Nasal Respiration Entrains Human Limbic Oscillations and Modulates Cognitive Function.

The need to breathe links the mammalian olfactory system inextricably to the respiratory rhythms that draw air through the nose. In rodents and other small animals, slow oscillations of local field potential activity are driven at the rate of breathing (∼2-12 Hz) in olfactory bulb and cortex, and faster oscillatory bursts are coupled to specific phases of the respiratory cycle. These dynamic rhythms are thought to regulate cortical excitability and coordinate network interactions, helping to shape olfactory coding, memory, and behavior. However, while respiratory oscillations are a ubiquitous hallmark of olfactory system function in animals, direct evidence for such patterns is lacking in humans. In this study, we acquired intracranial EEG data from rare patients (Ps) with medically refractory epilepsy, enabling us to test the hypothesis that cortical oscillatory activity would be entrained to the human respiratory cycle, albeit at the much slower rhythm of ∼0.16-0.33 Hz. Our results reveal that natural breathing synchronizes electrical activity in human piriform (olfactory) cortex, as well as in limbic-related brain areas, including amygdala and hippocampus. Notably, oscillatory power peaked during inspiration and dissipated when breathing was diverted from nose to mouth. Parallel behavioral experiments showed that breathing phase enhances fear discrimination and memory retrieval. Our findings provide a unique framework for understanding the pivotal role of nasal breathing in coordinating neuronal oscillations to support stimulus processing and behavior. SIGNIFICANCE STATEMENT: Animal studies have long shown that olfactory oscillatory activity emerges in line with the natural rhythm of breathing, even in the absence of an odor stimulus. Whether the breathing cycle induces cortical oscillations in the human brain is poorly understood. In this study, we collected intracranial EEG data from rare patients with medically intractable epilepsy, and found evidence for respiratory entrainment of local field potential activity in human piriform cortex, amygdala, and hippocampus. These effects diminished when breathing was diverted to the mouth, highlighting the importance of nasal airflow for generating respiratory oscillations. Finally, behavioral data in healthy subjects suggest that breathing phase systematically influences cognitive tasks related to amygdala and hippocampal functions.

Stress response in postpartum women with and without obsessive-compulsive symptoms: an fMRI study.

BACKGROUND: During the postpartum period, some women might be under a considerable amount of stress and at increased risk for on-set or exacerbation of obsessive-compulsive disorder (OCD). Little is known about the stress response correlates during the postpartum period and in patients with OCD. This study aimed to examine the cerebral, psychologic and endocrine correlates of the stress response in patients with OCD and during the postpartum period. METHODS: Women with postpartum OCD, healthy postpartum women and healthy mothers past the postpartum period underwent functional magnetic resonance imaging while facing a reliable psychosocial stressor (the Montreal Imaging Stress Task). Stress-related psychologic and endocrine responses (i.e., cortisol) were obtained. RESULTS: We enrolled 12 women with postpartum OCD, 16 healthy postpartum women and 11 healthy mothers past the postpartum period in our study. Compared with healthy postpartum counterparts, postpartum women with OCD had a heightened self-reported and endocrine stress response associated with a distinct brain activation pattern in response to psychosocial stress involving the orbitofrontal and temporal cortices. Moreover, compared with mothers assessed in a period of time beyond the postpartum period, healthy postpartum women did not differ in psychologic and cortisol response to stress, but recruited different brain regions, such as the dorsolateral prefrontal cortex and the anterior cingulate cortex, during exposure to stress. LIMITATIONS: Potential confounding factors, such as medication use, breastfeeding, parity and personality factors, may have modulated the stress-related endocrine response and could not be assessed in this study. CONCLUSION: Obsessive-compulsive disorder and the postpartum period differentially influence the brain circuitry underlying psychosocial stress as well as the psychologic and endocrine responses.

Cortisol awakening response and negative emotionality linked to asymmetry in major limbic fibre bundle architecture.

