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PubMed2004

Bladder spasm following transurethral surgery.

This article describes a study carried out to determine the incidence of bladder spasm and any common factors among patients presenting with bladder spasm in the recovery unit following transurethral surgery. Data was collected retrospectively from 200 sets of patient notes. The findings suggest that bladder spasm is common following transurethral surgery and that certain surgical procedures are more likely to result in bladder spasm.

Clinical Protocols↗
PubMed2004

Zonisamide treatment for symptomatic infantile spasms.

The authors evaluated zonisamide for symptomatic infantile spasms in 23 patients. Spasm cessation, EEG evolution, and tolerability were assessed for a mean duration of 6.5 months. Six patients (26%) had complete control with cessation of spasms and clearing of hypsarrhythmia. Mean latency time from onset of zonisamide treatment to complete spasm control was 19 days. There were no discontinuations due to adverse effects.

Anticonvulsants↗
PubMed1983

Focal facial spasm.

An unusual case of focal facial spasm modified by factors affecting the peripheral facial nerve was investigated in a 32-year-old woman with involuntary contractions at the left mouth and nasal area. Voluntary facial movements were normal. The involuntary spasms ceased with digital pressure over the facial nerve in the left stylomastoid area. A difference between voluntary and these involuntary facial movements occurred both with local anesthetic blockade and with crushing of the facial nerve. Blink reflexes demonstrated unilateral left synkinesis, and facial EMG showed clonic discharges and individual motor units that discharged rapidly (200 Hz). Treatment with diphenylhydantoin, carbamazepine, and prednisone was ineffective. Neurolysis of the peripheral facial nerve resulted in temporary relief, whereas biofeedback controlled the spasms. Focal facial spasms may represent a disorder of the facial nucleus influenced by both peripheral and central mechanisms.

Adult↗
PubMed1988

CT and hemifacial spasm.

Forty-six patients with typical hemifacial spasm had CT. Thirty-eight (83%) were abnormal, including two with surgically documented tumors. Thirty-six had a characteristic dolichoectatic vertebrobasilar artery, with the convexity pointing to the side of the spasm in 92% of the scans. This study suggests that CT is worthwhile procedure in the evaluation of hemifacial spasm and that dolichoectatic vertebrobasilar arteries are very frequently associated with hemifacial spasm.

Adult↗
PubMed1989

Treatment of infantile spasms with high-dose ACTH: efficacy and plasma levels of ACTH and cortisol.

Fifteen children with infantile spasms and a hypsarrhythmic EEG defined by EEG-videotelemetry monitoring received a regimen of high-dose (150 IU/m2/d) ACTH for their seizures. We carried out an endocrinologic evaluation before and after initiation of the ACTH and conducted a time course study of plasma ACTH and cortisol levels after ACTH dosing. Spasms were controlled and the EEG normalized in 14 of the 15 children. Prior to starting ACTH therapy all the patients had normal prolactin, insulin, cortisol, and ACTH levels in plasma and normal thyroid function. Although the pattern of rise of ACTH levels in plasma after ACTH dosing was similar in all the children, there was great individual variation in the absolute concentrations. However, both the pattern of rise and absolute level of cortisol in plasma after ACTH was highly predictable in all patients. Plasma cortisol rose rapidly within 1 hour of ACTH administration and continued a slower rise for 12 to 24 hours after the ACTH dose. High-dose ACTH therapy seems quite effective in infantile spasms, perhaps because of a sustained high level of plasma cortisol. This sustained plateau of cortisol may be more effective in controlling infantile spasms than the pulse effect expected with oral steroids or lower doses of ACTH.

Adrenocorticotropic Hormone↗
PubMed1992

Hemimasticatory spasm: clinical and electrophysiologic observations.

Hemimasticatory spasm is a rare disorder of the trigeminal nerve that produces involuntary jaw closure due to paroxysmal unilateral contraction of jaw-closing muscles. We report three patients with this disorder. Electrophysiologic studies demonstrated normal blink and masseter reflexes. The masseter inhibitory reflex was absent during periods of spasm. Needle electromyography demonstrated irregular bursts of motor unit potentials that were identical to the pattern observed in hemifacial spasm. The electrophysiologic findings suggest ectopic excitation of the trigeminal motor root or its nucleus, an abnormality that is analogous to ectopic excitation of the facial nerve in hemifacial spasm. One patient improved temporarily with surgery, one improved while on treatment with carbamazepine, and another responded favorably to botulinum toxin injection.

Adult↗
PubMed1984

Hemifacial spasm caused by a venule: case report.

