Vertigo associated with head position changes refers to vertigo that occurs when the head position is changed. It is not uncommon in clinical practice, and patients are often seen in neurology and orthopedics, and are often diagnosed with posterior circulation ischemia (PCI) cervical spondylosis, but in fact this is not the case. The most common of them is still vertigo caused by peripheral vestibular system lesions, benign paroxysmal positional vertigo, and studies have shown that benign paroxysmal positional vertigo accounts for about 86.61% of vertigo related to head position changes. However, many doctors are unable to distinguish the characteristics of the three types of vertigo, which leads to misdiagnosis and delays the treatment of patients who cannot be seen by otologists in time.
Benign paroxysmal positional vertigo (BPPV)
Benign paroxysmal positional vertigo, also known as canaloliths or otoliths, is an idiopathic peripheral vestibular disorder characterized by transient vertigo induced by changes in head position with a prevalence of about 64/10,000, mostly in middle-aged and elderly people. It was first described by Barany (1921) and further elaborated by Dix and Hallpike (1952). In most cases, there is no obvious trigger for the onset of the disease, while possible triggers are mostly seen in trauma and the rest in post-operative ear surgery, viral infections, tumors, prolonged bed rest, etc. It is also more commonly associated with Ménière’s disease. The posterior semicircular canal (PC) is in the most vulnerable position to gravity when the body is upright and lying down, so the incidence is the highest, accounting for 91%. This is followed by the horizontal semicircular canal, and the upper semicircular canal is the least.
I. Pathogenesis
It is believed that the otoliths located in the ellipsoidal sac degenerate and fall out into the semicircular canal, causing the semicircular canal, which originally only senses angular acceleration changes, to respond to the linear acceleration caused by the displacement of the otoliths by gravity during a specific head position change, and inducing vertigo, which is supported by the presence of basophilic material (otoliths) in the semicircular canal. Currently, there are two main theories to explain the pathophysiological process.
(i) cupulolithiasis, proposed by (Schuknecht 1969), suggests that a degenerated and dislodged otolith adheres to the apex of the posterior semicircular canal cupula.
(2) canalithiasis, first proposed by Hall (1979) and supported by Epley et al, suggests that the otoliths in the posterior semicircular canal are not in a state of adhesion but in a state of suspension. Thus, when the head position is changed, the otoliths in the above mentioned state are directly or indirectly led by gravity to the deviation of the jugular crest and symptoms appear.
Clinical characteristics
1. Onset characteristics: temporal and spatial: paroxysmal transient vertigo induced by specific head position changes, often induced during sleep turning and rising, and each time lasting less than 1 minute.
2. Characteristics of vertigo: ① latent period: symptoms appear only after a few seconds after the change of head position. (2) Duration – Gradually strong, gradually weak, brief, reversible, fatigue. ③Adaptability (easy fatigue).
3. Nystagmus characteristics: rotational or horizontal, groundward.
III. Diagnosis
Diagnostic criteria: History of transient vertigo attack induced by specific head position change. There is an incubation period of several seconds before the onset, and the duration is <60 seconds, usually 20-30 seconds.
Positive Dix-Hallpike test. The procedure of this test is as follows: the examiner helps the patient to quickly change from sitting position to lying head suspension position with the subject ear pointing to the ground; the patient is helped to sit up again quickly. The head is kept in a 45° sagittal position throughout the entire transfer process. Positive test performance: after a short latency period (2-5 seconds) in the suspended head position, a brief vertigo attack and/or nystagmus lasting <30 seconds, directed toward the subject's ear; after a sitting position, a nystagmus in the opposite direction. The test may be easily fatigable, i.e., after several sessions, vertigo and nystagmus may not be induced, and the test may be repeated at another time.
Dix-Hallpike test
IV. Treatment
Semont (1988) and Epley (1992) proposed their treatment methods: Semont’s canalith repositioning procedure (CRP) and Semont’s maneuver. Although many authors have made different modifications based on their methods, these two methods are still the classical and main methods of treating BPPV with comparable efficacy. The manual repositioning method is simple, noninvasive and has obvious complications, and can be performed on an outpatient basis, often with an efficiency of more than 90%. Vestibular rehabilitation can also be performed at home under the guidance of a physician.
Epley manual repositioning
Cervical vertigo
Cervical vertigo, also known as cervical syndrome, is mainly related to cervical diseases, such as cervical spine, muscles, ligaments, blood vessels and nerves, which can cause cervical vertigo. The disease is closely related to cervical spondylosis, and cervical instability plays an important role in the development of cervical spondylosis. According to the involvement of adjacent tissues and structures, cervical spondylosis can be clinically classified into four types: spinal, radicular, vertebral artery and sympathetic. Sympathetic cervical spondylosis caused by vertebral instability is more common, but the latter also has its own strict diagnostic criteria.
Sympathetic cervical spondylosis has a wide range of symptoms, most of which are sympathetic excitation symptoms and a few are sympathetic inhibition symptoms. The common symptoms are.
