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AIM: To assess the knowledge of Waikato medical practitioners concerning cardiac pacing and its indications. METHOD: Anonymous postal questionnaire. The responses received were compared with those of four New Zealand experts on cardiac pacing. RESULTS: 404 questionnaires were administered of which 204 (50%) were returned, (16.3% physicians, 22.7% JRMO's 61% general practitioners). Virtually all had ready access to diagnostic facilities and were satisfied with the service offered. Physicians were more likely to have referred patients and to have had personal experience with pacing. Practical matters, such as costs and length of the procedure were reasonably well appreciated. The complexity of the procedure, however, was overestimated. Pacemaker function was poorly understood. All practitioner groups were less likely to refer for pacing compared with the experts, but were more likely to refer in the presence of recurrent symptoms, particularly if the patient was elderly. CONCLUSION: A conservative approach to referral for permanent pacing exists in the Waikato region and this is unrelated to access to diagnostic facilities or referral difficulties.

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Quantitative EEG changes were studied during cocaine withdrawal in 36 subjects. All subjects had used cocaine orally (n = 28) or intravenously (n = 8) within 48 h of admission to an inpatient unit. EEGs were recorded 2 and 6 days following admission. Nine subjects returned for a 1-month follow-up EEG. Modal EEG frequency significantly decreased on day 6 compared to day 2. The most dramatic change in both absolute and relative power from day 2 to day 6 was a decrease in the beta 2 (18-26 Hz) band. Those subjects who returned for the 4-week follow-up showed a further decrease in beta 2 power. Power in the beta 2 band was significantly greater for the intravenous users than for the smokers, and the decrease in power from day 2 to day 6 was also significantly greater in this group. While acute effects of cocaine on the EEG have been reported to last only several hours, this study indicates that chronic use may cause longer lasting neuroadaptive changes, particularly in those who have used cocaine intravenously.

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Proposals suggesting monetary compensation of organ donors to increase donation rates for transplantation are founded on the ethical premise that the principal criterion for organ procurement policy should be patients' health and not the personal preferences and philosophies of policymakers. In this paper, we argue that a market-based organ procurement system is superior to both the current altruistic-based system and a system based on compensation without a market. A market system would address both the problem of potential donors refusing to donate and that of their never being asked, whereas the altruistic system addresses neither problem and a system of compensation addresses only the former. Empirical evidence suggests that the latter (not being asked) is the predominant cause of the current shortage of organs. Our discussion shows that collection rates are likely to be substantially higher under a market system.

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The frequency of shoulder disturbances, particularly frozen shoulder, has not been assessed previously in Parkinson's disease. In a survey of 150 patients compared with 60 matched control subjects a significantly higher incidence of both a history of shoulder complaints (43% vs. 23%) and frozen shoulder (12.7% vs. 1.7%) was found in the Parkinson's disease population. Those developing a frozen shoulder had initial disease symptoms indicative of akinesia twice as frequently as tremor while the ratio was reversed in those without frozen shoulder. In at least 8% of the patients frozen shoulder was the first symptom of disease, occurring 0-2 years prior to the onset of more commonly recognised features. Parkinson's disease should be added to the list of causes of frozen shoulder, and clinicians must be aware that the latter is often the presenting symptom of Parkinson's disease.

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The parkinsonism that occurs in some patients with olivopontocerebellar atrophy (OPCA) can cause diagnostic confusion with idiopathic Parkinson's disease (IPD). The response to levodopa is usually a distinguishing feature, the OPCAs either failing to benefit or losing efficacy relatively quickly. A fluctuating response to levodopa in those OPCA patients who do benefit has not been emphasized in the literature previously. Reported here are three patients with presumed OPCA, dominated by parkinsonian features, who eventually developed typical fluctuations with morning akinesia, wearing off, and periodic lack of response related to meals. These fluctuations were a major source of disability and an important reason for diagnostic confusion with IPD. The possible mechanisms of these fluctuations are discussed.

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This update reviews several important topics in the field of Parkinson's disease, including etiologic studies, the types and mechanisms of drug complications and their treatment, when and how to begin treatment, the association of dementia with Parkinson's disease, and the development of the newer research tools. The recent discovery of a highly selective neurotoxin (MPTP) that causes parkinsonism in humans and other primates and the use of positron emission tomography in living patients should improve our understanding of the cause of cell death in Parkinson's disease and assist in the development of more definitive treatment for this common, disabling neurologic condition.

