Subacute encephalopathy and seizures in alcoholics (SESA) presenting with non-convulsive status epilepticus

AbstractSubacute encephalopathy with seizures in chronic alcoholism (SESA) was first described in 1981 by Niedermeyer who reported alcoholic patients presenting with confusion, seizures and focal neurological deficits and is quite distinct from patients presenting with typical alcohol withdrawal seizures. EEG often reveals periodic discharges and spikes, but SESA presenting with non-convulsive status epilepticus has rarely been described.We report a case of SESA with non-convulsive status epilepticus in a patient who was initially suspected of having a typical alcohol withdrawal seizure.A 61 year old woman with a history of chronic alcoholism was admitted at an outside hospital for confusion thought to be secondary to an alcohol withdrawal seizure. She had right hemiparesis and later developed right facial twitching that did not respond to intravenous fosphenytoin and levetiracetam. She was transferred for further management. Upon arrival, lorazepam and fosphenytoin were given and right face clonic movements resolved. However, continuous EEG monitoring revealed ongoing non-convulsive status epilepticus (NCSE). Following treatment with IV valproate and lacosamide, there was resolution of NCSE.SESA is likely an under recognized clinical syndrome that is quite distinct from typical alcohol withdrawal seizures and requires a different diagnostic and management approach. NCSE is likely to account for the encephalopathy and focal neurological deficits seen in patients presenting with the clinical syndrome of SESA. Therefore, a high degree of suspicion is warranted and continuous EEG monitoring is recommended for alcoholic patients with encephalopathy and focal neurological deficits

Zonal organization of the climbing fiber projection to the flocculus and nodulus of the rabbit: A combined axonal tracing and acetylcholinesterase histochemical study

The localization and termination of olivocerebellar fibers in the flocculus and nodulus of the rabbit were studied with anterograde axonal transport methods [wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) and tritiated leucine] and correlated with the compartments in the white matter of these lobules delineated with acetylcholinesterase histochemistry (Tan et al. J. Comp. Neurol., 1995, this issue). Olivocerebellar fibers originating from the caudal dorsal cap travel through floccular compartments FC2 and FC4 to terminate as climbing fibers in floccular zones FZII and FZIV. Fibers from the rostral dorsal cap and the ventrolateral outgrowth traverse compartments FC1 and FC3, which are interleaved with compartments FC2 and FC4, and terminate in zones FZI and FZIII. Fibers from the rostral pole of the medial accessory olive traverse the C2 compartment and terminate in the C2 zone. FZI-II

A pill for the partner via the chlamydia patient? Results from a mixed method study among sexual health care providers in the Netherlands.

Chlamydia prevalence in the Netherlands remains high despite targeted efforts. Effective Partner Notification (PN) and Partner Treatment (PT) can interrupt transmission and prevent re-infections. Patient Initiated Partner Treatment (PIPT) may strengthen chlamydia control. This study explores the current practice of PN and PT, and benefits of, and barriers and facilitators for PIPT among professionals in sexual health care in the Netherlands

Comparison of the functional and structural characteristics of rare TSC2 variants with clinical and genetic findings

The TSC1 and TSC2 gene products interact to form the tuberous sclerosis complex (TSC), an important negative regulator of the mechanistic target of rapamycin complex 1 (TORC1). Inactivating mutations in TSC1 or TSC2 cause TSC, and the identification of a pathogenic TSC1 or TSC2 variant helps establish a diagnosis of TSC. However, it is not always clear whether TSC1 and TSC2 variants are inactivating. To determine whether TSC1 and TSC2 variants of uncertain clinical significance affect TSC complex function and cause TSC, in vitro assays of TORC1 activity can be employed. Here we combine genetic, functional, and structural approaches to try and classify a series of 15 TSC2 VUS. We investigated the effects of the variants on the formation of the TSC complex, on TORC1 activity and on TSC2 pre-mRNA splicing. In 13 cases (87%), the functional data supported the hypothesis that the identified TSC2 variant caused TSC. Our results illustrate the benefits and limitations of functional testing for TSC