Guide Mechanisms of Clinical Signs

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  1. Mechanisms of Clinical Signs BRAND NEW Textbook
  2. Mechanisms of Clinical Signs - Mark Dennis, William Talbot Bowen, Lucy Cho - Google книги
  3. Table of Contents
  4. Mechanisms of Clinical Signs

Video and audio content presents real life evaluation scenarios of clinical signs. New to this Edition Clinical Pearls highlight the main signs which students and trainees should look out for to help them identify conditions with which the patients present. A Student Consult eBook is available with the purchase of a print book, and provides access to a total of multiple choice questions covering the 7 body systems, to test students and trainees' knowledge of the content.

The eBook contains links to audio and video examples of particular signs which have to be heard or observed over a period of time in order to be identified correctly, e. Agonal respiration in Chapter 2 Respiratory Signs. New images are added to depict clinical signs where no images were present in the previous edition. The art and science of clinical examination is a vital component of patient assessment and management. The Mechanisms of Clinical Signs textbook aims to provide a more complete understanding of many clinical signs.

The book is structured in a way that allows it to be used for quick referencing: each clinical sign is assigned its own section and is grouped according to body system. Clinical signs are also indexed according to conditions. For each sign, a detailed explanation is provided, largely focused on the underlying pathophysiology or mechanism. The eBook version also includes videos, audio files and multiple-choice questions.

The analysis of each clinical sign is strengthened by the inclusion of a discussion of its supporting evidencebase. The textbook is meticulously referenced and a list of sources is provided at the end of each chapter. Overall, this textbook is successful in providing a sound understanding of the underlying mechanisms of clinical signs.

The information is presented in such a way that enables the reader to more easily remember the application of each clinical sign. The concise, structured layout of the book makes it a practical reference tool for those wishing to learn or review clinical signs. Both medical students and doctors will be able to benefit from this excellent resource. This is a very useful book as it helps to explain the underlying mechanism or processes of each clinical sign. Most books just state the sign this is commonly seen in each disease state, but this book expands on that and explains why it happens physiologically.

Great book for all students! Useful to help understand what we are doing, and why, when we examine patients. Only registered users can write reviews. Please, log in or register. Cookies are used by this site. To decline or learn more, visit our Cookies page. Login Create an account. A substantial part of the present knowledge of peripheral and central craniofacial pain mechanisms is derived from elaborate and well-designed animal studies for reviews see Dubner et al, 64 Sessle, 65—67 Capra and Dessem, 68 Hannam and Sessle, 69 and Lund and Sessle Injection of potent algesic substances such as mustard oil into deep craniofacial tissues has been particularly useful to document the neurobiology and neuropharmacology of brain stem reflex responses and hyperexcitability of central neurons.

Therefore, there is a need to apply experimental pain models in healthy human subjects, with the purpose of bridging the basic information obtained in animal studies with the data from clinical trials in patients. In summary, exogenous stimulation techniques help to characterize basic aspects of craniofacial muscle pain. The choice of model depends on the specific purpose of the study. For example, injection of specific algesic substances and excitatory neuropeptides may help outline the neuropharmacology involved in craniofacial muscle pain.

For the study of sensorimotor interaction in the human craniofacial region, it is important that the stimulus is safe and induces a robust pain sensation that can be maintained for several minutes or longer. Kellgren and Lewis 81—83 demonstrated that intramuscular injection or infusion of hypertonic saline is a suitable and reliable model to evoke experimental muscle pain in healthy subjects. Since hypertonic saline has been used extensively as a painful stimulus, this technique will be described in more detail in the next paragraphs.

Induction of Muscle Pain by Hypertonic Saline. Tonic infusion of hypertonic saline has advantages over bolus injection in that muscle pain can be maintained for up to 15 or 20 minutes at a fairly constant level, the evoked pain is more similar to clinical muscle pain, and more experimental registrations can be performed.

Hypertonic saline is unfortunately a non-specific painful stimulus, ie, not mediated by specific pharmacologic receptors, and non-nociceptive afferents may be activated concomitantly with the activation of nociceptive group III and IV afferents. It is unlikely that increased intramuscular pressure should be the cause of the pain during infusion of hypertonic saline, since the maximum pressure measured at the tube does not exceed to mmHg. In summary, the evidence strongly suggests that hypertonic saline is indeed a potent chemical stimulus for excitation of group III and IV muscle afferents and central neurons encoding nociceptive information along the neuroaxis.

