scholarly journals Assessing the capacity of the sympathetic nervous system to respond to a cardiovascular challenge in human spinal cord injury

Spinal Cord ◽  
2008 ◽  
Vol 46 (10) ◽  
pp. 666-672 ◽  
Author(s):  
R Brown ◽  
V G Macefield
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Human Spinal Cord ◽  
Cord Injury ◽  
Sympathetic Nervous

scholarly journals Alpha-1 Adrenoceptor Hyperresponsiveness in Three Neuropathic Pain States: Complex Regional Pain Syndrome 1, Diabetic Peripheral Neuropathic Pain and Central Pain States Following Spinal Cord Injury

2004 ◽  
Vol 9 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Robert W Teasell ◽  
J Malcolm O Arnold
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Peripheral Neuropathy ◽  
Sympathetic Nervous System ◽  
Complex Regional Pain Syndrome ◽  
Pain Syndrome ◽  
Cord Injury ◽  
Sympathetic Nervous

The pathophysiology of the pain associated with complex regional pain syndrome, spinal cord injury and diabetic peripheral neuropathy is not known. The pain of complex regional pain syndrome has often been attributed to abnormal sympathetic nervous system activity based on the presence of vasomotor instability and a frequently reported positive response, albeit a temporary response, to sympathetic blockade. In contrast, the pain below the level of spinal cord injury and diabetic peripheral neuropathy are generally seen as deafferentation phenomena. Each of these pain states has been associated with abnormal sympathetic nervous system function and increased peripheral alpha-1 adrenoceptor activity. This increased responsiveness may be a consequence of alpha-1 adrenoceptor postsynaptic hypersensitivity, or alpha-2 adrenoceptor presynaptic dysfunction with diminished noradrenaline reuptake, increased concentrations of noradrenaline in the synaptic cleft and increased stimulation of otherwise normal alpha-1 adrenoceptors. Plausible mechanisms based on animal research by which alpha-1 adrenoceptor hyperresponsiveness can lead to chronic neuropathic-like pain have been reported. This raises the intriguing possibility that sympathetic nervous system dysfunction may be an important factor in the generation of pain in many neuropathic pain states. Although results to date have been mixed, there may be a greater role for new drugs which target peripheral alpha-2 adrenoceptors (agonists) or alpha-1 adrenoceptors (antagonists).

Leptin response to short-term fasting in sympathectomized men: role of the SNS

2003 ◽  
Vol 284 (3) ◽  
pp. E634-E640 ◽  
Author(s):  
Justin Y. Jeon ◽  
Vicki J. Harber ◽  
Robert D. Steadward
Keyword(s):  
Body Mass Index ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Short Term ◽  
Cord Injury ◽  
Before And After ◽  
Sympathetic Nervous ◽  
Plasma Leptin

We studied plasma leptin levels in six people with high-lesion spinal cord injury [SCI; body mass index (BMI) 25.9 ± 1.5 kg/m2, age 37 ± 3.0 yr] and six able-bodied (AB) controls (BMI 29.1 ± 1.9 kg/m2, age 35 ± 3.5 yr) before and after 12, 24, and 36 h of fasting. The plasma leptin levels significantly decreased during 36 h fasting by 48.8 ± 4.5% (pre: 11.3 ± 2.3, post: 6.2 ± 1.5 ng/ml) and 38.6 ± 7.9% (pre: 7.6 ± 5.0, post: 4.2 ± 1.0 ng/ml) in SCI and AB, respectively. Plasma leptin started to decrease at 24 h of fasting in the SCI group, whereas plasma leptin started to decrease at 12 h of fasting in the AB group. The current study demonstrated that plasma leptin decreased with fasting in both SCI and AB groups, with the leptin decrease being delayed in the SCI group. The delayed leptin response to fasting in the SCI group may be because of increased fat mass (%body fat, SCI: 33.8 ± 3.0, AB: 24.1 ± 2.9) and sympathetic nervous system dysfunction.

Spinal Cord Injuries the Facts of Neuropathology: Opportunities and Limitations

2019 ◽  
Vol 1 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Byron A Kakulas
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Wallerian Degeneration ◽  
Spinal Cord Injuries ◽  
Neurological Status ◽  
Research Projects ◽  
Human Spinal Cord ◽  
The Third ◽  
Cord Injury

It is essential for research projects which are undertaken to find a “cure” for human spinal cord injury (SCI) to be consistent with the neuropathological facts of the disorder. In this respect there are three main points to be taken into account. Firstly, the researcher should be aware that simple transection of the spinal cord is not a feature of human SCI. The usual lesion is one of compression and disruption with haemorrhage. The second and most important aspect of human SCI is to understand that Wallerian degeneration inevitably ensues following disruption of the axon. Wallerian degeneration is progressive and inexorable and unlike the peripheral nervous system CNS axons do not regenerate. The third and more helpful fact is that in the majority (71%) of SCI autopsies a small amount of white matter, myelin and axons, was found to be preserved at the level of injury. Re-activation of these dormant, axons offers the opportunity for improvement of the SCI patient’s neurological status by means of restorative neurology (RN).

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