Body Temperature and Diaphoresis Disturbances in a Patient with Arachnoiditis

We report a case of a patient with chronic arachnoiditis who presented with temperature and sweating disturbances. Initially, the patient had a low grade fever (oral temperature of 37.9°C); the right side of his body was cold and wet; the left was hot and dry. Different temperatures were obtained on both sides at the forehead, thorax, and medial aspect of the knees. The patient later presented with the same temperature disturbances in different body areas, sometimes in the right or in the left side or in both sides at the same time. The disturbances always disappeared after epidural analgesia produced by bupivacaine, fentanyl, and iced saline. The possible mechanisms that produced these disturbances are discussed. Arachnoiditis (ARC) is a chronic, nonspecific, inflammatory and proliferative process of the arachnoid membrane (1–2). Depending on its grade of severity, it may produce a variety of symptoms such as neuropathic pain, fever, night sweating, hyperhidrosis, and vesical and digestive dysfunctions (1–2). We present a case of out of the ordinary skin temperature and sweating distribution in a patient with ARC. Case Report A 44-yr-old male, 1.65 m tall, 115 kg in body weight, was involved in a motor vehicle accident in 1983, after which he developed low back pain and sciatica in both legs. In 1991, he had a L5-S1 laminectomy for treatment of a herniated disk. One year later, the pain reappeared; he was unsuccessfully treated with a spinal cord stimulator. After its removal in 1995, he was sent to the pain clinic for evaluation and treatment. After a clinical history and examination, a severe case of arachnoiditis was suspected and later confirmed by a magnetic resonance imaging study, with clumped nerve roots at the L4 and L5 levels, more prominent on the right side. Initially, he was treated with analgesics, antidepressants, muscle relaxants, a lumbosacral orthosis, isometric exercises, and a series of six epidural blocks (3) with iced saline, bupivacaine, methylprednisolone, and fentanyl, which provided pain relief for 8–10 days. Subsequently, a lumbar epidural catheter was inserted and connected to a disposable infusion pump (controlled by the patient) for the intermittent infusion of analgesics (3–4) (bupivacaine, clonidine, ketamine, and fentanyl). Before the epidural infusion began it was noted that the patient complained of profuse sweating on the right side of the body; his arterial blood pressure was 155/77 mm Hg, the heart rate 80 bpm and the oral temperature 37.9°C. At touch, the left side of his body was dry and hot; the right side was humid and cold. Through a skin temperature indicator strip (Sham Inc., Tampa), the forehead temperature (<2 cm apart) was 37.5°C on the right and 38°C on the left side; in the thorax, just below the areola, it was 36°C on the right and 36.8°C on the left; in the medial aspect of the right knee it was 34.7°C and 35.3°C on the left knee. Five minutes after the onset of the epidural block, the disturbances disappeared. Thereafter, every time he returned to the clinic his oral temperature was approximately 37.7°C, with sweating disturbances and temperature disparities on both sides of his body. It was noted that while the patient had pain relief from the epidural infusion of analgesics, the temperature on both sides of his body became evenly distributed, but while in pain, the aberrant skin temperatures, as described, returned. Discussion Body temperature is usually under the control of the central nervous system (CNS), mainly through the hypothalamus (5–7). The thermoregulatory control mechanisms—shivering, nonshivering thermogenesis, skin blood flow, sweating, piloerection (5–8) —are not completely understood (6,9), but the sympathetic nervous system (SNS) appears to intervene in all except shivering (5–6,10). Temperature receptors in the skin generate afferent impulses carried by Aδ and C fibers to the CNS. Their cell bodies in the dorsal root ganglion send connections to the spinal cord and through the neospinothalamic or paleospinothalamic tracts to the supraspinal thermoregulatory centers, such as the thalamus and hypothalamus, for temperature control (5–6,10) and to the cerebral cortex for sensation (5,10). However, spinal cord temperature receptors, mainly in the cervical region in mammals (6), might also participate in the thermoregulatory activities. The exact mechanisms which produced the temperature and diaphoretic disturbances in this patient are unknown. Low grade fever is common in patients with arachnoiditis (1), but the disturbances observed in this patient are rare, probably due to a significant lesion of the spinal cord, posterior horn and rami communicants linking it to the autonomic nervous system (1,11). In our clinical experience, a combination of phenobarbital, ergotamine, and bella Foline (Bellergal®, Sandoz Pharmaceutical, East Hanover, NJ) reduces diaphoresis, probably by activating the normal regulatory cutaneous temperature mechanism and reducing sweat gland output (1). The cooling and burning sensations may be explained by C-nociceptor afferents stimulating a somathosympathetic vasoconstrictor reflex (12–13). When chronic denervation occurs such as after some spinal operations, damage to communicating sympathetic interganglia microscopic fibers may take place, resulting in alternating warm sensations, triggered by release of vasoactive substances from nociceptor afferentes 1(12), while cooling sensation may be elicited by intraneural stimulation with dominance of sympathetic vasoconstrictor effects over some vasodilator transmitters (14). This sympathetic versus parasympathetic “tug-of-war” imbalance can be responsible for the frequent diaphoresis, heat intolerance, and nocturnal hyperactivity of sweat glands noted in patients with arachnoiditis while in pain. The initial hemicorporal temperature and diaphoresis discrepancies could be explained by a hypothalamic afferent disturbance and consequent efferent discharges through the SNS. The later disturbances, when the patient had different temperatures and diaphoresis on one side of his body, may be more difficult to explain. A few hypotheses for the causes of this phenomenon are as follows: a) a hypothalamic disturbance resulting from abnormal afferent stimuli; b) disturbances of the spinal cord receptors and concomitant efferent reflexes; c) reflexes originated at the Rexed’s lamina I, II or V by the A-δ and C fibers; d) reflexes originated at the Rexed’s lamina V by the A-β fibers that carry impulses from the low-threshold mechanoreceptors, similar to the mechanisms postulated to explain allodynia (10). The disappearance of the disturbances after epidural analgesia are indeed perplexing but could be explained by the action of the medications on the spinal thermoregulatory and opioid receptors (15). In conclusion, the authors report a case of skin temperature and sweating disturbances in a patient with chronic arachnoiditis that reversed to normal during intervals of pain relief afforded by epidural analgesia.