Concomitant spontaneous spinal and posterior fossa subdural hematoma in an 11-year-old child with aplastic anemia: a case report and review of literature.

PURPOSE: The current article describes an 11-year-old male who has aplastic anemia with an extremely rare condition, that is, concomitant posterior fossa SDH and spinal SDH. METHODS: This is a case report and review of literature. CASE PRESENTATION: This case presents an 11-year-old male known to have aplastic anemia complained of neck and back pain, headache, and persistent vomiting for 3 days. He had no history of head or spine trauma at all. His parents are relatives "positive consanguinity," and his sister suffers from aplastic anemia. Clinical examination revealed severe pallor at the time of presentation, with no neurologic or locomotor deficit and positive Kernig's sign. CONCLUSION: Patients with aplastic anemia or any bleeding disorder conditions should be investigated thoroughly if symptoms denoted a CNS pathology. Concomitant cranial and spinal SDH rarely occurs, and more studies are advocated to be structured to investigate the specific pathophysiology and etiologies of this condition.

Holocordic Spinal Sbdural Hematoma: A Challenging Management In Emergency: Literature Review.

OBJECTIVE: Spinal subdural hematoma (SSH) is a rare entity and the etiology has yet to be elucidated. Holocordic spinal hematomas represent an exception. The management of these patients remains controversial, due to their rarity and their extremely poor prognosis. METHODS: Electronic databases (MEDLINE, Scopus, and PubMed) were analyzed for studies published through April 2021, searching holocordic spinal subdural hematoma. Case reports, case series, and literature reviews were included. RESULTS: We found only 7 cases describing holocordic SSH reported in the literature, and we added the description of 1 case we managed at our institution, reaching a total of 8 cases. We discuss clinical and radiologic features, etiologic hypothesis, treatment strategies, and prognostic factors. CONCLUSIONS: The correct treatment of holocordic hematomas is not yet well standardized. Complete evacuation is not amenable, but surgical evacuation based on magnetic resonance imaging has shown to be the most effective therapeutic option, crucial in terms of prognosis, even if performed with some delay.

Acute Spontaneous Spinal Subdural Hematoma: A Case Report.

BACKGROUND Spontaneous spinal subdural hematoma is a rare condition that can lead to devastating neurologic deficits, usually caused by coagulation abnormalities, trauma, underlying neoplasm, or arteriovenous malformation. The patient presents with local and/or radicular pain, followed by loss of sensory, motor, bladder, and bowel function. CASE REPORT A 25-year-old patient presented with left-sided weakness preceded by nontraumatic upper back pain. He denied any past medical illness and being on any regular medications. He had decreased strength in the left lower limb, left upper limb, and right lower limb, with intact strength in the right upper limb. The patient exhibited decreased sensation of pain and touch on the right side of the lower limb, bilateral loss of proprioception, and intact reflexes and anal tone. He had weakness on the left side of the body and contralateral decreased sensation of pain and touch on the right side. These symptoms were suggestive of Brown-Sequard syndrome, while the bilateral loss of proprioception suggested posterior cord syndrome. Magnetic resonance imaging showed an acute spinal subdural canal hematoma producing cord compression. The patient had an urgent laminectomy and hematoma evacuation. Afterward, his neurological function improved. CONCLUSIONS Spontaneous spinal subdural hematoma can occur without any known pathology or remarkable trauma. It can compress the spinal cord and produce cerebral stroke-like symptoms. Hence, spinal hematoma should be ruled out in any patient presenting with a neurological deficit.

Posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome associated spinal subdural hematoma: A case report.

