What are the primary symptoms of Parkinson’s disease. How is Parkinson’s disease diagnosed. What treatments are available for managing Parkinson’s disease. Who is at risk for developing Parkinson’s disease. How does Parkinson’s disease affect daily life. What are the latest research developments in Parkinson’s disease. How can caregivers support individuals with Parkinson’s disease.

Understanding Parkinson’s Disease: A Neurodegenerative Disorder

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that affects millions of people worldwide. It primarily impacts the brain’s ability to control movement, leading to a range of distinctive symptoms. To fully grasp the nature of this condition, it’s essential to delve into its underlying mechanisms and broader implications.

How does Parkinson’s disease affect the brain? At its core, PD causes the weakening and death of specific nerve cells (neurons) in the brain region responsible for movement control. These neurons typically produce dopamine, a crucial chemical for regulating movement. As these cells deteriorate, dopamine levels decrease, resulting in the characteristic motor symptoms associated with Parkinson’s.

Is Parkinson’s disease limited to dopamine-producing neurons? While dopamine deficiency is the primary focus, some patients also experience a decline in norepinephrine levels. This neurotransmitter plays a vital role in various bodily functions, including blood pressure regulation and heart rate control.

The Global Impact of Parkinson’s Disease

Parkinson’s disease affects a significant portion of the global population. According to the Parkinson’s Foundation, over 10 million people worldwide are currently living with PD. In the United States alone, nearly one million individuals will be diagnosed with the disease this year.

How rapidly is the prevalence of Parkinson’s disease increasing? While exact figures vary, research suggests that the number of people affected by PD is growing steadily. This increase is partly attributed to an aging global population, as age is a significant risk factor for the disease.

Risk Factors: Who Is Most Susceptible to Parkinson’s Disease?

Understanding the risk factors associated with Parkinson’s disease can help identify individuals who may be more susceptible to developing the condition. While PD can affect anyone, certain factors may increase one’s likelihood of diagnosis:

• Gender: Men are approximately 1.5 times more likely to develop Parkinson’s disease than women.
• Age: The risk of PD increases significantly with age, although early-onset cases (before age 50) do occur.
• Genetics: While most cases are not directly inherited, certain genetic variations can increase susceptibility.
• Environmental factors: Exposure to specific chemicals, pesticides, and pollutants has been linked to an increased risk of PD.
• Head trauma: Repeated head injuries may contribute to a higher risk of developing Parkinson’s disease.

Are there any preventative measures one can take to reduce the risk of Parkinson’s disease? While there’s no guaranteed way to prevent PD, some lifestyle choices may help reduce risk:

• Regular exercise
• A balanced, nutritious diet
• Avoiding exposure to environmental toxins
• Protecting the head from injuries
• Managing stress levels

Recognizing the Symptoms: Early Signs and Progression

Identifying the symptoms of Parkinson’s disease is crucial for early diagnosis and management. The onset of PD is often gradual, with symptoms progressively worsening over time. Common early signs include:

1. Tremor or shaking, often beginning in the hands or fingers
2. Muscle rigidity or stiffness
3. Bradykinesia (slowness of movement)
4. Postural instability and balance problems
5. Changes in gait, including shuffling or reduced arm swing while walking

Do all individuals with Parkinson’s disease experience the same symptoms? While these are considered the cardinal signs of PD, it’s important to note that the disease can manifest differently in each person. Some may experience a tremor as their first symptom, while others might initially notice stiffness or balance issues.

Advanced Symptoms and Non-Motor Manifestations

As Parkinson’s disease progresses, additional symptoms may emerge, affecting various aspects of daily life:

• Speech changes: Softening of voice or slurred speech
• Difficulty with chewing and swallowing
• Cognitive changes, including memory issues
• Autonomic dysfunction: Constipation, bladder control problems, and sexual dysfunction
• Sleep disturbances
• Mood disorders: Anxiety and depression
• Sensory changes: Decreased sense of smell
• Temperature regulation issues

How do non-motor symptoms impact the quality of life for individuals with Parkinson’s disease? Non-motor symptoms can significantly affect daily functioning and overall well-being. They may be as disruptive as motor symptoms and often require specific management strategies.

Diagnosing Parkinson’s Disease: Challenges and Approaches

Diagnosing Parkinson’s disease can be challenging, as there is no definitive test to confirm the condition. Neurologists rely on a combination of medical history, physical examination, and symptom assessment to make a diagnosis.

What are the key diagnostic criteria for Parkinson’s disease? According to the Parkinson’s Foundation, at least two of the following four symptoms must be present over time for a PD diagnosis to be considered:

1. Resting tremor
2. Bradykinesia (slowness of movement)
3. Rigidity in limbs or trunk
4. Postural instability or balance issues

Why is differential diagnosis important in Parkinson’s disease? Several conditions can mimic PD symptoms, making accurate diagnosis crucial. Some of these conditions include:

• Essential tremor
• Normal pressure hydrocephalus
• Dementia with Lewy bodies
• Multiple system atrophy
• Corticobasal syndrome
• Progressive supranuclear palsy

How do neurologists differentiate between Parkinson’s disease and these similar conditions? Careful observation of symptom patterns, response to medication, and sometimes advanced imaging techniques can help distinguish PD from other neurological disorders.

