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Objective: To evaluate a new climacteric symptom scale (SUMEVA) and to assess its correlation with follicle stimulating hormone (FSH) and estradiol (E2) levels., Methods: 115 healthy perimenopausal women who were not receiving, nor had received, hormone therapy were studied. They were asked to complete 3 questionnaires concerning climacteric symptoms: (1) Kupperman's index (KI), (2) Green scale (GS), and (3) SUMEVA, which is the sum of symptom evaluations done in an analog visual scale. FSH and E2 determinations were done by chemoluminiscence., Statistical Analysis: The comparison among the groups was done by Student's t test. Pearson correlation analysis was done between FSH and E2 levels and KI, the GS, and SUMEVA., Results: There were 60 women with FSH < or = 30 mIU/mL (group I) and 55 with FSH > 30 mIU/mL (group II). The KI average in the whole group was 13.2 +/- 8.1, the GS 20.6 +/- 13.1, and the SUMEVA 65.6 +/- 44.9. The three scales had a significant correlation between them., Conclusions: No correlation of KI, GS, or SUMEVA was found with FSH and E2 levels, but the SUMEVA was as effective as the other previously validated, scales for climacteric symptom evaluation.

Objectives: To establish the differences in Kupperman's index (KI) and hormone levels according to weight and body fat distribution in postmenopausal women, since obesity and fat distribution affect hormone levels., Material and Methods: One hundred and twenty-five postmenopausal women were studied and divided according to body mass index (BMI) and waist-hip ratio (WHR): normal weight (BMI < or = 27), obesity (BMI > 27); lower-level body fat distribution (WHR < or = 0.85) and upper-level body fat distribution (WHR >0.85). Afterwards four subgroups were created: (I) BMI < or = 27 and WHR < or = 0.85, (II) BMI < or = 27 and WHR > 0.85, (III) BMI > 27 and WHR < or = 0.85, and (IV) BMI >27 and WHR > 0.85. Climacteric symptoms were analyzed with Kupperman's index. Estrone, estradiol, testosterone, androstenedione, and dehydroepiandrosterone sulfate determinations were done by radioimmunoassay and verified by chemoluminescence. The androstenedione-estrone and testosterone-estradiol ratios were calculated. Statistical analysis was by Student's t test for independent samples, plus Pearson's correlation analysis., Results: Average age was 53.0 +/- 6.5 years, time since menopause 74.2 +/- 64.3 months. When comparing those with lower-level body fat distribution and those with upper-level body fat distribution, the A levels were significantly lower (P < 0.04) in those with upper-level distribution. Kupperman's index was significantly lower in subgroup I when compared with subgroups III and IV. The androstenedione level was lower in subgroup IV compared with subgroup III. In the whole sample, there was a correlation of the WHR with testosterone (0.297, P < .004) and the testosterone-estradiol ratio (0.209, P < .04)., Conclusion: It was shown that the testosterone-estradiol ratio has a better correlation with the symptoms, so it can be used to evaluate climacteric patients when they complain of menopausal symptoms.

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.

Background: Carpal tunnel syndrome results from entrapment of the median nerve in the wrist. Common symptoms are tingling, numbness, and pain in the hand that may radiate to the forearm or shoulder. Surgical treatment is widely preferred to non-surgical or conservative therapies for people who have overt symptoms, while mild cases are usually not treated., Objectives: The objective is to compare the efficacy of surgical treatment of carpal tunnel syndrome with non-surgical treatment., Search Strategy: We searched the Cochrane Neuromuscular Disease Group trials register and MEDLINE, EMBASE and LILACS (to October 2002). We checked bibliographies in papers and contacted authors for information about other published or unpublished studies., Selection Criteria: We included all randomised and quasi-randomised controlled trials comparing any surgical and any non-surgical therapies., Data Collection and Analysis: Two reviewers independently assessed the eligibility of the trials., Main Results: We found two randomised controlled trials involving 198 participants in total. The first trial included 22 participants, 11 allocated to surgery and 11 to splinting for one month. The trial was not blinded nor was it clear if allocation was properly concealed. In the second trial, 87 participants were allocated to surgery and 89 to splinting for at least six weeks. The trial was not blinded but allocation concealment was adequate. The second trial considered our primary outcome measure, relevant clinical improvement at three months. Sixty-two people out of 87 allocated to surgery (71%) qualified for treatment success. Forty-six people out of 89 allocated to splinting (51.6%) qualified for treatment success. The confidence interval favoured the surgical group (relative risk 1.38 95% confidence interval 1.08 to 1.75). We were able to pool data from both trials for two secondary outcomes. For clinical improvement at one year of follow-up, the pooled estimate favoured surgery (relative risk 1.27, 95% confidence intervals 1.05 to 1.53). For need for surgery during follow-up, the pooled estimate indicates that a significant proportion of people treated medically will require surgery while the risk of re-operation in surgically treated people is low (relative risk 0.04 in favour of surgery, 95% confidence intervals 0.01 to 0.17)., Reviewer's Conclusions: Surgical treatment of carpal tunnel syndrome relieves symptoms significantly better than splinting. Further research is needed to discover whether this conclusion applies to people with mild symptoms.

