Pulsatile tinnitus from a redundant arterial loop

Abstract

Abstract-Background: Distal sensory polyneuropathy (DSP) is the most common neurologic complication of human immunodeficiency virus (HIV) infection. Risk factors for DSP have not been adequately defined in the era of highly active antiretroviral therapy. Methods: The authors evaluated 101 subjects with advanced HIV infection over 48 weeks. Assessments included a brief peripheral neuropathy (PN) screen (BPNS), neurologic examination, nerve conduction studies, quantitative sensory testing (QST), and skin biopsies with quantitation of epidermal nerve fiber density. Data were summed into a Total Neuropathy Score (TNS). The presence, severity, and progression of DSP were related to clinical and laboratory results. Results: The mean TNS (range 0 to 36) was 8.9, with 38% of subjects classified as PN-free, 10% classified as having asymptomatic DSP, and 52% classified as having symptomatic DSP. Progression in TNS from baseline to week 48 occurred only in the PN-free group at baseline (mean TNS change ϭ 1.16 Ϯ 2.76, p ϭ 0.03). Factors associated with progression in TNS were lower current TNS, distal epidermal denervation, and white race. As compared with the TNS diagnosis of PN at baseline, the BPNS had a sensitivity of 34.9% and a specificity of 89.5%. Conclusions: In this cohort of advanced human immunodeficiency virus (HIV)-infected subjects, distal sensory polyneuropathy was common and relatively stable over 48 weeks. Previously established risk factors, including CD4 cell count, plasma HIV RNA, and use of dideoxynucleoside antiretrovirals were not predictive of the progression of distal sensory polyneuropathy (DSP). Distal epidermal denervation was associated with worsening of DSP. As compared with the Total Neuropathy Score, the brief peripheral neuropathy screen had relatively low sensitivity and high specificity for the diagnosis of DSP.

Disrupted neural activity in unilateral vascular pulsatile tinnitus patients in the early stage of disease: Evidence from resting-state fMRI

“…According to previous studies (Levine et al, 2008;Madani and Connor, 2009;Mehall et al, 1995;Otto et al, 2007;Signorelli et al, 2012;Sonmez et al, 2007;Waldvogel et al, 1998;Xue et al, 2012), abnormal blood flow induced by a focal bone defect in the region of the sigmoid sinus is a common cause of PT. Other etiologies may include sigmoid sinus diverticulum, persistent petrosquamosal sinus, mastoid emissary vein, paraganglioma, atherosclerosis, dural arteriovenous fistula, and involuntary contraction of muscles in the middle ear (Abdul-Baqi, 2004;Bento et al, 1998;Chan, 2009;Forte et al, 1989;Gultekin et al, 2008;Howsam et al, 2005;Krishnan et al, 2006;Libman and Johnson, 2006;Madani and Connor, 2009;Nowe et al, 2004;Otto et al, 2007;Sogawa et al, 2005;Sonmez et al, 2007;Waldvogel et al, 1998;Xue et al, 2012;Zhao et al, 2014). The relatively clear etiologies of PT provide a foundation for a contrasting study of the neural activities of NPT and PT patients.…”

Abnormal Baseline Brain Activity in Patients with Pulsatile Tinnitus: A Resting-State fMRI Study

“…Typically, symptomatic improvement could be achieved by external compression of the internal jugular vein in the neck on the symptomatic side. Possible etiologies include sigmoid sinus diverticulum, atherosclerosis, abnormal vascular loops, aneurysm of internal carotid artery, mastoid emissary vein, dural arteriovenous shunts, paraganglioma, involuntary contraction of muscles in the middle ear, and so forth [ 6 – 11 , 28 – 36 ]. The abnormal blood flow induced by a focal defect of mastoid bone shell in the region of the transverse-sigmoid junction is a common etiology according to our daily work.…”