Guillain-Barre Syndrome - Diagnosis

9/28/01 (Franco)

Question: What are the diagnostic criteria for Guillain-Barre syndrome?

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[Link Directly to Fulltext Article in OVID]

Unique Identifier: 21298931 / PubMed Identifier: 11405806

Authors: Gordon PH. Wilbourn AJ.

Institution: Department of Neurology, University of New Mexico School of Medicine, 915 Camino de Salud NE, Albuquerque, NM 87131, USA. pgordon@salud.unm.edu

Abstract: CONTEXT: Guillain-Barre syndrome (GBS) is the foremost cause of acute, generalized, peripheral neuropathic weakness. Although nerve conduction studies are a diagnostic aid, the characteristic electrical changes may not evolve for several weeks. Early diagnosis of GBS is important, however, because early treatment has been shown to improve outcome. OBJECTIVES: To describe the electrodiagnostic abnormalities detectable in the first week of GBS, to determine if there are early patterns suggestive of GBS, and to identify the percentage of patients whose condition can be diagnosed with reasonable certainty in the first week. DESIGN AND SETTING: We retrospectively reviewed the medical records of all patients admitted to the Cleveland Clinic Foundation, Cleveland, Ohio, having the discharge diagnosis GBS during the past 16 years. Patients who underwent nerve conduction studies within 7 days of muscle weakness were selected for this study. RESULTS: The H reflex was absent in 30 (97%) of 31 patients. Nineteen patients (61%) had low-amplitude or absent sensory nerve action potential (SNAP) in the upper extremity. Fifteen patients (48%) overall, including 21 (67%) of the 31 patients, including 14 (67%) of the 21 patients younger than 60 years, had an abnormal upper extremity SNAP combined with a normal sural SNAP. Other findings included an abnormal F wave (25 patients [84%]), reduced compound muscle action potential amplitude (22 patients [71%]), prolonged distal latency (20 patients [65%]), temporal dispersion (18 patients [58%]), slowed motor conduction velocity (16 patients [52%]), and motor conduction block (4 patients [13%]). Definite diagnosis was possible in 17 patients (55%), but not commonly until the fifth day. CONCLUSIONS: The H reflex is the most sensitive test for early GBS. Upper extremity SNAPs are also frequently abnormal in early GBS. Absent H response, abnormal F wave, and abnormal upper extremity SNAP combined with a normal sural SNAP are characteristic of early GBS. If multiple nerves are tested, definite diagnosis is possible in half the patients, but not until the fifth day after the onset of symptoms.

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Unique Identifier: 21203590 / PubMed Identifier: 11306855

Authors: Van der Meche FG. Van Doorn PA. Meulstee J. Jennekens FG. GBS-consensus group of the Dutch Neuromuscular Research Support Centre.

Institution: University Hospital, Rotterdam, The Netherlands. vandermeche@neur.azr.nl

Abstract: BACKGROUND: Diagnostic criteria for the Guillain-Barre syndrome (GBS) have been available since 1978. Since then, several variants have been described. More recently, a distinction has been made between pure motor forms, severe sensory forms, primary axonal and primary demyelinating varieties. Associations of clinical characteristics, and specific infections and the presence of antiganglioside antibodies have been found. For further studies on GBS, it is therefore necessary to reconsider the available diagnostic criteria and add additional criteria for subclassification. METHODS: A panel of (20) experts was formed. The literature representing the recent developments in GBS subclassification was reviewed. Following a consensus protocol, diagnostic and classification criteria were formulated. RESULTS: The diagnosis of GBS can usually be made on clinical characteristics. A schedule for subclassification has been made to cover also the clinical variants in a systematic manner. [References: 32]

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Unique Identifier: 20538621 / PubMed Identifier: 11085768

Authors: Seneviratne U.

Institution: Institute of Neurology, National Hospital of Sri Lanka, Colombo 8, Sri Lanka.

Abstract: Guillain-Barre syndrome is an autoimmune disorder encompassing a heterogeneous group of pathological and clinical entities. Antecedent infections are thought to trigger an immune response, which subsequently cross reacts with nerves leading to demyelination or axonal degeneration. Both intravenous immunoglobulin treatment and plasma exchange have been found to be equally beneficial. Several factors are useful in predicting the outcome of these patients. [References: 116]

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Unique Identifier: 20415129 / PubMed Identifier: 10959227

Authors: Meulstee J. van der Meche FG.

