Spinal epidural hematoma (SEH) represents the most frequent entity of acute or chronic spinal bleeding. Based upon pathogenesis, SEH can be classified as idiopathic, spontaneous, and secondary. The idiopathic forms are considered not to be attributed to any specific risk factors. Spontaneous SEH, accounting for 0.3–0.9% of all spinal epidural space occupying lesions, instead is associated with risk factors (such as substantial soft trauma or coagulation abnormalities). The chronic form, as our literature review revealed, is the rarest and its most frequent location is the lumbar spine. The pathophysiology of spontaneous and idiopathic SEH is still under debate: There are only a few reports in literature of chronically evolving SEH with progressively increasing pain and neurological impairment. Magnetic resonance imaging may be inconclusive for differential diagnosis. Here, we present two cases of lumbar chronic SEH with slow, progressive, and persistent lumbar radicular impairment. The first patient reported a minor trauma with slight back contusion and thus was classified as spontaneous SEH. In the second case not even a minor trauma was involved, so we considered it to be idiopathic SEH. In both cases preoperative blood and coagulation tests were normal and we did not find any other or co-factors in the patients’ clinical histories. MR imaging showed uncertain spinal canal obstructing lesions at L3 and L4 level in both cases. Surgical treatment allowed a correct diagnosis and resulted in full clinical and neuroradiological recovery after 1 year follow-up. Our aim is to discuss pathogenesis, clinical and radiological features, differential diagnosis and treatment options, on the background of relevant literature review.
Spontaneous; Idiopathic; Chronic; Hematoma; Epidural; Spinal
Although postoperative spinal epidural hematoma (SEH) is not uncommon, hematomas that require surgery are rare. Cauda equina syndrome (CES) may be associated with postoperative SEH. In these cases, early recognition and emergency decompression can prevent further damage and better neurologic recovery.
A 41-year-old man underwent two-level discectomy with insertion of an interspinous spacer at L3-4 and L4-5 because of low back pain and radiculopathy. Eight hours after the operation, the patient developed CES. MRI revealed SEH compressing posteriorly at the L3-4 level. On emergency decompression and hematoma evacuation, the interspinous spacer had obstructed the laminotomy site at L3-4 completely, blocking drainage to the drain. The patient experienced complete neurologic recovery by 2 months followup.
Many studies report risk factors for SEH. However, postoperative SEH can also be encountered in patients without these risks. One study reported a critical ratio (preoperative versus postoperative cross-sectional area) correlated with postoperative symptoms, especially in those with CES. The propensity to develop CES is likely dependent on a number of patient-specific factors.
Surgeons should be aware that patients without risk factors may develop acute CES. Wider laminotomy (larger than half of the device size) may help to prevent this complication when one uses the compressible type of device, especially in patients with relatively small lamina.
We report a series of epidural hematomas which cause neurologic deterioration after spinal surgery, and have taken risk factors and prognostic factors into consideration. We retrospectively reviewed the database of 3720 cases of spine operation in a single institute over 7 years (1998 April-2005 July). Nine patients who demonstrated neurologic deterioration after surgery and required surgical decompression were identified. Factors postulated to increase the postoperative epidural hematoma and to improve neurologic outcome were investigated. The incidence of postoperative epidural hematoma was 0.24%. Operation sites were cervical 3 cases, thoracic 2 cases, and lumbar 4 cases. Their original diagnoses were tumor 3 cases, cervical stenosis 2 cases, lumbar stenosis 3 cases and herniated lumbar disc 1case. The symptoms of epidural hematomas were neurologic deterioration and pain. After decompression, clinical outcome revealed complete recovery in 3 cases (33.3%), incomplete recovery in 5 cases (55.6%) and no change in 1 case (11.1%). Factors increasing the risk of postoperative epidural hematoma were coagulopathy from medical illness or anticoagulation therapy (4 cases, 44.4%) and highly vascularized tumor (3 cases, 33.3%). The time interval to evacuation of complete recovery group (29.3 hours) was shorter than incomplete recovery group (66.3 hours). Patients with coagulopathy and highly vascularized tumor were more vulnerable to spinal epidural hematoma. The postoperative outcome was related to the preoperative neurological deficit and the time interval to the decompression.
