🚀 go-pugleaf

Brian Sandle (bsandle@southern.co.nz) wrote:
: 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@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@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.

I've had & do have pain from the top of the back of my neck all the way
down to my toes.  As far as I can tell, this is caused by 'slipping' in
the relationship between my mandible and maxilla as when they 'slip' back
into place, the pain immediately goes away.  Feels like a joint problem at
the top of the back of my neck.  the original injury was from 30 minutes
in an orthodontic surgeon's chair with my mouth open entirely too wide so
that he could excise my wisdom teeth.  The ligaments streeetch too much.
Been loose every since.  I'm not blaming the doc - I'm sure he had to open
my mouth that wide.

The point:  a person may develop some weird compensatory postures to pain
that may cause more pain or pain in differnent places.  

:  
: 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@hotmail.com wrote in message <75p0a9$tug$1@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@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
:                               

--

sdoggett@.kent.edu

In sci.med.dentistry Doggett Sheryl <sdoggett@f1n06.kent.edu> wrote:
: Brian Sandle (bsandle@southern.co.nz) wrote:
[...]
: : 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.

: I've had & do have pain from the top of the back of my neck all the way
: down to my toes.  As far as I can tell, this is caused by 'slipping' in
: the relationship between my mandible and maxilla as when they 'slip' back
: into place, the pain immediately goes away.  Feels like a joint problem at
: the top of the back of my neck.  the original injury was from 30 minutes
: in an orthodontic surgeon's chair with my mouth open entirely too wide so
: that he could excise my wisdom teeth.  The ligaments streeetch too much.
: Been loose every since.  I'm not blaming the doc - I'm sure he had to open
: my mouth that wide.

: The point:  a person may develop some weird compensatory postures to pain
: that may cause more pain or pain in differnent places.  

I have been looking into the physiology now.

(You might see it on dejanews with some of my other problems!) I reported 
a less sensitive patch under the left ear some while back. I thought it 
might be due to jaw clenching. Now with my facial troubles - possibly the 
fifth or facial nerve - I though that might be an extension of the under 
ear problem. But as far as I can work out at present from Gray's Anatomy 
the under ear nerve come from further down the spine and rises up the neck.

Now I have been gently stretching my neck and things feel a bit better. I 
think the careful stretch and rotation of it may even massage the nerve 
exits from the base of the skull for the fifth nerve too? The face feels a 
bit better.

There is still the pressure which appeared at the time after the roots 
were cleaned out and filler was pushed through the apex of the tooth. I 
am just wondering what effect that has on sleep.

Did I ask whether it is normal to breathe when clenching the jaw? That 
sort of pressure on the maxillo bone may be part of the whole complex 
mechanism of jaw clenching - tooth sharpening aggression. So pressure 
from a tooth on it may say to the nervous system not to breathe.

Then what does happen to the body in sleep? It will not repair so well.

I used to have my computer screen to one side. I had it like that for a 
long time. I did not have a trouble till the dental work. Maybe it is 
that the body is not repairing so well. Now I have shifted the screen 
more straight on. I liked turnign my spine to the left becuase it seemed 
to improved circulation to the left hip. Now I am wondering about such 
things as cerbrospinal pressure and supply to nerves where they exit from 
the spine all the way down. I wonder how much lidocaine would drop 
cerebrospinal pressure when in dental use?

In case there was infection I started using propolis. My chest pains have 
mostly receded. No mouth guard in use at night. I have reduced TV 
watching and orchestral cello playing has started again. It was rather 
uncomfortable for the first few days - only just possible, but maybe the 
movement of the arms helps pump blood around. It was good after a concert 
when I was palying forcefully for some time.

I suppose I will think of something else to say.

I am still wondering whether to keep the root canal molar.

I am to see a neurologist sometime. I wonder if he or she will persuade 
the dentist not to use any more dental injections on me.

Brian Sandle

In sci.med.dentistry Brian Sandle <bsandle@southern.co.nz> wrote:
: In sci.med.dentistry Doggett Sheryl <sdoggett@f1n06.kent.edu> wrote:
: : The point:  a person may develop some weird compensatory postures to pain
: : that may cause more pain or pain in differnent places.  

Does that happen in MS?

