Progressive Polyradiculopathy in HIV

Progressive Polyradiculopathy in HIV

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Progressive polyradiculopathy typically occurs late in the course of HIV infection, unlike inflammatory demyelinating polyradiculoneuropathies in HIV, which usually occur earlier in the course of disease. [1, 2, 3] Progressive polyradiculopathy in HIV is extremely uncommon, however, is more prevalent in untreated patients with severe immunosuppression. Given its rare occurrence, incidence rate is unknown. HIV-infected patients become susceptible to progressive polyradiculopathy in advanced immunosuppression when the CD4 T-cell count is less than 50/µL. [4]  However, cases of progressive polyradiculopathy have been seen in varying degrees of immunosuppression. [5]  The lumbrosacral region is most often the affected site.

Polyradiculopathy typically results from cytomegalovirus (CMV) infection. The most common manifestation of neurological CMV disease in HIV infection is retinitis followed by encephalitis, myelitis, multifocal polyneuropathy, and polyradiculopathy. [6, 7] CMV co-infection of the retina and other sites is common. An idiopathic form of polyradiculopathy exists, which has a better prognosis than the CMV-related form.

Histologically, polyradiculopathy typically features necrosis of nerve roots and endoneurial and epineurial blood vessels, along with marked inflammation (most pronounced in the lumbar region). In CMV-associated cases, cytoplasmic and nuclear CMV inclusions may be apparent in Schwann cells and fibroblasts. 

CMV polyradiculopathy is rapidly fatal without treatment. Treatment with foscarnet or ganciclovir may improve or stabilize the condition. Clinical stabilization often occurs after initial worsening during the first 2 weeks of treatment. [2]  Even with treatment, mortality is 22%. In idiopathic polyradiculopathy, spontaneous improvement without treatment is common. [8]

Less common causes of polyradiculopathy in HIV infection include spinal lymphomas, diffuse infiltrative lymphocytosis syndrome, and CNS (central nervous system) opportunistic infections such as tuberculosis meningitis, syphilis, cryptococcosis, herpes simplex virus type 2, varicella-zoster virus, and toxoplasmosis. [5]  

Reactivation of HSV-2 after genital herpes with HIV infection can cause lumbosacral radiculitis. [9] Lumbosacral radiculopathy caused by tuberculous meningitis is due to infection of spinal leptomeninges characterized by granulomatous inflammation. This can compress nerve roots or the cord resulting in radiculopathy. [10] A single case of syphilitic lumbosacral radiculopathy has also been reported. [11]

Idanivir-induced epidural lipomatosis in the lumbar canal causing polyradiculopathy has been described, but resolved with discontinuation of the drug. [12]

Progressive polyradiculopathy presents as a cauda equina syndrome. CMV-related polyradiculopathy is characterized by rapidly progressive ascending numbness, pain, bowel dysfunction, and asymmetric weakness affecting the legs and later occasionally also the arms. [13] These symptoms can develop acutely over days or more subacutely in 1 to 6 weeks. Possibly co-existing CMV-related conditions include retinitis, colitis, and encephalitis. With idiopathic polyradiculopathy, symptoms are more benign and the clinical progression is slower. [14]

The following may be noted in CMV-related polyradiculopathy:

Rapidly progressive, ascending course


Sensory loss, invariable

Rarely, sensory level suggestive of spinal cord involvement

Flaccid paraparesis


Urinary retention, constipation, or incontinence

Rarely, cranial neuropathies

Severe pain

Often asymmetrical, especially in the early stage of disease

Late involvement of the upper extremities

Herpes zoster is characterized by pain and itching followed by rash. Trigeminal and thoracic dermatomes are most commonly affected. [15]

Cerebrospinal fluid analysis may be useful for differentiation between the various etiologies: the infectious forms (eg, CMV, cryptococcosis, tuberculosis, toxoplasmosis), the idiopathic form, and the neoplastic form (ie, lymphoma). In addition to routine studies, analysis of the CSF for cytology, CMV, Venereal Disease Research Laboratory test (VDRL), and cryptococcal antigen may be performed. The most sensitive techniques, including polymerase chain reaction (PCR), are required to rule out specific treatable infections.

In CMV-related polyradiculopathy, typical CSF findings are as follows:

Decreased glucose level

Markedly elevated protein level, but can be normal

Polymorphonuclear neutrophil (PMN)–predominant pleocytosis. One case report showed lymphocytic predominance.

Positive PCR for CMV

Absence of malignant cells

Pleocytosis usually comprises more than 60% PMNs, but the percentage is sometimes lower. In one study, only 50% of patients had PMN-preponderant pleocytosis. Positive CMV-PCR and elevated protein were the most common CSF findings. [16]

PCR of CSF has a 92% sensitivity and a 94% specificity in CMV-associated progressive polyradiculopathy. CMV culture is positive in only 50% of cases.

