Epilepsy is a common and serious chronic neurological disorder, with pharmacoresistance occurring in up to one third of cases of epilepsy. Temporal lobe is the most frequent site of epileptogenic lesions, and surgically resected specimens from patients with pharmacoresistant epilepsy reveal a broad spectrum of lesions, with hippocampal sclerosis as the most common pathology while glioneuronal hamartoma is a rare entity. We report a case of a 62 year-old woman with chronic pharmacoresistant epilepsy characterized by an unusual clinical picture of complex, partial and generalized tonic-clonic seizures with associated repetitive back and forth pelvic movements, not clinically typical for temporal lobe epilepsy. However, video EEG monitoring, MRI, and brain SPECT revealed a right temporal lobe epileptogenic focus. Temporal lobectomy was performed and revealed glioneuronal hamartoma in the white matter, characterized by the presence of immature oligodendroglial-like cells, dysmorphic/ dysplastic small neuronal cells, and hybrid cells with intermediate morphology in a hypomyelinated fibrillar background. No proliferative activity was present. Immunostain for CD34 highlighted intense bush-like ramifications of the cell processes in the dysplastic glioneuronal cells. The patient remained seizure free during the follow-up period of 32 months. Our case is noticeable for atypical clinical features of temporal lobe epilepsy, associated with the rare entity of glioneuronal hamartoma composed of an unusual immature cellular composition with CD34 positivity.
{"title":"Glioneuronal hamartoma with unusual clinical manifestations in a case of pharmacoresistant temporal lobe epilepsy","authors":"R. Makary, A. Mohammadi, S. Shuja","doi":"10.5580/588","DOIUrl":"https://doi.org/10.5580/588","url":null,"abstract":"Epilepsy is a common and serious chronic neurological disorder, with pharmacoresistance occurring in up to one third of cases of epilepsy. Temporal lobe is the most frequent site of epileptogenic lesions, and surgically resected specimens from patients with pharmacoresistant epilepsy reveal a broad spectrum of lesions, with hippocampal sclerosis as the most common pathology while glioneuronal hamartoma is a rare entity. We report a case of a 62 year-old woman with chronic pharmacoresistant epilepsy characterized by an unusual clinical picture of complex, partial and generalized tonic-clonic seizures with associated repetitive back and forth pelvic movements, not clinically typical for temporal lobe epilepsy. However, video EEG monitoring, MRI, and brain SPECT revealed a right temporal lobe epileptogenic focus. Temporal lobectomy was performed and revealed glioneuronal hamartoma in the white matter, characterized by the presence of immature oligodendroglial-like cells, dysmorphic/ dysplastic small neuronal cells, and hybrid cells with intermediate morphology in a hypomyelinated fibrillar background. No proliferative activity was present. Immunostain for CD34 highlighted intense bush-like ramifications of the cell processes in the dysplastic glioneuronal cells. The patient remained seizure free during the follow-up period of 32 months. Our case is noticeable for atypical clinical features of temporal lobe epilepsy, associated with the rare entity of glioneuronal hamartoma composed of an unusual immature cellular composition with CD34 positivity.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"55 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127693133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Mishra, R. Bhat, K. Sudeep, M. Nagappa, A. Swain, A. Badhe
The Posterior Reversible encephalopathy Syndrome (PRES) is a cliniconeuroradiologic entity. Eclampsia is one of the important causes of PRES. Most patients have severe hypertension, some have only mildly elevated or even normal blood pressure. Symptoms include headache, nausea, vomiting, altered mental status, seizures, stupor, and visual disturbances. On CT and MR studies, edema is relatively symmetrical pattern, typically in the sub cortical white matter and occasionally in the cortex of the occipital and parietal lobes. PRES is reversible when treatment is instituted early, delayed diagnosis and treatment can result in chronic neurological sequelae. Early recognition and controlled of blood pressure and seizure is the main stay of treatment. Anesthesiologist, intensivists and other physicians involved in the evaluation of patients with markedly elevated blood pressure, eclampsia, renal failure etc should presumed PRES and must be aware of the clinical spectrum of the associated conditions, its diagnostic modalities, and treatment.