Institution: Department of Neurology, University Hospital Rotterdam Dijkzigt, The Netherlands.

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Unique Identifier: 20154033 / PubMed Identifier: 10689443

Authors: Trojaborg W.

Institution: Institute of Neurology, Columbia Presbyterian Medical Center, Columbia University, New York, NY, USA.

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[Link Directly to Fulltext Article in OVID]

Unique Identifier: 20158265 / PubMed Identifier: 10695718

Authors: Hughes RA. Hadden RD. Gregson NA. Smith KJ.

Institution: Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Guy's Hospital, London, UK. richard.a.hughes@kci.ac.uk

Abstract: Recent neurophysiological and pathological studies have led to a reclassification of the diseases that underlie Guillain-Barre syndrome (GBS) into acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor and sensory axonal neuropathy (AMSAN) and acute motor axonal neuropathy (AMAN). The Fisher syndrome of ophthalmoplegia, ataxia and areflexia is the most striking of several related conditions. Significant antecedent events include Campylobacter jejuni (4-66%), cytomegalovirus (5-15%), Epstein-Barr virus (2-10%), and Mycoplasma pneumoniae (1-5%) infections. These infections are not uniquely associated with any clinical subtype but severe axonal degeneration is more common following C. jejuni and severe sensory impairment following cytomegalovirus. Strong evidence supports an important role for antibodies to gangliosides in pathogenesis. In particular antibodies to ganglioside GM1 are present in 14-50% of patients with GBS, and are more common in cases with severe axonal degeneration associated with any subtype. Antibodies to ganglioside GQ1b are very closely associated with Fisher syndrome, its formes frustes and related syndromes. Ganglioside-like epitopes exist in the bacterial wall of C. jejuni. Infection by this and other organisms triggers an antibody response in patients with GBS but not in those with uncomplicated enteritis. The development of GBS is likely to be a consequence of special properties of the infecting organism, since some strains such as Penner 0:19 and 0:41 are particularly associated with GBS but not with enteritis. It is also likely to be a consequence of the immunogenetic background of the patient since few patients develop GBS after infection even with one of these strains. Attempts to match the subtypes of GBS to the fine specificity of anti-ganglioside antibodies and to functional effects in experimental models continue but have not yet fully explained the pathogenesis. T cells are also involved in the pathogenesis of most or perhaps all forms of GBS. T cell responses to any of three myelin proteins, P2, PO and PMP22, are sufficient to induce experimental autoimmune neuritis. Activated T cells are present in the circulation in the acute stage, up-regulate matrix metalloproteinases, cross the blood-nerve barrier and encounter their cognate antigens. Identification of the specificity of these T cell responses is still at a preliminary stage. The invasion of intact myelin sheaths by activated macrophages is difficult to explain according to a purely T cell mediated mechanism. The different patterns of GBS are probably due to the diverse interplay between antibodies and T cells of differing specificities. [References: 296]

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Unique Identifier: 20013622 / PubMed Identifier: 10546299

Authors: Toyka KV.

Institution: Neurologische Universit&#x00E4;tsklinik, W&#x00FC;rzburg, Germany. k.toyka@mail-uni-wuerzburg.de

Abstract: It is now 83 years that Guillain, Barre and Strohl described the first two cases of an acute paralytic illness with the typical "dissociation albumino-cytologique" in the cerebrospinal fluid. Since then, the full spectrum of GBS has been documented in hundreds of cases ranging from acute inflammatory demyelinating polyneuropathy to the pure motor variants and the Miller Fisher syndrome. During the last 10 years, detailed immunopathologic features have been described and new triggering and possibly causative agents identified, the most prominent being the enteritic bacterium Campylobacter jejuni. Besides the pathogenic role of cell-mediated immunity, IgG antibodies have now been discovered which block neuromuscular transmission. Established treatments include plasma exchange therapy and intravenous immunoglobulin G. Together with sophisticated intensive care measures, mortality has now been reduced to below 5p. 100 with these treatment modalities. Several treatment strategies that proved effective in the animal model of GBS need to be studied in future clinical trials. [References: 59]

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Unique Identifier: 20022752 / PubMed Identifier: 10555826

Authors: Ho T. Griffin J.

