Trigger Point pain?

Discussion in 'Fibromyalgia Main Forum' started by lease79, Nov 20, 2006.

  1. lease79

    lease79 New Member

    I've gone to the beach the last two nights with my family. Yesterday I wore a hat.
    Woke up this morning feeling okay, but came to sit at my computer & very suddenly started having trouble 'tracking'. My eyes hurt really bad looking to the sides & then I had trouble with my balance. I felt that if I tipped my head slightly to either side that I would fall clean over. If I stand perfectly still. Or walk without turning my head at all I'm fine.
    Then the tension/muscle headache kicked in. Pain all up the back of my head on both sides & down into my shoulders. It's palpable. Eyes hot & sore.
    I jumped in a warm bath, but felt like it was rocking side to side, so I carefully got out & laid down. Felt quite nauseous too.
    Felt better whilst lying down, but couldn't have the back of my head touching the pillow, because it hurt so bad :(
    On trying to sit up I felt incredibly dizzy.
    Took panadol & diazepam & am feeling a little better (although extremely tired.)
    We've had a thunderstorm here today after 2 days of heat, & I've overdone it exercise wise. Does this sound like trigger point pain to you???
  2. PVLady

    PVLady New Member

    You may have some inner ear problem. Some years ago, my husband has similar symptoms. By a stroke of luck, I ran across a magazine article by Dr. Robert Baloh, professor at UCLA, Los Angeles. Luckily, we were able to see him in person and he treated my husband - and cured him.

    The information below is very technical but if you think you could have it, you can print it and take to your doctor.

    My husband suffered for months before we found Dr. Baloh. Doctors would give him Compazine for nausea and Valium - but that did not cure the problem.

    Basically, you can get tiny particles of calcium in your inner ear that causes dizziness, nausea, balance problems, etc. Your eyes also get weird. When my husband had a episode, it was triggered by any sudden movement of his head. Like looking up fast, turning the head fast, etc. He would feel dizzy and very nauseous.

    He had to be completely still for hours to recover.

    His eyes would also have a condition called "nystagmus" during the episode. The eyes would move around, like doll eyes.

    (His cure involved moving my husband's head to bring on a episode of dizziness etc. He then confirmed the problem. He then moved his head and body around to dislodge the calcium particles in his middle ear. He was then instructed to sleep upright for three days. He never had another episode of dizziness).

    The condition is called "Benign Positional Vertigo". Here is a article from Dr. Baloh's website:

    In a patient complaining of dizziness, an early and important step is to determine the type, because diagnostic evaluation and management differ markedly depending on the cause and type of dizziness (1). Therefore, the examining physician should complete careful history taking before starting any workup.

    The patient's description of symptoms and the circumstances in which they occur are often key to determining the general type of dizziness (table 1). Many drugs can cause dizziness (table 2), so use of potential offending drugs should be sought during the patient interview. Common nonvestibular causes (eg, hyperventilation, orthostatic hypotension, panic disorder) often can be identified on the basis of characteristic findings in the patient's history, and diagnostic evaluation can be immediately directed at the underlying cause.

    This article focuses on six vestibular causes of dizziness, all of which have vertigo as the predominant symptom: benign positional vertigo, acute unilateral vestibulopathy, chronic bilateral vestibulopathy, Meniere's disease, migraine, and vertebrobasilar insufficiency.

    Benign positional vertigo
    Benign positional vertigo is by far the most common cause of vertigo. Patients have brief episodes with positional change, typically when turning over in bed, getting in and out of bed, bending over and straightening up, or tipping the head back to look up (thus, the name sometimes used for the disorder, "top-shelf vertigo"). Benign positional vertigo can result from head injury, viral neurolabyrinthitis, or vascular occlusion. In most cases, though, it is an isolated disorder with no accompanying inner ear damage (2). It can occur at any age but is most common in older people.