RATIONALE: Posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) are separate clinical entities with distinct pathophysiological features. But in some special conditions PRES and RCVS can occur simultaneously. PATIENT CONCERNS: We report the unique case of a 40-year-old female presented with crescendo headache, blurred vision, and recurrent generalized tonic-clonic seizure. She had a minor neck injury 1 week before but attracted no more attention. Neurological tests on admission yielded a Glasgow Coma Scale score of 13. No obvious focal neurological deficit apart from positive signs of meningeal irritation was presented. DIAGNOSES: Xanthochromia and hemorrhagic cerebrospinal fluid with pleocytosis was found on lumbar puncture. Cranial computed tomography was negative but magnetic resonance imaging demonstrated bilateral areas of vasogenic edema in the parieto-occipital lobes and cerebellum consistent with PRES. An incidental subacute spinal subdural hematoma extending from the level of C6 to T1 was depicted by spinal magnetic resonance imaging, presumably as a complication of negligible neck trauma. Spinal digital subtraction angiography showed no evidence of spinal aneurysm, arteriovenous malformation, or dural arteriovenous fistula. Cerebral digital subtraction angiography showed segmental narrowing and dilatation of vessels, a potential feature of RCVS, involving the circle of Willis and their branches. INTERVENTIONS: The patient was treated with nimodipine for vasodilation and other symptomatic therapies. The spinal subdural hematoma was not warranted for surgical intervention and managed with simple analgesics. OUTCOMES: The patient experienced a dramatic improvement in neurological symptoms and was discharged without sequelae. Follow-up imaging showed complete resolution of all radiological changes. LESSONS: Clinician should be aware of spinal subdural hematoma as the potential trigger in development of PRES and RCVS. We speculate that endothelial dysfunction and vascular tone dysregulation may be implicated to play the major pathophysiologic role.

Acute spinal subdural hematoma: A case report of spontaneous recovery from paraplegia.

RATIONALE: Spontaneous spinal subdural hematoma (SSDH) is a rare disease that can cause severe permanent neurological dysfunction. Here we present a case of spontaneous SSDH, in which a series of magnetic resonance images (MRIs) taken through the course of the disease facilitated understanding of the resolution process of the hematoma and the diagnosis of SSDH. PATIENT CONCERNS: A 59-year-old male presented with sudden severe back pain and rapid onset of paraplegia. This symptom had continued developing while he was transferred to the emergency department. Initial physical examination showed flaccid paralysis of both lower limbs with areflexia and loss of all sensation below T6 bilaterally. MRI images showed an anterior subdural hematoma from C7 to T7 with spinal cord compression. DIAGNOSIS: Based on MRI findings, the diagnosis was SSDH. INTERVENTIONS: We chose conservative treatment of 1-week bed rest and intensive rehabilitation for the patient due to the presence of sacral sparing and the slight motor recovery at 24 hours after the onset. OUTCOMES: Frequent MRI images demonstrated that the spinal cord compression was surprisingly mitigated only 2 days and mostly absorbed 4 days after the onset. The patient's motor function was recovered completely and he was discharged after 8 weeks of hospitalization. LESSONS: Our chronological MRI findings provide crucial information for diagnosing SSDH and also suggest that spinal surgeons should consider the potential option of a conservative approach for treating SSDH. Although prompt selection of a therapeutic strategy for SSDH could be challenging, the surgeons could observe the course of the patient's neurological status for a few days to detect signs of spontaneous recovery.

Lumbar Subdural Hematoma Detected After Surgical Treatment of Chronic Intracranial Subdural Hematoma.

BACKGROUND: Spinal subdural hematoma (SSDH), which can cause lower back pain, leg pain, and leg weakness, is rare and will usually be associated with a bleeding tendency, trauma, spinal vascular malformation, intraspinal tumor, or iatrogenic invasion. Only a few cases of SSDH after intracranial chronic subdural hematoma (CSDH) have been reported. We report a case of lumbar SSDH in the absence of predisposing factors after reoperation for recurrent intracranial CSDH, which improved with conservative treatment. CASE DESCRIPTION: Approximately 1 month after falling, a 63-year-old woman was experiencing left hemiparesis and impaired orientation that was diagnosed as right intracranial CSDH using computed tomography. Surgical treatment of the CSDH led to immediate improvement of her symptoms. On postoperative day 29, the right CSDH had recurred with left hemiparesis, and successful reoperation relieved the symptoms within a few hours postoperatively. However, 1 day after the second operation, very small acute subdural hematomas in regions along the left tentorium cerebelli and left falx cerebri were found on computed tomography. On day 31, she complained of sitting-induced bilateral radiating lower limb pain. Magnetic resonance imaging on day 34 showed an acute SSDH at the L4-L5 level and a sacral perineural cyst filled with hematoma, although her radiating pain was showing improvement. She was treated conservatively and was discharged without symptoms on day 44. CONCLUSIONS: Although SSDH is rare, it is important for neurosurgeons and physicians to consider the possibility of a SSDH when lower limb pain or paresis occurs after procedures that will result in rapid intracranial pressure alterations such as drainage of an intracranial CSDH.

