Clinical and Neurophysiological Pattern of Guillain-Barré Syndrome in Diabetic and Non Diabetic Patients
|
|
- Shannon Randall
- 5 years ago
- Views:
Transcription
1 Clinical and Neurophysiological Pattern of Guillain-Barré Syndrome in Diabetic and Non Diabetic Patients Shereen Zakarya Department of Neurology, Mansoura University ABSTRACT Objective: To study the clinical and neurophysiological pattern of Guillain-Barré syndrome (GBS) in Diabetics and non diabetic Patients. Materials and Methods: The clinical records of consecutive GBS patients during a 6-year period between 2001 and 2006 were analyzed. 51 cases with GBS, were divided into 2 groups, Group I: 39 non diabetic patients, their ages ranged from years, with a mean age 41±16.8 years, 25 males and 14 females. Patients with other causes of peripheral neuropathy were excluded from the study. Group II: 12 diabetic patients with GBS, 6 males and 6 females, their ages above 50 years, only one female patient was below 20 years. All diabetic patients with past history of diabetic neuropathy were excluded from the study. Results: The majority of the cases presented during the winter months and a preceding infection was reported in two thirds of them. Group I: The pattern of weakness was ascending in 92.3%. Proximal lower limb (LL) weakness was the predominant clinical presentation (89.7%), sensory loss in 59%. Bilateral facial weakness was the commonest cranial nerve affection (64.1%). Autonomic disturbances 26.6%, and need for assisted ventilation in 8 cases (20.5%), nerve conduction studies (NCS) demonstrated a demyelinating pattern in 66.7%, and axonal pattern in 17.9% and no abnormality in 5.1%. 35.9% showed improvement in the 3 rd, the majority of patients (71.8%) improved with one course of intravenous immunoglobulin (IV IG), only 12.8% needed plasma exchange, some factors which indicate bad prognosis include severe autonomic disturbance (12.8%), axonal NCS (17.9%) also it was observed that distal weakness of LL (10.3%) and proximal weakness of UL (17.9%) also indicated bad prognosis. Group II: Ascending progression was reported in (91.7%), distal weakness of both UL (50%) and LL (66.7%) was the predominant clinical presentation, sensory loss was detected in only 33.3%, bilateral facial weakness was also the commonest cranial nerve affection (58.3%), bulbar palsy was detected in only 3.8%, autonomic disturbances in 33.3% which is higher than the detected in non diabetic patients but no one need assisted ventilation, NCS demonstrated also a demyelinating pattern in 66.7%, cerebrospinal fluid (CSF) protein showed mainly mild elevation (the protein was less than 2 gm in 33.3%), 75% improved with one course of IV IG, autonomic and axonal NCS indicate also bad prognosis. Conclusion: The main clinical pattern of weakness in non diabetic GBS patients is proximal weakness of LL, while distal weakness of LL is the main clinical pattern in diabetic GBS, sensory loss is less common in diabetic than in non diabetic patients cerebrospinal fluid (CSF) protein usually showed mild to moderate elevation (less than 2 gm) in diabetic patients, the need for assisted ventilation is less in diabetic patients than non diabetic ones. Autonomic disturbances and axonal type in NCS caused delayed recovery in both diabetic and non diabetic with GBS while predominant distal weakness in the LL and proximal weakness in the UL in non diabetic GBS patients and uncontrolled DM in diabetic GBS patients also caused delayed recovery. (Egypt J. Neurol. Psychiat. Neurosurg., 2008, 45(2): ) INTRODUCTION Guillain-Barré syndrome (GBS) is the most common cause of acute or subacute generalized paralysis. It occurs in all parts of the world and in all seasons affecting children and adults of all ages and both sexes. A mild respiratory or gastrointestinal infection precedes the neuropathic symptoms by 1 to 3 s in about 60 percent of cases 1. GBS is an acute immune mediated polyradiculoneuropathy. GBS is not a disease with variations but a group of syndromes with distinctive subtypes depending upon the site of the immune attack. The major subtypes are acute idiopathic demyelinating polyradiculoneuropathy (AIDP) if the primary target of attack is the myelin sheath, acute motor axonal neuropathy (AMAN) if it involves motor axons at the internodal area, and acute motor Correspondence to Shereen Zakarya, shereenzakarya@yahoo.com. Contact number:
2 Egypt J. Neurol. Psychiat. Neurosurg. Vol. 45 (2) July 2008 sensory axonal neuropathy (AMSAN) if both motor and sensory axons are affected 1. The triad of ataxia, areflexia and ophthalmoplegia, known as Miller Fisher syndrome (MFS), is due to predominant (demyelinating) attack on extraocular motor nerves and proprioceptive sensory fibers. The incidence of these 4 major subtypes differs from region to region with acute idiopathic demyelinating polyradiculoneuropathy predominating in the West, AMAN in China, and MFS in Japan and Taiwan 1,2. All of them are characterized by acute atonic areflexic motor weakness with albumino-cytological dissociation. With the exception of MFS the other subtypes cannot be easily distinguished by clinical features but can be differentiated by electrophysiological characteristics 1. The natural course of the disease is the progression of motor weakness (up to 4 s) that reaches the maximum deficit (nadir) and remains at nadir for several s before improvement starts 3,4. Early introduction (within 2 s of onset) of immunomodulatory therapy can arrest the progression and hasten the recovery. Aim of the present work is to study the clinical and neurophysiological pattern of Guillain-Barré syndrome (GBS) in Diabetic and non diabetic patients. MATERIALS AND METHODS The patients of the present work were admitted to the Neurology Department in IBN Sina Hospital, Kuwait between January 2001 & December They were divided into two groups: Group I: Thirty nine non diabetic patients presented with GBS their diagnosis was based on established clinical criteria of Asbury and Cornblath 5 and was verified by investigations, their ages ranged from 15 to 74 years with a mean 41±16.8, 25 males and 14 females Group II: Twelve diabetic patients satisfied the diagnostic criteria, there were equal numbers of males and females, their ages above 50 years, only one female patient was under the age of 20 years, 9 patients were known to be suffering from diabetes before the onset of motor weakness, the other two patients were detected to be diabetic after admission to the hospital. All the patients files included normal Electromyography (EMG), Nerve Conduction Studies (NCS) before illness i.e. no evidence of peripheral neuropathy before illness. All diabetic patients with past history of diabetic neuropathy before illness were excluded from the study. Both groups were subjected to: 1. History taking 2. Thorough neurological examination was performed at the onset of illness then at regular intervals. 3. The functional status of the patients was assessed using a modified objective scale of Miller published by Ammache et al Laboratory investigations to exclude infectious or metabolic causes of weakness, fasting blood sugar complete blood picture serum urea, creatinine, hepatic function enzymes and erythrocyte sedimentation rate. 5. Cerebrospinal fluid analysis for cells, glucose, and total protein. 6. Electrophysiological studies using standard techniques. The Italian Guillian-Barré study group electrodiagnostic criteria 7, 8 were used to classify the NCS as demyelinating, axonal or mixed type. 7.. Strict control of blood sugar in diabetic patients. 8. Immediately after diagnosis, every patient was given intravenous immunoglobulin (IV IG) 0.4 g/kg body weight for 5 days if the functional grading was more than 2 on Miller's scale. If the weakness persisted over 10 days after the first course of IV IG, a second course of IV IG was given. If the functional grade deteriorated, the patient was subjected to plasma exchange (PE). Statistical Analysis: Frequency, mean, standard deviation and standard error of mean were used to describe data. Chi-square test was used to test for association between groups and clinical categorical data. P value 700
