Ligamentum flavum hematomas: Why does it mostly occur in old Asian males Interesting point of reported cases: Review and case report

Kanat, Ayhan/0000-0002-8189-2877; GUCER, HASAN/0000-0002-9122-379XWOS: 000371637400003PubMed: 27041879Hematoma of the ligamentum flavum (LF) is a rare cause of neural compression and sciatica. Currently, the etiology and epidemiological characteristics of ligamentum flavum hematoma (LFH) are unknown and epidemiological investigations using rewieving of reported cases have not been performed. We report the case of a 63-year-old man with a LFH compressing the spinal canal at the left L2-L3 level, rewieved relevant literature. in Medline research, wefound a total of 50 reported cases with LFHs, and the interesting point of these cases were analyzed. Many of cases were old males. Interestingly, 39 of the 50 cases were reported from Asian countries. the ages of 42 patients could be verified. the youngest age was 45 years, oldest age was 81 years, and mean age was 66.07 years. Thirty-three out of these 42 patients (78.53%) were older than 60 years. An important aspect of the present review is to bring attention for occurrence in older Asian males. With an increasing number of elderly people in the general population, there is a need to investigate risk factors such as sexual gender, age, and geographic location for LFH

Vazospazmın indüklediği iskemiye bağlı spinal araknoidit ve spinal sinir köklerinin aksonal dejenerasyonu: Deneysel çalışma

Objective: Various reasons have been ascribed to arachnoiditis development, among which subarachnoid hemorrhage (SAH) may be an important factor in this process. In this experimental study, we investigated the effect of SAH on histopathological findings. The volumetric changes of the radicular arteries and the density of spinal nerve root axons of a SAH model on C4 roots in rabbits were measured. Materials and Methods: In this study, 18 rabbits were used. The animals were randomly divided into three groups: subarachnoid hemorrhage (SAH; n = 10), physiologic serum (SF; n = 4) and control (n = 4) groups. SAH was performed by injecting 0.5 cc of blood into cisterna magna taken from their auricular veins. Cervical spinal nerve roots at the C4 level were examined histopathologically. Results: Meningeal thickening and adhesions, reddish spinal cord and radices were detected macroscopically. Histopathologically, leptomeningeal adhesions, intimal lesions of radicular arteries and axonal injury were detected at the nerve radices. The mean radicular artery volume was found to be low on the arachnoiditis developing animals. The mean alive axon density of the C4 nerve root decreased and axonal degeneration was observed in the SAH group. Conclusion: Our study suggests that SAH may be an important etiologic factor in spinal arachnoiditis.Amaç: Araknoidit gelişiminde çeşitli nedenler suçlanmaktadır, subaraknoid kanama (SAK) da bu süreçte önemli bir öğe olabilir. Bu deneysel çalışmada (tavşan SAK modelinde) SAK'ın histopatolojik bulgular üzerine etkisini, radiküler arterlerin hacimsel değişikliklerini ve C4 spinal sinir kök aksonlarının dansitesini araştırdık. Materyal ve Metot: Bu çalışmada 18 tavşan kullanıldı. Tavşanlar rastgele üç gruba ayrıldı: subaraknoid kanama (SAK; n = 10), serum fizyolojik (SF; n = 4) ve kontrol (n = 4). SAK, kulak veninden alınan 0.5 ml kanın sisterna magnaya verilmesiyle oluşturuldu. C4 servikal spinal sinir kökleri histopatolojik olarak incelendi. Sonuçlar: Makroskopik olarak, meningeal kalınlaşma ve yapışıklıklar, kızılımsı spinal kord ve kökler saptandı. Histopatolojik olarak sinir köklerinde, leptomeningeal yapışıklıklar, radiküler arterlerde intimal lezyonlar ve aksonal hasar saptandı. SAK grubunda, radiküler arter ortalama hacmi araknoidit gelişen hayvanlarda düşük olarak bulundu. SAK grubunda, C4 kökünün ortalama canlı akson dansitesinde azalma ve aksonal harabiyet gözlendi. Yorum: Çalışmamızın sonuçlarına göre SAK, spinal araknoiditde önemli bir etyolojik etken olabilir

