How to diagnose and manage acute stroke with dizziness/vertigo?
Author: Li Ruijie
Source: " Neurology and Critical Care Medicine Literature Study" Public Account
Case (Wallenberg syndrome)
55-year-old male, with a previous history of hypertension , was given a 2-day medical treatment with acute attacks of persistent vertigo and unsteady walking. Vertigo is a dizzy feeling, walking tilted to the right, accompanied by nausea and blurred vision, denying hearing loss and tinnitus .
body check: BP160/100mmHg, spontaneous left-beating nystagmus, with the amplitude of nystagmus increased when gaze removed and left-beating nystagmus became, and when gaze was gaze to the right, it became right-beating nystagmus. After shaking your head horizontally for about 15 seconds, the nystagmus becomes a right-beating nystagmus. Scan the right and shrink the left, consistent with storing the right side, and smoothly tracking the abnormalities to the left. The head pulse test was normal, and the pharyngeal reflex was weakened. The right Horner syndrome , the pain and temperature sensation in the right face and left limbs are weakened. The right side refers to the measurement error of the nose test, and tilt to the right when standing.
clinical characteristics are consistent with acute persistent vertigo syndrome. Considering the presence of Horner syndrome, Horner syndrome, , altered orientation gaze-induced nystagmus (GEN), central shaking nystagmus (HSN), normal HIT, hyposensitivity and severe imbalance, Wallenberg syndrome was clinically diagnosed. MRI imaging confirmed acute infarction in the blood supply area of the right posterior inferior cerebellar artery (PICA), involving the right lateral medulla and the right inferior cerebellar lobe (Figure 1).
Figure 1 Brain MRI and MR angiography. Axial diffusion-weighted images (A, B) show acute infarction involves the lateral medulla and the lower cerebellar area including cerebellar nodules and cerebellar tonsils. MR angiography showed no right vertebral artery (C).
prevalence and pathogenesis
stroke may manifest as acute dizziness/vertigo. Vascular vertigo is mainly manifested as acute (AVS, acute persistent dizziness) or episodic (EVS, episodic dizziness) vestibular syndrome, and positional vestibular syndrome (recurrent positional dizziness) rarely occurs. About 20% of ischemic strokes occur in the posterior circulation area ( vertebral basal artery ), and dizziness/vertigo is the most common symptom of vertebral basal artery ischemia. Although there is a medical proverb that central lesions of isolated dizziness/vertigo, including stroke, are rare, with the improvement of clinical neurology and neuroimaging, it is increasingly believed that minor infarctions of the inferior cerebellar lobe and brainstem are responsible for isolated vertigo.
clinically is the most important thing to distinguish between isolated vascular dizziness and benign diseases involving the inner ear, because the treatment and prognosis of these diseases are different. Misdiagnosis of acute stroke can lead to severe morbidity and mortality, while overdiagnosis of vascular vertigo can lead to unnecessary examinations and medication. Stroke accounts for a small percentage of all dizziness symptoms present in the emergency department (ED). However, at 3 years of follow-up, the risk of stroke or cardiovascular events in patients with dizziness/vertigo was twice as high as in patients with no experience of ED due to dizziness/vertigo. In addition, during the 4-year follow-up, patients hospitalized for isolated vertigo had a three-fold higher risk of stroke than the general population. In particular, patients with 3 or more risk factors have a 5.5-fold higher risk of stroke than those without risk factors.
AVS accounts for about 10%-20% of patients with dizziness in ED. It is estimated that in the United States, there are about 400,000-800,000 ED visits every year. It is estimated that approximately 25% of AVS cases are caused by stroke. Most patients with dizziness and vertigo caused by ischemic stroke show AVS, but only about 20% of patients have focal neurological signs, while the rest are isolated AVS.
stroke with AVS may occur any segment of the vestibular pathway from the inner ear to the cerebral hemisphere, but mainly involves the structure of posterior circulation blood supply (Figure 2).
