cell body reorganization in the spinal cord after sympathectomy

The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Wednesday, August 14, 2013

cilio-spinal center can extend to T5


The ciliospinal reflex (pupillary-skin reflex) consists of dilation of the ipsilateral pupil in response to pain applied to the neck, face, and upper trunk. If the right side of the neck is subjected to a painful stimulus, the right pupil dilates (increases in size 1-2mm from baseline). This reflex is absent in Horner's syndrome and lesions involving the cervical sympathetic fibers. The enhanced ciliospinal reflex in asymptomatic patients with cluster headache is due to preganglionic sympathetic mechanisms.
http://en.wikipedia.org/wiki/Ciliospinal_reflex


The cilio-spinal center is not sharply confined to TI spinal level, but may extend downwards as low as T5

Tuesday, August 6, 2013

High plasma norepinephrine and depression

Copyright © 1999 Society of Biological Psychiatry. Published by Elsevier Science Inc.

Plasma norepinephrine and prediction of outcome in major depressive disorder
Timothy G. Johnstona, Christopher B. Kelly, a, Michael R. Stevensonb and Stephen J. Coopera 
a Department of Mental Health, Whitla Medical Building, The Queen’s University of Belfast, Belfast, UK (TGJ, CBK, SJC)
b Department of Medical Statistics, Mulhouse Building, The Queen’s Unversity of Belfast, Belfast, UK (MRS)
Received 1 February 1999; revised 17 May 1999; accepted 21 May 1999. Available online 30November 1999.
Background: Several epidemiologic and clinical factors have been shown to predict long term outcome in major depressive disorder (MDD). The value of biological predictors has not been extensively studied. This study examined whether plasma norepinephrine may be useful in predicting outcome in MDD.
Methods: Forty patients were followed up 8 years after an index major depressive episode. Three outcome variables were assessed: time to first recurrence (the primary outcome measure), the Lee and Murray criteria and the Depression Outcome Scale (DOS). The results were examined against plasma norepinephrine value, at the index episode, using survival analysis and linear regression.

Results: High plasma norepinephrine at the index episode was positively and significantly associated with time to first recurrence for patients with nonpsychotic MDD (n = 31, χ2 = 8.38, on 1 df, p < .01). Similarly, plasma norepinephrine was significantly associated with good global outcome, both using Lee and Murray criteria (n = 34, adjusted R2 = .24, p < .01) and DOS criteria (n = 31, adjusted R2 = .17, p < .01) for this group of patients. In contrast, plasma norepinephrine was not significantly related to outcome for MDD with psychotic features.
Conclusions: Plasma norepinephrine at index episode seems to be a predictor of outcome in MDD.

A neurotransmitter involved in emotional arousal enhances learning

A neurotransmitter involved in emotional arousal enhances learning by phosphorylating glutamate receptors.

Do you remember the song that was playing during your first kiss? Both positive and negative emotions influence learning and memory but researchers have not determined the mechanism. Now Hu et al. report that the neurotransmitter norepinephrine regulates glutamate receptor trafficking in a recent article in Cell.
Axon terminals containing norepinephrine synapse in the hippocampus and amygdala, which are important in emotional memory. In the hippocampus, norepinephrine reduces the threshold for long-term potentiation (LTP), which is thought to be a substrate of memory. Norepinephrine acts at pastedGraphic.pdf-adrenergic receptors, where it activates cAMP-dependent protein kinase (PKA) and calcium/calmodulin-dependent protein kinase II (CaMKII). These kinases phosphorylate serines 845 and 831, respectively, in the AMPA glutamate receptor type 1 (GluR1). The authors proposed that norepinephrine regulates learning by phosphorylating AMPA receptors.
Hu, H. et al. Emotion enhances learning via norepinephrine regulation of AMPA-receptor trafficking. Cell 131, 160–173 (2007). | Article | PubMed |


Emotional intelligence
Neuroscience Gateway (October 2007) | doi:10.1038/aba1787

Thursday, August 1, 2013

RSD due to nerve injury


According to the National Institute of Neurological Disorders and Stroke (NINDS), RSD is "a chronic pain condition that is believed to be the result of dysfunction in the central or peripheral nervous systems." According to MedicineNet, RSD involves "irritation and abnormal excitation of nervous tissue, leading to abnormal impulses along nerves that affect blood vessels and skin."
Animal studies indicate that norepinephrine, a catecholamine released from sympathetic nerves, acquires the capacity to activate pain pathways after tissue or nerve injury, resulting in RSD. Another theory suggests that RSD, which follows an injury, is caused by triggering an immune response and symptoms associated with inflammation (redness, warmth, swelling). RSD is not thought to have a single cause, but rather multiple causes producing similar symptoms.
http://arthritis.about.com/od/rsd/a/rsd.htm
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