MYOFASCIAL PAIN SYNDROME(OMOHYOIDEUS-4 patients reports)

The JOURNAL OF CRANIOMANDIBULAR PRACTICE June '84-Aug. 'b4, Vol. 2, No. 3 The Omohyoideus Myofascial Pain Syndrome: Report of Four Patients Abstract Pain in the shoulder, neck, arm, and hand, and in the scapular, supraclavicular, mandibular, and temporal regions may be caused by the omohyoideus myofascial pain syndrome. This may be primary, caused by vomiting or by other intense use of the muscle, or it may be secondary, occurring as a result of rheumatoid myositis, ankylosing spondylitis, nonankylosing rheumatoid spondylitis, gouty myositis, or other disorders. The syndrome can be successfully treated by gently injecting the inferior belly of the omohyoideus muscle and the secondary trigger points with a combination of medications that will break the pain/spasm cycle. Michael R. Rask, M.D. Michael R. Rask, M.D. After receiving his M.D. degree from the University of Oregon Medical School in 1955, Dr. Rask completed his internship at Kings County Hospital in Brooklyn and later returned to Oregon for his orthopedic residency. He is currently in private practice in Las Vegas, Nevada, specializing in neurological orthopedic surgery. Dr. Rask belongs to a number of regional and national medical societies, including the American academy of neurological and Orthopaedic Surgeons, the American Federation for Medical Accreditation, and the Neurological and Orthopaedic Institute. Dr. Rask is chairman of the Board of Neurological and Orthopaedic Surgeons and editor-in-chief of The Journal of Neurological and Orthopaedic Surgery. He is also chairman of the Neurological Orthopaedic Institute. Dr. Rask has published nearly 200 articles in numerous major medical journals, and he has also presented a number of lectures and scientific exhibits at major scientific meetings. CASE REPORT The Omohyoideus Myofascial Pain Syndrome: Report of Four Patients By Michael R. Rask, M.D. Abundant material has been written about the thoracic inlet (or outlet) syndrome, the scalenus anticus muscle syndrome, the scalenus medius or posterior muscle syndromes, and cervical disk disease, but no attention has been paid to a painful and not infrequent muscle syndrome that has come to my notice over the years. The inferior belly of the omohyoideus muscle can cause a painful and disabling cervical-glenoappendicular disorder. This article will discuss four cases of this disorder, give some notes on the problem's etiology, and suggest a method for conservative treatment. Patient One This 54-year-old businessman had injured his lower back many years ago while lifting heavy objects. His L4-5 disk was damaged, and he had received no conservative therapy. After two unsuccessful lumbar laminectomies done by two different neurosurgrons, the patient developed severe and unrelenting cauda equina claudication (without intermittency). The patient responded well to the conservative therapeutic program I generally use for postoperative arachnoradiculitis.1 (This consists of intravenous Colchicine,* sodium salicylate, calcium gluconate, oral Colchicine and Anturane,* 2 and trigger point injections with Marcaine,* Sarapin,* and gamma globulin.3) After this conservative therapy, the patient returned home without much lower back or lower limb pain. However, he later became ill with influenza, and while he was vomiting, he has a sudden onset of severe pain in the neck and left shoulder. After several days of intense discomfort, the patient also began having severe, unrelenting left-sided temporo-parietal headache. The patient went to several practitioners in his hometown, who conducted numerous radiographic and electrical testings. These clinicians simply told him that it was related to his previous unsuccessful lower spine surgery. When I first examined the patient for this painful cervical condition in July, 1983, he was unable to extend or rotate his head and neck to the right without experiencing severe pain in the left supraclavicular area. This burning pain radiated into the left shoulder anteriorly and into the upper left brachium/elbow regions. There was also pain in the scapular insertion of the levator scapulae superioris muscle. Chest x-rays showed no evidence of a superior sulcus tumor, while a CT scan revealed some C5-6 disk "build-up" beneath the posterior longitudinal ligament without significant asymmetry. All other testing was negative, including laboratory procedures. (The patient did have mild adult-onset diabetes, but this was under good control with Diabinese.*) Examination of the patient's neck revealed extreme tenderness in the inferior belly of the omohyoideus muscle where it traversed the upper brachial plexus (Figure 1). No lymphadenopathy was present, nor was there marked tenderness in the brachial plexus itself. The subclavian artery pulsation could not be altered with the various arm abduction elevation and Valsalva procedures (negative Adson's and hyperabduction tests)4 that I attempted. The patient also had tenderness in the anterior bicipital groove of the left shoulder, in the scapular insertion of the levator scapulae superioris tendon, in the belly of the brachioradialis muscle, and in the midbelly of the temporalis muscle (just above the aygomatic arch). I found no sensory deficit (for light touch, temperature, or pinwheel pain) and no deep-tendon reflex deficit in the limbs. Nor was there muscle weakness anywhere in the upper left limb. Manipulating the inferior belly of the patient's left omohyoideus muscle re-created the severe neck, shoulder, and arm pain and headache. I carefully injected this muscle belly with Marcaine (bupicacaine hydrochloride 0.5%), gamma gloubulin, and Sarapin, using a 30 gauge ½ inch atraumatic, disposable needle. This completely relieved the patient's pain. On two subsequent occasions, I injected the secondary trigger points (in the bicipital groove and the scapular insertion of the levator scapulae superioris muscle), the muscle belly of the brachioradialis (at the left elbow), and the trigger point in the temporalis muscle in a similar manner. The patient was then able to return to his home with no pain and with no limitations to the movement in his shoulder and neck. His headache was also gone. Six months later I saw this patient again and found him to be totally asymptomatic. Patient Two This 49-year-old teacher developed