Clinical outcome; risk factor; postoperative; spinal epidural hematoma; spine surgery
We present a rare case of spinal epidural hematoma (SEH) after thoracolumbar posterior fusion without decompression surgery for a thoracic vertebral fracture. A 42-year-old man was hospitalized for a thoracic vertebral fracture caused by being sandwiched against his back on broken concrete block. Computed tomography revealed a T12 dislocation fracture of AO type B2, multiple bilateral rib fractures, and a right hemopneumothorax. Four days after the injury, in order to promote early orthostasis and to improve respiratory status, we performed thoracolumbar posterior fusion surgery without decompression; the patient had back pain but no neurological deficits. Three hours after surgery, he complained of acute pain and severe weakness of his bilateral lower extremities; with allodynia below the level of his umbilicus, postoperative SEH was diagnosed. We performed immediate revision surgery. After removal of the hematoma, his symptoms improved gradually, and he was discharged ambulatory one month after revision surgery. Through experience of this case, we should strongly consider the possibility of preexisting SEH before surgery, even in patients with no neurological deficits. We should also consider perioperative coagulopathy in patients with multiple trauma, as in this case.
•Spontaneous epidural hematoma of the spine (SEHS) is an extremely rare entity.•Early diagnosis and treatment showed to have the best outcome.•SESH should be suspected in every acute medullary syndrome with spinal pain, motor and/or sensory deficit.
Spontaneous epidural hematoma of the spine (SEHS) is an extremely rare entity. Patients known to have thrombophilia or on anticoagulant drugs are the most affected. It is generally caused by a rupture of the postero-internal vertebral venous plexus secondary to minor barotrauma such as cough, peridural catheter insertion...
Early diagnosis and treatment showed to have the best outcome.
We report 3 cases of spontaneous epidural hematoma in patients treated by acenocoumarol, which occurred without any provocative factor. All 3 patients were treated with decompressive laminectomy.
We described the MRI findings and discussed the spontaneity of the entity. Our present case studies and the review of the literature showed that early diagnosis and management of SEHS can lead to improvement of the neurological state and avoid definitive motor and sensitive deficit.
This rare entity should be suspected in every acute medullary syndrome with spinal pain, motor and/or sensory deficit. In order to decrease the sequelae, neurologically unstable patients should benefit from early diagnosis and urgent surgical decompression.
Spontaneous epidural hematoma of the spine; Oral anticoagulants; Acenocoumarol
Spinal epidural abscess (SEA) and spinal epidural hematoma (SEH) are neurologic emergencies with distinct etiologies and treatment. Despite similarities on magnetic resonance imaging (MRI), their differentiation is usually possible with meticulous history taking and neurologic examinations. We report an unusual case of SEA that developed from preceding SEH, posing a diagnostic challenge to physicians. A 65-year-old diabetic man suddenly experienced back pain and weakness of both legs when he lifted heavy luggage. He was afebrile, and his laboratory tests were mostly unremarkable. Spinal MRI consisting of T1-weighted, T2-weighted, and fat-suppressed T2-weighted images revealed an epidural mass over the L2-L4 spinous process. He was diagnosed with SEH based on his symptoms and MRI findings, and was treated conservatively using steroid pulse therapy. Despite initial improvement, he suddenly developed into septic shock and coma on the 10th hospital day, and died shortly thereafter. An autopsy revealed massive pus accumulation in the lumbar epidural space and brain, and a postmortem diagnosis of infected SEH associated with invasive pneumococcal disease was established. Serial MRI studies, including diffusion-weighted and/or gadolinium-enhanced T1-weighted images are warranted in patients with a presumed diagnosis of SEH receiving steroid therapy to detect such infectious transformation.
Invasive pneumococcal disease; magnetic resonance imaging; spinal epidural abscess; spinal epidural hematoma
Study Design Case report.
Objectives To describe a case of delayed-onset spinal hematoma following the breakage of a spinal epidural catheter.
Methods The authors describe the clinical case review.
