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At least 487 records · Page 27Linked to original sources
PubMed1998

[Frequency and nature of atheroma at the site of spasm of angiographically normal or subnormal coronary arteries: an endocoronary ultrasonographic study].

Anatomical studies suggest that sites of coronary spasm are subject to early atherosclerosis. Coronary angiography is unable to confirm the lesions or provide information about their nature. On the other hand, endocoronary ultrasound is able to identify and, it is hoped, to determine the frequency and composition of the lesions. Nineteen patients with chest pain and angiographically normal or subnormal coronary arteries were included in a prospective study (16 men and 3 women: average age 53 +/- 10 years). Four patients had spontaneous spasm and in the other 15, spasm was induced by intravenous injection of ergometrine (6 micrograms/kg). After countering the spasm with isosorbide dinitrate, the site of spasm and adjacent segments were examined by endocoronary ultrasound. Localised vasospasm which was stenotic in 14 cases and obstructive in 5 cases, was observed. The ECG was unchanged in 4 cases and showed ST-T segment changes in 15 cases. The artery affected was the left anterior descending in 10 cases, the left circumflex in 2 cases and the right coronary in 7 cases. A plaque of atheroma, defined as significant intimal thickening, was detected in 18 out of the 19 cases. This atheroma was classified as soft in 17 cases and hard in one case. The authors conclude that vasospasm is not only associated with a plaque of atheroma, nearly always suspected at coronary angiography, but also its composition is nearly always soft (lipidic) from ultrasonographic data.

Adult↗
PubMed1999

The origin of hypsarrhythmia and tonic spasms in West syndrome: evidence from a case of porencephaly and hydrocephalus with focal hypsarrhythmia.

We report on a 3-year-old girl with West syndrome and with focal hypsarrhythmia. The left hemisphere of the patient was virtually completely defective and continuous hypsarrhythmia was only seen in the residual right frontal cortex, where an interictal single photon emission computed tomography (SPECT) showed hyperperfusion. Despite a focal epileptic pattern, the tonic spasms were quite symmetrical. In our patient, spasms might not require the sensorimotor cortex, but the brainstem containing the descending pathways that control spinal reflexes and other infratentorial structures seem to be essential for the occurrence of spasms. This is in accordance with the result of an ictal SPECT that showed hyperperfusion of the brainstem and cerebellum. These findings suggest that hypsarrhythmia originates from cortical lesions, while subcortical structures may be primarily responsible for the tonic spasms in this patient.

Brain↗
PubMed1991

Hemifacial spasm. Occurrence in multiple sclerosis.

We present six patients with hemifacial spasm and multiple sclerosis. To our knowledge, this association has not been described previously in the North American literature. Magnetic resonance imaging was obtained in all the patients and plaques consistent with multiple sclerosis were identified. In two patients the plaques were seen in the area of the facial nucleus on the involved side. We suggest that hemifacial spasm can be a manifestation of multiple sclerosis. These cases illustrate the utility of magnetic resonance imaging in the investigation of hemifacial spasm. Our findings also support a central (nuclear) origin in multiple sclerosis associated with hemifacial spasm.

Adrenocorticotropic Hormone↗
PubMed1982

Carotid artery spasm. A cause of postendarterectomy thrombosis?

Carotid endarterectomy is generally regarded as a durable repair, with a low incidence of postoperative thrombosis. However, unexpected, inexplicable occlusions and pressure-flow aberrations have been reported to occur during the period immediately after operation period. We studied 245 operative angiograms obtained during a series of 335 carotid endarterectomies. Among the various defects noted were 24 instances of mild to severe spasm of the middle and distal extracranial carotid artery. This spasm was remote from the endarterectomy site and often was entirely beyond the field of operative exposure. Early and late postoperative angiograms demonstrated that this may be a transient phenomenon, and repeated intraoperative films documented that spasm may progress without further direct instrumentation of the involved segment. The patient who demonstrated the most severe spasm later suffered immediate postoperative occlusion and stroke despite a technically satisfactory repair.

Carotid Artery Diseases↗
PubMed2005

Assessment of the efficacy of phentolamine to prevent radial artery spasm during cardiac catheterization procedures: a randomized study comparing phentolamine vs. verapamil.

