Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spasm”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2003

Induction of coronary artery spasm by two pharmacological agents: comparison between intracoronary injection of acetylcholine and ergonovine.

BACKGROUND AND OBJECTIVES: There have been few studies comparing the clinical usefulness for the induction of coronary artery spasm (CAS) between acetylcholine (ACh) and ergonovine (ER). This study is designed: (1) to examine the duration of effect after intracoronary injection of ACh on the responsible vessels using a 0.014 inch, 15 MHz Doppler guide wire, and (2) to evaluate the efficacy of two pharmacological agents, ACh and ER, for the induction of CAS in patients with <50% stenosis in the cardiac laboratory. METHODS: Phasic coronary flow velocity patterns were recorded at rest and during ACh tests in 22 patients with normal or near-normal coronary arteries. The tip of the guide wire was placed on the proximal right coronary artery (RCA) and mid-left anterior descending artery. We measured the time required to baseline level of average peak velocity after intracoronary injection of ACh. We performed selective intracoronary administration of both ER and ACh in the same 171 patients (106 men, 65 women, mean age of 62+/-10 years) with <50% stenosis. Under no medication, ACh was injected first in incremental doses of 20, 50, and 80 microg into the RCA and of 20, 50, and 100 microg into the left coronary artery (LCA). Ten minutes later, ER was administered at 10 microg/min for four minutes for a maximal dose of 40 microg on the RCA and at 16 microg/min over four minutes for a total dose of 64 microg on the LCA. Positive spasm was defined as > or =99% luminal narrowing. RESULTS: The time-averaged peak velocity returned to baseline after intracoronary injection of ACh within 10 minutes in all 120 procedures, consisted of 19 with positive spasm (RCA (n=10): 245+/-33 s; LCA (n=9): 351+/-187 s) and 101 with negative spasm (RCA (n=48): 155+/-62 s, LCA (n=53): 248+/-106 s). In the overall results, there was no difference concerning the incidence of provoked spasm between the two pharmacological agents (ACh: 33% versus ER: 32%, NS). Coronary spasms were induced by either pharmacological agent in 134 vessels. Concordance in this study was 94% in all vessels, whereas the remaining 6% of vessels were different from each other. The non-concordance rate of the right coronary artery was significantly higher than that of the left coronary artery (10% versus 4%, p<0.01). However, ER provoked more focal spasms, whereas ACh provoked more diffuse and distal spasms, compared with each other. Seventy-four (55%) of the 134 vessels had coronary spasms in the same coronary arteries. Concordance of both provoked spasm sites and spasm configurations in the same coronary artery was observed in only 18 (13%) vessels. No serious or irreversible complications were observed during the two sequential tests. CONCLUSIONS: As a spasm provocation test, there were no differences between ACh and ER. We recommend the supplementary use of these two pharmacological agents for the induction of CAS in the cardiac laboratory, if available.

Acetylcholine↗
PubMed1988

Multivessel coronary spasm in patients with variant angina: a study with intracoronary injection of acetylcholine.

Multivessel coronary spasm has been described but its incidence in patients with variant angina still remains unclear. Thirty-three patients with variant angina were studied during coronary angiographic examination with selective intracoronary injection of acetylcholine (ACh). In all but three patients, the location of ischemia during attack was determined by the electrocardiographic findings, by exercise 201Tl myocardial scintigraphy, and by two-dimensional echocardiography during a hyperventilation test, and the coronary artery (or arteries) responsible for the attack was predicted before the study. ACh induced spasm of at least one coronary artery in all but one patient. ACh induced spasm of both the left and right coronary arteries (i.e., multivessel coronary spasm) in 24 patients: in two of the four patients who were predicted to have spasm of the left coronary artery, in six of the 11 predicted to have spasm of the right coronary artery, in 13 of the 15 predicted to have spasm of both the left and right coronary arteries, and in three of the three in whom coronary artery responsible for attack had not been predicted. This ACh-induced spasm of the left and right coronary arteries occurred separately and no patients showed hemodynamic instability during attack. In one patient in whom multivessel coronary spasm had been predicted and ACh failed to induice coronary spasm, ergonovine maleate (0.2 mg) induced spasm of both the left and right coronary arteries simultaneously, resulting in severe prolonged hypotension. Nineteen of the 25 patients in whom multivessel coronary spasm was documented showed angiographically normal or nearly normal coronary arteries after administration of nitroglycerin.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1997

Electrophysiological investigation of hemifacial spasm after microvascular decompression: F waves of the facial muscles, blink reflexes, and abnormal muscle responses.

