Dizziness is one of the most common symptoms in neurology, otolaryngology, psychiatry, and internal medicine, and most dizziness can be definitively diagnosed by obtaining an accurate history through detailed questioning. It is common to encounter a group of dizzy patients who can only describe a vague sensation (including chronic dizziness, tightness in the head, and sensations of rising and falling from the floor) despite the physician’s efforts to obtain a history. These dizzy patients have no clear vestibular damage and are therefore referred to as “extra-vestibular symptoms” or “psychogenic dizziness”. For this reason, Wuehr et al. proposed the concept of phobic positional vertigo, which consists of two behavioral criteria.
(i) obsessive-compulsive personality, a sense of instability and mild depression.
② anxiety and vegetative disorders.
And Vaillancourt et al. proposed spatial-motor discomfort, with the main symptoms being.
① inability to perform normal spatial orientation based on visual or deep sensory information.
② Special sensitivity to normal motion.
Bronstein also proposed visual vertigo, in which patients with balance disorders and high visual field dependence induce vertigo or dizziness in the presence of complex visual stimuli. However, these concepts do not provide an accurate and comprehensive overview of the clinical features of “vague sensations” mentioned above. Therefore, based on previous studies, Staab proposed the concept of chronic subjective dizziness (CSD), which refers to prolonged (≥3 months) non-rotational dizziness; subjective instability; high sensitivity to motion stimuli; and exacerbation of these symptoms in complex visual environments (e.g., walking in crowded shopping malls, driving in the rain, etc.). Otological examination and balance function examination showed no active vestibular dysfunction. The research progress of CSD is reviewed.
Epidemiology
The age range of patients with CSD is from adolescence to old age, and the incidence of CSD increases with age. The incidence of CSD in patients with previous neuro-otologic disorders is approximately 25%. A study confirmed that of 189 patients with CSD aged 19-64 years, 68.2% had a psychiatric disorder (including somatization disorder, anxiety or depression disorder), 16% had both vestibular disorders and psychiatric disorders, and 51.1% had only psychiatric disorders.
Etiology and pathogenesis
The majority (93%) of CSDs have a primary cause of psychogenic factors. Among them, anxiety disorders are the most common psychiatric disorders, including acute anxiety and generalized anxiety disorder. Patients with excessive anxiety, obsessive-compulsive personality or panic attacks may present with dizziness similar to vestibular disorder.The pathophysiological mechanisms of CSD are related to the human’s own threat response system and anxiety temperament.CSD can also evolve from organic disorders. Studies have found that CSD frequently occurs in patients with neuro-otologic disorders (e.g., vestibular neuritis or benign positional vertigo), neurologic disorders (e.g., migraine, post-concussion syndrome), or other systemic disorders (e.g., cardiac arrhythmias). The vestibular system and the nervous system can influence the degree of anxiety through the activity of the limbic system. There are direct connections between the vestibular nuclei and brainstem regions, between sympathetic and parasympathetic nerves, and between some regions of the limbic system. Balance control information from the vestibule and other balance information reaches the central nervous system via a common upstream pathway for integrated analysis, and balance control information from the vestibule plays a key role in the development of conditioned taste aversion and anxiety. This pathway may explain why vestibular disorders and psychiatric disorders often coexist.
Autonomic dysfunction is another cause of chronic non-rotational dizziness. Studies have demonstrated that 80% of patients with chronic persistent dizziness have at least one autonomic dysfunction, manifested by postural hypotension, postural tachycardia syndrome, and mildly increased heart rate with decreased diastolic blood pressure. Autonomic dysfunction includes decreased sympathetic nerve function and sympathetic hyperexcitability. The mechanism of sympathetic dysfunction causing CSD may be that either decreased sympathetic function or hyperexcitation leads to central nervous system hypoperfusion, causing an imbalance in the sympathoadrenergic system, which eventually leads to the appearance of dizziness symptoms.
CSD classification
CSD often occurs in patients with a history of neuro-otologic disease (e.g., vestibular neuritis or benign positional vertigo) or neurologic disease (e.g., migraine, post-concussion syndrome), which is critical for clinicians to differentiate between symptoms of neuro-otologic disease (vertigo) and symptoms of CSD (chronic nonrotational dizziness). For example, a patient with Ménière’s disease may complain of persistent dizziness, but if the patient has more vague and persistent symptoms consistent with CSD (not uncommon in patients with Ménière’s disease), then irrational treatment may exacerbate the patient’s anxiety symptoms; similarly, patients with episodic dizziness, such as benign positional vertigo, and vestibular neuritis may trigger anxiety reactions and CSD symptoms even after a single episode is cured. There are also a few patients with CSD who suffer from primary anxiety disorders, and studies have confirmed that anxiety disorders and their associated disorders cause and/or maintain dizziness symptoms. In contrast, most anxiety disorders are triggered by or coexist with neuro-otologic disorders. Based on the previous interrelationship between CSD and neuro-otologic disorders and psychiatric disorders, they are classified into three types: neuro-otologic CSD, psychogenic CSD, and interactive CSD.
