Laparoscopic management of median arcuate ligament syndrome

Median arcuate ligament syndrome is a rare disorder resulting from luminal narrowing of the celiac trunk. The classic management of median arcuate ligament syndrome involves the surgical division of the median arcuate ligament fibers in order to decompress the celiac trunk. This has traditionally required an upper midline incision. A few authors have described a successful laparoscopic release of celiac artery compression syndrome. Laparoscopy provides a less invasive, but equally effective method for decompressing the celiac trunk.     

Exercise-related abdominal pain as a manifestation of the median arcuate ligament syndrome

Abdominal pain related to exercise, often loosely referred to as 'stitch', is not uncommon, particularly among participants in sports that involve running. The cause of this typically transient pain is poorly understood with several aetiologies proposed including diaphragmatic ischaemia (1, 2). Other gastrointestinal symptoms that are common during prolonged or high-intensity exercise include nausea, diarrhoea and gastrointestinal bleeding (3, 4). These symptoms are also usually transient and are thought to protect against critical organ damage by promoting cessation of exercise. Decreased gastrointestinal blood flow, increased motility and altered neuroendocrine modulation are postulated disease mechanisms (3). We report here a case of an elite runner with exercise-related severe abdominal pain and diarrhoea related to compression of the coeliac axis by the median arcuate ligament. Complete symptom relief was achieved with surgical division of the constricting ligament. The clinical characteristics and pathogenesis of coeliac axis compression syndrome are discussed.     

Exercise-related abdominal pain as a manifestation of the median arcuate ligament syndrome

Abdominal pain related to exercise, often loosely referred to as 'stitch', is not uncommon, particularly among participants in sports that involve running. The cause of this typically transient pain is poorly understood with several aetiologies proposed including diaphragmatic ischaemia (&;lt;citeref rid="b1"&;gt;1&;lt;/citeref&;gt;,?&;lt;citeref rid="b2"&;gt;2&;lt;/citeref&;gt;). Other gastrointestinal symptoms that are common during prolonged or high-intensity exercise include nausea, diarrhoea and gastrointestinal bleeding (&;lt;citeref rid="b3"&;gt;3&;lt;/citeref&;gt;,?&;lt;citeref rid="b4"&;gt;4&;lt;/citeref&;gt;). These symptoms are also usually transient and are thought to protect against critical organ damage by promoting cessation of exercise. Decreased gastrointestinal blood flow, increased motility and altered neuroendocrine modulation are postulated disease mechanisms (&;lt;citeref rid="b3"&;gt;3&;lt;/citeref&;gt;). We report here a case of an elite runner with exercise-related severe abdominal pain and diarrhoea related to compression of the coeliac axis by the median arcuate ligament. Complete symptom relief was achieved with surgical division of the constricting ligament. The clinical characteristics and pathogenesis of coeliac axis compression syndrome are discussed.     

The laparoscopic approach in the median arcuate ligament syndrome: report of a case

A malposition of the median arcuate ligament (MAL) is a rare entity causing the celiac axis compression syndrome (CACS), first described by Harjola in 1963. The presence of anomalous fibrous diaphragmatic bands of the diaphragm compresses the celiac axis, especially during the expiration. In this report we present the fourth case in literature that was ever successfully treated by laparoscopy. A 38-year-old male presented with a history of intermittent epigastric pain, 15 kg weight loss caused by inappetence and frequent diarrhoea, over a 5-year period. The clinical examination revealed only a loud systolic bruit in the epigastrium, with loss of intensity during deep inspiration. Suspecting CACS, a spiral CT angiography was requested. The CT demonstrated the MAL crossing anteriorly to the celiac artery (CA) and the sagittal and the tridimensional reconstructions demonstrated the CA narrowing due to compression, while the superior mesenteric artery (SMA) was normal. The MAL was laparoscopically divided, releasing the celiac axis. The surgical time was 130 minutes, without significant blood losses. At 3-months follow-up, the CT-scan demonstrated no evidence of CACS with complete recovery.     

Celiac axis compression by median arcuate ligament on computed tomography among asymptomatic persons

Background/Aim  

Compression of celiac artery by median arcuate ligament (MAL) may cause abdominal symptoms. This study looked at the prevalence of this finding in asymptomatic persons.     

Pancreaticoduodenal artery aneurysms associated with celiac axis stenosis due to compression by median arcuate ligament and celiac plexus

Celiac axis stenosis is frequently associated with pancreaticoduodenal artery aneurysms. Although the cause of stenosis was not clear in most of the reported cases, compression of the median arcuate ligament of the diaphragm was found to be responsible for the stenosis in 7 of 42 reported cases of this type of aneurysm. We report a case of aneurysm caused by compression of the median arcuate ligament of the diaphragm and celiac plexus. An asymptomatic 43-year-old Japanese man was admitted with a low echoic lesion in the uncus of pancreas. Computed tomographic scan and angiogram revealed stenosis of the celiac axis and two aneurysms in the inferior posterior pancreaticoduodenal artery. The celiac plexus and median arcuate ligament were divided surgically and normal flow was reestablished in the celiac axis. One of the aneurysms was resected and the afferent artery of the other aneurysm was ligated. In the setting of pancreaticoduodenal artery aneurysm associated with celiac axis stenosis, management of stenosis should be considered in addition to local treatment of the aneurysm. In this context, division of median arcuate ligament and celiac plexus or aorto-celiac bypass may normalize the flows in the pancreaticoduodenal arcade and could be effective in preventing aneurysm reformation. (Received May 12, 1997; accepted Sept. 26, 1997)     

