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.
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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.
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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.
Back Pain Specialist: Mike Melgoza is a very active person who is always engaging in physical activity, as a result, he occasionally suffers from debilitating back pain symptoms. Mike Melgoza was struggling to sleep properly due to his symptoms of back pain before receiving chiropractic care with Dr. Alex Jimenez. Mike Melgoza has already started experiencing tremendous relief from his back pain and he highly recommends Dr. Alex Jimenez as the non-surgical choice for back pain.
Back Pain Specialist
Back pain is one of the most common reasons people visit the doctor or miss work and it is also a leading cause of disability globally. The majority of people have back pain at least once throughout their lifetimes. Luckily, you can take steps to prevent or relieve back pain. If prevention fails, easy treatment and appropriate body mechanics frequently will heal your back in a few weeks and keep it operational for the long haul. Surgery is rarely required to treat back pain.
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As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
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Patellofemoral Syndrome: As the weather warms and spring is in full swing, more and more runners are heading outside, hitting the pavement to train for upcoming races or to just step up their game after a long winter. While there are some die hard runners who don�t let even the most brutal winter stop them, most tend to retreat indoors, waiting for warmer days and a more pleasant environment. Unfortunately, increased activity can also lead to an increased risk of injury, particularly patellofemoral pain syndrome (PFPS), also known as runner�s knee.
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What Is Patellofemoral Pain Syndrome?
Runner�s knee is often used to describe PFPS, but runner�s knee is actually a broader term describing several different knee injuries or ailments. PFPS is a painful condition that is caused when the tissue that is between the femur (thigh bone) and the patella (kneecap) becomes inflamed or irritated.
Most people will notice pain in the front portion or anterior part of the knee, but pain can be experienced in other parts of the knee and even back pain may occur. Running increases the discomfort, as does sitting for long periods and going up or down stairs.
The causes of PFPS can also vary widely. Overuse is often the first thing that people think, but a problem with the way the knee is aligned is actually the most common reason.
If the patella is not properly aligned, when it moves through the groove that is at the end of the femur, it causes irritation to the surrounding tissues. This usually happens because the muscles and joints are out of balance.
For instance, if the quad muscle on one side is weaker than the other side it throws the entire system out of balance, causing the knee to become misaligned. This leads to knee pain and discomfort.
Treatment For Patellofemoral Syndrome – Runner�s Knee
When treating PFPS, rest is usually first on the list, followed by icing the area to reduce inflammation. Once the pain is under control, the next step is to determine what is causing the problem. It is important to rule out more serious conditions or injuries first in order to determine the best course of treatment.
If it is indeed PFPS, strengthening the muscles in and around the knee is generally the first step in treatment. It is important that the muscle strength is balanced so that the knee can be properly aligned. Getting a good pair of running shoes is also recommended so that future injury can be prevented.
Chiropractic For Runner�s Knee
Runner�s knee, or PFPS, responds very well to chiropractic treatment. The chiropractor is able to do a complete exam and find the cause of the problem, then tailor the treatment accordingly. This is typically done on a case by case basis with treatment that is based on the individual�s unique needs. The chiropractor may do various chiropractic alignments and manipulations on the spine, hip, ankle, and knee in order to bring the body back into proper balance.
The chiropractor may also recommend other complimentary treatments including special supplements, dietary adjustments, and an exercise plan. The chiropractor may also recommend certain stretching exercises to aid in healing. Kinesio taping is another common treatment that may be used in conjunction with chiropractic care. It is particularly beneficial when there is a muscular strength imbalance. The tape can help support the weaker muscle group.
Chiropractic care is a very effective treatment for patellofemoral syndrome and the associated knee pain. It works to correct the problem by bringing the body back into proper alignment, allowing it to function as it should.
The cranial nerves are the nerves which come out straight from the brain, including the brainstem, in comparison to the spinal nerves, which come out from sections of the spinal cord. Of those, 10 out of 12 of these cranial nerves originate in the brainstem. Cranial nerves transfer information between the brain and parts of the human body, particularly to and from areas of the head and neck.
Spinal nerves exit from the spinal cord with the spinal nerve closest to the head (C1) exiting in the space above the first cervical vertebra. The cranial nerves, however, exit from the central nervous system above this region. Each cranial nerve is paired and is present on either side of the brain. Based on the definition in humans, there are twelve, sometimes thirteen, cranial nerve pairs, which have been assigned Roman numerals I-XII for identification, sometimes including cranial nerve zero as well. 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.
