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PubMed1986

Physiological abnormalities in hemifacial spasm studied during microvascular decompression operations.

The pathophysiology of hemifacial spasm was studied using electrophysiologic recordings made during neurosurgical operations to relieve it by microvascular decompression of the facial nerve near its entrance into the brain stem. Electrical stimulation of the temporal or the marginal mandibular branch of the facial nerve resulted in a response not only from the muscles that were innervated by the branch of the facial nerve that was stimulated, but also from other muscles, as evidenced by EMG recordings. This "lateral spread" of antidromic activity was facilitated by stimulation at a high rate (50 pps): the response increased five- to tenfold within a few seconds. When the repetition rate was reduced to the initial low stimulus rate (2 to 5 pps), facilitation continued for periods lasting from a few seconds to several minutes. The amplitude of the response of the supraorbital reflex (blink reflex), which can be elicited in patients with hemifacial spasm intraoperatively on the affected side despite the use of inhalation anesthesia, also increased after brief stimulation at a high rate (50 pps). After the facial nerve had been decompressed, both the lateral spread response and the blink reflex response were absent. These results support the hypothesis that hemifacial spasm is the result of hyperexcitability of the facial motor nucleus and facilitation of cross-transmissions between cells in the nucleus that innervate different parts of the face.

Electric Stimulation↗
PubMed1987

Hemifacial spasm: ephaptic transmission or hyperexcitability of the facial motor nucleus?

Hemifacial spasm is a rare disorder that is caused by a blood vessel cross-compressing the facial nerve near the nerve's entry into the brain stem. Electrical stimulation of one branch of the facial nerve on the affected side in patients elicits a response from muscles that are innervated by another branch. Intraoperative recording of this abnormal muscle response, together with measurements of conduction times in parts of the facial nerve, in earlier studies have shown evidence that the cross-transmission of antidromic activity that causes this response occurs central to the site of vascular compression of the facial nerve. In this study we show that in rare circumstances during microvascular decompression operations, a small EMG potential precedes the regular abnormal muscle response. This early response has a latency that is equal to the sum of the conduction times of the portions of the facial nerve that would have been involved if the cross-transmission had occurred at the site of vascular compression of the facial nerve, and it may thus be a result of ephaptic transmission in the nerve at that location. Thus, cross-transmission of antidromic activity can indeed occur in the facial nerve at the site of compression, although we have observed this early potential in only 3 of more than 50 patients who were operated upon for hemifacial spasm; further, in those three patients it occurred only for a short time and only during surgical manipulation of the facial nerve. In view of the fact that this early response occurs only after the nerve has been manipulated, and because it is of such small magnitude, it seems unlikely that such cross-transmission (ephaptic transmission) at the site of the vascular compression plays a direct role in generating the spasm and the antidromic activity that spreads from one branch of the facial nerve to another.

Electric Conductivity↗
PubMed1996

Effect of repetitive stimulation on lateral spreads and F-waves in hemifacial spasm.

The lateral spread (LS) response, which can be elicited in muscles innervated by other branches of the facial nerve, is electromyographycally specific for patients with hemifacial spasm (HFS), occurring about 10 ms after stimulus. The F-wave in facial muscles, which is a late response that antidromicaly propagates to the facial motonucleus and returns orthodromicaly down the same axon, revealed a trend toward enhancement in patients with HFS. The LSs were facilitated by repetitive stimulation during the microvascular decompression (MVD) operation, which has proved to be a successful treatment, and the F-waves were also facilitated by repetitive stimulation on the spasm side more than on the normal side. Greater facilitation of these responses was in direct proportion to higher stimulation rates and greater numbers of stimulations. The repetitive stimulation of the facial nerve may result in activation of the motoneuron pool and in the lowering of the threshold of somatic membranes. These results support the hypothesis that hemifacial spasm is caused by hyperexcitability of the facial motonucleus, which is increased by antidromic repetitive stimulation.

Electric Stimulation↗
PubMed1989

Treatment of muscle spasms with oral dantrolene sodium.

A case of severe muscle spasms relieved by oral administration of dantrolene sodium is presented. The patient had undergone full-mouth extraction 2 days prior to onset of her spasms. The treatment consisted of intravenous diazepam followed by oral dantrolene sodium. The spasms lasted for approximately 10 days.

