Diaphragmatic Cramp as a Possible Cause of Noncardiac Chest Pain and Referred Mandibular Pain.
The sudden onset of chest pain and the urgent admission to an emergency unit results in emotional trauma and justifiable concern in all those involved. However, not all chest pain is caused by cardiac ischemia. In about 30% of cases the physiological parameters and electrocardiograms are normal. These normal findings alone do not exclude myocardial infarction, particularly in the very early stages, but if a cardiac origin can be positively excluded, the patient is left with an unexplained pain where the treatment is often analgesia and reassurance. Noncardiac chest pain may be localized on either side of the anterior chest wall or appear to emanate from deeper within the chest cavity. Pain often radiates in a pattern similar to that of cardiac origin, extending to the back, shoulder or mandibular teeth. The duration of the episode may be from a few minutes to hours, during which time the patient is incapacitated from many normal functions. Various causes of noncardiac chest pain have been recorded, especially reflux of hydrochloric acid from the stomach into the lower esophagus (gastroesophageal reflux, reflux esophagitis or heart burn) which has been found in up to 60% of noncardiac chest pain patients. Other possible causes include musculoskeletal chest pain, pericarditis, pleural pain, thoracic nerve root pain and esophageal spasm. If pain of noncardiac origin persists for longer than a few minutes, one further possible cause might be diaphragmatic cramp.
A male in his early fifties suffered a thirty year history of noncardiac chest pain with referred mandibular pain which came on with no apparent cause. As a young man the attacks of pain were more common than later in life, with the onset of chest pain preceding the mandibular pain. Recently, however, unilateral then bilateral posterior (molar) dental pain often occurs first, providing a warning of the chest pain that follows. The pain lasts from fifteen to sixty minutes, with surges of intermittent severe pain with brief spells of relief. The pain has a cramp-like crescendo quality and is not relieved by changes of position, deep breathing or rest. All chest and dental examinations proved negative, including electrocardiograms (ECGs), and no diagnosis has ever been recorded. Quinidine was prescribed previously but this proved ineffectual. No recent treatments have been prescribed.
If the hypothesis of diaphragmatic cramp is true, it is likely to be a painful involuntary contraction of the skeletal muscle component of the diaphragm, akin to muscle cramps common to limb and trunk muscles. The causes of cramp are not well understood, but factors influencing the onset of cramp generally include muscle chilling, electrolyte imbalance, excessive nerve stimulation and overactive muscle excercise. Some of these factors, like chilling, do not apply to cramping of the diaphragm, but nerve stimulation may be an important factor.
Diagnosis of this condition is currently not possible because cramp is virtually undetectable in muscles to which there is no direct access. The inability to directly observe this phenomenon indicates that diaphragmatic cramp may be a previously unrecognized event. The diaphragm has a peripheral sheet of skeletal muscle inserted into a central aponeurotic tendon. Skeletal muscles in the limbs and elsewhere are prone to cramping. Some patients describe chest pains that have a "cramp-like" quality to them, ie, feelings of sporadic tightening with crescendos of pain, followed by relaxation associated with remissions of pain in repeated cycles, similar to that experienced in limb muscles. The autonomic innervation of the diaphragm is via the phrenic nerve, and intermittent and sporadic impulses from this nerve are known to cause hiccoughs, the result of twitching of the diaphragmatic muscle. It might be possible therefore that sustained impulses from a central source along the phrenic nerve could cause skeletal spasm akin to cramp. Further, skeletal muscle cramps at any site may arise from the intramuscular portion of the motor nerve terminal itself or from the peripheral portion of the nerve.
The phrenic nerve also contains many sensory fibers. Thus, the phrenic nerve, being derived from spinal nerves of mixed motor and sensory function, could be the innovator (motor) of the cramp at a local or central level and the bearer (sensory) of the pain.
Phrenic nerve motor impulses arise from the dorsal respiratory group (DRG) of nuclei which lie within the nucleus of the tractus solitarius (solitary nucleus) in the medulla (Fig 1). These impulses and are the main respiratory drive.[4,5] Action potentials are generated by the DRG to cause inspiration and expiration on a rhythmic basis. These action potentials are transmitted from the DRG down the solitariospinal tract to the grey matter of the phrenic nucleus in cervical cord segments 4-6. From here the path follows bilateral spinal nerves out via the cervical plexus to the phrenic nerve which arises from the third, fourth and fifth cervical spinal nerve rami.