The terminal nerves, olfactory nerves (I) and optic nerves (II) come out from the cerebrum, or forebrain, where the rest of the ten pairs of cranial nerves arise in the brainstem, which is the lower portion of the brain. The cranial nerves are considered components of the peripheral nervous system (PNS), though on a structural level, the olfactory, the optic and the trigeminal nerves are more accurately considered a portion of the central nervous system (CNS).
Most commonly, humans are believed to have twelve pairs of cranial nerves (I-XII). 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). There may be a thirteenth cranial nerve, known as the terminal nerve, or nerve N or O, which Is quite small and may or may not be functional in humans.
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Anatomy of the Cranial Nerves
The cranial nerves are usually named according to their structure or function. For instance, the olfactory nerve (I) supplies smell, and the facial nerve (VII) supplies motor innervation to the face. Since Latin was the common language of the study of anatomy once the nerves were documented, recorded, and mentioned, many nerves maintain Greek or Latin names, including the trochlear nerve (IV), named based on its arrangement, as it supplies a muscle which attaches to a pulley (Greek: trochlea). The trigeminal nerve (V) is named based on its three components (Latin: trigeminus meaning triplets), and the vagus nerve (X) is known because of its wandering course (Latin: vagus).
In addition, cranial nerves are numbered according to their rostral-caudal, or front-back, position, when looking at the brain. If the brain is carefully removed from the skull, the nerves are typically visible in their numeric order, with the exception of the final nerve, the CN XII, which seems to come out from above, into the CN XI.
Cranial nerves have pathways within and away from the skull. The pathways inside the skull are known as “intracranial paths” and the pathways outside the skull are known as “extracranial pathways”. There are a number of holes in the skull known as “foramina”, by which the nerves may exit from the skull. All cranial nerves are paired, meaning that they can be found on both the left and right sides of the human body. The skin, muscles, or other structural function provided by a nerve on the same side of the human body as the side it originates from, is referred to as an ipsilateral function. In case the function is on the other hand from the origin of the nerve, then this is referred to as a contralateral function.
Location of the Cranial Nerves
After coming out from the brain, the cranial nerves from inside the skull must leave this bony structure in order to arrive to their destinations. Several of the cranial nerves pass through the foramina,�holes in the skull, as they journey to their destinations. Other nerves pass through bony canals, longer pathways enclosed by bone. The foramina and canals might contain more than just one cranial nerve, and may also include blood vessels. Below is a list of the twelve cranial nerves and a brief summary of their function.
The olfactory nerve (I), composed of many small separate nerve fibers, which passes through perforations from the cribiform plate component of the ethmoid bone. These fibers end in the upper part of the nasal cavity and also operate to communicate impulses containing information about scents or odors into the brain.
The optic nerve (II) passes through the optic foramen from the sphenoid bone in order to reach the eye. It communicates visual information to the brain.
The oculomotor nerve (III), the trochlear nerve (IV), the abducens nerve (VI) and the ophthalmic division of the trigeminal nerve (V1) journey 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 maxillary division of the trigeminal nerve (V2) moves through the foramen rotundum from the sphenoid bone to supply the skin of the middle of the face.
The mandibular branch of the trigeminal nerve (V3) moves through the foramen ovale of the sphenoid bone to supply the lower face with sensory innervation. This nerve also extends to nearly all the muscles that control chewing.
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 using the stylomastoid foramen, also from the temporal bone. Its fibers then distribute 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, and therefore doesn’t reach the outside surface of the skull.
The glossopharyngeal (IX), the vagus nerve (X) and the accessory nerve (XI) all emerge from the skull via the jugular foramen to enter the neck. The glossopharyngeal nerve provides innervation to the upper throat and the back of the tongue, the vagus nerve offers innervation to the muscles at the voicebox, and proceeds down to provide parasympathetic innervation to the chest and abdomen. The accessory nerve controls the trapezius and sternocleidomastoid muscles at the neck and shoulder.
The hypoglossal nerve (XII) exits the skull using the hypoglossal canal at the occipital bone and also reaches the tongue to control virtually all the muscles involved in movements of this organ.