Results A 64-year-old woman had undergone epidural anesthesia 18 years before she was referred to our hospital because of lower-back pain and lower neurologic deficit with leg pain. The clinical examination showed the presence of a fragment of an epidural catheter in the thoracolumbar canal, as assessed by computed tomography, and a spinal hematoma that compressed the spinal cord at the same spinal level, as assessed by magnetic resonance imaging. Surgical removal of the epidural catheter and decompression surgery were performed. The patient exhibited substantial clinical improvement 1 month after surgery; she achieved a steady gait without the need for a cane and had no leg pain.
Conclusion This is the first report of delayed onset of spinal hematoma following the breakage of an epidural catheter. Generally, when the breakage of an epidural catheter occurs without symptoms, follow-up alone is recommended. However, because spinal hematoma might exhibit a late onset, the possibility of this complication should be considered when deciding whether to remove the catheter fragment. We believe that in our patient, there could be a relationship between the catheter fragment and subdural hematoma, and catheter breakage could have been a risk factor for the spinal hematoma.
epidural catheter; spinal interdural hematoma; breakage; complication
Spontaneous spinal epidural hematoma is a relatively rare but potentially disabling disease. Prompt timely surgical management may promote recovery even in severe cases.
We report a 34-year-old man with a 2-hour history of sudden severe back pain, followed by weakness and numbness over the bilateral lower limbs, progressing to intense paraparesis and anesthesia. A spinal magnetic resonance imaging scan was performed and revealed an anterior epidural hematoma of the thoracic spine. He underwent an emergency decompression laminectomy of the thoracic spine and hematoma evacuation. Just after surgery, his lower extremity movements improved. After 1 week, there was no residual weakness and ambulation without assistance was resumed, with residual paresthesia on the plantar face of both feet. After 5 months, no residual symptoms persisted.
The diagnosis of spontaneous spinal epidural hematoma must be kept in mind in cases of sudden back pain with symptoms of spinal cord compression. Early recognition, accurate diagnosis and prompt surgical treatment may result in significant improvement even in severe cases.
The addition of thoracic epidural anesthesia to general anesthesia during cardiac surgery may have a beneficial effect on clinical outcome. However, epidural catheter insertion in a patient anticoagulated with heparin may increase the risk of epidural hematoma. We report a case of epidural hematoma in a 55-year-old male patient who had a thoracic epidural placed under general anesthesia preceding uneventful mitral valve replacement and tricuspid valve annular plasty. During the immediate postoperative period and first postoperative day, prothrombin time (PT) and activate partial thromboplastin time (aPTT) were mildly prolonged. On the first postoperative day, he complained of motor weakness of the lower limbs and back pain. An immediate MRI of the spine was performed and it revealed an epidural hematoma at the T5-6 level. Rapid surgical decompression resulted in a recovery of his neurological abnormalities to near normal levels. Management and preventing strategies of epidural hematoma are discussed.
Analgesia; Epidural; Hematoma; Postoperative complications; Spinal
Iatrogenic or spontaneous spinal hematomas are rarely seen and present with multiple symptoms that can be difficult to localize. Most spontaneous spinal hematomas are multifactorial, and the pathophysiology is varied. Here, we present a case of a scattered, multicomponent, combined subdural and epidural spinal hematoma that was managed conservatively.
A 38-year-old woman came to the emergency department (ED) complaining of severe neck and back pain. She had undergone a caesarean section under epidural anesthesia 4 days prior to her arrival in the ED. She was placed on heparin and then warfarin to treat a pulmonary embolism that was diagnosed immediately postpartum. Her neurological examination at presentation demonstrated solely the existence of clonus in the lower extremities and localized cervical and low thoracic pain. In the ED, the patient's international normalized ratio was only mildly elevated. Spinal magnetic resonance imaging revealed a large thoracolumbar subdural hematoma with some epidural components in the upper thoracic spine levels. Spinal cord edema was also noted at the T6-T7 vertebral level. The patient was admitted to the neurosurgical intensive care unit for close surveillance and reversal of her coagulopathy. She was treated conservatively with pain medication, fresh frozen plasma, and vitamin K. She was discharged off of warfarin without any neurological deficit.
Conservative management of spinal hematomas secondary to induced coagulopathies can be effective. This case suggests that, in the face of neuroimaging findings of significant edema and epidural blood, the clinical examination should dictate the management, especially in such complicated patients.
