State-of-the-Art: Inflammatory and Metabolic Markers in Mood Disorders.

Mounting evidence highlights the involvement of inflammatory/immune systems and their relationships with neurotransmitters and different metabolic processes in mood disorders. Nevertheless, there is a general agreement that available findings are still inconclusive. Therefore, further investigations are required, aimed at deepening the role of possible alterations of biomarkers in the pathophysiology of mood disorders that might lead to more focused and tailored treatments.

Inflammatory and metabolic markers in patients with mood disorders.

Objectives: An increasing bulk of data underlined that mood disorders show alterations that are not confined to the brain, but involve several other systems. The aim of this retrospective study was to explore metabolic/inflammatory profiles, blood pressure, and BMI in patients affected by bipolar disorders (BDs) to better understand the role of peripheral biomarkers in mood disorders.

Methods: Different metabolic/inflammatory parameters and clinical characteristics were evaluated in 97 BD inpatients from Sicily, a southern Italian region, and compared with normative values from the same area.

Effectiveness of clozapine, oxcarbazepine and rivastigmine combination in a bipolar disorder patient with initial cerebral atrophy.

This paper reports the case of a 46-year-old woman suffering from bipolar disorder of type I with mixed features with initial fronto-temporal atrophy. Although considered treatment-resistant to conventional strategies, she successfully responded to a combination of rivastigmine, clozapine, and oxcarbazepine.

Frequency and phenotypic spectrum of KMT2B dystonia in childhood: A single-center cohort study.

Background: Childhood-onset dystonia is often genetically determined. Recently, KMT2B variants have been recognized as an important cause of childhood-onset dystonia.

Objective: To define the frequency of KMT2B mutations in a cohort of dystonic patients aged <18 years at onset, the associated clinical and radiological phenotype, and the natural history of disease.

Acute myelopathy selectively involving lumbar anterior horns following intranasal insufflation of ecstasy and heroin.

We report a patient who developed acute myelopathy after intranasal insufflation of amphetamines and heroin. The functional prognosis was very poor; after 4 months, she remained paraplegic. MRI imaging showed selective T2 hyperintensity and intense enhancement confined to the spinal anterior horns and lumbar nerve roots and plexus.

Loss of glial fibrillary acidic protein (GFAP) impairs Schwann cell proliferation and delays nerve regeneration after damage.

Axonal loss causes disabling and permanent deficits in many peripheral neuropathies, and may result from inefficient nerve regeneration due to a defective relationship between Schwann cells, axons and the extracellular matrix. These interactions are mediated by surface receptors and transduced by cytoskeletal molecules. We investigated whether peripheral nerve regeneration is perturbed in mice that lack glial fibrillary acidic protein (GFAP), a Schwann-cell-specific cytoskeleton constituent upregulated after damage.

Motor evoked potentials in a mouse model of chronic multiple sclerosis.

We tested cortical motor evoked potentials (cMEPs) as a quantitative marker for in vivo monitoring of corticospinal tract damage in a murine multiple sclerosis model (experimental autoimmune encephalomyelitis, EAE). The cMEPs, previously standardized in naive C57BL/6 developing and adult mice, were studied longitudinally in adult EAE mice. Central conduction times (CCTs) increased significantly shortly before the earliest clinical signs developed (10 days postimmunization, dpi), with peak delay in acute EAE (20-40 dpi).

Loss of Mtmr2 phosphatase in Schwann cells but not in motor neurons causes Charcot-Marie-Tooth type 4B1 neuropathy with myelin outfoldings.

Mutations in MTMR2, the myotubularin-related 2 gene, cause autosomal recessive Charcot-Marie-Tooth type 4B1 (CMT4B1). This disorder is characterized by childhood onset of weakness and sensory loss, severely decreased nerve conduction velocity, demyelination in the nerve with myelin outfoldings, and severe functional impairment of affected patients, mainly resulting from loss of myelinated fibers in the nerve. We recently generated Mtmr2-null(neo) mice, which show a dysmyelinating neuropathy with myelin outfoldings, thus reproducing human CMT4B1.

Mononeuropathies of the radial nerve: clinical and neurographic findings in 91 consecutive cases.

Retrospective features of 91 consecutive cases (68 men, 23 women; mean age 44.4 years) of radial mononeuropathy diagnosed over the last 8 years in two electromyography (EMG) services are reported to define the clinical and electrophysiological findings of radial neuropathies in relation to traumatic and non-traumatic causes and site of injury. The occurrence of radial neuropathy was 0.