I have just had a complaint not to keep this thread on the multiple 
sclerosis newsgroup and that has reminded me of some things I meant 
to say.
 
Actually a week ago on New Zealand National Radio program `Future 
Indicative' (probably avaible via www) I learned of how a woman 
developed MS after an epidural anesthetic for back injury. That 
made me write about this again. But when I was writing the article 
the system failed and I forgot to include that next time, didn't I?
 
Though the MS - lidocaine test abstract stayed in.
 
As well as searching Medline
http://www.ncbi.nlm.nih.gov/PubMed/boolean.html
for multiple and sclerosis and lidocaine, which produces a few 
interesting results and several not too relevant, I searched for 
multiple and sclerosis and sleep and apnea.
 
I shan't bother you all with another list of abstracts and I think 
it is easier to just do the search rather than type in what I think 
are relevant titles. I shall be interested to see if the same 
people who read the long list of abstracts also do the search and 
whether it is just as time of reader/bandwidth economic. These days 
with cheap memory and fast modems it is probably better to use them 
to save readers time in searching. Maybe you will comment on that.
 
I was wondering if I had multiple sclerosis. Once before from a 
post to the MS group I learned of unilateral coldness, which I have 
had - in the right leg. It may be something else in my case. I gave 
the wrong hip when I said turning to the left at the computer helps 
it - it is the right one. Is MS ever confused with spinal pressure 
on nerve exiting points?
 
I felt good this morning. When I woke I found my left chin muscles 
coming back into control. Do you know the feeling when you feel a 
little sad and pucker up the chin? I could only feel it in the 
right side of the face. The left side would only pucher with much 
more force. But now it has started to work much better again. But 
getting on the comnputer again, though I am sitting slightly skew, 
has worsened it slightly.
 
When it was fairly bad walking out in the street would make it worse.  
 
So there are a number of troubles I might have.

Apologies for not spelling out all the questions and everything but 
leaving it open ended. Sit and remember and think rather than read? 

Brian Sandle

I have also had SEVERE seizures from Lidocaine injections in Dental Offices. I
found that I don't have that reaction from it if it is the type WITHOUT
EPINEPHRINE!!! NO EPI...The injections usually are given with this included to
help keep the med localized for longer...without it, it takes about 30 minutes
before you have to have another shot! Tell the folks you deal with "NO EPI" and
your shakes can be "normal" terror from sounds of drilling and smells of YOUR
teeth being drilled!

Also, I recently had a root canal redone, and they told me that they weren't
gonna use Lidocaine at all because they preferred (?not sure heard exactly
rightly?) DARVOCAINE? for that?

Ask...

K. Bennett

"The more I know, the more I know I need to know more."
(By:  A Smart Person...?)

Rauni wrote:

> I have has seizures after shots of lidocaine. I don't know if that is
> common or not. Makes going to the dentist difficult. I need a melogram
> and can't get one because of my reaction to lidocaine.  BTW I also
> have a seizure disorder
>
> On Tue, 02 Feb 1999 00:38:12 GMT, Brian Sandle
> <bsandle@southern.co.nz> wrote:
>
> >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@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@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@hotmail.com wrote in message <75p0a9$tug$1@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@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
> >

Brian Sandle wrote:

> You should be using a threaded newsreader. Then each
> thread is like a little newsgroup. If you lose interest you
> don't have to read that thread.

I'ld be very surprised if Bear does not have a threaded newsreader.

> The reason this article is in all those groups is that it
> started in the pain & fibromyalgia groups, had a followup
> to earlier material of mine which had received replies on
> bionet.neuroscience, is on the sleep disorder group
> because it is asking whether people have considered
> sleep apnea as a cause for their pains, and it of course
> is asking whether the dentists have thought of any
> connection to their work and sleep disorder - troubles
> occurring after a night or so. It is on the mult-sclerosis
> group since it arose after a radio program on MS
> following local anesthetic and it also hopes to clarify
> more about MS and locals.

Yes, sleep disorders do cause many symptoms, not the least of which are
neurological.  But the correlation between these symptoms are related to (a)
sleep deprivation and (b) reduced saturated oxygen in the blood ... along
with increased CO2 levels.  Sorry, that's the correlating factor.

