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NOVEL MOLECULAR FACTORS IN THE PATHOCHEMICAL MECHANISMS SUPPORTING CHRONIC BACK PAIN?
IGOR G.BONDARENKO, MD, PHD; JUHANI TEVREN, DC; RAINER BOEGER, MD, PROF.; JUKKA CHYDENIUS,DC
Recurrent character of the chronic back pain often indicates that there are endogenous chemical mechanisms sustaining the local aseptic (non-microbial) inflammation in the connective tissue and, therefore, pain. The mechanism that has been described best is an overproduction of the mediators of inflammation in the tissues such as prostaglandins and leukotrienes. Pharmacological approach to the correction of that pathophysiological process is the use of non-steroidal anti-inflammatory drugs (“pain-killers”) supposed to inhibit cyclooxygenase and lipoxygenase, the enzymes catalysing the synthesis of the aforementioned pro-inflammatory chemicals.
There exists a different cohort of endogenous substances in the body which, although not behaving as direct inducers of the pain by acting on the nociceptors in the damaged area, may impair the structural integrity of the major proteins of connective tissue – collagen(s) and elastin. Homocysteine, a sulfur-containing amino acid, has been equivocally claimed to be associated with the higher risk of cardiovascular conditions. Hyperhomocysteinemia has been proven to be an independent risk factor of cardiovascular disease, including atherosclerosis and stroke, and is connected to insulin resistance. There is also a link between elevated levels of homocysteine and neurodegenerative diseases.
Evidence exists that homocysteine-induced damage to the vascular wall is due to the impairment in the structure of its collagen and elastin, both by the inhibition of the assembly/maturation of those proteins. Destructive effects of homocysteine are not restricted by vascular wall only. Hyperhomocysteinemia has been shown to be associated with the increased risk of hip fracture in the elderly. As early as in 1976, experiments by Griffiths et al. demonstrated that excess homocysteine can decrease the level of cross-linking of the collagen in the tendons, thus making collagen mechanically weaker. Twenty years later, Liu G. et al. (1997) confirmed the irreversible inhibition of lysyl oxidase, the enzyme responsible for strengthening collagen and elastin by cross-linking their filamentous chains, by homocysteine thiolactone – the product of homocysteine breakdown in the body. A single-point mutation in the gene leading to the elevation of homocysteine has been proven to be associated even with the decrease of bone mineral density.
Another endogenous chemical potentially involved in the labilisation of the major proteins of connective tissue is NG, NG-asymmetrical dimethylarginine (ADMA). This methylated derivative of the amino acid arginine, described by P. Vallance et al. (1992), is synthesised in the body from it’s own proteins and acts as a specific inhibitor of nitric oxide synthase family, therefore diminishing the production of nitric oxide in the tissues. Similar to homocysteine, elevation of ADMA level is associated with the increased risk of cardiovascular conditions – it has been reported in hypercholesterolaemia, peripheral arterial occlusive disease, hypertension, chronic heart failure, and coronary artery disease, as well as in diabetes mellitus. Moreover, higher values of ADMA in blood have been diagnosed in patients with hyperhomocysteinemia, which emphasises the pathophysiological proximity and interrelations between homocysteine and ADMA in the pathogenesis of cardiovascular diseases. Again, as in the case of homocysteine, it seemed plausible to suggest that the effects of ADMA on blood vessel wall could be, in particular, accounted for by its damaging action on the connective tissue proteins. In that case, the association between the elevation of ADMA and the possible impairment of collagen and/or elastin could result to other clinical conditions, in which structural integrity of collagen/elastin plays a primary role. Very few disperse data indirectly support the suggestion. Experimental studies by Lu R. et al. (2002) have demonstrated that age-related decrease in bone mineral density in the spine, tibias and femora correlated with the increase of serum levels of ADMA. In particular, it could be accounted for by the inhibition of osteoblastic differentiation by ADMA. In clinical studies, almost two-fold elevation of ADMA levels in the cerebrospinal fluid of the patients with lumbar spinal canal stenosis has been demonstrated.
In our preliminary study, levels of ADMA (analysed by high-performance liquid chromatography) in the blood serum of 10 patients (male: 8, female: 2, age: 31-69) with chronic back pain were found to be close to the upper reference limit (“upper normal value”) or to exceed it. If the hypothesis on the role of endogenous destabilisers of major connective tissue proteins in the mechanisms of chronic pain is supported in further studies, a specific nutritional supplementation can be developed to reduce the levels of ADMA and/or homocysteine in the body fluids and, therefore, to augment the efficiency of chiropractic treatment of chronic back pain.
DIMINISHMENT OF VERTIGO AND TIA SYMPTOMS IN A 67-YEAR-OLD FEMALE USING FUNCTIONAL NEUROREHABILITATION
Roope Chydenius1, Susan E. Esposito1* and Michael Pendleton2
Presentation: A 67-year-old female patient presented to a chiropractic neurology clinic with a primary complaint of mild to moderate vertigo. Additional complaints were transient ischemic attack (TIA) symptoms such as brain fogginess, pain in the right ear, blurry vision, rushing sensations and tinnitus. The patient reported feeling as if her right brain had been “poured out”, a feeling of emptiness. Her history included physical and verbal abuse from her parents and then from her spouse, 54 years of bulimia, and a diagnosis of ADD/ADHD by her primary care physician. Multiple tests had been taken prior to her visit to the chiropractic neurology clinic (EEG, EKG, MRI and MRA) and none of them showed any alarming abnormalities/pathologies.
