Rare disease Case report Hemiparesis in spontaneous spinal epidural haematoma: a potential stroke imitator Ravish Patel,1 Aravind Kumar,2 Kazuya Nishizawa,1 Naresh Kumar1 1 Orthopaedic Surgery, National University Hospital, Singapore, Singapore 2 Orthopaedic Surgery, Khoo Teck Puat Hospital, Yishun, Singapore Correspondence to A/Prof Naresh Kumar, ​dosksn@​nus.​edu.​sg Accepted 6 January 2018 Summary Spontaneous spinal epidural haematoma (SSEH) is a rare condition that requires urgent surgical intervention in order to prevent permanent neurological deficit. SSEH commonly presents as a paraparesis or tetraparesis. SSEH presenting as a hemiparesis is less common and in such situations, it can be mistaken for a cerebrovascular accident (CVA). Thrombolytic or anticoagulant treatment for CVA can potentially worsen the neurological deficit. We report one such case of SSEH misdiagnosed as a CVA. Treatment with tissue plasminogen activator led to worsening of his condition. On a subsequent cervical spine MRI, an epidural haematoma extending from C3 to C5 was detected and treated with laminectomy and evacuation. Surgical intervention led to significant improvement from American Spinal Injury Association Scale (ASIA) B to ASIA E. Presence of clinical features such as Horner’s syndrome, Brown-Sequard syndrome and the absence of cranial nerve palsies in acute hemiparesis are indicative of SSEH rather than CVA. Background Symptomatic spontaneous spinal epidural haematoma (SSEH) leading to spinal cord compression is a neurosurgical emergency that requires urgent decompression and haematoma evacuation. The clinical presentation depends on the location and the size of the SSEH. Patients with cervical SSEH usually present with axial neck pain that is occasionally associated with radicular arm pain, thus mimicking a prolapsed intervertebral disc. This is quickly followed by the onset of motor weakness, usually presenting as tetraparesis or paraparesis.1–3 Hemiparesis is an extremely rare presentation of SSEH and is frequently misdiagnosed as a cerebrovascular accident (CVA).4–15 It is very important to consider cervical spinal cord compression in patients presenting with acute neurological deficit and to perform an MRI scan if there is any doubt.16 17 It has been suggested that early diagnosis and decompression lead to better neurological recovery and a good outcome.18 Case presentation To cite: Patel R, Kumar A, Nishizawa K, et al. BMJ Case Rep Published Online First: [please include Day Month Year]. doi:10.1136/bcr-2017222686 A 51-year-old right-handed man with a history of hypertension presented with an acute onset of rightsided posterior neck pain in the early morning. The Visual Analogue Score for pain was 7. He had no weakness or loss of coordination, and he was able to walk. After about 45 min, he noticed the onset of right upper limb and right lower limb weakness with drooping of the eyelids on right side. There were no visual disturbances, change of voice or difficulty in swallowing. He was quickly rushed to the tertiary care hospital where his blood pressure (BP) was recorded to be 157/95 mm Hg with a pulse rate of 62 beats/min. Neurological examination revealed weakness of grade 2/5 throughout the right upper limb, grade 3/5 power of right hip flexion and knee extension (L2, L3 myotomes) and grade 4/5 power of right ankle dorsiflexion, big toe dorsiflexion and ankle plantar flexion (L4, L5 and S1 myotomes, respectively). The left upper limb and left lower limb power was grade 5/5. Reduced sensation with a sensory level of T12 was noted with hyper-reflexia, ankle clonus and Babinski’s sign in the right lower limb. The National Institutes of Health Stroke Scale score was 6 at the time of presentation. Hence, as per American Heart Association/American Stroke Association guidelines, a non-enhanced CT scan (NECT) and multiphasic CT angiography of the brain were done.19 A provisional diagnosis of acute territorial infarct of left middle cerebral artery was made with an Alberta Stroke Program Early CT Score of 9. However, no haemorrhage, no clot in the arterial system or any arterial dissection was detected on the CT-brain