{"title":"PRES (Posterior Reversible Encephalopathy Syndrome) and Eclampsia:-Review","authors":"S. Mishra, R. Bhat, K. Sudeep, M. Nagappa, A. Swain, A. Badhe","doi":"10.5580/c6","DOIUrl":"https://doi.org/10.5580/c6","url":null,"abstract":"The Posterior Reversible encephalopathy Syndrome (PRES) is a cliniconeuroradiologic entity. Eclampsia is one of the important causes of PRES. Most patients have severe hypertension, some have only mildly elevated or even normal blood pressure. Symptoms include headache, nausea, vomiting, altered mental status, seizures, stupor, and visual disturbances. On CT and MR studies, edema is relatively symmetrical pattern, typically in the sub cortical white matter and occasionally in the cortex of the occipital and parietal lobes. PRES is reversible when treatment is instituted early, delayed diagnosis and treatment can result in chronic neurological sequelae. Early recognition and controlled of blood pressure and seizure is the main stay of treatment. Anesthesiologist, intensivists and other physicians involved in the evaluation of patients with markedly elevated blood pressure, eclampsia, renal failure etc should presumed PRES and must be aware of the clinical spectrum of the associated conditions, its diagnostic modalities, and treatment.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132346634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
INTRODUCTION:Migraine is a painful neurological condition and the pathogenesis of migraine is not completely understood. Some researchers are of opinion that cortex may be involved whereas others hold the brainstem responsible.AIM:The aim of the present study was to evaluate the brainstem auditory evoked potentials in patients with migraine.METHODOLOGY:25 patients in the age range of 10-45 years, diagnosed as having migraine (with or without aura) were taken as the study group. Out of these 25 subjects, 6 (4 males, 2 females) subjects reported headache during the testing period. Control group consisted of 25 healthy subjects in the age range of 10 to 45 years with no complaint of migraine. Brainstem auditory evoked potentials were recorded using insert ear phones.RESULTS:There was a significant difference between absolute latencies of study group and control group. Similarly, significant results were obtained for interpeak latencies between control and study group. It was observed that prolongation in interpeak latency was reported in those subjects who had an acute attack of migraine during ABR testing.CONCLUSION :It is concluded that there is an involvement of brainstem structures during migraine attack and this is supported by the prolongation of interpeak latencies of waves in ABER. Therefore, Auditory brainstem evoked responses can be used as an effective tool in making the neurophysiological evaluation of the auditory pathway which further plays an important role in the explanation of pathophysiology of migraine.
{"title":"Auditory Brainstem Evoked Responses In Migraine Patients","authors":"D. Kaushaln, S. Munjal, M. Modi, N. Panda","doi":"10.5580/2183","DOIUrl":"https://doi.org/10.5580/2183","url":null,"abstract":"INTRODUCTION:Migraine is a painful neurological condition and the pathogenesis of migraine is not completely understood. Some researchers are of opinion that cortex may be involved whereas others hold the brainstem responsible.AIM:The aim of the present study was to evaluate the brainstem auditory evoked potentials in patients with migraine.METHODOLOGY:25 patients in the age range of 10-45 years, diagnosed as having migraine (with or without aura) were taken as the study group. Out of these 25 subjects, 6 (4 males, 2 females) subjects reported headache during the testing period. Control group consisted of 25 healthy subjects in the age range of 10 to 45 years with no complaint of migraine. Brainstem auditory evoked potentials were recorded using insert ear phones.RESULTS:There was a significant difference between absolute latencies of study group and control group. Similarly, significant results were obtained for interpeak latencies between control and study group. It was observed that prolongation in interpeak latency was reported in those subjects who had an acute attack of migraine during ABR testing.CONCLUSION :It is concluded that there is an involvement of brainstem structures during migraine attack and this is supported by the prolongation of interpeak latencies of waves in ABER. Therefore, Auditory brainstem evoked responses can be used as an effective tool in making the neurophysiological evaluation of the auditory pathway which further plays an important role in the explanation of pathophysiology of migraine.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133578121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A 54 year-old man presented with 3 years of progressive left foot drop and 4 months of proximal weakness in right leg. Hypoesthesia between left T8 and T10 levels. There was 0/5 strength of left ankle dorsiflexors, invertors and evertors. There was 3/5 strength of left hamstring, iliopsoas and right extensor digitorum brevis. No abdominal reflex but brisk ankle and knee jerks. Babinski’s signs with increased tone in both lower extremities. MRI (Figure: A-F) of thoracic spine showed T5/T6 anterior thoracic spinal cord herniation. It is uncommon and often diagnosed late or misdiagnosed as a presumed posterior intradural arachnoid cyst.1,2 Prompt diagnosis and treatment can prevent severe disability. Figure 1 Figure: Pre-operative images: Sagittal spin echo T1-WI (A), FSE T2-WI (B), Axial FSE T2-WI (C) – Left anterolateral herniation (C), There is anterior displacement of the thoracic cord at T5/T6 level within the ventral epidural space abutting directly the posterior aspect of the T5/T6 disc and the corresponding vertebral body. Post-operative images: Sagittal spin echo T1-WI (D), FSE T2-WI (E), Axial FSE T2-WI (F), showing resolution of thoracic cord herniation at T5/T6 disc level with gliotic anterior cord atrophy.
