Lateral Infarction Research Articles

Pure or predominant sensory stroke due to brain stem lesion.

Pure or predominant hemisensory symptoms can be seen in patients with brain stem stroke. However, there have been no reports in which sufficient numbers of patients were studied with detailed descriptions on the sensory patterns and imaging findings. We describe 17 patients presenting with pure or predominant hemisensory symptoms due to brain stem stroke in whom CT scan and/or MRI identified appropriate lesions. Eleven patients had an infarct and 6 had a hemorrhage. Aside from sensory deficit, the majority had dizziness and gait ataxia. Fifteen patients had paramedian dorsal pontine lesions associated with pure or predominant lemniscal sensory involvement, often in the cheiro-oral (n = 4) or leg dominance (n = 4) patterns. The lesions of the former group tended to be located more medially compared with those of other patients, which is in agreement with the sensory topography of the pontine lemniscal sensory tract. Bilateral facial or perioral sensory symptoms were noted in 6 patients. One patient with a dorsolateral pontine lesion had selective spinothalamic modality impairment, while one with a lateral midbrain infarct had sensory deficit of all modalities. Pure or predominant brain stem sensory stroke is most often produced by small infarcts or hemorrhages in the paramedian dorsal pontine area and may be differentiated from thalamic pure sensory stroke by the following characteristics: frequent association of dizziness/gait ataxia, predominant lemniscal sensory symptoms, occasional leg dominance or cheiro-oral pattern, and frequent bilateral perioral involvement.

Clinical significance of perioperative Q-wave myocardial infarction: The Emory Angioplasty versus Surgery Trial

Objective: The primary end point of the Emory Angioplasty versus Surgery Trial was a composite of three events: death, Q-wave infarction, and a new large defect on 3-year postoperative thallium scan. This study examines the clinical significance of Q-wave infarction in the surgical cohort (194 patients) of the Emory trial. Methods: Twenty patients (10.3%) with Q-wave infarctions were identified: 13 patients had inferior Q-wave infarctions and seven patients had anterior, lateral, septal, or posterior Q-wave infarctions (termed anterior Q-wave infarctions). Results: In the inferior Q-wave infarction group, postoperative cardiac catheterization (at 1 year or 3 years) in 11 patients revealed normal ejection fraction (ejection fraction >55%) in 10 (91%), no wall motion abnormalities in 10 (91%), and all grafts patent in 10 (91%). In the anterior Q-wave infarction group, postoperative catheterizatiOn in six patients revealed normal ejection fractions in five (83%), no wall motion abnormalities in three (50%), and all grafts patent in three (50%). Average peak postoperative creatine kinase MB levels were as follows: no Q-wave infarction ( n = 174) 37 ± 43 IU/L, inferior Q-wave infarction 40 ± 27 IU/L, and anterior Q-wave infarction 58 ± 38 IU/L. Mortality in the 20 patients with Q-wave infarctions was 5% (1/20) at 3 years; in patients without a Q-wave infarction it was 6.3% (11/174) ( p = 0.64). Of 17 patients with a Q-wave infarction who underwent postoperative catheterization, 11 (65%) had a normal ejection fraction, normal wall motion, and all grafts patent with an uneventful 3-year postoperative course. Conclusions: The core laboratory screening of postoperative electrocardiograms, particularly in the case of inferior Q-wave infarctions, appears to identify a number of patients as having a Q-wave infarction with minimal clinical significance. Q-wave infarction identified in the postoperative period seems to be a weak end point with little prognostic significance and therefore not valuable for future randomized trials. (J T horac C ardiovasc S urg 1996;112:1447-54)

The syndrome of posterior choroidal artery territory infarction.

Posterior choroidal artery (PChA) territory infarcts remain the least well-known type of thalamic infarcts. Our study of 10 personal cases, selected from 2,925 stroke patients admitted consecutively to a community-based primary care center, and 10 published cases of unilateral PChA territory infarct suggests that they can often be differentiated clinically from other thalamic infarcts. Patients with PChA territory infarct associated with superficial posterior cerebral artery territory infarct or with another infarct were excluded. Damage was characteristically limited to the lateral geniculate body, pulvinar, posterior thalamus, hippocampus, and parahippocampal gyros, without involvement of the upper midbrain and the anterior nucleus of thalamus. In lateral PChA territory infarct, the most common clinical manifestations included homonymous quadrantanopsia, with or without hemisensory loss and neuropsychological dysfunction (transcortical aphasia, memory disturbances). A homonymous horizontal sectoranopsia is exceptional but particularly suggestive of the involvement of the lateral geniculate body in this territory. Media] PChA territory infarct was less frequent. Its neurologic picture was dominated by eye movement disorders not particularly suggestive of thalamic involvement. Late disability was usually absent or slight, being related to pain and delayed abnormal movements. The most common stroke etiology was presumed small-vessel occlusive disease.

