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Locomotion analysis is now widely used across many animal species to understand the motor defects in disease, functional recovery following neural injury, and the effectiveness of various treatments. More recently, rodent locomotion analysis has become an increasingly popular method in a diverse range of research. Speed is an inseparable aspect of locomotion that is still not fully understood, and its effects are often not properly incorporated while analyzing data. In this hybrid manuscript, we accomplish three things: (1) review the interaction between speed and locomotion variables in rodent studies, (2) comprehensively analyze the relationship between speed and 162 locomotion variables in a group of 16 wild-type mice using the CatWalk gait analysis system, and (3) develop and test a statistical method in which locomotion variables are analyzed and reported in the context of speed. Notable results include the following: (1) over 90% of variables, reported by CatWalk, were dependent on speed with an average R(2) value of 0.624, (2) most variables were related to speed in a nonlinear manner, (3) current methods of controlling for speed are insufficient, and (4) the linear mixed model is an appropriate and effective statistical method for locomotion analyses that is inclusive of speed-dependent relationships. Given the pervasive dependency of locomotion variables on speed, we maintain that valid conclusions from locomotion analyses cannot be made unless they are analyzed and reported within the context of speed.

Two studies were conducted to explore the hypothesis that Broca's and Wernicke's aphasics have deficits arising from the processes involved in activating the lexicon from phonological form. The first study explored whether phonologically similar lexical entries differing only in their initial consonants show “rhyme priming.” Results revealed that Broca's aphasics failed to show facilitation when the target was identical to the prime (i.e. identity priming) and they showed significant inhibition when targets were preceded by rhyming words. Wernicke's aphasics showed a pattern of results similar to that of normal subjects, i.e., identity priming and rhyme priming as well as significantly slower reaction-times in the rhyming condition compared to the identity condition. The second study investigated form-based repetition priming in aphasic patients at a number of intervals including when no other stimuli intervened between repeated stimuli (0 lag) or when 4, 8, or 12 stimuli intervened. Results showed that, unlike old normal subjects who showed repetition priming for both words and nonwords, both Broca's and Wernicke's aphasics showed repetition priming for word targets only. Moreover, in contrast to old normal subjects who showed a greater magnitude of priming at 0 lag for word targets, neither Broca's aphasics or Wernicke's aphasics showed priming at 0 lag. Implications of these findings are considered with respect to the hypotheses that Broca's and Wernicke's aphasics have deficits in the nature of the activation patterns within the lexicon itself and in auditory (working) memory.

Two experiments were conducted exploring on-line processing of filler–gap constructions in aphasia. An auditory–auditory lexical decision paradigm was used to investigate whether Broca's and Wernicke's aphasic patients show, as do normals, reactivation of the filler at the gap site. Experiment I investigated the processing of a number of filler–gap constructions including wh-questions, relative clauses as subject, relative clauses as object, and embedded wh-questions. Broca's aphasics showed reactivation of the filler at the gap site, whereas Wernicke's aphasics did not. Experiment II examined object relative clauses and their processing by Broca's aphasics. In addition, we investigated whether the presence (or absence) of the relative pronoun played any role in on-line processing. Broca's aphasics performed as did normals. In addition, their performance was unaffected by the presence or absence of the relative pronoun. The results of these experiments suggest that Broca's aphasics do not have an impairment in processing or representing thematic relationships of NP arguments to predicates or relating traces to their antecedents.

The histochemical NADPH-diaphorase reaction has identified distinct neuronal populations in the nervous system of several species. Considerable evidence suggests that NADPH-d is a neuronal nitric oxide synthase (NOS). We examined spinal cords of adult and metamorphosing Xenopus laevis (XL) for developmental differences in NADPH-d reactivity. In adult XL, labeling was found in all dorsal root ganglia (DRGs) and in their termination sites within the dorsal horn (cutaneous afferent field) and intermediate gray (muscle afferent field). Cell bodies in the intermediate gray regions containing the autonomic preganglionic neurons were labeled in thoracic and sacral sections. Neurons located in the medial (MMC) and lateral motor columns (LMC) of the ventral horn were also stained. In metamorphosing XL, reactivity was detected in neurons in the intermediate gray, in the MMC and in the LMC as in the adult. Additionally, primary motoneurons including those innervating tail musculature were labeled. Neurons in the DRGs were stained at all stages; in the dorsal horn, the density of staining reflected the development of the sensory afferent fields. The conservation of NADPH-d reactivity in adult and metamorphosing XL spinal neurons suggests that NOS may be involved in processes independent of developmental changes occurring in XL spinal cord.

Lidocaine kinetics were examined during continuous infusions in five healthy subjects using stable isotope lidocaine labeled with two deuterium atoms. During phase 1, lidocaine and stable isotope lidocaine (50 mg IV each) were given as a bolus to confirm that the two species were kinetically identical. Phase 2 consisted of a long-term (30 hr) lidocaine infusion designed to produce a steady-state concentration equal to 1.5 microgram/ml. Twenty-four hours into the infusion, stable isotope lidocaine (50 mg) was given as an intravenous bolus and kinetic parameters were calculated. Phase 3 differed from phase 2 in that target steady-state lidocaine concentration was 4 microgram/ml and the stable isotope lidocaine dose was reduced to 40 mg. A gas chromatograph-mass spectrometer was used to determine lidocaine and stable isotope lidocaine serum concentrations. Compared to phase 1, clearance decreased (P less than 0.05) and half-life increased (P less than 0.025) during phases 2 and 3. The volume of distribution at steady-state remained constant during all three phases. Lidocaine cumulated in serum during long-term infusions in all five patients; repeated decreases in infusion rate were necessary to avoid exceeding desired target concentrations in phases 2 and 3.

A case that utilizes a pharmacokinetic approach to evaluate the need for withdrawal prophylaxis after a phenobarbital overdose is presented. To date, the practitioner has had to rely on an accurate drug-use history to predict which patients may be at risk for withdrawal symptoms. Since this information is often difficult to obtain, some other means of identifying potential withdrawal-syndrome patients would be useful. This case describes the successful use of kinetically determined parameters, the elimination rate constant and half-life, in predicting withdrawal potential. This easily used kinetic approach may provide practitioners with a useful tool for predicting those patients at risk for withdrawal symptoms following phenobarbital overdose.