food poisoning after eating some tainted fish. He became violently ill and was wretching and vomiting. Toward the end of the vomiting attack, he had a sudden burning pain in the right side of his neck and in his right shoulder blade, and aching in the right mandibular region. This pain persisted for three weeks. Buffered aspirin seemed to relieve the pain slightly. The patient found that turning his head to the left caused the pain in his neck and shoulder to become more intense. The pain also seemed worse in the morning. When I examined this patient three weeks after the onset of the syndrome, he had no sensory, motor, or deep-tendon reflex deficits. Radiographs of his neck showed no disk narrowing, and a chest x-ray showed no pathology there. The inferior belly of the patient's omohyoideus muscle was extremely tender to palpation, and the brachial plexus was slightly tender. There was also some tenderness at the cervical insertions of the lower three heads of the levator scapulae superioris muscle on the right side. The patient also had tenderness deep in the right levator scapulae superioris bursa on the inner upper aspect of the right scapula, and there was slight temporalis muscle tenderness above the aygomatic arch. Hyperextending the patient's head and turning it to the left (positive Spurling's test) aggravated his discomfort. (In Spurling's test for cervical radiculopathy, the pain and paresthesia can be reproduced by vertical compression of the head upon the neck. The neck may be extended, flexed, or bent laterally.4,8) I treated this patient by injecting the inferior belly of the right omohyoideus muscle with 2cc's of 0.5% Marcaine, ½ cc gamma globulin, and 1 cc Sarapin, taking great care not to anesthetize the right phrenic nerve (see Figure 2). This completely relieved the patient's discomfort. On the second visit, I injected the inferior belly of the omohyoideus muscle again, and I also injected the trigger points in the levator scapulae superioris muscle insertions and deep in the trapezius muscle (at the insertion of the omohyoideus muscle into the scapula). Three days later, the patient had no remaining symptoms. Patient Three After a severe rear-end collision in which her vehicle overturned, this 37-year-old secretary had developed Crohn's disease and nonankylosing rheumatoid spondylitis (NARS).5 (This had occurred 12 years before I saw her.) After seven years of chronic inflammatory disease in her neck, the patient began gradually to develop pain in the right supraclavicular area, the right shoulder, and the right upper brachium. She also experienced intense spasm of the levator scapulae superioris on the right side, and she had aching in her jaw, temporalis area headache, and burning in the inner upper aspect of the right scapula. She also had slight numbness in the tips of her fingers. Nonsteroidal anti-inflammatory medications afforded her only slight relief, and they often interfered with the Crohn's gastroenteritis. When I examined this patient, I found that she had the characteristic trigger point pain and tenderness in the inferior belly of the omohyoideus muscle. There was also tenderness of the brachial plexus. Radiographs of her neck revealed no disk narrowing, and there was no evidence of ankylosing spondylitis (the basis for the diagnosis of NARS).5 Spurling's test was positive for right shoulder and upper limb pain, but the patient's cervical movements were markedly limited, due to the inflammatory stiffness of her disease. I found no real sensory change or motor weakness and no deep tendon reflex abnormality in either upper limb. Maneuvers to identify thoracic inlet (or outlet) syndrome and scalenus anticus muscle syndrome were negative. I injected the inferior belly of the patient's right omohyoideus with 11/2 cc's of 0.5% Marcaine, 1 cc Sarapin, and ½ cc gamma globulin. This completely relieved the pain in her supraclavicular region and her right shoulder and mandibular areas for two to three months. The temporalis and levator scapulae superioris trigger points needed additional injections to give the patient greater pain relief. The usual ½ inch number 30 gauge disposable needle was used for all the injections. This helps to prevent the injection medication from escaping into the spinal nerve root dural sac and also eliminates the chance of injuring the cupola of the lung. Patient Four This patient is a 29-year-old concert pianist who had been in excellent health all of her life. Five months before she came to me, she was playing the piano fortissimo, when she suddenly felt an aching pain in the right cervical supraclavicular region, burning pain in the right shoulder, aching in the upper brachium, and pain in the upper inner shoulder blade. This pain waxed and waned for three months, occurring especially when she played the piano strenuously, and then it became constant. She also had some aching of her first digital web which had begun six weeks before she consulted me, and she had mandibular aching and intermittent headache. She had no numbness or tingling in her hand or upper limb. Left-sided neck movements increased her neck and arm discomfort. She had no history of neck injury. When I examined this patient in June, 1983, I found no sensory, motor, or deep-tendon reflex deficit in her right upper limb. There was extreme tenderness in the inferior belly of the omohyoideus muscle and some tenderness in the upper trunk of the brachial plexus (C5-6 roots). I found trigger points in the right bicipital groove, the brachioradialis muscle belly, the temporalis muscle belly (above the zygoma), the insertion of the levator scapulae superioris into the upper inner scapulae, and the first dorsal interosseous muscle. Moving her head to the left aggravated the patient's pain. Cervical and chest radiographs revealed no abnormalities, and CT scans of the C4-5, C5-6, and C6-7 disks showed no damage or tumor. HLA B-27 and antinuclear antibody titers were normal. I injected the inferior belly of the omohyoideus muscle carefully with the injection technique described above, and the patient's pain was completely relieved. I injected the other trigger points on two later occasions, and the patient returned to playing her piano fortissimo. Figure 1: Note how the inferior belly of the omohyoideus muscle traverses the upper portion of the brachial plexus. When this muscle