It has been compared to the worst possible type of pain anyone can imagine. Other people say it’s even worse than labor because the pain doesn’t seem to have an end to it. These are some of the most common descriptions of sciatica, where a severe case of this excruciating nerve pain can bring anyone to their knees. That’s why lots of patients don’t simply say they have sciatica, they’re victims of its symptoms.
Sciatic nerve pain, or sciatica, is associated with many well-known symptoms, however, is sciatica really that common? What type of treatments are available to help alleviate sciatic nerve pain?And does a person’s everyday activities play a part in whether they will develop sciatica in the first place? Dwight Tyndall, MD, FAAOS answers several of the most commonly asked questions patients need to know regarding their sciatica.�Dr. Tyndall is a pioneer in the area of outpatient spine surgery, however, he is also a strong proponent of non-surgical treatment methods, including chiropractic care, to manage back pain and sciatica. Dr. Tyndall shares his perspectives on sciatic nerve pain and discusses what may indicate a need for surgery in severe cases of sciatica.
Contents
What is Sciatica?
According to Dr. Tyndall, sciatica is both a spinal disorder and a catch-all term for a group of symptoms. Sciatic nerve pain, best referred to as sciatica, is a spinal condition characterized by nerve pain which radiates down the length of the sciatic nerve. The sciatic nerve is the largest nerve in the entire human body, and it’s made up of spinal nerves from the vertebrae level L4 in the lumbar spine down to the vertebrae level S1 in the sacrum. Anything which impacts those nerves can lead to sciatica. Moreover, sciatica’s symptoms may be grouped under the medical term dysesthesia, meaning any sort of abnormal sensation. Most patients describe sciatica as an odd feeling radiating out of their lower back into their buttocks and down to their thigh and calf, often radiating as far down into the foot.
What are the Symptoms of Sciatica?
Dr. Tyndall explains that sciatica’s hallmark symptom include pain in the low back or buttocks which radiates down one or both legs. Signs and symptoms which shouldn’t be ignored include pain which doesn’t respond to non-surgical treatment options and/or pain which greatly restricts an individuals activity level and quality of life. Some red flags which may signal the need for surgical interventions associated with sciatic nerve pain include: reduced motor function in one part of the leg, usually a drop foot at which the patient can’t lift thei foot off the ground, weakness in one or both legs and bladder or bowel changes.
Is Sciatica the Same as Lumbar Radiculopathy?
“Most people see sciatica to be more severe than lumbar radiculopathy, but radiculopathy, which comes from the Latin radix significance origin, is a condition that affects the nerve during its origin as it exits the spinal cord. Sciatica and lumbar radiculopathy can be brought on by a pinched nerve from the spinal column due to a disc herniation or stenosis, but kidney problems or a sinus issue, like endometriosis, may also pose sciatica-like symptoms,” states Dr. Dwight Tyndall.
Who’s at Risk of Developing Sciatica?
“By my clinical experience, men and women have exactly the same identical risk of developing sciatica. Obesity also doesn’t play a role, either. Concerning age classes, however, sciatica has been estimated to peak during the ages of 30 and 40, and the risk usually declines as people begin reach their 50’s,” added Dr. Tyndall.
How Common is Sciatica?
As mentioned by Dr. Dwight Tyndall, sciatica and low back pain frequently occur together, but sciatica is much less common. While 80 percent of individuals experience low back pain at any point in their lives, just 2 to 3 percent will actually develop sciatica.
When Should a Person with Sciatica See a Healthcare Professional?
According to Dr. Tyndall, an individual with symptoms of sciatic nerve pain will need to see a healthcare professional if their pain is not reacting to over-the-counter (OTC) medications, or if these create weakness in the leg. Also, a person ought to see a doctor if their pain is so severe that their well-being is affected. Should the sciatica include bladder or bowel changes, the individual must seek immediate medical attention for their health issues. Furthermore, it’s important for a person with sciatica to seek the help of a healthcare professional to rule out any possible underlying causes which may be responsible for their symptoms.
What Type of Healthcare Professional Can Help Treat Sciatica?
According to Dr. Tyndall, any healthcare professional qualified and experienced in spine health issues, such as a chiropractor, can help diagnose, treat and even prevent sciatica. A doctor of chiropractic, or chiropractor, is a healthcare professional who utilizes spinal adjustments and manual manipulations, among other non-invasive treatment methods, to help correct any spinal misalignments, or subluxations, which may be causing sciatic nerve pain. A chiropractor may also recommend a series of stretches and exercises, as well as lifestyle modifications, to help speed up the patient’s recovery process. Chiropractic care is often the preferred alternative treatment option to help alleviate sciatica without the need for drugs and/or medications or surgery. However, if a patient is experiencing any of the red flag symptoms mentioned above, it may be necessary to visit a spine surgeon in order to discuss the treatment options. Always make sure to consider surgical interventions as a final alternative if your sciatica doesn’t respond to non-surgical treatment methods.
What are the Causes of Sciatica?
“There are many external factors, but among the greatest is your occupation. Someone who operates in a manual labor industry, like construction, has a higher likelihood of developing sciatica since they put more wear and tear on their back. Tiger Woods is an example of this. He acquired sciatica because his career as a golfer placed significant stress on his spine. There is a genetic element as well, as a few young men and women who do not operate in a strenuous job develop sciatica, however, the genetic tie is not clearly defined. Lastly, pregnancy may also result in sciatica. As the infant develops, it can put pressure on the lumbar spine, pelvis, and sciatic nerve. However, delivering the infant is usually enough to eliminate sciatica caused by pregnancy,” says Dr. Tyndall.
How Often is Sciatica Likely to Re-Occur?
“This question isn’t easy to answer because many factors contribute to whether a person will develop sciatica more than once. Sciatica is likely to re-occur if the spinal disc that led to sciatica the very first time is severely damaged. The more damaged the disk, the more likely it is to re-herniate and lead to sciatica again. Also, if the patient continues to work in a high-physical stress environment, the risk of re-ocurrence increases.
How is Sciatica Diagnosed?
“The physical examination is essential to a sciatica diagnosis. The straight-leg raise test is the traditional diagnostic tool during a physical examination. In this test, a patient be asked to lift up their leg when lying down. If that induces pain down their leg, the patient could have sciatica. Other physical tests healthcare professionals frequently utilize are knee extension tests, where the patient expands their knee to a straight position, like a straight-leg lift. Additionally, healthcare professionals will as patients to walk on their tip toes or on their heel to measure their potency. Other healthcare professionals will also observe how strong they are going down stairs or simply walking. Many doctors can determine a sciatica analysis from a physical examination, but if imaging studies are needed to learn more, the physician may recommend a magnetic resonance imaging (MRI) scan.
What Treatments are Effective for Sciatica?
As mentioned before by Dr. Dwight Tyndall, there is a variety of treatment options available to help alleviate the symptoms of sciatica. Approximately 80 percent of patients will improve with non-surgical treatment options. Several OTC medications, such as NSAIDs (eg, ibuprofen), are also effective in the management of sciatic nerve pain. If the sciatica does not subside, the doctor may prescribe a low-dose steroid pack (to be obtained over one week). If this doesn’t manage the sciatic nerve pain, then the patient may receive an epidural steroid injection (you will first need an MRI to pin-point the injection region).
Other non-surgical treatment options which are commonly utilized to help alleviate the symptoms of sciatica, include, acupuncture, chiropractic care and physical therapy, and needless to say, time normally works wonders such as pain. Chiropractic care is the most commonly used alternative treatment option for the treatment of sciatica. Chiropractic care focuses on the diagnosis, treatment and prevention of a variety of injuries and/or conditions associated with the musculoskeletal and nervous system. Through spinal adjustments and manual manipulations, a doctor of chiropractic, or chiropractor, can help reduce unnecessary pressure in the structures surrounding the spine, improving strength, mobility and flexibility. Chiropractic care and physical therapy alike, can also help improve a patient’s overall health and wellness, aside from improving their sciatica, through physical activities and nutritional advice.
Is Surgery Ever Necessary to Treat Sciatica?
“It may certainly be so, however, the good thing is that the vast majority of people with sciatica don’t need surgery. And, your doctor may ask you to explore non-surgical treatment options, however, your tolerance for pain is the real predictor as to when you have to consider another option for treatment. Surgery may be necessary if symptoms worsen despite trying non-surgical alternatives, if you have weakness in your leg, or if you experience bladder and/or bowel changes,” explained Dr. Dwight Tyndall.
“The surgical procedure to treat sciatica is also called a lumbar microdiscectomy. It is a normal procedure with very positive individual outcomes when used accordingly. A lumbar microdiscectomy is similar to a traditional lumbar discectomy. Technological advances, like the advent of surgical microscopes, allow surgeons to create smaller incisions that are minimally traumatic to the body and result in a much quicker recovery for the patient”, added Dr. Tyndall.
Can Surgery be Performed in an Outpatient Setting?
“Yes, lumbar microdiscectomy can surely be carried out in an outpatient setting. Many patients like the cozy environment and are able to go home the exact same day of operation,” concluded�Dwight Tyndall, MD, FAAOS.
Is Sciatica Preventable?
As thoroughly explained by Dr. Dwight Tyndall, sciatica can be preventable if the individual doesn’t put significant and repeated stress in their back, which will reduce the chance of damaging or injuring a nerve. Nonetheless, in the present society, through our tasks and daily stresses of modern life, it’s difficult to accomplish that. Fortunately, with the abundance of treatment choices available, people can get relief from sciatic nerve pain with the appropriate healthcare professional’s help.
Dr. Alex Jimenez’s Insight
Many people will experience symptoms of low back pain at least once throughout their lifetime, however, only a few individuals will develop true sciatica symptoms. Sciatica is medically referred to as a collection of symptoms, rather than a single condition, and it’s generally characterized by pain and discomfort, followed by tingling or burning sensations and numbness along the length of the sciatic nerve. The sciatic nerve is the largest nerve in the human body and it travels from the lower back down the buttocks and thighs into the legs and feet. Sciatic nerve pain, or sciatica, has become a common health issue for many people, therefore, its important to be educated regarding this prevalent complaint in order to follow up with the most appropriate treatment.
The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Sciatica
Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.
Autoimmunity is the reaction of cells (lymphocytes) or antibodies�of the immune system along with the body�s own tissues leading to certain pathology. Autoimmunity can produce various conditions, which depend upon the target of the attack.�While intrinsic factors, which include age, sex, and genetics contribute to autoimmunity, it is believed that extrinsic factors such as drugs, chemicals, microbes, and/or the environment can trigger the initiation of autoimmune responses.
Contents
Autoimmune Disease & Environmental Toxicants
Educational Objectives
Review air pollution, cigarette smoking, and citrullination as models for the genesis of autoimmune disease
Explore the role of general cell stressors in autoimmune disease
Discuss the impact of lung and gut barrier disruption by environmental toxins and food additives in autoimmune disease
Utilize the Functional Medicine ATM model to illustrate the various mechanisms by which toxicants could contribute to the pathophysiology of autoimmune disease.
