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PubMed1984

[Prognostic value of coronary spasm threshold determined by the ergometrine test].

The prognosis of spastic angina is difficult to determine. The object of this study was to try to evaluate the prognosis of coronary spasm on the results of provocative, ergometrine testing. Out of 708 patients with angiographically normal or near-normal coronary arteries undergoing the ergometrine test for assessment of chest pain, 78 patients with positive results were retained for study. The threshold of spasm was established in every case: this was defined as the quantity of ergometrine per kilogramme body weight required to provoke spasm. The values ranged from 1 to 12.5 micrograms/kg (average 7.58 micrograms/kg +/- 3.84). The reproducibility of the ergometrine test appeared to be very satisfactory. In the short term, only 4 out of 32 tests became negative. The test remained positive in 28 cases and the mean value of the threshold of spasm did not change significantly (5.64 +/- 3.27 to 5.52 +/- 3.18 micrograms/kg). In the long term only 2 out of 18 tests became negative. The test remained positive in 16 cases and the mean value of the threshold of spasm did not change significantly (5.68 +/- 2.96 to 6.58 +/- 3.11 micrograms/kg). The ergometrine test with a reference threshold of positivity of 5 micrograms/kg is doubly useful: this threshold value helps predict a good response to calcium inhibitor drugs: the threshold of spasm was less than this value in 6 of the 41 patients whose tests became negative after diltiazem therapy, and in 12 of 14 patients in whom the test remained positive (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vasospasm↗
PubMed1981

[An approach to the diagnosis of coronary artery spasm in spontaneous angina pectoris (author's transl)].

Spontaneously occurring spasms are more likely to be detected by performing coronary angiography during an acute ischaemic attack. This was achieved in 28 out of 41 cases. Spasm was found to be present in 23/25 attacks with elevated S-T segment but in only 5/16 attacks with other changes on ECG. The difference was statistically significant (p less than 0.01). When coronary angiography was performed outside anginal attacks, arterial spasm was detected in 16 out of 1071 cases (1.48%). The percentage increased in patients with spontaneous angina: 13/15 cases (8.6%). These spontaneous spasms are painless and can be differentiated from catheter-induced spasms and organic stenosis by the nitroglycerin test. Spasms which do not occur spontaneously can be provoked by methylergometrine maleate. This was done 175 time with 16 positive results. The criteria of positivity of the test, as well as its value, indications and dangers are discussed.

Angina Pectoris↗
PubMed1993

[Changes in plasma endothelin during coronary spasm].

The role of endothelin, a powerful vasoconstrictor, was studied in coronary spasm. A methylergonovine stress test was performed in patients with normal coronary angiography. Patients who developed spasm (Group I, n = 6) were compared with those who did not (Group II, n = 6). Plasma endothelin was measured at 8, 11 a.m., 2 p.m., 4, 7, 9, 11 p.m. and 1 a.m. The stress test was carried out at 17 hours and an additional endothelin measurement was performed during spasm in positive cases. The clinical characteristics of the two groups were comparable especially with regards to cardiovascular risk factors. Except for the value recorded during coronary spasm, the plasma endothelin levels were significantly higher in the group with coronary spasm. A time-dependent variation was observed in both groups with higher endothelin levels in the morning. In group I the plasma endothelin levels were higher under basal conditions and during spasm in patients with spastic angina.

Adult↗
PubMed2005

Botulinum toxin type A therapy for hemifacial spasm.

BACKGROUND: Hemifacial spasm is characterised by unilateral involuntary contractions of muscles innervated by the facial nerve. The usual cause is a vessel touching the facial nerve near its origin from the brain stem. Although it is a benign condition it can cause significant cosmetic and functional disability. It is a chronic disease and spontaneous recovery is very rare. The two treatments routinely available are microvascular decompression and Botulinum Toxin type A (BtA) muscular injections. OBJECTIVES: To determine whether botulinum toxin (BtA) is an effective and safe treatment for hemifacial spasm. SEARCH STRATEGY: We searched the Cochrane Movement Disorders Group trials register, the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2004), MEDLINE (1977 to December 2003), EMBASE (1977 to December 2003), and reference lists of articles. We also contacted drug manufacturers and researchers in the field. SELECTION CRITERIA: Randomised studies comparing BtA with placebo in people with hemifacial spasm. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. Study authors were contacted for additional information. Adverse effects information was collected from the trials. MAIN RESULTS: We found only one small randomised, placebo-controlled trial involving 11 people. It was a crossover trial during which patients underwent four sets of injections, comparing placebo with three different doses of BtA - formulation Botox(r) (low dose: one-half of the intermediate dose; intermediate dose; and high dose: twice the intermediate dose), and one of placebo. In this trial BtA was superior to placebo. AUTHORS' CONCLUSIONS: The findings of this single eligible trial support the results of large, open, case-control studies showing a benefit rate between 76 and 100%. This effect size probably makes it very difficult to perform new large placebo controlled trials for hemifacial spasm. Despite the paucity of good quality controlled data, all the studies available suggest that BtA is effective and safe for treating hemifacial spasm. Future trials should explore technical factors such as the optimum treatment intervals, different injection techniques, doses, Bt types and formulations. Other issues include service delivery, quality of life, long-term efficacy, safety, and immunogenicity. BtA should be compared with surgical microvascular decompression.