Figure 2 Cerebrovascular anatomy of the posterior circulation (A) and cerebellar vascular area (B). The cerebellum receives three pairs of arterial blood supply. PICA is usually found in the distal segment of the vertebral artery. AICA is usually emitted from the mid- or proximal end of the basal artery in , and SCA is usually emitted from the distal basal artery. Generally speaking, proximal branches from all 3 cerebellar arteries supply parts of the brainstem, while longer spiral branches supply the cerebellum, anatomical variation is common.
Diagnosis and classification of stroke
Although the diagnosis of stroke is mainly based on neurologic examinations and abnormal manifestations of brain imaging including blood vessels, vascular vertigo with vascular risk factors should be the main consideration for diagnosis in patients with AVS. Vascular causes should also be suspected in EVS, especially when patients with stroke risk factors last only a few minutes. Vascular vertigo can be classified according to manifestations (persistent versus onset), vascular involvement areas, and underlying causes. Brain imaging helps determine the region and cause of stroke. Ischemic stroke accounts for about 80% of all cases. This article only involves vascular vertigo caused by cerebellar and medulla bulbar infarction.
small cerebral infarction
cerebellum is supplied by three arteries: posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), and superior cerebellar artery (SCA). Contrary to traditional beliefs, well-known cerebellar signs such as dysarthria and poor ranging often do not occur in localized cerebellar infarction. Therefore, detailed eye movement results are very important for the diagnosis of cerebellar infarction, which is the most common cause of isolated vascular vertigo (Table 1).
Table 1 Characteristics of acute vestibular syndrome caused by cerebellar infarction
posterior inferior cerebellar artery infarction
PICA regional infarction is the most common cause of isolated AVS. In a previous study, 25 of 240 isolated cerebellar infarctions developed isolated vertigo, and 24 of them were medial regional infarctions of PICA. A recent study using diffusion-weighted images found that 75% of patients with isolated AVS with at least one vascular risk factor were acute stroke, mainly involving the caudal cerebellar lobe in the medial area of PICA.
unidirectional spontaneous nystagmus and mild imbalances observed in some patients with PICA regional infarction were similar to those in patients with acute peripheral vestibule disease. However, with or without GEN, normal HIT can almost distinguish between PICA regional cerebellar infarction and acute peripheral vestibular lesions.
cerebellar nodes are involved in controlling eye movements and posture adjustments to gravity, and receive blood supply from the medial side of PICA. Patients with isolated cerebellar nodule infarction show isolated vertigo and moderate to severe imbalance. The most common manifestation is one-way spontaneous nystagmus and descending in the opposite direction, similar to peripheral vestibular disease. In unilateral lesions, the direction of spontaneous nystagmus is consistent. However, HIT and dual temperature tests are normal. Other abnormal signs include periodic alternating nystagmus, HSN abnormalities, paroxysmal positional nystagmus, and impaired tilt inhibition of nystagmus after rotation.
tonsillary infarction may be a cause of acute vestibule syndrome. In a previous study, patients with unilateral tonsillary infarction showed: (1) almost complete impairment of ipsilateral smooth tracking and contralateral visual tracking, (2) low amplitude ipsilateral spontaneous nystagmus without gaze, (3) impaired gaze and (4) moderate reverse tilt of subjective visual perpendicularity (SVV) with normal vestibular function.
Angular inferior cerebellar artery infarction
is similar to PICA infarction, and vertigo is a common symptom of AICA regional infarction. However, AICA infarction is mostly accompanied by unilateral or bilateral hearing loss, with or without brainstem signs, such as facial paralysis, Horner syndrome or cross-sensory loss. GEN similar to the change in direction of Bruns' nystagmus can be observed. Hearing loss is usually permanent, but dizziness and imbalance gradually improve as central compensation.
