Apologies for a lengthy article. Perhaps more attention should be given
to disturbance of the breathing stimulus mechanism in the sinus area.
I have ben asking about licdocaine neurological effects on
sci.med.dentistry and bionet.neuroscience.
Now I wonder whether lidocaine may affect a person with a tendency to
multiple sclerosis in the breathing centre, perhaps, then sleep apnea
could set in and produce more nerological symptoms.
Or the dental work might produce disturbance in the sinus which could
reduce breathing stimulus.
My left nostril gets a bit more blocked with pressure since an upper big
molar root canal. Now it is 6 days since and I woke with a more blocked
nostril than before. It has cleared a bit.
I have been having some of the neurological troubles mentioned by
stigmata1, but they have been clearing a bit since the root canal. The
dentist found a fair bit of pus under the root dressing which had been in
for a month.
Brian Sandle
***********************
Sleep Apnea
Author: prepster <prepster at mindspring.com>
Date: 1999/01/14
Forum: alt.support.sleep-disorder
I have had Sleep Apnea for a while and only recently took action on it. My
doctor says he wants to correct a deviated nasal septum, remove my tonsils
and do an UPPP.
I refuse to do the UPPP; it is painful with side effects and has a low
success rate...comments? Would it also help to have my adenoids removed?
**********************
Re: Chronic Pain Down Right since April
Author: Barry Kaplan <kaplanfamily at worldnet.att.net>
Date: 1998/12/22
Forums: alt.support.chronic-pain, alt.med.fibromyalgia
more headers author posting history prev next
_________________________________________________________________
Dave,
What did they fill the root canal with?
The most common root canal filling material is called "gutta percha" and it
is fairly innocuous.
In years past, two other materials were used. One is called "silver
points". They are not good, but they shouldn't cause the pain you are
reporting. They just corrode over time.
The other material that is out of favor is called "sargenti paste" This
stuff can be real bad news. I have heard of syptoms similar to yours, but
not NEARLY as bad nor widespread in distribution.
However, it is also possible that the thing causing the pain may not have
been of dental origin. The distribution of the nerves in the mouth has
nothing to do with the nerves in your arm and leg. If you reported the pain
and tic only in your face, I might suspect things like trigeminal neuralgia
(tic Douluoroeux).
I know you said you saw 23 doctors, but there are two things you need to be
certain to do (if you haven't already). First of all, I would make sure I
had a second opinion onthe root canal by a board certified endodontist (root
canal specialist)
Secondly, you might consider seeing a neurologist about your other
complaints.
It is possible that the tooth you had the root canal done on may not have
been the problem. I have never seen mouth pain refer farther than the
sinuses or neck. You may have had a different problem to begin with.
There are at least two physicians that often respond to posts an this
newsgroup. Hopefully Mike, Todd ,and anyone else with anything to add will
pipe up
Barry (DDS)
stigmata1 at hotmail.com wrote in message <75p0a9$tug$1 at nnrp1.dejanews.com>...
>I hope there's an answer! In April of 1998 I went to get some routine
dental
>work done, and found that I required a root canal, which I assented to.
>Almost immediately after the procedure, I started experiencing excrutiating
>pain in that tooth, which seemed to inflame the entire right side of my
face.
>It was so bad I wanted to be knocked out and have it removed on site.
>However, since I'm 23 all doctors advised me against removal and assured me
>that within a month the pain would subside. Well, the pain became so bad
>twice that I went to the emergency room because I couldn't take it, and
they
>gave me Percocet, Which I ended up being on for about two months. During
this
>time period, I started feeling a burning pain sensation "creeping" down my
>arm and my leg, as well as the already established pain in my face, eye,
>saggital plan, which led to a facial tic that I have to this day. But as
this
>pain started creeping down my extremities, I found it more and more
difficult
>to move my hand and my foot, writing was very difficult, I had trouble
>holding the pen. Gradually, the excruciating pain gave way to a lesser
pain,
>and I was moved off of Percocet down to Hydrocodone, Then just OTC pain
>relievers. I'm not lying prostrate in pain anymore, but I still have a
>constant, low level pain that's down the right side of my body. When I sigh
>or yawn or exhale deeply, I feel "bolts" of pain race down my right arm
until
>it 'hits' at the tips of the fingers. I also experience a phenomenon
when I
>hold my computer mouse, where my right hand will get 'cold shots' all over
>the top of my hand when surrounding the mouse. There seem to be pain focal
>points at the top of my spine and the bottom, and I feel the pain connected
>and start to run down what feels like the center of my leg and arm where
the
>limb is subumerged in a burning sensation. Anyone know what this is, how it
>came about, and the cure?
