Lawrence and Kuypers (1968a, b) revisited: copies of the original filmed material from their classic papers in Brain.

This article aims to reintroduce two classic papers on motor control published in Brain in 1968, in which Lawrence and Kuypers reported their systematic studies of the effects of lesions to the corticospinal system (Lawrence and Kuypers, 1968a), and subsequently to the descending brainstem pathways (Lawrence and Kuypers, 1968b) in the Old World macaque monkey. They showed that the capacity for independent movements of the digits was permanently lost after a complete, bilateral lesion of the corticospinal system. These studies also revealed that the brainstem pathways contribute to fundamentally different aspects of motor control, with one set of pathways (the ventromedial system) involved in the control of head, trunk and girdle movements, while the other, lateral set of fibres control movements of the extremity such as reach and grasp. There is still much to learn today from these papers. However, an important part of their scientific legacy, the films illustrating the different cases, has long been unavailable. Much of this filmed material is now made available again in video format accessible on the Brain web site, complete with supplementary notes and histological detail. This article summarizes this newly available material for these classic papers in Brain.

Modeling the rovibrationally excited C2H4OH radicals from the photodissociation of 2-bromoethanol at 193 nm.

This study photolytically generates, from 2-bromoethanol photodissociation, the 2-hydroxyethyl radical intermediate of the OH + ethene reaction and measures the velocity distribution of the stable radicals. We introduce an impulsive model to characterize the partitioning of internal energy in the C(2)H(4)OH fragment. It accounts for zero-point and thermal vibrational motion to determine the vibrational energy distribution of the nascent C(2)H(4)OH radicals and the distribution of total angular momentum, J, as a function of the total recoil kinetic energy imparted in the photodissociation. We render this system useful for the study of the subsequent dissociation of the 2-hydroxyethyl radical to the possible asymptotic channels of the OH + ethene reaction. The competition between these channels depends on the internal energy and the J distribution of the radicals. First, we use velocity map imaging to separately resolve the C(2)H(4)OH + Br((2)P(3/2)) and C(2)H(4)OH + Br((2)P(1/2)) photodissociation channels, allowing us to account for the 10.54 kcal/mol partitioned to the Br((2)P(1/2)) cofragment. We determine an improved resonance enhanced multiphoton ionization (REMPI) line strength for the Br transitions at 233.681 nm (5p (4)P(1/2) <-- 4p (2)P(3/2)) and 234.021 nm (5p (2)S(1/2) <-- 4p (2)P(1/2)) and obtain a spin-orbit branching ratio for Br((2)P(1/2)):Br((2)P(3/2)) of 0.26 +/- 0.03:1. Energy and momentum conservation give the distribution of total internal energy, rotational and vibrational, in the C(2)H(4)OH radicals. Then, using 10.5 eV photoionization, we measure the velocity distribution of the radicals that are stable to subsequent dissociation. The onset of dissociation occurs at internal energies much higher than those predicted by theoretical methods and reflects the significant amount of rotational energy imparted to the C(2)H(4)OH photofragment. Instead of estimating the mean rotational energy with an impulsive model from the equilibrium geometry of 2-bromoethanol, our model explicitly includes weighting over geometries across the quantum wave function with zero, one, and two quanta in the harmonic mode that most strongly alters the exit impact parameter. The model gives a nearly perfect prediction of the measured velocity distribution of stable radicals near the dissociation onset using a G4 prediction of the C-Br bond energy and the dissociation barrier for the OH + ethene channel calculated by Senosiain et al. (J. Phys. Chem. A 2006, 110, 6960). The model also indicates that the excited state dissociation proceeds primarily from a conformer of 2-bromoethanol that is trans across the C-C bond. We discuss the possible extensions of our model and the effect of the radical intermediate's J-distribution on the branching between the OH + ethene product channels.

Calibrated finger rub auditory screening test (CALFRAST).