[Figure 1 ILLUSTRATION OMITTED]
Muscle cramps possibly cause pain by mechanical shearing forces on nociceptors within the muscle as some muscle fibers cramp while other nearby fibers do not cramp. The possible reasons why normal respirations continue during diaphragmatic cramp may be that the intercostal muscles are innervated separately from the diaphragm, and thus not involved. Also, phrenic nerve involvement in cramp could vary in degree between the left and right branches, and could possibly be only unilateral, which would allow many muscle fibers on the affected side to function normally.
Mandibular Referred Pain
Mandibular referred pain may follow or precede the onset of the chest pain. The referred pain has characteristics similar to the corresponding chest pain, ie, surges of intense pain that correspond with the chest pain and which is perceived to affect the molar teeth on both sides, with brief periods of remission. Referred pain from the diaphragm is usually experienced in the shoulder due to commonly shared spinal roots in the cervical cord serving both the shoulder and the phrenic nerve. Mandibular referred pain probably involves the trigeminal nerve. Of the trigeminal's three main branches, the mandibular branch is the largest, with 78,000 myelinated axons compared to 26,000 and 50,000 of the other branches. The sensory component is dominant and connects with the trigeminal spinal nucleus of the medulla. The subnucleus caudalis (pars caudalis) is the lowest division of the trigeminal spinal nucleus, the neurons of which respond to tooth-pulp stimulation. However, the referred pain is perceived to emanate from this trigeminal branch only because the sensations are generated within the subnucleus caudalis in response to phrenic stimuli, and relayed from here to the cerebral cortex via the thalamus. Both areas allow pain to be experienced as a conscious phenomenon.
The link between this and the chest pain impulses arising from the phrenic nerve lies in largely unknown connections within the dorsal medulla. The DRG of the solitary nucleus lies at the same level as the trigeminal nucleus at the lowermost level of the medulla. As diaphragmatic and shoulder pain are linked by sharing a common cervical spine segment, diaphragmatic and mandibular pain are also linked by sharing the same medullary level. The nucleus raphe magnus and the periaquaductal gray matter, both of which exist higher in the medulla, connect with the trigeminal nucleus and influence pain perception. Stimulation of these higher nuclei can cause pain that appears to be of dental origin. The cerebral cortex receives both the diaphragmatic pain and the stimulation of the trigeminal nucleus, interpreting the latter as arising from the mandibular periphery.
Noncardiac chest pain is not life-threatening, but patients should be treated for their pain and not thought of as malingerers. Reassurance that the heart is not involved is helpful, but does little to relieve the pain. Since diaphragmatic cramp is not amenable to the normal methods of muscle cramp treatment, ie, massage and stretching, the only treatment available is quinidine and analgesia. Quinidine has been the treatment of choice for limb cramps for years,[3,8] but does not appear to be very effective for noncardiac chest pain. Muscle relaxants do not appear to have been used for noncardiac chest pain, and their effectiveness for cramps is limited at best. Chest pain is usually accompanied by fear and stress, so the treatment of noncardiac chest pain with analgesia is justified by the physical and psychological comfort it provides. Peripherally acting analgesics, such as nonsteroidal anti-inflammatory drugs (NSAIDs) may act at the neuromuscular level, but since the duration of most cramps tends to be limited to an average time of about ten minutes, the oral route of drug administration may not be fast enough to give pain relief before the cramp had resolved. Since the pain pathways involve medullary function, a centrally-acting analgesic, eg, pethidine, may be more appropriate, given by injection for faster action. It may be beneficial for the patient if they were offered the choice of the route of administration of the analgesia. They could be offered either a low-dose opiate derivative drug given by injection or an oral dose of an NSAID. This should be followed by a short period of observation until the cramp is relieved and the drug activity reduced. The effect of this would be to make the patient more comfortable and reduce anxiety in a situation where definitive diagnosis is not possible.
Diaphragmatic cramp as a potential cause of some noncardiac chest pains has not been previously identified. Mandibular referred pain associated with the chest pain may be due to the close relationship between the origins of the phrenic and trigeminal nerves within the medulla. Analgesia may be the only current option in the treatment of such an inaccessible cramp, but oral administration may act too late to be of benefit, and some patients may require a faster route.
I would like to thank Janet Vickers and Lynda Filer of the Division of Applied Biological Sciences of City University for their comments on this paper. Also my gratitude goes to Shelley Welsman of City University Audio Visual Aids Department for her assistance with the diagram.
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Questions or comments about this article may be directed to: William T. Blows, RMN, RGN, RNT, OStJ, BSc (Hons) PhD, Lecturer, Division of Applied Biological Sciences, St Bartholomew School of Nursing and Midwifery, City University, 20 Bartholomew Close, London, EC1A 7QN, England.
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|Author:||Blows, William T.|
|Publication:||Journal of Neuroscience Nursing|
|Date:||Jun 1, 1999|
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