Abstract: OBJECTIVE The diagnosis of growth hormone deficiency (GHD) in adults is established through growth hormone (GH) stimulation testing, which is often complex, expensive, time-consuming and may be associated with adverse side effects. The decision to perform GH provocative testing is influenced by clinical findings, medical history and biochemical evidence. We report in this study our experience using the glucagon stimulation test (GST) in assessing GHD in adult patients with traumatic brain injury (TBI) as it relates to baseline serum insulin-like growth factor-1 (IGF-1) concentrations. DESIGN A receiver operating characteristic (ROC) curve analysis was performed to determine the optimal IGF-1 cut-off for diagnosis of GHD at different potential diagnostic GST cut-off values (<3, <5, & <10 μg/l). PATIENTS One hundred and thirty-eight patients (98 men and 40 women) with a documented history of moderate to severe TBI were assessed for GHD using serum IGF-1 concentrations and the GST. MEASUREMENTS IGF-1 values were compared with peak GH values obtained following the GST. RESULTS An IGF-1 cut-off value of 175 μg/l minimized the misclassification of GHD patients and GH-sufficient patients and provided a sensitivity of 83% and specificity of 40%, as well as a negative predictive power of 90% considering a criterion for peak GH response of <3 μg/l. CONCLUSIONS Our current findings are consistent with previous work assessing peak GH response using the insulin tolerance test (ITT) in a non-TBI sample, suggesting that diagnostic accuracy may be optimized if the GST is used when obtained serum IGF-1 concentrations are below 175 μg/l. While the decision to perform provocative testing to assess GHD in adult patients should be based on the clinician's clinical impression, the findings from this retrospective study can provide useful clinical information and serve as a guide.

Abstract: Chronic illnesses are projected to affect 157 million individuals in the United States by the year 2020. Few studies have investigated the experience of chronic illnesses in minority groups. The pu...

Abstract: A 25-year-old woman with no significant medical history and who was not previously on medications is admitted to your inpatient rehabilitation unit. She sustained a traumatic brain injury due to a high-speed motor vehicle crash 4 weeks ago. She was restrained. There was prolonged extrication of 30 minutes, but no clear documentation of hemodynamic instability. The initial Glasgow Coma Scale (GCS) score was 3. She was intubated at the scene. The initial head computed tomography demonstrated bifrontal contusions, a left frontoparietal subdural hemorrhage, and evidence of diffuse axonal injury. No skull or facial fractures were noted. She underwent an emergent craniotomy for evacuation of the subdural hemorrhage. Intracranial pressure monitoring did not demonstrate elevations of intracranial pressure after surgery, and cerebral perfusion remained adequate. She was weaned from the ventilator after 3 weeks. Since then, she has reportedly been lethargic but occasionally lifts her thumb to command. She has been afebrile, with some tachycardia (100-110 beats per minute) but normotensive. Laboratory values have been notable for mild hyponatremia (sodium, 128-135 mmol/L). On admission, her pupils are responsive, her eyes are open, she appears to track objects, but she has a left cranial nerve VI palsy and does not follow any commands. She is afebrile, blood pressure is 140/80 mmHg, pulse 100 beats per minute, respirations 20 per minute. She has a tracheostomy, with minimal secretions. There has been recent literature that has suggested a rather high prevalence of endocrine abnormalities after brain injuries but no clear guidelines regarding who should be screened for these deficits, what tests should be ordered to evaluate, and, if present, when to treat deficits. The situation is complicated because many of the clinical signs and symptoms of endocrine abnormalities may also be due to a number of other neuromedical complications of traumatic brain injury or the brain injury itself. From the information presented, when should a laboratory workup for endocrinopathies be initiated for this patient and what tests (if any) should be ordered? Guest Discussants:

Abstract: Background: Balint's syndrome includes the clinical symptom triad of simultagnosia, ocular apraxia and optic ataxia. These symptoms, in combination, are rare and can be quite debilitating as they impact visuospatial skills, visual scanning and attentional mechanisms.Case Study: The literature addressing rehabilitation of individuals with Balint's syndrome is sparse. The current case report describes the outcome of a 58-year old male who presented with Balint's syndrome secondary to severe traumatic brain injury and following completion of a comprehensive post-acute brain injury rehabilitation programme. The patient was 4-months post-injury onset upon admission and received 6 months of rehabilitation services as an inpatient. The patient's comprehensive rehabilitation programme involved a 3-pronged approach including the implementation of (a) compensatory strategies, (b) remediation exercises and (c) transfer of learned skills in multiple environments and situations with implementation of psychoeducation a...