Usefulness of the 12-lead electrocardiogram in detection of myocardial infarction: electrocardiographic-anatomic correlations--Part II.

Part II of this two-part series on electrocardiographic-necropsy correlation of infarct location focuses on lateral and posterior ("inferior") infarctions. The value of infarct location regarding complications and prognosis is also discussed.

Usefulness of the 12-lead electrocardiogram in detection of myocardial infarction: electrocardiographic-anatomic correlations--part I.

This two-part review evaluates a 56-year period (1938-1994) of electrocardiographic-necropsy correlation studies. Part I focuses on definitions of infarct location and evaluates anterior infarctions. Part II will focus on lateral and posterior infarcts.

Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction

The role of the ECG in evaluating reperfusion status after thrombolytic treatment in acute myocardial infarction is not clear. Dramatic ST segment changes have been observed during recanalization of an infarct-related artery, but ST criteria have not been definitively established for prediction of coronary artery patency. Differences in ST segment changes in relation to infarct localization have not been evaluated, and further investigation is required into reciprocal ST depression, which provides information independent from ST elevation. Therefore, the aim of this study was to evaluate how early changes in ST segment elevations and depressions predict vessel patency after fibrinolysis for patients with anterior and inferior/lateral infarcts. Two hundred patients with a Pardee wave in the ECG and chest pain of less than 6 h duration were given thrombolytic treatment. The result of the therapy was assessed simultaneously with coronary angiography. Patients were divided into two groups: I (50 patients) without recanalization (TIMI grade 0, 1 or 2), and II (150 patients) with successful recanalization (TIMI grade 3). Before and after therapy, analysis of the 12 lead ECG included maximum ST elevation measurement (H1, H2 respectively), the sum of ST elevations (sigma H1, sigma H2), the sum of ST segment depressions (sigma h1, sigma h2), and the ratios of ST segment changes (R1 = H2:H1, R2 = sigma H2:sigma H1, R3 = sigma h2:sigma h1). The mean interval from the first to the second ECG was 3.5 +/- 1 h. Successive values of R1 and R2 were examined to find that which best distinguished between the two groups. The best values for prediction of reperfusion were: (1) For anterior wall infarct [table: see text] (2) For inferior and lateral infarct [table: see text] In 13 patients with a complete right or left bundle branch block in the first or second ECG, the result of treatment was predicted in 11 patients using criteria for factor R1 and in 12 patients using criteria for R2. Analysis of ST segment depressions revealed a significant correlation between normalization of ST segment depressions and elevations (R3 vs R1: r = 0.60, P < 0.05; R3 vs R2 r = 0.59, P < 0.05). Multivariate discriminant analysis showed an independent value of R3 for discrimination between the two groups, but only in patients with inferior/lateral infarcts. The overall accuracy of the common algorithm in predicting reperfusion was significantly better in patients with inferior/lateral infarcts (Chi2 test, P = 0.0078). When separate algorithms were used, there was no significant difference between patients with anterior or inferior/lateral infarcts because of the significant improvement in prediction of reperfusion in patients with anterior infarcts (McNemar's test: P = 0.041). We conclude that analysis of ST segments on the standard 12-lead ECG offers valuable help in the early identification of successful recanalization of infarct-related arteries after thrombolytic therapy in patients with acute myocardial infarction. Use of the ratio of ST segment normalization according to the separate criteria for anterior and inferior/lateral infarcts gives the test a high sensitivity and specificity, even in the presence of interventricular conduction disturbances.

Immunohistochemistry with an antibody to human liver carboxylesterase in human brain tissues

Human liver carboxylesterase (CE) is an enzyme capable of metabolizing drugs, and may also function as a regulator of lipid metabolism. We examined one isoform of CE by immunohistochemistry in the brains of neurologically normal, Alzheimer disease (AD), amyotrophic lateral sclerosis (ALS) and cerebral infarction cases. In all but the infarcted brains, the anti-CE antibody stained only capillary endothelial cells in the brain and spinal cord tissues. In infarct brain areas, intense immunoreac-tivity of the macrophages was seen. In contrast, the macrophages in the ALS lateral columns and the reactive microglia located in the center of classical senile plaques in AD, as well as other reactive microglial cells in the grey matter, showed no immunoreactivity. In the central nervous system, CE may function as a protective factor against foreign chemicals in capillary endothelial cells, and the antibody to CE may serve as a marker for invading macrophages from the systemic circulation.