The limbic system plays an important role in regulating the hypothalamic-pituitary-adrenal (HPA) axis as well as aspects of emotion, and both neuroendocrine disturbance and increased negative emotionality are associated with risk for developing affective disorders. However, the extent to which the architecture of connections between limbic structures may be linked to individual differences in basal HPA-axis reactivity and negative emotionality is unknown. Here we tested the hypotheses that microstructural asymmetry of the major limbic fibre bundles would be associated with cortisol awakening response (CAR) and neuroticism, a personality trait associated with the tendency to experience negative emotions. Sixty-nine healthy adults were studied with diffusion-weighted imaging, and fractional anisotropy (FA) was extracted from the cingulum and uncinate fasciculus. Higher neuroticism scores, which were associated with higher CAR, were also correlated with higher right relative to left cingulum FA. Elevated CAR was associated with the degree of FA asymmetry within both the cingulum and the uncinate fasciculus, but in opposing directions. These results suggest that the balance between left- and right-sided limbic circuits may bear an important relationship to hypothalamic-pituitary-adrenal axis reactivity, and to the tendency to experience negative emotions, and they raise important questions about the significance of limbic system architecture.

Forebrain projections to brainstem nuclei involved in the control of mandibular movements in rats.

Mandibular movements occur through the triggering of trigeminal motoneurons. Aberrant movements by orofacial muscles are characteristic of orofacial motor disorders, such as nocturnal bruxism (clenching or grinding of the dentition during sleep). Previous studies have suggested that autonomic changes occur during bruxism episodes. Although it is known that emotional responses increase jaw movement, the brain pathways linking forebrain limbic nuclei and the trigeminal motor nucleus remain unclear. Here we show that neurons in the lateral hypothalamic area, in the central nucleus of the amygdala, and in the parasubthalamic nucleus, project to the trigeminal motor nucleus or to reticular regions around the motor nucleus (Regio h) and in the mesencephalic trigeminal nucleus. We observed orexin co-expression in neurons projecting from the lateral hypothalamic area to the trigeminal motor nucleus. In the central nucleus of the amygdala, neurons projecting to the trigeminal motor nucleus are innervated by corticotrophin-releasing factor immunoreactive fibers. We also observed that the mesencephalic trigeminal nucleus receives dense innervation from orexin and corticotrophin-releasing factor immunoreactive fibers. Therefore, forebrain nuclei related to autonomic control and stress responses might influence the activity of trigeminal motor neurons and consequently play a role in the physiopathology of nocturnal bruxism.

Cortisol relates to regional limbic system structure in older but not younger adults.

We investigated if the relationship between age and regional limbic system brain structure would be moderated by diurnal cortisol output and diurnal cortisol slope. Participants aged 23-83 years collected seven salivary cortisol samples each day for 10 consecutive days and underwent magnetic resonance imaging. Age, sex, cortisol, and an age x cortisol interaction were tested as predictors of hippocampal and amygdalar volume and caudal and rostral anterior cingulate cortex (ACC) thickness. We found significant interactions between age and cortisol on left and right amygdalar volumes and right caudal ACC thickness. Older adults with higher cortisol output had smaller left and right amygdalar volumes than older adults with lower cortisol output and younger adults with higher cortisol output. Older and younger adults with lower cortisol output had similar amygdalar volumes. Older adults with a steeper decline in diurnal cortisol had a thicker right caudal ACC than younger adults with a similarly shaped cortisol slope. Hippocampal volume was not related to either cortisol slope or output, nor was pallidum volume which was assessed as an extra-limbic control region. Results suggest that subtle differences in cortisol output are related to differences in limbic system structure in older but not younger adults.

Two different mirror neuron networks: The sensorimotor (hand) and limbic (face) pathways.

The vast majority of functional studies investigating mirror neurons (MNs) explored their properties in relation to hand actions, and very few investigated how MNs respond to mouth actions or communicative gestures. Since hand and mouth MNs were recorded in two partially overlapping sectors of the ventral precentral cortex of the macaque monkey, there is a general assumption that they share a same neuroanatomical network, with the parietal cortex as a main source of visual information. In the current review, we challenge this perspective and describe the connectivity pattern of mouth MN sector. The mouth MNs F5/opercular region is connected with premotor, parietal areas mostly related to the somatosensory and motor representation of the face/mouth, and with area PrCO, involved in processing gustatory and somatosensory intraoral input. Unlike hand MNs, mouth MNs do not receive their visual input from parietal regions. Such information related to face/communicative behaviors could come from the ventrolateral prefrontal cortex. Further strong connections derive from limbic structures involved in encoding emotional facial expressions and motivational/reward processing. These brain structures include the anterior cingulate cortex, the anterior and mid-dorsal insula, orbitofrontal cortex and the basolateral amygdala. The mirror mechanism is therefore composed and supported by at least two different anatomical pathways: one is concerned with sensorimotor transformation in relation to reaching and hand grasping within the traditional parietal-premotor circuits; the second one is linked to the mouth/face motor control and is connected with limbic structures, involved in communication/emotions and reward processing.

