need prayer desperately

Discussion in 'Spirituality/Worship' started by sixtyslady, Dec 12, 2007.

  1. sixtyslady

    sixtyslady Member

    please everyone would you please pray for my healing from vertigo, I had it before and it ws terrible.i woke up this morning with it. I tried to lay back down and I could"t I was so dizzy.
    please help me storm heaven with my prayeer request.
    thank you all so much.
    blessings sixtyslady
  2. sixtyslady

    sixtyslady Member

    bless you Dear, for your prayers and advice.
    I"m going to try the tuermic and see if it will help.
    thanks again for taking the time to answer my post.

    Blessing sixtyslady
  3. sixtyslady

    sixtyslady Member

    I guess I have a virus because I keep having a low grade temp.
    I was watching Creflo Dollar early this morning and he said to get a hold of the fact that God Loves us.
    and not to let Satan put negative thoughts in our heads.
    so thats what I"m trying to do this morning every time I have a thought that I'm not going to get over this dizziness I rebuke it,and say Jesus loves me.
    I"m also trying the garlic. and would like to try the turmeric,but read that if one has gallbladder problems this could make it worse.
    I wish I could take vitamin c but had a bad time with it last year when I try it. sixtyslady.
  4. greatgran

    greatgran Member

    Oh, I will Pray for the healing of your vertigo..I have it from time to time and its horrible. Never know when its going to hit or how long it will last. I will be praying for you.

    God Bless,
  5. kgangel

    kgangel New Member

    Vertigo is a tough thing to deal with a good friend of my mom is having a tough time w/it too

    God Bless you, I am praying


  6. PVLady

    PVLady New Member

    I don't know where you are located but I know of a excellent doctor who helped my husband. You may have a condition called BPV "Benign Positional Vertigo"

    It is caused by calcium particles in your inner ear. If you have this condition, it might be cured by a doctor performing a series of movements that dislodge these particles.

    The doctor who writes about this is Dr.Robert Baloh at UCLA in Los Angeles, CA.

    The following article was written by Dr. Baloh. He is a professor at UCLA. I know the article is pretty technical but maybe you can take it to your doctor. I would see a neurologist.

    The dizzy patient

    Presence of vertigo points to vestibular cause
    Robert W. Baloh, MD


    Preview: Depending on the physiologic mechanism at fault, dizziness can represent several overlapping sensations--all of them uncomfortable.

    In cases with a vestibular cause (perhaps about half the cases of dizziness), vertigo is the predominant symptom, so patients have the unsettling feeling that their environment is spinning around them or that they are moving in space.

    Dr Baloh discusses pertinent findings to seek on history taking (eg, do certain movements elicit dizziness? did vertigo follow a blow to the head?) that may help establish the cause. He also describes further workup, treatment, and prognosis.


    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.

    Table 2. Drugs commonly associated with dizziness
    Class of drug Type of dizziness Mechanism


    Alcohol Positional vertigo Specific-gravity difference in endolymph vs cupula
    Intoxication CNS depression
    Disequilibrium Cerebellar dysfunction


    Tranquilizers Intoxication CNS depression


    Anticonvulsants Intoxication CNS depression
    Disequilibrium Cerebellar dysfunction


    Antihypertensives Near faint Postural hypotension


    Aminoglycosides Vertigo Asymmetric hair-cell loss
    Disequilibrium Vestibulospinal reflex loss
    Oscillopsia Vestibulo-ocular reflex loss


    CNS, central nervous system.


    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.

    Table 3. Specific treatment methods for vertigo from common vestibular causes
    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.

    Table 4. Commonly used antivertiginous and antiemetic drugs
    Classes and agents Dosage Comments



    Dimenhydrinate 50 mg orally q4-6h or 100-mg suppository q8h Available without prescription, mild sedation, minimal side effects
    Meclizine 25-50 mg orally q4-6h Mild sedation, minimal side effects
    Promethazine HCl (Phenergan) 25-50 mg orally, IM, or suppository q4-6h Good for nausea and vertigo, more sedation, rare extrapyramidal side effects


    Monoaminergic agents
    Amphetamine sulfate 5 or 10 mg orally q4-6h Stimulant, can counterbalance sedation of antihistamines, many potential side effects
    Ephedrine 25 mg orally q4-6h Available without prescription, fewer side effects than amphetamine


    Diazepam (Valium, Valrelease) 5 or 10 mg orally q6-8h Prominent sedation, little effect on nausea, avoid chronic use


    Prochlorperazine (Compazine) 5-25 mg orally, IM, or suppository q4-6h Good antiemetic; serious extrapyramidal side effects, particularly in young patients; do not use with benzamide


    Metoclopramide (Maxolon, Octamide PFS, Reglan) 5-10 mg orally, IM, or IV q4-6h Improves gastric emptying, watch for bowel obstruction, do not use with phenothiazine or in children


    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.