The objective of this study was to evaluate phentolamine as radial artery spasmolytic in transradial catheterization procedures. Radial artery spasm is a relatively frequent complication during transradial approach, causing patient discomfort or even making it impossible to continue the procedure. As radial artery spasm is mediated by the stimulation of alpha-adrenoreceptors, the use of the alpha-blocker phentolamine could make sense as spasmolytic. We designed a randomized double-blind study to compare phentolamine vs. verapamil, the standard spasmolytic agent. Five hundred patients (250 in each arm) submitted to a transradial cardiac catheterization were consecutively included and randomly assigned to receive 2.5 mg of verapamil or 2.5 mg of phentolamine after sheath insertion. Both vasodilator agents induced a significant radial artery diameter increase (from 2.22 +/- 0.53 to 2.48 +/- 0.57 mm, P < 0.001 for verapamil, and from 2.20 +/- 0.53 to 2.45 +/- 0.53 mm, P < 0.001 for phentolamine). However, verapamil was more efficacious to prevent radial artery spasm (13.2% compared with 23.2% in phentolamine-treated patients; P = 0.004). Follow-up (20 +/- 18 days) evaluation of the radial artery patency by plestismography and pulse oximetry showed no differences between the two groups in the rate of radial occlusion (3.0% vs. 3.2% in verapamil and phentolamine treated patients, respectively). Phentolamine was an effective radial vasodilator agent, although it showed less ability to prevent radial artery spasm than verapamil. Radial artery occlusion rate was almost identical for both vasodilators. Thus, phentolamine could be a valid alternative to verapamil as a radial artery spasmolytic agent.

Adrenergic alpha-Antagonists↗
PubMed1994

Familial hemifacial spasm.

Two brothers developed hemifacial spasm at 63 and 70 years of age. Spasms occurred on the left and right sides of the face, respectively. Computed tomography scan and magnetic resonance imaging failed to show any abnormality. In addition, a third sibling reported a history of a peripheral facial palsy, which remitted spontaneously without sequelae. This is the fourth description of familial hemifacial spasms. This family is unique in that hemifacial spasm presented on different sides in the two brothers, and involvement was limited to one generation. Age at onset was later than for other familial cases and similar to sporadic cases.

Aged↗
PubMed1994

Botulinum toxin treatment in patients with hemifacial spasm.

Hemifacial spasm is nearly always a unilateral disease of the facial musculature and is characterized by involuntary tonic or clonic cramps that considerably reduce the affected patient's quality of life. In the past, a number of different conservative and operative therapeutic procedures have been applied for the treatment of hemifacial spasm. In many cases these attempts failed to control the disease permanently or resulted in unwanted, sometimes strong, side effects. We report our own experiences with botulinum therapy in 29 patients with hemifacial spasm (78 therapeutic sessions). In our patients the mean duration of an effect after treatment with botulinum toxin was 18.2 weeks. Side effects were rare. Our results since 1990 at the University of Göttingen demonstrate that subcutaneous application of toxin from Clostridium botulinum to involved facial muscles represents a reliable method for successful treatment of hemifacial spasm.

Adult↗
PubMed1988

Lack of clinical-EEG effects of naloxone injection on infantile spasms.

In a previous study we found depressed ACTH and normal beta-endorphin values in the cerebrospinal fluid of patients with West's syndrome, whereas normal peptide levels were present in infants with secondary Infantile spasms. This prompted us to study the effects of naloxone administration in children with West's syndrome. After informed consent was obtained from the parents, the effects of naloxone administration on clinical and EEG findings were evaluated in five infants 5-9 months old (3 males, 2 females) with cryptogenic infantile spasms and hypsarrhythmia. The infants were studied at the onset of symptomatology before therapy. An average of 5-10 groups of spasms were present per day. Naloxone (12 micrograms/kg body weight) was administered as an intravenous bolus in two cases, as a slow venous drip in another two cases, and intramuscularly in the last case. EEG and polygraphic monitoring were performed for 2 h. Naloxone did not induce any acute behavioral changes and the number of seizures remained unchanged after treatment. These data reject the possibility that endogenous opioids tonically modulate infantile spasms. Further studies are required to ascertain the involvement of POMC peptides in West's syndrome.

Adult↗
PubMed1991

Intraspinal baclofen in the treatment of severe spasticity and spasms.

