[Psychogenic disorders].
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Diagnosis, Differential↗
Biomedical subjects
R J Verdugo
Publications and source records attributed to R J Verdugo.
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. METHODS: In this study, neurological and neurophysiological evaluation of 132 consecutive hyperalgesia patients using rigorous clinical and laboratory protocols were carried out. RESULTS: Two discrete semeiologic entities emerged: classic neurological vs atypical, fulfilling taxonomically complex regional pain syndrome (CRPS) II and I, respectively. The classic group (34.9%) exhibited sensorimotor patterns restricted to nerve distribution and documented nerve fiber dysfunction. Among them four (3.03%) had sensitization of C-nociceptors, seven (5.3%) had central release of nociceptive input, and 35 (26.52%) probable ectopic nerve impulse generation. The atypical group (65.1%) displayed weakness with interrupted effort; non-anatomical hypoesthesia and hyperalgesia; hypoesthesia or paresis reversed by placebo, or atypical abnormal movements, and physiological normality of motor and sensory pathways. CONCLUSIONS: Spatiotemporal features of neuropathic hyperalgesia constitute key criteria for differential diagnosis between CRPS II and I and, together with other behavioral sensorimotor features, signal psychogenic pseudoneurological dysfunction vs structural neuropathology. 'Neuropathic' hyperalgesias may reflect neuropathological or psychopathological disorders.
Adolescent↗
Surgical versus non-surgical treatment for carpal tunnel syndrome.
BACKGROUND: Carpal tunnel syndrome is the clinical condition resulting from the entrapment of the median nerve in the wrist. It has been accepted as the most frequent entrapment neuropathy. The most common symptoms are tingling, numbness, and pain in the hand that may radiate to the forearm or shoulder. There may be weakness and atrophy of the thenar muscles associated with sensory loss in the affected fingers. There is no universally accepted therapy for carpal tunnel syndrome. Surgical treatment is widely preferred to non-surgical or conservative therapies for overtly symptomatic patients, while mild cases are usually not treated. OBJECTIVES: The objective of this review is to compare the efficacy of surgical treatment of carpal tunnel syndrome with non-surgical treatment in improving clinical outcome. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group register for randomised or quasi-randomised trials as well as MEDLINE, EMBASE and LILACS (to July 2001). We checked the bibliographies in relevant papers and contacted the authors to obtain information about other published or unpublished studies. SELECTION CRITERIA: All randomised and quasi-randomised controlled trials comparing any surgical and any non-surgical therapies. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed eligibility of the trials. MAIN RESULTS: Only one randomised controlled trial was found. It included 22 female patients, 11 allocated to surgical section of the anterior carpal ligament and 11 to splinting for one month. The trial was not blinded and it is not clear if the allocation was properly concealed. Data reported allowed an intention-to-treat analysis on two secondary outcomes. The results favour surgery for both of them. There was a significant clinical improvement at one year follow-up in 10 out of 11 patients allocated to surgery and two out of 11 allocated to splinting (relative risk 5.00, 95% confidence interval 1.41, 17.76). Eight out of 11 patients allocated to splinting required surgery during follow-up, compared with apparently no re operation in the surgical group (relative risk 0.06, 95% confidence interval 0.00, 0.91). REVIEWER'S CONCLUSIONS: Surgical treatment of carpal tunnel syndrome seems to be better than splinting. There is a need for randomised controlled trials comparing surgical and non-surgical therapies for carpal tunnel syndrome, particularly in patients with mild symptoms in whom there is greater uncertainty concerning the balance of risks versus benefit of surgical therapy.
Carpal Tunnel Syndrome↗
Mechanisms of neuropathic pain: nerve, brain, and psyche: perhaps the dorsal horn but not the sympathetic system.
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Brain↗
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.
Adolescent↗
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.
Adult↗
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 groupl 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.
Adult↗
Reflex sympathetic dystrophy. A common clinical avenue for somatoform expression.
