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At least 217 records · Page 12Linked to original sources
PubMed1999

Randomised, placebo-controlled study of vigabatrin as first-line treatment of infantile spasms.

PURPOSE: Vigabatrin (VGB) has been shown to be an effective drug in the treatment of infantile spasms (West syndrome) in predominantly retrospective and open but also in prospective studies. This prospective, randomised, and placebo-controlled trial of VGB in infantile spasms was considered to be justified and feasible to confirm or refute these previous findings. METHODS: Forty children with newly diagnosed infantile spasms received either VGB or placebo for 5 days in a double blind, placebo-controlled, parallel-group study, after which all the infants continuing in the study were treated openly with VGB for a minimum of 24 weeks. RESULTS: Compared with baseline, at the end of the double-blind phase, the patients treated with VGB had a 78% (95% confidence interval, 55-89%) reduction in spasms compared with 26% (-56-65%) in the group treated with placebo (p = 0.020). Seven VGB-treated patients and two placebo-treated patients were spasm free on the final day of the double-blind period (p = 0.063). At the end of the study, 15 children (38% of the original 40 patients or 42% of the 36 patients who entered the open phase) were spasm free with VGB monotherapy. No patient withdrew from the study because of an adverse event. CONCLUSIONS: This unique randomized, placebo-controlled study is the first to demonstrate the efficacy of a specific drug in the treatment of West syndrome and supports the results of previously published open and prospective trials. It further confirms that VGB could be considered as the drug of first choice in treating infantile spasms.

Adolescent↗
PubMed1997

Computed tomographic analysis of hemifacial spasm: narrowing of the posterior fossa as a possible facilitating factor for neurovascular compression.

Hemifacial spasm can be caused by vascular compression of the facial nerve at the root exit zone from the brainstem. Several case reports suggest that narrowing of the cerebellopontine angle cistern caused by Paget's disease, abnormal elevation of the petrous bone caused by hyperplasia, or contralateral acoustic neurinoma may increase the chance of vascular compression of the facial nerve. Therefore, posterior fossa narrowness has been evaluated in 34 patients with hemifacial spasm by measuring the petrous angle and pons diameter index to elucidate whether narrowing of the posterior fossa can act as a facilitating factor for neurovascular compression. The petrous angle in the hemifacial spasm group was significantly smaller than that in the control group, which consisted of 33 patients with an unruptured supratentorial aneurysm, and the pons diameter index in the hemifacial spasm group was significantly greater than that in the control group. These results indicate that the cerebellopontine angle cistern of patients with hemifacial spasm is narrower resulting in more crowded cranial nerves and vascular structures compared with patients without hemifacial spasm. The narrowness of the cerebellopontine angle cistern may be a possible factor in facilitating neurovascular compression in hemifacial spasm.

Adult↗
PubMed2003

Influence of age on the association between primary hemifacial spasm and arterial hypertension.

OBJECTIVE: To investigate the association between primary hemifacial spasm and arterial hypertension. SUBJECTS: 114 patients with primary hemifacial spasm and 228 neurological controls, matched for age, sex, and referral centre, were recruited during an 18 month period from consecutive outpatients attending two neurological institutions. DESIGN: The association between exposure variables and case/control status was examined in conditional logistic regression models, adjusting simultaneously for disease duration and education level. RESULTS: Hypertension was more common among the patients with primary hemifacial spasm than among the controls. The association was independent of age, disease duration, years of schooling, and other diseases (adjusted odds ratio (OR) 2.76 (95% confidence interval (CI), 1.43 to 5.33); p = 0.002). Hypertension was associated with hemifacial spasm in both the left sided group (adjusted OR, 2.76 (1.18 to 6.44); p = 0.02) and the right sided group (adjusted OR, 3.02 (1.13 to 8.1); p = 0.03). The association of hypertension with hemifacial spasm was apparently greater in the age group < 60 years (adjusted OR, 4.2 (1.4 to 12); p = 0.008) than in the age group >/= 60 years (adjusted OR, 2.5 (CI 1.3 to 4.6); p = 0.005), but the difference in the OR estimates between the two age groups was not significant. Among hypertensive patients, mean age at the diagnosis of hypertension was significantly lower than mean age at the onset of hemifacial spasm in the age group >/= 60 years, but not significantly different in the age group < 60 years. CONCLUSIONS: The findings support the hypothesised association of primary hemifacial spasm with hypertension and raise the possibility that a different mechanism underlies the association in different age groups.