Important casual association of carotid body and glossopharyngeal nerve and lung following experimental subarachnoid hemorrhage in rabbits. First report

Gundogdu, Cemal/0000-0003-2857-923X; Kanat, Ayhan/0000-0002-8189-2877WOS: 000331025400038PubMed: 24267741Object: the glossopharyngeal nerves (GPNs) and carotid bodies (CBs) have an important role in the continuation of the cerebral autoregulation and cardiorespiratory functions. the relationship between degenerative injury of CB and the GPN in subarachnoid hemorrhage (SAH) was studied. Methods: Twenty rabbits were included in this study. Five of them (n = 5) were used as control group. the remaining animals (n = 15) were exposed to experimental SAH. in the six animals of the SAH group, severe signs of illness were observed, and these six animals were killed in the first week after SAH. Others animals (n = 9) were followed for 20 days and then sacrificed. GPNs and CBs were examined and, the live and degenerated GPN axon number, and of CB neuron numbers were stereologically estimated. Results: the mean number of live neurons in CBs was 4206.67 +/- 148.35 and live axons of GPNs were 1211.66 +/- 14.29 in the animals of the control group. the number of degenerated neurons of CBs was 2065 +/- 110.27 and the number of degenerated axons of GPNs was 530.83 +/- 43.48 in early killed animals with SAH. the number of degenerated neurons of CBs and the number of degenerated axons of GPNs were found as 1013.89 +/- 4184 and 2270.5 +/- 13438 in the living animals with SAH, respectively. Conclusions: High number of degenerated axons of GPN and neurons of CBs of the early killed animals suggest that the mortality in early SAH might be due to GPNs injury secondary to compression of their axons or supplying vessels by the probably herniated brainstem, and secondary denervation injury of CBs, and lung. Crown Copyright (c) 2013 Published by Elsevier B.V. All rights reserved

Vazospazmın indüklediği iskemiye bağlı spinal araknoidit ve spinal sinir köklerinin aksonal dejenerasyonu: Deneysel çalışma

Amaç: Araknoidit gelişiminde çeşitli nedenler suçlanmaktadır, subaraknoid kanama (SAK) da bu süreçte önemli bir öğe olabilir. Bu deneysel çalışmada (tavşan SAK modelinde) SAK'ın histopatolojik bulgular üzerine etkisini, radiküler arterlerin hacimsel değişikliklerini ve C4 spinal sinir kök aksonlarının dansitesini araştırdık. Materyal ve Metot: Bu çalışmada 18 tavşan kullanıldı. Tavşanlar rastgele üç gruba ayrıldı: subaraknoid kanama (SAK; n = 10), serum fizyolojik (SF; n = 4) ve kontrol (n = 4). SAK, kulak veninden alınan 0.5 ml kanın sisterna magnaya verilmesiyle oluşturuldu. C4 servikal spinal sinir kökleri histopatolojik olarak incelendi. Sonuçlar: Makroskopik olarak, meningeal kalınlaşma ve yapışıklıklar, kızılımsı spinal kord ve kökler saptandı. Histopatolojik olarak sinir köklerinde, leptomeningeal yapışıklıklar, radiküler arterlerde intimal lezyonlar ve aksonal hasar saptandı. SAK grubunda, radiküler arter ortalama hacmi araknoidit gelişen hayvanlarda düşük olarak bulundu. SAK grubunda, C4 kökünün ortalama canlı akson dansitesinde azalma ve aksonal harabiyet gözlendi. Yorum: Çalışmamızın sonuçlarına göre SAK, spinal araknoiditde önemli bir etyolojik etken olabilir.Objective: Various reasons have been ascribed to arachnoiditis development, among which subarachnoid hemorrhage (SAH) may be an important factor in this process. In this experimental study, we investigated the effect of SAH on histopathological findings. The volumetric changes of the radicular arteries and the density of spinal nerve root axons of a SAH model on C4 roots in rabbits were measured. Materials and Methods: In this study, 18 rabbits were used. The animals were randomly divided into three groups: subarachnoid hemorrhage (SAH; n = 10), physiologic serum (SF; n = 4) and control (n = 4) groups. SAH was performed by injecting 0.5 cc of blood into cisterna magna taken from their auricular veins. Cervical spinal nerve roots at the C4 level were examined histopathologically. Results: Meningeal thickening and adhesions, reddish spinal cord and radices were detected macroscopically. Histopathologically, leptomeningeal adhesions, intimal lesions of radicular arteries and axonal injury were detected at the nerve radices. The mean radicular artery volume was found to be low on the arachnoiditis developing animals. The mean alive axon density of the C4 nerve root decreased and axonal degeneration was observed in the SAH group. Conclusion: Our study suggests that SAH may be an important etiologic factor in spinal arachnoiditis

