Heat can also aid in relieving sore muscles by improving blood circulation to them. While the whole arm generally feels painful in TOS, some relief can be seen when ice or heat is intermittently applied to the thoracic region (collar bone, armpit, or shoulder blades). Medications
In a review, botox was compared to a placebo injected into the scalene muscles. No effect in terms of pain relief or improved movement was noted. However, in a six-months follow-up, paresthesia (abnormal sensations such as in pins and needles) was seen to be significantly improved. Surgery
Surgical approaches have also been used successfully in TOS. Microsurgery can be used approaching the area from above the collar bone (supraclavicular) followed by neurolysis of the brachial plexus, removal of the scalene muscle (scalenectomy), and the release of the underlying (subclavicular) blood vessels. This approach avoids the use of resection, and has been found to be an effective treatment. In cases where the first rib (or a fibrous band extending from the first rib) is compressing a vein, artery, or the nerve bundle, part of the first rib and any compressive fibrous tissue, can be removed in a first rib resection and thoracic outlet decompression surgical procedure; scalene muscles may also need to be removed (scalenectomy). This allows increased blood flow and the reduction of nerve compression.
Shorter episodes of occlusion can lead to what is referred to as silent myocardial ischemia due to its asymptomatic nature. These episodes can also be accompanied by arrhythmias. Longer episodes of occlusion can lead to stable or unstable angina, myocardial infarction, and sudden cardiac death. Risk factors
Unlike classical angina pectoris, traditional cardiovascular risk factors are not thought to be significantly associated with coronary vasospasm. The exception to this is with smoking, which is known to be a modifiable risk factor for vasospastic angina.There are several risk factors that are thought to precipitate, or trigger, episodes of coronary vasospasm. Many of these factors work by exerting effects on the autonomic nervous system. One of the mechanisms through which this occurs is via increasing sympathetic nervous system activity. The resulting increased sympathetic outflow leads to vasoconstrictive effects on blood vessels. For example, cocaine use can trigger vasospasm in coronary arteries through its actions on adrenergic receptors causing vasoconstriction. Exercise, cold weather, physical activity or exertion, mental stress, hyperventilation are additional precipitating factors. Pathophysiology
The exact pathophysiology behind coronary vasospasm has not been elucidated. Instead, a combination of different factors has been proposed to contribute to coronary vasospasm. In general, it is thought that an abnormality within a coronary artery causes it to become hyperreactive to vasoconstrictor stimuli. This abnormality can be located in one segment of the coronary artery, or it may be diffuse and present throughout the entire artery. If and when vasoconstrictor stimuli act upon the hyperreactive segment of the artery, then vasospasm can result.