12 research outputs found

    Transient ischemic attack (TIA) is an emergency

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    Transient ischemic attack (TIA) is a warning sign of stroke, and stroke is one of the leading causes of morbidity and mortality in the world. The assessment and management of TIAs can be difficult even for an experienced neurologist. The purpose of this article is to increase the awareness and establish a diagnostic and therapeutic approach to patientswith TIA. In terms of therapy, patients with TIA share the same recommendations as those with acute ischemic stroke. Based on the etiology, therapeutic measures for secondary prevention after a TIA include antithrombotic, antihypertensive, statins therapy, aswell as carotid intervention as appropriate. Itwas shown that early evaluation following appropriate treatment after TIA reduces the risk of the first and early recurrent stroke by about 80%, therefore TIA should be considered as an emergency and should be treated as such

    Stylocarotid syndrome: A case report

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    INTRODUCTION The American otolaryngologist Eagle was the first to describe styloid syndrome in 1937 and the syndrome was named after him (Eagle's syndrome). The original description of two separate syndromes is connected with his name: classical syndrome, which almost constantly occurs after tonsillectomy and carotid artery syndrome, which occurs without tonsillectomy and also in cases when stylohyoid complex compresses the carotid segments and perivascular sympathetic fibers. In the following years, two more syndromes were defined: stylohyoid and pseudostylohyoid, which according to their manifestations, correspond to the genuine classical form. CASE OUTLINE A 40-year old male is presented, with a history of 3-year duration of pains in the upper part of the left side of the neck, in the left eye and its surroundings. Pain occurrences were not regular. Throbbing pains were most often provoked by sudden head movements and neck compression. He was healthy until the onset of these problems. The findings of all examinations were normal. The applied prophylactic therapy, typical for cluster headache, was without any effect. On 64-MSCT (multislice computed tomography), the neck arteries did not show any intraluminal pathology. The styloid processes were of normal length. On the left side, the styloid process tip pressed the internal carotid artery disturbing its longitudinal axis. CONCLUSION In our presentation, the defined lengths of the styloid processes were normal. The medial angulation of the left styloid process was more expressed reaching 63.5 degrees (the right side angulation was normal). Persistent and throbbing pain in the region of the left eye with backward projection suggested compression on the internal carotid artery. Pains were most frequently provoked by head turning and neck compression. 64-MSCT diagnostics enabled us to determine the characteristics of styloid processes and their relation to the internal carotid artery. Improvement was achieved by administration of anti-epileptic (gabapentin) and antidepressant (amitriptyline) drugs

    Transient ischemic attack (TIA) is an emergency

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    Transient ischemic attack (TIA) is a warning sign of stroke, and stroke is one of the leading causes of morbidity and mortality in the world. The assessment and management of TIAs can be difficult even for an experienced neurologist. The purpose of this article is to increase the awareness and establish a diagnostic and therapeutic approach to patientswith TIA. In terms of therapy, patients with TIA share the same recommendations as those with acute ischemic stroke. Based on the etiology, therapeutic measures for secondary prevention after a TIA include antithrombotic, antihypertensive, statins therapy, aswell as carotid intervention as appropriate. Itwas shown that early evaluation following appropriate treatment after TIA reduces the risk of the first and early recurrent stroke by about 80%, therefore TIA should be considered as an emergency and should be treated as such

    Paroxysmal hemicrania: A case report

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    Paroxysmal hemicrania (PH) is one of the trigeminai autonomie cephalgias (TACs), a group of primary headache disorders characterized by unilateral trigeminal distribution pain that occurs in association with prominent ipsilateral cranial autonomy features. The TACs are relatively rare, which is likely to be why they are poorly recognized in primary care. TACs will thus be referred to neurologists eventually, offering an excellent opportunity to diagnose and treat these patients. PH responds in a dramatic and absolute fashion to indomethacin. The importance of recognizing these syndromes is underscored by their excellent but highly selective response to treatment. This is the case report of our patient with PH and the review of current knowledge about pathophysiology of TACs, as well as differential diagnosis of other entities from this headache group