Adolescent↗
PubMed1994

Asymmetric hypsarrhythmia and infantile spasms in west syndrome.

The video encephalograms (EEGs) of 77 consecutive infantile spasms patients were evaluated for the presence of focal or asymmetric hypsarrhythmia and infantile spasms, to determine whether these findings were useful in predicting the presence of focal structural brain disease and were of any additional diagnostic or prognostic significance. Of the 77 patients with infantile spasms, 38% had focal or lateralized features present on video-EEG studies. Unilateral hypsarrhythmia and asymmetric ictal EEG changes during infantile spasms often occurred together: each always indicated the side of a focal or asymmetric structural cerebral lesion that was visible on computed tomographic or magnetic resonance imaging brain scan and was usually large. Clinically asymmetric infantile spasms were less common, always occurred in the presence of asymmetric ictal EEG changes, and did not appear to have additional localizing value. Lateralized hypsarrhythmia, with or without asymmetric infantile spasms, occurred in the presence of bilateral structural lesions that were more abnormal in the area of the greater EEG abnormality. Partial seizures also indicated symptomatic etiologies but were less localizing to visible focal lesions. Patients with symmetric hypsarrhythmia and infantile spasms rarely had focal/lateralized lesions visible on imaging studies. Although the majority of the symmetric group had structural brain disease, these brain lesions were diffuse, not lateralized. This group also included all patients who had cryptogenic etiology and normal development.

Brain↗
PubMed1995

The use of felbamate to treat infantile spasms.

Based on the initial successful use of felbamate for infantile spasms in an infant with tuberous sclerosis, three additional infants with infantile spasms of different etiologies who had failed conventional therapies were treated with felbamate. Three of the four patients have shown complete resolution of infantile spasms. All responding patients did so within 1 week of starting felbamate. The one treatment failure had an initial reduction of seizure frequency and severity but has not maintained that response long term. Controlled studies are needed to firmly establish that felbamate is both safe and effective for the treatment of infantile spasms. As these cases document, felbamate is currently available for use in infantile spasms, and the frequent conversion of infantile spasms to Lennox-Gastaut syndrome, for which felbamate is approved, makes its use in infantile spasms logical.

Anticonvulsants↗
PubMed2002

Focal and global cortical hypometabolism in patients with newly diagnosed infantile spasms.

OBJECTIVE: To evaluate the occurrence and prognostic importance of focal defects in cerebral cortical glucose metabolism in infants with newly diagnosed symptomatic and cryptogenic infantile spasms. PATIENTS AND METHODS: Ten children with symptomatic and seven with cryptogenic infantile spasms underwent MRI, video-EEG, and PET using fluorodeoxyglucose as a tracer within 2 weeks of diagnosis. PET was repeated at 1 year of age in 12 patients. RESULTS: Cortical hypometabolic foci were found in 13 children (77%) with newly diagnosed spasms (six cryptogenic and seven symptomatic). The hypometabolic foci disappeared in seven of nine reexamined at age 1. The occipital foci disappeared in all (n = 6). Focal findings on PET correlated well with focal findings on video-EEG. There was no difference in quantitative cortical or subcortical glucose metabolic rate at the onset of infantile spasms between children with cryptogenic and symptomatic etiology of spasms. The glucose metabolic rate at the onset of spasms or focal lesions in glucose metabolism did not have prognostic value for seizure outcome. CONCLUSIONS: Infantile spasms are often associated with transient cortical, especially occipital, hypometabolic foci that are not necessarily associated with structural lesions and do not indicate a poor prognosis.

Cerebral Cortex↗
PubMed2004

Monitoring of the lateral spread response in the endovascular treatment of a hemifacial spasm caused by an unruptured vertebral artery aneurysm. Case report.