Treatment Strategies: Managing Parkinson’s Disease Symptoms

While there is currently no cure for Parkinson’s disease, various treatment options can help manage symptoms and improve quality of life. The approach to treatment is often multifaceted, combining medications, therapies, and sometimes surgical interventions.

Pharmacological Interventions

Medications play a crucial role in managing Parkinson’s disease symptoms. The primary goal of pharmacological treatment is to address the dopamine deficiency in the brain. Common medications include:

• Levodopa: Replenishes the brain’s dopamine supply
• Carbidopa: Often combined with levodopa to reduce side effects
• Dopamine agonists: Mimic the effects of dopamine in the brain
• MAO-B inhibitors: Help prevent the breakdown of dopamine
• COMT inhibitors: Prolong the effects of levodopa

How do doctors determine the most appropriate medication regimen for each patient? Treatment plans are highly individualized, taking into account the patient’s age, symptom severity, lifestyle, and potential side effects. Medication adjustments are often necessary as the disease progresses.

Surgical Options

For some individuals with Parkinson’s disease, surgical interventions may be considered when medications are no longer effectively managing symptoms. The most common surgical approach is Deep Brain Stimulation (DBS).

What is Deep Brain Stimulation, and how does it help manage Parkinson’s symptoms? DBS involves implanting electrodes in specific areas of the brain and connecting them to a stimulator device. This device sends electrical pulses to the brain, helping to regulate abnormal impulses and potentially improving motor symptoms.

Complementary Therapies

In addition to medications and surgical options, various therapies can help manage Parkinson’s disease symptoms and improve overall quality of life:

• Physical therapy: Improves mobility, balance, and flexibility
• Occupational therapy: Helps maintain independence in daily activities
• Speech therapy: Addresses speech and swallowing difficulties
• Exercise programs: Regular physical activity can help manage symptoms and slow progression
• Cognitive behavioral therapy: Assists in managing mood disorders and cognitive changes

How can a multidisciplinary approach benefit individuals with Parkinson’s disease? By combining various treatment modalities, patients can address multiple aspects of the disease, potentially leading to better symptom management and improved overall functioning.

Living with Parkinson’s Disease: Coping Strategies and Support

Managing Parkinson’s disease extends beyond medical treatments. Developing effective coping strategies and accessing support systems are crucial for maintaining quality of life and emotional well-being.

Lifestyle Modifications

Making certain lifestyle changes can help individuals with Parkinson’s disease better manage their symptoms and maintain independence:

• Adapting the home environment for safety and accessibility
• Establishing a regular exercise routine
• Maintaining a balanced, nutritious diet
• Practicing stress-reduction techniques, such as meditation or yoga
• Staying socially engaged and mentally active

How can these lifestyle modifications impact the progression of Parkinson’s disease? While they may not alter the underlying disease process, these changes can significantly improve symptom management, reduce complications, and enhance overall well-being.

Support Systems and Resources

Building a strong support network is essential for individuals with Parkinson’s disease and their caregivers. Valuable resources include:

• Support groups for patients and caregivers
• Educational programs and workshops
• Online communities and forums
• Professional counseling services
• Parkinson’s disease organizations and foundations

What role do caregivers play in supporting individuals with Parkinson’s disease? Caregivers provide essential physical and emotional support, helping with daily tasks, medication management, and serving as advocates in healthcare settings. It’s crucial for caregivers to also prioritize their own well-being and seek support when needed.

Research and Future Directions in Parkinson’s Disease

The field of Parkinson’s disease research is dynamic and rapidly evolving. Scientists and clinicians worldwide are working to better understand the disease mechanisms, develop new treatments, and ultimately find a cure.

Current Research Focus Areas

Several key areas of research are showing promise in advancing our understanding and treatment of Parkinson’s disease:

• Genetic studies to identify risk factors and potential therapeutic targets
• Investigation of biomarkers for earlier and more accurate diagnosis
• Development of neuroprotective therapies to slow or halt disease progression
• Exploration of cell replacement strategies, including stem cell therapies
• Refinement of surgical techniques and deep brain stimulation technologies
• Research into the gut-brain connection and its role in PD

What are some of the most promising recent developments in Parkinson’s disease research? While it’s important to approach new findings with cautious optimism, recent advances in areas such as alpha-synuclein targeting therapies, gene therapies, and personalized medicine approaches are generating excitement in the scientific community.

Clinical Trials and Patient Participation

Clinical trials play a crucial role in advancing Parkinson’s disease research and treatment. These studies help researchers evaluate new therapies, diagnostic tools, and interventions.

How can individuals with Parkinson’s disease contribute to research efforts? Participating in clinical trials can provide access to cutting-edge treatments and contribute to the broader understanding of the disease. However, it’s important for potential participants to carefully consider the risks and benefits in consultation with their healthcare providers.

