The parasympathetic innervation of the spleen: are we chasing a ghost?

2021 ◽  
Author(s):  
Laurent Gautron
2021 ◽  
Vol 11 (2) ◽  
pp. 455-474
Author(s):  
Per Borghammer

A new model of Parkinson’s disease (PD) pathogenesis is proposed, the α-Synuclein Origin site and Connectome (SOC) model, incorporating two aspects of α-synuclein pathobiology that impact the disease course for each patient: the anatomical location of the initial α-synuclein inclusion, and α-synuclein propagation dependent on the ipsilateral connections that dominate connectivity of the human brain. In some patients, initial α-synuclein pathology occurs within the CNS, leading to a brain-first subtype of PD. In others, pathology begins in the peripheral autonomic nervous system, leading to a body-first subtype. In brain-first cases, it is proposed that the first pathology appears unilaterally, often in the amygdala. If α-synuclein propagation depends on connection strength, a unilateral focus of pathology will disseminate more to the ipsilateral hemisphere. Thus, α-synuclein spreads mainly to ipsilateral structures including the substantia nigra. The asymmetric distribution of pathology leads to asymmetric dopaminergic degeneration and motor asymmetry. In body-first cases, the α-synuclein pathology ascends via the vagus to both the left and right dorsal motor nuclei of the vagus owing to the overlapping parasympathetic innervation of the gut. Consequently, the initial α-synuclein pathology inside the CNS is more symmetric, which promotes more symmetric propagation in the brainstem, leading to more symmetric dopaminergic degeneration and less motor asymmetry. At diagnosis, body-first patients already have a larger, more symmetric burden of α-synuclein pathology, which in turn promotes faster disease progression and accelerated cognitive decline. The SOC model is supported by a considerable body of existing evidence and may have improved explanatory power.


1994 ◽  
Vol 252 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Asunción Morán ◽  
Cristina Velasco ◽  
Maria-Luisa Martín ◽  
Luis San Román

2000 ◽  
Vol 42 (4) ◽  
pp. 219-224 ◽  
Author(s):  
Argenis TORRES ◽  
Diego F. DÁVILA ◽  
Carlos F. GOTTBERG ◽  
Jose H. DONIS ◽  
Gabriela ARATA DE BELLABARBA ◽  
...  

We administered arecoline to rats, with experimentally induced chagasic myocarditis, in order to study the sinus node sensitivity to a muscarinic agonist. Sixteen month old rats were inoculated with 200,000 T. cruzi parasites ("Y" strain). Between days 18 and 21 (acute stage), 8 infected rats and 8 age-matched controls received intravenous arecoline as a bolus injection at the following doses: 5.0, 10.0, 20.0, 40.0, and 80.0 mug/kg. Heart rate was recorded before, during and after each dose of arecoline. The remaining 8 infected animals and 8 controls were subjected to the same experimental procedure during the subacute stage, i.e., days 60 to 70 after inoculation. The baseline heart rate, of the animals studied during the acute stage (349 ± 68 bpm, mean ± SD), was higher than that of the controls (250 ± 50 bpm, p < 0.005). The heart rate changes were expressed as percentage changes over baseline values. A dose-response curve was constructed for each group of animals. Log scales were used to plot the systematically doubled doses of arecoline and the induced-heart rate changes. The slope of the regression line for the acutely infected animals (r = - 0.99, b =1.78) was not different from that for the control animals (r = - 0.97, b = 1.61). The infected animals studied during the subacute stage (r = - 0.99, b = 1.81) were also not different from the age-matched controls (r = - 0.99, b = 1.26, NS). Consequently, our results show no pharmacological evidence of postjunctional hypersensitivity to the muscarinic agonist arecoline. Therefore, these results indirectly suggest that the postganglionic parasympathetic innervation, of the sinus node of rats with autopsy proved chagasic myocarditis, is not irreversibly damaged by Trypanosoma cruzi.


