The following file is the result of a 11/95 search on the MEDLINE database
with the key words 'Vagus nerve stimulator epilepsy'.
 
MEDLINE is the US National Institute of Health searchable database of
medical publications from around the world. There are more than 7.5 million
citations, from over 4000 medical journals. Over 50% of the citations
include abstracts. No full text documents are available. 
 
A guide with information on accessing MEDLINE through various providers (it
is not free) is available on the WWW at
http://www.sils.umich.edu/~nscherer/Medline/MedlineGuide.html
 
A biomedical subset of MEDLINE is provided for free by the National Center
for Biotechnology Information located at
http://www3.ncbi.nlm.nih.gov/Entrez/. There is little clinical information,
but it provides a good demonstration of the database.
 
 
Further infor regarding vagal nerve stimulation can be gotten from Cyberon
Corporation, Mr. Shawn Lunney, 713-332-1375 x233
 
He indicated all US Studies are full, but 15-20 European countries do this 
implant.
 
 
The Greatful Med search of the National Library of Medicine showed the
following:
 
 
1
Murphy JV; Hornig G; Schallert G
Left vagal nerve stimulation in children with refractory 
epilepsy. Preliminary observations.
Section of Neurology, Children's Mercy Hospital, Kansas City, Mo., USA.
Arch Neurol 1995 Sep;52(9):886-9
Unique Identifier: MEDLINE 95390831
 
Abstract: 
 
OBJECTIVE: To observe the tolerance and efficacy of periodic left
vagal nerve stimulation in a group of children with medically
intractable epilepsies. DESIGN: A vagal nerve stimulator
(Cyberonics Inc, Webster, Tex) was implanted in 12 children with
medically and surgically refractory epilepsies. These children
were followed up for 2 to 14 months. OUTCOME MEASUREMENTS: (1)
The number of seizures recorded during the final month of
observation was compared with the number recorded during the
month before the implantation of the vagal nerve stimulator. (2)
Parents were asked to compare overall status of their child,
relative to the period prior to using the vagal nerve stimulator,
on a global rating scale. (3) The number of antiepileptic drugs
at the last visit was compared with the number before the use of
this device. (4) Adverse events were recorded. RESULTS: Five of
the 12 patients had a greater than 90% reduction in the number of
monthly seizures. Global evaluation scores indicated that there
were no deteriorations from baseline and that there was a
considerable number with improved status. Four patients were able
to reduce the number of antiepileptic drugs used. No significant
adversities were noted. CONCLUSIONS: The vagal nerve stimulator
is well tolerated in children with intractable epilepsies, and it
may have a role in their medical management. We were unable to
determine specific epilepsies or seizures that were sensitive to
this intervention.
 
2
Koeze TH
Neuromodulation for pain and epilepsy.
Academic Unit of Neurosurgery, London Hospital Medical College, UK.
REVIEW ARTICLE: 75 REFS.
Baillieres Clin Neurol 1995 Apr;4(1):167-83
Unique Identifier: MEDLINE 95360401
 
3
A randomized controlled trial of chronic vagus nerve stimulation 
for treatment of medically intractable seizures. The Vagus 
Nerve Stimulation Study Group.
Neurology 1995 Feb;45(2):224-30
Unique Identifier: MEDLINE 95157736
 
Abstract: 
 
Preliminary reports have suggested that chronic, intermittent
stimulation of the vagus nerve (VNS) is an alternative treatment
for patients with medically refractory seizures. We performed a
multicenter, randomized, controlled trial to evaluate the
efficacy and safety of adjunctive VNS in patients with poorly
controlled partial seizures. An implanted, programmable
pacemaker-like device was connected to two stimulating electrodes
wrapped around the left vagus nerve. One hundred fourteen
patients were randomized to receive 14 weeks of high-level
stimulation (presumed therapeutic dose) or low-level stimulation
(presumed subtherapeutic dose) using a blinded, parallel study
design. Seizure frequency was compared with a 12-week baseline.
Mean reduction in seizure frequency was 24.5% for the high
stimulation group versus 6.1% for the low stimulation group (p
= 0.01). Thirty-one percent of patients receiving high
stimulation had a seizure frequency reduction of > or = 50%,
versus 13% of patients in the low group (p = 0.02). Treatment
emergent side effects were largely limited to a transient
hoarseness occurring during the stimulation train. One patient
with no previous history of cardiac disease experienced a
myocardial infarction during the third month of vagal
stimulation. VNS may be an effective alternative treatment for
patients who have failed antiepileptic drug therapy and are not
optimal candidates for epilepsy surgery.
 
