A PET study of the neural systems of stuttering

The cause of stuttering is unknown. Failure to develop left-hemispheric dominance for speech is a long-standing theory although others implicated the motor system more broadly, often postulating hyperactivity of the right (language nondominant) cerebral hemisphere. As knowledge of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postulating hyperactivity of premotor cortex, either directly or through connectivity with the thalamus and basal ganglia. Alternative theories target the auditory and speech production systems. By contrasting stuttering with fluent speech using positron emission tomography combined with chorus reading to induce fluency, we found support for each of these hypotheses. Stuttering induced widespread overactivations of the motor system in both cerebrum and cerebellum, with right cerebral dominance. Stuttered reading lacked left-lateralized activations of the auditory system, which are thought to support the self-monitoring of speech, and selectively deactivated a frontal-temporal system implicated in speech production. Induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed the auditory-system underactivations and the deactivation of the speech production system. Thus stuttering is a disorder affecting the multiple neural systems used for speaking.     

An alternative method for the quantitation of neuronal damage after experimental middle cerebral artery occlusion in rats: analysis of behavioral deficit

We tested the hypothesis that increasing durations of focal ischemia that have been shown to result in enlargement of cortical infarct will be associated with progression of behavioral dysfunction that can be measured by a battery of tests sufficiently sensitive and reproducible to detect a positive effect of pharmacotherapy. Untreated or N-methyl-D-aspartate receptor antagonist (CNS-1102)-treated spontaneously hypertensive rats underwent 45, 60, 90, or 120 min of tandem middle cerebral and common carotid artery occlusion followed by reperfusion. We then evaluated the extent of damage and its recovery for up to 21 days using nine behavioral tests aimed at analyzing strength, coordination, and bilateral asymmetry. Also using a graded bioassay that employs a curve-fitting computer program (ALLFIT) to correlate duration of ischemia with degree of behavioral dysfunction, we calculated the average of maximal behavioral dysfunction and duration of ischemia required to produce half-maximal behavioral dysfunction and compared these values in untreated controls with analogous values obtained from animals treated with CNS-1102. Three behavioral tests, forearm flex, tape (somatosensory neutralization), and foot-fault placing, were each separately and combined able to distinguish between the degrees of damage produced by increasing durations of ischemia. The behavioral abnormalities assessed using the tape test were reversible within a week, whereas those using forearm flex or foot-fault tests persisted for at least 21 days. CNS-1102 significantly reduced behavioral dysfunction measured by all three tests. This analysis of behavioral dysfunction represents a useful experimental model to grade efficacy of therapies aimed at protecting the brain from damage produced by acute stroke and might also be used to assess recovery from preexisting ischemic damage.     

Whole-body kinetics and dosimetry of L-3--123I-iodo-alpha-methyltyrosine

BACKGROUND: Desflurane anesthesia can produce cerebral metabolic depression and increase cerebral blood flow. We evaluated the effect of desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2) and pH during neurosurgery. METHODS: Following a craniotomy, the dura was opened and a Paratrend 7 sensor, which measures PO2, PCO2, pH and temperature, was inserted into brain tissue. In 6 control patients in group 1, anesthesia was maintained constant with 3% end-tidal desflurane over 60 min, including a 30-min stabilization period. In group 2, 9 patients were ventilated with 3% desflurane under baseline conditions. After a 30-min stabilization period, baseline tissue gases and pH were measured and end-tidal desflurane was increased to 6% and then 9% for 15-min intervals. Mean arterial pressure (MAP) was maintained with intravenous phenylephrine. RESULTS: Under baseline conditions, cardiovascular and brain tissue measures were similar between the 2 groups. Increasing end-tidal desflurane from 3% to 9% produced burst-suppression EEG in all patients and significantly increased tissue PO2 and pH and decreased PCO2. No parameters changed significantly in the control group during steady-state anesthesia. CONCLUSION: These results show that 9% desflurane can improve brain tissue metabolic status before temporary brain artery occlusion if cerebral perfusion pressure is maintained. This may be particularly important in patients with symptoms of ischemia before surgery.     

Perceived dangerousness of recreational drugs

In Study One, a sample of 230 college students were asked to estimate the abuse potential and lethality of commonly used recreational drugs, both licit and illicit. In Study Two, a sample of 103 degreed nurses were asked to estimate the lethality of the same recreational drugs. The findings indicate that the illicit drugs under consideration are perceived as presenting the greatest danger to the user and that dangers attributed to the use of licit recreational drugs are generally minimized. Perception of danger was found to be unaffected by exposure to reported drug education programs. Results are discussed in terms of public health implications.     

Retrospective comparison of photorefractive keratectomy and radial keratotomy

BACKGROUND: The efficacy and predictability of photorefractive keratectomy and radial keratotomy become increasingly relevant. This retrospective study compares one surgeon's experience with photorefractive keratectomy and radial keratotomy over a 3-year period from 1990 to 1993. METHODS: Photorefractive keratectomy was performed on 103 eyes of 76 patients that met the inclusion criteria for the phase IIb, phase III, and phototherapeutic keratectomy studies as delineated by the United States Food and Drug Administration. Radial keratotomy was performed on 117 eyes of 81 patients with up to 9.00 diopters (D) of myopia. RESULTS: In the photorefractive keratectomy group, 83% of the eyes achieved uncorrected visual acuity of at least 20/40; 37% saw 20/20; 88% had a refraction within 1.00 D of emmetropia, and 63% within 0.50 D of emmetropia. For the radial keratotomy group, 85% of the eyes achieved an uncorrected visual acuity of 20/40 or better; 27% saw 20/20; 88% had a refraction within 1.00 D of emmetropia; and 55% within 0.50 D of emmetropia. There were no serious complications, and only one single eye in each of the photorefractive keratectomy and radial keratotomy groups lost two lines or more of spectacle-corrected visual acuity. CONCLUSION: Photorefractive keratectomy and radial keratotomy are both effective procedures, and result in similar refractive outcomes for myopia of -1.00 to -9.00 D.