1991 ◽  
Vol 23 (2) ◽  
pp. 181-186
Author(s):  
L. P. Voitenko ◽  
B. S. Polinkevich ◽  
T. V. Beregovaya ◽  
L. Ya. Shtanova ◽  
S. D. Groisman

2011 ◽  
Vol 14 (2) ◽  
pp. 94-97
Author(s):  
Irina Alekseevna Kurnikova ◽  
Tatiana Evgen'evna Chernyshova ◽  
Irina Vladimirovna Gur'eva ◽  
Guzyal' Ilgisovna Kliment'eva

Aim. To estimate dynamics of secretory and motor-evacuational functions of the stomach in patients with type 1 diabetes mellitus and gastrointestinalform of diabetic neuropathy. Materials and methods. 32 patients with DM1 without gastrointestinal pathology allocated to different groups depending on DM duration (gr. 1 lessthan 10 yr, gr. 2 over 10 yr). Vegetative equilibrium was estimated from the Kerdo index, rehabilitative potential from its basic constituent (morphophysiologicalindex). The motor-evacuational function of the stomach was studied with the use of a scintillation gamma-chamber, the gastric secretoryfunction by pH measurements. Results. Half of the patients in gr 2 presented with hypersympathicotony. The frequency of hypertonic form of gastric tone increased with durationof DM while the acid-producing and evacuational functions of the stomach decreased (as estimated by pH-measurement and gastroscintiographyrespectively). The propulsive function most significantly decreased in the pyloric part. The efficacy of rehabilitation of diabetic patients with gastrointestinalform of diabetic neuropathy was much lower than in those with preserved vegetative function of the stomach. Conclusion. Impairment of evacuational function of the stomach and duodenum with DM1 duration may be a cause of unstable blood glucose level.Hypomotor dyskinesia of the upper gastrointestinal tract due to DM1 and deficit of parasympathetic innervation occurs more frequently in patientswith low rehabilitative potential. Functional changes in the gastrointestinal tract of DM1 patients do not depend on the quality of compensation ofmetabolic disorders but correlate (r=-0.39) with DM duration. It is concluded that the gastrointestinal form of diabetic neuropathy impairs rehabilitativepotential of fhe patients.


2011 ◽  
pp. 158-161
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak ◽  
Robert B. Daroff

A tonic pupil is caused by a lesion affecting the postganglionic parasympathetic innervation of the pupil. It can be an incidental finding on examination or associated with visual symptoms, such as photophobia or blurred vision at near. We discuss the common causes and diagnostic evaluation of a tonic pupil in this chapter.


2010 ◽  
Vol 76 (3) ◽  
pp. 253-262 ◽  
Author(s):  
Petros Mirilas ◽  
John E. Skandalakis

We present surgicoanatomical topographic relations of nerves and plexuses in the retroperitoneal space: 1) six named parietal nerves, branches of the lumbar plexus: iliohypogastric, ilioinguinal, genitofemoral, lateral femoral cutaneous, obturator, femoral. 2) The sacral plexus is formed by the lumbosacral trunk, ventral rami of S1–S3, and part of S4; the remainder of S4 joining the coccygeal plexus. From this plexus originate the superior gluteal nerve, which passes backward through the greater sciatic foramen above the piriformis muscle; the inferior gluteal nerve also courses through the greater sciatic foramen, but below the piriformis; 3) sympathetic trunks: right and left lumbar sympathetic trunks, which comprise four interconnected ganglia, and the pelvic chains; 4) greater, lesser, and least thoracic splanchnic nerves (sympathetic), which pass the diaphragm and join celiac ganglia; 5) four lumbar splanchnic nerves (sympathetic), which arise from lumbar sympathetic ganglia; 6) pelvic splanchnic nerves (nervi erigentes), providing parasympathetic innervation to the descending colon and pelvic splanchna; and 7) autonomic (prevertebral) plexuses, formed by the vagus nerves, splanchnic nerves, and ganglia (celiac, superior mesenteric, aorticorenal). They include sympathetic, parasympathetic, and sensory (mainly pain) fibers. The autonomic plexuses comprise named parts: aortic, superior mesenteric, inferior mesenteric, superior hypogastric, and inferior hypogastric (hypogastric nerves).


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