4
Friedman M; Wernicke JF; Caldarelli DD
Safety and tolerability of the implantable recurrent laryngeal 
nerve stimulator.
Department of Otolaryngology and Bronchoesophagology, Rush 
Medical College, Rush-Presbyterian-St. Luke's Medical Center, 
Chicago, IL 60612.
Laryngoscope 1994 Oct;104(10):1240-4
Unique Identifier: MEDLINE 95020291
 
Abstract: 
 
The recurrent laryngeal nerve (RLN) stimulator has been implanted
on a limited basis since 1988 for control of spasmodic dysphonia.
A similar vagus nerve stimulator has been implanted in a larger
series of patients to control epilepsy. The safety and
tolerability of these two stimulators were evaluated. In 113
patients implanted with the vagus nerve stimulator, the
complication rate was 0.9%. All patients were monitored for vital
signs, electrocardiographic changes, and adverse effects. The
absence of changes in vital signs and electrocardiograms during
vagal stimulation establishes the safety of this treatment. Since
placement of the electrode around the vagus nerve is an easier
surgical technique than placement deep to the RLN, it seems
reasonable to change the technique to implant the stimulator on
the vagus in patients with spasmodic dysphonia.
 
5
Michael JE; Wegener K; Barnes DW
Vagus nerve stimulation for intractable seizures: one year follow-up.
Baylor College of Medicine, Department of Otolaryngology, 
Houston, Texas 77030.
J Neurosci Nurs 1993 Dec;25(6):362-6
Unique Identifier: MEDLINE 94149389
 
Abstract: 
 
Even with the best health care available, many patients with
epilepsy still suffer from poorly controlled seizures. Patients
with intractable partial seizures are often inhibited from
realizing their full potential and may experience a less than
optimal quality of life. Vagus nerve stimulation (VNS) is being
studied in a double-blind, controlled, randomized trial at 17
epilepsy centers throughout the U.S. and Europe as a potential
therapy for patients with refractory seizures. During a 14-week
controlled phase in three of the centers, the therapeutic group
(N = 10) experienced a mean seizure frequency percent reduction
(SFPR) of 33.1% as compared to baseline (p = 0.0084) while the
subtherapeutic group (N = 12) experienced an SFPR of 0.6% as
compared to baseline (p = 0.9183). After the controlled phase,
all patients were switched into the therapeutic group in an open
extension phase. Results after one year of therapeutic
stimulation (N = 15) reveal a mean SFPR of 35.6% (p = 0.0088)
with 6 of the 15 patients (40%) achieving at least a 50% seizure
reduction. Adverse effects included hoarseness, coughing and
nausea. There were no deaths or serious injuries related to the
device. Based on these limited data, VNS appears to be a safe and
efficacious new therapy for refractory partial seizures.
 
6
McLachlan RS
Suppression of interictal spikes and seizures by stimulation 
of the vagus nerve.
Department of Clinical Neurological Sciences, University 
of Western Ontario, London, Canada.
Epilepsia 1993 Sep-Oct;34(5):918-23
Unique Identifier: MEDLINE 94008874
 
Abstract: 
 
The effects of electrical stimulation of the vagus nerve, a
proposed treatment for patients with intractable epilepsy, on
focal interictal spikes produced by penicillin and EEG
secondarily generalized seizures induced by pentylenetetrazol
were assessed in rats. Interictal spike frequency was reduced by
33% during 20 s of stimulation (p < 0.001) and remained low for <
or = 3 min. Amplitude of residual spikes was also decreased.
Cardiac and respiratory rates were suppressed. Cooling the nerve
proximal to the point of stimulation abolished the EEG and
respiratory effects. A similar reduction in spike frequency of
39% was obtained by heating the animals' tail (p < 0.01). Vagal
stimulation at onset of seizures reduced mean seizure duration
from 30.2 +/- 15.7 s without stimulation to 5.0 +/- 1.8 s (p <
0.01). Only the EEG equivalent of the clonic phase of the seizure
was affected. These findings suggest that vagus nerve stimulation
can be a potent but nonspecific method to reduce cortical
epileptiform activity, probably through an indirect effect
mediated by the reticular activating system.
 