angiogram. In view of the strong clinical suspicion, no evidence of haemorrhage in brain and closing window of opportunity for effective thrombolysis tissue plasminogen activator (t-PA) was commenced 4.5 hours after the onset of symptoms.19 A subsequent MRI brain did not show any evidence of the brain infarct. His neurological deficit then gradually deteriorated along with the onset of acute retention of urine and he was shifted to a tertiary spine institute next day. On examination in the emergency department, he had grade 0/5 power of the C5, C6 myotomes, grade 1/5 power of C7–T1, L4–L5 myotomes, grade 2/5 power in L2 and grade 5/5 power in L3, S1 myotomes (table 1), all on the right side. The left upper limb and left lower limb had grade 5/5 power. The sensory examination revealed hypoesthesia below T4 on the left side and hyperaesthesia in right upper limb which was suggestive of a Brown-Sequard syndrome. There was no saddle anaesthesia and the anal tone was intact. The American Spinal Injury Association scale was grade C. He was noted to have ptosis, miosis (anisocoria) and anhidrosis on the right side of the face indicative of a Horner’s syndrome. The BP was 130/72 mm Hg, and the pulse rate was 59 beats/min. Patel R, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-222686 1 Rare disease Table 1 Evaluation of patient as per American Spine Injury Association Score Myotomal involvement Before t-PA Preoperative 6 weeks postoperative Right C5 elbow flexion 2 0 4 Right C6 wrist extension 2 0 4 Right C7 elbow extension 2 1 4 Right C8 finger flexion 2 1 4 Right T1 finger abduction 2 1 3 Right L2 hip flexors 3 2 5 Right L3 knee extensions 3 5 5 Right L4 ankle dorsiflexion 4 1 5 Right L5 long toe dorsiflexion 4 1 5 Right S1 ankle plantar flexion 4 5 5 t-PA, tissue plasminogen activator; 0, absent; 1, visible contractions; 2, active movement only if gravity eliminated; 3, active movement through range of motion against gravity; 4, active movement through range of motion against resistance; 5, normal. Investigations Radiographs and a CT scan of the cervical spine showed no fracture or malalignment. MRI of the whole spine showed a fusiform heterogeneous non-enhancing extradural mass along the right posterolateral aspect of central canal at C3–C5 level measuring 8 mm ×1.7 mm in maximum axial dimension (figure 1). The mass was isointense on T1-weighted and T2-weighted images with severe narrowing of the central canal and increased signal intensity of the spinal cord. MR angiogram did not reveal any vascular lesion but it showed that the left vertebral artery was the dominant artery. Full blood count, coagulation profile, platelet count and biochemistry profile were normal. Differential diagnosis ►► SSEH. ►► Prolapsed intervertebral disc. ►► Spondylodiscitis. ►► Epidural abscesses. ►► Transverse myelitis. ►► Epidural tumours. ►► Acute myocardial infarctions. ►► Cerebrovascular events. ►► Dissecting aortic aneurysms. Treatment Next morning (48 hours after onset of symptoms) the patient underwent bilateral spinous process C4 laminectomy and a right C3 and C5 hemilaminectomy (figures 2 and 3). The haematoma was evacuated and haemostasis was achieved. A malformed venous plexus was found overlying the spinal cord at C5 level. The intraoperative blood loss was 350 mL. Fresh frozen plasma was kept ready but was not required as the haemostasis was adequate. Histological examination of the haematoma showed a well-formed and organised clot without any evidence of malignancy. Outcome and follow-up The neurological status improved remarkably over the next 6 weeks. His urinary incontinence recovered by day 14. The motor power of all the lower limbs muscles recovered to MRC grade 5/5, and the upper limb recovered to MRC grade 4/5 except for right T1 which was grade 3/5. He recommenced work by the 9th postoperative week. Discussion Acute SSEH was first described by Jackson in 186920 and first treated surgically by Bain in 1897.21 The common sites for development of SSEH show a bimodal distribution between the lower cervical and thoracic regions with peaks at C6 and T12.22 The haematoma usually spans three to four cervical