posted
I had this symptom from babesia. It would get worse when herxing, but it gradually went away.
Posts: 925 | From California | Registered: Sep 2004
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lymeHerx001
Frequent Contributor (1K+ posts)
Member # 6215
posted
Sorry Ive had chronic vertigo and MCS for 3 years now.
I pray and forgive every day.
Antihistamines used to work
Posts: 2905 | From New England | Registered: Sep 2004
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Vanilla
Unregistered
posted
What kind of birth control? I would not take birth control pills if I had Lyme but that is me and everyone is different. I think birth control is always a good idea but not the pills or anything hormone related. I do not think hormones are good for you any way or safe but to add them to a lyme mix is not a great idea in my book. I believe they can cause cancer or be a trigger for cancer. My mother died young of breast cancer and she thought it had something to do with a bad reaction she had to birth control pills. She also was a chain smoker which is also a cancer trigger.
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Vertigo has probably been my most persistent symptom, almost from the beginning of my acute onset of Lyme / babs / bart. I am not sure which causes it the most.
I have found that the 4 hours antihistamine (chlor. maleate?) helps the most for this in conjunction with many other tools I have found over the years. Hyland's makes a motions sickness formula which helps a bit. It is homeopathic and sort of hard to find but it can't hurt to look at health food store. Also, I used to use sudafed when it was really bad, but I hate it because it wires me and wacks out my heart. Now I use chinese herbs - in particular "Bi Yan Pian" and "Er Chen Wan" - I think that you can find them both at asiachi.com. Bi Yan Pian I do about 5 pills as need or 3x day and the er chen wan is for when there is more blatant phlegm / congestion - I do about 8 pills as needed or 3x day. they are both for sinuses / phlegm congestion.
Usually the dizziness / vertigo is caused by inner ear infection or inflammation by the Lyme. It can also be caused by brain involvement. regardless of the cause, the anithistamine seems to reduce the inflammation.
With years of treatment this is almost no longer an issue for me. It does get retriggered when I am relapsing or hexing or when I am coming down with a cold / flu, and with allergies.
MCS is also commonly associated with it because of the inflammation caused by the sensitivities.
Hope this helps.
Good luck to you, but it will get better with time. This is one of my least favorite symptoms in the whole world.
I used to have to sleep with my feet on the floow or the wall to ground myself because I got the bed spins so badly. No more though.
Posts: 589 | From Rhode Island | Registered: Jun 2006
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pmerv
Frequent Contributor (1K+ posts)
Member # 1504
posted
Heather, I used to get vertigo attacks regularly before my Lyme diagnosis. They would incapacitate me for one day and then let up. After I was treated they gradually improved, becoming much less frequent.
The other thing I tried that worked was acupuncture. I was getting weekly treatments for aches and pains of Lyme, and we decided one week to concentrate on the vertigo. My dr stuck special needles around my ears and other places. The next day I had a vertigo attack.
The next week we repeated the treatment and the next day I had another attack.
After that I had no vertigo for years and years. That was decades ago and nowadays I only get vertigo if I go off antibiotics for a couple of months. So I stay on "maintenance" abx.
I can't explain it, but it might be worth trying.
-------------------- Phyllis Mervine LymeDisease.org Posts: 1808 | From Ukiah, California, USA | Registered: Aug 2001
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I went to my doc who is doing NAET allergy ellimination on me and he gave me a homeopathic vertigo pills to take sublingually.
PMERV- Its funny that you mentioned accupuncture because I already went it had it done. I had it done on Tuesday and like you said I had a back attack yesterday (Wednesday). So, will go next week and hopefully after a few weeks I will start to feel better.
Thanks so much for the support
Blessings, Heather
Posts: 74 | From Florida | Registered: May 2006
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I'm so sorry you are stuggling w/ this! Lyme can definately cause this by triggering any one of a number of disease processes.
