Rapid Responses to:
|
|
Rapid Responses: Rapid Responses published:
-
![[Read Rapid Response]](/icons/misc/sectionDOWN.gif)
Guillain-Barré and Cauda Equina Compression
- Ossie E Uzoigwe, Sheffield S10 1DG (27 July 2008)
-
Is Lumbar Puncture needed in Guillain Barré Syndrome?
- Peter D Gibson (27 July 2008)
-
Guillain-Barré Syndrome in Children
- Imran Mushtaq, Nasim Mehmood, Consultant Paediatrician (29 July 2008)
-
Vitamin B.12 and demyelination
- George Y Caldwell, Singapore 259858 (2 August 2008)
-
Rehabilitation: Vital component of management plan in Guillain Barre Syndrome
- Sabahat A Wasti, Numan Amir, Consultant Neurologist, Sheikh Khalifa Medical City, Abu Dhabi, UAE (6 August 2008)
-
Guillain-Barré syndrome, poliomyelitis surveillance and the U-shaped curve of neglect
- David N Durrheim (10 August 2008)
-
Guillain-Barré, enterovirus and hand,foot and mouth
- martin s knapp, Merilyn Mackenzie-Knapp (29 September 2008)
-
Guillain Barré Syndrome disease requires an effective and appropriate diagnosis and treatment.
- Dr Jose Maximo Carles Zerquera,, Dra Sorahy Santander Garcia, Family Doctor, Dr Ruben Rodriguez Rodriguez Anesthesiology, Dr Fernando Cabreales Lugones Anesthesiology, Dra Maria E Bravo Rodriguez Pediatric, Lic Ihosvany Castellanos Santos (5 December 2008)
|
|
|||
|
Ossie E Uzoigwe, Student 8 Harcourt Crescent, Sheffield S10 1DG
Send response to journal:
|
Dear Editor, Winer overlooks an important differential diagnosis in the clinical review on Guillain-Barré syndrome1. Cauda equina compression must be considered in all patients presenting with lower limb areflexic paralysis. Traditionally, back pain has been used to differentiate between the two diagnoses. However it is not a reliable discriminator. Back pain is a recognised feature of Guillain-Barré syndrome2,3. Both share a similar age distribution. A diagnostic delay can result in significant morbidity in cases of cauda equina compression. There is a temporal window of 48 hours within which any surgical intervention should be performed; after which permanent neurological deficit is likely4. If any suspicion exists urgent magnetic resonance imaging should be performed. MRI can have diagnostic utility in Guillain-Barré syndrome. Enhancement of the cauda equina and conus medullaris with gadolinium administration on T1 weighted images has been consistently demonstrated in cases of Guillain-Barré5. MRI should be used to exclude cauda equina compression and support the diagnosis of Guillain-Barré. 1. Winer JB, Guillain-Barré syndrome. BMJ 2008; 337:671 2. Clague JE, Macmillan RR, Backache and the Guillain-Barré syndrome: a diagnostic problem. Br Med J 1986; 293:325-326 3. Ropper AH, Shanani BT. Pain in Guillain-Barré syndrome. Arch Neurol 1984; 41:511-515. 4. Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JPCauda equina syndrome secondary to lumbar disc herniation: meta-analysis of surgical outcomes. Spine 2000; 25:1515-1522. 5. Garson KC, Ropper AH, Muriello MA, Blair R, Prospective evaluation of MRI lumbosacral nerve root enhancement in acute Guillain-Barré syndrome. Neurology 1996; 47: 813-817 Competing interests: None declared |
|||
|
|
|||
|
Peter D Gibson, Consultant Physician North Manchester General Hospital M8 5RB
Send response to journal:
|
This was a helpful article. However, (as with all diagnostic tests) it would be useful to know the sensitivity and specificity of a raised protein in the CSF. Also, is there evidence (ideally from a Randomised Controlled Trial) that performing a lumbar puncture in these patients improves the outcome for patients? I ask this, because Lumbar Puncture can be a painful procedure for patients and in some patients causes significant morbidity (e.g. post-lumbar puncture headache). Competing interests: None declared |
|||
|
|
|||
|
Imran Mushtaq, Associate Specialist-Child & Adolescent Psychiatrist Milton Keynes SP-CAHMS, Eaglestone Centre, Standing Way, Milton Keynes MK6 5AZ, Nasim Mehmood, Consultant Paediatrician
Send response to journal:
|