�Mild forms of the autoimmune response probably occur naturally in most people. But, for people with a predisposition to autoimmunity, environmental factors, such as toxic chemicals, drugs, bacteria or viruses, may trigger a full?fledged response.�
�NOVEL CRYSTAL BALL: One day Y?shaped molecules called autoantibodies in a patient�s blood may tell doctors whether a patient is �brewing� certain diseases and may even indicate roughly how soon the individual will begin to feel symptoms.�
Autoimmune Disease: �Delayed Gratification�
Scientific American, March, 2007
Many autoimmune diseases do not develop spontaneously, but instead evolve through an extended germination period before they become clinically evident…
Well over 10 million people test positive for ANA, years before they have any symptoms.
This implies the presence of additional environmental factors that dampen or amplify the process over time.
Arbuckle MR, et al, N Engl J Med. 2003 Oct 16;349(16):1526?33.
Elevated Levels Of Antibodies Against Xenobiotics In A Subgroup Of Healthy Subjects
Vojdani, A, Kharrazian, D, Mukherjee, PS
Some environmental chemicals, acting as haptens, can bind to a high? molecular?weight carrier protein such as human serum albumin (HSA), causing the immune system to misidentify self?tissue as an invader and launch an immune response against it, leading to autoimmunity
The levels of specific antibodies against 12 different chemicals bound to HSA were measured by ELISA in serum from 400 blood donors.
10% (IgG) and 17% (IgM) of tested individuals showed significant antibody elevation against aflatoxin?HSA adduct.
The percentage of elevation against the other 11 chemicals ranged from 8% to 22% (IgG) and 13% to 18% (IgM).
Detection of antibodies against various protein adducts may indicate chronic exposure to these chemical haptens in about 20% of the tested individuals
J Appl Toxicol. 2015 Apr; 35(4): 383�397.
Could Environmental Toxins Be A Key Missing Link That Pushes The Immune System Over The Brink To Permanently Lose Control Of Its Tolerance To Self?Antigens?
(A Corollary Question: Does The Persistent Presence Of Autoantibodies Or Autoreactive T Cells Imply An Inevitable Progression To Full?Blown Autoimmune Disease?)
Rheumatoid Arthritis: Swan neck deformity from chronic synovitis
Anti?Cyclic Citrullinated Peptide Antibody
Current method is 96% specific for RA
Elevated titers detected >10 years before onset of clinical disease
Sensitivity (likelihood of positive test) increases from 50% at Dx to >75% over course of disease
Likely involved in pathogenesis
Citrullinated Ags are highly expressed in inflamed joints
Citrulline is formed by posttranslational modification of arginine residues by peptidyl arginine deiminases (PADs)
PADs are upregulated by inflammation, injury, and toxicants
Inflammation and injury thus increases citrullination of multiple synovial proteins
Multiple HLA?DR variants (shared epitope) associated with RA preferentially display citrullinated Ags on MHCII � activating citrulline?specific autoreactive T cells
Smoking increases risk of +anti?CCP when coupled with HLR?DR shared epitope
Floris van Gaalen et al. J Immunol 2005;175:5575-5580
Autoimmunity To Specific Citrullinated Proteins Gives The First Clues To The Etiology Of Rheumatoid Arthritis
Four citrullinated whole protein antigens, fibrinogen, vimentin, collagen type II, and alpha?enolase, are now well established, with others awaiting further characterization All four proteins are expressed in the joint, and there is evidence that antibodies to citrullinated fibrinogen and collagen type II mediate inflammation by the formation of immune complexes Antibodies to citrullinated proteins are associated with HLA ‘shared epitope’ alleles
Porphyromonas gingivalis, pathogenic bacteria that is a major cause of periodontal disease, expresses endogenous citrullinated proteins
Thus, both smoking and Porphyromonas gingivalis are attractive etiological agents for further investigation into the gene/environment/autoimmunity triad of RA.
Wegner N, Lundberg K, Kinloch A, et al, Immunol Rev. 2010 Jan;233(1):34?54
�More than 20,000 physicians, after Luckies had been furnished them for tests, basing their opinions on their smoking experience, stated that Luckies are less irritating than other cigarettes.�
Mad Men?
Holy Smokes!!
Cigarette Smoking Has Been Strongly Linked To Numerous Autoimmune Diseases
Cigarette Smoking & Autoimmune Disease: What Can We Learn From Epidemiology?
Rheumatoid arthritis and cigarette smoking:
Risk is highest in men: OR up to 4.4 X
Smoking increases risk of seropositive RA 2.4X in women
Smoking intensity and duration both greatly increase risk
Smoking increases severity of symptoms
Increased risk remains for 20 yrs after cessation
�Cigarette smoking is the most conclusively established environmental risk factor for RA�
Smoking & Air Pollution As Pro?Inflammatory Triggers For The Development Of Rheumatoid Arthritis.
Smoking initiates chronic inflammatory events in the lungs.
These, in turn, promote the release of the enzymes, peptidylarginine deiminases 2 and 4 from smoke?activated, resident and infiltrating pulmonary phagocytes.
Peptidylarginine deiminases mediate conversion of various endogenous proteins to putative citrullinated autoantigens.
In genetically susceptible individuals, these autoantigens trigger the production of autoantibodies to anti?citrullinated peptide, an event which precedes the development of RA.
Anderson R, Meyer PW, Ally MM, Tikly M, Nicotine Tob Res. 2016 Jul;18(7):1556?65
Floris van Gaalen et al. J Immunol 2005;175:5575-5580
Cigarette Smoking & Autoimmune Disease: What Can We Learn From Epidemiology?
Systemic lupus erythematosis
Highest risk in current smokers
Current smokers have higher levels of anti?dsDNA Ab
Multiple sclerosis
Increased risk of MS in both current & past smokers
Risk increases with intensity of smoking (more cigarettes per day)
Increased severity of MS in current smokers
Cirtrullination of myelin?basic protein ?? antigenic
Graves� hyperthyroidism
Smoking is esp. strong risk factor for opthalmopathy
Industrial Air Emissions & Proximity To Major Industrial Emitters, Are Associated With Anti?Citrullinated Protein Antibodies.
Randomly sampled 1586 subjects out of 20,000 population from Quebec, Canada
After adjusting for age, sex, smoking, and ethnicity, found
Positive association between anti?CCPA and annual industrial PM 2.5 and sulfur dioxide emissions (i.e. living closer to emitters increases anti?CCPA)
Negative association between anti?CCPA and to a major industrial emitter of both PM 2.5 and SO2 (living further away from emitters decreases anti?CCPA)
�These analyses suggest that exposure to industrial emissions of air pollutants is related to ACCPA positivity.�
Bernatsky S, Smargiassi A, Joseph L, et al, Environ Res. 2017 Aug;157:60?63
Air Pollution As A Determinant of Rheumatoid Arthritis
The induction by air pollution of an inflammatory environment with high citrullination levels in the lung may induce iBALT formation, thereby causing a transition toward a more specific immune response via the production of anti?citrullinated peptide antibodies.
Air pollution not only triggers innate immune responses at the molecular level, increasing the levels of proinflammatory cytokines and reactive oxygen species, but is also involved in adaptive immune responses.
Thus, via the aryl hydrocarbon receptor (AHR), diesel exhaust particles can trigger a T?cell switch to the Th17 profile.
Sigaux J, et al Joint Bone Spine. 2018 Mar 7. pii: S1297?319X(18)30043?5
The Aryl Hydrocarbon Receptor Links TH17?Cell? Mediated Autoimmunity To Environmental Toxins
The aryl hydrocarbon receptor (AhR) is a ligand?dependent transcription factor that mediates a range of critical cellular events in response to halogenated aromatic hydrocarbons and non?halogenated polycyclic aromatic hydrocarbons such as dioxin (TCDD)
In a murine model of multiple sclerosis, which is mediated by Th17 cells, activation of cells using the AhR exacerbated disease, whereas mice deficient in the AhR had attenuated autoimmune disease.
This paper thus links activation of Th17 cells with environmental toxins, suggesting a plausible hypothesis for the increase in such diseases with industrialization.
Veldhoen, M., Hirota, K., Westendorf, A.M, et al Nature. 2008 May 1;453(7191):106?9
J Inflamm (Lond). 2015; 12: 48.
Does Rheumatoid Arthritis (& Other Autoimmune Diseases) Start In The Gut, Or In The Lungs?
Gomez?Mejiba SE, Zhai Z, Akram H, et al. Inhalation of Environmental Stressors & Chronic Inflammation: Autoimmunity and Neurodegeneration.
Mutation research. 2009;674(1?2):62?72.
Citrullination & Autoimmunity
Environmental exposure to cigarette smoke and nanomaterials of air pollution may be able to induce citrullination in lung cells prior to any detectable onset of inflammatory responses, suggesting that protein citrullination could be considered as a sign of early cellular damage
Citrullination has been reported to be a process present in a wide range of inflammatory tissues. Indeed, citrullinated proteins have been detected also in other inflammatory arthritides and in inflammatory conditions other than arthritides (multiple sclerosis, polymyositis, inflammatory bowel disease and chronic tonsillitis)
Histone hypercitrullination can activate neutrophil extracellular traps (NETS)� high inflammatory
These data support the hypothesis that rather than being a disease?dependent process, citrullination is an inflammatory?dependent condition that plays a central role in autoimmune diseases.
Valesini G, Shoenfeld Y, et al Autoimmun Rev. 2015 Jun;14(6):490?7 Wang S,
Wang Y.Biochim Biophys Acta. 2013 Oct;1829(10):1126?35
Air Pollution In Autoimmune Rheumatic Diseases: A Review
Environmental factors contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica dust in rheumatoid arthritis and systemic lupus erythematosus
Scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica dust.
Primary vasculitis associated with anti?neutrophil cytoplasmic antibody (ANCA) may be triggered by silica exposure
Air pollution is one of the environmental factors involved in systemic inflammation and autoimmunity
Farhat SC, et al, Autoimmun Rev. 2011 Nov;11(1):14?21
Silica, Silicosis & Autoimmunity
Exposure to respirable crystalline silica (<10 ?m in size) occurs most often in occupational settings � the �dusty� trades
Epidemiological studies link occupational exposure to crystalline silica dust with systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis
Findings from human and animal model studies are consistent with an autoimmune pathogenesis that begins with activation of the innate immune system leading to proinflammatory cytokine production (NLRP3 inflammasome), pulmonary inflammation leading to activation of adaptive immunity, breaking of tolerance, and autoantibodies and tissue damage
Pollard KM, Front Immunol. 2016; 7: 97.
Asbestos = Magnesium Silicate
Assessment Of Autoimmune Responses Associated With Asbestos Exposure In Libby, Montana, USA
The population in Libby, Montana, provides a unique opportunity for study because of both occupational and environmental exposures that have occurred as a result of the mining of asbestos?contaminated vermiculite near the community
Libby serum samples showed significantly higher frequency of positive ANA and ENA tests, increased mean fluorescence intensity and titers of the ANAs, and higher serum IgA, compared with Missoula serum samples
The results support the hypothesis that asbestos exposure is associated with autoimmune responses and suggests that a relationship exists between those responses and asbestos?related disease processes.