Many different meds are used to treat it and/or relieve symptoms depending on the nature of the offending material or disease process at work:
Inflammation, viral/bacterial infections, blood pressure changes, toxins, lesions, fluid, calcium crystals, growths, etc. You need a good ENT to discover that.
I have suffered w/this symptom due to lyme- triggered labyrinthitis for years, sometimes to a severe degree. Horrid! Not to scare you, but once it got so bad I collapsed and had to be paramediced to the hospital where I spent nearly a week hanging on to the bed, bathed in sweat, wretching. Also more hearing loss.
So, my best advice would be to find out cause!
For info, see text explaining vertigo below. Apologies in advance for the length of article, but its a good basic text.
Dizziness is a common complaint and too often the symptom is attributed to an "inner ear problem."
Numerous cochleovestibular, neurologic, cardiovascular, metabolic, ocular, and systemic diseases are capable of eliciting the sensation of dizziness; the ear, however, is responsible for only 50-60 percent of the known causes of dizziness.
I. ANATOMY AND PHYSIOLOGY OF THE LABYRINTH
The semicircular canals Anatomy: the semicircular canals (lateral, posterior, and superior) lie at right angles to one another and are encased within the otic capsule of the temporal bone.
Each canal contains perilymph (fluid) which bathes the membranous ducts within the canal. Each canal has an ampulla or a widening of the canal at the point it communicates with the vestibula.
The crista ampullaris is located in each respective ampulla. The crista contains specialized neuroepithelium with hair cells imbedded in a gelatinous material to form the cupula.
Physiology: the cupula extends into the ampulla to detect rotational movement of the endolymph.
The maculae of the utricle and saccule Anatomy: the utricle and saccule are located in the bony vestibula.
The endolymph contained within the utricle and saccule is continuous with the cochlear duct and the membranous duct of the semicircular canals.
Both the saccule and utricle have maculae which contain hair cells embedded in a gelatinous material covered with calcium carbonate crystals (otoconia).
Physiology: the maculae are responsive to the effect of gravity and linear movement.
Posture and movement
The labyrinth acts as a bilateral frequency modulator. Acceleration,deceleration, or rotational movement of the head leads to excitation of one system and inhibition of the opposite.
Sensory output is relayed to the vestibular nuclei and pathways for central interpretation.
The manifestation of disease: in order to maintain posture and move through the environment in an orderly and safe fashion,appropriate information from three sensory modalities is important: the visual axis, proprioception in the joints and muscles, and the labyrinths.
This input is integrated in the brain stem and cerebellum to adjust posture and motor activity and to maintain orientation.
A failure in sensory input, poor integration in the central nervous system, or diseased support systems (cardiovascular and metabolic), can provoke the feeling of disorientation or dizziness.
The interdependence of so many organ systems accounts for the large differential diagnosis of dizziness.