Serotonin transporter gene promoter methylation in peripheral cells in healthy adults: Neural correlates and tissue specificity.

Early adversity can influence gene expression via epigenetic mechanisms, including DNA methylation. Peripheral tissues are essential in psychiatric epigenetics, as methylation generally cannot be assessed in the living human brain. Several magnetic resonance imaging (MRI) studies show associations of peripheral serotonin transporter gene (SLC6A4) methylation with function and/or structure of frontal-limbic circuits and brain's resting-state. Commonly used samples are derived from blood, saliva or buccal cells. However, little is known regarding which peripheral tissue is most strongly associated with human brain processes. The aim of the current study was to compare the extent of the association between peripheral SLC6A4 promoter methylation and frontal-limbic function, structure and resting-state in healthy individuals across peripheral tissues. Forty healthy prospectively-followed adults underwent anatomical, resting-state and functional MRI. Saliva-, blood- and buccal-derived DNA methylation was assessed by pyrosequencing. Blood-derived SLC6A4 methylation was positively associated with superior frontal gray matter (GM) volume and with right lateral parietal area (RLP)-frontal pole regional resting-state functional connectivity (rsFC). Saliva-derived SLC6A4 methylation was positively associated with superior frontal GM volume. Buccal-derived SLC6A4 methylation was positively associated with superior and inferior frontal and anterior cingulate cortical (ACC) GM volumes, and with RLP-ACC, frontal pole and medial prefrontal regional rsFC. Current results confirmed the relevance of peripheral methylation for frontal-limbic processes in humans. Buccal cells may be the most sensitive cell type when studying SLC6A4 promoter methylation and its associated risk for neural vulnerability and resilience for psychopathologies in which serotonin is implicated. These data should be further validated in clinical populations.

Pain-induced analgesia mediated by mesolimbic reward circuits.

We tested the hypothesis that noxious stimuli induce pain modulation by activation of supraspinal structures. We found that intense noxious stimuli (i.e., subdermal injection of capsaicin or paw immersion in hot water) induced profound attenuation of the jaw-opening reflex in the anesthetized rat; forepaw subdermal capsaicin also elevated the mechanical hindpaw-withdrawal threshold in the awake rat. These antinociceptive effects were blocked by previous injection of either a dopamine antagonist (flupentixol) or an opioid antagonist (naloxone) into the nucleus accumbens. Additional experiments in anesthetized animals showed that the antinociceptive effect of noxious stimulation by either capsaicin (>/=100 micrograms) or hindpaw immersion in hot water (>/=45 degrees C for 4 min) correlated with the intensity of the stimulus. The maximal antinociceptive effect of capsaicin was similar in magnitude to that of a high dose of morphine (10 mg/kg) injected subcutaneously. Injection of the GABA(A)-receptor agonist muscimol, but not naloxone, into the rostroventral medulla, a major component of descending pain modulation systems, blocked capsaicin-induced antinociception. Although it is widely thought that painful stimuli may induce analgesia by activating forebrain structures, this is the first demonstration that such a mechanism exists. Furthermore, this mechanism can be engaged by naturalistic stimuli in awake animals. These observations imply that painful stimuli might under certain conditions be rewarding.

The clenching-grinding spectrum and fear circuitry disorders: clinical insights from the neuroscience/paleoanthropology interface.

This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8 percent of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry activation not present before the trauma). Grinding-induced incisor wear, and clenching-induced palpable masseter tenderness may be examples of such objective physical signs of persistent fear-circuitry activation (posttraumatic stress disorder Criterion D).

Orbital cortex neuronal responses during an odor-based conditioned associative task in rats.