Institution: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Abstract: The concepts of Guillain-Barre syndrome have changed substantially over the last 10 years, and the last 2 years have been no exception. Guillain-Barre syndrome is now recognized as a heterogeneous disorder with many clinical manifestations. Most current investigations are centered on the hypothesis of molecular mimicry. The major challenge now is to identify the precise mechanisms of nerve fiber injury and to determine how to prevent immune injury. [References: 65]

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Unique Identifier: 99064466 / PubMed Identifier: 9848000

Authors: Hartung HP. van der Meche FG. Pollard JD.

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Unique Identifier: 99087437 / PubMed Identifier: 9872432

Authors: Trojaborg W.

Institution: Institute of Neurology, Columbia Presbyterian Medical Center, Columbia University, New York, NY 10032, USA.

Abstract: During the last 15 years new information about clinical, electrophysiological, immunological and histopathological features of acute and chronic inflammatory neuropathies have emerged. Thus, the Guillain-Barre syndrome (GBS) is no longer considered a simple entity. Subtypes of the disorder besides the typical predominant motor manifestation, are recognized, i.e. a cranial nerve variant with ophthalmoplegia, ataxia and areflexia, an immune-mediated primary motor axonal neuropathy (AMAN), and a motor-sensory syndrome (AMSAN). Also, the clinical pattern of GBS is related to preceding viral or bacterial infections. Two types of acute motor paralysis have been described, one with slow and incomplete recovery, another with recovery times identical with acute inflammatory demyelinating polyneuropathy (AIDP). Histologically, the first is characterized by Wallerian degeneration of motor roots and peripheral motor nerve fibres. In the latter anti-GM antibodies bind to the nodes of Ranvier producing a failure of impulse transmission. Motor-point biopsies have shown denervated neuromuscular junctions and a reduced number of intramuscular nerve fibres. Molecular mimicry has been postulated as a possible mechanism triggering GBS. Thus, in the cranial variant antibodies to ganglioside GQ1b recognizes similar epitopes on Campylobacter jejuni strains and similar observations apply to anti-GM1 antibodies. Chronic inflammatory demyelinating polyneuropathy (CIDP) also has several different clinical presentations such as a pure motor syndrome, a sensory ataxic variant, a mononeuritis multiplex pattern, relapsing GBS, and a paraparetic subtype. Each of the acute and the subtypes have different, more or less distinct, electrophysiologic and pathological findings. Instructive patient stories are presented together with there electrophysiologic and biopsy findings. [References: 117]

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Unique Identifier: 98392697 / PubMed Identifier: 9725076

Authors: Steck AJ. Schaeren-Wiemers N. Hartung HP.

Institution: Department of Neurology, University of Basel, Switzerland. steck@ubaclu.unibas.ch

Abstract: The highly complex and multiple mechanisms responsible for the development of demyelinating neuropathies are reviewed, in particular Guillain-Barre syndrome and its variant Miller Fisher syndrome, chronic inflammatory demyelinating neuropathy, multifocal motor neuropathy, anti-myelin-associated glycoprotein neuropathy, as well as experimental models. Recent investigations into the role of auto antibodies against myelin proteins, or glycolipids have given insights into the pathogenesis of demyelinating inflammatory neuropathies. [References: 73]

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[Link Directly to Fulltext Article in OVID]

Unique Identifier: 98450941 / PubMed Identifier: 9779661

Authors: Wohrle JC. Spengos K. Steinke W. Goebel HH. Hennerici M.

Institution: Department of Neurology, Klinikum Mannheim of the University of Heidelberg, Germany. woehrle@neuro.ma.uni-heidelberg.de

