Definition of vertigo
Vertigo is a kind of motion hallucination or spatial misperception in which patients subjectively feel themselves or external objects rotating, swinging, lifting and tilting. It is often accompanied by nausea, vomiting, and nystagmus.
Vertigo is not a well-defined disease entity, but a multisensory disorder syndrome, which is a motion hallucination of the body itself or of an objective external object. It is an unpleasant, static gravity-distorting experience caused by dysfunction between the vestibular, visual and deep sensory systems.
Anatomical and physiological characteristics of the vertebral artery
The vertebral artery is the first branch from the subclavian artery, entering the transverse foramen at the level of C6 and then penetrating the dura above the posterior atlanto-occipital arch through the atlanto-occipital membrane. In approximately 6% to 8% of cases, the left vertebral artery emanates directly from the aortic arch
PCI clinical presentation and classification
Common symptoms: dizziness/vertigo, double or blurred vision, headache, nausea, vomiting, limb/head and perioral numbness, limb weakness, unsteady walking or sudden collapse
Rare symptoms: transient or episodic loss of consciousness, transient amnesia, sudden deafness with vertigo, rapid onset of unconsciousness, respiratory and cardiac arrest
Common signs of PCI
Crossed cranial nerve damage and contralateral motor and sensory long tract syndrome are the most common signs of PCI
Oculomotor impairment, limb paralysis, sensory abnormalities, gait/limb ataxia, dysarthria/swallowing, visual field defects, hoarseness, Horner’s syndrome, etc.
Posterior circulation TIA, cerebellar infarction, dorsolateral medullary syndrome, basilar artery cusp syndrome, Weber syndrome, atresia syndrome, posterior cerebral artery infarction, lacunar infarction (motor mild hemiparesis, ataxic mild hemiparesis, dysarthria-hand clumsiness syndrome, pure sensory stroke, etc.).
Often mistaken as a clinical manifestation of posterior circulation ischemia
Due to the dense structure of the brainstem and the non-one-to-one correspondence between vascular innervation and neural structures, the majority of posterior circulation ischemia presents as multiple overlapping clinical manifestations, rarely as a single symptom or symptom. Simple dizziness/vertigo, syncope, or transient loss of consciousness are rarely caused by posterior circulation ischemia.
Neuroimaging, mainly MRI, should be performed in all patients suspected of posterior circulation ischemia; DWI has the most diagnostic value for acute lesions, while CT examination is susceptible to bone artifacts and has little diagnostic value, and is only applicable to exclude bleeding and patients who cannot undergo MRI examination.
Then, various vascular examinations, such as MRA, CTA, DSA and other examinations should be actively carried out to help detect and clarify large intracranial and extracranial vascular lesions.
Prevention and treatment of posterior circulation ischemia
1.Acute treatment.
There is still a lack of randomized controlled studies in a large sample of patients with posterior circulation ischemia, so the acute management of posterior circulation ischemia is the same as that of anterior circulation ischemic stroke. An organized treatment model for stroke units should be actively pursued.
(1) Intravenous thrombolysis with recombinant tissue-type fibrinogen activator (rt-PA) can be performed in appropriate patients within 3 h of onset. The treatment window can be relaxed to 6 h. For all patients who are not suitable for thrombolysis and have no contraindications, they should be treated with aspirin 100-300 mg/d.
Treatment
(2) Other treatment measures Other treatment measures can be referred to the relevant treatment guidelines at home and abroad.
(3)Note: Patients with posterior circulation ischemia are sensitive to the changes in cerebral perfusion due to the decrease in blood pressure and blood volume, and dilation drugs should be used with caution.
Prevention and treatment of posterior circulation ischemia
Prevention.
Control various vascular risk factors with reference to relevant domestic and international guidelines for prevention and treatment. In view of the prevalence of embolism, etiologic investigations should be actively carried out. Antithrombotic therapy should be administered in those with a clear diagnosis. Antiplatelet agents alone or in combination have an important preventive role, and the efficacy of angioplasty stenting should be explored.
Education: actively carry out continuing re-education of posterior circulation ischemia especially for physicians to update the concept and knowledge and to stop using the concept of VBI. Education should be strengthened to correctly grasp the early manifestations of posterior circulation ischemia and achieve early detection and diagnosis. The risk factors of posterior circulation ischemia should be correctly understood and a scientific view of prevention should be established.
Problems that should be noted
1, unclear concept, arbitrary diagnosis (paper basket diagnosis);
2, A large number of so-called “VBI clinical studies reported”, in fact, many of them are BPPV;
3, 16% of all dizziness is caused by psychiatric etiology, while psychiatric factors account for 40% of long-term dizziness of unknown origin;
4, do not pay blind attention to the cause of “cervical spondylosis” and misdiagnose cervical dizziness or cervical vertigo;
5, basilar artery prolongation is one of the causes of long-term dizziness;
6.Blind medication→Drug dizziness is also one of the reasons why it has not been taken seriously for a long time;
7.For the diagnosis of simple vertigo with nausea and vomiting episodes in the elderly without other symptoms, lasting for a few hours to less than 48 hours, it may be an isolated vertigo episode or vestibular vertigo, and PCI should not be diagnosed;
8. The diagnosis of vestibular artery TIA has not been seen yet;
9.Some vertigo is related to autonomic regulation disorders, such as overwork, severe sleep deprivation, and high mental tension;
10. If necessary, occupying lesions should be excluded.
Summary
Several important understandings about posterior circulation ischemia
1, posterior circulation ischemia includes TIA and infarction in the posterior circulation.
2, The main etiology of posterior circulation ischemia is the same as that of anterior circulation ischemia, and cervical spondylosis is not the main etiology.
