Manifestations of HIV infection in the peripheral nervous system

doi:10.1016/S1474-4422(13)70002-4

The Lancet Neurology

Volume 12, Issue 3, March 2013, Pages 295-309

https://doi.org/10.1016/S1474-4422(13)70002-4 Get rights and content

Summary

Peripheral nerve disorders are associated with all stages of HIV infection. Distal sensory polyneuropathy is characterised by often-disabling pain that is difficult to treat. It is prevalent in both high-income and low-income settings. In low-income settings, use of potentially neurotoxic antiretrovirals, which are inexpensive and widely available, contributes substantially to incidence. Research has focused on identification of factors that predict risk of distal sensory polyneuropathy and elucidation of the multifactorial mechanisms behind pathogenesis. Sensorimotor polyneuropathies and polyradiculopathies are less frequent than distal sensory polyneuropathy, but still occur in low-income settings and have potentially devastating consequences. However, many of these diseases can be treated successfully with a combination of antiretroviral and immune-modulating therapies. To distinguish between peripheral nerve disorders that have diverse, overlapping, and frequently atypical presentations can be challenging; a framework based on a clinicoanatomical approach might assist in the diagnosis and management of such disorders.

Introduction

HIV invades the nervous system soon after primary infection, and affects both the CNS and peripheral nervous system (PNS). As the disease progresses, concentrations of HIV-infected CD4 cells steadily fall. CD4 cell count is used as a biomarker to assess immunocompetence. However, a preserved CD4 cell count does not equate to normal immune function, because the immune system is activated early during infection. An increased turnover of CD4 and CD8 cells (accompanied by polyclonal B-cell activation and immunoglobulin production) ensues, with increasing immune dysregulation.¹ Nonetheless, the duration of HIV infection and CD4 cell counts are useful guides for clinicians.² Immunologically mediated peripheral nerve syndromes (either parainfectious or postinfectious) occur more frequently in patients with preserved CD4 cell counts, whereas those with low counts are more likely to develop opportunistic infections.

In this Review, we use a clinicoanatomical approach as a guide to PNS presentations in HIV-infected patients (table 1). The range of PNS involvement described in patients with HIV has broadened since early in the epidemic, and disease manifestations vary between populations, largely on the basis of antiretroviral availability, selection, and adherence. Therefore, we discuss uncommon inflammatory, infective, vasculitic, and neoplastic peripheral nerve disorders in addition to the more prevalent distal sensory polyneuropathy. We have included disease presentations that, despite being documented only in older reports or small case series, remain important in regions with high burdens of disease, resource limitations, and incomplete antiretroviral coverage. In these settings, capacity for invasive or sophisticated diagnostic tests is restricted, which might necessitate empirical treatment. Corticosteroids are frequently used in patients in whom an inflammatory disorder is suspected and infectious or neoplastic causes have been excluded. However, concomitant initiation of combination antiretroviral therapy (cART) helps with effective immune restoration. These two strategies are frequently used in combination. When evidence is scarce, we offer insight from our experience in the management of these disorders.

A major difficulty in the diagnosis of neurological disease in HIV-infected patients, particularly as the infection advances, is that patients can have simultaneous involvement of the CNS and PNS that affects several anatomical levels, which should be kept in mind when taking histories of symptom evolution and using the clinical approach we outline in this Review (figure 1).² For instance, HIV-associated dementia (which might also encompass a motor disturbance) and distal sensory polyneuropathy often confound the assessment of superadded neurological syndromes.

