Ultrasound examination predicts 6-month progression in carpal tunnel syndrome patients.

Carpal tunnel syndrome (CTS) is a peripheral neuropathy resulting from chronic median nerve compression. Chronic compression leads to neurological changes that are quantified through nerve conduction studies (NCS). Although NCS represents the gold standard in CTS assessment, they provide limited prognostic value.

Blood flow velocity but not tendon mechanics relates to nerve function in carpal tunnel syndrome patients.

Carpal tunnel syndrome (CTS) develops from chronic compression of the median nerve. Chronic compression results in a number of vascular, structural and functional changes to the carpal tunnel tissues which ultimately manifest in the characteristic symptoms of CTS. The purpose of this study was to investigate the interplay of median nerve function, median nerve hemodynamics, and finger flexor tendon and subsynovial connective tissue (SSCT) mechanics in CTS patients.

Correction to: A review of electrophysiological studies of lower motor neuron involvement in amyotrophic lateral sclerosis.

The published version of this article unfortunately contained a mistake. The sequence of authorship and the corresponding author is incorrect. The correct sequence and corresponding author is presented here.

A review of electrophysiological studies of lower motor neuron involvement in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease involving both the upper and lower motor neuron diseases. In this review, we studied and compared different articles regarding the electrodiagnostic criteria for diagnosis of lower motor neuron pathology in ALS. We reviewed the most recent articles and metaanalysis regarding various lower motor neuron electrodiagnostic methods for ALS and their sensitivities.

Central Nervous System-Toxic Lidocaine Concentrations Unmask L-Type Ca²⁺ Current-Mediated Action Potentials in Rat Thalamocortical Neurons: An In Vitro Mechanism of Action Study.

Background: High systemic lidocaine concentrations exert well-known toxic effects on the central nervous system (CNS), including seizures, coma, and death. The underlying mechanisms are still largely obscure, and the actions of lidocaine on supraspinal neurons have received comparatively little study. We recently found that lidocaine at clinically neurotoxic concentrations increases excitability mediated by Na-independent, high-threshold (HT) action potential spikes in rat thalamocortical neurons.

Truths and misinformation: a qualitative exploration of myotonic dystrophy.

Background: Myotonic dystrophy (DM1) is an autosomal dominant, progressive, and multisystem condition that impacts affected individuals physically, socially, and emotionally. Understanding individuals' perceptions of their disease is critical to ensuring appropriate information, education, and counseling.

Methods: We conducted a content analysis of findings from a larger study that used a novel, qualitative research approach called photovoice to explore nine patients' experiences of living with DM1.

Revisiting the evidence for neuropathy caused by pyridoxine deficiency and excess.

Pyridoxine deficiency and excess have been implicated as a cause for peripheral neuropathy. As a result, unrelated neuropathies are often treated with pyridoxine based on questionable evidence. However, neurological practitioners frequently discourage patients from taking pyridoxine in excess of 50 mg/d given concerns around the development of a toxic sensory neuronopathy.

Management of patients with spontaneous intracranial hypotension causing altered level of consciousness: report of two cases and review of literature.

Background: Decreased level of consciousness is a rare neurological manifestation of spontaneous intracranial hypotension (SIH), which typically presents with orthostatic headache. The optimal management of this uncommon presentation remains uncertain.

Methods: We analyzed the presentation, management and outcome of two patients in our institution and reviewed 22 patients reported in the literature with SIH and decreased level of consciousness, defined as any decrease in the patient's Glasgow Coma Scale score.

Comparison of infectious and noninfectious intracranial caseating granulomas.

Although caseating granulomas are classically associated with infectious processes, a subgroup of intracranial caseating granulomas without identifiable infectious pathology (ICGN) is described. We aimed to identify clinical, laboratory, radiological and histological markers with potential to distinguish patients with ICGN from those with intracranial caseating granulomas with infectious etiology (ICGI) on tissue microbiological examinations. In a referral hospital setting, we identified 11 patients with ICGNs and 6 patients with ICGI over an 11-year period.

Intracranial caseating granulomas with no infectious organism detected.

Background: Caseating granuloma is a classic histopathological feature of mycobacterial infections. Occasionally, no infectious organism is demonstrated despite extensive examination of intracranial caseating granulomas. The pathogenesis and optimal management strategy for patients with such intracranial caseating granulomas with no detectable infectious organism (ICGNs) remain unclear.

Optimizing fluctuation analysis of GABAAergic IPSCs for accurate unitary currents.

Nonstationary fluctuation analysis of synaptic currents requires division of currents into bins of time, with little agreement on how to select an optimal bin width. We used simulated inhibitory postsynaptic currents (simIPSCs) in an empirical approach to establish the optimal bin width needed for estimation of the unitary current, ie. We found acceptable accuracy (< or = 5%) at bin widths shorter than the length of the stationary segment of simIPSCs that persisted when Gaussian noise was added to the simulated currents.

Distinctive glycinergic currents with fast and slow kinetics in thalamus.

We examined functional properties of inhibitory postsynaptic currents (IPSCs) evoked by medial lemniscal stimulation, spontaneous IPSCs (sIPSCs), and single-channel, extrasynaptic currents evoked by glycine receptor agonists or gamma-aminobutyric acid (GABA) in rat ventrobasal thalamus. We identified synaptic currents by reversal at E(Cl) and sensitivity to elimination by strychnine, GABA(A) antagonists, or combined application. Glycinergic IPSCs featured short (about 12 ms) and long (about 80 ms) decay time constants.