Winer’s clinical review on Guillain-Barré syndrome (GBS) deals with current views and clinical practice of a rare disorder and rightly emphasizes on recognition of its rapid progression to avoid high mortality due to respiratory failure (1). We find the spectrum of GBS interesting and thought provoking and wonder why an important group of patients, children were missed in this review. This would merit special mention, for number of reasons. GBS in children differs in many ways compare to adults. It is an acute, immune-mediated flaccid paralysis frequently associated with Campylobacter infection. Of two predominant GBS subtypes (three in adults), a demyelinating subtype (acute inflammatory demyelinative polyneuropathy [AIDP]) predominates in the United States and Europe, and axonal subtype (acute motor axonal neuropathy [AMAN]) is the predominant form in China. I t is considered relatively benign condition in children in comparison with adults (2). Similar to adult pattern, boys appear to be at greater risk for GBS than girls. The average age is in the range of 4-8 years. Individuals affected with GBS can be as young as 1 year. Estimates of annual incidence of GBS range from 0.5-1.5 per 100,000 in individuals younger than 18 years. Full recovery within 3-12 months is experienced by 90-95% of pediatric patients with GBS. Overall mortality rate in childhood GBS is much less then adults and is estimated to be less than 5% (2). Myasthenia Gravis, Lyme disease and HIV are among other differential diagnosis in children apart from those described by Winer (3). Treatment is generally same for children and adults. Contact a family, is an excellent resource for information, for parents and carers (4). References: 1. Winer JB. Guillain-Barré syndrome. BMJ 2008;337:a671 2. Nachamkin I, Barbosa PA, Ung H, Lobato C, Rivera AG, Rodriguez P. Patterns of Guillain-Barre syndrome in children: results from a Mexican population. Neurology. Oct 23 2007;69(17):1665-71. 3. Tseng BS. Guillain-Barre Syndrome in Childhood. Emedicine. Jan 2008. 4. Medical texts in The Contact a Family Directory, can be accesses through, http://www.cafamily.org.uk. Imran Mushtaq, Associate Specialist-Child & Adolescent Psychiatrist, Milton Keynes SP-CAHMS, Eaglestone Centre, Standing Way, Milton Keynes MK6 5AZ Nasim Mehmood, Consultant Paediatrician, Royal Liverpool Children’s NHS Trust Eaton Road Liverpool L12 2AP Competing interests: None declared |
|||
|
|
|||
|
George Y Caldwell, general practitioner 31 Balmoral Park, #18-33,, Singapore 259858
Send response to journal:
|
The neuro-pathology of "Demyelination" of Guillane-Barre syndrome is shared with Neuromyelitis Optica, Multiple Sclerosis, Motor Neurone Disease, Idiopathic Paroxysmal Vertigo and Herpes Zoster, together with other entitled syndromes. Vitamin B.12 (cyanocobalamin and hydroxocobalamin) has a known effectiveness in Herpes Zoster when given early. This has been known since 1944. It is certainly ineffective after three months and perhaps less. However, in many of these syndromes, by the time the ultimate dread diagnosis is made since it takes time before a Consultant's opinion is eventually obtained, it is very possible that Vitamin B.12 would then be quite ineffective. Cyanocobalamin is essential for the formation of Myelin: OVESEN, L. "DRUGS" 27 148 (1984). Martindale's Pharmacopoeia. A series of cases has been reviewed and there is evident instant relief from pain when Vitamin B.12 is given early to cases of Zoster and there is no Post Herpetic Neuralgia. In the suspected cases of these other demyelination syndromes, why not then adminster early intramuscular injections of B.12? Perhaps they have been tried, but perhaps too late to have any beneficial effect? Competing interests: None declared |
|||
|
|
|||
|
Sabahat A Wasti, Consultant in Rehabilitation Medicine Sheikh Khalifa Medical City Abu Dhabi UAE, Numan Amir, Consultant Neurologist, Sheikh Khalifa Medical City, Abu Dhabi, UAE
Send response to journal:
|
Editor The clinical review on Guillain-Barre Syndrome by Winer1 whilst mostly comprehensive leaves out a vital management component. The author omits to mention therapy support and rehabilitation as an essential adjuvant intervention to pharmaceutical and intensive measures. Rehabilitation must form an essential component of management plan for patients with the diagnosis of Guillain-Barre Syndrome2. We regularly see patients with Guillain-Barre Syndrome and do so at an early stage. Involvement of neurorehabilitation team must start as early as acute medical unit or Intensive Care stage. The role of the team at this stage is to prevent complications such as tissue shortening and pressure ulcers. Early swallow assessment by speech and language therapist is necessary to reduce the risk of chest infections. Maintenance of joint position and joint range of motion is essential for subsequent optimized functional outcome. Early commencement of sitting regime helps orthostatic retraining. Effective