The syndrome of hemifacial spasm occurs as a consequence of compression, almost universally by blood vessels, of the root entry zone of the facial nerve. The vascular compression is usually obvious at operation, but may be subtle. The author describes a case in which a venule running in an anterior-posterior direction across the caudal aspect of the root entry zone of the facial nerve, which was thought to be causing the spasm, was coagulated and divided. A small, more distal arteriole, probably not contributory, was decompressed away from the nerve. After operation, the patient improved gradually, and she remains free of facial spasm or weakness. This is the most subtle vascular compression seen by the author and his colleagues in over 400 microvascular decompressions for hemifacial spasm.

Brain Stem↗
PubMed1985

Microvascular decompression in hemifacial spasm: intraoperative electrophysiological observations.

Facial muscle responses in patients with hemifacial spasm undergoing microvascular decompression operations were recorded. Two peripheral branches of the facial nerve were stimulated and the electrical responses of muscles innervated by these branches were studied to see how the lateral spread of activity that is known to be present in these patients was affected by decompressing the facial nerve. In some of the patients the hemifacial spasm ceased when the dura mater was opened, in some it ceased when the arachnoid was opened, and in others the spasm persisted until the offending vessel was dissected away from the nerve. The lateral spread of activity elicited by antidromic stimulation of a branch of the facial nerve was less affected by opening of the dura mater or arachnoid: it usually persisted until the blood vessel that had been compressing the facial nerve was removed and reappeared when the vessel that had been compressing the facial nerve was allowed to slip back onto the nerve. This seems to indicate that microvascular decompression of the facial nerve is effective in alleviating hemifacial spasm because it removes the actual cause of the disorder rather than simply causing local injury to the nerve as a result of the procedure.

Electric Stimulation↗
PubMed1981

Coronary artery spasm: a mechanism of chest pain in selected patients with the mitral valve prolapse syndrome.

A group of 14 patients with mitral valve prolapse syndrome was referred for coronary angiographic study. The group was selected on the basis that all members had recurrent chest pain as their chief complaint and all had interpreted their chest pain as serious enough to warrant at lest two previous emergency visits to medical facilities in the six months preceding the study. All were found to have normal left ventricular function, and only one had a significant fixed obstructive coronary lesion. Seven of 14 patients (50 percent) showed evidence of coronary artery spasm during the catheterization study, five of whom had histories highly suggestive of coronary vasospasm. During the catheterization, spasm occurred spontaneously in three patients, ws ergonovine-induced in two, and was catheter-tip-induced in two. Ergonovine was administered to nine of the 14 patients. The drug induced vasospasm in two patients but failed in seven (two of whom had previously demonstrated catheter tip spasm). Of those seven patients who showed evidence of spasm, four had typical chest pain in association with reversible ST segment elevation and manifested a variant anginal syndrome.

Adult↗
PubMed2002

Efficacy of the ketogenic diet for infantile spasms.

OBJECTIVE: The objective of this study was to determine whether the ketogenic diet is safe, well-tolerated, and efficacious in the treatment of infantile spasms. METHODS: During a 4-year period, 23 children with infantile spasms, aged 5 months to 2 years, were started on the ketogenic diet; 9 (39%) had symptomatic infantile spasms, and 16 (70%) had hypsarrhythmia. Children had an average prediet exposure to 3.3 anticonvulsants. Two children were enrolled before any medication had been tried. Seizure reduction was analyzed retrospectively, using parent reports and electroencephalograms (EEGs) when available. RESULTS: At 3, 6, 9, and 12 months, 38%, 39%, 53%, and 46%, respectively, of all patients currently on the diet were >90% improved (3 were seizure-free at 12 months); 67%, 72%, 93%, and 100% were >50% improved. Fifty-six percent remained on the diet at 12 months, 46% of whom were >90% improved and 100% were >50%. Fifty percent of those with hypsarrhythmia and follow-up EEGs had EEG improvement. Fifty-seven percent had their medications reduced or discontinued by 12 months. Fifty-seven percent had improvement in development, which was correlated with seizure control. Independent factors that predicted improvement included age younger than 1 year and previous exposure to 3 or fewer anticonvulsants. No child has died, and 7 children had diet-related adverse reactions (nephrolithiasis, gastroesophageal reflux). DISCUSSION: The ketogenic diet is a safe, well-tolerated, and possibly effective potential alternative to other therapies for infantile spasms.

Child, Preschool↗
PubMed2001

Current concepts on pathophysiology, diagnosis and treatment of diffuse oesophageal spasm.