BACKGROUND: Determination of auditory function is a fundamental part of a complete neurologic examination. Disability from permanent hearing loss is common in the general population. Current bedside auditory tests are unreliable and cumbersome. We evaluated the calibrated finger rub auditory screening test (CALFRAST) as a routine diagnostic tool. METHODS: The sound spectrum and mean peak intensities of standard finger rub were measured, as well as background noise. CALFRAST overlapped the frequency spectrum of normal speech. Patients and companions were recruited from a neurology clinic. With arms extended, two stimulus intensities were presented: strong finger rub (CALFRAST-Strong 70) and the faintest rub that the examiner could hear (CALFRAST-Faint 70). With subjects' eyes closed, each ear's CALFRAST threshold was ascertained and then compared with its audiometric measure. The normal threshold was considered to be 25 dB. Validity, reliability, and discrimination abilities were obtained using standard methods. RESULTS: Two hundred twenty-one subjects (442 ears; 58% women) were examined. Ages ranged from 18 to 88 years, with a mean of 46 years. Eighty-five subjects (39%) had some degree of hearing loss. Both specificity and positive predictive value of CALFRAST-Strong 70 were 100%. Both sensitivity and negative predictive value of CALFRAST-Faint 70 were 99%, with a negative likelihood ratio <0.1. Area under the receiver operating characteristic curve was 0.94, consistent with excellent discrimination ability. Both intrarater and interrater reliability were excellent, both kappa >0.8. Subjects' self-assessment of hearing was unreliable. CONCLUSION: The calibrated finger rub auditory screening test (CALFRAST) is simple, accurate, inexpensive, and reliable. As a routine screening tool, CALFRAST may contribute to more efficient identification of auditory impairment.

Spinal cord and brain injury protection: testing concept for a protective device.

STUDY DESIGN: Test development for a device that could prevent both brain and spinal cord injuries during motorcycling and horseback riding. OBJECTIVE: The objective of this study was to develop a method and test a concept device that could protect against both spinal cord (SCI) and brain injuries (BI). SETTING: St Louis, Missouri, USA. METHODS: A Hybrid III dummy (that is, head, neck and torso) was used as a pendulum bob during three test conditions: (1) no protection, (2) standard motorcycle helmet and (3) SCI and BI test structure (SCIBITS). Triaxial accelerometers, a C1 force transducer and a video system were used to collect data as the dummy axially impacted a rigid barrier at speeds ranging from 10 to 605 cm s(-1). SCIBITS consisted of a fused fiberglass thoracic jacket/head shield unit. Separation between the dummy head and the head shield permitted freedom of head movement within safe limits as impact forces to the head shield were transferred from the head and neck to the upper thorax. The BI threshold was 200-300 g, and the SCI threshold was 3010 N. RESULTS: The SCIBITS protected against spinal cord injury, whereas the motorcycle helmet did not. The helmet protected against BI and the SCIBITS provided partial protection. CONCLUSIONS: The experiments describe the efficacy of an impact testing system utilizing an instrumented dummy suspended as a pendulum bob. The equipment will facilitate the design and construction of a functional device for protection against both SCI and BI in relation to both motorcycling and horseback riding.

Hereditary spastic paraplegia and hereditary ataxia, Part 2: A family demonstrating various phenotypic manifestations with the SCA3 genotype.

BACKGROUND: Clinical descriptions of the dominantly inherited ataxic motor syndromes in a 7-generation family of German origin were first reported in 1951. OBJECTIVE: To provide follow-up clinical, pathological, and genetic data for 9 patients in this family. DESIGN: Clinical histories and neurologic findings, gross and microscopic pathological features, and DNA analysis. RESULTS: Clinical presentations in this closely followed up portion of the family include fairly uniform ataxic and upper motor neuron symptoms. Nystagmus was a conspicuous and early sign, but generational anticipation was not evident. Although often present, amyotrophy was not a major source of disability. Major pathological degeneration was noted in the pons, spinal cord, and upper brainstem, where ubiquitin-immunoreactive intranuclear inclusion bodies were demonstrated. The diagnosis of Machado-Joseph disease (SCA3 [spinocerebellar ataxia type 3] genotype) was established from autopsy tissue in 1 patient and from blood specimens in 6 others. CONCLUSIONS: Clinical variation within this family and between this family and families with the SCA1 and SCA3 genotypes is so broad as to make the genetic diagnosis from clinical criteria alone practically impossible. The pathological definition of Machado-Joseph disease is more reliable, but some findings do overlap those of other genotypes. To our knowledge, the basis for the phenotypic variations in Machado-Joseph disease, genetic or otherwise, has not been established.