goes into spasm primarily, as from intense vomiting, or secondarily, as a result of disk disease or other damage, the muscle belly become extremely painful. This will then cause a painful syndrome of neck, shoulder, and limb pain, temporalis muscle headache, and, in some patients, mandibular pain. The syndrome can disable the patient if it is not treated correctly. (Illustration from Atlas of Orthopadeic Exposures. Toufick Nicola, M.D. Baltimore: The Williams and Wilkins Company, 1966, pg. 62. Reprinted with the permission of the Williams and Wilkins Company.) Figure 2:The phrenic nerve is in close proximity of the inferior belly of the omohyoideus (retracted). Note also the proximity of the subclavian artery, subclavian vein the cupola of the lung, and the brachial plexus. These vital structures must not be disturbed in the injection procedure used in the treatment. It is thus essential to employ atraumatic injection techniques, using a 30 gauge 1/2 inch needle and injecting only small amounts of the medication mixture. Long acting bupivacaine (marcaine 0.5%) seems to be ideal for breaking the muscle pain/spasm cycle. (Illustration from Atlas of Orthopaedic Exposures. Toufick Nicola, M.D. Baltimore: The Wilkins Company, 1966, pg. 63. Reprinted with the permission of the Wilkins Company.) Figure 3: View of the anterior neck. The Omohyoideus muscle is attached by a central tendon to the clavicle and first rib. The infrahyoid belly of the muscle is flat and straplike, but the inferior belly is bulky and fleshy. Primary inflammation and spasm of the inferior belly can cause supra clavicular pain, burning in the shoulder and upper arm, elbow and lateral hand pain, sholder blade pain(rhumboid and levator scapulae superioris muscles), temporalis headache, and the mandibular aching. The may also become inflamed secondarily as a result of disk disease, ankylosing spondylitis, nonankylosing rheumatoid spodylitis, gouty myositis, rheumatoid myositis, and sprains or strains of the neck and sholder girdle.(Illustration fromSobotta: Atlas of Human Anatomy. Helmut Ferner and Jochen Straubsand, eds. 10th English Ed. Baltimore: Urban and Schwarzenberg, 1983. Reprinted with the permission of Urban and Schwarzenberg.) Figure 4: Simplified drawing showing the attachments of the omohyoideus muscle. Notice the central tendon and the scapular attachment of this multi-functioning muscle. (Illustration of from Anson's Atlas of Human Anatomy. Barry J. Anson, ed. Philadelphia: The W.B. Sanuders Company, 1950. Reprinted with the permission of the W.B. Sanuders Company.) Anatomy of the Omohyoideus Muscle The omohyoideus muscle arises from the upper margin of the scalpula, near (and sometimes from) the suprascalpular ligament (see Figure 4). It attaches to the hyoid bone. The superior belly of the omohyoideus is like an infrahyoid “strap” muscle, while the inferior belly of the muscle is thick and fleshy. This inferior portion of muscle crosses over the upper trunk of the brachial plexus (C-5 and C-6) (se Figure 3). The central tendon of the omohyoideus muscle is beneath the sternocleidomastoid muscle and separates the two bellies (Figure 3). This central tendon is held in place by the strong process of the middle layer of cervical fascia. The fascial process helps attach the omohyoideus mid-muscular tendon to the posterior surfaces of the clavicle and first rib. The nerve supply for both the bellies of the omohyoideus muscle is derived from ansa cervicalis (C1-2-3, and sometimes C-4). (In older anatomy books, ansa cervicalis is called ansa hypoglossi). In the fetus, the omohyoideus muscle is longitudinal and starp-like (as is the rest of the infrahyoid musculature), but it moves with clavicle and scapula as they grow, taking on its unusual character. Its function is to assist in swallowing, vomiting, and respiration, and it also has some scapulo-clavicular actions. Etiology of the Omohyoideus Muscle Pain Syndrome This omohyoideus muscle pain disorder may be either primary or secondary. Any muscle can be the primary site for a painful contraction syndrome, 6 and if the muscle is located in a strategic place, then the muscle pain/spasm cycle that occurs will have even more wide spread results. The omohyoideus is of course such a case, since the brachial plexus is located beneath it. Because there is a great cross-over of the nerve supply for the muscle (the ansa cervicalis), there can also be referred pain in similarly innervated structures. This can create seemingly unrelated symptoms such as temporalis headache, sympathetic pain in the levator scapulae superioris muscle, the inframandibular pain on the affected side. (These structures share segmental innervation of the omohyoideus.) In addition, since the upper trunk of the brachial plexus (C5 and C6 spinal nerve roots) is so near, contiguous inflammation from the muscle may cause the patient’s neck and supraclavicular pain in progress into his or her entire upper limb. However, the trouble arises primarily from two-bellied omohyoideus muscle. Primarily isolated muscular disease may occur in the omohyoideus muscle as a result of the violent, intense vomiting (as in patients 1 and 2) or violent shoulder and neck movement (as in patient 4). However, the syndrome can also occur secondarily, as a result of rheumatoid myositis, ankylosing spondylitis, nonankylosing rheumatoid spondylitis (as in patient 3), gouty myositis, cervical spine injuries, or disk damage in the region. In addition to isolated viral inflammation of muscle or nerves, muscular inflammation may also occur as a result of joint diseases, trauma, spinal cord lesions brachial plexus neuropathy (Parsonnage-Turner syndrome), poliomyelitis, Guillain-Barré syndrome, polyneuropathies (alcoholism, porphyria, arsenic intoxication), polyneuritis nodosa, lupus, rheumatoid arthritis, diabetes, beriberi, B12 deficiency, or other problems. 