Administration, Oral↗
PubMed1990

Arteries in contact with the cisternal portion of the facial nerve in autopsy cases: microsurgical anatomy for neurovascular decompression surgery of hemifacial spasm.

The cisternal portion of the facial nerve and its contact arteries were examined anatomically in relation to neurovascular decompression surgery to treat hemifacial spasm. Thirty-five sides of brains from 20 autopsied adult patients were examined under a surgical microscope (x 5-x 25). One attaching point was found on 10 facial nerves, two points on 20 nerves, and three points on four nerves. More than two thirds of the facial nerves were attached at two points: the root exit zone and the distal cisternal portion. In a case of distal attachment, the contact artery formed an arterial-nerve complex with the distal portions of the facial and acoustic nerves. The arterial attachment at the root exit zone was evident on 24 of the 35 facial nerves (69%), and most of the contact arteries were the anterior inferior cerebellar artery and its branches. In five nerves, the root exit zone was attached at two points to arteries. The anatomy of autopsied brains without hemifacial spasm is not identical to that of actual clinical cases of hemifacial spasm; nevertheless, the results do aid in intraoperative anatomical orientations.

Adult↗
PubMed1992

Hemifacial spasm associated with a cerebellopontine angle arachnoid cyst in a young adult.

There are no reported cases of hemifacial spasm associated with an arachnoid cyst in the literature. We report the first case of hemifacial spasm with an ipsilateral cerebellopontine angle arachnoid cyst in a 25-year-old man. The patient underwent evacuation of the arachnoid cyst by a partial membranectomy without any beneficial effect, and finally got rid of the hemifacial spasm by reexploration and microvascular decompression of the facial nerve. The operative findings and results revealed that the cyst produced deviation of the ipsilateral posterior inferior cerebellar artery, which was secondarily in contact with the root exit zone of the facial nerve.

Adult↗
PubMed1984

The effect of epidural morphine on ureteral colic and spasm of the bladder.

Twenty-one patients suffering from severe pain associated with ureteric stones and spasm of the bladder which did not respond to repeated systemic injections of pethidine and papaverine received continuous epidural morphine. The morphine, 3-4 mg per dose, was injected into the lumbar-epidural space, and 15-20 min later all patients were pain free for at least 24 h. Administration of morphine was continued for periods ranging from 2 days to 2 weeks according to need. Eleven of the patients with ureterolithiasis passed the stone spontaneously. Epidural morphine analgesia is indicated for persistent ureteral colic and for spasm of the bladder when conventional treatment fails or systemic drugs are contraindicated. It abolishes pain and spasm for prolonged periods of time and does not interfere with the spontaneous elimination of stone.

Adult↗
PubMed1996

Efficacy and tolerance of repeated oral doses of tolperisone hydrochloride in the treatment of painful reflex muscle spasm: results of a prospective placebo-controlled double-blind trial.

The efficacy and safety of oral tolperisone hydrochloride (Mydocalm) in the treatment of painful reflex muscle spasm was assessed in a prospective, randomized, double-blind, placebo-controlled trial. A total of 138 patients, aged between 20 and 75 years, with painful reflex muscle spasm associated with diseases of the spinal column or proximal joints were enrolled in eight rehabilitation centers. Patients were randomized to receive either 300 mg tolperisone hydrochloride or placebo for a period of 21 days. Both treatment groups recovered during the 3 weeks rehabilitation program. However, tolperisone hydrochloride proved to be significantly superior to placebo: the change score of the pressure pain threshold as the primary target parameter significantly increased during therapy with tolperisone hydrochloride (P = 0.03, valid-case-analysis) compared to the results obtained on placebo treatment. The overall assessment of efficacy by the patient also demonstrated significant differences in favor of tolperisone hydrochloride. Best results were seen in patients aged between 40 and 60 years with a history of complaints shorter than 1 year and with concomitant physical therapy. The evaluation of safety data, i.e., adverse events, biochemical and hematological laboratory parameters, demonstrated no differences between tolperisone hydrochloride and placebo. As a conclusion tolperisone hydrochloride represents an effective and safe treatment of painful reflex muscle spasm without the typical side effects of centrally active muscle relaxants.

Administration, Oral↗
PubMedDate not supplied

A case of infantile spasms: epileptic apnea as partial seizures at onset.