Pfau JC, et al Environ Health Perspect, 2005, Vol 113: 25-30
Air Pollution, Oxidative Stress & Exacerbation Of Autoimmune Diseases
Particulate matter present in air pollution can induce oxidative stress and cell death, both by apoptosis and necrosis of human cells leading to aggravation of chronic inflammation, i.e. the tissue damaging reaction observed in autoimmune diseases.
Therefore, identification of strong inducers of oxidative stress among components of PM seems to be crucial for their neutralization and elimination from the ambient environment.
It seems likely that PM 2.5 may exacerbate the onset of the SLE because they were attributed to a significant increase of the level of anti?dsDNA antibodies, and the presence of the renal casts in SLE patients
Exposure to ozone, sulphates, and other pollutants present in the air has been associated with type 1 diabetes in children
MS occurrence and hospitalization was associated with exposure to air pollutants such as PM10, SO2, NO2, and NOx
In addition to tobacco smoke and silica, pollution emissions from road traffic may be an environmental factor responsible for exacerbation of RA
Gawda, A, et al, Central European Journal of Immunology 2017; 42(3)
What Do Environmental Pollutants, Toxins, Infections & Unhealthy Diets Have In Common?
Increase inflammation and additional free radical production,
Which damages tissues (bystander effect), disrupts barriers, and/or modifies DNA…
Creating �foreign?like� tissues that break immune tolerance (eg anti?nuclear antibodies)
Cell Stressors
Macario, A. J.L. et al. N Engl J Med 2005;353:1489-1501
Damage Associated Molecular Patterns
Molecular structures that activate immunologic receptors
Released with cellular injury and/or necrosis after exposure to cellular stressors
DNA fragments
Mitochondria
Misfolded proteins
Advanced glycation end products have similar biological effects
Initiate and perpetuate inflammatory response (esp NLRP3 inflammasome)
Ojcius D, Sai?d?Sadier N. Alarmins, inflammasomes and immunity. Biomedical Journal. 2012;35(6):437.
Vakrakou AG, Boiu S, Ziakas PD, et al, Systemic activation of NLRP3 inflammasome in patients with severe primary Sjo?gren’s syndrome fueled by inflammagenic DNA accumulations.
J Autoimmun. 2018 Mar 15. pii: S0896?8411(17)30789?8.
Environmental Xenobiotic Exposure & Autoimmunity
We argue that localized tissue damage and chronic inflammation elicited by xenobiotic exposure leads to the release of self?antigens and damage?associated molecular patterns …
As well as the appearance of ectopic lymphoid structures and secondary lymphoid hypertrophy,
Which provide a milieu for the production of auto-reactive B and T cells that contribute to the development and persistence of autoimmunity in predisposed individuals.
Pollard KM, Christy JM, Cauvi DM, Kono DH, Current Opinion in Toxicology, Volume 10, August 2018, Pages 15?22
The Functional Medicine Paradigm (Slightly Modified)
Immune disruption = increased susceptibility to triggers
Overload in hepatic detoxification pathways
Effect on triggers:
Synergistic action (immunotoxicant)
Adjuvant: chemical modification of self?antigen to make it appear foreign or immunogenic (neoantigens)
Enhanced apoptosis: danger/damage signals (DAMPs)
Effect on mediators:
Amplified inflammatory pathways
Increased oxidative stress
Disruption of pro?resolution counter?regulatory mechanisms
Functional Toxicology
Changes In Intestinal Tight Junction Permeability Associated With Industrial Food Additives Explain The Rising Incidence Of Autoimmune Disease
The incidence of autoimmune diseases and food additive consumption are both increasing in parallel
Dysfunction of intestinal tight junctions is common in multiple autoimmune diseases
Commonly used industrial food additives including glucose, salt, solvents, emulsifiers, gluten, microbial transglutaminase, and nanoparticles increase intestinal tight junction leakage.
Intestinal entry of foreign antigen activates the autoimmune cascade
Lerner A, Matthias T. Autoimmunity Reviews 14 (2015) 479�489
Autoimmunity Reviews 14 (2015) 479�489
Autoimmune Disease: �Two?Hit� Signal Theory
Barrier disruption allows immune system to be repeatedly exposed to a combination of an autoantigen & an �adjuvant� [Adjuvants can be toxicants, microbes, foods]
This triggers a genetically predisposed immune system to react to the autoantigen as a non?self �stranger�
�Danger� signals released at the site of clearance of dead cells amplify the process; shaping the features & severity of the resulting autoimmune disease
Persistent �Stranger + Danger� = loss of tolerance
Based on this model, strategies aimed at preventing the accumulation of dying cells lowering the adjuvant (toxic) load may be beneficial for the prevention & treatment of autoimmune disease
Anaya JM, Ramirez?Santana C, Alzate MA, Molano?Gonzalez N, Rojas?Villarraga A, The Autoimmune Ecology., Front Immunol. 2016 Apr 26;7:139
Oxidatively Modified Autoantigens In Autoimmune Diseases
Oxidative modification of proteins has been shown to elicit antibodies in a variety of diseases, including SLE, diabetes mellitus & RA.
Oxidatively modified DNA & LDL occur in SLE, a disease in which premature atherosclerosis is a serious problem. AGE pentosidine & AGE?modified IgG have been shown to correlate with RA disease activity.
In the face of overwhelming evidence for the involvement of oxidative damage in autoimmunity, the administration of antioxidants is a viable untried alternative for preventing or ameliorating autoimmune disease…�
Kurien BT, Hensley K, Bachmann M, Scofield RH., Free Rad Biol & Med, 2006, Vol 41: 549-556
Oxidative Stress In The Pathology & Treatment Of Systemic Lupus Erythematosus.
Oxidative stress is increased in SLE, and it contributes to immune system dysregulation, abnormal activation and processing of cell? death signals, autoantibody production and fatal comorbidities.
Oxidative modification of self antigens triggers autoimmunity, and the degree of such modification of serum proteins shows striking correlation with disease activity and organ damage in SLE.
Reactive oxygen intermediates (ROI) mostly originate from mitochondria, and T cells from patients with SLE exhibit mitochondrial dysfunction
In T cells from patients with SLE and animal models of the disease, glutathione, the main intracellular antioxidant, is depleted and serine/threonine?protein kinase mTOR undergoes redox?dependent activation.
In turn, reversal of glutathione depletion by application of its amino acid precursor, N?acetylcysteine, improves disease activity in lupus? prone mice; pilot studies in patients with SLE have yielded positive results that warrant further research.
Antioxidant therapy might also be useful in ameliorating damage caused by other treatments.
Oxidative stress (OS) plays an important role in the pathogenesis of a variety of autoimmune diseases (ADs) and many environmental agents participate in this process.
Environmental agents, including trichloroethylene (TCE), silica, pristane (TMPD in mineral oil), mercury, and smoke, are known to induce an autoimmune response, potentially through OS?mediated mechanisms.
Antioxidants can attenuate SLE disease activity by down regulating NLRP3 inflammasome activation and activating Nrf2 signaling.
Khan MF, Wang G. Curr Opin Toxicol. 2018 Feb;7:22?27.
Metals & Minerals Associated With Autoimmune Diseases
Heavy metals
Mercury
Cadmium
Lead
Gold
Minerals & Metalloids
Silica (crystalline silicon dioxide)
Asbestos (chrysotile = magnesium silicate)
Arsenic
Lithium
Iodine
Bigazzi PE., Metals and kidney autoimmunity. Environ Health Perspect. 1999 Oct;107 Suppl 5:753?65
Biologic Markers in Immunotoxicology National Research Council (US) Subcommittee on Immunotoxicology. Washington (DC): National Academies Press (US); 1992.
Anaya JM, et al, The Autoimmune Ecology., Front Immunol. 2016 Apr 26;7:139
Messages To Take Home
Autoimmune and autoinflammatory diseases are steadily increasing in our society
The rise in exposure to environmental pollutants and other toxins is increasing the total body burden of xenobiotics
A central theme in the development of autoimmune diseases is the loss of immune tolerance
Immune tolerance can be broken by disruption of barriers (skin, lung, gut, brain) and/or immune dysregulation
Numerous xenobiotics have been shown to disrupt healthy barriers and dysregulate immune responses
Xenobiotics may play a central role in the initiation and perpetuation of autoimmune disease
Explosion Of Autoimmune Diseases: The Mosaic Of Old & Novel Factors
Modern life and exposures to novel chemical and xenobiotic compounds may lead to the development of new complexes of symptoms that do not necessarily belong to one of the well?known autoimmune diseases
As physicians and scientists, we must continue to study novel pathogenic mechanisms and susceptible alleles to help us identify new therapeutic venues.
Agmon?Levin N, Lian Z, Shoenfeld Y. Cell Mol Immunol. 2011 May; 8(3): 189�192.
IFM Annual International Conference Hollywood, Florida May, 2018
Robert Rountree, MD
Robert Rountree, MD is a speaker, consultant, and advisory board member for Thorne and Balchem. He is also a clinical trial board member for Thorne Research.
Active release therapy, more specifically referred to as the active release technique, is a patented system designed by Dr. P. Michael Leahy which focuses on the treatment of developed scar tissue in damaged muscles all across the human body. When Dr. Leahy first developed the technique about two decades ago, he realized that the damage in the complex soft tissues of the muscles might perhaps be able to be sensed as well as addressed directly through movement in the form of specialized techniques. With its proven ability to cure pain, its own acronym, ART, provides the active release therapy with some ironical link to being a true art form in chiropractic care.
When athletes overwork their muscles from playing sports or even through just everyday activities, many individuals don’t understand how scar tissue can develop on our muscles in the first place. The scar issue forms in order to help heal damaged muscles, however, it can ultimately create painful symptoms which may last long after these have healed. Scar tissue most commonly develops as a result of pulled muscles or muscle tears, or even from a lack of oxygen, called hypoxia.
As the scar tissue builds in the damaged or injured muscles, if the individual does not maintain a proper level of mobility in the affected area, it can progressively cause muscles to become stiff or tight and weak, eventually leading to health issues such as tendonitis or nerve problems. This explains why some people with pain or limited range of motion, often will need to visit a healthcare professional immediately. Fortunately, many doctors are certified to treat these type of problems using active release therapy.
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Using the Active Release Technique to Relieve Pain
Together with providing tension to the targeted sore muscle and utilizing specific body motions, the painful symptoms associated with scar tissue improves through active release therapy. As of now, there are approximately 500 different active release techniques designed to alleviate the tightness or stiffness and weakness in all of the body’s soft tissues, from the muscles to the nerves. Many of these movements are particularly chosen for each individual based on the specific muscle issue and location.
Active release techniques can also be helpful for small traumatic injuries caused by accumulative trauma or repetitive strain. More specifically, ART functions to break up fibrous tissues called adhesions. These adhesions result from a tear onto a tendon, ligament or muscle. Adhesions commonly develop in different ways, including from trauma as a result of acute injury or from repetitive motion injury caused by overuse, most commonly from sports injuries. It may also be a result of poor posture which has been aggravated by continuous pressure in addition to tension produced in the soft tissues for extended amounts of time.