levels.23 24 The most common age at presentation is after fourth or fifth decade and the male-to-female ratio is 1.4:1.3 The cause of SSEH is idiopathic in up to 40% of cases and causes such as vascular malformation, coagulopathy, anti-platelet agents and excessive garlic ingestion have been reported in the rest.25 The source of bleeding can be either the epidural veins or the epidural arteries. It is hypothesised that activities such as coughing, sneezing, sudden twisting or lifting a heavyweight can trigger a rise in venous pressure and precipitate haemorrhage in the epidural venous plexus.26 A rise in intra-abdominal and intrathoracic pressure leads to an increase in spinal epidural venous pressure.22 25 Sudden increase of epidural venous pressure in this valveless system predisposes to a rupture. A pair of longitudinal veins in the posterior internal vertebral venous plexus is connected with multiple interconnecting veins and a rupture of these veins along the sides of interconnecting veins is believed to be the cause of SSEH.27 28 However, Beatty and Winston2 believed that the pressure in the epidural veins is less than the intrathecal pressure and so any form of venous bleeding should be tamponaded. A tear of the lateral longitudinal arterial system due to traction of cervical nerves during stretching of upper limbs has also been proposed to cause SSEH.2 It partially explains the higher incidences of SSEH at the mobile lower cervical spine and lower thoracic spine. This hypothesis is further supported by the fact that larger series of SSEH have shown a correlation between SSEH and arterial hypertension.23 Figure 1 Fusiform heterogeneous T2-weighted isointense non-enhancing extradural mass (white arrows)along the right posterolateral aspect of central canal extending from levels C3/4 to C5 and compressing the cord from right. (A) Sagittal T2-weighted image, (B) axial T2-weighted image at C3/4, (C) axial T2-weighted image at C4 and (D) axial T2-weighted image at C5. 2 Patel R, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-222686 Rare disease Figure 2 MRI after the spinous process preserving C4 laminectomy and C3, C5 right hemilaminectomy. Postoperative MRI shows no residual haematoma (white arrows) and decompressed spinal cord at the affected segments: (A) sagittal T2-weighted image, (B) axial T2-weighted image at C3-4, (C) axial T2-weighted image at C4 and (D) axial T2-weighted image at C5. The differential diagnosis of SSEH includes a prolapsed intervertebral disc, infections such as spondylodiscitis, epidural abscesses and transverse myelitis, epidural tumours, acute myocardial infarctions, cerebrovascular events and dissecting aortic aneurysms.1 11 SSEH with hemiparesis being mistaken for an acute ischaemic CVA is not uncommon and there are at least 11 such cases reported in the literature (table 2). Treatment with heparin, t-PA, aspirin or warfarin has been instituted in these patients with a severe risk of aggravating the clinical condition. In fact, mortality has been reported in one of the patients with SSEH that was misdiagnosed as a CVA.9 Several factors can lead to such a misdiagnosis. Hypertension has been associated with 3% of the SSEH patients.23 Frequently, anxiety at the time of presentation can increase their BP. In such a scenario, the first differential that physicians suspect is CVA. Patients with SSEH presenting with hemiparesis may also have dysarthria but the cause of it is not known.13 Elderly patients with SSEH may be using dentures and during the acute phase of disease when the dentures are removed, their speech might sound slurred.11 Thrombolysis and embolectomy are the two available treatments that have proven to be effective after CVA.19 29 Thrombolysis is non-invasive method that can be instituted early while embolectomy is an invasive procedure that is employed after extensive workup. There is a narrow window for administration of a thrombolytic agent for a CVA and this is the only available non-invasive treatment that has proven to be effective.19 29 Thus, a NECT brain with or without CT angiography or CT perfusion is the investigation of choice in the acute emergency