Due to problems with my 10 yr. old son and vns causing apnea I have copyed
and pasted this here for all to read. I sited all reports as they were published on
"MEDSCAPE from wed MD"
Cyberonics never acknowledged any of these studies being performed!

Epilepsia 2003 Dec;44(12):1588-91 (ISSN: 0013-9580)
Holmes MD; Miller JW; Voipio J; Kaila K; Vanhatalo S
Department of Neurology, Regional Epilepsy Center, University of Washington, Seattle, Washington, U.S.A. Department of Child Neurology, Hospital for Children and Adolescents Department of Biosciences, University of Helsinki, Helsinki, Finland.
Purpose: To study whether respiratory alteration caused by vagal nerve stimulation (VNS) can change end-tidal carbon dioxide (EtCO2) levels. Methods: We performed polygraphic recordings including capnographic monitoring during daytime sleep on adults with VNS therapy. Results: Ten of 13 patients showed VNS-induced alterations in the frequency or amplitude of respiration. Five patients had a consistent increase in respiratory rate with a simultaneous, consistent and significant decrease (p < 0.01; 5-22%) in EtCO2 during VNS. Three subjects showed occasional decreases in EtCO2 during VNS, and two showed no clearly detectable VNS-related EtCO2 changes. Conclusions: Our findings suggest that VNS may alter brain CO2 levels through changes in respiration. Because carbon dioxide (CO2) has potent effects on various brain functions, it is possible that these transient CO2 changes may have an effect on the state transitions between interictal and preictal states.
Language: English
MEDLINE Indexing Date: 200311
Publication Type: Owner: NLM
Publication Type: Journal Article
PreMedline Identifier: 0014636333
Journal Code: IM

ARTICLE # 2

Respiratory pattern changes in sleep in children on vagal nerve stimulation for refractory epilepsy.
Can J Neurol Sci 2003 Aug;30(3):224-7 (ISSN: 0317-1671)
Nagarajan L; Walsh P; Gregory P; Stick S; Maul J; Ghosh S
Department of Neurology, Princess Margaret Hospital for Children, PO Box D184, Perth,WA 6840, Australia.
BACKGROUND: An altered breathing pattern in sleep, over two to three weeks, reported by the parents of a child on Vagal Nerve Stimulation (VNS) therapy for refractory epilepsy, prompted a sleep study in him. His polysomnography (PSG) revealed respiratory irregularity concordant with VNS activation. Dyspnoea is a well recognised and reported side effect of the VNS. However there are only a few studies looking at respiration in sleep with VNS. We therefore undertook PSGs in seven other children on VNS. METHODS: Sleep studies were undertaken, in accordance with standard clinical practice. Sleep and apnoeas and hypopneas were scored in accordance with conventional criteria. Respiratory pattern changes in sleep (RPCS) with VNS were looked for. RESULTS: Respiratory pattern changes in sleep were seen during PSG in seven of eight children on VNS for refractory epilepsy. Decreased effort and tidal volume occurred in seven children, concordant with VNS activation. In one child, this was associated with a fall in respiratory rate, i the other six children with an increase. No study showed an apnoea/hypopnoea index in the abnormal range. The RPCS were not associated with significant hypoxia or hypercapnoea. CONCLUSION: Our results suggest that RPCS occur in most children with VNS. This is not surprising in view of the significant influence vagal afferents have on respiratory control centres. The RPCS did not appear to have a clinical impact in our group. However further investigations are suggested to explore this phenomenon, especially in patients with sleep apnoea syndromes or compromised respiratory function.
Major Subject Heading(s) Minor Subject Heading(s)
Electric Stimulation Therapy
Epilepsy [physiopathology] [therapy]
Respiratory Mechanics
Sleep
Vagus Nerve [physiopathology]
Adolescent
Child, Preschool
Child
Polysomnography
Tidal Volume
Work of Breathing


Indexing Check Tags: Female; Human; Male
Language: English
MEDLINE Indexing Date: 200309
Publication Type: Owner: NLM
Publication Type: Case Reports; Journal Article
PreMedline Identifier: 0012945946
Journal Code: IM

Here's another one I just found. FYI: BE AWARE I was told by cyberonics and my neuro that "they never heard of such problems".
And the next time you go to your NEURO, ask them if they own any stock in Cyberonics.