Ten patients with severe spasticity were evaluated according to a standardized protocol in order to be treated by intraspinal baclofen. Entry criteria in the protocol were the following: 1) Stable central nervous system lesion, 2) Severe spasticity and/or flexo-extensor spasms not controllable by oral treatment, 3) Normal CSF circulation and 4) Informed consent. All patients received a test dose of twenty-five micrograms of baclofen injected intrathecally. At intervals of at least one day, doses were increased in 10-25 microgram steps until total abolition of spontaneous spasms was achieved in complete spinal cord lesions. In patients with residual motor function, doses were titrated until the optimal dose was found that reduced spasms and enabled performance of maximum daily life activities according to the patient's neurological level. In nine patients a multidose reservoir was implanted to deliver intrathecal baclofen. Effective dosage was 60 +/- 31 micrograms in the entire group. Ashworth score was reduced from 4.6 +/- 0.7 to 1.2 +/- 0.4 (mean +/- SD) (p less than 0.0001) and spasms from 3.2 +/- 0.8 to 0.2 +/- 0.4 (p less than 0.0001). Follow-up of the nine patients in whom a reservoir was implanted has been 18 +/- 9 months. Initial dosage requirements and tolerance were significantly different in complete (Frankel's A grade) or incomplete lesions (Frankel's B, C and D grades). Complete spinal cord lesions required a greater initial dose (156 +/- 43) than incomplete lesions (44 +/- 24), these differences being statistically significant (Student's t-test, p less than 0.05). Tolerance was observed only in patients with complete motor and complete sensory lesions. In incomplete lesions, dose increase was insignificant.

Adolescent↗
PubMed1994

Infantile spasms combined with partial seizures: electroclinical study of eleven cases.

We studied 11 infants (7 males) with combined infantile spasms (IS) and partial seizures. The age of onset of the spasms ranged from 6 days to 9 months. All of the children had neurological or CT/MRI abnormalities, and five also had a family history of epilepsy. The clinical and polygraphic patterns of the clusters of spasms combined with partial seizures were analysed. Ten infants were followed-up for a mean period of 3 years, 4 months (range 1 year 10 months to 4 years 11 months). At the last check-up, the seizures were controlled in 2 patients; the others continued to have spasms and/or partial seizures. All of the patients developed mild to severe psychomotor retardation. This condition defines a subgroup of infants presenting with IS, which is distinct from West syndrome.

Electroencephalography↗
PubMed2006

No clinical or neurophysiological evidence of botulinum toxin diffusion to non-injected muscles in patients with hemifacial spasm.

Botulinum toxin injected into a muscle may diffuse to nearby muscles thus producing unwanted effects. In patients with hemifacial spasm, we evaluated clinically and neurophysiologically, whether botulinum toxin type A (BoNT-A) diffuses from the injection site (orbicularis oculi) to untreated muscles (orbicularis oris from the affected side and orbicularis oculi and oris from the unaffected side). We studied 38 patients with idiopathic hemifacial spasm. Botulinum toxin was injected into the affected orbicularis oculi muscle alone (at 3 standardized sites) at a clinically effective dose. Patients were studied before (T0) and 3-4 weeks after treatment (T1). We evaluated the clinical effects of botulinum toxin and muscle strength in the affected and unaffected muscles. We also assessed the peak-to-peak amplitude compound muscle action potential (CMAP) recorded from the orbicularis oculi and orbicularis oris muscles on both sides after supramaximal electrical stimulation of the facial nerve at the stylomastoid foramen. In all patients, botulinum toxin treatment reduced muscle spasms in the injected orbicularis oculi muscle and induced no muscle weakness in the other facial muscles. The CMAP amplitude significantly decreased in the injected orbicularis oculi muscle, but remained unchanged in the other facial muscles (orbicularis oris muscle on the affected side and contra-lateral unaffected muscles). In conclusion, in patients with hemifacial spasm, botulinum toxin, at a clinically effective dose, induces no clinical signs of diffusion and does not reduce the CMAP size in the nearby untreated orbicularis oris or contralateral facial muscles.

Action Potentials↗
PubMed2004

Extensor spasms triggered by imposed knee extension in chronic human spinal cord injury.

