Effects of lumbar sympathectomy: abolition of ejaculation, causalgia in 41, general morbidity of 0.6% and mortality rate of 0.6 %, arrhythmias, cardiac decompensation

Goldstein, reviewing the complications of 791 patients undergoing open lumbar sympathectomy reports 10% of specific complications, such as abolition of ejaculation in 22 patients and causalgia in 41, general morbidity of 0.6% (TEP and bleeding) and mortality rate of 0.6 % (arrhythmias, cardiac decompensation or bleeding) 15.

SIMPACTECTOMIA RETROPERITONEOSCÓPICA FOR TREATMENT OF LUMBAR plantar hyperhidrosis RETROPERITONEOSCOPIC lumbar sympathectomy FOR THE TREATMENT OF PLANT HYPERIDROSIS
Marcelo de Paula Loureiro, TCBC-PR ¹, ² Neomar Roman, Sheila Cristina Weigmann ³;
Aline ³ Fontana, Paulo Cesar Bufara Boscardim4
(Rev Bras ECR. Cir. 2007, 34 (4): 222-224).
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dynamic cerebral autoregulation is altered by ganglion blockade

We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29+/-6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (P <0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure.
Conclusions-: These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to-beat CBF in humans.
Circulation. 106(14):1814-1820, October 1, 2002.
http://www.problemsinanes.com/pt/re/dyslipidaemia/abstract.00003017-200210010-00017.htm;jsessionid=PX6phQHYFG5PD1p2DMS1cJLvG1TbtLLLH0bfJT6vKJgLLx1zn0Xf!1816077220!181195629!8091!-1?nav=reference

Horner syndrome, pneumothorax, hemothorax, asymmetry of results, intercostal neuralgia, causalgia, hypoesthesia, incomplete results, paresthesia in the anterolateral abdominal wall, dyspareunia

The complications and side effects are very significant, such as irreversible compensatory sweating (20% to 50%), low satisfaction with results, Claude-Bernard-Horner syndrome, pneumothorax, hemothorax, asymmetry of results, intercostal neuralgia, causalgia, incomplete results, and anesthetic complications^11-13.

Retroperitoneoscopic lumbar sympathectomy (video-assisted): this technique is effective in the treatment of isolated or persistent plantar hyperhidrosis (compensatory after thoracic sympathectomy). The treatment consists of removing the nerves of the sympathetic chain located in the abdomen, in the anterolateral portion of the lumbar vertebrae. It requires hospitalization and is carried out under general anesthesia. It may lead to complications such as lesions of structures adjacent to the sympathetic chain, light abdominal distension, neuralgia, and causalgia as well as hypoesthesia in the thighs and groin, limitation of leg movement,
paresthesia in the anterolateral abdominal wall, change in libido, dyspareunia, pulmonary thromboembolism, hemorrhages, arrhythmias, and cardiac decompensation, amongst others. It definitively eliminates plantar hyperhidrosis14,15.  
http://www.scielo.br/scielo.php?pid=S1983-51752011000400008&script=sci_arttext&tlng=en#end

Vasodilation; Vasomotor Disturbances

Complex regional pain syndromes (CRPS) are characterized by vascular disturbances primary affecting the microcirculation in the distal part of the involved extremity. In the acute stage inhibited sympathetic vasoconstriction and exaggerated neurogenic inflammation driven by central and peripheral mechanisms, respectively, seem to be the major pathophysiological mechanisms inducing vasodilation. During the chronic course of the disease as well as early in some patients vasoconstriction dominates the clinical picture induced by changes in the microcirculation itself such as endothelial dysfunction or vascular hyperreactivity, whereas sympathetic vasoconstrictor activity returns and neurogenic inflammation is less severe. It can be suggested that the interaction between different mechanisms underlying vasomotor disturbances as well as the severity of each single mechanism in the individual patient have a great impact on the variety of the overall clinical picture in CRPS. Irrespective of the underlying pathophysiology, measurements of skin temperature differences between the affected and the contralateral extremity can serve as a diagnostic tool in CRPS, in particular when sensitivity and specificity is increased by considering dynamic alterations in skin temperature asymmetries.
http://onlinelibrary.wiley.com/doi/10.1111/j.1526-4637.2010.00914.x/abstract

Epidemiology /Etiology

CRPS is found to result:^[1]
- After traumatic injury (65%)

• 1-2% of all fractures result in CRPS
• Largest risk of CRPS for fractures of the wrist

