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PubMed1986

Transition from peristaltic esophageal contractions to diffuse esophageal spasm.

A patient with dysphagia and chest pain was shown by manometry to have high-amplitude peristaltic esophageal contractions (nutcracker esophagus). Worsening symptoms over the next two years led to the performance of repeated manometric studies, which showed diffuse esophageal spasm. This demonstration of a transition from nutcracker esophagus to diffuse esophageal spasm lends further support for consideration of the nutcracker esophagus as a manometric disorder associated with chest pain or dysphagia. Furthermore, it suggests a pathophysiologic relationship between the nutcracker esophagus, a disorder with preserved peristalsis, and diffuse esophageal spasm, the classic dysmotility considered to be of neurogenic origin.

Deglutition Disorders↗
PubMed1986

[An anatomo-clinical case of sequelae of acute encephalopathy. Infantile spasm with hypsarrhythmia].

Clinico-pathological studies of West syndrome are rather rare. A case of sequelae of acute encephalopathy which involved a nine-month-old boy with post-mortem data is reported. Birth and postnatal development had been normal until the onset of illness. Laboratory examinations ruled out bacterial or viral meningo-encephalitis and metabolic disorders. After the recovery from a coma lasting several days, spastic quadriplegia, severe mental retardation and intractable epileptic attacks were present. The latter were made of tonic spasms and myoclonic seizures. EEG records showed hypsarrhythmia. Neuropathological examination revealed almost symmetrical bilateral cystic cavities in the pontine tegmentum and lateral nuclei of both thalami. The corpus callosum was very thin. No finding suggested a congenital anomaly. In a search of the pathological basis for infantile spasms, this case was compared with the published data. It would appear that the lesions of the pontine tegmentum play a significant role in the pathogenesis of hypsarrhythmia or infantile spasms.

Acute Disease↗
PubMed1986

[Spontaneous precordial pain: coronary spasm or esophageal pathology?].

Chest pain due to esophageal spasm or esophagitis may mimic pain of variant angina. Differential diagnosis of the two diseases is often difficult and requires various tests, the value of which is discussed. These problems are illustrated by three cases. The esophageal investigation should preferably be preceded by coronary arteriography. Chest pain or dysphagia due to iced drinks is not specific for esophageal spasm but may be due to coronary spasm.

Adult↗
PubMed1985

Incidence, significance and remission of tubal spasm during attempted hysteroscopic tubal sterilization.

Four hundred three attempted hysteroscopic tubal sterilizations were performed. Tubal spasm was encountered in 37 cases (9.2%) and prevented bilateral placement of tubal plugs in 16 of those cases. There was some evidence that glucagon was associated with a higher rate of remission and that women using barrier birth control methods experienced a lower incidence of tubal spasm. A number of other factors were found to be unrelated to tubal spasm and its remission.

Diazepam↗
PubMed1985

Transition from nutcracker esophagus to diffuse esophageal spasm.

The nutcracker esophagus is a newly defined subset of primary esophageal motility disorders that can be responsible for dysphagia and/or chest pain. Any possible relationship between this entity and diffuse esophageal spasm is poorly understood. Herein we report a case of nutcracker esophagus that showed a transition to classical diffuse esophageal spasm during 1 year follow-up. This transition supports the hypothesis that nutcracker esophagus and diffuse esophageal spasm may be related disorders.

Deglutition Disorders↗
PubMed1985

[Spasm or dimpling of the hypothenar eminence].

Bilateral hypothenar muscular spasm ("dimpling") was discovered in a 62 year-old man. The spasms consisted of recurrent arrhythmic contractions of the palmaris brevis muscle. E.M.G. showed no signs of denervation but the contractions could be stopped by infiltration of the ulnar nerve by xylocaine. Apparently, this syndrome has previously been reported in only two cases. Its clinical and electromyographic characteristics are similar to hemifacial spasm. Compression of the ulnar nerve after its division at the wrist could be a cause.

