CP is both the presence of something AND the absence of something.
In another article at this site, it was suggested that long explanations of CP with laypersons, or even with uninformed professionals, can lead to a lot of frustration. It is often better to just say, “I have Central Pain” and let the commenter realize there is something they don’t know; or, in the case of a professional, to hand them a printoff of something here or from a text. The unread professional may be more difficult, if they assume they would surely have learned about CP if it existed. The CP patient is not responsible for failings of the professional’s medical or nursing school. Former neglect is no excuse for future neglect. Information from the National Institutes of Health, from the journal “Pain” or from this website may be helpful in expanding the database of the professional, so that allowance for the reality of CP can occur. It is not back pain, it is the terrible result of thalamic injury.
There are occasions, such as with family, but not always then, when some explanation of the CP symptoms is needed. In these conversations, it may be helpful to state that CP is both the absence of something and the presence of something.
There is always a sensory loss with CP. This creates a kind of numbness, frequently also a weakness or heaviness, and loss of accurate sensation of the body surface (atopoesthesia) and extremities. The distinction between digits, or between feet and legs may be lost. Is this numbness purely numbness. It is not possible to tell in Central Pain, because interposed in the numbness is pain, or the presence of something. Thus CP is both the absence of something and the presence of something. The pain is extraordinary in amount and in quality. The presence of the pain is so pervasive that the sensation of numbness is not received with clarity. By comparison, the silence of your mate may be overshelmed by the noise of your children.
The pains of Central Pain can be divided into two presumptive varieties. The word presumptive is used here because recent studies give a hint that the motor tracts may somehow generate some of the pain of CP or may at least have a role in the modulation of CP pain. Electro or radiostimulation of the motor cortex inhibits central pain, but the attempt has also been associated with the creation of phantom limbs. Normally, when we say pain, we mean signal carried in the sensory tracts. The sensory tracts are of two varieties, that which is carried in the anterior cord, or spinothalamic tract pain (burning, cold, and touch) and that which is carried in the posterior cord, or posterior column pain (muscle pain and lancinating pain).
Function of the posterior columns can be measured with somatosensory evoked potentials. SSEP’s are not measuring pain, there are giving a general idea of how the posterior columns are doing. If there is prolonged latency on SSEP in the time for signal to pass through the posterior columns, the person is very likely to have muscle pains or electrical shooting pains. There is nothing to prevent a person having damage to the anterior AND posterior cord.
Events of cord compression or hypoxia from compression often injure both sides of the cord. Those with vessel injury only may have blockage of blood supply. The arterial vessels have stronger walls than the veins, so those with spinal cord injury and CP without full paralysis may have had compression of the more easily collapsed veins. This venous obstruction creates s damning of blood within the cord which prevents new blood from coming in via the arteries. If no new blood can enter a blood clogged cord, the cord will have no oxygen and will be damaged. All areas improperly drained of blood by veins, the so called “watershed areas”, will show affect. Arteries in the central nervous system are very prone to vasospasm, and that is also a concern as a cause of cord injury, but most compression being marginal, the veins are thought to be much more vulnerable.
The venous situation OR the arterial situation are both capable of injuring ONLY the anterior cord or the posterior cord. Thus, we see individuals with ONLY posterior column pain or ONLY anterior cord pain, but frequently we see injury in both, particularly when injury occurs when the neck is hyperextended or hyperflexed, when there is a pincer like effect from the ligamentum flavum in back and the disc/vertebraal margin and posterior longitudinal ligament in front of the cord. The cervical spinal canal narrows 2-3 mm when the neck is extended or flexed.
If there is less than 3mm clearance, the cord will be compromised by extension (drawn back) or flexion (drawn forward). These compressive forces are even more prevalent if there is a combined rotation of the neck with flexion or extension, which is known as translational movement. In most people a canal of 15 mm and cord no bigger than 9,5 mm can be expected, which gives 5.5 mm clearance, but this figure reflects ONLY the cord and the bony canal around it. The vessels and structures running with them are more susceptible to injury. The vessels run in the intervening space between bony canal and cord, and using the above averages of upper normal, compromises of less than 5.5 mm can cause arterial vasospasm, or swelling and injury around the veins, leading to compression. Of course, if there is a fracture of the vertebrae, then a bony frgament can be dislodged which compresses the cord itself.