Abstract: BACKGROUND: Chronic axonal polyneuropathy is a well-known clinical sequela of excessive alcohol consumption; however, acute axonal polyneuropathy related to alcohol abuse is less well recognized. OBJECTIVE: To describe alcohol-related acute axonal polyneuropathy in 5 chronic alcoholics who developed ascending flaccid tetraparesis and areflexia within 14 days. METHODS: Case series with clinical, laboratory, electrophysiological, and, in 1 patient, biopsy data. RESULTS: All 5 patients consumed a daily average of 250 g of alcohol, and 4 had lost a substantial amount of weight recently. Additional clinical features included painful paresthesia, myalgia, and glove and stocking-type sensory loss. Repeated cerebrospinal fluid examinations failed to show the marked increase of protein concentration with normal cell count typical of Guillain-Barre syndrome, although the protein level was mildly elevated in 1 patient. Blood laboratory findings were consistent with longstanding alcohol abuse. Compound muscle and sensory nerve action potentials were absent or reduced, while conduction velocities were normal or mildly reduced. Three to 4 weeks after onset, needle electromyography displayed moderate to severe fibrillations and positive sharp waves in addition to normal motor unit potentials, indicating an acute axonal polyneuropathy; this was confirmed by sural nerve biopsy in 1 patient. CONCLUSIONS: Excluding other factors, we assume that in these patients the combination of alcohol abuse and malnutrition caused severe acute axonal polyneuropathy. Its distinction from Guillain-Barre syndrome is important because treatment requires balanced diet, vitamin supplementation, and abstinence from alcohol, while immunotherapy may not be indicated.

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[Link Directly to Fulltext Article in OVID]

Unique Identifier: 98417122 / PubMed Identifier: 9746040

Authors: Hahn AF.

Institution: Clinical Neurological Sciences, University of Western Ontario, London Health Sciences Centre, Canada. angelika.hahn@lhsc.on.ca

Abstract: Guillain-Barre syndrome (GBS) is viewed as a reactive, self-limited, autoimmune disease triggered by a preceding bacterial or viral infection. Campylobacter jejuni, a major cause of bacterial gastroenteritis worldwide, is the most frequent antecedent pathogen. It is likely that immune responses directed towards the infecting organisms are involved in the pathogenesis of GBS by cross-reaction with neural tissues. The infecting organism induces humoral and cellular immune responses that, because of the sharing of homologous epitopes (molecular mimicry), cross-react with ganglioside surface components of peripheral nerves. Immune reactions against target epitopes in Schwann-cell surface membrane or myelin result in acute inflammatory demyelinating neuropathy (85% of cases); reactions against epitopes contained in the axonal membrane cause the acute axonal forms of GBS (15% of cases). Care for such patients may be challenging, yet the prognosis overall is favourable. Optimal supportive care and anticipation and prevention of complications are the mainstay of therapy. Admission to the intensive-care unit is necessary in 33% of patients who require intubation and assisted ventilation. Immunomodulation with infusions of IgG or plasma exchange treatments foreshorten the disease course. [References: 74]

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Unique Identifier: 98266427 / PubMed Identifier: 9605390

Authors: Ono S. Inoue K. Munakata S. Nagao K. Shimizu N.

Institution: Department of Neurology, Teikyo University School of Medicine, Ichihara Hospital, Chiba, Japan.

Abstract: Although many studies have been performed on nervous tissue pathology in Guillain-Barre syndrome (GBS), much less is known about pathological changes in skeletal muscle in this disorder. We have studied muscle biopsies from 5 patients with GBS, 5 patients with amyotrophic lateral sclerosis (control A), and 5 patients with polyarteritis nodosa (control B). We also examined muscle obtained after death from 7 patients without neurologic or muscular diseases (control C). By light microscopy, all specimens from patients with GBS exhibited necrosis and/or phagocytosis, none of which was observed in the other three controls. Neither small angulated fibers nor small group atrophy was found in patients with GBS and in control C, by contrast with controls A and B. Ultrastructurally, filamentous bodies, subsarcolemmal aggregates of mitochondria, accumulation of glycogen particles, and concentric laminated bodies were present much more frequently in patients with GBS than in all controls. Only GBS patients showed cytoplasmic bodies. These observation suggests that there is muscle involvement in the early stage of GBS and that these muscle changes may have an intimate and important relationship to the pathogenesis of GBS.

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Unique Identifier: 97250056 / PubMed Identifier: 9095881

Authors: McMahon-Parkes K. Cornock MA.

Institution: Faculty of Health &#38; Social Care, University of the West of England, Bristol, UK.