Therefore, it is reasonable to suggest that changes in somatosensory or motor function following hypertonic saline are primarily a result of activity evoked in nociceptive muscle afferents. Human experimental pain models can be used to describe the effects of craniofacial muscle pain on somatosensory sensitivity. This is important because it had earlier been suggested that a low psychophysical threshold could contribute to the complaints of TMD pain.

The next sections will review the evidence for somatosensory changes in superficial and deep tissues in relation to experimental and clinical muscle pain in the craniofacial region. Many human studies of experimental deep pain have reported increased cutaneous sensitivity to pricking mechanical or electrical stimuli in the local pain area, 35,83,94, but some reports have also shown decreased or unchanged sensitivity. The sites of superficial hyperesthesia involved either the local pain area at the injection site or even more distant regions. Steinbrocker et al reported that changes in superficial sensitivity were variable in occurrence following intramuscular injection of hypertonic saline, but that they usually consisted of hyperesthesia and rarely hypoesthesia in the local pain area.

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A recent detailed study showed that both hypoesthesia and hyperesthesia can occur, depending on the innervation area and the relation to the referred pain area. However, changes in somatosensory sensitivity in the referred pain area appear to be modality-specific, because both hyperalgesia to electrical stimuli and hypoalgesia to radiant heat stimuli can be observed. A number of studies have examined the sensitivity of superficial tissues in patients with craniofacial muscle pain to various non-painful and painful stimulus modalities.

It has been reported that the detection and pain thresholds to electrical stimulation of the facial skin or teeth are not significantly different between TMD patients and control subjects. Patients with craniofacial muscle pain may also demonstrate hyperalgesic responses to application of thermal heat within and outside the local pain area. Instead it was suggested that integrative mechanisms in the central nervous system participated because of an augmented temporal summation of thermal stimuli on the hand.

In patients who have significant hyperalgesia to superficial stimuli applied outside the segment containing the local pain area, it is unlikely that peripheral sensitization and sensitization of second-order neurons can explain the findings. Rather, sensitization is probably occurring at higher levels in the central nervous system, and it has been suggested that the ascending reticular formation could be involved. Secondly, the many nuclear groups in the brain stem and basal forebrain areas project to other brain areas related to a wide range of functions, such as regulation of sensory perception, emotional responses, arousal, endocrine responses, somatomotor output, and autonomic function.

In summary, there are contradictions in the clinical literature regarding the valence of changes in superficial sensitivity in patients with craniofacial muscle pain. Studies have reported both hypo- and hyperalgesic responses. This controversy may be explained partly by differences in psychophysical techniques and by differences in diagnostic criteria for the patient population.

However, the most recent studies with robust psychophysical techniques and the best described diagnostic criteria for inclusion have indicated both localized and generalized hyperalgesia to heat stimuli that is probably related to hyperexcitability of central neurons and deficiencies in the endogenous inhibitory control systems. Mechanical stimuli have been used extensively to assess the sensitivity of deep craniofacial tissues in humans.

The most widely used technique is pressure algometry. Provided that proper standardization methods are followed, approaches using pressure-pain thresholds are generally considered an improvement on the manual palpation of muscles. Nonetheless, a palpometer device has recently been developed and tested in patients with tension-type headache and fibromyalgia , ; this device might also provide useful information in, for example, TMD patients.

Several authors have reported increases in deep tenderness following injection of hypertonic saline. However, this finding could not be confirmed in a recent study with control injection of 0. The finding of deep hypoalgesia to intramuscular electrical stimulation proximal to the pain area in healthy subjects further complicates the interpretation of pain-induced effects on deep sensitivity, 7 as does the observation of deep hypoalgesia to pressure stimuli in referred pain areas and extra-segmental sites.

