Case 1, a 63-year-old female, felt dizziness, rotating vision, nausea and vomiting when walking in the morning for a few seconds 4 months ago, and then had repeated attacks, usually when turning her head left or right or turning sideways. Since then, the patient often felt drowsy and uncomfortable and walked unsteadily, but there was no fall attack and no headache. During the course of the disease, the patient had difficulty sleeping, excessive dreaming, spontaneous sweating, palpitations, shortness of breath, and was very worried about the symptoms of dizziness. He had previous hypertension for 8 years, coronary artery disease, type 2 diabetes mellitus for 3 years, hypertriglyceridemia for 1 year, and denied history of trauma surgery.
Examination: normal range of blood pressure in the prone position; NS (-); vestibular function test (-); Dix-Hallpike test: no typical nystagmus was induced, but the patient had dizziness and nausea discomfort.
External ancillary tests: day 3 of onset: varus test (+) – localized right posterior semicircular canal lithotripsy; electrical audiometry: mild neurological deafness in both ears; cervical vascular ultrasound: bilateral internal carotid artery sclerosis with plaque formation; cranial MRI: multiple lacunar infarcts; head and neck CTA: right vertebral artery slender (consider abnormal development); ECG: sinus rhythm with ST segment changes
Blood test: LDL 3.4 mmol/L; cervical lateral opening radiograph: cervical degenerative changes
Case 2: A 48-year-old male, a company employee, developed paroxysmal subjective instability after lumbar disc surgery 2 years ago, after which it gradually persisted and became apparent during exercise, ceiling viewing, and supermarket shopping, and gradually became reluctant to go out and stopped working. Multiple neurological, otologic, imaging, nystagmography, vestibular function, and dynamic postural examinations showed no specific findings; HAMD=24′, HAMA=18′. Previous history of migraine for more than 10 years, with 1-2 attacks per month, without preventive treatment.
I. Basic understanding
Chronic dizziness is essentially a pathological compensation caused by the interaction between vestibular dysfunction and psychogenic disorders, and is a concept based on the interaction pattern of vertigo. The core features manifest: persistent dizziness or subjective unsteadiness for more than 3 months, high sensitivity to motor stimuli, poor tolerance to complex visual stimuli or fine visual tasks, and no accompanying active vestibular dysfunction. Anxiety is a core component of the psychophysiological model of chronic dizziness, but anxiety is not included in the core features of chronic subjective dizziness because focusing first on the presence or absence of anxiety may prematurely lead to the conclusion that the patient’s dizziness has a psychiatric cause, thereby omitting coexisting neuro-otologic disorders.
II. Clinical typology of chronic subjective dizziness
Classification
Subgroups
Manifestations and criteria
Anxiety disorders
Neuro-otologic
Chronic dizziness and anxiety following organic lesions
Psychogenic
Chronic dizziness in the course of anxiety disorders
Intercurrent
Chronic dizziness and anxiety disorders in persons with psychogenic anxiety disorders that are aggravated by a transient, definite disorder
Other psychiatric disorders
Somatic symptom disorder of DSM-V, conversion disorder
Vestibular migraine
Exclude those with paroxysmal vertigo and select only those with dizziness
Post-traumatic injury
Exclude those with significant vertigo after concussion or whip-like injury
Autonomic disorders
Dizziness, panic, pre-syncope, and worsening of symptoms after postural exercise
Cardiac arrhythmia
Second, diagnostic ideas
Vertigo: (1) motor hallucination, which is a kind of “inner vertigo”, such as common rotational vertigo or true vertigo; (2) often accompanied by nystagmus, balance disorder, gait instability, nausea and vomiting; (3) suggests hemianopia or central nervous pathway lesion.
Dizziness: ① impaired or impaired spatial orientation sensation, no false or distorted sensation of movement; ② heavy head, shaking sensation, stepping on cotton-like, drunkenness-like description; ③ vestibular lesions, medical diseases or psychological disorders.
Analysis of chronic dizziness: identify “chronic dizziness” rather than gait disorder; multifactorial analysis: involvement of one or more systems; retrospective diagnosis: whether there is previous “true vertigo; try to confirm some clinical syndromes.
Clarify whether it is a head or leg problem
Associated symptoms
Suspected diagnosis
Screening options
Vibratory hallucinations during head movements
Bilateral vestibular dysfunction
Head toss test / hot and cold test
Persistent vibratory hallucinations
Vertical downward nystagmus
Cranial MRI
Any memory impairment, urinary incontinence
Hydrocephalus/small vessel lesions in the brain
CT or MRI of the skull and brain
Any hand anesthesia, clumsiness or lower limb muscle
Increased tension
Spinal cervical spondylosis
MRI of the neck
Motor incoordination, dysarthria
Cerebellar ataxia
MRI of the head
Numbness and weakness in the distal extremities of any limbs
Peripheral neuropathy
EMG, laboratory tests
Motor retardation, tremor
Parkinson’s disease
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Common conditions with previous true vertigo: vestibular neuronitis, BPPV, Ménière’s disease, migraine, brainstem stroke, etc.
Presence of other factors preventing compensatory action of vestibular function: visual impairment: strabismus, cataract surgery; proprioceptive impairment: peripheral neuropathy; fluctuating vestibular disorders: recurrent dizziness; bone and joint problems; fear of falling and other psychological disorders; age factors.
III. Clinical management
1. Psychoeducation is a critical first step in the successful treatment of patients with chronic dizziness and is completed by medical personnel familiar with the somatic symptoms and psychiatric manifestations of chronic dizziness, as well as the completion of a prescribed period of psychoeducation for the patient.
2. pharmacological treatment, avoidance of long-term application of vestibular depressants, and emphasis on pharmacological dizziness/syncope.
3, vestibular rehabilitation treatment: basis: control of balance is the result of integration of multiple sensory information. Vestibular compensation is a plastic process of CNS function; Objective: to stimulate the vestibular system and promote CNS compensation of impaired vestibular function; Methods: including simple to complex eye, head and postural movements.