Indusium griseum

Indusium griseum

The indusium griseum is a thin layer of grey matter which covers the superior surface of the corpus callosum, extending from the paraterminal gyrus anteriorly to the dentate gyrus and hippocampus posteriorly via the gyrus fasciolaris.

It continuous laterally with the grey matter of the cingulate gyrus.

It contains two longitudinally directed strands of fibers termed respectively the medial and lateral longitudinal striae (of Lancisi) on each side.

The supracallosal gyrus is prolonged around the splenium of the corpus callosum as a delicate lamina, the fasciola cinerea, which is continuous below with the fascia dentata hippocampi.


To uncover the ontogenesis of the human indusium griseum (IG), 28 post-mortem fetal human brains, 12-40 postconceptional weeks (PCW) of age, and 4 adult brains were analyzed immunohistochemically and compared with post-mortem magnetic resonance imaging (MRI) of 28 fetal brains (14-41 PCW). The morphogenesis of the IG occurred between 12 and 15 PCW, transforming the bilateral IG primordia into a ribbon-like cortical lamina. The histogenetic transition of sub-laminated zones into the three-layered cortical organization occurred between 15 and 35 PCW, concomitantly with rapid cell differentiation that occurred from 18 to 28 PCW and the elaboration of neuronal connectivity during the entire second half of gestation. The increasing number of total cells and neurons in the IG at 25 and 35 PCW confirmed its continued differentiation throughout this period. High-field 3.0 T post-mortem MRI enabled visualization of the IG at the mid-fetal stage using T2-weighted sequences. In conclusion, the IG had a distinct histogenetic differentiation pattern than that of the neighboring intralimbic areas of the same ontogenetic origin, and did not show any signs of regression during the fetal period or postnatally, implying a functional role of the IG in the adult brain, which is yet to be disclosed 1).

1)

Bobic Rasonja M, Oreškovic D, Knezovic V, Pogledic I, Pupacic D, Vukšic M, Brugger PC, Prayer D, Petanjek Z, Jovanov Miloševic N. Histological and MRI Study of the Development of the Human Indusium Griseum. Cereb Cortex. 2019 Feb 4. doi: 10.1093/cercor/bhz004. [Epub ahead of print] PubMed PMID: 30722016.

Acromegaly medical treatment

Acromegaly medical treatment

Medical treatment

Indications

Patients not cured by surgery.

Who cannot tolerate surgery.

Recurrence after surgery or radiotherapy.

More satisfactory surgical outcomes for noninvasive macroadenomas treated with presurgical SA may be achieved, although controversy of such adjuvant therapy exists. Combination of SA and pegvisomant or cabergoline shows advantages in some specific cases. Thus, an individual treatment program should be established for each patient under a full evaluation of the risks and benefits 1).


First-generation somatostatin receptor ligands (SRL) are the mainstay of acromegaly treatment, however the percentage of patients controlled with these drugs significantly varies in the different studies. Many factors are involved in the resistance to SRL.

In a review, Gadelha et al., updated the physiology of somatostatin and its receptors (sst), the use of SRL in the treatment of acromegaly and the factors involved in the response to these drugs. The SRL act through interaction with the sst, which up to now have been characterized as five subtypes. The first-generation SRL, octreotide and lanreotide, are considered sst2 specific and have biochemical response rates varying from 20 to 70%. Tumor volume reduction can be found in 36-75% of patients. Several factors may determine the response to these drugs, such as sst, aryl hydrocarbon receptor interacting protein (AIP), E-cadherinZAC1filamin A and β-arrestin expression in the somatotropinomas. In patients resistant to first-generation SRL, alternative medical treatment options include: SRL high dose regimens, SRL in combination with cabergoline or pegvisomant, or the use of pasireotide. Pasireotide is a next-generation SRL with a broader pattern of interaction with sst. In the light of the recent increase of treatment options in acromegaly and the deeper knowledge of the determinants of response to the current first-line therapy, a shift from a trial-and-error treatment to a personalized one could be possible 2).


The cost of treatment including medications and the possibility of major side effects represent important limitations of the medical therapy 3) 4).