Reflex sympathetic dystrophy (RSD) and causalgia appear to reflect identical pictures even though the latter is related to nerve injury and the former is not. Overriding past and present skepticism about a role for the sympathetic system in their cause and treatment, the International Association for the Study of Pain still recommends sympathetic blocks and sympathectomy for both causalgia and RSD. Such fallacy is traceable to fragmentary clinical observations, to ad-hoc experiments, and to traditional neglect of the placebo phenomenon in chronic "neuropathic" pain patients.
Causalgia↗
[Sympathetic denervation of an extremity as a presentation form of apical lung cancer].
We report a 56 years old male patient presenting with a sympathetic denervation of the right upper limb due to an apical lung cancer. Vasomotor paralysis of the limb was objectively documented with a contact termography. The clinical presentation of this patient was unusual, considering that the alteration occurred without sensory or motor changes of the limb or autonomic disturbances of the face. The absence of clinical and neurophysiological involvement of large and small caliber fibres of the brachial plexus and the lack of autonomic dysfunction of the face was explained by a predominant tumoral infiltration of T2 and T4 ventral roots, which supply autonomic innervation to the upper limbs.
Adenocarcinoma↗
'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 micrograms), 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 (> or = 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, pharmacologic 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.
Adult↗
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 i.v. 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 micrograms), 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.
Adult↗
Use and misuse of conventional electrodiagnosis, quantitative sensory testing, thermography, and nerve blocks in the evaluation of painful neuropathic syndromes.
A number of laboratory tests are critically important in the quest to diagnose presence or absence of organic neuropathic dysfunction and to establish the relevance of such to the subjective pain complaints. However, none of these tests has absolute diagnostic value and their results must be interpreted in the light of the clinical picture. Conventional electrophysiology evaluates function of large caliber afferent and motor fibers leaving the function of small caliber afferent fibers unexplored, and cannot explore the basis for positive sensory phenomena. The quantitative somatosensory thermotest is the best test available to explore function of small caliber afferents. It allows documentation of positive sensory phenomena in the form of thermal hyperalgesia. Because it is a psychophysical test, it lacks localizing value. Thermography sensitively detects and precisely delineates areas of cutaneous thermal change of neural origin. Three types of diagnostic neurologic blocks are used in the clinic: compression-ischemia, local anesthetic and sympathetic blocks. Although they may provide important information about the pathophysiology of pain and hyperalgesias, adequate placebo control is of the essence because chronic neuropathic pain patients may express a high incidence of placebo response.
Electrodiagnosis↗
Vasomotor innervation of the skin of the hand: a contribution to the study of human anatomy.
The sympathetic vasomotor innervation of the skin of the human hand was studied in 47 subjects who underwent local anaesthetic block of ulnar, median or radial nerves at elbow or wrist levels. Areas of cutaneous anaesthesia were compared with cutaneous territories of paralytic vasodilatation delineated by infrared telethermography. It was found that: (1) during ulnar nerve block the area of vasodilatation matched the area of anaesthesia in all 15 cases; (2) median nerve block induced paralytic vasodilatation which, in 14 of 15 cases, matched the area of cutaneous anaesthesia in median territory, but also extended to the unanaesthetised lateral part of the dorsum of the hand; (3) no vasodilatation developed during radial nerve block in 17 of 18 cases, whereas areas of sympathetic sudomotor paralysis matched the area of radial sensory loss in all 5 subjects in whom sweating function was studied. It is concluded that: (1) the ulnar nerve supplies vasomotor fibres to its cutaneous sensory territory, no less and no more; (2) the median nerve normally provides supplementary vasomotor innervation to the skin of the radial aspect of the dorsum of the hand; (3) the radial nerve supplies sudomotor innervation for the lateral aspect of the dorsum of the hand, but (4) does not normally contribute vasomotor sympathetic fibres to the skin of the hand.
Adult↗