Diffuse oesophageal spasm is a functional oesophageal motility disorder of unknown aetiology, which appears to be due to a disturbance of the normal pharmacological timing of propulsive contraction occurring in the oesophageal body after swallowing. The lack of pathophysiological understanding may be due to the fact that there is more than one pathophysiological pathway causing symptoms of diffuse oesophageal spasm. Barium studies, oesophageal scintigraphy and fiberoptic examination can be helpful in finding the correct diagnosis, but manometry is still the gold standard of diagnostic procedures. Similar to other spastic oesophageal motility disorders, pharmacological treatment of diffuse oesophageal spasm includes nitrates, calcium antagonists, anticholinergics and antidepressants with varying beneficial effects. Botulinum toxin, which provides sufficient treatment as measured by symptom score and manometric patterns in patients with achalasia, was recently evaluated for the treatment of diffuse oesophageal spasm in small patient selections with promising results.

Biofeedback, Psychology↗
PubMed2001

Hemifacial spasm due to cerebellopontine angle meningiomas--two case reports.

A 54-year-old female and a 49-year-old female presented with complaints of hemifacial spasm. Both patients underwent surgery to remove cerebellopontine angle meningiomas. In one case, no vascular compression was observed at the root exit zone. The tumor was removed subtotally leaving residual tumor adhered to the lower cranial nerves. The hemifacial spasm disappeared immediately after the operation. The residual tumor was treated using gamma knife radiosurgery. In the other case, the root exit zone of the facial nerve was compressed by both the tumor and anterior inferior cerebellar artery and the tumor was removed totally. Postoperatively, the hemifacial spasm disappeared, but the patient suffered facial nerve paresis and deafness that was probably due to intraoperative manipulation. However, the facial nerve paresis gradually improved. Cerebellopontine angle meningioma with hemifacial spasm must be treated by surgical resection limited to preserve cranial nerve function. Subtotal removal with subsequent radiosurgery to treat the remaining tumor tissue is one option for the treatment of cerebellopontine angle meningioma.

Cerebellar Neoplasms↗
PubMed2005

Disappearance of hemifacial spasm after ventriculoperitoneal shunting in a patient with achondroplasia--case report.

A 15-year-old boy with achondroplasia developed right hemifacial spasm associated with headache, vomiting, and hearing disturbance. Computed tomography showed hydrocephalus. A ventriculoperitoneal shunt was placed. His hydrocephalus subsequently resolved, the hemifacial spasm and headache disappeared, and his hearing disturbance improved. The episodes of hemifacial spasm were probably related to a small posterior cranial fossa volume, the so-called crowding of the posterior fossa. Increased intracranial pressure due to hydrocephalus apparently contributed to further reduction in the posterior cranial fossa volume and led to the hemifacial spasms. In addition, his hearing disturbance may have been the result of dysfunction of the cochlear nerve due to the increase in intracranial pressure caused by hydrocephalus.

Achondroplasia↗
PubMed1979

Arteriographic demonstration of spontaneous right coronary artery spasm in a patient with Prinzmetal's angina.

Coronary artery spasm may occur spontaneously during coronary angiography in patients with clinically documented or suspected Prinzmetal's angina. In other patients with Prinzmetal's angina, the spasm can be provoked by the administration of ergonovine. A patient with spontaneous spasm of the right coronary artery during coronary angiography is reported and some considerations for diagnosis and therapy of this entity is offered. Although intraoperative spasm has been reported in the cardiology literature, no such case has been described in the radiology literature.

Angina Pectoris↗
PubMed2004

Relationship between diffuse esophageal spasm and lower esophageal sphincter dysfunction on barium studies and manometry in 14 patients.

OBJECTIVE: We sought to reassess the function and clinical characteristics of the lower esophageal sphincter in a series of patients with radiographically defined diffuse esophageal spasm. MATERIALS AND METHODS: In reviewing records in the radiology database at our hospital, we identified 14 patients with diffuse esophageal spasm confirmed on barium studies who also underwent esophageal manometry. The radiographic findings were reviewed and correlated with the manometric findings. Medical records were also reviewed to determine the clinical presentation, treatment, and patient course. RESULTS: All 14 patients were symptomatic, presenting with dysphagia, chest pain, or both. All the barium studies revealed intermittently absent or weakened peristalsis, with nonperistaltic contractions that were moderate in six patients (43%) and marked in eight patients (57%) (contractions nearly obliterating the lumen in six and completely obliterating the lumen in two). Nine patients (64%) had impaired opening of the lower esophageal sphincter, manifested by beaklike narrowing of the distal esophagus, and five (36%) had normal opening of the lower esophageal sphincter. Manometry revealed abnormal peristalsis in all 14 patients, with repetitive simultaneous contractions in eight (57%) and lower esophageal sphincter dysfunction in 12 (86%). All eight patients with lower esophageal sphincter dysfunction or incomplete relaxation of the lower esophageal sphincter on barium studies or manometry who were treated with the Clostridium botulinum toxin or endoscopic balloon dilatation had a positive response. CONCLUSION: Our preliminary data show that diffuse esophageal spasm is characterized on barium studies by frequent lower esophageal sphincter dysfunction rather than a classic corkscrew appearance. Barium and manometric studies may have complementary roles in the evaluation of patients with diffuse esophageal spasm.

