Effect of slow, small movement on the vibration-evoked kinesthetic illusion.

The study reported in this paper investigated how vibration-evoked illusions of joint rotation are influenced by slow (0.3 degrees /s), small (2-4 degrees ) passive rotation of the joint. Normal human adults (n=15) matched the perceived position of the left ("reference") arm with the right ("matching") arm while vibration (50 pps, 0.5 mm) was applied for 30 s to the relaxed triceps brachii of the reference arm. Both arms were constrained to rotate horizontally at the elbow. Three experimental conditions were investigated: (1) vibration of the stationary reference arm, (2) slow, small passive extension or flexion of the reference arm during vibration, and (3) slow, small passive extension or flexion of the reference arm without vibration. Triceps brachii vibration at 50 pps induced an illusion of elbow flexion. The movement illusion began after several seconds, relatively fast to begin with and gradually slowing down to a stop. On average, triceps vibration produced illusory motion at an average latency of 6.3 s, amplitude of 9.7 degrees , velocity of 0.6 degrees /s, and duration of 16.4 s. During vibration, slow, small ( approximately 0.3 degrees /s, 1.3 degrees ) passive rotations of the joint dramatically enhanced, stopped, or reversed the direction of illusory movement, depending on the direction of the passive joint rotation. However, the subjects' perceptions of these passive elbow rotations were exaggerated: 2-3 times the size of the actual movement. In the absence of vibration, the subjects accurately reproduced these passive joint rotations. We discuss whether the exaggerated perception of slow, small movement during vibration is better explained by contributions of non muscle spindle Ia afferents or by changes in the mechanical transmission of vibration to the receptor.

Experimental benznidazole encephalopathy: I. Clinical-neurological alterations.

Benznidazole (N-benzyl-2-nitro-1-imidazoleacetamide) is an antiprotozoan agent of the nitroimidazole group used extensively in South America to treat Chagas' disease. In humans, its most important side effect is peripheral polyneuropathy, the frequency of which is dose related. To evaluate this effect, we administered benznidazole to adult, male, mongrel dogs at doses ranging from 5 to 40 mg/kg/day (0.5 to 4 times the dose used to treat chagasic patients). Subsequent neurological examination revealed apathy, ataxia, spastic tetraplegia with hyperreflexia of stretching reflexes, balance disorders and asymmetrical gait. These alterations appeared earlier and were more intense at the higher doses. Drug withdrawal also left dose- and time-dependent sequelae like ataxia, hypertonia, hyperreflexia and alterations of balance. No peripheral neuropathy was detected. The present findings suggest that a careful reevaluation of the side effects of benznidazole in humans is necessary.

Experimental benznidazole encephalopathy: II. Electroencephalographic and morphological alterations.

We describe electroencephalographic (EEG) and morphological alterations in the CNS of dogs treated with benznidazole. The relationship between dose, duration of treatment and intensity of lesions observed was examined and used to establish anatomo-clinical associations. Two predominant EEG patterns were noted in treated dogs. Most of the animals (Group I) that received acute treatment with high doses (30 mg/kg/day) for 15 days followed by treatment at a lower dose (10 mg/kg/day) exhibited a type 2, EEG pattern, i.e., low voltage desynchronized with fast activity (LVFA). In contrast, most of the animals (Group II) that received short-term acute treatment with high doses (40 mg/kg/day) for 7 days followed by chronic treatment at lower doses (20 and 5 mg/kg/day) presented a type 1 EEG pattern. high voltage diffuse with slow activity (HVSA). Even after the drug was discontinued, the animals presented mild EEG alterations. These alterations. observed during and after treatment with benznidazole, suggest the presence of encephalopathy with multifocal characteristics. Several morphological alterations were observed in the animals, the most important being: lymphocytic inflammatory infiltrate, neuronal degeneration, satellitosis, demyelination and axonal degeneration, microglial proliferation, necrosis and gliosis. Such alterations involved the meninges, cerebral cortex, hemispheric white matter and subcortical gray matter, brain stem, cerebellum, and, less frequently, the spinal cord. No histopathological alterations were detected in the peripheral nerves. All encephalic levels were involved in all animals treated although the use of the high doses for 15 days (Group I) appeared to result in more lesions in the subcortical gray matter and the lower brainstem when compared to the use of high doses for 7 days (Group II) which led to greater involvement of the cerebral cortex, hemispheric white matter, cerebellum and medulla.