    Diagnosis of benign positional vertigo rests on characteristic findings on the Dix-Hallpike maneuver: fatigable, torsional, vertical, paroxysmal positional nystagmus resulting from a rapid change from the sitting to the head-hanging position. If findings on history taking and physical examination are typical, no further evaluation is necessary; however, if findings are atypical, other causes (eg, tumor, posterior-fossa infarct) must be ruled out. Of course, more serious causes are almost always accompanied by additional neurologic symptoms and signs.

    The typical features of benign positional vertigo are explained by statoconial debris made up of calcium carbonate crystals that float freely within the posterior semicircular canal under the influence of gravity (so-called canalolithiasis) (3,4). When the patient sits upright, a "clot" of crystals forms at the most dependent portion of the posterior semicircular canal. When the patient moves back and to the side in the plane of the posterior canal, as during the standard Dix-Hallpike positioning test, the clot has a plunger effect as it moves in the canal, producing displacement of the cupula. Fatigability with repeated positioning is explained by dispersion of single particles from the clot, which reduces the plunger effect. The induced vertigo and nystagmus are brief because once the clot reaches its lowest position in the canal, the cupula, due to its elasticity, returns to its primary position. Latency before onset of nystagmus is explained by the delay before the clot is set into motion.

    Findings on surgical procedures to block the posterior semicircular canal with a bony plug have supported the theory of a causative canalolithiasis mechanism in benign positional vertigo. In the process of exposing the membranous labyrinth of the posterior canal, surgeons have observed a chalky white substance in the endolymph of the posterior semicircular canal (5).

    Probably the most convincing argument for the canalolithiasis mechanism is the dramatic response of benign positional vertigo to the positional maneuver (figure 1: not shown (6)) designed to relocate the clot. The patient's head is rotated in the plane of the posterior semicircular canal so the clot travels around the canal and enters the utricle. The maneuver is repeated until symptoms disappear. The patient is then instructed to avoid lying flat for at least 2 days to prevent the clot from reentering the posterior semicircular canal. About half of patients eventually have recurrence of benign positional vertigo, 10% to 20% of patients within a week or two of the maneuver. Patients can be taught to perform the maneuver at home to alleviate recurrent episodes.

    Acute unilateral vestibulopathy
    A common clinical presentation that can occur at any age is acute onset of vertigo, nausea, and vomiting lasting for several days and not associated with auditory or neurologic symptoms. Most patients gradually improve over a few weeks, but some, particularly older patients, can have persistent symptoms for months. About half of patients with acute unilateral vestibulopathy report having had an upper respiratory tract illness a few weeks before onset of vertigo. The disorder occasionally occurs in epidemics, may affect several members of a family, and erupts most often in spring and early summer.

    All of these features suggest a viral origin for acute unilateral vestibulopathy, but attempts to isolate a causative viral agent have been unsuccessful, except for an occasional finding of herpes zoster infection. Pathologic studies showing atrophy of one or more vestibular nerve trunks, with or without atrophy of associated sense organs, provide evidence of a vestibular nerve site and probably viral cause in many patients with the disorder (7,8). In about 20% of patients, attacks of acute vestibulopathy (usually less severe) recur months or years after the initial attack. Whether delayed recurrence represents reactivation of a latent virus or some other pathophysiologic mechanism is unknown.

    Occlusion of the internal auditory artery leads to sudden, profound loss of both auditory and vestibular function. However, ischemia confined to the distribution of the anterior vestibular artery can result in isolated vertigo due to infarction of only the vestibular labyrinth. Usually, an ischemic disorder should be considered only in older patients, particularly those with a history of transient ischemia, stroke, or known atherosclerotic vascular disease; occasionally, it may be seen in association with a hyperviscosity syndrome (eg, hyperlip-idemia, polycythemia, macro-globulinemia, sickle cell anemia).

    Vertigo can result from a blow to the head that does not cause temporal bone fracture (a so-called labyrinthine concussion). Fistulas of the oval and round windows should be considered when there is a clear relationship between onset of vertigo and sudden barometric change, blunt head trauma without skull fracture, impact noise, or severe physical exertion (9). Clinically, rupture leads to sudden onset of vertigo, hearing loss, or both.