In patients with hemifacial spasm, it has been said that the spasm is due to cross compression of the facial nerve by a blood vessel and that microvascular decompression (MVD) of the facial nerve is an effective treatment. The F waves, which result from backfiring of antidromically activated motor neurons of the facial motor nucleus, are indices of the excitability of the facial motor nucleus and are enhanced in patients with hemifacial spasm. Measuring blink reflexes and abnormal muscle responses (lateral spread), a characteristic sign of hemifacial spasm, has been used to investigate the mechanism of hemifacial spasm pathophysiologically. Thus the authors measured F waves of the facial muscle, blink reflexes, and abnormal muscle responses before and after MVD in patients suffering from hemifacial spasm to investigate the excitability of the facial motor nucleus and the course of the cure of hemifacial spasm after MVD. The authors obtained facial nerve-evoked electromyograms in 20 patients with hemifacial spasm before and after the MVD procedure. On the spasm side, the F waves and blink reflexes were enhanced preoperatively compared to those on the normal side and abnormal muscle responses were recorded in all patients. In 12 patients whose hemifacial spasm had not disappeared completely for 5.1 +/- 1.7 (mean +/- standard error) months following the MVD procedure, F waves were still enhanced significantly and abnormal muscle responses were still recordable, albeit at lower amplitude. Within 1 month after the hemifacial spasm had disappeared completely. F waves were still significantly enhanced in 17 patients and abnormal muscle responses were recorded in seven of 15 patients. Subsequently, the enhanced F waves and abnormal muscle responses disappeared completely. The authors' study supports the hypothesis that the cause of hemifacial spasm is hyperexcitability of the facial motor nucleus and suggests that additional surgery should not be performed for at least 2 years after MVD, because that period is necessary for the disappearance of the hyperexcitability of the facial motor nucleus.

Adult↗
PubMed1978

[A regional cerebral blood flow in patients with acute subarachnoid hemorrhage--with special references to spasm (author's transl)].

Measurements of the regional cerebral blood flow (rCBF) were performed 44 times on patients with subarachnoid hemorrhage, using the 133-Xe clearance method with aid of the 8 channel detector unit. The patients consisted of 31 preoperative cases within 3 weeks of the last subarachnoid hemorrhage. The sites of the ruptured aneurysms included 11 anterior communicating arteries, 8 middle cerebral arteries, 7 internal carotid arteries and 3 anterior cerebral arteries. In 2 cases, the aneurysms were not identified with the cerebral angiograms. The purpose of this study was to investigate the effect of spasm on the rCBF. The subjects were divided into two groups: those with and without spasm. Furthermore, the group with spasm was divided into three subgroups according to the degree of spasm. The findings obtained were as follows; The group with spasm showed a statistically significant decrease in the mean of the rCBF. The MrCBF was not influenced by the distribution of spasm, however. In the group without spasm, the MrCBF had a good correlation with the cerebrospinal fluid pressure (CSF-P) or the level of consciousness. In the group with spasm, there was no correlation between the MrCBF and the CSF-P or the level of consciousness. For example that marked reduction of the MrCBF were seen in some cases with low CSF-P or only slight disturbance of consciousness. The rCBF was measured 2 or 3 times in 5 cases with spasm. The decrease in MrCBF occured about one week after the incidence of the subarachnoid hemorrhage but MrCBF recovered with the disappearance of spasm 2 or 3 weeks after the attack. There was a poor correlation between spasm and relative flow patterns. The good correlation, however, was found in only one case with the severe spasm at the middle cerebral artery.

Acute Disease↗
PubMed2001

Infantile spasms.

