Persistent Postural-perceptual Dizziness: A Review

Abstract

Introduction:

Persistent postural-perceptual dizziness (PPPD) is characterized by chronic subjective dizziness, phobic postural vertigo, and related disorders. For at least 3 months, it exhibits varying symptoms of vertigo, unsteadiness, or dizziness.

Methods:

Research articles regarding PPPD were searched by viewing the Scopus, PubMed, Medline, and Google Scholar databases online. A search strategy using the Preferred Reporting Items for Systematic Reviews and Meta-Analysis was used.

Results:

It presents a typical chronic vestibular system and brain malfunction that result in persistent dizziness, nonspinning vertigo, and/or unsteadiness. Persistent nonvertiginous dizziness and hypersensitivity to motion and visual stimuli are the main signs and symptoms of PPPD. These symptoms appeared either when there were no active neuro-otologic illnesses or when an episodic vestibular condition was present but could not completely account for the symptoms. Psychological mechanisms that resemble cognitive models of health anxiety and panic disorder are involved in the PPPDs development and maintenance.

Conclusion:

Since PPPDs diagnostic criteria only involve symptoms, the patient's clinical history is crucial in making the diagnosis. Once diagnosed, effective communication and personalized treatment plans, such as serotonergic medicines, cognitive behavioral therapy, and specialized physical therapy (vestibular rehabilitation), help manage PPPD. Since PPPD is a relatively recent clinical diagnosis, many medical practitioners who treat patients who feel dizzy are unfamiliar with it.

Introduction

In primary care facilities and the neurology clinic, dizziness is the most frequently reported symptom; headache is the second-most frequently reported symptom.^[1],[2] Chronic neurological disorder called persistent postural-perceptual dizziness (PPPD) causes unsteadiness and nonspinning vertigo.^[3] A functional disorder called PPPD results in severe distress or functional impairment. PPPD, also known as chronic subjective vertigo, is frequently seen in patients who complain of vertigo at neuro-otology and neurology clinics.^[3] A number of clinical terms, including supermarket syndrome, visual vertigo, persistent subjective vertigo, space and motion discomfort, and phobic postural vertigo, have lately been combined under the umbrella term PPPD.^[4] Vertigo or unsteadiness with vestibular, neurological, or mental origins is a PPPD symptom. PPPD is dizziness that persists for more than 3 months without a medical cause.^[4] The patient's motor response pattern has changed, and the majority of them exhibit intense anxiety. This somatoform illness sits at the crossroads of neuro-otology and psychiatry. Patients with PPD are more likely to continue to feel queasy after experiencing physical or mental illness.

Methods of Literature Search

Research articles regarding PPPD were searched through multiple approaches. We began by doing an online search of the Scopus, PubMed, Medline, and Google Scholar databases. The Preferred Reporting Items for Systematic Reviews and Meta-Analysis criteria were used to design a search strategy. While additional research publications were manually found from the citations, our search method recognized the abstracts of published works. The eligibility included randomized controlled trials, observational studies, comparative studies, case series, and case reports that assessed adequately. A total of 46 articles were included such as 16 case reports, 12 case series, and 18 research articles [Figure 1]. The epidemiology, etiopathology, clinical profile, diagnosis, and available treatments for PPPD are covered in this article. This review article provides a starting point from which future prospective trials can be developed, and it could serve as a catalyst for more investigation into this clinical syndrome known as PPPD, for which there are currently very few studies available.

Figure 1

Flow chart showing methods of literature search

Epidemiology

There have not been any sizable epidemiological studies published yet that describe the prevalence or incidence of PPPD. Recent changes to the diagnostic terminology include PPPD.^[5] When it was introduced to the Barany Society's international classification of vestibular disorders in 2017, it was first described.^[6] It was also added to the International Classification of Diseases 11 by the World Health Organization.^[7] Validated statistics on the incidence and prevalence of PPPD are hard to come by. According to the UK research, 4% of all patients registered with general practitioners had chronic dizzy symptoms, and the majority of these individuals were rendered helpless by their symptoms.^[8] Approximately 2% of all secondary referrals in neurology outpatient clinics were detected mainly with vertigo or dizziness, and 50% of them were considered psychological/functional.^[9] In another study at a tertiary dizziness canter, about 15%–20% of all patients presented with PPPD.^[10]

