Subacute AIDS-related lumbosacral radiculopathy: a bacterial infection?

Igloffstein, J; Vogel, Peter

doi:10.1007/bf00314789

Cited by 8 publications

(5 citation statements)

References 10 publications

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“…In fact, all our patients with documented CMV PR had PMN pleocytosis. However, mycobacterial infections, as shown in this series, may also present with PMN pleocytosis, as may bacterial [8] or treponemal infections [11]. On the other hand, CMV PR may show mild lymphocytic or no pleocytosis in CSF [12].…”

Section: Discussionmentioning

confidence: 52%

“…CMV infection is the most frequently reported aetiology of this syndrome [5,10,15,16,19], but cases of lymphomatous meningitis [12,19], and isolated cases of syphilis [3,11], and cryptococcosis [4] have also been reported. A bacterial infection was thought to be the cause of acute PR in one reported case, but there was no microbiological confirmation [8]. Toxoplasmosis of the conus medullaris may also present as acute lumbosacral PR [9].…”

Section: Discussionmentioning

confidence: 95%

“…Two patients with cerebral lymphoma had contralateral Babinski signs, but no pyramidal signs were detected in the others. Eight patients were febrile at diagnosis (patients 1, 3,4,8,11,12,15,16).…”

Section: Resultsmentioning

confidence: 99%

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Acute polyradiculopathies in HIV-infected patients

Corral

Quereda

Casado

et al. 1997

Journal of Neurology

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We studied 17 consecutive cases of acute polyradiculopathy (PR) diagnosed in HIV-infected patients to investigate the possible causes of this syndrome in our milieu. Sixteen patients presented with lumbosacral PR and one patient had predominantly cervical PR. Electrophysiological study showed a predominantly motor axonal neuropathy in all patients examined. Six patients had a laboratory-confirmed aetiology for the PR: cytomegalovirus (CMV) was isolated from cerebrospinal fluid (CSF) in three cases, meningeal lymphomatosis was diagnosed by CSF cytology in two cases, and one patient had cryptococcal meningitis. Another patient was thought to have acute axonal polyradiculoneuritis associated with HIV infection. CMV and Mycobacterium tuberculosis were the probable agents in four and three patients, respectively. Finally, in three patients a cause could not be foscarnet were effective in the treatment of definite or probable CMV PR. The present study confirms that acute lumbosacral PR in HIV-infected patients must be considered a syndrome with different causes. CMV and M. tuberculosis infections were the most frequent causative agents in our series (41% and 18% of the cases, respectively). Early empirical therapy is often necessary as definite diagnosis may be delayed or never achieved. Our experience suggests that, at least in our milieu, anti-tuberculous drugs should be considered in some cases together with ganciclovir or foscarnet in the empirical therapy for PR in HIV-infected patients.

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Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 95%

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Acute polyradiculopathies in HIV-infected patients

Corral

Quereda

Casado

et al. 1997

Journal of Neurology

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“…Other minor forms of neuropathy associated with HIV infection have been documented. [7][8][9][10][11] DPSN is the commonest neuropathy and it occurs in up to 35% of individuals with advanced HIV infection. 3,6 Although the pathology of DPSN has been determined as retrograde distal axonal degeneration ('dying back' axonopathy) and drop out of dorsal root ganglion neurons, 12,13 little is known of its pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Eight different forms of HIV‐associated neuropathy have been described: 6 (i) distal predominantly sensory neuropathy (DPSN); (ii) vasculitic neuropathy; (iii) lymphomatous neuropathy; (iv) cytomegalovirus (CMV); lumbosacral polyradiculopathy; (v) Varicella zoster virus (VZV) polyradiculopathy; (vi) acute and chronic inflammatory demyelinating polyneuropathy (IDPN); (vii) autonomic neuropathy; and (viii) neuropathy induced by di‐deoxy‐inosine (ddI) and di‐deoxy‐cytidine (ddC) therapy. Other minor forms of neuropathy associated with HIV infection have been documented 7–11 …”

Section: Introductionmentioning

confidence: 99%

Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?

Petratos

Gonzales

2000

Neuropathology

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Neuropathology 2000; 20, 257-272 Of the eight clinically defined neuropathies associated with HIV infection, there is compelling evidence that acute and chronic inflammatory demyelinating polyneuropathy (IDPN) have an autoimmune pathogenesis. Many non-HIV infected individuals who suffer from sensorymotor nerve dysfunction have autoimmune indicators. The immunopathogenesis of demyelination must involve neuritogenic components in myelin. The various antigens suspected to play a role in HIV-seronegative IDPN include (i) P 2 protein; (ii) sulfatide (GalS); (iii) various gangliosides (especially GM 1 ); (iv) galactocerebroside (GalC); and (v) glycoproteins or glycolipids with the carbohydrate epitope glucuronyl-3-sulfate. These glycoproteins or glycolipids may be individually targeted, or an immune attack may be raised against a combination of any of these epitopes. The glycolipids, however, especially GalS, have recently evoked much interest as mediators of immune events underlying both non-HIV and HIV-associated demyelinating neuropathies. The present review outlines the recent research findings of antiglycolipid antibodies present in HIVinfected patients with and without peripheral nerve dysfunction, in an attempt to arrive at some consensus as to whether these antibodies may play a role in the immunopathogenesis of HIV-associated inflammatory demyelinating polyneuropathy.

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Acute lumbosacral polyradiculopathy in acquired immunodeficiency syndrome: Experience in 23 patients

Olney

1994

Annals of Neurology

105

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We reviewed our experience in 23 patients with acquired immunodeficiency syndrome (AIDS) who had acute lumbosacral polyradiculopathy. The patients developed a distinctive syndrome of rapidly progressive flaccid paraparesis and areflexia that was frequently associated with sphincter disturbances. Persuasive laboratory evidence of a cytomegalovirus polyradiculopathy (polymorphonuclear pleocytosis or confirmatory cerebrospinal fluid culture) was found in 15 of the 23 patients. Treatment with ganciclovir in these patients led to clinical stabilization, although worsening during the first 2 weeks of treatment was common. Most patients with cytomegalovirus polyradiculopathy had severe residual deficits. Metastasis from systemic lymphoma accounted for the polyradiculopathy in 2 other patients. A more benign syndrome was identified in the remaining 6 patients. They generally had slower clinical progression and less severe neurological deficits at their nadir than did patients with cytomegalovirus polyradiculopathy. Unlike patients with cytomegalovirus infection, their cerebrospinal fluid showed a predominantly mononuclear pleocytosis. Moreover, spontaneous improvement without treatment was common. Our experience together with the published experience of others suggests that the acute lumbosacral polyradiculopathy in AIDS is a clinical syndrome with different etiologies and variable clinical outcome. Recognition of this heterogeneity is necessary for the management of individual patients, as well as the interpretation of treatment results.

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Subacute AIDS-related lumbosacral radiculopathy: a bacterial infection?

Cited by 8 publications

References 10 publications

Acute polyradiculopathies in HIV-infected patients

Acute polyradiculopathies in HIV-infected patients

Can antiglycolipid antibodies present in HIV‐infected individuals induce immune demyelination?

Acute lumbosacral polyradiculopathy in acquired immunodeficiency syndrome: Experience in 23 patients

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