Subdural haematoma, the great imitator, mimicking acute spinal cord lesion
- Kensuke Shiga and
- Aiko Tamura
- Department of Neurology, Matsushita Memorial Hospital, Moriguchi, Japan
- Correspondence to Dr Kensuke Shiga; kenshiga@koto.kpu-m.ac.jp
Abstract
Acute non-traumatic paraparesis is usually caused by vascular, inflammatory or neoplastic myelopathies; however, it is sometimes caused by non-myelopathic pathologies, including polyradiculoneuropathies, myopathies, psychogenic aetiologies or parasagittal cortical pathologies. A 73-year-old woman reported weakness of the bilateral lower limbs and urinary incontinence. Together with the sensory level at the left T6 dermatome, we initially considered thoracic myelopathy as the most likely diagnosis. However, MRI of the cervicothoracic cord was negative and subsequent cranial CT revealed a bilateral subdural haematoma. A parasagittal cortical pathology should not be excluded from differential diagnoses as a rare cause of paraparesis until its possibility is carefully ruled out.
Background
A subdural haematoma (SDH), a collection of blood between the dura and arachnoid membrane, is caused by the tearing of bridging veins that drain from the surface of the brain to the dural sinuses. SDH, the great neurologic imitator,1 has a broad spectrum of manifestations, including headache, cognitive impairment, apathy, seizures, and focal deficits, such as either contralateral or ipsilateral hemiparesis. In rare cases, bitemporal SDH may present with paraparesis,2–6 challenging clinicians to localise the anatomical site of a lesion because the presence of acute paraplegia with urinary incontinence is usually suggestive of a thoracic cord lesion, another neurological emergency.7 We herein report a patient with bilateral SDH presenting with acute paraparesis, urinary incontinence and sensory loss below the T6 dermatome mimicking a spinal cord pathology, prompting us to perform a cervicothoracic MRI before brain CT.
Case presentation
A 73-year-old woman presented with acute-onset weakness of the bilateral lower limbs and urinary incontinence. Seven days prior to the presentation, one of her friends had commented that her manner of walking was strange; however, the patient herself did not feel it strange at that time. One day prior to presentation, she accidentally fell to the ground when she took out garbage and from then on, she began to feel difficulty walking. Her medical history included diabetes mellitus, hypertension and dyslipidaemia. She was taking metformin, teneligliptin, canagliflozin, azelnidipine and rosuvastatin. She denied any head trauma or headache. She regularly consumes one unit of alcohol a few days every week.
On presentation, her blood pressure was 143/81 mm Hg and the pulse was 70/min. Her temperature was 37°C and respiration was 20/min. On neurological examination, she was alert and well oriented regarding the date and place. Cranial nerves were normal. The strength and tone of the upper extremities were normal. The muscle tone of the lower extremities was slightly spastic. The Medical Research Council scores of bilateral iliopsoas, quadriceps femoris and hamstrings muscles were 3/5, and those of the bilateral tibialis anterior and gastrocnemius muscles were 4/5. There was a loss of superficial sensation in the left lower extremity up to the T6 dermatome with decreased vibratory sensation at the bilateral medial malleoli. The reflexes of the upper extremities were normal while those of the lower extremities were brisk. Babinski signs were negative on both sides. She was aware of urinary incontinence, and the tone of the anal sphincter muscles was decreased based on digital examination. The combination of acute paraplegia, urinary incontinence and the sensory level below the left T6 dermatome led to the diagnosis of an upper thoracic spinal cord lesion.
Investigations
MRI of the cervical and thoracic cord, however, did not reveal any causative pathology for paraplegia within the spinal cord (figure 1). In search of a possible parasagittal cortical pathology, cranial CT was subsequently performed, demonstrating massive fluid collection in the bifrontal subdural space, indicating SDH (figure 2).
(A) A sagittal T2-weighted image of the cervical cord showed a slightly narrow cerebrospinal fluid space at C4/5 and C5/6 without cord deformity. (B) A sagittal T2-weighted image of the thoracic cord showed a normal morphology.
(A) An axial image of plain head CT showed bilateral fluid collection in the bilateral subdural spaces, that is, bilateral subdural haematoma compressing both cerebral hemispheres. (B) A coronal section of the plain head CT revealed marked convexity as the parasagittal cortices were compressed from both sides.
Treatment
An urgent neurosurgical referral was made and she underwent a bilateral burr hole aspiration of blood.
Outcome and follow-up
On the days after surgery, her paraplegia, urinary incontinence and sensory deficit completely resolved. She became ambulant without imbalance.