Changes in number of water-filled vesicles of choroid plexus in early and late phase of experimental rabbit subarachnoid hemorrhage model; the role of petrous ganglion of glossopharyngeal nerve

AYDIN, Nazan/0000-0003-3232-7713; Gundogdu, Cemal/0000-0003-2857-923X; Kanat, Ayhan/0000-0002-8189-2877WOS: 000338195300008PubMed: 24752726Cerebrospinal fluid (CSF) secretion may be increased in the early phases of subarachnoid hemorrhage (SAH), possibly via ischemic glossopharyngeal nerve discharges, and decreased due to glossopharyngeal nerve degeneration in the late phase of SAH; but this reflex pathway has not been definitively investigated. We studied the relationship between petrous ganglion of the glossopharyngeal nerve (GPN) and water vesicles of the choroid plexus (CP) in the early and late phases of SAH. This study was conducted on 30 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 20 rabbits in the SAH group. in the SAH group, five of the animals were decapitated after 4 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 20 days of injections (Group IV). the Petrous Ganglia and CPs of lateral ventricles were removed and stained for stereological analysis. the mean number of follicles per cubic millimeter was 5.3 +/- 1.2 the in control group (Group I), 4.5 +/- 0.9 in the sham group (Group II), 16.60 +/- 3.77 the in early decapitated group (Group III), and 4.30 +/- 0.84 in the late decapitated group (Group IV). the mean number of degenerated neuron density of petrous ganglions was 6 +/- 2, 50 +/- 6, 742 +/- 96, and 2.420 +/- 350 in the control (Group I), sham (Group II), early decapitated (Group III), and late decapitated group (Group IV), respectively. the mean number of water vesicles was statistically different after SAH between the early decapitated group (group III) and the late decapitated group (group IV) (P < 0.05). We studied the relationship between petrous ganglion cells of the GPN and water vesicles of CP in the early and late phases of SAH, and found that CP vesicles are increased in the early phase of SAH due to irritation of GPN, and decreased in the late phase due to ischemic insult of the petrous ganglion and parasympathetic innervation of the CP

Unraveling of the Effect of Nodose Ganglion Degeneration on the Coronary Artery Vasospasm After Subarachnoid Hemorrhage: An Experimental Study