3. Neither the clinical manifestations nor the available imaging tests (CT, TCD, MRI, SPECT or PET) can reliably define the “relative ischemic state”.
4.Dizziness/vertigo is a common manifestation of posterior circulation ischemia, but the common cause of dizziness/vertigo is not posterior circulation ischemia.
5. The diagnosis, treatment and prevention of posterior circulation ischemia should be consistent with that of anterior circulation ischemia.
Vestibulocentric vertigo
Ischemic vagal stroke
1. Transient ischemic attack: The attack lasts for several minutes or hours and resolves completely within 24 hours;
2. Progressive stroke: symptoms peak within a few hours or days, combined with mild hearing loss and hemianopsia;
3.Complete stroke: symptoms peak rapidly, and symptoms of sudden deafness and vertigo are difficult to improve significantly with symptomatic treatment.
BPPV
Identification of the involved semicircular canals is based on the patient’s medical history, the head position at the time of vertigo attack and nystagmus appearance, and the direction of the nystagmus observed on Dix-Hallpike examination. The incidence of hallux valgus involvement varies depending on the anatomy of the hallux valgus, with the posterior hallux valgus being the most commonly involved and the superior and external hallux valgus being less commonly involved. When the body is standing, the posterior semicircular canal is located in the posterior and inferior position of the entire vestibular organ, and it is easier to fall into the posterior and basal part of the vestibule, where the posterior semicircular canal is located, when the debris is moved. Positional vertigo of the posterior semicircular canal often occurs when lying down in a sitting position or from lying down to sitting position, when bending over, lowering or tilting the head, and strong rotational vertigo with nystagmus, nausea and vomiting occurs when the head is excited. The vertigo and nystagmus attacks may be reduced or not occur with repeated excitation of the head position, and the entire course of the attack may last from a few hours to a few days, months or years. Because the posterior arm of the superior canal is directly connected to the common pedicle and vestibule, the otolithic fragments in the superior canal can be mostly eliminated by themselves, and thus BPPV of the superior canal rarely occurs.
How is BPPV diagnosed?
The position test (Dix-Hallpike test), also known as the varus nystagmus test. It is important to confirm the diagnosis of benign episodic positional vertigo (BPPV). The diagnostic criteria are: typical vertigo with rotation and vertical nystagmus in the position test; vertigo and nystagmus occurring 1 to 2 seconds after the position test and lasting 10 to 20 seconds; fatigue response in repeated position tests.
How to perform the position test of BPPV?
(Take benign episodic positional vertigo in the right ear as an example): Before the test, the patient should be warned that transient vertigo may occur in any position. The patient’s eyes must be kept open during the entire test. The patient is seated on the examination bed and is observed for spontaneous nystagmus. The examiner stands on the patient’s right side and asks the patient to deflect the head to the right side by 45. The right posterior hemianopia is aligned with the sagittal axis of the body. The examiner holds the patient’s head on the right and left side with both hands and asks the patient to lie down quickly in a supine position with the head still in a rightward deflected position (right ear down), with the head over the end of the examination bed and dangling outside the examination bed. Observe the presence of vertigo and nystagmus for 15 seconds. If nystagmus is present, observe the latency, duration, direction and type of nystagmus, understand the degree of vertigo and observe the vegetative reflexes. If there is no vertigo and nystagmus, let the patient return to sitting position and also observe whether there is vertigo and nystagmus for 15 seconds. Turn the head to the left for 45 seconds and repeat the above examination. For cases with positional vertigo and positional nystagmus, the patient should be examined 4 to 5 times in a row within a short period of time so that the symptoms and signs are repeated and the fatigue is observed.
BPPV treatment method
The treatment of BPPV is based on tubular stone repositioning therapy (CRT), and the efficiency of this therapy is 71% to 92%. Canalolith repositioning therapy (CRT) is mainly used for the treatment of BPPV in the posterior and superior semicircular canals, and the patient is made to change five positions by manipulation, thus allowing the canalolith fragments of the posterior and superior semicircular canals to enter the elliptical capsule through the common foot. Repositioning is currently used as the treatment of choice for this condition.
Resetting operation
Take the right ear as an example: first administer the right position to test the supine position, then rotate the patient’s head in the long axis of the body to the left ear downward after the vertigo and nystagmus it causes have stopped, and continue rotating the head and body (turning over) to the face downward, holding it for 10 to 30 seconds. Keep the head down during the rotation. This procedure often causes transient vertigo. Keep the head turned to the left and allow the patient to return to a sitting position. Return to the upright position and turn the head straight and
Manipulative repositioning of BPPV
1. Have the patient sit longitudinally on the bed with the examiner holding the head behind him/her.
2. Lie down quickly with shoulder pads and neck extended, and place the head on the bed surface with the affected ear down.
3.Turn the head gradually and continue to turn 45° to the opposite side so that the otolith moves closer to the total foot, maintaining the head position for more than 30 seconds.
4. Turn the head and torso simultaneously 90° to the healthy side so that the otolith returns to the oval capsule, maintaining this position for more than 30 seconds.
5.Turn the head to the front and have the patient sit up slowly in a head straight position.
Try to lie on the healthy side for the first and second night after repositioning. Avoid intense activities such as playing ball and swimming within one month after the reset, avoid washing hair after lying down, and keep sufficient sleep. Some patients may feel unstable walking or even slight vertigo for two to three days after the reset, no need to be nervous. Patients should be followed up in the first week after the repositioning, and if there is any recurrence or vertigo, repositioning treatment can be done again until the vertigo disappears completely and the test becomes negative. Most patients are completely cured after 1 or 2 treatments, but some patients may have recurrence after several months or years of treatment, and can just repeat the treatment with the same method.