Effects of vagus nerve stimulation on sleep-related breathing in epilepsy patients.
Epilepsia 2003 Jul;44(7):930-5 (ISSN: 0013-9580)
Marzec M; Edwards J; Sagher O; Fromes G; Malow BA
Michael S. Aldrich Sleep Disorders Laboratory and the Epilepsy Program, Clinical Neurophysiology Section, Department of Neurology, University of Michigan Medical School, Ann Arbor, Michigan, U.S.A.
PURPOSE: To describe the effects of vagus nerve stimulation (VNS) on sleep-related breathing in a sample of 16 epilepsy patients. METHODS: Sixteen adults with medically refractory epilepsy (nine men, seven women, ages 21-58 years) underwent baseline polysomnograms (PSGs). Three months after VNS therapy was initiated, PSGs were repeated. In addition, patient 7 had a study with esophageal pressure monitoring, and patient 1 had a continuous positive airway pressure (CPAP) trial. RESULTS: Baseline PSGs: One of 16 patients had an apnea-hypopnea index (AHI) >5 (6.8). Treatment PSGs: Five of 16 patients had treatment AHIs >5. Respiratory events were more frequent during periods with VNS activation (on-time) than without VNS activation (off-time; p = 0.016). Follow-up studies: Esophageal pressure monitoring in patient 7 showed crescendos in esophageal pressure during VNS activation, supporting an obstructive pattern. The CPAP trial of patient 1 showed that all respiratory events were associated with VNS stimulation at low CPAP levels. They were resolved at higher CPAP levels. CONCLUSIONS: Treatment with VNS affects respiration during sleep and should be used with care, particularly in patients with preexisting obstructive sleep apnea. The AHI after VNS treatment remained <5 in the majority of patients and was only mildly elevated (<12) in five patients. In one patient, CPAP resolved VNS-related respiratory events.
Major Subject Heading(s) Minor Subject Heading(s) CAS Registry / EC Numbers
Epilepsy, Complex Partial [physiopathology]
Epilepsy, Generalized [physiopathology]
Myoclonic Epilepsy, Juvenile [physiopathology]
Polysomnography
Pulmonary Ventilation [physiology]
Vagus Nerve [physiopathology]
Adult
Airway Resistance [physiology]
Anticonvulsants [therapeutic use]
Combined Modality Therapy
Electric Stimulation Therapy [adverse effects] [instrumentation]
Epilepsy, Complex Partial [therapy]
Epilepsy, Generalized [therapy]
Follow-Up Studies
Middle Aged
Myoclonic Epilepsy, Juvenile [therapy]
Oxygen [blood]
Prostheses and Implants
Solitary Nucleus [physiopathology]
0 (Anticonvulsants)
7782-44-7 (Oxygen)


Indexing Check Tags: Female; Human; Male; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.
Language: English
MEDLINE Indexing Date: 200309
Publication Type: Owner: NLM
Publication Type: Journal Article
Grant ID: KO2 NS 02099
PreMedline Identifier: 0012823576
Journal Code: IM

:blink:
DBillin,
Thank you for this interesting test study. It is my opnion that reports like these will only help us to understand more about our nifty little bosom buddy. Doctors cannot possibly keep up with all the different kinds of reasearch and it is up to ourselves to be kept informed.
I welcome all types of reports and studies regarding the VNS and I will now place a new forum for them
Birdbomb B)

Horner syndrome associated with implantation of a vagus nerve stimulator.
Am J Ophthalmol 2001 Mar;131(3):383-4 (ISSN: 0002-9394)
Kim W; Clancy RR; Liu GT
Division of Neurology, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.

PURPOSE: To report a case of Horner syndrome that occurred after implantation of a vagus nerve stimulator. METHODS: Case report. RESULTS: A 6-year-old female with cerebral dysgenesis and intractable partial seizures presented with Horner syndrome after vagus nerve stimulator implantation. CONCLUSION: Horner syndrome can occur as a result of the vagus nerve stimulator implant procedure and should be included as one of its possible surgical complications.

HORNER'S SYNDROME
SIGNS AND SYMPTOMS
Horner's syndrome is characterized by an interruption of the oculosympathetic nerve pathway somewhere between its origin in the hypothalamus and the eye. The classic clinical findings associated with Horner's syndrome are ptosis, pupillary miosis and facial anhidrosis. Other findings may include apparent enophthalmos, increased amplitude of accommodation, heterochromia of the irides (if it occurs before age two), paradoxical contralateral eyelid retraction, transient decrease in intraocular pressure and changes in tear viscosity.
Horner's syndrome has no predilection for age, race, gender or geographic location. Horner's syndrome of congenital origin is typically around the age of two years with heterochromia and absence of a horizontal eyelid fold or crease in the ptotic eye. Iris pigmentation (which is under sympathetic control during development) is completed by the age of two, making heterochromia an uncommon finding in Horner's syndromes acquired later in life. Old photographs can aid the clinician in distinguishing congenital Horner's by documenting heterochromia present at, or near, birth.
PATHOPHYSIOLOGY
Sympathetic innervation to the eye consists of a three neuron arc. The first neuron originates in the hypothalamus. It descends and travels between the levels of the eighth cervical and forth thoracic vertebrae (C8-T4) of the spinal cord. There, it synapses with second order neurons whose preganglionic cell bodies give rise to axons. These axons pass over the apex of the lung and enter the sympathetic chain in the neck, synapsing in the superior cervical ganglion. Here, cell bodies of third order neurons give rise to postganglionic axons that course to the eye via the cavernous sinus. These sympathetic nerve fibers course anteriorly through the uveal tract and join the fibers of long posterior ciliary nerves to innervate the dilator of the iris. Postganglionic sympathetic fibers also innervate the muscle of Mueller within the eyelid, which is responsible for the initiation of eyelid retraction during eyelid opening. Postganglionic sympathetic fibers, responsible for facial sweating, follow the external carotid artery to the sweat glands of the face. Interruption at any location along this pathway (preganglionic or postganglionic) will induce an ipsilateral Horner's syndrome.

DBillin168,

Thank you for the research find. It is interesting reading.

Herb