FDG PET-CT evaluation in neurolymphomatosis: imaging characteristics and clinical outcomes.

Neurolymphomatosis (NL) often represents unidentified non-Hodgkin lymphoma relapses. Considering its severity, early detection and treatment are crucial. We outline one hospital's 18F-FDG-PET-CT imaging findings of NL, along with the patients' clinical characteristics. Clinical records and imaging findings of 19 NL patients, PET-CT diagnosed, were retrospectively reviewed. Patient data, FDG-PET-CT findings and the presence of coexisting diseases, especially CNS involvement, were documented. Available MRI and clinical data verified the findings. All cases had increased linear FDG uptake along anatomic nerve sites. CTs showed varying degrees of corresponding soft-tissue-thickening. Clinical correlations also contributed to the diagnosis. In 4/19 patients, lymphoma presented with NL, in 15/19 it appeared with disease recurrence/progression. In 9/19, clinical symptoms suggested neural involvement while 10/19 had nonspecific symptoms. Eleven died of lymphoma within 0.9 years of diagnosis despite directed-therapy. Eight, however, survived up to 7.82 years post-diagnosis. Whole-body FDG-PET-CT can assist in early NL diagnosis, possibly enhancing survival.

Acetazolamide-enhanced neuroSPECT scan reveals functional impairment after minimal traumatic brain injury not otherwise discernible.

A patient suffering from aggressive personality changes and cognitive impairment following head trauma, without neurological or anatomical imaging findings, underwent neuroSPECT scans with and without acetazolamide injection, both before treatment and during treatment with valproate. Acetazolamide injection induced increased prefrontal perfusion not evident at baseline. Valproate treatment was associated with increased prefrontal perfusion concomitant with clinical improvement and abolished response to acetazolamide challenge.

Brain reactivity to specific symptom provocation indicates prospective therapeutic outcome in OCD.

A pertinent question in biological psychiatry is what differentiates responders and non-responders to pharmacological treatment. One possibility is that individual differences in the symptomatic spectrum as well as in the underlying biology of the disorder lead to the known 40% failure in pharmacological treatment. Our study aimed to maximize individual brain markers of obsessive-compulsive disorder (OCD) by applying single photon emission computed tomography (SPECT) during a provoked symptomatic state prior to and following treatment. Four brain SPECT scans were obtained from 26 OCD patients prior to and at 6 months of sertraline treatment. At each time point, two SPECT scans were performed in a counterbalanced order of two specific states; one a symptom-provoking condition and the other a relaxed condition. At 6 months of treatment, patients were divided into responders and non-responders according to a predetermined clinical criterion. Prospective responders showed significantly lower brain perfusion in the dorsal-caudal anterior cingulum and higher brain perfusion in the right caudate, when compared to non-responders, only during symptom provocation. When pre- and post-treatment scans during symptom provocation were compared, only responders showed significant change in brain response: increased perfusion in the left anterior temporal cortex and prefrontal cortex at 6 months' treatment. These findings suggest that obtaining functional brain imaging during specific symptom provocation emphasizes individual differences in brain reactivity. Thus can indicate prospective responders to symptom-related treatment in OCD and mark the relevant brain regions for effective response to treatment.