    Posterior reversibile encephalopathic syndrom: case report and review of literature

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    INTRODUCTION Reversible Posterior Leukoencephalopathy Syndrome was introduced into clinical practice in 1996 in order to describe unique syndrome, clinically expressed during hypertensive and uremic encephalopathy, eclampsia and during immunosuppressive therapy [1 ]. First clinical investigations showed that leucoencephalopathy is major characteristic of the syndrome, but further investigations showed no significant destruction in white cerebral tissue [2, 3,4]. In majority of cases changes are localize in posterior irrigation area of the brain and in the most severe cases anterior region is also involved. Taking into consideration all above mentioned facts, the suggested term was Posterior Reversible Encephalopathy Syndrome (PRES) for the syndrome clinically expressed by neurological manifestations derived from cortical and subcortical changes localized in posterior regions of cerebral hemispheres cerebral trunk and cerebellum [5]. CASE REPORT Patient, aged 53 years, was re-hospitalized in Cardiovascular Institute "Dedinje" two months after succesfull aorto-coronary bypass performed in June 2001 due to the chest bone infection. During the treatment of the infection (according to the antibiogram) in September 2001, patient in evening hours developed headache and blurred vision. The recorded blood pressure was 210/120 mmHg so antihypertensive treatment was applied (Nifedipin and Furosemid). After this therapy there was no improvement and intensive headache with fatigue and loss of vision developed. Neurological examination revealed cortical blindness and left hemiparesis. Manitol (20%, 60 ccm every 3 hours) and iv. Nytroglicerin (high blood pressure). Brain CT revealed oedema of parieto-occipital regions of both hemispheres, more emphasized on the right. (Figure 1 a, b, c). There was no sign of focal ischemia even in deeper sections (Figure 1d, e, f). Following three days enormous high blood pressure values were registered. On the fourth day the significant clinical improvement occurred with lowering of blood pressure, better mental state and better vision. There was no sign of left hemiparesis on the 7th day. On the 9th day there were no symptoms or sign of disease. Control brain CT (15th day) was normal. ETHIOPATHOGENESIS Most common causes of PRES are hypertensive encephalopathy [6-8], pre-eclampsia/eclampsia [9-12] cyklosporin A administration [13-22] and uremic encephalopathy [23]. There are several theories about the mechanism for PRES in hypertensive encephalopathy (reversible vasospasm and hyperperfusion) and administration of cyclosporin A (neurotoxic effect). CLINICAL PICTURE Most common symptoms are headache, nausea, vomiting, confusion, behavioural changes, changes of conciousnes (from somnolencia to stupor), vision disturbances (blurred vision, haemianopsia, cortical blindness) and epileptic manifestations (mostly focal attacs with secondary generalization). Mental functions are characterised with decreased activity and reactivity, confusion, loss of concentration and mild type of amnesia. Lethargy is often initial sign, sometimes accompanied with phases of agitation. Stupor and coma rarely occurred. DIAGNOSIS In patients with hypertensive ecephalopathy and eclampsia high blood pressure is registered. Neurological examination revealed vision changes and damages of mental function as well as increased reflex activity. Today, brain MRI and CT are considered the most important diagnostic method for the diagnosis and follow-up of patients with PRES [6]. Brain MRI better detects smaller focal parenhim abnormalities than brain CT.The most often neuroradiological finding is relatively symetrical oedema of white cerebral tissue in parieto-occipital regions of both cerebral hemispheres. Gray cerebral tissue is sometimes involved, usually in mild form of disease. Diagnosis of this "cortical" form of PRES is possible by MR FLAIR (Fluid-Attenuated Inversion Recovery) technique [5]. TREATMENT Therapeutic strategy depends on the cause of PRES and clinical picture. Most important are blood pressure regulation (labetalol, nitroprusid, diuretici), control of epileptic attacs (phenytoin), anti-oedema therapy. (Manitol), induction of vaginal delivery in eclampsia and discontinuation of cyclosporin therapy. In most cases there are no neurological manifestations after the 7th day but some studies showed normalization of clinical finding after one year and more