Function of the Cranial Nerves
The cranial nerves give motor and sensory innervation particularly to the structures found inside the neck and head. The sensory innervation contains both “overall” feelings, such as temperature and touch, and “particular” innervation, such as flavor, vision, smell, balance and hearing. For instance, the vagus nerve (X) gives sensory and autonomic, or parasympathetic, motor innervation to structures in the neck and to many of the organs in the chest and abdomen. Below, we will discuss the function of each cranial nerves in further detail.
Smell (I)
The olfactory nerve (I) communicates the sense of smell. Damage to the olfactory nerve (I) may cause an inability to smell, referred to as anosmia, a distortion in the sense of odor, referred to as parosmia, or even a distortion or absence of flavor. When there’s suspicion of a change in the sense of smell, every nostril is tested with compounds of known odors, such as coffee or soap. Intensely smelling chemicals, such as ammonia, can lead to the activation of pain receptors, known as nociceptors, of the trigeminal nerve which are situated in the nasal cavity, which may ultimately confound olfactory testing.
Vision (II)
The optic nerve (II) communicates visual information. Damage to the optic nerve (II) affects specific aspects of vision which are based on the area of the lesion. An individual may not be able to observe objects in their left or right sides, known as homonymous hemianopsia, or might have difficulty seeing objects on their outer visual areas, known as bitemporal hemianopsia, if the optic chiasm is included. Vision may be analyzed by examining the visual field, or simply by analyzing the retina with an ophthalmoscope, with a procedure called funduscopy. Visual field testing can be employed to pin-point structural lesions in the optic nerve, or further along the visual pathways.
Eye Movement (III, IV, VI)
The oculomotor nerve (III), the trochlear nerve (IV) and the abducens nerve (VI) coordinate eye motion. Damage to nerves III, IV, or VI can impact the movement of the eyeball globe. One or both eyes may be influenced; in either case, double vision, referred to as diplopia, will likely occur since the movements of the eyes are no longer synchronized. Nerves III, IV and VI are tested by observing the way the eye follows an object in different directions. This object may be a finger or even a pin, and may be moved at several directions to test for pursuit velocity. If the eyes don’t work together, the most likely cause is harm to a specific cranial nerve or its nuclei.
Damage to the oculomotor nerve (III) can lead to double vision, or diplopia, and inability to coordinate the movements of both eyes, known as strabismus, as well as eyelid drooping, referred to as ptosis, and pupil dilation, or mydriasis. Lesions may also lead to theinability to open the eye due to paralysis of the levator palpebrae muscle. People suffering from a lesion in the oculomotor nerve may compensate by leaning their heads to relieve symptoms because of paralysis of one or more of the eye muscles it regulates.
Damage to the trochlear nerve (IV) may also cause diplopia with all the eye adducted and raised. The result will be an eye which can’t move downwards properly, especially downwards when within an inward position. This is a result of impairment from the superior oblique muscle, which is innervated by the trochlear nerve.
Damage to the abducens nerve (VI) can also result in diplopia This is a result of impairment in the lateral rectus muscle, which is innervated by the abducens nerve.
Trigeminal nerve (V)
The trigeminal nerve (V) is made up of three different parts: The ophthalmic (V1), the maxillary (V2), as well as the Mandibular (V3) nerves. When put together, these nerves provide sensation to the skin of the face and also controls the muscles of mastication, or chewing. Conditions affecting the trigeminal nerve (V) include, trigeminal neuralgia, cluster headaches, and trigeminal zoster. Trigeminal neuralgia may occur later in life, from middle age onwards, most often after the age of 60, and it is a condition commonly associated with a very strong pain that spreads over the region innervated by the maxillary or mandibular nerve divisions of the trigeminal nerve (V2 and V3).
Facial expression (VII)
Lesions of the facial nerve (VII) may manifest as facial palsy. This is where a individual is unable to move the muscles on one or both sides of the face. An extremely frequent and generally temporary facial palsy is called Bell’s palsy. Bell’s Palsy is the end result of an idiopathic (unknown cause), unilateral lower motor neuron lesion of the facial nerve and is characterized by an inability to move the ipsilateral muscles of facial expression, including altitude of the eyebrow and furrowing of their forehead. Patients with Bell’s palsy frequently have a drooping mouth over the affected side and often have difficulty chewing since the buccinator muscle is affected. Bell’s palsy occurs very rarely, affecting around 40,000 Americans annually. Facial paralysis may be caused by other conditions including, stroke. Related conditions to Bell’s Palsy are sometimes misdiagnosed as Bell’s Palsy. Bell’s Palsy is a temporary condition usually lasting 2-6 months, but can have life-changing results and may reoccur often. Strokes typically also impact the cranial nerve by cutting off blood flow to nerves within the brain which is a clear indication that the nerve is present with similar symptoms.
Hearing and Equilibrium (VIII)
The vestibulocochlear nerve (VIII) divides into the vestibular and cochlear nerve. The vestibular region is in charge of innervating the vestibules and semicircular canal of the inner ear; this structure communicates information regarding equilibrium, and is a significant element of the vestibuloocular reflex, which keeps the brain stable and allows the eyes to track moving objects. The cochlear nerve communicates data from the cochlea, allowing sound to be heard. If damaged, the vestibular nerve can manifest the sensation of spinning and dizziness. Function of the vestibular nerve may be analyzed by placing warm and cold water in the ears and watching eye motions caloric stimulation. Damage to the vestibulocochlear nerve may also pose as repetitive and involuntary eye movements, previously described as nystagmus, particularly when looking in a horizontal plane. Damage to the cochlear nerve may cause partial or complete deafness in the affected ear.
Oral Sensation, Taste, and Salivation (IX)
The glossopharyngeal nerve (IX) innervates the stylopharyngeus muscle and supplies sensory innervation to the oropharynx and back of the tongue. The glossopharyngeal nerve additionally supplies parasympathetic innervation to the parotid gland. Unilateral absence of a gag reflex suggests a lesion of the glossopharyngeal nerve (IX), and perhaps the vagus nerve (X).
Vagus Nerve (X)
Reduction of function of the vagus nerve (X) can lead to a reduction of parasympathetic innervation to quite a high number of structures. Important consequences of damage to the vagus nerve could include an increase in blood pressure and heart rate. Isolated dysfunction of just the vagus nerve is rare, but can be diagnosed with a hoarse voice, because of dysfunction of one of its branches, the recurrent laryngeal nerve. Damage to this nerve may result in difficulties swallowing.
Shoulder Elevation and Head-Turning (XI)
Damage to the accessory nerve (XI) can lead to ipsilateral weakness in the trapezius muscle. This can be tested by asking the patient to elevate their shoulders or shrug, where the shoulder blade, or scapula, will protrude to a winged position. Additionally, if the nerve is damaged, weakness or an inability to elevate the scapula may be present because the levator scapulae muscle is only able to provide this function. Based on the location of the lesion, there may also be weakness within the sternocleidomastoid muscle, which then acts to reverse the head so that the face points to the other side.
Tongue Movement (XII)
The hypoglossal nerve (XII) is unique in that it is innervated in the motor cortices of both hemispheres of the brain. Damage to the nerve at lower motor neuron level may cause fasciculations or atrophy of the muscles of the tongue. The fasciculations of the tongue are sometimes said to look like a”bag of worms”. Upper motor neuron damage won’t cause atrophy or fasciculations, but only weakness of the innervated muscles. Once the nerve is damaged, it will lead to weakness of tongue movement on one side. When damaged and extended, the tongue will move towards the weaker or damaged side, as shown in the image.
Dr. Alex Jimenez’s Insights
The cranial nerves are a set of 12 nerves which emerge directly from the brain. The first two nerves, known as the olfactory nerve and the optic nerve, come out from the cerebellum, where the remaining ten cranial nerves emerge from the brain stem. The names of the cranial nerves relate directly to their function and they are also numerically identified in roman numerals I-XII by their specific location of the brain and by the order in which they exit the cranium. Damage to any of the above mentioned cranial nerves can cause health issues associated to the specific structure and function of each nerve. Common signs and symptoms in these regions can help healthcare professionals identify the affected cranial nerves.
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.
Human Cranial nerves are a set of 12 paired nerves that come directly from the brain. The first two (olfactory and optic) come from the cerebrum, with the remaining ten come from the brain stem. The names of the these nerves relate to what function they perform and are also numerically identified in roman numerals (I-XII).�The�nerves serve in functions of smell, sight, eye movement, and feeling in the face. These�nerves also control balance, hearing, and swallowing.