The lateral spread response (LSR) is used in the electrophysiological diagnosis of a hemifacial spasm or for monitoring during microvascular decompression. The authors used LSRs for intraoperative monitoring during endovascular surgery in a rare case of vertebral artery (VA) aneurysm that caused intractable hemifacial spasm. A 49-year-old woman presented with a right hemifacial spasm that had persisted for 9 months. No other clinical symptom was observed. Vertebral artery angiography revealed a saccular aneurysm of the right VA. Magnetic resonance (MR) imaging demonstrated that the aneurysm was compressing the root exit zone of the right facial nerve. Endovascular treatment of the VA aneurysm was performed while monitoring the patient's LSRs. During occlusion of the VA at sites distal and proximal to the aneurysm, the LSRs temporarily disappeared and then reappeared with a higher amplitude than those measured preceding their disappearance. The hemifacial spasm alleviated gradually and disappeared completely 6 months after treatment. The LSRs changed in parallel with the improvement in the patient's hemifacial spasms and eventually disappeared. No recurrence of symptoms has been noticed as of 18 months postoperatively. This is the first report of the use of LSR monitoring during endovascular surgery for an intracranial aneurysm that causes hemifacial spasm. Intraoperative and postoperative changes in the LSRs provided useful information regarding the pathophysiology of hemifacial spasm.

Electric Stimulation↗
PubMed1999

Use of botulinum toxin A in the treatment of hemifacial spasm and blepharospasm.

BACKGROUND: Hemifacial spasm and blepharospasm are both dystonic disorders. They may seriously affect individuals' lifestyle and social activities. In 1990, the Food and Drug Administration of the USA approved botulinum toxin A as a therapeutic agent in the treatment of hemifacial spasm and blepharospasm. We present a therapeutic review of botulinum toxin A in 80 patients in Taiwan. METHODS: Fifty-eight patients with hemifacial spasm and 22 with blepharospasm. Botulinum toxin A was prepared and injected into the facial and eyelid muscles. Patients were monitored every two weeks and classified into four groups (excellent, moderate, mild and no improvement) according to the clinical improvement scale. Complications were also recorded. RESULTS: A total of 86.2% of hemifacial spasm patients and 81.8% of blepharospasm patients had excellent improvement on the spasm intensity scale, while 6.8% of hemifacial spasm and 9.0% of blepharospasm patients had moderate improvement. The complication rate was low and included transient mild facial weakness (5%), ptosis (3.8%), eyelid swelling and/or ecchymosis (3.8%), nausea/vomiting (2.5%) and transient severe facial weakness (1.3%). CONCLUSION: Botulinum toxin A is an excellent therapeutic agent to improve spasm intensity and has a low complication rate.

Adult↗
PubMed2003

[Successful treatment of the backward-bending attack due to generalized spasm in stiff-person syndrome with intravenous immune globulin therapy].

We report a 63-year-old man with stiff-person syndrome, who dramatically responded to the treatment with high dose intravenous immunoglobulin (IVIG). He developed stiffness of the right leg and low back five years ago. He was treated with oral diazepam 6 mg/day and showed a marked improvement. He had been maintained on the same dose since then. In 2000, he began to have episodic generalized spasm and painful spasm of his left leg as well as persistent stiffness of his legs and low back. Findings on the physical examination were normal except for a prominent hyperlordosis with co-contracture of the lumbar paraspinal and abdominal muscles. Neurologic examination revealed stiffness in the lower limbs, more marked on the left side, and lower truncal muscles. The left leg had painful spasm, which was provoked by tactile stimuli. There was severe generalized spasm which made him suddenly bend backward. These backward-bending attacks were provoked spontaneously or reflexively by sudden tactile stimuli. He was unable to arise from a chair or stand without assistance. His deep tendon reflexes on both legs were brisk and Babinski sign was negative. He had no diabetes mellitus and thyroid function was normal. Antibodies against glutamic acid decarboxylase(GAD), antinuclear antibody, thyroid peroxidase autoantibody and antithyroglobulin autoantibody in the serum were present. His painful spasm was disappeared and muscle stiffness was moderately improved by treatment with oral diazepam and clonazepam, but backward-bending attacks due to generalized spasms were not controlled. He received IVIG. Three days after the administration of IVIG, these attacks disappeared completely. Subsequently muscle stiffness improved. One week after, he was able to walk without assistance. IVIG may be useful for treatment of generalized spasm, which had no response to treatment with diazepam or clonazepam.