3 was considered significant if less than These tests were run on an IPM compatible personal computer using the statistical package for social scientists (SPSS) for windows 7.5 (SPSS Inc, Chicago, IL, USA). RESULTS This is a retrospective comparative study between Non diabetic GBS patients (Group I) and Diabetic GBS (Group II) Most of the admissions (59%) were during the winter months of November to March. Twenty-seven (69%) patients gave history of preceding illness of which respiratory illness (44%) was the commonest. Of 7 (18%) patients with gastro-intestinal problems, 6 had Diarrhea and 1 nonspecific abdominal pain. No prior illness was reported by 14 (36%) patients. The patients were admitted within I day to a maximum of 21 days after the onset of the illness with an average of 8.3 days. Group I: Thirty nine (39) patients satisfied the diagnostic criteria; 25 males and 14 females with a male to female ratio of 1.8:1. The mean age was 41±16.8 years (range years). The distributions of age and sex are given in table (1). All the 39 patients had motor weakness. In most of them, the weakness started in the lower limbs (LL), then ascended to involve the upper limbs (UL). Combined involvement of both proximal and distal muscle was predominant in the UL, whereas in the LL predominant proximal muscle weakness (89.7%) was noted. The deep tendon reflexes were absent in 36 (92.3%) patients, sluggish in 2 (5.1%) and present in 1 (2.7%) throughout the course of the illness. There were no sensory complaints in 16 (41%) patients at presentation. The patterns of sensory disturbance and motor weakness are given in table (3). The other clinical features like cranial nerve affection, autonomic disturbance and respiratory failure are summarized in table (4). Ophthalmoplegia occurred in 1 GBS patient. Facial weakness was the commonest cranial nerve affection occurring in more than half of the patients. Bulbar weakness was noted in 6 patients (15.4%) and 5 of them developed autonomic disturbance and respiratory failure leading to prolonged ventilatory support and delayed recovery. In addition to these 5 patients, another 3 needed ventilatory support for a few hours and did not have either autonomic disturbance or bulbar palsy. Of the 8 patients requiring ventilatory support, (6 males and 2 females) all of them of different ages. The commonest autonomic disturbance was a combination of labile hypertension and urinary retention. One patient had tachycardia and none developed gastric disturbance or pulmonary edema. All the patients had undergone LP. The CSF protein was normal in 12 patients; the study was performed within 2 s of onset of the illness. The albumino-cytological dissociation was noted in 68%, with CSF protein elevation in 32 patients (Table 5); mean value and highest value g/l; the mean CSF cell count was <1 cell/ µl. All patients had undergone NCS. The most commonly encountered neurophysiological abnormalities were absent or prolonged F wave: 90%, prolonged distal latency: 80%, absent H reflex: 76%, delayed nerve conduction velocity: 73%, partial or complete conduction block: 63%, abnormal blink reflex: 60%, reduced compound muscle action potentials (CMAP): 38% and abnormal sensory nerve action potentials (SNAP): 28%. Demyelination was the predominant type in the neurophysiological work-up followed by axonal type (Table 5). Of the 7 patients with axonal forms, 4 had either absent or low SNAP, which characterizes the AMSAN variant and the other 3 had normal SNAP, typical for the AMAN type. Thirty-nine patients received IV IG. 10 patients was admitted and given IV IG in the first few days of illness onset; IV IG administration was delayed up to the third of admission in other patients because of the atypical progression of their illness. Recovery was accordingly delayed in these patients. Of the 39 patients, 28 (71%) improved with one course of IV IG, 4 (10.3%) required a second course after an interval of 10 days and 5 (12.8%) deteriorated rapidly and required PE. Upon initiation of the treatment, disease progression was arrested, the duration of the plateau phase was shortened and the recovery started in most of the patients (Table 6). In 9 patients, the progression continued up to 4 s, and 4 of them required ventilatory support and PE. Two (5%) patients, in whom the plateau 701
4 Egypt J. Neurol. Psychiat. Neurosurg. Vol. 45 (2) July 2008 phase was prolonged for more than 2 s, showed a delayed recovery. Once the improvement started from nadir, No acute relapses (within 2-3 s of treatment) or mortality were noted in our patients. There was no significant clinical difference between patients with or without prior illness; the admission and initiation of treatment within the first 3 s of illness did not alter the recovery pattern. Patients with predominant distal weakness in the LL, proximal weakness in the UL, autonomic disturbance and axonal type of GBS had a poor outcome (Table 7). Group II: Twelve diabetic patients satisfied the diagnostic criteria, there were equal numbers of males and females, their ages above 50 years, only one patient was under the age of 20 years, 9 patients were known to be suffering from diabetes before the onset of motor weakness, the other two patients were detected to be diabetic after admission to the hospital. All the patient s files included normal EMG, NCS before illness i.e. no evidence of peripheral neuropathy before illness. All diabetic patients with past history of diabetic neuropathy before illness were excluded from the study. Ascending progression was reported in (91.7%), distal weakness of both UL (50%) and LL (66.7%) was the predominant clinical presentation, sensory loss was detected in only 33.3%, bilateral facial weakness was also the commonest cranial nerve affection (58.3%), bulbar palsy was detected in only 3.8%, autonomic disturbances in 33.3% which is higher than the detected in non diabetic patients but no one need assisted ventilation, NCS demonstrated also a demyelinating pattern in 66.7%, CSF protein was normal in 2 patients, 75% showed mainly mild to moderate elevation (CSF protein was less than 2 gm). 9 patients (75%) improved with one course of IV IG, 16.7% needed second course of IV IG and only 8.3% needed plasma exchange. Autonomic, axonal NCS and uncontrolled diabetes mellitus (DM) had a poor outcome. Table 1. Age and sex distribution of non diabetic patients with GBS. Age Male Female Total NO. % NO. % NO. % < > Total Table 2. Age and sex distribution of diabetic patients with GBS. Age Male Female Total NO. % NO. % NO % > Total
5 Age and sex distribution of non diabetic patients with GBS < >70 MALE FEMALE Table 3. Patterns of motor weakness and sensory disturbances in diabetic & non diabetic patients with GBS. Clinical features Evolution of motor weakness Weakness in UL Weakness in LL Sensory loss Signs/pattern Non Diabetic Patients Diabetic Patients NO. % NO. % Ascending Descending Total Proximal > distal Distal > proximal Distal = proximal Total Proximal > distal Distal > proximal Total Paresthesia only Joint position sense only Glove and stocking only All 3 together Any combination of above Total
