Connellnewell1823

A CT-guided biopsy revealed a GN. Debulking surgery was performed and a small amount of residual tumor was left in the paravertebral nerve roots. The patient recovered well with no complications. The diagnosis of GN was confirmed with pathology, which was reviewed by the Tumor Board; the Board agreed that only follow-up in the Surgery Clinic was needed. During the patient's last visit, 10 months after surgery, a follow-up CT scan showed that the residual tumor was stable. CONCLUSIONS GNs are benign abdominal and retroperitoneal tumors that are typically asymptomatic and detected incidentally. Surgical resection is the treatment of choice and even when it is incomplete, the prognosis for patients is excellent.BACKGROUND Although several studies have shown that ultramarathon running causes severe physical and mental stress and harms organ systems, its effect on brain tissue remains unclear. The purpose of this study was to investigate the volumetric change of cortical and subcortical brain structures following 38.6-km and 119.8-km mountain races. MATERIAL AND METHODS A total of 23 healthy male runners (age, 49.05±5.99 years) were classified as short-trail (ST; n=9) and ultra-trail (UT; n=14) endurance running. Pre- and post-test scanning of brain tissue was performed by using a 3-Tesla magnetic resonance imaging (MRI). Pre- and post-race differences in cortical and subcortical volumes in the ST and UT groups were separately determined by Wilcoxon signed-rank test. RESULTS Cortical gray matter (GM) and cerebral GM volume significantly increased after the race in both ST and UT groups, whereas the volume of the thalamus, caudate, pallidus, and hippocampus significantly increased only in the UT group. Cerebrospinal fluid (CSF) and white-matter (WM) volumes did not change after endurance running and remained unaltered in both groups. CONCLUSIONS Endurance running has a site-specific acute effect on cortical and subcortical structures and may attenuate GM volume decrease in older adult male athletes. EGFR activity The increased volume of subcortical structures might be a response of physical exercise and additional physical stress experienced by ultramarathon runners.

Since its outbreak in Wuhan, China in late 2019, coronavirus disease-19 (COVID-19) has become a global pandemic. The number of affected cases and deaths continues to rise. Primarily a respiratory illness, COVID-19 is now known to affect various organ systems including peripheral nerve and skeletal muscle. The purpose of this review is to discuss the scope of neuromuscular manifestations and complications of COVID-19.

Several neuromuscular conditions, including Guillain-Barré syndrome, rhabdomyolysis, and myositis, have been reported in patients infected with COVID-19, but even with a temporal association, a causal relationship remains unproven. Direct invasion of neurons or myocytes by the virus, and immune-mediated injury have been speculated but not consistently demonstrated. In addition to potentially causing the above conditions, COVID-19 can trigger exacerbations of preexisting neuromuscular conditions such as myasthenia gravis, and severe infections can lead to critical illness myopathy/polyneuropathy.

COVID-19 appears to be potentially associated with a wide range of neuromuscular manifestations and complications. Further studies are needed to examine these possible associations, understand the pathogenesis, and develop preventive and treatment strategies.

COVID-19 appears to be potentially associated with a wide range of neuromuscular manifestations and complications. Further studies are needed to examine these possible associations, understand the pathogenesis, and develop preventive and treatment strategies.

Triphasic waves arising in patients with toxic metabolic encephalopathy (TME) are often considered different from generalized periodic discharges (GPDs) in patients with generalized nonconvulsive status epilepticus (GNCSE). The primary objective of this study was to investigate whether a common mechanism can explain key aspects of both triphasic waves in TME and GPDs in GNCSE.

A neural mass model was used for the simulation of EEG patterns in patients with acute hepatic encephalopathy, a common etiology of TME. Increased neuronal excitability and impaired synaptic transmission because of elevated ammonia levels in acute hepatic encephalopathy patients were used to explain how triphasic waves and GNCSE arise. The effect of gamma-aminobutyric acid-ergic drugs on epileptiform activity, simulated with a prolonged duration of the inhibitory postsynaptic potential, was also studied.

The simulations show that a model that includes increased neuronal excitability and impaired synaptic transmission can account for both the emergence of GPDs and GNCSE and their suppression by gamma-aminobutyric acid-ergic drugs.

The results of this study add to evidence from other studies calling into question the dichotomy between triphasic waves in TME and GPDs in GNCSE and support the hypothesis that all GPDs, including those arising in TME patients, occur via a common mechanism.

The results of this study add to evidence from other studies calling into question the dichotomy between triphasic waves in TME and GPDs in GNCSE and support the hypothesis that all GPDs, including those arising in TME patients, occur via a common mechanism.

Triphasic waves are intuitively distinctive waveforms that fall under the umbrella of generalized periodic discharges. The ability to distinguish these waveforms consistently could be helpful if a specific underlying pathophysiology could be identified. However, scalp EEG and clinical observation have been limited in their ability to elucidate the underlying cortical physiology that leads to triphasic waves. Evidence from intracranial physiologic data and computational modeling suggest that these and other periodic discharges should be viewed not as strictly ictal nor non-ictal but rather on the spectrum between these two. Triphasic waves in particular appear to result from an abnormal balance between cortical excitation and synaptic transmission with input from functionally connected brain networks, such as the thalamocortical pathways involved in arousal. The practical implication of triphasic waves begins with acknowledgement of uncertainty and a rational approach should ask whether the pattern-or its treatment-might be creating harm.