Treatment of the primary gastroenterological distress is the first concern, mitigation of gastric symptoms will also alleviate cardiac distress.

- Anticholinergics, magnesium, or sodium (to raise blood pressure) supplements

- Anticonvulsants have eliminated all symptoms in some RS sufferers; Lorazepam, Oxcarbazepine increase GI motility, reduce vagus "noise" (sodium channel blocking believed to contribute to positive effects)

- Alpha blockers may increase gi motility if that is an issue, also 5 mg to 10 mg amitriptyline if motility is an issue that can't be solved by other methods

- antigas - simethicone, beano, omnimax reduces epigastric pressure

- Antacids - nexium, tums, Pepcid AC, rolaids, etc. reduces acid reflux in the case of hiatal hernia or other esophageal type RS.

- Vagusectomy

- Beta blockers - reduces contractility and automaticity of the heart which reduces irregular rhythms but also lowers blood pressure when symptoms occur, and further reduces perfusion ex: Atenolol, this will control disarrhythmia, but can precipitate Prinzmetal Angina and Heart block substantially.

Roemheld syndrome is characterized strictly by abdominal maladies triggering reflexes in the heart. There are a number of pathways through which cardiac reflexes can occur: hormones, mechanical, neurological and immunological.

It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate).

Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. Sick sinus syndrome is also associated with azygos continuation of interrupted inferior vena cava.

Artificial pacemakers have been used in the treatment of sick sinus syndrome.

Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias respond well to medical therapy.

However, because both bradyarrhythmias and tachyarrhythmias may be present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia. Therefore, a pacemaker is implanted before drug therapy is begun for the tachyarrhythmia.

Treatment for Romano–Ward syndrome can "deal with" the imbalance between the right and left sides of the sympathetic nervous system which may play a role in the cause of this syndrome. The imbalance can be temporarily abolished with a left stellate ganglion block, which shorten the QT interval. If this is successful, surgical ganglionectomy can be performed as a permanent treatment.Ventricular dysrhythmia may be managed by beta-adrenergic blockade (propranolol)

Romano–Ward syndrome is the major variant of "long QT syndrome". It is a condition that causes a disruption of the heart's normal rhythm. This disorder is a form of long QT syndrome, which is a heart condition that causes the cardiac muscle to take longer than usual to recharge between beats; if untreated, the irregular heartbeats can lead to fainting, seizures, or sudden death

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

Individuals with LGL syndrome do not carry an increased risk of sudden death. The only morbidity associated with the syndrome is the occurrence of paroxysmal episodes of tachycardia which may be of several types, including sinus tachycardia, supraventricular tachycardia, atrial fibrillation, atrial flutter, or even ventricular tachycardia.

Lown–Ganong–Levine syndrome (LGL) is a pre-excitation syndrome of the heart due to abnormal electrical communication between the atria and the ventricles. Once thought to involve an accessory conduction pathway, it is grouped with Wolff–Parkinson–White syndrome as an atrioventricular re-entrant tachycardia (AVRT). Individuals with LGL syndrome have a short PR interval with normal QRS complexes and paroxysms of clinically-significant tachycardia. The syndrome is named after Bernard Lown, William Francis Ganong, Jr., and Samuel A. Levine.

Individuals with a short PR interval found incidentally on EKG were once thought to have LGL syndrome. However, subsequent studies have shown that a short PR interval in the absence of symptomatic tachycardia is simply a benign EKG variant.

In August 2016, researchers at the Instituto de Assistência dos Servidores do Estado do Rio de Janeiro used botulinum toxin as a method to block the acetylcholine release from the presynaptic neurons. Although they have seen a reduction in one sided flushing, sweating still occurs.

There have been case studies of individuals whom have experienced this syndrome after an operation. Two patients, a 37-year-old and 58-year-old female patients suffering from metastatic cancer were scheduled for placement of an intrathecal pump drug delivery system. After the intrathecal pump was placed, certain medications were given to the patients. Once the medications were administered, both patients had one sided facial flushes, closely resembling Harlequin Syndrome. Patients were given neurological exams to confirm that their nerves were still intact. An MRI was performed and showed no significant evidence of bleeding or nerve compression. After close observation for 16 hours, symptoms of the Harlequin syndrome was diminished and both patients did not have another episode.

Another case study was based on a 6-year-old male visiting an outpatient setting for one sided flushes during or after physical activity or exposed to heat. Vitals, laboratory tests, and CT scans were normal. Along with the flushes, the right pupil was 1.5 mm in size, while the left pupil was 2.5 mm in size; however, no ptosis, miosis, or enophthalmos was noted. The patient also had an MRI scan to rule out any lesion near the brain or spinal cord. No abnormalities were noted and the patient did not receive any treatments. The patient was diagnosed with idiopathic Harlequin syndrome.

