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1. |
Introduction |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 1-1
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ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02569.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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2. |
Current Concepts of Diabetes |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 2-12
J. Vallance‐Owen,
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ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02570.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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3. |
The Neuropathology of Parkinson's Disease |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 7-13
M. J. Eadie,
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摘要:
Summary:For almost 100 years after Parkinson's original description there was uncertainty as to whether there was any structural brain pathology in idiopathic Parkinsonism, or, if there was, whether the lesions were situated in(a) the spinal cord(b) the mid‐brain and substantia nigra(c) the striatum, pallidum, thalamus and mid‐brainThen, in 1913, Lewy2studied 20 Parkinsonian brains and found changes in the cerebral cortex, caudate nucleus, putamen, globus pallidus, certain fibre tracts in the basal ganglia, the substantia innominata and the dorsal vagal nucleus. As well as cell loss and gliosis there were neurofibrillary changes in neurons, and laminated inclusion bodies (Lewy bodies). Except for changes in the substantia nigra Lewy described practically all the microscopic lesions of idiopathic Parkinsonism. The nigral changes were emphasised by many later authors, and came to be regarded as the most common, if not the essential, lesions of Parkinsonism. However, the currently available evidence suggests that bilateral substantia nigra lesions alone are not a sufficient explanation for Parkinsonism.At the present time, at least three problems face those who would interpret the neuropathology of Parkinsonism:(i) what is the meaning of the Lewy body?(ii) what is the correlation between regional brain lesions and different aspects of Parkinsonian dysfunction ?(iii) could Parkinsonism be the clinical expression of a chemical disorder in monoaminergic neurons, with structural alterations a late effect of the underlying chemical chan
ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02559.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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4. |
Evidence for Intravenous Dipyridamole (Persantin) Producing a “Coronary Steal” Effect in the Ischaemic Myocardium |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 8-14
D. E. L. Wilcken,
H. J. Paoloni,
E. Eikens,
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摘要:
Summary:We studied thirteen patients before and after a five‐minute infusion of intravenous dipyridamole (Persantin) (0.6 mg/kg). In ten patients with no evidence of ischaemic heart disease there were only modest increases in cardiac output (+17%) and heart rate (+16%), and decreases in systemic resistance (‐24%), pulmonary capillary pressure (‐19%), and mean blood pressure (‐10%), five minutes after dipyridamole. Values returned towards control levels ten minutes later; there were no symptoms. By contrast, two patients with ischaemic heart disease developed acute coronary insufficiency after dipyridamole. ECG changes indicated acute ischaemia in the region of the previous infarct. Used diagnostically in a third patient, with the patient's consent, dipyridamole produced symptoms and haemodynamic changes of angina pectoris.We concluded that dipyridamole caused moderate peripheral vasodilatation in the patients without evidence of coronary artery disease. The findings in the patients with ischaemic heart disease are consistent with the hypothesis that dipyridamole produced a shunting of blood away from ischaemic areas in the myocardium by reducing coronary vascular resistance more in well perfused areas than in ischaemic areas–a “coronary steal” effect.Recent reports suggest that dipyridamole (Persantin) reduces platelet aggregation1–4. This effect has been the rationale for the use of dipyridamole with anticoagulants in the prevention of thromboembolic complications of prosthetic valve replacement5and in the treatment of acute renal failure due to glomerulonephritis6and rejection of the transplanted kidney7.It is possible that repeated attacks of “crescendo” angina pectoris and acute coronary insufficiency, which frequently culminate in myocardial infarction, could be due to recurrent embolisation of platelet aggregates forming on an atheromatous plaque in a major coronary vessel. If this hypothesis is correct, infusions of dipyridamole might be useful therapeutically. We undertook a study of the effects of dipyridamole on plateletss and in the course of this we noted important and unexpected circulatory effects of the drug in two patients with coronary artery disease. This prompted us to investigate the circulatory effects of dipyridamole and this paper reports our findings; some of the results have already been r
ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02254.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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5. |
Current Therapy of Diabetes and its Rationale |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 13-21
J. R. Turtle,
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ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02571.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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6. |
The Biochemistry of Catecholamines in Relation to Parkinson's Disease |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 14-18
H. Hinterberger,
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摘要:
Summary:The effect of oral doses of 2–9 g L‐3, 4‐dihydroxyphenylalanine (L‐dopa) on the metabolism of catecholamines was studied in 14 patients with Parkinson's Disease being treated simultaneously with cholinolytic medication.Comparison of the excretion in urine of free and conjugated noradrenalin and adrenalin showed no significant differences before and after three months of medication with L‐dopa. Vanilmandelic acid was moderately increased, indicating stimulation of catecholamine turnover well controlled by homeostatic mechanisms. The excretion of free and conjugated 3, 4‐dihydroxyphenylethyla‐mine (dopamine) and its acidic metabolites 3, 4‐dihydroxyphenylacetic acid and homovanillic acid was increased by a factor of 103‐104.Peak levels of L‐dopa in plasma were observed 1 ‐5‐3 hours after an oral dose and were found to vary considerably between patients. No relation between plasma levels and improvement scores could be observed.Levels of L‐dopa, homovanillic acid, 3, 4‐dihydroxyphenylacetic acid and 5‐hydroxyindoleacetic acid were measured in lumbar fluid obtained 4–6 hours after ingestion of an oral dose. These levels increased with increasing daily dose (mg/kg). Although the absolute amount of homovanillic acid did not closely follow clinical improvement, absence of homovanillic acid in the CSF was noted in two
ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02560.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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7. |
Autonomic Dysfunction with Orthostatic Hypotension1,2 |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 15-21
Richard J. Burns,
John A. Downey,
Derek B. Frewin,
Robert F. Whelan,
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摘要:
Summary:Three cases of orthostatic hypotension with autonomic failure are presented and the physiological tests which were performed to assess the extent of their autonomic loss discussed.In one patient, the diagnosis of widespread amyloid disease was made at autopsy, while in another patient, who is still living, amyloid material was found in a biopsy from the sural nerve. In both patients, rectal biopsy had been negative for amyloid. Rectal biopsy was also negative for amyloid in the third patient, though a sural nerve biopsy was not performed in her case.The treatment of orthostatic hypotension arising from autonomic failure is briefly discussed.Autonomic failure with orthostatic hypotension and loss of sweating was first described by Bradbury and Eggleston in 19251. Since then, several case reports have been published2,3of patients who also had loss of sphincter control and impotence. The patients may be divided into two groups, i.e. a group where the symptoms are secondary to a recognised disease, such as diabetes mellitus, amyloidosis or tabes dorsalis, and a second group for which no cause can be found. This paper describes three patients with autonomic dysfunction and the physiological tests which were performed to assess the extent of their autonomic loss. One of the patients died and, at autopsy, was found to have widespread amyloid disease. Studies on the two other patients, still living, are reported, and in one, a brother of the deceased patient, nerve biopsy shows the presence of amyloid.
ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02255.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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8. |
Pathophysiology of Parkinson's Disease |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 19-23
J. G. McLeod,
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摘要:
Summary:Parkinson's Disease is a disorder of the extrapyramidal system, and its major clinical manifestations are rigidity, tremor and akinesia.The extrapyramidal system takes origin from the cerebral cortex and from basal ganglia and other subcortical nuclei. It controls movement by its influence on the alpha and gamma motoneurones in the spinal cord through the reticulospinal, vestibulospinal and rubrospinal tracts.The rigidity of Parkinson's Disease is basically of a plastic type; the cogwheel effect is caused by the superimposed tremor. The increased muscle tone may be caused by an increase in the background gamma efferent activity to the muscle spindles, or by hyperexcitability of the alpha motoneurones.The frequency of the resting tremor in Parkinson's Disease is 3–5 cycles/sec. It is caused by an imbalance of excitatory and inhibitory activity to the ventrolateral nucleus of the thalamus which results from disease of the substantia nigra and globus pallidus. The spontaneous rhythmical activity is transmitted to the periphery by way of the pyramidal tract and section or disease of this tract will abolish the tremor.The mechanism of the akinesia, loss of postural control, and gait disturbance in Parkinson's Disease is not clear but is probably related to disease of the substantia nigra, since experimental lesions of the structure result in poverty of movemen
ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02561.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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9. |
The Pharmacology and Metabolism of Oral Antidiabetic Drugs |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 22-30
A. Bänder,
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ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02572.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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10. |
Electromyographic Studies of Parkinsonian Patients |
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Australian and New Zealand Journal of Medicine,
Volume 1,
Issue 1,
1971,
Page 24-28
C. J. Andrews,
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摘要:
Summary:A quantitative electromyographic study of rigidity in 20 Parkinsonian patients demonstrated that the stretch reflex in biceps was more affected than that of triceps, and of hamstrings more than quadriceps.Increasing disability from Parkinsonian rìgìdity was found to be associated with a lowered sensitivity of the stretch reflex to the dynamic phase of stretch and an increase in the static response to maintained stretch. Treatment with L‐dopa for six months reversed this pattern in extensor muscles much more readily than in flexor muscles. Since animal experiments have shown that L‐dopa diminishes the fusimotor activity of dynamic flexor muscles by its action on the spinal cord, and that the spinal action of L‐dopa can be blocked by phenoxy‐benzamine, the latter agent has been used in Parkinsonian patients who were under treatment with L‐dopa.Phenoxybenzamine was given to five Parkinsonian patients intravenously and one patient orally. In all patients the dynamic sensitivity of the stretch reflex in flexor muscles improved and rigidity was diminished. Three patients treated with oral phenoxybenzamine showed subjective and objective clinical improvement. This study suggests that the effect of L‐dopa on the spinal cord limits its effectiveness in the treatment of Parkinson's Disease and that this undesirable action may be eliminated by the concomitant use of phe
ISSN:0004-8291
DOI:10.1111/j.1445-5994.1971.tb02562.x
出版商:Blackwell Publishing Ltd
年代:1971
数据来源: WILEY
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