Spinal arachnoid web (SAW) is an abnormal thickening of the intradural arachnoid bands that extend to the pial surface of the posterior aspect of the spinal cord. The first case was described in 1997 by Mallucci et al. [1] It is a rare and probably underdiagnosed pathology characterized by focal thickening of arachnoid tissue causing dorsal compression of the spinal cord [2]. The SAW or arachnoid web (AW) is considered as a variant of spinal arachnoid cysts (SAC). According to Nisson et al., SAW predominantly affects men and is most commonly located in the thoracic spine, posterior to the spinal cord and frequently associated with syringomyelia [3]. SAW is sometimes regarded as the remnants of a ruptured or collapsed arachnoid cyst, or even resulting from incomplete formation of an arachnoid cyst. Post-traumatic, post-infectious and post-operative causes have been reported. Research into idiopathic forms remain ongoing. Patients with SAW present with neuropathic pain and signs of compressive myelopathy, accompanied by episodic lower limb weakness [2][3]. Typical MRI features include ventral displacement of the spinal cord, syringomyelia, and the characteristic “scalpel sign” [4]. Surgical decompression with adhesiolysis remains the most effective therapeutic option [5].

The aim of this study is to report three cases of arachnoid web managed in our department and to discuss diagnostic and therapeutic considerations in light of the literature.

CASE NUMBER 1:

A 49-year-old male with a history of multiple knee surgeries, including left leg pinning and right hallux valgus correction in 2018, presented in October 2020 to a peripheral hospital with reports. He reported progressive symptoms evolving over 2 years symptoms, including difficulty rising from a chair, rest-related radicular pain in the lower limbs while supine, gait and balance disturbances, and inability to climb or descend the stairs. Neurological examination revealed proprioceptive ataxia, bilateral pyramidal syndrome with hyperreflexia, and impaired deep sensation. Initial MRI (July 2020) demonstrated a dorsal syrinx at T5 - T7 associated with T5 - T6 myelopathy, anterior deviation of the spinal cord, and posterior cord impression at T6. A follow-up contrast-enhanced MRI 6 months later, confirmed a T2-hypointense oblique arachnoid band at T5 - T6 producing the cord impression and the classic “scalpel sign” diagnostic of spinal arachnoid web (SAW), and stable T2-hyperintense T6 myelopathy posterior to the vertebral body.

A T5-T6-T7 laminectomy was performed. After dural opening, a markedly thickened arachnoid membrane was identified displacing the spinal cord anteriorly. The SAW was completely resected, revealing a clear imprint on the decompressed cord, which was now freely mobile. Adhesions below were resected. Histological analysis confirmed fibroconnective tissue consistent with an arachnoid cyst wall. Immediate postoperative course was marked pain resolution. The patient neurologically plateaued and was discharged on postoperative day 3 to continue rehabilitation (Figure 1 and Figure 2).

Figure 1.Preoperative sagittal T2-weighted MRI showing myelopathy and syrinx (A) and the arachnoid web as a T2-hypointense band (arrow) (B) [Case 1].

Figure 2. Intraoperative photograph of Case 1 after durotomy showing the dura mater (blue arrow), the compressive arachnoid web with clear spinal cord imprint (black arrow), and normal spinal cord (green arrow) (A). Intraoperative photograph after arachnoid web resection showing adequate spinal cord decompression (B).

CASE NUMBER 2:

A 52-year-old male patient with no significant medical history presented in November 2021 with left-predominant lower limb weakness. A progressive gait disturbance had begun in July 2021, evolving into spastic paraparesis causing falls and difficulty climbing and descending stairs. Initial lumbar spine MRI was unremarkable and failed to explain the clinical findings. Subsequent thoracic spinal MRI revealed anterior spinal cord displacement with a posterior T3 myelomalacia. Neurological examination showed marked ankle spasticity, brisk knee jerks, left Babinski sign, spastic gait with left lower limb scissoring (particularly stiff ankle), and motor deficits (foot dorsiflexion 3/5, plantar flexion 4/5). Multidisciplinary neuroradiology review concluded on the diagnosis of SAW. Surgical intervention was indicated for spinal cord compression from SAW. Surgical procedure involved midline dural opening, exposing notably thickened arachnoid. Arachnoid incision revealed clear cord impression with severe anterior displacement. SAW was completely excised, restoring cord mobility and decompression. Intraoperative findings confirmed arachnoid remodelling. Postoperative course was uneventful. Neurologically, the patient stabilized. He was discharged on postoperative day 3 to rehabilitate. Four-month follow-up MRI was satisfactory (Figure 3andFigure 4).

Figure 3. Preoperative T2-weighted sagittal MRI (A) showing spinal cord deformation (scalpel sign: arrow) responsible for myelopathy (A) and axial view showing dorsal spinal cord flattening with anterior displacement (arrow) (B).

Figure 4.Preoperative sagittal T2-weighted MRI (A) and postoperative MRI at 4 months showing improvement of myelopathy and resolution of the arachnoid web (B). Note the incidental vertebral hemangioma (blue arrow).

CASE NUMBER 3:

A 68-year-old male with a history of traumatic brain injury and neck pain in 2018 presented in September 2021 with 6-month history of nocturnal upper limb dysesthesia with intermittent electric shock-like sensation. Neurological examination revealed no sensory or motor deficits. Cervical spine MRI (June 2021) demonstrated a large syrinx extending from C7 to T2, with a T2-level indentation suggestive of SAW and T2-hyperintensity at the inferior margin of the syrinx. Electrophysiological studies showed no radicular, plexus or trunk involvement on upper limb electromyography (EMG). Four-limb somatosensory evoked potentials (SSEPs) confirmed bilateral long-tract involvement with prolonged central conduction times consistent with syringomyelia. Follow-up MRI (October 2021) showed stable radiographic findings with no evidence of transdural herniated disc or thoracic spinal arachnoid cyst. Considering our patient’s clinical condition was stable and his symptoms were mild, and despite electrophysiological abnormalities associated with syringomyelia, a conservative management plan was put in place after consulting with the patient. However, regular clinical and radiological monitoring every six months (currently annual) has been prescribed to monitor the condition’s progression (Figure 5).

Figure 5. Preoperative T2 sagittal showing spinal cord deformation (scalpel sign, green arrow) and syringomyelic cavity “blue arrow” (A), and axial T1 view showing anterior displacement of the spinal cord (red arrow) (B). Axial T2-weighted image showing the syringomyelic cavity indicated by the green arrow.

SAW is a rare intradural meningeal pathology of uncertain etiology. The most widely accepted hypothesis suggests that AW represents an incomplete or disrupted form of arachnoid cyst development, possibly arising from collapsed or embryonic cystic structures. Its marked dorsal thoracic predominance supports the theory of origin from the diverticula of the septum posticum, a thin longitudinal membrane dividing the posterior subarachnoid space. Structural alterations of the septum posticum may generate complex arachnoid bands capable of obstructing cerebrospinal fluid (CSF) flow and producing focal cord compression, as hypothesized by Nisson [3].

Since its first description by Mallucci et al. in 1997, fewer than 300 cases have been reported, most within the last decade [1][6]. Increased MRI accessibility and heightened clinical awareness likely explain the rising number of diagnoses. Symptom onset typically occurs between the fourth and seventh decades. A male predominance has been reported by Nisson (72%) [3][7], whereas Laxpati et al. observed slight female predominance [8]. Our findings confirm the progressive and frequently insidious course of AW. The median duration of symptoms prior to consultation was 13 months which is consistent with previously published series that reported delays ranging from one to several years. Such delays are likely to contribute to irreversible spinal cord damage and may limit postoperative recovery.