Because AICA sends the inner ear artery to supply the inner ear, AICA infarction can cause typical peripheral and central vestibular lesions. However, elderly patients with sudden unilateral deafness and vertigo should consider isolated labyrinth infarction, especially those with a history of stroke or known vascular risk factors. Since current imaging techniques cannot identify isolated labyrinth infarctions, diagnosis should depend on clinical manifestations and concurrent vascular risk factors and be presumed in the absence of pathological studies.
pomophore lobes are also supplied by AICA and are involved in controlling smooth tracking, gaze preservation and eye movement caused by vestibular stimulation. Previous studies have found that patients with isolated unilateral lobular infarction have shown spontaneous nystagmus to the lesion, impaired visual tracking on the ipsilaterally, and reverse twisting and tilting of SVV. The rotation chair test was performed under low frequency stimulation, and the horizontal vestibular eye reflex (VOR) gain increased.In contrast, VOR gain decreases with higher frequency and higher speed HIT. Although HIT is usually normal in patients with central vestibular disease, the reduction in HIT response does not rule out that isolated cerebellar lesions involve lobular lobes as a cause of AVS.
Stroke of superior cerebellar artery
Since there is no obvious vestibular junction in the upper cerebellum supplied by SCA blood, SCA regional infarction rarely causes vertigo. The low incidence of vertigo in the SCA blood supply area may help clinically distinguish between PICA or AICA infarction in patients with acute imbalance. SCA lateral infarction usually presents with dizziness, imbalance and mild trunk ataxia, but severe limb ataxia can occur. In contrast, the most prominent feature of medial SCA infarction is severe gait ataxia accompanied by sudden falls or severe deviations.
Medite bulbar infarction
vertigo caused by brainstem stroke is usually accompanied by symptoms and signs that prompt central lesions, thus forming a typical syndrome.
dorsolateral medulla bulbar syndrome
As mentioned in the previous case, vertigo symptoms in patients with lateral medulla bulbar infarction usually appear at the same time as other nervous system symptoms or signs, including cross-sensory hypotension, Horner syndrome, limb ataxia and small ocular fission, and bedside diagnosis is easier. However, small infarctions involving the lateral medulla oblongata may lead to dizziness and imbalance without other localized symptoms.
Spontaneous nystagmus in patients with lateral medulla oblongata infarction have greatly changed. Usually horizontal nystagmus is beaten away from the lesion. The vertical components usually jump upwards, but may separate. Torsional nystagmus can occur on the ipsilateral or contralateral sides. GEN is visible in almost all patients and is mostly horizontal. HSN often appears, and the horizontal parts are mostly on the same side. Even in patients with spontaneous nystagmus, the horizontal HSN beats toward the lesion side. The eye tilt reaction is unchanged in the acute phase and is ipsilateral, that is, the head is tilted to the lesion side, the upper pole of the eye rotates to the ipsilateral shoulder, and the ipsilateral eye is lower than the contralateral eye. The patient also showed a bias towards the lesion side of the eye without restricting the eye movement (ipsilateral lateral impulse). The ipsilateral lateral impulse includes a steady-state eye shift towards the lesion side, a height ipsilateral movement opposite the lesion, a oblique deflection of the height lateral movement and a vertical movement. Neck and ocular vestibular induced myogenic potential (VEMP) may also be abnormal in patients with Wallenberg syndrome.
Medium bulbar infarction
In medial medulla infarction, vertigo and abnormal eye movement may be prominent when the lesion extends to the quilt side. In this area, the ascending efferent fibers from the vestibular nucleus, the medial longitudinal bundle (MLF), sublingual plexus replex of the sublingual nucleus, and the climbing fibers emitted from the medial ductile nucleus are from the anterior medial artery blood supply. Different patterns of abnormal eye movement can occur in medial medulla infarction. Spontaneous horizontal nystagmus usually beats toward the lesion. GEN usually looks stronger in the same area. Occasionally upskipping or semi-seesaw nystagmus is present, attributed to the involvement of the sublingual peripheral nucleus or MLF. Due to damage to the olive cerebellar fibers before crossing, eyeball misalignment can be observed. Impaired medial vestibulosyl tract in MLF may impair cervical VEMP on the lesion side.
