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PubMed2000

Intravascular ultrasound findings of negative arterial remodeling at sites of focal coronary spasm in patients with vasospastic angina.

BACKGROUND: There are few data about the intravascular ultrasound (IVUS) findings in patients with vasospastic angina, especially regarding patterns of vascular remodeling. METHODS AND RESULTS: Coronary spasm was documented by angiography and electrocardiographic evidence of ischemia in 36 patients after administration of ergonovine (cumulative doses up to 350 microg). After relief of spasm with 1000 microg of intracoronary nitroglycerin, quantitative angiography and IVUS imaging were performed and analyzed by standard methods. The 36 focal spasm sites were compared with the proximal and distal reference segments. The angiographic baseline minimum lumen diameter measured 1.78 +/- 0.66 mm, which decreased to 0.66 +/- 0.38 mm with ergonovine provocation (P <.0001), increased to 2.66 +/- 0.64 mm after intracoronary nitroglycerin (P <.0001 compared with baseline and after ergonovine), and did not change after IVUS imaging (2.66 +/- 0.63, P =.9). By IVUS, atherosclerotic lesions were observed at all coronary spasm sites; the mean plaque burden measured 56% at the spasm site and 35% at the reference. Spasm site plaque composition was hypoechoic in 31 and hyperechoic, noncalcific in 5; there was no calcium. The mean eccentricity index (maximum divided by minimum plaque thickness) was 6.7. Positive remodeling (spasm site arterial area greater than proximal reference) was present in 5; intermediate remodeling (proximal reference greater than spasm site greater than distal reference arterial area) was present in 7; and negative remodeling (spasm site arterial area less than distal reference) was present in 24. CONCLUSIONS: Sites of vasospasm in patients with variant angina showed characteristics of early atherosclerosis, except for an unusually high incidence of negative arterial remodeling.

Adult↗
PubMed1991

Importance of coronary spasm for recurrences following percutaneous transluminal coronary angioplasty (PTCA).

To examine the importance of coronary spasm for recurrences following coronary angioplasty, the incidence of spontaneous and ergonivine-provoked coronary spasm was studied, during initial and 6 months follow-up coronary angiography, in a consecutive series of 102 patients with single-vessel disease and successful coronary angioplasty. Repeat angiography demonstrated restenosis in 35 patients (34%). In patients with no demonstrable coronary spasm before and 6 months after PTCA, restenosis occurred in 23% (14/61). The recurrence rate for patients with spasms only before PTCA was similar (29%; 6/21). An increase of recurrences was observed in patients with coronary spasm before and 6 months after PTCA (69%; 9/13) and was extremely high in patients with detectable spasms only after PTCA (86%; 6/7). The importance of the severity of underlying coronary stenosis as regards the ergonovine testing result, demonstrated no relationship between the degree of underlying stenosis and the incidence of provokable coronary spasms. Thus, coronary spasms provokable only before PTCA do not increase the risk for recurrences. Spasms persisting after PTCA or seen only after the procedure are associated with a significantly higher rate of restenoses.

Angina Pectoris, Variant↗
PubMed1988

Syndrome of coronary artery spasm of normal coronary arteries. Clinical and angiographic features.

To define the clinical and angiographic features of the syndrome of spasm of angiographically normal coronary arteries, 77 patients with spasm and fixed angiographically normal coronary arteries, 77 patients with spasm and fixed coronary stenosis equal to or greater than 50% (group A) were compared with 35 patients with spasm and normal or minimally diseased coronary arteries (group B). Statistically significant differences between groups A and B were as follows: the incidence of rest angina (50.6% vs 85.7%; p less than 0.01) and mixed angina (32.5% vs 5.7%; p less than 0.01); the appearance of ST segment depression (53.3% vs 16%; p less than 0.01) and no electrocardiographic changes during stress test (35.6% vs 76%; p less than 0.01); and the tendency for arteriographically documented spasm to be focal (87.5% vs 71.4%; p less than 0.05) and to affect only one vessel (76.6% vs 57.1%; p less than 0.05). No differences were found between groups A and B in major coronary risk factors, history of previous myocardial infarction, electrocardiographic abnormalities at rest or during pain episodes, or arteries affected by spasm. Thus, angina appearing exclusively at rest is the main clinical feature of spasm of normal coronary arteries. The electrocardiogram, whether at rest or during pain episodes, has no value for predicting the existence of underlying coronary lesions, whereas stress testing does. Spasm of normal arteries tends to be more diffuse than that superimposed on organic lesions and to affect more than one artery, suggesting different mechanisms in the genesis of both types of spasm.

Adult↗
PubMed2002

Intracoronary administration of a thromboxane A2 synthase inhibitor relieves acetylcholine-induced coronary spasm.

This study sought to clarify the effectiveness of intracoronary administration of a thromboxane (TX) A2 synthase inhibitor, Ozagrel Na, to relieve coronary spasms induced by intracoronary injection of acetylcholine (ACh). An ACh spasm provocation test was performed in 92 consecutive patients with coronary spastic angina using incremental doses of 20, 50, and 80 microg into the right coronary artery, and 20, 50, and 100 microg into the left coronary artery within 20s. A coronary spasm was defined as TIMI 0 or 1 flow and an intracoronary injection of 20 mg Ozagrel Na was administered when it was provoked. Within 2 min of the administration of the TXA2 synthase inhibitor, ACh-induced coronary spasms were relieved (TIMI 3 flow) in 88.1% of procedures without complications. In only 4 cases (4.3%), it took more than 3 min to relieve the coronary spasms. Intracoronary administration of 20mg Ozagrel Na when ACh-induced spasms occurred, shortened the spasm relief time in all 7 patients (200 +/- 59s vs 111 +/- 23s, p < 0.01), improved the maximal ST segment elevation in 5 of them (3.9 +/- 3.7 mm vs 0.7 +/- 1.5 mm, p < 0.05), and stopped chest pain in 4 patients. In 4 patients who had ACh-induced coronary spasm of the left anterior descending artery, the TXB2 concentration in the coronary sinus decreased after intracoronary administration of Ozagrel Na into the left coronary artery (463 +/- 562 vs 96 +/- 45, p < 0.01). In conclusion, intracoronary administration of a TXA2 synthase inhibitor can relieve ACh-induced coronary spasms by inhibiting TXA2 synthesis in the local coronary circulation.

Acetylcholine↗
PubMed1995

Correlation between isolated negative U waves and the grade of coronary artery spasm.

The relation between isolated negative U waves and the severity of induced coronary artery spasm was investigated in 24 patients with variant angina to determine the grade of myocardial ischemia during the appearance of isolated negative U waves. Coronary artery spasm was induced by injections of either incremental doses of acetylcholine or ergonovine into the left coronary artery. Coronary spasm was quantified into 4 grades: Grade 0 = complete perfusion, Grade 1 = partial perfusion, Grade 2 = penetration without perfusion, and Grade 3 = no perfusion. Induction with acetylcholine was discontinued when a coronary spasm of Grade > or = 2 was induced. Electrocardiogram in leads V1 to V6 and systemic blood pressure were recorded continuously. Provocations of coronary spasm with at least 2 doses of acetylcholine could be performed in 15 patients. All acetylcholine-induced coronary spasms of Grade < or = 1 disappeared spontaneously within 3 min. Negative U waves developed in 19 (79%) patients, in whom 37 trials with acetylcholine or ergonovine injection were performed. Isolated negative U waves were detected in 10 trials, negative U waves and ST depression in 8 trials, and negative U waves and ST elevation in 14 trials. The induced coronary spasms associated with isolated negative U waves were of Grade 1 in 9 of the 10 trials. In contrast, all of the coronary spasms associated with negative U waves and ST elevation had a Grade of > or = 2. In conclusion, the coronary angiographic finding associated with isolated negative U waves is coronary spasm with delayed filling of the distal coronary artery, with opacification of the entire coronary bed.

Acetylcholine↗
PubMed2000

The preventive effect of magnesium on coronary spasm in patients with vasospastic angina.

