There is little medical information available about gamma-hydroxybutyrate (GHB) or gamma-butyrolactone (GBL) dependence or withdrawal. In this study the authors treated and reviewed multiple cases of GHB and GBL withdrawal in high-dose users. Five patients during nine hospitalizations were treated for GHB or GBL withdrawal. The authors describe a spectrum of GHB or GBL withdrawal from mild to severe and discuss medications used for treatment. They conclude that patients with GHB or GBL withdrawal may present with agitated psychosis, delirium, and autonomic instability. In this sample, relapse to GHB or GBL use occurred soon after treatment of withdrawal.

We describe what we believe is the first psychiatric hospitalization due to GHB-induced delirium reported in the medical literature. We examine the use of the substance gamma hydroxybutyric acid (GHB) and describe the clinical findings in a patient who presented to an acute inpatient psychiatric unit with a chief complaint of feeling suicidal and a 1-year history of GHB use. A review of the literature and GHB's availability through the Internet are discussed.

We compared the neuropathological changes of 6 patients with clinically diagnosed lobar dementia. In the 4 patients with histopathology consistent with frontotemporal dementia (FTD), moderate neuronal loss contrasted with marked cortical and subcortical gliosis. We found silver-positive, carbohydrate-rich, spheroidal enlargements of presynaptic terminals within the neuropil of specific central nervous system regions. The spheroids were immunopositive for the cytoskeletal proteins tau, the high molecular weight neurofilament subunit (NF-H), and beta-tubulin. No abnormal tau phosphorylation and only rare ubiquitin immunoreactivity were detected in these structures. Carbohydrate modifications, including advanced glycation end products within the spheroid matrix, were confirmed by lectin binding, and by anti-pentosidine immunoreactivity, an indicator of oxidative stress. Ultrastructurally, the spheroids consisted of unmyelinated, membrane-enclosed structures filled with randomly arrayed pairs of filaments, approximately 8 to 10 nm in diameter, that were sparsely labeled with antibodies to unmodified tau (T14) and NF-H. Despite clinical overlap, the central nervous systems of our FTD patients are distinguishable from those of other patients with other lobar dementias, including Pick's disease and corticobasal degeneration, by the absence of abnormally phosphorylated neuronal or glial tau inclusions. The neuropil spheroids are dystrophic changes of certain selectively vulnerable presynaptic terminals, suggesting a retrograde degenerative process in FTD.

We present a child with cardio-facio-cutaneous (CFC) syndrome with inadequate weight gain due to inadequate food intake. After correction of hyperemesis due to intestinal malrotation, she continued to fail to feed due to poor suck reflex. A review documented digestive system findings in 26 of 57 reported patients with CFC syndrome. Thus, digestive system dysfunction and malformation may represent an additional manifestation of the CFC syndrome.