{"title":"Thoracic Spinal Cord Herniation- Delayed Diagnosis is a Major Concern.","authors":"A. Hussain, A. Khorsandi, M. Gowan, J. Daniel","doi":"10.5580/92a","DOIUrl":"https://doi.org/10.5580/92a","url":null,"abstract":"A 54 year-old man presented with 3 years of progressive left foot drop and 4 months of proximal weakness in right leg. Hypoesthesia between left T8 and T10 levels. There was 0/5 strength of left ankle dorsiflexors, invertors and evertors. There was 3/5 strength of left hamstring, iliopsoas and right extensor digitorum brevis. No abdominal reflex but brisk ankle and knee jerks. Babinski’s signs with increased tone in both lower extremities. MRI (Figure: A-F) of thoracic spine showed T5/T6 anterior thoracic spinal cord herniation. It is uncommon and often diagnosed late or misdiagnosed as a presumed posterior intradural arachnoid cyst.1,2 Prompt diagnosis and treatment can prevent severe disability. Figure 1 Figure: Pre-operative images: Sagittal spin echo T1-WI (A), FSE T2-WI (B), Axial FSE T2-WI (C) – Left anterolateral herniation (C), There is anterior displacement of the thoracic cord at T5/T6 level within the ventral epidural space abutting directly the posterior aspect of the T5/T6 disc and the corresponding vertebral body. Post-operative images: Sagittal spin echo T1-WI (D), FSE T2-WI (E), Axial FSE T2-WI (F), showing resolution of thoracic cord herniation at T5/T6 disc level with gliotic anterior cord atrophy.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129434012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cerebral artery thrombosis is one of the major causes of death. It is usually not clear what kind of pathologic processes participate in this pathological entity. We report a case of a 47-year old female patient with recurrent episodes of cerebral arterial thrombosis, without permanent neurological deficits and history of heavy smoking, hypertension, hypothyroidism, hypercholesterolemia, metabolic syndrome and insulin resistant postprandial hyperglycemia. Brain magnetic resonance angiography (MRA) revealed total thrombosis of the left internal carotid artery (ICA) and partial thrombosis of the right ICA. Although, the extent of the cerebral arteries thrombosis due to the coexistence of many risk factors, the clinical symptoms are mild, because of the sufficient blood supply from the vertebrobasilar system and the efficient collateral circulation.
