Australian workers with back injury: a statistical overview.

This paper reviews international and Australian data concerning the occurrence of back injuries amongst the labour force. Analyses of Australian Bureau of Statistics data for the period 1977 to 1986 revealed substantial differences between Australian states in their rates of back injury claims for work injuries, with a decline in rates over the ten years surveyed. Analyses of WorkCare data from the State of Victoria in Australia revealed that claimants with back injury claims of greater than 12 months standing were very costly. A total of 8,633 claimants accounted for 68.7% of all payments for back injury ($362 million out of a total of $527 million) when these claimants represented only 10.7% of all back injury claimants for the period September 1985 to May 1989. Substantial variations were found in claim rates across occupations and age levels. An almost linear (r = 0.98) association was found between age and proportion of long term claimants at each age level. It is suggested that these data could be used to identify 'at risk' groupings with a view to the implementation of preventive measures.

Anticonvulsive and convulsive effects of lidocaine: comparison with those of phenytoin, and implications for mechanism of action concepts.

The anticonvulsive action of lidocaine was tested in mice against a series of convulsants, and its profile of action compared with that of phenytoin. Both agents antagonized seizures induced by ouabain or glutamate (injected i.c.b.), effects attributable to reduction of the sodium conductance of neuronal membranes. Lidocaine and phenytoin were relatively ineffective against convulsants that act on synaptic chloride channels via the GABA-ionophore receptor complex. At higher dose levels, both lidocaine and phenytoin are excitatory within limited ranges. Lidocaine-induced seizures were potentiated by phenytoin, and antagonized by chlordiazepoxide, phenobarbital, valproate, trimethadione and muscimol, but not by ethosuximide. This profile of action is similar to that of bicuculline, suggesting that lidocaine may bind to the GABA recognition site and to another site in the GABA-ionophore receptor complex. Phenytoin-induced excitation was antagonized by chlordiazepoxide, less effectively by phenobarbital or trimethadione, only minimally by valproate, and not by trimethadione or muscimol. Phenytoin is known to bind to picrotoxin and benzodiazepine receptor sites; these findings suggest that it may be excitatory at one or both of these sites.

Effects of anticonvulsants on K+-induced excitation and on penicillin-induced seizures.

Excitation induced in mice by intracerebral injection of KCl was antagonized by prior i.p. injection of phenytoin, chlordiazepoxide or phenobarbital, but was not significantly affected by muscimol, valproate, ethosuximide or trimethadione. In contrast, seizures induced by intracerebral injection of benzyl penicillin were antagonised by chlordiazepoxide, phenobarbital, valproate, ethosuximide and trimethadione, but not by phenytoin or muscimol. Implications with regard to mechanisms of action of the anticonvulsants and of penicillin are discussed.

Occupational repetitive strain injuries.

The incidence of repetitive strain injuries is rising; they are the most common cause of loss of time from work for women and third most common for men. A detailed history and careful examination are required to determine specifically the muscles and tendons affected by overuse; treatment is directed primarily at avoiding stress to these areas.

Repetitive strain injuries.

The semimechanized and repetitive nature of industry, the greater use of keyboards, and the need to boost production during an economic recession have led to a huge increase in repetitive strain injuries. The types of injury, their diagnosis and their treatment are discussed.

Effects of anticonvulsants and other agents on seizures induced by intracerebral L-glutamate.

Convulsions induced in mice by intracerebral injection of L-glutamate were antagonized by phenytoin, phenobarbital, chlordiazepoxide and valproic acid. Trimethadione had only a small effect at the dose used, and ethosuximide was ineffective. The profile of interaction of glutamate with these antiepileptic agents resembles that of ouabain, and differs considerably from the profiles of other convulsants previously tested. However, muscimol had a small potentiating effect on glutamate but not on ouabain. Neither L-glutamic acid diethyl ester nor L-nuciferine significantly altered the convulsive response to glutamate.

Interactions of phenytoin with ouabain and other chemical convulsants.

Phenytoin potentiated the convulsive actions of bicuculline and picrotoxin in mice, whereas the action of bemegride was neither potentiated nor antagonized. Seizures induced by intracerebral injection of ouabain were antagonized by phenytoin, as well as by phenobarbital, chlordiazepoxide and valproic acid; trimethadione had a possible small effect, not quite significant at the 5% level; ethosuximide and muscimol did not show significant effects. Seizures induced by intracerebral injection of pentylenetetrazol were antagonized by phenobarbital but not by phenytoin. Tests of phenytoin against other chemical convulsants are reviewed, and it is suggested that phenytoin may be specific for seizures that arise from a derangement of mechanisms involving sodium ions. This strengthens the view that such a derangement is likely in many cases of human epilepsy.

Vocational rehabilitation for industrially disabled workers.

The role of vocational rehabilitation services, which help to re-employ injured workers, is not well understood in Australia. The rehabilitation counsellor must be able to coordinate a wide variety of resources and to find the best possible socio-economic solution for the worker.

Muscimol as an antagonist of chemical convulsants.

