Sciatic Nerve Anatomy

The Sciatic Nerve is the largest nerve in the body (roughly the width of an adult thumb, around 2 cm at its origin), derived from the ventral rami of L4-S3 via the sacral plexus. It serves as the primary conduit for motor and sensory signals to the lower limb.

Functionally it is best understood as two nerves in one sheath: a medial tibial division (ventral rami) and a lateral common peroneal (fibular) division (dorsal rami). These two components are bound by a common epineurium but remain anatomically and clinically distinct from origin to the popliteal fossa, where they formally separate. This duality explains nearly every examination point on the topic: the peroneal division, being lateral, smaller, with fewer/larger fascicles, less protective connective tissue and tethered at the fibular neck, is selectively vulnerable to stretch, compression and ischaemia, so a "sciatic" injury often masquerades as an isolated foot drop.

Its relations in the gluteal region (resting on the bed of short external rotators, exiting beneath piriformis in most people) are critical for the posterior approach to the hip, acetabular fracture surgery and intramuscular injection safety. Its long course and the great distance from a proximal lesion to the foot muscles also dominate prognosis after laceration.

Differentiating High vs Low Lesion

Differential Diagnosis of "Sciatica" / Foot Drop

The clinical syndrome of buttock-to-leg pain or foot drop has several causes that must be separated, because management differs completely. The single most useful discriminators are the short head of biceps femoris (peroneal-division marker), the glutei (plexus/root marker) and the paraspinals (root marker).

Injection Injury Protocol

1. Immediate: Stop injection. Document drug and volume.
2. Acute Phase: Analgesia (Neuropathic agents). MRI to look for hematoma (compressive).
3. Chronic Phase: Serial EMG. If no recovery at 3-6 months, consider exploration and neurolysis (poor prognosis if intrafascicular injection occurred).

• Foot Drop: Most common manifestation of injury. Requires AFO (Ankle Foot Orthosis).
• Neuropathic Pain: Often severe (Type II CRPS).
• Pressure Sores: Insensate foot/heel.
• Contracture: Equinus deformity if not splinted.

• Splinting: Anti-drop foot splint (AFO) immediately.
• ROM: Passive ankle dorsiflexion to prevent contracture.
• Strengthening: Hamstrings and Glutes.
• Nerve Glides: Sciatic sliders flossing techniques.
• Return to Sport: Dependent on motor recovery (Variable).

• Stretch Injury: Good prognosis (neuropraxia).
• Injection Injury: Poor prognosis (chemical neurolysis).
• Laceration: Guarded. Rate of regeneration is 1mm/day, but the distance to the foot is distinctively long (causes motor endplate death before nerve arrives).
• Common Peroneal: Paradoxically worse prognosis than Tibial division (less vascular, more tethered).

• Does piriformis syndrome exist as a distinct entity? The variant anatomy is no commoner in symptomatic patients (Smoll 2010), and many authorities prefer the broader term deep gluteal syndrome. It remains a diagnosis of exclusion with no universally accepted diagnostic criterion.
• Timing and role of exploration after injection injury. There is no high-level evidence that early surgical washout or neurolysis changes outcome; most chemical injuries are established at the moment of injection. Management is therefore largely supportive, with exploration reserved for a compressive haematoma or non-recovery on serial EMG.
• Acute exploration after THA palsy. Whether to re-operate for an immediate post-operative palsy is debated; most are observed unless imaging shows a correctable compressive cause (haematoma) or gross overlengthening. Return of any motor function within two weeks predicts good recovery (Schmalzried 1997).
• Maximum "safe" lengthening in THA. A figure of around 4 cm is widely quoted, but the threshold is patient-specific; nerve tension, not an absolute number, is the determinant, and palsy occurs at lower lengthening in dysplasia.
• Tendon transfer vs orthotic for established foot drop. Choice between a permanent AFO and reconstructive transfer (e.g. tibialis posterior) depends on prognosis for spontaneous recovery, which is itself uncertain for high lesions.

Global Epidemiology

• Traumatic hip dislocation: Sciatic nerve injury complicates roughly 10% of adult posterior hip dislocations/fracture-dislocations and about 5% of paediatric cases worldwide, the peroneal division being most often affected (Cornwall & Radomisli, 2000).
• Total hip arthroplasty (THA): Pooled prevalence of nerve palsy is approximately 1%, rising to 3-5% in revision and developmental dysplasia of the hip (DDH) (Schmalzried 1991, 1997).
• Injection injury: Iatrogenic sciatic neuritis from dorsogluteal intramuscular injection remains a global problem, disproportionately affecting children and limited-resource/rural settings where ventrogluteal technique is under-used.
• Anatomical variant: A piriformis–sciatic anatomical anomaly is present in approximately 17% of the population (Smoll, 2010).

Side-by-Side Society Guidance

Registry Evidence

• Arthroplasty registries (NJR England & Wales, AJRR USA, AOANJRR Australia, Swedish SHAR) do not record nerve palsy as a primary endpoint, but capture the DDH and revision case-mix that drives higher palsy rates, and track leg-length restoration, the principal modifiable risk factor.
• Registry-level rises in revision and complex primary volume translate into a higher absolute burden of nerve injury even when the per-case rate is stable.

High- vs Limited-Resource Practice Variation

• High-resource: MR neurography, intra-operative neuromonitoring, and early EMG are available; ventrogluteal injection and ultrasound-guided blocks are standard.
• Limited-resource: Diagnosis rests on clinical examination; dorsogluteal injection persists and is a leading preventable cause of paediatric foot drop. Prevention (correct injection site, prompt reduction of dislocations) carries the greatest yield where reconstructive nerve surgery is scarce.