{"title":"Extensive cerebral arteries thrombosis.","authors":"S. Mourgela, A. Sakellaropoulos","doi":"10.5580/27b","DOIUrl":"https://doi.org/10.5580/27b","url":null,"abstract":"Cerebral artery thrombosis is one of the major causes of death. It is usually not clear what kind of pathologic processes participate in this pathological entity. We report a case of a 47-year old female patient with recurrent episodes of cerebral arterial thrombosis, without permanent neurological deficits and history of heavy smoking, hypertension, hypothyroidism, hypercholesterolemia, metabolic syndrome and insulin resistant postprandial hyperglycemia. Brain magnetic resonance angiography (MRA) revealed total thrombosis of the left internal carotid artery (ICA) and partial thrombosis of the right ICA. Although, the extent of the cerebral arteries thrombosis due to the coexistence of many risk factors, the clinical symptoms are mild, because of the sufficient blood supply from the vertebrobasilar system and the efficient collateral circulation.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"20 4","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"113971935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
An 83 year-old cigarette smoker presented with left sided weakness. Examination revealed a left homonymous hemianopsia, left hemiparesis affecting face and arm greater than leg, and left hemihypesthesia with intact graphesthesia and stereognosis. MRI showed an area of restricted diffusion corresponding to an infarct in the anterior choroidal artery distribution (figure). Anterior choroidal artery infarcts are uncommon accounting for 2% of ischemic stroke1. They are distinguished by a unique clinical syndrome of hemiparesis, hemihypesthesia, and visual field deficits but without other cortical signs1. The most common etiologies include cardioembolism (54%), arterial embolus (17%), and small vessel disease (6%)2. Figure: Diffusion weighted imaging (left) and corresponding apparent diffusion coefficient map (right) demonstrating acute infarction. The territory supplied by the anterior choroidal artery can include the posterior limb of the internal capsule, choroid plexus, initial segments of the optic radiations, and parts of amygdala, uncus, and globus pallidus.
{"title":"Anterior Choroidal Artery Infarct","authors":"B. Robottom, J. Cabassa, M. Wozniak, S. Reich","doi":"10.5580/1e01","DOIUrl":"https://doi.org/10.5580/1e01","url":null,"abstract":"An 83 year-old cigarette smoker presented with left sided weakness. Examination revealed a left homonymous hemianopsia, left hemiparesis affecting face and arm greater than leg, and left hemihypesthesia with intact graphesthesia and stereognosis. MRI showed an area of restricted diffusion corresponding to an infarct in the anterior choroidal artery distribution (figure). Anterior choroidal artery infarcts are uncommon accounting for 2% of ischemic stroke1. They are distinguished by a unique clinical syndrome of hemiparesis, hemihypesthesia, and visual field deficits but without other cortical signs1. The most common etiologies include cardioembolism (54%), arterial embolus (17%), and small vessel disease (6%)2. Figure: Diffusion weighted imaging (left) and corresponding apparent diffusion coefficient map (right) demonstrating acute infarction. The territory supplied by the anterior choroidal artery can include the posterior limb of the internal capsule, choroid plexus, initial segments of the optic radiations, and parts of amygdala, uncus, and globus pallidus.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"173 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2007-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115415750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lacune was a term first used in the European literature in the mid 19th century but was little used in English language medical literature until the publications of Charles Miller Fisher in the 1960's. The lacunar hypothesis is controversial and the terminology is best reserved for the pathological lesion. New clinical classifications of stroke such as that proposed in the TOAST study have demonstrated a high interphysician agreement rate and are widely employed. The term lacune was first used by the French physician, Amédée Dechambre (1812-1886) in his description of postmortem cerebral softenings in subcortical white matter [1]. His paper published in 1838 in the Gazette Médicale de Paris reported the pathology in a patient who had initially recovered from hemiplegia, ‘A number of small lacunes of variable size and form, more or less filled with milky fluid...’