Botulinum Toxins, Type A↗
PubMed2003

Evaluation of a spasmolytic cocktail to prevent radial artery spasm during coronary procedures.

Radial artery spasm is a frequent complication of the transradial approach for coronary angiography and angioplasty. Recently, we have been able to quantify spasm using the automatic pullback device. The objective of this study was to assess the efficacy of an intra-arterial vasodilating cocktail in reducing the incidence and severity of radial artery spasm. A hundred patients undergoing coronary procedures via the radial artery were divided into two groups of 50 each. Patients in group A received intra-arterial cocktail (5 mg of verapamil plus 200 micro g nitroglycerine in 10 ml of normal saline), while patients in group B did not receive any vasodilating drug. The pullback device was used for sheath removal at the end of the procedure. Seven (14%) patients in group A experienced pain (i.e., pain score of III-V) during automatic sheath removal, as compared to 17 (34%) in group B (P = 0.019). The mean pain score was significantly lower in group A than in group B (1.7 +/- 0.94 vs. 2.08 +/- 1.07; P = 0.03). The maximal pullback force (MPF) was also significantly lower for group A (0.53 +/- 0.52 kg; range, 0.10-3.03 kg) as compared to group B (0.76 +/- 0.45 kg; range, 0.24-1.99 kg; P = 0.013). Only 4 (8%) patients in group A had an MPF value greater than 1.0 kg, suggesting the presence of significant radial artery spasm, as opposed to 11 (22%) in group B (P = 0.029). Administration of an intra-arterial vasodilating cocktail prior to sheath insertion reduces the occurrence and severity of radial artery spasm.

Aged↗
PubMed1985

Electrophysiology of the facial nerve in hemifacial spasm: ectopic/ephaptic excitation.

Pathologic and pathophysiologic findings in hemifacial spasm are reviewed in connection with recent theoretical and experimental studies of ectopic/ephaptic excitation. The intracranial segment of the normal facial nerve is ensheathed by an arachnoid membrane only and shows no fascicular organization. In hemifacial spasm, this segment shows signs of demyelination. Several electrical phenomena relating to ectopic excitation, ephaptic transmission between facial nerve fibers, and autoexcitation can be reproduced in clinical electrophysiologic studies of hemifacial spasm. These abnormalities gradually disappear after facial nerve decompression in the cerebellopontine recess. It is concluded that the normal facial nerve is vulnerable to minor compression, the primary pathophysiologic mechanism in hemifacial spasm is ectopic/ephaptic excitation due to compression and demyelination of the intracranial segment of the facial nerve, and the facial nerve in hemifacial spasm is a useful model for the study of ephaptic transmission, which has provided new information about the resolution of abnormal electrical events after decompression.

Blinking↗
PubMed1992

Hemifacial spasm due to tumor, aneurysm, or arteriovenous malformation.

The authors report eight cases of so-called symptomatic hemifacial spasm. They had gross pathological lesions such as a tumor (one epidermoid, one neurinoma, and two meningiomas), vascular malformation (one medullary venous malformation and two arteriovenous malformations), and aneurysm. In all four cases with a tumor, no artery compressed the facial nerve at the root exit zone. In three of the four cases, the hemifacial spasm disappeared after removal of the tumor in contact with the facial nerve. Compression or encasement of the facial nerve by the tumor was the pathogenesis of the hemifacial spasm in these three cases. The remaining case with tumor (tentorial meningioma) did not have a mass or vessel that directly compressed the facial nerve at the root exit zone. However, the hemifacial spasm disappeared after the removal of the tumor. In a case with a medullary venous malformation with arterial component, an engorged draining vein compressed the root exit zone of the facial nerve. In the remaining three vascular cases--two cases of arteriovenous malformation and a case of saccular aneurysm--enlarged feeding arteries and an aneurysm directly compressed the root exit zone of the facial nerve. Not only arterial or venous but also mass compression can cause hemifacial spasm in some symptomatic cases. Surgical decompression of the facial nerve from the causative organic lesion is the primary choice of treatment.

