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Migrainous facial palsy (MFP): the introduction of a new concept of neurovascular conflict and its preliminary clinical evidence.

偏头痛性面神经麻痹 (MFP): 神经血管冲突新概念的引入及其初步临床证据。

  • 影响因子:1.76
  • DOI:10.1007/s10072-020-04370-0
  • 作者列表:"Bhatjiwale M","Bhatjiwale M
  • 发表时间:2020-04-01

BACKGROUND:Facial palsy and migraine have frequently been reported to occur in conjunction. We report a case series and propound a theory to explain the same. AIMS AND OBJECTIVES:To postulate an anatomico-pathophysiological association in the causative factor of lower motor neuron type of facial palsy in cases with migraine without aura. MATERIALS AND METHODS:Preliminary experiences and observations in 12 cases suffering from facial palsy following an attack of migraine without aura, mainly in the occipital and posterior auricular region, are elaborated. RESULTS:Facial palsy occurred on the ipsilateral side as the headaches in a majority of the cases (83.33%) and in rare cases of bilateral headaches (16.67%), it lateralised to the side the headaches were more severe. In most of these cases (75%), a complete clinical recovery was noted within 6 months. CONCLUSION:We concluded that neurogenic inflammation of the facial nerve trunk caused by its proximity to the dilated posterior auricular/stylomastoid/occipital and superficial temporal arteries during a migraine attack leads to a temporary lower motor neuron type of paresis of the muscles supplied by the facial nerve. SIGNIFICANCE:This pathophysiological understanding of the disease mechanism could open new avenues as to the treatment of this condition. This proposition indicates in clearer light than before, a possible mechanism to explain the higher incidence and risk of facial palsy in migraineurs.


背景: 面神经麻痹和偏头痛经常被报道合并发生。我们报告了一个病例系列,并提出了一个理论来解释同样的问题。 目的和目的: 在无先兆偏头痛的病例中,假设下运动神经元型面瘫的致病因素与解剖病理生理相关。 材料和方法: 对 12 例以枕部和耳后区为主的无先兆偏头痛发作后面瘫患者的初步经验和观察进行了阐述。 结果: 大部分病例 (83.33%) 的头痛发生在同侧面瘫,罕见的双侧头痛 (16.67%),它向侧面偏侧,头痛更严重。在大多数这些病例 (75%) 中,在 6 个月内观察到完全的临床恢复。 结论: 我们的结论是,偏头痛发作时面神经干靠近扩张的耳后/茎突肌/枕部和颞浅动脉引起的神经源性炎症导致暂时性下运动神经元型面神经供应的肌肉麻痹。 意义: 这种对疾病机制的病理生理学理解可以为这种疾病的治疗开辟新的途径。这一命题比以前更清晰地表明,这是解释偏头痛患者面瘫发病率和风险更高的可能机制。



作者列表:["Garabadu D","Singh D"]

METHODS::Multiple sclerosis (MS) is a chronic neurodegenerative disorder with clinical symptoms of neuroinflammation and demyelination in the central nervous system. Recently, herbal medicines are clinically effective against MS as the current disease-modifying drugs have limited effectiveness. Hence, the present study evaluated the therapeutic potential of Ocimum basilicum essential oil (OB) in ethidium bromide (EB)-induced cognitive deficits in the male rats. Further, the effect of OB (50, 100 and 200 μL/kg) was evaluated on EB-induced neuroinflammation, astrogliosis and mitochondrial dysfunction in the pre-frontal cortex (PFC) of the animals. The EB was injected through bilateral intracerebroventricular route into hippocampus to induce MS-like manifestations in the rats. OB (100 and 200 μL/kg) and Ursolic acid (UA) significantly reduced the EB-induced cognitive deficits in Morris water maze and Y-maze test paradigms. OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced neuroinflammation in terms of increase in the levels of pro-inflammatory cytokines (TNF-alpha and IL-6) in the rat PFC. Further, OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced astrogliosis in terms of increase in the levels of GFAP (Glial fibrillary acidic protein) and Iba-1 (Ionized calcium binding adaptor molecule-1) in the rat PFC. In addition, OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced decrease in the mitochondrial function, integrity, respiratory control rate and ADP/O in the PFC of the rodents. Moreover, OB (100 and 200 μL/kg) and UA significantly reduced the EB-induced mitochondria-dependent apoptosis in the PFC of the rat. Hence, it can be presumed that OB could be a potential alternative drug candidate in the pharmacotherapy of MS.

来源期刊:Experimental neurology
作者列表:["Bertrand SJ","Zhang Z","Patel R","O'Ferrell C","Punjabi NM","Kudchadkar SR","Kannan S"]

METHODS::Sleep fragmentation is an increase in sleep-wake transitions without an overall decrease in total sleep time. Sleep fragmentation is well documented during acute and chronic hospitalization and can result in delirium and memory problems in children. Sleep fragmentation is also often noted in neurodevelopmental disorders. However, it is unclear how sleep fragmentation independent of disease affects brain development and function. We hypothesized that acute sleep fragmentation during the neonatal period in otherwise healthy animals would result in neuroinflammation and would be associated with abnormalities in cognitive development. The orbital shaker method was used to fragment sleep for 72 h in postnatal day 3 New Zealand white rabbit kits (fragmentation group). To control for maternal separation, the sham group was separated from the dam and maintained in the same conditions without undergoing sleep fragmentation. A naïve control group remained with the dam. Kits underwent behavioral testing with novel object recognition and spontaneous alternation T-maze tests at 2-3 weeks post-fragmentation and were sacrificed 3-50 days after fragmentation. Sleep fragmentation resulted in acute and chronic changes in microglial morphology in the hippocampus and cortex, and regional differences in mRNA expression of pro- and anti-inflammatory cytokines at 3, 7 and 50 days post-fragmentation. Impaired novel object recognition and a longer latency in T-maze task completion were noted in the fragmented kits. This was in spite of normalization of sleep architecture noted at 2 months of age in these kits. The results indicate that transient neonatal sleep fragmentation results in short-term and long-term immune alterations in the brain, along with diminished performance in cognitive tasks long-term.

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来源期刊:World neurosurgery
作者列表:["Middlebrooks EH","Lin C","Okromelidze L","Lu CQ","Tatum WO","Wharen RE Jr","Grewal SS"]

METHODS:BACKGROUND:Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) is a recently approved therapy for patients with drug-resistant epilepsy. To date, there is a poor understanding of the mechanism of action and lack of in vivo biomarkers. We propose a method for investigating the in vivo stimulation effects using blood-oxygen-level dependent (BOLD) MRI and present the brain activation pattern associated with ANT DBS. METHODS:Two patients undergoing ANT DBS for epilepsy underwent BOLD MRI using a block design after the DBS was programmed to alternate ON/OFF in 30 second blocks. The scanner was triggered utilizing surface electrophysiological recording to detect the DBS cycle. Nine total runs were obtained and were analyzed using a general linear model. RESULTS:Active ANT stimulation produced activation within several areas of the brain, including the thalamus, bilateral anterior cingulate and posterior cingulate cortex, precuneus, medial prefrontal cortex, amygdala, ventral tegmental area, hippocampus, striatum, and right angular gyrus. CONCLUSIONS:Utilizing block-design BOLD MRI, we were able to show widespread activation resulting from ANT DBS. Overlap with multiple areas of both the default mode and limbic networks was shown suggesting that these nodes may modulate the effect of seizure control with ANT DBS.

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