Thus, in the normal somatosensory system, descending inhibitory controls and segmentally organized inhibitory mechanisms may partly counteract peripheral and central sensitization. Combined injection of BK and 5-HT or substance P and BK causes significantly lower pressure-pain thresholds, and injection of capsaicin into the masseter muscle also causes significant reductions in thresholds. In conclusion, the effect of intramuscular injection of hypertonic saline on deep sensitivity is relatively modest in healthy human subjects, probably because of little or no potency to induce peripheral sensitization and a concurrent activation of endogenous inhibitory control systems.

A large number of studies have consistently reported lower pressure-pain thresholds in the jaw-closing muscles of patients with TMD pain compared to control subjects. The pathophysiologic mechanism responsible for lower pain thresholds in deep craniofacial tissues could be a sensitization of peripheral nociceptors. Animal studies have shown that a deep noxious input causes sensitization of the peripheral receptors.

Although peripheral sensitization may cause deep tissue hyperalgesia, there is substantial evidence that sensitization of second-order neurons in the spinal cord or brain stem is also involved in the pathophysiologic process. Based on studies of capsaicin-induced cutaneous hyperalgesia, central summation of nociceptive inputs from muscles would be expected to be exaggerated in musculoskeletal pain conditions if central hyperexcitability is involved.

In line with this suggestion, the efficacy of temporal summation of intramuscular electrical painful stimuli is increased in fibromyalgia patients compared to control subjects. The site-specificity and extent of deep hyperalgesia has been examined in several papers. One study reported that the pressure-pain sensitivity in the finger was increased in patients with TMD pain. In accordance, Maixner et al , have presented good evidence that patients with TMD pain are hyperalgesic to stimulation of deep tissues outside the craniofacial region. They speculate that this state of generalized deep hyperalgesia could be caused by defects in endogenous inhibitory control systems, which could also account for observations of generalized hyperalgesia in tension-type headache patients , and fibromyalgia patients.

It is difficult to explain the observed differences, since strict inclusion criteria for the diagnosis of TMD pain were followed 3 and comparable pressure algometers were used in these studies. In contrast, more pronounced changes in deep pressure sensitivity were observed in the finger than in the anterior temporalis in patients with chronic tension-type headache compared to healthy controls. Moreover, graded responses corresponding to transitions from localized pain complaints to more widespread pain complaints might be of importance. An interesting observation is that many fibromyalgia patients have a preceding history of localized muscle pain that develops into a more generalized pain condition.

In summary, there is good evidence that the sensitivity to pressure stimuli within the local pain area is increased in patients with craniofacial muscle pain, ie, a localized deep hyperalgesia. One mechanism that could be responsible for the observation of deep hyperalgesia is sensitization of peripheral nociceptors. However, the observation of more generalized increases in sensitivity to pressure stimuli in some patients with craniofacial muscle pain suggests that changes in central hyperexcitability are involved as well. The finding of generalized deep hyperalgesia contrasts with the experimental muscle pain studies in healthy subjects, in which there is considerable evidence for deep hypoalgesia outside the local pain area.

The development of persistent muscle pain and generalized deep hyperalgesia could be associated with a gradual decrease in the efficacy of endogenous inhibitory control systems or an imbalance between descending facilitatory and inhibitory control systems. A practical implication of the psychophysical studies reviewed above is that stimulus intensity, stimulus modality, stimulus location, and rating scales must be carefully described and standardized to obtain useful information and allow comparisons between studies. There is a continual need to supplement the data from previous studies of craniofacial muscle pain with new data derived from extra-segmental stimulation to determine the extent and degree of somatosensory changes in well-defined subgroups of patients.

An important note is that many patients with craniofacial pain may also have unrecognized pains in other parts of their body. A wide variety of somatosensory changes can be expected in conditions with craniofacial muscle pain, ie, both hypo- and hyperalgesia and hypo- and hyperesthesia have been described in experimental and clinical pain studies. From a clinical point of view, psychophysical tests may nevertheless facilitate the differential diagnosis, eg, neurogenic pain disorders often have somatosensory deficits in discrete regions related to the nerve supply, whereas patients with craniofacial muscle pain are unlikely to demonstrate a strict somatotopic pattern of changes.

Furthermore, the psychophysical studies imply that both peripheral sensitization and hyperexcitability of central neurons may be responsible for the observed effects of muscle pain. This means that the management of craniofacial muscle pain should target both peripheral and central sites. Finally, the experimental pain studies have clearly indicated that deep and superficial somatosensory sensitivity can change in the presence of jaw muscle pain, , which suggests that patients with persistent muscle pain do not a priori have lower psychophysical thresholds. In contrast to superficial types of pain, pain from deep structures is typically described as diffuse and difficult to locate precisely.