    Patients may have typical episodes of benign positional vertigo months or years after recovery from acute manifestations of peripheral vestibulopathy. Presumably, the cause is damage to the utricular macule resulting in release of statoconial debris, which makes its way into the long arm of the posterior semicircular canal and produces canalolithiasis (2).

    Chronic bilateral vestibulopathy
    Unlike patients with acute unilateral vestibulopathy, those with chronic bilateral vestibulopathy often present with subtle symptoms of nonspecific dizziness and disequilibrium that may be difficult to differentiate from symptoms of other neurologic causes of disequilibrium (10). The associated oscillopsia (an illusion that the environment is moving when the head is moved) may be incorrectly interpreted as a vision problem, leading to unnecessary and unhelpful ophthalmologic evaluation.

    By far the most common cause of bilateral vestibulopathy is ototoxicity from aminoglycoside use. Patients may experience vertigo at first if the toxic effect is asymmetric, but more often they have progressive symmetric loss of vestibular function, leading to imbalance rather than vertigo. In many cases, patients being treated with ototoxic drugs are bedridden and therefore unaware of vestibular impairment until they recover from the acute illness and try to walk. They then note unsteadiness and oscillopsia. Aminoglycosides can produce both auditory and vestibular damage, but some, such as streptomycin sulfate and gentamicin (Garamycin, Jenamicin), are relatively specific to the vestibular system.

    When using such drugs, clinicians must be continually alert for early symptoms of vestibular ototoxicity. This is particularly important in patients who are seriously ill and confined to bed and those with renal impairment. Younger patients usually adapt to bilateral vestibular loss by using other sensory signals, but older patients may be permanently disabled. Early discontinuation of the offending drug may allow stabilization and even improvement of vestibular loss.

    Meniere's disease
    Meniere's disease is characterized by a triad of symptoms: vertigo, hearing loss, and tinnitus (11). Most patients also experience a sense of fullness and pressure in the area of the affected ear. Typically, an attack of vertigo reaches maximum intensity in minutes and then slowly subsides over several hours. In the early stages, hearing loss is completely reversible, but in later stages, residual hearing loss persists. Tinnitus is typically described as a roaring sound, like that of the ocean or that heard when a hollow seashell is held next to the ear. Episodes occur at irregular intervals for years, often with prolonged periods of remission. Eventually, severe permanent hearing loss develops and the episodic nature of the disease disappears (burned-out phase). In as many as one third of patients, bilateral Meniere's disease eventually develops.

    Variations on the typical picture occur, particularly in the early stages of the disease process, and the source of symptoms remains uncertain until the combination of fluctuating hearing loss and vertigo develops. Some patients have episodes of abruptly falling to the ground without loss of consciousness or neurologic symptoms. These drop attacks have been called otolithic catastrophes on the basis of the presumed sudden stimulation of the otolith membrane from endolymphatic hydrops (12). Delayed Meniere's disease can develop in an ear that was damaged years earlier, usually by viral or bacterial infection (13). When hearing loss is profound, as it often is, episodic vertigo is not accompanied by fluctuating hearing levels and tinnitus.

    The key to diagnosis of Meniere's disease is documentation of fluctuating hearing levels in patients with a characteristic clinical profile. In the early stages, sensorineural hearing loss is usually greater in the lower frequencies. Although results of caloric examination may be normal early in the disease process, in most patients, response to caloric stimulation becomes significantly decreased on the affected side. The principal pathologic finding in patients with Meniere's disease is an increase in the volume of endolymph, along with distention of the entire endolymphatic system (so-called endolymphatic hydrops).

    Vertigo is a common symptom of migraine, occurring in about 25% of patients, either along with headache or in separate, isolated episodes (14). Attacks of vertigo can predate the onset of headache, and in some cases vertigo is the only manifestation of migraine (the so-called migraine equivalent). Migraine should be suspected in any patient with chronic recurrent attacks of vertigo of unknown cause. Benign paroxysmal vertigo of childhood and benign recurrent attacks of vertigo in adults nearly always turn out to be due to migraine. The duration of vertigo with migraine varies widely. Therefore, migraine can mimic several common neuro-otologic syndromes that result in vertigo.