Caesarean section; hematoma; intensive care unit; subdural–epidural
Spinal epidural haemorrhage may present as back pain associated with radicular symptoms and can be a catastrophic clinical scenario with progression to paraplegia or even sudden death. Being a rare entity, it needs a high index of clinical suspicion to diagnose it. Fractures have been documented as a cause of hematorrachis but such hematomas only extend to one or two vertebral segments. Large epidural hematomas are usually associated with conditions like bleeding diathesis, arterio-venous malformations, plasma cell myeloma, and non-Hodgkin’s lymphoma. Surgical management with immediate evacuation of the hematoma is the usual line of management in patients with neurological deficits. Though rare, monitored and careful conservative management can lead to recovery of neurological symptoms and resolution of the hematoma. We report a case of a very large post traumatic epidural hematorrchis extending to 11 vertebral segments from D3 to L1 vertebral bodies, who had a gradual spontaneous recovery.
Compression fracture; Epidural hematoma; Hematorrachis
Spinal epidural hematoma (SEH) is an uncommon disorder, and chronic SEHs are rarer than acute SEHs. However, there is few reported involving the bone change of the vertebral body in chronic SEHs. We present a case report of lumbar epidural hematoma that required differentiation from extramedullary spinal tumors by a long process because the CT scan revealed scalloping of the vertebral body and review the relevant literature. A 78-year-old man had experienced a gradual onset of low back pain and excruciating pain in both legs. Lumbar MRI on T1-weighted images revealed a space-occupying lesion with a hyperintense signal relative to the spinal cord with no enhancement on gadolinium adminisration. Meanwhile, T2-weighted images revealed a heterogeneous intensity change, accompanying a central area of hyperintense signals with a hypointense peripheral border at the L4 vertebra. Moreover, the CT scan demonstrated scalloping of the posterior wall of the L4 vertebral body which is generally suspected as the CT finding of spainal tumor. During the epidural space exploration, we found a dark red-colored mass surrounded by a capsular layer, which was fibrous and adhered to the flavum and dura mater. Microscopic histological examination of the resected mass revealed a mixture of the relatively new hematoma and the hematoma that was moving into the connective tissue. Accordingly, the hematoma was diagnosed as chronic SEH. The particular MRI findings of chronic SEHs are helpful for making accurate preoperative diagnoses of this pathology.
chronic lumbar epidural hematoma; spontaneous spinal epidural hematoma; scalloping; MRI findings
Retrospective study on the results of microendoscopic decompression surgery for the treatment of cervical myelopathy. The purpose of this study was to describe the microendoscopic laminoplasty (MEL) technique as the surgical method in the treatment of cervical myelopathy, and to document the clinical outcomes for MEL surgery. Endoscopic surgery poses several challenges for the aspiring endoscopic surgeons, the most critical of which is mastering hand–eye coordination. With training in live animal and cadaver surgery, the technical progress has reduced the problem of morbidity following surgery. The authors have performed microendoscopic decompression surgery on more than 2,000 patients for lumbar spinal canal stenosis. Fifty-one patients underwent the posterior decompression surgery using microendoscopy for cervical myelopathy at authors’ institute. The average age was 62.9 years. The criteria for exclusion were cervical myelopathy with tumor, trauma, severe ossification of posterior longitudinal ligament, rheumatoid arthritis, pyogenic spondylitises, destructive spondylo-arthropathies, and other combined spinal lesions. The items evaluated were neurological evaluation, recovery rates; these were calculated following examination using the Hirabayashi’s method with the criteria proposed by the Japanese Orthopaedic Association scoring system (JOA score). The mean follow-up period was 20.3 months. The average of JOA score was 10.1 points at the initial examination and 13.6 points at the final follow-up. The average recovery rate was 52.5%. The recovery rate according to surgical levels was, respectively, 56.5% in one level, 46.3% in two levels and 54.1% in more than three levels. The complications were as follows: one patient sustained a pin-hole-like dura mater injury inflicted by a high-speed air-drill during surgery, one patient developed an epidural hematoma 3 days after surgery, and two patients had the C5 nerve root palsy after surgery. The epidural hematoma was removed by the microendoscopy. All two C5 palsy improved with conservative therapy, such as a neck collar. These four patients on complications have returned to work at the final follow-up. This observation suggests that the clinical outcomes of microendoscopic surgery for cervical myelopathy were excellent or showed good results. This minimally invasive technique would be helpful in choosing a surgical method for cervical myelopathy.
