East or west: to which subspecies does the type specimen of the Galah, Eolophus roseicapilla (Vieillot, 1817) (Aves: Cacatuidae), belong?

The Galah (Eolophus roseicapilla) is a pink-and-grey cockatoo, widespread in and endemic to Australia, and now familiar as a cage bird world-wide. It has three currently recognised subspecies: roseicapilla Vieillot, 1817 in the Australian west, kuhli Mathews, 1912 in the far north, and albiceps Schodde, 1989 in the east (Schodde 1997; Higgins 1999; Dickinson & Remsen 2013; del Hoyo & Collar 2014; Engelhard et al. 2015). The northern subspecies, kuhli, is not involved in the issue of type identity of roseicapilla, and so is not considered further here. First to distinguish east and west subspecies was G.M. Mathews (1912). Without explanation then or later, Mathews arbitrarily applied the senior specific name, Cacatua roseicapilla Vieillot, 1817 and its two objective synonyms based on the same type-eos Kuhl, 1820 and rosea Vieillot, 1822-to the eastern subspecies, and introduced the new name assimilis for the then supposedly undescribed western form. Mathews' lead was followed unquestioningly until the late 1980s when Schodde (1989) and Rowley (1990: 3) concluded that the type of Vieillot's roseicapilla was of the western subspecies, collected by the Baudin expedition in the region of Shark Bay on the mid-western Australian coast. Rowley (l.c.), but not Schodde (l.c.) contrary to Rowley's reference, went further to claim that it had been taken by François Péron in 1803, presumably on the brief return visit of Baudin in Le Géographe to Shark Bay en route to France. This left the eastern subspecies un-named, which Schodde (l.c.) accordingly described as albiceps.

Efficacy and safety of levetiracetam 1000-3000 mg/day in patients with refractory partial-onset seizures: a multicenter, open-label single-arm study.

PURPOSE: To evaluate the efficacy and tolerability of levetiracetam as add-on therapy in patients with refractory partial-onset seizures in a protocol designed to reflect clinical practice. METHODS: All patients in this open-label, single-arm study entered an 8-week baseline period followed by a 4-week titration period and a 12-week maintenance period. Patients initially received levetiracetam 1000 mg/day (administered bid) and could increase to 2000 mg/day after 2 weeks, and to 3000 mg/day after another 2 weeks, to obtain adequate seizure control. During the 12-week maintenance period, the dose of levetiracetam could not be increased but could be decreased once if tolerability warranted. Seizure count and adverse events were recorded by patients in a diary. Quality of life and global evaluation of disease evolution were also evaluated. RESULTS: Ninety-nine patients were enrolled and 91 completed the study. A steady dose was maintained over the last 8 weeks of treatment or longer in 84 patients, with 89.3% of these patients receiving 3000 mg/day, 9.5% receiving 2000 mg/day, and 1.2% receiving 1000 mg/day. A 35.9% median percent reduction from baseline in weekly frequency of partial-onset seizures was observed over the entire treatment period. The median partial-onset seizure count decreased from 2.3 per week during the baseline period to 1.3 per week over the treatment period. A total of 42.4% of patients were responders (> or = 50% reduction from baseline in weekly seizure frequency) over the treatment period; two patients were seizure-free from the first day of treatment throughout the treatment period. The most frequent drug-related adverse events were fatigue (27.3% of patients), somnolence (11.1%), headache (8.1%), and dizziness (8.1%). CONCLUSION: Levetiracetam as add-on therapy at doses up to 3000 mg/day effectively reduced the frequency of partial-onset seizures in patients with refractory epilepsy and was well-tolerated in this study, bridging conditions of placebo-controlled clinical trials and clinical practice.

Driving to distraction--certification of fitness to drive with epilepsy.

Assessment of medical fitness to drive can be a sensitive and difficult task, particularly when it involves a condition such as epilepsy, where impairment is intermittent. The patient, their doctor and the driver licensing authority (DLA) each have responsibilities, both to the patient and to the wider community of road users. DLAs in Australia have shifted most of the responsibility for determining fitness to drive to the treating doctor. This creates a conflict of interest and may lead to unsafe decisions, damage to the doctor-patient relationship, interference with medical management and legal vulnerability for the doctor. Australian neurologists have argued for a system in which the treating doctor provides objective information about the patient's condition, rather than an opinion on fitness to drive, and the DLA uses that information to determine fitness. This must be supported by an expert review process. Although drivers are legally obliged to notify the DLA when they become unfit, most people are unaware of this law. However, passing this responsibility to doctors in the form of mandatory reporting is counterproductive to road safety.

Long-term follow-up using a higher target range for lamotrigine monitoring.

The aims of the study were (1) to review the clinical application of the higher target plasma lamotrigine (LTG) concentration of 3-14 mg/L previously proposed by our therapeutic drug monitoring (TDM) laboratory following our initial study 7 years earlier, and (2) to survey clinical application of LTG assays by experienced neurologists (n = 11) who frequently use LTG. There was a 2.9-fold increase in LTG assay requests received by our laboratory from 1996 to 2003. By comparison, data for the number of LTG prescriptions filled throughout Australia were limited to the 4 years from 1997 to 2000, where a 1.7-fold increase was seen. LTG assay requests increased 1.5-fold in this same 4-year period (r2 = 0.97), indicating that the growth in assay requests paralleled the growth in prescriptions. The distribution of LTG concentrations measured in 2003 was compared with those for 1996 and 1997. This indicated there was a significantly increased (P < 0.01) clinical usage of the higher LTG target range. This result was reinforced by questionnaire responses. Respondents (100% of those surveyed), (1) considered the target LTG concentration (3-14 mg/L) to be one of the primary parameters applied in individualizing LTG dosage regimens, (2) were using target concentrations above 7 mg/L in 75% of patients, and (3) reported dose-limiting toxicities in some (but not all) patients typically at concentrations above, or well above, 13 mg/L. In conclusion, the growth in LTG assay requests received by our laboratory paralleled prescribing of this drug. The clinical use of the higher LTG target concentration range was increased during the 7 years since its introduction, indicating clinical acceptance and therapeutic benefit as well as the absence of long-term adverse effects associated with higher plasma LTG concentrations.