6 Egypt J. Neurol. Psychiat. Neurosurg. Vol. 45 (2) July 2008 Table 4. Cranial nerve affection, autonomic disturbance and breathing pattern of GBS in diabetic & non diabetic patients. Clinical features Cranial nerve involvement Breathing pattern Autonomic disturbances Signs/pattern Non diabetic Patients Diabetic Patients n % n % Ophthalmoplegia Unilateral facial involvement Bilateral facial involvement No facial involvement Bulbar palsy Total Ventilatory support No ventilatory support Total Labile hypertension alone Retention of urine alone Both together Total Table 5. Laboratory features of the disease in diabetic and non diabetic patients. Investigation CSF Nerve conduction Features Non diabetic Patients Diabetic Patients n % n % No cells Less than 10 cells/µd Protein normal (<0.45 g) Protein g g g >3 g Demyelination type Axonal type Mixed type H reflex abnormality alone Normal
7 Table 6. Treatment and outcome of the disease in both diabetic and non diabetic patients. Outcome Arrest of progression Plateau duration Improvement Treatment Features Non diabetic Patients Diabetic Patients n % n % 1st nd rd th I s >2 s In 2nd In 3rd In 4th In 5th In 6th In 7th In 8th One course of IV IG Two courses of IV IG Plasma exchange Clinical improvement in non diabetic GBS VS diabetic GBS In 2nd In 3rd In 4th In 5th In 6th In 7th In 8th Non diabetic Patients Diabetic Patients 705
8 Egypt J. Neurol. Psychiat. Neurosurg. Vol. 45 (2) July 2008 Table 7. Evaluation of poor prognostic factors in non diabetic patents with GBS. Prognostic factors Patients p n % value Age > 70 years NS Ventilatory support Grade 6 disability in <4 days Plateau duration >14 days CMAP of median nerve < I mv Proximal weakness in UL Distal weakness in LL Severe autonomic disturbance Axonal NCS DISCUSSION GBS is a disease with a worldwide distribution affecting all ages, gender and ethnic groups. Usually, the incidence of GBS increases with age and is more common in persons 50 years or older with a male to female ratio of 1.6:1 6,7-12 compared to 1.8:1 in non diabetic patients in our study, but equal ratio in diabetic patients. As regard age, in non diabetic GBS it occurred in all age groups with predominance above the age of 50 years but in diabetic GBS nearly all the patients were more than 50 years. GBS is a nonseasonal disease 11,14 but seasonal clustering has been reported during summer in Northern China 15, spring in Taiwan 16 and winter and spring (September to March) in many studies 10,13 and in the present study during the winter months of November to March. GBS patients present with a wide clinical spectrum. There are variations in the clinical pattern and differences in immunologic, electrophysiologic and pathologic findings 4. Pattern of weakness is manly proximal in both LL in non diabetic GBS patients but mainly distal in diabetic patients which considered clinical variants of GBS, distal weakness of LL in diabetic patients is difficult to be considered diabetic neuropathy because it is of a acute onset, associated with typical electrophysiological pattern of GBS, also CSF protein was above the normal level. The incidence of AMAN in our population is the same as that in Western countries in contrast to an incidence of 15-20% in Japan, 40% in Latin America and 60-70% in Northern China 1. Western studies indicate a poor recovery for AMSAN and a faster recovery for AMAN 1,17,18,19. Kuwabara et al 20. Reported a variable pattern of recovery (both fast and slow recovery) for AMAN. Both AMSAN and the axonal type showed a delayed recovery pattern in diabetic and non diabetic patients in our study. Our non diabetic patients with predominant distal weakness in LL and proximal weakness in UL had delayed recovery. This type of muscle weakness and recovery pattern were not reported in diabetic patients and most of the other studies. The increase of CSF protein is probably a reflection of the widespread inflammatory disease of the nerve roots but high values have had no clinical or prognostic significance, in less than10% of GBS patients the CSF protein values remain normal throughout the illness 5, in our study CSF protein was normal in 17.9% in non diabetic GBS patients and 16.7% in diabetic GBS patients, CSF protein showed only mild to moderate elevation (less than 2 gm) in diabetic GBS patients but it was reached to high levels in non diabetic GBS patients Bulbar weakness and dysautonomia were considered poor prognostic signs in a Spanish study 12 whereas they were not relevant in a 706
9 Taiwanese study 16. We observed that the development of bulbar weakness was a bad prognostic sign as these non diabetic patients went on to develop autonomic disturbance and respiratory failure needing prolonged ventilatory support. The 8 patients who required ventilatory support and the 5 patients who had a combination of urinary retention and labile hypertension had a prolonged course of their illness. The autonomic disturbances were more common in diabetic patients (33.3%), but no one of them needed ventilatory support. Most of the studies report autonomic disturbance in 66% and ventilatory support in 30% of GBS patients 7,11,12,21 The incidence of autonomic disturbance (25.6% in non diabetic patients and 33.3 in diabetic patients) and requirement for ventilatory support (20% in non diabetic patients) was much lower in our study. Though GBS is a monophasic illness, there are reports of acute and long-term relapses in several studies 8,11,21,22 but we did not observe any acute relapse. Mortality in GBS has decreased from 33 to 5% after the introduction of positive pressure ventilatory support and advanced intensive care management 7,11,23. No deaths were recorded in our study most probably due to the early initiation of treatment. Over the years, treatment of GBS moved from symptomatic to specific immunomodulatory therapy. PE and IV IG are of equal benefit and cost effectiveness 24. We chose IV IG as initial therapy because of its ease of administration. Several controlled clinical trials have shown that both PE and IV IG shorten the time to recovery when used in the early stages of the neuropathy 9. In our study, IV IG was effective up to 3 s after the onset of illness. There are numerous studies about long-term prognostic pointers in GBS 3,7,10,12,20,25,26. Although we concur with most of the commonly mentioned poor prognostic factors, they do not help in the early evaluation (within 2 s) of those patients who are not qualified for treatment at the outset. Hence a need exists for having clinical and electrophysiological pointers to institute early immunomodulatory therapy for the patients with less than grade 2 disability even when the weakness is still in the progressive phase. In some patients there may be late progression after 2 s and a favorable outcome will be denied to them if the treatment is delayed. The non diabetic patients with predominant distal weakness in the LL, proximal weakness in the UL, autonomic disturbance (both hypertension and urinary incontinence together) and those with an axonal type tend to have a delayed recovery but in diabetic patients only autonomic disturbances, axonal type and uncontrolled DM tend to have a delayed recovery but distal weakness of LL didn t indicate poor prognosis. We recommend that patients with any of these factors be given immunomodulatory therapy irrespective of other clinical factors. Since our study population was small especially for diabetic patients, studies with a larger number of patients are needed before making these factors a universal guide to early initiation of treatment. Conclusion The main clinical pattern of weakness in non diabetic GBS