As research continues to progress, the hope for more effective treatments and eventually a cure for Parkinson’s disease grows. While living with PD presents significant challenges, ongoing advancements in understanding and managing the disease offer promise for improved quality of life and outcomes for those affected.

The facts about Parkinson’s Disease

Parkinson’s disease is a progressive neurogenerative disease that causes nerve cells (or neurons) in the area of the brain that controls movement to weaken and/or die. While healthy neurons produce a chemical called dopamine, which the brain needs a certain amount of in order to regulate movement, weakened neurons produce lower levels of dopamine. What causes these neurons to weaken is currently unknown. 

Some patients with Parkinson’s disease also suffer from a decline in norepinephrine, a chemical that transmits signals across nerve endings and controls various functions, such as blood pressure and heart rate.

More than 10 million people worldwide are currently living with Parkinson’s disease and nearly one million will be living with the disease in the United States this year, according to the Parkinson’s Foundation.

Risk factors

One’s risk of developing PD can depend on the following factors:

• Gender. Men are 1.5 times more likely to have PD than women.
• Age. The risk of PD increases with age, although some people are diagnosed with early-onset PD before the age of 50.
• Genetics. Most cases occur in patients with no familial link to PD, but some have an inheritance pattern involving certain altered genes that could increase the risk of developing PD.
• Environmental causes. Studies have shown a link between exposure to chemicals used in pesticides and herbicides—as well as metals and organic pollutants—and Parkinson’s disease.
• Head injury. Repeated blows to the head can increase one’s risk of developing PD, however, it doesn’t guarantee a diagnosis.

Symptoms of Parkinson’s disease

These common symptoms of Parkinson’s disease often begin gradually and progress over time:

• Shaking or tremor
• Rigid muscles
• Difficulty walking
• Unsteady balance
• Poor posture
• Slowing of body movements (bradykinesia)

As the disease continues to progress, additional symptoms can occur such as slurred or soft speech, trouble chewing and/or swallowing, memory loss, constipation, trouble sleeping, loss of bladder control, anxiety, depression, inability to regulate body temperature, sexual dysfunction, decreased ability to smell, restless legs and muscle cramps.

Diagnosis

There are currently no blood or lab tests that can be used to diagnose Parkinson’s disease. Neurologists make a diagnosis based on their patient’s medical history and an examination.

According to the Parkinson’s Foundation, at least two of the four following symptoms must be present over a period of time for a neurologist to consider Parkinson’s disease as a diagnosis:

• Shaking or tremor
• Bradykinesia
• Stiffness in arms, legs and/or trunk
• Balance issues

There are a number of conditions that closely mimic Parkinson’s disease, such as:

• Essential tremor. Essential tremor is an action tremor, meaning that the involuntary shaking increases when you move and try to use your hands. In Parkinson’s disease, tremors occur mainly at rest, and activity reduces the symptoms.
   
• Normal pressure hydrocephalus. This condition, seen primarily in older people, happens when there is an excess of the fluid surrounding the brain and spinal cord. The classic symptoms are an unsteady gait, problems with memory and thinking, and urinary incontinence.
   
• Dementia with Lewy bodies. Symptoms seen early on in PD can also develop during the late stages of dementia with Lewy bodies, a disease that causes problems with mood, thinking and movement and is characterized by abnormal protein deposits called Lewy bodies in the brain.
   
• Multiple system atrophy. A progressive neurogenerative disorder, multiple system atrophy involves the death of different types of nerve cells in the brain and spinal cord. Symptoms include slowness of movement, tremor, stiffness, and impaired speech.
   
• Corticobasal syndrome. CBS is a condition that affects movement, language or both. The cause is currently unknown, but some people with CBS have a build-up of tau in their brains similar to that of Alzheimer’s disease patients.
   
• Progressive Supranuclear Palsy. This rare condition, which damages nerve cells in the brain, can cause loss of balance, eye problems, unexplained falls, and stiffness. 

Parkinson’s disease treatment

Although there is no cure for Parkinson’s disease, neurologists can recommend various medications, surgeries and/or therapies to relieve symptoms.

Medication. The most common medications used to treat Parkinson’s disease are formulated to help maintain, replenish or mimic dopamine and other chemicals in the brain:

• Levodopa replenishes the brain’s decreasing supply of dopamine,
• Carbidopa is used in combination with levodopa (e.g. Sinemet) to help reduce the side effects associated with levodopa, such as nausea, low blood pressure, and restlessness.
• Dopamine Agonists mimic the effects of dopamine. They can be used to delay starting levodopa or can be used in addition to it.
• Amantadine can boost levels of dopamine that are already present in the brain.
• Anticholinergic medications are prescribed to help reduce tremor.
• Catechol-O-methyltransferase (COMT) inhibitors block enzymes that break down dopamine and thereby prolong dopamine’s action in the brain.
• Monoamine Oxidase (MAO) B Inhibitors also blocks an enzyme that breaks down dopamine and allows it to function for a longer period.
• Adenosine Receptor Antagonist may keep muscles working more normally in what are known as “off” periods when patients are taking levodopa/carbidopa.  