Neuronal activity in the rat orbital cortex during discrimination of various odors [five volatile organic compounds (acetophenone, isoamyl acetate, cyclohexanone, p-cymene and 1,8-cineole), and food- and cosmetic-related odorants (black pepper, cheese, rose and perfume)] and other conditioned sensory stimuli (tones, light and air puff) was recorded and compared with behavioral responses to the same odors (black pepper, cheese, rose and perfume). In a neurophysiological study, the rats were trained to lick a spout that protruded close to its mouth to obtain sucrose or intracranial self-stimulation reward after presentation of conditioned stimuli. Of 150 orbital cortex neurons recorded during the task, 65 responded to one or more types of sensory stimuli. Of these, 73.8% (48/65) responded during presentation of an odor. Although the mean breadth of responsiveness (entropy) of the olfactory neurons based on the responses to five volatile organic compounds and air (control) was rather high (0.795), these stimuli were well discriminated in an odor space resulting from multidimensional scaling using Pearson's correlation coefficients between the stimuli. In a behavioral study, a rat was housed in an equilateral octagonal cage, with free access to food and choice among eight levers, four of which elicited only water (no odor, controls), and four of which elicited both water and one of four odors (black pepper, cheese, rose or perfume). Lever presses for each odor and control were counted. Distributions of these five stimuli (four odors and air) in an odor space derived from the multidimensional scaling using Pearson's correlation coefficients based on behavioral responses were very similar to those based on neuronal responses to the same five stimuli. Furthermore, Pearson's correlation coefficients between the same five stimuli based on the neuronal responses and those based on behavioral responses were significantly correlated. The results demonstrated a pivotal role of the rat orbital cortex in olfactory sensory processing and suggest that the orbital cortex is important in the manifestation of various motivated behaviors of the animals, including odor-guided motivational behaviors (odor preference).

Hippocampal responses evoked by tooth pulp and acoustic stimulation: depth profiles and effect of behavior.

Averaged evoked potentials and unitary discharges in response to tooth pulp and acoustic click stimuli were recorded from the hippocampus of freely moving rats. The spatial distribution of evoked field responses to tooth pulp stimulation and acoustic clicks were identical. Averaged evoked potentials consisted of a large negative deflection (N1) preceded by a small positive potential (P1). The shortest latency N1 in response to tooth pulp stimulation was recorded from the middle third of the dentate molecular layer and the outer portion of apical dendrites of CA3 (27 ms). The peak latency of N1 was significantly longer (34 ms) in the stratum radiatum of CA1. Laminar profiles of N1 in the dentate gyrus and CA3 were similar to that evoked by electrical stimulation of the medial entorhinal afferents; in CA1 the depth profiles of the potentials were similar to the response profile evoked by the Schaffer collaterals. Largest amplitude P1 was obtained from above the pyramidal layer of CA1 and the hilus. Both sensory modalities were able to modify the discharge rate of neurons in all hippocampal regions. The amplitude of evoked field potentials and cellular responses were dependent upon both the ongoing behavior of the animal and the nature of its response to the stimulus. The largest amplitude evoked potentials were recorded during immobility and slow wave sleep. On the other hand, virtually no potentials were obtained during exploratory behaviors associated with theta EEG activity. The findings indicate that information about sensory stimuli can reach the hippocampus by two distinctive pathways: a short latency inhibitory input via the fimbria-fornix and a longer latency path via the entorhinal cortex. It is suggested that neuronal mechanisms involved in theta EEG block the sequential activation of the unidirectional entorhinal-hippocampal circuitry.

Effects of stimulation of the substantia innominata upon attack behavior elicited from the hypothalamus in the cat.

Experiments were undertaken in order to determine the role of the substantia innominata and surrounding regions in quiet biting attack elicited from electrical stimulation of the hypothalamus in the cat. Stimulation from sites in the lateral aspect of the substantia innominata resulted in a suppression of quiet biting attack and in a constriction of the 'effective trigeminal sensory fields' established during hypothalamic attack site stimulation. Stimulation from sites situated more medially in the substantia innominata resulted in a facilitation of quiet biting attack and in an expansion of the 'effective trigeminal sensory fields'. The motor component of the jaw opening response was altered in only 50% of the cases in contrast to the consistent effects observed upon the 'effective sensory fields'. Electrical stimulation of the substantia innominata had little effect upon affective display elicited from the ventromedial hypothalamus. Stimulation from sites located in the nucleus accumbens had no effect upon hypothalamically-elicited quiet biting attack and inhibited the occurrence of affective display in 2 to 5 animals tested. These studied suggest that the substantia innominata differentially modulates quiet biting attack and accomplishes this, at least in part, through its effects upon sensory mechanisms associated with the jaw opening reflex.

An analysis of the mechanisms underlying septal area control of hypothalamically elicited aggression in the cat.