>>Any answers appreciated,
>>Dave Canova,
>stigmata1 at hotmail.com>*********************
Neurology 1992 Nov;42(11):2088-93
Lidocaine unmasks silent demyelinative lesions in multiple sclerosis.
Sakurai M, Mannen T, Kanazawa I, Tanabe H
Department of Neurology, School of Medicine, University of Tokyo,
Japan.
Blockage of a small number of sodium channels may prevent impulse
conduction in some demyelinated segments of nerve fibers with low
safety factors, thereby unmasking subclinical demyelinative lesions.
On the basis of this hypothesis, lidocaine, a sodium channel blocker,
was administered intravenously to 28 MS patients and to 19 normal
subjects and seven patients with nondemyelinating diseases. As
predicted, lidocaine (mean plasma level, 2.7 micrograms/ml) elicited
reversible subclinical symptoms in 23 of the MS patients, but it had
not effect on the control subjects. We made a quantitative study of
the visual functions (visual acuity, color vision, visual evoked
potential [VEP]) that were impaired in 15 MS patients. Of the 23
affected eyes, nine showed normal VEPs, indicative of the test's
sensitivity to focal lesions. This test should be useful in the
diagnosis of MS and in the evaluation of the subclinical activity of
MS as well.
PMID: 1331868, UI: 93063903
Masui 1998 May;47(5):570-5
[Midazolam for anesthetic induction in neonates].
[Article in Japanese]
Kawakami K, Ohata J, Kadosaki M, Saito I, Iwasawa K, Mitono H
Department of Anesthesiology, Nagano Children's Hospital.
The purpose of this study is to evaluate the effects of midazolam on
circulation, respiration, sedation, and liver function of the
neonates. The study subjects are 27 neonates (body weight 2.1 to 3.8
kg, gestational age at birth 34 to 41 weeks) who underwent surgery in
neonatal period. Of 27, 13 patients received lidocaine (1.5 mg.kg-1)
immediately before tracheal intubation (group L), and 14 had
midazolam (0.1 mg.kg-1) with lidocaine (group ML). We compared the
effects of midazolam in the presence of lidocaine on the following
parameters: (1) the incidence of hypotension (systolic blood pressure
< 50 mmHg) and bradycardia (heart rate < 100 beats.min-1), (2) the
incidence of apnea and desaturation of oxygen (< 80%), (3) the degree
of sedation, and (4) the serum levels of bilirubin and unbound
bilirubin after surgery. In group L, there were hypotension (1/13)
and desaturation (1/13). In group ML, there were desaturation (1/14)
and post-operative apnea (1/14). None in both groups developed
bradycardia or intracranial hemorrhage. A single-dose of lidocaine
induced sedation only in 4 neonates, while combination of midazolam
and lidocaine in 11. None had elevation of either total or unbound
bilirubin after surgery. In conclusion, the titrated dose of
midazolam with lidocaine is useful for anesthetic induction of
neonates, although cares should be taken on its adverse effects such
as hypotension, desaturation, and post-operative apnea.
Publication Types:
* Clinical trial
PMID: 9621667, UI: 98284687
_________________
Anesthesiology 1998 Mar;88(3):761-7
Hypoxia causes apnea during epidural anesthesia in rabbits.
Hogan QH, Amuzu J, Clifford PS, Bosnjak ZJ, Kampine JP
Department of Anesthesiology, Medical College of Wisconsin and the
Zablocki Veterans Administration Medical Center, Milwaukee 53226,
USA.
BACKGROUND: Although pulmonary function is minimally changed by
neuraxial blockade in most cases, ventilatory arrest may ensue in
rare cases. The authors examined the mechanism of apnea in a rabbit
model of sudden ventilatory arrest during the combination of epidural
anesthesia and hypoxia. METHODS: Rabbits were studied during
alpha-chloralose sedation and spontaneous ventilation through a
tracheostomy tube. Heart rate and mean arterial pressure were
monitored by intraarterial cannulation. Respiratory rate and tidal
volume were measured by pneumotachograph. Responses were recorded
during administration of oxygen at inspired oxygen concentrations of
11% for 2.5 min and 0% for 40 s, before and after either
thoracolumbar epidural blockade (0.4 ml/kg lidocaine, 1.5%) or
intramuscular lidocaine (15 mg/kg). In a third group of animals,
epinephrine was given intravenously during epidural blockade to
return mean arterial pressure to baseline values before hypoxia. In a
fourth group of animals, which did not get lidocaine, sympathetic
blockade and hypotension were produced with intravenously
administered trimethaphan rather than epidural blockade. RESULTS:
Thoracolumbar epidural anesthesia decreased mean arterial pressure
from 76 +/- 4 mmHg (mean +/- SE) to 42 +/- 2 mmHg. Apnea during
hypoxia occurred in 90% of these animals (nine of ten) but in only
11% of animals (one of nine) after intramuscularly administered
lidocaine (P < 0.01). Treatment of epidural hypotension with
epinephrine prevented apnea (zero of nine animals). Apnea during
hypoxia occurred in 50% (three of six) of animals given trimethaphan.