Expression of chromogranin A in lesions in the central nervous system from patients with neurological diseases

Expression of chromogranin A in various neurological diseases was examined immunohistochemically using purified anti-human chromogranin A antiserum. The antibody stained dystrophic neurites in senile plaques in Alzheimer disease brain, Pick bodies and ballooned neurons in Pick's disease brain, some Lewy bodies in the substantia nigra of Parkinson's disease, and axonal swellings in various neurological conditions including Parkinson's disease, striatonigral degeneration, Shy-Drager syndrome, amyotrophic lateral sclerosis and cerebral infarction. The present study shows that expression of chromogranin A is not an exclusive feature of Alzheimer disease or Pick's disease, and indicates that it could be a useful marker for various neurological diseases.

The clinical and topographic spectrum of cerebellar infarcts: a clinical-magnetic resonance imaging correlation study.

We studied 34 consecutive patients with non-mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical-MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.

Diagnosis of right ventricular infarction by overlap images of simultaneous dual emission computed tomography using technetium-99m pyrophosphate and thallium-201

The validity of dual energy single-photon emission computed tomography (SPECT) with technetium-99m pyrophosphate (Tc-99m PPi) and thallium-201 for the diagnosis of right ventricular (RV) infarction, and the clinical features of RV infarction, were investigated in 190 patients with acute myocardial infarction. Diagnosis of RV infarction was performed by Tc-99m PPi accumulation in the RV myocardium on thallium-201 and Tc-99m PPi overlay images at the dual SPECT with simultaneous imaging taken 2 to 9 days after the onset of myocardial infarction. Thirty RV infarctions were found among the 190 patients with left ventricular infarction (15.8%): 29 (97%) in association with the inferior and 1 (3%) with the lateral infarction. Tc-99m PPi accumulation was mostly observed in the posterior wall of the right ventricle. A total occlusion or a severe stenosis of the right coronary artery was demonstrated angiographically in 92% of the patients with RV infarction. The prevalence of RV infarctions was significantly lower in patients who achieved successful early reperfusion than in those who did not (26.7 vs 68.4%, respectively, p < 0.01). However, a successful early reperfusion therapy could not significantly decrease the rate of RV involvement in patients without significant collateral flow (p < 0.01). Thus, dual isotope SPECT with Tc-99m PPi and thallium-201 can be used as a reliable method for the diagnosis of RV infarction.

The levels of serum myoglobin in cardiac patients with elevated creatine kinase‐MB and suspected acute myocardial infarction

A monoclonal antibody enzyme immunoinhibition assay was used to quantitate serial serum myoglobin (Mb) levels in 121 patients who had > or = 5% creatine kinase-MB (CK-MB) and suspected acute myocardial infarction (AMI). Serum Mb levels higher than 0.16 micrograms/ml were considered abnormal. In 94% of these patients who were finally diagnosed with AMI, Mb levels were higher than 0.16 micrograms/ml, whereas all 30 normal control blood donors had lower Mb levels. Patients with anterior or inferior wall infarcts had higher Mb levels (> or = 0.64 micrograms/ml) than patients with lateral or subendocardial infarction. Only 68% (82/121) of patients evaluated by elevated CK-MB alone had a final diagnosis of AMI. In contrast, 94% (77/83) of patients who in addition showed elevated Mb had AMI. It is suggested that analysis of Mb levels allows a more accurate diagnosis of AMI in patients with elevated CK-MB than does reliance on CK-MB values alone.

Vimentin immunoreactivity in normal and pathological human brain tissue.

Vimentin immunoreactivity was examined in brain tissues from non-neurological and various human central nervous system disease cases. In all brain tissues examined, vimentin immunoreactivity was intensely positive in ependymal cells and subpial tissues, and weakly positive in some capillaries and some white matter astrocytes. In affected areas of Alzheimer's disease (AD), Pick's disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS) and cerebral infarction cases, numerous intensely vimentin-immunopositive astrocytes of both protoplasmic and fibrous morphology were demonstrated. A few such astrocytes were also observed in Parkinson's disease and progressive supranuclear palsy. ALS, MS and infarction brains also had numerous, strongly vimentin-positive, round and fat-laden microglia/macrophages. In AD and ALS, a few reactive microglia with irregularly enlarged shapes were vimentin positive. In AD, they were almost exclusively related to senile plaques.