STUDY OBJECTIVES: Previous studies have reported that magnesium (Mg) deficiency is associated with coronary spasm. However, little is known about the preventive effect of Mg on coronary spasm. The present study investigated whether Mg prevents coronary spasm in patients with vasospastic angina (VSA). DESIGN: Effectiveness trial. SETTING: University medical center. PATIENTS: Twenty-two patients with VSA. INTERVENTION: Coronary spasm was induced with an intracoronary infusion of acetylcholine (Ach). After spontaneous relief of the coronary spasm, Mg sulfate (0.27 mmol/kg body weight) was infused IV over 20 min in 14 patients and isotonic glucose was infused in 8 patients as control subjects. Intracoronary infusion of Ach was then repeated, and the diameter of the coronary arteries was measured quantitatively. MEASUREMENTS AND RESULTS: Mg infusion caused coronary artery dilatation at baseline in both the spastic (5. 9 +/- 2.3%) and nonspastic segments (5.5 +/- 1.5%). Mg infusion reduced the severity of chest pain and ST-segment deviations during coronary spasm. After the Mg infusion, the percent change in the diameter of the spastic segments improved from - 62.8 +/- 2.6% to - 43.7 +/- 4.7% during coronary spasm. Overall, 10 of 14 patients (71%) responded favorably to Mg infusion. Isotonic glucose infusion did not elicit changes in chest pain severity, ST-segment deviations, or the diameter of the coronary arteries during spasm. CONCLUSIONS: Mg infusion produces nonsite-specific basal coronary dilatation and suppresses Ach-induced coronary spasm in patients with VSA.

Acetylcholine↗
PubMed2003

Standardization of flow velocities with respect to age and sex improves the accuracy of transcranial color Doppler sonography of middle cerebral artery spasm.

OBJECTIVE: The overall accuracy of transcranial Doppler sonography in the diagnosis of middle cerebral artery spasm has not been established. Moreover, the factors of age and sex have not been addressed in most studies. In this article, we present receiver operating characteristic (ROC) curve analysis of the accuracy of transcranial color Doppler sonography in diagnosing middle cerebral artery spasm on the basis of flow velocities standardized for age and sex. SUBJECTS AND METHODS. We prospectively studied 214 consecutive patients (110 male, 104 female; age range, 12-77 years) who were routinely referred for cerebral angiography. Middle cerebral artery spasm was graded as mild (</= 25% of vessel caliber reduction) and moderate to severe (> 25% reduction). Angle-corrected blood velocity measurements were obtained using a 2.5-MHz probe. The velocity values were reexpressed as a percentage of the mean of normal reference values for the relevant age, for subjects younger than 40 years, and for sex. RESULTS: The prevalence of spasm among 335 arteries studied was 8.1% for mild and 12.8% for moderate to severe middle cerebral artery narrowing. For distinguishing all or moderate to severe vasospasm from lesser grades of vasospasm, peak systolic velocity was the best parameter. Areas under ROC curves for all and moderate to severe middle cerebral artery spasms were 0.83 and 0.92, respectively. After standardization, the ROC areas increased significantly (p < 0.05) for all, to 0.86, and only slightly, to 0.93, for moderate to severe spasms. For all grades of middle cerebral artery spasm, the best efficiencies were found at standardized velocity value of 170%. CONCLUSION: The accuracy of transcranial color Doppler sonography is high in the identification of middle cerebral artery spasm. Standardization of velocities with respect to age and sex increases the accuracy of the method in diagnosing mild middle cerebral artery spasms.

Age Factors↗
PubMed1975

[Experimental Subarachnoid hemmorrhage in dogs--effect of various drugs and sympathectomy on cerebral arterial spasm (author's transl)].