continence management regime must also be established. A well integrated multi-disciplinary rehabilitation team is vital for achieving early and thereafter long-term functional goals and improved out come for patients with Guillain-Barre syndrome. We understand that review articles are widely utilized by trainees to update themselves on current trends. It is therefore essential that such articles are comprehensive and contain all relevant clinical, pathophysiological, therapeutic and current management strategies. Rehabilitation forms an essential component of treatment in patients with Guillain-Barre and it must be included as part of management strategy in clinical reviews. 1. Winer JB, BMJ 2008;337:a671 2. Carroll A; McDonnell G; Barnes M, International Journal of Rehabilitation Research. 26(4):297-302, December 2003. Competing interests: None declared |
|||
|
|
|||
|
David N Durrheim, Professor of Public Health Medicine School of Public Health and Medical Practice, University of Newcastle, Newcastle, 2287, Australia
Send response to journal:
|
John Winer's clinical review of Guillain-Barre syndrome (GBS) provides an excellent summary of our current understanding of the neuropathology, associated infections and best practice management of this perplexing neurological condition.1 Surprisingly poliomyelitis was not mentioned in the differential diagnosis of GBS presented. This probably reflects the current exceedingly rare occurrence of poliovirus presentation in most countries due to the remarkable efforts of the polio eradication campaign. Sustained political commitment, health service energy and non- governmental organisation investment have driven confirmed poliovirus cases down to levels unthinkable just a few decades ago . Unfortunately as the end-game draws near, it is easy to become complacent, lose momentum and even neglect to consider poliomyelitis in GBS presentations. It is perilous to drop our surveillance guard now.2 While wild poliovirus continues to circulate in a small number of countries, all countries remain vulnerable to possible importation and a possible upswing in the number of cases (U-shaped curve) as demonstrated in 2005 and 2006 with 21 previously polio-free countries importing wild poliovirus.3 Although the acute motor weakness associated with poliomyelitis is more commonly asymmetrical in nature, and sensory and autonomic features are uncommon, it is hazardous to definitively exclude poliovirus infection on clinical grounds alone. Now is not the time to declare a premature victory against polio. It is essential that all countries, both developing and developed, maintain a high level of alertness and ensure that appropriate stool specimens are submitted from all cases of acute flaccid paralysis (~GBS), carefully maintaining the reverse cold chain of these specimens in transit to approved virological laboratories that can actively exclude poliovirus as the cause of the syndrome.4 References 1. Winer JB. Guillain-Barr Syndrome. BMJ 2008; 337: 227-231. 2. Durrheim D, Massey P, Kelly H. Re-emerging poliomyelitis – is Australia’s surveillance adequate? Commun Dis Intell 2006; 30: 275–277. 3. Centres for Disease Control and Prevention. Resurgence of wild poliovirus type 1 transmission and consequences of importation, 21 countries, 2002–2005. MMWR Morb Mort Wkly Rep 2006; 55: 145–150. 4. World Health Organization. Acute flaccid paralysis (AFP) surveillance: the surveillance strategy for poliomyelitis eradication. Wkly Epidemiol Rec 1998; 16: 113–117. Competing interests: None declared |
|||
|
|
|||
|
martin s knapp, consultant physician 12 Townsend St. Ivanhoe 3079, Australia, Merilyn Mackenzie-Knapp
Send response to journal:
|
The review article on Guillain-Barré syndrome (1) (July 26), the comprehensive review of the condition on the web-site http://neuromuscular.wustl.edu, and the rapid responses on bmj.com do not make comment on the established association with epidemics of enterovirus infections, most often EV71 and an association with human hand foot and mouth in some epidemics (2). Our interest in this developed when a family member, aged 30, developed neurological symptoms; initially a unilateral facial palsy progressing to Guillain-Barré syndrome syndrome with CSF and EMG confirmation. Ten days before the facial palsy there had been contact with a nephew (aged 1) at the time of an attack of hand, foot and mouth disease when other infants in his crèche had similar mouth and skin symptoms. One other adult member