PÄIVI POHJAVAARA
SOCIAL PHOBIA: AETIOLOGY, COURSE
AND TREATMENT WITH ENDOSCOPIC
SYMPATHETIC BLOCK (ESB)
A qualitative study of the development of social phobia
and its meaning in people's lives and a quantitative study
of ESB as its treatment
Academic Dissertation to be presented with the assent of
the Faculty of Medicine, University of Oulu, for public
discussion in the Väinö Pääkkönen Hall of the Department
of Psychiatry, on December 3rd, 2004, at 12 noon.
Thanks to modern research techniques, we know a lot of the location of attention, emo-
tion and arousal modulation in the brain. Arousal requires involvement of the brain stem,
the thalamus and the cortex, while attention is maintained by the function of the right
frontal lobe (Kaplan & Sadock 1998, Nagahama et al. 2001). The amygdala rates the
emotional importance of an experience, and the limbic system is the centre of human
drives, whose regulation appears to require an intact frontal cortex. Crude emotions are
produced and handled in the midbrain structures and the olfactory cortex, while distinct-
ly human emotions are generated in the cortex (Kaplan & Sadock 1998).
Homeostatic responses mediated by the autonomic
nervous system are achieved by altering the balance between the sympathetic, parasympa-
thetic and different hormonal systems (Mosqueda-Garcia 1996). The most apparent link
between the autonomic and endocrine systems is manifested by the interactions between
the adrenal cortex and the adrenal medulla.
The neuroanatomical circuits, which support fear and anxiety behaviour, are modulated
by a variety of chemical neurotransmitter systems (Charney 2003). These include the
peptidergic neurotransmitters, corticotrophin-releasing hormone (CRH), neuropeptide
Yand substance P, the monoaminergic transmitters, norepinephrine, serotonin and dopam-
ine, and the amino acid transmitters, gamma-aminobutyric acid and glutamate.
The connection between the sympathetic nervous system and the psyche is best seen in
anxiety and especially in social phobia. The observed usefulness of beta-adrenergic antag-
onists in performance phobia supports this hypothesis (Sutherland & Davidson 1995).
There are studies indicating possible supersensitivity of the central serotonin systems in
social phobia and schizophrenia patients (Tancer et al. 1995, Malhotra et al. 1998). It has
been shown using SPECT (Pirker et al. 2000) that, in a solitary case study, the decreased
5-HTT activity of a social phobic patient was normalized by a sympathetic block (Kuikka
et al. 2000). Among the many neurotransmitters implicated in social anxiety disorder, the
complex interactions between the noradrenergic and serotonergic systems and the HPA
axis overlap those found seen in fear and anxiety (Marcin & Nemeroff 2003).
The physical symptoms of social phobia might be treated by blocking the sympathetic
system at the upper thoracic level with a surgical procedure (Crozier 2001, Telaranta
1998). Sympathectomy was first used to treat the exophthalmos of Basedow disease
(Jonnesco 1896) and angina pectoris (Le Riche 1913, Jonnesco 1921) in the late 19th and
early 20th centuries. Its beneficial effect on the treatment of facial sweating was noticed
as early as the 1930s, and its impact on palmar sweating was reported in the 1950s, when
the procedure was already carried out endoscopically (Kux 1954).
"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding." Associate Professor Robert Boas, Faculty of Pain Medicine of the Australasian College of Anaesthetists and the Royal College of Anaesthetists, The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 258-260
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
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