Low back pain's etiology (cause) is one great example of the seeming impenetrable nature of reality. Is back pain caused by mechanical failure of discs and boney joints? Or is it caused by hypersensitivity in spinal nerves due to chemicals present with inflammation? Or is low back pain caused remotely by the body's executive center--the brain? Undoubtedly all these tissues and organs take some role in all back pain. But to definitively identify the one tissue or one organ which is principally responsible for back pain in a particular patient is unreasonable.
For example, I recently treated a woman who was diagnosed with a right groin strain. She has a history most significant for leukemia and treatment by radiation and stem cell transplant. Upon evaluation I noted that she was tender to touch over her pubic bones, her groin muscles and her outer hip muscles. Additionally when I had her lie on her back and applied a posterior (backward) shear stress through her right hip joint she complained of increased groin pain. I was immediately concerned about three things:
1) Possible stress fracture in her right hip which would occur due to post-menopausal osteoporosis;
2) Possible cancer metastasis to her pelvic girdle;
3) Possible low back pain referred to the right groin.
Her doctor ordered an MRI of her hips which revealed mild arthritic changes in both hips. Previous MRI of the lumbar spine had revealed mild spondylolisthesis (miniature spine fractures with no to minimal spinal bone displacement) at L4-5 and L5-S1. This data discourages the view that hip fracture is the cause (although MRI's can miss stress fractures) and ruled out a bone tumor. Possible causes of her hip pain would then be:
1) Mild hip arthritis;
2) Referred low back pain;
3) Muscle weakness and imbalance.
The doctor injected her outer hip area with carbocaine (a medicine in the lidocaine family) which immediately relieved that pain. The doctor ruled out low back pain at that point, stating that if it were low back pain the carbocaine would not have helped. Reflecting back on this just now I would beg to differ with his conclusion. Low back dysfunction causes hypersensitivity in sensory nerves distal to the low back. If her tender outer hip is caused by hypersensitive sensory nerves (versus a traditional bursitis or tendonitis) then carbocaine would have the affect of "numbing" these hypersensitive sensory nerves and render them inactive thus blocking the patients outer hip tenderness. In which case her hip pain would be from her back and not from her weak hip.
Medical professionals could spend a lifetime studying this patient and patients like her and may still be unable to determine which tissues or organs are responsible for her pain. Regardless of if we could identify whether it was the patient's back or hip or muscles which are causing her pain the causal question remains unsatisfactorily answered. For instance, if we determine it is muscle weakness on the right side causing her pain we do not definitively know what caused her right hip weakness. Why are both hips not weak? Why does a very active person who regularly exercises have this mysterious unilateral weakness? If we determine that it is her back causing the pain we do not definitively know what it is that causes her back pain. Is it her facet joints? Is it her disc? Is it her spinal nerves? Or, to beat all, is it because she has had this mysterious chronic weakness in the right hip?
And so it goes for the man asking the 'why' and 'how' questions. Just when he thinks he has gained some understanding he realizes that he has merely unearthed ten more questions about the nature of reality.
Saturday, June 21, 2008
Monday, June 16, 2008
Back pain and metaphor.
Last February I completed a class on the lumbar spine. One exciting epiphany for me was the thought that pain relief obtained through spinal manipulations are mediated not through mechanical "release" of joints, but rather through neurophysiological inhibition of pain neurons. Chiropractors and therapists in the past explained the efficacy of manipulations referring to poor spinal alignment due to capsular restrictions in the small spinal joints. Manipulations were purported to "adjust" the spine by "freeing" certain capsular restrictions. The idea of manipulations freeing restricted capsules has become decreasingly popular (although I would say at this time not decreasingly tenable) with a paradigm shift toward neurophysiologically decreased spinal pain via manipulations.
In particular two research studies with which I became familiar advanced my own understanding of spinal pain. One study was performed by chiropractors on cats. These cats had force transmitters surgically attached to their 6th lumbar spines. Additionally electrophysiologic readings were obtained from afferent mechanoreceptors (aka: nerves that sense muscle length) of spinal muscles. Oscillations were transmitted to the 6th lumbar spine and as the force on the lumbar bone approached that of a spinal manipulation an abrupt increase was sensed in electrical activity in the afferent mechanoreceptors. Doubtless this increased sensory input to the spianl cord has an effect on regulating the back. I would propose that stimulation of mechanoreceptors could be an initial step of a pathway of spinal reflexes to neurologically block the conduction of local pain sensations. In short, the vibrations from manipulations stimulate sensory nerves in spinal muscles which could in turn block pain conduction and recalibrate muscle resting tone. This theory (commonly referred to as the "gait theory" of pain inhibition) has been well developed in the medical field and there exist substantial scientific data which can be used to validate it.