. Lacune is derived from the Latin, lacuna, a pit or hole and in French, la lacune, a gap or empty space. Max Durand-Fardel in 1842 applied the term to these deep cavities and referred to the multiple small holes in the hemispheric white matter as ‘l'état cribalé' (sieve-like state) [2]. Pierre Marie correlated clinical findings with multiple lacunes and described sudden hemiplegia with good recovery and a slow gait with small steps ‘marche à petits pas de Déjérine', pseudo bulbar palsy and dementia [3]. He concluded that lacunae could be softenings caused by a ‘local arteriosclerotic process' or a process of ‘destructive vaginalitis', a dilatation of the perivascular space. During the first half of the twentieth century the terms were seldom used in the English-language medical literature. Charles Miller Fisher popularised the lacunar hypothesis with careful clinical and pathological studies published in the 1960's [4]. He proposed that lacunar infarcts were small (< 15 mm diameter) infarcts due to occlusion of a single penetrating branch of a large artery and associated with a number of well-defined clinical syndromes including pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis and dysarthria clumsy hand. Fisher's pathological studies established that the arteriopathy in lacunes was a segmental disorganisation of the arterial vessel wall associated with an eosinophilic deposit or lipohyalinosis which was principally due to chronic hypertension. He also described atherosclerotic plaques, stenoses or occlusions of the penetrating or parent artery whilst a small percentage demonstrated haemosiderin-laden macrophages representing old micro-haemorrhages. Brain imaging including CT and MRI has allowed the detection of lacunae in vivo. Newer MRI techniques employing diffusion weighted imaging (DWI) with measurement of the apparent diffusion co-efficient (ADC) have higher sensitivity for detecting small deep infarcts [5]. Imaging however is not able to demonstrate that an infarct is due to an occlusion of a single perforating artery. Many studies have also foun
Lacune这个词最早出现在19世纪中期的欧洲文献中，但在英语医学文献中很少使用，直到20世纪60年代查尔斯·米勒·费舍尔的出版物。腔隙假说是有争议的，该术语最好用于病理病变。TOAST研究中提出的新的脑卒中临床分类已显示出较高的医师间一致性，并被广泛采用。lacune这个词最早是由法国医生amsamdsamade Dechambre(1812-1886)在描述死后大脑皮层下白质软化时使用的[1]。1838年，他在《巴黎公报》上发表了一篇论文，报告了一位最初从偏瘫中康复的病人的病理情况:“许多大小和形状各异的小腔隙，或多或少充满了乳白色的液体……”Lacune一词来源于拉丁语lacuna(坑或洞)和法语la Lacune(空隙或空的空间)。1842年，Max Durand-Fardel将该术语应用于这些深空腔，并将半球白质中的多个小孔称为' l' samat cribal '(筛状状态)[2]。Pierre Marie将临床表现与多发凹痕相关联，并描述了恢复良好的突发性偏瘫和小步缓慢的步态“marche petits pas de dsamjsamrine”、假性球麻痹和痴呆[3]。他得出结论，腔隙可能是由“局部动脉硬化过程”或“破坏性阴道炎”(血管周围空间的扩张)引起的软化。在二十世纪上半叶，英语医学文献中很少使用这些术语。Charles Miller Fisher在20世纪60年代发表了仔细的临床和病理研究，普及了腔隙假说[4]。他提出腔隙性梗死是由于大动脉的单个穿透性分支闭塞而导致的小梗死(直径< 15mm)，并与许多明确定义的临床综合征相关，包括纯运动性偏瘫、纯感觉性卒中、感觉运动性卒中、共济失调性偏瘫和发音障碍性手笨拙。Fisher的病理研究证实，陷窝中的动脉病变是动脉血管壁的节段性紊乱，与嗜酸性粒细胞沉积或脂透明质沉积有关，主要是由慢性高血压引起的。他还描述了动脉粥样硬化斑块、穿透性动脉或母动脉狭窄或闭塞，同时一小部分表现为满载血黄素的巨噬细胞，代表陈旧性微出血。包括CT和MRI在内的脑成像已经可以在体内检测到腔隙。较新的MRI技术采用弥散加权成像(DWI)测量表观弥散系数(ADC)，对于检测小的深部梗死具有更高的灵敏度[5]。然而，影像学不能证明梗死是由于单个穿通动脉闭塞所致。许多研究还发现，经影像学证实的经典腔隙性梗死具有其他非腔隙性梗死机制，包括大血管或心脏栓塞。腔隙假说长期以来一直存在争议。它的批评者指出了多种病理生理机制，并在许多情况下证明了潜在的栓塞源[6]。该模型的倡导者指出，少数凹窝可能是由栓塞引起的，但有令人信服的临床和流行病学理由将凹窝保留为独特的缺血性卒中亚型[7]。腔隙性和腔隙性梗死是医学术语的一部分，已有150多年的使用历史。它们是应该继续使用，还是应该完全放弃?该概念最好用于病理病变和术语皮层下卒中或小腔隙和腔隙性梗死:该概念的历史和用于临床和放射学描述的3 / 2深度梗死的现代用法。急性缺血性卒中(TOAST)的ORG 10172试验开发了一种基于病因的卒中亚型分类新系统[8]。(1)大动脉粥样硬化、(2)心脏栓塞、(3)小血管闭塞、(4)其他原因确定的脑卒中和(5)原因不明的脑卒中5种亚型的医师间一致性较高。通过使用这一术语，医生可以避免某些先入为主的观念，并保持开放的心态，以最佳的调查和治疗个别中风患者。