Discussion
Acute non-traumatic paraplegia is a neurological emergency that requires a rapid diagnostic exploration to clarify not only the responsible site of the lesion, but also the aetiology in order to immediately commence therapeutic intervention. From a neuroanatomical perspective, non-traumatic paraplegia is commonly caused by inflammatory, vascular or neoplastic processes within the spinal cord, while it can also result from uncommon non-myelopathic pathologies, such as polyradiculitis, hyperkalaemic or hypokalaemic paralysis, or parasagittal cortical lesions.7 It is challenging for clinicians to consider uncommon non-myelopathic pathologies while they are urged to search for a possible cause of the myelopathic process as soon as possible. The diagnostic challenge grows when a paraplegic patient exhibits urinary incontinence and a thoracic sensory level, as seen in this patient.
The combination of paraplegia with brisk reflexes, urinary symptoms and sensory loss below the T6 dermatome led us to consider a myelopathic process at the thoracic cord, which was ruled out by spinal MRI (figure 1). Subsequently, we performed a brain CT in an attempt to explain the combination of her symptoms and signs, unexpectedly revealing bilateral SDH (figure 2).
When retrospectively reviewing our initial diagnosis of myelopathy, the typical constellation of paraparesis, urinary incontinence and the T6 sensory level together with the preserved level of consciousness might have resulted in us not considering a possible intracranial pathology. However, some patients with bilateral SDH resulting in paraparesis were fully conscious, with a Glasgow Coma Scale of 15/15,2 3 as seen in this patient. Therefore, SDH, the classic great neurologic imitator,1 should not be excluded from differential diagnoses in patients with paraparesis, even if they show preserved normal consciousness.
In rare instances, paraparesis can result from parasagittal cortical pathologies, such as parasagittal meningioma,8 aneurysm rupture of the unpaired anterior cerebral artery,9 bifrontal encephalitis with anti-myelin oligodendrocyte glycoprotein(MOG) antibodies10 and bilateral SDH.2–6 The weakness of the bilateral lower extremities in patients with parasagittal lesions is potentially explained by the anatomical proximity of the motor homunculi of the lower extremities within the parasagittal cortex, close to the falx cerebri. Several possible causes of paraparesis in patients with SDH have been proposed, such as direct compression or distortion of the bilateral hemispheres at the falx,11 subfalcine herniation by the haematoma2 or ischaemia of the corresponding cortical areas supplied by the anterior cerebral arteries.11 The exact mechanisms of bilateral SDH resulting in paraparesis are not fully understood; however, parasagittal cortical pathologies should not be excluded from possible causes of acute paraparesis.
The urinary incontinence in patients with SDH is most probably attributable to the damage in a putative supratentorial micturition centre whose components include bilateral cortical regions located in the anterior part of the frontal lobe near the midline.12 In a study comprising 500 consecutive cases of chronic SDH, urinary incontinence was a feature in 87 cases (17.4%), being associated with gait disturbance in 80 patients.13
The sensory level of the left T6 dermatome was another confusing sign in this patient, which led us to consider a thoracic myelopathy. Hellmann et al 14 reported 12 patients whose thoracic sensory level was a false localising sign with normal thoracic MRI. Among these, 10 patients had cervical spinal cord lesions, whereas two patients had intracranial lesions with a demyelinating pathology. In addition, Capasso et al 15 reported a patient with right parasagittal meningioma presenting a contralateral sensory level below T6, in which they argued the lesion affecting the postcentral gyrus in the areas corresponding to the lower limb and the lower part of the trunk may virtually result in a peculiar distribution of the sensory deficit mimicking a thoracic cord level. In this patient, the compression by the SDH to the right parietal sensory cortex could result in the sensory deficit below T6; however, it remains still unclear why this sensory level appeared only on the left side.
In summary, the view that paraparesis is most often caused by a myelopathic process may sometimes lead to an error in anatomical diagnosis that can delay the correct diagnosis. In patients with paraparesis, it is crucial to consider other anatomical possibilities including a parasagittal cortical pathology.
Learning points
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Acute paraplegia generally suggests a spinal cord lesion as a responsible site of lesion. This representative heuristics may lead to an erroneous anatomical diagnosis in a few exceptional cases, possibly delaying correct diagnoses.
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A parasagittal intracranial lesion is theoretically considered to be a textbook exception to the heuristics above; however, it is rarely encountered even in neurology clinics.
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Chronic subdural haematoma, the great imitator in neurology, can be a rare cause of acute paraplegia when occurring bilaterally.
Acknowledgments
We appreciate the patient for permitting the submission of this report.
Footnotes
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Contributors KS designed the study and wrote the initial draft of the manuscript. AT was involved in the management of the patient.
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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Competing interests None declared.
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Provenance and peer review Not commissioned; externally peer-reviewed.
- © BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.
References
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