Pain localized to the source of pain is termed local or primary pain, whereas pain felt in a different region away from the source of pain is termed referred or heterotopic pain. Experimental human studies with infusion of hypertonic saline into the midportion of the masseter muscle have shown diffuse areas of pain within the muscle, which spread toward the temporomandibular joint, temple, and eye region on the ipsilateral side 99,,,, Fig 3.

Preliminary maps of saline-induced pain from 6 different pericranial muscles showed that the masseter and anterior temporalis were consistently associated with referred pain patterns, whereas other pericranial muscles showed a less uniform pain distribution among subjects. In the craniofacial region it is clinically relevant that experimental jaw muscle pain can cause pain referred to the teeth. Likewise, it is well-established that odontogenic pain may mimic jaw muscle pain.

The frequency and area of referred pain is dependent on the perceived intensity of the experimental painful stimulus 96,,, and the duration of the stimulus.

Mechanisms of Clinical Signs BRAND NEW Textbook

Thus, it has been suggested that temporal summation of afferent inputs onto common central neurons may be involved in the development of referred pain. The increase in self-reported pain areas in human models of experimental muscle pain is paralleled by the findings of an increase in receptive field size of spinal cord and brain stem nociceptive neurons in animal models of myositis. It is likely that there is an association between the increases in referred pain areas and the increases in receptive field size related to changes of the excitability of central neurons in the brain stem and spinal cord.

The various theories on referred pain mechanisms have been reviewed recently. Mechanisms other than central convergence may also be involved in the expression of referred pain, since there is normally a time delay between the onset of local and referred pain. Thus, myositis-induced input from muscle nociceptors could lead to an expansion of the responding neuron population in the spinal cord or brain stem.

Mechanisms of Clinical Signs - Mark Dennis, William Talbot Bowen, Lucy Cho - Google книги

The neurobiology subserving such mechanisms is probably related to central sensitization of second-order nociceptive neurons and the development of hyperexcitability. Pain drawings have not been applied on a regular basis for assessment of TMD pain. Travell and Simons presented the classical topographic distributions of jaw muscle pain. These maps were drawn from the clinical experience of the pain patterns produced by activation of trigger points in the jaw muscles. Depending on the location of the trigger points in the superficial part of the masseter muscle, pain may be referred to the mandible or maxilla sinusitis-like pain , to the mandibular or maxillary molar teeth toothache , to the gingiva, to the temple and over the eyebrow, or preauricularly to the region of the temporomandibular joint earache.

11. Eye Clinical Signs - GP Clinics - Dr. Vaidya

From the deep part of the masseter, pain can be experienced in the mid-cheek area and the ear earache and tinnitus. In close accordance with this description, it has been found that the pain of trigger points in the deep part of the masseter may often However, this central mechanism may be modulated by chronic pain conditions. The referred pain area induced by hypertonic saline is enlarged in patients with chronic fibromyalgia and whiplash syndrome as compared to control subjects. Interestingly, referred pain proximal to the injection site has been observed in fibromyalgia and whiplash patients, whereas this is rarely found in healthy subjects.

Hence, central hyperexcitability is most likely involved in the facilitated response of referred pain. In line with this notion are findings that the NMDA antagonist ketamine reduces the increased areas of saline-induced referred pain in patients with fibromyalgia.

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Experimental jaw muscle pain evoked by injection of hypertonic saline shares many of the clinical features of persistent muscle pain in the craniofacial region, with spread of pain to the temporomandibular joint, jawbone, and teeth. The perceived intensity and duration of muscle pain seem to be important factors in the spread and referral of pain. The underlying mechanisms responsible for this spread and referral of pain are most likely related to central convergence of afferent fibers and unmasking of new synaptic connections resulting from central hyperexcitability.

Thus, human experimental pain models may be used to study in detail the underlying neural mechanisms of referred pain, eg, by blocking the peripheral input from the referred pain area. Pain drawings are useful tools in experimental and clinical research to map the extent of pain, but they cannot differentiate between local primary pain and referred pain heterotopic. Furthermore, the current versions of pain drawings do not distinguish sufficiently well between superficial or deep types of pain.