>> and has not solicited any interest on the ASSD news group.
>
> Which I find disappointing. I was hoping that someone might
> go back through my articles and say, yes I have had shihn
> cramps from sleep apnea, or neck cramps or whatever. Or
> maybe ASSD will deny any pains or physical effects other
> than sleepiness from sleep apnea. Though the receptionist
> I spoke to at the local hospital here said it does have
> neurological effects. You might tell me how one knows if one
> has it if one sleeps alone. She said wives mainly report it
> to husbands.

Sigh!  You obviously think a sleep disorder such as sleep apnea is just
something that can get better with a little more sleep.  Sarcastic.  Yes.
But you clearly have not done the research prior to including this newsgroup
in your post.

Sleep apnea (obstructive or caused by the central nervous system) results in
a host of typical symptoms.  They tend to cluster around two primary areas.

Neurological

This cluster includes depression, extreme daytime sleepiness (which kills
due to auto and industrial accidents), sleep deprivation, hypnogenic
hallucenations, short term memory loss, irratibility, to name a few.

Cardiovascular

This second cluster includes hypertension, stroke, heart attacks,
potentially congestive heart failure (the research on this is in progress),
leg cramps, night sweats, just to name a few symptoms.

By noting this, I'm not denying the possibility there may be a connection in
a few individuals.  Just the vast majority of us have far more common
causes.


Regards,
=jbf=

John B. Fisher

In sci.med.dentistry nospam@this bear <Nospam@spamfree.net> wrote:
: x-no-archive: yes


:  Once again, I will request politely that you please stop cross posting
: this thread to SIX different news groups. This a tremendous waste of
: bandwidth

There has been some waste as new users have forgotten to trim the long 
articles.

But cross posting does not waste. Only one copy is sent around the world. 
If your news server works well you should only see it once.

You should be using a threaded newsreader. Then each thread is like a 
little newsgroup. If you lose interest you don't have to read that thread.

The reason this article is in all those groups is that it started in the 
pain & fibromyalgia groups, had a followup to earlier material of mine which 
had received replies on bionet.neuroscience, is on the sleep disorder 
group because it is asking whether people have considered sleep apnea as 
a cause for their pains, and it of course is asking whether the dentists 
have thought of any connection to their work and sleep disorder - 
troubles occurring after a night or so. It is on the mult-sclerosis group 
since it arose after a radio program on MS following local anesthetic and 
it also hopes to clarify more about MS and locals.

: and has not solicited any interest on the ASSD news group.

Which I find disappointing. I was hoping that someone might go back 
through my articles and say, yes I have had shihn cramps from sleep 
apnea, or neck cramps or whatever. Or maybe ASSD will deny any pains or 
physical effects other than sleepiness from sleep apnea. Though the 
receptionist I spoke to at the local hospital here said it does have 
neurological effects. You might tell me how one knows if one has it if 
one sleeps alone. She said wives mainly report it to husbands.


 I
: suggest respectfully that you restrict this thread to where it
: belongs.....The dental news group

I think it is good to have a little communciation on certain topics from 
time to time. Not every little article has mentioned the sleep disorder, 
but a picture is being formed.

:  You co operation on this matter would be greatly appreciated.

Mostly when I get complaints about cross posting it is because some 
individual does not like or is threatened out of comfort by the content.

: 
........Bear.........

You are interested in stopping sleep disorders. You may even sucbscribe 
to some profit oriented approach and be disturbed by some new 
non-profit-taking thinking coming in. 

Has anyone tried fish oil for any of the problems? The DHA or some other 
component towards nerve growth?

Then have you had to avoid halibut or even cod liver oil to keep down any 
toxicity of excess vitamin A or D? That might swell joints and press on 
nerves.

Brian Sandle

In sci.med.dentistry K. Bennett <klmwb@cybergal.com> wrote:
: I have also had SEVERE seizures from Lidocaine injections in Dental Offices. I
: found that I don't have that reaction from it if it is the type WITHOUT
: EPINEPHRINE!!! NO EPI...The injections usually are given with this included to
: help keep the med localized for longer...without it, it takes about 30 minutes
: before you have to have another shot!

I was asking the dentist about that. He says he does not use epinephrine 
(also known as adrenaline). He says that it is a different thing from a 
vasoconstrictor. That puzzled me. I was saying that becuase he did not 
use adrenaline - a vasoconstrictor - that perhaps the mepivicaine or 
prilocaine that he uses would travel further into areas where it might 
cause other trouble.