Finding the right combination of PD medications can take time in order to find what works best with the least amount of side effects, which can include nausea, low blood pressure, dizziness, constipation, insomnia, hallucinations, and dyskinesia (uncontrolled body movements). Your doctor may prescribe additional medications to relieve some of these side effects or to relieve the non-motor symptoms commonly associated with Parkinson’s disease.

Deep Brain Stimulation. Typically reserved for those who don’t respond well enough to medication, deep brain stimulation is a surgical procedure where thin metal wires are placed in the brain and programmed to send electrical pulses that aid in controlling motor symptoms. In general, it is considered for patients who have had PD for four years or more and it is not recommended for patients with dementia.  

Focused Ultrasound. A non-invasive option that is FDA-approved to treat tremor-predominant Parkinson’s disease as well as essential tremor. Focused ultrasound for tremor destroys brain cells that cause motor problems. Unlike deep brain stimulation, focused ultrasound therapy is permanent and irreversible. It is also being tested for other PD symptoms. 

Other Therapies. Sports and exercise regimens, such as walking, non-contact boxing, biking, yoga and tai chi, have been shown to improve balance, motor control, and strength in PD patients. Physical and occupational therapy can also aid in improving gait, flexibility, speech and the ability to perform everyday activities, such as eating and dressing.

Image: MarianVejcik/Getty Images

Self-help videos to stop vertigo work for some, not all

Benign paroxysmal positional vertigo (BPPV)  makes people intensely dizzy from time to time. Some people are using Internet videos to self-treat the condition at home using a maneuver called the Epley maneuver. If at first it doesn’t help, below are some tips to improve the odds of success.

Blame it on crystals

BPPV happens when tiny crystals of calcium carbonate in one part of your inner ear become dislodged and float into another part. That doesn’t sound too serious, but small head movements cause the loose crystals to move, triggering your inner-ear sensors to send mixed messages to your brain. Simply looking up or rolling over in bed causes brief bouts of extreme dizziness. Some people experience nausea as well.

What causes the crystals to dislodge in the first place? “We don’t really know,” says Dr. Felipe Santos, an ear, nose, and throat specialist at Massachusetts Eye and Ear Infirmary and an assistant professor in otology and laryngology at Harvard Medical School. “There seems to be an association in a percentage of patients with head trauma, but for the most part, we don’t know.”

Vertigo treatment

Once BPPV has been diagnosed (abnormal eye movements are a giveaway), a clinician will lead you through an exercise to move the crystals into another ear chamber where they’ll be absorbed by the body. Think of the exercise as one of those water-filled puzzles that you shake in order to move small beads from one place to another. Research has shown that the most successful of these moves is called the Epley maneuver.

It’s a fairly simple exercise: You sit at the end of an exam table with your head turned 45 degrees toward the affected side. The clinician will then tilt you back quickly so you’re lying on your back with your head hanging off the table, still turned to the affected side. Your head is held in this position for 20 to 30 seconds, then rotated 90 degrees to the unaffected side and held for another 20 to 30 seconds. Then, looking in the same direction, you’ll quickly roll onto your side while the clinician rapidly rotates your head another 90 degrees, until you’re lying nearly facedown. You’ll stay like that for another 20 to 30 seconds before the clinician rapidly brings you back up to a sitting position.

The maneuver is easy enough to do at home—as long as you know how. Many people who recognize the onset of BPPV turn to Internet videos for instructions. One of the most popular is produced by the American Academy of Neurology.

Important steps

If the maneuver doesn’t work for you, you may be neglecting two important steps.

First: Identify which ear is causing the vertigo. If you get dizzy every time you roll left in bed, then your left ear is the likely culprit. Once you know which ear has some loose calcium crystals, it’s important that you look to that side when you begin the Epley maneuver.

Second: Try to stabilize your neck after the Epley maneuver. “Typically, we advise patients to avoid positions that invoke the vertigo,” says Dr. Santos. “You don’t have to wear a neck brace, but we ask patients to avoid extreme flexion of the neck that would induce vertigo for 48 hours. Eventually, the goal is to get patients to return to normal activity and not restrict their head movements.”

Some people don’t even need the maneuver. Medications also used for motion sickness may help relieve symptoms and the BPPV symptoms may resolve on their own within a few days.

If it does linger for weeks or even months, BPPV usually still does go away eventually.  If you don’t want to suffer through intense room spinning, you might want to consider looking at a video and trying the Epley maneuver yourself.

If it doesn’t help, it’s possible that you didn’t do it right, or that the crystals are in a part of your ear canal that requires another simple maneuver (called the Log Roll). But Dr. Santos says it’s best to leave it to the experts. “The advantage of seeing someone is that you can confirm you’re treating the correct side and the correct canal. We can pinpoint where the calcium crystals are and how to move them along,” says Dr. Santos.

Differential diagnosis and treatment of vertigo | Lyashenko E.A.

Dizziness is a common reason for visiting a doctor. It occurs in 5-30% of patients depending on the age group. Dizziness can be a symptom of a large number of diseases of varying severity. At the moment, about 80 different nosologies are known, accompanied by dizziness [1].

The systems responsible for maintaining balance in humans include the vestibular, visual, and proprioceptive systems.
The peripheral vestibular system is represented by the labyrinth and the vestibular nerve. The labyrinth consists of a vestibule and three semicircular canals located in three mutually perpendicular planes, the receptors of which respond to linear and angular accelerations. The impulses generated by the vestibular receptors of the labyrinths are sent along the vestibular nerve to the vestibular nuclei of the brainstem (superior, lateral, medial and inferior). The vestibular nuclei, in turn, are connected with five physiological systems: with the oculomotor nuclei through the longitudinal medial bundle, multisynaptic connections with the reticular formation, with the motor part of the spinal cord through the reticulospinal pathways and partially with the medial longitudinal bundle, with the cerebellum, with the autonomic nervous system. In addition, the vestibular nuclei interact with the cerebral cortex. After processing the information in the cerebral cortex, nerve impulses go to the skeletal and eye muscles, providing an optimal stable posture and the normal position of the eyeballs. Any disease that leads to a mismatch in the flow of impulses from the vestibular apparatus to the brain stem, and then to the cerebral cortex, causes dizziness [2].
However, dizziness is not always associated with damage to the vestibular apparatus. The whole question is what specific sensations the patient calls dizziness. Often, patients describe a feeling of lightheadedness, an approaching loss of consciousness, weakness, a feeling of “emptiness”, lightness in the head, unsteadiness when walking and gait disturbance. If the patient has true dizziness, he, as a rule, describes the rotation of objects around him in a certain direction or the patient himself in space [3].
Thus, all dizziness can be divided into two large groups: systemic and non-systemic.
Systemic (true, vestibular) vertigo is associated with damage to the vestibular system at various levels and is characterized by the illusion of rotation of one’s own body or surrounding objects in a certain direction in space. Such dizziness is often accompanied by autonomic symptoms (nausea, vomiting, increased sweating), fear, imbalance and nystagmus, is paroxysmal in nature. To determine the level of damage to the vestibular apparatus, it is necessary to conduct an otoneurological examination.
Peripheral vestibulopathy is characterized by horizontal rotatory nystagmus, which weakens when the gaze is fixed and does not change direction when looking in different directions, nausea and vomiting, moderate gait disturbances, hearing loss and tinnitus.
Central vestibular syndrome may be accompanied by vertical, horizontal, or rotatory nystagmus that does not improve with fixation of the gaze and may change direction when looking in different directions. Walking is often impossible. The severity of nausea and vomiting may vary. Several studies have noted that isolated vertigo is extremely rare with a central cause of vestibular involvement. As a rule, symptoms of damage to the brain stem are detected: double vision, impaired sensitivity on the face or limbs, etc. [4].
Additional methods of examination are used: tone audiometry, electrocochleography, MRI of the brain [5].
The causes of peripheral damage to the vestibular apparatus include labyrinthitis of various etiologies, exposure to ototoxic antibiotics, trauma to the temporal bone with a fracture of the pyramid, thrombosis or hemorrhage in the blood supply of the labyrinth artery, occupational diseases (noise, vibration), etc. [6].
Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder. BPPV is characterized by short-term attacks of dizziness, accompanied by nystagmus and provoked by a change in the position of the head. The cause of the disease is canalolithiasis, which causes a violation of the lymph flow in one of the semicircular canals. This form of vertigo develops spontaneously predominantly in the elderly and is more common in individuals with concomitant metabolic disorders (urolithiasis, cholelithiasis, dyslipidemia) or after traumatic brain injury. The diagnosis of BPPV is based on the anamnesis data and the results of the Dix-Holpike positional test, designed to provoke an attack of dizziness and nystagmus in the patient [2,5].
Meniere’s disease is a classic example of acute recurrent systemic vertigo and is considered an independent nosological form. This affects mainly the inner ear. Dizziness in Meniere’s disease can last up to 12-24 hours. External factors (light, sound, speech, flickering objects, eye movement) can lead to increased dizziness. The frequency of attacks ranges from once a year to several times a day. Meniere’s disease is characterized by hearing loss (most often unilateral) and the presence of autonomic symptoms.
Vestibular neuritis (acute peripheral vestibulopathy, vestibular neuronitis) is the third most common cause of acute vestibular vertigo after benign paroxysmal positional vertigo and Meniere’s disease. It is manifested by sudden severe and prolonged (up to several days) dizziness with nausea, vomiting, a sense of fear and imbalance. Patients have spontaneous and often positional nystagmus. Hearing is not impaired, but there may be noise and stuffiness in the ear. In half of patients, attacks recur after a few months or years. The etiology of this disease is not fully known.
Labyrinthitis also causes typical bouts of systemic vertigo and hearing impairment, which regress slowly over several weeks or even months as the underlying cause subsides. Known labyrinthitis bacterial (as a complication of inadequate therapy for otitis media) and viral (with measles, rubella, influenza, mumps). At the same time, balance disorder and systemic dizziness develop, which are accompanied by hearing loss.
Neurinoma of the VIII pair of cranial nerves is characterized by a gradual onset of the disease. Dizziness is rare. With the development of a tumor in the internal auditory canal, hearing loss quickly sets in, but more often it is localized in the region of the cerebellopontine angle, and hearing loss develops over the years. Neurinoma is characterized by a combined lesion of the facial, trigeminal nerves, signs of damage to the cerebellum, changes in the fundus. Magnetic resonance imaging has the greatest diagnostic value.
Also, the cause of peripheral vestibular syndrome can be an injury in which the thin bone membranes of the labyrinth are damaged. Immediately after the injury, vestibular dizziness, nausea, and vomiting occur due to the shutdown of one of the labyrinths. Less often, dizziness is caused by transverse or longitudinal fractures of the pyramid of the temporal bone, which are accompanied by hemorrhage in the middle ear or damage to the tympanic membrane. Horizontal spontaneous nystagmus and imbalance are characteristic. Symptoms are aggravated by sudden movements of the head.
With barotrauma (during diving, straining, coughing), a membrane rupture in the region of the oval or round holes is possible and the formation of a perilymphatic fistula, through which pressure changes in the middle ear are transmitted to the inner ear. At the same time, intermittent or positional vestibular vertigo and non-permanent sensorineural hearing loss develop. Perilymphatic fistula closes spontaneously, which is accompanied by the disappearance of symptoms.
Cholesteatoma is a tumor that develops in chronic bacterial inflammation of the inner ear. It destroys the walls of the tympanic cavity and leads to the formation of a perilymphatic fistula and, accordingly, to the appearance of systemic dizziness and hearing loss.
The defeat of the vestibular analyzer of the central level may be due to ischemia of the brain stem, multiple sclerosis, tumors of the posterior cranial fossa, as well as tumors in other departments. Any pathological processes that disrupt the connection of the vestibular system with the cerebral cortex (stem encephalitis, severe intracranial hypertension, vertebrobasilar insufficiency, with degenerative brain disease). Studies have shown that in 80% of cases a combination of symptoms of peripheral vestibulopathy with symptoms of damage to the pons varolii is detected, which is due to a single source of blood supply to peripheral vestibular structures and central tracts and nuclei from the branches of the anterior inferior cerebellar artery and penetrating arteries of the brain stem [7].