Adult mongrel dogs were used. The posterior communicating artery was punctured with a fine needle and subarachnoid hemorrhage was produced, which simulated aneurysmal rupture in human. The cerebral basal arteries were constricted remarkably after the puncture. However this vasospasm disappeared in about 60-120 minutes. After this restoration, the vessels began to be constricted again and reduced their diameter in greater degree with lapse of time. Effect of various drugs and sympathectomy on the experimental spasm induced by this method were studied utilizing the magnified vertebral angiography. The drugs used were papverine, isoxuprine, methysergide, phentolamine and propranolol. One of these drugs was given to each dog into the vertebral artery 15 minutes after the puncture of the artery for study of the early spasm, and the same procedure was carried out 24 hours after the late spasm. Vertebral arteriograms were taken immediately after and at 5, 10 and 30 minutes after injection of the drug. Diameter changes of the cerebral basal arteries were measured on the film. Smooth muscle relaxtants, papaverine and isoxsuprine, were effective on relieving the early and the late spasm. An antiserotonin agent, methysergide, relieved slightly the early spasm, but it had no effect on the late spasm. Phentolamine, that is an adrenergic blocking agent, relieved the early spam remarkably, but it was less effective on the late spam. A beta adrenergic blocking agent, propranolol, was effective on relieving neither the early nor the late spasm. Two weeks after the removal of the bilateral upper cervical ganglia, subarachnoid hemorrhage was produced by the smae method as mentioned above in four dogs. Arteriograms taken 24 hours after puncture of the posterior communicating artery in these dogs showed vasoconstriction as same as in the non-sympathectomized dogs. From these experimental results, it was suggested that an etiological difference in the early and the late spasm may exist, and that the occurence of the late spasm may not be influenced by the sympathetic system.

Animals↗
PubMed1987

[Coronary arterial spasm and symptomatology in ischemic and non-ischemic heart diseases: study of the ergonovine maleate provocative test in 3,000 consecutive patients].

We performed coronary angiography and ergonovine maleate provocative tests (EM test) for 3,000 consecutive patients to clarify 1) the incidence of coronary arterial spasm and significant fixed organic stenosis in ischemic and non-ischemic heart diseases, and 2) the relation of these angina-inducing mechanism(s) to rest (R), effort and rest (E & R), and effort (E) angina. Coronary arterial spasm was defined as total or subtotal occlusion induced by ergonovine test, and fixed stenosis was defined as stenosis with more than 70% narrowing of luminal diameter measured after administration of isosorbide dinitrate. Subjects consisted of 3,000 consecutive patients and were categorized in four groups including 1,145 patients who had typical angina pectoris (Group I: rest angina 653, effort angina 230, and combined rest and effort angina 262), 398 patients with myocardial infarction (Group II), 648 patients with atypical chest pain (Group III), and 809 patients who eventually had diagnostic catheterization for heart diseases other than of ischemic nature (Group IV). Results were as follows: 1. The incidence of coronary artery spasm was 22.2% in Group I, 22.9% in Group II, 1.2% in Group III, and 3.7% in Group IV. 2. In Group I, there was a close relationship between the mechanism of angina and the type of occurrence of typical chest pain; coronary artery spasm was more likely observed in rest angina, organic stenosis was observed in effort angina, and the combined type was observed in cases with both spasm and organic stenosis. Furthermore, the occurrence of coronary artery spasm was significantly more frequent in cases with single vessel disease compared with those with multivessel disease (50.7% vs. 26.7%, p less than 0.005). 3. In Group II, the most frequent angiographic evidence was fixed organic stenosis, and there was no relationship between spasm and the numbers of diseased vessels. 4. In Groups III and IV, the most common entity causing coronary artery spasm was hypertrophic cardiomyopathy. In conclusion, two major mechanisms of angina pectoris, i.e., coronary artery spasm and organic stenosis, are closely related to the symptomatology of this disease, such as rest, effort and combined rest and effort types.

Adult↗
PubMed1983

Coronary arterial spasm in ischemic heart disease and its pathogenesis. A review.