II. DIFFERENTIAL DIAGNOSIS OF DIZZINESS:
The cochleovestibular system
Infection Acute otitis media Chronic otitis media Serous otitis media Bacterial labyrinthitis Viral labyrinthitis Vestibular neuronitis Syphilis Herpes zoster oticus Trauma Perilymph fistula Temporal bone fracture Labyrinthine concussion Iatrogenic injury Barotrauma Cervical vertigo Tumor Cholesteatoma Acoustic neurinoma Glomus tumors Primary or metastatic carcinoma Vascular Infarction of labyrinthine artery Intralabyrinthine hemorrhage Degenerative Benign positional vertigo (cupulolithiasis) Aging Developmental Congenital anomalies of the inner ear Idiopathic Meniere's disease (Endolymphatic hydrops) Bell's palsy Disorders of bone metabolism Otospongiosis Osteopetrosis Ototoxins Aminoglycosides Salicylates Alcohol Loop diuretics: ethacrynic acid and furosemide Heavy metals: mercury, gold, lead, arsenic drugs Antineoplastics: nitrogen mustard, bleomycin, cis-platinum Nervous system
Infection Meningitis Encephalitis Brain abscess Demyelinating disorders Multiple sclerosis Other demyelinating processes Tumor Cerebellopontine angle tumors Benign and malignant neoplasia Metastatic carcinoma Developmental Malformations of the base of skull Peripheral neuropathy Diabetes mellitus Ethanol Pellagra Tabes dorsalis Vascular Hyperventilation Vertebrobasilar insufficiency Migraine variants Brain stem infarction or hemorrhage Cerebellar infarction or hemorrhage Vascular loop syndrome Seizure disorders Temporal lobe Petit mal Cardiovascular system Circulatory Hypovolemia Anemia Polycythemia Orthostatic hypotension Hypotension Cardiac Arrhythmias Valvular disease: AS/AI Stokes-Adams attacks Great vessels Subclavian steal Hypersensitive carotid sinus reflex Other Systems
Ocular/Oculomotor Changes in refraction Cataracts Glaucoma EOM neuropathy Muscle imbalance Endocrine or metabolic Diabetes mellitus Hyperlipidemia Hyperthyroidism Carcinoid syndrome Menstruation-pregnancy-menopause Pheochromocytoma Allergy/autoimmune Inhalant Food Drug Collagen vascular disorders Psychiatric Chronic anxiety Hysteria "Old age syndrome" Multisensory deficit
III. THE EVALUATION OF DIZZINESS
History Characterizing exactly what the patient means by "dizzy" is the most important step in the evaluation.
Vertigo is an illusion of movement and is specific for a lesion in the inner ear, vestibular nuclei, or vestibular pathways.
Momentary vertigo associated with rapid head movements typifies benign paroxysmal positional vertigo.
Vertigo lasting for several hours tends to occur with inner ear disorders. Persistent vertigo of greater than three weeks' duration is due to a problem within the central nervous system!
Imbalance or incoordination connotes disease in the cerebellum, brain stem, or vestibulospinal tracts.
Light-headedness or the feeling of faintness, although often benign, can implicate a problem in any of the systems listed in the differential diagnosis.
Peripheral vestibular disorders do not produce a loss of consciousness! Loss of consciousness associated with dizziness is most frequently due to vertebrobasilar insufficiency, cardiac arrhythmias, or seizures.
Examination
Resting pulse and blood pressure should be measured in the supine and standing positions to document presence or absence of orthostatic hypotension.
Complete head and neck exam
Otologic inspection is necessary to rule out disease of the external and middle ear.
The Weber and Rinne test are used to document sensorineural or conductive hearing losses.
A fistula test is performed with a pneumatic otoscope in order to ascertain the presence or absence of a perilymph fistula.
The patient is examined for the presence of spontaneous gaze and positional nystagmus.
Nasopharyngoscopy and indirect laryngoscopy are considered a part of the neurotologic examination.
Cranial nerve assessment is essential.
Vestibular and cerebellar assessment is made through rapid repetitive motion, past pointing, Romberg, tandem walk, and cold water caloric testing.
Auscultation of the precordium and the neck is necessary to detect carotid bruits, AV malformations, and valvular heart disease.
IV. LABORATORY STUDIES
Cochleovestibular Standard audiometry Pure tone studies Speech studies Recruitment Tone decay Impedance audiometry Tympanometry Acoustic reflex Auditory brainstem evoked response Electronystagmography Oculomotor testing Bithermal calorics Positional tests Rotary testing
Generation of the vestibular (slow) phase of different kinds of nystagmus. The thickness of the lines connecting the semicircular canal to the eye muscles is proportional to the intensity of nervous discharge along the nerve pathways.
