Distal symmetric polyneuropathy phenotype in patients with sensory neuronopathy at the time of electrodiagnosis.

Introduction/aims: It is unknown how often patients with sensory neuronopathy (SNN) present with a distal symmetric polyneuropathy (DSP) phenotype. In these cases, electrodiagnostic testing may discriminate SNN with a DSP phenotype from DSP.

Methods: We reviewed the records of patients who met SNN diagnostic criteria between January 2000 and February 2021 and identified patients with a DSP phenotype at the time of electrodiagnosis.

Patients who meet electrodiagnostic criteria for CIDP rarely present with a sensory predominant DSP phenotype.

Introduction: It is unknown how often patients with electrodiagnostic evidence of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), a potentially treatable condition, present with a distal symmetric polyneuropathy (DSP) phenotype.

Methods: We reviewed the records of patients who presented to our electrodiagnostic laboratory between January 1, 2011, to December 31, 2019, and fulfilled electrodiagnostic criteria for CIDP to identify those who presented with a sensory predominant DSP phenotype.

Results: One hundred sixty-two patients had a chronic acquired demyelinating neuropathy, of whom 138 met criteria for typical or atypical CIDP.

Minorities, men, and unmarried amyotrophic lateral sclerosis patients are more likely to die in an acute care facility.

Studies suggest that dying at home is a more favorable experience. This study investigated where amyotrophic lateral sclerosis (ALS) patients die and the patient demographics associated with dying in an acute care facility or nursing home compared to home or hospice. Centers for Disease Control and Prevention Multiple Cause Mortality Files from 2005 to 2010 were used to identify ALS patients and to classify place of death.

Multifocal motor neuropathy.

Multifocal motor neuropathy is an acquired disorder in which demyelination of motor axons, presumably due to autoimmune attack, results in progressive painless weakness without sensory loss. Motor axonal damage also occurs. It is a frequent mimic of motor neuron disease.

Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats.

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias.