scholarly journals Longitudinal volumetric MRI study of pituitary gland following severe traumatic brain injury

2012 ◽  
Vol 19 (3) ◽  
pp. 193-202 ◽  
Author(s):  
Sorin C. Craciunas ◽  
Carmen M. Cirstea ◽  
Hung-Wen Yeh ◽  
Lewis Hutfles ◽  
Joann Lierman ◽  
...  

Abstract Purpose: Previous studies have suggested that the hypopituitarism following traumatic brain injury (TBI) is more prevalent than traditionally thought. The objective of this study was to characterize longitudinal MRI morphometric changes of pituitary gland in patients with severe TBI. Materials and methods: Fourteen patients who had suffered a severe TBI (Glasgow Coma Score=3 - 8) underwent MRI at three time points: Time 1 (mean=31. 5 days), Time 2 (98. 0) and Time 3 (185. 5). The pituitary gland volume was quantified by manually tracing on T1-weighted magnetic resonance images. Data from TBI patients were compared to 14 age- and sexmatched uninjured controls. The relationships between pituitary volumetric measures and patient demographics, length of respiratory support and coma, and presence of intracranial hemorrhage or skull fractures were also analyzed. Results: Following TBI, the pituitary volumes were significantly greater at all three time points: Time 1: median=665mm3, range=460-830mm3, p=0. 007; Time 2: 694mm3, 467-866mm3, 0. 007; and Time 3: 655mm3, 444- 795mm3, 0. 015, compared with controls (504mm3, 433-591mm3). At Time 1, pituitary volume was increased in 10 out of 14 patients. Of these, early pituitary enlargements persisted up to six months in nine patients. Pituitary enlargements were negatively correlated with GCS, but not with other variables. Conclusion: Following a severe TBI, early pituitary enlargement found in most of our patients persisted in the chronic phases. Our data suggest a potential role of MRI morphometry in early prediction of pituitary dysfunction following head trauma, but further studies including hormonal measurements are necessary for validation.

2019 ◽  
Vol 180 (5) ◽  
pp. 281-290 ◽  
Author(s):  
Yamina Dassa ◽  
Hélène Crosnier ◽  
Mathilde Chevignard ◽  
Magali Viaud ◽  
Claire Personnier ◽  
...  

Objectives Childhood traumatic brain injury (TBI) is a public health issue. Our objectives were to determine the prevalence of permanent pituitary hormone deficiency and to detect the emergence of other pituitary dysfunctions or central precocious puberty several years after severe TBI. Design Follow-up at least 5 years post severe TBI of a prospective longitudinal study. Patients Overall, 66/87 children, who had endocrine evaluation 1 year post severe TBI, were included (24 with pituitary dysfunction 1 year post TBI). Main outcome measures In all children, the pituitary hormones basal levels were assessed at least 5 years post TBI. Growth hormone (GH) stimulation tests were performed 3–4 years post TBI in children with GH deficiency (GHD) 1 year post TBI and in all children with low height velocity (<−1 DS) or low IGF-1 (<−2 DS). Central precocious puberty (CPP) was confirmed by GnRH stimulation test. Results Overall, 61/66 children were followed up 7 (5–10) years post TBI (median; (range)); 17/61 children had GHD 1 year post TBI, and GHD was confirmed in 5/17 patients. For one boy, with normal pituitary function 1 year post TBI, GHD was diagnosed 6.5 years post TBI. 4/61 patients developed CPP, 5.7 (2.4–6.1) years post-TBI. Having a pituitary dysfunction 1 year post TBI was significantly associated with pituitary dysfunction or CPP more than 5 years post TBI. Conclusion Severe TBI in childhood can lead to permanent pituitary dysfunction; GHD and CPP may appear after many years. We recommend systematic hormonal assessment in children 1 year after severe TBI and a prolonged monitoring of growth and pubertal maturation. Recommendations should be elaborated for the families and treating physicians.


2020 ◽  
Vol 133 (5) ◽  
pp. 1559-1567 ◽  
Author(s):  
Hans Kristian Moe ◽  
Janne Limandvik Myhr ◽  
Kent Gøran Moen ◽  
Asta Kristine Håberg ◽  
Toril Skandsen ◽  
...  