Roentgenographic views of the internal auditory canal: plain or polytomography CT scanning Contrast High resolution Air-contrast
Arteriography
Nervous system Lumbar puncture/CSF studies EEG CT scanning with contrast NMR scanning
CBC with differential Fasting blood glucose Five-hour glucose tolerance test Lipid profile Thyroid function studies Rheumatoid factor and antinuclear antibody RPR, VDRL, or FTA-ABS Psychiatric testing
V. COMMON CAUSES OF DIZZINESS
Cochleovestibular system Benign paroxysmal positional vertigo.
Symptoms: a 15-30 second episode of vertigo induced byposition chang
Signs: the positional nystagmus may be observed by purposefullyinducing the position change and observing the eyes. Nystagmustends to be toward the involved ear and exhibits latency and fatiguability.
Laboratory: ENG documents the presence of positional nystagmus.
Treatment: reassurance and vestibular exercises. Singular nerve section for the recalcitrant and disabled patient.
Meniere's disease (See previous section on Hearing Loss).
Viral labyrinthitis
Symptoms: acute onset of vertigo usually associated with nausea and vomiting Hearing loss may or may not be present.
Signs: unilateral hearing loss, spontaneous nystagmus with the slow component toward the involved ear. Pass pointing and falling to the side of the lesion in the acute stages.
Laboratory: audiograms may show sensorineural hearing loss. ENG reveals nystagmus and often a caloric weakness.
Treatment: the condition is self-limited and the most effectivetherapy includes rest and sedation. Meclizine or diazepam often beneficial.
Vestibular neuritis
Symptoms and signs: presentation and physical findings can be identical to those of viral labyrinthitis except that hearing loss is not present.
Laboratory: ENG will show a unilateral weakness in theinvolved ear.
Treatment: same as for viral labyrinthitis. Vestibular neuronitis can be recurrent. A vestibular nerve section willcure the vertigo and preserve hearing.
Acoustic neurinoma. Patients rarely present with true vertigo secondary to acoustic neurinoma but more frequently complain ofunsteadiness, tinnitus, or hearing loss. See previous section on Hearing Loss.
Labyrinthine concussion
Symptoms: vertigo or dizziness with or without hearing loss following severe head injury.
Signs: spontaneous nystagmus with the slow component toward the involved ear may be present along with a sensorineural hearing loss.
Laboratory: a basic audiogram will document the presenc eof sensorineural hearing loss. The ENG may document the presenceof a caloric weakness or a positional nystagmus. Polytomography of the skull base or CT scanning is indicated when skull fractures are suspected.
Treatment includes the use of antivertiginous medications in the initial stages.
Labyrinthectomy or vestibular nerve sectionare indicated for a patient with symptoms persistent beyond six months.
Otosyphilis. See section on Hearing Loss. Cardiovascular
Orthostatic hypotension. Symptoms: the patient complains of light-headedness or thesensation of faintness upon sitting upright or standing.
Signs include an increased pulse rate or a fall of systolicpressure with the change in position.
Laboratory: none.
Treatment: reassurance and a change in medication whenindicate
Hyperventilation Symptoms: light-headedness, fullness in the throat, perioral paresthesias, chest tightness, anxiety.
Physical examination: normal.
Laboratory: if the patient is symptomatic, an arterial blood gas may reveal the presence of hypocarbia.
Treatment: reassurance along with methods to increase the pCO2 (paper bag).
Neurological systems
Vertebrobasilar insufficiency.
Symptoms: these patients can experience true vertigo but this is usually associated with visual disturbances, dysarthria, disorientation, and ataxia.
Signs: physical examination may be normal between attacks.
Laboratory: CT scan is usually normal. Findings on arteriography can be variable
Treatment: ASA, Persantine, anticoagulation in severe cases.
"Old age syndrome"
Symptoms: complaints of dizziness and disequilibrium withfrequent falls in the elderly population.
Signs: include orthostatic hypotension, diminished visual acuity, presbycusis, etc. Laboratory: findings tend to be nonspecific.
Treatment: ambulation with assistance and adjustment of any medications implicated in the production of orthostatic hypotension
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