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Clinical Case Report

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Spontaneous spinal epidural hematoma mimicking
transient ischemic attack
A case report
Chuqiao Li, MSa,c, Rui He, BSa, Xiaoqiang Li, MSb, Yulan Zhong, MSa, Li Ling, MD, PhDc,
∗
Fangming Li, MD, PhDc,
Abstract
Rationale: Spontaneous spinal epidural hematoma (SSEH) is a rare but highly disabling neurological emergency. The initial

presentations are variable. Most patients of SSEH present with paraplegia or tetraplegia clinically, but recurrent hemiparesis with
complete spontaneous recovery, mimicking transient ischemic attack (TIA), is a very rare initial presentation of SSEH.
Patient concerns: A 71-year-old female presented to the emergency department with 2 episodes of transient right hemiparesis in
5 hours. Two days later, above symptom reappeared and progressed to quadriplegia, dyspnea, and uroschesis quickly. The
neurological examination showed tetraplegia and hypalgesia below the C2 level, but neither facial palsy nor aphasia was found.
Diagnosis: The patient was initially misdiagnosed as TIA and treated with antiplatelet therapy. But during the hospital day, the
cervical magnetic resonance imaging showed a dorsal epidural hematoma extending from C2 to C6 level and she was diagnosed as
SSEH.
Interventions: She underwent surgical decompression and hematoma removal 1 week later.
Outcomes: One week after operation, the sensory deficit above C6 level improved, but there was no improvement in her muscle

strength and dyspnea. Unfortunately, she died 1 month later.
Lessons: Our case highlights recurrent hemiparesis with complete spontaneous recovery mimicking TIA is a rare initial presentation

of SSEH. It is important to perform careful clinical assessments and neuroimaging investigations for correct diagnosis. Neck pain and
hemiparesis sparing cranial nerve are important signs for distinction of SSEH from acute ischemic cerebrovascular diseases.
Abbreviations: MRI = magnetic resonance imaging, SSEH = spontaneous spinal epidural hematoma, TIA = transient ischemic

attack.
Keywords: hemiparesis, spontaneous spinal epidural hematoma, transient ischemic attack

the “spontaneous” refers to atraumatic etiology and lack of
iatrogenic procedure. Its etiology is related to vascular malformation, coagulopathy, anticoagulants, tumor, hypertension, and
pregnancy. The classic manifestations of SSEH are sudden onset of
back or neck pain followed by rapidly progressive spinal cord
compression syndrome. But the initial presentations of SSEH are
often miscellaneous and atypical. Recurrent hemiparesis with
complete spontaneous recovery, mimicking transient ischemic
attack (TIA), is a very rare initial presentation of SSEH. Here, we
report a rare case of SSEH who initially presented with recurrent
hemiparesis and was misdiagnosed as TIA.

1. Introduction
Spontaneous spinal epidural hematoma (SSEH) is a rare but highly
disabling neurological emergency, which accounts for <1% of all
spinal epidural space-occupying lesions.[1,2] The annual incidence
of SSEH was estimated to be 0.1 per 100,000 patients.[3] In SSEH,
Editor: Elena Cecilia Rosca.
CL and RH contributed equally to this work.
The authors report no conflicts of interest.
a
Department of Neurology, The Affiliated Guangzhou Red Cross Hospital, Jinan
University, Guangzhou, b Department of Neurology, Xiaolan Hospital of Southern
Medical University, Zhongshan, c Department of Neurology, Shenzhen Hospital,
Southern Medical University, Shenzhen, Guangdong, China.

2. Case report

∗

A 71-year-old woman presented with sudden neck pain and
weakness in her right upper and lower limbs while she was having
a bath at home. Her symptoms resolved spontaneously within
10 minutes. After half past 4 hours later, she had the same onset
of right hemiparesis and had full recovery within 15 minutes, and
then was immediately admitted to our emergency department.
The patient had a 30 years history of hypertension without wellcontrol. She had no previous history of taking any antiplatelet or
anticoagulant drugs. There was no recent history of head and
spinal trauma or surgery.
The initial blood pressure was 210/90 mm Hg. On neurological
examination, the patient had a normal cranial nervous system

Correspondence: Fangming Li, Department of Neurology, Shenzhen Hospital,
Southern Medical University, N0.1333 Xinhu Road, Shenzhen, Guangdong
518110, China (e-mail: lifly050413@163.com).
Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc.
This is an open access article distributed under the terms of the Creative
Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is
permissible to download, share, remix, transform, and buildup the work provided
it is properly cited. The work cannot be used commercially without permission
from the journal.
Medicine (2017) 96:49(e9007)

Received: 9 August 2017 / Received in final form: 8 November 2017 / Accepted:
9 November 2017
http://dx.doi.org/10.1097/MD.0000000000009007

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Figure 1. Cervical magnetic resonance imaging (MRI; sagittal) showed a longitudinal dorsal epidural hematoma (A: T2-weighted, B: T1-weighted) extending from
C2 to C6 level.