Cervical spine; Clinical outcome; Endoscopic surgery; Laminoplasty; Myelopathy
Although extravasations of polymethylmetharylate during percutaneous vertebroplasty are usually of little clinical consequence, surgical decompression is occasionally required if resultant neurologic deficits are severe. Surgical removal of epidural polymethylmetharylate is usually necessary to achieve good neurologic recovery. Because mobilizing the squeezed spinal cord in a compromised canal can cause further deterioration, attempts to remove epidural polymethylmetharylate in the thoracic region need special consideration. A 66-year-old man had incomplete paraparesis and radicular pain on the chest wall after percutaneous vertebroplasty for osteoporotic compression fracture of T7. Radiological studies revealed polymethylmetharylate extravasations into the right lateral aspect of spinal canal that caused marked encroachment of the thecal sac and right neuroforamina. Progressive neurologic deficit and poor responses to medical managements were observed; therefore, surgical decompression was performed 4 months later. After laminectomy and removal of facet joints and T7 pedicle on the affected side, extravasated polymethylmetharylate posterior and anterior to the thecal sac was completely removed without retracting the dura mater. Spinal stability was reconstructed by supplemental spinal instrumentation and intertransverse arthrodesis with banked cancellous allografts. Myelopathy and radicular pain gradually resolved after decompression surgery. The patient was free of sensory abnormality and regained satisfactory ambulation two years after surgical decompression.
Vertebroplasty; Polymethylmethacrylate; Epidural extravasations; Thoracic myelopathy; Surgical removal
Spinal epidural hematoma is a well known complication of spinal surgery. Clinically insignificant small epidural hematomas develop in most spinal surgeries following laminectomy. However, the incidence of clinically significant postoperative spinal epidural hematomas that result in neurological deficits is extremely rare. In this report, we present a 33-year-old female patient whose spinal surgery resulted in postoperative spinal epidural hematoma. She was diagnosed with lumbar disc disease and underwent hemipartial lumbar laminectomy and discectomy. After twelve hours postoperation, her neurologic status deteriorated and cauda equina syndrome with acute spinal epidural hematoma was identified. She was immediately treated with surgical decompression and evacuation of the hematoma. The incidence of epidural hematoma after spinal surgery is rare, but very serious complication. Spinal epidural hematomas can cause significant spinal cord and cauda equina compression, requiring surgical intervention. Once diagnosed, the patient should immediately undergo emergency surgical exploration and evacuation of the hematoma.
•In this article, reporting on the case of a huge 10 levels spontaneous spinal subdural hematoma treated with decompressive thoracic no-instrumented laminectomy in a 45-year-old woman with good neurological recovery, we would like to underline the importance of a timely surgical decompression as the mainstay option in the management of strongly symptomatic spontaneous idiopathic acute spinal subdural hematomas.•To our knowledge, 10 levels thoracic laminectomy for a SSDH removal have never been described. We performed “conservative” laminectomy by sparing of articular processes with no need to posterior fixation also considering the intrinsic stability of thoracic chest.
Spontaneous idiopathic acute spinal subdural hematoma (SSDH) is a rare cause of acute back pain followed by signs and symptoms of nerve root and/or spinal cord compression, frequently associated with coagulopathies, blood dyscrasias and arterio-venous malformations. Standard management includes non-operative treatment and timely (within 24 h) surgical decompression.
Presentation of case
We report on the case of a huge 10 levels SSDH treated with decompressive thoracic no-instrumented laminectomy in a 45-year-old woman with good neurological recovery (from ASIA A to D).
Spontaneous SSDHs without detectable structural lesion or anticoagulant therapy are very rare. Among 26 cases documented the literature harbouring SSDHs, the thoracic spine was found to be the preferred site, and the compression was usually extending over several vertebral levels. Nonoperative treatment for SSDH may be justified in presence of minimal neurologic deficits, otherwise, early decompressive laminectomy along with evacuation of hematoma are considered the treatment of choice in presence of major deficits.
