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Vertigo cases: Vertigo | Conditions | UCSF Health


Vertigo | Conditions | UCSF Health

Vertigo, dizziness and balance-related conditions are among the most common health problems in adults. Nearly 40 percent of U.S. adults experience vertigo at least once in their lifetime, with women slightly more likely to get it than men. It can occur because of a problem with the body’s vestibular system, which includes structures of the inner ear, vestibular nerve, brain stem and cerebellum, a region of the brain that integrates sensory perception, coordination and motor control. This system regulates balance, posture and the body’s orientation in space.


Although the cause is unknown in many cases, a number of disorders can cause vertigo, dizziness and imbalance. Those conditions include:

Benign Paroxysmal Positional Vertigo(BPPV)

In people with BPPV, head or body movements — particularly when lying in bed or leaning over — can cause a brief vertigo attack that lasts less than one minute. BPPV occurs when microscopic calcium deposits called otoliths are trapped in one of the three semicircular canals that make up the vestibular system. BPPV is the most common cause of vertigo and can be treated effectively.

Meniere’s Disease

Meniere’s Disease results from an imbalance of fluids in the inner ear, which can cause periods of vertigo lasting from minutes to hours. It’s frequently accompanied by fluctuating, low-frequency hearing loss, tinnitus and a feeling of fullness or pressure in the ears, known as aural fullness.

Viral and Bacterial Labyrinthitis

Labyrinthitis results from inflammation within the inner ear, and may cause vertigo attacks lasting from hours to days.

Other Causes

Various neurological conditions can also cause vertigo. These include:

Other, non-neurological causes include:

  • Diabetes
  • Heart arrhythmias
  • Hyperventilation
  • Orthostatic hypotension, a sudden decrease in blood pressure when you stand up
  • Psychiatric or emotional problems such as panic attacks and anxiety
  • Use of multiple prescription and non-prescription medications

Our Approach to Vertigo

UCSF offers state-of-the-art evaluation and treatment for vertigo, dizziness and other balance problems. Our team includes specialists in audiology, otolaryngology (ear and throat disorders), neurology and physical therapy, who collaborate to identify the cause of an individual’s symptoms and design a plan to address them. Treatment for vertigo depends on the diagnosis and may include medications or surgery, as well as physical therapy to improve stabilization, retrain the brain and relieve symptoms.

What Causes Vertigo and Who Is at Risk for It?

The Most Common Reasons People Get Vertigo

About 93 percent of all vertigo cases are caused by one of the following conditions: (1)

  • Benign Paroxysmal Positional Vertigo (BPPV) BPPV is the most common cause of vertigo. (2) It happens when small crystals break free and float inside the tubes of your inner ear, which are called semicircular canals. BPPV typically results in short episodes of vertigo that come on suddenly and last a few seconds to a few minutes. Certain head movements trigger episodes of vertigo in people with BPPV. Most of the time, doctors can’t identify exactly what causes BPPV, but it’s sometimes associated with a minor or severe blow to the head.
  • Labyrinthitis This condition, which is also referred to as “vestibular neuritis,” is characterized by irritation and swelling of the inner ear. It’s typically caused by an inner ear infection or virus. Sudden vertigo symptoms and hearing loss are common in people with labyrinthitis.
  • Meniere’s disease This disease is caused by excess fluid buildup in your inner ear. People with Meniere’s often experience sudden, intense episodes of vertigo that last a long time. They may also have symptoms like ringing in the ears, hearing loss, or “plugged” ears. Doctors aren’t sure exactly what causes Meniere’s disease, but it’s linked to viral infections of the inner ear, allergies, and head injuries. Hereditary factors are also thought to play a role.

Less Common Reasons People May Get Vertigo

Other causes of vertigo may include:

  • Cholesteatoma This condition is characterized by irregular skin growth in the middle ear, behind the eardrum. It can be brought on by repeated, chronic ear infections.
  • Otosclerosis Otosclerosis causes abnormal bone growth in the middle ear that can result in hearing loss.
  • Stroke A blood clot or bleeding in the brain — otherwise known as a stroke — can cause symptoms of vertigo.
  • Perilymphatic Fistula With this condition, an abnormal connection (usually a tear or defect) between the middle ear and the inner ear allows fluid to leak into the middle ear.
  • Acoustic neuroma This is a noncancerous tumor that develops on the main nerve leading from your inner ear to your brain.
  • Multiple sclerosis (MS) Many people with the neurological disease known as MS experience vertigo episodes at some point.
  • Parkinson’s Disease Parkinson’s can affect movement and balance. People with this disease may also experience vertigo.
  • Migraine About 40 percent of people who have migraines also have problems with dizziness or balance at some time. (3) There’s even a condition known as “migraine-associated vertigo.”
  • Diabetes Sometimes, complications from diabetes can cause hardening of the arteries and less blood flow to the brain, which leads to vertigo symptoms.
  • Pregnancy Dizziness and vertigo may crop up during pregnancy due to hormone changes, low blood sugar levels, pressure on blood vessels caused by an expanding uterus, or the baby pressing on a vein that carries blood to the heart.
  • Chiari Malformation This condition, where brain tissue extends into the spinal canal, can cause symptoms of vertigo.
  • Syphilis This sexually-transmitted infection (STI) can lead to hearing loss and dizziness.
  • Anxiety Disorders Anxiety and panic attacks may cause people to feel symptoms of vertigo. Stress can also worsen the condition.
  • Brain Tumor A tumor in an area of the brain called the cerebellum can cause vertigo symptoms.
  • Air Pressure Changes Pressure differences between the middle ear cavities are commonly experienced when flying or diving underwater. This can cause a condition called alternobaric vertigo.
  • Allergies Some people have dizziness or vertigo attacks when they’re exposed to certain allergens, such as dust, molds, pollens, dander, or foods.
  • Medication Dizziness and vertigo are sometimes side effects of medicines. Anti-seizure drugs, antidepressants, sedatives, blood pressure meds, and tranquilizers are common culprits.

Related: MS and Vertigo: When the Earth Moves, but Not in a Good Way

Head and Neck Injuries May Cause Vertigo

About 5 percent of the population suffers from a head injury each year, according to the American Hearing Research Foundation. (4)

These injuries can damage the inner ear and lead to vertigo, which is often referred to as “post-traumatic vertigo.” People with head injuries who experience vertigo might have symptoms like dizziness, headaches, hearing changes, pain, balance problems, and even mental disturbances.

Cervical vertigo happens after a severe neck injury. While experts agree that this condition exists, there’s debate over how often it occurs.

When Doctors Can’t Find the Cause for Vertigo

Sometimes, doctors aren’t able to identify a specific source for vertigo symptoms. For instance, there’s often no known trigger for BPPV.

While not knowing exactly what’s causing your vertigo symptoms can be frustrating, it doesn’t mean that you can’t get proper treatment and care. Your healthcare provider will help you find ways to control your episodes, even if a cause isn’t identified.

Some Factors Put You at Increased Risk for Vertigo

Anyone can develop vertigo symptoms, but certain risk factors might raise your chances. These include:

  • Being over age 50
  • Being a woman
  • Suffering a head injury
  • Taking certain drugs, especially antidepressants or antipsychotics
  • Having any medical condition that affects balance or your ears
  • Experiencing a previous episode of vertigo
  • Having a family member who has vertigo
  • Having an inner ear infection
  • Experiencing high levels of stress
  • Drinking alcohol

Having these risk factors doesn’t mean you will develop vertigo — they just put you at an increased risk for the condition.

Benign Paroxysmal Positional Vertigo – StatPearls

Continuing Education Activity

Vertigo is the perception of motion in the absence of motion, which may be described as a sensation of swaying, tilting, spinning, or feeling unbalanced. Due to highly variable descriptions of vertigo, it is often consolidated into the umbrella descriptor ‘dizziness’, a very common complaint that accounts for over three million emergency department visits annually. Vertigo can be of vestibular or peripheral origin or be due to non-vestibular or central causes. Benign paroxysmal positional vertigo (BPPV) is the most common cause of peripheral vertigo, accounting for over half of all cases. It is of great importance to distinguish BPPV from other causes of vertigo as the differential diagnosis includes a spectrum of disease processes ranging from benign to life-threatening. This activity describes the evaluation and management of benign paroxysmal positional vertigo and highlights the role of the interprofessional team in improving care for affected patients.


  • Describe how to properly evaluate for benign paroxysmal positional vertigo.

  • Outline the differential diagnosis of benign paroxysmal positional vertigo.

  • Review how to properly manage a patient affected by benign paroxysmal positional vertigo.

  • Explain the importance of improving care coordination, with particular emphasis on communication between interprofessional medical teams, to enhance prompt and thorough delivery of care to patients with benign paroxysmal positional vertigo.

Access free multiple choice questions on this topic.


Vertigo is the allusion of movement, perception of motion though none exists. It is a sensation of swaying, tilting, spinning, or feeling unbalanced, which may be experienced as self-motion to some versus movement of the surrounding environment to others. Due to highly variable descriptions of the vertigo experience, it is often consolidated into the umbrella term “dizziness,” which is a very common complaint, accounting for over three million emergency department (ED) visits annually. Vertigo can be of vestibular or peripheral origin or be due to non-vestibular or central causes. With regards to peripheral vertigo, benign paroxysmal positional vertigo (BPPV) is the most common cause, accounting for over one-half of all cases. It is of great importance to identify BPPV versus other causes of vertigo as the differential diagnosis includes a spectrum of diseases processes ranging from benign to life-threatening.[1][2][3]


Benign paroxysmal positional vertigo occurs due to the displacement of calcium-carbonate crystals or otoconia within the fluid-filled semicircular canals of the inner ear. These otoconia are essential to the proper functioning of the utricle of the otolithic membrane by helping deflect the hair cells within the endolymph, which relays positional changes of the head including tilting, turning, and linear acceleration.[4]


Dizziness, including vertigo, affects 15 to 20% of adults yearly based on population studies. The lifetime prevalence of BPPV specifically was found to be 2.9%, and the incidence increases with age due to age-related degeneration of the otolithic membrane. Additionally, BPPV is about two to three times more common in women versus men. [5]


With BPPV, otoconia (also known as “otoliths” or “canaliths”) dislodge and settle within the endolymph of the semicircular canals. When the head remains static, there is no stimulus causing the hair cells to fire. With motion, however, the displaced otoconia shift within the fluid, and the subsequent stimulus is unbalanced with respect to the opposite ear, inappropriately causing symptoms of dizziness, spinning, and/or swaying. Hence, symptoms of BPPV are profound with movement but classically lessen with rest.

History and Physical

A detailed history and physical are imperative to the evaluation of vertigo since differentiating vestibular versus central, potentially life-threatening, processes is of critical importance. Ask open-ended questions to obtain the best possible description of symptoms. Ask regarding the timing of symptoms and context, as well as exacerbating and alleviating factors. Inquire about recent viral infections due to association with labyrinthitis and about trauma, recent neurosurgery, and medications that may be ototoxic as this may suggest an alternate diagnosis. Relapses are common, so a history of recurrent vertiginous spells suggests BPPV. Due to age-related degeneration of the otolithic membrane, BPPV frequently occurs in the elderly population, though close consideration must be made for central causes of vertigo, which also correlate with increasing age and cerebrovascular disease.