patients is proximal weakness of LL, while distal weakness of LL is the main clinical pattern in diabetic GBS, sensory loss is less common in diabetic than in non diabetic patients CSF protein usually showed mild elevation (less than 2 gm) in diabetic patients, the need for assisted ventilation is less in diabetic patients than non diabetic ones. Autonomic disturbances and axonal type in NCS caused delayed recovery in both diabetic and non diabetic patients with GBS while predominant distal weakness in the LL and proximal weakness in the UL in non diabetic GBS patients and uncontrolled DM in diabetic GBS patients also caused delayed recovery. Hence, patients with any of these features should be given immunotherapy early in the course of the disease, In addition to good control of glucose in diabetic patients with GBS. REEFRENCES 1. Asbury AK: New concepts of Guillain-Barre syndrome. J Child Neurol 2000;15: Leone M, Giordana MT. Guillain-Barre` syndrome: A prospective, population- based incidence and outcome survey. Neurology 2003; 60(7): Me Khann GM: Guillain-Barre syndrome clinical and therapeutic observations. Ann Neurol 1990; 27(suppl): S I 3 S
10 Egypt J. Neurol. Psychiat. Neurosurg. Vol. 45 (2) July Van des Meche FGA, Van Doon PA. GBS and chronic inflammatory demyelinating polyneuropathy: immune mechanisms and update on current therepies. Ann Neurol 1995; 37 (suppl); s14-s31 5. Asbury AK, Comblath DR: Assessment of current diagnostic criteria for Guillain-Barre syndrome. Ann Neurol 1990;27(suppl):S2 I S Ammache Z, Afifi AK, Brown CK, Kimura J: Childhood Guillain-Barre syndrome: clinical and elect rophys iologic features predictive of outcome. J Child Neurol 2001;16: Albers JW, Kelly JJ: Acquired inflammatory demyelinating polyneuropathies: clinical and electrodiagnostic features. Muscle Nerve 1989; 12: The Italian Guillain-Barre Study Group: The prognosis and main prognostic indicators of Guillain-Barre syndrome. A multicentre prospective study of 297 patients. Brain 1996; 119: Winer JB: Guillain-Barra syndrome. J Clin Pathol 2001;54: Ropper AH, severe acute Guillain-Barre` Syndrome. Neurology 1986; 36: Bosch EP, Smith BE: Acute inflammatory demyelinating polyradiculoneuropathy; in Bradley WG: Neurology in Clinical Practice, ed 4. Philadelphia, Butterworth, Heinemann, 2004, pp Seneviratne U: Guillain-Barre syndrome. Postgrad Med J 2000;76: Singh NT, Jaiswal AR, Misra S, et al. prognostic factors in Guillain-Barre` Syndrome. J Assoc physicians, India 1994; 42: Sedano MJ, Calleja J, Canga E, Berciano J: Guillain-Barre syndrome in Cantabria, Spain. An epidemiological and clinical study. Acta Neurol Scand 1994;89: McKhann GM, Comblath DR, Griffin JW, Ho TW, Li CY, Jiang Z, Wu HS, Zhaori G, Liu Y, Jou LP, Gao CY, Mao JY, Blaster MJ, Mishu B, Asbury AK: Acute motor axonal neuropathy: A frequent cause of acute flaccid paralysis in China. Ann Neurol 1993;33: Lyu RK, Tang LM, Cheng SY, Hsu W, Chen S: Guillain-Barre syndrome in Taiwan: a clinical study of 167 patients. J Neurol Neurosurg Psychiatry 1997;63: Ropper AH: The Guillain-Barre syndrome. N Eng] J Med 1992;326: Mori M, Kuwabara S, Fukutake T, Yuki N, Hattori T: Clinical features and prognosis of Miller Fisher syndrome. Neurology 2001;56: Ho TW, Li CY, Cornblath DR, Gao CY, Asbury AK, Griffin JW, McKhann GM: Patterns of recovery in the Guillain-Barre syndromes. Neurol 1997;48: Kuwabara S, Mori M, Ogawara K, Hattori T, Yuki N: Indicators of rapid clinical recovery in Guillain-Barra syndrome. J Neurol Neurosurg Psychiatry 2001;70: Barohn RJ, Saperstein DS: Guillain-Barra syndrome and chronic Inflammatory demyelinating polyneuropathy. Semin Neurol 1998;18: Koul R, Chacko A, Ahamed R, Varghese T, Javed H, Al-Lamki Z: Ten year prospective study (clinical spectrum) of childhood Guillain-Barre syndrome in the Arabian Peninsula: comparison of outcome in patients in the pre-and postintravenous immunoglobulin eras. J Child Neurol 2003; 18: Kleyweg RP, Van Der Meche FGA, Loonen MCB, De Jonge J, Nip BK: The natural history of the Guillain-Barre syndrome in 18 children and 50 adults. J Neurol Neurosurg Psychiatry 1989;52: Plasma Exchange/Sandoglobulin GuillainBarre Syndrome Trial Group. Randomized trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barre syndrome. Lancet 1997;349: Cornblath DR: Electrophysiology in Guillain- Barre Syndrome. Ann Neurol 1990;27(suppl): S17 S Hiraga A, Mori M, Ogawara K, Hattori T, Kuwabara S: Difference in patterns of progression in demyelinating and axonal Guillain-Barre syndromes. Neurol., 2003;61: انممخص انعربى 708
11 اننمط االكه ن كى وانفس ونوج انعصب نمتالزمة ج الن بار ه ف انمرضى انمصابون وانغ ر مصابون بانبول انسكري
Electrophysiology in the Guillain-Barré Syndrome: Study of 30 Cases
Journal of Bangladesh College of Physicians and Surgeons Vol. 24, No. 2, May 2006 Electrophysiology in the Guillain-Barré Syndrome: Study of 30 Cases NC KUNDU Summary: Thirty consecutive patients diagnosed
More informationComparison of electrophysiological findings in axonal and demyelinating Guillain-Barre syndrome
Iranian Journal of Neurology Original Paper Iran J Neurol 2014; 13(3): 138-143 Comparison of electrophysiological findings in axonal and demyelinating Guillain-Barre syndrome Received: 9 Mar 2014 Accepted:
More informationGuillain-Barré Syndrome
Guillain-Barré Syndrome Ouch! www.philippelefevre.com Guillain-Barré Syndrome Acute post-infective polyneuropathy Heterogeneous condition with several variant forms Lipid A Neuronal Ganglioside Pathogenesis
More informationRisk Factors of Respiratory Failure in Children with Guillain-Barré Syndrome
Pediatrics and Neonatology (2012) 53, 295e299 Available online at www.sciencedirect.com journal homepage: http://www.pediatr-neonatol.com ORIGINAL ARTICLE Risk Factors of Respiratory Failure in Children
More informationSupplementary Online Content
Supplementary Online Content Stevens O, Claeys KG, Poesen K, Veroniek S, Van Damme P. Diagnostic challenges and clinical characteristics of hepatitis E virus associated Guillain- Barré syndrome. JAMA Neurol.
More informationInternational Journal of Basic & Applied Physiology
ELECTRODIAGNOSTIC FEATURES IN CLINICALLY SUSPECTED GUILLAIN BARRE SYNDROME Asha Shrivastava*, Rashmi Dave**, Sanjeev Shrivastava ***, Brajesh Sharma **** *Professor, ** JR III, *** Assistant Professor,
More informationClinical and electrophysiologic features of childhood Guillain-Barré syndrome in Northeast China
Journal of the Formosan Medical Association (2014) 113, 634e639 Available online at www.sciencedirect.com journal homepage: www.jfma-online.com ORIGINAL ARTICLE Clinical and electrophysiologic features
More informationPrediction of Functional Outcome in Axonal Guillain-Barre Syndrome Eun Jung Sung, MD, Dae Yul Kim, MD, Min Cheol Chang, MD, Eun Jae Ko, MD
Original Article Ann Rehabil Med 2016;40(3):481-488 pissn: 2234-0645 eissn: 2234-0653 http://dx.doi.org/10.5535/arm.2016.40.3.481 Annals of Rehabilitation Medicine Prediction of Functional Outcome in Axonal
More informationImmunopathology of Guillain- Barré syndrome. L. Magy Service de Neurologie Centre de Référence 'Neuropathies Périphériques Rares' CHU Limoges, France
Immunopathology of Guillain- Barré syndrome L. Magy Service de Neurologie Centre de Référence 'Neuropathies Périphériques Rares' CHU Limoges, France What is Guillain-Barré syndrome? An immune-mediated
More informationThe Role of Cytomegalovirus, Haemophilus Influenzae and Epstein Barr Virus in Guillain Barre Syndrome
ORIGINAL REPORT The Role of Cytomegalovirus, Haemophilus Influenzae and Epstein Barr Virus in Guillain Barre Syndrome Shahriar Nafissi 1, Zahra Vahabi 1, Maryam Sadeghi Ghahar 2, Ali Akbar Amirzargar 2,