    The diagnosis of migraine-associated vertigo is straightforward when an aura occurs and is followed by a typical unilateral throbbing headache. It becomes more problematic when attacks of vertigo and headache occur independently or vertigo occurs without headache. Long-standing motion sensitivity, including car sickness and boat sickness, and a clear family history of migraine point to migraine.

    Some patients have typical visual aura or other focal neurologic symptoms of migraine without headache. Basilar migraine is characterized by posterior-fossa symptoms (eg, vertigo, ataxia, dysarthria, tinnitus) together with visual phenomena consistent with ischemia in the distribution of the posterior cerebral arteries (15). This symptom complex is particularly common in adolescent girls, but it can occur at any age and in either sex. The possibility of basilar migraine should be considered in any patient presenting with transient vertigo and other posterior-fossa symptoms. Sometimes, headache is mild and is adequately controlled with sleep or mild analgesics and sedatives, and the patients are much more bothered by the aura signs and symptoms.

    The mechanism of migraine-associated vertigo is poorly understood. Vasoconstriction of the internal auditory artery may explain some symptoms, particularly when onset of vertigo or hearing loss is abrupt. Although sudden hearing loss occurs with migraine, it does so infrequently compared with the incidence of vertigo. Phonophobia and tinnitus are much more common than hearing loss with migraine; phonophobia is particularly prominent during the period of severe headache. Recently, mutation in a gene coding for a subunit of a neuronal calcium channel was discovered in families who have hemiplegic and basilar migraine. Mutations in similar ion channel genes are prime candidates as explanations of the metabolic defects in the brain and inner ear that contribute to other types of migraine (16).

    Vertebrobasilar insufficiency
    Cerebrovascular disease is a common cause of vertigo, particularly in older patients (17). Whether the vertigo results from ischemia of the labyrinth, brain stem, or both is not always clear, since the blood supply to the labyrinth, eighth cranial nerve, and vestibular nuclei originates at the same source--the vertebrobasilar circulation.

    Typically, vertigo associated with transient ischemia in the vertebrobasilar system has an abrupt onset, lasts for several minutes, and is accompanied by nausea, vomiting, and severe imbalance. Associated symptoms resulting from ischemia in the remaining territory supplied by the posterior circulation include visual blurring or blackouts, diplopia, drop attacks, weakness and numbness of the extremities, and headache. These symptoms occur in episodes, with or without vertigo. Vertigo may be an isolated initial symptom of transient ischemic attacks, but repeated episodes of vertigo in the absence of other symptoms suggest a different problem.

    Atherosclerosis of the subclavian, vertebral, and basilar arteries is the most common cause of transient ischemic attacks associated with the vertebrobasilar system. Emboli in the posterior circulation are probably more common than is generally known. Caplan (18) estimated that about one fifth of posterior-circulation infarcts are cardiac and another one fifth are intra-arterial emboli arising most often from occlusive lesions of the extracranial and intracranial vertebral arteries. Less common causes of arterial occlusion include dissection, arteritis, polycythemia, and hypercoagulation syndromes. Rarely, tumors (eg, acoustic neuroma) compress arterial circulation to the inner ear and produce acute vertigo. Acoustic neuromas usually present as slowly progressive unilateral hearing loss.

    Diagnosis of transient ischemia or stroke associated with the posterior circulation can usually be made on the basis of a characteristic combination of symptoms and signs. History taking should identify risk factors for atherosclerosis, including coronary artery disease, hypertension, diabetes mellitus, and hyperlipidemia. In young patients without obvious risk factors for atherosclerosis, traumatic dissection and systemic illness (eg, arteritis, hypercoagulation syndromes) should be considered.

    Magnetic resonance imaging is the study of choice for obtaining images of brain structures supplied by the posterior circulation (19). It easily identifies specific stroke syndromes, such as Wallenberg's syndrome, in the distribution of a single vessel. Magnetic resonance angiography can be used to identify occlusive disease in the large vessels of the neck and base of the brain.

