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I read with interest the paper by Abe et al1 on occipital and posterior parietal hypoperfusion in 28 Parkinson’s disease (PD) patients without dementia. These findings suggest that there was a reduced regional cerebral blood flow (rCBF) in the intraparenchymal territory of the posterior cerebral arteries (PCAs) probably due to the presence of atheromatous plaques located in the distal end of the basilar artery.2 Atherosclerotic changes are of considerable importance because they can cause stenosis and/or occlusion at the origin of the terminal (PCAs) or collateral (superior cerebellar arteries) branches, as well as of the posterior perforating arteries (PPAs).
Based on the fact that in situ the donor tissues of catecholamines are normally highly vascularised and by contrast in PD the rCBF is reduced in the neostriatum, from February 1988 to December 2002 we have used two surgical procedures to treat PD:3–5 (1) transplantation of adrenal medulla into the putamen by a transinsular pathway, and (2) omental transplantation on the interpeduncular fossa, anterior perforated space, and insular cortex in 16 patients with moderate or advanced stages of PD. Thus, omental tissue revascularises to the catecholaminergic (dopaminergic and noradrenergic) nuclei, as well as to the surrounding structures, and moreover prolongs the survival of the graft implanted in the putamen. In all patients, neurological improvement was better during the first weeks after surgery than in the following months or years. Our third patient is the same case previously reported by us.3 At present, 15 years postoperatively, she has only slight tremor on the left leg and does not require anti-parkinsonian medication. She occasionally receives 1 mg of clonazepam at night. Her quality of life is good and she manages the daily living activities similar to any normal woman of her age.
In conclusion, the vascular impairment described by Abe and colleagues supports the autopsy findings2 and neurosurgical results.3–5 Clinical data suggest that PD is initiated in the intraparenchymal territory of the PPAs caused by atherosclerotic plaques located at the mouths of these arteries. Therefore, we believe that Parkinson’s disease is wrongly classified as a neurodegenerative disorder.
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