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The neuropathy is not responsive to treatment with antiretroviral medications and therapy is largely symptomatic We usually initiate treatment with lidoderm patches and neurontin
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HIV-RELATED INFLAMMATORY DEMYELINATING POLYRADICULONEUROPATHY
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Both AIDP and CIDP can occur as a complication of HIV infection39,57 AIDP usually develops at the time of seroconversion, while CIDP can occur anytime in the course of the infection Clinical features are indistinguishable from idiopathic AIDP or CIDP
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CSF is abnormal, demonstrating an increased protein along with reduced glucose concentration and notably a neutrophilic pleocytosis CMV can be cultured from the CSF, blood, and urine NCS often demonstrate an asymmetric reduction of amplitudes of the SNAPs and CMAPs, with active denervation changes on EMG in muscles innervated by affected nerve roots and nerves60,61 These abnormalities are quite distinct from those found in both CIDP and DSP helping to differentiate these various disorders
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In addition to elevated protein levels, lymphocytic pleocytosis is evident in the CSF a nding that helps distinguish this HIV-associated polyradiculoneuropathy from idiopathic AIDP/CIDP Motor and sensory NCS are similar to that seen in idiopathic AIDP and CIDP (s 11 and 12)26,57 59 Motor and sensory NCS may demonstrate slow conduction velocities, prolonged distal latencies and F-waves, conduction block or temporal dispersion
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In ammatory in ltrates associated with varying degrees of axonal loss are evident in the ventral and dorsal roots, particularly in the lumbar regions Occasionally, the cranial nerve root exiting from the brainstem may be involved with adjacent myelitis CMV inclusions may be found in endothelial cells and macrophages on the nerve biopsy specimens62
HISTOPATHOLOGY
Nerve biopsies are identical to that of idiopathic AIDP and CIDP26,51
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NEUROPATHIES ASSOCIATED WITH INFECTIONS
PATHOGENESIS
The polyradiculoneuropathy may be caused by the direct infection of neurons by CMV or ischemia secondary to associated vasculitis
darabine), or -interferon Short courses of prednisone and cyclophosphamide may be necessary If CMV is suspected, treatment with gancyclovir or foscarnet should be initiated
TREATMENT
The polyradiculoneuropathy may improve with gancyclovir or foscarnet, if treatment is started early61,63 However, the prognosis is poor, and most patients die within several weeks or months
HIV-RELATED AUTONOMIC NEUROPATHY
CLINICAL FEATURES
An autonomic neuropathy characterized by orthostatic hypotension, impaired sweating, diarrhea, impotence, and bladder dysfunction can develop acutely or insidiously in patients with HIV infection66 68 Clinical features are similar to those seen with idiopathic autonomic neuropathy
HIV-RELATED MULTIPLE MONONEUROPATHIES
CLINICAL FEATURES
Multiple mononeuropathies can also develop in patients with HIV infection, usually in the context of AIDS39 Weakness, numbness, paresthesia, and pain are evident in the distribution of affected nerves
LABORATORY FEATURES
CSF can reveal pleocytosis and increased protein Most patients have electrodiagnostic features similar to that noted in DSP In addition, autonomic function testing is usually abnormal67
LABORATORY FEATURES
Elevated CSF protein and mononuclear pleocytosis may be seen EMG and NCS demonstrate features seen with other forms of multiple mononeuropathies caused by vasculitis (see 13)64
PATHOGENESIS
An immune-mediated mechanism similar to that suspected in idiopathic autonomic neuropathy is likely
HISTOPATHOLOGY
Nerve biopsies can reveal axonal degeneration with necrotizing vasculitis or perivascular in ammation65 CMV inclusions may be seen in endothelial cells and macrophages on62
TREATMENT
A trial of corticosteroids IVIG or PE may be tried Symptoms of autonomic neuropathy are treated symptomatically
PATHOGENESIS
The pathogenic basis for this disorder is likely multifactorial The neuropathy may be caused by vasculitis related to deposition of HIV antigen antibody complexes in the walls of blood vessel, concomitant hepatitis B or C infection, or CMV infection
HIV-RELATED SENSORY NEURONOPATHY/ GANGLIONOPATHY
Dorsal root ganglionitis is a very rare complication of HIV infection, and neuronopathy can be the presenting manifestation69 Patients develop sensory ataxia similar to idiopathic sensory neuronopathy/ganglionopathy Autopsies have demonstrated in ammatory cell in ltrate in the dorsal root ganglia along with the loss of cell bodies and degeneration of myelinated nerve bers in the peripheral nerves NCS reveal amplitudes or absence of SNAPs Again, a trial of corticosteroids, IVIG, or PE may be warranted
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