7
Uthman BM; Wilder BJ; Penry JK; Dean C; and others
Treatment of epilepsy by stimulation of the vagus nerve.
Neurology Service, Veterans Administration Medical Center, 
Gainesville, FL 32608-1197.
Neurology 1993 Jul;43(7):1338-45
Unique Identifier: MEDLINE 93317190
 
Abstract: 
 
We treated 14 patients with medically refractory partial seizures
by stimulation of the vagus nerve in two single-blind pilot
studies. Patients received stimulation through an implantable,
programmable NeuroCybernetic Prosthesis, consisting of a pulse
generator and a lead-electrode assembly. The mean reduction in
seizure frequency after 14 to 35 months of vagal stimulation was
46.6%. Of the 14 patients, five (35.7%) had a 50% or greater
reduction in seizure frequency. Two patients, one of whom had had
10 to 100 seizures per day before stimulation, have been
seizure-free for over 1 year. Adverse events were primarily
limited to initial hoarseness and a tingling sensation at the
electrode site in the neck when the device was activated. Most
patients tolerated the device and stimulation well. There were no
permanent adverse events. Some cases of medically refractory
partial seizures are improved by vagal stimulation.
 
8
Tougas G; Hudoba P; Fitzpatrick D; Hunt RH; Upton AR
Cerebral-evoked potential responses following direct vagal 
and esophageal electrical stimulation in humans.
Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Am J Physiol 1993 Mar;264(3 Pt 1):G486-91
Unique Identifier: MEDLINE 93212826
 
Abstract: 
 
Cerebral evoked responses following direct electrical stimulation
of the vagus and esophagus were compared in 8 epileptic subjects
and with those recorded after esophageal stimulation in 12
healthy nonepileptic controls. Direct vagal stimulation was
performed using a left cervical vagal pacemaker, which is used in
the treatment of epilepsy. Esophageal stimulation was obtained
with the use of an esophageal assembly incorporating two
electrodes positioned 5 and 20 cm orad to the lower esophageal
sphincter. Evoked potential responses were recorded with the use
of 20 scalp electrodes. The evoked potential responses consisted
of three distinct negative peaks and were similar with the use of
either vagal or esophageal stimulation. The measured conduction
velocity of the afferent response was 7.5 m/s in epileptic
subjects and 10 m/s in healthy controls, suggesting that afferent
conduction is through A delta-fibers rather than slower C
afferent fibers. We conclude that the cortical-evoked potential
responses following esophageal electrical stimulation are
comparable to direct electrical stimulation of the vagus nerve
and involve mostly A delta-fibers. This approach provides a
method for the assessment of vagal afferent gastrointestinal
sensory pathways in health and disease.
 
9
McIntosh S; Da Costa D; Kenny RA
Outcome of an integrated approach to the investigation of 
dizziness, falls and syncope in elderly patients referred 
to a 'syncope' clinic [see comments]
Department of Geriatric Medicine, Royal Victoria Infirmary, 
Newcastle upon Tyne.
Age Ageing 1993 Jan;22(1):53-8
Unique Identifier: MEDLINE 93175257
Comment in: Age Ageing 1993 Sep;22(5):391
 
Abstract: 
 
Sixty-five consecutive elderly patients (mean age 78 years)
referred to a 'syncope' clinic over a six-month period were
prospectively studied. Initial evaluation included ambulatory
electrocardiography, carotid sinus massage before and after
atropine and prolonged head-up tilt. Diagnostic criteria for
causes of syncope were assigned at the beginning of the study.
Overall, a diagnosis was attributed to symptoms in 92% of
patients; overlap was present in a quarter. Diagnoses were
cardioinhibitory carotid sinus syndrome (CSS; 5%), vasodepressor
CSS (26%), mixed CSS (14%), orthostatic hypotension (32%),
vasodepressor vasovagal syncope (11%), cardiac arrhythmia (21%),
epilepsy (9%), cerebrovascular disease (6%) and others (12.5%).
Sixty per cent of patients with vasodepressor CSS also had
orthostatic hypotension or vasodepressor vasovagal syncope
suggesting a common aetiology. Using an integrated approach
incorporating head-up tilt and carotid sinus massage in a
selected group of elderly patients referred to a 'syncope'