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Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Bulbar palsy: Myasthenia gravis.Posterior fossa tumors or aneurysms involving medulla or lower cranial nerves.Syringobulbia.Polyneuritis cranialis: low-grade basal meningitis, vasculitis.X-linked recessive bulbar and SMA (Kennedy's syndrome).Creutzfeldt–Jakob disease (amyotrophic form).
Examine the cranial nerves
Published in Hani TS Benamer, Neurology for MRCP PACES, 2019
Q: What are the causes of bulbar palsy? Motor neurone disease.Syringobulbia.Skull base lesion which is usually due to cancer (nerve VII could also be involved).Brainstem tumour.
Questions and Answers
Published in David Browne, Brenda Wright, Guy Molyneux, Mohamed Ahmed, Ijaz Hussain, Bangaru Raju, Michael Reilly, MRCPsych Paper I One-Best-Item MCQs, 2017
David Browne, Brenda Wright, Guy Molyneux, Mohamed Ahmed, Ijaz Hussain, Bangaru Raju, Michael Reilly
Answer: A. Signs B to E, along with increased or normal gag reflex, are indicative of a pseudobulbar palsy (bilateral upper motor neuron lesion of IX, X and XII cranial nerves). Bulbar palsy has absent gag, wasted or fasciculations of the tongue, absent or normal jaw jerk, nasal speech and normal emotions. [AO. p. 345]
Infant botulism: an underestimated threat
Published in Infectious Diseases, 2021
Luca Antonucci, Cristian Locci, Livia Schettini, Maria Grazia Clemente, Roberto Antonucci
Once diffused into extracellular fluid and absorbed by blood and lymphatic vessels, BoNT reaches neuromuscular junctions of voluntary motor and autonomic muscles [35,39], where it binds irreversibly to cholinergic receptors on presynaptic cell membranes, causing flaccid paralysis [40]. Constipation is an early sign of IB, possibly due to the proximity of the intestinal muscular layer to the source of toxin. The musculature of head, face and throat are also involved early in the course of illness, leading to a bulbar palsy. A progressive descending flaccid paralysis follows that involves the respiratory muscles and diaphragm and may lead to respiratory failure and arrest, when more than 90-95% of muscular receptors are blocked [36,40]. BoNT does not cross the blood-brain barrier, however, evidences from clinical and experimental use of BoNT/A support a direct influence of the neurotoxin on central circuits [41]. It has been hypothesised that BoNT/A may undergo long-range axonal transport [42], followed by a transcytosis process by which it may gain access to second-order neurons in the central nervous system [43,44].
Mechanical ventilation in Guillain–Barré syndrome
Published in Expert Review of Clinical Immunology, 2020
Pei Shang, Mingqin Zhu, Matthew Baker, Jiachun Feng, Chunkui Zhou, Hong-Liang Zhang
As a main factor triggering hospital-acquired pneumonia (HAP) in GBS patients, oropharyngeal dysphagia was clinically attributed to cranial nerve involvement and could be predicated via electrophysiology [33]. Bulbar palsy could result in dysphagia, dysarthria and/or asphyxiation, ineffective cough, or aspiration pneumonia, further dampening respiratory capacity. Severe dysphagia impedes decannulation in about 60% tracheotomized GBS patients and persisted dysphagia deteriorates laryngeal sensory deficits [27]. Interestingly, a previous study demonstrated that the presence of IgG anti-GQ1b antibody and cranial nerve involvement heralded respiratory muscle weakness in patients with GBS [34], indicating that ophthalmoplegia merits attention from caregivers to avert respiratory failure.
Tracheostomy ventilation in motor neurone disease: a snapshot of UK practice
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
Jonathan Palmer, Ben Messer, Michelle Ramsay
Median survival for patients who were not weaned and continued TV was 24 months (range 1–60) post intubation. For those eight patients extubated and successfully weaned onto NIV, the median survival post decannulation was 37 months (range 7–46). Only one of these patients had a diagnosis of progressive bulbar palsy, the remainder had ALS. For patients who chose elective tracheostomy, an increase in survival of 10 months was demonstrated compared to those receiving emergency TV with known MND (34 vs. 24 months). This was further improved when compared to those who received emergency tracheostomy before a formal diagnosis of MND (34 vs. 22 months).