    Leptomeningeal carcinomatosis can be presenting manifestation of breast carcinoma

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    Introduction. Leptomeningeal carcinomatosis (LC) is a serious complication occuring in solid cancer patients with rather poor prognosis. Case report. We presented a 47-yearold woman with the 6-month history of diffuse headache, nausea and visual obscuration. Initially, clinical status and brain magnetic resonance imaging (MRI) indicated syndrome of idiopathic intracranial hypertension. Due to clinical progression and high papillary stasis, cerebrospinal fluid (CSF) examination was performed only after ventriculoperitoneal shunt was implanted. This led to a significant although transient clinical improvement. Futher investigations led to the diagnosis of invasive lobular breast carcinoma and repeated CSF analysis revealed malignant breast carcinoma cells. In this case LC was an initial presentation of a malignant disease. Conclusion. In the presence of a high clinical suspicion of LC, in spite of initially negative findings, a clinician should persist in repeating relevant tests, such are MRI with larger amounts of gadolinium and high-volume cytological CSF analyses in order to make the diagnosis. [Projekat Ministarstva nauke Republike Srbije, br. 175022

    Transcranial Doppler test for evaluation of cerebral artery embolism: Microemboli detection

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    About one third of ischaemic cerebrovascular diseases have embolic properties. Because of that, transcranial Doppler (TCD) test for detection of microembolic signals (MES), as the only one method for detection of microemboli, is a very important test for the evaluation of cerebral artery embolism. Cerebral emboli are particles of thrombus or atheromatous plaque, platelet aggregates, lipid or air particles in cerebral circulation, which can occlude arterioles and cause ischemic transient attack (TIA) or stroke. Most frequently, they derive from exulcerated plaques of the carotid bifurcation or the aortic arch, from the atrial thrombus, prosthetic heart valves, as well as during carotid endarterectomy, arterial stent, aortocoronary by-pass. For MES detection, bilateral monitoring of a. cerebri mediae (ACM) is performed with each probe held in place over a temporal bone. MES are represented as brightly coloured embolic tracks as they pass through the insonated arteries. A computer hard disk provides continuous recording that is replayed for counting embolic signals. Colour intensity or acoustic range indicate the size and structure of MES. MES in the range of one ACM indicate the source of embolism on the ipsilateral carotid artery, while the bilateral detection of MES suggests a cardiogenic source. Indications for TCD detection of MES are the evaluation of pathogenesis and risk for embolic stroke or TIA and assessing the source of embolism. We started applying this method at the Institute of Neurology in Belgrade 2 years ago. We have investigated 78 patients till today and detected MES in 23 patients (28.7%). The Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology, 2004, considers that TCD is probably useful for detection of cerebral MES in various cardiovascular and cerebrovascular disorders and procedures

    Changes in the retrobulbar arterial circulation after decrease of elevated intraocular pressure in patients with primary open angle glaucoma

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    Introduction. An altered perfusion of the optic nerve head has been proposed as a pathogenic factor in glaucoma. Objective. To evaluate changes of haemodynamic parameters in the retrobulbar arterial circulation after a decrease of elevated intraocular pressure (IOP) in patients with primary open angle glaucoma (POAG). Methods. Twenty-six patients were examined, 14 men and 12 women, 21 up to 50 years old and 5 below, all with previously diagnosed and treated POAG, and all examined at the Eye Clinic, Clinical Centre of Serbia. IOP was measured both with a Goldmann aplanation tonometer and dynamic contour tonometer. Central corneal thickness was measured with ultrasound pachymeter. Imaging of the retrobulbar arterial circulation by colour Doppler was performed at the Neurology Clinic, Clinical Centre of Serbia. It involved measuring of haemodynamic parameters of the ophthalmic artery, central retinal artery, and posterior ciliary arteries. Peak systolic velocity (PSV) and end-diastolic velocity (EDV) were measured, and resistive index (RI) and pulsatility index (PI) were calculated. Results. Haemodynamic arterial parameters PSV and EDV in the ophthalmic and central retinal artery after decrease of IOP were lower, while RI and PI were higher. In the posterior ciliary arteries PSV, EDV and PI were lower, and RI was higher. Conclusion. Changes of the retrobulbar arterial circulation after elevated IOP in POAG patients are important for approach and treatment, while the role of vascular factors in the supplement of the optic disc neuroretinal rim could be a key for progression backlash of glaucoma and the radix of neuroprotection