Classically, the symptoms of BPPV are sudden in onset, provoked by movement, and decreased with rest. The Dix-Hallpike test is a diagnostic maneuver that can be performed quickly and easily to evaluate for BPPV. It is based on the anatomical properties of the inner ear, which predispose displaced otoconia to settle in the posterior semicircular canal. Theoretically, otoconia may settle in the superior or lateral semicircular canals, leading to a negative test, though with a sensitivity of 79% and specificity of 75%, this maneuver does have clinical utility. The Dix-Hallpike helps localize the affected ear by exacerbating both symptoms and clinical signs such as nystagmus. Subsequently, the Epley maneuver can be performed, coercing the crystals back into the utricle and removing the disturbance from the otolithic membrane. The Epley can promptly relieve symptoms, though relapses are common. Additionally, the Epley is often not tolerated by elderly patients as well as those with active nausea/vomiting and those with profound symptoms who cannot cooperate. The Epley is contraindicated in cervical spine injury/abnormality, such as possible atlantoaxial subluxation, as well as in patients with possible carotid or vertebral artery dissection. In addition to these special tests, it is imperative to perform a full neurological exam, including cranial nerves, coordination, and gait. The neurological exam is expectedly normal in BPPV with a few exceptions. Patients with BPPV can demonstrate nystagmus, which is typically horizontal and unidirectional as well as fatigable, meaning it peaks in intensity but subsequently tapers off. Vertical, torsional, or direction-changing nystagmus should raise concern for the central cause. With BPPV, there is a latency period of 30 seconds or less between provocative head movement and the onset of nystagmus. Also, the otoconia in BPPV cause aberrant impulses to be fired from the semicircular canals via cranial nerve VIII, impairing the vestibular-ocular reflex. Patients with BPPV will have issues coordinating head movement with extra-ocular movement, leading to an abnormal head impulse test. The HiNTS exam, which includes nystagmus and head impulse testing, is a sequence of tests to help discern central versus peripheral causes of dizziness. It would be of value to perform in the physical exam of patients being evaluated for possible BPPV.


BPPV is largely a clinical diagnosis, and often the battery of laboratory and imaging tests ordered only helps rule out other possibilities. As above, obtaining a good history and performing a thorough neurological exam is imperative. Laboratory studies are not found to be helpful. Imaging of the head in BPPV is unremarkable. Head CT and MRI are useful to rule out infarct, hemorrhage, masses/tumors, or other pathology that would suggest alternative causes of vertigo. The Dix-Hallpike, if it can be tolerated, should be performed as a provocative test to observe for expected changes in symptoms and to localize which inner ear is involved.[6][7][8]

Treatment / Management

After using the Dix-Hallpike maneuver to localize which side is problematic, the Epley maneuver can be performed. This series of positional changes helps dislodge otoconia from the otolithic membrane and back into the utricle, removing the disturbance and symptomatology. As aforementioned, the Dix-Hallpike and Epley are not always tolerated by patients with BPPV, in which case treatment is symptomatic. Antihistamines address vertigo by suppressing labyrinth excitability and vestibular end-organ receptors. The antihistamine best supported in the literature for vertigo is Meclizine, 25 mg to 100 mg daily. Vertigo associated with BPPV is typically abrupt in onset, very brief, and truly paroxysmal, just as the name suggests, and medications may not be particularly beneficial. Hence, routine medical management with Meclizine is not indicated unless the frequency of vertigo spells is high and disruptive to daily function. Nausea and vomiting is another common complaint with BPPV and can be treated with anti-emetics as needed: ondansetron, metoclopramide, or promethazine/prochlorperazine. Patients with recurrent BPPV should be provided with ENT referral for further evaluation as there are lateral and horizontal canal variants of BPPV that require specific re-positioning maneuvers different from the Epley.[1][9]

Differential Diagnosis

Vestibular neuritis, labyrinthitis, brainstem or cerebellar infarction, brainstem or cerebellar hemorrhage, traumatic vestibulopathy, cerebellopontine angle neoplasm, vestibular migraine, medication ototoxicity, herpes zoster oticus, decompression sickness, brainstem encephalitis, vertebrobasilar insufficiency, vertebral artery dissection.


Persistent nausea and vomiting can become an issue for some patients.

Enhancing Healthcare Team Outcomes

BPPV is a very common presentation in primary care. It is estimated that at least 20% of patients will complain of vertigo during a clinic visit. Tragically, the condition is often misdiagnosed and patients are erroneously treated for some other disorder, leading to very high morbidity. Primary care physicians, nurse practitioners, urgent care providers, and emergency department physicians must be aware of this disorder and know how to manage it. Once the diagnosis is made and treatment initiated, the prognosis is good. Most people develop symptom resolution in 4 to 6 weeks, although in some patients the symptoms persist. Despite optimal treatment, there is a recurrence rate of 5 to 25%. The risk of recurrence is higher in females, older patients, and those with psychiatric comorbidities. [10][11] [Level 5]


Parker IG, Hartel G, Paratz J, Choy NL, Rahmann A. A Systematic Review of the Reported Proportions of Diagnoses for Dizziness and Vertigo. Otol Neurotol. 2019 Jan;40(1):6-15. [PubMed: 30439765]
Alimoğlu Y, Altın F, Açıkalın RM, Yaşar H. Two-Hour Follow-Up is Equivalent to One-Day Follow-Up of Posterior Canal Benign Paroxysmal Positional Vertigo. J Int Adv Otol. 2019 Apr;15(1):141-145. [PMC free article: PMC6483436] [PubMed: 30411707]
Male AJ, Ramdharry GM, Grant R, Davies RA, Beith ID. A survey of current management of Benign Paroxysmal Positional Vertigo (BPPV) by physiotherapists’ interested in vestibular rehabilitation in the UK. Physiotherapy. 2019 Sep;105(3):307-314. [PubMed: 30389100]
Zamergrad MV, Grachev SP, Gergova AA. [Acute vestibular disorder in the elderly: stroke or peripheral vestibulopathy]. Zh Nevrol Psikhiatr Im S S Korsakova. 2018;118(6. Vyp. 2):46-49. [PubMed: 30346433]
Bruintjes TD, van der Zaag-Loonen HJ, Eggelmeijer F, van Leeuwen RB. The prevalence of benign paroxysmal positional vertigo in patients with osteoporosis. Eur Arch Otorhinolaryngol. 2018 Dec;275(12):3083-3086. [PubMed: 30315360]
Power L, Murray K, Szmulewicz D. Early experience with a multi-axial, whole body positioning system in the treatment of Benign Paroxysmal Positional Vertigo (BPPV). J Clin Neurosci. 2019 Mar;61:186-188. [PubMed: 30377044]
Lloyd M, Mackintosh A, Grant C, McManus F, Kelly AM, Karunajeewa H, Tang CY. Evidence-based management of patients with vertigo, dizziness, and imbalance at an Australian metropolitan health service: an observational study of clinical practice. Physiother Theory Pract. 2020 Jul;36(7):818-825. [PubMed: 30332324]
Luryi AL, LaRouere M, Babu S, Bojrab DI, Zappia J, Sargent EW, Schutt CA. Traumatic versus Idiopathic Benign Positional Vertigo: Analysis of Disease, Treatment, and Outcome Characteristics. Otolaryngol Head Neck Surg. 2019 Jan;160(1):131-136. [PubMed: 30324864]
Pérez-Vázquez P, Franco-Gutiérrez V, Soto-Varela A, Amor-Dorado JC, Martín-Sanz E, Oliva-Domínguez M, Lopez-Escamez JA. Practice Guidelines for the Diagnosis and Management of Benign Paroxysmal Positional Vertigo Otoneurology Committee of Spanish Otorhinolaryngology and Head and Neck Surgery Consensus Document. Acta Otorrinolaringol Esp (Engl Ed). 2018 Nov – Dec;69(6):345-366. [PubMed: 28826856]
Britt CJ, Ward BK, Owusu Y, Friedland D, Russell JO, Weinreich HM. Assessment of a Statistical Algorithm for the Prediction of Benign Paroxysmal Positional Vertigo. JAMA Otolaryngol Head Neck Surg. 2018 Oct 01;144(10):883-886. [PMC free article: PMC6233832] [PubMed: 30178063]
Luryi AL, Lawrence J, Bojrab D, LaRouere M, Babu S, Hong R, Zappia J, Sargent E, Chan E, Naumann IC, Schutt CA. Patient, disease, and outcome characteristics of benign paroxysmal positional vertigo with and without Meniere’s disease. Acta Otolaryngol. 2018 Oct;138(10):893-897. [PubMed: 30016894]

An approach to vertigo in general practice


Dizziness is a common and very distressing presentation in general practice. In more than half of these cases, the dizziness is due to vertigo, which is the illusion of movement of the body or its surroundings. It can have central or peripheral causes, and determining the cause can be difficult.


The aim of this article is to provide a clear framework for approaching patients who present with vertigo. A suggested approach to the assessment of vertigo is outlined.


The causes of vertigo may be central (involving the brainstem or cerebellum) or peripheral (involving the inner ear). A careful history and physical examination can distinguish between these causes. The most common causes of vertigo seen in primary care are benign paroxysmal positional vertigo (BPPV), vestibular neuronitis (VN) and Ménière’s disease. These peripheral causes of vertigo are benign, and treatment involves reassurance and management of symptoms.

Vertigo is a common, distressing presentation in general practice and constitutes approximately 54% of cases of dizziness. 1 Classically, vertigo presents as a sensation of movement of the environment around the patient.2 Often patients describe a ‘spinning’ sensation of either their body or their surroundings. This sensation can be confused with dizziness, which is a non-specific term, so an adequate history is required to differentiate this symptom. Dizziness can be classified into four groups:

  • vertigo (spinning sensation)
  • disequilibrium (feeling of imbalance)
  • light-headedness (sensation of giddiness)3
  • presyncope (sensation of feeling faint).

Vertigo can be classified as central or peripheral on the basis of vestibular symptom pathology.4 Vestibular symptoms originating from pathology in the cerebellum or brain stem are classified into the central type. Conversely, symptoms arising in the inner ear or from the vestibular nerve are classified as peripheral.