A second study looked at the use of lumbar spinal manipulations for patients who satisfied a clinical prediction rule. This rule was developed to help clinicians predict which patients would benefit from manipulations. One interesting side note in this study was that each patient was manipulated at the same spinal level regardless of the location of "reduced capsular tightness". The location of the manipulation was not the determining factor in the success of the manipulation. One could conclude that it doesn't mater at which lumbar joint the manipulation was performed. This does not bode well for the older idea of "freeing" capsular restrictions at specific joints to relive pain. It does, however, fit well with the idea of neurophysiological reductions in pain sensation via a mechanically stimulated reduction of resting muscle tone and a lowering of resting membrane potentials in pain neurons.
My parting thoughts relates to truth and metaphor. As mentioned above, chiropractors and therapists used the idea of "freeing" capsular restrictions when performing manipulations. This is a prime example of the use of metaphor to convey powerful meaning to a patient about returning to health. The patient feels that something is "stuck" in her back and the therapist says he is "freeing" that which is "stuck." Regardless of whether or not this metaphor has been a true description of the biomechanical and neurophysiological reality or not, it has been helpful in conveying a sense of efficacy. During my career as a therapist I regularly am asked for explanations about function of the human body. "Why does my leg hurt when I walk?" "Why is my arm muscle weak some days but not others?" The questions are always personal and always difficult to answer in a meaningful and helpful way. Often times I employ metaphor for the purposes of encouraging the patient's understand of procedures and increase motivation towards compliance in therapy. The ethical qualm for me has become, how do I speak in metaphor while honestly tipping my hat to the ambiguity present in human understanding. Currently I am beginning to steer away from answers to 'how' questions and focusing on 'what' questions. I'll give anecdotes of what others have done to successfully overcome spinal pain and just skip over the how altogether. Intellectually these are dull answers but they are more true than any metaphor I can dream up to describe the latest theory. I do not deem the linguistic tool of metaphor to be intrinsically misguiding; rather I deem metaphor that construes fiction as fact to be false in the worst way--deception.
In particular two research studies with which I became familiar advanced my own understanding of spinal pain. One study was performed by chiropractors on cats. These cats had force transmitters surgically attached to their 6th lumbar spines. Additionally electrophysiologic readings were obtained from afferent mechanoreceptors (aka: nerves that sense muscle length) of spinal muscles. Oscillations were transmitted to the 6th lumbar spine and as the force on the lumbar bone approached that of a spinal manipulation an abrupt increase was sensed in electrical activity in the afferent mechanoreceptors. Doubtless this increased sensory input to the spianl cord has an effect on regulating the back. I would propose that stimulation of mechanoreceptors could be an initial step of a pathway of spinal reflexes to neurologically block the conduction of local pain sensations. In short, the vibrations from manipulations stimulate sensory nerves in spinal muscles which could in turn block pain conduction and recalibrate muscle resting tone. This theory (commonly referred to as the "gait theory" of pain inhibition) has been well developed in the medical field and there exist substantial scientific data which can be used to validate it.
A second study looked at the use of lumbar spinal manipulations for patients who satisfied a clinical prediction rule. This rule was developed to help clinicians predict which patients would benefit from manipulations. One interesting side note in this study was that each patient was manipulated at the same spinal level regardless of the location of "reduced capsular tightness". The location of the manipulation was not the determining factor in the success of the manipulation. One could conclude that it doesn't mater at which lumbar joint the manipulation was performed. This does not bode well for the older idea of "freeing" capsular restrictions at specific joints to relive pain. It does, however, fit well with the idea of neurophysiological reductions in pain sensation via a mechanically stimulated reduction of resting muscle tone and a lowering of resting membrane potentials in pain neurons.