Adult↗
PubMed1990

The spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases.

This communication will discuss the spasm of resistance vessel concept of ischemic heart disease and other ischemic diseases, and will focus on ischemic heart disease. The hypothesis is regarded as a separate model or paradigm, and is based on the principle that spasm of resistance vessels directly induces symptoms in these conditions. Resistance vessels help maintain vascular homeostasis through autoregulatory mechanisms, and spasm of resistance vessels is considered to represent 'inappropriate' activation of these mechanisms by disease states, which are equated with risk factors. For ischemic heart disease, the most important risk factor is stenotic coronary artery disease, and the concept asserts that severe ischemia secondary to coronary artery disease causes sufficient tissue injury to incite injury-spasm of resistance vessels. While it is universally accepted that occlusions of epicardial arteries by stenotic coronary artery disease, spasm, and thromboses directly induce clinical symptoms, the hypothesis suggests that these occlusions have other roles. The concept accepts all current treatments of ischemic heart disease, but as this disorder is viewed differently, a significantly different direction of research is proposed for improving its treatment and prevention.

Coronary Vasospasm↗
PubMedDate not supplied

Studies on CSF tryptophan metabolism in infantile spasms.

Cerebrospinal fluid from 8 patients with infantile spasms (mean age: 6.1 months) was collected before treatment. The concentration of cerebrospinal fluid tryptophan metabolites was analyzed using high-performance liquid chromatography and compared to metabolite concentrations in cerebrospinal fluid from 20 age-matched controls (mean age: 5.8 months). The levels of cerebrospinal fluid serotonin, 5-hydroxyindoleacetic acid, and kynurenine were significantly lower in infantile spasm patients compared to controls (P less than .05). In contrast, the levels of cerebrospinal fluid 3-hydroxykynurenine were significantly higher in infantile spasm patients than in controls (P less than .05). There were no significant differences in the levels of cerebrospinal fluid tryptophan and 5-hydroxytryptophan. Although the study population was small, these findings suggest that the presence of seizures in infantile spasms is associated with a decrease in serotonergic metabolites which, in turn, may indicate a decrease in serotonergic activity, altered clearance of these metabolites, or altered turnover in the direction of 3-hydroxykynurenine. The perturbance caused by increased 3-hydroxykynurenine and decreased kynurenine in the homeostatic balance between these 2 tryptophan metabolites could further contribute to the pathogenesis of infantile spasms.

5-Hydroxytryptophan↗
PubMedDate not supplied

Changes in CSF neurotransmitters in infantile spasms.

Cerebrospinal fluid (CSF) from 7 patients with infantile spasms (mean age: 6.7 months) was collected before and after treatment with adrenocorticotropic hormone (ACTH). The concentration of neurotransmitter metabolites was analyzed using high-performance liquid chromatography and compared to the metabolite concentration in the CSF from 7 age-matched controls (mean age: 6.1 months). Pretreatment levels of CSF 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid, 3-methoxy-4-hydroxyphenyl glycol (MHPG), and kynurenine were significantly lower in infantile spasm patients compared to controls. Following treatment, marked increases in 5-HIAA and decreases in kynurenine levels were observed in the CSF of the 5 infants whose seizures were eliminated or reduced by ACTH. In the 2 nonresponders 5-HIAA levels decreased. The level of MHPG was reduced slightly in 5 infants, including the 2 nonresponders, and was increased in 2 responders. CSF homovanillic acid levels increased in 4 infantile spasm infants and decreased in 3 following ACTH. These data demonstrate that the presence of seizures in infantile spasms is associated with a significant decrease in serotonergic activity and that elimination of seizures by ACTH is accompanied by increased serotonin turnover. The simultaneous increase of 5-HIAA and decrease of kynurenine, an alternate metabolite of tryptophan, suggests an underlying disturbance of tryptophan metabolism in infantile spasms. The possibility that elimination of seizures by ACTH may be related to decreased production of certain kynurenine metabolites, particularly quinolinic acid, is discussed.