Muscimol (MU) was tested on mice for anticonvulsive action against chemical convulsants. 3-Mercaptopropionic acid (3-MP) was more sensitive to inhibition by MU (1.5 mg/kg) than was either pentylenetretrazol (PTZ) or bicuculline (BIC); picrotoxin (PIC) and kainic acid were not measurably antagonized; aminophylline was potentiated. The profile of action of MU closely resembles that of aminooxyacetic acid (AOAA), except that the latter strongly antagonizes kainic acid. MU distinguished more clearly than did AOAA between the action of 3-MP and that of either PTZ or BIC, inasmuch as the differences between the respective potency ratios were larger with MU than with AOAA. The results are consistent with the view that MU acts as a GABA agonist, that GABA antagonism is not a sufficient basis on which to explain the convulsive action of BIC or PIC, and that the antagonism of AOAA toward seizures induced by kainic acid may not be due to an action on the GABA system.

Aminophylline and imidazole as convulsants.

The convulsive actions of aminophylline (APH) and imidazole (IDZ) have been tested against a series of anticonvulsants, and their patterns of sensitivity to these agents are compared with those of other convulsants. APH was antagonized by phenobarbital and chloridiazepoxide, but less effectively than is pentylenetetrazol. Antagonism by trimethadione was not significant. Ethosuximide, phenytoin and aminooxyacetic acid potentiated APH, an effect not seen with other convulsants in our previous studies. IDZ-induced seizures were found to be relative refractory to anticonvulsants, but were antagonized to a small degree by all of those mentioned above except phenytoin; aminooxyacetic acid was relatively the most effective. Phenytoin potentiated IDZ-induced seizures. Subconvulsive doses of APH potentiated pentylenetetrazol- and 3-mercaptopropionic acid-induced seizures about equally, as did IDZ. Possible mechanism of action are discussed.

Effects of anticonvulsants and glutamate antagonists on the convulsive action of kainic acid.

In its pattern of sensitivity to anticonvulsants, kainic acid (KA) showed little resemblance to pentylenetetrazol (PTZ), 3-mercaptopropionic acid (3-MP), bicuculline, picrotoxin or bemegride. That KA may have an action on the gamma-aminobutyrate system is suggested by the following: it is strongly antagonized by aminooxyacetic acid; ethosuximide is ineffective against KA as it is against 3-MP; and a subconvulsive dose of KA potentiated 3-MP but not PTZ. However, KA is to some extent comparable to PTZ in that it is antagonized by trimethadione, phenobarbital and chlordiazepoxide more effectively than is 3-MP. The convulsive action of KA is potentiated by the glutamate antagonists l-glutamate diethyl ester (GDEE) and l-nuciferine. GDEE also slightly potentiated bicuculline, but not other convulsants tested; it slightly antagonized PTZ. Nuciferine potentiated all except PTZ and bemegride. The failure of these agents to antagonize KA-induced seizures is consistent with the view that KA and glutamate act at separate excitatory receptor sites. The potentiation might possibly be due to a blocking of glutamergic activation of neurons that are inhibitory.

Quantitative evaluation of the actions of anticonvulsants against different chemical convulsants.

Anticonvulsants were tested on mice for their effectiveness against different chemical convulsants. Ethosuximide is very effective against pentylenetetrazol (PTZ), but ineffective against 3-mercaptopropionate (3-MP) which is an inhibitor of gamma-aminobutyrate (GABA) synthesis. Trimethadione, chlordiazepoxide and mesuximide are less effective against 3-MP than against PTZ. The same tendency was apparent, though falling short of statistical significance, with phenobarbital, mephenytoin, carbamazepine and valproic acid, whereas aminooxyacetic acid (AOAA) appeared to be somewhat more effective against 3-MP than against PTZ. Several anticonvulsants were tested also against bicuculline (BIC), picrotoxin (PIC) and bemegride (BEM), and profiles depicting their relative capacities to antagonize the convulsants were constructed. These show major differences and few resemblances. Likewise the convulsants show little resemblance to each other in their patterns of sensitivity to different anticonvulsants. The data do not support the concept that PTZ, BEM, BIC or PIC induce seizures primarily by blockading GABA-mediated inhibition, since their patterns are so unlike that of 3-MP. The profiles of clinically used anticonvulsants suggest that none of those tested acts primarily on the GABA system, since all are so unlike that of AOAA.

Research training in psychiatric residency programs: a survey.

Although it seems reasonable to assume that the absence of research training may account for the fact that few psychiatrists involve themselves in research, there is at present little, if any, objective data regarding the extent of research training in psychiatric residency programs. Accordingly, an 11-item questionnaire designed to assess training opportunities and staff and resident interest in research was sent to 400 training facilities in general and child psychiatry. An 82% return rate was obtained. In general, findings suggest that while in many training centers research is viewed as unimportant and frequently given the lowest priority, most facilities appear to have ample personnel to provide adequate research training. While opportunities for research training may be "available" in most training programs for those students sufficiently motivated to seek them out, the low priority assigned to this aspect of training may deflect most residents from becoming involved in research. This is likely to leave the resident poorly equipped to engage in research activities after the completion of training. The implications of the findings for residency training are discussed.