My parting thoughts relates to truth and metaphor. As mentioned above, chiropractors and therapists used the idea of "freeing" capsular restrictions when performing manipulations. This is a prime example of the use of metaphor to convey powerful meaning to a patient about returning to health. The patient feels that something is "stuck" in her back and the therapist says he is "freeing" that which is "stuck." Regardless of whether or not this metaphor has been a true description of the biomechanical and neurophysiological reality or not, it has been helpful in conveying a sense of efficacy. During my career as a therapist I regularly am asked for explanations about function of the human body. "Why does my leg hurt when I walk?" "Why is my arm muscle weak some days but not others?" The questions are always personal and always difficult to answer in a meaningful and helpful way. Often times I employ metaphor for the purposes of encouraging the patient's understand of procedures and increase motivation towards compliance in therapy. The ethical qualm for me has become, how do I speak in metaphor while honestly tipping my hat to the ambiguity present in human understanding. Currently I am beginning to steer away from answers to 'how' questions and focusing on 'what' questions. I'll give anecdotes of what others have done to successfully overcome spinal pain and just skip over the how altogether. Intellectually these are dull answers but they are more true than any metaphor I can dream up to describe the latest theory. I do not deem the linguistic tool of metaphor to be intrinsically misguiding; rather I deem metaphor that construes fiction as fact to be false in the worst way--deception.
Saturday, June 7, 2008
Advocacy: Blood, Sweat and Tears.
Eight months now I have been treating a worker injured on the job. Currently she is at risk of losing workers compensation benefits related to her recent cognitive decline. Losing the benefits would be a devastating blow to this mother of four*. Her husband is unable to work full time due to caring for their six children and now his wife.
She suffered her injuries when a large stack of wooden pallets fell on her causing immediate neck and arm pain. She was admitted to the hospital and discharged shortly thereafter. Subsequently her symptoms became worse, she was re-hospitalized and fell into a coma for several days. Unfortunately diagnostic work-up focused mostly on her neck and shoulder and neglected her brain. She was discharged from the hospital after awaking from her coma. She was able to live at home with her husband and family, but unable to work due to pain.
Approximately four months after her injury the patient's husband noticed a rapid change in her behavior: drowsiness, paranoia, memory loss, inappropriate speech. A neurologist was consulted and he recommended physical and occupational therapy. My evaluation revealed marked deficits in the patient's neck and shoulder function and acute onset of vertigo with neck motion. Interestingly I found the patient's cognitive deficits to be more profound than her orthopaedic deficits. Those deficits matched those of a brain injured patient: poor attention span, short-term memory loss, decreased executive function. Apparently no MRI was performed on her brain and so I was unable to understand what was the underlying cause for this patient's decline.
She has made excellent progress with her shoulder and neck function. Sadly, though, her cognitive status prevents her from being safe when unattended and will possibly prevent her from ever being able to work again. Workers compensation is looking to deny any coverage for cognitive related disabilities claiming that her cognitive decline is not associated with the accident, but is rather a combination of the patient's diabetes and her poor diet since the injury. Neuropsychiatric evaluation revealed that the patient does have profound cognitive deficits in the realms of attention span, short term memory, safety judgement. In their conclusion, the psychiatrists stopped short of directly implicating her work injury for this patient's cognitive decline. I plan on advocating for workers compensation coverage for this patient. Below is the beginning of my line of argument.
Rational for explaining my patient's cognitive decline boil down to two: 1) traumatic brain injury with chronic cognitive sequela; 2) diet induced diabetic encephalopathy. I will develop the former rational as workers compensation is developing the later.
Traumatic brain injury typically results in an immediate and significant cognitive loss followed by a steady but small cognitive decline over the life of the patient. Given that my patient experienced a coma after her injury she likely suffered at least mild brain injury if not moderate or severe. Unfortunately no MRI is available from that time period and no MRI has been performed since. Consequently brain damage cannot be assessed. The lack of an MRI is very surprising in a case such as this one. A brain MRI has not been performed either due to medical mismanagement or due to the patient's haste to exit the hospital (she has expressed a strong phobia of dying in the hospital due to past family experience). Because no MRI is available certain brain injury diagnoses can not be ruled out and therefore should be considered as possible causes.
My patient experienced significantly increased appetite after her work injury. Increased appettite is associated with injury to the ventro-medial aspect of the hypothalamus. In such a case the patient's increased appetite (and subsequent diabetic encephalopathy) would then be a direct result from the work related injury. Magnetic resonance imaging of the brain would reveal the status of my patients hypothalamus. Damage in the hypothalamus means that the patient's increased appetite is a symptom as well as a cause. Increased food consumption would lead to diabetic encephalopathy. This entire process would then be a work related injury. Workers compensation would then be warranted for her cognitive issues.