Balance is controlled by the cerebellum, which receives input from the vestibular nuclei in the brain stem. 5 This in turn receives input from the visual pathway, proprioception and inner ear. The vestibular apparatus of the inner ear consists of three semicircular canals, and two otolith organs called the utricle and the saccule.6 The utricle and saccule contain hair cells embedded in calcium carbonate crystals. These cells control vertical and non-rotational movements. Receptors in the semicircular canals respond to the position of the head. When the head tilts, receptors on the ipsilateral ear are stimulated and receptors in the contralateral ear are inhibited. These send impulses to the brain stem and cerebellum to control balance. Any disruption of this pathway can lead to vertigo.7


Often, patients presenting with dizziness are unable to describe the sensation and can be vague, particularly if it is the initial presentation. It is important to differentiate vertigo from other non-rotational forms of dizziness. Once the diagnosis of vertigo is determined, this needs to be differentiated into a central or peripheral subtype. 3

More serious central causes, such as cerebrovascular accidents (CVAs), tumours and multiple sclerosis (MS), need to be considered. Central causes are suspected if the patient presents with associated neurological symptoms such as weakness, dysarthria, sensory changes, ataxia or confusion. It may be difficult to distinguish between central and peripheral causes in patients who present with vertigo as their only symptom. Risk factors for vascular disease, including smoking, diabetes, obesity, hypertension and hypercholesterolaemia, need to be assessed to rule out CVAs, which can lead to vertigo from ischemia or infarction.8

Peripheral pathology is associated with symptoms of nausea, vomiting and hearing loss. Vertigo can be triggered by a change in the position of the head, recent upper respiratory tract infection (URTI), stress or trauma. Patients who experience anxiety or panic attacks can have vertigo as a result of hyperventilation.8 Loud noises can precipitate vertigo in patients with peripheral causes in a phenomenon called Tullio phenomenon.9 Medications, including frusemide, salicylates and antihypertensive agents, can affect the vestibular system, which in turn causes vertigo.10,11 Perilymphatic fistula should be considered if there is a history of recent head injury.

Vertigo with hearing loss is seen in labyrithitis and Ménière’s disease, whereas hearing loss is not seen in benign paroxysmal positional vertigo (BPPV) and vestibular neuronitis (VN). A brief approach to assessing vertigo is outlined in Figure 1.

Physical examination

A physical examination can assist in differentiating between central and peripheral subtypes of vertigo. Examination should involve the following:

  • Ear examination: an otoscopic examination should be performed to visualise the tympanic membranes for any vesicles that can be seen in a Herpes zoster infection or retraction pockets as seen in cholesteotoma.2 Vertigo triggered by pushing on the tragus or with the Valsalva manoeuvre is seen in a perilymphatic fistula. A hearing assessment should be performed.
  • Neurological examination: initially, a focused neurological examination including gait, balance and coordination needs to be performed. A gait and balance assessment (Romberg’s sign and the heel-toe test),12 and examination for cerebellar signs can exclude central causes.
  • Eye examination: eyes need to be examined for nystagmus and papilledema. Nystagmus is quick, jerky, involuntary movements of the eye. Vertical nystagmus is only seen if the cause is central.7 Nystagmus due to central causes may be horizontal, rotational or vertical, and does not disappear on fixing the gaze.13 Nystagmus in the peripheral type disappears with fixation of the gaze.
  • Cardiovascular examination: pulse, blood pressure, heart rate and rhythm should be checked.14 Carotid examination to identify bruits (in the case of a CVA) is necessary. Further imaging to rule out CVA can be performed if this is clinically suspected.

A number of specialised tests are required to determine the causes of vertigo. These are highlighted in Table 1.

Table 1. Interview schedule: key topics and questions
Physical examination Description
Dix−Hallpike manoeuvre The patient sits at the edge of the bed and the examiner turns the patient’s head 30–45 degrees to the side being tested. The patient needs to keep their eyes open and focus on a stable point, and then quickly lie supine and hyperextend the neck. Horizontal nystagmus denotes a positive test. This test can induce vertigo, so patients should be warned about this before the test is performed.2,7
Orthostatic blood pressure testing A drop in the systolic blood pressure by more than 20 mm/Hg from a lying down to standing position is significant for a postural drop. This is seen in patients who are dehydrated or who present with autonomic dysfunction.2 Autonomic dysfunction can occur acutely and be driven by vertigo.
Head impulse test The patient is asked to look at the examiner’s nose and the examiner quickly turns the patient’s head 10–20 degrees. It is abnormal if eyes move rapidly and repetitively, failing to re-fixate to the examiner’s nose. A positive test indicates disrupted vestibule-ocular reflex.7


The most common causes of vertigo seen in primary care are BPPV, VN and Ménière’s disease (Table 2).2 While most of the causes of vertigo are benign, more serious causes, including CVAs, MS, tumours, psychogenic causes and perilymphatic fistula, need to be considered,2 particularly in patients who are older or have risk factors for vascular diseases.

Table 2. Most common differential diagnoses of vertigo
Differential diagnosis Onset and duration of each attack of vertigo Provoking factors Special features Physical exam findings
Labyrinthitis Few seconds to minutes Change in the head position Tinnitus Hearing loss present
Vestibular neuronitis Seconds to minutes Recent upper respiratory tract infection Imbalance, while nystagmus is horizontal or rotational, the direction of the fast component is away from the side of the lesion Absence of hearing loss
Benign paroxysmal positional vertigo Seconds Change in the head position Positional Positive Dix−Hallpike
Ménière’s disease Hours Spontaneous Hearing loss and tinnitus Hearing assessment for sensorineural hearing loss


BPPV is the most common cause of vertigo in clinical practice.15 It is caused by an accumulation of calcium crystals in the posterior semicircular canal. These crystals affect the movement of the endolymph in the semicircular canals, which causes vertigo.15 The classic symptoms of BPPV are brief episodes of vertigo, associated with nausea and nystagmus.

The episodes of vertigo are triggered by rapid changes in the position of the head.1 Symptoms can last for weeks and recur after remission. Nystagmus seen in BPPV has a rotational nature.1 The Dix−Hallpike manoeuvre is used to diagnose BPPV. In contrast, the Epley manoeuvre can be used to treat BPPV (Box 1).1 This procedure is performed in an attempt to dislodge the otoliths from the semicircular canals. It has a 77% success rate on the initial attempt and 100% on further attempts.15

Box 1. Epley manoeuvre for treatment of BPPV
  1. Sit the patient on the bed.
  2. With the neck hyperextended and laterally rotated to 45 degrees, the patient is asked to lie supine.
  3. The patient is required to maintain the supine position for one minute.
  4. The head is turned to the opposite side with lateral rotation of 45 degrees, and remains in this position for one minute.
  5. The head, chest and pelvis are tilted downwards to 135 degrees (almost prone), and this position is maintained for one minute.
  6. Quickly sit the patient upright with their head tilted to the affected side.

This manoeuvre should not be performed in patients with neck injury, carotid stenosis and heart disease1

Acute labyrinthitis

The inner ear is composed of the bony and the membranous labyrinth. Acute labyrinthitis is inflammation of this labyrinth. It presents with vertigo and hearing loss, preceded by a viral infection.16 Middle ear infections can spread to the inner ear and cause labyrithitis. The duration of symptoms ranges from days to weeks. Hearing loss is the main distinguishing factor between labyrithitis and BPPV. Typically, no treatment is required for labyrithitis. However, if suppurative labyrinthitis is suspected, the patient should be referred to the emergency department for drainage of otitis media.17

Ménière’s disease

Ménière’s disease is an uncommon cause of vertigo.18 It is thought to be caused by increased fluid in the endolymph part of the cochlea, which eventually affects the semicircular canals.18 In most patients, the aetiology is unknown.18 Ménière’s disease is commonly seen in women, and the incidence increases in men and women after the age of 60 years.18

Ménière’s disease classically presents with episodes of vertigo lasting longer than 20 minutes, tinnitus, sensorineural hearing loss and aural fullness. Eventually, hearing loss becomes permanent. Pure tone audiometry is the most useful test to assess sensorineural hearing loss.

There is no known cure for Ménière’s disease and treatment is primarily symptomatic.19 Betahistine is the current mainstay of treatment. Surgical treatment options exist; however, most patients are adequately managed with medical treatment.

Vestibular neuronitis

VN is caused by inflammation of the vestibular nerve. This inflammation precedes a viral URTI or herpes zoster infection and is caused by immune-mediated sequelae following the viral illness.15 It is commonly seen in middle-aged adults of both sexes.8 VN often occurs in epidemics during outbreaks of respiratory infections.15 The main characteristic of VN is an acute onset of vertigo without hearing loss or tinnitus. Similarly to BPPV, symptoms of vertigo are aggravated by a change in the position of the head. Loss of balance is more prominent in VN, compared with other causes of vertigo, and patients may commonly present with falls.

Initially, the vertigo is severe, lasts for two to three days and is followed by gradual recovery, which may take two to six weeks.20 Bed rest and antiemetics can be used in the first 24–72 hours. Patients can be reassured that symptoms will improve with time.20


Blood tests are not routinely ordered for patients presenting with vertigo. However, it is recommended that glucose levels of all patients with vertigo should be checked.21 Radiological tests including computed tomography (CT), magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) are indicated if:

  • the examination is not consistent with a peripheral lesion
  • prominent risk factors for CVA are present
  • neurological signs and symptoms are present, or
  • symptoms of vertigo are accompanied by a headache.

In these cases, referral to a neurologist is recommended.22,23


Treatment is tailored to the specific causes of vertigo. Antiemetic medications such as betahistine are used for symptomatic management of acute vertigo. These medications should not be used long term. Patients should be warned about the side effects of drowsiness, dry mouth and blurred vision. Benzodiazepines are not indicated and should be avoided because of their addictive nature.16,24

Lifestyle changes including salt restriction and avoiding alcohol and coffee are recommended.24 Assessment and management of the patient’s risk of falls is important in vertigo. Referral to an experienced physiotherapist for vestibular rehabilitation can help prevent recurrences.16 Exercises prescribed by physiotherapists involve moving the eye balls up and down and sideways in a supine or sitting position. Balance stabilisation exercises help to regain normal activities faster.24

Patients should be referred for specialist review if they have symptoms of continuous vertigo, progressive hearing loss, severe ongoing headache, cerebellar signs or if the diagnosis is not clear.7

Key points

  • Vertigo is a common presentation in general practice.
  • A careful history is required to elicit features of central or peripheral causes of vertigo.
  • Serious causes including CVAs and MS need to be considered.
  • Physical examination involves a neurological, cardiovascular, eye and ear examination.
  • Treatment is specific to the cause of vertigo.

Sindhu Dommaraju MBBS, FRACGP, DCH, General Practitioner, University of Newcastle, Callaghan, NSW. [email protected]

Eshini Perera MBBS, BMedSci, MMed, MPH, FRACGP, Dermatology Registrar, University of Melbourne, Parkville, VIC

Competing interests: None.
Provenance and peer review: Not commissioned, externally peer reviewed.


AFP Clinical Dommaraju Vertigo updated (PDF 144 KB)

Post-COVID-19 Benign Paroxysmal Positional Vertigo

Background. COVID-19 is a disease caused by a new strain of coronavirus (SARS-COVID-19). The WHO first learned about this new virus on December 31, 2019, following a report on a group of cases of “viral pneumonia” in Wuhan, People’s Republic of China, and declared a pandemic in March 2020. The disease was an almost complete unknown at the outset, but knowledge of its pathophysiology, clinical picture, and treatment options grew and developed rapidly. Objective. Dizziness is a very common symptom that patients report in routine clinical practice and one of the significant clinical manifestations of COVID-19. This short report investigated a possible connection between COVID-19 and benign paroxysmal positional vertigo (BPPV). Methods. We present two cases of benign paroxysmal positional vertigo (BPPV), which developed within two weeks of SARS-COVID-19 infection, manifesting with mild disease severity in early November 2020. Results. In both cases, the disease manifested by severe, short-lived attacks of vertigo, objective-circular type, with accompanying nausea and vomiting. The symptoms occurred when lying in bed and turning to the right and assuming an upright position. The diagnosis of posterior semicircular canal BPPV (PC-BPPV) was made based on a subjectively and objectively positive right-sided Dix–Hallpike test. Conclusions. The pathophysiology of post-COVID BPPV is probably similar to that of other viral infections, with some of its specificities such as inducing hypercoagulation and microthrombus formation, which can cause significant circulatory disorders possibly affecting its pathogenesis.

