Symptomatic Spasm Research Articles

Radial artery spasms - angiographic morphology, risk factors and management.

Radial artery is the preferred access for coronary interventions. However, the procedure is sometimes interrupted by a spasm which causes pain, prolongs the procedure, and can force the access crossover. To observe factors contributing to a symptomatic radial artery spasm. In this prospective study, we present results of 103 consecutive patients regarding radial artery spasm and angiographic image of the punctured artery. Angiography of the radial artery was performed in 70 (68.0%) patients. Potential risk factors for radial artery spasm were evaluated. The overall incidence of the radial artery spasm was high - 25 (24.3%). Signs of spasm were present in 37.1% of radial artery angiographies before the procedure and 60.1% after, however, it did not always indicate a symptomatic spasm. Risk factors related to radial artery spasm included female sex (OR = 2.94, p = 0.02), failure of the first puncture attempt (OR = 3.12, p = 0.014) and use of non-hydrophilic sheath (OR = 9.56, p = 0.036). Radial artery narrowing at the tip of the sheath was also a risk factor for spasm (p = 0.022). No spasms were observed after hydrophilic sheath application (n = 13). The administration of a radial cocktail was not observed to significantly decrease the spasm odds. Risk factors for radial artery spasm include female sex and multiple puncture attempts. Hydrophilic sheath coating protects against radial artery spasm. Overall signs of a spasm in the angiography are common and do not imply a symptomatic spasm, which can be predicted by a tight narrowing at the tip of the sheath.

Impact of strict fluid management on the treatment outcome of clazosentan for cerebral vasospasm

ObjectiveClazosentan (CLA) reduces cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). However, adverse events including pulmonary edema were reported. We examined whether the strict management of fluid balance reduces the adverse events and improves patient outcomes. MethodsPatients with aSAH between 2020 and 2023 were included. They were divided into pre-CLA (before CLA approval) and post-CLA (after approval) groups. The patients in the post-CLA group were further divided into the post-CLA1 (before the change in fluid management) and post-CLA2 (after the change) groups. To achieve fluid balance of 0–500 ml/day according to the modified protocol, the infusion volume was restricted. ResultsThe daily fluid balance increased from the pre-CLA to the post-CLA1 periods (p = 0.01). The protocol changes decreased the pulmonary edema (post-CLA1 vs. post-CLA2, 44 vs. 22 %, p = 0.09) and discontinuation of CLA (44 vs. 9 %, p < 0.01). The incidence of symptomatic spasm (SS) and delayed cerebral infarction (DCI) in the post-CLA2 were slightly reduced without significant differences (SS: 17 vs. 13 %, p = 0.69; DCI: 11 vs. 9 %, p = 1.00). ConclusionStrict management of fluid balance during CLA treatment reduced the adverse events and discontinuation of CLA administration. Fluid restriction may positively affect the management of cerebral vasospasms.

Impact of immediate general anesthesia in the emergency room on prevention of rebleeding after subarachnoid hemorrhage.

Aneurysm rebleeding is fatal in patients with aneurysmal subarachnoid hemorrhage (aSAH). We aimed to investigate whether immediate general anesthesia (iGA) management in the emergency room, upon arrival, prevents rebleeding after admission and reduces mortality following aSAH. The clinical data of 3033 patients with World Federation of Neurosurgical Societies (WFNS) grade 1, 2, or 3 aSAH from the Nagasaki SAH Registry Study between 2001 and 2018 were retrospectively analyzed. iGA was defined as sedation and analgesia using intravenous anesthetics and opioids combined with intubation induction. We calculated crude and adjusted odds ratios to evaluate the associations between iGA and the risk of rebleeding/death using multivariable logistic regression models with fully conditional specification for multiple imputations. In the analysis of the relationship between iGA and death, we excluded patients with aSAH who died within 3days after the onset of symptoms. Of the 3033 patients with aSAH who met the eligibility criteria, 175 patients (5.8%) received iGA (mean age, 62.4years; 49 were male). Heart disease, WFNS grade, and lack of iGA were independently associated with rebleeding in the multivariable analysis with multiple imputations. Among the 3033 patients, 15 were excluded due to death within 3days after the onset of symptoms. After excluding these cases, our analysis revealed that age, diabetes mellitus, history of cerebrovascular disease, WFNS grade, Fisher grade, lack of iGA, rebleeding, postoperative rebleeding, no shunt operation, and symptomatic spasm were independently associated with mortality. Management by iGA was associated with a 0.28-fold decrease in the risks of both rebleeding and mortality in patients with aSAH, even after adjusting for the patient's history of diseases, comorbidities, and aSAH status. Thus, iGA can be a treatment for the prevention of rebleeding before aneurysmal obliteration treatment.

