Neurological dysfunction of the bladder in workers exposed to dimethylaminopropionitrile

Neurogenic bladder dysfunction, characterized by hesitancy, need to strain, decreased stream, and increased duration of urination, developed in 104 (63%) of 166 employees working in the manufacture of polyurethane foam. Highest rates of illness (69%) occurred in production workers, and no illness occurred in office or warehouse workers. Onset of the epidemic coincided with introduction of a catalyst, dimethylaminopropionitrile (DMAPN), and monthly case incidence rates increased as DMAPN use increased. Outbreak ceased abruptly when DMAPN use was stopped. Of eight patients who underwent neurourologic testing during recovery, seven lacked either detrusor reflex or normal sensation of bladder filling; seven had a subclinical sensory abnormality; three had prolonged sacral-evoked responses; and two of these three had limb motor neuropathies. Dimethylaminopropionitrile is unique among known neurotoxins in producing urinary symptoms more frequently than limb nerve symptoms.     

Controlled trial of clinical utility of serum salicylate monitoring in rheumatoid arthritis

A crossover double-blind controlled trial was performed on 36 patients with rheumatoid arthritis to assess the necessity for serum salicylate monitoring in determining optimal dosage. There was no clinically or statistically significant increase in the clinical improvement of patients associated with serum monitoring but potentially toxic serum levels occurred without tinnitus when serum monitoring was not used.     

Drug driving from a user's perspective

The bulk of research into drug driving in Australia has been undertaken from a road safety orientation where drug driving is viewed within the broader context of road safety and driver behaviour. Such a specific focus precludes the broader behavioural, contextual and cultural issues associated with substance use. This study aimed to address this issue by focusing on drug driving behaviour within the context of illicit substance use. A series of focused interviews were conducted with 211 illicit drug users from urban and regional centres. A consistent theme identified in the interviews was that drug driving was not necessarily viewed as risky behaviour but rather as an outcome of illicit substance use. Further, some interviewees saw their drug use as enhancing their driving skills and frequently the motor vehicle was viewed as a safe place to use. Overall there was agreement among interviewees that the likelihood of being apprehended for drug driving by police was minimal; this perception was reinforced by past experience. The lack of concern for detection of drug driving behaviour suggests that research should continue into the development and implementation of enforcement programs and roadside detection.     

Spontaneous neuronal hyperactivity in the medial and intralaminar thalamic nuclei of patients with deafferentation pain

Electrical activity was recorded from single cells in the thalamus of 10 patients with chronic pain associated with deafferentation. Under local anesthesia, these patients underwent either electrode implantation or thalamotomy for treatment of their pain. In eight of the 10 patients, single units were identified as discharging spontaneously in high-frequency, often rhythmic, bursts. The discharges were of two types: short bursts comprised of two to six spikes with a burst frequency of one to four per second; and long trains of 30 to 80 spikes of similar frequency. Reconstruction of electrode trajectories indicated that recordings were made from the region corresponding to the lateral aspect of the mediodorsal thalamic nucleus, the central lateral nucleus, a small part of the central median nucleus, and the parafascicular nucleus. In the eight patients in whom spontaneous neuronal burst activity was exhibited, it was impossible to study activity evoked by natural cutaneous stimulation due to the continuous spontaneous neuronal discharges. Both animal and human studies have suggested that pain related to deafferentation is accompanied by spontaneous hyperactivity in the dorsal horn of the spinal cord and in the ventral posterior thalamic nuclei. The authors present evidence of spontaneous neuronal hyperactivity in the intralaminar thalamic nuclei of patients with pain related to deafferentation. The findings suggest that spontaneous neuronal discharge in patients with pain related to deafferentation is more widespread in the central nervous system than has been previously appreciated. The results have important implications for the surgical treatment of chronic pain.     