To our knowledge, the present case is the most extensive laminectomy for a SSDH removal never described before. No postoperative instability occurs in 10 levels thoracic laminectomy in case the articular processes are spared. When major neurological deficits are documented, early decompressive laminectomy with evacuation of hematoma should be considered the best treatment for SSDH.
Spinal epidural hematoma is a rare complication associated with pain control procedures such as facet block, acupuncture, epidural injection, etc. Although it is an uncommon cause of acute myelopathy, and it may require surgical evacuation. We report four patients with epidural hematoma developed after pain control procedures. Two procedures were facet joint blocks and the others were epidural blocks. Pain was the predominant initial symptom in these patients while two patients presented with post-procedural neurological deficits. Surgical evacuation of the hematoma was performed in two patients while in remaining two patients, surgery was initially recommended but not performed since symptoms were progressively improved. Three patients showed near complete recovery except for one patient who recovered with residual deficits. Although, spinal epidural hematoma is a rare condition, it can lead to serious complications like spinal cord compression. Therefore, it is important to be cautious while performing spinal pain control procedure to avoid such complications. Surgical treatment is an effective option to resolve the spinal epidural hematoma.
Spinal epidural hematoma; Pain control procedure; Surgical evacuation
Spontaneous spinal epidural hematoma is an uncommon but disabling disease. This paper reports a case of spontaneous spinal epidural hematoma and treatment by surgical management. A 32-year-old male presented with a 30-minute history of sudden headache, back pain, chest pain, and progressive quadriplegia. Whole-spinal sagittal magnetic resonance imaging (MRI) revealed spinal epidural hematoma on the ventral portion of the spinal canal. Total laminectomy from T5 to T7 was performed, and hematoma located at the ventral portion of the spinal cord was evacuated. Epidural drainages were inserted in the upper and lower epidural spaces. The patient improved sufficiently to ambulate, and paresthesia was fully recovered. Spontaneous spinal epidural hematoma should be considered when patients present symptoms of spinal cord compression after sudden back pain or chest pain. To prevent permanent neurologic deficits, early and correct diagnosis with timely surgical management is necessary.
Spontaneous spinal epidural hematoma; Quadriplegia; Surgical treatment; Functional recovery
We intend to report the largest series of spinal epidural cavernomas (SEC), discuss their clinical features, imaging characteristics, surgical findings, outcome analysis and compare them with similar reports in the literature.
Among the cases of spinal tumors treated surgically by the authors, there have been nine cases of SEC’s. All the data were collected prospectively and the cases have been followed after surgery up to the time of this analysis.
There were six female and three male patients with the ages ranging between 13 and 74 years. The lesions were located in the thoracic spine (4 cases), lumbar spine (4 cases) and one at the sacral level. Clinical presentations included acute spinal pain and paraparesis in two, low back pain and radiculopathy in five, and slowly progressive myelopathy in the other two cases. The lesion was iso-intense with the spinal cord in T1W images and hyperintense in T2W images and showed strong homogeneous enhancement after contrast medium injection in most of our cases. In the presence of hemorrhage inside the lesion, it was hyperintense in both T1W and T2W MR sequences as in our case 6. In the single case presenting with acute hemorrhage, epidural hematoma was the only finding, our case 1. Complete surgical removal was achieved in all our cases, and confirmed by postoperative MRI.
SEC is hard to be differentiated from other epidural spinal lesions before intervention but should be considered in the list of differential diagnosis regarding its favorable outcome.
Cavernous angioma; Magnetic resonance imaging; Spinal epidural cavernoma; Spinal epidural lesion
Spontaneous spinal epidural hematoma (SSEH) is a rare idiopathic condition that leads to acute onset of neurological deficits, which if not recognized early can have catastrophic consequences. The definition and pathophysiology of this condition remain controversial. High index of suspicion followed by T2-weighted gradient echo sequences are particularly useful in early diagnosis. Management consists of prompt surgical decompression of the hematoma though a recent trend is toward non-surgical treatment.
A 70-year-old man presented with acute onset neck pain with a radicular component and rapidly progressive quadriparesis. Magnetic resonance imaging revealed a posteriorly located cervical extradural hematoma with cord compression that was promptly evacuated. Functional recovery to near normal function occurred within 24 hours of surgery.