1. Introduction

Coronavirus disease-19 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-COVID-19). The WHO declared a pandemic of this virus in March 2020 after its rapid spread from the city of Wuhan, in the province of Hubei in China [1]. It has been shown that, in addition to the most common clinical symptoms of the disease, such as dry cough, fever, and general weakness, some patients develop taste and smell disorders, headaches, congestion of the nasal mucosa, gastrointestinal disorders, and dizziness. A small proportion of patients may develop significant complications such as bilateral pneumonia, accompanied by shortness of breath, chest pain, and a characteristic finding of ground-glass opacity on CT, which indicates severe viral pneumonia [2, 3].

The infection can affect the central nervous system, and neurological symptoms can appear both in the initial disease stages and in the protracted recovery period. Most patients experience, to a greater or lesser extent, neurological and psychological symptoms, ranging from insomnia, anxiety, and depression to disturbances of consciousness, confusion, and epileptic seizures.

Among neurological complications, the most common are encephalopathy and cerebrovascular stroke, disorders of consciousness, seizures, and hypoxic brain injuries. Dysosmia and dysgeusia and nonspecific symptoms such as headache, dizziness, and paresthesia have been reported. Dizziness is a very common symptom that patients report in routine clinical practice [4].

Numerous studies, appearing daily from various parts of the world, have revealed vertigo as one of the significant clinical manifestations of COVID-19. One of them cites vertigo as the most common neurological manifestation of COVID-19, thought to follow the neuroinvasive potential of the virus [5]. Some researchers hypothesized that the virus enters neuronal tissue from the circulation and binds angiotensin-converting enzyme 2 receptors (ACE2), which are located in the capillary endothelium. Other mechanisms that lead to dizziness during COVID-19 infection are direct inflammatory action of the virus on nervous tissue, indirect immune response, hypoxia, and hypercoagulopathy [5].

After performing a literature search of PubMed and Google Scholar databases to identify published cases of vertigo associated with COVID-19, three case reports and 11 studies listing vertigo and COVID-19 were identified. Out of these 14 studies, only two investigated vertigo as a presenting symptom, and only one noted vestibular rehabilitation treatment details and disease outcome [6]. Vertigo presented as an initial COVID-19 symptom in three patients and followed respiratory symptoms in two patients [7].

The most important element in this case report is the consideration of possible causes and disease course of post-COVID BPPV. A thorough literature review shows that BPPV may be associated with COVID-19 by a specific mechanism of etiopathogenesis.

Our case report was assembled following CARE (CAse REport) guidelines and the Institutional Review Board according to the Helsinki Declaration of 1983. Written informed consent for publication was obtained from both patients.

2. Case Presentation
2.1. Case 1

This report lists two very similar cases of post-COVID-19 BPPV. The first is a 41-year-old female patient that was diagnosed with COVID-19 in early November 2020. She was tested for SARS-COVID-19 using a PCR test (nasopharyngeal swab) positive on November 5 and 20, 2020, and tested negative on November 30, 2020. Apart from fever up to 37.2 °C and severe pain in her legs, she did not develop most of the common symptoms of COVID-19, such as high fever, dry cough, shortness of breath, and a sudden loss of smell and taste. She did not receive any drugs, and a chest CT scan was not performed because she did not have any significant respiratory problems. She returned to work in early December, and a week later developed severe, short-lived attacks of objectively circular dizziness, usually when getting out of bed or turning on her right side that lasted for six days, followed by nausea and vomiting. Initially, she also had severe occipital headaches that spread to her neck, which subsided after the first few days of illness. Upon initial examination by her GP, she was referred to a neurologist. Dizziness subsided after the first few days of illness. Among the laboratory findings, only serum K+ level was decreased (3.7 mmol/L), attributed to a loss of body fluid by vomiting. She was afebrile, normotensive, independently mobile, and eupneic. Her neurological status was normal. The neurologist concluded that it is a case of peripheral vertigo and referred the patient to an otorhinolaryngologist. The patient did not have hearing problems, denied tinnitus, and complained of a moderate occipital headache. She was on bisoprolol therapy previously due to tachycardia, diagnosed after her third pregnancy in 2017. A neurotological assessment showed negative spontaneous nystagmus, and head impulse and skew deviation tests were also negative. The Romberg test with the open and closed eyes was without lateralization, as well as the Fukuda test. A diagnosis of right-sided posterior semicircular canal canalithiasis (PC-BPPV) was made based on a positive Dix–Hallpike test [8, 9]. In the right position, after a latency of ten seconds, dizziness and nausea occurred, and objectively, a small vertical-torsional geotropically directed positional nystagmus (PN) was observed, lasting for 5 seconds. When returning to a sitting position, dizziness increased, with nausea and PN becoming more pronounced. A right-sided Epley repositioning procedure was performed twice in one session, after which the patient no longer had symptoms [10]. The patient was alerted to the possible occurrence of an otolithic crisis during the first 24 h after performing the Epley procedure. The patient was advised to test her serum vitamin D3 levels and to follow up in a week.

2.2. Case 2

Similarly, the second 28-year-old female patient was also diagnosed with a mild form of COVID-19 on November 7 and tested negative on November 20, 2020. She underwent an antigen test using the SARS-COVID-19 IgG method: Abbott Architect i2000-CMIA 18.12. 2020, which was positive, at the level of 8.18 (recommended values: <1.4). In the first days of the disease, the dominant symptom was a moderate frontal headache, followed by muscle and joint pain, diarrhea, vomiting, and general weakness. Therefore, she occasionally took 400 mg of ibuprofen p.o. As with the former patient, she did not experience the most common symptoms of coronavirus disease, such as fever, dry cough, shortness of breath, loss of smell and taste, or a change in taste. Short-lived, but intense attacks of objectively circular dizziness, accompanied by nausea when turning to the right side and getting out of bed, occurred on December 20, 2020, about one month after being diagnosed with COVID-19. She is otherwise healthy, does not have hearing complaints, denies tinnitus, and sometimes has moderate frontoparietal headaches. During the clinical examination, a test of spontaneous nystagmus, head impulse, and skew deviation were negative. The Romberg test with the open and closed eyes was without lateralization, as well as the Fukuda test. The Dix–Hallpike test was subjectively and objectively positive on the right side upon a return to the sitting position. After a latency of a few seconds, dizziness and nausea occurred, and a rough, geotropically oriented vertical-torsional PN is observed, lasting about 15 seconds. A diagnosis of PC-BPPV was made, and a right-sided Epley repositioning procedure was performed on two occasions in one session. After the second iteration, the patient was symptom-free, and PN could not be observed. This patient was also advised to test her serum vitamin D3 levels and to follow up in a week. The patient was also alerted to the possible occurrence of an otolithic crisis during the first 24 h after performing the Epley procedure.

3. Discussion

The COVID-19 pandemic has brought with it many new issues and intensified many previously known health-related, economic, and social problems. The disease is predominantly characterized by an acute respiratory disorder but also causes several neurological symptoms, including disorders of smell and taste, headache, and dizziness (up to 20% of patients). Treatment of the infection itself has so far been largely limited to attempts to coadminister azithromycin and hydroxychloroquine, as well as symptomatic treatment and management of complications, while corticosteroids are used often, but mostly nonrationally, as they should be reserved for more severe disease instances [11]. Similarly, treatment of vertigo during COVID-19 is primarily concerned with symptomatic treatment using antiemetics, antihistamines, and sedatives.

The emergence of post-COVID-19 vertigo, alongside other post-COVID-19 conditions, is a new development. In this article, we presented two very similar cases of PC-BPPV a few weeks after overcoming the milder clinical form of COVID-19. In the future, we can expect a greater number of post-COVID vertigo patients, and the differential diagnosis of acute-onset vertigo should include BPPV and vestibular neuronitis as a consequence of SARS-COVID-19 infection. In the case of chronic persistent postural-perceptive vertigo (PPPD) and other functional vestibular disorders, a significant increase in patients seen by vestibular specialists may also be expected, due to the pronounced impact of the COVID-19 pandemic on both physical and mental health.

BPPV represents 17.1% of the total number of dizziness complaints in the general population, while in the elderly this share rises to approximately 50% [12, 13]. von Brevern et al. found that BPPV is responsible for 8% of moderate or severe vertigo, with a lifetime prevalence of 2.4%, while a one-year prevalence is 1.6%, and an incidence of 0.6% [14].

The BPPV pathophysiology may be explained by two cardinal theories, cupulolithiasis and canalithiasis. The understanding of metabolic mechanisms that regulate the level of calcium, proteins, and mucopolysaccharides involved in the construction of the otolithic membrane, which disrupts the rupture of adhesive bonds that hold otoliths together may also shed new light on the emergence of post-COVID BPPV [15–17]. It is known that the elderly suffer the most from BPPV due to degenerative changes in the macula of the utriculus, probably due to lower calcium levels in the endolymph and reduced number and volume of otoliths. Most cases of BPPV are idiopathic in origin and probably result from a degeneration of the macula. The secondary BPPV causes refer to the identifiable causes of otoconial dislodgement. Apart from otologic and nonotologic surgery, head trauma, vestibular neuritis, Meniere’s disease, and a sudden sensorineural hearing loss may also cause the BPPV. However, in younger patients, such as our two cases, other pathophysiological mechanisms come into consideration [18, 19].

Viral labyrinthitis is responsible for the occurrence of about 15% of BPPV which occurs due to the detachment of otoliths from the utriculus, either by the direct action of inflammatory elements near the macula or indirectly, due to disorders of labyrinthine microcirculation, representing viral ganglionitis. Neuropathologic changes (focal axonal degeneration and vestibular ganglion cell loss) and a high incidence of cupular basophilic deposits seen in the patients’ temporal bones with a known BPPV weaken a purely mechanistic concept of BPPV symptoms. A recently reported quantitative study involving five patients with the BPPV has revealed a significant degeneration (50%) of both the superior and the inferior divisions of the vestibular ganglion and a small cupular deposit in only one patient, supporting neural injury as the principal etiopathogenetic pathway, easily caused by viral neurotoxicity [19, 20]. In the case of COVID-19, it is a very specific viral infection, accompanied by the formation of microthrombi in the circulation, possibly explaining the occurrence of BPPV after the initial phase of the SARS-COVID-19 infection. However, as the blood supply to the inner ear courses through the a. labyrinthi (a. auditoria interna), the end branch of the anterior inferior cerebellar artery (a. cerebelli anterior inferior-AICA), its loss of function would cause hearing loss, which challenges this concept of BPPV attributed to microcirculation issues. However, there are reports of otoconia being displaced due to vasospasms in the circulation of the inner ear [21]. The mechanisms behind the otoconia degeneration and displacement are still unclear. The proinflammatory regulators are activated during a viral inflammatory process. Nuclear factor kappa-light-chain-enhancer of the activated B cells (NF-κB) is one of the most widely known mediators controlling proinflammatory signaling and has been correlated with an increased expression in various inflammatory conditions, including viral infections such as the COVID-19 [22]. A possible cause of post-COVID BPPV could be prolonged bed rest, as it has long been known that otoconia rupture can occur due to insufficient movement, probably due to hypercoagulability. Although Mao et al. state that neurological symptoms occur much more frequently in patients with a more severe acute respiratory syndrome, both of our patients had a very mild COVID-19 and yet developed BPPV a few weeks after the resolution of disease symptoms [23].

