Sciatic Nerve[4][5]:

The sciatic nerve innervates the posterior thigh, including the biceps femoris, semitendinosus, semimembranosus, and the ischial aspect of the adductor magnus which allow for knee flexion and hip adduction. Via the tibial nerve, the sciatic nerve innervates the muscles of the posterior leg, including the flexor hallucis longus, flexor digitorum longus, tibialis posterior, popliteus, gastrocnemius, soleus, and plantaris and the sole of the foot, including. The common peroneal nerve innervates the muscles of the anterior and lateral leg, including tibialis anterior, extensor hallucis longus, extensor digitorum longus, fibularis tertius, fibularis longus, and fibularis brevis.

Superior gluteal nerve:

Innervates the gluteus medius, gluteus minimus, and tensor fascia lata. The gluteus medius and minimus function together to abduct the hip, internally rotate the flexed hip, and externally rotate the extended hip. The tensor fascia lata flexes, medially rotates and abducts the hip while also externally rotating the leg at the knee.

Inferior gluteal nerve:

After exiting the pelvis, the inferior gluteal nerve immediately pierces into the only muscle it innervates, the gluteus maximus. The gluteus maximus externally rotates and extend the thigh at the hip joint. It attaches to the iliotibial tract laterally to support the extended knee.

The nerve to internal obturator and superior gemellus muscles:

As the name implies, this nerve innervates the internal obturator and superior gemellus muscles. The internal obturator is responsible for abducting the thigh and externally rotating the extended thigh. It is a major stabilizer of the hip during walking. The superior gemellus helps with externally rotating the thigh.

The nerve to quadratus femoris and inferior gemellus muscles:

The quadratus femoris externally rotates and adducts the thigh. The inferior gemellus is an external rotator of the thigh.

The nerves of the lumbosacral trunk have shown variance in terms of how they arise from the roots, how they exit the pelvis and associate with the piriformis, and their course the body.[1][2][4][5]

The majority of patients who present with lower extremity radiculopathy improve with nonoperative management alone.[6][7][8][7]  Even in the setting of acute injuries with MRI evidence of a lumbar disc herniation and correlating clinical symptoms in the motor/sensory distribution of the specific nerve root(s) involved, nonoperative management remains the mainstay of initial treatment.[9]  Greater than 95% of lumbar disc herniations involves the L4/L5 and/or L5/S1 disc spaces, with patients typically presenting with low back pain with sharp, stabbing pain often traceable from the lower lumbar region to the lower leg and foot.[10][11][9]

The most common indication for surgical intervention is persistent, intractable pain following exhaustion of all possible nonoperative treatment options (physical therapy, rest, non-steroidal anti-inflammatory drugs) for a minimum of a dedicated 6 weeks period.[12]

Lower extremity radiculopathy, often ambiguously ill-defined even by healthcare providers and physicians as "sciatica," is frequently attributable to nerve root(s) compression and impingement at one or multiple nerve roots in the lumbosacral plexus. These nerve roots ultimately contribute innervation (motor/sensory) peripherally as the sciatic nerve, manifests as shooting, stabbing, and/or burning pain radiating from the back to the ipsilateral or contralateral lower extremity.  Accurate clinical diagnosis is critical to ensure the utilization of the ideal management modalities for each patient.

Diabetes Mellitus

Clinical differentiation and accurate delineation of underlying sources of pain in adult patients presenting with chronic low back pain and radicular symptoms are further fraught with ambiguity in the setting of diabetes.  Diabetic lumbosacral radiculoplexus neuropathy (DLSRPN) is easily confused with lower extremity radiculopathy.  Etiologically, long-standing, poorly controlled, diabetes can lead to widespread stenosis affecting the microvasculature, including the vaso nevorum, that supplies peripheral nerves in many regions of the body. 

The patient often complains of pain, tingling, numbness, and hypersensitivity. The treatment of diabetic neuropathy is multimodal and may include the use of tricyclic antidepressants.  The actual benefit of these agents remains debated in the literature.  The primary concern of diabetic neuropathy is the development of ulcers which often go undetected because patients lack the appropriate sensory feedback that is physiologically present in non-diabetics.[13]

Other pertinent clinical conditions

Sacral tumors can also cause lumbosacral plexopathy.[14]  Surgery may be necessary within the setting of progressive neurologic deficits or debilitating pain and neurologic symptoms secondary to mass effect.   

Trendelenburg gait occurs secondary to weakness and dysfunction of the gluteus medius and minimus.  The former normally functions as a critical stabilizing force for the pelvis during the stance phase of the gait cycle.  Hip abductor compromise results in a characteristic "lurching" gait pattern as the patient compensates to shift their center of gravity toward the side of the stance limb; Trendelenburg gait pathology can be summarized as follows:

• Right-sided hip abductor dysfunction results in:
  • Compromise to the hip abductor pelvic stabilizing function during the gait
  • When the right limb is the stance limb during gait, the left side of the pelvis will "droop"
  • The patient compensates for the left-sided "droop" by leaning toward the side of the lesion (in this case, the right side)
    • Leaning toward the right side thereby shifts the center of gravity during ambulation
  • A cane improves gait biomechanics and is helpful when used on the contralateral (i.e., unaffected) side

Hip abductor dysfunction leading to Trendelenburg gait can occur in the setting of lesions in the superior gluteal nerve, often by a needle hitting the nerve during a gluteal injection, or via L5 radiculopathy etiologies.[2] Neuropraxia following surgery about the hip can also result in a Trendelenburg gait (e.g., following total hip replacement, hemiarthroplasty, or approaches to the hip/pelvis for open reduction internal fixation of various fracture patterns).[15][16]