Such adhesions, when left untreated, can also limit blood flow as well as shorten muscles, causing the well-known symptoms. Worsened symptoms can also result in pain, discomfort or weakness and at times numbness, most notably when scar tissue applies pressure on the nerves. When adhesions occur, the patient will surely complain of distress much more due to the simple fact that they will not be able to engage in the physical activities they were used to performing in before.
The active release technique, or ART,� works by implementing a couple of movements and motions on the affected muscle, tendon or fascia. In comparison to other soft tissue therapies, it’s said to achieve better end results. Primarily, ART aims to help improve the symptoms of the damaged or injured area by applying pressure and force on it. From there, the individual will be tasked to perform a technique which will help release the tension from the treatment. This can essentially improve motion for the treated region.
The combination of this tension out of the active release technique and that of the movement of muscles and its soft tissues will loosen and break up the adhesions. Because of this, there’ll be lesser pain felt on the injured region. This technique works well with active strengthening in addition to biomechanics training. The combination of these therapies will make patients feel improved body awareness, strength, flexibility and mobility even after a few ART sessions.
How Different is ART from Traditional Soft Tissue Treatments?
When compared with traditional manners of soft tissue therapy, ART boasts of a very comprehensive strategy. The active release technique is performed by certified healthcare practitioners who’ve underwent a very rigorous training procedure. Healthcare professionals must participate in sit-in classes and they must also have hands-on testing. Their certificate doesn’t stop after they pass the 90 percent mark on the hands on test though. They’ll also have to maintain their ART certification by getting annual recertification. This may work by honing the healthcare professional’s abilities and at the exact time, this will boil to the benefit of patients undergoing the therapy.
How Successful is ART as a Treatment?
Current research has demonstrated how effective the procedure is when it comes to treating hamstring pain and dysfunction in addition to hip pain, turf toe and lymph nodes. While the efficacy of ART has been demonstrated along these areas, several studies are still being made to check into its potential for treating disorders for other body components.
Using the Active Release Technique for Sciatica
Sciatica is an issue which affects a large number of people. It is essentially a pain syndrome, characterized by a collection of common symptoms which are caused when the sciatic nerve, the largest and most important nerve supplying the lower spine and the lower extremities, is compressed by the small muscles in the pelvis. The piriformis muscle is the one most implicated in the compression of the sciatic nerve, particularly because it moves through this muscle when emerging from the pelvis and entering the lower limbs. The active release technique, or ART, may be used in the treatment of sciatica brought on by piriformis syndrome.
Pathophysiology of Sciatica
When sciatica is caused by the compression of the sciatic nerve by the piriformis muscle, the latter generally goes into a spasm for an extended period of time, leading to the compression of this fundamental nerve. The spasm may result in a compromise in the blood supply to the muscle itself as well as the nerve, which will further complicate the issue. Nerve communications are important in order for the human body to maintain its outmost efficiency. Sciatica often can also be caused by disc injuries and herniations, as generally is a differential diagnosis to piriformis syndrome. Specific orthopedic tests can help, doctors of chiropractic, or chiropractors, evaluate the source of the patient’s sciatica prior to commencing any type treatment.
Consequences of Sciatic Nerve Pain
There are a number of effects that could arise as a result of sciatica. Reduction in overall body ranges of movement can be anticipated, accompanied by searing or sharp pain that can be excruciating. This can make it very difficult for an individual’s quality of life, especially when carrying out daily tasks like going to school and work, might become impossible due to the seriousness of the health issue. When the issue isn’t treated on time, it might cause permanent damage to the sciatic nerve.
Conventional Treatments for Sciatic Nerve Pain
There are a range of conventional treatments that may be utilized based on the intensity of the sciatic nerve pain, or sciatica. One of these is an injection of a drug/medication that can relax the muscle so that it stops compressing the nerve. Additionally, it has been proven that drugs and/or medications, such as steroids, may also have an impact on reducing the pain and impairment related to the symptoms. When the pharmacological methods don’t result in any progress, surgical ones can be attempted. The most usual of these is a surgery to release the nerve from the muscle by cutting away a portion of it. Although these have been listed as conventional treatments which may be used to treat sciatica, alternative treatment options and secondary opinions should be considered before considering surgical interventions. Only when no other treatment has demonstrated any improvements, should surgery be considered by a patient.
The Role of Active Release Techniques for Sciatica
The active release technique, or ART, is a form of therapy that focuses on the manipulation of soft tissues, including nerves, fascia and muscles, so as to achieve relief of painful symptoms, in this case for sciatica. For sciatic nerve pain, ART is utilized to reduce spasm and remove adhesions of the muscle that may be entrapping the sciatic nerve. Since the adhesions are removed through specific manual methods, the nerve can slide under the soft tissues, and sciatica symptoms can solve relatively quickly. There are a range of things that a patient can do in order to increase the efficacy of the active release technique. Early start to treatment assists in long-term resolution of sciatica symptoms.
Dr. Alex Jimenez’s Insight
The active release technique, also known as active release therapy or ART, is a soft tissue treatment based on a series of movement and motion techniques utilized to relieve pain and discomfort as well as promote the healing of muscles, joints and nerves, among other soft tissues. When performed by a certified healthcare professional, including a chiropractor, ART can help break down adhesions which may have developed following scar tissue formation after a damaged or injured muscle has healed. The active release technique has become one of the most common therapy for soft tissue treatment.
ART therapy is usually provided by skilled therapists like chiropractors, who have to keep their accreditation through continuing education on a yearly suface. This treatment is a specialized procedure that needs quite a bit of expertise and skill so as to work and supply rapid results. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Sciatica
Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.
Whiplash Injuries: If you have ever had to deal with the pain of whiplash, you know how it can impact every aspect of your life. Whiplash can cause chronic pain and keep you from doing many activities you enjoy. Daily tasks can be painful or even impossible to carry out. Even milder cases can make turning your head from side to side complex.
Chiropractic is a very effective treatment for whiplash injuries that helps with pain management and enables you to heal faster. Your chiropractor can recommend exercises you can do at home between treatments and other lifestyle changes that will facilitate your healing and improve flexibility.
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Whiplash Injuries
What Is Whiplash?
Whiplash is a term that describes an injury that is typically focused on the neck and spine. It is caused when the head and neck are thrown in one direction unexpectedly and quickly, then thrust in the opposite direction. The head is rapidly whipped, usually front to back. It can be whipped from side to side, though.
Most people associate whiplash with car accidents, but even turning one way while a child tugs your arm in another direction can cause it. Anything that jerks your head suddenly can cause whiplash.
What Damage Does Whiplash Cause?
The damage that is caused by whiplash is called vertebral subluxation. This type of subluxation is caused by injury, and a chiropractor can diagnose the injury and treat it. It is the most common source of discomfort and pain caused by injuries due to whiplash. There are different kinds caused by tension and emotional stress, poor sleeping, lousy posture, weak muscles, and inadequate diet.
The injury from whiplash is in the neck and spine, but the pain can extend to the head, arms, shoulders, hips, and legs. You can experience frequent headaches, numbness, and tingling in your hands and have difficulty walking or moving about. The pain can range from stiffness and soreness to stabbing and sharpness. The injury can affect various nerves, causing blurred vision, dizziness, low back pain, ear ringing, and even problems with your internal organs.
Chiropractic Treatment For Whiplash
Chiropractors will use different techniques to relieve the pain of whiplash and help with healing.
Chiropractic Adjustment The chiropractor performs spinal manipulation to move the joints into alignment gently. This will help to align the body to relieve pain and encourage healing.
Muscle Stimulation and Relaxation This involves stretching the affected muscles, relieving tension, and helping them relax. Finger pressure techniques may also be combined with trying to alleviate pain.
McKenzie Exercises These exercises help with disc derangement that whiplash causes. They are first performed in the chiropractor’s office, but the patient can be taught how to do them at home. This helps the patient have some degree of control in their healing.
Each whiplash case is different. Instances of varying whiplash have various symptoms. A chiropractor will evaluate the patient and determine the appropriate treatment case-by-case basis. The chiropractor will determine the best course of treatment that will relieve your pain and restore your mobility and flexibility.
Whiplash can be far more severe than you may realize. Any accident that causes whiplash injuries can result in the vertebrae moving out of alignment. This can damage and irritate the spinal nerves. Even whiplash from years ago can still affect you if you never saw a chiropractor. Your spine can still be out of alignment, and injury or trauma from years ago can cause problems that seem unrelated.
Injury Medical Clinic: Accident Treatment & Recovery
The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular
syndromes for the non-neurologist.
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The Rule Of 4 & The Brainstem
The rule of 4 is a simple method developed to help �students of neurology� to remember the anatomy of the brainstem and thus the features of the various brainstem vascular syndromes. As medical students, we are taught detailed anatomy of the brainstem containing a bewildering number of structures with curious names such as superior colliculi, inferior olives, various cranial nerve nuclei and the median longitudinal fasciculus. In reality when we do a neurological examination we test for only a few of these structures. The rule of 4 recognizes this and only describes the parts of the brainstem that we actually examine when doing a neurological examination. The blood supply of the brainstem is such that there are paramedian branches and long circumferential branches (the anterior inferior cerebellar artery (AICA), the posterior inferior cerebellar artery (PICA) and the superior cerebellar artery (SCA). Occlusion of the paramedian branches results in medial (or paramedian) brainstem syndromes and occlusion of the circumferential branches results in lateral brainstem syndromes. Occasionally lateral brainstem syndromes are seen in unilateral vertebral occlusion. This paper describes a simple technique to aid in the understanding of brainstem vascular syndromes.
Any attempt to over simplify things runs the risk of upsetting those who like detail and I apologize in advance to the anatomists among us, but for more than 15 years this simple concept has helped numerous students and residents understand, often for the first time, brainstem anatomy and the associated clinical syndromes that result.
In The Rule Of 4 There Are 4 Rules:
There are 4 structures in the �midline� beginning with M.
There are 4 structures to the side beginning with S.
There are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain).
The 4 motor nuclei that are in the midline are those that divide equally into 12 except for 1 and 2, that is 3, 4, 6 and 12 (5, 7, 9 and 11 are in the lateral brainstem).
If you can remember these rules and know how to examine the nervous system, in particular the cranial nerves, then you will be able to diagnose brainstem vascular syndromes with ease.
Figure 1 shows a cross-section of the brainstem, in this case at the level of the medulla, but the concept of 4 lateral and 4 medial structures also applies to the pons, only the 4 medial structures relate to midbrain vascular syndromes.
The 4 Medial Structures & The Associated Deficit Are:
The Motor pathway (or corticospinal tract): contra lateral weakness of the arm and leg.
The Medial Lemniscus: contra lateral loss of vibration and proprioception in the arm and leg.
The Medial longitudinal fasciculus: ipsilateral inter- nuclear ophthalmoplegia (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally).