This experiment was performed in order to examine several of the underlying mechanisms by which the septal area and adjacent regions regulate quiet biting attack behavior elicited from electrical stimulation of the hypothalamus in the cat. The results clearly indicate that stimulation of the septal area and anterior cingulate gyrus increased the latency for the occurrence of quiet biting attack behavior. Those sites within the septal area from which inhibition of attack can be produced are linked to sensory mechanisms associated with trigeminal reflexes activated during hypothalamic stimulation. Stimulation of these septal area sites decreased the lateral extent of the 'effective sensory fields' of the lipline established during hypothalamic stimulation, but did not appear to have any affect upon the latency of the hypothalamically elicited jaw-opening response. Deoxyglucose autoradiography revealed that the inhibition resulting from stimulation of the lateral septal area may be due to either the monosynaptic activation of the lateral hypothalamus or the disynaptic activation of this area utilizing a circuit involving the nuclei of the diagonal band of Broca.

Collateral axonal projections to limbic structures from ventrolateral medullary A1 noradrenergic neurons.

Experiments were done to investigate whether catecholaminergic neurons within the ventrolateral medulla (VLM) send collateral axonal projections to the central nucleus of the amygdala (ACe) and the bed nucleus of the stria terminalis (BST). Unilateral microinjections of the fluorescent retrograde tracers fluorogold (FG) or rhodamine labelled latex micro-beads (Rd) were made into either ACe or BST in the rat. Brainstem sections were then processed immunohistochemically for the identification of cell bodies containing the catecholamine biosynthetic enzymes tyrosine hydroxylase, dopamine beta-hydroxylase (DBH) or phenylethanolamine-N-methyltransferase (PNMT). Retrogradely labelled cell bodies projecting to either ACe or BST were found throughout the rostrocaudal extent of VLM, bilaterally. Approximately 44% of these retrogradely labelled neurons were found to contain both retrograde tracers. In addition, approximately 91% of the VLM neurons that send collateral axonal projections to ACe and BST were also immunoreactive to DBH. None were found to contain PNMT immunoreactivity. These results demonstrate that noradrenergic neurons of the A1 cell group in VLM innervate ACe and BST via collateral axonal projections and suggest that these VLM neurons may be directly involved in relaying cardiovascular afferent and/or visceral afferent information directly to these limbic structures.

FMRI brain activation in response to odors is reduced in primary olfactory areas of elderly subjects.

Olfactory function is affected by aging and deficits often result in decreasing quality of life, health and safety. The present study investigated the cortical substrate of olfactory deficits related to aging with functional Magnetic Resonance Imaging (fMRI), with a retronasal olfactory stimulation protocol using flavored aqueous solutions presented to the mouth. Activation was found in young subjects in the piriform/amygdalar region and in the orbitofrontal cortex and in other areas previously found activated in neuroimaging studies using odorized air, including insula and cerebellum. Activation was seen in similar areas in old subjects but the degree of activation was significantly lower in regions receiving primary olfactory projections (piriform cortex, entorhinal cortex, and amygdala). This result supports the hypothesis of dysfunction and/or degeneration in areas critical to olfactory processing as a major cause of olfactory deficits in the older population.

Glucocorticoid feedback increases the sensitivity of the limbic system to stress.

In the hypothalamus, corticotropin-releasing hormone (CRH) has a well-described role initiating the hypothalamic-pituitary-adrenal (HPA) axis response to stress. Cortisol, released from the adrenal gland, exerts negative feedback on this axis. The role of extrahypothalamic CRH in stress responses is less well known. The purpose of this study was to measure the response of CRH in the amygdala to acute and repeated stress and to examine if cortisol had any effect on this response. Immunosensor-based microdialysis probes were used to measure CRH and cortisol in the amygdala and cortisol systemically in sheep exposed to a predator stress (a dog). Upon presentation of a dog, CRH increased in the amygdala of the sheep and then fell off. Cortisol levels rose both systemically and in the amygdala, and as they peaked, a second CRH response was observed. Repeated stress changed this response, with the magnitude of the first CRH peak decreasing while the second peak increased. Repeated stress also produced an exaggeration in both of the CRH peaks to presentation of a subsequent novel stress (a forelimb electric shock). Animals that had an escape route from the repeated dog stress did not show this exaggeration when faced subsequently with the novel stress. Administration of mifepristone, a glucocorticoid receptor antagonist, prior to the delivery of the repeat stress prevented subsequent changes in the CRH response. The data suggest that the amygdala shows a CRH response to presentation of a stressor acutely and repeatedly and that repeated stress can alter subsequent amygdala responsiveness to the same or a different stressor. This alteration appears dependent on circulatory glucocorticoids.