One week after operation, the sensory deficit above C6 level
improved, but there was no improvement in her muscle strength
and dyspnea. Unfortunately, she died 1 month later.

and sensory system. Her muscle strength was grade 5/5 in
bilateral upper and lower limbs, but the right knee reflex was
hyperactive and Hoffman’s sign was positive. Laboratory
investigations showed that a complete blood cell count,
prothrombin time, and partial thromboplastin time were within
normal limits. An emergency brain computed tomography and
cervical x-ray scans were unremarkable. A clinical diagnosis of
TIA was considered. Then the patient was hospitalized in the
neurological wards and treated with antiplatelet therapy (100 mg
aspirin and 75 mg clopidogrel, once daily). She did not complain
any other symptoms except a mild neck pain in the following 2
days after admission.
On the third hospital day, the brain magnetic resonance
imaging (MRI) and cervical MRI were performed. The brain MRI
showed no signs of acute cerebral infarction. The cervical MRI
revealed a spinal epidural hematoma located in the posterior
spinal epidural space extending from the C2 to C6 spinal
vertebral level. The hematoma was isointense on T1-weighted
images and hyperintense on T2-weighted images (Fig. 1). Just
after returning to the wards, the patient recurred the right
hemiplegia (muscle strength was grade 3/5 in right upper and
lower limbs), and developed rapidly progressive quadriplegia,
loss of pain and temperature sensation, dyspnea, and uroschesis.
Neurological examination revealed tetraplegia (the muscle
strength was grade 2/5 in left limbs and 1/5 in right limbs)
and loss of pain below the C2 level bilaterally. She had neither
aphasia nor abnormal cranial nerve signs. Given her progressive
symptoms and imaging findings, the diagnosis of spinal cord
compression was considered. The patient was transferred to the
intensive care unit immediately and treated with trachea cannula
and ventilator-assisted ventilation. Her family members did not
consent to emergency surgical decompression and the patient
became worse in the following days. After a week later, her family
members finally consented to the surgical decompression. The
findings of operation confirmed a hematoma arising on the dorsal
spinal epidural surface and extended from the C2 to C6 spinal
vertebral level, and the right was more serious.

3. Discussion
SSEH is a rare clinical emergency which was first described by
Jackson in 1869.[4] Holtas et al[3] reported that the annual
incidence of SSEH was approximately 0.1 patient per 100,000
patients. But in the last years, the number of diagnosed and
reported cases of SSEH has been increased due to the progress of
neuroradiological investigations and neurosurgery. Patients with
SSEH usually present with sudden onset of severe back or neck pain
followed by rapidly progressive symptoms and signs of nerve root
or spinal cord compression. The clinical symptom severity is
significantly correlated with the rate of bleeding, the extent of
hematoma, and the length of time of onset. However, the initial
manifestations of SSEH are sometimes atypical, even mimicking
an onset of ischemic stroke. Among the initial presentations of
patients with SSEH, hemiparesis is a less common symptom
compared with other motor deficits such as paraplegia or
tetraplegia.[5,6] But with the rapid development of MRI technology, there are increasing cases of SSEH who presented with
hemiparesis initially have been reported in the last years. In clinical
practice, when patients of SSEH presented with sudden onset of
hemiparesis, even they complained of back pain or neck pain, they
are often been suspected to have an acute cerebral infarction during
the initial assessment.[7] Moreover, hemiparesis with complete
spontaneous recovery, mimicking TIA, is a rare initial symptom of
SSEH. Only a few patients with complete spontaneous recovery
due to SSEH have been reported in the last decades.[8,9] For
example, Hernandez et al[8] reported that a patient had 3 relapsing
paraplegia and complete spontaneous recovery in 5 hours, and
myelography and computed tomography confirmed a posterior
epidural hematoma extending from T11 to T12 level. The initial
presentation of our patient was 2 episodes of right hemiparesis with
complete spontaneous recovery within 5 hours. The present patient
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treated with the antiplatelet drugs due to her initial manifestation
mimicking TIA, which may result in the rapid development of
hematoma and poor outcome. In clinical practice, physicians
tend to consider TIA as the first diagnosis for patients with acuteepisodic neurological disorders. If the patient complained of
persistent neck or back pain and recurred or fluctuating
hemiparesis, neck or back pain should not be overlooked as
an important sign for the diagnosis of SSEH, especially in the
patients without cranial nerve signs.
Spinal MRI is the preferred diagnostic tool for SSEH. Spinal
MRI can show the segmental and range of epidural hematoma,
and the extent of spinal cord compression. However, the super
acute or acute hemorrhage has atypical MR manifestations. The
hematoma shows isointense on T1-weighted and hyperintense on
T2-weighted images. It should combine the onset time to analyze
the MR signs of hematoma. If physicians’ lack of the realization
of early imaging changes, it can easily lead to a misdiagnosis. For
subactue hemorrhage, it shows characteristic hyperintense on T1weighted and low signal intensity on T2-weighted images. In our
patient, the findings of spinal MRI were consistent with the signs
of acute hemorrhage.
Emergency surgical spinal decompression is the main treatment
of SSEH, which should be performed within 12 hours and not
later than 36 hours for a favorable outcome.[12,21] Conservative
management can also be considered in those SSEH patients with
minimal neurological deficits or who have rapidly improving
neurological function.[22] Delayed surgical decompression was
performed in our patients, and her condition deteriorated due to
hematoma expansion.
Although our patient presented with mild and recurrent
hemiparesis with complete spontaneous recovery at the initial
stage, she developed rapidly progressive neurological deficits within
a short time after admission. We considered that the causes of her
rapid exacerbation were multifactorial, including old age, uncontrolled hypertension, the location of hematoma in the cervical area,
the antiplatelet therapy, and delayed surgical spinal decompression.
Among above factors, the use of antiplatelet agent may be the major
cause of hematoma expansion and poor outcome.
In conclusion, our case highlights recurrent hemiparesis with
complete spontaneous recovery mimicking TIA is a rare initial
presentation of SSEH. It is important to perform careful clinical
assessments and neuroimaging investigations for diagnosis. Neck
pain and hemiparesis sparing cranial nerve are important signs for
distinction of SSEH from acute ischemic cerebrovascular diseases.