As prevention of recurrence of BPPV, and with limited rationale, in preventing severe forms of COVID-19, vitamin D3 is used to a greater extent worldwide, due to its low level in the general population, and also very small side effects [24, 25].

Although the neurotropic nature of SARS-COVID-19 has been known since the beginning of the pandemic, data on neurologic symptoms have been scarce to date, save dysosmia. Few studies evaluated vertigo as a presenting symptom. There is currently no evidence of post-COVID-19 BPPV in the available medical literature, and this report aims to encourage others to evaluate post-COVID-19 patients presenting with vestibular symptoms comprehensively, reducing the number of delayed referrals and misdiagnosed patients.

Data Availability

The data used to support the findings of this study are available from the corresponding author upon request.


Consent was obtained from all participants in this study.


All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Conflicts of Interest

All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work.


In compliance with the ICMJE uniform disclosure form, all authors declare the following: payment/services info: all authors have declared that no financial support was received from any organization for the submitted work.

Vertigo – an overview | ScienceDirect Topics


Vertigo is an illusion of motion, usually rotational, of the patient or the patient’s surroundings. The clinician responsible for evaluating this problem should consider a differential diagnosis, with special attention to whether the vertigo is central or peripheral in origin. A large number of entities cause vertigo, ranging from benign and self-limited causes such as vestibular neuritis and BPPV to immediately life-threatening causes such as cerebellar infarction or hemorrhage. In general, the more violent the sensation of vertigo and the more spinning, the more likely that the lesion is peripheral. Central lesions tend to cause less intense vertigo and more vague symptoms. Peripheral causes of vertigo or nystagmus include irritation of the ear (utricle, saccule, semi-circular canals) or the vestibular division of the eighth cranial (acoustic) nerve caused by toxins, otitis, viral infection, or cerumen or a foreign body lodged against the tympanic membrane. The term labyrinthitis should be reserved for vertigo with hearing changes, and the term vestibular neuronitis should be reserved for the common, transient vertigo, without hearing changes, that is sometimes associated with upper respiratory tract viral infections. Paroxysmal positional vertigo may be related to inappropriate particles (free-floating debris or otoliths) in the endolymph of the semicircular canals. If it occurs after significant trauma, suspect a basal skull fracture with leakage of endolymph or perilymph, and consider otolaryngologic referral for further evaluation.

The vestibular nerve is unique among the cranial nerves in that the neurons in this nerve, on each side, are firing spontaneously at 100 spikes/sec with the head still. With sudden loss of input from one side, there is a strong bias into the brain stem from the intact side. This large bias in neural activity causes nystagmus. The direction of the nystagmus is labeled according to the quick phase, but the vestibular deficit is actually driving the slow phase of nystagmus.

Vestibular neuritis is preceded by a common cold 50% of the time. The prevalence of vestibular neuritis peaks at 40 to 50 years of age. Vestibular neuritis is probably similar to Bell’s palsy and is thought to represent a reactivated dormant herpes infection in the Scarpa’s ganglion within the vestibular nerve. Viral labyrinthitis can be diagnosed if there is associated hearing loss or tinnitus at the time of presentation, but the possibility of an acoustic neuroma should be kept in mind, especially if the vertigo is mild.

Central causes include multiple sclerosis, temporal lobe epilepsy, basilar migraine, and hemorrhage or infarction or tumor in the posterior fossa. Patients with a slow-growing acoustic neuroma in the cerebellopontine angle usually do not present with acute vertigo but rather with a progressive, unilateral hearing loss, with or without tinnitus. The earliest sign is usually a gradual loss of auditory discrimination.

Vertebrobasilar arterial insufficiency can cause vertigo, usually with associated nausea, vomiting, and cranial nerve or cerebellar signs. It is commonly diagnosed in dizzy patients who are older than 50 years of age, but more often than not the diagnosis is incorrect. The brain stem is a tightly packed structure in which the vestibular nuclei are crowded in with the oculomotor nuclei, the medial longitudinal fasciculus, and the cerebellar, sensory, and motor pathways. It would be unusual for ischemia to produce only vertigo without accompanying diplopia, ataxia, or sensory or motor disturbance. Although vertigo may be the major symptom of an ischemic attack, careful questioning of the patient commonly uncovers symptoms implicating involvement of other brain stem structures. Objective neurologic signs should be present in frank infarction of the brain stem.

Nystagmus occurring in CNS disease may be vertical and disconjugate, whereas inner-ear nystagmus never is. Central nystagmus is gaze directed (beats in the direction of gaze), whereas inner-ear nystagmus is direction fixed (beats in one direction, regardless of the direction of gaze). Central nystagmus is evident during visual fixation, whereas inner-ear nystagmus is suppressed.

A peripheral vestibular lesion produces unidirectional postural instability with preserved walking, whereas an inferior cerebellar stroke often causes severe postural instability and falling when walking is attempted.

If vertebrobasilar arterial insufficiency is suspected in an elderly patient who has no focal neurologic findings, it is reasonable to place such a patient on aspirin and provide him with prompt neurologic follow-up.

Either central or peripheral nystagmus can be caused by toxins, most commonly alcohol, tobacco, aminoglycosides, minocycline, disopyramide, phencyclidine, phenytoin, benzodiazepines, quinine, quinidine, aspirin, salicylates, NSAIDs, and carbon monoxide.

Vertigo in an otherwise healthy young child is usually indicative of benign paroxysmal vertigo that may be a migraine equivalent, especially when associated with headache.

Benign Paroxysmal Positional Vertigo Treatment NYC | Mount Sinai

Benign paroxysmal positional vertigo (BPPV) is a very common cause of vertigo, or head spinning, caused by loose particles (“crystals”) of calcium in the inner ear. The vertigo is brief, disturbing, and brought on by a change in head position. It is abrupt, intense, and sometimes violent, and is occasionally accompanied by nausea. It lasts for a few seconds, but the after-effect can be longer.

The typical attack is brought on by lying back quickly with the head turned to one side. It can also be brought on by bending, stooping, turning in bed, reaching for the top shelf, or working under a car. It does not occur while stationary.

At Mount Sinai, our hearing and balance exerts have been treating BPPV for decades and find that in most cases, BPPV can be treated effectively. Other causes for vertigo exist, however, and a neurotologist specialized in balance disorders can usually make the proper diagnosis and prescribe an effective treatment.

Causes of BPPV

BPPV is caused by loose particles of calcium in the inner ear. The calcium particles are microscopic crystals that are normally attached to one of the balance organs in the inner ear. In BPPV, these particles drift into one of the balance canals, where they don’t belong. Tilting the head quickly causes the particles to move, stimulating the nerve receptors in that balance canal and creating the false sensation of movement (vertigo).

The condition usually comes about for no known reason. Occasionally it can be caused by a head injury or an ear infection. BPPV should be differentiated by other causes of vertigo that may not be as easy to treat.

Treatments for BPPV

BPPV can be effectively treated in most cases by a physical maneuver that is performed in the office. The particle repositioning maneuver (also called the Epley maneuver, after the doctor who devised it) redistributes the particles of calcium that cause the vertigo. The procedure is effective in a single session in a large percentage of cases. The remainder usually improve after a second session.

The particle repositioning maneuver is illustrated below. With the patient seated, the head is first brought into the position that triggers the vertigo. After the vertigo is allowed to pass, the head is then rotated 180o to the opposite position, allowing the calcium crystals to disperse into an area of the ear where they no longer cause vertigo. The patient is then brought upright, and after a pause, the maneuver is repeated to be certain that it was effective in clearing the problem.

After the procedure, the patient is instructed to sleep at home in a semi-reclining position (two pillows under the back), for at least two nights.

If the procedure doesn’t work, the procedure is effective in most cases. If the vertigo persists after one treatment, a second maneuver in the office is usually effective. In a few cases, the vertigo will not respond to this treatment, or it may improve temporarily and then recur. In these cases, home balance exercises or treatment by a physical therapist may be prescribed. In rare cases that don’t respond to these measures, surgical treatment can be effective.

90,000 Thoughts that can kill you

  • David Robson
  • BBC Future

Photo author, Getty

Sometimes the very thought that a person is sick can kill him. As David Robson found out, we can unconsciously pick up fears that will have dire consequences for us.

Beware of alarmists. Their words, like the spells of a shaman, can turn into epidemics.

It is well known that waiting for illness can be more dangerous than it is.For example, voodoo shamans harm their victims with the power of suggestion, making the person believe they are sick, which often causes actual symptoms of the disease.

The power of persuasion can cause vomiting, dizziness, headaches and even death. This phenomenon is called the “nocebo effect” (a drug that has no real pharmacological effect, but causes a negative reaction in the patient. – Red .).

Today we understand how easily these dangerous beliefs can be spread through gossip and be devastating.This explains why some families seem to be doomed to serious illness, and why people living near wind turbines suffer mysterious bouts of dizziness, insomnia, and nausea.

If after vaccination you feel that you will soon fall ill, your mobile phone

causes a headache or you suffer from an unexpected food allergy, you may also be a victim of the nocebo effect.

“The nocebo effect demonstrates the power of the brain,” says Dimos Mitsikostas of the Athens Naval Hospital in Greece.“We cannot fully explain it yet.” They decided to teach the annoying assistant a lesson and warned him that a block was waiting for him. They blindfolded the poor man, bent his head and threw a damp cloth around his neck. Convinced that a steel blade had touched him, the man “died on the spot.”

Although there are many such stories, modern researchers tend to focus on the ability of the mind to heal disease rather than harm the body. This is the so-called “placebo effect” – from the Latin “I will like”.

Photo by Thinkstock

During clinical trials, patients are randomly assigned to either a real drug or a placebo pill that has no pharmacological effect. Patients who take false medications and do not know it often see improvement in their condition solely due to their faith in the treatment.

But along with the improvement, people who take a placebo often report mysterious side effects – nausea, headache, discomfort, which are unlikely to cause an “empty” pill. The point is that patients receive the same warning of possible side effects during clinical tests, whether they are receiving a real drug or a placebo.

So, waiting for symptoms in some patients causes them to appear. “It’s a systematic phenomenon, but medicine has never really addressed it,” says Ted Kapchuk of Harvard Medical School.

Over the past decade, doctors have proven that the nocebo effect – from the Latin for “I will harm” – is quite common. After reviewing the medical literature, Dr. Mysticostas found that the nocebo effect often appears during the treatment of headaches, multiple sclerosis, or depression.

Photo author, Getty

In progress

studies 65% of patients with Parkinson’s disease reported negative side effects of placebo. “About one in ten subjects dropped out of the study because of the nocebo effect, which is very high,” says the researcher.

