CASE STUDy:Chiropractic Care of a Patient with Amyotrophic Lateral Sclerosis
Jennifer James Padrta, BS, Chiropractic Intern . June 2002
ABSTRACT
This study examined the effects of chiropractic adjustments in a patient with Amyotrophic Lateral Sclerosis (ALS). The adjustments were performed manually in most cases, with the exception of the atlas adjustments performed by a mechanical spring loaded chiropractic adjusting device. Further studies are needed to examine the long-term effects of chiropractic adjustments on patients with ALS.
BACKGROUND
Amyotrophic Lateral Sclerosis (ALS) is part of a group of motor neuron diseases with degeneration of the lower cranial nerves, corticospinal and corticobulbar tracts. The onset is usually between 30-60 years of age and progresses at different rates. Most cases are sporadic, even though there are some familial cases. ALS is often referred to as “Lou Gehrig’s Disease.” Lou Gehrig was a baseball player for the New York Yankee’s that died from the disease in 1941 at 38 years old. (1) Lou Gehrig made the disease well known, although it was actually described by Charcot in 1874. (6)
ALS is usually characterized by a combination of upper and lower motor neuron lesion signs. Fasciculations and muscle atrophy are noticeable, as well as brisk deep tendon reflexes are apparent with the upper motor lesion portion. Sensory function is completely normal. (3)
Lower Motor Neuron and Upper Motor Neuron Signs in Four CNS Regions:
​
​
​
​
​
​
There is no single definitive diagnostic test for ALS. To diagnose ALS, it requires the presence of upper and lower motor neuron degeneration by clinical, electrophysiological or neuropathologic examination and the progression of the symptoms to other regions or within the same one. To determine the diagnosis of ALS, there must be an absence of any other disease that might explain the upper and lower motor neuron degeneration. (10)
Recently, there has been interest in looking deeper into a phenomenon called “apoptosis” which means, programmed cell death. Researchers are trying to uncover if apoptosis is responsible for the neurodegenerative processes in ALS, by checking for levels of certain oncoproteins and their possible link with a predisposition of apoptosis. (4) No solid research has proven this theory, as of yet.
Research has recently shown an enterovirus in the motor neurons of the anterior horn cells of people with ALS. (5) There have been many studies theorizing the same point, but this is the first time it has been scientifically proven. Of course, not all ALS patients have an enterovirus in their brain tissue, so there is not one cause of ALS. Some proposed underlying causes of ALS include genetic susceptibility, heavy metal exposure, environmental toxins (pesticides), head trauma, viral infections and autoimmunity. (6)
The prevailing cause of familial cases of ALS is a defective superoxide dismutase (SOD1) gene on chromosome 21. The normal function of SOD1 is to limit the production of intracellular free radicals. The mechanism of the defect is not known, but it is theorized the defective enzyme has an unwanted neurotoxic property. (11)
Excessive amounts of the amino acid glutamate (glutamic acid) along with MSG, may also play a role in the progression of ALS. Cyclooxygenase-2 (COX-2) produces prostaglandins that cause astrocytes in the CNS to release glutamate. In turn, glutamate may induce the formation of free radicals. (8)
Dr. Alf Breig’s work on skull traction and cervical cord injury is another approach to the possible treatment of ALS. Dr. Breig has written about how surgically setting the cervical spine in slight extension, thereby allowing slack in the pons cord tract, could successfully treat ALS and number of other neurogenic problems. (2, 15)
According to most references, there is no cure or treatment for ALS, as it is considered a fatal disease. Most ALS patients die within 2-2 ½ years of their diagnosis. The 5-year survival rate is only 20%. (3)
In the late 1970’s, the New England Journal of Medicine published an account by Norman Cousins, about how he used humor to recover from ALS. Mr. Cousins stated that 10 minutes of belly laughter produced an anesthetic effect lasting at least two hours.
Right up the same alley, a study by Martin & Lefcourt showed that heavy laughter increased levels of enkephalins and endorphins in the brain. And yet, another study by Dillon, Minchoff, and Baker reports that finding something funny results in a significant increase in IgA antibodies.
At this point science has no concrete answers of how to treat ALS, so one approach may work for one person, but not the next.
INTRODUCTION
The patient is a 62 year-old male who, in 1992, began having muscle spasms in his left leg and left arm. In 1994 he was diagnosed with Amyotrophic Lateral Sclerosis (ALS). Muscle atrophy continued and included all limbs beginning in the hands, then to the upper arms and into the shoulder region. He has been wheelchair bound for the past five years. Current symptoms include dysarthria and dysphagia, acid reflux, fasciculations, and periodic spells of gagging or coughing after having swallowed food or drink. Edema is present in his hands, legs, and feet.
It is necessary to note that the patient suffered trauma at the age of 19 years, when he fell 30+ feet off of a railroad trestle and landed on his head, breaking both wrists and right elbow.