Vertebrobasilar insufficiency is a common cause of dizziness in the elderly with vascular risk factors [8,9]. Dizziness begins acutely, lasts several minutes, is accompanied by imbalance, nausea and vomiting. If we talk about vertebrobasilar insufficiency as the main cause of dizziness, then it should be accompanied by other symptoms of damage to the brain stem and cerebellum: impaired coordination, gait, double vision, dysarthria, dysphonia, weakness and numbness in the extremities [10]. Vertigo attacks are often the first symptom of vertebrobasilar insufficiency, but if these episodes are repeated for many months and even more years, and other symptoms do not appear, then the diagnosis of vertebrobasilar insufficiency is doubtful [1]. Signs such as osteochondrosis of the cervical spine, sometimes the bending of one or both vertebral arteries, detected by ultrasound examination of the vessels of the neck, are also not sufficient grounds for concluding that the vertebrobasilar circulation is insufficiency. It has now been proven that isolated systemic vertigo, not accompanied by focal neurological symptoms, in the overwhelming majority of cases is a sign of damage to the peripheral parts of the vestibular system [10].
Occasionally, systemic vertigo can be caused by subclavian steal syndrome, caused by occlusion of one of the subclavian arteries proximal to the origin of the vertebral artery. In subclavian steal syndrome, retrograde blood flow occurs, as a result of which blood from the vertebral artery is directed to the distal subclavian artery.
To clarify the diagnosis between the peripheral and central mechanisms of development of vestibulopathy in the case of systemic vertigo that has arisen for the first time in middle-aged and elderly people with risk factors for developing cerebral stroke, an MRI of the brain is required [3,11].
All vertigo that does not fall under the description of systemic vertigo is classified as non-systemic vertigo. They are also divided into several types, depending on the causes of their causes.
The 1st group includes dizziness in the form of a feeling of weakness, lightheadedness, an approaching loss of consciousness. Dizziness occurs with sharp turns of the head, in stuffy rooms, ringing in the ears, fuzziness of the environment appear. This condition occurs with orthostatic hypotension, hypoglycemia, lipothymic (pre-syncope) reactions resulting from various cardiac diseases, such as sick sinus syndrome, atrial or ventricular tachyarrhythmias, atrioventricular blockade, aortic stenosis, etc. Pregnancy is a common physiological cause of non-systemic dizziness in women. Dizziness of this type often occurs as a manifestation of peripheral autonomic failure, with neurological diseases such as Shye-Drager syndrome and other degenerative diseases of the central nervous system [2,7].
To clarify the nature of dizziness and fainting, a cardiological examination is necessary to exclude cardiac pathology. The Dagnini-Ashner test, the Valsalva test have a certain diagnostic value. These tests indicate an increased reactivity of the vagus nerve. Such patients do not tolerate tight collars and stuffy rooms [7].
The second group of causes of non-vestibular vertigo includes conditions associated with instability. The cause of instability can be peripheral nerve damage, such as diabetic polyneuropathy, spinal cord disease, such as funicular myelosis, or cerebellar lesions. Balance and gait disorders (dysbasia) associated with paretic, atactic, hyperkinetic, akinetic, apractical or postural disorders are sometimes perceived and described by patients as conditions resembling vertigo. However, an analysis of the patient’s sensations shows in such cases that the patient may not have dizziness in the literal sense of the word, but there is a decrease in control over his body in the process of its orientation in space.
Dizziness can occur with pathological processes in the neck. These include dizziness in congenital bone pathology (Arnold-Chiari anomaly), in cervical osteochondrosis and osteoporosis (for example, in the picture of the posterior cervical sympathetic syndrome), and whiplash.
The third group is psychogenic dizziness. Complaints of dizziness are among the most common complaints in patients with neurotic disorders. Psychogenic dizziness is necessarily accompanied by severe fear and anxiety, as well as autonomic disorders – tachycardia, cardialgia, hyperventilation, increased sweating, etc. At the same time, patients define their sensations as lightheadedness, lightness in the head, often the symptoms of dizziness are combined with noise and ringing in the ears, increased sensitivity to sound stimuli, and unsteadiness when walking [7].
To diagnose the cause of dizziness, a detailed history is the most important. The following tests will also help a general practitioner: a complete blood count (hemoglobin), glucose levels, an ECG, and an x-ray of the cervical spine. As a more detailed examination, tone audiometry, electrocochleography, brain MRI are performed.
Treatment for dizziness depends on the underlying cause. With non-systemic dizziness, treatment of the underlying disease is necessary: ​​cardiological, psychogenic, etc. The treatment of vestibular disorders is a very urgent problem, especially considering the frequency of their occurrence and the impact on the quality of life of patients. Treatment of systemic vertigo consists of non-drug methods and drug therapy. Patients suffering from vestibular vertigo undergo a certain training. For this, special sets of exercises (vestibular gymnastics) have been developed that develop the ability of patients to control dizziness. Drug therapy includes symptomatic and pathogenetic therapy. Antiemetics, anxiolytics, diuretics are used to relieve acute conditions and alleviate the patient’s condition. Pathogenetic therapy includes taking both drugs that optimize cerebral circulation and specific drugs that act mainly on the structures of the vestibular analyzer. The histaminergic system plays an important role in the functioning of the vestibular structures, since transmission of impulses from vestibular receptors and vestibular nuclei is provided mainly by histaminergic neurons. Currently, three types of histamine receptors are distinguished: postsynaptic H1 and H2, as well as presynaptic H3 [2].
To date, the drug of choice for the treatment of vestibular vertigo is betahistine dihydrochloride. It was first used in 1962 for the treatment of cluster headache, and in 1965 its positive effect was noted in Meniere’s disease. In the last 20 years, a large number of studies have been carried out to evaluate the effectiveness of the drug, including a number of double-blind studies. The mechanism of action of betahistine is associated with an effect on histamine receptors. Betahistine acts primarily on histamine H1 and H3 receptors in the inner ear and vestibular nuclei of the CNS. By direct agonistic effect on the H1 receptors of the vessels of the inner ear, as well as indirectly through the effect on the H3 receptors, it improves microcirculation and capillary permeability, normalizes the pressure of the endolymph in the labyrinth and the cochlea. However, betahistine increases blood flow in the basilar arteries. It also has a pronounced central effect due to the effect on the H3 receptors of the nuclei of the vestibular nerve, normalizes the conductivity in the neurons of the vestibular nuclei at the level of the brain stem.
A number of studies have shown that the effectiveness of betahistine is associated with a decrease in both spontaneous and evoked impulses from vestibular receptors and vestibular nuclei. In the experiment, it was found that betahistine reduced the intensity and amplitude of firing of neurons in the lateral vestibular nucleus, both at rest and during stimulation [12].
Along with the effect on histamine receptors of peripheral and central vestibular formations, betahistine dihydrochloride has a vasoactive effect. The drug causes dilation of the arterioles and capillaries of the inner ear, which leads to a selective increase in blood flow. In addition, against the background of taking the drug, there is some increase in cerebral blood flow in the vertebrobasilar and carotid systems. The vasoactive effect of betahistine is presumably due to the blocking of H3-histamine receptors and, possibly, the effect on presynaptic adrenergic receptors.
One of the betahistine preparations is Tagista (Stada). Indications for its use are: dropsy of the labyrinth of the inner ear, vestibular and labyrinth disorders: dizziness, noise and pain in the ears, headache, nausea, vomiting, hearing loss; vestibular neuritis, labyrinthitis, benign positional vertigo (including after neurosurgical operations), Meniere’s disease. As part of complex therapy – vertebrobasilar insufficiency, post-traumatic encephalopathy, cerebral atherosclerosis. Depending on the duration and severity of dizziness, the drug is prescribed in a daily dose of 16-48 mg in 2-4 doses for a period of 2 months. Tagista has virtually no side effects. In rare cases, mild dyspepsia, skin allergic reactions and headache are observed.
Studies have shown the effectiveness of Tagist not only in peripheral vestibular syndrome, but also in the treatment of vestibular disorders in vertebrobasilar insufficiency. The results of these studies show almost the same effectiveness of Tagysta in peripheral and central vestibular syndromes, as well as in their combination. Complete disappearance of symptoms within 2 months. at a daily dose of 48 mg was observed in 35% of patients, a decrease in symptoms – in 60%. Thus, the drug showed its effectiveness in 95% of cases [7,12].