CSF findings are different in non-CMV-related progressive polyradiculopathy.

in lymphoma, CSF findings include lymphocytic pleocytosis.

In TB-related cases, CSF findings usually include (but not always) elevated protein, decreased protein and glucose, as well as PMN’s often mixed with lymphocytes. Mycobacterial cultures as well as lymph node biopsies may also assist in diagnosis.

In idiopathic cases, CSF findings include:

Moderate mononuclear pleocytosis

Mildly elevated protein

Absence of identifiable infectious agents or malignant cells

A complete blood count may indicate very low CD4 lymphocyte counts. Blood and urine cultures may indicate CMV and other possible etiologic agents.

MRI with contrast or myelography is useful to exclude cauda equina or spinal cord compressive lesions resulting from lymphoma, syphilis, or toxoplasmosis. Possible findings include the following:

Meningeal enhancement consistent with arachnoiditis

Thickened nerve roots or root enhancement in cauda equina can be seen. This finding is nonspecific and inconsistently seen in CMV- associated polyradiculopathy.

Electromyography and nerve conduction studies may indicate the following:

Differentiation from other rapidly progressive neuropathies such as Guillain-Barré syndrome

Widespread denervation

Prolonged or absent F-waves

Low-amplitude or unobtainable tibial or peroneal compound muscle action potentials and sural nerve action potentials

Treatment strategies depend on the etiology. In idiopathic polyradiculopathy, spontaneous improvement without treatment is common. [8]

For CMV, prompt initiation of therapy is critical. Combination treatment with ganciclovir and foscarnet may be preferred as initial therapy to stabilize disease and maximize response, although it has substantial rates of adverse effects. [17] Ganciclovir-resistant CMV may respond to foscarnet, but mortality remains high. CMV polyradiculopathy can be fatal within 2 months making early treatment extremely important. 

CMV polyradiculopathy responds to cidofovir in combination with highly active antiretroviral therapy (HAART). [18] Acyclovir inhibits activity of both HSV-1 and HSV-2.

In cases of subacute lumbosacral radiculopathy in immunocompetent individuals, symptoms can resolve spontaneously over weeks. Others have responded to corticosteroids. [19]

Symptomatic treatment for neuropathic pain include agents such as gabapentin, pregabalin, nortriptyline, amitriptyline, lamotrigine, venlafaxine, and duloxetine. Physical therapy is also recommended.


What is progressive polyradiculopathy in HIV infection?

Which clinical history findings are characteristic of progressive polyradiculopathy in HIV infection?

Which physical findings are characteristic of progressive polyradiculopathy in HIV infection?

What is the role of CSF analysis in the workup of progressive polyradiculopathy in HIV infection?

Which CSF findings are characteristic of CMV-related progressive polyradiculopathy in HIV infection?

Which CSF findings are characteristic of non-CMV-related progressive polyradiculopathy in HIV infection?

What is the role of CBC count in the workup of progressive polyradiculopathy in HIV infection?

What is the role of MRI in the workup of progressive polyradiculopathy in HIV infection?

What is the role of EMG and NCS in the workup of progressive polyradiculopathy in HIV infection?

How is progressive polyradiculopathy in HIV infection treated?

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Florian P Thomas, MD, PhD, MA, MS Chair, Neuroscience Institute and Department of Neurology, Director, Multiple Sclerosis Center and Hereditary Neuropathy Centers, Hackensack University Medical Center; Founding Chair and Professor, Department of Neurology, Hackensack Meridian School of Medicine at Seton Hall University; Professor Emeritus, Department of Neurology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine

Florian P Thomas, MD, PhD, MA, MS is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, Sigma Xi

Disclosure: Nothing to disclose.

Erik Z Krause, DO Resident Physician, Department of Neurology, St Louis University School of Medicine

Erik Z Krause, DO is a member of the following medical societies: American Academy of Neurology, American Osteopathic Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Glenn Lopate, MD Associate Professor, Department of Neurology, Division of Neuromuscular Diseases, Washington University in St Louis School of Medicine; Consulting Staff, Department of Neurology, Barnes-Jewish Hospital

Glenn Lopate, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, Phi Beta Kappa

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Alnylam Pharmaceuticals<br/>Received income in an amount equal to or greater than $250 from: Alnylam Pharmaceuticals; GLG.

Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM Adjunct Associate Professor of Neurology, University of Missouri-Columbia School of Medicine; Medical Director of St Mary’s Stroke Program, SSM Neurosciences Institute, SSM Health

Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Headache Society

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Mandeep Garewal, MD and Sofia Yahya, MD,to the development and writing of the source article.

Progressive Polyradiculopathy in HIV

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