Infantile spasms constitute both a distinctive seizure type and an age-specific epilepsy syndrome that have been extensively described for over a century. Standardization of the classification of infantile spasms has evolved, culminating in recent recommendations for separately recognizing and distinguishing the seizure type (spasms or epileptic spasms) and the epilepsy syndrome of infantile spasms (West syndrome). More-detailed descriptions of the clinical and electrographic features of epileptic spasms and hypsarrhythmia have emerged. Advances in neuroimaging techniques have revealed clues about pathophysiology and increased the etiologic yield of the diagnostic evaluation of patients with infantile spasms. Adrenocorticotrophic hormone remains the treatment of choice for many neurologists. Recent controlled studies support vigabatrin as first-line therapy, and open-label studies suggest that topiramate, lamotrigine, and zonisamide may be useful in treating spasms. Recent reports of visual-field constriction with vigabatrin may limit its use. Surgical treatment has been used successfully in a select subgroup of patients with secondarily generalized spasms from a single epileptogenic zone. Although the prognosis for most patients with infantile spasms remains poor, further studies identifying predictors of favorable prognosis and recent advances in understanding the pathophysiology of infantile spasms offer hope of safer and more-effective therapies that improve long-term outcome.

Adrenocorticotropic Hormone↗
PubMed2002

Microvascular decompression to treat hemifacial spasm: long-term results for a consecutive series of 143 patients.

OBJECTIVE: The concept of neurovascular decompression for the treatment of hemifacial spasm is now widely accepted. In this study, we report our long-term results for 145 cases treated with this procedure. METHODS: The results of 145 microvascular decompressions to treat hemifacial spasm (performed between 1980 and 1998) among 143 patients (62.2% female patients and 37.8% male patients; mean age, 54.5 yr) are presented. The onset of symptoms was typical in 95.9% of cases and atypical in 4.1%. Platysma muscle involvement was observed for 24.5% of patients, with a higher incidence among female patients (74.3%). Patients were monitored with annual questionnaires. Twenty-six patients were lost to follow-up monitoring, and 117 are still undergoing follow-up monitoring, with an average period of 9.6 years (range, 1-17.6 yr). RESULTS: At discharge, 69 patients (59%) were spasm-free and 48 patients (41%) experienced further spasm. At 6 months, the number of spasm-free patients had increased to 108 (92.3%), whereas only 9 patients (7.7%) complained of hemifacial spasm; 44 patients were spasm-free at an average time of 15 weeks. In follow-up examinations (average period, 9.4 yr), 106 patients were spasm-free. Seven patients experienced only temporary relief, with recurrence after 4.5 years. Two patients were spasm-free after 4 or 6 weeks, and the recurrence of spasm was observed 1 year later. Two patients were never completely spasm-free. Among the patients who did not undergo previous surgery elsewhere, only two experienced recurrence. CONCLUSION: Deafness was the main postoperative complication (8.3%); most of those cases (66%) occurred before the routine use of intraoperative evoked potential monitoring. Analysis of our series demonstrates that this surgical procedure involves very low risk, is well tolerated by elderly patients, is associated with very low recurrence rates, and is a definitive treatment for more than 90% of cases.

Adult↗
PubMed2004

A proposal for case definitions and outcome measures in studies of infantile spasms and West syndrome: consensus statement of the West Delphi group.

PURPOSE: To reach a broad consensus on case definitions, outcomes, and outcome measures that will ease future study design and facilitate comparison of data from different studies of infantile spasms and West syndrome. METHODS: Persons who had recently presented or published first-author original research in this field were invited to participate in an e-mail Delphi process and to invite other investigators or clinicians who they thought might participate. RESULTS: The process consisted of six rounds, anonymous except to the facilitator. In total, responses were received from 46 participants. The final statement was approved by 31 participants from 15 countries. It concluded that the primary clinical outcome, cessation of spasms, should denote absence of witnessed spasms from within 14 days of commencement of treatment, and for > or =28 consecutive days from the last witnessed spasm. Primary electroclinical outcome denotes cessation of spasms with resolution of hypsarrhythmia. West syndrome should be a defined subset of the syndrome of infantile spasms. An infantile spasms single-spasm variant should be recognized. Ways are suggested of handling subtle spasms in the context of clinical studies. It proposes a standard for reporting modifying and atypical features of hypsarrhythmia, a minimal set of baseline characteristics and outcomes that should be reported in trials of infantile spasms, and suggests a standard definition of relapse. Consensus was not reached on a definition of hypsarrhythmia. CONCLUSIONS: We reached a clear consensus on many aspects of study design for the investigation of infantile spasms, although incomplete consensus was found on how to define EEG criteria.