Adrenocorticotropic Hormone↗
PubMed1996

Infantile spasms: cerebral blood flow abnormalities correlate with EEG, neuroimaging, and pathologic findings.

This ongoing study examines abnormalities of cerebral perfusion in a consecutive series of children with infantile spasms and correlates cerebral blood flow (CBF) abnormalities with electroencephalographic (EEG), neuroimaging, and pathologic findings. A consecutive series of children with infantile spasms, diagnosed by standard clinical and EEG criteria, had cerebral perfusion studies using 99Tc-HmPAO single photon emission computed tomography (SPECT), together with neuroimaging studies using computed tomography (CT) and/or magnetic resonance imaging (MRI), interpreted independently and correlated with surgical pathologic findings. Twenty children aged 2-13 months (mean 9.3 months) were studied over a 4-year period; 60% had symptomatic infantile spasms due to cerebral dysgenesis (33%), other congenital lesions (25%), tuberous sclerosis (17%), or other causes (25%), and the remaining patients were cryptogenic (40%). CBF abnormalities were present in 85%: multifocal decrease (40%), focal increase (25%), diffuse decrease (15%), and focal increase (10%), while the remaining 15% had normal cerebral blood flow. Focal cortical lesions may lead to infantile spasms, even in cryptogenic patients diagnosed by functional neuroimaging such as 99Tc-HmPAO SPECT. In selected patients, surgical excision of the cortical lesions leads to improved seizure control and possibly outcome. The localization and surgical excision of focal cortical lesions in infantile spasms required further investigation with functional and structural neuroimaging, EEG, and intraoperative electrocorticography.

Brain↗
PubMed2005

Childhood-onset hemifacial spasm: successful treatment with botulinum toxin.

Hemifacial spasm is a disorder characterized by involuntary contractions of muscles innervated by the ipsilateral facial nerve. The majority of cases are of adult-onset. However, a few cases have been described in children. Detectable causes of pediatric hemifacial spasm include facial nerve compression by vasculature and brainstem masses. In the treatment of hemifacial spasm, surgical decompression of the facial nerve has been used with good results in both adults and children. However, surgical procedures have serious risks and should be used only in selected cases. Although injections of botulinum toxin type A have been successfully used in adult hemifacial spasm patients, to our knowledge there is no report of use of this indication in children. This report presents the first case of a pediatric patient with childhood-onset hemifacial spasm successfully treated with periorbital botulinum toxin injections. The literature on the subject is also reviewed.

Botulinum Toxins, Type A↗
PubMed2002

Hemifacial spasm caused by vertebral artery dolichoectasia.

PURPOSE: To display the characteristic magnetic resonance imaging (MRI) abnormalities associated with hemifacial spasm caused by compression of the seventh cranial nerve by a dolichoectatic vertebral artery. DESIGN: Interventional case report. METHODS: Correlation of imaging and clinical findings. RESULTS: In a 36-year-old man with mild left hemifacial spasm, MRI showed an enlarged (dolichoectatic) vertebral artery that compressed the seventh cranial nerve at its exit from the caudal pons. Manifestations of hemifacial spasm were relieved with periocular botulinum toxin injections. CONCLUSION: In hemifacial spasm, MRI may show compression of the ipsilateral seventh cranial nerve or other structural abnormalities. Relief of hemifacial spasm may occur with botulinum toxin injection or with neurosurgical intervention designed to relieve the compression.

Adult↗
PubMed1995

Hemifacial spasm and osteitis deformans.

PURPOSE/METHODS: A patient with osteitis deformans (Paget's disease) and hemifacial spasm underwent magnetic resonance tomographic angiography. Bone-modulating bisphosphonates and botulinum injection were administered to treat the hemifacial spasm. RESULTS/CONCLUSIONS: Computed tomography showed marked temporal bone overgrowth. Magnetic resonance tomographic angiography showed no vascular compression of the facial nerve root. The hemifacial spasm failed to resolve with intravenous pamidronate. Subsequent botulinum injection rendered the patient spasm free for 22 weeks. Further research on the use of bisphosphonates in the treatment of pagetoid hemifacial spasm is required.

Aged↗
PubMed1986

Hemifacial spasm: results of microvascular decompression of the facial nerve in 54 patients.