歩いて来たSAH

To prevent rebleeding of a subarachnoid hemorrhage (SAH) due to intracranial artery aneurysms, early treatment is indispensable. We investigated such cases at the time of initial diagnosis of walk-in patients in hospitals. The study covered 293 patients with SAH caused by ruptured intracranial artery aneurysms who were hospitalized in our department between 1996 and 2005. The individuals were treated at the Yamagata University between 1996 and 2005. All 293 cases had a sudden onset. In 89 cases (30.3%), the individuals consulted physicians at various medical facilities without the use of ambulances. In 129 of these cases (44%), the individuals presented with headache only, including Hunt & Kosnik (H&K) Grade I: 27 (9.2%) and Grade II: 102 (34.8%). These findings revealed that headache is common in such cases. Moreover, 24 of the 27 (88.9%) cases of H&K Grade I and 65 of 102 (63.7%) cases of Grade II were walk-in patients, and the consultation rate of walk-in patients presenting only a headache was very high. The average number of days that individuals waited before consulting a physician was 2.2 (0–35 days). Of the 89 cases of walk-in patients, 24 were very difficult to diagnose (26.9%). Two cases (both H&K I) were difficult to diagnose even under CT examination, and 22 cases (H&K I: 8, II: 14) were not suspected to be SAH cases, and their CT were not examined. These difficult cases were first diagnosed as follows: common cold, 4; high blood pressure, 2; facial palsy for oculomotor nerve paralysis, 1; and ordinary headache, 17. Of these 24 cases for which a confirmed diagnosis was difficult, upon subsequent visits, 18 were diagnosed as having persistent headache; 5, rerupture of SAH (admitted by ambulance); and 1, symptomatic spasm (admitted by ambulance). The location of aneurysms of the walk-in 89 patients were ICA: 21, MCA: 22, ACA: 34, VBA: 3, and other: 9. The overall results of the walk-in 89 patients were GR: 73 (82%), MD: 9 (10%), SD: 1 (1%), D: 6 (7%). Our investigation indicated that difficulty in making a confirmed diagnosis is not rare when only the symptoms are considered.

Symptomatic diffuse esophageal spasm as a major ictal manifestation of post-traumatic epilepsy: a case report

Post-traumatic epilepsy (PTE) can create diagnostic confusion when typical epileptic seizures are not manifest. Abdominal symptoms as a manifestation of PTE are rare in this setting. We present a 43-year-old female with paroxysmal chest and abdominal pain, nausea, salivation, and intermittent dysphagia. Esophageal testing demonstrated diffuse esophageal spasm, but smooth muscle relaxants provided no relief. Finally, after history revealed that a motor vehicle accident temporally preceded symptom onset, video electroencephalography confirmed PTE. Therapy with anti-epileptic drug completely resolved symptoms, and the esophageal motor pattern normalized. We speculate that abnormal epileptiform discharges from the seizure focus altered cerebral input to intrinsic esophageal innervation, resulting in inhibitory dysfunction and a picture resembling diffuse esophageal spasm. This is the first report of symptomatic esophageal spasm as a major ictal manifestation of PTE.

74. 脳梗塞症状 (Symptomatic spasm) 発現時の破裂脳動脈瘤の治療

74. 脳梗塞症状 (Symptomatic spasm) 発現時の破裂脳動脈瘤の治療

Endovascular Management of Symptomatic Spasm of Radial Artery Bypass Graft

To describe the technique of endovascular access for treatment of vasospasm of a radial artery bypass graft from the occipital artery to the M3 branch of the middle cerebral artery (MCA) in a patient with moyamoya disease. A 32-year-old woman presented with recurrent right-sided ischemic symptoms in the territory of a previous stroke. Angiographic findings were consistent with moyamoya disease, and a perfusion deficit was identified on computed tomography (CT) perfusion imaging. The patient underwent a left MCA bypass graft for flow augmentation. She returned with an occluded bypass graft, collateralization of the anterior MCA territory through a spontaneous synangiosis, and a severe perfusion deficit in the posterior MCA territory. She underwent a revision bypass graft procedure with the radial artery from the occipital artery stump to the MCA-M3 branch. She developed repeated symptomatic vasospasm of the radial artery graft postoperatively. After systemic anticoagulation, the graft was accessed through the occipital artery, and intra-arterial verapamil was injected. When this failed to resolve the graft spasm, the radial artery graft was accessed with a 0.14-inch Synchro-2 microwire (Boston Scientific, Natick Massachusetts), and sequential angioplasties were performed using over-the-wire balloons from the proximal to distal anastomosis and in the occipital artery stump. A nitroglycerin patch was applied cutaneously over the graft to relieve the vasospasm. No complications occurred. Graft patency with robust flow was observed on the 5-month follow-up angiogram. Endovascular techniques can be safely used for salvage of spastic extracranial-intracranial grafts.

