Internal carotid artery dissection(ICAD) results from disruption of the intima of the arterial wall, and can lead to intrusion of blood into the arterial wall and form an intramural hematoma. The hematoma can compress...Internal carotid artery dissection(ICAD) results from disruption of the intima of the arterial wall, and can lead to intrusion of blood into the arterial wall and form an intramural hematoma. The hematoma can compress the true lumen of the vessel, causing functional stenosis or occlusion. The classic triad signs of ICAD include pain in the ipsilateral neck, head and orbital regions; a(partial) Horner syndrome; and cerebral or retinal ischemia. However, not all ICAD patients present with this classic signs. In some cases, ocular manifestations are the initial(and sometimes the only) findings. We summarize the ocular manifestations associated with ICAD in 3 categories: visual symptoms, oculosympathetic palsy, and ocular motor nerve palsy.展开更多
Objective:To study the effects of butyphthalide combined with antioxidant therapy on neurotrophic status and cellular oxidative damage in patients with cerebral infarction complicated by diabetic peripheral neuropathy...Objective:To study the effects of butyphthalide combined with antioxidant therapy on neurotrophic status and cellular oxidative damage in patients with cerebral infarction complicated by diabetic peripheral neuropathy.Methods: The patients with cerebral infarction complicated by diabetic peripheral neuropathy admitted to our hospital between January 2017 and December 2017 were selected and randomly divided into the control group receiving conventional therapy and the observation group receiving butyphthalide combined with antioxidant therapy. The contents of cytokines and oxidative damage markers in serum were measured before treatment and 4 weeks after treatment.Results: Serum brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), vascular endothelial growth factor (VEGF), platelet-derived endothelial cell growth factor (PD-ECGF) and total antioxidant capacity (T-AOC) levels of both groups significantly increased whereas macrophage migration inhibitory factor (MIF), tumor necrosis factor-α (TNF-α), chemokine ligand 16 (CXCL16), activated leukocyte cell adhesion molecule (ALCAM), platelet endothelial cell adhesion molecule-1 (PECAM-1), malondialdehyde (MDA), 8-iso-prostaglandin F2 (8-iso-PGF2 ) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels significantly decreased after treatment, and serum BDNF, IGF-I, VEGF, PD-ECGF and T-AOC levels of the observation group after treatment were significantly higher than those of the control group whereas MIF, TNF-α, CXCL16, ALCAM, PECAM-1, MDA, 8-iso-PGF2 and 8-OHdG levels were significantly lower than those of the control group.Conclusion: Butyphthalide combined with antioxidant treatment of cerebral infarction complicated by diabetic peripheral neuropathy can improve the neurotrophic status and alleviate the cellular oxidative damage.展开更多
基金Supported by Research and Development Program of Shaanxi Province, China (No.2017SF-279)Science and Technology Planned Projects of Xi’an, China [No.2017116SF/YX010(8)]Science and Technology Planned Projects of Xi’an, China [No.201805104YX12SF38(2)]
文摘Internal carotid artery dissection(ICAD) results from disruption of the intima of the arterial wall, and can lead to intrusion of blood into the arterial wall and form an intramural hematoma. The hematoma can compress the true lumen of the vessel, causing functional stenosis or occlusion. The classic triad signs of ICAD include pain in the ipsilateral neck, head and orbital regions; a(partial) Horner syndrome; and cerebral or retinal ischemia. However, not all ICAD patients present with this classic signs. In some cases, ocular manifestations are the initial(and sometimes the only) findings. We summarize the ocular manifestations associated with ICAD in 3 categories: visual symptoms, oculosympathetic palsy, and ocular motor nerve palsy.
文摘Objective:To study the effects of butyphthalide combined with antioxidant therapy on neurotrophic status and cellular oxidative damage in patients with cerebral infarction complicated by diabetic peripheral neuropathy.Methods: The patients with cerebral infarction complicated by diabetic peripheral neuropathy admitted to our hospital between January 2017 and December 2017 were selected and randomly divided into the control group receiving conventional therapy and the observation group receiving butyphthalide combined with antioxidant therapy. The contents of cytokines and oxidative damage markers in serum were measured before treatment and 4 weeks after treatment.Results: Serum brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), vascular endothelial growth factor (VEGF), platelet-derived endothelial cell growth factor (PD-ECGF) and total antioxidant capacity (T-AOC) levels of both groups significantly increased whereas macrophage migration inhibitory factor (MIF), tumor necrosis factor-α (TNF-α), chemokine ligand 16 (CXCL16), activated leukocyte cell adhesion molecule (ALCAM), platelet endothelial cell adhesion molecule-1 (PECAM-1), malondialdehyde (MDA), 8-iso-prostaglandin F2 (8-iso-PGF2 ) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels significantly decreased after treatment, and serum BDNF, IGF-I, VEGF, PD-ECGF and T-AOC levels of the observation group after treatment were significantly higher than those of the control group whereas MIF, TNF-α, CXCL16, ALCAM, PECAM-1, MDA, 8-iso-PGF2 and 8-OHdG levels were significantly lower than those of the control group.Conclusion: Butyphthalide combined with antioxidant treatment of cerebral infarction complicated by diabetic peripheral neuropathy can improve the neurotrophic status and alleviate the cellular oxidative damage.