Radiologists are sometimes guilty of assuming that because there is sufficient room for the cord, that there is sufficient room for the vessels supplying the cord. This is simply not true. The anterior spinal artery, which supplies the lower cervical cord, has its origins in the carotid arteries which come off the aorta, and runs as the anterior spinal artery which is right at the front of the cord, going up toward the head. It is correct that a branch of the anterior spinal artery dips into a groove in the front of the cord at each level, but the anterior spinal artery branch must receive its blood supply from the more superficial vessel, which may have been compressed.
The vessels are too small to be imaged, even on MRI, and the comprsssion and swelling may have gone down by the time of the study, leading the radiologist to conclude incorrectly that the cord was not damaged. This error is especially common when the whitish hue of swelling (caused by water in the cord) has resolved and no bright areas can be seen. This feature explains why it is more common NOT to see bright lesions in injuries which cause central pain. Deformations of the cord substance are not uncommon, but radiologists typically do not comment on this unless it is severe. A compression ratio, or ratio of the front to back diameter vs. the side to side diameter of the cord is desirable, but rarely included with the interpretation.
The Japanese have begun to have the computer calculate the AREA of the cross sectional cord at each level, for comparison, but this is not usually done in the United States at the present time. One does see the better radiologists taking note of a “kidney bean” shaped cord, but we would prefer to see AP/transverse numbers which pick up lesser compressions and deformations, since the cord must really be damaged before it is perceived as “kidney bean” shaped. A practice cf calculating ratios by number would allow marching down the percentage of compression and correlating that with clinical symptoms. There will not be jump from no injury to total injury, but a gradual scale of symptoms which correlate to some degree with gradually declining values in the compression ratio. (See McHenry, K., Petrizze D., “Clinical and Radiologic Features of Central Pain” Controversies in Neuroscience V p. 13, Dow Institute, 1994, Portland)
These measurements would go far toward eliminating the central pain patient who is subjected to doubt over the injury. A negative film is often seen to be positive when viewed by an expert neuroradiologist with a background in compression ratios. Whether or not the readiologist performs this evaluation, the neurologist and neurosurgeon should be familiar with it. If you are congronted with a doubting Thomas, it is entirely appropriate to ask what the compression ratio of the cord is.
If the clearance for cord is only one or two millimeters and you have central pain, a compressive episode is highly likely. The radiologist may not agree, but the radiologist only rarely sees patients, and even if he/she does visit the patient, most of them will have no pain, or may be seen BEFORE central pain has had time to develop, possibly leading to a false impression of the frequency of nerve injury pain. Since MRI is new and always changing, the surgeon may be somewhat intimidated by the big powerful magnet and may defer to the radiologist more than is the practice with plain xrays. The patient should not be left in the gap, but both professionals should confer together for the patient’s sake. To their credit, many neuroradiologist are attempting to fill this gap, but there is still room for better communication and more precise clinical evaluation.
The inclusion of functional MRI in pain patients will go far toward eliminating the skepticism that often attaches to central pain symptoms with “normal” MRIs. This easy calculation, the compression ratio, can be done with a ruler, even if the MRI technologist failed to have the computer do it during the MRI. When the injury is near C4 or C5 the anterior spinal artery may temporarily fail to supply cord, or may never have supplied it in the first place. In the neck, vessels coming in through the foramina, or opening for the spinal nerve, which are called the “radicular arteries” or “medullary arteries” may supply both sides of the cord even though the radicular artery typically enters from only one side.
Injuries to the neck which lead to central pain nearly always cause bilateral pain, suggesting a problem with the more superficial core arteries, which ultimately supply the smaller vessels embedded in the cord proper. The superficial arteries are closer to the compressive forces, ie. the vertebrae and disc up front and the ligamentum flavum in back. The vsssel which supplies the back of the cord penetrates the ligamentum flavum (which joins the vertebrae above with the vertebrae beneath. Any swelling in the lig. flavum will compress the penetrating artery or veins.
Those with CP who are not paralyzed nearly always have some weakness or problems of control. This is called paresis. IF paralysis is involved, it is called plegia. Both terms refer to motor consequences. There really are no satisfactory terms for partial sensory loss or degrees of nerve injury pain. Injured motor nerves simply fire less, but injured sensory nerves fire more, much more, even if the discriminating ability has been lost from the pain nerve. What remains is a poorly localized burn which is known as protopathic burning. It is the most durable feature in a nerve and the last sensation to be lost in an injured nerve. A nerve which cannot feel touch at all can definitely fire wildly with a protopathic pain signal.