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.

Background: HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a defined entity. However, there are many patients not well characterized with a similar clinical picture who are HTLV-I seronegative., Objective: Clinical and neurophysiological description of patients with HTLV-I seronegative idiopathic paraparesis., Patients and Methods: Seventeen patients (4 women and 13 men aged 24-67 years, average 52.3) were evaluated including clinical assessment, vibratory sensory analysis, quantitative somatosensory thermotest (QST), somatosensory evoked potentials (SSEPs), electromyography (EMG) and motor and sensory nerve conductions., Results: In addition to the spastic paraparesis, 3 (17.6%) patients had pseudobulbar symptoms. Ten (58.8%) patients had a spastic gait but could walk unaided, 6 (35.2%) needed support and 1 patient could not walk. Bladder dysfunction was found in 10 (58.8) patients and sensory symptoms in 7 (41.1%). There was mild distal impairment of vibration and position sense, distal tactile and pinprick hypoesthesia in 4 (23.4%) patients. Tibial SSEPs were abnormal in 11 (64.7%). Nerve conduction studies and EMG were normal. QST showed cold hypoesthesia in 14 (82.4%) patients. Warm sensation and beat pain appeared unimpaired., Conclusions: All sensory abnormalities found were restricted to sensations carried by myelinated (A beta and A delta) channels. Sensory and motor abnormalities are similar to HAM/TSP patients suggesting a common pathogenesis.

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., (Copyright 2000 John Wiley & Sons, Inc.)

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.

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.

Background: Idiopatic or HTLV-1 associated progressive spastic paraparesis does not have a clear etiology or treatment., Aim: To assess the effects of a medication containing cytidinmonophosphate, uridintriphosphate and vitamin B 12 in the treatment of progressive spastic., Patients and Methods: Patients with the disease were randomly assigned to receive the Nucleus CMP forte (containing dysodic cytidinmonophosphate 5 mg, trisodic uridintriphosphate 3 mg and hydroxicobalamin 2 Mg) tid or placebo during six months. Gait, spasticity, degree of neurogenic bladder and somatosensitive evoked potentials were assessed during treatment., Results: Forty six patients aged 25 to 79 years old were studied, 24 were female and 29 HTLV-1 positive. Twenty two were treated with the drug and the rest with placebo. Gait and spasticity improved in 7 of 22 patients receiving the drug and 1 of 24 receiving placebo (p < 0.05). Neurogenic bladder improved in 10 of 22 receiving the drug and 4 of 24 receiving placebo (NS) Somatosensitive evoked potentials improved in four of seven patients treated with the drug and in two of seven treated with placebo., Conclusions: The medication caused a modest improvement in patients with progressive spastic paraparesis and was free of side effects.

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.

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.

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.

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.

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.

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.

The quantitative somatosensory thermotest (QST) assesses the function of afferent channels concerned with sensory submodalities served by small calibre fibres. Measured ramps of ascending or descending temperature are applied to the skin through a Peltier contact thermode, and detection thresholds are recorded as the subject signals the onset of a particular sensation. The present study describes underlying principles, methodological aspects and normal reference values for the QST. In patients, measurement of thresholds for cold sensation, warm sensation, cold-induced pain and heat-induced pain, applied to 465 individuals, yielded 13 abnormal patterns segregated into three main groups: (i) thermal (cold or warm) hypoaesthesia; (ii) thermal hyperalgesia (abnormally reduced threshold for cold and/or heat induced pain); (iii) thermal hypoaesthesia combined with thermal hyperalgesia. Critical analysis of these results yielded a number of observations of general relevance: (i) thermal specific (warm or cold) hypoaesthesia and thermal (heat or cold) hyperalgesia may occur in the absence of hypoaesthesia for tactile submodalities served by large calibre afferents; (ii) cold hypoaesthesia and warm hypoaesthesia may dissociate from each other; (iii) thermal pain hyperalgesias may occur in the absence of hypoaesthesias for specific cold or warm sensations; (iv) cold hyperalgesia and heat hyperalgesia may dissociate from each other. Thus, a negative routine sensory examination and unimpaired sensory nerve action potentials do not exclude possible somatosensory dysfunction. Furthermore, while most methods of sensory testing only document normality or deficit, the QST permits additional documentation of hyperalgesia, a positive sensory phenomenon that implies unusual pathophysiologies such as sensitization of receptors, central hyperexcitability, disinhibition or, possibly, ectopic nerve impulse discharge. This psychophysical test does not specify the level within afferent channels, between skin and brainmind, where the abnormality resides. It is recommended that the QST for all four thermal specific and thermal pain functions be incorporated in routine neurological assessment.

