Search Results (5)

Drug-induced gingival overgrowth is associated with various systemic diseases, including epilepsy. Among antiepileptic medications, phenytoin is commonly reported to cause this condition. In contrast, sodium valproate (VPA), another widely used antiepileptic drug, rarely induces gingival overgrowth. This difference in side effects highlights the variability in drug-induced oral complications among different antiepileptic medications. This case study presents a patient who developed significant gingival overgrowth after using VPA for over 10 years. The study aims to identify VPA as the causative agent and observe changes during long-term administration and after dose reduction. Our findings demonstrate that even long-standing gingival overgrowth can improve rapidly following discontinuation of the causative medication, providing valuable insights for managing similar cases in the future. Full article

Background/Objectives: This study aimed to develop and validate a stratified risk model for predicting high opioid use in patients with acute brain injury due to stroke or traumatic brain injury (TBI) admitted to a neurocritical care intensive care unit. Methods: We examined the factors associated with the use of high-opioids (≥75th quartile, ≥17.5 oral morphine equivalent/ICU day) in a retrospective cohort study including patients with acute ischemic stroke, spontaneous intracerebral hemorrhage, spontaneous subarachnoid hemorrhage, and TBI. We then developed, trained, and validated a risk model to predict high-dose opioids. Results: Among 2490 patients aged 45–64 years (β = −0.25), aged 65–80 years (β = −0.97), and aged ≥80 years (β = −1.17), a history of anxiety/depression (β = 0.57), a history of illicit drug use (β = 0.79), admission diagnosis (β = 1.21), lowest Glasgow Coma Scale Score (GCSL) [GCSL 3–8 (β = −0.90], {GCS L 9–12 ((β = −0.34)], mechanical ventilation (β = 1.21), intracranial pressure monitoring (β = 0.69), craniotomy/craniectomy (β = 0.6), and paroxysmal sympathetic hyperactivity (β = 1.12) were found to be significant predictors of high-dose opioid use. When validated, the model demonstrated an area under the curve ranging from 0.72 to 0.82, accuracy ranging from 0.68 to 0.91, precision ranging from 0.71 to 0.94, recall ranging from 0.75 to 1, and F1 ranging from 0.74 to 0.95. Conclusions: A personalized stratified risk model may allow clinicians to predict the risk of high opioid use in patients with acute brain injury due to stroke or TBI. Findings need validation in multi-center cohorts. Full article

Spinal cord injury (SCI) is a catastrophic event with multiple comorbidities including spastic paralysis, sensory loss, autonomic dysfunction with sympathetic blunting, neurogenic orthostatic hypotension, neurogenic restrictive and obstructive lung disease, neuropathic pain, spasticity, neurogenic bladder, neurogenic bowel, immobilization hypercalcemia, osteopenia/osteoporosis, neurogenic obesity, and metabolic dysfunction. Cervical and thoracic SCI is all too often accompanied by traumatic brain injury (TBI), which carries its own set of comorbidities including headaches, seizures, paroxysmal sympathetic hyperactivity, aphasia, dysphagia, cognitive dysfunction, memory loss, agitation/anxiety, spasticity, bladder and bowel incontinence, and heterotopic ossification. This manuscript will review the etiology and epidemiology of dual diagnoses, assessment of both entities, and discuss some of the most common comorbidities and management strategies to optimize functional recovery. Full article

Traumatic brain injury (TBI) and its potential long-term consequences are of major concern for public health. Neurorehabilitation of affected individuals has some specific characteristics in contrast to neurorehabilitation of patients with acquired brain lesions of other aetiology. This review will deal with the clinical consequences of the distinct lesions of TBI. In severe TBI, clinical course often follows a typical initial sequence of coma; followed by disturbed consciousness; later, post-traumatic agitation and amnesia; and finally, recovery of function occurs. In the different phases of neurorehabilitation, physicians should be aware of typical medical complications such as paroxysmal sympathetic hyperactivity, posttraumatic hydrocephalus, and posttraumatic neuroendocrine dysfunctions. Furthermore, we address questions on timing and on existing evidence for different rehabilitation programmes and for holistic neuropsychological rehabilitation approaches. Full article

Traumatic brain injury is not a discrete event but an unfolding sequence of damage to the central nervous system. Not only the acute phase but also the subacute and chronic period after injury, i.e., during inpatient rehabilitation, is characterized by multiple neurotransmitter alterations, cellular dysfunction, and medical complications causing additional secondary injury. Neuroendocrine disturbances also influence neurological outcome and are easily overlooked as they often present with diffuse symptoms such as fatigue, depression, poor concentration, or a decline in overall cognitive function; these are also typical sequelae of traumatic brain injury. Furthermore, neurological complications such as hydrocephalus, epilepsy, fatigue, disorders of consciousness, paroxysmal sympathetic hyperactivity, or psychiatric-behavioural symptoms may mask and/or complicate the diagnosis of neuroendocrine disturbances, delay appropriate treatment and impede neurorehabilitation. The present review seeks to examine the interrelation between neuroendocrine disturbances with neurological complications frequently encountered after moderate to severe TBI during rehabilitation. Common neuroendocrine disturbances and medical complications and their clinical implications are discussed. Full article