He wears a BI-PAP breathing apparatus at night to ensure continued respiration. His lower extremity muscle strength is intact and can shuffle out of his wheelchair with assistance for short distances. Most of his time is spent on a computer using a specialized program which is operated by one knee, allowing him to open programs, write letters, and surf the web. His mind is completely intact.
The following medications are taken daily and prescribed by a medical doctor at an ALS facility:
Neurontin manufactured by Parke-Davis Pharmaceuticals, also known as gabapentin, is an anti-epileptic seizure medication. Neurontin is a glutamate blocker, but it has no apparent affect on ALS. According to Parke-Davis in a press release, “The results of this longer, larger, higher dose study of gabapentin in ALS provides no evidence of effectiveness of this drug for patients with this disease." (7)
The patient has been taking Neurontin for approximately 4 years and states that he feels “disconnected and doesn’t feel good” when he does not take it. Oddly enough, another research journal finds that Neurontin is used successfully with patients with chronic neuropathic pain used with diabetics, but it seems that ALS patients are finding relief with the Neurontin as well. (12)
Rilutek (Riluzole) is also a glutamate blocker and has been proven to be able to slow the progression of ALS and extend the survival of ALS patients. It is the first medication to have an effect on the progression of ALS and approved by the FDA. There is the possibility of liver injury, and patients should have lab tests performed as a baseline before beginning Rilutek and during the drug treatment period.
Celebrex is a cyclooxygenase-2 (COX-2) inhibitor. Inhibition of the COX-2 mechanism provides protection for spinal motor neurons in SOD1 mouse models. GI problems, kidney, and liver problems are potential concerns. (8)
Quinine is used widely for muscle cramps.
Prilosec is commonly used for acid reflux disease or gastroesophageal reflux disease (GERD). Prilosec is indicated for short-term treatment of active duodenal ulcers. Most patients heal within four weeks, but an additional four weeks may be necessary. (13) The patient has been taking Prilosec for much longer than 8 weeks.
Prozac is a commonly used anti-depressant. The patient states that it is difficult to have a quick mind and a body that won't comply. He has been taking Prozac for 4 years.
Amitriptyline HCL is used as an anti-depressant, but the patient states that he takes it as an anti-inflammatory drug.
Ambien is a hypnotic and allows the patient to sleep when he has difficulties.
The patient introduced approximately 900mg of calcium lactate chelated with magnesium and noticed an immediate decrease in fasciculations to the point of almost non-existence. He also began taking d-alpha-tocopherol (vitamin E), betaine hydrochloride with pepsin, vitamin A, phenylalanine, glutamine, N-acetyl cysteine (NAC) to help the body produce glutathione, coQ-10, essential fatty acids, ginseng, gingko biloba and creatine.
The patient entered the Life Chiropractic College West Health Center with a complaint regarding his speech due to ALS, but after receiving some musculoskeletal relief, complained of "butt pain" from being unable to ambulate on his own and being confined to his wheelchair.
He had upper motor neuron lesions of the lower extremities and lower motor neuron lesions of the upper extremities. The fasciculations were so extreme that getting a pulse and blood pressure readings were nearly impossible. His muscle strength in the lower extremities had complete range of motion against gravity, either with some or all resistance. The lower extremity reflexes were either average of hyperactive. There was no evidence of contractility or joint motion in the upper extremities and either had no response or an average response unilaterally when performing reflex exam.
All cranial nerves appeared to be intact. Heart, lung and abdominal exams all appeared normal.
The only sensory exam that was abnormal was differentiation of dull from sharp on face.
Motion palpation revealed taut and tender fibers and/or fixations at the occipital and atlas region on the right, bilaterally at T2-T7 and bilaterally at T10.
Cervical range of motion was decreased overall without pain.
All other tests were either within normal limits or were unable to be performed.
Radiographic studies concluded spondylosis from C2-C6, lower thoracic spine and entire lumbar spine with a transitional segment at L5 with accessory articulation on the right. Chest films were taken which demonstrated a chronic degenerative cyst and other findings suggest a chronic lung disease, which may be associated with the history of ALS.
METHODS
Conservative manual adjustments of the spine and its articulations were administered usually at one week interims and then extended to two week interims, as the patient had difficulty commuting such a distance when it was necessary to rely on others to drive him to the health center.
A persistent subluxation complex of the coccyx was apparent, possibly due to the time spent in the wheelchair. Other subluxation complexes included T2, T8, T12/L1, sacrum and on occasion C1 was adjusted using a mechanical spring loaded chiropractic adjusting device. Both shoulders were chronically subluxated anterior inferior, possibly due to the extreme muscle wasting in the upper extremities and chest.
RESULTS
The patient involved with this study did not follow all recommendations for home exercises and frequency of adjustments. The distance between his home and the health center was excessive for is condition to be seen more than 1-2 times per month.
Upon a re-evaluation, the patient noticed that he has less pain when in a supine position. Also noted was the cervical range of motion increased in all directions except for lateral flexion bilaterally.
