper gastrointestinal hemorrhage. At autopsy there was extensive replacement of spinal cord and medulla by CHB as well as multiple solid and cystic cerebellar tumors. Both kidneys were enlarged and largely replaced by renal cell carcinomas and simple cysts. Additionally she had small pancreatic cysts and microscopic pulmonary hamartomas were observed. There was no evidence of retinal lesions clinically or at autopsy. Light microscopic and immunohistochemical studies of the lesions are presented. The early onset of this disease in a female, with such extensive spinal cord involvement, in addition to other CNS and visceral manifestations of von Hippel-Lindau disease, is unusual and has not been previously reported.

A case of the myeloblastoma involving brain and spinal cord in a patient with acute myelomonocytic leukemia is reported. Numerous mitoses within the tumor provide an evidence for local cell proliferation in the neoplasm. Surgery combined with radiotherapy is suggested as the most efficient modality of the treatment.

The incidence of tumours in the irradiated cervical region in female Wistar (WU) rats after retreatment of part of the volume with hyperthermia was examined retrospectively. The cervical spinal cord (cervical 5-thoracic 2) was irradiated with a single dose of 15, 18 or 20 Gy. Ninety days thereafter, the cervical region was heated by means of a microwave applicator at a maximum temperature of 43 degrees C for 50-90 min measured at the vertebral column. Over a period of 18 months after treatment, animals were regularly observed. Neurological complications and the development of neoplasms were noted. From the 354 animals included in the study, 82 animals developed a tumour. Hyperthermia alone was not carcinogenic, but enhanced the carcinogenesis induced by radiation. The percentage of animals that developed a tumour inside the volume treated with hyperthermia 90 days after irradiation was significantly higher relative to radiation alone (33 +/- 5 per cent versus 4 +/- 2 per cent, P less than 0.001). The duration of the latent period before appearance of these tumours was not affected (355 +/- 18 days versus 425 +/- 54 days). No significant differences in the percentage of animals that developed a tumour at another site were observed between different treatment groups. Histology revealed that 88 per cent (14/16) of the examined tumours found inside the treated volume after hyperthermia and irradiation were soft tissue rhabdomyosarcomas. Outside the treated volume, most tumours were tumours of the mammary gland.

Radiation induced neoplasms of the spinal cord are rare lesions. This report details the MR evaluation of a patient with radiation induced astrocytoma of the cervical cord. The diagnosis of second primary neoplasm should be considered in patients with prior radiation therapy when MRI demonstrates an intramedullary lesion.

Spinal cord involvement in AIDS is not uncommon. Different types of lesions corresponding to varying pathogenetic mechanisms have been reported. Vacuolar myelopathy is the most frequently found. The symptoms and pathological changes resemble those of subacute combined degeneration; however, cobalamine or folate levels have always been found normal. Its frequent association with the multi-nucleated giant cells characteristic of HIV encephalitis makes it likely that the virus plays a role in its pathogenesis. Cytomegalovirus may be responsible for acute myeloradiculitis involving the spinal roots of the cauda equina and inferior part of the spinal cord. In cases of Herpes simplex virus myelitis has been reported; they are usually associated with cytomegalovirus infection and are due to herpes simplex virus type II. Secondary spread from systemic lymphomas may involve the subarachnoid space of the cord and the spinal roots. Compression of the spinal cord by epidural lymphomatous masses has also been described. Spinal infarcts may be secondary to acute or chronic vasculitis or to less specific vascular processes such as disseminated intravascular coagulation.

This paper is the report of three cases of spinal deformities connected to a paravertebral ganglioneuroma: The first case was discovered during the anterior approach of a thoracic scoliosis of more than 100 degrees at the age of twelve; the child had been treated before the age of one year for a thoracic neuroblastoma; eleven years after removal of the ganglioneuroma and fusion of the spinal curve, the evolution is satisfactory. The second case was similar, but the initial findings during infancy were not well known; the result is good two years after excision of the tumor and fusion of the spine. The third case is simply a progressive kyphosis after removal of a thoracic ganglioneuroma by laminectomy at the age of five years. The sister of this child suffered of a malignant thoracic neuroblastoma. Are pointed out here below the nature of these ganglioneuromas, non-secreting tumors from neuroectodermic origin, their rarity in relation with spinal deformities, the difficulties of their detection by modern imaging, and the requirement of a close survey of these patients and their family.

A case of an intraspinal cyst following a lumbar puncture is described. A 57 year-old man had a myelography at the level of L-2 revealing a disc herniation of L-4. About two years later he had another myelography for recurrent back pain, which disclosed an intradural extramedullary tumor at the level of L-2. Pathological diagnosis of the tumor was epidermoid cyst. From the topographical standpoint of the tumor, the previous lumbar puncture was thought to be the most likely cause of the epidermoid cyst. This is the third case report, to the best of our knowledge, which had a normal myelogram prior to the development of epidermoid cyst in the spinal canal.

