Cerebral syncope in a patient with spinal cord injury

An 80-year-old patient suffering from traumatic paraplegia due to spinal cord compression was admitted due to recurrent orthostatic syncope. Tilt table testing revealed that the patient lost consciousness without hypotension. Doppler flow measurements of the middle cerebral arteries showed a significant decrease in diastolic velocity during syncope without systemic hypotension. Treatment with beta-blockers was highly effective. The patient suffered from cerebral blood flow disregulation probably due to abnormal baroreceptor responses triggered during orthostatic stress. This is the first reported case of a patient with spinal cord injury suffering from such an unusual cause of syncope.     

Hyperventilation-induced syncope: no need to panic

Accurately diagnosing and treating adult patients presenting with recurrent syncope can be extremely problematic. We present the case of a patient who presented with recurrent syncope. We propose that many cases currently classified as idiopathic may in fact be due to orthostatic hypotension secondary to hyperventilation, or simply hyperventilation-induced syncope. The presence of undiagnosed psychiatric disorders should be considered in these patients.     

Tilt table testing,methodology and practical insights for the clinic

Tilt table testing (TTT) has been used for decades to study short-term blood pressure (BP) and heart rate regulation during orthostatic challenges. TTT provokes vasovagal reflex in many syncope patients as a background of widespread use. Despite the availability of evidence-based practice syncope guidelines, proper application and interpretation of TTT in the day-to-day care of syncope patients remain challenging. In this review, we offer practical information on what is needed to perform TTT, how results should be interpreted including the Vasovagal Syncope International Study classification, why syncope induction on TTT is necessary in patients with unexplained syncope and on indications for TTT in syncope patient care. The minimum requirements to perform TTT are a tilt table with an appropriate tilt-down time, a continuous beat-to-beat BP monitor with at least three electrocardiogram leads and trained staff. We emphasize that TTT remains a valuable asset that adds to history building but cannot replace it, and highlight the importance of recognition when TTT is abnormal even without syncope. Acknowledgement by the patient/eyewitness of the reproducibility of the induced attack is mandatory in concluding a diagnosis. TTT may be indicated when the initial syncope evaluation does not yield a certain, highly likely, or possible diagnosis, but raises clinical suspicion of (1) reflex syncope, (2) orthostatic hypotension (OH), (3) postural orthostatic tachycardia syndrome or (4) psychogenic pseudosyncope. A therapeutic indication for TTT in the patient with a certain, highly likely or possible diagnosis of reflex syncope, may be to educate patients on prodromes. In patients with reflex syncope with OH TTT can be therapeutic to recognize hypotensive symptoms causing near-syncope to perform physical countermanoeuvres for syncope prevention (biofeedback). Detection of hypotensive susceptibility requiring therapy is of special value.     

Adaptive Rate Pacing Controlled by Right Ventricular Preejection Interval for Severe Refractory Orthostatic Hypotension

A 72-year-old African-American man with frequent recurrent syncope was found to have severe refractory orihostatic hypotension with concomitant supine hypertension. Pharmacotherupy was successful in controlling his supine hypertension but was unable to resolve his severe orihostatic hypotension. Temporary fixed rate tachypacing was only minimally effective in preventing syncope during upright tilt, while variable rate pacing based on degree of blood pressure fall was far superior. Following these observations, an adaptive rate pacing system controlled by right ventricular preejection interval was implanted (Precept DR Model 1200). The system adequately sensed the patient's fall in blood pressure when sitting or standing and augmented its rate accordingly, thus preventing syncope. While supine, the pacing rate fell to 60 ppm, thereby, avoiding an exacerbation of his concomitant supine hypertension. Over a 3-nionth follow-up period, he has had no further orthostatic or syncopal episodes. We conclude that adaptive rate pacing using right ventricular preejection interval may be an effective treatment for severe refractory orthostatic hypotension.     