The Motor nucleus and nerve: ipsilateral loss of the cranial nerve that is affected (3, 4, 6 or 12).
The 4 Lateral Structures & The Associated Deficit Are:
The Spinocerebellar pathways: ipsilateral ataxia of the arm and leg.
The Spinothalamic pathway: contra lateral alteration of pain and temperature affecting the arm, leg and rarely the trunk.
The Sensory nucleus of the 5th: ipsilateral alteration of pain and temperature on the face in the distribution of the 5th cranial nerve (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla).
The Sympathetic pathway: ipsilateral Horner�s syndrome, that is partial ptosis and a small pupil (miosis)
These pathways pass through the entire length of the brainstem and can be likened to �meridians of longitude� whereas the various cranial nerves can be regarded as �parallels of latitude�. If you establish where the meridians of longitude and parallels of latitude intersect then you have established the site of the lesion.
Figure 2 shows the ventral aspect of the brainstem.
The 4 Cranial Nerves In The Medulla Are:
9 Glossopharyngeal: ipsilateral loss of pharyngeal sensation. 10 Vagus: ipsilateral palatal weakness. 11 Spinal accessory: ipsilateral weakness of the trapezius and sternocleidomastoid muscles. 12 Hypoglossal: ipsilateral weakness of the tongue.
The 12th cranial nerve is the motor nerve in the midline of the medulla. Although the 9th, 10th and 11th cranial nerves have motor components, they do not divide evenly into 12 (using our rule) and are thus not the medial motor nerves.
The 4 Cranial Nerves In The Pons Are:
5 Trigeminal: ipsilateral alteration of pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw. 6 Abducent: ipsilateral weakness of abduction (lateral movement) of the eye. 7 Facial: ipsilateral facial weakness. 8 Auditory: ipsilateral deafness.
The 6th cranial nerve is the motor nerve in the pons.
The 7th is a motor nerve but it also carries pathways of taste, and using the rule of 4 it does not divide equally in to 12 and thus it is not a motor nerve that is in the midline. The vestibular portion of the 8th nerve is not included in order to keep the concept simple and to avoid confusion. Nausea and vomiting and vertigo are often more common with involvement of the vestibular connections in the lateral medulla.
The 4 Cranial Nerves Above The Pons Are:
4 Olfactory: not in midbrain. 5 Optic: not in midbrain. 6 Oculomotor: impaired adduction, supraduction and infraduction of the ipsilateral eye with or without a dilated pupil. The eye is turned out and slightly down. 7 Trochlear: eye unable to look down when the eye is looking in towards the nose.
The 3rd and 4th cranial nerves are the motor nerves in the midbrain.
Thus a medial brainstem syndrome will consist of the 4 M�s and the relevant motor cranial nerve, and a lateral brainstem syndrome will consist of the 4 S�sand either the 9�11th cranial nerve if in the medulla, or the 5th, 7th and 8th cranial nerve if in the pons.
MEDIAL (PARAMEDIAN) BRAINSTEM SYNDROMES
Let us assume that the patient you are examining has a brainstem stroke. If you find upper motor neurone signs in the arm and the leg on one side then you know the patient has a medial brainstem syndrome because the motor pathways is paramedian and crosses at the level of the foramen magnum (decussation of the pyramids). The involvement of the motor pathway is the �meridian of longitude�. So far the lesion could be anywhere in the medial aspect of the brainstem, although if the face is also affected it has to be above the mid pons, the level where the 7th nerve nucleus is.
The motor cranial nerve �the parallels of latitude� indicates whether the lesion is in the medulla (12th), pons (6th) or midbrain (3rd). Remember the cranial nerve palsy will be ipsilateral to the side of the lesion and the hemiparesis will be contralateral. If the medial lemniscus is also affected then you will find a contra lateral loss of vibration and proprioception in the arm and leg (the same side affected by the hemiparesis) as the posterior columns also cross at or just above the level of the foramen magnum. The median longitudinal fasciculus (MLF) is usually not affected when there is a hemiparesis as the MLF is further back in the brainstem.
The MLF can be affected in isolation �a lacunar infarct� and this results in an ipsilateral internuclear ophthalmoplegia, with failure of adduction (movement towards the nose) of the ipsilateral eye and leading eye nystagmus on looking laterally to the opposite side of the lesion in the contra lateral eye. If the patient had involvement of the left MLF then, on being asked to look to the left, the eye movements would be normal, but on looking to the right the left eye would not go past the midline, while there would be nystagmus in the right eye as it looked to the right.
Figure 3 shows the clinical features of the medial brainstem syndromes.
LATERAL BRAINSTEM SYNDROMES
Once again we are assuming that the patient you are seeing has a brainstem problem, most likely a vascular lesion. The 4 S�s or �meridians of longitude� will indicate that you are dealing with a lateral brainstem problem and the cranial nerves or �parallels of latitude� will indicate whether the problem is in the lateral medulla or lateral pons.
A lateral brainstem infarct will result in ipsilateral ataxia of the arm and leg as a result of involvement of the Spinocerebellar pathways, contralateral alteration of pain and temperature sensation as a result of involvement of the Spinothalamic pathway, ipsilateral loss of pain and temperature sensation affecting the face within the distribution of the Sensory nucleus of the trigeminal nerve (light touch may also be affected with involvement of the spinothalamic pathway and/or sensory nucleus of the trigeminal nerve). An ipsilateral Horner�s syndrome with partial ptosis and a small pupil (miosis) is because of involvement of the Sympathetic pathway. The power tone and the reflexes should all be normal. So far all we have done is localize the problem to the lateral aspect of the brainstem; by adding the relevant 3 cranial nerves in the medulla or the pons we can localize the lesion to this region of the brain.
The lower 4 cranial nerves are in the medulla and the 12th nerve is in the midline so that 9th, 10th and 11th nerves will be in the lateral aspect of the medulla. When these are affected, the result is dysarthria and dysphagia with an ipsilateral impairment of the gag reflex and the palate will pull up to the opposite side; occasionally there may be weakness of the ipsilateral trapezius and/or sternocleidomastoid muscle. This is the lateral medullary syndrome usually resulting from occlusion of the ipsilateral vertebral or posterior inferior cerebellar arteries.
The 4 cranial nerves in the pons are: 5th, 6th, 7th and 8th. The 6th nerve is the motor nerve in the midline, the 5th, 7th and 8th are in the lateral aspect of the pons, and when these are affected there will be ipsilateral facial weakness, weakness of the ipsilateral masseter and pterygoid muscles (muscles that open and close the mouth) and occasionally ipsilateral deafness. A tumour such as an acoustic neuroma in the cerebello-pontine angle will result in ipsilateral deafness, facial weakness and impairment of facial sensation; there may also be ipsilateral limb ataxia if it compresses the ipsilateral cerebellum or brainstem. The sympathetic pathway is usually too deep to be affected.
If there are signs of both a lateral and a medial (paramedian) brainstem syndrome, then one needs to consider a basilar artery problem, possibly an occlusion.
In summary, if one can remember that there are 4 pathways in the midline commencing with the letter M, 4 pathways in the lateral aspect of the brainstem commencing with the letter S, the lower 4 cranial nerves are in the medulla, the middle 4 cranial nerves in the pons and the first 4 cranial nerves above the pons with the 3rd and 4th in the midbrain, and that the 4 motor nerves that are in the midline are the 4 that divide evenly into 12 except for 1 and 2, that is 3, 4, 6 and 12, then it will be possible to diagnose brainstem vascular syndromes with pinpoint accuracy.
P. GATES
The Geelong Hospital, Barwon Health, Geelong, Victoria, Australia
Everyone has stiff, sore muscles now and then. From overdoing it at the gym to sleeping in an awkward position, there are many reasons you might feel some muscular aches and pains. Some medical conditions or illnesses can also cause soreness. Several studies have found a remarkable, effective, inexpensive cure that is natural and safe � magnesium.
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Pain � It�s All In Your Head
Well, it�s in your brain, anyway. A chemical in the brain, NMDA, is responsible for pain. When this brain chemical is overly stimulated, the body experiences pain. The way the brain processes pain in an individual determines how that person will experience it and manage it.
There are very few medications that deal directly with NMDA, balancing it and decreasing its production. However, the side effects of these drugs are usually significant and undesirable. Magnesium has been found to calm production of NMDA without causing the side effects or toxicity. What�s more, magnesium is very inexpensive. It is far cheaper than pharmaceuticals at just pennies a dose. One drawback is that the FDA has not yet put its stamp of approval on the mineral that is often called the �gateway to health.�
Clinical Studies Find Magnesium Is An Effective Way To Relieve Pain
A study published in The Journal of Physiology in October 2010, explores the effectiveness of magnesium in decreasing nerve pain. The study, conducted on rats, found a strong link between magnesium deficiency and pain. In fact, that authors of the study suggest that pain is increased, or the sensitivity to pain is increased, due to magnesium deficiency.
As people are moving away from fresh foods, processed foods are becoming more prevalent. While processed foods offer easy, quick preparation and gratification, the trade-off has been a significant decrease in nutrition, leaving most people magnesium deficient. However, adding a magnesium supplement that provides 250 to 500 mg of the mineral will not only eliminate the deficiency, but decrease the pain as well. This usually happens surprisingly quickly � after only a few weeks you will notice a definite difference.
Chia Seeds Are High In Magnesium.
Other Benefits Of Magnesium
Magnesium has a wide range of uses and benefits for the entire body. It has long been used to treat indigestion as well as constipation when taken by mouth. For heartburn and indigestion, magnesium hydroxide has been noted as the fastest acting. It is also given to pregnant women to treat high blood pressure (pre-eclampsia and eclampsia). When given as a shot or by IV, magnesium helps lower blood pressure during pregnancy. It is also the treatment of choice for eclampsia because it reduces the risk of seizures that accompany the condition.
Magnesium, given intravenously, is effective in treating torsades de pointes, a type of irregular heartbeat. Additionally, it is believed to help these other conditions:
Various types of pain including nerve damage associated with certain cancers, pain after surgery, pain after hysterectomy, and chest pain.
A healthy diet, regular exercise, and reducing the stress in your life will also help with your pain management. When your body is properly nourished it functions at a more optimal level, meaning not just less pain, but better management of it. Exercise causes your brain to produce endorphins which not only minimize pain, but also boost your mood.
Stress can make you more sensitive to pain, causing you to feel it more and experience it on a more intense level. It decreases your ability to tolerate pain and manage it. Even learning relaxation techniques and breathing exercises can help you better manage stress that you may not be able to eliminate completely. Adding magnesium to your diet can help improve your overall wellbeing as well as decrease your pain.
Foods: Arthritis pain can be debilitating. According to the Centers for Disease Control (CDC), between the years of 2010 and 2012, an estimated 22.7 percent, or 52.5 million, adults in the United States alone were diagnosed by a doctor with arthritis, rheumatoid arthritis, lupus, gout, or fibromyalgia � annually. Also during that time, almost 50 percent of adults 65 or older were diagnosed with arthritis. It is estimated that by the year 2040, 78 million Americans ranging in age from 18 years old to 85-year-old will be diagnosed with arthritis. What�s more, nearly 1 in every 250 (around 294,000) children in the U.S. under 18 years old suffer from a form of arthritis or rheumatic condition.
