Neurological complications in HIV

Hogan, Celia; Wilkins, Ed

doi:10.7861/clinmedicine.11-6-571

Cited by 40 publications

(20 citation statements)

References 11 publications

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“…Over 40 million people worldwide are infected by HIV-1 (UNAIDS/WHO) [1], and while HIV-1 is most well known for its devastating effects on the immune system and the resulting AIDS, it can involve any level of the neuro-axis [2]. In this review, we will focus on updates related to HIV-associated neurocognitive disorders (HAND).…”

Section: Introductionmentioning

confidence: 99%

Update on HIV-Associated Neurocognitive Disorders

Alfahad

Nath

2013

Curr Neurol Neurosci Rep

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Neurocognitive disorders are a feared complication of HIV infection, especially in the post anti-retroviral era as patients are living longer. These disorders are challenging in terms of diagnosis and treatment. The clinical syndrome has evolved driven in part by comorbidities such as aging, drug abuse, psychiatric illnesses, and a metabolic syndrome associated with the use of antiretroviral drugs. Additionally some individuals may develop a fulminant immune reconstitution syndrome. Hence management of these patients needs to be individualized. The focus of research in the HIV field has recently switched towards elimination of the HIV reservoir as a means of combating long-term HIV complications. However these approaches maybe suitable for limited populations and might not be applicable once the HIV reservoir has been established in the brain. Further, all clinical trials using neuroprotective or anti-inflammatory drugs for treatment of HIV-associated neurocognitive disorders have been unsuccessful. Hence neurological complications of HIV infection represent the biggest challenge facing HIV researchers and there is a critical need for developing new diagnostics and approaches to treatment for these disorders.

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Section: Introductionmentioning

confidence: 99%

Update on HIV-Associated Neurocognitive Disorders

Alfahad

Nath

2013

Curr Neurol Neurosci Rep

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“…Raised intracranial pressure (ICP) can occur at different stages of HIV infection, mostly arising in advanced stages attributed to opportunistic infections such as cryptococcus meningitis, tuberculosis, and syphilis or from neoplasms [1]. Elevation in ICP occurs much less frequently in early stages of illness during a lymphocytic meningitis acute HIV infection (AHI) [2].…”

Section: Introductionmentioning

confidence: 99%

Acute HIV Infection Masquerading as Idiopathic Intracranial Hypertension: A Case Report and Literature Review

et al. 2020

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We describe a previously healthy 21-year-old man who presented acutely with signs and symptoms of raised intracranial pressure (ICP). Lumbar puncture yielded an elevated opening pressure and an acellular CSF analysis. Radiological images showed bilateral flattening of the posterior eye globes and an empty sella turcica. His serum HIV antigen/antibody was reactive. We provide a review of published cases that have been labeled as idiopathic intracranial hypertension (IIH) in HIV-infected patients, addressing the appropriateness of labeling such cases as truly idiopathic. We also discuss the importance of a thorough clinical evaluation of raised ICP in those who do not fulfil the typical IIH demographic.

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“…HIV-1 (HIV) affects both the central nervous system (CNS) and peripheral nervous system (PNS) 1,2 . Nervous system infection with HIV produces a range of clinical disorders, with peripheral neuropathy as a frequent neurological complication 3 .…”

Section: Introductionmentioning

confidence: 99%

Peripheral Neuropathy in Primary HIV Infection Associates With Systemic and Central Nervous System Immune Activation

Wang

Grill

et al. 2014

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Background Peripheral neuropathy (PN) is a frequent complication of chronic HIV infection. We prospectively studied individuals with primary HIV infection (PHI, <1 year after transmission) to assess the presence of and laboratory associations with PN in this early stage. Methods Standardized examination and analysis of blood and cerebrospinal fluid (CSF) was performed in participants with laboratory-confirmed PHI. PN was defined as ≥1 of the following unilateral or bilateral signs: decreased distal limb position, vibration, or temperature sense, or hyporeflexia; symptomatic PN (SPN) as presence of these signs with symptoms. Analysis employed nonparametric statistics. Results 20/58 (35%) antiretroviral-naïve male subjects without diabetes evaluated at a median 107 days post HIV transmission (dpt) met criteria for PN. 13/20 (65%) of PN subjects met criteria for SPN; 6/20 (30%) had bilateral findings. PN subjects and no PN subjects (NPN) did not differ in median age, dpt, blood CD4 or CD8 counts, CSF or plasma HIV RNA levels, CSF white blood cell counts, or CSF:blood albumin ratio. PN and SPN subjects had elevated CSF neopterin (p=0.003 and p=0.0005), CSF MCP-1 (p=0.006 and p=0.01) and blood neopterin (p=0.006 and p=0.009) compared to NPN. PN subjects had a higher percentage of activated phenotype CSF CD8+ T lymphocytes than NPN subjects (p=0.009). Conclusions Signs of PN were detected by detailed neurologic exam in 35% of men enrolled in a neurological study at a median 3.5 months after HIV transmission. PN during this early period may be mediated by systemic and nervous system immune responses to HIV.

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Neurological complications in HIV

Cited by 40 publications

References 11 publications

Update on HIV-Associated Neurocognitive Disorders

Update on HIV-Associated Neurocognitive Disorders

Acute HIV Infection Masquerading as Idiopathic Intracranial Hypertension: A Case Report and Literature Review

Peripheral Neuropathy in Primary HIV Infection Associates With Systemic and Central Nervous System Immune Activation

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