We report a 2-month-old boy who presented with apneic attacks as a manifestation of epileptic seizures at onset and eventually progressed to infantile spasms. At onset, at 2 months of age, apneic attacks were the sole symptom of epileptic fits. Although these seizures were accompanied by cyanosis, bradycardia was not noted. An ictal electroencephalogram showed focal paroxysmal discharges in the temporal area. Treatment with sodium valproate was not effective to control his seizures. By 6 months of age, he progressed to infantile spasms. Although his seizures could be completely controlled with the use of zonisamide, vitamin B6 or high-dose immunoglobulin, his mental and behavioral development was retarded severely. There have been no previously published cases with infantile spasms that evolved from epileptic apnea as partial seizures.

Apnea↗
PubMed1986

Esophageal spasm following propranolol overdose relieved by glucagon.

A case of propranolol overdose complicated by esophageal spasm preventing extrication of an orogastric lavage tube and relieved by intravenous glucagon is presented. Esophageal spasm is an infrequent complication of beta-adrenergic over-dose. Possible mechanisms of esophageal spasm and its relief with glucagon are discussed.

Esophageal Diseases↗
PubMedDate not supplied

Treatment of infantile spasms.

Although the syndrome of infantile spasms has been known for 150 years and its treatment described since 1958, controversy still surrounds the appropriate therapy for this devastating disorder. The rationale, dosage, and side effects of ACTH treatment of infantile spasms is described. The recommended treatment regimen is placed in the context of the literature on the therapy of spasms and its relation to outcome.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Vitamin B6 and valproic acid in treatment of infantile spasms.

Twenty patients with infantile spasms were treated with high doses of vitamin b6, valproic acid, or both. Three of 13 patients (23%) treated initially with high doses of vitamin B6 demonstrated a definite reduction in seizures; 2 patients had no improvement on electroencephalography. Vitamin B6 therapy alone was continued in a single patient (8%) who remained seizure-free during the 15-month follow-up period. Initial treatment with vitamin B6 and valproic acid improved the electroencephalogram significantly more (P less than 0.05) than initial vitamin B6 treatment alone. The group which had valproic acid added to vitamin B6 therapy had significantly fewer seizures (P less than 0.05) and better electroencephalograms (P less than 0.01) than did the group treated initially with vitamin B6 alone. There were no significant differences among the group treated initially with vitamin B6, the group treated initially with valproic acid, and the group in which valproic acid was substituted for vitamin B6. ACTH was more effective in abolishing seizures than was valproic acid or vitamin B6 and valproic acid. ACTH had an excellent effect on seizures in 86% of patients who did not respond well to vitamin B6, valproic acid, or both; however, many of these patients had later recurrence of infantile spasms. The combination of vitamin B6 and valproic acid is effective and safe in the treatment of infantile spasms.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Infantile spasms in COFS syndrome.

Cerebro-oculo-facial-skeletal (COFS) syndrome is a rare, autosomal recessive syndrome characterized by microcephaly, microphthalmia and/or cataracts, neurogenic arthrogryposis, and multiple congenital anomalies. A term female infant with COFS syndrome who developed infantile spasms at the age of 3 months is reported. The patient had a good response to intramuscular ACTH with disappearance of infantile spasms and resolution of the hypsarrhythmic pattern on electroencephalography succeeded by a slow, synchronous pattern. Modified hypsarrhythmia returned after ACTH therapy was discontinued. Infantile spasms have not previously been reported in association with COFS syndrome and are a potentially treatable aspect of the disease. This patient may add to the clinical spectrum of COFS syndrome or may have a variant.

Abnormalities, Multiple↗
PubMed1995

Cerebrospinal fluid corticotropin and cortisol are reduced in infantile spasms.

Infantile spasms respond to ACTH, and levels of the hormone in cerebrospinal fluid of untreated infants with this disorder were found to be lower than in age-matched controls. In this study we analyzed cerebrospinal fluid cortisol and ACTH using improved immunoassays in a larger cohort of infants with infantile spasms. Analysis of 20 patients and 15 age-matched controls revealed significantly lower levels of both ACTH and cortisol in the cerebrospinal fluid. These data, combined with the efficacy of ACTH and glucocorticoids for infantile spasms, support an involvement of the brain-adrenal-axis in this disorder.