Extensor spasms, which are a significant component of spasticity in spinal cord injury (SCI), are still incompletely understood. In this study, contributions of knee proprioceptors to the origination of extensor spasms were examined in fifteen subjects with SCI. Ramp and hold knee extension perturbations were imposed to one leg while the hip and ankle were held in an isometric position using an instrumented leg brace. Isometric joint torques of knee, ankle and hip, and electromyograms (EMGs) from six muscles of the leg were recorded following controlled knee extension at four different velocities. Tests were conducted with the hip in both flexed and extended positions. A stereotypical torque response consisting of hip flexion, knee extension, and ankle plantar flexion was observed following knee perturbations, although not all components were demonstrated in every subject. During the hold periods with the knee extended, EMG activity recorded from the vastus medialis, medial gastrocnemius and rectus femoris demonstrated patterns consistent with clinical observations of extensor spasms. Furthermore, larger responses were observed with the hip in the extended vs. flexed position (p<0.05). Such behaviors emphasize the role of knee and hip proprioceptors in the initiation of extensor spasms in human SCI. This knowledge may be especially helpful in identifying rehabilitation strategies for producing functional movements in human SCI.

Adult↗
PubMed1978

Coronary artery spasm and mitral valve prolapse.

Ten patients, representing 1.34 per cent of those patients undergoing selective coronary arteriography, were found to have unequivocal evidence of coronary artery spasm. This involved the proximal right coronary artery in eight patients, the mid-left anterior descending branch in one, and the left main coronary artery in one. Eight of these 10 patients had otherwise normal coronary arteries. Of these 10 patients with coronary artery spasm, nine had evidence of mitral valve prolapse. This involved the posteromedial scallop in six patients; the anterolateral and posteromedial scallops in one; the middle and posteromedial scallops in one; and the anterolateral, middle, and posteromedial scallops in one. These data suggest an association between coronary artery spasm and mitral valve prolapse. Coronary artery spasm may thus be an important factor in the pathogenesis of the chest pain, arrhythmias, electrocardiographic abnormalities, and sudden death, that have already been described in some patients with mitral valve prolapse.

Adult↗
PubMed1980

Exercise-induced coronary arterial spasm: angiographic demonstration, documentation of ischemia by myocardial scintigraphy and results of pharmacologic intervention.

Exercise-induced coronary arterial spasm is an infrequently recognized phemonemon whose mechanism and management are not well established. In two patients with reproducible exercise-induced S-T segment elevation and angina pectoris thallium-201 scintigraphy showed areas of reversible anteroapical hypoperfusion, and gated radionuclide ventriculography revealed anteroapical hypokinesia with a decrease in left ventricular ejection fraction at peak exercise. During coronary arteriography supine exercise provoked occlusive spasm of the left anterior descending coronary artery, which at rest had only minimal plaques. Consequently, treadmill testing was performed with five different pharmacologically provoked interventions: direct vasodilatation (nitrates), alpha adrenergic blockade (phenmoxybenzamine), beta adrenergic blockade (propranolol), calcium flux blockade (verapamil), and prostaglandin inhibition (indomethacin). Exercise-induced coronary arterial spasm, manifested as S-T segment elevation and angina, was prevented by nitrates, but was not eliminated by short-term oral administration of an alpha or beta blocking agent, a calcium antagonist or a prostaglandin inhibitor. Further, beta adrenergic blockade appeared to be detrimental. Thus, this study demonstrates (1) that coronary arterial spasm may be the underlying mechanism of at least some cases of exertional angina associated with transient perfusion deficits and left ventricular dysfunction, and (2) that it may be prevented by oral nitrates.

Angina Pectoris, Variant↗
PubMed1980

Syndrome of symptomatic coronary arterial spasm with nearly normal coronary arteriograms.

The clinical manifestations of symptomatic coronary arterial spasm were analyzed in 30 patients whose coronary arteriograms demonstrated no fixed severe obstructions. The study group consisted of 14 men and 16 women (average age, 47 years). Angina at rest was invariable and it was usually typical in quality, location, duration and response to nitroglycerin. Exertional angina occurred in 23 percent and syncope with angina in 33 percent. Spontaneous remission of angina for at least 1 month occurred in 57 percent of patients. Prinzmetal's variant angina occurred in 77 percent of patients and only S-T segment depression or T wave changes during angina occurred in 23 percent. Major arrhythmias during ischemia developed in 47 percent. Exericse tests were positive in 24 percent. Myocardial infarction, probably due to coronary spasm, occurred in 7 percent of patients. Isosorbide dinitrate and propranolol were effective therapy in only 39 percent and 6 percent of patients, respectively. Nifedipine, a calcium flux antagonist, was effective in 80 percent of patients. Patients with normal coronary arteriograms who have clinical features suggestive of coronary arterial spasm should be considered for further investigation, including long-term electrocardiographic monitoring and provocative testing for spasm.