Multiple Spinal Chronic Subdural Hematomas Associated with Thoracic Hematomyelia: A Case Report and Literature Review.

BACKGROUND: Chronic subdural hematoma (CSDH) is uncommon in the spine. Most spinal CSDHs occur as solitary lesions in the lumbosacral region. We report a rare case of multiple spinal CSDHs associated with hematomyelia. The diagnostic and therapeutic management of these complex spinal CSDHs is reviewed as well as the pertinent literature. CASE DESCRIPTION: A 79-year-old woman on warfarin therapy presented with lower back pain and progressive lower extremity weakness that had developed in the previous 2 weeks. She subsequently developed paraplegia and urinary incontinence. Thoracolumbar magnetic resonance imaging showed a CSDH from T12-L3 compressing the cauda equina. Single-shot whole-spine magnetic resonance imaging showed another CSDH and hematomyelia at T2-3. She underwent L2-3 hemilaminectomy, which revealed a liquefied subdural hematoma. Delayed T2 laminectomy exposed an organized subdural hematoma and xanthochromic hematomyelia. After each surgery, the patient showed significant motor recovery. Finally, the patient could walk, and the urinary catheter was removed. CONCLUSIONS: Spinal CSDH may occur in multiple regions and may be associated with hematomyelia. Whole-spine magnetic resonance imaging is useful to examine the entire spine for CSDH accurately and thoroughly. Comprehensive surgical exploration of all symptomatic hematomas may restore neurologic functions even with delayed surgery.

Management of Spinal Emergencies in Patients on Direct Oral Anticoagulants.

OBJECTIVE: Spine surgeons increasingly encounter acute spinal pathologies in patients treated with direct oral anticoagulants (DOACs), but only limited data on the management of these patients are currently available. METHODS: We retrospectively analyzed patients who presented to our department with acute spinal pathology during treatment with DOAC and who required urgent surgical therapy. Patient characteristics and treatment modalities were studied, with specific focus on the management of hemostasis and surgical therapy. Furthermore, we analyzed 19 cases of spinal emergencies during DOAC treatment reported in the literature. RESULTS: A total of 12 patients were identified and included in the present analysis. Patients suffered from acute spinal cord compression caused by spinal tumor manifestation (n = 5), empyema (n = 4), degenerative spinal stenosis (n = 1), hematoma (n = 1), and vertebral body fracture/dislocation (n = 2). All patients underwent emergency surgical treatment. Prohemostatic substances were administered perioperatively in 10 patients (83%) and included administration of prothrombin complex concentrates (83%), tranexamic acid (17%), and transfusion of platelets (8%). A total of 9 patients (75%) showed postoperative improvement of neurologic symptoms, and the in-hospital mortality in this patient cohort was 17%. CONCLUSIONS: Emergency spine surgery is feasible and should be considered in patients on treatment with DOAC. The (low) risk of intraoperative bleeding complications has to be weighed against the risk of permanent disability if surgical decompression is delayed. Administration of prothrombin complex concentrates and tranexamic acid may improve the coagulation before surgery, especially in cases of unavailable specific antidotes.

Spontaneous Spinal Subdural Hematoma: Case Report of 2 Years' Clinical and Radiologic Findings.