I think he uses longer acting anesthetics to compensate.

On the sci.med.dentistry thread I have been making some comments about 
allergy to dental filling composite material and also putting some 
questions about the cerebrospinal pressure (and its pulse).

 Tell the folks you deal with "NO EPI" and
: your shakes can be "normal" terror from sounds of drilling and smells of YOUR
: teeth being drilled!

: Also, I recently had a root canal redone, and they told me that they weren't
: gonna use Lidocaine at all because they preferred (?not sure heard exactly
: rightly?) DARVOCAINE? for that?

: Ask...

Actually I don't feel much difference in discomfort with or without 
injection.

 : K. Bennett

Brian Sandle

"K. Bennett" <klmwb@cybergal.com> wrote:

>I have also had SEVERE seizures from Lidocaine injections in Dental Offices. I
>found that I don't have that reaction from it if it is the type WITHOUT
>EPINEPHRINE!!! NO EPI...The injections usually are given with this included to
>help keep the med localized for longer...without it, it takes about 30 minutes
>before you have to have another shot! Tell the folks you deal with "NO EPI" and
>your shakes can be "normal" terror from sounds of drilling and smells of YOUR
>teeth being drilled!

>Also, I recently had a root canal redone, and they told me that they weren't
>gonna use Lidocaine at all because they preferred (?not sure heard exactly
>rightly?) DARVOCAINE? for that?

Carbocaine.

Cheers,

Joel

-----------


>Ask...

>K. Bennett

>"The more I know, the more I know I need to know more."
>(By:  A Smart Person...?)

>Rauni wrote:

>> I have has seizures after shots of lidocaine. I don't know if that is
>> common or not. Makes going to the dentist difficult. I need a melogram
>> and can't get one because of my reaction to lidocaine.  BTW I also
>> have a seizure disorder
>>
>> On Tue, 02 Feb 1999 00:38:12 GMT, Brian Sandle
>> <bsandle@southern.co.nz> wrote:
>>
>> >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@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@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@hotmail.com wrote in message <75p0a9$tug$1@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@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
>> >

In sci.med.dentistry Brian Sandle <bsandle@southern.co.nz> wrote:
: In sci.med.dentistry Brian Sandle <bsandle@southern.co.nz> wrote:
: : In sci.med.dentistry Doggett Sheryl <sdoggett@f1n06.kent.edu> wrote:
: : : The point:  a person may develop some weird compensatory postures to pain
: : : that may cause more pain or pain in differnent places.  

: Does that happen in MS?

And might check the relation of these topics to herpes sorts of things.

Check thread
Allergic response to local anesthetic?
in a search of alt.med.allergy and anesthetic
on
http://www.dejanews.com/home_ps.shtml

See also more on sci.med.dentistry thread `siezure'

Brian Sandle

Hey you guuuuuuyyyyyys!  When you "reply to group" to this Bear guys
messages, you are cross-posting to all the groups he/she cross-posted
to in the first place!  (In this case,
alt.support.sleep-disorder,sci.med.dentistry,alt.support.chronic-pain,
alt.med.fibromyalgia,bionet.neuroscience,alt.support.mult-sclerosis).

--
Jean
ICQ#  19761807
xjeahharris@mindspring.com    remove the x to reply

Breathe life into this feeble heart
Lift this mortal veil of fear
Take these crumbled hopes, etched with tears
We'll rise above these earthly cares

Cast your eyes on the ocean
Cast your soul on the sea
When the darK night seems endless
Please remember me

                  -- Loreena McKennitt

In sci.med.dentistry John B. Fisher <john_b_fisher@bellsouth.net> wrote:
: Brian Sandle wrote:

:> You should be using a threaded newsreader. Then each
:> thread is like a little newsgroup. If you lose interest you
:> don't have to read that thread.

: I'ld be very surprised if Bear does not have a threaded newsreader.

Then what is the reason it bothers Bear to have this connecting 
sub-newsgroup? Is it that this thread is not just about some technique 
sold by doctors?

And I had an email from the chronic pain group saying the thread is not 
wanted by a reader there.