Clinical profile and response to oral prednisolone in infantile spasm.

To evaluate the clinical profile and response to oral prednisolone in infantile spasms. Case series. Neurology Department, The Children Hospital and Institute of Child Health, Multan, from July 2005 to June 2007. Fifty patients of infantile spasms were studied. Age, gender, age at onset of seizures, type of spasms (flexor, extensor or mixed), history of intrapartum asphyxia, developmental history, dysmorphic facial features, any hypopigmented/ hyperpigmented skin lesions, computed tomogram and electroencephalogram findings and response to oral prednisolone was noted. Data was analyzed statistically by SPSS 10. Descriptive statistics was used to find out frequencies and percentages of all above mentioned variables. Chi-square test was applied to determine the association between these variables and response to treatment. P-value of less than 0.05 was taken significant. Male to female ratio was 2.1:1. Mean age of babies was 6.5+/-3.35 months. Mean age at onset of seizures was 5.35+/-3.52 months. Flexor spasms was seen in 32 (64%), extensor spasms in 8 (16%) and mixed spasms in 10 babies (20%). Symptomatic infantile spasms were noted in 48 (96%) babies while two babies (4%) were having cryptogenic infantile spasm. History of intrapartum asphyxia was noted in 54% of symptomatic cases. Favourable response to oral prednisolone was seen in 27 babies (54%). Except male gender, none of the other variable reached the statistical significance for favourable response to treatment. Infantile spasms were found more common in males, flexor spasms were the commonest type noted. Symptomatic spasm was noted in 96% of cases and intrapartum asphyxia was the commonest cause of symptomatic group. Response to oral prednisolone was noted in more than half of cases of infantile spasms.

Non-saccular aneurysms of the supraclinoid internal carotid artery trunk causing subarachnoid hemorrhage: acute surgical treatments and review of literatures

Non-saccular aneurysms (NSAs) of the internal carotid artery trunk include blood blister-like aneurysms (BBAs) and dissecting aneurysms (DAs), which are susceptible to disastrous intra- and postoperative bleeding. This study was conducted to clarify the clinical features of NSAs and the results of early bypass and trapping. Nineteen ruptured NSAs were identified in 937 patients with subarachnoid hemorrhage (SAH). The principal treatment was to trap the aneurysm following bypass surgery as soon as possible after SAH onset. Angiography revealed nine BBAs and ten DAs. Eight patients (four BBA and four DA) were treated in the chronic stage because of delayed arrival (n = 3) or lack of aneurysm on initial angiography (n = 3), or other reasons (n = 2). The remaining 11 patients underwent early surgery using trapping after bypass, except for one BBA-type (clipped). During surgery, corresponding intraoperative findings were confirmed for each aneurysm type. There were six preoperative reruptures; five were determinant of patient outcome. In 14 patients without preoperative rerupture influencing outcome, 11 patients were independent at discharge and three patients dependent due to surgical complication. There was one case of minor intraoperative bleeding; no postoperative rerupture occurred. There was no delayed vasospasm-related deficit, although temporary symptomatic spasm occurred in three patients. Early bypass and trapping appeared to be an acceptable treatment strategy for these NSAs eliminating intra- and postoperative bleeding and not increasing a chance of delayed vasospasm.