To stand on one's own legs

A fundamental human expectation is to stand upright. This exposes the cardiovascular system to gravitational forces, with a fall in pressure above heart level exposing organs such as the brain to impaired perfusion if adequate adaptive mechanisms are not activated. The autonomic nervous system plays an important role in the initial response to standing upright, and can be affected by several disorders, some rare, some common. Autonomic failure can result in orthostatic hypotension with hypoperfusion of vital organs, causing a variety of symptoms including syncope. Thus, it is important to recognise orthostatic hypotension, determine its aetiology, evaluate and treat it. Intermittent autonomic dysfunction (such as neurally mediated syncope without chronic neurogenic failure) also results in falls and syncope; various forms include the 'common faint' (vasovagal syncope) and carotid sinus hypersensitivity (especially in the elderly). Orthostatic intolerance without orthostatic hypotension is increasingly recognised as due to an autonomic disturbance. New techniques are helping to unravel the functional anatomy of cerebral autonomic centres and their pathways in the causation of orthostatic intolerance.     

直立倾斜试验诊断不明原因晕厥的价值

目的探讨直立倾斜试验在不明原因晕厥诊断中的价值。方法不明原因晕厥患者366例,均行直立倾斜试验检查。结果直立倾斜试验阳性252例,阳性率68．9％;直立性不耐受综合征类型中以血管迷走性晕厥多见,其次为体位性心动过速、直立性低血压;血管迷走性晕厥中血管减压型比例女性高于男性（P〈O．05）;年龄≥60岁15例患者中直立倾斜试验阳性10例,均表现为血管迷走性晕厥;13例发生假性晕厥。结论直立倾斜试验阳性者并非为反射性晕厥,直立位3～45min发生晕厥的阳性患者,须结合年龄、性别及病史确诊是体位性晕厥或反射性晕厥。     

Successful Treatment of Severe Orthostatic Hypotension with Erythropoietin

KAWAKAMI, K., et al .: Successful Treatment of Severe Orthostatic Hypotension with Erythropoietin. A 71-year-old man, who was diagnosed with familial amyloidosis type I, was admitted for treatment of severe orthostatic hypotension associated with recurrent syncopal attacks. Head-up tilt testing demonstrated severe orthostatic hypotension (114/72 mmHg in the supine position and 62/34 mmHg in the upright position) with syncope or presyncope. Oral midodorine and fludrocortisone therapies failed to prevent his symptoms. After administration of subcutaneous erythropoietin, his blood pressure drop in the upright position was decreased and symptoms disappeared unassociated with improvement of anemia. Although previous reports have shown that the mechanism by which erythropoietin improves orthostatic hypotension is related to improvement in anemia, other mechanisms may also play a role. (PACE 2003; 26[Pt. I]:105–107)     

Syncope and Headache

Purpose of Review

We review the literature on co-occurrence of syncope and headache and share clinical experience.

Recent Findings

Headache in relation to syncope has been the subject of recent interest.

Summary

Orthostatic intolerance has an expanding spectrum with three well-defined entities: orthostatic hypotension (OH), neurally mediated hypotension (NMH), and postural tachycardia syndrome (PoTS). Syncope occurs in patients with OH as well as in patients with episodically occurring NMH. Headache of OH is called coat-hanger ache (CHA) because it affects the neck and shoulders in a coat-hanger pattern. It can serve as a warning symptom of OH as well as a parameter to gauge the benefit of treatment. Awareness of CHA avoids inappropriate tests. Headache type occurring in NMH has not been fully delineated. A questionnaire-based study describes migraine leading to syncope and treatment of migraine to reduce syncope. Laboratory studies in NMH patients provide evidence for only short-duration headache. The author’s approach to such patients is presented.

     

Prevalence of orthostatic hypotension among patients presenting with syncope in the ED

We sought to determine the prevalence of orthostatic hypotension as a cause of syncope in the emergency setting, and describe the characteristics of patients diagnosed with this condition. Blood pressure orthostatic changes were measured prospectively in a standardized fashion up to 10 minutes, or until symptoms occurred, in all consecutive patients with syncope as a chief complaint presenting in the emergency department (ED) of a primary and tertiary care hospital. Patients unable to stand-up were excluded. Hypotension was considered to be the cause of syncope when there was: (1) a decrease in systolic blood pressure (SBP) >or= 20 mm Hg with simultaneous symptoms; (2) a decrease in SBP between 10 and 20 mm Hg, but a SBP or= 20 mm Hg were found in 10% of patients with syncope attributed to other causes. Compared with patients with vasovagal disorder, those with orthostatic hypotension were older; had more comorbid conditions including hypertension, organic heart disease, and abnormal electrocardiogram; were taking more hypotensive medications; and required more frequently hospitalization (P <.01). We concluded that standardized blood pressure measurement in the ED enabled to strongly implicate orthostatic hypotension as a cause of syncope in 24% of patients with this symptom. Drug-related hypotension was the most frequent cause for this disorder.     