Coronary arterial spasm plays an important role iun the production not only of variant angina but, also, of resting angina other than variant angina, of some exertional angina, and of some acute myocardial infarction. Coronary arterial spasm is most likely to occur at rest, particularly from midnight to early morning, and is usually not provoked by exercise in the daytime. This is related to the fact that the tone of coronary artery is increased from midnight to early morning, whereas it is decreased in the daytime after physical activities. Coronary arterial spasm can be induced by exercise, cold pressor test, hyperventilation, Valsalva maneuver, and the administration of pharmacological agents such as sympathomimetic agents (epinephrine, norepinephrine, etc.), beta-blocking agents (propranolol, etc.), parasympathomimetic agents (methacholine, pilocarpine, etc.), ergot alkaloids (ergonovine, ergotamine, etc.), alcohol, and others, particularly in the morning when spontaneous coronary arterial spasm is most likely to occur. Diltiazem and nifedipine, calcium-blocking agents, prevent coronary arterial spasm induced by these procedures in almost all patients. Phentolamine, an alpha-blocking agent, also suppresses coronary arterial spasm induced by these procedures in 81% of the patients. On the other hand, propranolol, a beta-blocking agent, is not only ineffective in suppressing coronary arterial spasm in 82% of the patients, but aggravates coronary arterial spasm in 41% of the patients. The acute attack of coronary arterial spasm can be promptly relieved by the administration of nitroglycerin.

Angina Pectoris, Variant↗
PubMed1983

[Incidence of induced coronary artery spasm in recent acute transmural myocardial infarction].

A number of studies have suggested that coronary spasm may play a role in the genesis of myocardial infarction. We carried out a provocation test with 0,4 mg intravenous methylergometrine in 131 patients undergoing routine coronary angiography at least 6 weeks after transmural myocardial infarction. The 124 men and 7 women of equal mean age of 49,6 years underwent the investigation on average 27 +/- 9 days after the date of onset of myocardial infarction. Seventy four patients had anterior infarcts (antero septal, anterior, apical), 55 had inferior infarcts (inferior, diaphragmatic and true posterior) and 2 had lateral wall infarcts. Thirty two patients with anterior infarcts (45 p. cent) had a single vessel disease of the left anterior descending artery, 19 had double vessel disease (25 p. cent), 16 had triple vessel disease (21,6 p. cent). During the provocation test with methylergometrine, 13 patients (17,6 p. cent) developed a spasm, 6 on the left anterior descending, 6 on the right coronary and 1 on the left circumflex artery. The patients with insignificant coronary lesions (7 cases) did not develop focal spasm. Twenty seven patients with inferior infarcts (49 p. cent) had single vessel disease, 19 had double vessel disease (34,6 p. cent) and 9 patients had triple vessel disease (16,4 p. cent). The provocation test induced spasm in 14 of the 55 patients (25,5 p. cent). The spasm was localised on the right on the right coronary artery in 9 cases, on the left circumflex in 3 cases and the left anterior descending artery in 2 cases. Therefore, in the whole population studied, 27/131 patients (21 p. cent) developed focal spasm after methylergometrine. In 13 cases, the spasm was observed in the coronary artery presumed to be responsible for the infarct, and in 14 cases on a vessel which did not correspond to the infarcted territory. Resting angina preceded myocardial infarction in only 6 of these 27 patients. This study does not confirm that coronary spasm was the cause of myocardial infarction. It does show the presence of a certain degree of reactivity of the coronary vessels after recent myocardial infarction. Half of the cases of spasm occurred on the vessel presumed responsible for the infarct but the other cases occurred in another zone, which suggests the possibility of post-infarction angina or even a recurrent myocardial infarction. This would be an indication for prophylactic treatment with calcium antagonist drugs.

Adult↗
PubMed1995

Aortocoronary vein graft spasm during angiography.

OBJECTIVE: To determine the frequency and clinical significance of aorto-coronary vein graft spasm during angiography. DESIGN: Retrospective review of angiograms and subsequent correlation with clinical outcome. PATIENTS: A total of 1264 patients having bypass surgery between 1971 and 1986. MAIN RESULTS: Twenty-four men, aged 31 to 54 years, demonstrated spasm in 31 vein grafts at angiography. Vein graft spasm occurred in 13 anterior descending, 12 right coronary, four marginocircumflex and two diagonal grafts. Spasm occurred less than six months after surgery in six cases, six to 12 months after surgery in 18 cases and five or more years after surgery in two cases. There was technical difficulty associated with the intubation of 15 of the 31 grafts. In all but two of the cases, the graft spasm was proximal. There was ischemic discomfort and/or electrocardiographic changes in nine patients, with ventricular fibrillation in three cases. Three cases of very severe vein graft spasm could be reversed with vasodilators, but in three others it could not be relieved and the grafts occluded irreversibly, leading to myocardial infarction in two patients. CONCLUSION: Aortocoronary vein graft spasm may occur during angiography and may be associated with more technically difficult graft intubation. Severe vein graft spasm may respond to vasodilators but can progress to graft occlusion with myocardial infarction. Aortocoronary vein graft spasm during angiography is not related to any higher incidence of spontaneous graft closure or recurrent angina.