In this review of the acquired immunodeficiency syndrome (AIDS), the authors have evaluated a total of 352 homosexual patients with AIDS or generalized lymphadenopathy managed at the University of California, San Francisco (UCSF), between 1979 and 1984. Of an initial unselected group of 318 patients, 124 (39%) were neurologically symptomatic, and one-third already had their neurological complaints at the time of presentation. An additional 210 AIDS patients with neurological symptoms have been reported in the literature. Thus, a total of 366 neurologically symptomatic patients with AIDS or lymphadenopathy are reviewed. Central nervous system (CNS) complications, encountered in 315 patients, included the following viral syndromes: subacute encephalitis (54), atypical aseptic meningitis (21), herpes simplex encephalitis (nine), progressive multifocal leukoencephalopathy (six), viral myelitis (three), and varicella-zoster encephalitis (one). Non-viral infections were caused by Toxoplasma gondii (103), Cryptococcus neoformans (41), Candida albicans (six), Mycobacteria (six), Treponema pallidum (two), coccidioidomycosis (one), Mycobacterium tuberculosis (one), Aspergillus fumigatus (one), and Escherichia coli (one). Neoplasms included primary CNS lymphoma (15), systemic lymphoma with CNS involvement (12), and metastatic Kaposi's sarcoma (three). Cerebrovascular complications were seen in four patients with hemorrhage and five with infarction. Five patients in the UCSF series had multiple intracranial pathologies, including two cases of simultaneous Toxoplasma gondii infections and primary CNS lymphoma, two cases of coexistent Toxoplasma gondii and viral infections, and one case of combined Toxoplasma gondii and atypical mycobacterial infection. Cranial or peripheral nerve complications, seen in 51 patients, included cranial nerve syndromes secondary to chronic inflammatory polyneuropathy (five), lymphoma (five), and Bell's palsy (five). Peripheral nerve syndromes included chronic inflammatory polyneuropathy (12), distal symmetrical neuropathy (13), herpes zoster radiculitis (six), persistent myalgias (two), myopathy (two), and polymyositis (one). In light of the protean behavior of AIDS and the problems related to the clinical, radiological, and serological diagnosis of the unusual and varied associated nervous system diseases, patients with AIDS and neurological complaints require a rigorous and detailed evaluation. The authors' experience suggests that biopsy of all CNS space-occupying lesions should be performed for tissue diagnosis prior to the institution of other therapies.

On the basis of neuropathologic studies in 22 patients died from ML it was found that lymphoma cells in the brain and spinal cord were in the form of leukostasis, infiltrations usually limited to perivascular spaces, infiltrations in hemorrhagic foci and their vicinity. In cerebrospinal meninges, spinal roots and peripheral nerves we observed leukostasis and intraparenchymatous infiltrations. It was found that the most important role in the development of lymphoma infiltrations in the nervous system was played by hematogenic metastases whose development in the brain and spinal cord was promoted by leukemic conversion with high leukocytosis. In contrast, marked dissemination of lymphoma cells to peripheral blood is not indispensible for the development of infiltrations in the cerebrospinal meninges and peripheral nervous system.

A direct causal relationship between a human virus and malignant transformations in target cells (sensory neuronal precursors) was suggested by the development of a medulloepitheliomatous neoplasm in the central nervous system. Twenty-six newborn Sprague-Dawley rats were given a single intracerebral inoculation of 0.05 ml of adenovirus fluid, 10(3.5) to 10(4.5) TCID(50) HeLa cells/0.1 ml, in the left frontal lobe. Within 37 to 151 days after the virus inoculation, 23 (88.7%) rats autochthonously developed an adenovirus-typical neoplasm in the central nervous system. Nine animals developed a multicentric neoplasm closely related to the ventricular system. Nine others developed solid variously sized neoplasms along the ventricular lumen. Some neoplasms showed multiple foci connected with the stratum subependymale ventriculi olfactorii and the velum medullare of the fourth ventricle. Six spinal cord tumors, located chiefly in the dorsal sensory column, developed within 37 to 61 days after intracerebral inoculation. The remarkably uniform histopathologic appearance of all 23 cases was attributed to a medulloepitheliomatous neoplasm derived from the ependymal anlage. Electron microscopy clearly revealed a solitary cilium within the apical region of many tumor cells. It consisted of a typical ring of nine doublets with no axial pair (a 9+0 pattern), the typical structure of cilia of sensory neuronal origin. The appearance of exuberant neuron-like tumor cells with argyrophile cytoplasmic expansions, neurosyncytial mosaic alignment and myelin-like configurations also suggested a neuronal origin. A paucity of mesenchymal stroma in the neoplastic tissue was noted. No control animals developed tumors.

We report a case of a 21-year-old white woman with a three-week history of rapidly progressive paresis and paresthesias of her extremities presenting as an intramedullary cervical cord lesion. Computer-assisted tomography and magnetic resonance imaging demonstrated a normal brain with a cervical cord enlargement suggestive of a primary spinal cord tumor. Her neurological deficits progressed despite dexamethasone; hence, laminectomy was performed with open biopsy of the cord lesion. The pathological specimens were sent to the Mayo Clinic and Kansas University for cell-type determination, due to their bizarre morphology. Both institutions concluded the biopsy specimens were demyelinated axonal plaques consistent with multiple sclerosis. This case illustrates that demyelinating disease can mimic spinal cord tumor, even with MRI scanning. Multiple sclerosis is a chronic demyelinating disease of the central nervous system. The clinical diagnosis requires documentation of lesions occurring on more than one occasion and at more than one site in the central nervous system. To improve the accuracy of the diagnosis of multiple sclerosis, spinal fluid analysis, visual and auditory evoked responses and radiologic imaging have been proposed. We report a patient with multiple sclerosis who presented with symptoms and physical findings suggesting a primary cervical cord tumor. Localized enlargement of the cervical cord was documented on magnetic resonance imaging. This is the first reported description of histopathologically confirmed spinal cord demyelination presenting as an intramedullary cervical cord tumor.