Electrocardiographic abnormalities in aluminium phosphide poisoning with special reference to its incidence, pathogenesis, mortality and histopathology

Ninety-five patients out of total 190 cases of aluminium phosphide (ALP) poisoning, who exhibited ECG changes were studied for incidence, type and pattern of ECG abnormalities, their effect on mortality and their relationship with histopathology of heart. Its incidence in the present study was 50%. The arrhythmias, conduction disturbances and ischaemic pattern occurred more or less in equal frequency. Certain ECG abnormalities which had not been reported previously ie, early repolarisation syndrome, varied sino-atrial blocks, bradycardia-tachycardia syndrome and electrical alternans were observed in this study. The clinical profile of these cases was similar irrespective of whether patients had ECG abnormalities or not. Shock was the cardinal feature. There was no effect of ECG abnormalities on mortality. The mortality which was otherwise high, depended upon severity of poisoning, dose of poison consumed, duration of shock, failure of response of shock to resuscitative measures and severe hypomagnesaemia. The pathogenesis of ECG abnormalities is still obscure. Hypomagnesaemia was observed in all the 18 cases studied, irrespective of ECG abnormalities. However, these were common when hypomagnesaemia was severe. Hypoxaemia and shock were not the contributory factors for these abnormalities. Autopsy revealed stereotyped histopathological changes of toxic myocarditis independent of ECG findings.     

The effects of hyponatraemia and subarachnoid haemorrhage on the cerebral vasomotor responses of the rabbit

Impairment of cerebral autoregulation and development of hyponatraemia are both implicated in the pathogenesis of delayed cerebral ischaemia and infarction following subarachnoid haemorrhage (SAH) but the pathophysiology and interactions involved are not fully understood. We have studied the effects of hyponatraemia and SAH on the cerebral vasomotor responses of the rabbit. Cerebrovascular reactivity to hypercapnia and cerebral autoregulation to trimetaphan-induced hypotension were determined in normal and hyponatraemic rabbits before and 6 days after experimental SAH produced by two intracisternal injections of autologous blood. Hyponatraemia (mean plasma sodium of 119 mM) was induced gradually over 48 h by administration of Desmopressin and intraperitoneal 5% dextrose. Sham animals received normal saline. The cerebrovascular reactivity (% change +/- SD in cortical CBF/mm Hg PaCO2, measured by hydrogen clearance) of hyponatraemic (4.8 +/- 3.0%) and SAH (1.3 +/- 2.0%) animals was significantly less (p less than 0.05) than control (11.6 +/- 4.0%) and sham (8 +/- 2.0%) animals, whereas the reactivity of hyponatraemic-SAH animals was preserved (9.8 +/- 6.0%). Hyponatraemia and SAH alone each significantly impaired CBF autoregulation but their combined effects were not additive. Systemic hyponatraemia impairs normal cerebral vasomotor responses but does not augment the effects of experimental SAH in the rabbit.     

Relationships of plasma viscosity, coagulation and fibrinolysis to coronary risk factors and angina

Plasma viscosity, molecular markers of activated coagulation and fibrinolysis (fibrinopeptides A and B beta 15-42), coagulation factors (fibrinogen and factor VII) and antiplasmins were measured in 529 men aged 35-54 years and related to new angina pectoris (n = 117) and to coronary risk factors in controls without angina (n = 412). Five major risk factors (cigarette-smoking, blood pressure, cholesterol, triglyceride and body mass index) were each associated with increases in plasma viscosity, coagulation factors, and imbalance of coagulation over fibrinolysis (increased ratio of fibrinopeptide A/fibrinopeptide B beta 15-42). Increased viscosity and fibrinogen in smokers were partly reversed in ex-smokers, but the imbalance of coagulation and fibrinolysis persisted. Cholesterol and triglyceride were also associated with increased antiplasmin activity. In men with angina, only fibrinogen was elevated compared to controls. We suggest that increased plasma viscosity and an imbalance of coagulation over fibrinolysis may be mechanisms by which known risk factors promote arterial thrombosis, but are not present in stable angina.