6 For older patients, the cliician must also consider the possibility of polymyalgic rheumatica. (Temporary arteritis is a peculiar component of that disorder.) Diagnosis A diagnosis of primary omohyoideus myofascial pain syndrome should be made only after careful tactile examination of the patient’s supraclavicular fossa, and after other causes for the cervical, supraclavicular, scapular, temporomandibular, and limb pain have been excluded. One example of another cause can be seen in the patient who has Horner’s syndrome (meiotic pupil, ptosis of the eyelid, narrowing of the palpebral fissure, and anhidrosis and flushing of the affected side of the face) with a cloudy radiologic lesion in the cupola of the lung. These symptoms would indicate that the patient has a sulcus neoplasm, and we must assume this to be the case until proven otherwise. The clinician must search for all such possible cervical disease, brachial plexus problems, and cervical spinal nerve root abnormalities and exclude them in order to arrive at diagnosis of primary omohyoideus myofascial pain syndrome. However, whether omohyoideus muscular inflammation or spasm is diagnised as a primary or secondary, the conservative therapy used is the same. Contradictions for this treatment would include malignant infiltration of the brachial plexus (and omohyoideus muscle), carries sicca, or any other treatable inflammatory condition. If any of these conditions are present, the clinician must not inject this area of the body to relieve the pain. Although omohyoideus muscle in the supraclavicular fossa will be extremely teder, there should be little, if any, sensory abnormality in the upper limb, and there should be no deep tendon reflex changes. In addition, the brachial plexus should not be more tender than the omohyoideus muscle. There may also be trigger points found in the bicipital groove of the shoulder, the insertion of the deltoid into the humerus, the brachioradialis muscle belly at the elbow, the first dorsal interosseous muscle, the levator scalpulae superioris muscle (both proximal and distal attachments), the rhumboid muscles, deep in the supraspinatus muscle where omohyoid attaches to the transverse scapular ligament, the mid-cervical apophyseal joints, the temporalis muscle, or even temporomandibular joint itself. Treatment The injection treatment must be performed gently with a technique as atraumatic as possible. I use a number 30 gauge ½ inch needle to deliver a small amount of the following mixture: 1 ½ cc’s of bupivocaine (Marcaine 0.5%), 1 cc Sarapin, and ½ cc globulin. This anesthetizes the fleshy inferior belly of omohyoideus muscle, which breaks the spasm /inflammatory cycle that has caused the trouble. The simpler and gentler the technique used, the better and more effective it is for the patient Although it is not necessary to infiltrate the brachial plexus in primary omohyoideus muscle pain syndrome, spinal nerve root blocks are quite effective in muscle spasm, that is secondary to cervical disk disease. The clinician must also inject the secondary trigger point areas described above with the same mixture of medications and same gentle technique. It is acceptable to use small amount of triamcinolone acetonide with medication mixture, but I have found that dexamethasone and other long-acting, slow-dissolving synthetic gluconeocorticoids are irritating and not too effective in the lon run. In addition to this injection, it often helps to give the patient prostaglandin inhibitors. I use a mixture of intravenous Colchcine, sodium salicylate, and calcium gluconate for this. Non steroidal oral anti-inflammatory medications such as Naprosyn* (naproxen), Clinoril,* and Tolectin* also seem to help. Narcotics, Muscle relaxants, and tranquilizers such as Valium* (diazepam), should not be used in treating this painful syndrome. These drugs are habit-forming, and they do nothing to relieve the disorder. Once the spastic muscle has been treated by injection, it is no longer for the patient to rest the neck and limb. Although I have not found surgical therapy to be necessary in treating the omohyoideus myofiscial pain syndrome, it is possible that a resistant and recurrent spastic muscle condition would make it necessary to divide the omohyoideus muscle. If this has to be dome, the muscle should be excised from the central tendon past the point where it crosses the patient's brachial plexus. At the same time, muscle and lymph nodes may be taken for biopsy. Summary The omohyoideus myofascial pain syndrome described here can cause severe pain in the neck, shoulder, arm, elbow, and hand, and in the scapular, supraclavicular, mandibular, and temporal regions. The syndrome is due to spastic inflammation of the fleshy inferior belly of the omohyoidues muscle. Once it has been determined that other more serious problems have not been the cuase of the spasm and pain, the condition can be treated easily with a gentle, atraumatic injection technique. Reprint requests to: Dr. Michael R. Rask Sahara Raincho Medical Center 2320 Rancho Dr., Suite 108 Las Vegas, Nevada 89102-4592 References 1. Rask, M.R. Postoperative arachnoradiculitis: report of 24 patients and the conservative treatment therefore. J Neurol Orthop Surg 1980: 1: 157-166. 2. Rask, M.R. The occurrence of acute gout in a patient with a healing fractured metatarsal. J Neurol Orthop Surg 1983: 4(3): 263-267. 3. Rask, M.R. On the use of gamma globulin for local triggerpoint, intra-anticular and spinal nerve root injections. J Neurol Orthop Surg 1983: 4(1): 92. 4. Rask, M.R. Signs of our neurological-orthopaedic times. J Neurol Orthop Surg 1980: 1: 251-255. 5. Rask, M.R. Non-ankylosing rheumatoid splondylitis (NARS): report of 11 patients. Orthop Rev 1982: 9: 21-33. 6. Nakano, K.K. Neurology of Musculoskeletal and Rheumatic Disorders. Boston: Houghton-Mifflin Professional Publishers. 1979, pp.11-12 7. Rask, M.R. Ipsilateral hip, knee and shin pain in a rheumatoid with an artificial hip. J Neurol Orthop Surg 1983: 4: 129-142. 8. Nakano, K.K. Entrapment neuropathies. In textbook. Kelley. Ed. Philadelphia: W.B. Saunders Company. 1982. 9. Travell, J.G., and Simons, D.G. Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore: The Williams and Wilkins Company. 1983. pp. 354-355. *Colchicine-Eli Lilly and Company, Indianapolis, Indiana. *Anturane-GEIGY Pharmaceuticals, Ardsley, New York. *Marcaine-Winthrop Laboratories, New York, New York. *Sarapin-High Chemical Co., Division of Day Frick, Inc., Philadelphia, Pennsylvania *Diabinese-Pfizer Laboratories Division, Pfizer Inc., New York, New York. *Naprosyn-Syntex Laboratories, Inc., Palo Alto, California. *Clinoril-Merck Sharp & Dohme, West Point, Pennsylvania. *Tolectin-McNeil Pharmaceutical, Spring House, Pennsylvania. *Valium-Roche Laboratories, Division of Hoffman-LaRoche, Inc., Nutley, New Jersy. Home

