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Inducible laryngeal obstruction has been described under at least 40 different monikers, including vocal cord dysfunction, paroxysmal vocal fold motion, and irritable larynx. The etiology of this condition is believed to be laryngeal hyperactivity in response to psychological issues or acid reflux. Most patients are treated with some combination of proton pump inhibitors, speech therapy, and psychotherapy. However, a small cohort of patients remains refractory to all medical interventions. The authors describe a novel condition, hemi-laryngopharyngeal spasm (HELPS), which can cause severe episodic stridor leading to unconsciousness in association with cough. The first recognized and surgically cured patient with HELPS was reported in an earlier issue of this journal. Three additional patients have been followed up for at least a year postoperatively, and their cases are reported here. Each patient presented with a similar pattern of episodic coughing and choking that increased in frequency, severity, and duration over years. The episodes eventually occurred while sleeping and could cause severe stridor with loss of consciousness. All three patients were initially misdiagnosed with a psychiatric illness and subjected to multiple intubations and one tracheostomy. Unilateral botulinum toxin injections in the vocal fold eased the severity of the throat contractions but not the cough. Magnetic resonance imaging showed a looping posterior inferior cerebellar artery juxtaposed to a vagus nerve in each case. Microvascular decompression (MVD) of that vessel relieved all symptoms. The introduction of this new medical condition may help a small cohort of patients with inducible laryngeal obstructions that have not responded to the current standard treatments. Patients are asymptomatic between episodes of progressively severe coughing and choking with stridor that may lead to intubation. Severe anxiety about the unpredictable symptoms is expected and may contribute to a psychiatric misdiagnosis. Microvascular decompression for HELPS is more difficult than that for trigeminal neuralgia because the involved nerve is more susceptible to manipulation. Ultimately, the final proof that HELPS is a real and distinct syndrome will require its recognition and successful treatment by colleagues around the world.

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Oxidized low density lipoprotein (LDL) has been found to exhibit numerous potentially atherogenic properties, including transformation of macrophages to foam cells. It is believed that high density lipoprotein (HDL) protects against atherosclerosis by removing excess cholesterol from cells of the artery wall, thereby retarding lipid accumulation by macrophages. In the present study, the relative rates of HDL-mediated cholesterol efflux were measured in murine resident peritoneal macrophages that had been loaded with acetylated LDL or oxidized LDL. Total cholesterol content of macrophages incubated for 24 h with either oxidized LDL or acetylated LDL was increased by 3-fold. However, there was no release of cholesterol to HDL from cells loaded with oxidized LDL under conditions in which cells loaded with acetylated LDL released about one-third of their total cholesterol to HDL. Even mild degrees of oxidation were associated with impairment of cholesterol efflux. Macrophages incubated with vortex-aggregated LDL also displayed impaired cholesterol efflux, but aggregation could not account for the entire effect of oxidized LDL. Resistance of apolipoprotein B (apoB) in oxidized LDL to lysosomal hydrolases and inactivation of hydrolases by aldehydes in oxidized LDL were also implicated. The subcellular distribution of cholesterol in oxidized LDL-loaded cells and acetylated LDL-loaded cells was investigated by density gradient fractionation, and this indicated that cholesterol derived from oxidized LDL accumulates within lysosomes. Thus impairment of cholesterol efflux in oxidized LDLloaded macrophages appears to be due to lysosomal accumulation of oxidized LDL rather than to impaired transport of cholesterol from a cytosolic compartment to the plasma membrane. -Dhaliwal, B. S., and U. P. Steinbrecher. Cholesterol delivered to macrophages by oxidized low density lipoprotein is sequestered in lysosomes and fails to efflux normally.

Objectives: A patient is presented with neurogenic cough due to a unilateral vascular compression of a vagus nerve rootlet at the brainstem with complete resolution of cough following microvascular decompression of that nerve. This etiology of a neurogenic cough has not been previously reported to our knowledge. The proportion of patients with neurogenic cough refractory to all current therapies and suffering with this treatable condition remains to be defined. We introduce the concept of Vagus Associated Neurogenic Cough Occurring due to Unilateral Vascular Encroachment of its Root (VANCOUVER syndrome) and present the salient features of this condition. Methods: A case review is presented with details of the patient’s history, examination, imaging, laryngoscopy, intraoperative findings, and long-term clinical outcome. Results: A 60-year-old man presented with a 15-year history of non-productive cough refractory to antibiotics, and anti-reflux medications. Investigations by an allergist, a cardiologist, a gastroenterologist, two pulmonologists, and an otolaryngologist were negative. MRI demonstrated a vascular compression of his left vagus nerve and microvascular decompression of that nerve resolved his symptoms. There were no surgical complications and the patient remains asymptomatic at 1 year. Conclusions: Neurogenic cough has been likened to a vagus nerve neuropathy in a similar way that trigeminal neuralgia is a trigeminal nerve neuropathy. Both cause intermittent sensory phenomena in their distribution and can be ameliorated with neuropathic medications. We demonstrate that neurogenic cough, like trigeminal neuralgia, may be caused by a vascular compression of its nerve root. A proposed mechanism of this type of neurogenic cough is presented along with a potential diagnostic paradigm for these patients.