Although the mechanism is still unclear, the pathophysiology of this condition, close monitoring, and reassurance are vital factors for successful management.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

As there is no known cure, Loeys–Dietz syndrome is a lifelong condition. Due to the high risk of death from aortic aneurysm rupture, patients should be followed closely to monitor aneurysm formation, which can then be corrected with interventional radiology or vascular surgery.

Previous research in laboratory mice has suggested that the angiotensin II receptor antagonist losartan, which appears to block TGF-beta activity, can slow or halt the formation of aortic aneurysms in Marfan syndrome. A large clinical trial sponsored by the National Institutes of Health is currently underway to explore the use of losartan to prevent aneurysms in Marfan syndrome patients. Both Marfan syndrome and Loeys–Dietz syndrome are associated with increased TGF-beta signaling in the vessel wall. Therefore, losartan also holds promise for the treatment of Loeys–Dietz syndrome. In those patients in which losartan is not halting the growth of the aorta, irbesartan has been shown to work and is currently also being studied and prescribed for some patients with this condition.

If an increased heart rate is present, atenolol is sometimes prescribed to reduce the heart rate to prevent any extra pressure on the tissue of the aorta. Likewise, strenuous physical activity is discouraged in patients, especially weight lifting and contact sports.

Reducing the dosage of the antipsychotic drugs resulted in gradual improvement in the abnormal posture. In some cases, discontinuing the use of those drugs resulted in complete disappearance of the syndrome. The time it took for the improvement and the disappearance of the syndrome depended on the type of drug being administered or the specific cause of the syndrome itself.

Anticholinergic drugs have been reported to be extremely effective in 40% of the patients with the Pisa syndrome. Patients with Pisa syndrome that is resistant to anticholinergic drugs is mostly resolved by the reduction of the administration of the antipsychotic drugs as previously mentioned. While the specific pathology underlying idiopathic Pisa syndrome is unknown, the administration of anticholinergic drugs has provided resolution in known cases.

Surgery is typically used to correct structural heart defects and syndactyly. Propanolol or beta-adrenergic blockers are often prescribed as well as insertion of a pacemaker to maintain proper heart rhythm. With the characterization of Timothy syndrome mutations indicating that they cause defects in calcium currents, it has been suggested that calcium channel blockers may be effective as a therapeutic agent.

Holt–Oram syndrome (also called Heart and Hand Syndrome, atrio-digital syndrome, atriodigital dysplasia, cardiac-limb syndrome, heart-hand syndrome type 1, HOS, ventriculo-radial syndrome) is an autosomal dominant disorder that affects bones in the arms and hands (the upper limbs) and may also cause heart problems. The syndrome includes an absent radial bone in the arms, an atrial septal defect, and a first degree heart block. Thalidomide syndrome can produce similar morphology to Holt–Oram syndrome, sufficient to be considered a phenocopy.

After the first discovery and description of Marshall–Smith syndrome in 1971, research to this rare syndrome has been carried out.

- Adam, M., Hennekam, R.C.M., Butler, M.G., Raf, M., Keppen, L., Bull, M., Clericuzio, C., Burke, L., Guttacher, A., Ormond, K., & Hoyme, H.E. (2002). Marshall–Smith syndrome: An osteochondrodysplasia with connective tissue abnormalities. 23rd Annual David W. Smith Workshop on Malformations and Morphogenesis, August 7, Clemson, SC.

- Adam MP, Hennekam RC, Keppen LD, Bull MJ, Clericuzio CL, Burke LW, Guttmacher AE, Ormond KE and Hoyme HE: Marshall-Smith Syndrome: Natural history and evidence of an osteochondrodysplasia with connective tissue abnormalities. American Journal of Medical Genetics 137A:117–124, 2005.

- Baldellou Vazquez A, Ruiz-Echarri Zelaya MP, Loris Pablo C, Ferr#{225}ndez Longas A, Tamparillas Salvador M. El sIndrome de Marshall-Smith: a prop#{243}sito de una observad#{243}n personal. An Esp Pediatr 1983; 18:45-50.

- Butler, M.G. (2003). Marshall–Smith syndrome. In: The NORD Guide to Rare Disorders. (pp219–220) Lippincott, Williams & Wilkins, Philadelphia, PA.

- Charon A, Gillerot T, Van Maldergem L, Van Schaftingen MH, de Bont B, Koulischer L. The Marshall–Smith syndrome. Eur J Pediatr 1990; 150: 54-5.