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MRI white matter lesions: does it represent MS?

15May08

MRI white matter lesions

Many times I get consulted by patients or their relatives when their MRI brain report reads multiple scattered white matter lesions seen. The radiologist’s report usually further reads that these can be seen in primary demyelinating conditions like multiple sclerosis or in vascular disorders. Patient’s and caregivers are naturally worried when they get this MRI report and do not know what to do and how to proceed further. So I thought that here I shall talk about these white matter abnormalities seen on the MRI. What is their significance? Do they represent evidence of multiple sclerosis?
White matter signal changes on the MRI essentially means that on the MRI, the white matter showed some scattered bright spots. White matter in the brain refers to the fiber tracts that carry information to and fro from the brain.
My first question when somebody asks me what next and what does this mean is to ask them why was the MRI done in the first place. If the MRI was done because there was a clinical suspicion of multiple sclerosis then these white matter lesions may indeed have significance and may represent radiological evidence of MS plaques. Let me explain this with an example. You go to your doctor, you have signs and symptoms that suggest MS (example you may have had an attack of optic neuritis), when the doctor examines you he is able to elict signs in the examination compatible with a diagnosis of MS, then he orders an MRI to see if you do have evidence of white matter lesions in the brain. In a case like this the presence of white matter lesions/ signal changes in the MRI is obviously important. Here it likely does suggest the presence of MS. That said and done I again want to re-emphasize that the diagnosis of MS is made on the basis of clinical history of previous attacks, CSF (spinal fluid) examination and MRI, not just on the basis of the MRI alone. Also there are certain criteria which have to be satisfied on MRI to make a definite diagnosis of MS. These radiological criteria for MS include the number of lesions on the MRI, their location and their size.
Thus it is important to remember that a person who is noted to have white matter lesions on a brain MRI does not necessarily have MS. White matter lesions can be seen in numerous other conditions and they are more commonly seen as we grow older. The thinking behind this is that they represent microvascular ischemic changes in the brain (the smaller caliber blood vessels in the brain showing signs of ischemia or decreased blood flow). Hence these white matter abnormalities on MRI are more commonly seen in patients who have microvascular and macrovascular risk factors such as a history of hypertension, diabetes and high cholesterol (dyslipidemia/ bad lipid profile).
White matter signal changes on MRI may also be seen in patients who have infectious and other inflammatory conditions. They have been reported in the MRI of patients with a history of migraine headaches (migraine too is a vascular disorder and that may explain the connection).
So I want to end by saying that the presence of these white matter signal changes on brain MRI has to be correlated to the history, clinical examination and other ancillary investigations. Your doctor shall help you in going about this in a methodical manner. I repeat these white matter lesions do not suggest MS in each and every case they are found.

Dr. Sethi

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THIS IS VERY INTERESTING, SINCE I DO HAVE WHITE MATTER ALL IN MY MRI BRAIN SCAN. IT IS A TERRIBLE PLACE TO BE, WHEN NOT TAKEN SERIOUSLY AND A PERSON HAS TO FIGHT TO GET AN ANSWER TO WHAT IS GOING ON.

I RECENTLY WENT TO A NEUROLOGIST THAT DIDN'T TAKE ME SERIOUSLY, FOR APPARENTLY WAS MOCKING ME AT MY LAST VISIT. IF IT ISN'T HARD ENOUGH TO MAKE IT THERE AND STAY IN THE LOBBY FOR 2 HOURS, THEN ANOTHER HOUR IN HIS ROOM, THEN WHEN HE FINALLY DOES COME IN, HE IS RUSHING AND GETTING THROUGH WITH THE OFFICE VISIT SO THAT HE CAN RUSH OVER TO ANOTHER ROOM. I KNOW, I HAVE BEEN THERE AND I AM TIRED OF THESE SO CALLED DOCTORS...WHO, ARE SUPPOSE TO HAVE OUR BEST INTEREST AT HEART. INSTEAD, THEY RIDICULE YOU AND SEND YOU OUT OF THEIR OFFICE WITH MORE QUESTIONS THAN, ANSWERS.

I JUST WANTED TO POST MY BRAIN MRI HERE, SO THAT WHEN I DO GET DIAGNOSED, I WILL HAVE EVIDENCE THAT THIS DOCTOR FOUND, WHAT HE SAW ON MY MRI, AS INSIGNIFICANT. IT IS WRONG AND BAD ENOUGH FOR A DOCTOR TO SEEM NOT TO CARE, BUT WHEN THEY ACTUALLY MAKE COMMENTS THAT ARE CONDESCENDING AND OFFENDING, THEN SOMETHING HAS TO BE DONE. THIS DOCTOR, THE LAST TIME, I WAS THERE, TOLD ME THIS, "YOU DON'T HAVE LEPROSY DO YOU?" AND  "DO YOU HAVE A PROSTATE PROBLEM, DO YOU?" I TOLD HIM, AFTER HE SAID THAT, THAT "I DON'T KNOW, HAVE YOU CHECKED?"..HE SAID, "WOMEN DON'T HAVE PROSTATES.". THEN, I REPLIED, "I DO KNOW THAT!"
THIS OFFICE VISIT WAS UNREAL. I HAVE NEVER HEARD ANY DOCTOR TALK TO ME, THE WAY THAT HE DID. HE WAS VERY CONDESCENDING AND IT WAS VERY OFFESSIVE AND HURTFUL, TO ME, SINCE I DEAL WITH A GREAT AMOUNT OF PAIN. I STRUGGLE TO GET THROUGH EVERYDAY, AS IT IS AND I DON'T NEED SOMEONE WHO IS SUPPOSED TO BE PROFESSIONAL TREATS YOU LIKE YOU DON'T MATTER.
HE WAS TELLING ME THAT I HAD TOO MANY SYMPTOMS AND I TOLD HIM THAT I KNEW THAT I HAD A LOT AND ALL OF THE SYMPTOMS, AFTER A WHILE WILL MAKE ANY PERSON DEPRESSED. IF I DIDN'T HAVE ALL OF THIS PAIN AND SUFFERING AS I DO, EACH AND EVERYDAY...I WOULD NOT BE DEPRESSED, AT ALL. I WOULD BE TO BUSY LIVING MY LIFE, TO BE THAT WAY.
THE LAST TIME I WAS THERE HE GAVE ME A PRESCRIPTION FOR CYMBALTA, BUT I DID TAKE ONE AND MY SYMPTOMS INCREASED. IT SAID ON THE INSTRUCTIONS NOT TO CONTINUE, IF SYMPTOMS WORSENED. I TOLD HIM THAT. HE ACTUALLY GAVE ME ANOTHER PRESCRIPTION TO TRY AND I TOLD HIM THAT I DIDN'T WANT IT AND HE ASKED ME WHAT IT WAS THAT I WANTED. I TOLD HIM THAT ALL I WANTED WAS TO FIND OUT WHAT IT IS THAT FEELS LIKE IT'S KILLING ME.
SOMETHING HAS TO BE DONE AND THE ANSWERS HAVE TO BE FOUND. IF, WE...THE  PATIENTS, DON'T PUSH TO FIND THE ANSWERS, TO WHAT IT IS THAT IS PLAGUING US, THEN WE ARE VERY POSSIBLY TAKING THE CHANCE ON BEING A STATISTIC. I DON'T KNOW @ YOU, BUT I DON'T WANT TO BE ONE...I JUST WANT MY LIFE BACK.