Although most side effects are subjective, such as nausea or pain, the nocebo effect sometimes appears physically in the form of rashes, itching, or even changes in physiological parameters. “It’s hard to believe. People take sugar pills, and their liver enzymes increase,” says Dimos Mitsikostas.

If you think patients are just imagining side effects, you are wrong.

Measurements of neural activity in the nocebo effect have shown that the spinal cord begins to respond to increased pain before a person can realize it.

Author of the photo, Getty

Consider the almost fatal incident with Mr. A, which was reported by Dr. Roy Reeves in 2007. Mr. A, who was suffering from depression, drank a whole bottle of pills. But immediately repenting, he rushed to the hospital and passed out right in the waiting room. The situation looked serious – a sharp drop in blood pressure, hyperventilation. The victim was immediately given an intravenous infusion.

However, blood tests did not reveal any traces of drugs in his body.Four hours later, Dr. Reeves was informed that the man was participating in a medical experiment and the only “overdose” that could happen was an overdose of sugar pills. Hearing this news, Mr. A was greatly relieved and soon recovered.

It is not known if the nocebo effect could actually kill Mr. A, but Dr. Fabrizio Benedetti of the University of Turin School of Medicine believes it is possible.

Brain scans of subjects who were under the influence of the nocebo effect showed a chain reaction in the hypothalamus, pituitary and adrenal glands – areas of our body that respond to extreme threats.If the fear and beliefs are strong enough, the hormone cocktail that is produced in the body can be deadly, he says.

Rumors of sickness

The idea that your doctor might accidentally make you sick is rather disturbing. More recently, scientists have found that it doesn’t take much to spread the nocebo effect. Even ordinary rumors can tune your mind to illness.


of the experiment, Dr. Benedetti invited about 100 students to a hike in the Italian Alps, which included an ascent of 3 thousand meters.meters. A few days before the trip, he told one participant that thin air can trigger migraines. On the day of the trip, it turned out that more than a quarter of the participants found out about this, and it was they who had the most headache during the trip.

Photo Credit, Getty

Moreover, analyzes of their saliva showed an overreaction to low oxygen levels, in particular increased levels of enzymes associated with altitude sickness. “The brain biochemistry of the ‘socially infected’ participants changed,” explains Dr. Benedetti.

In other words, harmful opinions that speak of illness can be contagious. “Negative expectations that are conveyed by friends, neighbors and others are spreading rapidly, causing a social nocebo effect for a large number of people,” says Benedetti.

One study found that watching another patient feel pain during treatment makes the treatment more painful. So, the nocebo effect is transmitted from person to person just through observation.Even more disturbing is that

the fact that the nocebo effect can spread unconsciously.

Photo author, Getty

History has many examples. the most famous is the dance plague of 1518 (about 400 people danced non-stop for almost a month, with the result that some died of heart attack or exhaustion. – Ed. ).

Another example is the so-called June Beetle, an epidemic in an American textile factory in the 1960s that caused widespread cases of dizziness and vomiting, although none of the poisonous insects rumored to have caused the disease were found.

Often, fear of new technology has a similar effect. In the late 19th century, early telephone users reported dizziness and pain after using the device. And Scandinavian workers in the 1980s often had rashes of obscure origin, which they believed were caused by computer monitors.

Today, the nocebo effect is manifested in such controversial diseases as ”

wind turbine syndrome “(discomfort and insomnia, which are mainly complained of by residents of Canada).Or “electro-sensitivity” – an allergic reaction to signals from mobile phones and Wi-Fi.

Some people even sleep in metal cocoons to avoid constant ringing in their ears. However, dozens of experiments have shown that people report the same symptoms when they are near a dummy device that does not actually emit any electromagnetic waves.

While nocebo is not a true disease, we should not underestimate the physical distress it causes.

Photo by Thinkstock

“I have no doubt that people do experience physical symptoms,” says James Rubin of King’s College London. Even the former head of the World Health Organization suffered from this syndrome. She

banned the use of cell phones in her office because she believed they caused her migraines. “

Other cases of nocebos include mysterious food intolerances. For example, 20% of British people say that their stomachs do not accept certain types of food, although medical tests show that only a tenth of them actually have nutritional problems.Nocebo may also explain why people often suffer from side effects after a placebo vaccine and are confident that

birth control pills cause depression, headache and chest pain, although scientific studies have largely found no evidence of this.

What can be done? Of course, it is very difficult to overcome long-standing beliefs, but responsible media action can at least stop the spread of poisonous new rumors.

Photo author, Getty

What about doctors? Rebecca Wells of Wake Forest University Medical Center in North Carolina believes this is the most important dilemma in modern medicine.On the one hand, doctors are required to report possible side effects of the drug – they must obtain “informed consent” from the patient, but on the other, this

information can be harmful.

In the future, the researcher believes, physicians will need to develop new procedures for how to tell patients about side effects, and what exactly they can tell them. Adequate attention to this issue is critical, as side effects in one person can be epidemic.

Communication and education are beneficial. Dr. Mitsikostas, for example, tries to explain to patients that they must beware of their own expectations. “Our patients need to understand that they have to fight their inner fear,” he says.

We cannot ignore the connection between mind and body, despite the amazing advances in modern medicine. “For millennia, medicine has been a placebo – magicians have used the power of persuasion and hope to strengthen the patient’s will to get better,” says Dr. Mitsikostas.“This is not enough to overcome the disease, but this strength is an integral part of the cure.”


the original of this article in English you can visit the website

BBC Future.

Meniere’s disease

Meniere’s disease is a non-inflammatory disease of the inner ear, in which excess fluid accumulates in the ear. The name of the disease comes from the name of the doctor who first described its symptoms.Mostly middle-aged people suffer from this disease; Meniere’s disease is rare among children.


Experts identify several possible causes leading to the disease:
• Consequence of an infectious disease, after which the body’s immune system malfunctions;
• Injuries, osteochondrosis of the cervical spine, in which the circulation of fluid in the inner ear cavity is impaired;
• Vascular disorders;
• Increased production of endolymph;
• Heredity.


The main symptoms of Meniere’s disease are dizziness, nausea and vomiting. The dizziness is so strong that it is difficult for the patient to stand and sit, he wants to lie with his eyes closed. Any movement increases the nausea and increases the retching urge.
There is a lack of coordination of movements and loss of balance. The patient’s hearing worsens, his ears are noisy and seem to be bursting inside.
The duration of an attack lasts a few hours on average, but may even last for several days.After an attack, the symptoms do not disappear sharply, tinnitus, hearing impairment, loss of coordination, and weakness persist. As the disease progresses, the symptoms described become more pronounced. The frequency of attacks fluctuates: some may recur several times a day, others suffer once a month or a year.
Above, we examined the possible cause of Meniere’s disease itself. Along with this, experts identify possible causes of the manifestation of the attack itself. It should be noted that in each patient, dizziness can be provoked by various reasons.The most common of them:
• stress and overwork;
• loud sound, pungent odor, bright light;
• infections and diseases of ENT organs, fever;
• tobacco smoke;
• overeating.

Diagnostics and treatment

If you suspect you have Meniere’s disease, you need to consult a neurologist or an otorhinolaryngologist. Before visiting the doctor, try to remember how you felt during the attack, before and after it, as well as what could have provoked it.
The specialist will conduct an examination, analyze the general clinical picture, anamnesis, conduct several tests, including checking the hearing, and diagnose vestibular disorders.
It is very important to distinguish Meniere’s disease from other diseases with similar symptoms. In addition, cases of dizziness in which hearing loss does not occur are referred to as Meniere’s syndrome. In this case, it is necessary to find the underlying disease.

Be healthy!

Vascular surgery

Vascular surgery
Is a branch of medicine aimed at diagnostics, treatment and prevention of diseases of large great vessels and the lymphatic system.

The most common problem with which a vascular surgeon is consulted is atherosclerosis and its complications.

Atherosclerotic vascular lesions, the formation of cholesterol plaques leads to a narrowing of their lumen, which impedes blood flow. This causes a disruption in the blood supply to the organ whose vessels are affected by the disease, which in turn can lead to loss of functionality and tissue necrosis.

In addition to atherosclerosis, the vascular surgeon is engaged in:

  • arterial diseases
  • vein problems
  • vascular injuries, embolism of arteries and veins
  • vascular lesions responsible for the blood supply to the brain
  • Contact a vascular surgeon should appear:

  • headache
  • noise in the head and ears
  • frequent dizziness
  • cases of loss of consciousness
  • edema
  • convulsive manifestations
  • tingling in the legs
  • burning sensation in the muscles
  • violation of sensitivity
  • spider veins
  • fast fatigability
  • feeling of heaviness in the limbs
  • Don’t wait until illness forces you to see a cardiovascular surgeon.Vein problems are severe with long-term treatment.

    It is important to remember that a timely visit to the doctor’s cardiovascular surgeon will help to identify the disease at the earliest stages and prevent its progression.

    For more information and to make an appointment with a doctor, call (88712) 29-26-47

    Prices for a doctor’s consultation at the AyMed clinic:

    Appointment (examination, consultation) of a cardiovascular surgeon, primary 2000



    Primaxetin® is intended only for men with premature ejaculation.The safety of using the drug in men without premature ejaculation has not been established, there is no data on delayed ejaculation.

    Taking together with narcotic drugs

    Patients should be advised not to take Primaxetin® together with narcotic drugs. Concomitant use of Primaxetin® with drugs with serotonergic activity, such as ketamine, methylenedioxymethamphetamine (MDMA) and lysergic acid diethylamide (LSD), can lead to potentially serious reactions, including but not limited to arrhythmia, hyperthermia, and serotonin syndrome.Taking Primaxetin® together with sedatives such as opiates or benzodiazepines may increase drowsiness and dizziness.


    The combination of Primaxetin® with alcohol may increase the effect of the latter on the central nervous system and the neurocardiogenic side effects of alcohol, such as fainting, which increases the risk of accidental injury. Therefore, patients should be advised to refrain from drinking alcohol while taking Primaxetin®.


    The frequency of fainting in clinical trials of Primaxetin® depended on the category of patients and ranged from 0.06% (for a dose of 30 mg) to 0.23% (for a dose of 60 mg) to 0, 64% (for both doses combined) in a study in healthy volunteers.

    Patients receiving Primaxetin® were more likely to have prodromal symptoms, including nausea, dizziness / lightheadedness, and sweating, than those receiving placebo.At a dose of Primaxetin® 30 mg, the frequency of nausea was 11.0%, the frequency of dizziness was 5.8%, and hyperhidrosis was 0.8%. At a dose of the drug Primaxetin® 60 mg, these figures were 21.2%, 11.7% and 1.5%, respectively. The incidence of syncope and possible prodromal symptoms was dose-dependent, as evidenced by the higher rates in patients receiving higher doses than the maximum recommended daily dose of 60 mg. The cases of syncope observed in clinical studies were regarded as having a vaso-vagal nature.Most of these cases occurred within the first 3 hours after taking the first dose, or were associated with conducting research procedures in a clinical setting (for example, taking a blood sample, standing up suddenly, measuring blood pressure). Possible prodromal symptoms, such as nausea, dizziness, lightheadedness, palpitations, asthenia, confusion and sweating, were usually also observed in the first 3 hours after taking the drug and often preceded fainting.Patients should be informed that during the period of treatment with Primaxetin® at any time, fainting may develop with or without prodromal symptoms. The clinician should educate the patient about the importance of adequate water loading and recognizing prodromal signs and symptoms to reduce the risk of serious fall injury due to loss of consciousness. If possible prodromal symptoms appear, the patient should immediately lie down so that the head is below the torso, or sit with the head bowed between the knees, and should remain in this position until the symptoms disappear.If fainting or other effects on the part of the central nervous system occurs, the patient should be warned about the need to avoid potentially traumatic situations, including driving a car and operating dangerous machinery.