Should the MRI demonstrate no damage to the hypothalamus I would argue that the patient's appetite changes are at the least an indirect symptom of depression related to her injury. Depression, unless treated, leads to increased appetite and hence the diabetic encephalopathy. Additionally, brain damage from the accident would predispose the patient toward onset of encephalopathy due to uncontrolled glucose levels. In other words, had she not had a brain injury, diabetic encephalopathy would be no where near as pronounced as it is now.
*I have changed various non-medical details about this patient to ensure privacy.
She suffered her injuries when a large stack of wooden pallets fell on her causing immediate neck and arm pain. She was admitted to the hospital and discharged shortly thereafter. Subsequently her symptoms became worse, she was re-hospitalized and fell into a coma for several days. Unfortunately diagnostic work-up focused mostly on her neck and shoulder and neglected her brain. She was discharged from the hospital after awaking from her coma. She was able to live at home with her husband and family, but unable to work due to pain.
Approximately four months after her injury the patient's husband noticed a rapid change in her behavior: drowsiness, paranoia, memory loss, inappropriate speech. A neurologist was consulted and he recommended physical and occupational therapy. My evaluation revealed marked deficits in the patient's neck and shoulder function and acute onset of vertigo with neck motion. Interestingly I found the patient's cognitive deficits to be more profound than her orthopaedic deficits. Those deficits matched those of a brain injured patient: poor attention span, short-term memory loss, decreased executive function. Apparently no MRI was performed on her brain and so I was unable to understand what was the underlying cause for this patient's decline.
She has made excellent progress with her shoulder and neck function. Sadly, though, her cognitive status prevents her from being safe when unattended and will possibly prevent her from ever being able to work again. Workers compensation is looking to deny any coverage for cognitive related disabilities claiming that her cognitive decline is not associated with the accident, but is rather a combination of the patient's diabetes and her poor diet since the injury. Neuropsychiatric evaluation revealed that the patient does have profound cognitive deficits in the realms of attention span, short term memory, safety judgement. In their conclusion, the psychiatrists stopped short of directly implicating her work injury for this patient's cognitive decline. I plan on advocating for workers compensation coverage for this patient. Below is the beginning of my line of argument.
Rational for explaining my patient's cognitive decline boil down to two: 1) traumatic brain injury with chronic cognitive sequela; 2) diet induced diabetic encephalopathy. I will develop the former rational as workers compensation is developing the later.
Traumatic brain injury typically results in an immediate and significant cognitive loss followed by a steady but small cognitive decline over the life of the patient. Given that my patient experienced a coma after her injury she likely suffered at least mild brain injury if not moderate or severe. Unfortunately no MRI is available from that time period and no MRI has been performed since. Consequently brain damage cannot be assessed. The lack of an MRI is very surprising in a case such as this one. A brain MRI has not been performed either due to medical mismanagement or due to the patient's haste to exit the hospital (she has expressed a strong phobia of dying in the hospital due to past family experience). Because no MRI is available certain brain injury diagnoses can not be ruled out and therefore should be considered as possible causes.
My patient experienced significantly increased appetite after her work injury. Increased appettite is associated with injury to the ventro-medial aspect of the hypothalamus. In such a case the patient's increased appetite (and subsequent diabetic encephalopathy) would then be a direct result from the work related injury. Magnetic resonance imaging of the brain would reveal the status of my patients hypothalamus. Damage in the hypothalamus means that the patient's increased appetite is a symptom as well as a cause. Increased food consumption would lead to diabetic encephalopathy. This entire process would then be a work related injury. Workers compensation would then be warranted for her cognitive issues.
Should the MRI demonstrate no damage to the hypothalamus I would argue that the patient's appetite changes are at the least an indirect symptom of depression related to her injury. Depression, unless treated, leads to increased appetite and hence the diabetic encephalopathy. Additionally, brain damage from the accident would predispose the patient toward onset of encephalopathy due to uncontrolled glucose levels. In other words, had she not had a brain injury, diabetic encephalopathy would be no where near as pronounced as it is now.
*I have changed various non-medical details about this patient to ensure privacy.
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