- Dernedde, G., Pendeville, P., Veyckemans, F., Verellen, G. & Gillerot, Y. (1998). Anaesthetic management of a child with Marshall–Smith syndrome. Canadian Journal of Anesthesia. 45 (7): 660. Anaesthetic management of a child with Marshall-Smith syndrome

- Diab, M., Raff, M., Gunther, D.F. (2002). Osseous fragility in Marshall–Smith syndrome. Clinical Report: Osseous fragility in Marshall-Smith syndrome

- Ehresmann, T., Gillessen-Kaesbach G., Koenig R. (2005). Late diagnosis of Marshall Smith Syndrome (MSS). In: Medgen 17.

- Hassan M, Sutton T, Mage K, LimalJM, Rappaport R. The syndrome of accelerated bone maturation in the newborn infant with dysmorphism and congenital malformations: (the so-called Marshall–Smith syndrome). Pediatr Radiol 1976; 5:53-57.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. Western Society for Pediatric Research, Carmel, California, February, 1987. Clin Res 35:68A, 1987.

- Hoyme HE and Bull MJ: The Marshall-Smith Syndrome: Natural history beyond infancy. David W. Smith Morphogenesis and Malformations Workshop. Greenville, SC, August, 1987. Proceedings of the Greenwood Genetics Center 7:152, 1988.

- Hoyme HE, Byers PH, Guttmacher AE: Marshall–Smith syndrome: Further evidence of an osteochondrodysplasia in long-term survivors. David W. Smith Morphogenesis and Malformations Workshop, Winston-Salem, NC, August, 1992. Proceedings of the Greenwood Genetic Center 12:70, 1993.

- .

- Tzu-Jou Wang (2002). Marshall–Smith syndrome in a Taiwanese patient with T-cell immunodeficiency. Am J Med Genet Part A;112 (1):107-108.

It is named for Mary Holt and Samuel Oram, who published a paper on it in 1960.

The prognosis for patients diagnosed with Timothy syndrome is very poor. Of 17 children analyzed in one study, 10 died at an average age of 2.5 years. Of those that did survive, 3 were diagnosed with autism, one with an autism spectrum disorder, and the last had severe delays in language development. One patient with atypical Timothy syndrome was largely normal with the exception of heart arrhythmia. Likewise, the mother of two Timothy syndrome patients also carried the mutation but lacked any obvious phenotype. In both of these cases, however, the lack of severity of the disorder was due to mosaicism.

Functional gastrointestinal disorders (FGID) include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and impaired gastrointestinal motility.

As of 2017, data on optimal treatment was limited. Therapies with hormones is the standard of care, namely adrenocorticotrophic hormone (ACTH), or oral

corticosteroids such as prednisone. Vigabatrin is also a common consideration, though there is a risk of visual field loss with long term use. The high cost of ACTH leads doctors to avoid it in the US; higher dose prednisone appears to generate equivalent outcomes.

As of 2017 data from clinical trials of the ketogenic diet for treating infantile spams was inconsistent; most trials were as a second-line therapy after failure of drug treatment, and as of 2017 it had not been explored as a first line treatment in an adequately designed clinical trial.

In the United States, sarcoidosis has a prevalence of approximately 10 cases per 100,000 whites and 36 cases per 100,000 blacks. Heerfordt syndrome is present in 4.1–5.6% of those with sarcoidosis.

Respiratory complications are often cause of death in early infancy.

Loeys–Dietz syndrome (LDS) is an autosomal dominant genetic connective tissue disorder. It has features similar to Marfan syndrome and Ehlers–Danlos syndrome. The disorder is marked by aneurysms in the aorta, often in children, and the aorta may also undergo sudden dissection in the weakened layers of the wall of aorta. Aneurysms and dissections also can occur in arteries other than the aorta. Because aneurysms in children tend to rupture early, children are at greater risk for dying if the syndrome is not identified. Surgery to repair aortic aneurysms is essential for treatment.

There are four types of the syndrome, labelled types I through IV, which are distinguished by their genetic cause. Type 1, Type 2, Type 3, and Type 4 are caused by mutations in "TGFBR1", "TGFBR2", "SMAD3", and "TGFB2" respectively. These four genes encoding transforming growth factors play a role in cell signaling that promotes growth and development of the body's tissues. Mutations of these genes cause production of proteins without function. Although the disorder has an autosomal pattern of inheritance, this disorder results from a new gene mutation in 75% of cases and occurs in people with no history of the disorder in their family.

Loeys-Dietz syndrome was identified and characterized by pediatric geneticists Bart Loeys and Harry Dietz at Johns Hopkins University in 2005.

If a contracture is less than 30 degrees, it may not interfere with normal functioning. The common treatment is splinting and occupational therapy. Surgery is the last option for most cases as the result may not be satisfactory.