Adrenocorticotropic Hormone↗
PubMed2004

Levetiracetam in the treatment of infantile spasms.

An 11-month-old infant with a 5-month history of seizures and a 3-month history of infantile spasms is described. EEG showed epileptic encephalopathy. The infantile spasms were resistant to treatment with clobazam. Following the introduction of levetiracetam, there was clinical cessation of seizures with resolution of seizure activity on the EEG. This is the second report in the literature of effective treatment of infantile spasms with levetiracetam.

Anticonvulsants↗
PubMed2006

The influence of etiology upon ictal semiology, treatment decisions and long-term outcomes in infantile spasms and West syndrome.

Studying infantile spasms is challenging because there are so many aspects of variation that introduce potential bias. These might relate to the many underlying etiologies, and variations in clinical semiology and electroencephalographic features that relate more to age or timing of investigation than to the underlying epilepsy or seizures type. New gene defects associated with the CDKL5/STK9 and ARX genes are associated with infantile spasms, but these illustrate that, when studying neurodevelopmental outcomes, it is necessary to deal also with heterogeneity at the level of genotype-phenotype correlation. We discuss these design issues with consideration of data from the United Kingdom infantile spasms study (UKISS)--in which neurodevelopmental outcomes show evidence of an interaction between underlying etiologic classification and randomised treatment--and with consideration to proposals on study design from the recent consensus statement of the West Delphi group. In the continual debate about whether we should "lump" or "split" when studying epilepsy syndromes, we propose the adoption of study designs using valid and consistent methods that permit both lumping and splitting.

Electroencephalography↗
PubMed2006

Comparative study of nicorandil and a spasmolytic cocktail in preventing radial artery spasm during transradial coronary angiography.

BACKGROUND: Radial artery spasm is one of the most common complications during coronary angiography via the transradial approach, causing patient discomfort or sometimes interrupting the procedure. This study was designed to compare the spasmolytic effect between nicorandil and a cocktail during transradial coronary angiography. METHODS: A randomized study to compare 4 mg of nicorandil and a cocktail (mixture of normal saline, 200 microg of verapamil) was performed in 150 patients. We examined vasospasms of the radial artery that were expressed as stenosis of the radial artery vessel diameter after the procedure. RESULT: The reductions of systolic and diastolic blood pressures showed no significant differences between the two groups (15.4+/-11.5/7.7+/-7.8 mmHg for nicorandil and 16.3+/-13.4/6.2 mmHg for cocktail). Both agents induced a significant radial artery vasodilation after transradial administration at proximal and mid segments (P < 0.001 for all). Nicorandil showed a significant increase of the mean change of the radial artery diameter compared to the cocktail at mid-segment (0.32+/-0.23 mm for nicorandil and 0.24+/-0.15 mm for a cocktail, P < 0.05). There was no statistically significant difference between the two groups in radial artery spasm (50.7% vs. 52.0% in nicorandil and a cocktail, respectively) after catheterization. CONCLUSION: Nicorandil with vasodilator effects by a dual mechanism was effective as the cocktail in preventing radial artery spasm during transradial coronary angiography.

Coronary Angiography↗
PubMed2006

Maternal IgG suppresses NMDA-induced spasms in infant rats and inhibits NMDA-mediated neurotoxicity in hippocampal neurons.

Maternal immunoglobulin G (IgG) was derived from Wistar rats that just delivered the new offsprings. We examined the effect of this maternal IgG on infantile spasms induced by N-methyl-d-aspartate (NMDA) in immature rats. Pup animals were treated subcutaneously with 10 mg/kg/day maternal IgG from day 11 to day 15 after birth followed by a single intraperitoneal dose of NMDA (15 mg/kg). Administration of maternal IgG decreased the severity and increased the number of ACTH immunoreactive cells in the cortex of rats with NMDA-induced spasms. Furthermore, maternal IgG inhibited NMDA-induced intracellular LDH activity in cultured hippocampal neurons in a dose-dependent manner. The results indicate that maternal IgG can attenuate NMDA-induced seizures. In infantile spasms, some factors may during pregnancy negatively affect the transfer of maternal IgG from mother to fetus thereby causing a decrease in the amount of protective maternal IgG.

Adrenocorticotropic Hormone↗