In central pain, protopathic firing is known as “dysesthesia”. Paresis is an imprecise term, which may mean mere tingling, or it may mean weakness, loss of muscle memory or control, and pain. For unknown reasons, those with paresthesia nearly always have severe CP, possibly because more of the cord remains functionally able to transmit abnormal signal. Some unfortunate plegics also have fully evolved CP, and this is an unimaginable state.
Such people can only be wished well, with the hope that they will have sufficient support from the medical profession, helping agencies, and family. This site is motivated to acknowledge such individuals in any way possible. Just as cancer patients are extended orphan drugs, there should not be excessive regulatory scrutiny of doctors attempting to help CP with medications. These really are extreme cases, and doctors who treat them should be extended some leeway, without fear they will be censured. “My greatest privilege as a doctor is to help my patients in pain.”–Albert Schweitzer.
Plegics tend to have the central pains in zones or areas where sufficient sensation remains as an incomplete injury, such as the ends of extremities, or at the level of injury. Many plegics have what is called “sunburn” on the body, which means they have some of the dysesthetic burning, which may nevertheless permit them to wear clothing. A full blown CP subject cannot tolerate clothing on the distal extremities, or tolerates it only with considerable agony. The inability to wear appropriate clothing causes considerable loss of identity and public rejection.
It is impossible to quantify Central Pain. This must await better brain scans and knowledge of pain mechanisms generally. Possibly the new tensor MRI will allow better correlation of the paths of pain fibers so that multiple centers in the brain may be studied to evaluate and measure pain. Existing theory is that the painfulness of pain is served by the insular cortex of the brain. The surrounding brain areas outgrow the insula and overlap it so that it appears buried unless the overlying masses of tissue are lifted away. Slightly above and more forward of the insula in the operculum of the parietal cortex, which serves the quality of the pain, and the location on the body is detected by the postcentral gyrus, a ridge behind a groove which runs from side to side about halfway back on the brain, the postcentral sulcus. “Central” refers to the center top of the brain. The motor cortex is the ridge in front of the groove. This is the area stimulated to inhibit pain.
Injury to the cord in the neck may give the central pains in the face since pain from the face travels down to the cord in the neck and then ascends again with body pain tracts.
It is often better to explain that CP involves both a loss of sensation and the imposition of a variety of painful sensations. It is also appropriate to tell an interested listener that severe CP is the most severe pain state known to man, both because of the sensation and the amount of the body involved.
In stroke, the pain is usually on one half of the body, with only one side of the thalamus being affected. In multiple sclerosis, the fatty sphingomyelin of the myelin which encases and insulates nerves is attacked. When the nerve insulation fails, the transmission is disordered. Since demyelination can occur anywhere, MS subjects can have a spotty loss, often leading to a general loss. MS frequently involves some motor sensation, leading to the so-called MS Hug, which means tightening of the chest muscles.
In Parkinsons, there is abnormality of the subthalamic nucleus, which sits below the thalamus. Since the subthalamic nucleus has some pain function, Parkinsons subjects often have pain, but it tends to be less severe, usually much less severe than with thalamic dysfunction. Pain is always severe to the person who has it, but Parkinsons sufferers can generally wear clothes, something denied to classical severe CP. The point is not to minimize the pain of Parkinsons, but merely to point out that a range of severity is possible in CP. Pain is minor only to someone who does not have it.
It has sometimes been said that the amount of pain does not correlate with the amount of damage. This is probably a bad statement as it stands. The nervous system puts a very high priority on the nervous system. The brain does not feel pain it is true, but will certainly respond to injury to nerves, with a tremendously strong pain response. One must make a judgment to say that injury to a hand is more or less significant than nerve injury. Different kinds of pain result, but there is no basis to say nerve injury pain is meaningless compared to injury to bone or muscle. Pain from injury to body parts ends, but pain from injury to nerves quickly travels to the thalamus and never ends, even if the nerve is severed. “Peripheral damage leads to central injury.”–Patrick Wall This may merely mean that even if the brain attempts to quiet peripheral nerves, it cannot if the peripheral nerves cannot move chloride to the membrane. In the case of stroke, it may mean that the thalamus is signalling its own damage. The brain receives orderly software written on the fly from the thalamus. If the brain receives anything other than the expected signal, it may read it as pain. CP can be incredibly painful.
With syringomyelia, a pocket or chamber develops in the middle of the spinal cord, where spinal fluid normally pulsates in response to the heartbeat. Either through some congenital weakness or through injury, the canal in the center of the cord expands. This presumably puts pressure on the veins in the cord, creating the watershed affect described above.
