Cauda equina syndrome (CES) is a well-recognized and potentially serious, though rare, neurological complication of spinal anesthesia. It presumably results from injury to the sacral roots in the spinal canal, which can also cause bilateral radiculopathy and progressive neurological deficits in the legs. These symptoms are typically evident after recovery from the subarachnoid block.

Transient radicular irritation syndrome, renamed as transient neurological toxicity or transient neurological symptoms (TNS), is another neurological syndrome that can follow spinal anesthesia. It has been described as a non-permanent complication in which patients complain of pain radiating from the lower back to the dorsolateral thighs and calves. It occasionally presents with dysesthesia in the buttocks and legs without motor symptoms starting less than 24 hours after spinal anesthesia. It persists for more than 24 hours and is self-limiting, typically resolving within one week.

Numerous possible etiological factors have been proposed for both syndromes. One common hypothesis is that both CES and TNS are direct neurotoxic effects of local anesthetics (LAs), a greater incidence correlating with higher LA concentrations. Initially, only lidocaine was blamed; subsequently, most LAs have been implicated in CES and TNS. It has also been suggested that the hyperosmolarity of hyperbaric solutions could be related to increased axon membrane permeability, but this hypothesis has been challenged by others. The lithotomy position during surgery has also been implicated in stretching the sacral nerve roots and increasing the vulnerability of those nerves that were in contact with LA. The use of spinal microcatheters was proposed as an etiology through uneven distribution of LA within the cerebrospinal fluid (CSF), exposing some nerve roots to high concentrations of LA and enhancing the neurotoxic effect. The ‘jet effect’ of injection through these catheters has also been mentioned. Finally, direct or indirect lesions in the spinal cord, compression or ischemia of the spinal cord, contamination of LAs, and pre-existing neuropathology have also been included in the list of potential CES etiologies.

However, the true etiology of these neurological conditions after neuraxial anesthesia has never been ascertained conclusively. Despite avoiding lidocaine, high concentrations of other LAs, microcatheters, and traction on the spinal nerves, the incidence of these complications has not diminished markedly and continues to be a subject of debate.

In 1999 and again in 2008, our team described a tubular structure enveloping single or groups of intrathecal nerve roots.^1,2 At the time, we named these tubular structures ‘arachnoid sleeves’ and proposed a new anatomical hypothesis to explain the post-spinal anesthesia complications. Recently we reported after experimental research³ that is possible to introduce a spinal needle - in particular its distal opening - completely inside this tubular subarachnoid structure and, by extension, to inject LA preferentially into it.

We extracted the full spinal dural sac and its contents from each of four fresh, unembalmed, cryopreserved human cadavers.³ The full samples were then immersed in a similar saline solution and different needle types were deliberately inserted into the nerve roots under direct vision to simulate lumbar punctures, penetrating the cauda equina root nerves traveling almost vertically downwards.³

After using 27G and 25G Whitacre pencil-point spinal needles, simulating clinical practice for lumbar punctures and spinal anesthesia, we performed deliberately needle insertions on the nerve roots of Cauda Equina. The positions of the needle tips and their orifices relative to the arachnoid sleeves were recorded under direct vision of the cauda equina roots samples. The nerve root and surrounding tissue offered no resistance to needle penetration. During the dissection, the translucent arachnoid sleeves in the specimens could not be identified with the naked eye. However, they could be easily visualized under stereoscopic microscopy.

The translucency of the arachnoid sleeves made it possible to visualize in detail whether the needle tip had entered the compartment they enclosed and to verify the position of the needle tip opening. In cases where the tip of the needle was introduced into the parenchyma of the nerve root itself, the complete needle tip opening was not consistently observed inside the arachnoid sleeve.

The photographic images³ allowed us to determine whether the entire needle tip opening or only part of it was located within the arachnoid sleeves. This was observed in high number of samples after using the both needle type. In the remaining punctures, the needle orifices were not observed inside the arachnoid sleeve, either because the needle tips were positioned inside the nerve root parenchyma, or because the orifices were outside the arachnoid sleeves.

This in vitro study of human cauda equina nerve roots under stereoscopic microscopy showed that the distal needle orifice of a 27- and 25-G Whitacre pencil-point spinal needle can be placed inside an arachnoid sleeve.

The arachnoid mater is a complex structure that includes the arachnoid layer and trabeculae arachnoid. The arachnoid layer occupies the internal surface of the spinal dural sac. ⁴ Inside it is the subarachnoid space filled with CSF and occupied by spinal cord and nerve roots. It is a semipermeable structure formed by cells tightly joined together.⁴ In contrast, the arachnoid sleeves have their origin in the trabeculae arachnoid, which is formed by interlacing collagen fibers and is permeable. In vivo, the arachnoid sleeves could be filled with a small amount of CSF, considering their permeability, with a larger volume of CSF inside the subarachnoid space but outside the arachnoid sleeves. Even using stereoscopic microscopy, it was challenging to distinguish the arachnoid sleeves as structures independent of the nerve root because, being translucent, they were in close contact with the nerve root surfaces, though they did not adhere to them.

We now know that the entire needle tip orifice can be placed inside arachnoid sleeves and an LA thus injected into it. Although we cannot say with certainty that placing the orifice of the needle and injecting LA is the cause of CES and TNS, we are reasonably certain that if the entire needle tip orifice is positioned inside an arachnoid sleeve, LA can be injected preferentially here. Anatomical variation must also be considered; injection pressure could possibly rupture the arachnoid sleeves in patients in whom they are very fragile structures.

It then becomes plausible to speculate that, alone or in combination with intraparenchymal injection of LA, this could well be the cause of neurological complications following subarachnoid block. This could be a toxic effect due to under- or non-dilution of the LA. If the entire needle orifice is positioned inside the arachnoid sleeve, the bulk of the LA will be injected into the sleeve with only minimal back leakage into the greater pool of CSF via the needle perforation. We thus propose that LA injected into this small pool of CSF inside the arachnoid sleeve would be less diluted than if it were injected into the larger pool of CSF, therefore most likely exposing the naked and unprotected nerve fibers to a relatively high and potentially toxic concentration of LA.

More distally, the arachnoid sleeves are simple tubular structures, but closer to the conus medullaris they form complex branching structures. At this level, the arachnoid sleeves have multiple interconnections where LA spread could affect more nerve roots, thus increasing the extent of neurological injury.

References

1. Reina MA, López A, De Andrés JA. Hypothesis concerning the anatomical basis of cauda equina syndrome and transient nerve root irritation after spinal anesthesia. Rev Esp Anestesiol Reanim 1999;46:99–105.

2. Reina MA, Maches F, López A, De Andrés JA. The ultrastructure of the spinal arachnoid in humans and its impact on spinal anesthesia, cauda equina syndrome, and transient neurological syndrome. Tech Reg Anesth Pain Manag 2008;12:153–60.

3. Riquelme I, Reina MA, Boezaart AP, Tubbs RS, Carrera A, Reina F. Spinal Arachnoid Sleeves and their Possible Causative Role in Cauda Equina Syndrome and Transient Radicular Irritation Syndrome. Clin Anat 2021;34:748–56.

4. Reina MA, Prats-Galino A, Sola, RG, Puigdellívol-Sánchez A, Arriazu Navarro R, De Andrés JA. Structure of the arachnoid layer of the human spinal meninges: a barrier that regulates dural sac permeability. Rev Esp Anestesiol Reanim 2002;57:486–92.