The effects of a home exercise program on pain and perceived dysfunction in a woman with TMD: a case study.

There are few reports analyzing the effects of exercise on patients with temporomandibular disorders. This paper presents a case study examining whether there were additional benefits from performing neuromuscular control home exercises (NMCHE) in a patient with temporomandibular disorder who was already receiving conventional treatment. A woman, 41 years of age, completed a health status questionnaire called the TMJ Scale prior to being accepted. She completed additional TMJ Scales after receiving conventional treatment and again after conventional treatment was combined with neuromuscular control home exercises. Based on the TMJ Scale's best subscore indicator of the presence or absence of a temporomandibular disorder, the patient did not derive benefit from conventional treatment without exercise. However, she received a large benefit from the addition of NMCHE. It was concluded that exercises for patients with temporomandibular disorders may be beneficial to those who do not improve with conventional treatment alone.

Relative frequency of a subclavian vs. a transverse cervical origin for the dorsal scapular artery in humans.

BACKGROUND: The origin of the dorsal scapular artery to the rhomboid muscles in humans has been the subject of uncertainty. The present study sought to clarify which of its two most common sources (the transverse cervical artery or the subclavian artery) is the major source of the dorsal scapular artery. METHODS: Gross anatomical dissection was used to visualize the origin and course of the dorsal scapular artery in human cadavers. RESULTS: We found that the dorsal scapular artery typically arises from either of two main sources: the subclavian artery (about 75% of all sides) or the transverse cervical artery (about 25% of all sides). Subclavian origins were approximately equally divided between its second and third part. Other origins for the dorsal scapular artery were negligible in frequency. Those dorsal scapular arteries that arose from the subclavian artery passed between the upper and middle or middle and lower trunks of the brachial plexus to course to the rhomboid muscles. In the case of transverse cervical artery origin, the dorsal scapular artery arose as a branch that passed deep to the levator scapulae muscle before coursing to the rhomboid muscles. No noteworthy differences were observed between males and females. CONCLUSIONS: These results strongly support the simple view, which does not appear widely accepted, that the subclavian artery is the most common source of the dorsal scapular artery to the rhomboid muscles and the transverse cervical artery a major but secondary source.

Cholecystokinin antagonists inhibit in vivo voltammetric signals generated by KCl-induced slow wave depolarization in rat caudate.

The effect of sulfated cholecystokinin octapeptide (CCK-8S) on the generation of slow wave depolarisation in the rat caudate-putamen (CPu) was studied using in vivo voltammetry. Pressure-ejection of 50 microM CCK-8S into the CPu induced voltammetric signals recorded at widely spaced Nafion-coated carbon fiber microelectrodes. Based on the in vitro selectivity properties of the electrodes, the signals were predominantly due to increases in extracellular concentrations of dopamine (DA). The similar propagation rates of the signals induced by CCK-8S and 100 mM KCl suggests that the CCK-8S-induced signals represent a slow wave depolarization (SWD). Since the CPu was refractory to a second CCK-8S stimulus, the effects of CCK antagonists on DA signals associated with 100 mM KCl-induced SWD were evaluated. Proglumide (4-64 mg/kg) and lorglumide (20-640 micrograms/kg), administered intravenously, decreased KCl-induced DA signals in the CPu in a dose-dependent manner. The antagonistic effect of lorglumide on the KCl-induced signals was partly reversed 130 min after drug administration. The generation of a SWD by CCK-8S and the inhibitory effects of CCK-8S antagonists on KCl-induced signals suggest that the susceptibility of the CPu to KCl-induced SWD may be enhanced by CCK-8S.

One year of continuous treatment with haloperidol or clozapine fails to induce a hypersensitive response of caudate putamen neurons to dopamine D1 and D2 receptor agonists.

In a "blind" experimental design, the sensitivity of caudate-putamen (CPu) cells to the selective dopamine (DA) D1 receptor agonist SKF-38393 and D2 receptor agonist LY171555 (quinpirole) in rats treated with either haloperidol (HAL), clozapine or tap water for 1 year was compared using the techniques of single cell recording and microiontophoresis. Although the maximum binding value for D2 receptors was elevated in chronic HAL-treated rats, there was no sign of electrophysiological supersensitivity of CPu neurons to the selective DA D1 and D2 receptor agonists. CPu cells were subsensitive to LY-171555 in HAL-treated rats without a drug withdrawal period. This suggests that residual HAL in the rat brain actively blocked the D2 DA receptors. In contrast, in clozapine-treated rats with or without a drug withdrawal period, the sensitivity of CPu cells to either the D1 or D2 agonists was not altered. Coadministration of SKF-38393 and LY-171555 onto the CPu neurons primarily produced an additive effect and only two cells both from the HAL group showed a synergistic action. The majority of CPu cells failed to respond to iontophoretic application of CCK-8S in either the control or antipsychotic drug-treated rats. If these findings can be extended to humans, they do not support the view that tardive dyskinesia is the result of CPu DA receptor supersensitivity.