With toxic exposures or viral infections, it is thought that another mechanism may be at play. Although not yet well studied, there is thought to be a system of pain which involved acetylcholine and the nicotinic receptors whereby peripheral signal may be sufficiently disordered to precipitate central pain. Some of these tracts are different from the classical spinothtalamic ST and posterior column tracts and may represent a subset of Central Pain. Little is known at this point, except that the pain in these individuals seems to be less severe than with conventional CP. It is not known how they respond to treatment. Those with posterior column pain can expect benefit from pain medicines, while those with injury to the spinothalamic tracts may not benefit from any known treatment.
The public has a very hard time grasping the concept of CP because those few who know anything about nerves tend to think in terms of electrical cords. Incomplete damage to an electrical cord simply results in less current. Thin wire carries less than thick wire. However, pain transmission does not occur with a volume of electrons. Pain is more complicated. First, the signal is created by ions with an electrical charge flowing through channels in the membrane of a neuron. If there is damage, two things happen. One, surrounding cells release chemicals (growth and repair chemicals) which hypersensitize both surrounding neurons and the dorsal root ganglion just outside the cord, where the nerve signals congregate.
Oversignal, or excessive gain from this hypersensitization can damage a sensitive thalamus. These areas are ALARM areas which signal risk of harm, or actual harm. Attempts by the brain to shut down the alarms fail in nerve injury because injured neurons cannot make the protein carrier of chloride, which is necessary to inhibit nerve signal. The inward flow of positive ions generates energy in mitochondria (the energy factory of cells), while the flow of negative ions consumes it. It is possible, but not well studied, that there are problems with energy within the neuron. Proton pumps may have failed. it is known that the VR-1 channel which controls Calcium flow at the neuronal membrane, is kept open by the changes of CP. Drugs which open the VR-1 channel, such as capsaicin, cause a diffuse burning pain in a zone around the injection site. Local C fibers are sensitized by the capsaicin, which then send signal to the dorsal root ganglion and cord, where normally unresponsive pain fibers, the big powerful A fibers are recruited and begin a spontaneous firing, which is part of the hypersensitization described.
The hypersensitization is to such a degree that no stimulus at all is required for the injured nerve fibers to fire. It is automatic and continual. This is surely torture. What is responsible for the fixed hypersensitization is not clear. The virtual endless hypersensitization can be confirmed by patch clamping of the nerve and it is also known that the chemicals of hypersensitization persist. However, there is more to the story. In Parkinsons the dopamine II receptor becomes locked. Chemicals embed and are locked in forever which disable the DII receptor. Stem cell therapy envisions injection of new DII receptors into the brain. Permanent destruction of receptors by a pain chemical may be present in CP. It is also possible that pain acids denature the configuration of certain receptors, rendering them inoperative or locked. It is possible that some of the pain chemical receptors are locked and cannot turn off, or that surrounding cells continue to produce new growth and repair factors which overproduce pain chemicals, maintaining the hypersensitization. This second process is known as “exciter toxicity” and is described in more detail at this site. (Use SEARCH for “exciter toxicity” to find more information).
Blocking central pain with drugs only half succeeds. The muscle pains and shooting pains usually respond to opiates or other pain meds, including antiepileptic drugs which quiet the central nervous system generally. The burning dysesthesia and visceral pain is more troublesome and there is no really satisfactory treatment for this. The ST damaged person must receive supportive help, including counseling on how to reduce stress and demands. The central nervous system can be quieted by reducing stress and expectations. It is really the only therapy available for severe ST pain. The apparently “lazy” lifestyle may cause resentment by others who do not realize that the mere withstanding of pain is terrifying, exhausting and demoralizing. We do not expect someone to work after a severe shock or stress. This impact from severe pain continues each day and through the night. Nights are actually the most difficult time in CP because the skin cannot bear contact with the sheets. The exhausting stepping from sleep to wakefulness, and back again, with times of extreme agony from touch burning, through a long and lonely night is emotionally devastating and discouraging. Days are punctuated by pain in the muscles or viscera. Small movements may cause pain in the gut, or minimal amounts of urine can cause overshelming burning in the bladder. Frequent emptying of the bladder can actually become a life style. Attempts at movement may cause such severe pain in the muscles that the person is functionally paralyzed. Those who move may collapse at periods in the day with aching, burning soreness throughout the body. There is no more genuinely disabled person than one in the grip of severe central pain. They are not only disabled physically, they are disabled emotionally. Paralytics with CP confirm this. (see “Reality CP Update” at this site). The emotional disablity is the result, not the cause, of Central Pain.