OBJECTIVEThe authors investigated the association between the cause of injury and the occurrence and grade of traumatic axonal injury (TAI) on clinical MRI in patients with moderate or severe traumatic brain injury (TBI).METHODSData for a total of 396 consecutive patients, aged 7–70 years, with moderate or severe TBI admitted to a level 1 trauma center were prospectively registered. Data were included for analysis from the 219 patients who had MRI performed within 35 days (median 8, IQR 4–17 days) and for whom cause of injury was known. Cause of injury was registered as road traffic accident (RTA) or fall (both with respective subcategories), alpine skiing or snowboarding accident, or violence. The MRI protocol consisted of T2*-weighted gradient echo, FLAIR, and diffusion-weighted imaging scans. TAI lesions were evaluated in a blinded manner and categorized into 3 grades, hemispheric/cerebellar white matter (grade 1), corpus callosum (grade 2), and brainstem (grade 3). The absence of TAI was analyzed as grade 0. Contusions and mass lesions on CT were also registered.RESULTSCause of injury did not differ between included and nonincluded patients. TAI was found in 83% of patients in the included group after RTAs and 62% after falls (p < 0.001). Observed TAI grades differed between the subcategories of both RTAs (p = 0.004) and falls (p = 0.006). Pedestrians in RTAs, car drivers/passengers in RTAs, and alpine skiers had the highest prevalence of TAI (89%–100%) and the highest TAI grades (70%–82% TAI grades 2–3). TAI was found in 76% of patients after falls from > own height (45% TAI grade 2–3), 63% after falls down the stairs (26% TAI grade 2–3), and 31% after falls from ≤ own height (12% TAI grade 2–3). Moreover, 53% of patients with TAI after RTAs and 68% with TAI after falls had cortical contusions or mass lesions on CT.CONCLUSIONSThis prospective study of moderate and severe TBI is to the authors’ knowledge the first clinical MRI study to demonstrate both the high prevalence and grade of TAI after most of the different types of RTAs, alpine skiing accidents, and falls from a height. Importantly, TAI was also common following more low-energy trauma such as falls down the stairs or from own height. Physicians managing TBI patients in the acute phase should be aware of the possibility of TAI no matter the cause of injury and also when the CT scan shows cortical contusions or mass lesions.


2021 ◽  
Author(s):  
Anke W. van der Eerden ◽  
Thomas L. A. van den Heuvel ◽  
Marnix C. Maas ◽  
Priya Vart ◽  
Pieter E. Vos ◽  
...  

Abstract Introduction In order to augment the certainty of the radiological interpretation of “possible microbleeds” after traumatic brain injury (TBI), we assessed their longitudinal evolution on 3-T SWI in patients with moderate/severe TBI. Methods Standardized 3-T SWI and T1-weighted imaging were obtained 3 and 26 weeks after TBI in 31 patients. Their microbleeds were computer-aided detected and classified by a neuroradiologist as no, possible, or definite at baseline and follow-up, separately (single-scan evaluation). Thereafter, the classifications were re-evaluated after comparison between the time-points (post-comparison evaluation). We selected the possible microbleeds at baseline at single-scan evaluation and recorded their post-comparison classification at follow-up. Results Of the 1038 microbleeds at baseline, 173 were possible microbleeds. Of these, 53.8% corresponded to no microbleed at follow-up. At follow-up, 30.6% were possible and 15.6% were definite. Of the 120 differences between baseline and follow-up, 10% showed evidence of a pathophysiological change over time. Proximity to extra-axial injury and proximity to definite microbleeds were independently predictive of becoming a definite microbleed at follow-up. The reclassification level differed between anatomical locations. Conclusions Our findings support disregarding possible microbleeds in the absence of clinical consequences. In selected cases, however, a follow-up SWI-scan could be considered to exclude evolution into a definite microbleed.


Cephalalgia ◽  
2013 ◽  
Vol 33 (12) ◽  
pp. 998-1008 ◽  
Author(s):  
William C Walker ◽  
Jennifer H Marwitz ◽  
Amber R Wilk ◽  
Jessica M Ketchum ◽  
Jeanne M Hoffman ◽  
...  

Background: Headache (HA) following traumatic brain injury (TBI) is common, but predictors and time course are not well established, particularly after moderate to severe TBI. Methods: A prospective, longitudinal cohort study of HA severity post-TBI was conducted on 450 participants at seven participating rehabilitation centers. Generalized linear mixed-effects models (GLMMs) were used to model repeated measures (months 3, 6, and 12 post-TBI) of two outcomes: HA density (a composite of frequency, duration, and intensity) and HA disruptions to activities of daily living (ADL). Results: Although HA density and ADL disruptions were nominally highest during the first three months post-TBI, neither showed significant changes over time. At all time points, history of pre-injury migraine was by far the strongest predictor of both HA density and ADL disruptions (odds ratio (OR) = 8.0 and OR = 7.2, averaged across time points, respectively). Furthermore, pre-injury non-migraine HA (at three and six months post-TBI), penetrating-type TBI (at six months post-TBI), and female sex (at six and 12 months post-TBI) were each associated with an increase in the odds of a more severe HA density. Severity of TBI (post-traumatic amnesia (PTA) duration) was not associated with either outcome. Conclusion: Individuals with HA at three months after moderate-severe TBI do not improve over the ensuing nine months with respect to HA density or ADL disruptions. Those with pre-injury HA, particularly of migraine type, are at greatest risk for HA post-TBI. Other independent risk factors are penetrating-type TBI and, to a lesser degree and post-acutely only, female sex. Individuals with these risk factors should be monitored and considered for aggressive early intervention.