SSEH in its true idiopathic form is a rare pathologic entity. Because of the high risk of poor outcome without treatment, SSEH should be a diagnostic possibility when presentation is even slightly suggestive. Prompt surgical evacuation of the hematoma leads to a favorable neurological outcome, whereas delay in treatment can be disastrous. The role of conservative management needs to be proven and should be tailored on an individual basis.
Tetraparesis; Tetraplegia; Paralysis; Myelopathy; Laminectomy; Neurologic manifestations; Progressive; Spinal cord compression; Cervical; Hematoma; Idiopathic spontaneous spinal epidural hematoma
We report three cases of spontaneous spinal epidural hematoma (SSEH) with hemiparesis. The first patient was a 73-year-old woman who presented with left hemiparesis, neck pain, and left shoulder pain. A cervical MRI scan revealed a left posterolateral epidural hematoma at the C3–C6 level. The condition of the patient improved after laminectomy and evacuation of the epidural hematoma. The second patient was a 62-year-old man who presented with right hemiparesis and neck pain. A cervical MRI scan revealed a right posterolateral dominant epidural hematoma at the C6-T1 level. The condition of the patient improved after laminectomy and evacuation of the epidural hematoma. The third patient was a 60-year-old woman who presented with left hemiparesis and neck pain. A cervical MRI scan revealed a left posterolateral epidural hematoma at the C2–C4 level. The condition of the patient improved with conservative treatment. The classical clinical presentation of SSEH is acute onset of severe irradiating back pain followed by progression to paralysis, whereas SSEH with hemiparesis is less common. Our cases suggest that acute cervical spinal epidural hematoma should be considered as a differential diagnosis in patients presenting with clinical symptoms of sudden neck pain and radicular pain with progression to hemiparesis.
Spontaneous spinal epidural haemorrhage is a rare condition. The initial clinical manifestations are variable. Nonetheless, most spinal cord lesions result in paraparesis or quadriparesis, but not hemi-paresis, if motor function is involved. We report on a 69-year-old man who presented initially with right-side limb weakness. He was initially misdiagnosed at emergency room with a cerebral stroke and treated inappropriately with heparin. One day after admission, correct diagnosis of acute spinal epidural haematoma was based on the repeated neurological examination and cervical magnetic resonance imaging study. The patient underwent emergency surgical decompression and hematoma removal. The pathogenesis of the haematoma could have been due to hypertension, increased abdominal pressure and anticoagulant therapy. We emphasize that patients with hemi-paresis on initial presentation could have an acute spinal epidural haemorrhage. We also draw the misdiagnosis to the attention of the reader because early recognition of spontaneous spinal epidural haematoma is very important for prompt and appropriate treatment to improve the overall prognosis.
Spontaneous spinal epidural haemorrhage; Hemi-paresis; Cerebrovascular disease
Spontaneous spinal epidural hematoma (SSEH) is a rare spinal cord compression disorder. Thunderclap headache mimicking subarachnoid hemorrhage as an initial manifestation of this disorder has been scarcely reported. Moreover, the neurological outcome of conservative treatment is satisfactory only in some clinical settings. The unusual presentation and mechanisms for spontaneous recovery of SSEH are discussed.
To report a case of SSEH that presented with acute severe headache that mimicked subarachnoid hemorrhage. After a period of neurological deficit, spontaneous improvement was seen, which progressed to full recovery without neurosurgical intervention.
A 62-year-old man presented with acute occipital headache and neck stiffness for which subarachnoid hemorrhage was initially suspected. An emergency computed tomographic brain scan and cerebrospinal fluid analysis excluded subarachnoid hemorrhage. Later, he developed acute paraparesis, hypoesthesia up to the fourth thoracic dermatomal level (T4) as well as bowel and bladder dysfunction. The magnetic resonance imaging eventually revealed spinal epidural hematoma, located anterior to C7 through T4 spinal level. He had no previous history of spinal injury, systemic, and hematological disorders. The neurological recovery began 20 hours after the onset and continued until complete recovery, 4 months after the onset without neurosurgical intervention.
SSEH could sometimes imitate subarachnoid hemorrhages when it located in the cervical region. Spontaneous recovery of SSEH without surgical intervention might be possible in cases with continuing neurological recovery, although the recovery began much later in the clinical course.
