Does That Go There? A Rare Occurrence of Spontaneous Sternocleidomastoid Abscess without Trauma in a Diabetic Individual.

BACKGROUND Spontaneous abscesses are generally typical in patients with significant risk factors and have been linked to numerous muscle groups. The sternocleidomastoid muscle, however, piqued our interest as an unusual location, especially in this patient who, other than diabetes mellitus, had no associated risk factors or signs of trauma. CASE REPORT A 61-year-old man appeared with neck pain, erythema, and swelling that had been present for 9 days and for which he had previously been examined in the Emergency Department. He was discharged on oral doxycycline after initial computed tomography (CT) of the neck revealed infiltration without collection. He returned with worsening symptoms and new-onset fever and chills. Vital signs were normal on assessment, with no evidence of trauma. Swelling was observed near the right sternocleidomastoid muscle insertion. A repeat CT scan of the neck revealed an abscess 2.5 cm in diameter. He was originally treated with empiric antibiotics before being moved to targeted medications. Incision and drainage were completed without complication. The patient was given a 6-week course of oral antibiotics. CONCLUSIONS Spontaneous intramuscular abscesses are uncommon in people who have had no previous trauma or other known risk factors, but could be encountered in diabetic patients with non-optimal blood glucose levels, due to bacteremia. As a result, these cases require a high level of suspicion to be recognized and treated early. The scarcity of literature on this illness makes determining the cause challenging. However, by highlighting this case, we intend to raise awareness and facilitate early diagnosis and treatment.

Group A Streptococcus Pneumonia in a Previously Healthy Individual: Is It Still a Thing?

Group A streptococcus (GAS) is known to cause many different kinds of infections, including invasive pneumonia in rare cases. When it is the causative agent, it is associated with a more severe disease course, but it can often be adequately treated if caught early enough. We hereby present the case of a 32-year-old male with no past medical history who presented with fever, hemoptysis, and tachycardia. Laboratory results showed leukocytosis, hyponatremia, mild transaminitis, and elevated creatine kinase. Initial imaging findings and clinical presentation were concerning for tuberculosis (TB) vs. community-acquired pneumonia (CAP), as it yielded a consolidation in the right upper lobe. The patient had no obvious risk factor except for imprisonment two years prior to symptoms onset. Empirical antibiotics and steroids were started. Quantiferon and acid-fast bacteria (AFB) were negative, but sputum and blood cultures were positive for Streptococcus pyogenes, ruling out TB. Antibiotic therapy was narrowed down. The patient responded well to therapy, with subsequent resolution of symptoms. The current body of knowledge regarding respiratory infections caused by GAS is limited by multiple factors, including its relative rarity and the diversity of how it can present, especially in a developed country. Its mimicry characteristics of other clinical entities, such as TB, can be deceiving, which can delay appropriate treatment if it occurs in settings where the diagnostic tools are not readily available. By sharing more cases and atypical presentations of this disease, the clinical presentations of this pathogen can be more fully understood, and it can be more rapidly identified and treated.

Methanol Intoxication-Associated Brain Hemorrhages: Can Early Detection Be Life-Saving? A Case Report.

BACKGROUND Methanol can cause many acute complications when ingested, either intentionally or accidentally. One rare complication is cerebral hemorrhage, which can present with focal neurologic deficits, decreased consciousness, and fixed, dilated pupils. With vigilant monitoring of patients in the acute period of toxicity, rapid identification, and initiation of treatment, outcomes can potentially be improved in these patients. CASE REPORT We present a case of a 42-year-old man who presented after ingestion of windshield wiper fluid. Initial symptoms started with fatigue and altered mental status, but he quickly developed abdominal pain and became obtunded. CT initially showed no acute hemorrhage or other pathology, but on day 2, despite receiving fomepizole, bicarbonate, and dialysis, the patient became hypotensive and showed loss of cranial nerve reflexes, and repeated CT head scans showed acute intracranial hemorrhage with mass effect. CONCLUSIONS Although the exact mechanism of intracranial hemorrhage and necrosis following methanol intoxication remains uncertain, we know beyond doubt that it can progress rapidly and lead to severe and irreversible complications, so identifying and treating it immediately is essential. In this case, methanol ingestion was known on presentation, antidote and renal replacement therapy were initiated within hours of ingestion, yet our patient still suffered fatal brain hemorrhage. Important warning signs of acute hemorrhage include loss of cranial nerve reflexes and decrease in consciousness, so these findings warrant further evaluation and prompt neuroimaging, especially in high-risk patients like the one in this report.