Adult↗
PubMed2003

Spinally generated electromyographic oscillations and spasms in a low-thoracic complete paraplegic.

We have measured some oscillatory properties of severe lower limb spasms experienced by a low-thoracic complete paraplegic during assisted standing. Electromyograms (EMG) were recorded from the leg muscles while the patient stood passively in a standing frame. The patient also stood using functional electrical stimulation (FES) while ground and handle reaction force vectors were measured together with EMG activity. During passive standing, spasms appeared simultaneously in all leg muscle groups on one side. The interval between spasms varied between 3 and 30 seconds. Within the spasms, there was a tendency of repetitive grouped discharge of motor units as well as a strong 10-Hz component in the EMG that was coherent across ipsilateral muscle groups. Thus, the spasms were inherently oscillatory. During FES-assisted standing, clinically similar spasms were observed. However, the interspasm interval became relatively fixed at around 16 seconds, which may indicate entraining of the spasm cycle by FES. There are similarities between this patient's spasms and the pathological motor activities seen in other movement disorders that may also be of spinal origin.

Adult↗
PubMed2005

Varied patterns of postoperative course of disappearance of hemifacial spasm after microvascular decompression.

BACKGROUND: The precise course of resolution of postoperative residual HFS after a single MVD has not been well categorised quantitatively in the literature. Not all patients with HFS were cured immediately after a single MVD; some of them exhibited a gradual disappearance of the HFS over a period of time. The time course of the gradual resolution of HFS is categorised and the situation of re-exploration in a few patients whose HFS persisted or recurred is determined. METHODS: The results of 547 MVDs in 545 Chinese patients were reviewed using the database from the author's personal records between January 1992 and December 2002. Different outcomes were observed and divided into four categories according to the variable convalescent period: type 1, spasm cured immediately; type 2, spasm persisted with milder severity and faded away gradually from 7 days to as long as 2 years; type 3, spasm ceased immediately but recurred after 3 days and ran the same course as in type 2; type 4, failed. FINDINGS: Four hundred and seventy-nine patients followed a type 1 course, which constituted an 87.9% immediate success rate. Forty-one patients (7.5%) followed a type 2 course, including three whose spasm persisted for more than 2 years. Twenty-three patients (4.2%), including one with venous compression, followed a type 3 course with their spasm ceased within three months. All of them had typical vascular loop compression. Another patient with a venous contact failed to respond positively to the first MVD underwent re-operation within 2 months. Re-operation was also performed in one patient four days after the first MVD due to persisting and even more severe spasm. These two patients were categorized type 4 as they failed the first MVD (0.4%). Late recurrence was noted in five patients from 1 to 2 years after the first MVD, only one of whom underwent re-exploration and was then cured again. CONCLUSIONS: Approximately 80% of the patients with HFS achieved immediate excellent results after a single MVD, the rest of the patients exhibited residual but usually milder spasms, which resolved gradually over a period of time. According to the patterns of the residual or persisting spasms, the situation and timing of re-exploration can be determined without difficulty. The surgeon should be concerned about missing the responsible vessels in patients with typical HFS who completely failed the first MVD.

Adult↗
PubMed1980

The effect of ACTH therapy upon infantile spasms.