Vestibular nerve nuclear infarction
Infarction localized to vestibular nerve nucleus can cause isolated vertigo and nystagmus, similar to acute peripheral vestibular disease. The vestibular nucleus is supplied by AICA and PICA. Recent analysis of isolated persistent vertigo, spontaneous horizontal torsional nystagmus (usually away from the lesion), HIT-positive, and unilateral double-temperature abnormalities in patients with isolated vestibular nuclear infarction. Neck and eye VEMP decrease or disappears when irritating the ipsilateral ear. All of these abnormalities are consistent with vestibular neuritis. However, the patient showed a change in direction, a typical sign of central vestibular lesions. Isolated vestibular nuclear infarction should be considered in the differential diagnosis of AVS with perivestibulum and central vestibular lesions, especially in the case of hearing retention.
Bedside and laboratory diagnostic examination
When other neurological symptoms and signs are associated with acute dizziness/vertigo, the diagnosis of stroke is simple in most cases even without neuroimaging.However, acute vascular dizziness/vertigo is not accompanied by other obvious neurological deficits, even using MRI imaging, and it is a challenge for experts. However, recent advances in clinical neurology demonstrate that systematic bedside assessments outperform neuroimaging in the diagnosis of acute persistent vertigo caused by stroke.
Bedside Assessment of
Acute persistent vertigo patients should be evaluated for spontaneous and induced nystagmus; eyeball misalignment, including reverse skew, saccades and smooth tracking in horizontal and vertical directions; HITs and balance functions.
bedside HIT is a useful tool to distinguish central vascular vertigo syndrome from benign diseases involving the inner ear. Normal HIT is a reliable marker of complete peripheral vestibular function, suggesting that patients with acute persistent vertigo are centrally lesions. If other central signs are combined, the diagnostic accuracy of bedside HIT differentiates central vascular vertigo and acute peripheral vestibular disease will be further improved. A modified bedside examination protocol combining HIT, transdirectional nystagmus and reverse skew (HINTS to INFARCT [head pulse normal, fast-phase alternating or occlusion trial re-gaining]) showed that in patients with acute persistent vertigo for more than 24 hours and with a vascular risk factor, the sensitivity to identify stroke was 100% and specificity was 96%, while the initial diffusion-weighted magnetic resonance imaging was 12%. However, for AICA infarction, HITS tests are mostly positive, and the diagnosis is insufficient. In fact, among the 18 patients with AICA infarction, 5 did not indicate central lesions. In this case, additional horizontal shaking and finger friction hearing tests (HINTS plus) may help detect central lesions.
Because mild directional skews may be ignored during bedside examinations, and patients with cerebellar stroke usually do not have GEN, so bedside HIT may be the best tool to distinguish isolated vertigo caused by cerebellar stroke from acute peripheral vestibular disease. However, bedside HIT may be false negative, especially when partial vestibular neurological deficits or corrective saccades (recessive saccades) occur during HIT. In this regard, a video-based device recently developed for HIT will facilitate objective measurement of head pulse VOR gain.
Laboratory examination
Generally speaking, routine laboratory studies, including whole blood count, electrolytes and thyroid function tests, do not have much significance in diagnosing the cause of dizziness. In an meta-analysis of , only 26 of 4538 patients (0.6%) had laboratory abnormalities that could explain their dizziness symptoms. The ischemic stroke guidelines also recommend that hematological, coagulation and biochemical tests be minimized to avoid time delays during the initial emergency assessment and that only blood glucose assessments are required at the start of intravenous recombinant tissue plasminogen activator (rtPA). Baseline ECG and troponin tests are also recommended for patients with acute ischemic stroke, but the initiation time of intravenous rtPA should not be delayed.
Neuroimaging is essential for the diagnosis of stroke. Computed tomography (CT) has limited value in detecting post-circulatory infarction and is recommended to exclude bleeding only. Even diffusion-weighted MRI imaging cannot detect 1/5 strokes in the posterior fossa within the initial 24 to 48 hours. Mass-weighted MRI showed lower sensitivity (47% vs 100%, P0.001) in detecting small strokes than HINTSplus (HINTS plus bedside hearing through finger friction). Initial MRI false negatives (6–48 hours) were more common in patients with small stroke than in patients with large stroke (53% vs. 7.8%, P 0.001). Therefore, when initial diffusion-weighted imaging is normal, a series of evaluations are needed for patients suspected of vascular vertigo to determine whether stroke is required (Figure 3).