Humans↗
PubMedDate not supplied

Relationship between reflex excitability and symptom duration in hemifacial spasm.

Changes in excitability and symmetry characteristics have been analyzed with blink reflex recovery curve method applied with dual stimuli at 200, 600 and 1000 ms in patients with hemifacial spasm (HFS), spasm duration shorter than 1 year (HFS 1), spasm duration longer than 8 years (HFS 2), and control group. When compared with controls, while HFS cases with short symptom duration had significant decreases in inhibition at 200 ms in the spasm and healthy sides, those with long symptom duration had this finding only in the spasm side at the 200 ms interval. When HFS groups were compared with each other, in cases with HFS 1, decreased inhibition in the spasm side was significant at 200 and 600 ms, while this was significant only at 200 ms in HFS 2 cases. HFS groups were not found to be different in terms of R2 recovery grade. In conclusion, in cases with HFS, decreased inhibition attributed to facial motor neuron and brain stem interneurons is more predominant on the side of the spasm and this was shown to be present also, to some extent, in the contralateral side. It can be said from our findings that the abnormalities of the blink reflex recovery do not progress in cases with HFS when the symptom duration becomes longer.

Adult↗
PubMed1987

Persistent accommodative spasm nine years after head trauma.

Spasm of the near reflex is most often seen on a functional basis in young adults with underlying emotional problems. In particular, when convergence spasm is associated with miosis on attempted lateral gaze, a functional basis for the disorder should be suspected. Patients who experience spasm of the near reflex following trauma commonly follow a benign course with spontaneous resolution of their ocular complaints within 1-2 years. Accommodative spasm, manifested by pseudomyopia, or spasm of convergence, alone, or in combination with miosis, may be found as isolated signs of spasm of the near reflex. We report a patient who continues to demonstrate accommodative spasm 9 years after a motor vehicle accident.

Accommodation, Ocular↗
PubMed1983

[Cerebellopontile angle epidermoid presenting as hemifacial spasm].

A rare case of CP angle epidermoid presenting as hemifacial spasm was reported. The patient was a 48-year-old woman with left hemifacial spasm of 4 years duration. Preoperative CT films showed some low density area in the left CP angle, however, this finding was thought to be within normal variation. The diagnosis of CP angle epidermoid was made at the time of craniectomy aimed for microvascular decompression. The epidermoid was extending from the lower cranial nerves up to the midbrain level and successfully removed with the same craniectomy opening. Postoperative follow up during 16 months period disclosed complete disappearance of hemifacial spasm and no other neurological deficit. So far, the authors have experienced 425 cases of microvascular decompression for hemifacial spasm and there was only 1 case in whom a CP angle epidermoid was found (0.24%). A review of the literature revealed that hemifacial spasm due to CP angle epidermoid was very rare (1.2%). It was also reported that if there is CP angle epidermoid, hemifacial spasm may appear in the incidence of 7.7-10%. A possibility of CP angle epidermoid should be kept in mind when performing microvascular decompression for hemifacial spasm particularly in younger patients.

Cerebellar Neoplasms↗
PubMed1981

Hemifacial spasm: treatment by microvascular decompression of the facial nerve at the pons.

Hemifacial spasm is a syndrome of intermittent and tonic unilateral facial muscular contraction; mild facial weakness on the same side is also frequently present. Hemifacial spasm can be differentiated clinically from habit spasms, blepharospasm, facial synkinesis following Bell's palsy, facial myokymia, and masticatory spasm. The syndrome of hemifacial spasm is caused by a variety of lesions; the common feature appears to be compression of the facial nerve at the pons. Diagnostic studies do not usually add significant information to that gained from the history and physical examination. The best current treatment (aside from removing an etiologic lesion such as a posterior fossa tumor in the small percentage of cases with such lesions) is microvascular decompression of the facial nerve at the pons through a retromastoid craniectomy. Of 30 patients treated in this manner, 28 have been satisfied with the results. On the most recent follow-up examination, 16 had no hemifacial spasm, nine had only slight periodic twitching about the eye, and three had occasional mild episodes of hemifacial spasm.