Adult↗
PubMed1982

Auditory brain stem responses in infantile spasms.

Auditory brain stem evoked responses (ABRs) and behavioral thresholds were studied in 30 infants with infantile spasms to determine the level of the lesion causing their inattention to sound stimuli. ABR thresholds, peak latencies of waves I and V and the peak interval latency of wave V-I were measured; behavioral audiometric thresholds were determined through conditioned-orientation-reflex (COR) audiometry. Thirty per cent of the infants (9 cases) with infantile spasms showed ABR abnormalities with respect to age-matched controls. The ABR abnormalities were classified into partial disappearance of latter waves (5 cases), prolongation of the wave V-I peak interval (3 cases) and no response (1 case). These findings are clear evidence that brain stem involvement may occur in infantile spasms. Eighty-six per cent of the patients showed threshold elevation by behavioral audiometry which may reflect by cortical dysfunction inherent in psychomotor retardation, as there was no peripheral hearing loss. Our results reveal that brain stem involvement can occur in patients with infantile spasms and their poor responses to sound are due to psychomotor retardation.

Adolescent↗
PubMedDate not supplied

Merosin-negative congenital muscular dystrophy, occipital epilepsy with periodic spasms and focal cortical dysplasia. Report of three Italian cases in two families.

We report clinical, EEG and neuroimaging findings of three patients in two Italian families with merosin-negative congenital muscular dystrophy (CMD), drug-resistant occipital epilepsy, diffuse persistent cerebral white matter changes and focal cortical dysplasia. Clinical and epilepsy histories, EEG and neuroimaging findings were very similar in all patients. Seizures started in childhood and mainly consisted of periodic spasms, a particular type of partial seizure characterized by clusters of epileptic spasms. The motor expression of the spasms was very mild so that they had been frequently missed or misinterpreted as non-convulsive generalized absence seizures. Interictal EEG showed occipital spike-waves and bilateral synchronous slow spike-wave discharges. Ictal EEG showed prolonged periodic sequences of slow waves with associated fast rhythm complexes, characteristic of periodic spasms. Two patients had normal intelligence, one patient presented moderate mental retardation. Focal cortical dysplasia in the posterior areas of the brain, in addition to marked diffuse white matter alterations, was detected in the magnetic resonance images of all patients. Findings in these patients indicate that in merosin-negative CMD brain involvement can include cortical dysplasia, in addition to white matter changes. In such cases the brain damage can lead to a childhood-onset localization-related symptomatic occipital epilepsy. Epileptic seizures and cortical dysplasia can be, however, difficult to detect in CMD. The clinical semiology of epileptic seizures may in fact be modified because of muscular weakness. This implies that epilepsy may be misdiagnosed or even missed and EEG-polymyographic recordings may be necessary to identify it. Similarly, cortical dysplasia may be very localized and visible by neuroimaging only if it is carefully investigated on the basis of epileptological and EEG-polymyographic findings.

Child↗
PubMed1995

Brain tumors associated with infantile spasms.

Two patients with brain tumors associated with infantile spasms are reported. Both infants displayed typical clinical features of infantile spasms, comprising tonic spasms manifesting in series and hypsarrythmia. In Patient 1, magnetic resonance imaging revealed a tumor in the hypothalamic region, suggestive of hypothalamic hamartoma. In Patient 2, cranial computed tomography and magnetic resonance imaging indicated the existence of a primary brain tumor with calcification in the right temporal lobe. Adrenocorticotropic hormone therapy combined with clonazepam relieved seizures in both infants. In Patient 1, resection of the hypothalamic tumor is impossible because the tumor lacks a stalk. In Patient 2, pathologic investigation of removed tumor tissue demonstrated mixed-oligoastrocytoma. It is suggested that focal lesions, like those in our patients, are involved in the development of infantile spasms.

Brain Neoplasms↗