{"title":"Lacune and lacunar infarct: A history of the concept and modern use","authors":"D. Todman","doi":"10.5580/d31","DOIUrl":"https://doi.org/10.5580/d31","url":null,"abstract":"Lacune was a term first used in the European literature in the mid 19th century but was little used in English language medical literature until the publications of Charles Miller Fisher in the 1960's. The lacunar hypothesis is controversial and the terminology is best reserved for the pathological lesion. New clinical classifications of stroke such as that proposed in the TOAST study have demonstrated a high interphysician agreement rate and are widely employed. The term lacune was first used by the French physician, Amédée Dechambre (1812-1886) in his description of postmortem cerebral softenings in subcortical white matter [1]. His paper published in 1838 in the Gazette Médicale de Paris reported the pathology in a patient who had initially recovered from hemiplegia, ‘A number of small lacunes of variable size and form, more or less filled with milky fluid...’. Lacune is derived from the Latin, lacuna, a pit or hole and in French, la lacune, a gap or empty space. Max Durand-Fardel in 1842 applied the term to these deep cavities and referred to the multiple small holes in the hemispheric white matter as ‘l'état cribalé' (sieve-like state) [2]. Pierre Marie correlated clinical findings with multiple lacunes and described sudden hemiplegia with good recovery and a slow gait with small steps ‘marche à petits pas de Déjérine', pseudo bulbar palsy and dementia [3]. He concluded that lacunae could be softenings caused by a ‘local arteriosclerotic process' or a process of ‘destructive vaginalitis', a dilatation of the perivascular space. During the first half of the twentieth century the terms were seldom used in the English-language medical literature. Charles Miller Fisher popularised the lacunar hypothesis with careful clinical and pathological studies published in the 1960's [4]. He proposed that lacunar infarcts were small (< 15 mm diameter) infarcts due to occlusion of a single penetrating branch of a large artery and associated with a number of well-defined clinical syndromes including pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis and dysarthria clumsy hand. Fisher's pathological studies established that the arteriopathy in lacunes was a segmental disorganisation of the arterial vessel wall associated with an eosinophilic deposit or lipohyalinosis which was principally due to chronic hypertension. He also described atherosclerotic plaques, stenoses or occlusions of the penetrating or parent artery whilst a small percentage demonstrated haemosiderin-laden macrophages representing old micro-haemorrhages. Brain imaging including CT and MRI has allowed the detection of lacunae in vivo. Newer MRI techniques employing diffusion weighted imaging (DWI) with measurement of the apparent diffusion co-efficient (ADC) have higher sensitivity for detecting small deep infarcts [5]. Imaging however is not able to demonstrate that an infarct is due to an occlusion of a single perforating artery. Many studies have also foun","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2007-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129908824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cyclopes are rare congenital abnormalities; a severe form of holoprosencephaly resulting in children being born with just one eye. It results from failure of the cerebral hemisphere to separate during fetal development. The incidence is 1 in 13,000 live births but present in 1 in 2500 pregnancies that end up as miscarriage. It is incompatible with life. In this report we present a Cyclops delivered via cesarean section on account of ante partum hemorrhage secondary to placental previa type 11a.
{"title":"Cyclops Deformity In Benin City, Nigeria: A Case Report","authors":"P. Otuaga, A. O. Eweka, A. O. Oni, L. Chris-ozoko","doi":"10.5580/22ea","DOIUrl":"https://doi.org/10.5580/22ea","url":null,"abstract":"Cyclopes are rare congenital abnormalities; a severe form of holoprosencephaly resulting in children being born with just one eye. It results from failure of the cerebral hemisphere to separate during fetal development. The incidence is 1 in 13,000 live births but present in 1 in 2500 pregnancies that end up as miscarriage. It is incompatible with life. In this report we present a Cyclops delivered via cesarean section on account of ante partum hemorrhage secondary to placental previa type 11a.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"725 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2007-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130362796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This article describes the observations collected from the dissection of nonformalinized cadavers analyzed in respect to the anatomical relation variations of facial nerves. Other findings reported on the medical literature are analyzed.