Diagnosis, Differential↗
PubMed1985

[Posterior fossa microvascular decompression for hemifacial spasm and trigeminal neuralgia--some improvements on operative devices and technique].

Microvascular decompression has been widely used as a method for the treatment of hemifacial spasm and trigeminal neuralgia. We have experienced 30 such cases in the last 2 years; 25 of them were hemifacial spasm and 5 trigeminal neuralgia. Excellent results were obtained in 26 cases; the remaining two cases, both hemifacial spasm, were partially cured. Mild facial paresis appeared several days after the operation in 3 patients. In all the cases, the facial paresis recovered completely within several weeks. The cause of the facial paresis was not known. In 2 cases a slight hearing deficits were noticed after surgery, which has been gradually improving over several months. As this operation is functional surgery, operative complications must be avoided as much as possible. It has been our policy that we first try medical treatment and/or some kinds of nerve block and if no effects are obtained, we recommend the microvascular decompression. For microvascular decompression, suboccipital craniectomy is performed in lateral position. From the point of view of surgical technique, we stress several important points as follows: The head is elevated about 30 degrees, and it is kept approximately horizontal and should not be excessively rotated. Craniectomy is made as far laterally as the sigmoid sinus; its shape is elongated oval. Retraction of the cerebellum should not be done in the direction of the cranial nerves to avoid post-operative hearing deficit. Two tapered retractors are effectively used for cerebellar retraction. A third slim, tapered retractor is useful for holding an offending artery when exploring the root exit zone or placing a sponge for decompression.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1979

Achalasia, diffuse esophageal spasm, and related motility disorders.

From 1972 to 1977, the authors observed 156 patients with primary esophageal motility disorders which caused such a severe degree of dysphagia that treatment by pneumatic dilatation was deemed necessary. Before dilatation, 24% of the patients presented with motility disorders that did not fit well into the two classical disease entities, diffuse esophageal spasm and achalasia (absence of peristalsis with presence of lower esophageal sphincter (LES) relaxations or presence of peristalsis with absence of LES relaxations). After treatment with pneumatic dilatation, these "intermediate" forms constituted 45% of the motor disorders. This was due mainly to the reappearance, on manometric tracings, of peristaltic contractions and of LES relaxations. Radiologic and manometric observations suggest that in many patients, this "return of peristalsis" may be an apparent change in pressure pattern rather than a real change in motility. In 6 of the 156 patients, a deterioration of the esophageal motility disorder was observed, which was characterized by the loss of peristalsis and of LES relaxations over a period of a few months or years. The frequent occurrence of intermediate types of motility disorders and the transition from diffuse spasm to achalasia suggest that achalasia and diffuse esophageal spasm are part of a spectrum of related motor disorders.

Adolescent↗
PubMed1979

[Spasm of the coronary arteries in acute myocardial infarct].

Emergency coronarography was performed in 36 patients with myocardial infarction. Spasms of the coronary artery supplying the area of the infarction were observed in some cases. The fact that the vessel was demonstrated along its entire length after 0.5 mg of nitroglycerine was placed under the tongue confirmed the existence of the spasm. In most patients with acute myocardial infarction the vessel supplying the area of the affected muscle has the appearance of a stump, i.e. its peripheral segments are not demonstrated. At the same time, in some patients, who died some time after the examination, anatomical study of the heart showed that these segments of the vessel were not occluded. Such an angiographic picture may also be explained by the spasm of the coronary arteries. The angiographic pattern of the coronary channel in patients with acute myocardial infarction suggests that coronarolytics and spasmolytics injected both intravenously and into the coronary vessel in coronarography may be used still more extensively.

Acute Disease↗
PubMed1979

Sphenopalatine (nasal) ganglion: remote effects including "psychosomatic" symptoms, rage reaction, pain, and spasm.

