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Syndrome of the trephined (SoT) is a severe complication following decompressive craniectomy resulting in neurological decline which can progress to aphasia, catatonia, and even death. While cranioplasty can reverse neurological symptoms of SoT, awareness of SoT is poor outside of the neurosurgery community. The authors performed a systematic review of the literature on SoT with a focus on reconstructive implications. Search terms “syndrome of the trephined” and “sunken flap syndrome” were applied to PubMed to identify primary studies through October 2021. Full-text review yielded 11 articles discussing SoT and reconstructive techniques or implications with 56 patients undergoing cranial reconstruction. Average age of the patients was 41.8±9.5 years. Sixty-three percent of the patients were male. The most common indication for craniectomy was traumatic brain injury (43%), followed by tumor resection (23%), intracerebral hemorrhage (11%), and aneurysmal subarachnoid hemorrhage (2%). Patients most commonly suffered from motor deficits (52%), decreased wakefulness (30%), depression or anxiety (21%), speech deficits (16%), headache (16%), and cognitive difficulties (2%). Time until presentation of symptoms following decompression was 4.4±8.9 months. Patients typically underwent cranioplasty with polyetheretherketone (48%), titanium mesh (21%), split thickness calvarial bone (16%), full thickness calvarial bone (14%), or split thickness rib graft (4%). Eight percent of patients required free tissue transfer for soft tissue coverage. Traumatic Brain Injury (TBI) was a risk factor for development of SoT when adjusting for age and sex (odds ratio: 8.2, 95% confidence interval: 1.2–8.9). No difference significant difference was observed between length until initial improvement of neurological symptoms following autologous versus allograft reconstruction (P=0.47). SoT can be a neurologically devastating complication of decompressive craniectomy which can resolve following urgent cranioplasty. Familiarity with this syndrome and its reconstructive implications is critical for the plastic surgery provider, who may be called upon to assist with these urgent cases.

This review examines various aspects of traumatic brain injury (TBI) and its potential role as a causative agent for type 2 diabetes mellitus (T2DM) in the veteran population. The pituitary glands and the hypothalamus, both housed in the intracranial space, are the most important structures for the homeostatic regulation of almost every hormone in the human body. As such, TBI not only causes psychological and cognitive impairments but can also disrupt the endocrine system. It is well established that in addition to having a high prevalence of chronic traumatic encephalopathy (CTE), veterans have a very high risk of developing various chronic medical conditions. Unfortunately, there are no measures or prophylactic agents that can have a meaningful impact on this medically complex patient population. In this review, we explore several important factors pertaining to both acute and chronic TBI that can provide additional insight into why veterans tend to develop T2DM later in life. We focus on the unique combination of risk factors in this population not typically found in civilians or other individuals with a non-military background. These include post-traumatic stress disorder, CTE, and environmental factors relating to occupation and lifestyle.

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