Findings: Positive dysdiadochokinesia and ataxia of the left upper extremity was seen on alternating palms up/palms down testing and immediate leftward sway after closing her eyes on balance testing. Finger tapping test revealed decreased amplitude throughout on the left. Gait analysis showed decreased left arm swing with bilateral cantilevering. In smooth pursuit eye movement testing, saccadic intrusions were observed upon vertical eye movement upwards and downwards as well as to the left (horizontally). Dysmetric saccades were noted upon vertical saccadic testing both upwards and, downwards as well as to the left (horizontally). Patient had a left inward and upward convergence spasm with right beating nystagmus. Chiropractic analysis showed subluxations with myospasm and hypo-mobility in specific spinal and rib joints. Benign paroxysmal positional vertigo (BPPV) was evidenced by Dix-Hallpike testing of the left posterior canal. Computerized assessment of postural systems (CAPS) testing showed 39% stability on a perturbed surface with eyes closed and head position in extension (PSEC-HE).
Methods: The treatment plan was aimed to increase the frequency of firing to the right parietal lobe while increasing central integrative state of the vestibulocerebellum. Passive cerebellar exercises were performed on the left side for left cerebellar and right cortical activation. Computerized right brain eye exercises were done using diagonal microsaccades from the lower right to the upper left field of vision, followed immediately by diagonal smooth pursuits from the upper left to the lower right field of vision. Optokinetic stimulations were performed in the following directions: left horizontally, down/left and up/left for three passes in each direction, to treat left inward and upward convergence spasm and right beating nystagmus. Head-Eye Vestibular Stimulation (HEVM) therapy was done using horizontal smooth pursuits and passive forward pitch head movements at 10 degrees to the left of midline. Additionally, HEVM therapy was used for vertical smooth pursuits and passive right yaw movements. Anti-saccades were performed using the Focus Builder application. Gait therapy was preformed utilizing turns to the left while having a tone pacer set at 100 Hz in the left ear and 500 Hz in the right ear. Cranial Nerve Non-Invasive Neuromodulation (CN-NINM) therapy was used on the left V1, V2 and bilateral V3/hypoglossal cranial nerve. Epley maneuver was done with vibracussor application to the bilateral mastoids and occipital bones to address BPPV symptoms. Additionally, each treatment session included one hour of neurofeedback therapy.
Results: The patient received treatment for a total of 14 days within a 3-month period, consisting of two treatments per day. After the 14 visits, the patient reported feeling 75-85% improvement since her first visit. Her vertigo had almost diminished but some short-lived episodes persisted. Her additional complaints, (TIA) symptoms, brain fogginess, pain in the right ear, blurry vision, rushing sensations and tinnitus were all decreased but did not resolve completely. CAPS result for PSEC-HE increased to 64% stability. Some difficulties in oculomotor tracking and saccades persisted, but patient will continue her treatment to address the remaining symptoms.
Conclusion: In this patient case, employing neurorehabilitation strategies proved effective in decreasing vertigo and other neurological symptoms. These results promote the need for further research of functional neurorehabilitation in the treatment of vertigo.
IMPROVEMENTS IN BALANCE AND THE APPREHENSION OF FALLING IN A POST-STROKE PATIENT
Roope Chydenius1, Susan E. Esposito1* and Michael Pendleton2
Background: A 49-year-old female patient presented to a chiropractic neurology clinic with primary complaint of balance problems and a strong apprehension of falling. She had an ischemic stroke in 2009 caused by carotid dissection. The stroke resulted in a partial left sided paralysis. The patient reported feeling her left foot twisting during gait, necessitating the use of a cane for ambulation. Additional complaints were increased emotionality, insomnia, moderate fatigue and low energy.
Methods: Upon examination, she revealed decreased sensation to sharp touch, light touch, vibration and position sense in the upper and lower left extremities. She reported diminished sensation on the entire left side of her face. Weber’s testing revealed sound lateralized to the right side. Tongue protrusion was midline but strength was weaker on the left. Point localization showed consistent inaccuracy by 3 inches on the left arm. Her left foot was cold to the touch. She was able to perform a squatting position but displayed a dysfunctional gait. The patient received treatment for a total of 6 days at a frequency of 3 times a day. Treatments consisted of mirror therapy involving marching and stepping up and down was utilized to provide visual feedback to improve her motor patterns. Gait training exercises were used with and without a mirror. Eye movement therapy was performed with saccades up and left and pursuits down and left. Repetitive peripheral sensory stimulation (RPSS) was performed on the left peroneal nerve, left posterior tibial nerve, along the dermatomes for L3 and L4. Between treatments, patient followed a home exercise protocol which consisted of computerized eye movement exercises. These eye exercises focused on right sided cortical activation in an effort to improve left sided movement.
Results: After 6 days of treatment, the patient reported an improvement in perceived balance problems, which decreased from severe to mild. Her gait had significantly improved, such that she was no longer reliant on the cane for ambulation, although she continues to use it as she reports, “just in case”. She no longer had anxiety nor a fear of falling. The patient had an increase in her perception of sharp and light touch as well as vibration in her upper and lower left extremities. She reported a concomitant increase in energy and diminished fatigue.
Conclusion: In this patient case, employing chiropractic neurology strategies proved very effective in treating a post stroke patient’s severe balance and sensory symptoms. These results promote further research of functional neurorehabilitation in the treatment of post stroke patients.
https://www.frontiersin.org/10.3389/conf.fneur.2018.60.00121/event_abstract