I AM SO TIRED, OF HOW SOME PEOPLE TREAT THOSE WHO ARE SUFFERING, JUST BECAUSE THEY DON'T UNDERSTAND OR WANT TO UNDERSTAND, DOESN'T GIVE THEM THE RIGHT TO PUNISH THE PERSON ANY FURTHER. WHY DO THEY RIDICULE THE PERSON WHO IS ALREADY HAVING SUCH A HARD TIME TRYING TO LIVE THEIR LIFE? LIFE IS HARD ENOUGH, BESIDES HAVING TO DEAL WITH AN "ASS"..(sorry, it is sad, but true) 

I AM PRETTY SURE THAT THE MRI'S THAT I HAVE POSTED SHOW EVIDENCE ENOUGH OF WHITE MATTER. DO DOCTORS EVEN LOOK AT THESE THINGS????  I DO HAVE MORE THAT SHOW EVEN MORE THAT I FOUND AFTER I POSTED THESE, SO I DON'T UNDERSTAND WHY IS IT SO HARD TO EVEN GET INTO SEE A DOCTOR THAT CAN HELP YOU. I HAVE BEEN TRYING AND IT IS LIKE PULLING TEETH...NO, WORSE.

GOD BLESS EVERYONE AND I PRAY THAT IF THERE IS ANYONE ELSE LOOKING FOR ANSWERS, DON'T GIVE UP. WE HAVE TO FIGHT TO STAY ALIVE THESE DAYS.:)))<3 Karen

Lumbar Puncture information just in case I do have Idiopathic Intracranial Hypertension

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Lumbar puncture

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Lumbar puncture
Intervention
A patient undergoes a lumbar puncture at the hands of a neurologist. The reddish-brown swirls on the patient's back are tincture of iodine (an antiseptic).
ICD-9-CM	03.31
MeSH	D013129

In medicine, a lumbar puncture (or LP, and colloquially known as a spinal tap) is a diagnostic and at times therapeutic procedure that is performed in order to collect a sample of cerebrospinal fluid (CSF) for biochemical, microbiological, and cytological analysis, or very rarely as a treatment ("therapeutic lumbar puncture") to relieve increased intracranial pressure.

Contents [hide] 1 Indications 2 Contraindications 3 Procedure 4 Risks 5 Diagnostics 6 History 7 References 8 External links

[edit] Indications

The most common purpose for a lumbar puncture is to collect cerebrospinal fluid in a case of suspected meningitis, since there is no other reliable tool with which meningitis, a life-threatening but highly treatable condition, can be excluded. Young infants commonly require lumbar puncture as a part of the routine workup for fever without a source, as they have a much higher risk of meningitis than older persons and do not reliably show signs of meningeal irritation (meningismus). In any age group, subarachnoid hemorrhage, hydrocephalus, benign intracranial hypertension and many other diagnoses may be supported or excluded with this test.
Lumbar punctures may also be done to inject medications into the cerebrospinal fluid ("intrathecally"), particularly for spinal anesthesia or chemotherapy. It may also be used to detect the presence of malignant cells in the CSF, as in carcinomatous meningitis or medulloblastoma.

[edit] Contraindications

Lumbar puncture should not be performed in the following situations

• Idiopathic (unidentified cause) increased intracranial pressure (ICP)
  • Rationale: lumbar puncture in the presence of increased ICP may cause uncal herniation
  • Exception: therapeutic use of lumbar puncture to reduce ICP
  • Precaution
    • CT brain is advocated by some, especially in the following situations
      • Age >65
      • Reduced GCS or conscious state
      • Recent history of seizure
      • Focal neurological signs
    • Ophthalmoscopy for papilledema
• Bleeding diathesis
  • Coagulopathy
  • Decreased platelet count (<50 x 10⁹/L)
• Infections^[1]
  • Skin infection at puncture site
  • Sepsis
• Abnormal respiratory pattern
• Hypertension with bradycardia and deteriorating consciousness
• Vertebral deformities (scoliosis or kyphosis), in hands of an inexperienced physician.^[2][3]

[edit] Procedure

Spinal needles used in lumbar puncture.