Defining Vasospasm After Subarachnoid Hemorrhage

Vasospasm is an important complication of subarachnoid hemorrhage, but is variably defined in the literature. We studied 580 patients with subarachnoid hemorrhage and identified those with: (1) symptomatic vasospasm, defined as clinical deterioration deemed secondary to vasospasm after other causes were eliminated; (2) delayed cerebral ischemia (DCI), defined as symptomatic vasospasm, or infarction on CT attributable to vasospasm; (3) angiographic spasm, as seen on digital subtraction angiography; and (4) transcranial Doppler (TCD) spasm, defined as any mean flow velocity >120 cm/sec. Logistic regression analysis was performed to test the association of each definition of vasospasm with various hospital complications, and 3-month quality of life (sickness impact profile), cognitive status (telephone interview of cognitive status), instrumental activities of daily living (Lawton score), and death or severe disability at 3 months (modified Rankin scale score 4-6), after adjustment for covariates. Symptomatic vasospasm occurred in 16%, DCI in 21%, angiographic vasospasm in 31%, and TCD spasm in 45% of patients. DCI was statistically associated with more hospital complications (N=7; all P<0.05) than symptomatic spasm (N=4), angiographic spasm (N=1), or TCD vasospasm (N=1). Angiographic and TCD vasospasm were not related to any aspect of clinical outcome. Both symptomatic vasospasm and DCI were related to reduced instrumental activities of daily living, cognitive impairment, and poor quality of life (all P<0.05). However, only DCI was associated with death or severe disability at 3 months (adjusted OR, 2.2; 95% CI, 1.2-3.9; P=0.007). DCI is a more clinically meaningful definition than either symptomatic deterioration alone or the presence of arterial spasm by angiography or TCD.

Cilostazol May Prevent Cerebral Vasospasm Following Subarachnoid Hemorrhage

Cilostazol is an antiplatelet aggregation inhibitor drug associated with increased cerebral blood flow and inflammation suppression. This study evaluated administration of cilostazol to prevent cerebral vasospasm following subarachnoid hemorrhage (SAH) in 50 patients treated surgically from December 2004 to November 2006. All patients, excluding those with Hunt and Kosnik grade 5 or who had undergone late surgery, were classified into two groups: 26 patients who received 200 mg/day cilostazol from postoperative day 1 to day 14 and 24 control patients. The frequency and the degree of cerebral vasospasm, occurrence of ischemic lesion, and clinical symptoms due to vasospasm were compared between the two groups. The appearance of severe vasospasm on angiography, persistent symptomatic spasm, and new cerebral infarction due to vasospasm demonstrated by neuroimaging were apparently lower in the cilostazol group than in the control group, suggesting that cilostazol may significantly suppress cerebral vasospasm following SAH.

Medical treatment of patients with infantile spasms.

Infantile spasms are the main feature in West syndrome, an age-related epilepsy syndrome that affects 1 in every 2,000-4,000 infants. The authors provide a comprehensive review of the literature about infantile spasms and their therapy. In the United States, the drug of choice for infantile spasms, at least the cryptogenic cases, has been adrenocorticotropic hormone (ACTH). It is generally considered to be more effective than corticosteroids. Adrenocorticotropic hormone appears to alter long-term prognosis of cryptogenic infantile spasms, and helps in some cases of symptomatic infantile spasm. Vigabatrin has been considered the drug of choice for infantile spasms secondary to tuberous sclerosis, and possibly, according to many neurologists, for all cases of infantile spasm. Recent concerns regarding retinopathy associated with vigabatrin therapy are, however, limiting the use of this drug. Valproic acid benefits 40%-70% of patients who failed a trial of ACTH. Nitrazepam is as effective as ACTH in acutely controlling infantile spasms; however, its long-term effects on prognosis have not been studied. Pyridoxine, lamotrigine, topiramate, zonisamide, ketogenic diet, immunoglobulin therapy, felbamate, and thyrotropin-releasing hormone have all been used for the treatment of infantile spasms, but are usually reserved for cases refractory to vigabatrin and/or ACTH.

Rapid natriuresis and preventive hypervolaemia for symptomatic vasospasm after subarachnoid haemorrhage.

To prevent symptomatic cerebral vasospasm, we have used hypervolaemia (HV) or volume expansion in patients with aneurysmal subarachnoid haemorrhage (SAH) in recent years. In these patients we could not perform effective fluid and sodium (Na) replacement because of rapid and overwhelming water and Na loss. Although this phenomenon is characteristic under hypervolaemic states, we regard it important to elucidate the mechanism underlying initiation of vasospasm after aneurysmal SAH. Patients with aneurysmal SAH, operated on within 24 hours of onset, were analysed prospectively. We selected 17 patients in good pre-operative condition. Intravascular volume expansion was accomplished with plasma fractionate or albumin and crystalloid solutions in all patients. We divided the 17 patients into two groups; symptomatic spasm group (S-group) consisting of 4 cases developing transient ischaemic symptoms and non-symptomatic spasm group (NS-group) consisting of 13 cases. In S-group, rapid and marked natriuresis developed characteristically before the onset of ischaemic symptoms. The differences in daily Na balance between the two groups were significant on the 3rd and 5th days (p < 0.05). The mean cumulative Na balance in S-group during the 10 days of the study (-375 +/- 159 mEg) was higher than that of NS-group (-24.4 +/- 225 mEq) (p < 0.05). Rapid natriuresis preceded the development of ischaemic symptoms, and was important as a trigger for symptomatic vasospasm after SAH. We considered that hormonal disorders were implicated in this phenomenon, and atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), renin, and aldosterone were each measured three times during the period, with no significant differences, found between the two groups. It was speculated that another potent natriuretic factor, similar to ANP, induced a rapid selective natriuresis resulting in symptomatic vasospasm.