Diagnostic criteria
CSD is a specific clinical syndrome that is fundamentally characterized by persistent nonspecific dizziness that cannot be explained by existing medical conditions, and it is not an exclusionary diagnosis.The diagnostic criteria for CSD are as follows.
Persistent nonrotational dizziness: persistent (≥3 months) nonrotational dizziness that may include one or more of the following symptoms: dizziness; light-headedness; frequent unsteadiness that is not apparent to others; sensation of “internal” rotation of the head without any perception of movement of visible objects around; sensation of the floor moving from bottom to top; and sensation of movement between oneself and the environment. The severity of the above symptoms may fluctuate.
(ii) Persistent motion stimulus sensitivity: persistent (≥ 3 months) high sensitivity to own motion (no direction specificity) or high sensitivity to movement of objects in the environment.
(iii) Visual vertigo: exacerbation of symptoms in environments with complex visual stimuli (e.g., grocery stores or shopping malls) or when performing delicate visual tasks (e.g., operating a computer).
(iv) Past medical history: including possible episodes of true vertigo or ataxia, with symptoms changing to those described in ① to ③ above after improvement.
⑤ Imaging: cranial imaging findings excluding anatomical lesions of neuro-otological importance.
⑥ Balance function examination: balance function examination results are within the reference range or no diagnostic findings are found. This criterion includes patients who have reached clinical recovery from previous neuro-otological disease, balance function tests suggesting complete compensation of vestibular function, and other examination abnormalities that do not explain the current symptoms.
Differential diagnosis
1. Vestibular migraine
Vestibular migraine occurs mostly in elderly patients and can be manifested as rotational or non-rotational vertigo, which can last for seconds, minutes, hours or days. 10%-30% of patients have typical vestibular aura, such as visual aura (intensification, solid or false dark spots, visual field defects) or somatosensory aura (such as sensory dullness, sensory abnormalities), which lasts for 5-60 min. migraine has established diagnostic criteria, many of its symptoms are variable, such as vertigo or dizziness that can occur before, during, or after a migraine. Less than 25% of patients have dizziness or vertigo with each headache episode, and nearly 30% of vestibular migraines are not associated with a migraine. Sometimes vertigo may present as the main symptom, when the patient often complains of only a slight tightness in the head without the typical migraine complaints. Not all patients have vertigo and headache at the same time, but the typical migraine-related symptoms (such as photophobia, photophobia, nausea and vomiting, exacerbated by exercise or relieved by rest) are an important basis for diagnosis.
Vestibular migraine is triggered by the same factors as migraine, such as the menstrual cycle, sleep restriction, stress, diet (cheese, red wine, glutamate), and possibly climate change. Treatment recommendations for vestibular migraine are similar to those for migraine, with zolmitriptan being the first choice for acute vestibular migraine attacks. Patients with excessive nausea or vomiting may be treated by non-oral means (i.e., nasal sprays, suppositories, or subcutaneous injections) or by intravenous administration [e.g., acetylsalicylic acid (1000 mg) and metoclopramide (10 mg) or cyproheptadine tablets (62.5 mg)]. Prophylactic medication is different from aura migraine or migraine without aura, including propranolol 80~240mg/d, metoprolol 50~200mg/d, bisoprolol 5~10mg/d or flunarizine 10mg/d, also topiramate 25~100mg/d and valproic acid 500~600mg/d.
2.Benign paroxysmal positional vertigo (BPPV)
BPPV is the most common cause of peripheral vertigo and is caused by the dislodgement of oval sac of the inner ear (commonly known as “otolith”), which is free in the lymphatic fluid in the semicircular canal or adheres to the cap of the jugular ridge and causes episodes of vertigo related to head position changes, accompanied by nystagmus, autonomic symptoms and balance disorders. It is associated with nystagmus, autonomic symptoms, and balance disturbances. The typical presentation is a brief episode of vertigo associated with a change in head position (e.g., lying down, sitting up, turning over in bed, or raising, lowering, or turning the head), lasting less than 1 minute and accompanied by autonomic symptoms such as nausea, vomiting, panic, and sweating. Patients with interictal episodes may have no manifestations or a few patients may have dizziness and a mild sense of imbalance. Unless other ear disorders are present, patients with BPPV do not have tinnitus, stuffiness, or hearing loss during episodes or intervals, and vestibular function tests are mostly normal. According to the involved semicircular canal, BPPV can be divided into superior semicircular canal BPPV, horizontal semicircular canal BPPV, posterior semicircular canal BPPV, and mixed BPPV, and the treatment of BPPV is preferred to otolith repositioning.
3.Ménière’s disease
Meniere’s disease is the most common form of acute onset vertigo causing hearing loss, and the recognized pathological change is membrane vagal effusion. The clinical diagnosis relies on a series of symptoms, signs and tests with diagnostic significance. The typical clinical manifestations are unilateral fullness, tinnitus, fluctuating hearing loss in the ipsilateral ear and severe vertigo with nausea and vomiting lasting 20 min to 12 h. Low to mid-frequency sensorineural deafness in the affected ear can be detected on electroaudiometry. In severe cases, hearing loss may occur, while the dizziness may be reduced. Medication is preferred for Ménière’s disease, while restriction of salt intake and diuretics can slow down the progression of Ménière’s disease. For intractable Ménière’s disease, endolymphatic bursa surgery is preferred, followed by intra-dural injection of gentamicin.