Adult↗
PubMed1996

Recurrence of hemifacial spasm after microvascular decompression.

The success of medical and surgical treatment for hemifacial spasm, and involuntary paroxysmal unilateral contraction of the facial muscles, has been mixed. Although microvascular decompression has the greatest reported success, symptom recurrence affects many patients in whom treatment was initially successful. In this study, we report the results of 34 patients who underwent microvascular decompression of the facial nerve from 1976 to 1989 as well as review the literature concerning the incidence and timing of recurrence in more than 600 patients who underwent microvascular decompression. In this series, 94% of 34 patients had continuous relief of spasm after surgical treatment (mean duration, > 6 yr). Of those patients whose spasms were completely initially relieved, 10.3% developed some degree of recurrent spasm; however, no patient developed a recurrence after 24 months without spasm. Our review of the literature discloses that 86% of all recurrences occurred within 2 years of surgery. Patients who have no recurrence of symptoms 2 years after surgical treatment have only a 1% chance of developing recurrent hemifacial spasm. We also comment on possible causes of treatment failure and recurrence of hemifacial spasm after surgical treatment.

Adult↗
PubMed1996

[Periodic decerebrate spasm with ocular dipping, Cheyne-Stokes respiration and hypersympathetic activity].

Decerebrate spasm is a generalized muscular spasm produced by some stimuli on decerebrate posture. Such spasm are called "tonic fit" or "decerebrate extensor spasm". We reported a 50-year-old man with periodic decerebrate spasm after cerebral hemorrhage. On admission, the patient was comatose. The pupils were round but anisocoric and did not react to light. Corneal reflexes were absent. The face, arms, and legs did not move voluntarily. Two weeks after admission, he was found in decerebrate rigidity. Periodic decerebrate spasms were also observed and were accompanied by ocular dipping. Cheyne-Stokes respiration, and hypersympathetic activity (transiently dilated pupils, hypertension, tachycardia). These symptoms persisted for two months and were induced by painful or sonic stimuli and suppressed by sleep, sedative or antiedematous drugs. The cycle was 0.6 approximately 0.7 per minute in accord with that of Cheyne-Stokes respiration. Magnetic resonance imaging revealed an area of low signal intensity in the midbrain to the bottom of the pons caused by the tentorial herniation on T1-weighted images. From the the clinical features and results of MRI studies, we considered that dysfunction of the midbrain to the pons in addition to diffuse cerebral dysfunction played some role in the manifestation of periodic decerebrate spasm with ocular dipping.

Cerebral Hemorrhage↗
PubMed1997

Preventing gastroepiploic artery spasm: papaverine vs calcium channel blockade.

UNLABELLED: The gastroepiploic artery (GEA) is a highly vasoactive artery gaining wider acceptance as a conduit for coronary artery bypass surgery. A variety of agents are used to dilate the GEA prior to grafting; however, little is known about the duration of their effect in the immediate postoperative period. This study evaluated three calcium channel blockers and papaverine in preventing graft spasm. METHODS: Porcine GEA segments (10-12 cm in length) were connected to a computer-controlled perfusion system with a constant in-flow pressure and distal resistance to simulate bypass flow (80-100 ml/min). Norepinephrine (NE; 10(-9) to 10(-5) M) was given in incremental doses at baseline before the vasodilator, immediately after (0 hr), and again at 2 hr after the vasodilator. Changes in flow and ED50 were recorded. Group INT (N = 25) received papaverine (PAP), diltiazem, nifedipine (NFP), or verapamil (VPL) intraluminally, while group EXT (N = 25) received the same dilators externally. RESULTS: All arteries showed dose-dependent vasoconstriction to NE prior to treatment. Immediately after receiving the vasodilator, arteries in both groups (INT and EXT) showed initial protection against NE-induced spasm with the exception of arteries receiving NFD externally. However, at 2 hr, for group INT, only VPL and NFD prevented NE-induced graft spasm (VPL: 40.4 +/- 6.8 ml/min vs 17.9 +/- 3.3 ml/min and NFD: 27.0 +/- 6.5 ml/min vs 13.1 +/- 0.9 ml/min, P < 0.02). In group EXT, after 2 hr, only VPL- and PAP-treated grafts showed resistance to NE-induced vasospasm (VPL: 35.6 +/- 7.3 ml/min vs 15.0 +/- 6.9 ml/min and PAP: 47.4 +/- 15.1 ml/min vs 8.0 +/- 2.0 ml/min, P < 0.001). CONCLUSIONS: Papaverine, a lipophilic vasodilator, when given externally on the perivascular fat of the GEA, prevented graft spasm for up to 2 hr. In contrast, intraluminally applied papaverine did not show graft protection against NE-induced spasm. Nifedipine prevented NE-induced spasm only when given intraluminally. Verapamil proved to be the most potent and versatile vasodilator with effective graft protection of up to 2 hr whether applied externally or internally and was the preferred agent for protecting against GEA spasm.

