The prevalence and clinical significance of inhalant withdrawal symptoms among a national sample

BACKGROUND: Inhalants are among the most common and dangerous forms of substance use, but very little research on inhalant use disorders exist. Unlike other substances, the Diagnostic and Statistical Manual, 4th edition (DSM-IV) indicates that inhalants do not have an associated withdrawal syndrome among persons who meet criteria for inhalant dependence. METHODS: Using data from the National Epidemiologic Survey on Alcohol and Related Conditions, this study examines the prevalence of withdrawal symptoms among inhalant users. Prevalence of inhalant withdrawal symptoms for inhalants was also compared with the prevalence of cocaine withdrawal symptoms to help determine the presence of an inhalant withdrawal syndrome. RESULTS: Approximately 47.8% of persons who met criteria for inhalant dependence reported experiencing three or more inhalant-related withdrawal symptoms that were clinically significant. Among those with inhalant dependence, almost half of the withdrawal symptoms were as common as the corresponding withdrawal symptoms experienced by persons with cocaine dependence. Furthermore, the percentage of persons with inhalant dependence reporting clinically significant inhalant withdrawal symptoms was almost equal to the percentage of persons with cocaine dependence reporting clinically significant cocaine withdrawal symptoms. CONCLUSIONS: These data provide evidence for an inhalant-related withdrawal syndrome among persons with inhalant dependence. Revisions to DSM-IV should consider including inhalant withdrawal as a diagnostic criterion for this disorder.     

Microglia are more susceptible than macrophages to apoptosis in the central nervous system in experimental autoimmune encephalomyelitis through a mechanism not involving Fas (CD95)

Morphological studies have shown that macrophages and microglia undergo apoptosis in the central nervous system (CNS) in acute experimental autoimmune encephalomyelitis (EAE) in the Lewis rat. To assess the relative levels of macrophage and microglial apoptosis, and the molecular mechanisms involved in this process, we used three-colour flow cytometry to identify CD45lowCD11b/c+ microglial cells and CD45highCD11b/c+ macrophages in the inflammatory cells isolated from the spinal cords of Lewis rats 13 days after immunization with myelin basic protein (MBP) and complete Freund's adjuvant. Simultaneously, we analyzed the DNA content of these cell populations to assess the proportions of cells undergoing apoptosis and in different stages of the cell cycle or examined their expression of three apoptosis- regulating proteins, i.e. Fas (CD95), Fas ligand (FasL) and Bcl-2. Microglia were highly vulnerable to apoptosis and were over-represented in the apoptotic population. Macrophages were less susceptible to apoptosis than microglia and underwent mitosis more frequently than microglia. The different susceptibilities of microglia and macrophages to apoptosis did not appear to be due to variations in Fas, FasL or Bcl- 2 expression, as the proportions of microglia and macrophages expressing these proteins were similar, and were relatively high. Furthermore, in contrast to T cell apoptosis, apoptosis of microglia/macrophages did not occur more frequently in cells expressing Fas or FasL, or less frequently in cells expressing Bcl-2. These results indicate that the apoptosis of microglia and CNS macrophages in EAE is not mediated through the Fas pathway, and that Bcl-2 expression does not protect them from apoptosis. Expression of FasL by macrophages and microglia may contribute to the pathogenesis and immunoregulation of EAE through interactions with Fas+ oligodendrocytes and Fas+ T cells. The high level of microglial apoptosis in EAE indicates that microglial apoptosis may be an important homeostatic mechanism for controlling the number of microglia in the CNS following microglial activation and proliferation.      

Axonal neurofilaments are resistant to calpain-mediated degradation in the WLD(S) mouse.

The biological basis for the phenotype of delayed Wallerian degeneration in the WLDs mouse has yet to be elucidated, although it is known that the characteristic is intrinsic to the axon. Previous data suggested that nerves from the WLD(S) are relatively resistant to proteolytic degradation. We investigated the time-course of neurofilament degradation in response to addition of the calcium-activated protease m-calpain, comparing nerves from WLD(S) and wild-type mice. During 10 min of in vitro proteolysis, neurofilaments from the WLD(S) were consistently slower to degrade than were neurofilaments from wild-type mice. Direct comparisons were performed on Western blots, with statistically significant differences in neurofilament immunoreactivity at 2, 4, and 6 min of reaction time (p < 0.01). These findings suggest that the mutation leading to the WLD(S) phenotype may affect the proteolytic interaction between calpain and neurofilaments.     