- After surgical intervention (19%)
- Infection (4%)
- Prior inflammation (2%)
- No clear cause (10%)
A review stated that women are predominantly affected, by a factor of 3,5 and a genetic predisposition has also been theorized.
The disease affects all ages, though most cases are between 50 and 70 years old, and it is generally believed to occur mainly in caucasian and Japanese people.^[4]

Characteristics/Clinical Presentation

The following symptoms have been found in literature:^[5]
- Autonomic and trophic disorders:

• Distal Edema in 80% of the patients
• Skin temperature changes at the affected body part in 80% of the patients, initially warmer and in 40% of patients gradually cools down until colder in comparison to the rest of the body as the disease progresses. Another review mentioned that 30% of the patients start off from the primarily cold stage.3
• In 40% of the patients skin at the affected body part starts showing redness, but becomes pale or livid in later stages
• In 55% altered sweating takes place, with hyperhydrosis being more common than hypohydrosis.
• Hair and nail growth possibly increase in early stages
• Atrophy of skin and muscles in later stages, as well as contractures may severely restrict movement

- Sensory disturbances (90%) typically in a glove or stocking-like distribution

• Spontaneous pain occurs in 75%, usually burning dragging or stinging

• 68% felt in deep structures
• 32% felt in skin
• In 77% pain shows fluctuating intensity, lesser proportion shows shooting pain
• Pain can be increased by orthostasis, anxiety, exercise or temperature changes.
• In many cases, pain is more pronounced at night

• Sensory gain (Mechanical hyperalgesia, allodynia, ...) or sensory loss (hypaesthesia, hypalgesia, …) may be present.

- Motor dysfunction

• Motor weakness
• Severe impairment of complex movements
• Impairment of range of motion, initially by concomitant edema, later by contractures and fibroses
• Neglect like symptoms have been found in some patiënts, described as the body part in question feeling foreign.
• Enhanced physiological tremor in around 50%
• Myoclonus or dystonia, especially in type II CRPS

http://www.physio-pedia.com/Complex_Regional_Pain_Syndrome

Sympathectomy involves division of adrenergic, cholinergic and sensory fibers which elaborate adrenergic substances during the process of regulating viscera

http://pharmrev.aspetjournals.org/content/18/1/611.full.pdf+html

effect of bilateral cervical sympathetic ganglionectomy on the architecture of pial arteries

The influence of the cranial sympathetic nerves on the architecture of pial arteries in normo- and hypertension was examined. For this purpose the effect of bilateral superior cervical ganglionectomy was evaluated in normotensive rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). The operations were performed at the age of 1 wk, which is just prior to the onset of ganglionic transmission. The length of the inner media contour was measured and the media cross-sectional area was determined planimetrically, with computerized digitalization of projected photographic images of transversely sectioned pial arteries. Four wk after sympathectomy there was a 20% reduction in media cross-sectional area and a consequent reduction in the ratio between media area and calculated luminal radius in the major pial arteries at the base of the brain in WKY but not in SHRSP. Conversely, in small pial arteries linear regression analysis showed that in WKY subjected to ganglionectomy the relationship between media cross-sectional area and luminal radius was significantly larger in arteries with a radius less than 21 microns compared to untreated WKY. No such effect was seen in the corresponding SHRSP vessels. In addition, the cross-sectional area of the internal elastic membrane (IEM) in the basilar arteries of WKY was measured by means of a computerized image-analysing system. Mean cross-sectional area of the IEM was approximately 45% larger following SE than in control animals. The present findings propose a 'trophic' role for the sympathetic perivascular nerves in large pial arteries of the rat. The increased media-radius ratio in the small pial arteries of the WKY following sympathectomy might reflect a compensatory hypertrophy due to reduced protection from the larger arteries against the pressure load. The inability to detect any morphometrically measurable effect of the sympathectomy in the cerebral arteries of SHRSP is probably explained by a marked growth-stimulating effect of the high pressure load in these animals.
http://www.ncbi.nlm.nih.gov/pubmed/7701941

Causes of orthostatic hypotension - surgical sympathectomy

Causes of orthostatic hypotension (modified from Simon et al9).
Hypovolemia or hemorrhage Addison’s disease Drug-induced hypotension • Antidepressants • Antihypertensives • Bromocriptine • Diuretics • Levodopa • Monoamine oxidase (MOA) inhibitors • Nitroglycerin • Phenothiazines Polyneuropathies • Myeloid neuropathy • Diabetic neuropathy • Guillain-Barre syndrome • Porphyric neuropathy • Vincristine neuropathy 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 (syphilis) • Wernicke’s encephalopathy Cardiovascular disorders Prolonged bed rest or immobilization
http://www.scribd.com/doc/15030687/Dizziness-Classification-and-Pathophysiology