Many articles implicate the nasal ganglion in the production of remote symptoms and discuss treatment. Symptoms are primarily spastic, involving both visceral and voluntary muscles including muscle spasm in the neck, shoulder, and low back; asthma, hypertension, intestinal spasm; diarrhea, angina pectoris, uterine spasm; intractable hiccup, and many others. All these symptoms appear to have 2 common denominators. They are mediated by the autonomic nervous system and at least in some instances can be "psychosomatic." The sphenopalatine ganglion (SPG) is a major autonomic ganglion located superficially in the pterygopalatine fossa, with major afferent distribution to the entire nasopharynx and important connections with the trigeminal nerve, facial nerve, internal carotid artery plexus of the sympathetic nervous system and, as shown in the rat, direct connection with the anterior pituitary gland. This paper presents arguments supporting the following hypotheses: 1. The SPG probably has a crucial role in lower animals in declenching the reflex responses known collectively as the rage reaction. 2. The SPG is a major point of entry to the autonomic system exposed to pathologic influences and readily accessible for therapeutic influences and readily accessible for therapeutic intervention. 3. A wide variety of symptoms are produced or maintained by alteration in autonomic system tonus and some of these may be affected by intervention on the SPG. 4. The possible relationship of some symptoms and "psychosomatic" conditions to the autonomic nervous system and the rage reaction must be considered.20

Anger↗
PubMed1984

[Infantile spasms in children under 1-year-old].

In the period of 1977 to 1982, 72 children suffering from infantile spasms and aged 10 days to 12 months were observed. Studies of the neurologic status over time were supplemented with echoencephalography, diaphanoscopy, cranial roentgenography and ophthalmoscopic examination. Furthermore, 58 children were subjected to electro-encephalographic investigations. The clinical findings and data provided by additional methods were evaluated over time, i.e., prior to, during and after the course of treatment. An analysis is presented of the results of corticosteroid therapy of two groups of patients: 1) "idiopathic"-where the medical history showed no previous nervous system impairments prior to the development of the spasms; 2) patients with a history of various damaging factors (pregnancy pathology in the mother, new-born asphyxia, intracranial birth injury, intrauterine infection, neuroinfection in the early postnatal period, etc.). The clinical picture of infantile spasms is extensively described. Before the initiation of hormonal therapy, the patients received anticonvulsive drugs for 1-10 months. The use of ACTH, synacthen and hydrocortisone proved to be fairly effective provided the treatment is instituted early. Possible mechanisms of the action of hormonal drugs are analyzed.

Adrenocorticotropic Hormone↗
PubMed1984

Pattern reversal evoked potentials in infantile spasms.

Visual evoked potentials in response to sinusoidal gratings of various spatial frequencies, alternating in contrast at 8 Hz were recorded from infants affected by an idiopathic form of infantile spasms (West syndrome). In two infants in whom the spasms began at 3 and 5 months of age, respectively, the VEP's were found to be depressed in amplitude at and around a spatial frequency of 3 and 5 c/deg, respectively. This midfrequency depression, which has never been reported in the literature for normal infants, suggests that infantile spasms in idiopathic patients may interfere at least temporarily with the development of visual function.

Evoked Potentials, Visual↗
PubMed1984

Neurovascular decompression for hemifacial spasm.

Results of 23 cases of facial spasm operated on by posterior fossa exploration were reviewed. In all cases, but one, vessels were found to impinge on the facial nerve root exit zone from the brain stem. All cases in which the facial nerve had been liberated from the vessel had satisfactory results and there was no recurrence of spasm. Significant sensorineural hearing loss occurred postoperatively in 11 cases. The hearing loss greatly improved within a month and persisted as permanent loss greater than 10 dB in 6 cases (26.0%). The complication has been lessened by approaching to the nerve from caudal direction and by retracting the cerebellum to oblique direction to the acoustic nerve. Microvascular decompression is the best procedure available for hemifacial spasm.

Adult↗
PubMed1983

Symptomatic hemifacial spasm: case report and review of literature.