BACKGROUND: Spontaneous spinal subdural hematoma (SDH) is rare but leads to severe nerve compression. According to the symptoms, surgery decompression and conservative treatment are justified options. We present a spontaneous spinal SDH case treated by decompression surgery for the lumbar region and conservative observation for the thoracic region. A series of images of the disease course is available. CASE DESCRIPTION: A 55-year-old woman without malignancy or coagulopathy history presented with progressive low back pain for the past 2 weeks. Progressive bilateral leg weakness happened 1 week ago. On the day she called for help, she presented with bilateral leg grade 2 muscle power and generalized back pain. There was no headache or meningeal sign. An absent bilateral knee reflex was found. Magnetic resonance imaging showed a space-occupying lesion at the T2-T6 and T12-L1 levels in the ventral and dorsal spinal canal, leading to cord compression. Due to rapid neurologic function deterioration, emergent T12-L1 laminectomy was performed. We found a T12-L1 tense dura sac with subdural hematoma ventral to the cord. Removal of the SDH was performed. T2-T6 levels were treated conservatively. She returned ambulant 1 week after operation. Magnetic resonance images at 3 months and 1 year later showed the SDH being absorbed and replaced by adhesive arachnoid cysts along the whole T and L spine. However, these lesions are asymptomatic for at least 2 years. CONCLUSIONS: Surgical intervention is recommended in patients presenting with severe neurologic deficits. Conservative treatment is a reasonable option for asymptomatic patients.

Surgical treatment of progressive cauda equina compression caused by spontaneous spinal subdural hematoma: A case report.

RATIONALE: Spontaneous spinal subdural hematoma (SSDH) without an underlying pathology is a very rare condition. The treatment protocol for SSDH is early diagnosis and treatment before irreversible damage to neural tissue. However, there is no agreement on the etiopathogenesis, as well as the need for surgery to treat spontaneous SSDH. Here, we report a rare case of spontaneous SSDH with progressive deterioration and symptoms of cauda equina syndrome after ineffective conservative treatment. PATIENT'S CONCERN: A 38-year-old male patient presented with sudden lower back and bilateral leg pain. DIAGNOSIS: A magnetic resonance imaging (MRI) scan on the third day after the onset of symptoms revealed a subdural hematoma from L1 to S1, presenting as hyperintensities on T1 weighted sequences and hypointensities to isointensities on T2 weighted sequences. INTERVENTION: Laminectomy and subdural evacuation were performed immediately. OUTCOMES: An abnormal ligamentum flavum was observed intraoperatively. A histological examination revealed extravasation of blood in the degenerated ligamentum flavum. Postoperatively, the lower limb pain improved immediately. At the 6-month follow-up, the pain and numbness of the lower limb disappeared, and the muscle strength of both legs recovered completely with normal gait. LESSONS: Spontaneous SSDH with ligamentum flavum hematoma was caused by a sudden increase of intravenous pressure, resulting from a marked surge in the intra-abdominal or intrathoracic pressure. Consecutive MRI scans provided valuable information, leading to a diagnosis of spontaneous SSDH. The treatment protocol for spontaneous SSDH should be determined based on the location and stage of the hematoma, as well as the subject's neurological status.

Clival SubduralHematoma after Drainage of Concomitant Intracranial and Spinal Cord Subdural Hematomas ­ Rare Case Report

Concomitant traumatic spinal cord and intracranial subdural hematomas associated with a retroclival hematoma are very uncommon. Their pathophysiology is not totally elucidated, but one hypothesis is the migration of the hematoma from the head to the spine. In the present case report, the authors describe the case of a 51-year-old man presenting with headache, nauseas and back pain after a head trauma who presented with intracranial and spinal cord subdural hematomas. Drainage was performed but, 1 week later, a retroclival subdural hematoma was diagnosed. The present paper discusses the pathophysiology, the clinical presentation, as well as the complications of concomitant traumatic spinal cord and intracranial subdural hematomas associated with a retroclival hematoma, and reviews this condition.

Acute idiopathic spinal subdural hematoma: What to do in an emergency?