    The combination of the drug Primaxetin® with alcohol intake may increase neurocardiogenic side effects, including fainting, which increases the risk of accidental injury; therefore, patients should be advised to refrain from alcohol intake during treatment with Primaxetin®.

    Patients at risk of cardiovascular diseases

    Patients with cardiovascular diseases did not participate in clinical trials of the drug. In patients with organic diseases of the heart and blood vessels (for example, obstruction of the ejection of blood from the heart, damage to the valve apparatus, stenosis of the carotid artery, atherosclerosis of the coronary artery), the risk of undesirable cardiovascular consequences of syncope of cardiac and other origin is increased.However, there is currently insufficient data to determine whether this risk extends to vasovagal syncope in patients with cardiovascular disease.

    Orthostatic hypotension

    Cases of orthostatic hypotension have been described in clinical studies. The doctor should inform the patient in advance that if possible prodromal symptoms appear, for example, a feeling of lightness in the head immediately after standing up, immediately lie down so that the head is lower than the body, or sit with the head bowed between the knees and remain in this position until disappearance of symptoms.In addition, the patient should be informed about the need to avoid getting up suddenly after prolonged lying or sitting. In addition, the drug Primaxetin® should be prescribed with caution to patients taking vasodilating drugs (for example, alpha-blockers, nitrates, PDE5 inhibitors), because of the possible reduced tolerance of such patients to the orthostatic effect of the drug. Moderately active CYP3A4 inhibitors

    When Primaxetin® is taken simultaneously with moderately active CYP3A4 inhibitors (erythromycin, clarithromycin, fluconazole, amprenavir, fosamprenavir, aprepitant, verapamil, diltiazem should be reduced to 30 mg) the dose of the drug should be reduced to 30 mg.

    Active CYP2D6 inhibitors

    It is recommended to exercise caution when increasing the dose of Primaxetin® to 60 mg in patients receiving active CYP2D6 inhibitors and in patients with low CYP2D6 activity, as this may increase the level of systemic exposure to the drug with a corresponding increase in the frequency and severity of dose-related adverse events.

    Suicide / suicidal ideation

    Short-term studies of antidepressants, including SSRIs, compared with placebo have shown an increased risk of suicide and suicidal ideation in children and adolescents with generalized depression and other psychiatric disorders.In adults over 24 years of age, this effect was not found. In clinical studies of the drug Primaxetin® for the treatment of premature ejaculation, clear data on the relationship of suicidal thoughts with treatment have not been obtained.


    The drug Primaxetin® should not be taken by patients with a history of mania / hypomania or bipolar disorder; if symptoms of these diseases appear, the drug should be discontinued.


    Due to the ability of SSRIs to lower the seizure threshold, Primaxetin® should be avoided in patients with unstable epilepsy; if seizures occur, the drug should be discontinued.Patients with controlled epilepsy should be closely monitored.

    Admission to children and adolescents under 18 years of age

    Primaxetin® should not be taken to patients under 18 years of age.

    Concomitant depression and mental disorders

    If the patient has signs and symptoms of depression, before using Primaxetin®, an examination should be carried out to exclude the presence of undiagnosed depressive disorder.The drug Primaxetin® should not be taken simultaneously with antidepressants, including SSRIs and serotonin and norepinephrine reuptake inhibitors. It is not recommended to discontinue treatment for depression or anxiety before starting treatment with Primaxetin®. The drug Primaxetin® is not intended for the treatment of mental disorders (for example, schizophrenia or depression), and should not be taken by men with these diseases, since this cannot exclude an increase in the symptoms of depression. You should immediately inform your doctor about any disturbing thoughts or sensations, and if signs and symptoms of depression appear during treatment, Primaxetin® should be discontinued.


    Cases of bleeding have been reported with SSRIs. It is recommended to exercise caution when taking Primaxetin® simultaneously with drugs that affect platelet function (for example, atypical antipsychotics, phenothiazines, acetylsalicylic acid, non-steroidal anti-inflammatory drugs (NSAIDs), anticoagulants), as well as in patients with bleeding or blood clotting disorders.

    Renal impairment

    Primaxetin® is not recommended for patients with severe renal failure, patients with mild to moderate renal failure should be careful.

    Withdrawal syndrome

    There is evidence that abrupt withdrawal of SSRIs, which have been used for a long time to treat chronic depressive disorders, leads to the following symptoms: decreased mood, irritability, agitation, dizziness, sensitivity disorders (for example, paresthesia in the form of a sensation of electric shock), anxiety, confusion, headache, lethargy, emotional instability, insomnia, hypomania.

    In a clinical study conducted to evaluate the effect of discontinuation of dapoxetine after 62 days of administration at a dose of 60 mg (daily or as needed) in patients with premature ejaculation, no signs of withdrawal were found.After transferring patients to placebo after daily dapoxetine intake, only minor symptoms were found in the form of mild to moderate insomnia and dizziness. Similar results were obtained in another double-blind clinical study with a one-week period to evaluate withdrawal effects after 24 weeks of 30 mg or 60 mg as needed.

    Influence on the ability to drive vehicles and mechanisms

    When taking dapoxetine, cases of dizziness, impaired attention, fainting, blurred vision, drowsiness are described.The patient should be warned about the need to refrain from driving vehicles and mechanisms, as well as engaging in other activities that require increased concentration of attention and speed of psychomotor reactions.

    90,000 Authorities responded to article on deaths after vaccination with “Sputnik V” – RBC

    “We can confirm that all reports are seriously considered by the EMA and are assessed,” an EMA spokeswoman told EUobserver earlier, commenting on the Rospotrebnadzor files on deaths and other complications.

    Deaths were reportedly related to heart, lung or blood sugar problems and were not caused by the Sputnik V vaccine.

    Read on RBK Pro

    The material contains links to photocopies of three reports on deaths of patients addressed to the head of Rospotrebnadzor Anna Popova. In one case, we are talking about a woman from the Leningrad region who received the first dose of the vaccine on January 26 and was hospitalized on February 2 complaining of weakness, nausea and thirst.The PCR test showed that she was infected with a coronavirus, the deceased had diabetes mellitus complicated by ketoacidosis.

    Another document entitled “Information on a sudden death that has a temporary connection with vaccinations” concerns the death of a woman in Perm who received the first dose of vaccination on March 1, and died on March 3 with symptoms of “weakness, shortness of breath, temperature 37.5”. An autopsy revealed that she had coronary heart disease. The report says that four more people were vaccinated from the same ampoule without any side effects.

    Austrian Chancellor Allows Registration of Sputnik V Before EU Regulator

    The third death also occurred in the Leningrad Region.The diagnosis indicated in the document: post-vaccination complication, sudden death on the street. “On 03/04/2021, she suddenly fell on the street – convulsions, foam at the mouth, blue face, loss of consciousness, death,” the document says. The first component of the vaccination was introduced on February 10, the date of the second vaccination is on the back of the sheet, which is not visible.

    The six patients who had complications were younger men and women, one of whom was “only” 25 years old. After being vaccinated, they suffered from a number of symptoms, including shortness of breath, cramps, swelling, muscle weakness, high blood pressure, headaches, dizziness, and fever.

    The authenticity of one of the materials of Rospotrebnadzor was confirmed to the publication by Denis Logunov, senior virologist at the N.N. Gamalei. “I asked for information about this case and received a response. This case is not fake, ”he told EUobserver, referring to a 51-year-old woman who died suddenly after a second dose of Sputnik V. “The case has been investigated. No connection with vaccination was found, ”added Logunov.

    Peskov called the comparison of “Sputnik V” with Russian roulette incorrect

    The article states that the total number of cases (ten) in the leaked files is “tiny” compared to the millions of people vaccinated with Sputnik V.

    RBC sent inquiries to the press services of the Rospotrebnadzor departments in the Perm Territory and the Leningrad Region. Natalya Voldschmidt, chief specialist-expert of the epidemiological surveillance department of Rospotrebnadzor in the Perm Territory, whose signature is in the appeal to the head of Rospotrebnadzor Anna Popova in connection with a sudden death after vaccination with “Sputnik V” in the region, declined to comment on RBC.

    Earlier, the head of the EMA Christa Virtumer-Hohe, commenting on the possible approval of Sputnik V in Austria, compared such actions to Russian roulette.She did not recommend using the Russian vaccine until the official permission of the regulator, but allowed her to enter the European market in the future.

    Presidential press secretary Dmitry Peskov called her words incorrect. “As for this annoying statement, it is, at least, from our point of view, incorrect. We know that RDIF has made certain statements. The demand for this vaccine, the vaccination process shows the demand for this drug and its popularity, ”said Peskov.

    90,000 Symptoms of Havana Syndrome Identified in Employees of the US Embassy in Vienna | News from Germany on world events | DW

    US authorities are investigating reports of multiple cases of the so-called “Havana Syndrome” at the American Embassy in Vienna. Embassy officials complain of sudden dizziness, headaches and hearing problems, the German edition of Der Spiegel writes on Saturday, July 17.

    Symptoms, which have not yet been accurately explained, were recorded in at least 20 people working in the US diplomatic mission in the Austrian capital. Complaints were last heard on July 16, but, according to the American New Yorker magazine, the first cases were noted shortly after Joe Biden took over as president in January 2021. Experts from the US Department of Health and CIA officials are involved in the investigation.

    “Havana Syndrome”

    For the first time, American diplomats complained of similar symptoms in Cuba in 2016-2017.Then at least 19 employees of the US Embassy in Havana were injured, who were diagnosed with “minor injuries and cerebral edema”, hearing loss, severe headaches, loss of balance and cognitive impairment. Initially, the US authorities expressed assumptions about some “acoustic attacks”, but this version has not been accurately confirmed. It was reported at that time and about the victims at the Canadian Embassy.

    In 2017, American diplomats complained about similar problems in the Chinese city of Guangzhou, later they were noted in Russia, Poland, and several European countries, Taiwan, Australia, and the Middle East.In total, about 130 people – American diplomats and their families, CIA employees and the military – could have suffered from the mysterious ailment.

    Different versions

    In 2018, The New York Times published a hypothesis about microwave radiation, which the Russian special services may be behind. In 2019, the UK Brain Recovery Center and the Nova Scotia Canadian Health Authority reported that the problems could be caused by neurotoxins in anti-mosquito pesticides.In 2020, the US National Academy of Sciences, Engineering and Medicine (NASEM) released a version of directed radio frequency radiation. Other versions were also expressed, including about a massive psychogenic illness.