Animals↗
PubMed2001

Spinal cord stimulation and early experimental cerebral spasm: the "functional monitoring" and the "preventing effect".

BACKGROUND: Clinical and experimental data on cerebral blood flow (CBF) changes during spinal cord stimulation (SCS) were published since 1986. The aims of the present work are: 1. To find an experimental model of reliable, simple and in vivo monitoring of "early" basilar artery spasm after subarachnoid haemorrhage (SAH) and 2. To investigate the effects of cervical spinal cord stimulation (CSCS) on it. Vasospasm due to SAH is both "acute" and "recurrent". Early spasm occurs within minutes of the SAH. its duration is approximately 1 hour. The need of different morphological and haemodynamic methods to evaluate experimental early spasm is reported. To overcome intracranial surgical manipulations and biological effects of contrast and fixation media we designed a model that allows "in vivo" functional monitoring of basilar blood flow far away from the spasm without direct surgical and chemical interference. Subsequently we investigated the effects of CSCS on the new model of "functional monitoring" of the "early" cerebral vasospasm. METHOD: 29 adult Burgundy rabbits were studied. Group 1: under homeostatic monitoring, "on-line" carotid blood flow (carotid BF) changes produced by SAH in cisterna magna of 12 (plus 5 sham treated) animals were studied from the common carotid artery after external carotid artery occlusion before, during SAH and up to the end of the experiments. All the animals underwent digital subtraction cerebral panangiography (CPA) after SAH obtaining a significant increase of carotid BF only when basilar vasospasm was shown by CPA. Carotid BF increase during basilar vasospasm was defined "functional monitoring" of early spasm. Group 2: Twelve animals wearing a cervical epidural electrode underwent carotid BF "functional monitoring" of early basilar spasm before and during CSCS. FINDINGS: Carotid BF changes during CSCS occurred in 10 animals. No carotid BF changes (i.e. no basilar vasospasm) occurred after SAH up to the end of the experiments in all the stimulated animals. INTERPRETATION: CSCS is able to prevent "early spasm" due to SAH in all the animals studied with the new model of "functional monitoring" described, independently from the occurence and the sign for stimulation-induced carotid BF variations. The role and the limits of reversible functional sympathectomy in mediating the effect of CSCS on early vasospam are discussed.

Acute Disease↗
PubMed1993

Plasmin and thrombin inhibitors in essentially untreated patients with coronary artery spasm.

We examined activities or levels of plasmin and thrombin inhibitors in essentially untreated patients with angiographically documented coronary artery spasm. The patients received the ergonovine malate provocation test and were classified into two groups: (a) those with significant coronary artery spasm that produced reduction of the internal luminal diameter of 50% or greater with chest pain and change of electrocardiography (n = 18), and (b) those without coronary artery spasm (n = 17). There was no significant differences in alpha 1-antitrypsin and alpha 2-macroglobulin levels, and C1-inactivator activity between the control and patients with coronary artery spasm. On the other hand, the lower antithrombin III and alpha 2-plasmin inhibitor activities were noted in patients with coronary artery spasm than the control. Thrombin/antithrombin III complex and alpha 2-plasmin inhibitor/plasmin complex levels were significantly higher in coronary artery spasm patients. These results suggest that the coagulation and fibrinolytic systems may maintain their equilibrium in untreated patients with coronary artery spasm.

Antifibrinolytic Agents↗