The relationship between 1-year mortality and infarct location in patients with non-Q wave myocardial infarction

The association between 1-year mortality and infarct location was evaluated in 544 patients with acute non-Q wave myocardial infarction. Infarcts were anterior (alone or including other locations) in 51.1% ( n = 278) of cases, localizable but not anterior 29.6% ( n = 161) of the time, and nonlocalizable in 19.3% ( n = 105) of patients. One-year actuarial mortality (73 deaths) was 16.9% in the anterior group, 13.3% in the nonanterior group, and 6.8% in nonlocalizable patients ( p = 0.037). Anterior and localizable nonanterior mortality were similar ( p = 0.367). However, there were differences when mixed location infarcts were excluded. Mortality in the inferior infarction only group (2.8%, n = 36) was less than in the lateral infarction only group (16.8%, n = 79, p = 0.041) and almost significantly less than in the anterior only group (15.1%, n = 62, p = 0.064). The positive prognosis in the inferior infarction only group may be associated with the low rate of ST depression among these patients compared with those with other infarct locations ( p < 0.0001). Mortality among localizable infarcts (15.5%) was greater than among those that were nonlocalizable (6.8%, p = 0.021). Despite the low overall risk of the nonlocalizable infarcts, 41.9% ( n = 44) of these patients developed at least one important risk factor while in hospital. We conclude that among patients with relatively small non-Q wave myocardial infarction: (1) anterior mortality is similar to localizable nonanterior mortality; (2) inferior only infarcts have a better prognosis than infarcts with other non-mixed locations; (3) infarct localizability implies increased risk; and (4) nonlocalizable infarcts define a heterogeneous group among which a substantial proportion will develop in-hospital risk factors that are associated with decreased survival.

Ocular tilt reaction following lateral pontomedullary infarction

Ocular tilt reaction following lateral pontomedullary infarction

Detection and localization of prolonged epicardial electrograms with 64-lead body surface signal-averaged electrocardiography.

Prolonged, fractionated ventricular electrograms often are detectable after myocardial infarction and are a marker for an arrhythmia-prone state. QRS late potentials detected on the body surface with signal-averaged electrocardiography (SAECG) are thought to arise from the diseased tissue that generates prolonged ventricular electrograms and as such are also a marker for arrhythmias. A limitation of the current SAECG technique is that recordings are obtained from only three bipolar lead pairs. Because late potentials probably arise from multiple small sources in the heart, more extensive sampling of the body surface may contribute additional information to the SAECG: The present study investigates the additional sensitivity of SAECG using 64 body surface leads in detecting prolonged epicardial electrograms and examines its use in determining the epicardial location of prolonged electrograms. Dogs were studied before and 5-10 days after either lateral left ventricular (n = 13) or right ventricular (n = 8) myocardial infarction. Greater prolongation of signal-averaged QRS duration was detected with 64-lead SAECG (postinfarction QRS duration, 100.3 +/- 16.3 msec) than with three-lead SAECG (postinfarction QRS duration, 89.4 +/- 10.1, p = 0.0005). Nineteen of the 21 dogs (90%) had prolonged epicardial electrograms detected over the infarct. The correlation between epicardial electrogram duration and signal-averaged QRS duration calculated from individual leads was much better for 64-lead SAECG (r = 0.88, p less than 0.0001) than for three-lead SAECG (r = 0.53, p = 0.01), and the difference was most marked in cases with longer electrogram durations (more than 100 msec). Local late potential maxima on the thorax after lateral left ventricular infarction were located to the left and inferior compared with those after right ventricular infarction (p = 0.006). SAECG with more extensive recording from the body surface using 64 leads detects greater QRS prolongation than three-lead SAECG, and the longer QRS durations detected correspond to the duration of prolonged epicardial electrograms. Body surface location of late potentials corresponds to the epicardial location of the prolonged electrograms. This application of body surface mapping techniques to SAECG may permit more sensitive detection of arrhythmia-prone states and may aid in identifying arrhythmia sources.

Thrombolytic Therapy Within One Hour of the Onset of Acute Myocardial Infarction

Between 1986 and 1988, 239 consecutive patients with acute myocardial infarction received thrombolytic therapy up to 285 minutes after onset of symptoms; in 39 (17 with anterior infarction, 21 inferior, one lateral infarction) recombinant tissue plasminogen activator or anistreplase was administered a mean of 51 minutes (range 20-60 minutes) after the onset of symptoms. The patency rates (26 of 30; 87 per cent), rapid ST segment resolution (36 of 38; 95 per cent) and QRS score of less than or equal to 3 (28 of 38; 74 per cent) were statistically significantly higher for those seen and treated in the first hour in comparison with those seen and treated later. For those treated within the first hour mean peak creatine kinase was 1264 U/l for those with TIMI grade 2 or 3 (partial or complete perfusion) compared with 3005 U/l for those with TIMI grade 0 or 1 (no perfusion or penetration without perfusion) (p = 0.02): mean peak creatine kinase-MB for those with TIMI grade 2 or 3 perfusion was 115 U/l compared with 312 U/l for those with TIMI grade 0 or 1 (p = 0.01). Four of the 39 patients developed ventricular fibrillation following thrombolytic therapy, three within 24 hours of infarction and one following reinfarction on day 15. There were no significant bleeding complications. One patient died. Thrombolytic therapy within 1 hour of the onset of symptoms led to a very high angiographic patency rate, rapid ST segment resolution with preservation of left ventricular function. This therapy is without significant complications.