Child, Preschool↗
PubMed1998

A pilot study of topiramate in the treatment of infantile spasms.

PURPOSE: West syndrome is a rare epileptic syndrome associated with infantile spasms, a specific abnormal electroencephalographic pattern (termed hypsarrhythmia), and mental retardation. Management of this disorder is difficult because current treatment regimens, including many anticonvulsants and hormones, are often ineffective. Topiramate (TPM) is a new antiepileptic drug that may be effective in pediatric epilepsies. We conducted a pilot study to test the effects of rapid TPM dosing in patients with refractory infantile spasms. METHODS: Eleven children with refractory infantile spasms were given an initial dose of 25 mg TPM per day in addition to their current therapy. Dosage was increased by 25 mg every 2-3 days until spasms were controlled, the maximal tolerated dose was reached, or the maximal dose of 24 mg/kg/day was achieved. Efficacy was primarily assessed by video EEG and secondarily by parental count of spasm frequency. RESULTS: Five (45%) subjects became spasm free during the study, with absence of infantile spasms and hypsarrhythmia (either classic or modified) proven by video EEG. Nine subjects, including the five spasm free, achieved a spasm reduction of > or =50%. Spasm frequency decreased from 25.6+/-19.3 to 6.9+/-5.9 spasms/day. Sixty-four percent of the subjects were able to achieve TPM monotherapy. CONCLUSIONS: Results in this cohort of 11 patients with refractory disease show TPM to be a promising new agent for the treatment of infantile spasms.

Adult↗
PubMed2007

Arterial hypertension in patients with left primary hemifacial spasm is associated with neurovascular compression of the left rostral ventrolateral medulla.

The aim of the study was to clarify the relationship between neurovascular compression of the rostral ventrolateral medulla and arterial hypertension in patients with primary hemifacial spasm. We enrolled 82 patients with primary hemifacial spasm and 82 age- and sex-matched magnetic resonance imaging (MRI) controls of the posterior cranial fossa. Neurovascular compression of the rostral ventrolateral medulla was assessed by MRI, and its association with arterial hypertension was investigated. No significant differences were found in prevalence of arterial hypertension between patients with primary hemifacial spasm and control subjects (39.0 vs. 29.3%, p=0.19). Thirty-two percent of the patients with left primary hemifacial spasm (n=44) and 47% of the patients with right primary hemifacial spasm (n=38) were hypertensive. Neurovascular compression of the left rostral ventrolateral medulla was observed in 86% of those with left (ipsilateral) primary hemifacial spasm with arterial hypertension (n=14) and 33% of those with left (ipsilateral) primary hemifacial spasm without (n=30). The association between neurovascular compression of the left rostral ventrolateral medulla and arterial hypertension was significant in patients with left (ipsilateral) primary hemifacial spasm (p=0.0012), but not in patients with right (contralateral) primary hemifacial spasm (p=0.18). Neurovascular compression of the left rostral ventrolateral medulla was more frequently observed in hypertensive patients with left primary hemifacial spasm, and neurovascular compression of the left rostral ventrolateral medulla correlated with arterial hypertension in these patients. These results are of potential clinical importance for the treatment of primary hemifacial spasm with arterial hypertension.

Adult↗
PubMed2003

Infantile spasms.