{"title":"Facial nerve: Anatomical revision","authors":"G. Rodriguez, LdeF Ibañez Valdes, H. F. Sibat","doi":"10.5580/f17","DOIUrl":"https://doi.org/10.5580/f17","url":null,"abstract":"This article describes the observations collected from the dissection of nonformalinized cadavers analyzed in respect to the anatomical relation variations of facial nerves. Other findings reported on the medical literature are analyzed.","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"65 3 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2007-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127410315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The discipline of sleep medicine has grown dramatically over the past 30 years with diagnostic sleep laboratories now established in most countries. An understanding of sleep physiology and sleep disorders developed through the twentieth century. This review highlights some of the key developments and milestones in the establishment of this relatively new field of sleep medicine. EARLY CONCEPTS REGARDING SLEEP There has been an interest in the nature of sleep and dreams throughout recorded history. Insomnia was reported in ancient Egyptian texts and opium was used as possibly the first hypnotic medication. Our knowledge of ancient Egyptian medicine comes from the Edwin Smith papyrus, the Ebers papyrus and Kahun papyrus [1]. These medical papyri make reference to many Egyptian treatments including poppy seeds (opium) to relieve insomnia as well as an anaesthetic. Hippocrates in his texts refers to disordered sleep and dreams. Although the Hippocratic corpus is multiauthored, there are numerous references to sleep in its volumes. The text, De Victo IV, also known as, On Dreams, elaborates on sleep and dreams as a diagnostic tool for somatic complaints [2]. Dreams also played an important role in the writings of Galen. His treatise, On Diagnosis from Dreams (De Dignotione ex Insomnis Libellis) describes dreams, which may mirror the conditions of the body [3]. Dreams and interpretation of dreams are also prominent in sacred texts including the Old and New Testaments of the Bible. Despite these early references, the scientific interest in sleep has emerged over the past 100 years and the field of sleep medicine itself has only existed since the 1970's. The monograph, The Philosophy of Sleep was written by the Scottish physician, Robert MacNish in 1830 with the first American edition in 1834 [4]. MacNish regarded sleep as a passive process during which the brain had a recuperative function associated with reduced sensory input. Wakefulness on the other hand, represented the activated state of the brain. This dichotomy in which sleep was seen as a passive process and wakefulness as an active state was the prevailing view until scientific discoveries of the mid twentieth century. MacNish's text approached sleep from a philosophical rather than experimental position. The first text to analysis sleep from a physiological perspective was Henri Pieron's text entitled, Le Probleme Physiologique Du Sommeil [5]. Peiron was a French scientist who published his text in 1913 and the volume is regarded as the beginning of the modern approach to sleep research. A variety of theories were advanced in the late nineteenth and early twentieth century with regard to the nature of sleep. A vascular theory was popular and proposed that during sleep the blood flow to the brain was reduced and accumulated in the digestive tract. Around the end of the nineteenth century, a chemical process gained popularity with the theory that toxins developed during wakefulness and were gra