Diffuse esophageal spasm

Objective: As recently suggested, nitric oxide (NO) may play an important role in the regulation of esophageal motility, being partly responsible for the latency period and latency gradient between the onset of a swallow and contractions of esophageal circular smooth muscles. Diffuse esophageal spasm appears to be a classical example in which the mechanisms normally responsible for the physiologic timing of the contractions occurring in the esophageal body after swallowing are disturbed. Methods: Five patients (one male and four female; age, 18-48 years) with symptomatic esophageal spasm were given glyceryl trinitrate (GTN) intravenously in gradually increasing doses or L-arginine on two separate occasions and underwent manometric measurements of esophageal motility after wet swallows, using a multilumen perfused catheter system (Synectics Medical, Stockholm, Sweden). The amplitude, duration, and propagation of the contractions and the latency period were analyzed, using specially designed software. Addit...

Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management.

Perioperative management of aneurysmal subarachnoid hemorrhage: Part 2. Postoperative management.

Update on Calcium Antagonists in Cerebrovascular Diseases

Clinical management of patients affected by subarachnoid hemorrhage has been modified by the use of nimodipine. Although no differences in overall neurologic outcome and rates of symptomatic spasm have been observed between nimodipine and control patients, severity of permanent neurologic deficits consequent to cerebral vasospasm is reduced in the former. On the other hand, clinical trials with nimodipine in ischemic stroke did not substantiate the expected neurologic benefits. A meta-analysis of the two phase IV studies published thus far shows that of 350 patients examined, mortality rate was 11.5% and 19% in subjects given nimodipine and placebo, respectively (n.s.). Cerebral death accounted for 30% of cases in both groups, whereas a lower percentage of cardiac and pulmonary fatal events were observed among nimodipine-treated subjects. Moreover, neurologic outcome of survivors was not significantly different. These results may be associated with the notion that the voltage-operated channel blockade exerted by calcium antagonists is only a part of the complex events leading to the enhancement of calcium ion intracellular concentration as a "common final pathway." However, difficulties encountered in planning clinical trials in acute ischemic stroke also might explain the lack of conclusive results. The feasibility of randomization of an adequate sample of patients and of very early therapeutic intervention after stroke onset are discussed.

Symptomatic Spasm の治療

Symptomatic Spasm の治療

Prevention of symptomatic vasospasm by topically applied Nimodipine

A 2.4 x 10(-5) M solution of the Calcium-antagonist Nimodipine was administered to the exposed cerebral vessels in 17 patients intraoperatively clipping of a ruptured aneurysm. The interval between subarachnoid haemorrhage and operation was 48 to 72 hours. The CT investigation had revealed blood accumulation in the basal cisterns in all cases. Vasodilatation was observed in all instances; the percentage being greater in small vessels as compared to large vessels. Postoperatively, a neurological deficit combined with angiographically verified vasospasm occurred in two patients, but was reversible in both. Fifteen patients remained free from symptomatic vasospasm and were discharged without neurological deficit. In 13 of these patients and 3 additional cases, a plastic cannula was placed intraoperatively so that postoperative topical administration of Nimodipine was possible. Postoperative control-angiograms after a mean interval of 7 days from SAH did not show severe spasm in any of the patients; localised moderate asymptomatic spasm was found in 8 cases and was reserved in 5. Moderate postoperative symptomatic spasm was observed in 2 patients, treated and reversed in one patient. In 5 of 7 cases without evidence of spasm in the angiogram postoperative topical administration of Nimodipine caused vasodilatation. It is concluded, that topical intracisternal administration of Nimodipine reverses intraoperative vascular spasm and decreases the probability of postoperative symptomatic vasospasm after early surgery.