Brain single-photon emission tomography with99mTc-HMPAO in neuropsychiatric systemic lupus erythematosus: relations with EEG and MRI findings and clinical manifestations

Abstract

Central nervous system (CNS) involvement in patients with systemic lupus erythematosus (SLE) is often difficult to evaluate because of protean neuropsychiatric (NP) manifestations and lack of reliable diagnostic markers. In the reported study the role of single-photon emission tomography (SPET) with technetium-99m hexamethylpropylene amine oxime (HMPAO) in the evaluation of CNS involvement in SLE was assessed and the relations between SPET perfusion defects, EEG examination, magnetic resonance imaging (MRI) findings and clinical presentation were examined. Twenty SLE patients with different NP manifestations were studied. Multiple areas of hypoperfusion, especially in the territory of the middle cerebral artery, were demonstrated by SPET analysis in all 20 patients. The number of hypoperfused areas and the degree of hypoperfusion, expressed by an asymmetry index (AI), were more marked in patients with multiple NP manifestations. MRI and EEG evaluations were positive for 14 of 18 and for 12 of 20 patients, respectively. In the patients with positive SPET and MRI, 87 MRI focal lesions and 63 hypoperfused areas were found, and for 51 of these 63 at least one MRI lesion was found in the same anatomical region. SPET examination of patients with a normal EEG showed fewer hypoperfused areas and a lower degree of asymmetry compared to patients with an abnormal EEG. SPET of patients with focal EEG abnormalities showed more hypoperfused areas (difference not statistically significant) and a higher AI than did SPET of the patients with diffuse EEG abnormalities. Seven of 11 anatomical regions with focal EEG abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Perfusion MRI in neuro‐psychiatric systemic lupus erthemathosus

“…To date, no significant associations or correlations between (regional) CBF and NP involvement have been reported (8,(10)(11)(12)(13)(14)(15). Rubbert et al (13) reported that they did not find any association between clinical SLE manifestations and also found no relation between CBF observations and NP symptoms.…”

“…However, they found no correlation with overall disease activity or serological disease parameters and poor correlation with the expert NP diagnosis. So far, no significant associations or correlations between (regional) CBF and NP involvement have been reported (8,(10)(11)(12)(13)(14)(15). To our knowledge, no perfusion weighted MR studies are available in NPSLE patients to date.…”

“…Patchy hypoperfusion has been implicated in the past as a possible cause of NP symptoms in SLE. On the one hand, previous investigators suggested patchy or random focal hypoperfusion, using single photon emission computed tomography (SPECT) in NPSLE patients (8). A recent study with SPECT suggested that the gray matter in SLE patients was relatively hypoperfused compared to healthy controls (9).…”

Neuroimmunopathology in a murine model of neuropsychiatric lupus

“…Approximately 40% of the NP-SLE manifestations develop before the onset of SLE or at the time of diagnosis and about 60% within the first year after diagnosis (van Dam, 1991). While a histologically normal brain with no specific pathognomonic brain lesions is a possible finding in NP-SLE, various abnormalities include hypoperfusion (Colamussi et al, 1995;Handa et al, 2003;Huang et al, 2002;Lopez-Longo et al, 2003) and regional metabolic abnormalities (Komatsu et al, 1999;Sibbitt and Sibbitt, 1993;Brooks et al, 1997;Volkow et al, 1988). Brain atrophy, however, is the most frequent observation on CT scans (Gonzalez-Scarano et al, 1979;Kaell et al, 1986;Miguel et al, 1994;Omdal et al, 1989;Ainiala et al, 2005;Waterloo et al, 1999) and is proposed to reflect widespread and progressive neuronal loss (Sibbitt and Sibbitt, 1993;Sibbitt et al, 1994).…”

Proliferating brain cells are a target of neurotoxic CSF in systemic autoimmune disease

“…Neurologic and psychiatric (NP) manifestations of unknown etiology are common in SLE and have been proposed to represent a more severe form of the disease, often denoting a graver prognosis (Bombardier et al, 1992;Rubin et al, 1985). Contemporary imaging techniques indicate that profound metabolic alterations and neuronal loss accompany neuropsychiatric lupus, or NP-SLE (Colamussi et al, 1995;Sibbitt et al, 1994). Periventricular lesions, cerebral atrophy, and ventricular enlargement of unknown etiology occur in up to 50% of patients (Baum et al, 1993;Bosma et al, 2000).…”