Section snippets

Distal sensory polyneuropathy

Distal sensory polyneuropathy is the most prevalent sensory neuropathy associated with HIV infection. An antiretroviral toxic neuropathy that is clinically similar to, and difficult to differentiate from, distal sensory polyneuropathy can arise after initiation of cART with dideoxynucleoside reverse transcriptase inhibitors (dNRTIs)—eg, stavudine.3, 4

Most estimates of prevalence of distal sensory neuropathy fall between 30% and 60% worldwide in patients with HIV-1 infection, but reported

Acute inflammatory demyelinating polyneuropathy

Acute inflammatory demyelinating polyneuropathy, or Guillain-Barré syndrome, evolves usually as an ascending polyradiculoneuropathy within hours or days; less frequently it occurs within several (but less than 8) weeks. It presents as symmetrical weakness and areflexia, with or without paraesthesiae. Even in the absence of weakness, acute inflammatory demyelinating polyneuropathy almost invariably results in areflexia. In HIV-infected people, the disorder is thought to occur more frequently in

Atypical (segmental) variants of acute and chronic inflammatory demyelinating polyneuropathies

Progressive multifocal radiculoneuropathy can be confined to either the legs or arms. Involvement of limbs might be asymmetrical.⁹⁶ A demyelinating polyneuropathy might be suspected when patients have areflexia in regions with preserved strength. Electrodiagnostic studies are a sensitive and reliable way to detect demyelination. However, mixed axonal and demyelinating features might be identified.³⁹ Such segmental variants respond to intravenous immunoglobulin.³⁹ An unusual case was that of a

Lumbosacral radiculopathy

Lumbosacral radiculopathy presents with rapidly progressive weakness of both legs (patients become paraplegic within days to weeks), hyporeflexic or areflexic legs, sparing of the arms, and no evidence of spasticity. Symptoms of urinary retention or incontinence are usually but not invariably present.⁹⁶ Although clinical overlap is apparent between this phenotype and that of an evolving ascending polyradiculopathy, we discuss presentations confined to the lumbosacral nerve roots (or plexus).

Signs confined to the arms

Brachial plexus neuritis, with the typical acute onset of pain in the shoulder girdle followed by atrophy and weakness, has been described as an HIV seroconversion illness.117, 118 Pronounced neurological recovery with cART was noted in two patients.¹¹⁷

Pure motor syndromes

This Review concerns the PNS, and thus we will not discuss amyotrophic lateral sclerosis or similar disorder, in which both upper and lower motor neurons are affected. HIV-associated lower-motor-neuron syndromes seem more frequently reported than are amyotrophic lateral sclerosis or similar disorders. A review of patients in whom lower motor neurons were affected and who were described between 1988 and 2005 included nine patients with generalised involvement (CD4 cell counts ranged from 44/μL

Cranial neuropathies

HIV-infected patients frequently develop cranial mononeuropathies, mostly affecting the facial nerve. Such cases of Bell's palsy, whether unilateral or bilateral, most often occur as peri-inflammatory or postinflammatory palsies around the time of primary HIV infection (within 6 weeks preseroconversion, or in the first weeks of seroconversion, respectively). Recovery is similar to that in patients who are not infected with HIV. Cases of facial diplegia accompanying a seroconversion illness of

Autonomic neuropathy

Because painful distal sensory polyneuropathy frequently implicates small nerve fibres, an associated autonomic neuropathy can be expected. Several groups have studied quantitative measures of autonomic function in HIV-infected cohorts, but findings have been inconsistent and so far no evidence of significant autonomic dysfunction has been reported.³⁹ A community study showed that HIV-infected patients often complained of symptoms possibly related to autonomic dysfunction, but objective

Conclusions

Much of the published work cited in this paper dates back several years and comes from areas where HIV/AIDS was first described. However, the burden of HIV disease is now in sub-Saharan Africa, where millions of HIV-infected individuals have not yet started cART. The clinical range of the disease has shifted in high-income countries, where clinical issues are largely complications of long-term cART and the effects of this treatment on an ageing population living with HIV. By contrast,

Search strategy and selection criteria

We searched PubMed for papers published in English between Jan 1, 2002, and Sept 30, 2012 with the terms AIDS[sb] in combination with (nerve OR neuropathy OR mononeuropathy OR polyneuropathy OR “mononeuropathy multiplex” OR “mononeuritis multiplex” OR “neuropathic pain” OR root OR radiculopathy OR plexus OR plexopathy OR “ataxic neuropathy” OR “diffuse infiltrative lymphocytosis syndrome” OR DILS OR vasculitis OR vasculitic OR vasculopathy). We also selected references from manual searches of