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A Case For Healthy Eating
As medications and treatments get more expensive and drugs have significant unpleasant (and sometimes horrifying) side effects, more people are looking toward natural ways to treat their arthritis pain. In most cases they need look no further than the foods that they eat. While there is not nutritional magic bullet, studies have shown that getting the right nutrition from certain foods can help to minimize inflammation and pain that comes from arthritis. It can also help with your overall health and influence the symptoms as well as progression of conditions that may be related to arthritis.
There are certain foods that act as anti-inflammatories while other can increase inflammation. Arthritis sufferers who learn what foods to eat and which ones to avoid can enjoy better pain management, improved mobility, a more active lifestyle, and a more positive outlook on life. These foods provide great benefits for patients with rheumatoid arthritis, osteoarthritis, osteoporosis, gout, and other forms of inflammation caused by arthritis.
Foods That Fight Arthritis Inflammation
Different types of foods seem to affect different types of arthritis. The Arthritis Foundation offers some very good guidelines on dietary recommendations for arthritis sufferers based on their type of arthritis.
Foods rich in omega-3 fatty acids, phytochemicals, and antioxidants have powerful anti-inflammatory properties. These types of foods are the core of the Mediterranean style diet which consists of olive oil, fish, fresh vegetables, fruits, beans, seeds, and nuts. It should be stressed that choosing fresh foods in these categories is best. The key is to select foods that are as minimally processed as possible and contain no additives or preservatives. This means that most canned foods should be excluded. However, many supermarkets now have olive bars and other fresh, healthier food options that direct consumers away from processed, unhealthy food items. Fiber also plays a significant part in reducing arthritic inflammation.
Specific foods to incorporate into your diet to combat arthritis pain include:
Salmon
Extra virgin olive oil
Tuna
Mackerel
Egg yolks
Milk
Green tea
Oatmeal
Wild and brown rice
Barley
Quinoa
Beans
Tart cherries
Berries � blueberries, blackberries, raspberries, and strawberries
Broccoli
Brussels sprouts
Cabbage
Foods That Increase Arthritis Inflammation
Just as there are foodstuff that help alleviate arthritis pain, there are also foods that increase it. The Arthritis Foundation offers advice on foods that should be avoided by arthritis sufferers as they have been shown to increase pain and inflammation.
Sugar � Read the labels! Anything ingredient that ends in �ose� is a form of sugar. This includes sucrose and fructose.
Saturated fat � Cheese, pizza, red meat, pasta dishes, full fat dairy
Trans fats � Processed snacks, cookies, crackers, stick margarine, fast food, donuts, anything fried, frozen breakfast products
Refined carbs � Crackers, rolls, bread, white potatoes, white rice
MSG � A food additive found in soy sauce and many Asian prepared meals, deli meats, prepared soups, salad dressings
Gluten and casein � Dairy and wheat products, whey protein, rye, and wheat
Aspartame � Most diet sodas, artificial sweeteners, many �diet� or �sugar free� products
Alcohol
Paying attention to what you put into your body will not only help you better manage pain and inflammation, it will also help you feel better both physically and emotionally. A healthy, fresh diet can literally change your life.
Injury Medical Clinic: Elderly & Geriatric Fitness
Physicians, neurologists, and other healthcare professionals may often run a cranial nerve examination as part of a neurological evaluation to analyze the operation of the cranial nerves. This involves a highly formalized series of tests that evaluate the status of each cranial nerve. A cranial nerve test begins with observation of the patient partly due to the fact that cranial nerve lesions may ultimately affect the symmetry of the face or eyes, among other signs and symptoms.
The visual fields for neural lesions or nystagmus�are tested via an evaluation of particular eye movements. The sensation of the face is tested by asking patients to execute different facial movements, like puffing out their cheeks. Hearing is tested through voice and tuning forks. The position of the individual’s uvula is also examined because asymmetry in its placement could indicate a lesion of the glossopharyngeal nerve. After the capability of the individual to use their shoulder to test the accessory nerve (XI), the patient’s tongue operation is generally assessed by detecting various tongue movements.
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Damage or Injury of the Cranial Nerves
Compression
Cranial nerves may be compressed due to increased intracranial pressure, a profound effect of an intracerebral haemorrhage, or tumour which presses against the cranial nerves and interferes with the communication of impulses along the length of a nerve. In some instances, a loss of functionality of one cranial nerve may on occasion be the first symptom of an intracranial or skull base cancer.
An increase in intracranial pressure can lead to dysfunction of the optic nerves (II) because of the compression of the surrounding veins and capillaries, resulting in swelling of the eyeball, known as papilloedema. A cancer, such as an optic glioma, can also affect the optic nerve (II). A pituitary tumour can compress the optic tracts or the optic chiasm of the optic nerve (II), causing visual field loss. A pituitary tumour may also extend into the cavernous sinus, compressing the oculuomotor nerve (III), the trochlear nerve (IV) and the abducens nerve (VI), often leading to double-vision and strabismus. These cranial nerves may also be impacted by herniation of the temporal lobes of the brain via the falx cerebri.
The cause of trigeminal neuralgia, where one side of the face experiences painful signs and symptoms, is believed to be due to the compression of a cranial nerve by an artery as the nerve exits from the brain stem. An acoustic neuroma, especially at the junction between the pons and medulla, may compress the facial nerve (VII) and the vestibulocochlear nerve (VIII), resulting in hearing and sensory loss on the affected side.
Stroke
Occlusion of blood vessels which supply the cranial nerves or their nuclei, or an ischemic stroke, might cause specific signs and symptoms which could localize where the occlusion happened. A clot in a blood vessel draining the cavernous sinus, also known as the cavernous sinus thrombosis, may affect the oculomotor (III), the trochlear (IV), and the opthalamic branch of the trigeminal nerve (V1) and the abducens nerve (VI).
Inflammation
Inflammation caused by an infection may impair the operation of any of the cranial nerves. Infection of the facial nerve (VII), for instance, can result in Bell’s palsy. Multiple sclerosis, an inflammatory process which can produce a loss of the myelin sheathes that encircle the cranial nerves, may cause a variety of shifting signs and symptoms which can ultimately affect multiple cranial nerves.
Other
Trauma to the skull, bone disease like Paget’s disease, and damage or injury to the cranial nerves through neurosurgery, by way of instance, through tumor removal, are other potential causes of cranial nerve health issues.
Dr. Alex Jimenez’s Insight
There are 12 pairs of cranial nerves which exit the brain, one in each side. These cranial nerves are named and numbered (I-XII) according to their location in the brain as well as their specific function in the body. Common conditions, such as multiple sclerosis, may affect one or more of the cranial nerves, resulting in dysfunction of the specific regions innervated by them. Signs and symptoms associated with health issues affecting specific cranial nerves can help healthcare professionals determine the source of the problem. Testing the cranial nerves involves a number of steps in order to be certain which function of the human body has been ultimately affected.
Clinical Significance of the Cranial Nerves
Most commonly, humans are believed to have twelve pairs of cranial nerves which have been assigned Roman numerals I-XII for identification. The numbering of the cranial nerves is based on the order in which they emerge from the brain, or from the front to the back of the brainstem. These include: the olfactory nerve (I), the optic nerve (II), the oculomotor nerve (III), the trochlear nerve (IV), the trigeminal nerve (V), the abducens nerve (VI), the facial nerve (VII), the vestibulocochlear nerve (VIII), the glossopharyngeal nerve (IX), the vagus nerve (X), the accessory nerve (XI), and the hypoglossal nerve (XII). Below we will narrow down the clinical significance of the cranial nerves.
Olfactory Nerve (I)
The olfactory nerve (I) communicates the sensation of smell to the brain. Lesions resulting in anosmia, or loss of the sense of smell, have been previously described to occur through trauma, damage or injury to the head, especially in the instance that a patient hits the back of their head. In addition, frontal lobe masses, tumors, and SOL have also been associated with the loss of the sense of smell. Healthcare professionals have previously identified that the loss of the sense of smell is one of the first symptoms seen in Alzheimer’s and early dementia patients.
Healthcare professionals may test the function of the olfactory nerve (I) by having the patient close their eyes and cover one nostril at a time in order to have them breathe out through their nose while placing a scent under the nostril and having them breathe in. The doctor will ask the patient, “do you smell anything?”, and record the findings. This tests whether the nerve is operating appropriately. If the patient says yes, the doctor will then ask the patient to identify the scent. This tests whether the processing pathway, known as the temporal lobe, is functioning accordingly.
Optic Nerve (II)
The optic nerve (I) communicates visual information to the retina. Lesions to this cranial nerve can be the result of CNS disease, such as MS, or CNS tumors and SOL. Most health issues associated with the visual system emerge from direct trauma, metabolic or vascular diseases. FOV lost in the periphery can also indicate that SOL may be affecting the optic chiasm, including a pituitary tumor.
A healthcare professional will often test the function of the optic nerve (II) by asking whether the patient can see. If the patient describes having vision in each eye, the optic nerve is functional. Doctors may also perform visual acuity testing using the Snellen chart, first one eye at a time, then the two eyes together, or they may perform distance vision testing. Near vision testing will often involve the Rosenbaum chart, first one eye at a time, then the two eyes together. Additional associated testing for the visual system can include, the ophthalmoscopic or funduscopic exam, which assess the A/V ratio and vein/artery health as well as assess cup to disc ratio of the visual system. Other testing methods include field of vision testing, intraoccular pressure testing and the iris shadow test.
Oculomotor Nerve (III), Trochlear Nerve (IV), and Abducens Nerve (VI)
The oculomotor nerve (III), the trochlear nerve (IV), the abducens nerve (VI) and the ophthalmic division of the trigeminal nerve (V1) travel through the cavernous sinus to the superior orbital fissure, passing out of the skull into the orbit. These cranial nerves control the tiny muscles that move the eye and also offer sensory innervation to the eye and orbit.
The clinical significance of the oculomotor nerve (III) includes diplopia, lateral strabismus (unopposed lateral rectus m.), head rotation away from the side of the lesion, a dilated pupil (unopposed dilator pupillae m.), and ptosis of the eyelid (loss of function of the levator palpebrae superioris m.). Lesions to the oculomotor nerve (III) can occur due to inflammatory diseases, such as syphilitic and tuberculous meningitis, aneurysms of the posterior cerebral or superior cebellar aa., and SOL in the cavernous sinus or displacing the cerebral peduncle to the opposite side. Testing this cranial nerve is performed by moving a light in front of the patient’s pupil from the lateral side and hold for 6 seconds. The doctor should watch for direct (ispilateral eye) and consensual (contralateral eye) pupillary constriction in order to distinguish dysfunction of the oculomotor nerve (III).