:> The reason this article is in all those groups is that it
:> started in the pain & fibromyalgia groups,

Stigmata1's pain (alt.support.chronic-pain) started from dental work but
it was different from mine in that it started straight away. It did move
further over his body than Barry Kaplan had noted before, from dental
work. So did mine. 

I suppose I should have done more research on this but hoped to get some
ideas back. Maybe the chronic pain group or bionet.neuroscience could send
out some ideas on pain referral. What organ does it happen through? Is it
the thalamus or what? 


 had a followup
:> to earlier material of mine which had received replies on
:> bionet.neuroscience,

About lidocaine and seizures, thanks. I don't think dentists come across 
that much, but see the sci.med.dentistry `siezure' thread. Maybe it can 
happen if there is some brain injury or treatment which has weakened the 
blood brain barrier. I have not posted to the epilepsy group. It may have 
been  worth it to do so.

 is on the sleep disorder group
:> because it is asking whether people have considered
:> sleep apnea as a cause for their pains,

But that question seems intrusive to the sleep apnea group. But thanks 
for your reply here.

 and it of course
:> is asking whether the dentists have thought of any
:> connection to their work and sleep disorder - troubles
:> occurring after a night or so. It is on the mult-sclerosis
:> group since it arose after a radio program on MS
:> following local anesthetic and it also hopes to clarify
:> more about MS and locals.

: Yes, sleep disorders do cause many symptoms, not the least of which are
: neurological.  But the correlation between these symptoms are related to (a)
: sleep deprivation and (b) reduced saturated oxygen in the blood ... along
: with increased CO2 levels.  Sorry, that's the correlating factor.

:>> and has not solicited any interest on the ASSD news group.
:>
:> Which I find disappointing. I was hoping that someone might
:> go back through my articles and say, yes I have had shihn
:> cramps from sleep apnea, or neck cramps or whatever. Or
:> maybe ASSD will deny any pains or physical effects other
:> than sleepiness from sleep apnea. Though the receptionist
:> I spoke to at the local hospital here said it does have
:> neurological effects. You might tell me how one knows if one
:> has it if one sleeps alone. She said wives mainly report it
:> to husbands.

: Sigh!  You obviously think a sleep disorder such as sleep apnea is just
: something that can get better with a little more sleep.  Sarcastic.  Yes.
: But you clearly have not done the research prior to including this newsgroup
: in your post.

I learned a bit, but sometimes newsgroup posts bring up other points than 
what is in the traditional line. Also rather than have one person 
(myself) propound it is interesting to have others educating us all. I am 
sure some sci.med.dental persons have learned somewhat from your reply here.

: Sleep apnea (obstructive or caused by the central nervous system) results in
: a host of typical symptoms.  They tend to cluster around two primary areas.

: Neurological

: This cluster includes depression, extreme daytime sleepiness (which kills
: due to auto and industrial accidents), sleep deprivation, hypnogenic
: hallucenations, short term memory loss, irratibility, to name a few.

Well MS is neurological. There is some Medline stuff on apnea and MS when 
the breathing control centre gets involved.

But I am interested more in whether MS could be worsened by sleep apnea. 
Do any of the MS people have experience with sleep apnea testing? My 
theory is to examine whether conditions which predispose to MS worsening 
might be similar to ones which predispose to increased sleep apnea, for 
some individuals. It may not be of significance. 

: Cardiovascular

: This second cluster includes hypertension, stroke, heart attacks,
: potentially congestive heart failure (the research on this is in progress),
: leg cramps, night sweats, just to name a few symptoms.

I did not have hypertension but I thought of stroke, heart attack, and 
had leg cramp, wanting explanation for the deames of certain nerve 
branches, even motor trouble.

: By noting this, I'm not denying the possibility there may be a connection in
: a few individuals.  Just the vast majority of us have far more common
: causes.

That is a little unclear as to whether you mean most people have more 
common causes than sleep apnea for those things, or whether you are 
referring back to my possible causes for sleep apnea - dental work or 
local anesthetics, or perhaps infections.

Yes, the sales approach to medicine works with applying the treatment
which works for the average. Trying to mop up if that doesn't help. 
is where I am at with this thread. It is for some sort of minority of
people. Maybe a few from the newsgroups I have posted to will be wondering
if they might come into a subgroup who should be careful about local
anesthetics, or about messing around with the sinuses.