The most widely used criteria for neurosurgical outcome assessment were combined measurements of IGF-1 and GH levels after oral glucose tolerance test (OGTT) 3 months after surgery. Ninety-eight percent of respondents stated that primary treatment with somatostatin receptor ligands (SRLs) was indicated at least sometime during the management of acromegaly patients. In nearly all centers (96%), the use of pegvisomant monotherapy was restricted to patients who had failed to achieve biochemical control with SRL therapy. The observation that most centers followed consensus statement recommendations encourages the future utility of these workshops aimed to create uniform management standards for acromegaly 5)

Current pharmacotherapy includes somatostatin analogs (SAs) and GH receptor antagonist; the former consists of lanreotide Autogel (ATG) and octreotide long-acting release (LAR), and the latter refers to pegvisomant. As primary medical therapy, lanreotide ATG and octreotide LAR can be supplied in a long-lasting formulation to achieve biochemical control of GH and IGF-1 by subcutaneous injection every 4-6 weeks. Lanreotide ATG and octreotide LAR provide an effective medical treatment, whether as a primary or secondary therapy, for the treatment of GH-secreting pituitary adenoma; however, to maximize benefits with the least cost, several points should be emphasized before the application of SAs. A comprehensive assessment, especially of the observation of clinical predictors and preselection of SA treatment, should be completed in advance. A treatment process lasting at least 3 months should be implemented to achieve a long-term stable blood concentration. More satisfactory surgical outcomes for noninvasive macroadenomas treated with presurgical SA may be achieved, although controversy of such adjuvant therapy exists. Combination of SA and pegvisomant or cabergoline shows advantages in some specific cases. Thus, an individual treatment program should be established for each patient under a full evaluation of the risks and benefits 6).

Somatostatin treatment can induce extensive fibrosis in GH secreting pituitary adenoma 7).

References

1)

Wang JW, Li Y, Mao ZG, Hu B, Jiang XB, Song BB, Wang X, Zhu YH, Wang HJ. Clinical applications of somatostatin analogs for growth hormone-secreting pituitary adenomas. Patient Prefer Adherence. 2014 Jan 6;8:43-51. eCollection 2014. Review. PubMed PMID: 24421637; PubMed Central PMCID: PMC3888346.
2)

Gadelha MR, Wildemberg LE, Bronstein MD, Gatto F, Ferone D. Somatostatin receptor ligands in the treatment of acromegaly. Pituitary. 2017 Feb;20(1):100-108. doi: 10.1007/s11102-017-0791-0. Review. PubMed PMID: 28176162.
3)

Chanson P, Salenave S, Kamenicky P, Cazabat L, Young J. Pituitary tumours: Acromegaly. Best Pract Res Clin Endocrinol Metab. 2009;23:555–74.
4)

Gondim JA, Ferraz T, Mota I, Studart D, Almeida JP, Gomes E, et al. Outcome of surgical intrasellar growth hormone tumor performed by a pituitary specialist surgeon in a developing country. Surg Neurol. 2009;72:15–9.
5)

Giustina A, Bronstein MD, Casanueva FF, Chanson P, Ghigo E, Ho KK, Klibanski A, Lamberts S, Trainer P, Melmed S. Current management practices for acromegaly: an international survey. Pituitary. 2011 Jun;14(2):125-33. doi: 10.1007/s11102-010-0269-9. PubMed PMID: 21063787.
6)

Wang JW, Li Y, Mao ZG, Hu B, Jiang XB, Song BB, Wang X, Zhu YH, Wang HJ. Clinical applications of somatostatin analogs for growth hormone-secreting pituitary adenomas. Patient Prefer Adherence. 2014 Jan 6;8:43-51. Review. PubMed PMID: 24421637.
7)

Kerschbaumer J, Pinggera D, Moser P, Hofmann A, Thomé C, Freyschlag CF. Somatostatin treatment can induce extensive fibrosis in growth hormone-producing adenoma. Acta Neurochir (Wien). 2016 Mar;158(3):441-3. doi: 10.1007/s00701-016-2714-7. Epub 2016 Jan 23. PubMed PMID: 26801514.
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