A Narrative Review of Stroke of Cortical Hand Knob Area.

The cortical hand knob region of the brain is a knob-like segment of the precentral gyrus, projecting into the middle genu of the central sulcus. This anatomic landmark is responsible for intricate control of hand motor movements and has often been implicated in motor weakness following stroke. In some instances, damage to this area has been mistaken for peripheral causes of hand weakness. Our article aims to consolidate clinically relevant information on the cortical hand knob area in a comprehensive review to guide clinicians regarding diagnosis and treatment strategies. We conducted a systematic search within the Medline/PubMed database for reports of strokes in the cortical hand knob region. All studies were published electronically up until December 2023. The search was conducted using the keyword "hand knob". A total of 24 reports containing 150 patients were found. The mean and median ages were 65 and 67 years, respectively. Sixty-two percent of the individuals were male. According to the TOAST criteria for the classification of the stroke, 59 individuals had a stroke due to large-artery atherosclerosis, 8 had small-vessel occlusion, 20 had cardioembolism, 25 were determined, and 38 were undetermined. The most common etiologies for stroke in the hand knob area can be attributed to large vessel occlusions, small vessel occlusions, or cardioembolism. Presentations following damage to this area can mimic ulnar, median, or radial neuropathy as well. Our comprehensive review serves as a resource for recognizing and managing stroke in the cortical hand knob area.

Chemokine signaling mediated monocyte infiltration affects anxiety-like behavior following blast injury.

The activation of resident microglia and infiltrated monocytes are known potent mediators of chronic neuroinflammation following traumatic brain injury (TBI). In this study, we use a mouse model of blast-induced TBI (bTBI) to investigate whether microglia and monocytes contribute to the neuroinflammatory and behavioral consequences of bTBI. Eight-ten week old mice were subject to moderate TBI (180 kPa) in a shock tube. Using double transgenic CCR2RFP/+: CX3CR1GFP/+ mice, we were able to note that in addition to resident Cx3CR1+ microglia, infiltrating CCR2+ monocytes also contributed to the expanding macrophage population that was observed after bTBI. The microglia activation and monocyte infiltration occurred as early as 4 h and lasted up to 30d after blast exposure, suggesting chronic inflammation. The infiltration of monocytes may be partly mediated by chemokine CCL2-CCR2 signaling axis and compromised blood brain barrier permeability. Hence, bTBI-induced infiltration of monocytes and production of IL-1ß were prevented in mice lacking CCR2 (CCR2 KO). Finally, this study showed that interference of monocyte infiltration using CCR2 KO, ameliorated the chronic effects of bTBI such as anxiety-like behavior and short-term memory decline. Taken together, these data suggest that bTBI leads to activation of both resident microglia and infiltrated monocytes. The infiltration of monocytes was partly mediated by CCL2-CCR2 signaling, which in turn contributes to increased production of IL-1ß leading to behavioral deficits after bTBI. Furthermore, bTBI induced behavioral outcomes were reduced by targeting CCL2-CCR2 signaling, highlighting the significance of this signaling axis in bTBI pathology.