More informationImmune Mediated Neuropathies
Immune Mediated Neuropathies Hernan Gatuslao, M.D. Assistant Professor Department of Neurology Virginia Commonwealth University School of Medicine AIDP and CIDP Acute inflammatory demyelinating polyneuropathy
More informationDiagnosis and Management of Immune-mediated Neuropathies
Continuing Medical Education 39 Diagnosis and Management of Immune-mediated Neuropathies Sung-Tsang Hsieh Abstract- Immune-mediate neuropathies, or inflammatory neuropathies are neuropathies due to the
More informationHyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-gm1 antibody
18 Department of Neurology, Chiba University School of Medicine, Chiba, Japan S Kuwabara K Ogawara M Mori T Hattori Department of Neurology, Dokkyo University School of Medicine, Tochigi, Japan M Koga
More informationMiller Fisher Syndrome A variant of Guillan Barré Syndrome. Sarah I. Sheikh, BM BCh, MRCP
Miller Fisher Syndrome A variant of Guillan Barré Syndrome Sarah I. Sheikh, BM BCh, MRCP History of GBS 1859 Jean Baptiste Octave Landry de Thézillat (1826-1865) published his observation on ascending
More informationGuillain-Barré syndrome and related disorders
Guillain-Barré syndrome and related disorders Dr Benjamin Wakerley Department of Neurology Gloucestershire Royal Hospital Disclosures Novartis - educational grant Guillain-Barré syndrome and related disorders
More informationDetection of Autoantibodies against Gangliosides in Guillain-Barré Syndrome
ISSN 1735-1383 Iran. J. Immunol. September 2010, 7 (3), 198-201 Hong-Liang Zhang, Su-Jie Gao, Yi Yang, Jiang Wu Detection of Autoantibodies against Gangliosides in Guillain-Barré Syndrome Article Type:
More informationAssociation of Campylobacter jejuni infection and Guillain- Barré syndrome: a cohort study in the northwest of Iran
The Turkish Journal of Pediatrics 2008; 50: 443-448 Original Association of Campylobacter jejuni infection and Guillain- Barré syndrome: a cohort study in the northwest of Iran Mohammad Barzegar 1, Asghar
More informationFrom the Department of Neurology, University Hospital Birmingham, Birmingham, UK
Q J Med 2002; 95:717 721 Review QJM Treatment of Guillain-Barré syndrome J.B. WINER From the Department of Neurology, University Hospital Birmingham, Birmingham, UK Introduction Although there are earlier
More informationNeuromuscular Respiratory Failure in Guillain-Barre Syndrome: Evaluation of Clinical and Electrodiagnostic Predictors
Original Article Neuromuscular Respiratory Failure in Guillain-Barre Syndrome: Evaluation of Clinical and Electrodiagnostic Predictors Uma Sundar, Elizabeth Abraham, A Gharat, ME Yeolekar, Trupti Trivedi,
More informationGuillain Barré Syndrome: Profile of 120 Patients with respect to Response to Various Modalities of Treatment
IJPMR ORIGINAL ARTICLE 10.5005/jp-journals-10066-0022 Guillain Barré Syndrome Guillain Barré Syndrome: Profile of 120 Patients with respect to Response to Various Modalities of Treatment 1 Vishal A Chafale,
More informationValidity of Neurophysiological Study Inprediction of Severity of Guillain-Barre Syndrome and the Indication for Mechanical Ventilation
IOSR Journal Of Pharmacy And Biological Sciences (IOSR-JPBS) e-issn:2278-3008, p-issn:2319-7676. Volume 14, Issue 1 Ser. II (Jan Feb 2019), PP 43-47 www.iosrjournals.org Validity of Neurophysiological
More informationEvaluation of Peripheral Neuropathy. Evaluation of Peripheral Neuropathy - Introduction
Evaluation of Peripheral Neuropathy Chris Edwards, MD Ochsner Neurology, Main Campus Evaluation of Peripheral Neuropathy - Introduction A very common complaint in the clinic Presentation is variable Multiple
More informationDysphagia as initial manifestation of Guillan-Barrè Syndrome in a child Elda Pitrolo, Simona Santucci, Chiara Cuzzupè, Filippo De Luca
Clinical Case Seminar A7(1-5 ) Dysphagia as initial manifestation of Guillan-Barrè Syndrome in a child Elda Pitrolo, Simona Santucci, Chiara Cuzzupè, Filippo De Luca Department of Human Pathology of Adulthood
More informationLE SYNDROME DE GUILLAIN-BARRE
FORMATION UNIVERSITAIRE SPECIFIQUE (FUS) Enseignement interuniversitaire MASTER DE SPECIALISATION EN MEDECINE INTERNE Samedi 19 dećembre 2015 Institute of Neurosciences LE SYNDROME DE GUILLAIN-BARRE Peter
More informationGuillain Barre Syndrome: A clinical observational study in Indian paediatric patients
Guillain Barre Syndrome: A clinical observational study in Indian paediatric patients *Shikha Swaroop 1, Bakul B Javadekar 2 Sri Lanka Journal of Child Health, 2017; 46(3): 238-242 Abstract Background:
More informationElectrodiagnostic studies comprising of electromyography (EMG) and nerve
INTRODUCTION AND TERMINOLOGY Electrodiagnostic studies comprising of electromyography (EMG) and nerve conduction studies (NCS) are well-established objective methods for the diagnosis, quantification and
More informationCritical Illness Polyneuropathy CIP and Critical Illness Myopathy CIM. Andrzej Sladkowski
Critical Illness Polyneuropathy CIP and Critical Illness Myopathy CIM Andrzej Sladkowski Potential causes of weakness in the ICU-1 Muscle disease Critical illness myopathy Inflammatory myopathy Hypokalemic
More informationCase Report An Unusual Case of Recurrent Guillain-Barre Syndrome of a Different Subtype Five Years after Initial Diagnosis
Case Reports in Neurological Medicine Volume 2013, Article ID 356157, 4 pages http://dx.doi.org/10.1155/2013/356157 Case Report An Unusual Case of Recurrent Guillain-Barre Syndrome of a Different Subtype
More informationA comparison between plasmapheresis and intravenous immunoglobulin in children with Guillain Barré syndrome in Upper Egypt
610471TAN0010.1177/1756285615610471Therapeutic Advances in Neurological DisordersK. Saad research-article2015 Therapeutic Advances in Neurological Disorders Original Research A comparison between plasmapheresis
More informationThe clinical spectrum of Malaysian patients with. Chronic inflammatory demyelinating polyneuropathy
Neurology Asia 2004; 9 : 39 45 The clinical spectrum of Malaysian patients with chronic inflammatory demyelinating polyneuropathy Khean Jin GOH, Wai Keong NG, Nee Kong CHEW, Chong Tin TAN Division of Neurology,
More informationrole of antiganglioside antibodies
J Neurol Neurosurg Psychiatry 2000;68:191 195 191 Department of Neurology, Chiba University School of Medicine, 1 8 1 Inohana, Chuo-ku, Chiba 260 8670, Japan S Kuwabara K Ogawara K Mizobuchi M Mori T Hattori
More informationGuillain-Barre Syndrome and its Prognosis with Hyponatremia
Original Article RUHS Journal of Health Sciences, Volume 2 Number 4, October -December 2017 Guillain-Barre Syndrome and its Prognosis with Hyponatremia Jerin Romeol, Hemant Mahur2, D P Singh3, Nitesh Pansari4,
More informationGUILLAIN BARRE SYNDROME IN EARLY INFANCY: A CASE REPORT. Rajkumar M. Meshram*, S. Abhisheik, Hina Agrawal, Samadhan Dhakne Abstract
Paediatrics Case Report International Journal of Clinical And Diagnostic Research ISSN 2395-3403 Volume 4, Issue 6, Nov-Dec 2016. Glorigin Lifesciences Private Limited. GUILLAIN BARRE SYNDROME IN EARLY
More informationORIGINAL CONTRIBUTION. Continuous Spectrum of Pharyngeal-Cervical-Brachial Variant of Guillain-Barré Syndrome
ORIGINAL CONTRIBUTION Continuous Spectrum of Pharyngeal-Cervical-Brachial Variant of Guillain-Barré Syndrome Takahide Nagashima, MD, PhD; Michiaki Koga, MD, PhD; Masaaki Odaka, MD, PhD; Koichi Hirata,
More informationSevere Chronic Inflammatory Demyelinating Polyneuropathy Ameliorated following High-dose (3 g/kg) Intravenous Immunoglobulin Therapy
doi: 10.2169/internalmedicine.1723-18 http://internmed.jp CASE REPORT Severe Chronic Inflammatory Demyelinating Polyneuropathy Ameliorated following High-dose (3 g/kg) Intravenous Immunoglobulin Therapy