Apnea in all groups was sudden in onset, with no preceding decreases
in respiratory rate or tidal volume. CONCLUSIONS: Epidural anesthesia
results in a narrowed margin of safety for oxygen delivery to the
brain and predisposes subjects to ventilatory arrest during hypoxia.
This results from the combined effects of decreased blood oxygen
content, which is due to decreased inspired oxygen concentration
superimposed on circulatory depression due to neural blockade.
PMID: 9523821, UI: 98181995
Am J Respir Crit Care Med 1995 Jun;151(6):1857-61
Effect of upper airway anesthesia on obstructive sleep apnea.
Berry RB, Kouchi KG, Bower JL, Light RW
Department of Medicine, Long Beach VA Medical Center, CA 90822, USA.
We hypothesized that upper airway mechanoreceptors contribute to the
arousal stimulus that occurs with upper airway occlusion in
obstructive sleep apnea (OSA). If so, upper airway anesthesia (UAA)
should reduce the arousal stimulus and impair the arousal response.
To test this hypothesis, we studied the effects of UAA on apnea
duration and the esophageal pressure deflection before arousal in a
group of patients with severe OSA. On two study nights separated by
one week, subjects were monitored for 2 h after lights out. They were
then awakened and either 5 cc of 4% lidocaine or saline (random
order) was dripped into the upper airway via the nose over 10 min.
Another 2 h of monitoring was then performed. Variables on the first
and second parts of the control (C1 and C2) and lidocaine nights (L1
and L2) were compared during non-rapid eye movement sleep using the
analysis of variance. With lidocaine, the mean (+/- SEM) apnea
duration increased from 24.2 +/- 2.6 (L1) to 30.7 +/- 2.3 (L2) s but
with saline the apnea length was unchanged from 23.3 +/- 1.5 (C1) to
23.4 +/- 1.6 (C2) (L2 > [L1, C1, C2], p < 0.01). In addition, the
maximum esophageal pressure deflection (cm H2O) before arousal
increased after lidocaine from 63.6 +/- 14.5 (L1) to 84.1 +/- 14.7
(L2) but after saline was unchanged from 62.1 +/- 15.4 (C1) to 60.0
+/- 15.2 (C2), (L2 > [L1, C1, C2], p < 0.05). We conclude that UAA
impairs the arousal response to airway occlusion. This suggests that
input from upper airway mechanoreceptors during obstructive events
contributes to the total arousal stimulus in patients with OSA.
Publication Types:
* Clinical trial
* Randomized controlled trial
PMID: 7767531, UI: 95285040
_____________________________________________________
Am J Respir Crit Care Med 1995 Apr;151(4):1108-12
Topical oropharyngeal anesthesia in patients with obstructive sleep apnea.
Deegan PC, Mulloy E, McNicholas WT
Department of Respiratory Medicine, University College, Dublin,
Ireland.
Topical oropharyngeal anesthesia (TOPA) increases obstructive sleep
apnea (OSA) frequency in both normal subjects and loud snorers. The
effects of TOPA in established OSA were assessed in six male patients
with a mean age (+/- SEM) of 50 +/- 5.3 yr. Following an
acclimatization night, each subject underwent two overnight sleep
studies, randomly assigned to TOPA (10% lidocaine spray and 0.25%
bupivocaine gargle) and control (C) (saline placebo). Patients
demonstrated sleep efficiencies of 93 +/- 2.9% (mean +/- SEM) during
C and 88 +/- 2.9% during TOPA. Overall apnea-hypopnea (AH) frequency,
using inductance plethysmography, showed little change: 21.2 +/- 3.6
on C versus 25.1 +/- 3.5 events/h on TOPA nights (p = 0.12). There
was no significant increase in AH duration with TOPA, and oxygen
desaturation (> or = 4%) frequency was similar: 21.1 +/- 3.9 per hour
during TOPA versus 23.6 +/- 5.9 during C. However, obstructive AHs
showed a change in thoracoabdominal motion from C to TOPA nights,
with an increase in events with abdominal paradox from 3.1 +/- 1.1 to
10.3 +/- 3.1 per hour (p = 0.03), and a reduction in events with
ribcage paradox from 13.1 +/- 1.6 to 8.2 +/- 2.4 per hour (p = 0.08).