As with all nerves, symptoms describe the location of the lesion
Lesion in the lingual nerve will result in loss of taste, general sensation in tongue & salivary secretion
Lesion proximal to the branching of the chorda tympani such as in the facial canal will result in the same symptoms without the loss of general sensation of the tongue (because V3 has not yet joined the CN VII)
Corticobulbar innervation is asymmetric to the upper and lower parts of the Facial Motor Nucleus
If there is an UMN lesion (lesion to the corticobulbar fibers) the patient will have paralysis of the muscles of facial expression in the contralateral lower quadrant
If there is a LMN lesion (lesion to the facial nerve itself) the patient will have paralysis of the muscles of facial expression in the ipsilateral half of the face
Bell�s Palsy
Testing Cranial Nerve CN VII
Ask the patient to mimic you or follow instructions to make certain facial expressions
Be sure to assess all four quadrants of the face
Raise eyebrows
Puff cheeks
Smile
Close eyes tightly
Check for strength of the buccinator muscle against resistance
Ask patient to hold air in their cheeks as you press gently from the outside
Patient should be able to hold air in against resistance
Cranial Nerve VIII – Vestibulocochlear
Cranial Nerve VIII Clinically
Changes in hearing alone are most often due to
Infections (otitis media)
Skull fracture
The most common lesion to this nerve is caused by an acoustic neuroma
This affects CN VII and CNVIII (cochlear AND vestibular divisions) due to proximity in the internal auditory meatus
Symptoms include nausea, vomiting, dizziness, hearing loss, tinnitus, and bell�s palsy etc.
Testing Cranial Nerve CN VIII
Otoscopic Exam
Scratch Test
Can the patient hear equally on both sides?
Weber Test
Tests for lateralization
256 Hz tuning fork placed on top of the patient�s head in the center, is it louder on one side than the other?
Rinne Test
Compares air conduction to bone conduction
Normally, air conduction should last 1.5-2 as long as bone conduction
Almost everyone can say that they’ve experienced a feeling of unsteadiness or a spinning/whirling sensation in their heads at one point in their lifetimes. Usually it’s narrowed down to dizziness, however, dizziness is a broad term that can mean different things to different individuals. It is a prevalent complaint which can also be serious. Dizziness has no specific medical definition, but there are four common conditions which can be considered types of dizziness:
Vertigo. The feeling of motion where there is no movement, as if you were spinning or your environment is whirling. Spinning/whirling yourself around and around, then abruptly stopping, can produce temporary vertigo. However, when it occurs throughout an individual’s regular course of living, it could mean that there’s an underlying health issue in the vestibular system of the inner ear, the body’s equilibrium system which tells you which way is up or down and senses the position of your head. About half of all dizziness complaints are diagnosed as vertigo.
Lightheadedness. Also referred to as near syncope or pre-syncope, lightheadedness is the feeling that you’re about to faint. It is commonly believed to occur from standing up too fast or by breathing deeply enough times to generate the sensation.
Disequilibrium. A problem with walking. People with disequilibrium feel unsteady on their feet or feel as if they will fall.
Anxiety. Individuals who are scared, worried, depressed, or fearful of open spaces can use the term “dizzy” to imply feeling frightened, depressed, or anxious.
Individuals who frequently suffer from dizziness may also ultimately complain of more than one type of dizziness. For instance, people with vertigo may also feel anxious. Dizziness may be a one-time event, or it can be a chronic, long-lasting issue. Nearly everyone who experiences some form of dizziness will recover over time. This is because an individual’s sense of balance is an intricate interaction between the brain, each ear’s different vestibular system, sensors in the muscles, and sense of vision. When one component experiences dysfunction, others can generally learn how to compensate. Below, we will be narrowing down the four common types of dizziness.
Vertigo, the sensation of spinning or whirling, can be divided into two different categories: peripheral vertigo and central vertigo. Peripheral vertigo is more common than central vertigo and it typically develops due to damage to the inner ear or CN VIII. This type of vertigo produces abnormal eye movements, referred to as nystagmus, which may be horizontal or rotary.
Nystagmus is usually jerky in nature with a fast and slow phase, however it is often named for the direction of the fast phase. Peripheral vertigo may worsen when the patient looks to the side of the fast phase of nystagmus. Furthermore, the severity of nystagmus can correlate with the severity of the patient’s vertigo. Peripheral vertigo is also characterized as having no other signs and/or symptoms of CNS dysfunction. Patient may describe having symptoms of nausea or may present difficulty when walking, but only due to vestibular dysfunction. The patient may also have hearing loss or tinnitus if the CN VIII or auditory mechanism function is damaged.