More informationElectrodiagnostic Variations in Guillain-Barré Syndrome - Retrospective Analysis of 95 Patients
Original Article GCSMC J Med Sci Vol (VI) No (II) July-December 2017 Electrodiagnostic Variations in Guillain-Barré Syndrome - Retrospective Analysis of 95 Patients Chilvana Patel*, Surya Murthy Vishnubhakat**
More informationGUILLAIN BARRÉ syndrome is the most common
1374 THE NEW ENGLAND JOURNAL OF MEDICINE Nov. 23, 1995 CAMPYLOBACTER JEJUNI INFECTION AND GUILLAIN BARRÉ SYNDROME JEREMY H. REES, PH.D., M.R.C.P., SARA E. SOUDAIN, B.SC., NORMAN A. GREGSON, PH.D., AND
More informationNovember 16-18, 2017 Hotel Monteleone New Orleans, LA. Provided by
November 16-18, 2017 Hotel Monteleone New Orleans, LA Provided by Diabetic Neuropathy: A Global and Growing Problem John D. England, MD Louisiana State University Health Sciences Center School of Medicine
More informationComparison of diabetes patients with demyelinating diabetic sensorimotor polyneuropathy to those diagnosed with CIDP
Comparison of diabetes patients with demyelinating diabetic sensorimotor polyneuropathy to those diagnosed with CIDP Samantha K. Dunnigan 1, Hamid Ebadi 1, Ari Breiner 1, Hans D. Katzberg 1, Leif E. Lovblom
More informationGuillain Barré syndrome associated with normal or exaggerated tendon reflexes
J Neurol (2012) 259:1181 1190 DOI 10.1007/s00415-011-6330-4 ORIGINAL COMMUNICATION Guillain Barré syndrome associated with normal or exaggerated tendon reflexes Nobuhiro Yuki Norito Kokubun Satoshi Kuwabara
More informationChanges in the severity and subtype of Guillain-Barré syndrome admitted to a specialist Neuromedical ICU over a 25 year period
J Neurol (2017) 264:564 569 DOI 10.1007/s00415-016-8380-0 ORIGINAL COMMUNICATION Changes in the severity and subtype of Guillain-Barré syndrome admitted to a specialist Neuromedical ICU over a 25 year
More informationPeripheral Neuropathies
Peripheral Neuropathies ELBA Y. GERENA MALDONADO, MD ACTING ASSISTANT PROFESSOR UNIVERSITY OF WASHINGTON MEDICAL CENTER Objectives Definition Neurophysiology Evaluation of polyneuropathies Cases Summary
More informationGuillain - Barre Syndrome - is an acute frequently severe and
12 JAPI march 2013 VOL. 61 Original Article Clinical Profile of Guillain Barre Syndrome Shubhangi Vithal Dhadke 1, Vithal Narayan Dhadke 2, Sachin S Bangar 1, Milind B Korade 3 Abstract Objectives: To
More informationGUILLAIN-BARRE SYNDROME
GUILLAIN-BARRE SYNDROME tarek.sharshar@rpc.aphp.fr University of Versailles Saint-Quentin en Yvelines Raymond Poincaré Teaching Hospital Garches - France STATEMENTS 1. Guillain-Barré Syndrome (GBS) is
More informationPeripheral neuropathies, neuromuscular junction disorders, & CNS myelin diseases
Peripheral neuropathies, neuromuscular junction disorders, & CNS myelin diseases Peripheral neuropathies according to which part affected Axonal Demyelinating with axonal sparing Many times: mixed features
More informationCorrelative study between C-reactive protein, clinical severity, and nerve conduction studies in Guillain-Barrè syndrome
Altaweel et al. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery (2018) 54:4 https://doi.org/10.1186/s41983-018-0006-2 The Egyptian Journal of Neurology, Psychiatry and Neurosurgery RESEARCH
More informationGuillain-Barré syndrome: subtypes and predictors of outcome from India
Journal of the Peripheral Nervous System 19:36 43 (2014) RESEARCH REPORT Guillain-Barré syndrome: subtypes and predictors of outcome from India Jayantee Kalita, Usha K. Misra, Gaurav Goyal, and Moromi
More informationA descriptive study of patients with Guillain-Barré syndrome: Experience from an Australian tertiary level hospital
A descriptive study of patients with Guillain-Barré syndrome: Experience from an Australian tertiary level hospital Emma Foster 1, Luke Bonavia 1, Ashwin Subramaniam 2-4, Cameron Green 1, Ernest Butler
More informationTHE ROLE OF THE ANTI GQ1B ANTIBODY IN DIFFERENTIAL. DIGNOSIS OF ACUTE OPTHALMOPARESIS
THE ROLE OF THE ANTI GQ1B ANTIBODY IN DIFFERENTIAL. DIGNOSIS OF ACUTE OPTHALMOPARESIS Abstract Miller Fisher syndrome has a triad of total external ophthalmoplegia, ataxia and areflexia, Botulism is caused
More informationMyasthenia gravis (MG) is an autoimmune disorder
Brief Communication The clinical features of patients concurrent with Guillain-Barré syndrome and myasthenia gravis Junliang Yuan, MD, Juan Zhang, MD, ABSTRACT Bingwei Zhang, MD, Wenli Hu, MD. Objectives:
More informationA comparison of two patients with Guillain-Barre Syndrome J O H N C O R S I N O, S P T
A comparison of two patients with Guillain-Barre Syndrome J O H N C O R S I N O, S P T Guillain-Barre Acute inflammatory demyelinating polyneuropathy Highly diverse presentation, course, outcome Miller-Fisher:
More informationParaparetic Guillain-Barré syndrome
Paraparetic Guillain-Barré syndrome Bianca van den Berg, MD Christiaan Fokke, MD Judith Drenthen, MD Pieter A. van Doorn, MD, PhD Bart C. Jacobs, MD, PhD Correspondence to Dr. Jacobs: b.jacobs@erasmusmc.nl
More informationCIDP + MMN - how to diagnose and treat. Dr Hadi Manji
CIDP + MMN - how to diagnose and treat Dr Hadi Manji Outline Introduction CIDP Diagnosis Clinical features MRI Nerve conduction tests Lumbar puncture Nerve biopsy Treatment IV Ig Steroids Plasma Exchnage
More informationInfection-Associated Neurological Syndromes
Infection-Associated Neurological Syndromes Anand P, MD PhD Medical Director, BloodCenter of Wisconsin Assistant Professor, Medical College of Wisconsin ASFA Annual Meeting San Antonio, TX, May 8th, 2015
More informationACUTE SYMMETRICAL MOTOR NEUROPATHY IN DIABETES MELLITUS
Prize-Winning Paper Summary ACUTE SYMMETRICAL MOTOR NEUROPATHY IN DIABETES MELLITUS A distinct clinical entity M. Gourie Devi* The main clinical features in 12 patients with acute motor neuropathy associated
More informationA STUDY OF ASSESSMENT IN PERIPHERAL NEUROPATHY IN PATIENTS WITH NEWLY DETECTED THYROID DISORDERS IN A TERTIARY CARE TEACHING INSTITUTE
A STUDY OF ASSESSMENT IN PERIPHERAL NEUROPATHY IN PATIENTS WITH NEWLY DETECTED THYROID DISORDERS IN A TERTIARY CARE TEACHING INSTITUTE Rajan Ganesan 1, Marimuthu Arumugam 2, Arungandhi Pachaiappan 3, Thilakavathi
More informationCOMPARISON OF ELECTRODIAGNOSTIC CRITERIA FOR PRIMARY DEMYELINATION IN CHRONIC POLYNEUROPATHY
Three sets of electrodiagnostic criteria for establishing primary demyelination in chronic polyneuropathy are evaluated. Sensitivity is assessed in 7 patients with clinically established chronic inflammatory
More informationRecurrent miller fisher: a new case report and a literature review
e208 F. Barbato et al. Review Clin Ter 2017; 168 (3):e208-213. doi: 10.7417/T.2017.2008 Recurrent miller fisher: a new case report and a literature review F. Barbato 1, A. Di Paolantonio 1, M. Distefano
More informationAppendix B: Provincial Case Definitions for Reportable Diseases
Ministry of Health and Long-Term Care Infectious Diseases Protocol Appendix B: Provincial Case Definitions for Reportable Diseases Disease: West Nile Virus Illness Revised March 2017 West Nile Virus Illness
More informationGuillain-Barré Syndrome Beth A. Rosen. DOI: /pir
Guillain-Barré Syndrome Beth A. Rosen Pediatrics in Review 2012;33;164 DOI: 10.1542/pir.33-4-164 The online version of this article, along with updated information and services, is located on the World
More informationS everal antibodies against gangliosides have been detected
568 PAPER Central motor conduction in patients with anti-ganglioside antibody associated neuropathy syndromes and hyperreflexia Y Oshima, T Mitsui, H Yoshino, I Endo, M Kunishige, A Asano, T Matsumoto...