Hypothalamo-limbic involvement in modulation of tooth-pump stimulation evoked nociceptive response in rats.

The hypothalamo-limbic system has been implicated in recognizing the affective significance of pain and elicitation of related emotional responses. Several evidences from different studies support a role of these areas in endogenous analgesic mechanisms for pain modulation as elucidated by different pain tests in more than one animal model. In the above context, the aim of this study was to investigate the relative effectiveness of the pain modulatory action of hypothalamic and limbic structures in rat using similar stimulation parameters, and studying the effect on tooth pulp stimulation evoked jaw opening reflex (TP-JOR). To achieve the objective, unilateral stimulation of hypothalamic (lateral = LH; ventromedial = VMN; anterior = AH) and limbic areas (amygdala = AMYG; hippocampus = HIPP) was done on the TP-JOR test. A significant reduction in the amplitude of EMG recorded from the digastric muscle (dEMG) as a result of tooth-pulp stimulation was observed on stimulation of LH, VMN, AMYG and HIPP but not from AH. Also, the magnitude of this effect was almost similar from these areas. The results suggest that these areas (except AH) have an antinociceptive role in tooth-pulp stimulation evoked pain response.

[A case of Cheyne-Stokes respiration with cyclic mutism during apneic period].

A 77-year-old man showed Cheyne-Stokes respiration (CSR) without a consciousness disturbance. In each apneic period of CSR, he became mute. In the apneic and mute state, he could open his mouth or protrude his tongue, but he could not breath or speak. In this patient, it was evident that not only phonation but also speech was under the control of respiration. Neuroimaging technique revealed an infarction in the right anterior cingulate gyrus and supplementary motor area as well as the entire perfusion area of the right middle cerebral artery. Marked atrophy of bilateral cerebral hemispheres was also observed. In this case, destruction of the right cingulate gyrus was thought to manifest occult functional fluctuation of the left cingulate gyrus influenced by the respiratory control mechanisms. This case suggested that the limbic system integrates the speech mechanism and the respiratory mechanism.

Synaesthetic restorations: a psychological perspective for surpassing aesthetic dentistry.

Dentistry is often described as a fusion of art and science. While the scientific aspect is well documented, the artistic component is nebulous and often subject to interpretation. The use of the word "aesthetic" as a description of artistic dentistry is essentially flawed. While it forms part of artistic concepts, aesthetics is not the quintessential description of what constitutes art or its perception by the human brain. This article redresses this balance by emphasizing the artistic nature of dentistry and rationalizing the criteria that constitute artistic perception.

Acute vs. chronic pain.

The differences between acute and chronic pain are many and varied. They are so different from one another that they must be considered separate entities. The chronic pain patient does not fit the traditional acute illness model as conceptualized by patients and healthcare providers. Because of the complex nature of the pain mechanism as a protective "reflex" and the fact that the pain response gets caught up in emotional expression, pain becomes a learned behavior pattern. When the patient who presents to the dental office suffering from pain is found not to respond to conventional methods of treatment, the dentist should first consider the nature of the pain response and the fact that the patient may not meet all the requirements for the acute illness model. The manner in which the patient describes his or her pain can be a major clue as to the temporal classification of the pain, thus allowing the dentist the advantage of better decision-making. Great discernment on the part of the dental practitioner must be exercised in order to provide the optimum care for the patient. It is important for the dentist to consider the fact that there may be no underlying cause for the pain and it may be necessary to make proper referrals for management of this type of patient. At a more practical and human level, patients want to know if their pain will ever completely go away. Patients are frightened that their pain is attributable to some unrecognized pathology (catastrophic thinking). This drives them to search for the ultimate cure. Going from practitioner to practitioner worsens the confusion as the patient hopes that someone will be able to illuminate the problem. By being able to classify the pain into a recognizable and explainable syndrome, the pain practitioner is often able to offer hope to the patient. Although treatment often does not yield a completely pain-free state, understanding the basis for the pain can provide significant relief through proper management.