The effect of intraventricular administration of the 5-HT3 receptor agonist 2-methylserotonin on the release of dopamine in the nucleus accumbens: an in vivo chronocoulometric study.

In the present study we have examined the effects of the serotonin3 (5-HT3) agonist 2-methylserotonin (2-Me-5HT) on the dopamine (DA) release in the nucleus accumbens (NAc) of rats using in vivo chronocoulometric recording. The intraventricular (i.c.v.) administration of 2-Me-5HT dose-dependently increased the DA release in the NAc. This effect was blocked by the selective 5-HT3 antagonist BRL-43694 (granisetron), but not by the 5-HT1/5-HT2 antagonist metergoline. The i.c.v. injection of 8-hydroxydipropylaminotetraline (8-OHDPAT, a selective 5-HT1a agonist) or (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI, a 5-HT2/5-HT1c agonist) failed to alter the DA release in the NAc. The increase in the DA release produced by 2-Me-5HT was abolished in animals that had received acute bilateral injections of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our results suggest that the 2-Me-5HT-induced DA release in the NAc is mediated by 5-HT3 receptors. In addition, 2-Me-5HT induced effect is dependent upon the impulse flow of DA cells.

Electrophysiological characterization of 5-hydroxytryptamine2 receptors in the rat medial prefrontal cortex.

The aim of the present study was to characterize 5-hydroxytryptamine2 (5-HT2) receptors in the rat medial prefrontal cortex (mPFc) by single cell recording and microiontophoretic techniques. This was accomplished using 5-HT2 receptor agonists 1-[2,5-dimethoxy-4-iodophenyl]-2-aminopropane [(+/-)-DOI] and 1-[2,5-dimethoxy-4-bromophenyl]-2-aminopropane [(+/-)-DOB]. DOI ejected at a low current (0.5 nA) potentiates glutamate (GLU)-induced activation of mPFc neurons and this effect is blocked by spiperone. At higher currents. DOI invariably inhibits GLU-induced neuronal activity. The microiontophoretic ejection of both DOI and DOB predominantly inhibits spontaneously active mPFc cells. The inhibitory action of DOI on spontaneously active cells is dose-dependent and is blocked by putative 5-HT2 receptor antagonists, with a rank order of potency as follows: ritanserin greater than metergoline approximately LY-53857 greater than spiperone greater than mesulergine greater than mianserin approximately ketanserin. Interestingly, ketanserin and mianserin only weakly block the effect of DOI. The suppressant action of DOI is probably not related to its interaction with 5-HT10 sites as spiperone, which has low affinity for these sites, potently blocks the effect of DOI. The suppressant effect of DOI is not blocked by other receptor antagonists such as BRL-43694 (5-HT3), (+/-)-pindolol (5HT 1a,1b, beta adrenergic, beta), prazosin (adrenergic1, alpha-1), pyrilamine (histamine1, H1), l-sulpiride (dopamine2, D2) or SR 95103 (gamma-aminobutyric acid, GABAA). Overall our results indicate that DOI predominantly inhibits mPFc cells in a direct manner and this effect is mediated by 5-HT2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Spreading depression induced by 100 mM KCl in caudate is blocked by local anesthesia of the substantia nigra.