More informationDiagnostic investigation of patients with chronic polyneuropathy: evaluation of a clinical guideline
J Neurol Neurosurg Psychiatry 2001;71:205 209 205 Department of Neurology, Academic Medical Centre, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands N R Rosenberg P Portegies M
More informationMedian-ulnar nerve communications and carpal tunnel syndrome
Journal of Neurology, Neurosurgery, and Psychiatry, 1977, 40, 982-986 Median-ulnar nerve communications and carpal tunnel syndrome LUDWIG GUTMANN From the Department of Neurology, West Virginia University,
More informationOriginal Paper. Iran J Neurol 2014; 13(1): 7-12
Iranian Journal of Neurology Original Paper Iran J Neurol 2014; 13(1): 7-12 Correlations between cytomegalovirus, Epstein-Barr virus, anti-ganglioside antibodies, electrodiagnostic findings and functional
More informationA Case of Acute Sensory Neuropathy Associated with Contrast Enhancement of the Cauda Equina on Magnetic Resonance Imaging
61 Case Report St. Marianna Med. J. Vol. 33, pp. 61 66, 2005 A Case of Acute Sensory Neuropathy Associated with Contrast Enhancement of the Cauda Equina on Magnetic Resonance Imaging Toshinari Kobayashi
More informationEvaluation of nerve conduction abnormalities in type 2 diabetic patients
Original article: Evaluation of nerve conduction abnormalities in type 2 diabetic patients 1Kannan K, 2 Sivaraj M 1Asst Professor, Dept of Physiology, kilpauk Medical College, Kilpauk, Chennai, Tamil Nadu,
More informationCompound Action Potential, CAP
Stimulus Strength UNIVERSITY OF JORDAN FACULTY OF MEDICINE DEPARTMENT OF PHYSIOLOGY & BIOCHEMISTRY INTRODUCTION TO NEUROPHYSIOLOGY Spring, 2013 Textbook of Medical Physiology by: Guyton & Hall, 12 th edition
More informationWorld Journal of Pharmaceutical Research
World Journal of Pharmaceutical research Al-Aubaidy et al. Volume 3, Issue 2, XXX-XXX. Research Article ISSN 2277 7105 RESPONSE OF ANTI-CARDIOLIPIN ANTIBODIES TO VARIOUS TREATMENT MODALITIES IN GUILLAIN
More informationIl ruolo della diagnostica di laboratorio
Cremona 9 giugno 2017 DIAGNOSI DIFFERENZIALE DELLE MALATTIE DEL SISTEMA NERVOSO PERIFERICO Il ruolo della diagnostica di laboratorio No conflicts of interest Wang Y et al. Mediators of Inflammatory 2015
More informationMultifocal motor neuropathy: diagnostic criteria that predict the response to immunoglobulin treatment
Multifocal motor neuropathy: diagnostic criteria that predict the response to immunoglobulin treatment 7 MMN RM Van den Berg-Vos, H Franssen, JHJ Wokke, HW Van Es, LH Van den Berg Annals of Neurology 2000;
More informationAppendix I (a) Human Surveillance Case Definition (Revised July 4, 2005)
Section A: Case Definitions Appendix I (a) Human Surveillance Case Definition (Revised July 4, 2005) The current Case Definitions were drafted with available information at the time of writing. Case Definitions
More informationCase Number 1 Guillain-Barré Syndrome (GBS)
Case Number 1 Guillain-Barré Syndrome (GBS) Maria Angela Grima Reviewed by: Dr. Nicola Aquilina Case summary: Demographic details: Mr. JS, male, Gudja Referred from: GP A 57-year-old Caucasian gentleman
More informationORIGINAL CONTRIBUTION. Nicholas D. Lawn, FRACP; Dade D. Fletcher, MD; Robert D. Henderson, FRACP; Troy D. Wolter, MS; Eelco F. M.
ORIGINAL CONTRIBUTION Anticipating Mechanical Ventilation in Guillain-Barré Syndrome Nicholas D. Lawn, FRACP; Dade D. Fletcher, MD; Robert D. Henderson, FRACP; Troy D. Wolter, MS; Eelco F. M. Wijdicks,
More informationCASE REPORT. Abstract. Introduction. Case Report. Tetsuya Miyagi, Katsuyuki Higa, Miwako Kido, Satoshi Ishihara, Ryo Nakachi and Syugo Suwazono
CASE REPORT The Sequential Ultrasonographic, Electrophysiological and MRI Findings in a Patient with the Pharyngeal-cervicalbrachial Variant of Guillain-Barré Syndrome from the Acute Phase to the Chronic
More informationGuillain-Barré syndrome and related disorders
Guillain-Barré syndrome and related disorders Artículo Amato AA RESUMEN En 1859, Landry describió una neuropatía caracterizada por parálisis severa ascendente. Posteriormente, Guillain, Barré y Strohl
More informationSEMESTER Suriname study. The Suriname Meningo- encephalitis Study (SMS) Introduction. SMS- protocol version 3.4. Principal investigators:
SEMESTER Suriname study The Suriname Meningo- encephalitis Study (SMS) Principal investigators: E.C.M. van Gorp 1,2 and S. Vreden 3 Participating investigators: H. Alberga 4, M. Baptista 5, R. Cruden 4,
More informationA Case of Fisher Syndrome Complicated by Maxillary Sinus Cysts
Showa Univ J Med Sci 22 3, 193 198, September 2010 Case Report A Case of Fisher Syndrome Complicated by Maxillary Sinus Cysts Yukiomi KUSHIHASHI 1, Go TAKAHASHI 1, Miyuki SUZUKI 1, Yoshihiro YAMADA 1,
More informationMULTIPLE SCLEROSIS PROFILE
MULTIPLE SCLEROSIS PROFILE What is Multiple Sclerosis? Multiple sclerosis (MS) is a chronic, inflammatory disease of unknown etiology that involves an immune-mediated attack on the central nervous system
More informationClinical electrophysiological characteristics and prognosis of acute motor axonal neuropathy in Uygur children of Xinjiang.
Biomedical Research 2017; 28 (22): 9696-9700 ISSN 0970-938X www.biomedres.info Clinical electrophysiological characteristics and prognosis of acute motor axonal neuropathy in Uygur children of Xinjiang.
More informationClinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh
Original Article Clinical Profile of Guillain Barre Syndrome-Observations from a Tertiary Care Hospital of Bangladesh Habib R a, Saifuddin M b, Islam R c, Rahman A d, Bhowmik NB e, Haque MA f Abstract
More informationNIH Public Access Author Manuscript Neurol Clin. Author manuscript; available in PMC 2014 May 01.
NIH Public Access Author Manuscript Published in final edited form as: Neurol Clin. 2013 May ; 31(2): 491 510. doi:10.1016/j.ncl.2013.01.005. Guillain-Barré Syndrome and Variants Mazen M. Dimachkie, M.D.
More informationGuillain-Barré Syndrome in a Patient with Pneumococcal Meningitis
Guillain-Barré Syndrome in a Patient with Pneumococcal Meningitis An Uncommon Complication of a Common Infection ACP Wisconsin, September 2017 Jesse Maupin, MD (PGY-2) University of Wisconsin Hospital
More informationCOPYRIGHT 2012 THE TRANSVERSE MYELITIS ASSOCIATION. ALL RIGHTS RESERVED
The Transverse Myelitis Association...advocating for those with acute disseminated encephalomyelitis, neuromyelitis optica, optic neuritis and transverse myelitis ACUTE DISSEMINATED ENCEPHALOMYELITIS (ADEM)
More informationChildhood Guillain-Barré Syndrome: Comparing Intravenous Immunoglobulin Treatment with Supportive Care
TSMJ Volume 6: Cases Childhood Guillain-Barré Syndrome: Comparing Intravenous Immunoglobulin Treatment with Supportive Care Sarah McLean, Sheng F. Oon, 6 th Year Medicine Abstract Objectives: Guillain-Barré
More informationGuillain-Barré Syndrome Mazen M. Dimachkie, M.D 1,* Richard J. Barohn, M.D 2
Current Treatment Options in Neurology (2013) 15:338 349 DOI 10.1007/s11940-013-0231-z NEUROIMMUNOLOGY (RP LISAK, SECTION EDITOR) Guillain-Barré Syndrome Mazen M. Dimachkie, M.D 1,* Richard J. Barohn,
More informationPitfalls in electrodiagnosis of Guillain-Barré syndrome subtypes
Pitfalls in electrodiagnosis of Guillain-Barré syndrome subtypes Antonino Uncini, Claudia Manzoli, Francesca Notturno, Margherita Capasso To cite this version: Antonino Uncini, Claudia Manzoli, Francesca
More informationComparison of Sudomotor and Sensory Nerve Testing in Painful Sensory Neuropathies
138 Original Article Comparison of Sudomotor and Sensory Nerve Testing in Painful Sensory Neuropathies James M. Killian, MD,* Shane Smyth, MD,* Rudy Guerra, PhD, Ishan Adhikari, MD,* and Yadollah Harati,
More informationALBUMINOCYTOLOGICAL DISSOCIATION IN DIFFERENT ELECTROPHYSIOLOGICAL GBS VARIANTS
O R I G I N A L A R T I C L E ALBUMINOCYTOLOGICAL DISSOCIATION IN DIFFERENT ELECTROPHYSIOLOGICAL GBS VARIANTS Ali ZohairNomani, Mansoor Iqbal, Haris Majid Rajput, Mazhar Badshah, Sumaira Nabi, Zakir Jan,
More informationAhmed Abbas, Mark Cook, Liong Hiew Fu, Alistair Lewthwaite, Colin Shirley, Yusuf A. Rajabally
2016, Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International http://creativecommons.org/licenses/by-nc-nd/4.0/ Accepted Manuscript A case of POEMS mimicking
More informationRisk factors for respiratory failure in Guillain-Barre syndrome in Bangladesh: a prospective study
RESEARCH ARTICLE Risk factors for respiratory failure in Guillain-Barre syndrome in Bangladesh: a prospective study Zhahirul Islam 1, *, Nowshin Papri 1, *, Gulshan Ara 2, Tanveen Ishaque 1,3, Arafat U.
More informationElectrodiagnostic criteria for polyneuropathy and demyelination: application in 135 patients with Guillain-Barre syndrome
482 48ournal of Neurology, Neurosurgery, and Psychiatry 1995;59:482-486 Department of Neurology, University Hospital Dijkzigt and Erasmus University Rotterdam, The Netherlands J Meulstee F G A van der
More informationAnti-GD1a Antibody Is Associated with Axonal But Not Demyelinating Forms of Guillain-Barré Syndrome
Anti-GD1a Antibody Is Associated with Axonal But Not Demyelinating Forms of Guillain-Barré Syndrome T. W. Ho, MD,* H. J. Willison, FRCP, I. Nachamkin, DrPH, C. Y. Li, MD, J. Veitch, FIMLS, H. Ung, BS,
More informationIN CONTRAST to the chronic distal
ORIGINAL CONTRIBUTION Alcohol-Related Acute Axonal Polyneuropathy A Differential Diagnosis of Guillain-Barré Syndrome Johannes C. Wöhrle, MD; Konstantinos Spengos, MD; Wolfgang Steinke, MD; Hans H. Goebel,
More informationA Comparison of Nerve Conduction Properties in Male and Female of 20 to 30 Years of Age Group
A Comparison of Nerve Conduction Properties in Male and Female of 20 to 30 Years of Age Group Gakhar 1, M., Verma 2, S.K. and Lehri 3, A. 1 Research Scholar, Department of Sports Science, Punjabi University,
More informationGuide to the use of nerve conduction studies (NCS) & electromyography (EMG) for non-neurologists
Guide to the use of nerve conduction studies (NCS) & electromyography (EMG) for non-neurologists What is NCS/EMG? NCS examines the conduction properties of sensory and motor peripheral nerves. For both
More informationMotor and sensory nerve conduction studies
3 rd Congress of the European Academy of Neurology Amsterdam, The Netherlands, June 24 27, 2017 Hands-on Course 2 Assessment of peripheral nerves function and structure in suspected peripheral neuropathies
More informationGandhi et al., IJPSR, 2012; Vol. 3(11): ISSN: GENERAL CONSIDERATION OF GUILLIAIN BARRE SYNDROME
IJPSR (2012), Vol. 3, Issue 11 (Review Article) Received on 11 July, 2012; received in revised form 06 August, 2012; accepted 21 October, 2012 GENERAL CONSIDERATION OF GUILLIAIN BARRE SYNDROME Zeel A.
More informationPediatric Aspects of EDX
Pediatric Aspects of EDX Albert C. Clairmont, MD Associate Professor-Clinical The Ohio State University February 25, 2013 Objectives Overview of Pediatric Electrodiagnosis (EDX) Understand the different
More informationThis is a repository copy of Anti-MAG negative distal acquired demyelinating symmetric neuropathy in association with a neuroendocrine tumor..
This is a repository copy of Anti-MAG negative distal acquired demyelinating symmetric neuropathy in association with a neuroendocrine tumor.. White Rose Research Online URL for this paper: http://eprints.whiterose.ac.uk//
More information