scholarly journals A case of primary diffuse leptomeningeal gliomatosis predominantly involving the cervical spinal cord and mimicking chronic meningitis

Author(s):  
Dilara Savci-heijink ◽  
Kamran Urgun ◽  
Aydin Sav ◽  
Askin Seker ◽  
Deniz Konya
2006 ◽  
Vol 2 (3) ◽  
pp. 202 ◽  
Author(s):  
Sung-Hun Kim ◽  
Dong-Chul Jun ◽  
Jin Se Park ◽  
Jae-Hyeok Heo ◽  
Sung-Min Kim ◽  
...  

1993 ◽  
Vol 15 (3) ◽  
pp. 275-283 ◽  
Author(s):  
P. -Y. Dietrich ◽  
M. S. Aapro ◽  
A. Rieder ◽  
G. R. Pizzolato

Author(s):  
L. Vacca-Galloway ◽  
Y.Q. Zhang ◽  
P. Bose ◽  
S.H. Zhang

The Wobbler mouse (wr) has been studied as a model for inherited human motoneuron diseases (MNDs). Using behavioral tests for forelimb power, walking, climbing, and the “clasp-like reflex” response, the progress of the MND can be categorized into early (Stage 1, age 21 days) and late (Stage 4, age 3 months) stages. Age-and sex-matched normal phenotype littermates (NFR/wr) were used as controls (Stage 0), as well as mice from two related wild-type mouse strains: NFR/N and a C57BI/6N. Using behavioral tests, we also detected pre-symptomatic Wobblers at postnatal ages 7 and 14 days. The mice were anesthetized and perfusion-fixed for immunocytochemical (ICC) of CGRP and ChAT in the spinal cord (C3 to C5).Using computerized morphomety (Vidas, Zeiss), the numbers of IR-CGRP labelled motoneurons were significantly lower in 14 day old Wobbler specimens compared with the controls (Fig. 1). The same trend was observed at 21 days (Stage 1) and 3 months (Stage 4). The IR-CGRP-containing motoneurons in the Wobbler specimens declined progressively with age.


1992 ◽  
Vol 158 (6) ◽  
pp. 1413-1413
Author(s):  
T E Barros ◽  
R P Oliveira ◽  
L A Rosemberg ◽  
A C Magalhães

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Michael D. Sunshine ◽  
Antonino M. Cassarà ◽  
Esra Neufeld ◽  
Nir Grossman ◽  
Thomas H. Mareci ◽  
...  

AbstractRespiratory insufficiency is a leading cause of death due to drug overdose or neuromuscular disease. We hypothesized that a stimulation paradigm using temporal interference (TI) could restore breathing in such conditions. Following opioid overdose in rats, two high frequency (5000 Hz and 5001 Hz), low amplitude waveforms delivered via intramuscular wires in the neck immediately activated the diaphragm and restored ventilation in phase with waveform offset (1 Hz or 60 breaths/min). Following cervical spinal cord injury (SCI), TI stimulation via dorsally placed epidural electrodes uni- or bilaterally activated the diaphragm depending on current and electrode position. In silico modeling indicated that an interferential signal in the ventral spinal cord predicted the evoked response (left versus right diaphragm) and current-ratio-based steering. We conclude that TI stimulation can activate spinal motor neurons after SCI and prevent fatal apnea during drug overdose by restoring ventilation with minimally invasive electrodes.


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