Figure 3 Diagnostic strategies based on HINTS results that may be AVS
Patients with suspected vascular vertigo should immediately use CT, magnetic resonance or conventional angiography to evaluate cerebrovascular. Perfusion imaging may help diagnose vascular vertigo, especially in patients with normal routine neuroimaging and determine the extent of inadequate perfusion. However, the diagnostic effect of perfusion imaging in patients with isolated vascular vertigo remains to be verified.
Various laboratory tests that can be used to evaluate vestibular and ocular motor function in stroke patients are beyond the scope of this article.
Selection of acute treatment for stroke
General Principles
Since there are currently no randomized trials for posterior circulatory stroke (including cerebellar infarction), the treatment of vascular vertigo should generally follow the guidelines for acute stroke.
It is crucial to closely monitor signs of worsening of the condition regardless of the patient's admission method. If worsening occurs, primary brainstem ischemia caused by the original vascular lesions must be distinguished from secondary brainstem compression or hydrocephalus , because the treatment regimen is different for each condition. MRI may help make this distinction. Patients with acute cerebellar infarction should ideally be treated in stroke centers and neurointensive care units that can undergo close clinical monitoring, rapid brain imaging and timely neurosurgery support.
drug treatment for
patients with severe vomiting should monitor and correct liquid and electrolyte imbalance. Vestibulo nerve inhibitors and restricted head movements can be applied to patients with severe vertigo, nausea and vomiting in the first few days. Once symptoms improve, medication should be gradually reduced and vestibular recovery begins. According to current guidelines, isolated vascular vertigo is not suitable for thrombolytic treatment due to its low disability score. However, future stroke events should be prevented by strict control of risk factors and the use of antiplatelets or anticoagulants.
Surgical treatment
Carotid endarterectomy/stent implantation is beneficial for certain patients with dizziness/vertigo and complicated vascular mutations or abnormalities, such as permanent trigeminal artery or permanent sublingual artery, which directly connects the carotid system and posterior circulation. Patients with large-area cerebellar infarction have a high risk of cerebral edema and increased intracranial pressure. Decompression should be considered for patients with direct brainstem compression or hydrocephalus leading to worsening of the condition. For patients with severe symptoms of vertebral artery stenosis, subclavian blood thief, or rotating vertebral artery syndrome and ineffective medication, stent or surgery may be considered.
Rehabilitation
stroke rehabilitation should begin as soon as possible, although most functional recovery is within the first few months, rehabilitation treatment can last for several days to more than a year. Vestibular rehabilitation can effectively reduce the symptoms of vestibular disorder patients and improve their function. The goal of vestibular recovery is to promote compensation of in the central nervous system through exercise-based strategies. The involvement of the vestibular central structure may limit compensation, so the recovery of patients with vestibular central dysfunction may be limited. For patients with vestibular central dysfunction, treatment time usually takes longer.
Triage and Treatment
During 4.5 hours of stroke (ultra-acute period), if the National Institutes of Health stroke score (NIHSS) is greater than 4 or the NIHSS score is lower but obviously leads to severe disability, intravenous thrombolysis or emergency endovascular surgery should be considered. Conservative treatments such as conservative treatments including antiplatelet drugs, strict risk factor management and ongoing monitoring of the disease are sufficient for isolated AVS or mild neurological dysfunction (such as internuclear ophthalmia). 4.5 hours after
stroke, AVS caused by basal artery occlusion can still be considered for intravenous thrombolysis or emergency endovascular treatment. Otherwise, conservative treatment is the main treatment method. Because approximately 25% of patients may experience neurological deterioration within the first 24-48 hours after stroke, it is difficult to predict which patients will worsen, stroke patients should be admitted to the hospital for treatment. Similarly, patients with transient ischemia attacks in posterior circulation can benefit from rapid assessment and close observation in hospital admission. Patients who have worsened by cerebral edema, hydrocephalus and brainstem compression should undergo decompression surgery immediately to prevent and treat secondary injuries in previous uninfarcted areas.