The purpose of this article is to discuss a case of hemifacial spasm due to a fusiform basilar aneurysm. The hemifacial spasm was successfully treated by decompression of the facial nerve in the facial canal 14 months before death due to aneurysmal rupture. The literature on symptomatic hemifacial spasm is reviewed, the pathophysiology discussed and the therapeutic options presented. Since the pathophysiology is poorly understood, conservatism is recommended.

Basilar Artery↗
PubMed1984

Blepharospasm--oromandibular dystonia (Meige's syndrome) misdiagnosed as secondary hemifacial spasm.

Orofacial dyskinesia (Meige's syndrome) is a rare clinical entity. This disorder was first described in 1910 by Henry Meige as "spasm facial median," a disabling spasm of the facial musculature which had frequently been misdiagnosed and inappropriately treated. This report concerns a patient who presented with tonic hemifacial spasm twenty-two years after contracting Bell's palsy. The condition was initially thought to be secondary to faulty regeneration of the facial nerve until Meige's syndrome became fully manifested over a period of two years. The diagnostic characteristics as well as the forms of treatment for this unusual disorder are presented.

Blepharospasm↗
PubMed1984

The role of intimal hyperplasia in arterial spasm.

It has been postulated that even moderate spasm in an artery with intimal hyperplasia can produce organ hypoxia because there is an excessive reduction in the diameter of the lumen. To test this hypothesis we created intimal hyperplasia in one femoral artery in five pigs and then induced arterial spasm by administering ergonovine maleate. Arterial spasm did not produce a greater reduction in the luminal diameter of the femoral artery with intimal hyperplasia than it did in the normal femoral artery. Until further evidence appears this hypothesis must be viewed with caution.

Animals↗
PubMed1982

[Physiopathology and treatment of vascular spasms].

Vasomotricity and tonus of arterial and arteriolar vessels yield to nervous regulation (central and peripheral, hormonal, metabolic) as well as to local myogenic regulation. The main mediators of vasomotricity are catecholamines which, by their alpha and beta effects, have an effect on the second mediator (3'5' AMP) and on calcic exchanges, angiotension, serotonin and prostaglandins which "modulate" vasomotor reactions. Metabolic factors: pH, PO2, PCO2 and electrolytes balance: Na, K, Mg, Ca have to be considered. The role of the metabolism of the wall and the role of red blood corpuscles (ADP) and of platelets (released substances of granules) have to be mentioned. The physiopathology of spasm must take into account topographic variations. One can distinguish spasms by nervous regulation, by catecholamines discharge and by extreme and lasting muscular contraction. Medicines of the spasm can have an effect on the peripheral sympathetic nervous system, catecholamines, the 3'5' AMP and especially on the smooth muscular fibre, more accessorily on red blood corpuscles, platelets and coagulation. Na nitroprussiate and calcium chelating agents are the most active substances to-day.

Animals↗
PubMed1983

[Influence of cold-stimuli on hemodynamics and coronary diameters. Provocation of coronary artery spasm].

In 32 patients with coronary heart disease the influence of different cold-stimuli on hemodynamic parameters and coronary artery diameter was examined during left heart catheterization. The cold pressor test (CPT) and the cold air inhalation test (CAIT) were applied to 16 patients in random sequence. 16 patients served as control group. Systolic and diastolic blood pressure increased more under CPT (by 15 and 10 mm Hg respectively) than under CAIT (by 10 and 3 mm Hg). Heart rate and left ventricular enddiastolic pressure did not change. Proximal and distal coronary segment diameters showed a slight, not statistically significant increase under cold-stimuli. All 4 patients with a history of angina pectoris at rest developed coronary spasm, some with ischemic ECG changes; spasm and symptoms disappeared spontaneously when the cold-stimulus was withdrawn. Patients with a history of angina pectoris under cold conditions showed no pathological reactions. It is concluded that two different mechanisms may cause angina pectoris under cold-stimuli. First, the oxygen-consuming effect of an increase in blood pressure, and secondly, an immediate coronary vasospastic reaction. The combined use of CPT and CAIT seems to be an effective and safe means of identifying patients with a tendency to coronary artery spasms.

Adult↗