Headache; Spontaneous spinal epidural hematoma; Subarachnoid hemorrhage; Paraparesis
Osteoporosis is the most common contributing factor of spinal fractures, which characteristically are not generally known to produce spinal cord compression symptoms. Recently, an increasing number of medical reports have implicated osteoporotic fractures as a cause of serious neurological deficit and painful disabling spinal deformities. This has been corroborated by the present authors as well. These complications are only amenable to surgical management, requiring instrumentation. Instrumenting an osteoporotic spine, although a challenging task, can be accomplished if certain guidelines for surgical techniques are respected. Neurological deficits respond equally well to an anterior or posterior decompression, provided this is coupled with multisegmental fixation of the construct. With the steady increase in the elderly population, it is anticipated that the spine surgeon will face serious complications of osteoporotic spines more frequently. With regard to surgery, however, excellent correction of deformities can be achieved, by combining anterior and posterior approaches. Paget's disease of bone (PD) is a non-hormonal osteometabolic disorder and the spine is the second most commonly affected site. About one-third of patients with spinal involvement exhibit symptoms of clinical stenosis. In only 12–24% of patients with PD of the spine is back pain attributed solely to PD, while in the majority of patients, back pain is either arthritic in nature or a combination of a pagetic process and coexisting arthritis. In this context, one must be certain before attributing low back pain to PD exclusively, and antipagetic medical treatment alone may be ineffective. Neural element dysfunction may be attributed to compressive myelopathy by pagetic bone overgrowth, pagetic intraspinal soft tissue overgrowth, ossification of epidural fat, platybasia, spontaneous bleeding, sarcomatous degeneration and vertebral fracture or subluxation. Neural dysfunction can also result from spinal ischemia when blood is diverted by the so-called "arterial steal syndrome". Because the effectiveness of pharmacologic treatment for pagetic spinal stenosis has been clearly demonstrated, surgical decompression should only be instituted after failure of antipagetic medical treatment. Surgery is indicated as a primary treatment when neural compression is secondary to pathologic fractures, dislocations, spontaneous epidural hematoma, syringomyelia, platybasia, or sarcomatous transformation. Five classes of drugs are available for the treatment of PD. Bisphosphonates are the most popular antipagetic drug and several forms have been investigated.
Osteoporosis; Fractures; Neurological deficit; Deformity; Paget's disease; Back pain; Spinal stenosis; Myelopathy; Treatment
Idiopathic hypertrophic spinal pachymeningitis (IHSP) is a rare inflammatory disease characterized by hypertrophic inflammation of the dura mater and various clinical courses that are from myelopathy. Although many associated diseases have been suggested, the etiology of IHSP is not well understood. The ideal treatment is controversial. In the first case, a 55-year-old woman presented back pain, progressive paraparesis, both leg numbness, and voiding difficulty. Initial magnetic resonance imaging (MRI) demonstrated an anterior epidural mass lesion involving from C6 to mid-thoracic spine area with low signal intensity on T1 and T2 weighted images. We performed decompressive laminectomy and lesional biopsy. After operation, she was subsequently treated with steroid and could walk unaided. In the second case, a 45-year-old woman presented with fever and quadriplegia after a spine fusion operation due to lumbar spinal stenosis and degenerative herniated lumbar disc. Initial MRI showed anterior and posterior epidural mass lesion from foramen magnum to C4 level. She underwent decompressive laminectomy and durotomy followed by steroid therapy. However, her conditions deteriorated gradually and medical complications occurred. In our cases, etiology was not found despite through investigations. Initial MRI showed dural thickening with mixed signal intensity on T1- and T2-weighted images. Pathologic examination revealed chronic nonspecific inflammation in both patients. Although one patient developed several complications, the other showed slow improvement of neurological symptoms with decompressive surgery and steroid therapy. In case of chronic compressive myelopathy due to the dural hypertrophic change, decompressive surgery such as laminectomy or laminoplasty may be helpful as well as postoperative steroid therapy.
Idiopathic hypertrophic spinal pachymeningitis; Spinal cord compression; Chronic nonspecific inflammation; Dural thickening