In what way are neurogenic claudication and vascular claudication similar? In what ways do they differ?
Neurogenic claudication and vascular claudication are distinct clinical entities that share a similar clinical symptom: pain and impaired walking. (The word claudication comes from the Latin word, claudicare, meaning “to limp.”) Additionally, they share a common basic pathological mechanism, ischemia, although the targets of ischemia are different.
Neurogenic claudication is caused by nerve ischemia in the spine. The most common etiology is spinal stenosis, namely degenerative spondylosis and its associated potentially-compressive phenomena (bone overgrowth, disc protrusion, facet arthritis).
Decreased space in the spinal canal compresses the thoracic spinal cord or lumbar nerve roots (Figure 1) and impedes perfusion accordingly. The resultant ischemia can lead to pain and weakness in the buttock and posterior thigh; the calf can be involved, but the symptoms are usually proximal.
Spinal stenosis is often diagnosed with MRI or CT scan, as axial imaging can show it best.
Neurogenic claudication is often exacerbated by prolonged upright standing or laying down and is relieved with bending over, such as on a bicycle or pushing a shopping cart. These latter positions of spinal flexion, riding a bicycle or pushing a shopping cart, tend to maximally open the spinal canal, whereas extension of the spine as seen with upright standing tends to compress the central canal. (This is analogous to Phalen’s maneuver compressing the carpal tunnel, with pressure relieved by holding the wrist in a neutral position.)
Vascular claudication is also caused by ischemia, but in this instance, the ischemic tissue is not nerve but is instead muscle. Vascular claudication is a symptom of peripheral artery disease; that is, the pain caused by poor circulation to the muscles in the calf.
Because the disease is mediated by decreased blood flow, the symptoms appear first distally in the calf. This stands in contrast to neurogenic claudication, which causes symptoms in the buttock and posterior thigh primarily.)
Also, because the disease is mediated by decreased blood flow, vascular claudication presents with pain in a “dose-dependent” fashion, meaning that pain is initiated and worsened with increased movement and is alleviated by rest. The crescendo/decrescendo pattern usually has specific distance markers, e.g. the pain starts at one block of walking and becomes intolerable at three blocks. For that reason, patients can be described as having “3 block claudication.” (The symptoms of neurogenic claudication are less related to distance walked or duration of activity and more to spinal position in flexion and extension.)
There is a molecule that explains the dose-dependent relationship between activity and pain: lactate (also known as lactic acid). Lactate is produced when a muscle undergoes anaerobic metabolism. The more exercise in the setting of peripheral artery disease, the more anaerobic metabolism; and the more anaerobic metabolism, the more lactate. Lactate is an acid, so it burns! With rest, lactate is metabolized and the pain resolves.
Peripheral artery disease can be diagnosed with measurement of a patient’s ankle-brachial index (see Figure 2), namely the ratio of blood pressure in the leg to that of the arm. An ankle-brachial index of 0.9 or less signifies peripheral artery disease, with of course lower numbers implying more severe disease.
Because vascular claudication is a symptom is provoked by activity it may be masked in patients with arthritis or cardio-pulmonary disease who don’t walk for other reasons besides poor leg perfusion.