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Most workers have found use of shunts unworkable as a means of access for home parenteral nutrition. Our experience using arteriovenous loop vein grafts for this purpose is described including any problems encountered. One shunt could not be established. In four other patients arteriovenous loop vein grafts have been used successfully. They are in our opinion superior to indwelling catheters as a means of access in long-term patients.

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The segmented EMG activity in flexor carpi radialis to imposed wrist movements was studied in 18 hemiplegic subjects with vascular lesions of the sensorimotor cortex or internal capsule and compared to that in age-matched normal subjects. The segmented EMG activity in the stretched muscle was normalized against the maximum M response elicited by electrical stimulation of its peripheral nerve in hemiplegic and normal subjects. This M response was used to estimate the maximal activity of the motoneuron pool. Twelve of the hemiplegic patients showed a stereotyped abnormal segmentation pattern of the EMG activity characterized by: an increased M1 segment of prolonged duration with both an increased sensitivity to low initial velocities of displacement and an increased slope of the input-output relationship for the range of velocities tested; absent or diminished activity during the interval of the normal M2-3 segment; and a late component not evident in normal subjects. The increased magnitude of the EMG activity during the M1 interval, markedly exceeded the normal range of control values. A method to demonstrate the response distribution of the interrelationship of the magnitude of the M1 segment using two variables (background EMG activity and initial velocity) for individual responses rather than average responses is presented. The results of the study indicate that: the increased excitability, reflected in the enhanced EMG over the M1 segment does not result from increased levels of resting alpha motoneuron activity and may result from disruption of polysynaptic internuncial influences on alpha motoneurons; the absent or diminished activity over the interval of the normal M2-3 segment may partially result from the interruption of a transcortical reflex by the vascular lesions.

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The amplitude and temporal modulation of the segmented EMG activity in flexor carpi radialis, evoked by imposed angular wrist extension, was studied with respect to the level of pre-existing background activity in rigid parkinsonian (PK) and dystonia musculorum deformans (DMD) patients. The interdependence of the evoked M1 and M2-3 segments on pre-existing background EMG activity and initial velocity of imposed displacement was established previously for a normal population. Individual responses of 21 parkinsonian and 12 dystonic patients were compared to the established normal "response volume". The augmented magnitude of the M2-3 segment in rigid PK patients, which correlates to the measure of rigidity, could not be accounted for by the low level of pre-existing EMG activity. Therefore, increased descending facilitation does not impinge directly on alpha motoneurons. Paradoxical excitation in the shortened muscle and resetting of tonic tremor of the stretched muscle by the imposed wrist extension are two other demonstrated abnormalities which may also contribute to PK rigidity. In contrast, DMD patients demonstrated normal amplitude modulation of the M1 and M2-3 segments, but exhibited a disturbance of normal temporal mechanisms that result in constant duration of the M1 and M2-3 responses with imposed force step loads.

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The electromyographic (EMG) activity following a sudden stretch applied to wrist flexor or extensor muscles was investigated using a method which enabled the individual records and cumulative results of 30 trials to be observed simultaneously. The results showed that in each case the spinal reflex EMG burst was followed by one or two additional reflex bursts. The second of these latter bursts, when present, occurred in one of two distinct latency ranges. Thus, three distinct latency ranges were observed for reflex bursts following the spinal reflex burst. A possible explanation for these results is that there are three distinct long-loop reflexes, one or two of which may be active following a muscle stretch. The present results do not distinguish whether any or all of these long-loop reflexes are segmental or supraspinal in origin.

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Evidence has recently been presented indicating that muscle stretch reflexes have a large supraspinal component. The finding introduces the possibility that stretch reflex parameters may be modifiable by stimuli involving other modalities besides stretch. In this investigation, the effects of a visual cue on the reflex portions of the EMG activity following a sudden muscle stretch were examined. The results, obtained from the flexor carpi radialis muscles of six normal awake subjects, failed to show any significant change in the EMG parameters as a result of visual cues occurring at the instant of onset of muscle stretch. This was interpreted as indicating that visual inputs do not reach the areas of brain involved in the supraspinal reflex in sufficient time to modify the reflex.

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