The clinical implications are the use of diagnostic blocks to differentiate between local and referred pain areas and early treatment to avoid the spread of jaw muscle pain. There are good reasons to believe that jaw motor function and muscle pain are interrelated, mainly because the cardinal symptoms of TMD include both pain and tenderness in craniofacial muscles and restrictions and deviations in jaw movements.

An important problem with clinical cross-sectional trials is the difficulty in identifying what is the cause and what is the effect of muscle pain. Experimental muscle pain models may therefore provide important insight into the nature of such sensorimotor interactions. The following sections will review the literature on the interaction between craniofacial muscle pain and various jaw motor functions, with the exception of jaw reflexes, which have recently been reviewed. The completely resting muscle is characterized by the absence of any EMG activity ; however, with the jaws at rest, there is weak EMG activity present in the human jaw-closing muscles.

In the trigeminal system, the jaw-closing muscles serve as the physiologic extensors and the jaw-opening muscles as the flexors. To avoid a discussion of cause-effect relationship between muscle pain and surface EMG activity at rest, a number of human experimental studies have directly measured EMG activity in response to deep injection of hypertonic saline. However, no surface EMG activity could be detected in 2 of 7 subjects; 1 subject demonstrated increases in EMG activity before the onset of pain, and no increases in intramuscular EMG could be found.

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Nevertheless, the authors saw no reason to challenge the well-accepted concept of the pain-spasm-pain theory. Graven-Nielsen et al found an increase in intramuscular EMG activity following infusion of isotonic or hypertonic saline into the tibialis anterior muscle but reported no difference in EMG activity between the 2 infusions. Finally, it has been shown that hypertonic saline injection into the masseter and tibialis anterior causes a transient increase in both surface and intramuscular EMG activity, but this activity is not correlated to the perceived pain intensity as measured on visual analog scales.

Overall, these studies suggest that a number of factors may influence postural EMG activity, eg, electrode type and mimetic muscle activity. There is little experimental evidence to suggest a long-lasting increase in EMG activity in human subjects during ongoing experimental muscle pain.

The weak and inconsistent signs of EMG increases in humans are in direct contrast to the robust EMG increases observed in the jaw muscles of animals exposed to injection of algesic substances into deep craniofacial tissues. It should be noted that the jaw muscle responses evoked by noxious stimulation of deep craniofacial tissues involve strong responses in both the jaw-opening and jaw-closing muscles. This can be interpreted as a "splinting" reaction, with the physiologic purpose to limit jaw movements and allow rapid healing.

Mechanisms of Clinical Signs

There is no consensus on the level of EMG activity recorded by surface EMG electrodes overlying the jaw-closing muscles in conditions with craniofacial muscle pain. A number of studies have indicated no significant difference in postural activity between patients with TMD pain and control subjects.

For a long time, increased postural EMG activity has been believed to play a very important role in the pathophysiologic mechanisms in many musculoskeletal pain disorders, including pain in the craniofacial region. Increased EMG activity in painful muscles would also intuitively explain the clinical impression of increased tension or hardness in the same muscles.

Recently, evidence was presented for increased hardness of pericranial muscles in patients with tension-type headache.

In this respect, confusion regarding terminology has long existed, since the terms "muscle tension," "muscle spasms," "muscle contractures," and "muscle hyperactivity" have been used interchangeably but may represent entirely different conditions. Later, Johansson and Sojka presented a model to explain the muscle tension and pain that integrated the gamma motoneuron system in the pathophysiologic mechanisms. Mense 11 discussed a modified vicious cycle concept in which the critical component was local ischemia.

However, it was pointed out that at present there is no evidence for the suggested chain of events. Finally, Simons and Mense have proposed that tension in painful muscles is electrically silent and that muscle contracture and not contraction could cause tension. The minute loci of trigger points could be associated with localized EMG activity, but the question of increased EMG activity in trigger points of jaw-closing muscles has not yet been unambiguously answered.

The topic of postural EMG activity in painful musculoskeletal disorders has for decades caused much speculation and discussion and continues to do so.