Pressure-ejection of 100 mM KCl was used to induce voltammetric signals in the rat caudate. The signals, detected chronoamperometrically with Nafion-coated carbon fiber microelectrodes, were reproducibly generated at 20-min intervals up to distances of 1600 micron from the KCl stimulus site. Unilateral 6-hydroxydopamine lesions of the substantia nigra (SN) demonstrated that over 90% of the voltammetric signal generated was dopamine. Evaluation of the signal onset at two widely spaced electrodes suggested that injection of nl volumes of 100 mM KCl into the rat caudate generates voltammetric signals which resemble spreading depression (SD) produced by more classical methods (e.g. 1 M KCl). We further investigated this phenomenon by simultaneous evaluation of extracellular K+ ion concentration changes, field potential (FP) and voltammetric signals or multiunit activity following stimulation with 100 mM or 1 M KCl. The results show that the signals generated by 100 mM KCl have many of the attributes of 'classical' SD, although the extracellular K+ ion concentration changes and FP changes were smaller in magnitude. However, the characteristic burst of multiunit activity followed by a marked quiescent period found during 1 M KCl stimulation was not observed with 100 mM KCl stimulation. Furthermore, application of 0.5% lidocaine to the SN reversibly blocked all signals generated by 100 mM KCl in the caudate while similar treatment with up to 2% lidocaine was ineffective when 1 M KCl was used as the stimulus. The results suggest that the signals generated by 100 mM KCl may represent an attenuated form of SD which requires a functioning SN, and that this stimulation could be a useful model for studying neurotransmitter interactions in the propagation of the SD phenomena.

Cholecystokinin antagonist lorglumide reverses chronic haloperidol-induced effects on dopamine neurons.

Intravenous administration of the cholecystokinin (CCK) antagonist lorglumide (LORG) reversed chronic haloperidol (CHAL)-induced depolarization inactivation (DI) of dopamine (DA) cells in both the A9 and A10 areas. Moreover, microinjection of LORG, but not naloxone, directly into the medial nucleus accumbens (mNAc) dose-dependently reversed CHAL-induced effect. LORG injected into other brain regions was without effect. These results suggest that CCK receptors in the mNAc form an important link for maintaining CHAL-induced DI of DA cells and that CCK is involved in the therapeutic action of antipsychotic drugs.

Electrocoating carbon fiber microelectrodes with Nafion improves selectivity for electroactive neurotransmitters.

A method which improves carbon fiber microelectrode selectivity for cationic amines by electrocoating the fiber with a thin film of the ionic polymer, Nafion, is described. The selectivity and response speed of these electrodes for the detection of electroactive cationic and anionic species found in brain extracellular fluid was evaluated using differential pulse voltammetry and chronoamperometry and compared to uncoated fibers. Carbon fiber microelectrodes electrocoated with Nafion are highly sensitive to cationic amines such as dopamine and serotonin and have minimal sensitivity to anions such as ascorbic acid and uric acid at physiological concentrations.

Effects of acute thioridazine, metoclopramide and SCH 23390 on the basal activity of A9 and A10 dopamine cells.

Extracellular single-unit recording techniques were employed to examine the effects of various dopamine (DA) antagonists on the basal activity of spontaneously active DA cells. Metoclopramide and thioridazine were both effective in reversing apomorphine-induced suppression of A9 and A10 DA cells. SCH 23390 produced only a partial reversal of this suppression. When the antagonists were given without any pretreatment, thioridazine preferentially increased the firing rate of A10 DA cells, and was relatively ineffective in altering A9 activity. Metoclopramide, on the other hand, increased the activity of most A9 DA cells, but was less effective in doing so with A10 cells. SCH 23390 did not significantly affect the basal activity of either cell subpopulation. These data support the hypothesis that the so-called 'atypical' antipsychotic drugs act preferentially on the A10 DA system. Taken together with previous results, they also suggest that the acute effects of DA antagonists on DA cell subpopulations coincide with their chronic effects.

Effects of DFP on unit activity in rat superior colliculus.

The effect of systemically administered diisopropylfluorophosphate (DFP) on the spontaneous firing rate and light-evoked responses of rat superior colliculus neurons was determined from average histograms of single unit and multiunit activity. DFP produced a dose-dependent increase in superior colliculus spontaneous activity, and a decrease in light evoked activity. In many experiments, light evoked responses were completely abolished. The changes in spontaneous activity were reversible over a period of about 5 hours following DFP injection. These results establish the retino-tectal pathway as a major target of DFP toxicity.

DFP action on rat superior colliculus: localization and role of cholinergic receptors.

