Front Neurol
November 2024
Objective: Neuronal loss in the somatosensory, as well as the motor cortex in amyotrophic lateral sclerosis (ALS), indicative of a structural abnormality has been reported. Previously we have shown that afferent inhibition was impaired in ALS, suggestive of sensory involvement. In this study, we aimed to evaluate excitability changes in the somatosensory cortex of ALS patients.
View Article and Find Full Text PDFJ Clin Neurophysiol
September 2022
Purpose: In addition to motor cortex involvement, sensory abnormalities have been demonstrated in amyotrophic lateral sclerosis (ALS), including structural and metabolic alterations in the occipital cortex. The aim of this study was to examine occipital excitability changes in ALS.
Methods: Twenty-one patients with ALS and 16 healthy subjects were enrolled into the study.
Introduction: We sought a combination of abnormalities to define a more sensitive measure of cortical excitability in amyotrophic lateral sclerosis (ALS).
Methods: The automatic threshold tracking method was employed to assess the resting motor threshold, intracortical facilitation (ICF), short-interval intracortical inhibition (SICI), and short-interval intracortical faciilitation (SICF) in patients and controls.
Results: SICF at interstimulus intervals (ISI) between 1 and 1.
Introduction: To test the hypothesis of impaired cholinergic activity in amyotrophic lateral sclerosis (ALS), we studied short- and long-latency afferent inhibition (SAI and LAI).
Methods: The ulnar nerve was stimulated at the wrist preceding transcranial magnetic stimulation (TMS), 21 ms for SAI and 200 ms for LAI, in 21 patients and 17 control subjects. Short-interval intracortical inhibition (SICI) and cognitive function was assessed in ALS patients using automatic threshold tracking and the Montreal Cognitive Assessment (MoCA).
Introduction: We studied spinal excitability and its relation to motor unit action potential (MUAP) changes in the thenar and hypothenar muscles in patients with amyotrophic lateral sclerosis (ALS).
Methods: Quantitative MUAP and peak ratio interference analyses were performed, and cutaneous silent period (CutSP) was measured in the abductor digiti minimi (ADM) and first dorsal interosseous (FDI) muscles of patients with ALS and controls.
Results: Patients with ALS revealed more prominently increased duration (P = 0.
Objective: The imbalance between neurotoxic cytokine tumor necrosis factor-α (TNF-α) and neurotrophic cytokines epidermal growth factor (EGF) and interleukin-6 (IL-6) plays a role in the pathogenesis of cobalamin (Cbl) deficiency-induced neuropathy. The aim of this study was to evaluate autonomic nervous system dysfunction and to look for any relationship between autonomic nervous system disturbances and serum cytokine levels (TNF-α, EGF, IL-6) in patients with Cbl deficiency.
Methods: Serum levels of TNF-α, EGF and IL-6 were studied in patients with Cbl deficiency (n=41) and a healthy control group (n=17) and after 3 months in patients who underwent Cbl replacement therapy (n=22).
Chronic lymphocytic leukemia (CLL) is a frequent hematological malignancy, with meningeal or peripheral nerve infiltrations being the most commonly encountered neurological complications. In this report, we describe a CLL patient with Miller-Fisher syndrome (MFS) who responded to immune modulation with plasmapheresis. A 47-year-old man diagnosed as B-cell CLL admitted with neutropenic fever.
View Article and Find Full Text PDFObjective: To report a patient with coeliac disease (CD) associated with primary biliary cirrhosis (PBC) who presented with myopathy without classical symptoms of CD.
Clinical Presentation And Intervention: A 42-year-old woman presented with inability to walk and marked loss of motor function. She had elevated liver enzymes with a cholestatic pattern.
Sleep related respiratory dysfunction and vocal cord paralysis are considered to be the major factors responsible for respiratory failure in multiple system atrophy (MSA). We report a patient initially presenting with alveolar hypoventilation culminating in respiratory failure, ultimately diagnosed as MSA. No central sleep apnea or marked paralysis of the vocal cords was noted.
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