Pathophysiology

PPPD's pathogenesis is complex and poorly understood.^[11] Multisensory maladjustment causing alterations of the sensory response pattern, such as vestibular, visual, and motion stimuli, is the key factor for explaining the pathophysiological correlation of this disorder.^[12] The diagnosis of PPPD as a functional condition distinguishes it from mental reasons as well as vestibular symptoms brought on by structural vestibular system deficits.^[13] PPPD is a clinical condition that affects the vestibular-thalamic circuits, which are in charge of body movement awareness.^[14] Anxiety and fear are predisposing variables for the sensitivity of the structures connected to the vestibular-thalamic pathways, which define the beginning of symptoms. Data from physiological studies and structural and functional neuroimaging studies of patients with phobic postural vertigo, chronic subjective dizziness, and PPPD itself show three key mechanisms by which this disorder is thought to develop, even though the exact pathophysiology of PPPD is still unknown.^[15]

These include tightened postural control, a preference for visual over vestibular inputs in the processing of spatial orientation information, and a failure of higher cerebral mechanisms to modify the first two processes. As seen in healthy individuals exposed to great heights or slippery surfaces, the physiological response to the onset of dizziness, vertigo, or fear of falling is to activate high-risk postural control strategies (e.g., shorter strides and stiffened stance), which rely more on visual or somatosensory inputs than vestibular signals.^[16] An acute behavioral response, including high anxiety, excessive vigilance about vestibular and balance sensations, and prolonged high dependence on visual cues for spatial orientation, is predictive of failure of symptomatic recovery in cases of persistent dizziness following acute vestibular syndromes.^[17],[18]

Clinical Manifestations

More women experience PPPD, a disorder caused by psychological and somatic connections, throughout the menopause period.^[19] One study showed a higher prevalence of PPPD with a ratio of females to males of 1.67:1, particularly in the age range of 46–55 years.^[19] Hormonal alterations are thought to be the cause of the increased prevalence of PPPD in females.^[20] This is often associated with metabolic disorders and migraine.^[21] The average length of the condition in PPPD patients is around 4.5 years, although in some cases, it can last for several decades, placing a significant burden on the patients and their families.^[3] Patients with PPPD bear a physical as well as a psychological and financial burden. PPPD's physical symptoms can frequently be incapacitating. Gait problems, anxiety, avoidance behavior, and severe impairment are common in PPPD patients.^[22] Visual conflict, head motions, stress, and sleep loss are the main PPPD triggers. When patients retain upright postures and in environments with complex or moving visual stimuli, the symptoms of PPPD are aggravated. Cinemas, oddities, and highly visual places like supermarkets are common vestibulo-visual conflict triggers. Walking, standing, staring at traffic, or sitting in a crowded restaurant are additional typical provocating elements that could be interpreted as offensive or menacing. Patients frequently experience functional gait irregularities and unnaturally high levels of awareness of their balance.^[17] The second-most frequent condition diagnosed in dizziness clinics is PPPD, which is more common in middle age.^[10] PPPD is chronic in nature and can endure for months or years.^[23] Consistent sway or instability that cannot be seen on a physical examination, worsening symptoms while standing, symptoms that are aggravated by head movements or complex visual stimuli, the presence of an underlying illness or emotional shock at the time of symptom onset, concurrent diseases that contribute to the symptoms, and anxiety are defining characteristics of PPPD.^[24] Episodes of vertigo or unsteadiness that have a vestibular, neurological, or mental disorders lead to PPPD. The use of high-demand postural control methods and an overreliance on visual cues for specific orientation appear to be brought on by these triggering variables. Vertigo, unsteadiness, dizziness, or balance issues are the initial triggers for this illness. There is no other illness or pathology that can more adequately explain the symptoms.^[25] According to the theories put forth by Staab and Ruckenstein, PPPD can result in three distinct manifestations: psychogenic, where worry is the only factor contributing to dizziness; otogenic: An otoneurologic condition that acts as a catalyst for the onset of anxiety, and an otoneurologic condition that causes dizziness interacts with preexisting anxiety symptoms to make them worse.^[26] According to reports, the degree of the initial unbalance and the anxiety that was brought on by physiological sensations throughout the incident is closely related to how long the dizziness lasts.^[27] Anxiety impairs eye tracking, motor coordination, and postural control.^[28]