Transient retrocochlear low‐frequency sensorineural hearing loss: A new clinical entity

Sensorineural hearing loss (SNHL) of varying types and extent developed in a number of the 963 patients who underwent microvascular decompression for hemifacial spasm. Fourteen of the patients with hearing loss had transient low-frequency SNHL. Low-frequency SNHL is seldom noted in patients with retrocochlear hearing loss, but five of these patients had Horner's syndrome or bulbar palsy. The results of Békésy audiometry, auditory brainstem response, and electrocochleography in the patients were also suggestive of brainstem pathology. Surgical records revealed that all of them had excessively short perforating arteries surrounding the entry zone of nerves VII and VIII, so that they had to be stretched during surgery. Occlusion of perforating arteries is suspected to have caused lateral brainstem infarction around the entry zone of nerves VII and VIII, and resulted in low-frequency SNHL.

Postinfarction rupture of the left ventricular free wall: Clinicopathologic correlates in 100 consecutive autopsy cases

Among 100 consecutive autopsied cases of postinfarction rupture of the left ventricular free wall, 51% of the deaths were inhospital and 49% were out of hospital. There were 51 men (mean age, 72 years) and 49 women (mean age, 76 years); 81% had multivessel disease. All had severe obstruction of at least one major epicardial coronary artery (98 atherosclerotic, one thrombotic, and one embolic). Acute coronary thrombosis was present in 73 cases and occurred on an atherosclerotic plaque in 72, 49 (68%) of which had associated plaque rupture. In 83 cases, the ruptured infarction represented the subject's first myocardial infarction. Despite a history of hypertension in 55 cases, appreciable left ventricular hypertrophy was observed in only 19 cases. By histopathologic age of infarction, 13 ruptures occurred during the first day, 45 between days 2 and 5, and 22 on days 6 and 7; thus, 58% occurred within 5 days and 80% within 7 days. The midventricle was the most frequent site of rupture (66%). Ruptures most frequently involved thelateral aspect of the left ventricular free wall (44%). In 66 cases, the rupture tract occurred along the interface between viable and necrotic myocardium. Our findings support the observations of others that the risk factors for postinfarction left ventricular free wall rupture include age greater than 60 years, female gender, preexisting hypertension, absence of left ventricular hypertrophy, first myocardial infarction, and midventricular or lateral wall transmural infarctions.

Social outcome related to cognitive performance and computed tomographic findings after surgery for a ruptured intracranial aneurysm

A series of 83 patients was examined with a battery of cognitive tests, a clinical interview, and computed tomography 1 year after surgery for a ruptured intracranial aneurysm. Disability on the Glasgow Outcome Scale (33%), failure to return to work (25%), impaired social relations (25%), and subjective or clinical mental impairment (56%) were found to be related to each other and to poor performance on cognitive tests, especially to verbal impairments in patients with left lateral infarctions and to memory deficits and cognitive inflexibility in patients with frontal medial infarctions. Furthermore, cognitive deficits and poor outcome were associated with diffuse brain damage. Depression and anxiety were unrelated to test performances, but were frequently reported by patients with right lateral infarctions.

Social Outcome Related to Cognitive Performance and Computed Tomographic Findings after Surgery for a Ruptured Intracranial Aneurysm

Abstract A series of 83 patients was examined with a battery of cognitive tests, a clinical interview, and computed tomography 1 year after surgery for a ruptured intracranial aneurysm. Disability on the Glasgow Outcome Scale (33%), failure to return to work (25%), impaired social relations (25%), and subjective or clinical mental impairment (56%) were found to be related to each other and to poor performance on cognitive tests, especially to verbal impairments in patients with left lateral infarctions and to memory deficits and cognitive inflexibility in patients with frontal medial infarctions. Furthermore, cognitive deficits and poor outcome were associated with diffuse brain damage. Depression and anxiety were unrelated to test performances, but were frequently reported by patients with right lateral infarctions.