Annals of neurology
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Annals of neurology · Oct 1993
Case ReportsDiffuse noxious inhibitory controls in humans: a neurophysiological investigation of a patient with a form of Brown-Séquard syndrome.
In normal subjects, the application of heterotopic painful stimuli induces simultaneous and parallel decrease in the sensation of pain and of the spinal nociceptive flexion (RIII) reflex evoked by electrical stimulation of the sural nerve. This inhibition of the RIII reflex is absent in tetraplegic patient with clinically complete spinal cord transections and can be triggered only from the analgesic hand in patients with Wallenberg's syndrome. These findings suggest that the inhibitory phenomena observed in normal subjects are likely to be examples of diffuse noxious inhibitory controls (DNICs), being sustained by a loop involving supraspinal structures, the ascending part of which is localized in the spinoreticular tract. ⋯ Nociceptive flexion (RIII) reflexes elicited by stimulation of cutaneous afferents in the ulnar and sural nerves were studied in the upper and lower limbs by recording from the biceps brachialis and biceps femoris muscles, respectively. For each limb, the RIII reflex threshold was determined. The reflex was then elicited regularly by stimuli of 1.2 times threshold before, during, and after periods of nociceptive electrical conditioning stimulation (15 mA; 4 Hz; 1 min) applied successively to the other three limbs.(ABSTRACT TRUNCATED AT 250 WORDS)
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Annals of neurology · Oct 1993
Cerebrospinal fluid inhibits Alzheimer beta-amyloid fibril formation in vitro.
Alzheimer's disease is characterized by the deposition of beta-protein (A beta) as amyloid. Recently, it was found that A beta is a normal component of serum and cerebrospinal fluid. Synthetic peptides homologous to A beta form amyloid-like fibrils spontaneously in water or physiological solutions. Using a peptide homologous to A beta 1-40, we find that fibril formation is inhibited by the presence of cerebrospinal fluid.
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Annals of neurology · Jul 1993
Clinical Trial Controlled Clinical TrialMyoblast transfer in Duchenne muscular dystrophy.
One biceps muscle of 8 patients with Duchenne muscular dystrophy was injected at 55 sites with a total of 55 million viable, purified, and contamination-free normal myoblasts (myoblast transfer). The other biceps of each patient was injected with a placebo to serve as a control. The procedure was blinded to the patients, parents, and investigators. ⋯ No serious complications were observed after myoblast transfer, indicating that the procedure is safe. The overall therapeutic efficiency of myoblast transfer was poor as judged by the results in maximal voluntary force generation, dystrophin content of the muscle, magnetic resonance imaging of the muscle, and the lack of donor-derived DNA and dystrophin messenger RNA in the injected muscle. An improved efficiency of the take of myoblasts might be achieved by using younger cells and injecting the myoblasts with a myonecrotic agent (to increase the prevalence of regeneration) and a basal laminal fenestrating agent.
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Annals of neurology · May 1993
Mechanical hyperalgesias in neuropathic pain patients: dynamic and static subtypes.
Two behavioral kinds of mechanical hyperalgesia can be clearly discerned by clinical criteria in patients with neuropathic syndromes, i.e., a dynamic type, elicitable by lightly stroking the symptomatic skin, and a static type, elicitable by steadily applying gentle pressure on it. Of 28 patients studied, 19 had dynamic and 18 had static type mechanical hyperalgesia (9 expressed both types). Experimental compression-ischemia nerve block totally abolished the dynamic hyperalgesia in all patients except in 2, in whom it was markedly diminished. ⋯ Static hyperalgesia, however, outlasted A-fiber block in 15 of 18 patients; the phenomenon persisted during the stage when only unmyelinated fibers were available for impulse conduction. It is thus concluded that, at the primary afferent level, dynamic hyperalgesia is mediated by myelinated fibers, whereas static hyperalgesia depends on unmyelinated afferents. These two kinds of hyperalgesia represent discrete pathophysiological entities with distinct clinical connotations.