During thoracoscopy, the thoracic sympathetic chains are readily visualized in each hemithorax in their posterior paravertebral locations. The sympathetic nerve chain is an elongated, white structure often visible underneath the chest wall pleura, running parallel to the vertebral column and just lateral to the heads of the thoracic ribs. Although the location of the sympathetic chain is generally constant from patient to patient, the width and size of the sympathetic chain can be quite variable. As well, the cephalad-to-caudal course of the chain can be rather straight in many patients and meander somewhat in others. Notably, there does not appear to be any correlation between the size of the sympathetic chain and the severity of symptoms experienced by the patient.

Proper identification of chain level is determined by counting the ribs from an intrathoracic approach at the time of surgery. Commonly, each ganglion is located within the intercostal space of its paired rib—hence, the second thoracic ganglion is found below the second rib in the second intercostal space. In the vast majority of persons, the first thoracic ganglion fuses with the inferior cervical ganglion to form the stellate ganglion and is located high above the level of the second rib. At thoracoscopy, the stellate ganglion is often surrounded or hidden by a series of small pads of fat-laden tissue at the apex of the hemithorax. Careful cadaveric dissections of the sympathetic chain have confirmed that there are occasionally normal anatomic variations to the sympathetic chain that are important to appreciate in sympathetic nerve surgery. For example, Singh et al.¹⁴ found, in their series, that although the second thoracic ganglion lies within the second intercostal space over 90% of the time, in the small number of remaining cases, the second thoracic ganglion may lie over the neck of the second rib and cross into the first intercostal space (2.5%), be fused to a discrete and separate first thoracic ganglion (2.5%), or fuse directly to the stellate ganglion and span both the first and second intercostal spaces (5%). A comparable distribution of normal anatomic variation was also found by Chung et al.³; in their series, the second thoracic ganglion was fused to the stellate ganglion in approximately 7% cases. Noteworthy in the latter series was that a discrete second thoracic ganglion was not identifiable in 7% of cases.

Functionally, the thoracic sympathetic chains are part of the body’s autonomic nervous system and provide sensorimotor innervations to the visceral organs of the chest. Structurally, the source of the nerve fibers comprising the sympathetic chain is from preganglionic sympathetic fibers that arrive via white rami communicantes of the ventral primary rami of spinal nerves T1–L2. The preganglionic cell bodies are located in the intermediolateral gray matter of the spinal cord of the corresponding levels. Within the sympathetic chain, preganglionic fibers synapse (or may pass through to synapse higher, lower, or peripherally) and postganglionic sympathetic fibers depart via gray rami communicantes at all spinal cord segments. The sensory component is responsible for the detection of pain from the viscera, while the motor component innervates organs such as the vascular smooth muscle, erector pili muscles, and sweat glands of the skin, the heart, and the lungs.

The stellate ganglion is formed by the fusion of the lower cervical and first thoracic ganglia. At this level, the oculosympathetic pathway can be interrupted as a result of trauma to the stellate ganglion, where neurons project postganglionic axons
to the eye to innervate the dilator of the iris, the Muller muscle of the eyelid, and follow the external carotid artery to regulate the sweat glands of the face. Classic Horner’s syndrome, as described historically in 1869 by the Swiss ophthalmologist Johann Friedrich Horner, includes miosis, ptosis, and apparent enophthalmos. The functional impact of Horner’s on everyday vision is minimal. Issues of cosmesis in severe cases can arise in Horner’s. Interestingly, Palumbo¹¹ noted that these facial sympathetics do not pass through the entire stellate ganglion. When only the lower half of the ganglion was removed as a treatment for hyperhidrosis, hyperhidrosis was relieved without the development of Horner’s syndrome.

The primary indication for thoracic sympathectomy is primary hyperhidrosis of the upper extremity. Primary palmar hyperhidrosis is a disorder of excessive sweat production of the palms. Hyperhidrosis can also affect the axillae, soles of the feet, and head and face. As described by Rex and coworkers,¹² an apparently related disorder is social phobia with its associated facial blushing. There are no identifiable triggers for sweating in primary hyperhidrosis. Although some have previously attributed hyperhidrosis to manifestations of emotional etiologies, it is now clear that this is probably incorrect, as the great majority of individuals afflicted with hyperhidrosis are otherwise self-confident, professionally successful, socially well-adjusted individuals. However, extremely stressful situations or heat and exercise may exacerbate their baseline symptoms. In hyperhidrosis, sweating can be visibly profuse and palpable to the patient and others. It can be socially debilitating, with patients being extremely self-conscious about shaking hands, and adolescents may refrain from many normal social activities. It may be that the emotional trauma of hyperhidrosis during the adolescent years ultimately contributes to shaping the more introverted adult personality type previously described as occasionally being associated with hyperhidrosis. For some, the symptoms of hyperhidrosis can begin in childhood and become more pronounced with adolescence and young adulthood. Employment selection can be limited by the severity of experienced symptoms. Even the simple process of writing or doing homework may be difficult, with sweat soiling the paper or smearing the ink. Contrary to previous opinion, hyperhidrosis has no demonstrable sex or race predilection. And only in a minority of cases is there a family history of hyperhidrosis—the vast majority of cases appear to be sporadic. Medical treatment, as reviewed by White,¹⁶ may consist of topical therapy with aluminum chloride, iontophoresis, systemic or topical anticholinergic therapy, or biofeedback. Excision of axillary sweat glands has also been performed, although this procedure is probably no longer indicated for hyperhidrosis, given the superior and less surgically traumatic thoracoscopic procedures now available.

Thoracoscopic sympathetic nerve surgery is highly effective in the treatment of primary hyperhidrosis and should be considered for all patients with the disorder who have not responded to medical treatment. As reported by Edmondson,⁴ Gossot,⁵ Krasna,⁶ and Kwong⁸ and their associates, thoracoscopic sympathectomy has a success rate of >90% in the treatment of hyperhidrosis. The complication rates are low, with the most troublesome source of patient dissatisfaction being compensatory sweating.