Nasojejunal Tube Placement for Levodopa-carbidopa Intestinal Gel Treatment by Neurologists in Patients with Advanced Parkinson's Disease: A Retrospective Observational Study.

Introduction Short-term levodopa-carbidopa intestinal gel (LCIG) treatment using nasojejunal (NJ) tubes (NJ-LCIG test) is recommended for patients with advanced Parkinson's disease to ensure compatibility with this treatment system prior to permanent percutaneous endoscopic gastrojejunostomy. However, there have been no studies on NJ tube insertion by neurologists or on possible differences in treatment efficacy based on the NJ tube insertion method or tube tip position. We therefore investigated the effects of LCIG with NJ tube placement performed by a neurologist.

Axon terminal hypertrophy of striatal projection neurons with levodopa-induced dyskinesia priming.

Background: A rat model of levodopa-induced dyskinesia (LID) showed enlarged axon terminals of striatal direct pathway neurons in the internal segment of the globus pallidus (GPi) with excessive gamma-aminobutyric acid (GABA) storage in them. Massive GABA release to GPi upon levodopa administration determines the emergence of LID.

Objectives: We examined whether LID and axon terminal hypertrophy gradually develop with repeated levodopa treatment in Parkinsonian rats to examine if the hypertrophy reflects dyskinesia priming.

Altered amantadine effects after repetitive treatment for l-dopa-induced involuntary movements in a rat model of Parkinson's disease.

Background: l-3,4-dihydroxyphenylalanine (l-dopa) is the most effective drug for Parkinson's disease (PD); however, most PD patients develop motor fluctuations including wearing-off and l-dopa-induced dyskinesia (LID). Amantadine is beneficial for improving the motor symptoms, reducing "off" time, and ameliorating LID, although its long-term efficacy remains unknown.

Objectives: To investigate the effects of amantadine on PD and LID using a rat model with repetitive drug treatment.

An autopsy case of amyotrophic lateral sclerosis with striatonigral and pallidoluysian degeneration and cat's-eye-shaped neuronal nuclear inclusions.

We report the case of a Japanese woman with sporadic amyotrophic lateral sclerosis (ALS) of 28 months' duration who died at the age of 66 years. Postmortem examination revealed moderate loss of neurons and phosphorylated TDP-43 (p-TDP-43)-immunoreactive neuronal and glial cytoplasmic inclusions in the upper and lower motor neurons. Additionally, marked neuronal loss was observed in the neostriatum, globus pallidum, subthalamic nucleus, and substantia nigra.

Accumulation of Nonfibrillar TDP-43 in the Rough Endoplasmic Reticulum Is the Early-Stage Pathology in Amyotrophic Lateral Sclerosis.

Transactivation response DNA-binding protein 43 (TDP-43)-immunoreactive neuronal cytoplasmic inclusions (NCIs) are the histopathological hallmarks of amyotrophic lateral sclerosis (ALS). They are classified as skein-like inclusions, round inclusions, dot-like inclusions, linear wisps, and diffuse punctate cytoplasmic staining (DPCS). We hypothesized that TDP-43-immunoreactive DPCS may form the early-stage pathology of ALS.

Cabergoline, a long-acting dopamine agonist, attenuates L-dopa-induced dyskinesia without L-dopa sparing in a rat model of Parkinson's disease.

Intermittent administration of L-dopa in Parkinson's disease is associated with L-dopa-induced dyskinesia (LID). Long-acting dopamine agonists may reduce the risk of LID by continuous dopaminergic stimulation. We examined the LID-like behavior, preprodynorphin messenger ribonucleic acid (mRNA) expression in the striatum (a neurochemical LID hallmark), and the volume of the entopeduncular nucleus (a pathological LID hallmark) in Parkinson's disease rat models that were treated with L-dopa and cabergoline.

Effects of Aging on Levo-Dihydroxyphenylalanine- Induced Dyskinesia in a Rat Model of Parkinson's Disease.

Background: It remains unclear why patients with young-onset Parkinson's disease more often develop levo-dihydroxyphenylalanine (L-dopa)-induced dyskinesia (LID) and have a more severe form than patients with old-onset Parkinson's disease. Previous studies using animal models have failed to show young-onset Parkinson's disease enhances LID.

Objectives: To evaluate the association of age at dopaminergic denervation (onset age) and initiation of L-dopa treatment (treatment age) with LID development in model rats.