Chronic Ischemic Changes Research Articles

Cefepime-induced encephalopathy without renal impairment

Cefepime is an extended-spectrum, fourth-generation cephalosporin that has been widely used for approved indications such as febrile neutropenia. Common adverse events of cefepime include headache, skin rash, gastrointestinal problems, and fever. However, encephalopathathy caused by cefepime has been sporadically reported worldwide over the last decade. We experienced a rare case of cefepime-induced encephalopathy. A 75-year-old man with a 30-year history of chronic obstructive pulmonary disease was admitted to the medical intensive care unit under a diagnosis of pneumonia. Initial antibiotic therapy was started with piperacillin/sulbactam and ciprofloxacin. His condition was improved with this treatment. About 2 months later, his condition was aggravated again, with mild fever and purulent sputum. Intravenous cefepime was selected on the basis of antibiotic susceptibility to Pseudomonas aeruginosa isolated from his sputum. However, his mentality became drowsy 48 hours after cefepime adminstration. He showed tremors and right facial paralysis. Neurologic examination for motor power and sensory function revealed normal findings. Laboratory tests, including serum electrolytes, glucose, osmolality, and ammonia, gave normal results. Brain magnetic resonance imaging showed chronic ischemic and atropic changes, and an electroencephalography revealed triphasic waves. The administration of cefepime was stopped, and his symptoms started to improve within 48 hours. Electroencephalography results became normalized, and he completely recovered within 48 hours after discontinuation of cefepime. (Allergy Asthma Respir Dis 2014;2:213-217)

Letter by Pescini et al Regarding Article, “Peripheral Artery Disease as a Manifestation of Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) and Practical Implications”

We read with interest the case report by Briceno et al,1 describing a 48-year-old man who was diagnosed with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) based on a skin biopsy after the disease was suspected because of migraine, dementia, a positive family history for cognitive decline, and chronic ischemic changes on brain MRI. Genetic testing was not reported. The patient developed dry gangrene of the right …

Vascular burden in acute stroke: An MRI study

Background: Intracranial atherosclerotic disease (ICAD) is the most common mechanism of ischemic stroke worldwide, particularly among Asians. Magnetic resonance angiography (MRA) is a reliable modality for diagnosis. Utilizing magnetic resonance imaging (MRI) as the primary neuroimaging tool for all patients with suspected acute stroke, we prospectively evaluated the association of acute stroke with background ICAD, chronic microvascular ischemic changes (CMI) and microhemorrhages (MH).

Peripheral Artery Disease as a Manifestation of Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy (CADASIL) and Practical Implications

48-year-old white man was seen in November in the emergency room of a county hospital in Houston with cold blue toes on both feet after exposure to temperatures that were above freezing, and with no snow on the ground. Besides the blue toes, the foot pulses were diminished. The skin over the feet was intact. An arteriogram revealed the absence of flow in multiple digital arteries (Figure 1). Subsequently over the following 2 months, the worst affected toes developed dry gangrene (Figure 2).One month earlier, in October, the patient had been admitted to the same hospital with migranous headaches and memory loss. He had severe dementia on cognitive testing, ataxia, and resting tremors. He had mildly impaired renal function that reversed with hydration. We noted transient, easy to control hypertension and asymptomatic bradycardia. A 12-lead ECG showed sinus bradycardia with no evidence of conduction pathway abnormalities or ongoing acute ischemia (Figure 3). A pharmacological stress test suggested nonreversible single vessel disease in the right coronary artery territory. MRI of the brain showed chronic ischemic changes involving the watershed areas of the frontal and the parietal lobes (Figure 4). On direct questioning, the patient recalled a half-brother who volunteered that they shared the same father, also with severe dementia.With this history of a familial dementia, and ruling out other commoner causes of dementia, a skin biopsy was performed. Electron microscopy showed granular osmiophilic material, confirming the diagnosis of cerebral autosomal dominant arte-riopathy with subcortical infarcts and leukoencephalopathy (CADASIL; Figure 5).At 3 months follow-up after the first encounter, the patient was still severely demented and with dry gangrene of the right 1st through 3rd toes. Unfortunately, he left unannounced from a personal care home before completion of the process of making him a ward of state.

Reversible Confluent Deep White Matter Abnormalities: A New Variant of Posterior Reversible Encephalopathy Syndrome

We describe a confluent deep white matter abnormalities variant of PRES, further strengthening the notion that PRES is a disorder of radiological heterogeneity. We present 2 cases of PRES with findings of diffuse but reversible vasogenic edema located in the deep periventricular white matter regions of bilateral hemispheres without a clearly posterior distribution. We feel that this represents a rare variant of PRES on imaging, thus adding to the existing radiological spectrum for this entity. Both of our patients presented with malignant hypertension (mean arterial blood pressure of 200 mmHg) and developed neurological symptoms that included encephalopathy, seizure, headache, and vision changes. Additionally, both patients presented with significant subcortical white matter edema that improved dramatically on follow-up imaging. The clinical and radiological improvement in both patients occurred following successful blood pressure management. It is possible that the deep white matter changes of PRES are seen exclusively in the setting of severe accelerated hypertension. Our case reports reveal that, in patients with hypertensive encephalopathy, a deep white matter pattern of diffuse signal changes may not necessarily indicate chronic ischemic changes and follow-up imaging studies are essential to rule out a diagnosis of PRES.

A vascular approach to mild amnestic cognitive impairment: a pilot study

Mild cognitive impairment (MCI) is a subtle memory disorder not matching criteria for dementia. There is evidence for vascular comorbidity in several types of dementia. We hypothesized that neurovascular workup would detect a high degree of vascular disease in patients with MCI. In cooperation with our memory clinic, patients with amnestic MCI were referred to our department for neurovascular investigation. The workup encompassed ultrasound examination with carotid duplex including Intima-Media-Thickness (IMT) measurement, and transcranial Doppler (TCD) including one-hour microemboli monitoring, cerebrovascular reactivity measurement and Bubble test. Cerebral MRI for the evaluation of vascular and white-matter lesions, brain atrophy, hippocampal volumes, and amyloid angiopathy was performed. Ten patients were included. Vascular risk factors were present in six patients. Four patients had atherosclerotic lesions, three classified as mild, and one as moderate carotid stenosis. IMT > 1 mm was found in two patients, with a maximum IMT of 1.11 mm. None of the patients with acceptable bone window had intracranial stenosis in TCD. Vasoreactivity was pathologically low in one patient. Permanent right-left shunt was found in three patients, of which one showed spontaneous cerebral microembolism. Hippocampal volume reduction and cortical atrophy were found in four patients. Chronic ischemic changes in MRI were present in one patient, and three patients had subcortical infarctions. Cortical infarctions, microbleeds, or amyloid angiopathy were not found. Pure amnestic MCI is probably less associated with cerebrovascular disease and may be more consistent with evolving Alzheimer's disease. However, vascular risk factors are common in these patients.

Left-sided ventricular cardiomyopathy with minimal right ventricular involvement

Left-sided ventricular arrhythmogenic cardiomyopathy is rare and represents a rather different expression of the arrhythmogenic right ventricular (RV) cardiomyopathy (ARVC). Among sudden cardiac deaths, ARVC plays a significant role. ARVC is considered as a cardiomyopathy of unknown aetiology that primarily involves the right ventricle (RV) and is characterized by progressive replacement of myocytes by fibro-fatty tissue, complicating a spectrum of arrhythmias. Predominant ARVC with left ventricular (LV) involvement is also reported. The LV variant of arrhythmogenic cardiomyopathy with minimal or no RV involvement is rare. A 31-year-old previously healthy young man, without a significant family history, was found dead in bed. Autopsy revealed an enlarged heart and asymmetrical LV hypertrophy with widely patent coronary arteries. LV myocardium demonstrated evidence of prominent epicardial fibro-fatty tissue that is predominantly fatty in nature and infiltrates into the myocardium. Microscopy of the LV free wall showed fibro-fatty tissue infiltration into the epicardial aspect of the LV that extends well into the mid-myocardium. A moderate to marked degree of interstitial fibrous tissue deposition was noted about adipocytes and cardiomyocytes. There was no evidence of chronic ischaemic changes or of significant myofibre disarray. The RV showed minimal fibro-fatty infiltration with normal myocytes. This report highlights a rare case which confirms previous observations that the LV variant of arrhythmogenic cardiomyopathy could occur with minimal or no involvement of the RV. Further studies are required in this context to elicit the spectrum and the exact nature of this disease.

Treatment Efficacy in Vertebrobasilar Transient Ischemic Attacks Presenting as Isolated Vertigo: A Retrospective Case Study

Background: Vertigo without other neurological symptoms is usually not supposed to be due to a vascular cause. How-ever, hypoperfusion of the anterior cerebellar artery can lead to ischemia of the vestibular labyrinth and/or vestibular nuclei in the pontomedullary region whereas hypoperfusion of the posterior cerebellar artery can cause ischemia of the vestibulocerebellum, all resulting in isolated vertigo. Methods: We retrospectively reviewed the clinical records of pa-tients with vertebrobasilar ischemic attacks referred to our outpatient dizziness clinic during the years 1999-2009. Pa-tients who presented only with vertigo (+/– vomiting and unsteadiness) were selected. Their clinical data, findings and treatment responses were recorded. Results: Amongst about one hundred patients with vertebrobasilar TIA we found 24 patients with monosymptomatic presentation. Their mean age was 67.3 years, fifteen were men. In most of the patients the vertigo attacsk were multiple and lasted from minutes to hours. All but four patients had at least one vascular risk factor at the time of presentation ,among them 13 had multiple vascular risk factors. Seven patients had evidence of chronic ischemic changes on brain CT or MRI .Aspirin (100 - 325 mg/die) was started in 15 patients. Three patients were started on clopidogrel (75 mg/die) because of aspirin intolerance and two patients on warfarin due to atrial fibrilla-tion. In two patients who were treated with aspirin prior to their vertigo attack, clopidogrel or dipyridamol were added. The mean time period from first attack to treatment initiation was 5.2 months. The mean follow up period was 27.4 months. In 18 patients the attacks have completely resolved after treatment initiation. Three patients had further vertigo attacks despite treatment. Two patients with vertigo episodes where a vascular etiology was not suspected, developed later an ischemic stroke in the vertebrobasilar territory (anterior cerebellar artery and vertebral artery infarct). Conclusions: The differential diagnosis of a vertigo attack presenting in a monosymptomatic form should include vertebrobasilar TIA, especially in individuals with vascular risk factors. In view of lack of a specific test for establishing the diagnosis antiplatelets should be administered on empirical grounds since early administration of therapy can abolish further attacks and prevent a vertebrobasilar stroke. Warfarin should be preserved for patients with cardiac conditions that warrant antiocoagulation for stroke prevention.

A comment on impaired peri-nidal cerebrovascular reserve in seizure patients with brain arteriovenous malformations

Sir, We read with great interest the article by Fierstra et al . (2011), recently published in your journal. This article reopens the debate regarding the unsolved problem of the origin of seizures in patients with brain arteriovenous malformations, the pathophysiology of which remains poorly understood. Although angiographic studies have shown some associations between different brain arteriovenous malformation angioarchitectural features and epilepsy, they have not elucidated the underlying pathophysiology (Turjman et al ., 1995 a , b ; Hoh et al ., 2002). Similarly, MRI studies have often shown gliosis and chronic ischaemic changes in peri-nidal tissue as well as in remote regions, but any significant correlation has been demonstrated between extent of gliosis and clinical symptoms (Essig et al ., 2000). The main pathophysiological hypotheses to date include: (i) focal cerebral ischaemia attributable to a steal phenomenon as described by Spetzler et al . (1992) and Taylor et al . (2002); (ii) gliosis, demyelination and haemosiderin deposits in peri-nidal tissue; and (iii) secondary epileptogenesis in ipsilateral temporomesial cortex (Yeh et al ., 1990), or at a distant site, attributable to a ‘kindling’ phenomenon, in which epileptic discharges are enhanced by excitatory synaptic connections from brain arteriovenous malformations (Hoh et al ., 2002). Bleeding was deemed responsible for triggering seizure activity by Turjman et al . (1995 a ) and Stein and Wolpert (1980); in contrast, in the study by Hoh et al . (2002), intracranial haemorrhage was not a statistically significant factor associated with epilepsy. Fierstra et al . (2011) studied in vivo the possible haemodynamic effect …

Homozygous mutation in SAMHD1 gene causes cerebral vasculopathy and early onset stroke

We describe an autosomal recessive condition characterized with cerebral vasculopathy and early onset of stroke in 14 individuals in Old Order Amish. The phenotype of the condition was highly heterogeneous, ranging from severe developmental disability to normal schooling. Cerebral vasculopathy was a major hallmark of the condition with a common theme of multifocal stenoses and aneurysms in large arteries, accompanied by chronic ischemic changes, moyamoya morphology, and evidence of prior acute infarction and hemorrhage. Early signs of the disease included mild intrauterine growth restriction, infantile hypotonia, and irritability, followed by failure to thrive and short stature. Acrocyanosis, Raynaud's phenomenon, chilblain lesions, low-pitch hoarse voice, glaucoma, migraine headache, and arthritis were frequently observed. The early onset or recurrence of strokes secondary to cerebral vasculopathy seems to always be associated with poor outcomes. The elevated erythrocyte sedimentation rate (ESR), IgG, neopterin, and TNF-α found in these patients suggested an immune disorder. Through genomewide homozygosity mapping, we localized the disease gene to chromosome (Chr) 20q11.22-q12. Candidate gene sequencing identified a homozygous mutation, c.1411-2A > G, in the SAMHD1 gene, being associated with this condition. The mutation appeared at the splice-acceptor site of intron 12, resulted in the skipping of exon 13, and gave rise to an aberrant protein with in-frame deletion of 31 amino acids. Immunoblotting analysis showed lack of mutant SAMHD1 protein expression in affected cell lines. The function of SAMHD1 remains unclear, but the inflammatory vasculopathies of the brain found in the patients with SAMHD1 mutation indicate its important roles in immunoregulation and cerebral vascular hemeostasis.

Brief Manic Episode After Rituximab Treatment of Limbic Encephalitis

Brief Manic Episode After Rituximab Treatment of Limbic Encephalitis

Chronic Liver Failure and Progressive Neurologic Decline due to Mitochondrial Depletion

Purpose: A 43-year-old African American female presented to the GI Clinic for follow-up of chronic liver disease after a prolonged hospitalization for neurologic complaints of vision disturbance, transient left-sided facial droop, left-sided weakness, and dysphagia. She experienced cognitive deficits, which improved over time. Past medical history includes chronic liver disease with a biopsy in 2002 consistent with small duct sclerosing cholangitis, history of esophageal varices with banding, hepatic and metabolic encephalopathy, achalasia status post multiple Botox injections and Heller Myotomy, chronic pelvic pain, depression. She does not smoke or drink. She has had multiple abdominal surgeries. Family history is outlined in the pedigree as shown in Figure 1. The patient uses a wheelchair and speaks slowly and softly, though coherently. She has external ophthalmoplegia with marked strabismus, as demonstrated in Figure 2. Abdomen reveals multiple healed surgical scars and is diffusely tender to palpation, no ascites. Neurological exam reveals generalized weakness. Pertinent labs include WBC 2.3, Hgb 8.7, Plt 68, T bili 1.6, INR 1.3. Creatinine 0.7. MELD 11. A liver biopsy from 2002 shows features of chronic cholestasis with portal fibrosis, ductal proliferation, periductal fibrosis and loss of some bile ducts. MRCP reveals poor visualization of the intrahepatic ductal system and a 9 mm CBD without filling defect. MRI of the brain reveals Manganese deposition in the basal ganglia, abnormal signal intensity in the splenium of the corpus callosum and minimal gliotic or small vessel chronic ischemic changes involving the cerebral white matter. Genetic studies for mitochondrial disorders detected a heterozygous novel variant in the DNA polymerase gamma 1 gene (POLG1), c.1837C>T (p. H613Y). There were a total of 7 heterozygous DNA polymorphisms identified, including the novel variant, H613Y, in exon 9 of this gene. Family member studies of our patient's sister (her deceased affected nephew's mother) for this variant was negative. Further testing for mitochondrial depletion on repeat liver biopsy were declined by the patient, and no other family members would consent to genetic analysis. This case represents a complicated mixture of chronic liver disease, neurologic manifestations, and a complex family history of liver disease. Genetic testing in this patient's case is abnormal, but not diagnostic. However, the conglomeration of findings including hepatic encephalopathy, liver failure, chronic progressive external ophthalmoplegia, and abnormal neurologic features suggestive of metabolic stroke with an abnormal MRI, are strongly suggestive of a mitochondrial syndrome.