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Neuropathogenesis of HIV-associated neuropathic pain
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Despite effective antiretroviral therapy in people living with HIV (PLWH), HIV-related sensory neuropathy (HIV-SN) continues to affect many individuals. Around 30% of PLWH suffer neurological complications. Neuropathic pain in PLWH remains prevalent, causing a significant disability and lowering quality of life. Various mechanisms are involved in the pathogenesis of HIV-associated neuropathic pain. While global HIV research has been carried out for four decades, the exact cellular and network mechanisms of HIV chronic pain are complex and have not been fully elucidated. As PLWH now live longer, patients often harbor comorbid disorders that can influence neuropathic pain development and treatments. This chapter reviews the HIV pathogenesis related to neuropathic pain and summarizes the in vivo and in vitro models that have been developed to investigate the pathogenesis of HIV-SN and neuropathic pain for preclinical research. This chapter may provide insights into novel therapeutic targets of HIV chronic pain.
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2023, Manson's Tropical Diseases, Fourth Edition
Acute encephalitis can be infectious, post-infectious, or antibody-mediated. Mortality and morbidity from tuberculous meningitis remain high. Tuberculomas may present as focal brain lesions with a wide range of appearances on brain imaging. Complex interactions between tuberculosis and human immunodeficiency virus (HIV) in co-infected subjects present diagnostic and therapeutic challenges. Paradoxical clinical worsening or new symptoms consistent with an inflammatory process after antiretroviral treatment initiation in HIV-infected patients suggests an immune reconstitution inflammatory syndrome. HIV-associated neurological complications may simultaneously affect the nervous system at multiple anatomical levels and involve more than one pathogenic process. Cerebral malaria is best treated with artesunate. Zika virus is spreading through the tropical Americas and can manifest with an inflammatory syndrome affecting the peripheral and central nervous system within 4 months of exposure.
Treatment and Management of Infectious, Granulomatous, and Toxic Neuromuscular Disorders
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The neuromuscular apparatus is susceptible to medications, toxins, granulomatous diseases, and infections by organisms like bacteria, parasites, and viruses. This chapter examines the most common and relevant neuromuscular disorders associated with these susceptibilities. The changes in the treatment of human immunodeficiency virus (HIV) infection have modified the profile of neuromuscular complications associated with HIV, but they continue to be an important cause of disability. Neurotropic viruses like West Nile virus represent the modern version of the old poliovirus-associated polymyelitis. Other viruses like human T-lymphotrophic virus type I can result in clinical phenotypes that resemble neurodegenerative conditions and must be excluded for accurate diagnosis. Neuroborreliosis must be considered in patients from endemic areas and will require a high degree of suspicion for proper diagnosis and treatment. Leprosy continues to be an important cause of neuropathy in developing nations, or in areas with high levels of poverty in more developed countries. A treatable cause of neuropathy, it requires early recognition and treatment to avoid incapacitating damage and deformities. The parasitic myositis from Trichinella and cysticercosis, although not as frequent in developed nations, must still be considered in areas with prevalent ingestion of wild game. Toxicities from heavy metals must still be considered in industrialized settings or suspicious circumstances. New medications and approaches in the fight against cancer have expanded the types of neuromuscular toxicities, from disruption of physiologic processes in neurons, axons, and muscles, to actual autoimmune responses against different neuromuscular components. These have resulted in an expanded profile of toxicities and clinical syndromes that clinicians must recognize.
Peripheral neuropathy in HIV patients on antiretroviral therapy: Does it impact function?