Acute spinal cord compression usually results from trauma, infection, or cancer. Spinal subdural hematoma is an uncommon cause of spinal cord compression that occurs after spine trauma or spinal invasive procedure, especially in context of coagulopathy. In the following reported case, an 82-year-old woman with a history of rapidly progressive paraparesis after a sudden middle back pain, with no previous trauma or coagulopathy, due to an acute spontaneous spinal subdural hematoma. In fact, the main difficulty was to determine, in an emergency situation, the right strategy to identify both the lesion and its cause to adapt therapeutics. This case not only provides an illustrative unusual condition in an emergency department but also a challenging discussion to choose the right treatment for a sudden neurological impairment. According to a literature review of the idiopathic cases of spinal subdural hematomas without coagulopathy, the clinical outcome depends on severity of neurological impairment. MRI is the main examination to perform in an emergency. Thus surgical evacuation should be performed in emergency in patients presenting with severe neurological impairment.

Traumatic Subacute Spinal Subdural Hematoma Concomitant with Symptomatic Cranial Subdural Hematoma: Possible Mechanism.

BACKGROUND: Spinal subdural hematoma (SDH) concomitant with cranial SDH is extremely rare. Although some theories have been proposed, the pathophysiology underlying this condition remains unclear. We present a case of traumatic subacute spinal SDH followed by symptomatic subacute cranial SDH. CASE DESCRIPTION: A 56-year-old woman was admitted with severe back pain 2 weeks after sustaining a minor head injury. The pain was worse with walking or standing and was relieved a little bit by sitting. There was no clinical evidence of back injury. There was no neurologic deficit. Magnetic resonance imaging of the spine showed subacute spinal SDH from T12 to S1. Owing to progressive worsening of back pain, bilateral laminectomy of L1-S1 and drainage of subacute spinal SDH were performed. The pain was completely relieved after surgery. On postoperative day 4, the patient was noted to be unconscious with Glasgow Coma Scale score of 10 (E2V3M5). Computed tomography scan of the head showed subacute bilateral cranial SDH. Burr hole drainage was performed. The patient experienced a complete recovery. CONCLUSIONS: This case suggests the possibility that spinal SDH can develop as a result of cranial SDH migration to the most dependent spinal subdural space. The physician should be aware of the possibility of symptomatic cranial SDH developing following spinal SDH evacuation.

A delayed-onset intracranial chronic subdural hematoma following a lumbar spinal subdural hematoma: A case report.

RATIONALE: A spinal subdural hematoma (SDH) is rarely complicated with an intracranial SDH. We found only 7 cases of spontaneous concurrent lumbar spinal and cranial SDHs, in which lumbar symptoms occurred before head symptoms. PATIENT CONCERNS: We describe a 77-year-old man with spontaneous concurrent spinal and cranial SDHs, in whom the spinal SDH was identified 30 days before the intracranial chronic SDH. DIAGNOSIS: Magnetic resonance imaging showed a spinal SDH at L4/L5. There was no paralysis, and the patient was managed conservatively. About 30 days after the onset of back pain, he experienced tinnitus and visual hallucination. Brain computed tomography showed a chronic SDH and midline shift. INTERVENTIONS: Burr-hole evacuation was performed, and the patient's condition improved. OUTCOMES: At 5 months of follow-up, there was no recurrence of the spinal or intracranial SDH. LESSONS: It is important to consider the possibility of intracranial hemorrhage when a spinal SDH is identified.

Concomitant Intracranial and Lumbar Chronic Subdural Hematoma Treated by Fluoroscopic Guided Lumbar Puncture: A Case Report and Literature Review.