The clinical significance of the trochlear nerve (IV) is characterized where the patient presents diplopia and difficulty while maintaining a downward gaze, often complaining of having difficulties when walking down stairs, resulting in more frequent tripping and/or falling, followed by extortion of the affected eye (unopposed inferior oblique m.) and a head tilt to the unaffected side. Lesions to the trochlear nerve (IV) can commonly be the result of inflammatory diseases, aneurysms of the posterior cerebral or superior cerebellar aa., SOL in the cavernous sinus or superior orbital fissure and surgical damage during mesencephalon procedures. Head tilts in superior oblique palsy (CN IV failure) may also be identified.
The clinical significance of the abducens nerve (VI) includes diplopia, medial strabismus (unopposed medial rectus m.), and head rotation towards the side of the lesion. Lesions to this cranial nerve can be the result of aneurysms of the posterior inferior cerebellar or basilar aa., SOL in the cavernous sinus or 4th ventricle, such as a cerebellar tumor, fractures of the posterior cranial fossa, and increased intracranial pressure. Testing this cranial nerve is performed through the H-Pattern testing, where the healthcare professional will have the patient follow an object no bigger than 2 inches. It’s essential for the doctor to follow these specific guidelines as patient’s can have difficulties focusing on items that are too large, and it’s also important for the doctor not to hold the object too close to the patient. Convergence and accommodation testing is performed by bringing the object close to the bridge of the patient’s nose and back out at least 2 times. The physician must look for pupillary constriction response as well as convergence of the eyes.
Trigeminal Nerve (V)
The trigeminal nerve (V) is made up of three different parts: The . When put together, these nerves provide sensation to the skin of the face and also controls the muscles of mastication, or chewing. Cranial nerve dysfunction along any of the separate sections of the trigeminal nerve (V) can manifest as decreased bite strength on the ipsilateral side of the lesion, loss of sensation along the distribution of V1, V2, and V3, and loss of corneal reflex. Lesions to the trigeminal nerve (V) can be the result of aneurysms or SOL affecting the pons, particularly tumors at the cerebellopontine angle, skull fractures on the facial bones or damage to the foramen ovale, and Tic doloureux, most frequently referred to as trigeminal neuralgia, characterized by sharp pain along the distributions of the different parts of the trigeminal nerve (V). Physicians may utilize analgesic, anti-inflammatory or contralateral stimulation to control the signs and symptoms.
Testing the trigeminal nerve (V) includes pain & light touch testing along the ophthalmic (V1), the maxillary (V2), as well as the Mandibular (V3) nerves of the cranial nerve.�Testing is best done toward the more medial or proximal areas of
the face, where the V1, the V2 and the V3 are better delineated. A healthcare professional may also assess dysfunction along this cranial nerve using the blink/corneal reflex testing, performed by puffing air or doing a small tissue tap from the lateral side of the eye on the cornea. If normal, the patient blinks. The CN V provides the sensory (afferent) arc of this reflex. Bite strength may also be tested by having the patient bite down on a tongue depressor while the doctor tries to remove it. The jaw jerk/Masseter reflex may also be performed with the patient�s mouth slightly open, by placing the thumb on a patient�s chin and tapping the own thumb with a reflex hammer. Strong closure of the mouth indicates UMN lesion. CN V provides both the motor and sensory of this reflex.
Facial Nerve (VII) and Vestibulocochlear Nerve (VIII)
The facial nerve (VII) and the vestibulocochlear nerve (VIII) both input the inner auditory canal in the temporal bone. The facial nerve subsequently extends to the side of the face then distributes to control and reach all of the muscles in charge of facial expressions. The vestibulocochlear nerve reaches the organs which control equilibrium and hearing in the temporal bone.
As with all cranial nerves, signs and symptoms along the facial nerve (VII) describe the location of the lesion. Lesion in the lingual nerve will manifest as loss of taste, general sensation in the tongue and salivary secretion. Lesion proximal to the branching of the chorda tympani, such as in the facial canal, will result in the same signs and symptoms, without the loss of general sensation of the tongue, partly due because the V3 has not yet joined the facial nerve (VII). Corticobulbar innervation is asymmetric to the upper and lower parts of the facial motor nucleus. In the instance of an UMN lesion, or a lesion to the corticobulbar fibers, the patient will experience paralysis of the muscles in charge of facial expression in the contralateral lower quadrant. If there is an LMN lesion, or a lesion to the facial nerve itself, the patient will experience paralysis of the muscles of facial expression in the ipsilateral half of the face, otherwise known as Bell’s palsy.
A healthcare professional will test the facial nerve (VII) initially by asking the patient to mimic or follow specific instructions to make certain facial expressions. The doctor should make sure to evaluate all four quadrants of the face by asking the patient to raise their eyebrows, puff their cheeks, smile and then close their eyes tightly. Subsequently, the doctor will test the facial nerve (VII) by checking the strength of the buccinator muscle against resistance. The healthcare professional will achieve this by asking the patient to hold air in their cheeks as they press gently from the outside. The patient should be able to hold air in against the resistance.
Signs and symptoms of dysfunction in the vestibulocochlear nerve (VIII) often involve changes in hearing alone, most commonly as a result of infections in the otitis media and/or as a result of skull fractures. The most common lesion to this nerve is caused by an acoustic neuroma which affects the CN VII and the CN VIII, particularly the cochlear and vestibular divisions, as a result of proximity in the internal auditory meatus. Signs and symptoms of the health issue include nausea, vomiting, dizziness, hearing loss, tinnitus, and Bell’s palsy, etc.
Testing the vestibulocochlear nerve (VIII) for dysfunction commonly involves an otoscopic exam, the scratch test, which determines whether a patient can hear equally on both sides, the Weber test, tests for lateralization, a 256 Hz tuning fork placed on top of the patient�s head in the center, which can help point out whether a patient hears it louder on one side than the other, and finally the Rinne test, which compares air conduction to bone conduction. Normally, air conduction should last twice as long as bone conduction.
Glossopharyngeal Nerve (IX), Vagus Nerve (X) and Accessory Nerve (XI)
The glossopharyngeal (IX), the vagus nerve (X) and the accessory nerve (XI) all emerge from the skull to enter the neck. The glossopharyngeal nerve (IX) provides innervation to the upper throat and the back of the tongue, the vagus nerve (X) offers innervation to the muscles at the voicebox, and proceeds down to provide parasympathetic innervation to the chest and abdomen. The accessory nerve (XI) controls the trapezius and sternocleidomastoid muscles at the neck and shoulder.
The glossopharyngeal nerve (IX) is rarely damaged alone, due to it�s proximity to the CN X and XI. A healthcare professional should perform a test to look for signs of CN X & XI damage as well if CN IX involvement is suspected.
Patients with clinical signs and symptoms caused by vagus nerve (X) dysfunction may experience dysarthria, or difficulty speaking clearly, as well as dysphagia, or difficulty swallowing. These may present as food or liquid coming out of their nose or frequent chocking or coughing when eating and/or drinking. Further clinical presentations include hyperactivity of a visceral motor component, leading to the hypersecretion of gastric acid and resulting in ulcers. Hyper-stimulation of the general sensory component can cause coughing, fainting, vomiting and reflex visceral motor activity. The visceral sensory component of this nerve only provides general feelings of un-wellness but visceral pain may transfer on to the sympathetic nerves.
Testing for the glossopharyngeal nerve (IX) and the vagus nerve (X) can include the gag reflex, where the�CN IX provides the afferent (sensory) arc and the�CN X provides the efferent (motor) arc. Approximately 20 percent�of patients have a minimal or absent gag reflex. Other tests may include wwallowing, gargling, etc., as it requires CN X function. Healthcare professionals may also test palatal elevation because it requires CN X function. Furthermore, the doctor will see whether the palate elevates and uvula deviates
contralateral to damaged side. Finally, the healthcare professional will test the auscultation of the heart, since the R CN X innervates SA node (more rate regulation) and the L CN X the AV node (more rhythm regulation).
Lesions in the accessory nerve (XI)�may occur due to radical surgeries in the neck area, such as the removal of the laryngeal carcinomas. Testing for the accessory nerve (XI) may include the strength test SCM m. Patients with clinical signs and symptoms due to lesions in the accessory nerve (XI) will experience difficulties turning their head against the resistance of a healthcare professional, particularly toward the side opposite of the lesion. Testing for the accessory nerve (XI) may also include the strength test trapezius m. Patients with clinical signs and symptoms due to lesions in the accessory nerve (XI) will experience difficulties with shoulder elevation on the side of the lesion.
Hypoglossal Nerve (XII)
The hypoglossal nerve (XII) originates from the skull to reach the tongue in order to control essentially all of the muscles involved in the movements of the tongue. The clinical significance of health issues associated to the hypoglossal nerve (XII) can manifest as a deviating tongue towards the side of an inactive genioglossus m. upon tongue protrusion. This may often be contralateral to a corticobulbar, or UMN, lesion or from an ipsilateral to a hypoglossal n., or LMN, lesion.
Testing for the hypoglossal nerve (XII) involves the healthcare professional asking a patient to stick out their tongue. The doctor will look for any deviation which may signal a health issue along the length of the hypoglossal nerve (XII). Another test the doctor may perform as a part of the evaluation may include the physician asking the patient to place their tongue inside their cheek and apply light resistance, one side at a time. The patient should be able to resist moving their tongue with pressure.
The clinical significance of the signs and symptoms which manifest as a result of cranial nerve dysfunction are essential in order for the healthcare professional to properly diagnose the patient’s specific health issue. The clinical findings described above are often unique to the affected cranial nerve and the tests and evaluations for each can help confirm a diagnosis. Proper diagnosis is fundamental in order for the doctor to continue with the patient’s appropriate treatment. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .
Curated by Dr. Alex Jimenez
Additional Topics: Sciatica
Sciatica is medically referred to as a collection of symptoms, rather than a single injury and/or condition. Symptoms of sciatic nerve pain, or sciatica, can vary in frequency and intensity, however, it is most commonly described as a sudden, sharp (knife-like) or electrical pain that radiates from the low back down the buttocks, hips, thighs and legs into the foot. Other symptoms of sciatica may include, tingling or burning sensations, numbness and weakness along the length of the sciatic nerve. Sciatica most frequently affects individuals between the ages of 30 and 50 years. It may often develop as a result of the degeneration of the spine due to age, however, the compression and irritation of the sciatic nerve caused by a bulging or herniated disc, among other spinal health issues, may also cause sciatic nerve pain.
Ataxia is a degenerative disease of the nervous system. Symptoms can mimic those of being inebriated/intoxicated, with� slurred speech, stumbling, falling, and unable to maintain coordination. This comes from degeneration of the cerebellum, which is the part of the brain responsible for coordinating movement. It is a disease that affects people of all ages. However, age of symptom onset can vary, from childhood to late adulthood. Complications from the disease can be serious, even debilitating and life shortening.
Symptoms can vary from person to person, as well as, the type of Ataxia. Symptom onset and progression can vary as well. Symptoms can worsen slowly, over decades or quickly, over a few months. The common symptoms are lack of coordination, slurred speech, trouble eating, swallowing, eye movement abnormalities, motor skill deterioration, difficulty walking, gait abnormalities, tremors, and heart problems. People with Ataxia usually require wheelchairs, walkers, and/or scooters to aid in mobility.