Kanat, Ayhan/0000-0002-8189-2877; altas, enver/0000-0001-9351-6986WOS: 000369625300036PubMed: 26365883BACKGROUND: Cardiac arrest is a major life-threatening complication of subarachnoid hemorrhage (SAH). Although medullary cardiocirculatuar center injury and central sympathetic overactivity have been suspected of initiating coronary artery spasm-induced cardiac arrest, we aimed to elucidate the effects of vagal ischemia at the brainstem on coronary vasospasm and sudden death in SAH. METHODS: Twenty-six rabbits were randomly divided into 3 groups. Control (n = 5); SHAM (n = 8), and SAH group (n = 13). Experimental SAH was applied by injecting homologous blood into the cisterna magna, and the SHAM group was injected with isotonic saline solution also in the cisterna magna., Twenty-one days after the injection, histopathologic changes of the neuron density of nodose ganglia, the vasospasm index values of the coronary arteries, and the electrocardiographic events were analyzed. RESULTS: Increased vasospasm index of the coronary arteries and degenerated neuron density of nodose ganglion were significantly different between animals with SAH, control, and SHAM groups (P < 0.005). If neurons of the nodose ganglia are lesioned due to ischemic insult during SAH, the heart rhythm regulation by vagus afferent reflexes is disturbed. CONCLUSIONS: We found that there is causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with SAH. Vagal pathway paralysis induced by indirect sympathetic overactivity may trigger coronary vasospasm and heart rhythm disturbances. Our findings will aid in the planning of future experimental studies and in determining the clinical relevance of such studies

Predictive Role of External Carotid Artery Vasospasm on Cerebral Ischemia After Subarachnoid Hemorrhage: Experimental Study

AIm: Cerebral vasospasm after subarachnoid hemorrhage (SAH) may lead to a devastating neurological outcome by inducing cerebral ischemia. However the role of external carotid artery (ECA) vasospasm has been rarely reported in the literature. The aim of this study was to elucidate the effect of ECA vasospasm on cerebral ischemia related neurodegeneration in the cerebral cortex after SAH. mATERIAl and mEThODS: This study was performed on 23 rabbits, divided into three groups: control (n=5), sham (n=5), and SAH (n=13). Experimental SAH was performed by injecting 0.75 mL auricular arterial homologous blood into the cisterna magna. After three weeks, the animals were decapitated and the common carotid arteries with their external and internal branches and the brains were examined histopathologically. Vasospasm indexes (VSI) of ECAs and internal carotid arteries (ICAs) and degenerated glial cell numbers of temporal cortices (n/mm3) were estimated stereologically and the results were compared statistically. RESUlTS: Temporal cortex glial cell density was estimated as 136.950±9.257/mm3 in normal rabbits, 131.324±7.987/mm3 in sham, 112.320±6.112/mm3 in light, and 97.543±5.432/mm3 in severe ECA vasospasm. The mean VSI values of ECA of all groups were 1.95±0.21, 2.15±0.29, 2.95±0.65 and 3.12±0.276, respectively. Statistical differences between the VSI values of ECA and degenerated neuron densities in temporal cortices were significant (p<0.005). CONClUSION: ECA vasospasm was observed to have a more important predictive role on the serious cerebral ischemia and neuronal degeneration after SAH. The mechanism may be related to ischemia of the parasympathetic ganglia of the lower cranial nerves and dorsal root ganglio

Spinal Subarachnoid Hemorrhage Induced Intractable Miotic Pupil. A Reminder of Ciliospinal Sympathetic Center Ischemia Based Miosis: An Experimental Study

AIM: To examine ischemic neurodegeneration of the ciliospinal center on permanent miosis following subarachnoid hemorrhage (SAH). MATERIAL and METHODS: Nineteen rabbits were examined in this study. The animals were divided into three groups, as control (GI, n=5), sham (GII, n=5) and study group (GIII, n=9). Pupil diameters were measured after giving 0.5 mL physiological saline for sham and autologous arterial blood for the study group into the cervico-thoracic subarachnoid space. After three weeks of follow up, the cervico-thoracic cord and bilateral superior cervical sympathetic ganglia were removed. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia and degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods. RESULTS: The mean pupil diameter was 5180 ± 370 µm and the mean degenerated neuron density of the ciliospinal center was 4 ± 1/mm3 in animals of the control group (GI). These values were 9850 ± 610 µm, 10 ± 3/mm3 in sham (GII), and 7.010 ± 440 µm and 98 ± 21/mm3 in the study (GIII) groups. There was an inverse relationship between degenerated neuron density of the ciliospinal nuclei and pupil diameters. CONCLUSION: We showed and reported for the first time that ciliospinal sympathetic center ischemia-induced neurodegeneration may have been responsible for permanent miosis following SAH