2005 ◽  
Vol 11 (1) ◽  
pp. 84-98 ◽  
Author(s):  
CATHY CATROPPA ◽  
VICKI ANDERSON

Limited research has investigated specific attentional sequelae following pediatric traumatic brain injury (TBI), such as sustained, selective, and shifting attention, as well as speed of processing. Little is known about the pattern of recovery of these skills or their interaction with ongoing development. The present study examined attentional abilities at acute, 6-, 12-, and 24-month time points postinjury in a group of 71 children who had sustained a mild, moderate, or severe TBI. Results indicated that children who sustained a severe TBI generally performed poorest, but showed most recovery over time. The pattern of recovery was dependent on the attentional component being measured. Specifically, deficits were most evident on more complex and timed tasks. While a number of areas showed recovery over time, for some attentional components, difficulties persisted to 24 months postinjury. (JINS, 2005,11, 84–98.)


2014 ◽  
Vol 99 (6) ◽  
pp. 2052-2060 ◽  
Author(s):  
Claire Personnier ◽  
Hélène Crosnier ◽  
Philippe Meyer ◽  
Mathilde Chevignard ◽  
Isabelle Flechtner ◽  
...  

Context: Traumatic brain injury (TBI) in childhood is a major public health issue. Objective: We sought to determine the prevalence of pituitary dysfunction in children and adolescents after severe TBI and to identify any potential predictive factors. Design: This was a prospective longitudinal study. Setting: The study was conducted at a university hospital. Patients: Patients, hospitalized for severe accidental or inflicted TBI, were included. The endocrine assessment was performed between 6 and 18 months after the injury. Main Outcome Measures: Basal and dynamic tests of pituitary function were performed in all patients and GH dynamic testing was repeated in patients with low stimulated GH peak (&lt;7 ng/mL). The diagnosis of proven severe GH deficiency (GHD) was based on the association of two GH peaks less than 5 ng/mL on both occasions of testing and IGF-I levels below −2 SD score. Initial cranial tomography or magnetic resonance imaging was analyzed retrospectively. Results: We studied 87 children and adolescents [60 males, median age 6.7 y (range 0.8–15.2)] 9.5 ± 3.4 months after the TBI (73 accidental, 14 inflicted). The second GH peak, assessed 4.9 ± 0.1 months after the first evaluation, remained low in 27 children and adolescents. Fifteen patients had a GH peak less than 5 ng/mL (mean IGF-I SD score −1.3 ± 1.5) and five (5.7%) strict criteria for severe GHD. Two children had mild central hypothyroidism and one had ACTH deficiency. We did not find any predictive factors associated with existence of GHD (demographic characteristics, growth velocity, trauma severity, and radiological parameters). Conclusion: At 1 year after the severe TBI, pituitary dysfunction was found in 8% of our study sample. We recommend systematic hormonal assessment in children and adolescents 12 months after a severe TBI and prolonged clinical endocrine follow-up.


2006 ◽  
Vol 155 (5) ◽  
pp. 663-669 ◽  
Author(s):  
Carlo L Acerini ◽  
Robert C Tasker ◽  
Simonetta Bellone ◽  
Gianni Bona ◽  
Christopher J Thompson ◽  
...  

Pituitary dysfunction is now well recognised after traumatic brain injury (TBI) in adults; however, little except anecdotal evidence is known about this potential complication in childhood and adolescence. Histopathological evidence exists for both hypothalamic and pituitary damage, but few data specific to children have been published. We review the available paediatric data, which shows that after both mild and severe TBI, hypopituitarism may occur, with GH and gonadotrophin deficiencies appearing to be most common. Precocious puberty has also been documented. Road-traffic accidents, falls, sport and child abuse are the most common aetiological factors for paediatric TBI. There are no published data on the incidence or prevalence, neither within a population of children with TBI, of hypopituitarism, nor on its natural history or response to hormone replacement. We urge paediatric endocrinologists, in collaboration with adult endocrinologists, to perform formal prospective research studies in patients suffering from TBI to clarify these questions.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A583-A583
Author(s):  
Shubham Agarwal ◽  
Sabah Patel ◽  
Faiza Hammad ◽  
Janice L Gilden

