ABSTRACT
We present an unusual case of a 62-year-old male presenting with contralateral hypoglossal and recurrent laryngeal nerve palsies following endotracheal intubation for emergency cardiac surgery. Postoperative, the patient was referred to Speech and Language Therapy due to concerns regarding the safety of his swallow. Oromotor assessment revealed left-sided tongue weakness and aphonia. Flexible endoscopic evaluation of swallowing (FEES) revealed a right vocal cord palsy and severe oropharyngeal dysphagia. There were no other focal neurological signs. An MRI head did not demonstrate a medial medullary stroke or other intracranial lesion. CT neck showed no abnormality identified in relation to the course of the right vagus nerve or recurrent laryngeal nerve at the skull base or through the neck respectively. The patient required a gastrostomy for nutrition and hydration. He continued to be assessed at several month intervals over the course of a year using FEES to obtain a range of voice, secretion and swallowing outcome measures. The patient commenced intensive dysphagia therapy targeting pharyngeal drive, hyolaryngeal excursion and laryngeal sensation. Swallow manoeuvres were trialled during FEES and a head-turn to the side of the vocal cord palsy during deglutition reduced aspiration risk which expedited return to oral intake. The patient had partial recovery over twelve months. Hypoglossal nerve palsy completely resolved. The right vocal cord remained paralysed however the left vocal cord compensated enabling the patient to produce a normal voice. The patient was able to take thin fluids and regular diet and the gastrostomy was removed.
ABSTRACT
OBJECTIVES: Traumatic brain injury (TBI) is a major cause of long-term disability with variable recovery. Preclinical studies suggest that vitamin D status influences the recovery after TBI. However, there is no published clinical data on links between vitamin D status and TBI outcomes. The aim was to determine the (i) prevalence of vitamin D deficiency/insufficiency, and associations of vitamin D status with (ii) demographic factors and TBI severity, and with (iii) cognitive function, symptoms and quality of life, in adults after TBI. DESIGN: Retrospective audit of patients seen between July 2009 and March 2015. Serum vitamin D (25-hydroxy-cholecalciferol) was categorized as deficient (<40 nmol/l), insufficient (40-70 nmol/l) or replete (>70 nmol/l). PATIENTS: A total of 353 adults seen in tertiary hospital clinic (75·4% lighter skinned, 74·8% male, age median 35·1 year, range 26·6-48·3 year), 0·3-56·5 months after TBI (74·5% moderate-severe). MEASUREMENTS: Serum vitamin D concentrations; Addenbrooke's Cognitive Examination (ACE-R), Beck Depression Inventory-II (BDI-II), SF-36 Quality of Life, Pittsburgh Sleep Quality Index. RESULTS: In total, 46·5% of patients after TBI had vitamin D deficiency and 80·2% insufficiency/deficiency. Patients with vitamin D deficiency had lower ACE-R scores than those of vitamin D replete (mean effect size ± SEM 4·5 ± 2·1, P = 0·034), and higher BDI-II scores than those of vitamin D insufficient (4·5 ± 1·6, P = 0·003), correcting for age, gender, time since TBI and TBI severity. There was no association between vitamin D status and markers of TBI severity, sleep or quality of life. CONCLUSION: Vitamin D deficiency is common in patients after TBI and associated with impaired cognitive function and more severe depressive symptoms.