The Internet Journal of Neurology最新文献

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}

{"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}