was an old woman with a previous history of uncontrolled
hypertension, so she is easy to be misdiagnosed as having a TIA at
the early stage and consequently administrated with antiplatelet
drugs. This patient did complain of neck pain on admission, but
this symptom did not be attached great importance by physicians
due to the findings of cervical x-ray scans was unremarkable.
Similar to the previous reported cases of SSEH with complete
spontaneous recovery, the length of spinal epidural hematomas
was not long in our patient. In addition, the cervical MRI of our
patient showed that the shape of spinal epidural hematomas was
cylindrical, which might have less pressure on the spinal cord.
These may be the reasons why our patient presented with less
severely neurological deficits and had complete spontaneous
recovery at the early stage. In addition, we think that at the
beginning of the stage, the hematoma may spread along spinal
epidural space containing fat, areolar tissue, and vascular network,
which would result in the subsequent decompression of internal
pressure. Hence, our patient had the manifestation of recurrent
hemiparesis with complete spontaneous recovery mimicking TIA.
We emphasize that it is important to collect a comprehensive case
history and perform neurological examination in the course of
diagnosis. Radicular pain should not be ignored as an important
sign of SSEH. When patients have sudden neck pain with
neurological deficits, it is highly suggestive of a possible cervical
spinal cord hemorrhagic disease, and SSEH should be considered
as a common stroke mimic.
So far, the actual source of bleeding has not been well defined in
patients with SSEH. Most authors support the venous origin
hypothesis due to the anatomical characteristics of the posterior
internal vertebral venous plexus and the most common location
was the posterior of the thoracic region in the spinal canal.[1,10,11]
They believed that it is prone to resulting in veins rupture and
bleeding when patients had a suddenly increasing pressure effect
from the thoracic or abdominal cavity, especially in the older
patients or the patients with slow progression of neurological
decline. The present patient had the onset when she was having a
bath, whereas many patients of SSEH have been reported to be
initially triggered by actions that suddenly increase venous
pressure.[12,13] On the contrary, some authors support the arterial
origin of bleeding, especially when the hematomas was located in
the cervical region.[14] They think that the intrathecal pressure is
higher than the venous pressure at the cervical level, which would
prevent bleeding from veins in the epidural space. Considering
that the hematoma of our patient was located at the cervical
region, our patient had rapidly deteriorating neurological deficit
after admission, as well as she had an uncontrolled hypertensive
condition, we speculated that the hematoma may be of arterial
origin in the present patient.
The precise etiology remains unclear. Increasing age, hypertension, anticoagulants, thrombolytics, antiplatelet agents,
vascular malformation, and systemic diseases have been considered as possible predisposing factors in some patients with
SSEH.[1,12,15–18] However, there are 40% to 60% of cases could
not find any underlying cause.[19,20] SSEH could occur at any age,
but most of the patients are in their fourth or fifth decades of life.
A recent individual patient data meta-analysis revealed the
median age is 58 years.[16] Hypertension has been observed in a
range from 3% to 21.4% of patients with SSEH, but whether
hypertension is a risk factor of SSEH or not is still controversial.[1,16] Evidences from current meta-analysis could not suggest
the relationship between hypertension and the development of
SSEH.[16] We thought that old age and uncontrolled hypertension
may be risk factors of our case. Moreover, this patient was

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