In patients with rheumatoid arthritis (RA), ischaemic stroke frequently leads to an unexplained remission of the arthritis in the paretic limb. Here we present two cases which suggest that neurovascular mechanisms contribute to the asymmetry of inflammation by impairing the microcirculation in the paretic extremity.

CASE REPORTS

A 47 year old man developed RA in 1988. In 1990, he had an apoplectic insult, resulting in a complete, left sided hemiplegia. The right hand had a marked ulnar drift of the metacarpophalangeal (MCP) joints and an inflamed wrist with impaired motion, whereas the left hand showed no inflammation or deformity. An x ray analysis of the right hand demonstrated carpal ankylosis and subluxation and erosion of all MCP joints. The left hand showed no erosive changes (fig 1A⇓). Thermal imaging indicated marked temperature differences between both hands, most obvious at the wrists (fig 1B⇓). Duplex sonography measured no detectable flow of the left radial artery. Electrophysiological investigation suggested demyelination that was slightly more pronounced on the paralytic side. The sympathetic skin response was negative.

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Figure 1

 (A) A radiograph of the first patient, showing marked differences in the erosive changes between the paralytic left side and the non-paretic right side. The patient had had the tip of the right thumb amputated owing to a work related accident. (B) Thermographic image of both hands obtained by an AGEMA 550 thermographic camera (FLIR SYSTEMS, Portland, OR, USA).

The second case involved a 66 year old woman who had had RA since 1982. In 1988 she had an ischaemic stroke with right sided hemiparesis that later recovered, leaving merely somewhat diminished muscle strength and minor hyperaesthesia. The left wrist and all MCP joints had active arthritis, whereas on the right, only two MCP joints were inflamed. An x ray analysis of the left hand disclosed carpal ankylosis, subluxation of all MCP joints, and erosions of all carpometacarpal (CMC), MCP, and proximal interphalangeal (PIP) joints. The right hand showed erosions at one CMC joint and one PIP joint only. Thermal imaging showed a decreased skin temperature on the left wrist. However, the difference was not as marked as in the first patient. Interleukin 2, 4, 5, 10, tumour necrosis factor α, and interferon γ were determined in plasma on three consecutive days for each arm separately, but did not show differences between the two sides. Duplex sonography and electrophysiological investigation showed no asymmetry.

DISCUSSION

The mechanism by which RA is modified by hemiparesis is poorly understood. Our observations suggest a link between the severity of paralysis and the extent of the remission of arthritis. This agrees with biopsy findings of a mild arthritis in a knee joint after the restoration of the motor function of the paralysed leg.¹

It has been suggested that the remission of arthritis after paralysis is due to the absence of mechanical factors.¹ However, rheumatoid vasculitis and scleroderma can develop on the non-paretic side after hemiplegia,^2,3 arguing against a mechanical link.

A role for the autonomic nervous system in inflammation has been discussed.⁴ Neurogenic peptides might contribute to the asymmetry of arthritis after stroke.^5,6 In patients with RA with hemiplegia, there are no reports of different concentrations of neurogenic peptides on the two sides. In our patients, measurement of the sympathetic skin response did not suggest differences in autonomous innervation between the sides.

Another mechanism by which neurogenic factors might contribute to the asymmetry of arthritis is an impaired perfusion of the paretic limb.⁵ Our patients are the first in whom the skin temperature and the limb perfusion was assessed quantitatively. In our first case, no flow signal of the radial artery was detectable. The marked difference in skin temperature also indicates impaired microcirculation in both patients. Significantly, this phenomenon was most obvious in the patient with complete paralysis. Changes in skin temperature frequently occur after hemiplegic stroke.⁷ This may be accompanied by a reduced blood flow in the affected extremity.⁸ However, this phenomenon is not seen in all patients.⁷ This might explain why in rare cases the arthritis even flares after a stroke.⁵ So far, the influence of perfusion and temperature on the intensity of joint inflammation has not been investigated in detail. Hyperthermia and increased perfusion are usually seen as mere byproducts of inflammation. However, it is tempting to speculate that differences of temperature and perfusion might also actively contribute to the remission of arthritis after hemiplegia.