Unraveling of the effect of nodose ganglion degeneration on the coronary artery vasospasm after subarachnoid hemorrhage: an experimental study

altas, enver/0000-0001-9351-6986; Kanat, Ayhan/0000-0002-8189-2877WOS: 000369625300036PubMed: 26365883BACKGROUND: Cardiac arrest is a major life-threatening complication of subarachnoid hemorrhage (SAH). Although medullary cardiocirculatuar center injury and central sympathetic overactivity have been suspected of initiating coronary artery spasm-induced cardiac arrest, we aimed to elucidate the effects of vagal ischemia at the brainstem on coronary vasospasm and sudden death in SAH. METHODS: Twenty-six rabbits were randomly divided into 3 groups. Control (n = 5); SHAM (n = 8), and SAH group (n = 13). Experimental SAH was applied by injecting homologous blood into the cisterna magna, and the SHAM group was injected with isotonic saline solution also in the cisterna magna., Twenty-one days after the injection, histopathologic changes of the neuron density of nodose ganglia, the vasospasm index values of the coronary arteries, and the electrocardiographic events were analyzed. RESULTS: Increased vasospasm index of the coronary arteries and degenerated neuron density of nodose ganglion were significantly different between animals with SAH, control, and SHAM groups (P < 0.005). If neurons of the nodose ganglia are lesioned due to ischemic insult during SAH, the heart rhythm regulation by vagus afferent reflexes is disturbed. CONCLUSIONS: We found that there is causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with SAH. Vagal pathway paralysis induced by indirect sympathetic overactivity may trigger coronary vasospasm and heart rhythm disturbances. Our findings will aid in the planning of future experimental studies and in determining the clinical relevance of such studies

Cervical disc hernia operations through posterior laminoforaminotomy

Kanat, Ayhan/0000-0002-8189-2877WOS: 000376130600006PubMed: 27217655Objective: the most common used technique for posterolateral cervical disc herniations is anterior approach. However, posterior cervical laminotoforaminomy can provide excellent results in appropriately selected patients with foraminal stenosis in either soft disc prolapse or cervical spondylosis. the purpose of this study was to present the clinical outcomes following posterior laminoforaminotomy in patients with radiculopathy. Materials and Methods: We retrospectively evaluated 35 patients diagnosed with posterolateral cervical disc herniation and cervical spondylosis with foraminal stenosis causing radiculopathy operated by the posterior cervical keyhole laminoforaminotomy between the years 2010 and 2015. Results: the file records and the radiographic images of the 35 patients were assessed retrospectively. the mean age was 46.4 years (range: 34-66 years). of the patients, 19 were males and 16 were females. in all of the patients, the neurologic deficit observed was radiculopathy. the posterolaterally localized disc herniations and the osteophytic structures were on the left side in 18 cases and on the right in 17 cases. in 10 of the patients, the disc level was at C5-6, in 18 at C6-7, in 2 at C3-4, in 2 at C4-5, in 1 at C7-T1, in 1 patient at both C5-6 and C6-7, and in 1 at both C4-5 and C5-6. in 14 of these 35 patients, both osteophytic structures and protruded disc herniation were present. Intervertebral foramen stenosis was present in all of the patients with osteophytes. Postoperatively, in 31 patients the complaints were relieved completely and four patients had complaints of neck pain and paresthesia radiating to the arm (the success of operation was 88.5%). on control examinations, there was no finding of instability or cervical kyphosis. Conclusion: Posterior cervical laminoforaminotomy is an alternative appropriate choice in both cervical soft disc herniations and cervical stenosis