Fifty-five infants with infantile spasms and hypsarrhythmia, who were treated with ACTH using 80 units im every other day for a mean period of ten months, were studied retrospectively and showed better results than infants using so-called nonsteroidal anticonvulsants or ACTH and steroids in other doses and with other time intervals. The study showed that the treatment with ACTH within the first month of onset of spasms produced a higher incidence of spasm-free state while on treatment, a shorter duration of spasms while on treatment, and a higher incidence of spasm-free state while on treatment, a shorter duration of spasms while on treatment, and a higher incidence of a spasm-free state when off treatment, compared to a similar regimen of ACTH begun after seizures had persusted for more than a month. The value of early treatment of infantile spasms suggests that the treatment of this disease should be regarded as a medical emergency.

Adrenocorticotropic Hormone↗
PubMed2002

Familial hemifacial spasm: report of cases and review of literature.

We describe clinical characteristics of 10 patients (five families) with familial hemifacial spasm, with reviews of 13 patients hitherto reported in the literature. There is no clear difference in clinical manifestations between sporadic and familial hemifacial spasms. There is no definite inheritance pattern, but may be autosomal dominant with low penetrance. The ages of onset of familial hemifacial spasm are variable, but occasionally can occur at early years of life. There is a left-side predominance with respect to the affected side of cases with familial hemifacial spasm. Similar to sporadic hemifacial spasm, vascular decompression was effective, suggesting that vascular compression is involved in generating hemifacial spasm even in the familial cases. Familial hemifacial spasm may not be a rare disorder, but may possibly be overlooked. Clarifying the role of genetic susceptibility in pathophysiological mechanisms underlying hemifacial spasm is an important approach toward better understanding of the pathogenesis of cranial rhizopathies.

Adult↗
PubMed1999

Cognitive deficits after cryptogenic infantile spasms with benign seizure evolution.

Between 1989 and 1994, 18 children with cryptogenic infantile spasms-defined by normal development before onset of spasms, symmetrical hypsarrhythmia or multifocal spikes, and typical spasms on presentation, and no abnormal findings on aetiological studies including neuroradiology-were diagnosed and treated. To assess the risk of cognitive impairment later in life, 15 of these 18 children whose spasms completely resolved within the first year of life were studied. Age at onset of spasms varied between 4.4 and 9.8 months (mean 6.5 months). Children were effectively treated with adrenocorticotrophic hormone (10 children), pyridoxine (three), vigabatrin (one), or sodium valproate (one). Spasms lasted between 11 and 138 days (mean 50 days) and stopped between the age of 6.3 and 10.2 months(mean 8.1 months). EEGs normalized between the age of 7.1 and 13.2 months (mean 9.4 months). Early development was assessed on presentation and within a few months after spasms had stopped. A detailed neuropsychological assessment was performed between the age of 4.0 and 5.9 years. Twelve children had normal intelligence; specific cognitive deficits were found in five. Three children had mild learning disability. Abnormal developmental status at age 8 to 15 months after complete resolution of spasms and EEG abnormalities was associated with cognitive deficits at age 4 to 6 years.

Anticonvulsants↗
PubMed2005

Spasm of accommodation in a patient with increased intracranial pressure and pineal cyst.

BACKGROUND: In the setting of a normal neurological examination, accommodation spasm is frequently attributed to a non-organic etiology. Occasionally, organic disorders are associated. In particular, central lesions involving the dorsal midbrain and quadrigeminal plate have been described with disorders of accommodation. HISTORY AND SIGNS: A 36-year-old woman with idiopathic intracranial hypertension (IIH) had visual blur from pseudo-myopia due to accommodative spasm. Magnetic resonance imaging (MRI) revealed a pineal cyst that was reported to be an incidental finding. The patient had persistent papilledema and recurrent episodes of unilateral and bilateral visual blur from accommodative spasm despite medical management. THERAPY AND OUTCOME: A lumboperitoneal shunt effectively lowered her intracranial pressure (ICP). Thereafter, all symptoms of increased ICP, accommodative spasm and papilledema resolved. A functional, non-organic cause for accommodation spasm was not suspected. CONCLUSIONS: To our knowledge, this is the first report of isolated accommodative spasm as a presenting symptom in a patient with IIH. The patient's accommodative spasm resolved with lowering of the ICP. It remains speculative whether her pineal cyst played a role in triggering the accommodative spasm.

Accommodation, Ocular↗