4. Bilateral loss of vestibular function
By far, bilateral vestibular function loss is most commonly caused by aminoglycoside ototoxicity. The main clinical manifestation of aminoglycoside-associated vestibular loss is episodic vertigo lasting several minutes to several hours per episode, often accompanied by renal failure, without deafness, which resolves after a few days with severe vibratory hallucinations and balance disorders, and is easily misdiagnosed as a cerebellar stroke.
Treatment
1.Psychotherapy
Psychotherapy is the first step in the treatment of CSD and the most critical step for success. Appropriate education of the patient is the key to the success of subsequent interventions. One modality in psychotherapy is autonomy training. A German psychiatrist created autonomy training, which alleviates mental disorders caused by high levels of mental stress by affecting the autonomic nervous system. Autonomy training can improve subjective symptoms in patients with refractory CSD (other interventions are less effective).
2.Pharmacological treatment
Selective 5-hydroxytryptamine reuptake inhibitors have replaced tricyclic antidepressants, monoamine oxidase inhibitors, and benzodiazepines as the first-line treatment for most anxiety-depression disorders. There are currently five 5-hydroxytryptamine reuptake inhibitors, namely fluoxetine hydrochloride, sertraline hydrochloride, paroxetine hydrochloride, fluvoxamine maleate, and citalopram hydrobromide. Compared with traditional drugs, 5-hydroxytryptamine reuptake inhibitors have the advantages of being well tolerated, easy to prescribe, safer to overdose, no need to test serum drug concentrations, less adverse effects, weaker withdrawal reactions, and non-addictive. The efficacy of 5-hydroxytryptamine reuptake inhibitors was found to be independent of the severity of psychiatric symptoms and was related to the duration of CSD, with patients with a duration of 3 to 31 months being more effective than those with a duration of 36 to 336 months. Patients with inactive neuroscientific diseases (e.g., BPPV, vestibular neuritis, etc.) are effective with 5-hydroxytryptamine reuptake inhibitors alone; patients with Ménière’s disease, autoimmune diseases, and migraine can be treated with maintenance regimens for the respective diseases; patients with CNS diseases and cardiogenic arrhythmias are less effective and can be treated with a combination of benzodiazepines if necessary. If necessary, benzodiazepines can be combined with the drugs.
3.Cognitive-behavioral therapy
Cognitive behavioral therapy is an effective treatment for anxiety disorders and includes psychoeducation about dizziness, education about the adverse effects of excessive attention to dizziness, exposure exercises to reduce avoidance and safety behaviors, optional strategies for coping with dizziness (e.g., distraction and ignoring dizziness symptoms), and encouragement by telling patients that they are “back to their normal lifestyle” regardless of the presence or absence of symptoms. “EJ Mahoney et al. showed that cognitive behavioral therapy is also effective for anxiety-related dizziness, significantly reducing anxiety, depressive symptoms, and dizziness disability, and can be effective within days to weeks, but only in the short term (1-6 months), so the longer the intervention, the greater the benefit; and cognitive behavioral therapy is significant for patients with interactive CSD patients, as these patients do not respond well to pharmacological treatment alone.
4. Vestibular and balance rehabilitation therapy
Vestibular and balance rehabilitation is indicated for patients with mild anxiety-depression disorder with chronic vestibular deficits, complaints of unsteadiness and fear of falling, but who do not present with panic attacks and agoraphobia. Vestibular and balance rehabilitation consisted of hospital treatment and subsequent home treatment, where patients attended a 15-d rehabilitation course of 2-h sessions with 2- to 3-minute training intervals, including training to improve vestibulo-ocular reflexes and/or alternative habituation, followed by a final 10-minute pause followed by stabilizing platform exercises on a sidewalk using rehabilitation software to restore correct static and dynamic stability. The execution and duration of the training were individualized by the therapist according to the clinical symptoms and dysfunction of each patient, and the patients were taught how to perform the rehabilitation training at home. after discharge, the patients were asked to adhere to the home exercise for 1 month, which was performed twice daily for 20-30 min. the results of the study showed that after 2-3 weeks of adherence to the training, it was found that the balance function of the patients was improved, and the dizziness and instability were alleviated, but the degree of anxiety disorder was not reduced and could only be improved by cognitive behavioral therapy.
Since the first report in the literature of a patient with complaints of chronic dizziness, sensitivity to motor stimuli, discomfort in open spaces, varying degrees of anxiety, and fearful posture, researchers have continued to learn, recognize, and study the disorder. In turn, the definition of CSD will be internationally recognized by the Vestibular Disorders Classification Committee of the Barany Society.CSD is a major challenge to diagnose and treat in neurological outpatient clinics, and most patients’ dizziness symptoms can be relieved by interventional treatment targeting the underlying psychiatric disorder.