Episodic cauda equina compression from an intradural lumbar herniated disc: a case of ‘floppy disc’

Abstract

INTRODUCTION

In 1942, Dandy (2) first reported on an intradural disc herniation among 300 patients who underwent surgery for lumbar disc herniation. IDDH are usually seen at L4-L5 and L3-L4. However, intradural disc herniation at L5-S1 is quite rare. There are approximately nine reports in the English literature of intradural disc herniation at L5-S1 (3).

We present a case of intermittent, painless cauda equina compression due to IDDH at L5-S1. We will review the relevant literature, discuss pathogenesis, diagnosis, and treatment.

CASE REPORT

A 53-year-old man was referred to the Emergency Department by his GP with a 3 week history of paraesthesia and weakness in his left lower limb. This was associated with 3 episodes of urinary and faecal incontinence. Interestingly he had no pain and the course of symptoms was intermittent. The symptoms followed a regular pattern of lower limb paraesthesia, weakness and then incontinence for urine and faeces. This would last for a few hours followed by complete resolution.

His past medical history was significant for “sciatica” 3 years prior to presentation, at which time, MRI scans showed ‘a protruding disc’ The symptoms resolved with physiotherapy.

Neurological examination revealed weakness of left foot dorsiflexors (Grade 4/ 5). Sensory examination revealed impaired pinprick from L1 to S1 dermatomes.

Anal tone and perianal sensation were normal.

Magnetic resonance imaging (MRI) revealed an intra-dural mass lesion at L5-S1 level with no contrast enhancement. He underwent an L5/S1 laminectomy. The dura was swollen and immobile. Subsequent durotomy demonstrated a 1×3 cm mass occupying the spinal canal with peripheral displacement of the nerve roots. Careful excision of the disc fragment revealed a small defect in the anterior thecal sac, which was firmly adherent. An anterior dural defect was found communicating with the L5-S1 interspace. Postoperative period was uneventful and patient gained full recovery in 4 months.

DISCUSSION

The physiologic and pathologic features that cause IDDH are not quite clear. Migration of the Nucleus Pulposus intra-durally requires perforation of the Annulus Fibrosus and the posterior longitudinal ligament. Adhesions between the Annulus Fibrosus, posterior longitudinal ligament and the ventral dura mater are therefore thought to predispose to this. Indeed at the L4-5 and slightly less at the L5-S1 levels, the two layers that normally compose the posterior longitudinal ligament are firmly connected to each other and the annulus fibrosis, thus favouring disc herniation and perforation of the dura mater (4). An autopsy study has also shown that the ventral dura is most frequently and firmly attached to the posterior longitudinal ligament at the L4-5 level and that these adhesions may be congenital. Post operative adhesions between these layers may also be contributory. Other predisposing anatomic factors include congenital narrowing of the spinal canal (5).

The most peculiar feature of the clinical presentation in this case is the clear intermittent course of the patient’s symptoms. This has not been clearly reported previously with transdural disc herniation.

We think that the intra-dural location of the disc fragment may have caused the fragment to be more mobile causing a ball and valve-like effect which could explain the intermittent nature of the clinical presentation.

It is usually not difficult with current MRI techniques to differentiate lumbar disc herniation from other conditions. Contrast-enhanced MRI scans are useful to differentiate a herniated disc from a disc space infection or tumour. Peripheral enhancement around the non-enhancing disc fragment is commonly seen on contrast MRI. A herniated disc fragment will rarely be enhanced centrally, which is attributed to vascular granulation tissue infiltrating the fragment. The potential presence of an intra-dural disc herniation must always be considered preoperatively on a patient whose magnetic resonance imaging study demonstrates abrupt loss of continuity of the posterior longitudinal ligament.

Mut (3) suggested classifying IDDH into, Type A: Herniation of a disc into the dural sac. Type B: Herniation of a disc into the dural sheath in the pre-ganglionic region of the nerve root. Type A intra-dural disc herniation at L5-S1 is quite rare. This report presents a case of Type A intra-dural disc herniation at L5-S1 mimicking an intra-dural extramedullary spinal tumour.

Lumbar intra-dural disc rupture must be considered in the differential diagnosis of mass lesions causing nerve root or cauda equina syndromes. The clinical course may be intermittent which may be due to the relatively more free movement of the fragment inside the thecal sac in comparison to tumours or extradural disc prolapse.

Neurological prognosis appears to be closely related to preoperative duration of neurological symptoms and therefore prompt preoperative diagnosis and prompt surgical intervention is crucial.

REFERENCES