of the family had concurrent oral symptoms. An internet search located well documented “epidemic” outbreaks of neurological illness reviewed by Huang and colleaugues (2), including patients with features of Guillain-Barré syndrome, in association with epidemics of human hand, foot and mouth disease. Small epidemics were reported from Victoria (3) and from Western Australia(4) and large outbreaks in South-East Asia (2) were associated with mortality and permanent neurological disability. Neither enterovirus 71 or other known pathogens were identified from our family member. Her illness did follow shortly after discharge from an admission with gastro-intestinal symptoms, including diarrhea, from a hospital that had other wards closed due to an epidemic of gastro- intestinal infection. It is also of interest that conversations with physiotherapists involved with rehabilitation indicated an unusually large number of patients reporting for rehabilitation to Victorian units at that time. There is no reporting of neither Guillain-Barré syndrome nor of hand, foot and mouth disease in our state so no formal epidemiological data is available. The association of Guillain-Barré syndrome with entero-virus infections and with hand, foot and mouth disease merited inclusion in Winer’s review. Clinicians and microbiologists should be aware of the association, especially those working in SE Asia and Australia. Martin Knapp FRCP Consultant Physician
1. John B Winer Guillain-Barré syndrome BMJ 2008;337 227-231 2. Huang CC, Liu CC, Chang YC et al. Neurologic complications of children with enterovirus infection N Eng J Med 1999, 341: 936-942 3. Gilbert GL, Dickson KE Waters M, et al. Outbreak of enterovirus infection in Victoria with a high incidence of neurologic involvement. 1988 Paediatr Infect Dis J; 7: 484-488 4. McMinn, P Stratov I ,Nagarajan L, Davis S, Neurological Manifestations of enterovirus 71 infection in children during an outbreak of hand, foot and mouth disease in Western Australia. Clinical Infectious Diseases , 2001;15: 236-242 Competing interests:
None declared
|
|||
|
|
|||
|
Dr Jose Maximo Carles Zerquera,, Internal Medicine, General Hospital Trinidad. Cuba., Dra Sorahy Santander Garcia, Family Doctor, Dr Ruben Rodriguez Rodriguez Anesthesiology, Dr Fernando Cabreales Lugones Anesthesiology, Dra Maria E Bravo Rodriguez Pediatric, Lic Ihosvany Castellanos Santos
Send response to journal:
|
We read your Clinical Review about Guillain Barré Syndrome and we consider it very important to the medical knowledge due to its low incidence in the daily life medical practice, but with a high seriousness which requires an effective and appropriate diagnosis and treatment. In some studies done about this disease in the last ten years in our Trinidad City with a population of 70283 people, the incidence was 15 cases with the predominance of female sex and young people, in the 65% of these cases their ages were between 6 and 12 years old. The infection of the respiratory tract preceded the appearance of this disease mainly by cytomegalovirus. In our study did not exist recurrence of this disease. The clinical spectrum was of an acute inflammatory demyelinating polyradiculoneuropathy with cramp, muscular pains in the limbs, non reflex, sings of dysfunction of the nervous system such as a persistent tachycardia, orthostatic hypotension, urinary retention, ataxic walk. The dissociation albuminocytologic occur in the study of the cerebrospinal fluid. There were some diseases such as polymyositis, metabolic and toxic polineuropathy, which offer confusion in the diagnosis. The seriousness of the disease was higher in adult patient with comorbility of disease. The 100 % of patients were seen in Intensive Care Units where a 45% received control ventilation, everyone used Immunoglobulin EV (Intaglobin) regimen of 400 mg/kg body weight each day for 5 consecutive day, plasma exchange in 5 sessions the first 15 days, vitamin B1-B6. The subcutaneous Heparin was used in the prophylaxis of the pulmonary embolism; a patient presented an acute vein thrombosis. The respiratory infection was a complication in the 34 % of the ventilated patients, who used antibiotics according to the established protocols. In the 10 % of the patients there were motor and sensitive squealers besides there were disorders to walk which have become permanent in two cases in spite of the rehabilitation. There was not any a dead man or woman in our study. Competing interests: None declared |
|||