Abstract: Guillain-Barre syndrome is a complex disorder that affects around 0.5-2 individuals per 100,000 per year (Hund et al 1993). The outcome can range from a sensation of paraesthesia to death. This article discusses the biological nature of Guillain-Barre syndrome, major diagnostic criteria and the treatment that is available. It highlights the nurse's role in management of the syndrome and describes how the extent of the syndrome in individual patients may be evaluated in the clinical area. [References: 17]

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Unique Identifier: 97005638 / PubMed Identifier: 8852937

Authors: Griffin JW. Li CY. Macko C. Ho TW. Hsieh ST. Xue P. Wang FA. Cornblath DR. McKhann GM. Asbury AK.

Institution: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

Abstract: The axonal patterns of Guillain-Barre syndrome, associated in many cases with antecedent Campylobacter jejuni infection, are now recognized as frequent causes of acute flaccid paralysis in some regions of the world. This study examined ultrastructurally the PNS of seven cases of the acute motor axonal neuropathy form of Guillain-Barre syndrome. In this disorder previous studies of advanced cases have found Wallerian-like degeneration of motor fibres in the spinal roots and peripheral nerves, with little lymphocytic inflammation or demyelination. The present study was focused on identifying early changes and establishing the sequence of changes. By electron microscopy the earliest and mildest changes consisted of lengthening of the node of Ranvier with distortion of the paranodal myelin, and in some instances with breakdown of the outermost myelin terminal loops. At this stage many nodes had overlying macrophages which extended their processes through the Schwann cell basal lamina covering the node and apposed the axolemma. Macrophage processes then extended beneath the myelin terminal loops, and the whole macrophage entered the periaxonal space at the paranode. Macrophage processes dissected the axon from the adaxonal Schwann cell plasmalemma and the macrophages advanced into the internodal periaxonal space, where they typically surrounded a condensed-appearing axon. At this stage the adaxonal Schwann cell cytoplasm regularly degenerated and disappeared, so that the periaxonal space was bounded by the innermost myelin lamella, and the axolemma of many fibres could not be seen. The internodal myelin sheath and the abaxonal Schwann cell cytoplasm remained normal. This arrangement appeared to be stable for some time, but in many fibres the axon subsequently underwent Wallerian-like degeneration. By interfering with impulse conduction, these nodal and periaxonal changes may explain paralysis in some pathologically mild cases. In addition, at early stages, these changes may be reversible, thus explaining the rapid recovery of some patients who become paralysed with acute motor axonal neuropathy. These observations, taken together with previous studies, suggest that acute motor axonal neuropathy is an antibody- and complement-mediated disorder in which the relevant epitopes are present on the nodal and internodal axolemma.

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Unique Identifier: 96285298 / PubMed Identifier: 8677835

Authors: Dematteis JA.

Institution: Hamot Medical Center, Erie, Pennsylvania, USA.

Abstract: Guillain-Barre syndrome is the most frequently acquired demyelinating peripheral polyneuropathy. In approximately two-thirds of cases, Guillain-Barre syndrome is preceded by a viral respiratory or gastrointestinal infection. The mechanism of injury is unclear but is believed to be immunologic. The cardinal clinical feature is symmetric and rapidly progressive weakness. Aspiration and respiratory failure are the major concerns. Sensory symptoms, such as paresthesias, are common. The most severe stage of the disease is reached two to four weeks after onset. Dysautonomia has replaced respiratory failure as the most common cause of death. Recovery is variable: 50 percent of patients recover completely, about 35 percent experience permanent neurologic sequelae, and 15 percent are significantly and permanently damaged. About 10 percent relapse before complete recovery, and 2 to 5 percent experience recurrence after full recovery. Laboratory confirmation of Guillain-Barre syndrome includes the typical cerebrospinal fluid cytoalbumin dissociation (elevated protein without white blood cells). Treatment is primarily symptomatic and preventive. Convalescent patients require intensive inpatient physical and occupational therapy to improve strength and prevent disabling contractures. [References: 19]

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Unique Identifier: 94310892 / PubMed Identifier: 8036879

Authors: van der Meche FG.

Institution: Department of Neurology, University Hospital, Dijkzigt, Rotterdam.

Abstract: The diagnosis of Guillain-Barre syndrome is usually not difficult, but criteria and possible pitfalls have been discussed. General care is still very important, but at present specific treatments are also available. For practical reasons high-dose immunoglobulins may be preferred above plasma-exchange. Moreover in a large study in the Netherlands of 150 patients it was shown that immunoglobulins were significantly superior with respect to the main outcome criterion and several secondary outcome criteria. In treating individual patients it is important to know that many patients do not have a favourable course and that such a course may be predicted. Also the individual patient may deteriorate further during and after treatment. In general this should not lead to a switch in treatment modality.

