Growth hormone deficiency and hypopituitarism in adults after complicated mild traumatic brain injury.

PURPOSE: Traumatic brain injury is considered the main cause of hypopituitarism in adults, and GH deficiency appears to be the most frequent pituitary deficit. Most of the available studies have included all degrees of severity of trauma. We aimed to assess pituitary function and GH deficiency in adult patients at different time lengths after complicated mild TBI according to Glasgow Coma Scale. We also aimed to evaluate whether mild TBI patients with GH deficiency had developed alterations in the glycolipid profile. METHODS: Forty-eight patients (34 men and 14 women) with complicated mild TBI were included in the study. Twenty-three patients were evaluated at 1 year (Group A) and 25 patients at 5 years or longer after the injury (Group B). All patients underwent basal hormonal evaluation for pituitary function. GH deficiency was investigated by the combined test (GH releasing hormone + arginine). The glycolipid profile was also evaluated. RESULTS: GH deficiency occurred in 8/23 patients (34.7 %) of Group A and in 12/25 patients (48 %) of Group B. In addition, two patients, one in each group, showed evidence of central hypothyroidism. Patients with GH deficiency, especially in Group A, presented a higher frequency of visceral adiposity and adverse metabolic profile as compared to no-GH deficiency patients. CONCLUSIONS: Patients examined at 1 year or several years from complicated mild TBI had a similarly high occurrence of isolated GH deficiency, which was associated with visceral adiposity and metabolic alterations. Our findings suggest that patients undergone complicated mild TBI should be evaluated for GH deficiency even after several years from trauma.

Complete oculomotor palsy caused by persistent trigeminal artery.

Primitive trigeminal artery (PTA) is the most frequent embryonic communication between the carotid and vertebro-basilar system. PTA is a pathophysiology phenomenon which has been implicated as a rare cause of cranial nerve dysfunction. We report the case of a 40-year-old woman who developed a complete oculomotor nerve palsy caused by a persistent ecstatic trigeminal artery. Brain MRI and MRA studies documented a neurovascular conflict between the oculomotor nerve and a PTA. To the best of our knowledge there is no report about complete third cranial nerve palsy NC due to a PTA. A role of this rare vascular condition is discussed.

Glucose metabolism in the idiopathic blepharoptosis: utility of the Oral Glucose Tolerance Test (OGTT) and of the Insulin Resistance Index.

BACKGROUND: Diabetes mellitus (DM), neuromuscular, hereditary or immunological disorders are the most common identified causes of blepharoptosis. However, in about 15-25% they remained uncertain. OBJECTIVE: To determined the role of glucose metabolism abnormality in idiopathic blepharoptosis. METHODS: We identified 162 patients with unilateral idiopathic blepharoptosis and 128 control subjects. In all we evaluated a glucose and insulin levels at fasting and after 2 h-OGTT. In addition we determined insulin resistance (IR), by HOMA-index. RESULTS: Following a 2 h-OGTT the prevalence of undiagnosed glucose metabolism abnormality was significantly higher in blepharoptosis patients vs. control group (P<.001). The IR was documented in 129 patients (78%), of whom 55 (34%) had Impaired Glucose Tolerance (IGT), 36 (22%) newly diagnosed DM (NDDM) and 38 (30%) only IR. The Body Mass Index, blood pressure, serum lipids, triglycerides and smoking were not associated with an increased risk of developing ptosis. Conversely, waist circumference were significantly increased in blepharoptosis patients (P=.003). CONCLUSIONS: In this study we focused on emerging evidence that prediabetic status may represent a risk factor for developing blepharoptosis. We propose that 2 h-OGTT and mainly HOMA-index should be determined as a rule in all patients with idiopathic blepharoptosis.