Carl Marincowitz and Will Townend
Background: Head injury represents an extremely common presentation to Emergency Departments (ED), but not all patients present immediately after injury. There is evidence that clinical deterioration following head injury will usually occur within 24 hours. It is unclear whether this means that head injury patients that present in a delayed manner, especially after 24 hours, have a lower prevalence of significant traumatic injuries.
Methods: This is a commentary on a systematic review that we conducted with the aim of identifying all studies that assess the risk of significant injuries in delayed ED presentation head injury populations. We postulated that the risk of injury may be different in this group compared to patients that present immediately.
Results: Three studies were eligible for inclusion. They were all of poor methodological quality, and heterogeneity prevented meta-analysis. The reported prevalence of traumatic intra-cranial injury on CT was between 2.2% and 6.3%.
Conclusion: Available evidence suggests that head injury patients who present in a delayed fashion to the ED may have lower rates of intra-cranial injury compared to non-delayed head injury patients. However, the evidence is sparse and it is of too low quality to guide clinical practice. Further research is required to help the clinical risk assessment of this group.
DOI: 10.29245/2572.942X/2016/1.1006 View / Download PdfKurt A. Jellinger
Multiple system atrophy (MSA) is a fatal orphan neurodegenerative disorder that manifests with autonomic, parkinsonian, cerebellar, and pyramidal features. It is characterized by the accumulation of misfolded α-synuclein (αSyn) in oligodendroglia and neurons, affecting multiple parts of the central, autonomic and perípheral system. Both the etiology and pathogenesis of MSA are unknown, although a genetic component has been proposed. Accumulation of aberrant αSyn in oligodendrocytes, preceded by relocation of p25α protein from myelin into oligodendroglia, results in the formation of insoluble glial cytoplasmic inclusions (GCIs). These changes are associated with proteasomal, mitochondrial and lipid transport dysfunction, oxidative stress, reduced trophic transport, neuroinflammation and other noxious factors. Their interaction induces dysfunction of the oligodendroglial-myelin-axon-neuron complex, resulting in the system-specific pattern of neurodegeneration characterizing MSA as a synucleinopathy with oligodendroglio-neuronopathy. Propagation of modified toxic αSyn species from neurons to oligodendroglia by "prion-like" transfer and its spreading to associate neuronal pathways result in multi-system involvement. No reliable biomarkers are currently available for the clinical diagnosis and prognosis of MSA and neither effective neuroprotective nor disease-modifying therapies of MSA are available, although novel treatment strategies targeting αSyn are under discussion. Multidisciplinary research to elucidate the genetic and molecular background of the deleterious cycle of noxious processes to develop reliable diagnostic biomarkers and to deliver targets for effective treatment of this hitherto incurable disorder is urgently needed.
DOI: 10.29245/2572.942X/2016/1.1002 View / Download PdfWolfgang H Jost
For years we have been injecting botulinum toxin relying mainly on our clinical experience and, in some cases, on the use of electromyography. Within that time some therapists introduced sonography for guidance and emphasize the advantages of this technique. Schramm et al., for example, pointed out the relevance of sonography for botulinum toxin treatment in cervical dystonia. Within a short time the importance of sonography has been well documented in this indication. Even assuming a critical distance, the significance of this technique has become largely indisputable.
DOI: 10.29245/2572.942X/2016/1.1010 View / Download Pdf