I included prepster's article from that point of view. Since Lidocaine in 
the nasal passages can cause sleep apnea by spoiling the air movement 
sense, can operations? prepster wanted comments about UPPP. I do not know 
what that is, but if it has a low success rate could that be the reason?

: Regards,
: =jbf=

: John B. Fisher

Thanks, John.

Have had no repsonse from fibromyalgia group. Any knowledge of sleep 
apnea there?

Brian Sandle

This message is to refer anyone interested in the continuation of this 
saga to the alt.support.mult-sclerosis forum for a new abstract on MS 
implicating herpes plus articles on a herpes-like reaction to lidocaine, 
the latter having been on sci.med.dentistry and alt.med.allergy.

The thread is Lidocaine and MS (Was:...

Below it is claimed that herpes can cause just about any effect, I 
thought to suggest a followup to alt.support.herpes as a future meeting 
point, though some of the MS stuff might not have been referred there.

But I see there is a group alt.support.disorders.neurological which may have 
been more appropriate for me to use than bionet.neuroscience originally, 
in my lidocaine quest, though it is rather low readership. That could be 
an intersection point, and maybe this will increase its readership.

Brian Sandle

From 
debwild@aol.com Sat Feb 13 14:52:07 1999 From: debwild@aol.com (Debwild)
Newsgroups: alt.support.herpes
Subject: Re: Pains
Date: 12 Feb 1999 18:54:48 GMT
References: <19990212070033.04994.00000472@ng19.aol.com>
Message-ID: <19990212135448.16414.00000364@ng-ft1.aol.com>


>i am having these really horrible back pains, is it associated with herpes? i
>was diagnosed with herpes many years ago. i was just wondering if these
>severe
>pains have anything to do with it? they are so bad i can hardly walk.. my
>legs
>hurt as well. it feels like i pulled a muscle. nothing i take helps get rid
>of
>the pain.. 
>
>
>
Hi,

With herpes anything is possible.  The back and leg pains you are describing
are very typical for me during an outbreak.  In fact, as some people know on
this ng, I literally am paralyzed for approximately 24 - 48 hours of my attack.
 I cannot walk or drive a car for that period of time till the antivirals kick
in and start working.  Sometimes the pain is so strong I cry.  Forget sleeping
- it is relentless.  Unfortunately pain relievers don't even touch this kind of
pain - I know, I have tried them all - even the heavy duty darvons etc.  The
best advice I can give is when you have the start of an attack - start
antivirals as soon as you can.  It helps shorten the duration of pain and the
attack itself.  Also, I have lingering pain after it is over and it can last
for weeks before it is gone.  To be sure it is related to herpes - go and talk
to a STD specialist and tell him your concerns.  There is a possibility you
could be suffering from a pinched nerve in your back like sciatica for
instance.  Check it out and good luck to you.

Deb


In sci.med.dentistry Brian Sandle <bsandle@southern.co.nz> wrote:
: In sci.med.dentistry John B. Fisher <john_b_fisher@bellsouth.net> wrote:
: : Brian Sandle wrote:

: :> You should be using a threaded newsreader. Then each
: :> thread is like a little newsgroup. If you lose interest you
: :> don't have to read that thread.

: : I'ld be very surprised if Bear does not have a threaded newsreader.

: Then what is the reason it bothers Bear to have this connecting 
: sub-newsgroup? Is it that this thread is not just about some technique 
: sold by doctors?

: And I had an email from the chronic pain group saying the thread is not 
: wanted by a reader there.


: :> The reason this article is in all those groups is that it
: :> started in the pain & fibromyalgia groups,

: Stigmata1's pain (alt.support.chronic-pain) started from dental work but
: it was different from mine in that it started straight away. It did move
: further over his body than Barry Kaplan had noted before, from dental
: work. So did mine. 

: I suppose I should have done more research on this but hoped to get some
: ideas back. Maybe the chronic pain group or bionet.neuroscience could send
: out some ideas on pain referral. What organ does it happen through? Is it
: the thalamus or what? 


:  had a followup
: :> to earlier material of mine which had received replies on
: :> bionet.neuroscience,

: About lidocaine and seizures, thanks. I don't think dentists come across 
: that much, but see the sci.med.dentistry `siezure' thread. Maybe it can 
: happen if there is some brain injury or treatment which has weakened the 
: blood brain barrier. I have not posted to the epilepsy group. It may have 
: been  worth it to do so.

