there are no reports of phantom sweating without a prior sympathectomy

Phantom sweating - a novel autonomic paresthesia

L. L. Lair, C. Gibbons, R. Freeman
Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA
Objective: To report a novel autonomic paresthesia in a patient with an idiopathic sensory and autonomic neuropathy.
Phantom sweating is the sensation of sweating in the absence of actual sweating. This symptom is reported in 40% of patients after sympathectomy. To our knowledge there are no reports of phantom sweating without a prior sympathectomy.

Quantitative sudomotor axon reflex testing revealed absent sudomotor activity in the dorsal foot with preserved activity in the distal thigh. Skin biopsy showed a loss of epidermal nerve fibers, nerve fiber swellings, and denervation of sweat glands.
Conclusions: We report a patient with symptoms of phantom sweating in the setting of a sensory and post-ganglionic autonomic neuropathy. The pathophysiologic mechanisms underlying this autonomic paresthesia are not known. Possible mechanisms include aberrant reinnervation, ephaptic communication between nerve fibers, ectopic discharges from injured nerve fibers, and a central
response to autonomic deafferentation.
Clin Auton Res (2007) 17:264–327

hypotension-related poorer mental ability is also reflected in diminished cortical activity

EEG studies have demonstrated that the hypotension-related poorer mental ability is also reflected in
diminished cortical activity. Contrary to convention, more recent research has suggested a deficient regulation of cerebral blood flow in persons with low blood pressure. In addition to reduced tonic brain perfusion, studies demonstrated insufficient adjustment of blood flow to cognitive requirements.

Chronically low blood pressure is accompanied by a variety of complaints including fatigue, reduced drive, faintness, dizziness, headaches, palpitations, and increased pain sensitivity [1–4]. In addition, hypotensive individuals report cognitive impairment, above all deficits in attention and memory.
Clin Auton Res. 2007 April; 17(2): 69–76.

Nitric Oxide synthesis contributes to the regulation of vasomotor tone

These findings indicate that NO is involved in the central regulation of sympathetic outflow in humans and suggest that both neuronal and endothelial NO synthesis may contribute to the regulation of vasomotor tone.
Circulation. 1997 Dec 2;96(11):3897-903.

hypoxaemia, a potentially serious complication of Sympathectomy

Consecutive series of patients (n = 210), suffering from upper limb hyperhidrosis, anaesthetised for TES.

SpO2 decreased below 98% in 58 patients. Sudden hypotension and bradycardia in two patients.
The mean PaO2 was significantly (p = 0.03) decreased during two-lung ventilation (TLV), after reinflation of the right lung, compared with TLV after endobronchial intubation. There was no significant difference in mean PaO2 during one-lung ventilation of both lungs. Lowest PaO2 observed during one-lung ventilation was less than 13.3 kPa in three sympathectomies. Postoperative pain, severe on awakening and mainly retrosternal, was relieved with i.v. opiates. CONCLUSION: Controlled ventilation with 100% inspired O2, SpO2 monitoring and one to two gentle manual ventilations when it decreases is the cornerstone of the management of hypoxaemia, a potentially serious complication of TES.
Eur J Surg Suppl. 1994;(572):23-5.

Haemodynamic changes following denervation of the heart

Bilateral cardiac sympathectomy significantly decreased the heart rate and the systemic arterial blood pressure from 191 + 8 to 124 + 6 beats min-' and from 121 + 10 to 88 + 9 mmHg, respectively. These variables increased to 129 + 7 beats min-' and to 103 + 10 mmHg, respectively, following bilateral vagotomy.
Journal of Physiology (1996), 490.3, pp.793-803

inhibition of sympathetic activity and a possible impairment of endothelial function

Alterations in skin microcirculation induced by brachial plexus block can be evaluated by wavelet transform of the laser Doppler flowmetry signal. Brachial plexus block reduces the oscillatory components within the 0.0095- to 0.021- and 0.021- to 0.052-Hz intervals of the perfusion signal. These alterations are related to inhibition of sympathetic activity and a possible impairment of endothelial function.

Anesthesiology:

September 2006 - Volume 105 - Issue 3 - pp 478-484

Clinical Investigations

Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and often leads to atherosclerosis.
http://en.wikipedia.org/wiki/Endothelium

Surgical sympathectomy listed as neurologic disorder (surgically induced)

Other neurologic disorders
- Idiopathic orthostatic hypotension
- Multiple sclerosis
- Parkinsonism
- Posterior fossa tumor
- Shy-Drager syndrome
- Spinal cord injury with paraplegia
- Surgical sympathectomy
- Syringomyelia
- Syringobulbia
- Tabes dorsales (syphillis)
- Wernicke's encephalopathy
Dizziness: Classification and Pathophysiology
The Journal of Manual and Manipulative Therapy, Vol. 12, No 4 (2004)

Sympathectomy: "suppression of the neuroendocrine stress response"

p.254

Neuraxial blocks typically produce variable decrease in blood pressure that might be accompanied by a decrease in heart rate and cardiac contractility. These effects are generally proportional to the degree (level) of the sympathectomy. Vasomotor tone is primarily determined by sympathetic fibres arising from T5 to L1, innervating arterial and venous smooth muscle. Blocking these nerves causes vasodilation of the venous capacitance vessels, pooling of blood, and decreased vvenous terurn to the heart; in some instances, arterial vasodilation may also decrease systemic vascular resistance. The effects of arterial vasodilation may be minimized by compensatory vasoconstriction above the level of the block. A high sympathetic block not only prevents compensatory vasoconstriction but also blocks the sympathetic cardiac accelerator fibres that arise at T1-T4.
Profound hypotension may result from vasodilation combined with bradycardia and decreased contractility. These effects are further exaggerated if venous return is further compromised by a head-up position or from the weight of a gravid uterus. Unopposed vagal tone in some persons may explain cardiac arrest with spinal anesthesia.
p.261

The sympathetic system normally maintains some tonic vasoconstriction on the vascular tree. Loss off this tone following induction of anesthesia or sympathectomy frequently contributes to perioperative hypotension.
p.375

AV conduction abnormalities are usually manifested by abnormal ventricular depolarization (bundle-branch block) prolongation of the P-R interval (first degree AV block) failure of some atrial impulses to depolarize the ventricles (second degree AV block) or AV dissociation (third degree AV block or complete heart block).
p.428

Clinical anesthesiology

By G. Edward Morgan, Maged S. Mikhail, Michael J. Murray
McGraw-Hill, Edition: 3 - 2002

SUPERSENSITIVITY TO NE AFTER ADRENERGIC DENERVATION

H-NOREPINEPHRINE UPTAKE
Portal veins were incubated for 1 hour with 3H-NE 1,3, and 5 days after chemical sympathectomy with 6-OHDA (Fig. 3). Preparations treated with cocaine (10~5 M) were exposed to this drug 15 minutes before 3H-NE incubation and maintained in a cocaine-containing solution throughout the entire incubation period. One day after 6-OHDA treatment, NE uptake was reduced to approximately 21 %
of control; at 3 days it was 33% of controls and 5 days after 6-OHDA it was approximately 39% of controls. The decrease in NE uptake caused by 6-OHDA treatment was comparable to that caused by cocaine.

SUPERSENSITIVITY TO NE AFTER ADRENERGIC DENERVATION

CATECHOLAMINE DEPLETION AFTER CHEMICAL SYMPATHECTOMY

1977;41;198-206 Circ. Res.
Trophic influence of the sympathetic nervous system on the rat portal vein