Neurogenic Claudication

Neurogenic claudication is a clinical syndrome caused by compression of neural structures in the lumbar spine, resulting in pain and weakness in the lower limbs during walking or standing. It is in practice a typical manifestation of lumbar spinal stenosis, usually of degenerative origin, and differs substantially from vascular intermittent claudication, which is due to ischaemia of the muscles of the lower limbs.

Definition and pathophysiology

Neurogenic intermittent claudication describes the patient’s inability to walk a satisfactory distance because of pain, a feeling of heaviness, or numbness in the legs, which forces the person to stop, sit down, or bend slightly forward, after which the symptoms gradually subside. The symptomatology is caused by a reduction of the available space in the spinal canal and/or the foramina, resulting in mechanical compression of the nerve roots.

Causes and risk factors

The most common cause is degenerative lumbar spinal canal stenosis, due to osteoarthritic changes, hypertrophy of the facet joints, thickening of the ligamentum flavum, degenerative disc disease, and osteophyte formation. A congenitally narrow spinal canal, deformities such as scoliosis, trauma, spondylolisthesis, or spinal tumours can also cause a compressive effect in the canal and lead to neurogenic claudication. The syndrome occurs more often in individuals over 50 years of age, as an expression of degenerative spine disease, but it can also appear in younger people with pre‑existing anatomical particularities.

Clinical presentation

The main symptoms include:

• Low back pain that often accompanies the lower limb symptoms.

• Pain, a feeling of heaviness, burning, or cramping in the buttocks, calves, or the whole lower limb, which worsens with walking or prolonged standing.

• Numbness, paraesthesias, and sometimes weakness in the lower limbs, with a characteristic limitation of the “walking distance” before the need to stop.

Patients often report that they can walk further when bending forward (for example leaning on a supermarket trolley) or when walking uphill, whereas walking downhill or standing upright in extension worsens the symptoms. In advanced cases there may be neurological deficits (muscle weakness, hypoaesthesia, reduced reflexes) and, more rarely, disturbances of urination, defecation, or sexual function, indicating more severe root compression.

Diagnosis

Diagnosis is based on:

• A detailed history, with emphasis on the relationship of symptoms to walking and standing and on relief with flexion or sitting, as well as on distinguishing from vascular claudication (pain mainly in the calves, relief with standing without necessarily bending, abnormal distal pulses).

• Clinical examination with assessment of neurological status (strength, sensation, reflexes) and specific walking and lumbar flexion–extension tests.

On imaging, lumbar spine MRI is the examination of choice for demonstrating stenosis and the relationship of bony, disc, and ligamentous structures to the dural sac and roots. CT and, in selected cases, CT myelography help assess bony structures or are used when MRI is not feasible. Vascular studies (e.g. lower limb duplex ultrasound) are required when there is suspicion of coexisting or purely vascular claudication.

Differential diagnosis

Key conditions that must be differentiated include:

• Vascular intermittent claudication due to peripheral arterial disease.

• Peripheral neuropathies (e.g. diabetic), radiculopathies from an isolated disc herniation, myopathies, or hip/knee arthropathies that limit walking.

The clinical picture, pulse palpation, response to postural change, and imaging findings are crucial for distinction.

Conservative management

In mild to moderate cases, or when symptoms are tolerable, initial conservative treatment is recommended:

• Medication with analgesics, anti‑inflammatories, and, when needed, neuropathic‑type analgesics.

• Physiotherapy and exercise focused on core strengthening, improving flexibility, and posture training (promoting slight flexion when helpful).

• Epidural or transforaminal corticosteroid injections in selected patients to reduce inflammation and provide short‑term relief.

At the same time, activity modification, weight management, and control of comorbid conditions (e.g. diabetes, vascular disease) contribute to improved function.

Surgical treatment

Surgical decompression is considered when:

• There is severe limitation of walking distance and quality of life despite adequate conservative therapy.

• There are progressive neurological deficits or signs of cauda equina syndrome (severe urinary/bowel disturbances, saddle anaesthesia), which constitute an indication for urgent intervention.

The classic approach is lumbar decompressive laminectomy, with or without concurrent fusion when there is instability or significant spondylolisthesis. Newer, less invasive techniques (microdecompression, minimally invasive laminectomies in carefully selected cases) aim to reduce surgical trauma and recovery time without compromising effectiveness. The choice of technique is individualised based on anatomy, number of levels, associated deformities, and the patient’s overall condition.

Prognosis and follow‑up. Many patients maintain stable or mild symptoms with appropriate conservative management and lifestyle adaptations. In those undergoing indicated surgical decompression, improvement rates in walking distance and quality of life are high, although complete disappearance of all symptoms is not always achievable, especially in very advanced degenerative changes or in the presence of multiple comorbidities. Long‑term follow‑up is useful for early recognition of symptom recurrence, development of stenosis at adjacent levels, or progression of associated conditions.

Practical clinical points

• Careful distinction between neurogenic and vascular claudication is critical, since the former directs towards spinal investigation, whereas the latter requires vascular assessment and evaluation for arterial disease.

• Patient assessment should be holistic, taking into account age, functional demands, comorbidities, and expectations, in order to choose the appropriate mix of conservative and, if necessary, surgical treatment.

Image source: J Pain 2021 (Sep); 22 (9): 1015–1039.