Cerebral Syncope: Loss of Consciousness Associated with Cerebral Vasoconstriction in the Absence of Systemic Hypotension

Transcranial Doppler (TCD) ultrasonography done during headupright tilt induced neurocardiogenic syncope has demonstrated that cerebral Vasoconstriction occurs concomitant with (or precedes) loss of consciousness. This article demonstrates evidence that cerebral blood flow changes alone (vasoconstriction), in the absence of systemic hypotension, may result in syncope. Five patients (4 men, 1 woman; mean age 41 ± 17 years) with recurrent unexplained syncope were evaluated by use of an upright tilt table test for 45 minutes with or without an infusion of low dose isoproterenol. TCDoppler ultrasonography was used to assess middle cerebral artery systolic velocity (Vs); diastolic velocity (Vd); mean velocity (Vm); and pulsatility index (PI = Vs = Vd/Vmean). Syncope occurred in five patients during the baseline tilt and in one patient during isoproterenol infusion. During tilt induced syncope, at an average mean arterial pressure of 89 ± 16 mmHg, TCD sonography showed a 2%± 10% increase in systolic velocity; a 51%± 27% decrease in diastolic velocity; and a 131 %± 87% increase in pulsatility index. One patient underwent continuous electroencephalographic recording during tilt, which demonstrated diffuse slow wave activity (indicating cerebral hypoxia) at the time of syncope concomitant with the aforementioned TCD changes in the absence of systemic hypotension. These fndings reflect an increase in cerebrovascular resistance secondary to arteriolar vasoconstriction distal to the insonation point of the middle cerebral artery, that occurred concomitant with loss of consciousness and in the absence of systemic hypotension. We conclude that in some individuals abnormal baroreceptor responses triggered during orthostatic stress may result in a derangement of cerebral autoregulation leading to cerebral vasoconstriction with resultant cerebral hypoxia in the absence of systemic hypotension.     

Review of orthostatic tests on the safety of tamsulosin, a selective alpha1A-adrenergic receptor antagonist, shows lack of orthostatic hypotensive effects

Two phase III studies with tamsulosin, a selective alpha1A-adrenergic receptor antagonist, were conducted to evaluate the safety and efficacy of the standard treatment doses of 0.4 mg/day and 0.8 mg/day in patients with symptoms of benign prostatic hyperplasia (BPH). These large-scale clinical trials were the first to include extensive testing for possible drug-induced orthostatic hypotension (OH). The frequency of positive orthostatic tests and magnitude of vital sign changes were compared among tamsulosin and placebo-treated groups. The results indicate that tamsulosin up to 0.8 mg/day does not induce higher risk of OH than that of placebo. Data from post-marketing surveillance (PMS) studies of tamsulosin indicate that the incidence of hypotension and syncope is extremely low in community-dwelling elderly men treated for BPH. From the results of the phase III studies, PMS studies and an active-controlled clinical pharmacology study, we conclude that the orthostatic test is a useful and convenient method to evaluate the risk of OH and syncope during the investigational stage.     

改善循环治疗加重帕金森病患者体位性低血压1例

目的 提醒临床医生加强对于帕金森病(Parkinson’s disease,PD)患者非运动症状的关注。方法 追踪报道1例帕金森病合并高血压患者,接受调整抗PD药物、降压及改善循环治疗的效果。结果 该患者治疗过程中出现了严重的体位性低血压、晕厥。结论 临床医生应重视PD患者的体位性低血压等非运动症状。     

Orthostatic hypotension occurring after discontinuation of long-term minoxidil therapy