In performing a lumbar puncture, first the patient is usually placed in a left (or right) lateral position with his/her neck bent in full flexion and knees bent in full flexion up to his/her chest, approximating a fetal position as much as possible. It is also possible to have the patient sit on a stool and bend his/her head and shoulders forward. The area around the lower back is prepared using aseptic technique. Once the appropriate location is palpated, local anaesthetic is infiltrated under the skin and then injected along the intended path of the spinal needle. A spinal needle is inserted between the lumbar vertebrae L3/L4 or L4/L5 and pushed in until there is a "give" that indicates the needle is past the ligamentum flavum. The needle is again pushed until there is a second 'give' that indicates the needle is now past the dura mater. Since the arachnoid membrane and the dura mater exist in flush contact with one another in the living person's spine (due to fluid pressure from CSF in the subarachnoid space pushing the arachnoid membrane out towards the dura), once the needle has pierced the dura mater it has also traversed the thinner arachnoid membrane and is now in the subarachnoid space. The stylet from the spinal needle is then withdrawn and drops of cerebrospinal fluid are collected. The opening pressure of the cerebrospinal fluid may be taken during this collection by using a simple column manometer. The procedure is ended by withdrawing the needle while placing pressure on the puncture site. In the past, the patient would often be asked to lie on his/her back for at least six hours and be monitored for signs of neurological problems, though there is no scientific evidence that this provides any benefit. The technique described is almost identical to that used in spinal anesthesia, except that spinal anesthesia is more often done with the patient in a seated position.
The upright seated position is advantageous in that there is less distortion of spinal anatomy which allows for easier withdrawal of fluid. It is preferred by some practitioners when a lumbar puncture is performed on an obese patient where having them lie on their side would cause a scoliosis and unreliable anatomical landmarks. On the other hand, opening pressures are notoriously unreliable when measured on a seated patient and therefore the left or right lateral (lying down) position is preferred if an opening pressure needs to be measured.
Patient anxiety during the procedure can lead to increased CSF pressure, especially if the person holds their breath, tenses their muscles or flexes their knees too tightly against their chest. Diagnostic analysis of changes in fluid pressure during lumbar puncture procedures requires attention both to the patient's condition during the procedure and to their medical history.^{[citation needed]}
Reinsertion of the stylet may decrease the rate of post lumbar puncture headaches.^[3]

[edit] Risks

Post spinal headache with nausea is the most common complication; it often responds to analgesics and infusion of fluids. It was long taught that this complication can often be prevented by strict maintenance of a supine posture for two hours after the successful puncture; this has not been borne out in modern studies involving large numbers of patients. Merritt's Neurology (10th edition), in the section on lumbar puncture, notes that intravenous caffeine injection is often quite effective in aborting these so-called "spinal headaches." Contact between the side of the lumbar puncture needle and a spinal nerve root can result in anomalous sensations (paresthesia) in a leg during the procedure; this is harmless and patients can be warned about it in advance to minimize their anxiety if it should occur. A headache that is persistent despite a long period of bedrest and occurs only when sitting up may be indicative of a CSF leak from the lumbar puncture site. It can be treated by more bedrest, or by an epidural blood patch, where the patient's own blood is injected back into the site of leakage to cause a clot to form and seal off the leak.
Serious complications of a properly performed lumbar puncture are extremely rare.^{[citation needed]} They include spinal or epidural bleeding, and trauma to the spinal cord or spinal nerve roots resulting in weakness or loss of sensation, or even paraplegia. The latter is exceedingly rare, since the level at which the spinal cord ends (normally the inferior border of L1, although it is slightly lower in infants) is several vertebral spaces above the proper location for a lumbar puncture (L3/L4). There are case reports of lumbar puncture resulting in perforation of abnormal dural arterio-venous malformations, resulting in catastrophic epidural hemorrhage; this is exceedingly rare.
The procedure is not recommended when epidural infection is present or suspected, when topical infections or dermatological conditions pose a risk of infection at the puncture site or in patients with severe psychosis or neurosis with back pain. Some authorities believe that withdrawal of fluid when initial pressures are abnormal could result in spinal cord compression or cerebral herniation; others believe that such events are merely coincidental in time, occurring independently as a result of the same pathology that the lumbar puncture was performed to diagnose. In any case, computed tomography of the brain is often performed prior to lumbar puncture if an intracranial mass is suspected.
Removal of cerebrospinal fluid resulting in reduced fluid pressure has been shown to correlate with greater reduction of cerebral blood flow among patients with Alzheimer's disease. Its clinical significance is uncertain.

[edit] Diagnostics

Lumbar puncture in a newborn suspected of having meningitis.

Increased CSF pressure can indicate congestive heart failure, cerebral edema, subarachnoid hemorrhage, hypo-osmolality resulting from hemodialysis, meningeal inflammation, purulent meningitis or tuberculous meningitis, hydrocephalus, or pseudotumor cerebri.
Decreased CSF pressure can indicate complete subarachnoid blockage, leakage of spinal fluid, severe dehydration, hyperosmolality, or circulatory collapse. Significant changes in pressure during the procedure can indicate tumors or spinal blockage resulting in a large pool of CSF, or hydrocephalus associated with large volumes of CSF. Lumbar puncture for the purpose of reducing pressure is performed in some patients with idiopathic intracranial hypertension (also called pseudotumor cerebri.)
The presence of white blood cells in cerebrospinal fluid is called pleocytosis. A small number of monocytes can be normal; the presence of granulocytes is always an abnormal finding. A large number of granulocytes often heralds bacterial meningitis. White cells can also indicate reaction to repeated lumbar punctures, reactions to prior injections of medicines or dyes, central nervous system hemorrhage, leukemia, recent epileptic seizure, or a metastatic tumor. When peripheral blood contaminates the withdrawn CSF, a common procedural complication, white blood cells will be present along with erythrocytes, and their ratio will be the same as that in the peripheral blood.
The finding of erythrophagocytosis,^[4] where phagocytosed erythrocytes is observed, signifies haemorrhage into the CSF that preceded the lumbar puncture. Therefore, when erythrocytes are detected in the CSF sample, erythrophagocytosis suggests causes other than a traumatic tap, such as intracranial haemorrhage and haemorrhagic herpetic encephalitis. In which case, further investigations are warranted, including imaging and viral culture.
Several substances found in cerebrospinal fluid are available for diagnostic measurement.