Training Residents in the Use of Telepsychiatry: Review of the Literature and a Proposed Elective

Many regions in the United States are deficient in mental health services, especially those in rural areas. As a result of these deficiencies, many patients in need of psychiatric services are often left untreated. Although it is clear that telepsychiatry has great potential in improving patient access to mental health care in areas where psychiatric services are deficient, the lack of familiarity with the technology and inadequate training are current barriers to expanding the use of telepsychiatry. A review of telepsychiatry, its clinical applications, and evidence-based literature regarding competencies in graduate medical education related to telepsychiatry are provided. An approach to implementing telepsychiatry into a curriculum is suggested. We also propose an elective clinical experience with resources for didactics or independent study that will enable residents to develop a knowledge base and competence in the practice of telepsychiatry.     

Effective Intervention Programming: Improving Maternal Adjustment Through Parent Education

This study assessed the secondary effects of a parent training intervention program on maternal adjustment, with a focus on understanding ways in which program efficacy differed for participants as a function of whether or not their children had behavior problems. Mothers (N = 99) of toddlers (2–3 years of age) were randomly assigned to receive one of three levels of intervention: (1) informational booklet (2) booklet + face-to-face parent training sessions, or (3) booklet + web-based parent training sessions. Findings indicated that all levels of intervention were associated with increases in maternal well-being for participants with typically developing children. Mothers of toddlers with behavior problems, however, did not benefit from receiving only the booklet but significantly benefitted from receiving either the face-to-face or web-based interventions. Findings are discussed in terms of efficient and efficacious program dissemination and the resulting implications for public policy.     

Facts and Meaning

The fee expresses the analyst's desire. Money struggles between patient and analyst offer an outstanding opportunity for conflicting subjectivities to be revealed and understood. Alternatively, avoiding fee conflicts can lead to treatment stagnation and analytic poverty. Nevertheless, analysts frequently fear and avoid this discussion, knowing that the fee is an intrusion of their own need. Jessica Benjamin's particular perspective on intersubjectivity suggests that this either/or dilemma of competing needs can be resolved through a both/and exploration process that establishes mutual recognition. Indeed, productive fee negotiations can expand intimacy between patient and analyst and increase the patient's capacity with money, limit setting, ambition, desire, and mutuality in his outside life. Analysts' resistances to asking for more, as well as patients' resistances to paying, are described. There are two clinical examples, one that shows the pitfalls of sidestepping this treacherous interaction, and one that illustrates the transformational power of a fee confrontation.     

Indeterminate dendritic cell neoplasm of the skin: A 2‐case report and review of the literature

Indeterminate dendritic cell neoplasm (IDCN) is an exceedingly rare and mostly cutaneous histiocytosis, frequently associated with other hematopoietic malignancies. We report 2 cases of multilesional cutaneous IDCN. A 55‐year‐old male with no associated malignancy and complete response to ultraviolet phototherapy; and a 72‐year‐old male with chronic myelomonocytic leukemia (CMML). Both cases showed histiocytoid cytology, positivity for CD1a and no expression of langerin or BRAF^V600E. With our patients, the literature describes 79 cases of IDCNs, including 65 (82%) with only skin involvement, 7 cases (9%) with involvement of skin and a second site, 5 cases (6%) involving lymph nodes only, 1 splenic lesion and 1 systemic disease. Seventeen cases (22%) were associated with other hematopoietic malignancies, most commonly CMML (6 cases), follicular lymphoma (4 cases) and acute myeloid leukemia (3 cases). All IDCNs associated with myeloid malignancies were limited to the skin, while most cases associated with lymphoma were limited to lymph nodes. Reported responses of cutaneous lesions to ultraviolet phototherapy are encouraging, while systemic chemotherapy is appropriate for clinically aggressive cases and treatment of associated malignancies. Recognition of the clinico‐morphologic spectrum of IDCNs should prevent misdiagnoses and prompt investigation of possible associated neoplasms.     

Late-onset epilepsy and occult cerebrovascular disease

The interface between cerebrovascular disease (CVD) and epilepsy is complex and multifaceted. Late-onset epilepsy (LOE) is increasingly common and is often attributed to CVD, and is indeed associated with an increased risk of stroke. This relationship is easily recognizable where there is a history of stroke, particularly involving the cerebral cortex. However, the relationship with otherwise occult, subcortical CVD is currently less well established yet causality is often invoked. In this review, we consider the diagnosis of LOE in clinical practice—including its behaviour as a potential mimic of acute ischemic stroke and transient ischemic attack; evidence for an association between occult CVD and LOE; and potential mechanisms of epileptogenesis in occult CVD, including potential interrelationships between disordered cerebral metabolism and perfusion, disrupted neurovascular unit integrity, blood–brain barrier dysfunction, and inflammation. We also discuss recently recognized issues concerning antiepileptic drug treatment and vascular risk and consider a variety of less common CVD entities associated with seizures.