Infantile spasms is a catastrophic form of epilepsy found only in infants and young toddlers, with the peak incidence between 4 - 7 months of age. Estimated prevalence is 1 in 2000 - 6000 live births. There are many causes of infantile spasms, including tuberous sclerosis, hypoxic-ischaemic injury, congenital infectious diseases, inborn errors of metabolism, malformations of cortical development, genetic syndromes such as Aicardi's syndrome and chromosomal abnormalities. A small percentage of patients have idiopathic infantile spasms, with normal growth and development prior to the onset of infantile spasms and no known aetiology. Because of the poor prognosis of infantile spasms, treatment is usually aggressive and immediate, with the hopes of altering the natural history of the disease. The majority of patients with infantile spasms have a poor prognosis with intractable epilepsy, severe developmental delays and/or significant cognitive impairments. Of all patients with infantile spasms, 70 - 90% have mental retardation. Furthermore, 20 - 50% of patients with infantile spasms develop Lennox-Gastaut syndrome with multiple seizure types, cognitive impairments and a markedly abnormal electroencephalogram, arguably one of the most difficult epilepsy syndromes to treat. Infantile spasms are resistant to most of the standard antiepileptic drugs. Adrenocorticotropin hormone (ACTH) or oral steroids result in a significant reduction of seizures, as well as an improvement in the electroencephalogram. Some studies have indicated that infants treated with ACTH within the first month of onset have a more favourable prognosis. Vigabatrin has also been shown to be effective in the treatment, although it is not yet FDA-approved in the US. Valproate has also been used in the treatment of infantile spasms, with an efficacy of approximately 25 - 40%. However, in the very young infant, it does carry a high risk of fatal hepatotoxicity. Surgical resection may be the treatment of choice for those infants with focal cortical dysplasia and intractable infantile spasms. Emerging therapeutic possibilities include topiramate, felbamate, lamotrigine, zonisamide and perhaps levetiracetam. With the advancements in molecular biology, genetics and neuroimaging, there is the hope of novel therapies in the future.

Anti-Inflammatory Agents↗
PubMed1994

Coupling of focal electrical seizure discharges with infantile spasms: incidence during long-term monitoring in newly diagnosed patients.

To investigate the coupling of focal electrical seizure discharges (FS) and infantile spasms, we analyzed the video/polygraphic monitoring studies performed on 96 consecutive patients newly diagnosed with infantile spasms and hypsarrhythmic EEGs. A FS was considered to be coupled with infantile spasms if it occurred during a cluster of spasms (a series of individual spasms separated by < 1 min) or within 10 s of spasm onset or cessation. Ten patients demonstrated FS. In five patients (5% of the entire population) an apparent coupling of some FS with infantile spasms was observed during the baseline monitoring study. However, in three patients (only 3% of the entire population) was the observed coupling of FS and infantile spasms significant (p < 0.05). These results indicate that coupling of FS and infantile spasms occurs rarely, and that, in some instances, apparent couplings of FS and infantile spasms are best explained by chance coincidence. These findings do not support the hypothesis that the generation of infantile spasms at a subcortical level is dependent on a focal cortical discharge.

Cerebral Cortex↗
PubMed1989

Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus.

To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

[Cardiac events in vasospastic angina: site and morphology of coronary artery spasm is related to the long-term prognosis of vasospastic angina].

To determine whether the site and morphology of coronary artery spasm provoked with acetylcholine can predict the long-term prognosis of vasospastic angina, coronary artery spasm (more than 90% narrowing) provoked with acetylcholine was studied in 66 consecutive patients (56 males, 10 females, mean age 56 +/- 9 years) with vasospastic angina. All patients were followed for 6.7 +/- 0.9 years and the incidence of cardiac events such as sudden death, myocardial infarction or worsened unstable angina was compared with the site and morphology of provoked spasm. The site of spasm was regarded as proximal when spasm occurred in the proximal site of 3 major coronary arteries which was designated as segment 1, 6 or 11, according to the classification of the American Heart Association, and distal in other segments. The morphology of spasm was classified into 3 types, focal (12 cases, localized more than 90% narrowing with adjoining parts constricting less than 25%), diffuse (17 cases, diffuse more than 90% narrowing), and intermediate (37 cases, localized more than 90% narrowing with adjoining parts constricting 25-90%). The site of spasm was classified into 2 types, the proximal group (24 cases) and the distal group (42 cases). Cardiac events occurred in 7 patients during the follow-up period: sudden death in 2, myocardial infarction in 2, and worsened unstable angina in 3. As to the site of spasm, the incidence of cardiac events was 21% (5/24 patients) in the proximal group, significantly higher than 5% (2/42) in the distal group (p < 0.05). As to the site of spasm, the incidence of cardiac events was 41% (5/12) in the focal group, significantly higher than 3% (1/37) in the intermediate group and 6% (1/17) in the diffuse group (p < 0.001). The presence of proximal and focal coronary artery spasm was associated with a significantly higher incidence of cardiac events. The site and morphology of coronary artery spasm provoked with acetylcholine is related to the long-term prognosis of vasospastic angina.