睡眠医学这门学科在过去的30年里发展迅速，现在大多数国家都建立了睡眠诊断实验室。对睡眠生理学和睡眠障碍的理解贯穿了整个20世纪。这篇综述重点介绍了睡眠医学这一相对较新的领域的一些关键发展和里程碑。关于睡眠的早期概念在有记载的历史中，人们对睡眠和梦的本质一直很感兴趣。古埃及文献中有失眠的记载，鸦片可能是第一种催眠药物。我们对古埃及医学的了解来自埃德温·史密斯纸莎草、埃伯斯纸莎草和卡洪纸莎草[1]。这些医学纸莎草记载了许多埃及的治疗方法，包括罂粟种子(鸦片)来缓解失眠和麻醉。希波克拉底在他的文献中提到了睡眠和梦的紊乱。虽然希波克拉底语料库是多作者的，但在它的卷中有许多关于睡眠的引用。《德·维克托四世》(De Victo IV)，也被称为《论梦》(On Dreams)，详细阐述了睡眠和梦作为躯体疾病的诊断工具[2]。梦在盖伦的著作中也扮演了重要的角色。他的专著《论梦的诊断》(De Dignotione ex Insomnis Libellis)描述了梦，这可能反映了身体的状况[3]。梦和梦的解释在包括《圣经》的旧约和新约在内的神圣文本中也很突出。尽管有这些早期的参考文献，但科学对睡眠的兴趣在过去的100年里才出现，睡眠医学领域本身直到20世纪70年代才出现。这部专著《睡眠的哲学》是由苏格兰医生Robert MacNish于1830年撰写的，1834年在美国出版了第一版[4]。MacNish认为睡眠是一个被动的过程，在这个过程中，大脑有一个与减少的感觉输入相关的恢复功能。另一方面，清醒代表了大脑的激活状态。在20世纪中期科学发现之前，这种将睡眠视为被动过程而将清醒视为主动状态的二分法一直是主流观点。MacNish的文章从哲学而非实验的角度来探讨睡眠。第一篇从生理学角度分析睡眠的文章是亨利·皮耶罗(Henri Pieron)的《Le problem Physiologique Du Sommeil》[5]。佩龙是一位法国科学家，他在1913年出版了这本书，这本书被认为是现代睡眠研究方法的开端。在19世纪末和20世纪初，关于睡眠的本质提出了各种各样的理论。一种流行的血管理论提出，在睡眠期间，流向大脑的血液减少并积聚在消化道。大约在19世纪末，一种化学过程开始流行，该理论认为毒素在清醒时产生，在睡眠时逐渐消除。法国生理学家勒让德(Legendre)和皮耶罗(Pieron)对睡眠不足的狗进行了实验[6]。当他们将这些狗的血清注射到清醒的狗身上时，它们就会感到疲劳。他们创造了“催眠毒素”这个词来解释这种内源性睡眠因素
{"title":"A History Of Sleep Medicine","authors":"D. Todman","doi":"10.5580/146b","DOIUrl":"https://doi.org/10.5580/146b","url":null,"abstract":"The discipline of sleep medicine has grown dramatically over the past 30 years with diagnostic sleep laboratories now established in most countries. An understanding of sleep physiology and sleep disorders developed through the twentieth century. This review highlights some of the key developments and milestones in the establishment of this relatively new field of sleep medicine. EARLY CONCEPTS REGARDING SLEEP There has been an interest in the nature of sleep and dreams throughout recorded history. Insomnia was reported in ancient Egyptian texts and opium was used as possibly the first hypnotic medication. Our knowledge of ancient Egyptian medicine comes from the Edwin Smith papyrus, the Ebers papyrus and Kahun papyrus [1]. These medical papyri make reference to many Egyptian treatments including poppy seeds (opium) to relieve insomnia as well as an anaesthetic. Hippocrates in his texts refers to disordered sleep and dreams. Although the Hippocratic corpus is multiauthored, there are numerous references to sleep in its volumes. The text, De Victo IV, also known as, On Dreams, elaborates on sleep and dreams as a diagnostic tool for somatic complaints [2]. Dreams also played an important role in the writings of Galen. His treatise, On Diagnosis from Dreams (De Dignotione ex Insomnis Libellis) describes dreams, which may mirror the conditions of the body [3]. Dreams and interpretation of dreams are also prominent in sacred texts including the Old and New Testaments of the Bible. Despite these early references, the scientific interest in sleep has emerged over the past 100 years and the field of sleep medicine itself has only existed since the 1970's. The monograph, The Philosophy of Sleep was written by the Scottish physician, Robert MacNish in 1830 with the first American edition in 1834 [4]. MacNish regarded sleep as a passive process during which the brain had a recuperative function associated with reduced sensory input. Wakefulness on the other hand, represented the activated state of the brain. This dichotomy in which sleep was seen as a passive process and wakefulness as an active state was the prevailing view until scientific discoveries of the mid twentieth century. MacNish's text approached sleep from a philosophical rather than experimental position. The first text to analysis sleep from a physiological perspective was Henri Pieron's text entitled, Le Probleme Physiologique Du Sommeil [5]. Peiron was a French scientist who published his text in 1913 and the volume is regarded as the beginning of the modern approach to sleep research. A variety of theories were advanced in the late nineteenth and early twentieth century with regard to the nature of sleep. A vascular theory was popular and proposed that during sleep the blood flow to the brain was reduced and accumulated in the digestive tract. Around the end of the nineteenth century, a chemical process gained popularity with the theory that toxins developed during wakefulness and were gra","PeriodicalId":232166,"journal":{"name":"The Internet Journal of Neurology","volume":"73 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2007-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127261872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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