2019, Journal of the Neurological Sciences
Citation Excerpt :
Although HIV-DSP is characterized by signs of small fibre dysfunction with increasing loss of pin sensibility in a length-dependent manner, in addition to large fibre dysfunction [6,9], there are few studies enquiring about autonomic dysfunction in these individuals. Early studies showed autonomic dysfunction in patients with advanced HIV infection [1]. However, more recently, evidence of autonomic dysfunction was found in 61% of HIV-positive patients in a North American cohort, of whom 95% were on ART [10].
HIV-associated distal sensory polyneuropathy (DSP), with or without neuropathic symptoms, can develop after anti-retroviral therapy (ART). Symptoms frequently involve small fibres but reports on autonomic dysfunction in HIV-DSP are sparse. We studied an HIV-infected cohort after 5 years of ART, and report on the frequency and severity of autonomic symptoms and the impact of DSP on everyday function. This cross-sectional study comprised of participants from a community-based South African HIV-clinic. The Brief Peripheral Neuropathy Screen and reduced Total Neuropathy Score evaluated neuropathic symptoms/signs. DSP was defined as ≥2 symmetrical DSP-signs, and symptomatic DSP when accompanied by neuropathic symptoms. Autonomic symptoms questionnaires, heart rate variability and postural blood pressure changes were assessed. The Lower Extremity Functional Scale (LEFS) was completed. The 67 participants had a median age of 42 years and median ART exposure of 7 years with viral suppression in 84%. Most (81%) met our criteria for DSP and 36% had additional neuropathic symptoms. Autonomic symptoms and signs (above normative values) were present in 15% and more likely in those with symptomatic DSP (P < .001). Participants with DSP, even without symptoms, had lower LEFS scores (P ≤ .039) than those without. HIV-DSP is prevalent and impacts on daily living.
Sensitivity and specificity of the Neuropad for distal sensory peripheral neuropathy (DSPN) in subjects with HIV-Infection: A case controlled observational study
2019, International Journal of Osteopathic Medicine
Citation Excerpt :
DSPN predominately affects the small sensory fibres, and is characterised by distal axonal degeneration [4]. Symptoms of burning or stabbing pain, paraesthesia, and numbness are reported in a symmetrical distribution affecting the feet more commonly than the hands [5–7]. Reduced vibration and pressure perception are found in a similar distribution, and ankle tendon reflexes are diminished or absent [7–12].
The aim of the current study was to assess the diagnostic accuracy of the Neuropad for detecting distal sensory peripheral neuropathy (DSPN) related to human immunodeficiency virus (HIV)-infection.
Single-gate observational case-control study.
A convenience sample of 30 HIV-infected subjects with a mean age of 48.9 years (95% CI 45.6–52.3) and no other potential causes of neuropathy were recruited from the Ian Charleson Day Centre (London, UK). Sudomotor function was assessed with the Neuropad, an adhesive patch designed to measure sweat production, using a 10-min cut-off. Vibration perception threshold (VPT) testing with a neurothesiometer and the painDETECT questionnaire (PD-Q) were used as reference standard measures of DSPN.
16 participants with sudomotor dysfunction and 14 with healthy sudomotor function were included in analysis. Compared to VPT (>25 V) the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of the Neuropad yielded 66.7%, 48.1%, 12.5% and 92.9% respectively. For the PD-Q (>12) sensitivity of the Neuropad was 100% and specificity was 58.3%, with PPV and NPV of 37.5% and 100% respectively.
The Neuropad may be a suitable screening tool for HIV-related DSPN, and can reliably exclude healthy individuals in the clinical setting. Abnormal Neuropad results require referral to confirm diagnosis. Limitations exist in the sampling method and study size. The use of reference standard measures of small nerve fibre function and continuous Neuropad quantification would strengthen future research.
Chronic Morphine Treatment and Antiretroviral Therapy Exacerbate HIV-Distal Sensory Peripheral Neuropathy and Induce Distinct Microbial Alterations in the HIV Tg26 Mouse Model
2024, International Journal of Molecular Sciences

