Cranial subdural migrating to lumbar subdural space in a toddler

Abstract

Migrated spinal subdural haematoma (sSDH) is a significantly uncommon finding. This case involves a paediatric patient representing after cranial trauma with new abnormal gait and leg pain who was found to have a migrated sSDH. Literature review for reported cases of pathogenesis theories, causes and management was performed and summarised in this report. The authors concluded that new abnormal gait and leg pain in a paediatric patient with previous cranial trauma is an indication for spinal MRI if migrated subdural haematoma is suspected. Non-surgical management is generally tolerated, and steroids can be trialled for radiculopathy if clinically indicated.

Background

Spinal Subdural Haematoma (sSDH) is an uncommon phenomenon. Known factors for the development of spinal SDH include trauma, pre-existing coagulopathies, anticoagulant therapy and invasive spinal procedures.^{1 2} However, idiopathic causes of spinal SDH have also been reported.³ Few studies have described the development of spinal SDH as a result of the migration of an intracranial SDH.^{2 4–8} The proposed mechanism of intracranial SDH resolution and SDH migration has been linked to elastic cerebral tissues as well as the anatomic continuity between the cranial and spinal subdural spaces.^{5 9} Combined with dilution with CSF from small arachnoid tears, the elasticity of the brain is thought to aid in the redistribution of the blood.⁴ This phenomenon is observed to be more common in children and young adults.⁴

Case presentation

In this report, we present a case of cranial subdural haematoma migrating to the lumbar spine and causing gait disturbance with radiculopathy. The patient is a female toddler with a medical history of post-traumatic stress disorder in the foster system who presented to the emergency department after reportedly falling off a stool with episode of emesis, unresponsiveness and eyes rolling in the back of her head. Glasgow Coma Sale was noted to be 12 on arrival, and CT scan of the head was noted to have a 0.5 cm acute right sided subdural haematoma with 0.5 cm of midline shift (figure 1). The patient was admitted to the paediatric intensive care unit and underwent a repeat CT of the head 6 hours from the initial CT, which revealed redistribution of subdural haemorrhage with improvement of midline shift to 0.3 cm (figure 1). The patient was also found to have a normal coagulation profile, bruising on her body and retinal haemorrhages.

Figure 1.

Coronal CT of the head on presentation (A, B) and 6 hours later (C, D). Initial scan demonstrates a thin laminar right convexity subdural haematoma. Follow-up scan shows interval decrease in size of the convexity subdural haematoma with redistribution to the right tentorial leaflet. There is an interval improvement in right to left midline shift from 0.5cm to 0.3 cm.

After discharge to a new foster family, the patient returned 9 days post injury with abnormal gait, arched back, and lower back and left lower extremity pain. Physical therapy notes documented an improving ‘scissoring gait’, ataxia, as well as left medial knee pain, all concerning for myelopathy and radiculopathy (possibly L4 distribution). Spinal MRI obtained 12 days post injury revealed a circumferential sSDH from T5-S2 (figure 2). The patient was started on 7 days of dexamethasone and discharged from the hospital with neurosurgical follow-up. No follow-up imaging was obtained, but symptoms resolved with 7-day steroid course. She was seen 1 month following the initial cranial SDH diagnosis and was asymptomatic at that time. She returned 7 months after initial injury to discuss shuffling gait, for which she was treated with physical therapy. She has been asymptomatic since.

Figure 2.

Select images from spinal MRI obtained on day 12 post injury. Sagittal T1 (A), sagittal constructive interference in steady state sequence (CISS; B), sagittal gradient echo sequence (GRE; C) and axial T1 (D–F) of the spine demonstrating a long segment spinal subdural haematoma surrounding the thecal sac, extending from T5-T6 to the tip of the thecal sac at S2, causing mild compression of the thecal sac and roots of the cauda equina. The spinal subdural haematoma is hyperintense on T1-weighted and T2-weighted images with mild susceptibility signal loss on the GRE sequences and demonstrates the inverted ‘Mercedes-Benz’ sign on axial T1-weighted image.