Minoxidil (Loniten), a potent predominant arteriolar vasodilator, provides prompt and effective reduction of blood pressure in many patients with severe hypertension. Minoxidil results, however, in profound reflex tachycardia and increased plasma volume almost always necessitating concomitant use of beta-adrenergic blocking agents and diuretics. Hypertrichosis and massive fluid retention are troublesome adverse reactions that may require discontinuation of minoxidil and initiation of an alternative antihypertensive agent. When minoxidil is discontinued, diuretic dosage requires re-evaluation and possible tapering to prevent volume depletion. Volume depletion is a risk factor in patients with persistent peripheral edema, sodium deprivation or dehydration; these states may interfere with physiologic mechanisms that maintain adequate cerebral perfusion upon standing, triggering orthostatic hypotension and potential syncope. Hypertension clinic visits should routinely include supine followed by sitting and standing blood pressure determinations to ensure detection of orthostatic hypotension. Described in the article is a case study in which a patient developed severe orthostatic hypotension one month after minoxidil was discontinued. Pathophysiologic mechanisms are discussed.     

Orthostatic vital signs do not predict 30 day serious outcomes in older emergency department patients with syncope: A multicenter observational study

BackgroundSyncope is a common chief complaint among older adults in the Emergency Department (ED), and orthostatic vital signs are often a part of their evaluation. We assessed whether abnormal orthostatic vital signs in the ED are associated with composite 30-day serious outcomes in older adults presenting with syncope.MethodsWe performed a secondary analysis of a prospective, observational study at 11 EDs in adults ≥ 60 years who presented with syncope or near syncope. We excluded patients lost to follow up. We used the standard definition of abnormal orthostatic vital signs or subjective symptoms of lightheadedness upon standing to define orthostasis. We determined the rate of composite 30-day serious outcomes, including those during the index ED visit, such as cardiac arrhythmias, myocardial infarction, cardiac intervention, new diagnosis of structural heart disease, stroke, pulmonary embolism, aortic dissection, subarachnoid hemorrhage, cardiopulmonary resuscitation, hemorrhage/anemia requiring transfusion, with major traumatic injury from fall, recurrent syncope, and death) between the groups with normal and abnormal orthostatic vital signs.ResultsThe study cohort included 1974 patients, of whom 51.2% were male and 725 patients (37.7%) had abnormal orthostatic vital signs. Comparing those with abnormal to those with normal orthostatic vital signs, we did not find a difference in composite 30-serious outcomes (111/725 (15.3%) vs 184/1249 (14.7%); unadjusted odds ratio, 1.05 [95%CI, 0.81–1.35], p = 0.73). After adjustment for gender, coronary artery disease, congestive heart failure (CHF), history of arrhythmia, dyspnea, hypotension, any abnormal ECG, physician risk assessment, medication classes and disposition, there was no association with composite 30-serious outcomes (adjusted odds ratio, 0.82 [95%CI, 0.62–1.09], p = 0.18).ConclusionsIn a cohort of older adult patients presenting with syncope who were able to have orthostatic vital signs evaluated, abnormal orthostatic vital signs did not independently predict composite 30-day serious outcomes.     

Vertigo and dizziness related to migraine: a diagnostic challenge

Vertigo and dizziness can be related to migraine in various ways: causally, statistically or, quite frequently, just by chance. Migrainous vertigo (MV) is a vestibular syndrome caused by migraine and presents with attacks of spontaneous or positional vertigo lasting seconds to days and migrainous symptoms during the attack. MV is the most common cause of spontaneous recurrent vertigo and is presently not included in the International Headache Society classification of migraine. Benign paroxysmal positional vertigo (BPPV) and Ménière's disease (MD) are statistically related to migraine, but the possible pathogenetic links have not been established. Moreover, migraineurs suffer from motion sickness more often than controls. Persistent cerebellar symptoms may develop in the course of familial hemiplegic migraine. Dizziness may also be due to orthostatic hypotension, anxiety disorders or major depression which all have an increased prevalence in patients with migraine.     