(1) Head symptoms: such as dizziness, headache or migraine, head sinking, occipital pain, memory loss and difficulty concentrating. Occasionally, people fall down due to dizziness.
(2) Eye symptoms: eye swelling, dryness, changes in vision, blurred vision, and fog in front of the eyes.
(3) Ear symptoms: tinnitus, hearing loss.
(4) Gastrointestinal symptoms: nausea or even vomiting, bloating, diarrhea, indigestion, belching, and foreign body sensation in the throat, etc.
(5) Main vascular symptoms: palpitations, heart rate changes, arrhythmias, blood pressure changes, etc.
(6) Excessive sweating, no sweating, chilliness on the face or a certain limb, sometimes feeling pain and numbness but not distributed according to nerve segments or travels.
The above symptoms are often clearly related to body position or activity, aggravated when sitting or standing, and alleviated or disappeared when lying down. If the symptoms are accompanied by neck discomfort or pain and stiffness, sympathetic cervical spondylosis is highly suspected. If cervical spine orthogonal and lateral radiographs and cervical spine magnetic resonance imaging (MRI) are performed, and if obvious compression of the spinal cord is found, and most of the compression comes from the anterior intervertebral disc or the bone spur at the posterior edge of the vertebral body and the ossified posterior longitudinal ligament, and if it is accompanied by symptoms such as pain, numbness and weakness of the extremities and unsteadiness in walking, then the diagnosis can be basically clear.
Posterior circulation ischemia
The posterior circulation, also known as the vertebrobasilar system, consists of the vertebral artery, the basilar artery and the posterior cerebral artery, which mainly supplies blood to the brainstem, cerebellum, thalamus, occipital lobe, part of the temporal lobe and the upper spinal cord. Posterior circulation ischemia (PCI) is a common ischemic cerebrovascular disease, accounting for approximately 20% of ischemic strokes. PCI refers to TIA and cerebral infarction of the posterior circulation. Its synonyms include ischemia of the vertebrobasilar system, TIA of the posterior circulation with cerebral infarction, vertebrobasilar artery disease, and vertebrobasilar artery thromboembolic disease.
The main etiologies of posterior circulation ischemia include (1) atherosclerosis is the most common vascular pathology manifested by PCI. The mechanisms leading to PCI include: large artery stenosis and occlusion causing hypoperfusion, thrombosis, and arterial-derived embolism. Atherosclerosis is more likely to occur in the beginning and intracranial segments of the vertebral artery. (2) Embolism is the most common pathogenesis of PCI, accounting for about 40% of emboli, which mainly originate from the heart, aorta and vertebral basilar artery. The most common sites of embolism are the intracranial segment of the vertebral artery and the distal basilar artery. (3) Penetrating small artery lesions, including vitreous lesions, microaneurysms, and atherosclerotic lesions at the beginning of small arteries, occur in the pontine, midbrain, and thalamus.
Cervical osteophytes are not the main cause of posterior circulation ischemia: It was previously thought that turning the head/neck could cause compression of the vertebral artery by the osteophytes, resulting in posterior circulation ischemia and dizziness/vertigo because the vestibular nucleus is sensitive to ischemia. This model of hypothesis instead of evidence is a major cause of confusion in the diagnosis of VBI. In contrast, clinical studies have demonstrated that cervical spine osteophytes are by no means a major risk factor for PCI, as there is no significant difference in the degree of cervical spine osteophytes between middle-aged and elderly populations with or without PCI, but only in vascular risk factors; serial vertebral artery dynamic angiograms only show isolated arterial compression due to osteophytes; Doppler ultrasonography after turning the neck is performed, and vertebral artery compression ratios are not seen between those with or without posterior circulation symptoms The rate of extracranial segment compression did not differ between those with and without posterior circulation symptoms.
The main manifestations of posterior circulation ischemia
The brainstem is an important site of neurological activity, with cerebral nerves, the reticular superior activating system, and important upstream and downstream conduction bundles passing through it. When the blood supply is impaired and neurological impairment occurs, a variety of different but overlapping clinical manifestations can occur. The clinical manifestations of PCI are therefore diverse, lacking a stereotypical or fixed form, and are difficult to recognize clinically. common clinical symptoms of PCI include dizziness, vertigo, numbness of the limbs or head and face, limb paralysis, sensory abnormalities, gait or limb ataxia, dysarthria or dysphagia, fall episodes, hemianopia, hoarseness, and Horner’s syndrome. The presence of crossover manifestations of neurological damage on one side of the brain and motor-sensory damage on the other side is a characteristic manifestation of PCI. Although dizziness and vertigo are common symptoms of PCI, the common etiology of dizziness and vertigo is not PCI. current evidence suggests that the overall prognosis of PCI is not worse than that of anterior circulation ischemia, e.g., 79% of 407 patients in the NEMC-PCR had a good prognosis.