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Unique Identifier: 93187660 / PubMed Identifier: 8383190

Authors: McEneaney D. Hawkins S. Trimble E. Smye M.

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Unique Identifier: 92392070 / PubMed Identifier: 1325767

Authors: Ropper AH. Adelman L.

Institution: Division of Neurology, St Elizabeth's Hospital, Boston, MA 02135.

Abstract: A patient with typical acute Guillain-Barre syndrome died 72 hours after his first symptoms occurred, and an autopsy was performed 8 hours after his death. Extensive sampling of cranial and peripheral nerves, sensory ganglia, and autonomic nerves showed only minimal inflammatory lymphocytic and macrophage infiltrates. This case, one of the earliest studied extensively, represents an extreme example of a noninflammatory mechanism that has been proposed in some cases of Gullain-Barre syndrome.

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Unique Identifier: 90302958 / PubMed Identifier: 2194423

Authors: McFarlin DE.

Institution: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

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Unique Identifier: 90302957 / PubMed Identifier: 2194422

Authors: Asbury AK. Cornblath DR.

Institution: Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia.

Abstract: Criteria for the diagnosis of Guillain-Barre syndrome are reaffirmed. Electrodiagnostic criteria are expanded and specific detail added. [References: 13]

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Unique Identifier: 90302955 / PubMed Identifier: 2194420

Authors: Cornblath DR.

Institution: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD.

Abstract: Clinical electrophysiological studies are important in the evaluation of patients with Guillain-Barre syndrome. Physiological evidence of demyelination occurs in almost all patients with Guillain-Barre syndrome, especially if serial studies are performed. Criteria for demyelination are proposed. Prognostic information concerning patient outcome can be deduced from computation of the mean of the summed motor evoked compound muscle action potential amplitudes from distal stimulation. Future studies of the electrophysiology of Guillain-Barre syndrome should allow increased use of the data for prognostication and should enhance our understanding of the mechanisms of the disease. [References: 34]

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Unique Identifier: 89021872 / PubMed Identifier: 3262981

Authors: Halls J. Bredkjaer C. Friis ML.

Institution: Department of Neurology, Gentofte Hospital, Copenhagen, Denmark.

Abstract: Thirty-four patients were identified with Guillain-Barre syndrome (GBS) on review of 266 neuropathy cases admitted to a Copenhagen county hospital from June 1977 to January 1984. The age-adjusted incidence rate of GBS is 2.0 x 10(-5) years-1. The natural history of the disease, antecedent events, symptoms and signs, autonomic dysfunction, sequelae, CSF findings and mortality are described. Six cancer patients with GBS differed significantly from the non-cancer patients in a more protracted disease course and failure to improve. The National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for the diagnosis of GBS are discussed, and it is concluded that the criteria, although useful in comparative studies, are too restrictive when used in clinical practice.

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Unique Identifier: 88014516 / PubMed Identifier: 3309710

Authors: Reich SG.

Institution: Department of Neurology, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Ohio.

Abstract: Harvey Cushing developed an illness in the last months of World War I that made it impossible for him to operate and forced him to bed for over a month. The features of Cushing's malady included symmetrical weakness, numbness, and paresthesias of the hands and feet, areflexia, bilateral facial paresis, diplopia, and fever. Neither Cushing nor his physicians were able to make a diagnosis. John Fulton, Cushing's biographer, misdiagnosed the condition as a "vascular polyneuritis," and Harry Zimmerman, who performed Cushing's autopsy, incorrectly attributed his symptoms to occlusion of the abdominal aorta. Based on extensive notes in Cushing's war diary describing the illness, it is readily recognized today as Guillain-Barre syndrome.

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Unique Identifier: 87120106 / PubMed Identifier: 3468607

Authors: Hagberg L. Malmvall BE. Svennerholm L. Alestig K. Norkrans G.

Abstract: Two cases of HIV infection associated with Guillain-Barre syndrome are described. The neurologic symptoms started 1 week and 20 weeks, respectively, after the primary HIV infection. Seroconversion for anti-HIV occurred during the disease. A rapid spread of virus to the central nervous system was shown.