    Baloh RW. Dizziness, hearing loss, and tinnitus. New York: Oxford University Press, 1998:107-25
    Baloh RW, Honrubia V, Jacobson K. Benign positional vertigo: clinical and oculographic features in 240 cases. Neurology 1987;37(3):371-8
    Epley JM. The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992;107(3):399-404
    Brandt T, Steddin S. Current view of the mechanism of benign paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis? J Vestib Res 1993;3(4):373-82
    Parnes LS, McClure JA. Free-floating endolymph particles: a new operative finding during posterior semicircular canal occlusion. Laryngoscope 1992;102(9):988-92
    Foster CA, Baloh RW. Episodic vertigo. In: Rakel RE, ed. Conn's current therapy. Philadelphia: Saunders, 1995:839
    Schuknecht HF. Neurolabyrinthitis: viral infections of the peripheral auditory and vestibular systems. In: Nomura Y, ed. Hearing loss and dizziness. New York: Igaku-Shoin, 1985:1-15
    Baloh RW, Lopez I, Ishyama A, et al. Vestibular neuritis: clinical-pathologic correlation. Otolaryngol Head Neck Surg 1996;114(4):586-92
    Gacek RR. Perilymphatic fistula. In: Cummings CW, ed. Otolaryngology: head and neck surgery. 2d ed. Vol 4. St Louis: Mosby-Year Book, 1993:3017-9
    Hess K. Vestibulotoxic drugs and other causes of acquired bilateral peripheral vestibulopathy. In: Baloh RW, Halmagyi GM, eds. Disorders of the vestibular system. New York: Oxford University Press, 1996:360-73
    Andrews JC, Honrubia V. Meniere's disease. In: Baloh, Halmagyi, eds,(10) pp 300-17
    Baloh RW, Jacobson K, Winder T. Drop attacks with Meniere's syndrome. Ann Neurol 1990;28(3):384-7
    Schuknecht HF. Delayed endolymphatic hydrops. Ann Otol Rhinol Laryngol 1978;87(6 Pt 1):743-8
    Kayan A, Hood JD. Neuro-otological manifestations of migraine. Brain 1984;107(Pt 4):1123-42
    Harker LA, Rassekh CH. Episodic vertigo in basilar artery migraine. Otolaryngol Head Neck Surg 1987;96(3):239-50
    Baloh RW. Neurotology of migraine. Headache 1997;37(10):615-21
    Grad A, Baloh RW. Vertigo of vascular origin: clinical and electronystagmographic features in 84 cases. Arch Neurol 1989;46(3):281-4
    Caplan LR. Brain embolism, revisited. Neurology 1993;43(7):1281-7
    Bogousslavsky J, Fox AJ, Barnett HJ, et al. Clinico-topographic correlation of small vertebrobasilar infarct using magnetic resonance imaging. Stroke 1986;17(5):929-38
    Herdman SJ. Vestibular rehabilitation. In: Baloh, Halmagyi, eds,(10) pp 583-98
    Dr Baloh is professor, department of neurology and head and neck surgery, University of California, Los Angeles, UCLA School of Medicine. Correspondence: Robert W. Baloh, MD, Department of Neurology and Head and Neck Surgery, UCLA School of Medicine, Box 951769, Los Angeles, CA 90095-1769. E-mail:


    [This Message was Edited on 12/30/2007]
  7. dolphin59

    dolphin59 New Member

    dear lady prayers from the uk from dolly xx
  8. jinlee

    jinlee Member

    Dr. Epley practives here in Oregon , and ENT. Look up his website and there are many with pictures or videos telling how to do the procedure in your own home.

    My husband suffered terribly from it and had to take meclizine all the time which only made him sicker. This takes just five minutes or so and he has only had to perform this three times or so.

    It is worth a try.

    Hope you find a cure as dizziness, vertigo is the pits.