Vocal Quality Complication Following Chondrolaryngoplasty: A Reported Case.

INTRODUCTION: Few studies have evaluated complications from chondrolaryngoplasty related to postoperative changes in voicing. This study adds to the literature a presentation of voice changes experienced by a patient following chondrolaryngoplasty. METHODS: Case-report. RESULTS: We present the case of a transgender female who experienced significant changes to pitch, vocal range, intensity, and vocal quality following chondrolaryngoplasty. Changes may be attributed to a surgical technique that failed to identify the level of the vocal folds during the operation. DISCUSSION: Chondrolaryngoplasty is a complex operation. This case illustrates the potential complications resulting from a surgical technique that fails to appropriately identify the level of the true vocal folds' to avoid destabilization of the anterior commissure. CONCLUSIONS: We reported this case of significant complication related to voicing following chondrolaryngoplasty. Future studies are necessary to explore potential long-term voice complications from this procedure. Surgeons performing this procedure must be aware of this potential complication.

No false elevation in ankle brachial index in patients with tibial plateau fractures and vascular risk factors.

Objectives: The ankle brachial index (ABI) is a useful tool in detection of lower extremity vascular injury. However, diabetes mellitus (DM), chronic kidney disease (CKD), and peripheral vascular disease (PVD) may affect extremity perfusion leading to possible false elevation of the ABI value. If true in trauma patients, this can affect initial evaluation, diagnostics, and management. We therefore explored mean ABI values in tibial plateau fractures of patients with vascular risk factors to help determine whether there is a difference. Design: This is a retrospective chart review of patients sustaining tibial plateau fractures with a specific ABI value recorded in the medical record. Patients were identified as either having vascular risk factors or not and data analysis performed to determine if their ABI differed and whether they were more likely to have a vascular injury. Results: 282 acute tibial plateau injuries with specific ABI values were identified, 46 of which carried the risk factors in question. The average risk factor group ABI was 0.95 ±â€¯0.15 versus those without risk factors 1.0 ±â€¯0.15 (p = 0.057). No patient with risk factors required a vascular intervention or four-compartment fasciotomy. Conclusions: This study shows no statistical significance between the presenting ABI of patients with risk factors such as DM, CKD, or PVD and those without those risk factors who sustained acute tibial plateau fractures. Therefore, in general the ABI still holds as a useful screening tool for evaluation of vascular insult in the setting of acute lower extremity trauma.

An emergent neural coactivity code for dynamic memory.

Neural correlates of external variables provide potential internal codes that guide an animal's behavior. Notably, first-order features of neural activity, such as single-neuron firing rates, have been implicated in encoding information. However, the extent to which higher-order features, such as multineuron coactivity, play primary roles in encoding information or secondary roles in supporting single-neuron codes remains unclear. Here, we show that millisecond-timescale coactivity among hippocampal CA1 neurons discriminates distinct, short-lived behavioral contingencies. This contingency discrimination was unrelated to the tuning of individual neurons, but was instead an emergent property of their coactivity. Contingency-discriminating patterns were reactivated offline after learning, and their reinstatement predicted trial-by-trial memory performance. Moreover, optogenetic suppression of inputs from the upstream CA3 region during learning impaired coactivity-based contingency information in the CA1 and subsequent dynamic memory retrieval. These findings identify millisecond-timescale coactivity as a primary feature of neural firing that encodes behaviorally relevant variables and supports memory retrieval.

A stable home-base promotes allocentric memory representations of episodic-like everyday spatial memory.

A key issue in neurobiological studies of episodic-like memory is the geometric frame of reference in which memory traces of experience are stored. Assumptions are sometimes made that specific protocols favour either allocentric (map-like) or egocentric (body-centred) representations. There are, however, grounds for suspecting substantial ambiguity about coding strategy, including the necessity to use both frames of reference occasionally, but tests of memory representation are not routinely conducted. Using rats trained to find and dig up food in sandwells at a particular place in an event arena (episodic-like 'action-where' encoding), we show that a protocol previously thought to foster allocentric encoding is ambiguous but more predisposed towards egocentric encoding. Two changes in training protocol were examined with a view to promoting preferential allocentric encoding-one in which multiple start locations were used within a session as well as between sessions; and another that deployed a stable home-base to which the animals had to carry food reward. Only the stable home-base protocol led to excellent choice performance which rigorous analyses revealed to be blocked by occluding extra-arena cues when this was done after encoding but before recall. The implications of these findings for studies of episodic-like memory are that the representational framework of memory at the start of a recall trial will likely include a path direction in the egocentric case but path destination in the allocentric protocol. This difference should be observable in single-unit recording or calcium-imaging studies of spatially-tuned cells.

Purkinje cell loss in experimental autoimmune encephalomyelitis.

Gray matter atrophy observed by brain MRI is an important correlate to clinical disability and disease duration in multiple sclerosis. The objective of this study was to link brain atrophy visualized by neuroimaging to its underlying neuropathology using the MS model, experimental autoimmune encephalomyelitis (EAE). Volumetric changes in brains of EAE mice, as well as matched healthy normal controls, were quantified by collecting post-mortem high-resolution T2-weighted magnetic resonance microscopy and actively stained magnetic resonance histology images. Anatomical delineations demonstrated a significant decrease in the volume of the whole cerebellum, cerebellar cortex, and molecular layer of the cerebellar cortex in EAE as compared to normal controls. The pro-apoptotic marker caspase-3 was detected in Purkinje cells and a significant decrease in Purkinje cell number was found in EAE. Cross modality and temporal correlations revealed a significant association between Purkinje cell loss on neuropathology and atrophy of the molecular layer of the cerebellar cortex by neuroimaging. These results demonstrate the power of using combined population atlasing and neuropathology approaches to discern novel insights underlying gray matter atrophy in animal models of neurodegenerative disease.

Cerebellar cortical atrophy in experimental autoimmune encephalomyelitis.

Brain atrophy measured by MRI is an important correlate with clinical disability and disease duration in multiple sclerosis (MS). Unfortunately, neuropathologic mechanisms which lead to this grey matter atrophy remain unknown. The objective of this study was to determine whether brain atrophy occurs in the mouse model, experimental autoimmune encephalomyelitis (EAE). Postmortem high-resolution T2-weighted magnetic resonance microscopy (MRM) images from 32 mouse brains (21 EAE and 11 control) were collected. A minimum deformation atlas was constructed and a deformable atlas approach was used to quantify volumetric changes in neuroanatomical structures. A significant decrease in the mean cerebellar cortex volume in mice with late EAE (48-56 days after disease induction) as compared to normal strain, gender, and age-matched controls was observed. There was a direct correlation between cerebellar cortical atrophy and disease duration. At an early time point in disease, 15 days after disease induction, cerebellar white matter lesions were detected by both histology and MRM. These data demonstrate that myelin-specific autoimmune responses can lead to grey matter atrophy in an otherwise normal CNS. The model described herein can now be used to investigate neuropathologic mechanisms that lead to the development of gray matter atrophy in this setting.