Clinically, symptomatic AW most often manifests as progressive thoracic myelopathy with gait disturbance and imbalance. MRI remains the diagnostic cornerstone. The characteristic “scalpel sign,” first described by Reardon et al., reflects focal dorsal indentation of the spinal cord and is considered highly suggestive of AW. However, this sign alone does not reliably distinguish AW from arachnoid cysts or ventral spinal cord herniation. Advanced MRI sequences (phase-contrast cine MRI, CISS, T2-TrueFISP) may further delineate CSF flow obstruction and arachnoid membranes [2][4][7].

The pathophysiology of spinal arachnoid web is still not fully understood. It has been hypothesized that these lesions may represent an arachnoid remnant, a focal arachnopathy, or a variant within the spectrum of spinal meningeal disorders. Whatever the exact mechanism, the resulting focal obstruction of CSF flow appears to be a key driver of cord deformation and syrinx formation [7].

Syringomyelia is a frequent association. Voglis et al. reported syrinx formation in 83% of cases, while Nisson et al. observed it in 67% [3][9]. Lower rates were described by Laxpati [8]. The syrinx may extend rostrally, caudally, or bidirectionally relative to the web, likely reflecting unidirectional CSF flow dynamics [10][11].

The MRI-based classification proposed by Carr et al. (Type 1: cord deformation; Type 2: deformation with myelomalacia; Type 3: deformation with myelomalacia and syringomyelia) provides a pragmatic framework for therapeutic decision-making. In contrast to prior series where Type 1 predominated, our cohort was mainly Type 3, reflecting more advanced disease at diagnosis [11].

Management should be individualized. Conservative treatment is limited to symptomatic control and does not appear to halt progression. Surgical decompression with intradural microsurgical excision remains the treatment of choice in patients with progressive myelopathy or associated syrinx [2][12][13]. Nisson et al. reported neurological improvement in 91% of surgically treated patients [3]. Conversely, isolated cord indentation without myelopathy or syrinx may be observed, as suggested by Carr et al. [11]. In our series, two patients underwent laminotomy with intradural web excision due to progressive neurological deterioration, while one pauci-symptomatic patient was managed conservatively. Laminotomy may offer theoretical advantages over laminectomy in selected thoracic cases, potentially reducing postoperative pain, CSF leakage, and hospital stay, although high-level comparative data are lacking [14].

No recurrence was observed during a mean follow-up of 7.5 months. Although recurrence is rarely reported, longer follow-up and larger prospective studies are necessary to define true recurrence rates and long-term functional outcomes. Postoperative outcomes showed modest functional improvement, particularly in gait, but persistent spastic paraparesis. The prolonged preoperative symptom duration and established myelopathy likely limited neurological recovery, underscoring the critical importance of early diagnosis and timely surgical intervention. Notably, surgery appeared to halt further neurological decline in both progressive cases [8][15]. As in the case of the third patient in this study, conservative treatment may be offered to patients who do not have a disabling neurological disorder. As the risk of post-operative neurological deterioration is not negligible in this context, patients without neurological symptoms should be kept under observation with regular clinical and radiological monitoring. Let us remember that we operate on patients, not on images.

Spinal arachnoid web is a rare and underestimated cause of spinal cord injury that is complex to diagnose due to subtle MRI findings and similarities to other well-known diseases. Early recognition of SAW is essential since delay in diagnosis can lead to potentially deleterious neurological sequelae. Increased awareness among clinicians and radiologists is key to improve diagnostic accuracy and outcomes.

All authors contributed to the study conception and design. Data collection and analysis were performed by M.M.O Onifade, the first draft of the manuscript was written by M.M.O Onifade and F. Gbenou. The review of the literature, including the selection of abstracts and full-text articles, was carried out by H.G. Atakla and El C. N. Sy. And all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

The study was approved by the institutional review board of National teaching hospital Fann of Dakar. The patients/relatives, provided informed consent for the inclusion of their clinical data in this study.

Informed consent was obtained from the patients.

Informed consent was obtained from the patients.

The authors would like to thank the participant and the ethics committee for consenting to this study.