DFP, an irreversible acetylcholinesterase inhibitor, markedly increases spontaneous unit activity and reduces light-evoked responses in the superficial layers of the rat superior colliculus (Cheney et al., 1987). The purpose of this study was to investigate: (1) the sites of DFP action within the retino-tectal pathway (retinal, central or both), and (2) the types of cholinergic receptors (muscarinic, nicotinic, or both) involved. DFP increased SGS unit activity when injected intraocularly, confining its action to the retina, or when given systemically in bilateral enucleate rats. Thus, DFP acts at both retinal and central sites to increase unit activity in the SGS. Pretreating with muscarinic receptor antagonists such as atropine or scopolamine blocked DFP's effects at both sites whereas the nicotinic receptor antagonist mecamylamine was ineffective. Moreover, DFP's actions were mimicked by injections of the muscarinic receptor agonist, oxotremorine. The oxotremorine effects were also blocked or reversed by treatment with atropine or scopolamine. We conclude that DFP acts at both retinal and central sites to influence SGS unit activity and, at both sites, muscarinic receptors mediate DFP's effects.

Characteristics of corticomotoneuronal postspike facilitation and reciprocal suppression of EMG activity in the monkey.

In this study we present further evidence supporting the reciprocal nature of output effects on forearm flexor and extensor muscles from single corticomotoneuronal (CM) cells. Spike-triggered averaging of rectified EMG activity was used to test the output effects of 105 motor cortex cells in two rhesus monkeys (Macaca mulatta) trained to perform alternating wrist movements and power grip. The electromyographic (EMG) activity was recorded from six forearm flexor and six forearm extensor muscles through pairs of percutaneously inserted intramuscular stainless steel wires. CM cells were identified by their characteristic postspike facilitation (PSF) in spike-triggered averages of agonist muscle EMG activity. Agonist muscles are those which coactivate with the cortical cell during movement. Of 105 motor cortex cells tested, 56 (53%) had no effect on either agonist or antagonist muscles. Of 49 cells that produced PSF of the agonist muscles, 14 (29%) also produced clear postspike suppression (PSS) of the antagonist muscles. Reproducibility of postspike effects was demonstrated by comparing spike-triggered averages of full-wave rectified EMG with averages of the same EMG activity triggered from randomly generated pulses. Consecutive averages from random triggers never showed consistent postspike effects. As a further test that our postspike effects were real, we computed averages of simulated EMG activity from the spikes of CM cells with reciprocal output effects. None of these averages showed consistent postspike effects. The mean onset latency of PSF calculated from 14 reciprocal CM cells yielding 51 PSF effects was 6.3 ms compared with 10.1 ms for 28 PSS effects from the same cells. PSS effects from a particular CM cell were nearly always longer in latency than the cell's PSF effects; only 2 of 28 PSS onset latencies were shorter than the longest latency PSF onset from the same cell. Average peak latencies for PSF and PSS were 8.6 and 11.6 ms, respectively. The magnitude of postspike effects was expressed as the percent of peak facilitation above the base-line mean for PSF or peak suppression below the base-line mean for PSS. With this measure, the average magnitude of PSF was 7.0% compared with 4.1% for reciprocal PSS. There was no correlation between onset latency and magnitude of PSF or PSS, although strong PSFs tended to have shorter latencies. Concerning the distribution of postspike effects, the average reciprocal CM cell facilitated 3.8 agonist muscles and suppressed 2.1 antagonist muscles. EDC was facilitated by all extension-related reciprocal CM cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Double-barreled electrode for simultaneous iontophoresis and single unit recording during movement in awake monkeys.

A double-barreled electrode for simultaneous glutamate iontophoresis and chronic single unit recording from cortical neurons in awake monkeys during voluntary movement is described. Electrode assembly consists of pulling a heated, partitioned capillary tube over a sharpened tungsten rod. Glutamate iontophoresis increased the firing rates of wrist movement related cells an average of 34 Hz during the agonist phase of movement and 27 Hz during the antagonist phase of movement. However, in no case did glutamate iontophoresis alter the detailed structure of the cell's response pattern during wrist movement. This electrode is well suited to chronic recording applications that involve methods such as cross-correlation requiring overlapping activity of neurons and/or muscles. Other applications might involve activation of totally 'silent' neurons to avoid possible sampling bias or to detect effects in post-stimulus time histograms that would otherwise be subliminal.

Duration of task: an indicator of differentiation between motoneuron pools.

Sustaining an isometric contraction at a percentage of maximum contraction value prior to fatigue is significantly longer for the dominant arm than the non-dominant arm as reanalysis of data shows. This peripheral motor parameter which differentiates handedness as reflected in motoneuron pools may clarify the relationship between contralateral motor function and functional cerebral lateralizations.