Renato J. Verdugo

Abnormal movements in complex regional pain syndrome : Assessment of their nature

Abnormal movements may be a clinical feature in complex regional pain syndrome (CRPS), but their basic nature is unclear. Between August 1989 and September 1998, patients fulfilling diagnostic criteria for CRPS (I or II) and displaying abnormal movements were entered into a prospective study. Fifty‐eight patients, 39 women and 19 men, met entry criteria; 47 had sustained a minor physical injury at work. The patients exhibited various combinations of dystonic spasms, coarse postural or action tremor, irregular jerks, and, in one case, choreiform movements. Patients underwent rigorous clinical and laboratory evaluation aimed at characterizing their neurological disturbance. Surprisingly, no case of CRPS II but only cases of CRPS type I displayed abnormal movements. In addition to an absence of evidence of structural nerve, spinal cord, or intracranial damage, all CRPS I patients with abnormal movements typically exhibited pseudoneurological (nonorganic) signs. In some cases, malingering was documented by secret surveillance. This study highlights abnormal movements in CRPS as constituting a key clinical feature that differentiates CRPS I from CRPS II. They are consistently of somatoform or malingered origin, signaling an underlying psychoneurological disorder responsible for the entire CRPS profile.

‘Sympathetically maintained pain’ I. Phentolamine block questions the concept

Patients with “reflex sympathetic dystrophy” or “causalgia” underwent sympathetic blocks. In protocol A (77 patients), we infused placebo (saline) for 30 minutes followed by phentolamine (35 mg). In protocol B (23 patients), the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 μg), a second phase of saline, and then the other active drug. We assessed magnitudes of pain and mechanical hyperalgesias on a 0-to-10 pain scale and monitored sensory and sympathetic effects. With protocol A, pain diminished significantly (≥ 50%) during placebo in 22 patients (28.9%) and during phentolamine in seven (9.2%). With protocol B, four patients (17.3%) had relief of pain during placebo, four (17.3%) during phenylephrine, and two (8.7%) during phentolamine. All “phentolamine responders” had progressive pain relief from placebo. Two patients expressed relief during phenylephrine and worsening during phentolamine. Most patients did not respond significantly to saline or drugs. Thus, pharmacologica manipulation of the alpha-1 adrenergic receptor by either agonist or antagonist drug does not influence neuropathic pains. These results raise questions about the existence of “sympathetically maintained pain,” as diagnosed by sympathetic blocks improperly controlled for placebo.

Phentolamine sympathetic block in painful polyneuropathies II. Further questioning of the concept of ‘sympathetically maintained pain’

To test for the presence of “sympathetically maintained pain” (SMP), we administered placebo-controlled phentolamine sympathetic blocks to 14 patients with painful polyneuropathies. Six received IV infusion of saline for 30 minutes, followed by phentolamine (35 mg). In eight patients, the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 μg), a second saline phase, and then the other active drug. We measured magnitudes of spontaneous pain and mechanical hyperalgesias on a 0-to-10 pain scale every 5 minutes and monitored sensory and sympathetic effects clinically and through quantitative thermotest and thermography. Five patients reported significant diminution of pain (> 50%), all in response to placebo. Neither phentolamine nor phenylephrine provided relief, although all patients had signs of physiologic abnormalities reputed to be determinants or predictors of SMP. These results complement previous studies demonstrating the nonexistence of SMP among “reflex sympathetic dystrophy” patients and further question the concept of SMP.

HTLV-I POSITIVE SPASTIC PARAPARESIS IN A TEMPERATE ZONE

Tropical spastic paraparesis and myelopathy caused by human T-lymphotropic virus type 1 formerly reported from Japan has now been found in 32 patients of European Mestizo and Indian descent in Santiago Chile. 14 of the patients were seropositive for human T-lymphotropic virus 1 and 13 had antibodies in the cerebrospinal fluid. This is the 1st group of patients who are not black or Japanese and do not live in a tropical climate. Patients presenting with chronic peripheral or central nervous system disorders should be tested for antibodies to human T-lymphotropic virus type 1.