Central and mixed AHs demonstrated similar frequencies on both
nights. These data support an impairment of upper airway (UA)
protective reflexes among patients with OSA.
Publication Types:
* Clinical trial
* Randomized controlled trial
PMID: 7697239, UI: 95211324
Brain Res 1991 Sep 27;560(1-2):321-5
Trigeminal mediation of the diving response in the muskrat.
Panneton WM
Department of Anatomy and Neurobiology, St. Louis School of Medicine,
MO 63104.
Stimulation of the nasal cavity elicits powerful cardiorespiratory
responses similar to the diving response. In the present study,
bradycardia and apnea were elicited in muskrats by stimulation of the
nasal cavity with ammonia vapors. These responses could be blocked by
injections of 2% lidocaine made bilaterally into the medullary dorsal
horns of the trigeminal sensory complex. However, the bradycardia due
to activation of the baroreceptor reflex with intravenous
phenylephrine was retained. These data implicate trigeminal neurons
in the medullary dorsal horn as modulators of autonomic activity,
especially in the cardiorespiratory adjustments after nasal
stimulation.
PMID: 1760738, UI: 92103521
________________________________________________________________
Other Formats: [Citation Format] [MEDLINE Format]
Links: [114 medline neighbors]
Am Rev Respir Dis 1991 Apr;143(4 Pt 1):810-3
Obstructive sleep apnea following topical oropharyngeal anesthesia in loud
snorers.
Chadwick GA, Crowley P, Fitzgerald MX, O'Regan RG, McNicholas WT
Department of Respiratory Medicine, University College, Dublin,
Ireland.
Previous studies support the presence of an upper airway reflex
mechanism that contributes to the maintenance of upper airway patency
during sleep. We investigated the possibility that interference with
this reflex mechanism contributes to the development of obstructive
sleep apnea. Eight otherwise asymptomatic snorers (seven male and one
female), age 39 +/- 5.3 yr (mean +/- SEM), underwent overnight sleep
studies on three successive nights. An acclimatization night was
followed by two study nights randomly assigned to control (C) and
oropharyngeal anesthesia (OPA). On the OPA night topical anesthesia
was induced using 10% lidocaine spray and 0.25% bupivacaine gargle. A
saline placebo was used on night C. All subjects slept well on both
study nights (mean sleep duration was 6.2 h on both study nights),
and sleep stage distribution was similar on both nights. Obstructive
apneas and hypopneas (OAH) rose from 114 +/- 43 during C to 170 +/-
49 during OPA (p less than 0.02). Central apneas and hypopneas (CAH)
were unchanged between the two nights (8 +/- 4.9 versus 7 +/- 3). The
duration of OAH was similar on both study nights (20 +/- 1.9 s during
C versus 20 +/- 1.5 s during OPA). The frequency of movement arousals
terminating OAH tended to be higher during OPA (7 +/- 2.9/h) than
during C (3 +/- 0.7); P = NS. The frequency of oxyhemoglobin
desaturations was also higher during OPA (5 +/- 2.1/h) than during C
(3 +/- 1.4), p less than 0.07.
PMID: 2008992, UI: 91181783
________________________________________________________________
Other Formats: [Citation Format] [MEDLINE Format]
Links: [109 medline neighbors]
Am Rev Respir Dis 1985 Nov;132(5):972-5
The effects of nasal anesthesia on breathing during sleep.
White DP, Cadieux RJ, Lombard RM, Bixler EO, Kales A, Zwillich CW
Inability to breathe through the nose is an increasingly recognized
cause of disordered breathing during sleep. To test the hypothesis
that this respiratory dysrhythmia could result from loss of neuronal
input to respiration from receptors located in the nose, we
anesthetized the nasal passages of 10 normal men during sleep. Each
subject spent 4 consecutive nights in the sleep laboratory while
sleep stages, breathing patterns, respiratory effort, and arterial
oxygen saturation were monitored. Night 1 was for acclimatization
with Nights 3 and 4 being randomized to nasal spraying with either 4%
lidocaine or placebo. On the lidocaine and placebo nights (Nights 3
and 4) the nasal passages were also sprayed with a decongestant to
prevent increased nasal air-flow resistance resulting from mucosal
swelling. To control for the possible effects of this decongestant,
an additional night (Night 2) was included during which the nasal
passages were sprayed with room air. Parallel studies conducted
during wakefulness demonstrated low nasal resistance during the
lidocaine-decongestant regimen. Because of the short duration of
anesthesia with lidocaine, spraying was done at lights out and 2.5
and 5 h later. On the placebo night (decongestant plus saline) there
were 6.4 +/- 1.8 (SEM) disordered breathing events (apneas plus
hypopneas) per subject, whereas with lidocaine (plus decongestant)
this increased fourfold to 25.8 +/- 7.8 events per subject (p less
than 0.05). The majority of the disordered breathing events were
apneas and were fairly evenly distributed between central and
obstructive events. The magnitude of these changes is similar to that
previously reported with complete nasal obstruction. These results
suggest that nasal receptors sensitive to air flow may be important
in maintaining breathing rhythmicity during sleep.