Anthropometric measurements collected from black and white men in the 1960 (n = 946) and 1963 (n = 456) examinations of the Charleston Heart Study cohort (Charleston County, South Carolina) were examined as predictors of all cause and coronary heart disease mortality. Anthropometric measurements included body mass index, chest girth (at the third intercostal space), abdominal girth (at the umbilicus) and midarm circumference. Vital status of 98 percent of the cohort was determined through 1988. Body mass index was not associated with mortality in the white men; however, it was predictive of all cause and coronary heart disease mortality in the black men. Analyses conducted separately in the lower and upper range of body mass index in black men showed the adjusted relative hazard at the 50th versus the 10th percentile of body mass index was 0.54 for all cause mortality, but was not significant for coronary heart disease mortality; whereas the adjusted relative hazard for the 90th relative to the 50th percentile was 1.7 for coronary heart disease deaths, but not significant for deaths from all causes. The circumference measurements were not predictive of all cause or coronary heart disease mortality in the white men. In the black men, the adjusted relative hazard ratios for all cause mortality for the 85th relative to the 15th percentiles were 0.22 for midarm circumference and 2.0 for abdominal circumference.

Changes in body weight and shape with 25 years of aging were examined using anthropometric measurements collected in the biracial Charleston Heart Study cohort. Measurements were available from 370 men and women who were in both the 1963 and 1988 examinations. Over the 25 year interval, mean weight increased 5.4 kg in subjects who were 37-46 years of age, while mean weight decreased by 2.6 kg in 55-74 year old subjects. Nevertheless, subjects in both age categories increased in abdominal girth (10.3 cm in the younger groups vs 4.7 cm in the older subjects). There was a positive linear relationship between changes in BMI and changes in the girth measurement. With no change in body mass index (BMI), estimated increases in abdominal circumference were 2.8 cm in white women, 6.6 cm in black women, 6.3 cm in white men and 7.5 cm in black men. This longitudinal study confirms cross-sectional studies that have shown increases in trunk girth with age, and in addition shows that girths change with aging, even in the absence of changes in BMI.

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. SSEP's 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 less than 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.

We screened 140 patients with different neurological diseases for the presence of anti HTLV-1 virus antibodies. ELISA test confirmed with Western Blot analysis was performed in CSF and blood. Positive findings were obtained in 23 out of 52 patients with progressive spastic paraparesis (44%). All patients with multiple sclerosis, polymyositis, amyotrophic lateral sclerosis or chronic polyneuropathy were negative. Patients with progressive spastic paraparesis and positive HTLV-1 antibodies were most commonly women (78%) and middle aged (mean 46 years old), with a history of surgical interventions (70%) or blood transfusion (35%). A slowly progressive spastic paraparesis with asymmetric onset and minimal sensory complaints was observed in some cases. Mononuclear pleocytosis in the CSF was observed in 35% with an increased IgG index in 88%. A delayed latency and low amplitude of somatosensory evoked potentials was observed in 89% of patients.

The population of neurons and the neuronal size in the nucleus basalis of Meynert (nbM) were studied in 20 patients with definite Creutzfeldt-Jakob disease (CJD). When compared with a normal control group, the 20 CJD brains showed a significant loss of neurons and reduction of neuronal size, mainly in the middle level of the nbM and mostly affecting the right side. Since these findings show some parallelism with the amount of cortical damage and given the scarce gliosis and spongiosis found in only six of the 20 CJD brains, we postulate that the involvement of the nbM in CJD is a retrograde abnormality secondary to the damage of the neocortex.