Vitamin B-12 treatment of asymptomatic, deficient, elderly Chileans improves conductivity in myelinated peripheral nerves, but high serum folate impairs vitamin B-12 status response assessed by the combined indicator of vitamin B-12 status

BACKGROUND It is uncertain whether vitamin B-12 supplementation can improve neurophysiologic function in asymptomatic elderly with low vitamin B-12 status or whether folate status affects responses to vitamin B-12 supplementation. OBJECTIVE We assessed the effects of a single intramuscular injection of 10 mg vitamin B-12 (which also contained 100 mg vitamin B-6 and 100 mg vitamin B-1) on vitamin B-12 status and neurophysiologic function in elderly community-dwelling Chileans with low serum vitamin B-12 concentrations who were consuming bread fortified with folic acid. DESIGN A pretreatment and posttreatment study was conducted in 51 participants (median ± SD age: 73 ± 3 y; women: 47%) with serum vitamin B-12 concentrations <120 pmol/L at screening. Vitamin B-12 status was defined by combining vitamin B-12, plasma total homocysteine (tHcy), methylmalonic acid (MMA), and holotranscobalamin into one variable [combined indicator of vitamin B-12 status (cB-12)]. The response to treatment was assessed by measuring cB-12 and neurophysiologic variables at baseline and 4 mo after treatment. RESULTS Treatment increased serum vitamin B-12, holotranscobalamin, and cB-12 (P < 0.001) and reduced plasma tHcy and serum MMA (P < 0.001). Treatment produced consistent improvements in conduction in myelinated peripheral nerves; the sensory latency of both the left and right sural nerves improved on the basis of faster median conduction times of 3.1 and 3.0 ms and 3.3 and 3.4 ms, respectively (P < 0.0001). A total of 10 sensory potentials were newly observed in sural nerves after treatment. Participants with high serum folate at baseline (above the median, ≥33.9 nmol/L) had less improvement in cB-12 (P < 0.001) than did individuals whose serum folate was less than the median concentration (i.e., with a concentration <33.9 nmol/L). CONCLUSION Asymptomatic Chilean elderly with poor vitamin B-12 status displayed improved conductivity in myelinated peripheral nerves after vitamin B-12 treatment and an interaction with folate status, which was detected only with the use of cB-12. This trial was registered at www.controlled-trials.com as ISRCTN02694183.

Spectrum of cutaneous hyperalgesias/allodynias in neuropathic pain patients

Objectives – The aim of this study was to discern the pathophysio‐logical bases for neuropathic hyperalgesias.

Reversal of hypoaesthesia by nerve block, or placebo: a psychologically mediated sign in chronic pseudoneuropathic pain patients

OBJECTIVES To gain understanding of the mechanism and meaning of improvement of hypoaesthesia after a diagnostic intervention, and of the nature of the population that displays such a sign. METHODS Patients with chronic “neuropathic” pain underwent rigorous clinical and laboratory investigations, including placebo controlled local anaesthetic block. Patients displaying profound regional cutaneous hypoaesthesia and pain entered the study through either of two criteria: (a) reversal of hypoaesthesia after diagnostic block, (b) nerve injury as the cause of hypoaesthesia and pain. The semeiology displayed by these patients together with the behaviour of their sensory phenomena in response to blocks were compared. Three groups were expected: (1) patients with “neuropathic” pain with profound hypoaesthesia reversed by block, but without neuropathy; (2) patients whose hypoaesthesia did not reverse and who had neuropathy as the cause of their sensory dysfunction; and (3) patients whose hypoaesthesia reversed, and had neuropathy. RESULTS Two groups emerged: (1) patients with profound hypoaesthesia reversed by block, but without neuropathy (27 patients), and (2) patients whose hypoaesthesia did not reverse and who had a neuropathy (13 patients). No patient with neuropathy was found whose cutaneous hypoaesthesia improved with block. The first group displayed the sensory-motor characteristics of psychogenic pseudoneuropathy. The semeiology of the second group was in keeping with organic neuropathy and displayed no pseudoneurological features. Spontaneous pain was relieved by placebo in 66.6% of the patients in group1 and 53.8% in group 2. CONCLUSIONS Such reversal of hypoaesthesia is due to a placebo effect, acting on a psychogenic symptom because: (a) 27 of 27 patients in which the sign occurred had absence of nerve disease behind the “neuropathic” symptoms, (b) In 26 of 27 patients the area of hypoaesthesia was non-anatomical, (c) 16 of 27 patients had other sensory-motor signs that could not be explained as a result of organic pathology (give way weakness and punctual denial of hypoaesthesia), and (d) the phenomenon was not found in patients with organic neuropathy.

