Traumatic spondyloptosis of the dorsal spine with incomplete neurological deficit

Injury ◽  
1983 ◽  
Vol 15 (1) ◽  
pp. 35-37 ◽  
Author(s):  
W.S.El Masri ◽  
J.R. Silver
Keyword(s):  
Neurological Deficit ◽  
Dorsal Spine

scholarly journals Excision of intra-dural dorsal spine meningioma with intra-operative neuromonitoring in a patient with post-pneumonectomy status- an anaesthetic challenge

2021 ◽  
Vol 8 (4) ◽  
pp. 615-618
Author(s):  
Amruta M Kulkarni ◽  
Vijay L Shetty
Keyword(s):  
Evoked Potentials ◽  
Female Patient ◽  
Neurological Deficit ◽  
Dorsal Spine ◽  
Anaesthetic Technique ◽  
Physiological Changes ◽  
Neurological Damage ◽  
Complete Excision ◽  
Optimal Monitoring ◽  
Anaesthetic Agents

Post-pneumonectomy status is associated with various anatomical and physiological changes. Intra-operative neuromonitoring allows for safe neurosurgery with minimal neurological damage. Intra-operative neuromonitoring requires that the anaesthetic technique be modified taking into considerations the effects of various anaesthetic agents on evoked potentials to allow for optimal monitoring. We present a case of 65 year old female patient, with post-pneumonectomy status posted for excision of intra-dural D10 meningioma with intra-operative neuromonitoring. The case was successfully conducted with meticulous planning and preparation with complete excision of lesion and no neurological deficit post-operatively.

Effect of age on outcome in patients with cerebral stroke

2020 ◽  
pp. 41-45
Author(s):  
G. R. Kuchava ◽  
E. V. Eliseev ◽  
B. V. Silaev ◽  
D. A. Doroshenko ◽  
Yu. N. Fedulaev
Keyword(s):  
Ischemic Stroke ◽  
Neurological Deficit ◽  
Neurological Status ◽  
Statistical Correlation ◽  
Multiple Organ ◽  
The Body ◽  
Social Adaptation ◽  
Cerebral Stroke ◽  
Septic Complications ◽  
Risk Of Death

The aim of the study was to assess the course and outcome of cerebral infarction, depending on the age factor and duration of stay in the neuroblock. Materials and methods: a dynamic observation of 494 patients, men and women, aged 38–84 years with acute ischemic stroke of hemispheric localization, which were divided into the three groups depending on age, was performed. Group 1 – younger than 60 years old, group 2–60–70 years old, group 3 – older than 60 years. All patients underwent standard therapy, according to the recommendations for the treatment of ischemic stroke. The patients underwent comprehensive clinical and instrumental monitoring, which included assessment of somatic and neurological status according to the NIH‑NINDS scales at 1st, 3rd, 10th days and at discharge or death; assessment of the level of social adaptation according to the Bartel scale on 1st, 3rd, 10th days and at discharge, clinical and biochemical blood tests, computed tomography of the brain. Assessment of the quality of therapy was carried out according to specially developed maps using methods of statistical correlation analysis. Results: the most pronounced positive dynamics of neurological status was in the 1st group of patients. The regression of neurological deficit in the 2nd group was worse. The minimal dynamics of neurological deficit was in the 3rd group of patients with cerebral stroke. Most often, the death of patients with cerebral stroke occurred from the development of multiple organ disorders. Conclusions: patients over 70 years of age have the greatest risk of death, due to: a decrease in the reactivity of the body, the presence of initially severe concomitant somatic pathology in patients with admission to hospital; accession of secondary somatic and purulent‑septic complications.

Decrease of blood flow velocity in the middle cerebral artery after stellate ganglion block following aneurysmal subarachnoid hemorrhage: a potential vasospasm treatment?

2020 ◽  
Vol 133 (3) ◽  
pp. 773-779
Author(s):  
Christopher Wendel ◽  
Ricardo Scheibe ◽  
Sören Wagner ◽  
Wiebke Tangemann ◽  
Hans Henkes ◽  
...  
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Neurological Deficit ◽  
Blood Flow Velocity ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Stellate Ganglion ◽  
Stellate Ganglion Block ◽  
Ganglion Block

OBJECTIVECerebral vasospasm (CV) is a delayed, sustained contraction of the cerebral arteries that tends to occur 3–14 days after aneurysmal subarachnoid hemorrhage (aSAH) from a ruptured aneurysm. Vasospasm potentially leads to delayed cerebral ischemia, and despite medical treatment, 1 of 3 patients suffer a persistent neurological deficit. Bedside transcranial Doppler (TCD) ultrasonography is used to indirectly detect CV through recognition of an increase in cerebral blood flow velocity (CBFV). The present study aimed to use TCD ultrasonography to monitor how CBFV changes on both the ipsi- and contralateral sides of the brain in the first 24 hours after patients have received a stellate ganglion block (SGB) to treat CV that persists despite maximum standard therapy.METHODSThe data were culled from records of patients treated between 2013 and 2017. Patients were included if an SGB was administered following aSAH, whose CBFV was ≥ 120 cm/sec and who had either a focal neurological deficit or reduced consciousness despite having received medical treatment and blood pressure management. The SGB was performed on the side where the highest CBFV had been recorded with 8–10 ml ropivacaine 0.2%. The patient’s CBFV was reassessed after 2 and 24 hours.RESULTSThirty-seven patients (male/female ratio 18:19), age 17–70 years (mean age 49.9 ± 11.1), who harbored 13 clipped and 22 coiled aneurysms (1 patient received both a coil and a clip, and 3 patients had 3 untreated aneurysms) had at least one SGB. Patients received up to 4 SGBs, and thus the study comprised a total of 76 SGBs.After the first SGB, CBFV decreased in 80.5% of patients after 2 hours, from a mean of 160.3 ± 28.2 cm/sec to 127.5 ± 34.3 cm/sec (p < 0.001), and it further decreased in 63.4% after 24 hours to 137.2 ± 38.2 cm/sec (p = 0.007). A similar significant effect was found for the subsequent SGB. Adding clonidine showed no significant effect on either the onset or the duration of the SGB. Contralateral middle cerebral artery (MCA) blood flow was not reduced by the SGB.CONCLUSIONSTo the authors’ knowledge, this is the largest study on the effects of administering an SGB to aSAH patients after aneurysm rupture. The data showed a significant reduction in ipsilateral CBFV (MCA 20.5%) after SGB, lasting in about two-thirds of cases for over 24 hours with no major complications resulting from the SGB.

Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

2020 ◽  
Vol 23 (3) ◽  
pp. 214-224 ◽  
Author(s):  
Esra Cakir ◽  
Ufuk Cakir ◽  
Cuneyt Tayman ◽  
Tugba Taskin Turkmenoglu ◽  
Ataman Gonel ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Brain Damage ◽  
Neurological Deficit ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Cortex Cell

Background: Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. Objective: The aim of this study was to investigate the role of ASX on brain IRI. Methods: A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. Results: In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Conclusion: Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.

Hypoglycemic Hemiparesis Masquerading As Ischemic Stroke: When Guideline Fails

2020 ◽  
Vol 15 (4) ◽  
pp. 420-422
Author(s):  
Dhruvkumar M. Patel ◽  
Mukundkumar V. Patel ◽  
Jayanti K. Gurumukhani ◽  
Maitri M. Patel ◽  
Himal J. Mahadevia ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Thrombolytic Therapy ◽  
Neurological Deficit ◽  
Clinical Case ◽  
Complete Recovery ◽  
Acute Onset ◽  
Diabetic Patients ◽  
Focal Neurological Deficit ◽  
Random Blood Sugar ◽  
Resident Doctor

Background: Hypoglycemia may rarely present as hemiparesis and sometimes it is difficult to differentiate from ischemic stroke. When random blood sugar (RBS) value is between 50 and 80 mg % in patients presenting with focal neurological deficit, no guideline exists to consider the possibility of hypoglycemia before initiating thrombolytic therapy. Clinical Case: A 58-year-old male, who was a known case of diabetes and hypertension, was brought to the emergency room with acute onset of right hemiparesis and dysarthria of 90 minutes duration. His NIHSS Score was 9, blood pressure was 150/90 mm of Hg and RBS was 79 mg% on admission. His CT scan brain was normal and was considered for thrombolysis. Resident doctor not aware of previous sugar repeated RBS before thrombolysis which was surprisingly 60 mg% 60 minutes after the first RBS. Even though he was a candidate for thrombolysis, intravenous 25 % dextrose was administered considering the possibility of hypoglycemia. He made a complete recovery within 20 minutes and thrombolytic therapy was withheld. : In Diabetic patients with focal neurological deficit and RBS less than 80 mg% on admission, RBS should be rechecked and in appropriate cases should be challenged with IV dextrose considering the possibility of hypoglycemia before commencing thrombolytic therapy.

FGF10 Attenuates Experimental Traumatic Brain Injury through TLR4/MyD88/NF-κB Pathway

2021 ◽  
pp. 1-9
Author(s):  
Qinhan Hou ◽  
Hongmou Chen ◽  
Quan Liu ◽  
Xianlei Yan
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Expression ◽  
Water Content ◽  
Neurological Deficit ◽  
Neuronal Apoptosis ◽  
Neuronal Damage ◽  
Intraventricular Injection ◽  
Brain Water Content ◽  
Brain Water

Traumatic brain injury (TBI) can induce neuronal apoptosis and neuroinflammation, resulting in substantial neuronal damage and behavioral disorders. Fibroblast growth factors (FGFs) have been shown to be critical mediators in tissue repair. However, the role of FGF10 in experimental TBI remains unknown. In this study, mice with TBI were established via weight-loss model and validated by increase of modified neurological severity scores (mNSS) and brain water content. Secondly, FGF10 levels were elevated in mice after TBI, whereas intraventricular injection of Ad-FGF10 decreased mNSS score and brain water content, indicating the remittance of neurological deficit and cerebral edema in TBI mice. In addition, neuronal damage could also be ameliorated by stereotactic injection of Ad-FGF10. Overexpression of FGF10 increased protein expression of Bcl-2, while it decreased Bax and cleaved caspase-3/PARP, and improved neuronal apoptosis in TBI mice. In addition, Ad-FGF10 relieved neuroinflammation induced by TBI and significantly reduced the level of interleukin 1β/6, tumor necrosis factor α, and monocyte chemoattractant protein-1. Moreover, Ad-FGF10 injection decreased the protein expression level of Toll-like receptor 4 (TLR4), MyD88, and phosphorylation of NF-κB (p-NF-κB), suggesting the inactivation of the TLR4/MyD88/NF-κB pathway. In conclusion, overexpression of FGF10 could ameliorate neurological deficit, neuronal apoptosis, and neuroinflammation through inhibition of the TLR4/MyD88/NF-κB pathway, providing a potential therapeutic strategy for brain injury in the future.

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