Enhancement of a robust arcuate GABAergic input to gonadotropin-releasing hormone neurons in a model of polycystic ovarian syndrome

Polycystic ovarian syndrome (PCOS), the leading cause of female infertility, is associated with an increase in luteinizing hormone (LH) pulse frequency, implicating abnormal steroid hormone feedback to gonadotropin-releasing hormone (GnRH) neurons. This study investigated whether modifications in the synaptically connected neuronal network of GnRH neurons could account for this pathology. The PCOS phenotype was induced in mice following prenatal androgen (PNA) exposure. Serial blood sampling confirmed that PNA elicits increased LH pulse frequency and impaired progesterone negative feedback in adult females, mimicking the neuroendocrine abnormalities of the clinical syndrome. Imaging of GnRH neurons revealed greater dendritic spine density that correlated with increased putative GABAergic but not glutamatergic inputs in PNA mice. Mapping of steroid hormone receptor expression revealed that PNA mice had 59% fewer progesterone receptor-expressing cells in the arcuate nucleus of the hypothalamus (ARN). To address whether increased GABA innervation to GnRH neurons originates in the ARN, a viral-mediated Cre-lox approach was taken to trace the projections of ARN GABA neurons in vivo. Remarkably, projections from ARN GABAergic neurons heavily contacted and even bundled with GnRH neuron dendrites, and the density of fibers apposing GnRH neurons was even greater in PNA mice (56%). Additionally, this ARN GABA population showed significantly less colocalization with progesterone receptor in PNA animals compared with controls. Together, these data describe a robust GABAergic circuit originating in the ARN that is enhanced in a model of PCOS and may underpin the neuroendocrine pathophysiology of the syndrome.Gonadotropin-releasing hormone (GnRH) neurons, located in the hypothalamus, control fertility by driving the secretion of the gonadotrophins, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) from the pituitary gland. The pulse amplitude and frequency of LH and FSH shape the sequence of events that occur at the ovary, including follicular development, gonadal steroid synthesis, and ovulation. Hormones secreted from the ovary, in turn, provide critical feedback signals to GnRH neurons through a network of hormone-sensitive neurons. Gonadal hormone feedback directs both the firing of GnRH neurons and pulsatile release of the GnRH peptide (1).Polycystic ovarian syndrome (PCOS), the most common form of anovulatory infertility (2), is estimated to affect more than 100 million women worldwide (3). Most women diagnosed with PCOS exhibit increased LH pulse frequency and decreased FSH release, suggestive of rapid GnRH pulse frequency (4). High LH, in turn, contributes to increased androgen production from ovarian theca cells, whereas decreased FSH disrupts follicle maturation and ovulation. Elevated GnRH/LH secretion in women with PCOS is less responsive to exogenous estrogen and progesterone (P4) administration (5, 6), suggesting that steroid hormone negative feedback to GnRH neurons is impaired. In animal models, elevated androgens are associated with blunted P4 negative feedback in particular (7, 8).Although the origin of GnRH/LH hypersecretion in PCOS is unknown, impaired steroid hormone negative feedback may lie within the hormone-sensitive afferent neuronal network to GnRH neurons. Identifying the specific neuronal elements affected is challenging in women; however, discoveries can be made in animal models (9, 10). PCOS is most commonly modeled through exposure to androgens during critical periods of development (11). Women exposed to elevated prenatal androgens (PNAs) develop the cardinal reproductive and endocrine features of PCOS in adulthood (12, 13), and PNA treatment produces a PCOS-like phenotype in all mammalian species studied to date (11). In the mouse, PNA elicits many of the key neuroendocrine features of the syndrome, suggestive of impaired steroid hormone feedback to the GnRH pulse generator (14, 15), however, it remains to be determined directly whether P4 negative feedback and LH pulse frequency are modified.P4 modulation of GnRH neurons via classical progesterone receptors (PRs) is most likely transsynaptic, as GnRH neurons do not express PRs. Many P4-sensitive populations have been identified throughout the hypothalamus, including neurons expressing gamma-aminobutyric acid (GABA) (16), glutamate (17), and various neuropeptides (18, 19). Both endogenous GnRH neuron firing activity and GABAergic postsynaptic currents are increased in PNA mice (15, 20). However, the specific P4-sensitive neuronal phenotype that relays feedback signals to GnRH neurons is so far unknown. The aim of the present study was to characterize whether LH pulse frequency and P4 negative feedback are impaired in a mouse model of PCOS and to investigate what modifications exist in the GnRH neuronal network that may impair negative feedback.     

Ossification of the posterior longitudinal ligament of the cervical spine and SAPHO syndrome

We describe a case of cervical cord compression due to ossification of the posterior longitudinal ligament of the spine (OPLLS) in a 43-year-old Vietnamese patient with SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis). Idiopathic OPLLS is mainly reported in 50- to 60-year-old men, particularly in Japanese, with a prevalence of 2%. Cervical myelopathy may occur. In addition to OPLLS in patients of Asian origin, the condition has also been described in association with ossifying diseases, including ankylosing spondylitis (AS) and diffuse idiopathic skeletal hyperostosis (DISH) but not previously, to our knowledge, with SAPHO syndrome.