• Measurement of chloride levels may aid in detecting the presence of tuberculous meningitis.
• Glucose is usually present in the CSF; the level is usually about 60% that in the peripheral circulation. A fingerstick or venipuncture at the time of lumbar puncture may therefore be performed to assess peripheral glucose levels in order to determine a predicted CSF glucose value. Decreased glucose levels can indicate fungal, tuberculous or pyogenic infections; lymphomas; leukemia spreading to the meninges; meningoencephalitic mumps; or hypoglycemia. A glucose level of less than one third of blood glucose levels in association with low CSF lactate levels is typical in hereditary CSF glucose transporter deficiency also known as De Vivo disease.
• Increased glucose levels in the fluid can indicate diabetes, although the 60% rule still applies.
• Increased levels of glutamine are often involved with hepatic encephalopathies, Reye's syndrome, hepatic coma, cirrhosis and hypercapnia.
• Increased levels of lactate can occur the presence of cancer of the CNS, multiple sclerosis, heritable mitochondrial disease, low blood pressure, low serum phosphorus, respiratory alkalosis, idiopathic seizures, traumatic brain injury, cerebral ischemia, brain abscess, hydrocephalus, hypocapnia or bacterial meningitis.
• The enzyme lactate dehydrogenase can be measured to help distinguish meningitides of bacterial origin, which are often associated with high levels of the enzyme, from those of viral origin in which the enzyme is low or absent.
• Changes in total protein content of cerebrospinal fluid can result from pathologically increased permeability of the blood-cerebrospinal fluid barrier, obstructions of CSF circulation, meningitis, neurosyphilis, brain abscesses, subarachnoid hemorrhage, polio, collagen disease or Guillain-Barré syndrome, leakage of CSF, increases in intracranial pressure or hyperthyroidism. Very high levels of protein may indicate tuberculous meningitis or spinal block.
• IgG synthetic rate is calculated from measured IgG and total protein levels; it is elevated in immune disorders such as multiple sclerosis, transverse myelitis, and neuromyelitis optica of Devic.
• Numerous antibody-mediated tests for CSF are available in some countries: these include rapid tests for antigens of common bacterial pathogens, treponemal titers for the diagnosis of neurosyphilis and Lyme disease, Coccidioides antibody, and others.
• The India ink test is still used for detection of meningitis caused by Cryptococcus neoformans, but the cryptococcal antigen (CrAg) test has a higher sensitivity.
• CSF can be sent to the microbiology lab for various types of smears and cultures to diagnose infections.
• Polymerase chain reaction (PCR) has been a great advance in the diagnosis of some types of meningitis. It has high sensitivity and specificity for many infections of the CNS, is fast, and can be done with small volumes of CSF. Even though testing is expensive, it saves cost of hospitalization.

[edit] History

The first technique for accessing the dural space was described by the London physician Dr Walter Essex Wynter. In 1889, he developed a crude cut down with cannulation in 4 patients with tuberculous meningitis. The main purpose was the treatment of raised intracranial pressure rather than for diagnosis.^[5] The technique for needle lumbar puncture was then introduced by the German physician Heinrich Quincke, who credits Wynter with the earlier discovery; he first reported his experiences at an internal medicine conference in Wiesbaden in 1891.^[6] He subsequently published a book on the subject.^[7][8]
The lumbar puncture procedure was taken to the United States by Arthur H. Wentworth M.D., an assistant professor at the Harvard Medical School, based at Children's Hospital. In 1893, he published a long paper on diagnosing cerebro-spinal meningitis by examining spinal fluid. His career took a nosedive, however, when antivivisectionists prosecuted him for having obtained spinal fluid from children. He was acquitted, but he was disinvited from the then forming Johns Hopkins Medical School where he would have been the first professor of pediatrics.^{[citation needed]}

[edit] References

1. ^ Mary Louise Turgeon (2005). Clinical hematology: theory and procedures. Lippincott Williams & Wilkins. pp. 401–. ISBN 9780781750073. http://books.google.com/books?id=cHAjsUgegpQC&pg=PA401. Retrieved 28 October 2010.
2. ^ Roos KL (March 2003). "Lumbar puncture". Semin Neurol 23 (1): 105–14. doi:10.1055/s-2003-40758. PMID 12870112.
3. ^ ^{a b} Straus SE, Thorpe KE, Holroyd-Leduc J (October 2006). "How do I perform a lumbar puncture and analyze the results to diagnose bacterial meningitis?". JAMA 296 (16): 2012–22. doi:10.1001/jama.296.16.2012. PMID 17062865.
4. ^ Harald Kluge (2007). Atlas of CSF cytology. Thieme. pp. 45–46. ISBN 9783131431615. http://books.google.com/books?id=HDLv-LAfqHoC&pg=PA45. Retrieved 28 October 2010.
5. ^ Wynter WE (1891). "Four cases of tubercular meningitis in which paracentesis of the theca vertebralis was performed for the relief of fluid pressure". Lancet 1 (3531): 981–2. doi:10.1016/S0140-6736(02)16784-5.
6. ^ Quincke HI (1891). Verhandlungen des Congresses für Innere Medizin, Zehnter Congress, Wiesbaden. 10. pp. 321–331.
7. ^ Quincke HI (1902). Die Technik der Lumbalpunktion. Berlin & Vienna.
8. ^ Heinrich Irenaeus Quincke at Who Named It?

[edit] External links

• eMedicine: Lumbar puncture
• Medstudents: Procedures: Lumbar puncture
• Video of lumbar puncture

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