Investigations

A basic coagulation profile was obtained at the time of admission. Relevant laboratory values are activated partial thromboplastin time of 25.0 s, prothrombin time of 13.3 s, international normalised ratio of 1.2 and platelet count of 386 ×10⁹/L.

Outcome and follow-up

The patient is now over 2 years out from the head trauma and migrated sSDH. She has returned to normal function and is now performing well in age-appropriate schooling.

Discussion

There have been many reports of sSDH, which can be separated into spontaneous, traumatic and migrated. Our focus is on migrated sSDH. Of the cases reviewed, migrated spinal sSDH can arise from aneurysm rupture,⁷ cerebral venous sinus thrombosis with haemorrhage,¹⁰ haemorrhagic metastatic brain lesions⁹ and trauma.4 8 11 12 sSDHs can present in a variety of ways, from radiculopathy and back pain to paraparesis and cauda equina syndrome.¹⁰ Of the reviewed migrated sSDHs, symptoms presented in a delayed fashion, from post injury day 4 to day 14.2 4 6 12 13 Management occurs on a case-by-case basis, with decompression and evacuation generally reserved for significant weakness and sacral nerve dysfunction. Of the cases reviewed, the majority of patients had resolution of their symptoms over time without surgical intervention. There was one case of evacuation due to bilateral lower extremity weakness and one due to progressive pain and parasthesias.^{1 4}

The mechanism by which cranial SDHs migrate to the spine is still speculated. Some theorise that elevated intracranial pressure from calvarial trauma results in the subdural being ‘pushed’ out of the cranial space and into the lumbar subdural space.⁵ This is the most likely mechanism for our patient’s sSDH. On her interval scan (figure 1), she was noted to have some right tentorial subdural haematoma, indicating a caudal migration of the blood. Indeed, it seems that gravity plays a role in the majority of migrating subdurals as all the reports of migrated subdural land in the most dependent portion of the spine.^{2 4–8} The cranial and spinal subdural spaces are continuous anatomically, making it only a question of pressure differentials.¹⁰ Several studies of migrated sSDHs have occurred in cerebrospinal fluid (CSF) diversion, which may have resulted secondary to lowering of the subarachnoid pressure and therefore opening of the potential space the subdural haematoma occupies.^{6 14}

The spinal subdural space is not vascular and generally is not the primary source of haemorrhage in the absence of local trauma. However, violation of either the arachnoid after subarachnoid bleeding or dura in the case of epidural bleeding can result in blood in the spinal subdural space. If there is communication between the cranial subdural and subarachnoid space, there is also a possibility of the subdural being redistributed into the subarachnoid space and mixing with CSF.²

Our case is unique in that it involved a paediatric patient who had difficulty expressing her symptoms secondary to age and developmental delay. She was noted to have arched back and back pain, which is why she returned to the hospital. This is also the only report to trial decadron for treatment of radiculopathy secondary to sSDH. It may be coincidental, but the patient experienced significant pain relief at the start of the decadron course and was able to be discharged that same day.

Patient’s perspective

Adoptive Mother: After the head trauma, she came home with us. We noticed within a day or two that it was difficult for her to bend over to put her socks and shoes on and get out of bed in the morning. She got out of bed like an elderly person (really slow and stiff). She couldn't sit cross-legged and when she was sitting she had an arch in her back that looked odd. She was also walking and running without bending her knees, sort of shuffling. Her daycare noticed it as well. It was hard to determine what was going on because of her trauma history and being so new to us (recently moved into our home). She cried a lot and couldn't tell us what was going on. But after she started the steroid, we noticed an immediate change in her mood and her ability to bend over and move with more mobility. Now, she’s doing great!

Learning points

• Although rare, cranial subdural haematomas can migrate to the spinal subdural compartment and become symptomatic in the form of lumbar radiculopathy or cauda equina syndrome.

• In the paediatric population, new abnormal gait is an indication for spinal MRI and suspicion for migrated subdural should prompt spinal imaging in patients with recent cranial trauma.

• Non-surgical management is generally tolerated, and steroids can be trialled for radiculopathy if clinically indicated.

Ethics statements

Patient consent for publication

Consent obtained from parent(s)/guardian(s)