Methanol Intoxication

The nervous system has increased susceptibility for methanol intoxication. The aim of this study is to investigate various central nervous system lesions of methanol intoxication in 17 cases autopsied in the mortuary department of the Council of Forensic Medicine in Istanbul, Turkey. The reasons of methanol intoxication in the cases was likely the unwitting ingestion of methanol while drinking illegal alcohol. Survival times ranged from several hours to days. In 8 cases (47%), cerebral edema and in 9 cases (53%) at occipital, temporal and parietal cortex, basal ganglia and pons, petechial bleeding was observed. In addition to these findings, hemorrhagic necrosis were observed in thalamus, putamen, and globus pallidus in 5 cases (29.4%) and, in cerebral cortex in another 3 cases (17.6%). In 3 of the cases (17.6%) in which cerebral edema was found, herniation findings accompanied to the situation and in 2 cases (11.7%), pons bleeding was observed. Around the basal ganglia, in 2 of the cases with hemorrhagic necrosis, the situation ended with a ventricular compression. In 7 cases (41%), the associated findings of chronic ischemic changes in cortical neurons, lacunae formation, degeneration of granular cell layer of the cerebellum, and reactive gliosis were considered as the results of chronic alcoholism.

Altered mental status in a case of multiple myeloma not related to a metabolic cause.

Sir, Altered mental status (AMS) in a patient with multiple myeloma (MM) is generally attributed to uremia, hypercalcemia, hyperviscosity and/or increased serum ammonia. We present an unusual case of altered mental status that could not be attributed to metabolic encephalopathy. Our patient was a 68-year-old African American male who was admitted for AMS. The patient was asymptomatic 1 week prior to admission. On examination, no focal neurologic deficit other than altered sensorium was found. The rest of his physical examination was normal. Routine laboratory analysis revealed elevated BUN of 58 mg/dl (7–25 mg/dl), creatinine of 4.9 mg/dl (0.7–1.4 mg/dl), calcium of 12.1 mg/dl (8.5–10.3 mg/dl), total protein of 9.6 g/ dl (5.5–9 g/dl) and serum ammonia of 65 mcg/dl (35–65 mcg/dl) with normal liver function tests. A toxicology screen was negative. Intravenous hydration with normal saline was initiated. Magnetic resonance imaging (MRI) of brain showed chronic microvascular ischaemic changes with no acute infarct. On cerebrospinal fluid (CSF) analysis, he was found to have elevated protein of 172 g/dl (15–45 g/dl), no pleocytosis and a negative gram stain. Polymerase chain reaction on CSF for herpes simplex was negative. Electroencephalogram (EEG) showed no seizure activity. Though all metabolic parameters normalized by the third day (creatinine of 1.3 mg/dl and calcium of 9.3 mg/dl), there was no improvement in his sensorium. To rule out paraneoplastic syndrome of unknown aetiology, a whole body CT scan was done. It showed a soft tissue mass in the pre-sacral area with multiple diffuse lytic bone lesions. The bone marrow was diagnostic for plasma cell myeloma. Serum immunofixation revealed 5050 mg/dl (700–1600 mg/dl) of monoclonal IgG. The serum viscosity was normal. A repeat lumbar puncture revealed a CSF with negative cytology, but abnormal bands of high intensity in the immunoglobulin region identical to the serum electrophoresis pattern. Four days after the normalization of all his metabolic parameters, there was still no improvement in his sensorium. The patient was started on intravenous dexamethasone for MM. After the first cycle, his sensorium returned to normal. The most common cause of AMS in a patient with MM and acute renal failure (ARF) is metabolic encephalopathy. Though rare, direct invasion of CNS by the myeloma cells has been reported. Currently, 70 cases of leptomeningeal myelomatosis (LMM) and intraparenchymal plasmacytoma have been published [1,2]. Schluterman et.al. published a case series of 23 patients. They were diagnosed up to 29 months (median, 13 months) after the initial diagnosis of MM. The presenting symptom in 65% of the patients was AMS. The CSF analysis revealed pleocytosis and/or increased protein (generally >100 g/dl) similar to our case. CSF cytology showed myeloma cells; however, it was negative in 4 out of the 23 patients at initial presentation. Unlike our patient, cranial leptomeningeal contrast enhancement was seen on MRI in as many as 70% of the cases. Our patient did not fulfil all the diagnostic criteria of LMM but did have a dramatic recovery of his sensorium after the first cycle of dexamethasone therapy. His altered mental sensorium may represent a paraneoplastic manifestation of MM or alternatively, the patient falls into the spectrum of disease activity before fully evolved LMM. He was discharged from the hospital and was referred to an oncologist for further management of MM. In conclusion, altered mental status in a patient with multiple myeloma may be due to a paraneoplastic manifestation of MM or due to direct invasion of the CNS by myeloma cells. Intrathecal chemotherapy should be used for patients that meet the diagnostic criteria of LMM. However, even those who do not may still show a significant improvement in their neurologic status after treatment with intravenous dexamethasone. Conflict of interest statement. None declared.