Acetylcholine↗
PubMed2000

Catheter-induced coronary spasm--a view of mechanical factors and experience with selective left coronary arteriography.

BACKGROUND: Coronary spasm during cardiac catheterization is not unusual. The mechanism of spasm remains uncertain, but is considered to be multifactorial. Many researchers believe that coronary spasm that develops during catheterization is partly spontaneous and partly catheter-induced. Because catheter-induced spasm results from mechanical irritation, we tried to find the iatrogenic factors that predispose patients to coronary spasm during coronary angiography. METHODS: Retrospectively, we reviewed the records of 7,295 patients who underwent coronary angiography at our hospital from June, 1983 to November, 1997; coronary spasm was documented in 30 patients, who became the study group. We randomly selected 41 patients who had normal coronary arteries as the normal control group. After reviewing cine films of coronary angiography, we compared these two groups for several parameters. These parameters included the length and diameter of the left main coronary artery (LMC), the angle between the LMC and the aorta, the angle between the catheter tip and the LMC, whether the catheter tip came into contact with the vascular wall and whether there was vessel wall bulging, catheter size and catheter/LMC ratio. This angiographic data and the demographic features, including age, sex, history of hypertension, diabetes mellitus, smoking, previous myocardial infarction, family history of coronary artery disease, cholesterol and triglyceride levels and chest pain character (exertional or rest pain) were compared between the study patient group and the control group. RESULTS: The results disclosed that larger catheter size (7.1 +/- 0.6 mm vs 6.4 +/- 0.7 mm, p < 0.001), smaller LMC diameter (4.2 +/- 0.9 mm vs 4.9 +/- 1.0 mm, p = 0.004), larger catheter/LMC ratio (0.07 +/- 0.05 vs 0.05 +/- 0.03, p = 0.022), catheter contact with the vessel wall (27/30 vs 20/41, p < 0.001) and vessel bulging (18/30 vs 5/41, p < 0.001) were related to catheter-induced coronary spasm. We found that the catheter tip coming into contact with the vessel wall, vessel wall bulging and catheter/LMC ratio (odds ratio 8.92 x 10(14)) were statistically significant factors predisposing patients to catheter-induced coronary spasm. CONCLUSIONS: Multiple factors contribute to coronary spasm. Of those, mechanical or iatrogenic factors might predispose patients to spasm during coronary catheterization. These facts deserve our attention, because iatrogenically induced spasms may be avoided by meticulously selecting catheters and manipulating them gently.

Adult↗
PubMedDate not supplied

Ictal clinical electroencephalographic findings of spasms in West syndrome.

The electroencephalographic/video recordings of 955 spasms in children with cryptogenic and symptomatic West syndrome (WS) were reviewed to define the relation between a clinical manifestation of a spasm and its EEG pattern, and to examine whether these features reflect the etiology and prognosis of WS. The review confirmed the spasm to be a distinct type of seizure, with a unique clinical and EEG pattern unlike that of all other recognized seizures. Symmetric spasms were present in cryptogenic and symptomatic patients. In contrast, asymmetric spasms, or focal signs recognizable during a spasm, strongly indicated the existence of a cerebral lesion. In both etiological groups, the characteristic ictal EEG pattern of the spasms consisted of a positive-vertex slow wave. The other two patterns apparently correlated to a spasm, were fast activity, here called spindle-like, and decremental activity. The fast activity corresponded to a clinical stare, and the decremental activity, when present, represented a postictal event. Although it was independent from the etiology of the spasms, persisting hypsarrhythmia during a cluster of spasms appeared to be an EEG pattern that correlated with a favorable outcome.

Electroencephalography↗
PubMed1980

Relation of coronary arterial spasm to sites of organic stenosis.