Adult↗
PubMed1995

Diffuse esophageal spasm: a malfunction that involves nitric oxide?

OBJECTIVE: As recently suggested, nitric oxide (NO) may play an important role in the regulation of esophageal motility, being partly responsible for the latency period and latency gradient between the onset of a swallow and contractions of esophageal circular smooth muscles. Diffuse esophageal spasm appears to be a classical example in which the mechanisms normally responsible for the physiologic timing of the contractions occurring in the esophageal body after swallowing are disturbed. METHODS: Five patients (one male and four female; age, 18-48 years) with symptomatic esophageal spasm were give glyceryl trinitrate (GTN) intravenously in gradually increasing doses or L-arginine on two separate occasions and underwent manometric measurements of esophageal motility after wet swallows, using a multilumen perfused catheter system (Synetics Medical, Stockholm, Sweden). The amplitude, duration, and propagation of the contractions and the latency period were analyzed, using specially designed software. Additionally, during the GTN infusion period arterial blood pressure was measured every 5 min, RESULTS: GTN infusion given at a dose of 100 to 200 micrograms/kg-h intravenously caused the occurrence of and a dose-dependent elongation of the latency period after swallowing. The mean amplitude of the contractions did not show any significant alterations, whereas the mean duration of the contractions decreased significantly, from 11.2 +/- 4.8 sec to 5.4 +/- 0.8 sec. These effects were accompanied by significant alleviation of symptoms during swallowing. Interestingly, no adverse side effects such as headache or flush were observed at any dose of GTN. The blood pressure did not show any changes during the studies in any of the five patients. Administration of L-arginine (300 mg/kg-h intravenously) did not cause any significant alterations of motility pattern or alleviation of dysphagia. CONCLUSIONS: 1) NO may play an important role in the control of human esophageal motility, being involved in the mechanisms responsible for the timing of propulsive contractions in the body after swallowing; 2) GTN may to be of benefit in the treatment of diffuse esophageal spasm in symptomatic patients; and 3) patients with diffuse esophageal spasm may have a malfunction in endogenous NO synthesis and/or degradation.

Adolescent↗
PubMed1985

Loss of auditory function in microvascular decompression for hemifacial spasm. Results in 143 consecutive cases.

Auditory function was studied before and after surgery in 143 consecutive patients who were operated on for hemifacial spasm by microvascular decompression of the intracranial portion of the facial nerve. The acoustic middle ear reflex was abnormal preoperatively in 41% of the patients, indicating that the vascular abnormalities that caused the hemifacial spasm also affected the auditory nerve. Three patients suffered a profound hearing loss in the ear on the operated side, and one lost hearing function totally. In addition, 24 patients had a moderate elevation in the pure-tone threshold at one or more octave frequencies. Of these, 16 patients experienced a hearing loss at only one frequency (8000 Hz), while eight had a threshold evaluation of no more than 20 dB in the speech frequency range (500, 1000, and 2000 Hz). Two patients were deaf on the side of the spasm before the operation. Three patients were not tested postoperatively, and one patient was tested only after surgery. Thus, in this series of 143 patients, only 2.8% suffered a significant hearing loss as a complication of facial nerve decompression to relieve hemifacial spasm.

Adult↗
PubMed1991

Familial hemifacial spasm associated with arterial compression of the facial nerve. Case report.

This report of an 88-year-old woman with familial hemifacial spasm includes the first published postmortem description of hemifacial spasm with cross-compression of the seventh cranial nerve root exit zone by a redundant loop of the anterior inferior cerebellar artery and associated vascular plexus. Histological examination of the seventh and eighth cranial nerve complex suggested nerve degeneration because increased numbers of corpora amylacea were present just distal to the compression concavity. There was no evidence of demyelination or gliosis of the nerve. This case suggests that vascular compression of the nerve root exit zone is an important condition in the etiology of most of these cases. This is the third reported case of familial hemifacial spasm; to date, all such patients have had left facial involvement. The family pedigree in this case suggests a pattern of autosomal-dominant inheritance with partial penetrance. The genetic basis for familial hemifacial spasm may involve anatomical variants or anomalies of the posterior circulation, since both posterior inferior cerebellar arteries were congenitally absent in this case.

Aged↗