Contents
Ataxia
The Loss Of Full Control Of Bodily Movements, Especially Gait
History Of Ataxia
How long has it been present?
Slow onset ? Degenerative disease?
Acute onset ? Stroke?
When does it occur?
If worsened by walking on uneven surfaces, or with limited vision ? Sensory ataxia?
Are there any coexisting symptoms?
Vertigo, weakness, stiffness, cognitive changes, etc.
Have others noticed this gait disturbance?
If no, consider psychogenic cause
Is the gait change explainable by physical problems such as pain or weakness?
Antalgic gait, limp, etc.
Weakness
Proximal muscle weakness�? Myopathy?
Distal muscle weakness ? Neuropathy?
UMN signs?
LMN signs?
Has the patient fallen? Or at risk for fall?
Is ataxia limiting ADLs?
Balance
Utilizes
Vestibular system
Cerebellar system
Conscious proprioceptive information (joint position sense)
Visual information
Motor strength and coordination
Vestibular System
Generally, if the problem lies in the vestibular system the patient will experience dizziness, possibly having vertigo or nystagmus
Does the dizziness feel similar to when you stand up too fast?
Pre-Syncope
�Light-headedness�
CardiacOrigin
Output disorders
Arrhythmias
Holter monitor testing
Postural/Orthostatic hypotension
May be secondary to other problems (diabetic neuropathy, adrenal hypofunction, Parkinsons, certain medications, etc.)
Vasovagal episodes
Slow heart rate with low blood pressure
Often brought on by stress, anxiety or hyperventilation
Migraine
Due to cerebrovascular instability
Blood sugar dysregulation
Disequilibrium Hx Questions
Does the dizziness only occur when you�re on your feet?
Does it get better if you touch/hold onto something?
Disequilibrium
Common in the elderly
Due to sensory deficits
Gradual onset
Worsened by reduced vision
Dark
Eyes closed
Visual acuity losses
Improved by touching a stationary object
Subjective of dizziness often improves with a gait assistive device (cane, walker, etc.)
Other Causes
Psychological stress
Often patient will describe dizziness as �floating�
Rule out hyperventilation and other types of dizziness
Sources
Blumenfeld, Hal. Neuroanatomy through Clinical Cases. Sinauer, 2002.
Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
You have been diagnosed with Benign Paroxysmal Positional Vertigo. This brochure is designed to help increase your understanding of this disorder and its potential treatments.
Contents
Benign Paroxysmal Positional Vertigo
What Is BPPV?
Benign paroxysmal positional vertigo (BPPV) is a disorder of the inner ear. People with BPPV typically experi�ence brief episodes of vertigo (dizziness) when they change the position of their head with respect to gravity. Approximately 20 percent of all vertigo is due to BPPV.
What Causes BPPV?
Benign Paroxysmal Positional Vertigo is thought to be due to tiny crystals, called otoconia, that have collected within a sensitive part of the inner ear. Otoconia are crystals of calcium carbonate that are normally located in a structure of the ear called the utricle.
Dizziness occurs when the crystals are displaced from the utricle into the semicircular canals of the inner ear.
Otoconia may become displaced when the utricle is injured, if there is an infection or other disorder of the inner ear, or simply due to advanced age. When you change the position of your head, the otoconia move within the semicircular canals and this causes the dizziness. The dizziness subsides when the otoconia stop moving.
The most common cause of BPPV in people under age 50 is head injury. In older people, the most common cause is degeneration of the vestibular system of the inner ear. BPPV becomes much more common with advancing age. Other causes include minor strokes, Meniere’s disease, and viruses such as those causing vestibular neuritis. In approximately half of all BPPV cases, no cause can be determined.
What Are The Symptoms?
The symptoms of BPPV include dizziness or vertigo, lightheadedness, imbalance, and nausea. Activities that
bring on symptoms vary among individuals, but symptoms are usually associated with a change in the position of the head with respect to gravity. Getting out of bed, rolling over in bed, and tipping the head back to look up are common “problem” motions. The use of shampoo bowls in hair salons may bring on symptoms. An intermittent pattern is common. BPPV may be present for a few weeks, then stop, and then come back again.
How Is Benign Paroxysmal Positional Vertigo (BPPV) Diagnosed?
BPPV is diagnosed with the Dix-Hallpike test. This test involves observing the eyes with the head and body positioned in specific ways. It can be performed either by the clinician, or as part of a laboratory test called an electronystagmography, or ENG. If the Dix-Hallpike test is abnormal and the findings are “dassic” for BPPV, then additional testing is not necessary. If the results are normal or not “classic” then the diagnosis of BPPV is less certain and other tests may be suggested.
What Are The Treatments For BPPV?
There are four approaches to treating BPPV.
1. Do Nothing And Wait For It To Go Away By Itself
BPPV symptoms sometimes go away within six months of onset, therefore you might want to wait and see if your symptoms subside on their own. During this waiting period, medications to prevent motion sickness or nausea are sometimes helpful in controlling the nausea associated with BPPV.
2. Physical Maneuvers Performed In The Clinic
(The Epley and Semont Maneuvers)
The Epley and Semont maneuvers, named for their inventors, are treat�ments that are performed in the clinic. These treatments are specifi�cally intended to move the otoconia from the semicircular canals to a less sensitive location within the inner ear. Your clinician will select the treatment that is most appropriate for you.
Each of these treatments takes about 15 minutes and alleviates symptoms in about 80 percent of patients. In the remaining 20 percent, a second treatment may be necessary, or you may be instructed to perform the Brandt-Daroff exercises (see “Home Treatment”).
The Epley maneuver, also called the canalith reposi�tioning procedure (CRP) and particle repositioning, is a procedure in which the clinician moves your head into five positions, maintaining each position for ap�proximately 30 seconds. The Semont maneuver (also called the liberatory maneuver) is a procedure in which the clinician rapidly moves you from lying on one side to lying on the other side. These maneuvers may not be appropriate for patients with neck or back problems. Pa�tients who experience nausea or anxiety may wish to take medication prior to the treatment.
INSTRUCTIONS FOR PATIENTS AFTER CLINIC TREATMENTS
Follow these instructions after the Epley or Semont maneuver. B.Y doing so you will minimize the opportunity for otoconia to return to the semicircular canals of the inner ear and reduce the potential that your dizziness will recur.
Wait at least 10 minutes after the maneuver before going home.
This is to avoid “quick spins” or brief bursts of vertigo as the otoconia reposition themselves immedi�ately after the maneuver. If possible, arrange to have someone drive you home.
The following two days:
Sleep semi-recumbent for the next two nights. This means sleeping with your head halfway between flat and upright, at a 45-degree angle. This is most easily done by sleeping in a recliner chair or by sleeping with pillows appropriately arranged on a couch.
During the day, try to keep your head vertical. A soft neck brace may be helpful.
Do not go to the barber, hairdresser or dentist.
When shaving, keep your head vertical by bending forward at your hips with your neck extended.
If you need to administer eye drops, try to keep your head as vertical as possible.
Sham�poo only under the shower.
During the following week, avoid provoking head positions that might bring on BPPV.
Use two pillows when you sleep.
Avoid sleeping on the affected side.
Don’t turn your head far up or far down.
Avoid tilting your head back especially when lying on your back with your head turned toward the affected side.
If possible, postpone elective surgery and going to the beauty parlor or the dentist’s office.
Avoid far head-forward positions and exercises where the head is not kept upright, for example toe touches.
The effectiveness of the clinic treatment cannot be determined for one week.
Wait one week after treatment to test the effectiveness of treatment. Place yourself in the position that usually makes you dizzy. Be sure to position yourself cautiously and under conditions in which you can’t fall or hurt yourself.
3. Home Treatment Of Benign Paroxysmal Positional Vertigo (Brandt-Daroff Exercises)
When the clinic treatment (Epley or Semont) fails, when the involved side is not determined, or when a case is mild, the Brandt-Daroff exercises may be recommended. These exercises succeed in 95 percent of cases but take longer to work than the clinic treatments. You should perform these exercises only if instructed to do so by your clinician. If your clini�cian performed the Epley or Semont maneuver, you must wait one week after that treatment before you begin the Brandt-Daroff exercises.
These exercises should be performed on a flat surface, without a pillow.
Start sitting upright on the edge of the bed or on the floor.
(Position 1)�Turn your head 45 degrees to the left and lie down on your right side.
(Position 2)�When in the right side-lying position, your head should be at a 45-degree angle turned halfway between the flat surface and the ceiling. Stay in the side-lying position for at least 30 seconds. If you are still dizzy, stay until the dizziness subsides or one minute, whichever is less.
Then sit up (Position 3} and stay in the sitting posi�tion for 30 seconds. Turn your head 45 degrees to the right and lie down on your left side.
(Position 4)�Again keeping your head turned halfway toward the ceiling for 30 seconds or until the dizziness subsides. Return to Position 1 (sit upright) for 30 seconds. This is one repetition.
One set (five repetitions) takes about 10 minutes to complete and should be performed each morning, mid-day and evening.
The Brandt-Daroff exercises should be performed for two weeks, three sets each day, or for three weeks, two sets each day (52 sets total). In most individuals, complete relief from symptoms is obtained after 30 sets, or about 10 days. In approximately 30 percent of patients, BPPV will recur within one year. If BPPV recurs you may wish to add one 10-minute exercise (one set) to your daily routine.
If the maneuvers or exercises do not control symptoms that have persisted for a year or longer and the diagnosis is very clear, surgery may be recommended. The most common surgical procedure, called posterior canal plugging, blocks most of the posterior canal’s function without affecting the functions of the other canals or parts of the ear. There is, however, a small risk of hearing loss. This surgery is effective in about 90 percent of individuals who have not responded to other treatments and when symptoms are severe and long-standing.
�?2000 Northwestern University. Authors: Timothy C. Hain, MD, Janet Odiry Helminski, PhD, PT.
This information is for educational purposes and is not intended as a substitute for examination, diagnosis, or medical care provided by a licensed and qualified health professional. This work was supported by the Center for Sensory and Communicotion Disorders at Northwestern University, a national research and training center funded by the National Institute on Deafness and Other Communication Disorders.
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IFM Annual International Conference Hollywood, Florida May, 2018
LATERAL BRAINSTEM SYNDROMES
The lower 4 cranial nerves are in the medulla and the 12th nerve is in the midline so that 9th, 10th and 11th nerves will be in the lateral aspect of the medulla. When these are affected, the result is dysarthria and dysphagia with an ipsilateral impairment of the gag reflex and the palate will pull up to the opposite side; occasionally there may be weakness of the ipsilateral trapezius and/or sternocleidomastoid muscle. This is the lateral medullary syndrome usually resulting from occlusion of the ipsilateral vertebral or posterior inferior cerebellar arteries.
May develop spontaneously, especially in the elderly
Sleep semi-recumbent for the next two nights. This means sleeping with your head halfway between flat and upright, at a 45-degree angle. This is most easily done by sleeping in a recliner chair or by sleeping with pillows appropriately arranged on a couch.