Among 63 patients with Prinzmetal's variant angina, coronary arterial spasm responsible for attacks of variant angina was documented arteriographically in 9 patients. In each observed episode (11 attacks in nine patients), coronary spasm producing myocardial ischemia occurred at and was superimposed on a site of preexisting organic stenosis. Measurements of normal portions of "spastic" and "nonspastic" vessels suggested a generalized uniform constriction of all major coronary arteries during attacks, with "spasm" limited to the site of an organic lesion in most cases. In two cases the magnitude of constriction in all vessels was consistent with generalized coronary hypercontractility or spasm. Among 104 patients with organic coronary artery disease and documented single vessel coronary spasm (foregoing 9 patients combined with 95 others from published reports), there were 70 patients with essentially single vessel organic coronary disease in 90 percent of whom the spasm involved the diseased vessel. Of 60 cases abstracted from the literature in which the relation of coronary spasm to the site of organic disease was described, 88 percent had the spasm causing ischemia localized to the site of an organic lesion. Hypotheses attempting to describe the pathophysiologic aspects of coronary spasm in variant angina must account for the intimate association of spasm with sites of organic stenosis in the majority of cases.

Angina Pectoris↗
PubMedDate not supplied

Therapeutic efficacy of ACTH in symptomatic infantile spasms with hypsarrhythmia.

The records of twenty-six infants with both symptomatic infantile spasms and classic hypsarrhythmia were reviewed to determine the efficacy of various ACTH dosages and time of initiation of therapy. Mean age of infantile spasm onset was 6.4 months. Most patients (13) had sustained perinatal hypoxic-ischemic insults. Seventeen patients (65%) had complete cessation of spasms. Between these responders and the 9 nonresponders there was no difference in duration of spasms prior to treatment (2.6 and 2.0 months) or mean ACTH dose (87.4 and 84.5 U/m2, respectively). Infants treated with high-dose ACTH (> 100 U/m2) did not have an improved response rate. The most favorable outcomes were associated with spasm onset at > 8 months of age (all of whom were responders, regardless of dose) or when treatment was started within 1 month of onset of infantile spasms with > 80 U/m2 ACTH (88% responders). Infants treated more than 2 months after onset often did not respond (57%) regardless of dose. Nonresponders with spasm onset at < 4 months of age had the worst prognoses; all had poorly controlled seizures and regressed developmentally. Although all infants in the study were neurologically abnormal, development either improved or did not deteriorate in most responder infants following spasm resolution and one-half remained seizure free. Nonresponder infants continued to have infantile spasms or other seizure types. These data suggest that ACTH is valuable in the treatment of significantly impaired infants with symptomatic infantile spasms, but the most important determinants of outcome may be age of onset and rapidity of treatment rather than dosage.

Adrenocorticotropic Hormone↗
PubMed1989

Infantile spasms.

Infantile spasms constitute a relatively rare disorder of infancy and early childhood; their onset is usually within the first 6 to 8 months of life. A large percentage of patients with this disorder (85-90 per cent) show various degrees of retardation. Infantile spasms typically occur in clusters immediately on arousal, or soon thereafter, but rarely occur while the infant is actually asleep. The usual interictal EEG pattern associated with infantile spasms is hypsarrhythmia, but infantile spasms may occur in the absence of this EEG pattern. The pathophysiology of infantile spasms is not known, but recent evidence suggests that certain regions in the brain stem that are associated with sleep cycling may be responsible for the clinical and EEG manifestations of this disorder. At present, the only known effective treatment for infantile spasms is ACTH or corticosteroids. The therapeutic efficacy of these two agents is relatively equal, and one drug may be effective if the other drug fails. The effectiveness of certain traditional anticonvulsants (valproic acid and the benzodiazepines) and pyridoxine in the treatment of infantile spasms has not been adequately assessed. The long-term mental and developmental outcome of patients with infantile spasms is poor. The only factor that appears to be important in terms of long-term outcome is whether the patient is initially classified as cryptogenic or symptomatic, with the cryptogenic patients having the better outcomes. Approximately half of the infantile spasm patients will continue to have other types of seizures after their spasms stop.

Adrenal Cortex Hormones↗