Complaints changed, as he found relief for his left hip pain, low back pain and tail bone pain. It appeared as though once a problematic area was relieved, he would notice another area that he hadn't noticed prior.
There were no other objective changes obtained, as many of the initial objective tests were unable to be performed during the physical exam.
Subjectively, the patient received some relief for periods of time. Immediately after an adjustment, his speech was noticeably different to everyone in the room. Musculoskeletal complaints varied due to multiple variables including sleep, activity, adjustment frequency and psychosocial attitude.
​
CONCLUSION
Recent research findings suggest that a chiropractic adjustment or SMT may produce hypoalgesic and sympathoexcitatory effects leading to the activation of the descending inhibitory pathways from the periaqueductal grey area of the midbrain. (14) We know from basic neurology that the periaqueductal grey area has an analgesic effect when stimulated.
After reviewing some of Dr. Alf Breig's work, it is possible that chiropractic adjustments along with Chiropractic Biophysics care, could induce the amount of extension or cervical lordosis necessary to stop spinal cord tethering and allow some relief or even resolution of some of the symptoms that are common to ALS patients.
Chiropractors have long approached patients with a variety of conservative manual adjustments, dietary and lifestyle changes. Since there are no absolute treatments for ALS that are efficient across the board, a large-scale study should be explored in regards to chiropractic care and the treatment of ALS patients.
ACKNOWLEDGEMENTS
I would like to thank Jerry Steele for his unrelenting support, both physically and mentally, by helping with movement of the patient on each visit. Also, for bouncing ideas off me in regards to ALS and sharing ideas and research with me. I would also like to thank Dr. Gregory Plaugher for showing me how to look for reliable research information, as well as the faculty at Life Chiropractic College West.
REFERENCES
1. McGuire V, Longstreth WT Jr, Nelson LM, Koepsell TD, Checkoway H, Morgan MS, van Belle G. Occupational exposures and amyotrophic lateral sclerosis. A population-based case-control study. American Journal of Epidemiology 1997 Jun 15;145(12):1076-88.
2. Breig A.Chapter 6. Pathological stress in the pons-cord tissue tract and its alleviation by neurosurgical means. Clinical Neurosurgery 1973;20:85-94.
3. Souza. Differential Diagnosis for the Chiropractor: Second Edition, pg 402-3
4. Neuropathologies and Applied Neurobiology Aug:27 (4):257-74
5. Giraud P, Beaulieux F, Ono S, Shimizu N, Chazot G, Lina B. Detection of enteroviral sequences from frozen spinal cord samples of Japanese ALS patients. Neurology. 2001 Jun 26;56(12):1777-8.
6. Rowland LP, Shneider NA. Amyotrophic lateral sclerosis. New England Journal of Medicine. 2001 May 31;344(22):1688-700.
7. Miller, Roger G. Phase III double-blind, placebo-controlled study of gabapentin (Neurontin) in patients. ALS Meeting of the American Neurological Association in Seattle, Washington on October 13, 1999.
8. Drachman, DB. and Rothstein, JD. Inhibition of cyclooxygenase-2 protects motor neurons in an organotypic model of amyotrophic lateral sclerosis. Annals of Neurology. 2000 Nov, 48(5): p.792-795.
9. Oey PL, Vos PE, Wieneke GH, Wokke JH, Blankestijn PJ, Karemaker JM. Subtle involvement of the sympathetic nervous system in amyotrophic lateral sclerosis. Muscle Nerve 2002 Mar;25(3):402-8
10. Subcommittee on Motor Neuron Diseases/Amyotrophic Lateral Sclerosis of the World Federation of Neurology Research Group on Neuromuscular Diseases and the El Escorial "Clinical limits of amyotrophic lateral sclerosis" workshop contributors. El Escorial World Federation of Neurology criteria for the diagnosis of amyotrophic lateral sclerosis, Journal of the Neurological Sciences 1994 Jul;124: 96-107.
11. Mitsumoto, H. and Munsat, T, Amyotrophic Lateral Sclerosis: A Guide for Patients and Families: Second Edition. Pgs 37-45
12. Backonja M, Beydoun A, Edwards KR, Schwartz SL, Fonseca V, Hes M, LaMoreaux L, Garofalo E. Gabapentin for the symptomatic treatment of painful neuropathy in patients with diabetes mellitus: a randomized controlled trial, JAMA 1998 Dec 2;280(21):1831-6
13. National Committee for Clinical Laboratory Standards. Summary Minutes, Subcommittee on Antimicrobial Susceptibility Testing, Tampa FL, January 11-13, 1998.
14. Sterling M, Jull G, Wright A. Cervical mobilisation: concurrent effects on pain, sympathetic nervous system activity and motor activity. Manual Therapy 2001 May;6(2):72-81
15. Breig, A. Overstretching of and circumscribed pathological tension in the spinal cord – a basic cause of symptoms in cord disorders. Journal of Biomechanics 1970 Vol 3, pg 7-9