setting to detect intracranial haemorrhage or early ischaemic CVA. In most centres, an MRI brain takes a longer time to organise. Thus, thrombolytic treatment is commenced in the presence of clinical suspicion of stroke after ruling out haemorrhagic CVA on NECT even though an MRI is found superior to a CT scan in diagnosing a cerebral infarct.30 Hence, in situations when the window of opportunity for t-PA is closing, an MRI brain is usually done after the commencement of thrombolytic treatment. An alternate diagnosis is considered only when subsequent MRI brain or a CT angiogram turns out to be normal. Two issues are of importance in patients with SSEH: (1) to prevent a delay in diagnosis and (2) to anticipate and avoid blood loss during subsequent surgery. A careful assessment of the patient in the emergency department is important. SSEH should be considered when patients with hemiparesis also have back or neck pain with/without radiculopathy.15 Other factors that point towards SSEH rather than CVA are the presence of a Brown-Sequard syndrome,4 10 12 Horner’s syndrome,7 12 the absence of cranial nerve palsies or facial weakness,4 11 15 a normal MRI brain,15 no improvement or a deterioration of neurology after starting thrombolytic therapy and a positive Lhermitte’s sign.31 After diagnosing SSEH, an urgent surgical evacuation is warranted unless the symptoms are mild and non-progressive. Non-operative management is feasible if spontaneous recovery is seen or if the neurological deficits are mild.1 3 25 However, haematoma evacuation is preferred in patients with profound deficit as there is inverse correlation between time to surgery and recovery.1 A study by Shin et al with a series of 14 patients showed that 84% of patients recovered if operated within 12 hours while only 64% of them recovered if operated between 12 and 24 hours. Only 47% of those who were operated more than 24 hours later showed recovery.16 Surgical decompression that is delayed more than 12 hours in the presence of a profound neurological deficit may lead to permanent neurological disability.25 Reversal agents and appropriate blood products should be made available so surgery is not delayed.32 Surgeries carried out immediately after t-PA infusions are rare and guidelines for these situations do not exist. The half-life of t-PA is approximately 5 min Figure 3 Postoperative CT scan showing (B) C3 right hemilaminectomy, (C) C4 laminectomy and (D) C5 right hemilaminectomy. The haematoma was decompressed through limited laminectomies preserving the spinous processes and posterior ligaments. Patel R, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-222686 3 4 Sex F M M F M F F M M F M F M Presenting symptoms Neck pain, shoulder pain, right hemiparesis Right hemiparesis, neck pain Right hemiparesis, neck pain Right hemiparesis, neck pain, shoulder pain, nausea Neck pain, right hemiparesis, right paraesthesia and speech disorder Left hemiparesis and neck pain Left hemiparesis and neck pain Right hemiparesis with neck and shoulder pain Left hemiparesis, neck pain, shoulder pain Left hemiparesis Left lower limb weakness Right hemiparesis, neck pain Left hemiparesis; neck pain – – No No No Yes Yes No – – No – – No No No No No No No No No No No No No Cranial nerve palsy – Yes Yes – – – Yes Yes – – – – – BrownSequard syndrome Antiplatelet agent was started Heparin Heparin 32 hours after onset Not described Warfarin Argatroban Aspirin Heparin Thrombolytic treatment started within 2 hours 30 min of onset t-PA Antiplatelet therapy Oral aspirin for 3 days t-PA administered 2 hours after onset Treatment offered for misdiagnosis Subsequent events Underwent C1–T1 decompression and C2–C7 posterior instrumented fusion same day Conservative Conservative Was operated after 24 hours of t-PA Conservative Urinary retention developed within 12 hours of starting antiplatelet Worsening of hemiparesis and BS Nil FFP and vitamin K, operated on the same day FFP, protamine, dexamethasone Laminectomy after 55 hours Worsening of hemiparesis and Laminoplasty after new sensory deficits 4 days C3–C7 Complete C4–C5 C6–C7 C2–T1 C3–C4 Complete recovery C3–C4 Good recovery