:  is on the sleep disorder group
: :> because it is asking whether people have considered
: :> sleep apnea as a cause for their pains,

: But that question seems intrusive to the sleep apnea group. But thanks 
: for your reply here.

:  and it of course
: :> is asking whether the dentists have thought of any
: :> connection to their work and sleep disorder - troubles
: :> occurring after a night or so. It is on the mult-sclerosis
: :> group since it arose after a radio program on MS
: :> following local anesthetic and it also hopes to clarify
: :> more about MS and locals.

: : Yes, sleep disorders do cause many symptoms, not the least of which are
: : neurological.  But the correlation between these symptoms are related to (a)
: : sleep deprivation and (b) reduced saturated oxygen in the blood ... along
: : with increased CO2 levels.  Sorry, that's the correlating factor.

: :>> and has not solicited any interest on the ASSD news group.
: :>
: :> Which I find disappointing. I was hoping that someone might
: :> go back through my articles and say, yes I have had shihn
: :> cramps from sleep apnea, or neck cramps or whatever. Or
: :> maybe ASSD will deny any pains or physical effects other
: :> than sleepiness from sleep apnea. Though the receptionist
: :> I spoke to at the local hospital here said it does have
: :> neurological effects. You might tell me how one knows if one
: :> has it if one sleeps alone. She said wives mainly report it
: :> to husbands.

: : Sigh!  You obviously think a sleep disorder such as sleep apnea is just
: : something that can get better with a little more sleep.  Sarcastic.  Yes.
: : But you clearly have not done the research prior to including this newsgroup
: : in your post.

: I learned a bit, but sometimes newsgroup posts bring up other points than 
: what is in the traditional line. Also rather than have one person 
: (myself) propound it is interesting to have others educating us all. I am 
: sure some sci.med.dental persons have learned somewhat from your reply here.

: : Sleep apnea (obstructive or caused by the central nervous system) results in
: : a host of typical symptoms.  They tend to cluster around two primary areas.

: : Neurological

: : This cluster includes depression, extreme daytime sleepiness (which kills
: : due to auto and industrial accidents), sleep deprivation, hypnogenic
: : hallucenations, short term memory loss, irratibility, to name a few.

: Well MS is neurological. There is some Medline stuff on apnea and MS when 
: the breathing control centre gets involved.

: But I am interested more in whether MS could be worsened by sleep apnea. 
: Do any of the MS people have experience with sleep apnea testing? My 
: theory is to examine whether conditions which predispose to MS worsening 
: might be similar to ones which predispose to increased sleep apnea, for 
: some individuals. It may not be of significance. 

: : Cardiovascular

: : This second cluster includes hypertension, stroke, heart attacks,
: : potentially congestive heart failure (the research on this is in progress),
: : leg cramps, night sweats, just to name a few symptoms.

: I did not have hypertension but I thought of stroke, heart attack, and 
: had leg cramp, wanting explanation for the deames of certain nerve 
: branches, even motor trouble.

: : By noting this, I'm not denying the possibility there may be a connection in
: : a few individuals.  Just the vast majority of us have far more common
: : causes.

: That is a little unclear as to whether you mean most people have more 
: common causes than sleep apnea for those things, or whether you are 
: referring back to my possible causes for sleep apnea - dental work or 
: local anesthetics, or perhaps infections.

: Yes, the sales approach to medicine works with applying the treatment
: which works for the average. Trying to mop up if that doesn't help. 
: is where I am at with this thread. It is for some sort of minority of
: people. Maybe a few from the newsgroups I have posted to will be wondering
: if they might come into a subgroup who should be careful about local
: anesthetics, or about messing around with the sinuses.

: I included prepster's article from that point of view. Since Lidocaine in 
: the nasal passages can cause sleep apnea by spoiling the air movement 
: sense, can operations? prepster wanted comments about UPPP. I do not know 
: what that is, but if it has a low success rate could that be the reason?

: : Regards,
: : =jbf=

: : John B. Fisher

: Thanks, John.

: Have had no repsonse from fibromyalgia group. Any knowledge of sleep 
: apnea there?

: Brian Sandle