Diagnosis

Patients with PPPD will require many doctors and frequently be encouraged to undergo a number of tests without receiving a solution to their symptoms. Although PPPD is not an excluding diagnosis, it must be the only possible explanation for the symptom in order for the diagnosis to be made. Long-term nonrotational dizziness, unsteadiness, fluctuations in symptoms with stimulus-triggered provocation, and/or exacerbation (e.g., visual stimuli), with a distinct feature of short episodes of momentarily worsening dizziness, are among the significant clinical presentations aiding in the diagnosis of PPPD.^[29] The identification of primary clinical symptoms and exclusion of other neurological or active medical conditions requiring treatment is the first steps in the diagnosis of PPPD, which is inherently interdisciplinary. Barany Society criteria [Table 1] must be met for the diagnosis of PPPD. The patient's history is the primary factor in the diagnosis. Clinical manifestations of PPPD that are significant include unsteadiness and nonspinning vertigo. The diagnosis of PPPD is achieved by gathering enough historical information to identify patients who meet the diagnostic requirements for this condition. It is not an exclusionary diagnosis. Standing up straight, moving around actively or passively (such as walking or riding in a car), or being exposed to environments with complex or moving visual stimuli (such as a hallway with intricately patterned carpet, a supermarket aisle, or traffic) can all exacerbate the clinical symptoms. Visual vertigo might cause these visual sensitivities as a symptom.^[30] With the increasing intensity of visual stimuli in the current period, visual vertigo is a defining hallmark of PPPD. Although the symptoms frequently wax and wane, they are typically thought of as persistent. There are no statistics on the interclinical agreement and no objective test to validate or disprove the diagnosis. As a result, a false positive rate in patients is unknown, and it is also impossible to quantify it for a segment of the general population that does well on the questionnaires. Functional magnetic resonance imaging (fMRI) testing, a recent advancement in brain imaging, has revealed abnormal changes in the brain. The change in visual and vestibular information, in particular, has been frequently seen. Visuospatial emotional and vestibular-navigational brain networks, which combined visual, vestibular, and emotional responses to assist spatial mobility, have reduced functional connectivity in PPPD patients with subclinical agoraphobia more than in healthy individuals.^[31] In PPPD patients, increased visual cortex activity is linked to how dizzy they feel.^[32] Patients with PPPD have significantly lower values for the amplitude of low-frequency fluctuation and regional homogeneity at the right precuneus and cuneus, suggesting that changes in the spontaneous functional activity of the cuneate lobe and anterior cuneate lobe may lead to abnormal integration of visual and vestibular information.^[33] Microcirculatory alterations are visible in the radiological results, which may be significant in the development of PPPD. Patients with PPPD typically experience reduced blood flow to the cortical regions with altered anatomical and functional connections, especially in the visual-vestibular network.^[34] The changes in cerebral blood flow shown by the blood-oxygen-level–dependent signal in fMRI and the photon emission patterns in single photon emission computed tomography may be brought on by the metabolic demands of the brain tissue.^[35]

Table 1

Barany Society diagnostic criteria for persistent postural-perceptual dizziness

Treatment

Some fundamental ideas are taken into account in the therapeutic strategy for PPPD. Correct symptom identification is the initial step, which is followed by adequate dietary guidance, medication, vestibular rehabilitation, and psychotherapy. Vestibular rehabilitation treatment (VRT) is a self-administered habituation program that can be tailored to the needs of the individual to adequately relieve symptoms without having any negative side effects. In individuals with PPPD, VRT dramatically lowers the functional, physical, and overall scores on the dizzy handicap inventory.^[36] The standard procedures of adaptation and substitution do not apply because vestibular rehabilitation is dependent on the accurate diagnosis of problematic movements and on showing the patient that their anxiety of performing these movements is unwarranted. The preferred kind of psychotherapy is short cognitive behavioral therapy. This therapy enables the patient to express the distressing circumstances and select the appropriate response.^[37] Psychometric testing is used to assess the degree of perceived harm caused by dizziness and to aid in mental screening. So far, there have not been any extensive, randomized, and controlled trials for the treatment of PPPD. However, for the treatment of PPPD, a few small-scale controlled studies of vestibular rehabilitation and psychotherapy were undertaken.^[38] The drugs used for the treatment of PPPD are selective serotonin reuptake inhibitors (SSRIs). Through anxiety circuits and central vestibular neurons that respond to movement, these medicines alter and modulate neuronal conduction. As many as 70% of patients can experience symptom decrease with the proper SSRI use after about 3 months of medication.^[1] Long-lasting symptoms of PPPD can affect patients at an early age, placing a heavy burden on children and adolescents, many of whom are unable to attend school. In addition, cognitive behavioral therapy, SSRIs, and vestibular rehabilitation are used to treat young children with PPPD.^[39]

Conclusion

A chronic condition known as PPPD is characterized by varying sensations of vertigo, unsteadiness, and dizziness for at least 3 months. This functional disorder, known as PPPD, is quite distressing. The pathogenic mechanism of PPPD is complex, and it is a highly diverse condition with a wide range of triggering variables and comorbidities. In addition to exposure to moving visual stimuli or intricate visual patterns, upright posture, active or passive movements without attention to location or direction, and these factors may make the symptoms worse. PPPD is diagnosed clinically based on the patient's history, the symptomatological pattern, the clinical manifestations, and the results of any available tests. Different treatment approaches and philosophies are available, but it is difficult to determine whether they are clinically helpful. Cognitive behavioral therapy, vestibular rehabilitation exercises, and serotonergic medications are all possible treatments for PPPD.