The causes of peripheral vertigo are typically benign, including: benign paroxysmal positional vertigo, or BPPV, cervicogenic vertigo, acute labyrinthitis/vestibular neuronitis, Meniere’s disease, perilymph fistula, and acoustic neuroma. Identifying a patient’s cause of vertigo can be determined by narrowing down the symptoms through proper diagnosis from a healthcare professional. If movements, especially of the neck and head, aggravate vertigo, it may be attributed to BPPV, vertebrobasilar artery insufficiency or cervicogenic vertigo. If noise manifests episodes of vertigo, it may be attributed to Meniere’s disease or perilymph fistula.
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Common Causes of Dizziness
Vertigo can be Brought on by many things:
Infections, such as the ones which cause the frequent cold or diarrhea, can lead to temporary vertigo through an ear infection. This inner ear disease is generally viral, benign, and usually goes away in one to six weeks, however, drugs and/or medications are readily available if these become too severe.
Benign paroxysmal positional vertigo, or BPPV, is caused by the motion of a misplaced otolith, a tiny calcium particle the size of a grain of sand, from the component of the inner ear which senses gravity into the part that senses head position. The individual feels as if their head is turning when it isn’t. After diagnosis of BPPV using a special methods known as the Dix-Hallpike test, treatment done right in the doctor’s office can help move the otolith back where it belongs and fix the health issue. This therapy, known as the Epley maneuver, has been accounted to cure vertigo 80 percent of the time.
Meniere’s disease is a disorder characterized by long-lasting episodes of severe vertigo. Other symptoms of Meniere’s disease are tinnitus, or ringing in the ears, hearing loss, and fullness or pressure in the ear.
Dandy’s syndrome is a feeling of everything bouncing up and down. It may occur to individuals who take an antibiotic that is toxic to the ear. However, it usually improves over time.
Less frequent, deadly diseases may also result in vertigo, like tumors or stroke.
Below, we will be narrowing down some of the common causes of vertigo, described above, in further detail.
Benign Paroxysmal Positional Vertigo (BPPV)
Benign paroxysmal positional vertigo, or BPPV, may develop spontaneously, particularly in the elderly. It may also commonly develop as a result of head trauma or head injury, such as that resulting from an automobile accident. Vertiginous episodes associated with BPPV may manifest through specific movements, including, looking at a high shelf, referred to as top-shelf vertigo, bending over, and rolling over in bed at night. The onset of vertigo with BPPV can begin a few seconds after movement and often resolves within a minute. As mentioned above, the diagnostic test commonly utilized to diagnose BPPV is the Dix-Hallpike maneuver. Treatment procedures to treat BPPV include the Epley maneuver and Brandt-Daroff Exercises. Furthermore, benign paroxysmal positional vertigo may also resolve on its own as the loose crystals in the inner ear dissolve, however, it may take months and new otoliths can also become displaced.
Cervicogenic vertigo occurs after a neck or head injury, however, it is not very common. It’s generally accompanied by pain and/or joint restriction where vertigo and nystagmus are less severe than that in BPPV. Cervicogenic vertigo manifests with changes in head position but does not subside as quickly as it does with benign paroxysmal positional vertigo.
Vertebrobasilar Artery Insufficiency
Vertebrobasilar artery insufficiency occurs if the vertebral artery is compressed during head rotation or extension. In this instance, the onset of vertigo is delayed more than in BPPV or cervicogenic vertigo due to the fact that ischemia often takes up to 15 seconds to occur. Orthopedic tests for vertebrobasilar artery insufficiency may help in its diagnosis. Diagnostic tests include the�Barre?-Lie?ou sign, DeKlyn Test or Dix-Hallpike Maneuver, Hautant test, Underberg test and the vertebrobasilar after functional maneuver.
Acute Labyrinthitis and Vestibular Neuronitis
Acute labyrinthitis and vestibular neuronitis are not well understood, however, they’re believed to develop as a result of inflammation. These conditions generally follow after a viral infection or may occur seemingly without a cause.�Acute labyrinthitis and vestibular neuronitis are characterized by a single, monophasic attack of vertigo which typically resolves in days to a few weeks and generally does not reoccur.
Meniere’s Disease
Meniere’s disease is characterized by increased pressure in the endolymph which causes membrane ruptures and a sudden mixture of endolymph and perilymph. With Meniere’s disease, episodes of vertigo can last from 30 minutes to several hours, or until equilibrium between the fluids in the inner ears to be reached. Over time, these episodes can damage vestibular and cochlear hair cells, resulting in low-pitch buzzing tinnitus and the loss of hearing of low tones. In comparison to Meniere’s disease, Meniere’s syndrome is when the symptoms of Meniere’s disease are found to be secondary to another condition, such as: hypothyroidism, acoustic neuroma, superior semicircular canal dehiscence or SCDS, or perilymph fistula. True Meniere’s disease is idiopathic.