Incomplete recovery Dead due to aspiration pneumonia Incomplete recovery; residual right hemiparesis Good recovery C4–C7 C4–C5 C4–T2 Complete recovery C1–T1 Good recovery Laminoplasty done after Moderate 32 hours disability Worsened to tetraparesis, Laminoplasty after articulation disorder improved 18 hours after mouth care Newly presented Horner’s syndrome Urinary retention, Horner’s syndrome and C6 BS Worsening of hemiparesis, Was operated after new appearance of sensory 27 hours of onset deficits and exaggerated DTR Location C4–C6 Complete recovery C4–C6 Good recovery Timing of surgical intervention after the onset of symptoms Outcome Stopped within 1 hour as MRI Clotting screen was Incomplete shows SSEH normal and was recovery operated within 2 hours 45 min of t-PA Tetraparesis Left shoulder pain and weakness of left upper limb extremity No change for 3 days Worsening of neurology, urinary retention FFP, fresh frozen plasma; SSEH, spontaneous spinal epidural haematoma; t-PA, tissue plasminogen activator; BS, Brown-Sequard syndrome; DTR, Deep Tendon Reflex. 75 Sakamoto et al5 74 Tanaka et al7 66 42 So et al12 Adamson et al10 69 Wang et al4 65 63 Son et al6 Hseih et al14 69 Yurter et al13 74 84 Ueba et al17 Kadota et al9 64 Tsukita et al16 80 71 Usami et al8 Age Morimoto et al15 Horner’s syndrome Reported cases of SSEH that were misdiagnosed and treated as stroke Author Table 2 Rare disease Patel R, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2017-222686 Rare disease but the fibrinolytic activity persists for 24 hours.33 Adamson et al used fresh frozen plasma, protamine and dexamethasone before surgery,10 whereas Son et al operated on SSEH about 2 hours and 45 min after t-PA infusion without using any supplements as the coagulation profile remained normal.6 In our case report, the coagulation profile was normal. Hence, the patient could be managed without any supplementation of clotting factors. In an immediate surgery following t-PA infusion when the clotting factors are deranged, administration of fresh frozen plasma or cryoprecipitate can be used for effective haemostasis.34 For patients presenting with hemiparesis, the emergency physicians and neurologists are under pressure to institute thrombolytic treatment within 3 hours as it is the only effective non-invasive treatment for ischaemic CVA. Hence, our suggestion to consider SSEH in a small subgroup may not always be justified. However, it is prudent to continue monitoring a patient on thrombolytic therapy and an urgent MRI cervical spine should be sought in those who deteriorate after thrombolysis or who present with atypical features of stroke. A proactive consideration of SSEH as a differential diagnosis for CVA is essential.11 A high index of suspicion, prompt and appropriate investigation and immediate intervention can reduce morbidity when SSEH mimics CVA. Learning points ►► Spontaneous spinal epidural haematoma should be considered in patients presenting with hemiparesis and neck or back pain with or without radiculopathy. ►► Epidural haematoma should be ruled out before initiating thrombolytic treatment. ►► Presence of Horner’s syndrome, Brown-Sequard syndrome, absence of cranial nerve palsies, positive Lhermitte’s sign and a normal brain MRI are indicators of a spinal pathology in patients presenting with hemiparesis. Contributors RP contributed in planning, reporting, acquisition of data, preparing the manuscript and editing the manuscript. AK played a cardinal role in critically reviewing and editing the manuscript. KN aided in acquisition of data (review of Japanese articles) and in editing the manuscript. NK held a paramount position in conceptualisation, planning and construction of the manuscript. Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors. Competing interests None declared. Patient consent Obtained. Provenance and peer review Not commissioned; externally peer reviewed. © BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted. References 1 Raasck K, Habis AA, Aoude A, et al. Spontaneous spinal epidural hematoma management: a case series and literature review. 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