Magnetic resonance imagingIn vivo proton magnetic resonance spectroscopy (MRS) and single photon emission computerized tomography (SPECT) in systemic lupus erythematosus (SLE)
Introduction
SLE is a common connective tissue disease that involves almost all organ systems. Neuropsychiatric involvement (NP-SLE) is seen in as many as 11-60% of SLE patients [1]. NP-SLE may cause transient neurologic deficits or chronic brain injury with mortality rate ranging from 7-40% [2]. The diagnosis of NP-SLE is difficult because of several reasons, namely, protean manifestations, need to differentiate NP-SLE from secondary causes of neurologic involvement like central nervous system (CNS) infections, metabolic encephalopathy etc., and last but not the least, confusion over nomenclature. In addition, the lack of reliable surrogate serum markers and an ideal imaging modality compound the problem. Magnetic resonance imaging (MRI) is the currently preferred anatomic imaging modality [3]. MRI is more likely to show abnormalities if there are focal neurologic deficits, seizures, chronic cognitive dysfunction, or the antiphospholipid syndrome (APS). However, in many patients with obvious NP-SLE, the MRI may not exhibit any changes especially patients with affective disorders, confusional states or headache [3], [4]. Another drawback of MRI is the difficulty in differentiating lesions of active NP-SLE from old lesions [5], [6]. Neuroimaging frequently (25-50% cases) reveals chronic lesions in patients even without active disease. The frequency of these lesions increases with age, disease severity and past history of NP-SLE [3], [6].
In this setting of a lack of gold standard imaging modality in NP-SLE, techniques to detect functional brain abnormalities can serve as useful adjuncts. Regional cerebral blood flow (rCBF) abnormalities detected by SPECT and non-invasive assessment of tissue metabolites in vivo by MRS can supplement information provided by MRI in patients with NP-SLE. We undertook a prospective study to evaluate the role of MRS and SPECT in picking up neuropsychiatric involvement in patients with SLE.
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Patients
Twenty patients of SLE, 10 with clinical evidence of neuropsychiatric involvement (cases) and 10 without any neuropsychiatric features (disease controls) were prospectively recruited into the study after informed consent. All patients with SLE fulfilled the American College of Rheumatology (formerly American Rheumatism Association) criteria for SLE [7]. NP-SLE was diagnosed when SLE patients manifested definite neurologic &/or psychiatric events currently or in the past provided other causes
Results
The 20 lupus patients included in our study included 10 with NP-SLE (female 9, male 1; mean age 27.3 ± 10.07 years) and 10 disease controls without clinical neuropsychiatric involvement-(female 9, male 1; mean age 26.9 ± 8.19 years) with disease duration ranging from 4 months to 9 years. The spectrum of NP-SLE included seizures, peripheral neuropathy, movement disorder, stroke, depression psychosis, anxiety disorder and headache.
MRI was abnormal in 5 out of 10 NP-SLE patients while all the 10
Discussion
The diagnosis of NP-SLE continues to be a major clinical problem. It is mandatory to exclude central nervous system infections, drug effects (e.g., due to corticosteroids and chloroquine), and metabolic alterations before attributing neurologic or psychiatric events to SLE. Apart from a wide list of differential diagnoses, the other difficulty is that there is no single confirmatory diagnostic test. Anti ribosomal and anti neuronal antibodies are neither sufficiently specific nor sensitive to
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2014, Neurologic ClinicsCitation Excerpt :Cortical atrophy and parenchymal calcifications are other possible findings in long-standing lupus. However, structural imaging studies in lupus may also be unremarkable; MRI has been found to be abnormal in only 50% of patients.115,116 In these instances, advanced imaging techniques may be of value.
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2013, Handbook of Clinical NeurologyCitation Excerpt :One MRI study suggested that there was a correlation of increased cerebral abnormalities with increased neurocognitive abnormalities (Appenzeller et al., 2007). Similarly abnormalities of technetium-99m-HMPAO or ECM single-photon emission computerized tomography (SPECT), perfusion-weighted imaging (PWI), magnetization transfer imaging (MTI), diffusion-weighted imaging (DWI), proton magnetic resonance spectroscopy (MRS), and fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) have all been reported but lack specificity for clinically diagnosed NPSLE or cognitive dysfunction in adult SLE or pSLE (Grunwald et al., 1995; Colamussi et al., 1997; Lin et al., 1997; Lass et al., 1998; Kao et al., 1999; Waterloo et al., 2001; Handa et al., 2003; Liu et al., 2003; Govoni et al., 2004; Jennings et al., 2004; Castellino et al., 2005; Olazaran et al., 2009). MRI, MRS, and SPECT studies in pSLE also demonstrated a lack of specificity of neuroimaging abnormalities and neuropsychiatric involvement (Szer et al., 1993; Reiff et al., 1997; Falcini et al., 1998; Russo et al., 1998; Mortilla et al., 2003).
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2011, Systemic Lupus ErythematosusNeuropsychiatric Systemic Lupus Erythematosus: Mechanisms of Injury
2010, Systemic Lupus Erythematosus, Fifth EditionDisturbed distribution of proliferative brain cells during lupus-like disease
2009, Brain, Behavior, and ImmunityCitation Excerpt :Systemic autoimmune disease lupus erythematosus (SLE) is frequently accompanied by neurologic and psychiatric complications (Bosma et al., 2002). Brain imaging reveals lesions in the periventricular and subcortical white matter (Jennings et al., 2004), hypoperfusion (Handa et al., 2003), and regional metabolic abnormalities (Appenzeller et al., 2006). The damaged blood–brain barrier (Abbott et al., 2003), brain atrophy, and ventricular enlargement (Kozora et al., 1998; Waterloo et al., 1999) further suggest that SLE progression induces a widespread neuronal loss by unknown pathogenic mechanisms (Sibbitt et al., 1994).