    Tolosa-Hunt syndrome: is it really necessary to show granuloma? - The report of eight cases

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    Introduction. Tolosa–Hunt syndrome (THS) is a rare entity, characterized by unilateral orbital pain associated with paresis of one or more of the oculomotor cranial nerves and caused by a granulomatous inflammation in the cavernous sinus, superior orbital fissure or orbit. The low prevalence of THS with a broad spectrum of other disorders that could cause painful ophtalmoplegia resulted in a stricter diagnostic criteria of THS in the latest edition of the International Classification of Headache Disorders. Current criteria require demonstration of granuloma by magnetic resonance imaging or biopsy. The diagnosis could be difficult and the initiation of treatment delayed due to a high variablity of clinical presentation of TSH. Reducing the number of patients that, based on clinical presentation, could be classified as having THS, but do not fullfil all diagnostic criteria further complicates establishing of correct diagnosis. Case report. Hereby we presented eight patients diagnosed with and treated for THS. Inspite the exclusion of other causes of painful ophtalmoplegia, granuloma could not be demonstrated in a half of patients. Clinical presentation of THS in patients with and without shown granuloma, did not significantly differ concerning headache characteristics (localization, intensity, quality, duration preceding cranial nerve palsy, response to steroids), the affected cranial nerve, disease course and response to the treatment, as well as types of diagnostic procedures that were performed in ruling out other diseases from the extensive differential diagnosis of painful ophthalmoplegia. Conclusion. There is no significant difference between the THS patients with and without demonstrated granuloma

    Plasminogen activator inhibitor-1 in the evolution of stroke

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    Fibrinolytic activity in the acute stroke was examined by monitoring the level of plasminogen activator inhibitor-1 (PAI-1), as one of the indicators of fibrinolytic activity. Given the role of PAI-1 in the processes of atherogenesis and thrombogenesis, plasma PAI-1 level was measured in 59 patients (up to 50 years of age) with atherothrombotic stroke (verified by computed tomography scanning or magnetic resonance imaging of brain) in the period from 12 to 24 hours (I analysis) and 30 days after the onset of stroke (II analysis); then, it was correlated with plasma PAI-1 level in the control group (57 healthy subjects), which was 2.86±0.70 U/ml. It was found that PAI-1 level was significantly higher in the acute stroke (I analysis: PAI-1 =4.10±1.40 U/ml, p<0.001; II analysis: PAI-1 =3.64+0.90 U/ml, p<0.001), while fibrinolytic activity was lower, especially on the first day from the stroke that was not completely increased even after 30 days. There was no difference in PAI-1 levels between the subgroups of patients with infarction and lacunar cerebral ischemia (p>0.05), as well as between females and males (p>0.05). Along with significantly increased fibrinogen level (4.65±1 g/l, in the controls - 2.83±0.64 g/l, p<0.001), significantly higher triglycerides (2.04±0.76 mmol/l, in the controls - 1.38+0.54 mmol/l, p<0.001) and lipoproteins(a) (0.405±0.29 g/l, in the controls -0.172±0.14 g/l, p<0.001) were found, correlating with higher plasma PAI-1 level in these patients. The increased plasma level of PAI-1 pointed to possibility of decreased fibrinolytic activity in pathogenesis of ischemie stroke, as well as, risk of reinsult, which had been the greatest after the onset of stroke and declined gradually within several weeks
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