High-frequency repetitive transcranial magnetic stimulation enhances layer II/III morphological dendritic plasticity in mouse primary motor cortex.

High-frequency repeated transcranial magnetic stimulation (HF-rTMS) is a safe non-invasive neuromodulatory technique and there is a body of evidence shows that it can modulate plasticity in different brain areas. One of the most interesting application of HF-rTMS is the modulation of plasticity in primary motor cortex (M1) to promote recovery after brain injuries. However, the underlying mechanism by which HF-rTMS modulates motor cortex plasticity remain to be investigated. In this study, we investigated the effects of HF-rTMS treatment on morphological plasticity of pyramidal neurons in layer II/III (L2/3) of the primary motor cortex in mice. Our results show that the treatment did not increase anxiety in mice in the open field test and the elevated plus-maze test. Treated mice displayed increased total spine density in apical and basal dendrites, with a predominance of thin spines. The treatment also increased dendritic complexity, as assessed by Sholl analysis at both apical and basal dendrites. Collectively, the results show that HF-rTMS induced remarkable changes in dendritic complexity in primary motor cortex L2/3 connections which may strengthen corticocortical connections increasing integration of information across cortical areas. The data support the use of HF-rTMS as a circuit-targeting neuromodulation strategy.

Reduced Reelin Expression in the Hippocampus after Traumatic Brain Injury.

Traumatic brain injury (TBI) is a relatively common occurrence following accidents or violence, and often results in long-term cognitive or motor disability. Despite the high health cost associated with this type of injury, presently there are no effective treatments for many neurological symptoms resulting from TBI. This is due in part to our limited understanding of the mechanisms underlying brain dysfunction after injury. In this study, we used the mouse controlled cortical impact (CCI) model to investigate the effects of TBI, and focused on Reelin, an extracellular protein that critically regulates brain development and modulates synaptic activity in the adult brain. We found that Reelin expression decreases in forebrain regions after TBI, and that the number of Reelin-expressing cells decrease specifically in the hippocampus, an area of the brain that plays an important role in learning and memory. We also conducted in vitro experiments using mouse neuronal cultures and discovered that Reelin protects hippocampal neuronal cells from glutamate-induced neurotoxicity, a well-known secondary effect of TBI. Together our findings suggest that the loss of Reelin expression may contribute to neuronal death in the hippocampus after TBI, and raise the possibility that increasing Reelin levels or signaling activity may promote functional recovery.

Angiotensin II Causes Neuronal Damage in Stretch-Injured Neurons: Protective Effects of Losartan, an Angiotensin T1 Receptor Blocker.

Angiotensin II (Ang II) is a mediator of oxidative stress via activation/induction of reactive oxygen and nitrogen species-generating enzymes, NADPH oxidase (NOX) and inducible nitric oxide synthase (iNOS). We investigated the hypothesis that overproduction of Ang II during traumatic brain injury (TBI) induces the activation of the oxidative stress, which triggers neuroinflammation and cell apoptosis in a cell culture model of neuronal stretch injury. We first established that stretch injury causes a rapid increase in the level of Ang II, which causes the release of pro-inflammatory cytokines, IL-1ß and TNF-α, via the induction of oxidative stress. Since angiotensin-converting enzyme (ACE) mediates the production of Ang II via the conversion of Ang I into Ang II, we analyzed the expression of ACE by western blotting. Further, we analyzed caspase-3-mediated apoptosis by TUNEL staining and annexin V western blotting. Angiotensin type I (AT1) receptor antagonist losartan attenuated Ang II-induced oxidative stress and associated neuroinflammation and cell death in cultured neurons. Remarkably, we noticed that the expression of Ang II type 1 receptor (AngT1R) upregulated in neuronal stretch injury; losartan mitigates this upregulation. Findings from this study significantly extend our understanding of the pathophysiology of TBI and may have significant implications for developing therapeutic strategies for TBI-associated brain dysfunctions.