"Penumbra sign" in knee pain: a case of distal femur osteomyelitis

"Penumbra sign" is a characteristic finding in magnetic resonance imaging (MRI) of Brodie's abscess, a rare variant of subacute osteomyelitis. We aimed to discuss the imaging finding penumbra sign that will help in the diagnosis of osteomyelitis and may be useful to clinicians in differential diagnosis. A 26-year-old male patient presented to the emergency department with complaints of pain and limping in the right knee that did not go away. He had a history of arthroscopic debridement and percutaneous fixation surgery due to osteochondral fragment 3 years ago. There were no additional findings in the patient's vital parameters, physical examination, and medical history. X-ray imaging revealed two screws in the distal femur and a well-defined sclerotic rim surrounding a radiolucent lesion anterior to the screws. MRI revealed a lesion in the distal femoral metaphysis with low-density fluid and hyperintense granulation tissue surrounding it. After surgical abscess drainage and local debridement, bone cement was placed in the resulting cavity. Teicoplanin treatment was started. The patient was discharged and complete recovery was achieved in the second month. The diagnosis of osteomyelitis is often missed or confused with bone tumors in non-traumatic cases presenting with persistent bone pain. MRI imaging is frequently used in differential diagnosis, and detection of characteristic imaging signs such as the penumbra sign accelerates the diagnosis. In this context, emergency department clinicians, in particular, should be cautious and not forget that early treatment can be started by recognizing these signs.

Penumbra aspiration thrombectomy of the superior mesenteric artery for mesenteric ischemia.

Acute mesenteric ischemia from thromboembolic occlusion is a life-threatening emergency associated with a high mortality rate. Prompt diagnosis and intervention are vital to preserve viable bowel and prevent mortality. In the past decade, a shift has occurred toward minimally invasive alternatives such as endovascular therapies. We present a case of acute mesenteric ischemia from superior mesenteric artery thrombosis treated promptly with the Penumbra suction thrombectomy device (Penumbra Inc).

Assessing the influence of migraine on ischemic penumbra and on the prognosis of ischemic stroke: A prospective cohort study.

INTRODUCTION: There is controversy as to whether migraine affects the behavior of ischemic penumbra during the acute phase of an ischemic stroke, thereby accelerating the formation of cerebral infarction. OBJECTIVES: To assess whether migraine modifies the existence and volume of the divergence between the areas of diffusion and perfusion in the stroke (the penumbra) and whether migraine implies a poorer prognosis after the stroke. METHODS: This was a prospective cohort study. We included hospitalized patients with ischemic stroke within 72 h of symptom onset (convenience sampling). A semi-structured questionnaire, the National Institute of Health Stroke Scale, and the modified Rankin Scale (mRS) were used. Patients underwent magnetic resonance imaging (MRI) of the brain with diffusion and with perfusion. Patients were assessed by telephone 3 months after the stroke to determine the prognosis. Scores of > 2 on the mRS were considered to have a poor prognosis. RESULTS: A total of 221 patients were included, 131/221 (59%) of whom were male, and with a mean (SD) age of 68.2 (13.8) years. Ischemic penumbra analysis was performed in 118 patients. There was no association between migraine and the absence of ischemic penumbra (16/63 [25%] vs. 12/55 [22%]; odds ratio 1.22, 95% confidence interval 0.52-2.87; p = 0.64). There was no difference in stroke volume between those with and without migraine (median [interquartile range] 1.0 [0.4-7.9] vs. 1.8 [0.3-9.4] cm3 ; p = 0.99). Migraine was not associated with the stroke prognosis after multivariable analysis. CONCLUSION: Migraine is not associated with the absence of ischemic penumbra, the volume of the ischemic penumbra, or the stroke prognosis.

Neurotrauma: The Crosstalk between Neurotrophins and Inflammation in the Acutely Injured Brain.

Traumatic brain injury (TBI) is a major cause of morbidity and mortality among young individuals worldwide. Understanding the pathophysiology of neurotrauma is crucial for the development of more effective therapeutic strategies. After the trauma occurs, immediate neurologic damage is produced by the traumatic forces; this primary injury triggers a secondary wave of biochemical cascades together with metabolic and cellular changes, called secondary neural injury. In the scenario of the acutely injured brain, the ongoing secondary injury results in ischemia and edema culminating in an uncontrollable increase in intracranial pressure. These areas of secondary injury progression, or areas of "traumatic penumbra", represent crucial targets for therapeutic interventions. Neurotrophins are a class of signaling molecules that promote survival and/or maintenance of neurons. They also stimulate axonal growth, synaptic plasticity, and neurotransmitter synthesis and release. Therefore, this review focuses on the role of neurotrophins in the acute post-injury response. Here, we discuss possible endogenous neuroprotective mechanisms of neurotrophins in the prevailing environment surrounding the injured areas, and highlight the crosstalk between neurotrophins and inflammation with focus on neurovascular unit cells, particularly pericytes. The perspective is that neurotrophins may represent promising targets for research on neuroprotective and neurorestorative processes in the short-term following TBI.

Menstrual blood transplantation for ischemic stroke: Therapeutic mechanisms and practical issues.

Cerebrovascular diseases are a major cause of death and long-term disability in developed countries. Tissue plasmin activator (tPA) is the only approved therapy for ischemic stroke, strongly limited by the short therapeutic window and hemorrhagic complications, therefore excluding most patients from its benefits. The rescue of the penumbra area of the ischemic infarct is decisive for functional recovery after stroke. Inflammation is a key feature in the penumbra area and it plays a dual role, improving injury in early phases but impairing neural survival at later stages. Stem cells can be opportunely used to modulate inflammation, abrogate cell death and, therefore, preserve neural function. We here discuss the possible role of stem cells derived from menstrual blood as restorative treatment for stroke. We highlight the availability, proliferative capacity, pluripotentiality and angiogenic features of these cells and explore their present and future experimental and clinical applications.

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain

Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed the effects of HT induced after recirculation of focal brain ischemia on infarct size during long survival times. Adult male Wistar rats underwent intra-luminal occlusion of the left middle cerebral artery for 60 min followed by HT (39.0-39.5°C) or normothermia. Control procedures included none and sham surgery with and without HT, and middle cerebral artery occlusion alone. Part I: 6-h HT induced at recirculation. Part II: 2-h HT induced at 2-, 6-, or 24-h recirculation. Part III: 2-h HT initiated at recirculation or 6-h HT initiated at 2-, 6- or 24-h recirculation. Survival periods were 7 days, 2 or 6 months. The effects of post-ischemic HT on cortex and striatum were evaluated histopathologically by measuring the area of remaining tissue in the infarcted hemisphere at -0.30 mm from bregma. Six-hour HT initiated from 6-h recirculation caused a significant decrease in the remaining cortical tissue between 7-day (N = 8) and 2-month (N = 8) survivals (98.46 ± 1.14 to 73.62 ± 8.99 percent, respectively). When induced from 24-h recirculation, 6-h HT caused a significant reduction of the remaining cortical tissue between 2- (N = 8) and 6-month (N = 9) survivals (94.97 ± 5.02 vs 63.26 ± 11.97 percent, respectively). These data indicate that post-ischemic HT triggers chronic neurodegenerative processes in ischemic penumbra, suggesting that similar fever-triggered effects may annul the benefit of early recirculation in stroke patients over the long-term.