Abstract Background: Pituitary dysfunction and panhypopituitarism remain underdiagnosed in penetrating and blunt head trauma and can occur in both acute and chronic settings. Case: A 56 years old male with no significant PMH was admitted with a gunshot wound to the left T9 rib paraspinally with bullet deflection cranially along the left lung, left sternocleidomastoid, and resting anterior to the suprasellar cistern just above the midline of the sphenoid sinus close to the pituitary gland. Moderate volume pneumocephalus, chest hemopneumothorax, and sudden loss of right-sided vision required neurosurgical and pulmonary intervention. Endocrinology was consulted to evaluate pituitary function in the context of the bullet within the cranium. Physical examination showed intact mental status, non-focal exam, right-sided blindness, and foley catheter with normal urine output. Laboratory hormonal assessment for hypothalamic-pituitary axis (HPA) was performed consistent with normal sodium, potassium, FSH of 14.2 mIU/ml (1.0-13.0 mIU/ml), LH of 4.5 mIU/ml (1.0-9.0 mIU/ml), AM cortisol of 13.6 ug/dl (5-25 ug/dl), free cortisol of 2.06, ACTH of 10 pg/ml (10-60 pg/ml), IGF-1 of 80 ng/ml (78-220 ng/ml), TSH 1.93 mIU/L (0.5-5.0 mIU/L), FT4 1.05 ng/dl (0.8-1.8 ng/dl), Prolactin of 14.2 ng/ml (4-23 ng/ml) and HbA1c 5.1%. He reported no symptoms of adrenal insufficiency and remained hemodynamically stable. He was monitored for symptoms of pituitary insufficiency and suppression of the HPA axis along with urine output which remained normal and reassuring for the absence of central DI. The patient will continue outpatient endocrine surveillance. Discussion: The development of hormone deficiencies is directly related to the severity of head trauma. Mild traumatic brain injury (TBI) patients discharged from the ED, without loss of consciousness or post-traumatic amnesia less than 30 minutes do not require endocrine surveillance. Pituitary dysfunction occurs in 20-40% of patients with moderate to severe TBI. Pituitary ischemia leads to pituitary injury, due to changes in cerebral blood flow, cerebral hypoxia, and increased intracranial pressure. Compressive effects on the stalk from increased intracranial pressure is another indirect mechanism for pituitary dysfunction. Hospitalizations longer than 48 hours following TBI, require pituitary screening at 3-6 months. Chronic hypopituitarism develops in 15-20% of patients within 2-3 years with ACTH and GH deficiencies. Other changes in LH, FSH, TSH, and development of central diabetes insipidus can occur. However, despite severe TBI, acute pituitary hormonal involvement may not always occur, as in our patient. References: Tan CL, Alavi SA, Baldeweg SE, et al. The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance. J Neurol Neurosurg Psychiatry. 2017 Nov;88(11):971-981.


2018 ◽  
Vol 22 (4) ◽  
pp. 369-374 ◽  
Author(s):  
Ryan R. Metzger ◽  
Xiaoming Sheng ◽  
Christian M. Niedzwecki ◽  
Kimberly S. Bennett ◽  
Denise C. Morita ◽  
...  

OBJECTIVETraumatic brain injury (TBI) is the leading cause of acquired disability among children. Brain injury biomarkers may serve as useful diagnostic and prognostic indicators for TBI. Levels of ubiquitin C-terminal hydrolase-L1 (UCH-L1) and the 145-kDa alpha II-spectrin breakdown product (SBDP-145) correlate with outcome in adults after severe TBI. The authors conducted a pilot study of these biomarkers in children after severe TBI to inform future research exploring their utility in this population.METHODSThe levels of UCH-L1 and SBDP-145 were measured in serum, and UCH-L1 in CSF from pediatric patients after severe TBI over 5 days after injury. Both biomarkers were also measured in age-matched control serum and CSF.RESULTSAdequate numbers of samples were obtained in serum, but not CSF, to assess biomarker temporal response profiles. Using patients with samples from all time points, UCH-L1 levels increased rapidly and transiently, peaking at 12 hours after injury. SBDP-145 levels showed a more gradual and sustained response, peaking at 48 hours. The median serum UCH-L1 concentration was greater in patients with TBI than in controls (median [IQR] = 361 [187, 1330] vs 147 [50, 241] pg/ml, respectively; p < 0.001). Receiver operating characteristic (ROC) analysis revealed an AUC of 0.77. Similarly, serum SBDP-145 was greater in children with TBI than in controls (median [IQR] = 172 [124, 257] vs 69 [40, 99] pg/ml, respectively; p < 0.001), with an ROC AUC of 0.85. When only time points of peak levels were used for ROC analysis, the discriminability of each serum biomarker increased (AUC for UCH-L1 at 12 hours = 1.0 and for SBDP-145 at 48 hours = 0.91). Serum and CSF UCH-L1 levels correlated well in patients with TBI (r = 0.70, p < 0.001).CONCLUSIONSFindings from this exploratory study reveal robust increases of UCH-L1 and SBDP-145 in serum and UCH-L1 in CSF obtained from children after severe TBI. In addition, important temporal profile differences were found between these biomarkers that can help guide optimal time point selection for future investigations of their potential to characterize injury or predict outcomes after pediatric TBI.


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