Symptomatic Chiari-I Malformation in a Patient With Acromegaly

LeMar, Homer J.; Perloff, Jan J.; Merenich, John A.

doi:10.1097/00007611-199402000-00031

Cited by 25 publications

(12 citation statements)

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“…An association of acromegaly and Chiari malformation has been reported in the literature. 1,2,8 A hypothesis for this association might be that the bony overgrowth reduces posterior fossa volume. 2 At least supratentorially, we could not confirm this phenomenon: both the outer anterior-posterior and lateral-lateral skull diameters increased but not the corresponding inner diameters, thus the intracranial volume itself does not appear to diminish.…”

Section: Discussionmentioning

confidence: 99%

Craniometric changes in patients with acromegaly from a surgical perspective

Ebner¹,

Kürschner²,

Dietz

et al. 2010

FOC

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Object The objective of this study was to evaluate and analyze morphometric and volumetric changes of the skull due to acromegaly in areas relevant for neurosurgical practice, focusing on the surgical implications. Methods On preoperatively acquired CT scans, cephalometric and volumetric measurements were performed on 45 patients with acromegaly (Group A) and 45 control patients (Group B). The authors determined thickness of the cranial vault, inner and outer diameters of the skull, and the diameter of sphenoidal and maxillary sinus, as well as frontal and maxillary sinus volumetry. The morphometric and volumetric CT data of the patients with acromegaly were compared with the data of a control group and correlated with clinical parameters. Results Cranial vault thickness differed significantly (p < 0.0001) between the 2 groups. A correlation of the vault thickness with preoperative human growth hormone, insulin-like growth factor–I levels, and duration of clinical history in acromegaly could not be established. The outer anterior-posterior skull diameter of Group A (18.47 ± 0.94 cm) differed significantly (p = 0.0146) from Group B (17.98 ± 0.93 cm) and correlated significantly with preoperative human growth hormone (r = 0.3277; p = 0.0299) and insulin-like growth factor-–I serum levels (r = 0.3756; p = 0.0120). Measurements of the anterior-posterior diameter of the sphenoidal sinus differed significantly (p = 0.0074) between patients with acromegaly and controls. Volumetric analysis of the frontal sinus resulted in a statistically significant difference (p = 0.0382) between patients with acromegaly (14.89 ± 10.85 cm3) and controls (10.06 ± 6.93 cm3). Conclusions Significant craniometric changes and volumetric remodelling of the paranasal sinus occur in acromegaly. The bone alterations are of surgical importance for using the transsphenoidal approach. Detailed preoperative diagnostic examination and planning as well as selection of appropriate instruments are mandatory for safe and successful pituitary adenoma removal in patients with acromegaly.

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Section: Discussionmentioning

confidence: 99%

Craniometric changes in patients with acromegaly from a surgical perspective

Ebner¹,

Kürschner²,

Dietz

et al. 2010

FOC

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“…Finally, acromegaly patients have increased risk of neuropathies due to hypertrophy of perineural and endoneural tissue. One striking example is a case study report of a patient presenting with symptoms of both acromegaly and the rare Chiari-I malformation, likely due to neural covering and bony tissue changes from increased GH secretion [57].…”

Section: Gh Dysregulation and The Human Brain: Acromegaly Ghd And Lamentioning

confidence: 99%

GH in the Central Nervous System: Lessons from the Growth Hormone Receptor Knockout Mouse

Gosney¹,

Jara²,

Basu

et al. 2012

TOEJ

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Various central nervous system (CNS) tissues express both growth hormone (GH) and its receptor (GHR), including those involved in memory and cognition. Studies show the presence of GHR in the pituitary, choroid plexus, hypothalamus, hippocampus, pituitary and the spinal cord during development and, to a lesser extent, in adults. This expression implies a role of GH signaling in growth, development and functionality of the CNS. While data on the function of GH in the CNS is sparse, several studies have been conducted using the GHR knockout (-/-) mouse in order to better understand this role. Abnormal growth hormone signaling in humans is the cause of various diseases that include Laron syndrome, GH deficiency and acromegaly. This article will review the research conducted using the GHR-/-mouse on the role of GH signaling in the CNS. Where possible, we will attempt to contextualize the animal data with respect to human disease.

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“…Whereas CM-II and CM-III are gross defects of neuroectodermal origin, there is accumulating evidence that CM-I is a disorder of the paraaxial mesoderm that results in underdevelopment of the posterior cranial fossa (PCF) and overcrowding of the hindbrain [19, 25, 30]. However, CM-I can also occur in association with disorders that appear to be unrelated to skull base hypoplasia such as hydrocephalus [4], intracranial mass lesions [12, 22], cerebrospinal fluid (CSF) leaks [2], prolonged lumboperitoneal shunting [5], hereditary disorders of connective tissue (HDCT) associated with occipitoatlantoaxial joint instability (OAAJI) and cranial settling [20], tethered cord syndrome [19], and miscellaneous conditions such as craniosynostosis [6], acromegaly [13], and Paget’s disease [7]. This raises the possibility that generically defined CM-I may have more than one causal mechanism.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of cerebellar tonsil herniation in patients with Chiari malformations as guide to clinical management

et al. 2010

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BackgroundThe pathogenesis of Chiari malformations is incompletely understood. We tested the hypothesis that different etiologies have different mechanisms of cerebellar tonsil herniation (CTH), as revealed by posterior cranial fossa (PCF) morphology.MethodsIn 741 patients with Chiari malformation type I (CM-I) and 11 patients with Chiari malformation type II (CM-II), the size of the occipital enchondrium and volume of the PCF (PCFV) were measured on reconstructed 2D-CT and MR images of the skull. Measurements were compared with those in 80 age- and sex-matched healthy control individuals, and the results were correlated with clinical findings.ResultsSignificant reductions of PCF size and volume were present in 388 patients with classical CM-I, 11 patients with CM-II, and five patients with CM-I and craniosynostosis. Occipital bone size and PCFV were normal in 225 patients with CM-I and occipitoatlantoaxial joint instability, 55 patients with CM-I and tethered cord syndrome (TCS), 30 patients with CM-I and intracranial mass lesions, and 28 patients with CM-I and lumboperitoneal shunts. Ten patients had miscellaneous etiologies. The size and area of the foramen magnum were significantly smaller in patients with classical CM-I and CM-I occurring with craniosynostosis and significantly larger in patients with CM-II and CM-I occurring with TCS.ConclusionsImportant clues concerning the pathogenesis of CTH were provided by morphometric measurements of the PCF. When these assessments were correlated with etiological factors, the following causal mechanisms were suggested: (1) cranial constriction; (2) cranial settling; (3) spinal cord tethering; (4) intracranial hypertension; and (5) intraspinal hypotension.

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Symptomatic Chiari-I Malformation in a Patient With Acromegaly

Cited by 25 publications

References 0 publications

Craniometric changes in patients with acromegaly from a surgical perspective

Craniometric changes in patients with acromegaly from a surgical perspective

GH in the Central Nervous System: Lessons from the Growth Hormone Receptor Knockout Mouse

Mechanisms of cerebellar tonsil herniation in patients with Chiari malformations as guide to clinical management

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