Perilymph Fistula
Perilymph fistula is an abnormal connection, or tear, which causes a small leak within the inner ear due to trauma or injury, especially barotrauma. Perilymph fistula can look very similar symptomatically to Meniere’s disease/syndrome and it’s often aggravated by changes in pressure causes by airplane rides or driving uphill. Another symptom of perilymph fistula includes Hennebert’s sign, where a vertigo or nystagmus episode is brought on by sealing pressure of the ear, such as by inserting an otoscope.
Central vertigo, another category of vertigo, is less common than peripheral vertigo, as described above. It is caused by damage to the processing center of vestibular information in the brain stem and the cerebral cortex. However, episodes of dizziness are considered to be less severe than with peripheral vertigo while episodes of nystagmus are more severe than the patient’s complaint or description. This specific nystagmus associated with central vertigo may go in multiple directions, including vertical. Central vertigo may or may not have other CNS findings upon diagnosis or examination and no changes in hearing can be expected with this form of vertigo. The most common causes of central vertigo include: cerebrovascular disease, such as transient ischemic attacks, multiple sclerosis, Arnold-Chiari malformation, damage to caudal brainstem or vestibulocerebellum and/or migraine condition.
Lightheadedness, or pre-syncope dizziness, is generally caused by some surrounding circumstance impairing blood flow into the brain when an individual is standing up. Blame this problem on our ancestors who learned to walk upright, placing our brain above our heart. It is a challenge for your heart to keep the brain supplied with blood and it is easy for this system to break down. When blood vessels in the brain become dilated, or enlarged, as a result of elevated fever, excitement or hyperventilation, alcohol ingestion, or prescription drugs and/or medications, such as antidepressants, it’s no wonder someone may commonly get lightheaded. There can also be serious causes, however, such as a stroke and cardiovascular disease.
Pre-syncope dizziness is specifically from cardiac origin, such as output disorders, arrhythmias, Holter monitor testing. It may also be caused by postural/orthostatic hypotension, which may be secondary to other health issues like diabetic neuropathy, adrenal hypofunction, Parkinsons, certain drugs and/or medications, etc. Light-headedness can involve vasovagal episodes accompanied by slow heart rate with low blood pressure often caused by stress, anxiety or hyperventilation. Finally, pre-syncope dizziness can be caused by migraine headaches due to cerebrovascular instability and blood sugar dysregulation.
Disequlibrium, can be caused by:
A type of arthritis in the neck called cervical spondylosis, which puts stress on the spinal cord.
Parkinson’s disease or related disorders that cause an individual to stoop forward.
Disorders involving part of the brain known as the cerebellum. The cerebellum is the part of the brain responsible for coordination and balance.
Diseases like diabetes that can lead to lack of sensation in the legs.
Disequilibrium is most common in the elderly and it generally occurs due to sensory deficits. In addition, disequilibrium has a gradual onset which worsens with reduced vision, darkness, eyes closed and visual acuity losses. However, it is improved by touching a stationary object which is often subjective as dizziness improves with a gait assistive device like a cane, walker, etc.
Dr. Alex Jimenez’s Insights
If you’ve ever experienced a sudden spinning or whirling sensation or even felt faint, woozy or unsteady, you’re not alone. Dizziness is a term used to describe a range of sensations and it is one of the most common reasons why many adults visit their healthcare professionals. While these false sensations can rarely signal a life-threatening condition, frequent episodes can significantly affect an individual’s quality of life. Diagnosis and treatment of dizziness can depend largely on the cause of the symptoms. Fortunately, many treatment methods used to treat dizziness are considered safe and effective.
Other causes of dizziness can be attributed to psychological stress. In this instance, the patient will describe their dizziness as a “floating” sensation.�Dizziness in the kind of anxiety is frequently, but not always, caused by depression. In addition, it can be attributed to an anxiety disorder or anxiety. Various medications can also cause dizziness as a side effect. It’s essential for a healthcare professional to rule out this type of dizziness caused by hyperventilation as well as other types of dizziness. 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.
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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.
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Testing Cranial Nerve CN II & III
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