    See also:

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      Double agent, dancer and courtesan

      In the 1910s, the young Margareta Gertrude Zelle from the Netherlands began her career as a dancer Mata in Paris under the pseudonym Harrison.She moved in high society in France and entered into contact with officers and politicians. In view of this, she was recruited by German intelligence, and after a while – by French counterintelligence: when Mata Hari agreed to become a double agent, the French exposed her.

    • High-profile spy scandals in the history of special services

      Spouses Rosenberg

      In the early 1950s, the case of the communists Julius and Ethel Rosenberg split American society. The spouses were accused of transferring secret information about the US nuclear program to Moscow.While some saw his death sentence as a necessary measure, in the eyes of others, they were innocent victims who suffered for their beliefs. Despite international protests, the couple were executed in 1953.

    • Loud spy scandals in the history of special services

      A spy in the Chancellor’s department

      What began in Germany as an espionage scandal soon escalated into a national crisis. The personal assistant of ex-chancellor Willy Brandt Gunther Guillaume (pictured in the center) turned out to be an agent of the GDR and handed over secret documents from the Chancellor’s office to the Stasi.The fact of the penetration of the GDR spy into the very center of the FRG policy shocked the public and contributed to Willie Brandt’s resignation.

    • High-profile spy scandals in intelligence history

      The Cambridge Five

      In 1979, former Cambridge University student Anthony Blunt found himself at the center of one of the UK’s biggest spy scandals. He admitted that he was part of a group of five agents who had access to the highest government circles and supplied the USSR with information of strategic importance.Four agents were exposed; the identity of the fifth has not yet been established.

    • Loud spy scandals in the history of special services

      From intelligence to the podium

      In 2010, the daughter of a Russian diplomat, Anna Chapman, was arrested in the United States on charges of spying for Russia. Chapman and nine other alleged Russian agents were then traded for Russians convicted of spying for Western countries. Returning to Moscow, Chapman began her career there as a model and TV presenter on the REN TV channel, and also starred in an erotic photo shoot in Maxim magazine.

    • Loud spy scandals in the history of the special services

      Spy Full House

      Every Tuesday the imaginary housewife Haidrun Anshlag sat down at her shortwave radio in the city of Marburg and listened to instructions from the headquarters of the special services in Moscow. This went on for over 20 years. Living in Germany under the guise of Austrian citizens, she and her husband handed over several hundred NATO and EU strategy documents to the Russian side. In 2013, both were found guilty of espionage.

    • Loud spy scandals in the history of special services

      Spy Strauss?

      The former head of the Christian Social Union, Franz Josef Strauss, managed to attract press attention even many years after his death. Strauss was allegedly an agent of the US military intelligence service OSS, the predecessor of the FBI. The Federal Center for Political Education of the Federal Republic of Germany released this information to the 100th anniversary of the birth of the politician. The results of the report, however, remain controversial.

    • High-profile spy scandals in the history of special services

      Espionage: version 2.0

      If during the Cold War, governments feared double agents, today it is wiretapping by intelligence services. An interview with Edward Snowden and 1.7 million secret FBI documents released in 2013 serve as proof of how the United States, together with other countries, is conducting global surveillance: intelligence services wiretap telephone conversations and store the data of millions of Internet users.

      Author: Nina Nibergal, Alexandra Yolkina

    90,000 Dizziness. Treatment in the clinic of osteopathy “Ostmed”

    Osteopathy: radical treatment of vertigo without medication and side effects

    “Oh, how dizzy … How dizzy!” These lines of a well-known song evoke in many not tenderness and nostalgia, but despair. Frequent dizziness, despite the seeming “frivolity” of this disease, can seriously complicate life.

    Causes of dizziness

    The first and most common cause is disruption of the vestibular system .

    The vestibular apparatus is responsible for a clear orientation in space and maintaining balance. It is located in the inner ear, which is located in the temporal bone. The vestibular apparatus consists of semicircular canals filled with fluid. The device for determining the horizontal level used by builders is just an analogue of semicircular canals.

    Changing the position of the fluid within the channels sends certain signals to the brain. Thanks to these signals, we are able to restore balance and a stable focus of vision. In cases when the work of the vestibular apparatus fails, it seems to a person that objects are circling around him or he himself is rotating around objects. Such sensations are familiar to everyone since childhood: they arose after a long ride on the merry-go-round. This phenomenon is called true vertigo.

    Unfortunately, in adulthood, the causes of chronic dizziness are not carousels at all.

    According to statistics, 90% of dizziness is caused by problems in the vestibular system. Most often it is the appearance of salt stones – otoliths – in the semicircular canals themselves, the receptors of the vestibular apparatus. When the position of the head or body changes, the otoliths cause abnormal “turbulence” in the fluid that fill the canals.

    In medical terminology, this phenomenon is called benign paroxysmal positional vertigo (BPPV).By “benign” we mean a non-dangerous course of the disease that does not threaten health deterioration. Paroxysmal means the symptom appears suddenly. And “positional” indicates that dizziness occurs at the moment of turning the head in a certain direction.

    There are other reasons:

    • Inflammation or clamping of the vestibular nerve , which connects the vestibular apparatus with the corresponding area of ​​the brain. As a result, signals about body position are distorted to the brain.
    • Disruption of the vestibular nuclei in the brain. As a rule, this is due to a violation of blood circulation at the level of the cervico-vertebral and basilar arteries that supply blood to the brain stem. This problem is called vertebrobasilar insufficiency .
    • Meniere’s disease . It is also true vertigo combined with noise in one ear, nausea, and vomiting. According to one version, the reason is an increase in fluid pressure (endolymph) in the inner ear.
    • Brain tumors . Tumors can compress both the semicircular canals themselves and the nerves, as well as the vestibular centers of the brain.

    The second group of reasons is psychogenic.

    In 10% of cases, dizziness is of a psychosomatic nature. That is, their main reason is severe stress, psychological trauma. Often such dizziness occurs with vascular dystonia.

    In this case, the mechanism of the appearance of dizziness is different.On a nervous basis, a person’s pressure drops sharply. And as a result of this, it seems to him that he is about to faint, there is nausea, clouding of consciousness, the visual image begins to float. This condition is also called dizziness.

    How is vertigo usually treated?

    As a rule, a neurologist, based on a subjective description of symptoms, determines the exact cause of dizziness. When it comes to whirling objects, i.e. true dizziness, the vestibular apparatus is “to blame”.If faintness, fainting occurs, then the matter is in the psyche. Accordingly, therapy is prescribed.

    In the treatment of psychogenic dizziness, antidepressants, tranquilizers, sedatives are prescribed. Psychotherapy is also carried out.

    Vascular and antihistamines are used in the treatment of vertigo. Vascular drugs are designed to normalize blood microcirculation at the channel level or at the level of the brain stem. Antihistamines reduce the activity of the vestibular nuclei in the brainstem, inhibiting the passage of the impulse.

    To influence the salt crystals (otoliths) formed in the semicircular canals, a special gymnastics is prescribed, which “loosens” and dissolves these crystals.

    If the problem of the vestibular apparatus has arisen due to an infectious process in the inner ear or vestibular nerve, antibiotic therapy is prescribed.

    Quite often, thanks to these measures, blood flow is restored, the work of the vestibular apparatus improves, and the condition returns to normal.True, often after some time, the symptoms return. In other cases, medications have to be drunk constantly, otherwise the dizziness does not go away. Finally, there are times when therapy does not work at all. Why it happens?

    Osteopathy: Finding the True Causes

    As a rule, the point is that the initial problems that caused the violations were not obvious. Unlike the studies of classical medicine, osteopathic methods allow you to find the underlying causes.

    In the case of vertigo, osteopaths have found that most often malfunctions of the vestibular apparatus are caused by a violation of the micromobility of the bones of the skull, sacrum and tension of the dura mater. The dura is a ligament inside the spinal canal, running from the sacrum to the skull, lining the skull from the inside and forming 2 membranes inside the skull: the sickle of the brain and the tent of the cerebellum.

    This usually occurs after accidents, falls, other injuries.They disrupt the conduction of nerve impulses from the vestibular nuclei to the semicircular canals, blood circulation in the brain stem through the vertebral arteries, blood circulation in the inner ear, and the flow of cerebrospinal fluid. Often, due to injury, there is a physical blockage of the vestibular nerve.

    Using environmentally friendly manual methods, an osteopath can remove clamps and blocks, balance the entire body, and then the pressure and microcirculation of blood and lymph throughout the body are restored without any drugs. In conditions of good blood supply and natural cleansing, the semicircular canals begin to work in an optimal mode, and the salt crystals formed in them dissolve without additional effort.Special manual techniques can also release the pinched vestibular nerve.

    In the case of vertigo caused by psychological reasons , the help of an osteopath will also be invaluable. Severe stress causes chronic tension in the body, most often in the so-called emotionally associated zones. An osteopath can relieve this tension by normalizing intracranial pressure. The psychological problems themselves begin to be perceived more easily.At least so much so that work with a psychologist is quick and effective.

    Unfortunately, there is one reason why osteopathy is powerless. These are tumor formations . Such cases are very rare, however, they cannot be ruled out. If osteopaths have similar suspicions, patients are referred for MRI.

    Examples from the experience of an osteopath

    Male, 45 years old. Dizziness within 8 years after serious injury with fracture of the temporal bone. Against the background of drug treatment, there are temporary improvements, then relapses occur . Neurological tests have shown that dizziness is caused by disturbances at the level of the vestibular apparatus. Osteopathic diagnostics showed a rigid blockage of the temporal bone at the level of all sutures. Together with intraosseous tension, this created an imbalance in the entire skull-spine-sacrum connection. Osteopathic treatment freed the temporal bone, relieved intraosseous tension, balanced the entire body structure, and normalized the functioning of the vestibular apparatus.After 5 sessions with a frequency of once a week, the complaints disappeared and did not recur until now (2 years have passed).

    Woman, 40 years old. After severe stress, suffered six months ago, periodically there were bouts of nausea and dizziness . During the seizures, everything floated before my eyes, there was a light-headed feeling. He was also tormented by attacks of fear and panic attacks. Vascular drugs and antidepressants did not have a measurable effect. Osteopathic examination revealed a pronounced spasm at the level of the abdominal diaphragm and pericardium.This spasm significantly obstructed blood flow and caused low blood pressure. During three sessions of osteopathic treatment, the spasm was completely relieved, the whole body was balanced. In parallel, work was carried out with a psychologist. When the psychological problem was resolved, the body was able to recover. The attacks did not recur.

    Patient reviews

    I am writing this review to express my gratitude to Svetlana Yuryevna Kolyazina and share information with those who are looking for help in the wilds of osteopathy.Last year I went to the Ostmed clinic to see S.Yu. Kolyazina. I am very pleased with the result. Based on my experience, I advise those who need the help of a good osteopathic neurologist. Svetlana Yurievna is a wonderful specialist, a master of her craft. Anonymous

    Dear Alexander Grigorievich! I want to express my gratitude to you for your help. Before getting to you, I was worried about headaches, dizziness and insomnia. There were also pressure surges, disturbed by noise in the ears and in the head. Antonina

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