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ReviewManifestations of HIV infection in the peripheral nervous system

Summary

Introduction

Section snippets

Distal sensory polyneuropathy

Acute inflammatory demyelinating polyneuropathy

Atypical (segmental) variants of acute and chronic inflammatory demyelinating polyneuropathies

Lumbosacral radiculopathy

Signs confined to the arms

Pure motor syndromes

Cranial neuropathies

Autonomic neuropathy

Conclusions

Search strategy and selection criteria

J Pain Symptom Manage

J Neurol Sci

Virology

Brain Behav Immun

Pain

Neurol Clin

Pain

Psychosomatics

J Pain Symptom Manage

J Neurol Sci

J Infect

Rheum Dis Clin North Am

Mitochondrion

Human immunodeficiency virus-associated neurocognitive disorders: mind the gap

Ann Neurol

The peripheral nerve complications of human immunodeficiency virus (HIV) infection

Muscle Nerve

Nucleoside analogue-associated peripheral neuropathy in human immunodeficiency virus infection

J Acquir Immune Defic Syndr Hum Retrovirol

The risk of developing peripheral neuropathy induced by nucleoside reverse transcriptase inhibitors decreases over time: evidence from the Delta trial

Antivir Ther

HIV neuropathy natural history cohort study: assessment measures and risk factors

Neurology

Prevalence of and risk factors for HIV-associated neuropathy in Melbourne, Australia 1993–2006

HIV Med

Can we predict neuropathy risk before stavudine prescription in a resource-limited setting?

AIDS Res Hum Retroviruses

Neurologic disorders are prevalent in HIV-positive outpatients in the Asia-Pacific region

Neurology

Age and height predict neuropathy risk in patients with HIV prescribed stavudine

Neurology

Continued high prevalence and adverse clinical impact of human immunodeficiency virus-associated sensory neuropathy in the era of combination antiretroviral therapy: the CHARTER Study

Arch Neurol

HIV neuropathy in South Africans: frequency, characteristics, and risk factors

Muscle Nerve

High prevalence of distal sensory polyneuropathy in antiretroviral-treated and untreated people with HIV in Tanzania

Trop Med Int Health

Sex differences in the incidence of peripheral neuropathy among Kenyans initiating antiretroviral therapy

Clin Infect Dis

Peripheral neuropathy in HIV: prevalence and risk factors

AIDS

Influence of age and neurotoxic HAART use on frequency of HIV sensory neuropathy

AIDS Res Treat

Neurologic manifestations of human immunodeficiency virus-2: dementia, myelopathy, and neuropathy in West Africa

J Neurovirol

Clinical toxicity of highly active antiretroviral therapy in a home-based AIDS care program in rural Uganda

J Acquir Immune Defic Syndr

Incidence of treatment-limiting toxicity with stavudine-based antiretroviral therapy in Cambodia: a retrospective cohort study

PLoS One

The use of a triple nucleoside-nucleotide regimen for nonoccupational HIV post-exposure prophylaxis

HIV Med

Toxicities associated with dual nucleoside reverse-transcriptase inhibitor regimens in HIV-infected children

J Infect Dis

Distal symmetric polyneuropathy: limitations of the proposed case definition

Muscle Nerve

Evaluation of a clinical screening tool for HIV-associated sensory neuropathies

Neurology

HIV neuropathy: insights in the pathology of HIV peripheral nerve disease

J Peripher Nerv Syst

Pathogenesis of HIV-associated sensory neuropathy: evidence from in vivo and in vitro experimental models

J Peripher Nerv Syst

Schwann cell chemokine receptors mediate HIV-1 gp120 toxicity to sensory neurons

Ann Neurol

Spatially distinct and functionally independent mechanisms of axonal degeneration in a model of HIV-associated sensory neuropathy

Brain

HIV-1 viral protein R causes peripheral nervous system injury associated with in vivo neuropathic pain

Review
Manifestations of HIV infection in the peripheral nervous system