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            C-flumazenil PET in patients with refractory temporal lobe epilepsy and normal MRI

Koepp, MJ; Hammers, Alexander; Labbé, Claire; Woermann, FG; Brooks, David J.; Duncan, John S.

doi:10.1212/wnl.54.2.332

Cited by 111 publications

(63 citation statements)

References 26 publications

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“…For assessment of medial temporal changes, statistical parametric maps were re-thresholded at P = 0.01 uncorrected, assessed using a medial temporal lobe mask, and significant changes assessed at a threshold of Z > 2.5 and characterized in terms of Z score, extent (k), and coordinates, as described and used previously (Hammers et al, 2001(Hammers et al, , 2002Koepp et al, 1997aKoepp et al, , 1997bKoepp et al, , 2000. This combination of thresholds has a theoretical foundation in the correction for approximately four independent comparisons at the smoothing level of the final SPM (7Z = 2.5 corresponds to a P of 0.0124, that is B0.05/4, a traditional Bonferroni correction for multiple comparisons) and has been empirically validated by approximately yielding the expected false-positive rates in our previous studies.…”

Section: Discussionmentioning

confidence: 99%

[¹¹C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

Hammers

Panagoda

Heckemann

et al. 2007

J Cereb Blood Flow Metab

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11 C]FMZ PET datasets and arterial plasma input functions were available for 15 patients with medically refractory medial temporal lobe epilepsy (TLE) and histologically verified unilateral HS and for 13 control subjects. SPM2 was used for analysis. ADD1020 and ADD2040 images showed decreased FMZ uptake ipsilateral to the epileptogenic hippocampus in 13/15 cases; 6/13 had bilateral decreases in the ADD1020 analysis and 5/13 in the ADD2040 analysis. BP-SRTM images detected ipsilateral decreases in 12/15 cases, with bilateral decreases in three. In contrast, VD images showed ipsilateral hippocampal decreases in all 15 patients, with bilateral decreases in three patients. Bilateral decreases in the ADD images tended to be more symmetrical and in one case were more marked contralaterally. Full quantification with an image-independent input should ideally be used in the evaluation of FMZ PET; at least in TLE, intrasubject correlations do not predict equivalent clinical usefulness.

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Section: Discussionmentioning

confidence: 99%

[¹¹C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

Hammers

Panagoda

Heckemann

et al. 2007

J Cereb Blood Flow Metab

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“…Hippocampal asymmetry (right minus left hippocampal volume) is significantly correlated with right minus left intracarotid amobarbital memory scores. 92 Hippocampal volumetry has also been used to determine region of interest, [93][94][95] or partial volume correction 96 for PET in temporal lobe epilepsy. A number of studies have also examined methodological issues in hippocampal volumetry in epilepsy such as, optimizing hippocampal volume determination, 17,97 the necessity of hippocampal volume normalization, 98-100 the comparability and reliability of manual and digitizer measurements, 49 the correlation of hippocampal body with total hippocampal volume, 101 the intra-and interobserver variability, 102 and the utility of automated methods.…”

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confidence: 99%

MR-based in vivo hippocampal volumetrics: 2. Findings in neuropsychiatric disorders

2004

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Magnetic resonance imaging (MRI) has opened a new window to the brain. Measuring hippocampal volume with MRI has provided important information about several neuropsychiatric disorders. We reviewed the literature and selected all English-language, human subject, data-driven papers on hippocampal volumetry, yielding a database of 423 records. Smaller hippocampal volumes have been reported in epilepsy, Alzheimer's disease, dementia, mild cognitive impairment, the aged, traumatic brain injury, cardiac arrest, Parkinson's disease, Huntington's disease, Cushing's disease, herpes simplex encephalitis, Turner's syndrome, Down's syndrome, survivors of low birth weight, schizophrenia, major depression, posttraumatic stress disorder, chronic alcoholism, borderline personality disorder, obsessive-compulsive disorder, and antisocial personality disorder. Significantly larger hippocampal volumes have been correlated with autism and children with fragile X syndrome. Preservation of hippocampal volume has been reported in congenital hyperplasia, children with fetal alcohol syndrome, anorexia nervosa, attention-deficit and hyperactivity disorder, bipolar disorder, and panic disorder. Possible mechanisms of hippocampal volume loss in neuropsychiatric disorders are discussed.

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“…[ 11 C]FMZ binds to the GABA-related central benzodiazepine receptor and can be used in vivo to detect remaining neurons in sclerotic hippocampi. In many cases, however, [ 11 C]FMZ showed poor spatial correlation with neuronal cell loss and therefore has not been proven consistently helpful in localizing the epileptic foci (Koepp et al, 2000). …”

Section: Discussionmentioning

confidence: 99%

Untitled

Sauvageau

Desjardins

Lozeva

et al. 2002

Metabolic Brain Disease

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Increased binding sites for "peripheral-type" benzodiazepine receptor (PTBR) ligands have been described in a wide range of neurological disorders including both human and exper-imental epilepsy. This study was undertaken to assess PTBR expression in relation to the presence of hippocampal sclerosis in human temporal lobe epilepsy (TLE). For this pur-pose, hippocampal CA1 subfields were dissected from surgical samples from patients with therapy-refractive TLE with (n D 5) or without (n D 2) hippocampal sclerosis and from age-matched nonepileptic postmortem controls (n D 5). PTBR expression was assessed by immunohistochemistry and reverse-transcription polymerase chain reaction. Receptor sites were evaluated using an in vitro binding assay and the selective PTBR ligand [ 3 H]PK11195. Epileptic patients with hippocampal sclerosis showed increases in PTBR binding sites, im-munoreactivity, and mRNA expression compared to both nonsclerotic TLE patients and postmortem nonepileptic controls. Induction of PTBR expression and binding sites were directly correlated with the presence of hippocampal sclerosis and the accompanying reac-tive gliosis.

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¹¹ C-flumazenil PET in patients with refractory temporal lobe epilepsy and normal MRI

Abstract: 11C-FMZ PET showed focal increases as well as decreases of FMZ binding in 80% of patients with refractory TLE and normal high-quality MRI but was not consistently helpful in localizing the epileptic foci.

Cited by 111 publications

References 26 publications

[¹¹C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

[¹¹C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

MR-based in vivo hippocampal volumetrics: 2. Findings in neuropsychiatric disorders

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11 C-flumazenil PET in patients with refractory temporal lobe epilepsy and normal MRI

Abstract: 11C-FMZ PET showed focal increases as well as decreases of FMZ binding in 80% of patients with refractory TLE and normal high-quality MRI but was not consistently helpful in localizing the epileptic foci.

Cited by 111 publications

References 26 publications

[11C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

[11C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

MR-based in vivo hippocampal volumetrics: 2. Findings in neuropsychiatric disorders

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¹¹ C-flumazenil PET in patients with refractory temporal lobe epilepsy and normal MRI

[¹¹C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?

[¹¹C]Flumazenil PET in Temporal Lobe Epilepsy: Do We Need an Arterial Input Function or Kinetic Modeling?