Publication Types:
* Clinical trial
* Randomized controlled trial
PMID: 4062052, UI: 86048887 this document
Am J Perinatol 1987 Apr;4(2):164-6
Lidocaine toxicity after maternal pudendal anesthesia in a term infant with
fetal distress.
Bozynski ME, Rubarth LB, Patel JA
There have been many reports of lidocaine toxicity especially after
maternal paracervical block anesthesia. We recently treated a term
infant with evidence of fetal distress who presented with symptoms of
lidocaine toxicity after maternal pudendal anesthesia. The infant
developed apnea and bradycardia soon after birth which responded to
mechanical ventilation and epinephrine. A prolonged Q-T interval was
noted on day 1 which normalized by day 3. Cord blood was assayed and
revealed an elevated lidocaine level. Lidocaine toxicity has been
associated with fetal distress secondary to fetal ion trapping in the
presence of acidosis. Although good response to supportive therapy
occurred in our patient, other methods of therapy such as exchange
transfusion and treatment of seizures may be required in some cases.
Awareness of this now uncommon syndrome will lead to prompt
diagnosis, appropriate work-up, and management.
PMID: 3566884, UI: 87184830
________________________________________________________________
Other Formats: [Citation Format] [MEDLINE Format]
Links: [169 medline neighbors]
Am J Physiol 1977 Jul;233(1):R30-6
Properties of the laryngeal chemoreflex in neonatal piglets.
Lee JC, Stoll BJ, Downing SE
Cardiorespiratory reflex responses to laryngeal chemoreceptor
stimulation were studied in 62 piglets of both sexes varying in age
from 1 to 79 days. The distal trachea was cannulated to provide a
free airway and the proximal end used to introduce fluids into the
laryngeal area. Introduction of either water or milk produced apnea,
bradycardia, and hypertension. Swab application of test fluids to the
laryngeal epithelium produced similar responses. The reflex could be
interrupted by flushing the laryngeal region with saline, by cutting
the superior laryngeal nerves (SLN) or by anesthetizing the laryngeal
epithelium with lidocaine. Electrical stimulation of SLN elicited
identical responses. Respiratory inhibition by the reflex was
enhanced following central depression with chloralose and overridden
by administration of the respiratory stimulant, aminophylline. The
relative potency of the laryngeal reflex was estimated to be
equivalent to about 40% of the dose of chloralose which produced
permanent respiratory arrest. It is concluded that in circumstances
where respiratory drive is reduced the laryngeal inhibitory reflex is
capable of caused persistent apnea and asphyxial death in the young
piglet.
PMID: 18025, UI: 77219523
________________________________________________________________
Other Formats: [Citation Format] [MEDLINE Format]
Links: [102 medline neighbors]
Rev Bras Pesqui Med Biol 1976 Dec;9(5-6):229-37
Lethal effect of the serotonin-xylocaineR association in ganglion-blocked
rats.
Valle LB, Oliveira-Filho RM, Armonia PL, Saraceni G Jr, Nassif M, De
Lucia R
In rats anestetized with urethane and under ganglionic blockade by
hexamethonium (20 mg/kg, i.v.), the i.v. injection of serotonin (60
mug/kg) determined apnea, ECG alterations and a brief hypotensive
response which is similar to that as elicited when 5-HT is given to
intact rats. During the hypertension which follows that initial
response, apnea is still present along with more severe ECG changes.
After that, blood pressure falls into a prolonged hypotension, which
is invariably accompanied by death. Neither norepinephrine, nor
respiratory analeptics (CoramineR, RemeflinF) were able to prevent
the fatal outcome. Only artificial respiration was found to be useful
in some instances. It was concluded that the association serotonin
plus lidocaine becomes lethal when given to ganglion-blocked rate,
and this toxic effect can be ascribed mainly to the respiratory
depressor activity of the drugs.
PMID: 1013401, UI: 77103742
___________________________
Z Orthop Ihre Grenzgeb 1974 Oct;112(5):1053-62