A 40-year-old man presented with a severe headache, lower back pain, and lower abdominal pain 1 month after a head injury caused by falling. Computed tomography (CT) of the head demonstrated bilateral chronic subdural hematoma (CSDH) with a significant amount in the left frontoparietal region. At the same time, magnetic resonance imaging (MRI) of the lumbar spine also revealed CSDH from L2 to S1 level. A simple drainage for the intracranial CSDH on the left side was performed. Postoperatively, the headache was improved; however, the lower back and abdominal pain persisted. Aspiration of the liquefied spinal subdural hematoma was performed by a lumbar puncture under fluoroscopic guidance. The clinical symptoms were dramatically improved postoperatively. Concomitant intracranial and spinal CSDH is considerably rare so only 23 cases including the present case have been reported in the literature so far. The etiology and therapeutic strategy were discussed with a review of the literature. Therapeutic strategy is not established for these two concomitant lesions. Conservative follow-up was chosen for 14 cases, resulting in a favorable clinical outcome. Although surgical evacuation of lumbosacral CSDH was performed in seven cases, an alteration of cerebrospinal fluid (CSF) pressure following spinal surgery should be reminded because of the intracranial lesion. Since CSDH is well liquefied in both intracranial and spinal lesion, a less invasive approach is recommended not only for an intracranial lesion but also for spinal lesion. Fluoroscopic-guided lumbar puncture for lumbosacral CSDH following burr hole surgery for intracranial CSDH could be a recommended strategy.

Delayed Posttraumatic Subacute Lumbar Subarachnoid Hematoma: Case Report and Review of the Literature.

BACKGROUND: Traumatic spinal subarachnoid hematoma, associated or not with a concurrent subdural hematoma, has rarely been described. The evolution of such hematomas is heterogeneous. This study aims at defining the most accurate management, which is currently not standardized. CASE DESCRIPTION: A 20-year-old man, victim of a high-kinetic road accident 5 days before and with several nonneurologic nonsurgical vertebral fractures, experienced a sudden dorsolumbar pain radiating to his lower limbs. A rapidly progressive asymmetric paraparesis with loss of reflexes was noticed, associated with bilateral global hypoesthesia of the lower limbs and with acute urinary retention, whereas the anal tonicity was preserved (American Spinal Injury Association C). Magnetic resonance imaging scan revealed a conus medullaris compression at the level of the L1-L2 vertebrae by an intradural expansive mass. Immediate surgical decompression revealed a strictly subarachnoid hematoma. Venous bleeding was seen at the level of the conus medullaris and controlled. Pathologic examination of the clot excluded an underlying tumor or vascular abnormality. The complete coagulation profile was normal. CONCLUSION: Six weeks after surgery, the neurologic examination revealed only a slight tactile hypoesthesia of the left thigh. With only 4 reported cases, purely subarachnoid spinal hematomas remain widely rarer than epidural hematomas. The reported case possesses a certain number of peculiarities: young age, pure subarachnoid location, lumbar location, occurrence after a car accident, subacute onset, and excellent neurologic recovery. In our opinion, a symptomatic subarachnoid spinal hematoma should be surgically evacuated at the early phase so neurologic recovery can be expected.

Lumbosacral Subdural Hematoma After Glioblastoma Multiforme Resection: Possible Radiographic Evidence for the Downward Migration of Intracranial Blood.

BACKGROUND: Spinal subdural hematomas (SSDHs) are rare and usually associated with bleeding diatheses, trauma, iatrogenic injury, spinal vascular malformations, or intraspinal tumors. CASE DESCRIPTION: We report a case of a 75-year-old man who developed a symptomatic lumbosacral SSDH after undergoing resection of a right temporal glioblastoma multiforme. The patient subsequently recovered and was discharged home. Over the next 2 weeks, he developed progressively worsening symptoms of lower back pain, lower extremity weakness, and urinary retention. Although the patient had no known risk factors for developing a SSDH, magnetic resonance imaging on postoperative day 16 revealed an extensive L2-sacrum SSDH. The patient underwent L2-L5 total laminectomies for evacuation of the SSDH. His symptoms resolved after surgery. Literature review produced 26 other cases of SSDHs after intracranial surgery in patients without obvious risk factors. In our case, the lumbosacral SSDH may have originated from downward migration of intracranial blood in a gravity-dependent fashion. Radiographic evidence of blood within the posterior thecal sac of the patient's cervical spine supports this hypothesis. CONCLUSIONS: In most cases, SSDHs after intracranial surgery resolve with conservative treatment; however, as shown in our case, surgery may be required if there is progressive neurologic decline. Neurosurgeons should be aware of this potential complication after intracranial surgery; a magnetic resonance imaging of the spine may be indicated if there is unexplained lower extremity pain or weakness.