Update on the theory and management of orthostatic intolerance and related syndromes in adolescents and children

Orthostasis means standing upright. One speaks of orthostatic intolerance (OI) when signs, such as hypotension, and symptoms, such as lightheadedness, occur when upright and are relieved by recumbence. The experience of transient mild OI is part of daily life. ‘Initial orthostatic hypotension’ on rapid standing is a normal form of OI. However, other people experience OI that seriously interferes with quality of life. These include episodic acute OI, in the form of postural vasovagal syncope, and chronic OI, in the form of postural tachycardia syndrome. Less common is neurogenic orthostatic hypotension, which is an aspect of autonomic failure. Normal orthostatic physiology and potential mechanisms for OI are discussed, including forms of sympathetic hypofunction, forms of sympathetic hyperfunction and OI that results from regional blood volume redistribution. General and specific treatment options are proposed.     

Diagnosis and management of vasovagal syncope and dysautonomia

Vasovagal syncope is a condition better known as neurocardiogenic or neurally mediated syncope. Dysautonomic syncope is the irregular neuroautonomic response during the body's attempt to maintain homeostasis. Both types of syncope are associated with orthostatic hypotension and are nonlethal. The underlying pathophysiology manifests the vast symptoms suffered by the individual. Research continues to develop new markers to improve diagnostic testing and therapies for treatment. Advanced practice nurses now have a new tool with Head-Up Tilt Training Programs to offer the patients who suffer from frequent and refractory neurocardiogenic and dysautonomic syncope.     

Is Home Orthostatic Self‐Training Effective in Preventing Neurally Mediated Syncope?

BACKGROUND: Repeated orthostatic stress may prove to be of benefit in the regulation of neurally mediated syncope. But the role of home orthostatic self-training is not established to prevent symptoms in patients with neurally mediated syncope. We performed a prospective and randomized study to evaluate the effectiveness of repeated home orthostatic self-training in preventing tilt-induced neurally mediated syncope. METHODS AND RESULTS: Fourty-two consecutive patients (24 males and 18 females, mean age 39 years, 16-68 years) with recurrent neurally mediated syncope were randomized into the tilt training and control groups. The home orthostatic self-training program consisted of daily sessions for 7 days a week for 4 weeks. In order to determine the effects of home orthostatic self-training, we repeated the head-up tilt test in both groups 4 weeks later. Among the tilt-training group, 9 of 16 patients (56%) had a positive response on follow-up head-up tilt test. Among the untreated control group, 9 of 17 patients (53%) had a positive response on follow-up head-up tilt test. In subgroup analyses according to the number of tilt-training sessions or the classified type, we found no differences in the follow-up head-up tilt test responses. Spontaneous syncope or presyncope over mean follow-up of 16.9 months were observed in 42.9% versus 47.1% in the tilt-training and control group, respectively. CONCLUSIONS: Home orthostatic self-training was ineffective in reducing the positive response rate of head-up tilt test in patients with recurrent neurally mediated syncope.     

Incidence and Predictors of Syncope in Paced Patients with Sick Sinus Syndrome

In spite of a normal pacemaker/unction, syncope still occurs in some patients with sick sinus syndrome (SSSJ. Causes often remain unknown. To identify predictors and etiologies of this bothersome symptom, we studied 507 patients who received atrial, ventricular, and dual-chamber pacemakers for SSS. During a mean follow-up of 62 ± 38 months, actuarial incidence of syncope was 3% at 1 year, 8% at 5 years, and 13% at 10 years. Causes were vasovagal (18%), orthostatic hypotension (25.5%), rapid atrial tachyarrhythmias (11.5%), ventricular tachycardia (5%), acute myocardial ischemia (2.5%), and pacemaker/lead malfunction (6.5%), In 13 patients (29.5%), syncope remained unexplained. The only preimplant predictor for syncope was syncope as primary indication for pacemaker implant. Electrocardiographic correlation with bradycardia was not a predictor of relief of syncope during the follow-up. In conclusion: (1) syncope in paced patients with SSS has multiple etiologies and may be multifactorial; (2) the only predictor of syncope after pacemaker implant is the occurrence of preimplant syncope as the main indication for pacing; (3) extensive Holier monitoring is not useful to document bradycardic origin of syncope nor to predict its recurrence; (4) SSS probably overlaps with other entities such as autonomic dysfunction, vasovagal syncope, carotid sinus hypersensitivity, and venous pooling, which would provide an explanation for recurrent syncope in patients with normal pacemaker function.