Déficit de vitamina B-12 en adultos mayores: ¿Un problema de salud pública en Chile?

BACKGROUND There is a correlation between aging and the decrease of plasma levels of vitamin B-12. AIM To determine the prevalence of vitamin B-12 and folate deficiency and its hematological impact among older adults (AM). MATERIAL AND METHODS Cross-sectional study, in 1028 subjects aged 65 to 87years, living in community and evaluated between 2005 and 2008. Percentile distribution of vitamin B-12, folate, hemoglobin, packed red cell volume and mean cell volume by gender and age were analyzed. Deficiency was defined as vitamin B-12 levels < 148 pmol/L, marginal deficiency as vitamin B-12 levels < 221 pmol/L, anemia was defined as a hemoglobin < 13 and 12 g/dL among men and women, respectively. RESULTS The prevalence of vitamin B-12 deficiency was 12% and the figure for marginal deficiency was 25.4%. Males were more affected than females (p < 0.001). The frequency of anemia was 8.6%o, and was higher among women (p = 0.004). CONCLUSIONS There is a high prevalence of full blown and marginal deficit of vitamin B-12 among the elderly. This deficiency should be considered for correction through public nutrition policies.

Sensory dysfunction in HTLV-I-associated myelopathy/tropical spastic paraparesis. A comprehensive neurophysiological study.

We performed a comprehensive clinical and neurophysiological evaluation of function of the large- and small-caliber afferent pathways in 29 patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Sensory symptoms, particularly cutaneous paresthesias, were present in 11 (37.9%) patients. On examination, a mild distal impairment of vibration and sense of position were found in 14 (48.2%) and 5 (17.2%) patients, respectively. Ten (34.4%) patients had distal tactile hypoesthesia and 7 (24.1%) presented pinprick hypoesthesia. Quantitative somatosensory thermotest showed cold hypoesthesia in 58.6% of patients. Nerve conduction studies and electromyography were normal. Tibial somatosensory evoked potentials were abnormal in 88.5% of patients. All of the sensory abnormalities found were restricted to sensations carried by myelinated (A-beta and A-delta) fibers. Unmyelinated C fibers mediating warm sensation and thermal pain appeared unimpaired. Our findings indicate that the sensory dysfunction in HAM/TSP patients is probably due to a lesion restricted to the central nervous system.

Evoked potential abnormalities in progressive spastic paraparesis associated to HTLV-1.

The electrophysiological features of progressive spastic paraparesis (PSP) associated with HTLV‐1 in Chile, a non‐tropical country, are presented. Twenty‐two of 45 PSP subjects were positive for HTLV‐1 antibodies. Trimodal evoked potentials were all normal in only 2 of these cases (9.1%). Somatosensory evoked potentials (SSEPs) were abnormal in 19 patients (86.3%) with a mean amplitude of 1.31 uV SD 0.92. Visual evoked potentials (VEPs) and brainstem auditory evoked potentials (BAEPs) were normal in all patients except four. Peripheral nerve conduction was normal in all but one who showed discrete slowness of the motor conduction velocity in the peroneal nerves. EMG was normal in 15 cases in whom it was performed. SSEPs were abnormal in 2 (8.7%) of 23 HTLV‐1 negative cases with a mean amplitude of 2.4 uV SD 1.5, which is statistically different with respect to the positive cases (p < 0.001). These results support an involvement of the spinal cord not restricted to the pyramidal tracts but also including subclinical damage of the posterior columns in PSP associated to HTLV‐1.