Literature
1. Solovieva A.D. Vertigo // Consilium Medicum. Neurology. T. 6. No. 2. 2004.
2. Diks M.R., Khuda D.D. Dizziness. M.: Medgiz, 1989.
3. Gorbacheva F.E., Natyazhkina., G.M., Chuchin M.Yu. Vertigo // Consilium Medicum. The most important symptoms and syndromes. T. 4. No. 2. 2002.
4. Lilenko S.V. Nystagmometry in the diagnosis of vertebrogenic dizziness: Abstract of the thesis. dis. … cand. honey. Sciences. SPb., 2000.
5. Yakovleva I.Ya., Alekseeva N.S. Modern methods of complex otoneurological examination in the diagnosis and pathogenesis of ischemic circulatory disorders of the inner ear and brain. All-Russian Congress of Neurologists, 4th: Proceedings. Kazan, 2001. 191 s.
6. Caplan L.R. Posterior Circulation Ischemia: Then, Now, and Tomorrow. The Thomas Willis Lecture. Stroke 2000; 31: 2011-2023.
7. Veselago O.V. Dizziness. M.: Triada-Pharm, 2001. 96 p.
8. Kamchatnov P.R. Vertebrobasilar insufficiency: Abstract of the thesis. dis. … Dr. med. Sciences. M., 2001.
9. Vereshchagin N.V. Circulatory failure in the vertebrobasilar system // Consilium medicum. 2001, pp. 15–18.
10. Alekseeva N. S. Cochleovestibular syndromes in vertebrobasilar insufficiency // Journal of Neurology and Psychiatry. S.S. Korsakov. No. 10. 2004.
11. Schick B., Brors D., Koch O. et al. Magnetic resonance imaging in patients with sudden hearing loss, tinnitus and vertigo Otol Neurootol 2001; 22:6:808–812.
12. Lavrov A.Yu. The use of Betaserc in neurological practice // Neurological journal. 2001. No. 2. T. 6. S. 10.

