Uterine Cervical Metastasis From Primary Rectal Adenocarcinoma on PET/CT and MRI.

FDG avid uterine cervical masses are most commonly due to primary cervical carcinoma; however, history and differential diagnoses are critical when interpreting FDG PET/CT studies. A 51-year-old woman with newly diagnosed moderately differentiated adenocarcinoma of the rectum underwent FDG PET/CT for staging, which revealed the hypermetabolic primary rectal tumor and nodal metastases. Additionally, FDG avid focus in the anterior cervix without a CT correlate was present. Cervical metastasis was suspected, and further evaluation with MRI and histopathologic correlation was recommended, which confirmed cervical metastasis. This case illustrates an unusual case of FDG-avid cervical metastasis from rectal adenocarcinoma.

Natalizumab-induced progressive multifocal leukoencephalopathy.

A 55-year-old woman with known relapsing-remitting multiple sclerosis (RRMS) on natalizumab (Tysabri®) for 3 years was admitted to the hospital with worsening word-finding difficulties and gait instability. Neurologic examination revealed right hemianopia, right arm hemiplegia, right-sided sensory loss, and global aphasia. The patient underwent MRI and PET imaging with concurrent electroencephalogram. She was subsequently diagnosed with natalizumab-induced progressive multifocal leukoencephalopathy (PML) and treated with plasmapheresis, intravenous immunoglobulin, and high-dose intravenous steroids. Steroids were continued over a 3-month hospital course and tapered upon discharge. Speech, arm strength, and ambulation have since improved.

An overview of PET neuroimaging.

Over the past 35 years or so, PET brain imaging has allowed powerful and unique insights into brain function under normal conditions and in disease states. Initially, as PET instrumentation continued to develop, studies were focused on brain perfusion and glucose metabolism. This permitted refinement of brain imaging for important, non-oncologic clinical indications. The ability of PET to not only provide spatial localization of metabolic changes but also to accurately and consistently quantify their distribution proved valuable for applications in the clinical setting. Specifically, glucose metabolism brain imaging using (F-18) fluorodeoxyglucose continues to be invaluable for evaluating patients with intractable seizures for identifying seizure foci and operative planning. Cerebral glucose metabolism also contributes to diagnosis of neurodegenerative diseases that cause dementia. Alzheimer disease, dementia with Lewy bodies, and the several variants of frontotemporal lobar degeneration have differing typical patterns of hypometabolism. In Alzheimer disease, hypometabolism has furthermore been associated with poorer cognitive performance and ensuing cognitive and functional decline. As the field of radiochemistry evolved, novel radioligands including radiolabeled flumazenil, dopamine transporter ligands, nicotine receptor ligands, and others have allowed for further understanding of molecular changes in the brain associated with various diseases. Recently, PET brain imaging reached another milestone with the approval of (F-18) florbetapir imaging by the United States Federal Drug Administration for detection of amyloid plaque accumulation in brain, the major histopathologic hallmark of Alzheimer disease, and efforts have been made to define the clinical role of this imaging agent in the setting of the currently limited treatment options. Hopefully, this represents the first of many new radiopharmaceuticals that would allow improved diagnostic and prognostic information in these and other clinical applications, including Parkinson disease and traumatic brain injury.

Frequency and clinicopathological characteristics of presenilin 1 Gly206Ala mutation in Puerto Rican Hispanics with dementia.

The frequency and clinical and pathological characteristics associated with the Gly206Ala presenilin 1 (PSEN1) mutation in Puerto Rican and non-Puerto Rican Hispanics were evaluated at the University of Pennsylvania's Alzheimer's Disease Center. DNAs from all cohort subjects were genotyped for the Gly206Ala PSEN1 mutation. Carriers and non-carriers with neurodegenerative disease dementias were compared for demographic, clinical, psychometric, and biomarker variables. Nineteen (12.6%) of 151 unrelated subjects with dementia were discovered to carry the PSEN1 Gly206Ala mutation. Microsatellite marker genotyping determined a common ancestral haplotype for all carriers. Carriers were all of Puerto Rican heritage with significantly younger age of onset, but otherwise were clinically and neuropsychologically comparable to those of non-carriers with AD. Three subjects had extensive topographic and biochemical biomarker assessments that were also typical of non-carriers with AD. Neuropathological examination in one subject revealed severe, widespread plaque and tangle pathology without other meaningful disease lesions. The PSEN1 Gly206Ala mutation is notably frequent in unrelated Puerto Rican immigrants with dementia in Philadelphia. Considered together with the increased prevalence and mortality of AD reported in Puerto Rico, these high rates may reflect hereditary risk concentrated in the island which warrants further study.