During the 10-year period between January 1975 and December 1984, 367 patients with hemifacial spasm were examined at our institution. Because of the severity of the spasm, 54 patients underwent surgical management that consisted of microvascular decompression of the facial nerve. Postoperatively, the hemifacial spasm was completely resolved in 44 patients (81%), but 6 of these patients had subsequent recurrence of the condition. An additional five patients (9%) experienced improvement but were not totally free of the spasm. Five patients (9%) received no benefit from the procedure. Complications occurred in 19 patients (35%) but were usually transient. The most serious complication was permanent ipsilateral hearing loss, which occurred in eight patients (15%). Thus, in general, microvascular decompression of the facial nerve effectively alleviates hemifacial spasm.

Adult↗
PubMedDate not supplied

Botulinum-A toxin in the treatment of craniocervical muscle spasms: short- and long-term, local and systemic effects.

Botulinum toxin has become the initial treatment of choice for the management of essential blepharospasm, hemifacial spasm and other craniocervical dystonias. Numerous studies have confirmed a 90% to 95% response rate. Although a number of common side effects have been reported, the occurrence and incidence of rare local complications remains poorly understood. More importantly, the acute and chronic distant effects of botulinum toxin have not been clearly elucidated. A better understanding of such effects is essential if clinicians are to appropriately advise patients on the use of this therapeutic modality. This article is based on the Duke University experience in the management of over 500 patients with craniocervical spasm disorders, combined with a review of the published literature. These disorders include essential blepharospasm, oromandibular dystonia, hemifacial spasm, and torticollis. The incidence of side effects following more than 6000 treatments with botulinum toxin is presented. Pertinent research relating to the causes of these complications is also reviewed. The most common complications of treatment with botulinum toxin are related to acute local effects resulting from chemodenervation. The most important clinical effect in this group is weakening of the levator muscle resulting in ptosis, and the corneal consequences of lagophthalmos. The latter includes exposure keratitis, dry eyes, blurred vision, and hypersecretion epiphora. Less common local effects include facial numbness, diplopia, and ectropion. Some distant effects are being observed with increasing frequency. These include pruritus, dysphagia, nausea, and a flu-like syndrome. Most significant, however, are the rare reports of generalized weakness and the documentation of EMG abnormalities distant to the site of toxin injection. This has been seen with injections for both blepharospasm and torticollis. Until further studies on the long-term distant complications of botulinum toxin are available, it is recommended that patients receive as few life-time doses of toxin as possible, consistent with adequate management of their spasms. The practice of reinjecting patients routinely every three months, or at the first return of mild spasms should be discouraged.

Blepharospasm↗
PubMed2002

Neurosteroids and infantile spasms: the deoxycorticosterone hypothesis.

Deoxycorticosterone (DOC) is a mineralocorticoid precursor that has anticonvulsant properties in animals and possibly also in humans. Studies indicate that the anticonvulsant activity of DOC requires its enzymatic conversion to 5 alpha,3 alpha-tetrahydrodeoxycorticosterone (THDOC), a neurosteroid that lacks classical hormonal properties but acts as a powerful positive allosteric modulator of GABAA receptors. DOC can be considered a stress hormone because its synthesis is under the control of ACTH. Therefore, stress-induced fluctuations in seizure susceptibility could in part result from alterations in DOC availability. Also, the therapeutic activity of ACTH in infantile spasms could partially relate to its stimulatory effects on the synthesis of DOC, which then undergoes biotransformation to neurosteroids. The recent demonstration that the synthetic neurosteroid analog ganaxolone reduces spasm frequency in children with intractable infantile spasms suggests that neurosteroid-related anticonvulsants may offer a potential new nonhormonal approach for the treatment of infantile spasms and other developmental epilepsies. In addition, it further confirms the utility of pharmacological enhancement of GABA-mediated inhibition in the control of infantile spasms.

Anticonvulsants↗
PubMed2002

Infantile spasms versus myoclonus: is there a connection?

Infantile spasms (IS) is usually classified as a form of "myoclonic epilepsy," but the nosology of this whole group of disorders is unclear. Evidence suggests that the spasms are subcortically mediated, but can be modified by input from the cortex, which is believed to be abnormally excitable and disorganized. The latter features may give rise to hypsarrhythmia. The whole issue of myoclonus rests on the phenotype of IS and precise measurements of the length of electromyographic (EMG) bursts. Based on scant EMG data, it would appear that the bursts during flexor spasms are too long for epileptic myoclonus. The nature of tonic spasms of even longer duration is not myoclonic. However, the infrequent spontaneous myoclonic jerks, which can occur without spasms, and head nodding could represent positive and negative myoclonus, respectively. Data can be collected easily through techniques such as back-averaging to resolve the issue of classification and localization of motor phenomena.

Brain Diseases↗