    Treatment methods
    Treatment of vertigo can be divided into three categories: specific, symptomatic, and rehabilitative (6). Specific therapies for the vertigo that accompanies common vestibular causes of dizziness are summarized in table 3.

    Cause Treatment


    Benign positional vertigo Maneuver to remove debris from semicircular canal (see figure 1: not shown)


    Acute unilateral Antivertiginous drugs for first few days; vestibular vestibulopathy rehabilitation as soon as possible


    Chronic bilateral Discontinuation of ototoxic agent; vestibular vestibulopathy rehabilitation


    Meniere's disease Low-salt diet (1-2 g sodium daily) with or without diuretic; antivertiginous drugs during attack; surgery in the few (<5%) intractable cases


    Migraine Control of potential triggers (eg, foods, stress); antimigraine drugs (beta blockers, calcium channel blockers, acetazolamide [AK-Zol, Diamox])


    insufficiency Antiplatelet drug (aspirin or ticlopidine HCl [Ticlid]); anticoagulant drug (heparin or warfarin sodium [Coumadin]) if spells continue


    When possible, of course, treatment of vertigo should be directed at the underlying disorder. However, in many cases, treatment of symptoms is the only method available or must be combined with specific therapy. Several classes of drugs have been found to have antivertiginous and antiemetic properties (table 4), although in most instances, their exact mechanism of action is unknown. All these agents produce potentially unpleasant side effects. The choice of drug or combination of drugs is made on the basis of known complications and the severity and duration of the vertigo.

    When the vestibular system has been permanently damaged, the initial state of imbalance at the level of the brain stem vestibular nuclei causes severe vertigo. Gradually, the patient adapts to the imbalance through a process of compensation if vision, depth perception, and sensation in the lower extremities are intact and proprioception in the neck and limbs are normal. Central pathways are also integral to compensation; recovery is diminished if these areas are damaged.

    Clinicians have long been aware that vestibular compensation is more rapid and more complete when patients begin exercising promptly. A vestibular exercise program should be instituted as soon as possible after injury to the vestibular system, and use of vestibular suppressants should be limited to the acute stage (20). While nystagmus is present, patients should attempt to focus the eyes and should move and hold them in the direction that provokes the most dizziness. When nystagmus has diminished to the point that the patient can clearly focus on a target in all directions, eye-head coordination exercises should be started. A useful exercise is to stare at a target while oscillating the head from side to side and up and down. Another helpful technique is to use combined eye and head movements to quickly move the focus back and forth between two widely separated visual targets.

    Patients should attempt to stand and walk while nystagmus is still present. As improvement occurs, head movements should be added while standing and walking, beginning with slow side-to-side and up-and-down movements and progressing to quick head turns in all directions. Compensation typically requires several months, and the degree of recovery depends on the age of the patient and the severity of the lesion.

    A patient's history usually contains key information regarding the type of dizziness and the best way to direct diagnostic workup. In dizziness with a vestibular cause (benign positional vertigo, vestibular neuritis, Meniere's disease, migraine, vertebrobasilar insufficiency), patients often describe their world as spinning, whirling, or tilting. Treatment should be directed at the underlying cause whenever possible, and various antivertiginous and antiemetic medications can be used to suppress symptoms. Initiation of a vestibular exercise program as soon as possible after injury helps ensure the best compensation possible.

    There is more information as to drugs that can cause this problem, etc. You may be able to locate the same website I found this info on with a search.

    Hope you are feeling better soon...

  3. lease79

    lease79 New Member

    This came on really suddenly, so I'm beginning to wonder if it was the storm?? Still feeling a bit rough now.
  4. charlenef

    charlenef New Member

    when i over do it it makes me dizzy/off balance and i usually can feel the tightness any where from my whole back or just my shoulders and neck. charlene
  5. lease79

    lease79 New Member

    Thanks heaps for the advice ;)
    Feeling a little better today. Just the 'truck ran over me' thing going on mainly, but balance is a little better ;)

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