Dizziness, what kind of disease, symptoms, diagnosis, treatment

Adamant
medical clinic

St. Petersburg, embankment of the Moika River, 78.

+7 (812) 740-20-90

Content:

Dizziness is a disorientation in space, in which you get the impression that objects are rotating around him or yourself. You may experience various sensations when dizzy – weakness, feeling drunk, lightheaded, etc.

The most common cause of dizziness are banal causes – hunger, fatigue, motion sickness, etc. However, in some cases, the condition is a symptom of a dangerous disease. To avoid the severe consequences of a possible illness, contact Adamant Medical Clinic. You are guaranteed a comprehensive diagnosis and effective treatment.

Causes of dizziness

There are many causes of dizziness. From simple hunger or fatigue to dangerous diseases.

Any cause has associated symptoms:

• Inflammation of the inner ear – discharge from the ear and hearing impairment.
• Meniere’s syndrome – dizziness is accompanied by nausea, vomiting, tinnitus and hearing loss.
• Vestibular neuritis – regular vomiting, dizziness increases when trying to stand up or rotating the head.
• Periliphatic fistula – tinnitus, unilateral deafness, vomiting.
• Cranio-cerebral or whiplash injury – regular dizziness after trauma.
• Inflammation of the brain, swelling – dizziness is accompanied by pain in the head, which gradually increases in certain positions of the body, there is a violation of coordination of movements, speech disorders, loss of consciousness, etc.

As you can see, dangerous diseases of the internal organs can be the cause of dizziness. In the absence of timely medical care, they cause severe complications – up to death. Therefore, it is extremely important to seek diagnosis for regular dizziness.

Doctors of Adamant Medical Clinic will conduct a comprehensive diagnosis and provide effective treatment. This guarantees you the preservation of hearing and normal brain activity.

Treatment of dizziness

In the event that you are suddenly overtaken by dizziness, then calm down and sit down, try not to panic.