Cognitive deterioration due to GH deficiency in patients with traumatic brain injury: A preliminary report

León-Carrión, José; Leal‐Cerro, Alfonso; Cabezas, F. Murillo; Atutxa, Ainara Madrazo; Gómez, Saleky García; Cordero, J. M. Flores; Moreno, Alfonso Soto; Ferrari, M.D. Rincón; Domínguez-Morales, M. R.

doi:10.1080/02699050701484849

Cited by 44 publications

(20 citation statements)

References 24 publications

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“…For example, Leon-Carrion et al (2007) showed a GH-related cognitive impairment in patients who develop a GH deficiency post-TBI. These patients also had deficits in memory and attention.…”

Section: Implications Of Gh=igf-1 Deficiency In Tbi Subjectsmentioning

confidence: 99%

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Kasturi

Stein

2009

Journal of Neurotrauma

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In humans, traumatic brain injury (TBI) causes pathological changes in the hypothalamus (HT) and the pituitary. One consequence of TBI is hypopituitarism, with deficiency of single or multiple hormones of the anterior pituitary (AP), including growth hormone (GH). At present no animal model of TBI with ensuing hypopituitarism has been demonstrated. The main objective of this study was to investigate whether cortical contusion injury (CCI) could induce long-term reduction of serum GH in rats. We also tested the hypothesis that TBI to the medial frontal cortex (MFC) would induce inflammatory changes in the HT and AP. Methods: Nine young adult male rats were given sham surgery (n ¼ 4) or controlled impact contusions (n ¼ 5) of the MFC. Two months postinjury they were killed, trunk blood collected and their brains and AP harvested. GH was measured in serum and AP using ELISA and Western blot respectively. Interleukin-1b (IL-1b) and glial fibrillary acidic protein (GFAP) were measured in the cortex (Cx), HT, and AP by Western blot. Results: Lesion rats had significantly (p < 0.05) lower levels of GH in the AP and serum, unaltered serum IGF-1, and significantly (p < 0.05) higher levels of IL-1b in the Cx and HT and GFAP in the Cx, HT, and AP compared to that of shams. Conclusion: CCI leads to a long-term depletion of serum GH in male rats. This chronic change in GH post-TBI is probably the result of systemic and persistent inflammatory changes observed at the level of HT and AP, the mechanism of which is not yet known.

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“…For example, Leon-Carrion et al (2007) showed a GH-related cognitive impairment in patients who develop a GH deficiency post-TBI. These patients also had deficits in memory and attention.…”

Section: Implications Of Gh=igf-1 Deficiency In Tbi Subjectsmentioning

confidence: 99%

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Kasturi

Stein

2009

Journal of Neurotrauma

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“…GH deficiency has been associated with more severe deficits in memory, attention, executive function, mood, and sleep, as well as being associated with fatigue, many of which are often reported as postconcussive symptoms. [3][4][5][6][7][8][9][10] GH also may play a critical role in recovery, as it is involved in both myelin formation [11][12][13] and neuronal plasticity. [14][15][16][17] A number of potential pathophysiological mechanisms have been suggested as to how the pituitary gland is damaged.…”

mentioning

confidence: 99%

The Effects of Repeat Traumatic Brain Injury on the Pituitary in Adolescent Rats

Greco¹,

Hovda²,

Prins³

2013

Journal of Neurotrauma

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Adolescents are one of the highest groups at risk for sustaining both traumatic brain injury (TBI) and repeat TBI (RTBI). Consequences of endocrine dysfunction following TBI have been routinely explored in adults, but studies in adolescents are limited, and show an incidence rate of endocrine dysfunction in 16-61% in patients, 1-5 years after injury. Similar to in adults, the most commonly affected axis is growth hormone (GH) and insulin-like growth hormone 1 (IGF-1). Despite TBI being the primary cause of morbidity and mortality among the pediatric population, there are currently no experimental studies specifically addressing the occurrence of pituitary dysfunction in adolescents. The present study investigated whether a sham, single injury or four repeat injuries (24 h interval) delivered to adolescent rats resulted in disruption of the GH/IGF-1 axis. Circulating levels of basal GH and IGF-1 were measured at baseline, 24 h, 72 h, 1 week, and 1 month after injury, and vascular permeability of the pituitary gland was quantified via Evans Blue dye extravasation. Changes in weight and length of animals were measured as a potential consequence of GH and IGF-1 disruption. The results from the current study demonstrate that RTBI results in significant acute and chronic decreases in circulation of GH and IGF-1, reduction in weight gain and growth, and an increase in Evans Blue dye extravasation in the pituitary compared with sham and single injury animals. RTBI causes significant disruption of the GH/IGF-1 axis that may ultimately affect normal cognitive and physical development during adolescence.

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“…Leon-Carrion demonstrated cognitive impairments in GH deficient patients after traumatic brain injury (TBI) and suggested that treatment with GH could improve cognition [8]. Preliminary results from our ongoing study assessing the effects of rhGH replacement on neuropsychological function in GH deficient adults with moderate to severe traumatic brain injury (TBI) indicate positive trends in processing speed index, memory, and integration in the community.…”

Section: Gh Replacement and Cognitionmentioning

confidence: 89%

What are critical outcome measures for patients receiving pituitary replacement following brain injury?

et al. 2008

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There are scant prospective studies defining improvements in critical outcome measures with hormone replacement in hypopituitarism secondary to brain injury. We review the tests of cognition and physical function and summarize their use for subjects that are deficient in anterior hormone production during anterior pituitary hormone replacement in brain injury and propose these as the minimal tests that are feasible for a physician to perform in a clinical setting. We summarize the studies conducted to assess outcome measures after brain injury and also report preliminary findings for improvements in cognition and physical function in subjects with brain injury and GH deficiency.

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Cognitive deterioration due to GH deficiency in patients with traumatic brain injury: A preliminary report

Cited by 44 publications

References 24 publications

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

The Effects of Repeat Traumatic Brain Injury on the Pituitary in Adolescent Rats

What are critical outcome measures for patients receiving pituitary replacement following brain injury?

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