Computed Tomography Imaging in the Management of Headache in the Emergency Department: Cost Efficacy and Policy Implications

To evaluate the economic impact and diagnostic utility of computed tomography (CT) in the management of emergency department (ED) patients presenting with headache and nonfocal physical examinations. Computerized medical records from 2 major community hospitals were retrospectively reviewed of patients presenting with headache over a 2.5-year period (2003-2006). A model was developed to assess test outcomes, CT result costs, and average institutional costs of the ED visit. The binomial probabilistic distribution of expected maximum cases was also calculated. Of the 5510 patient records queried, 882 (16%) met the above criteria. Two hundred eighty-one patients demonstrated positive CT findings (31.8%), but only 9 (1.02%) demonstrated clinically significant results (requiring a change in management). Most positive studies were incidental, including old infarcts, chronic ischemic changes, encephalomalacia, and sinusitis. The average cost of the head CT exam and ED visit was $764 (2006 dollars). This was approximately 3 times the cost of a routine outpatient visit (plus CT) for headache ($253). The incremental cost per clinically significant case detected in the ED was $50078. The calculated expected maximum number of clinically significant positive cases was almost 50% lower than what was actually detected. Our results indicate that emergent CT imaging of nonfocal headache yields a low percentage of positive clinically significant results, and has limited cost efficacy. Since the use of CT for imaging patients with headache in the ED is widespread, the economic implications are considerable. Health policy reforms are indicated to better direct utilization in these patients.

OP04.11: MR diagnosis of ischemia/infarct in the fetal brain; spectrum of appearance and significance of findings

Objectives: Fetal stroke is defined as fetal intracranial hemorrhage that occurs between 14 weeks of gestation and the onset of labor. It has been associated with postnatal epilepsy, mental retardation, and cerebral palsy and may be caused by antenatal ischemic, thrombotic, or hemorrhagic injury. Maternal alloimmune thrombocytopenia and trauma are common predisposing conditions, but there are many unknown risk factors. MRI can depict intracranial hemorrhage, infarct, porencephaly, cystic encephalomalacia, and ischemia. Methods: This was a retrospective, chart review of cases performed between January 1, 2000 through February 2008. A comparison of CNS findings on prenatal ultrasound and fetal MRI was performed to assess potential differences in the two imaging modalities Results: Review of fetal MRI’s revealed 23 cases of diagnosed CNS hemorrhage, ischemia, and infarcts. MRI can delineate the features and extent of the cerebral injury and can define acute and chronic ischemic changes. This is extremely important for predicting prognosis and decision making. Prior studies have shown that major destructive lesions, diffuse excessive high signal intensity within the white matter, cerebellar hemorrhage, and ventricular dilatation after intraventricular hemorrhage are associated with adverse outcomes, but punctate white matter lesions, hemorrhage, or ventricular dilatation without intraventricular hemorrhage are not necessarily correlated with unfavorable results. Conclusions: We present the spectrum of CNS injury diagnosed at our institution. Accurate diagnosis of CNS injury was valuable in prenatal counseling and decision making. It is hoped that additional studies will be performed with long term outcomes assessment to assist in prognostication of fetuses diagnosed with CNS ischemia/infarct.

Incidence, Topography, Predictors and Long-Term Survival After Stroke in Patients Undergoing Coronary Artery Bypass Grafting

Previous studies on stroke after coronary artery bypass grafting (CABG) provide limited data about the timing (early vs delayed) of this event and findings of brain imaging analysis. This information is of significant importance because it provides insight into the etiology of stroke, potentially allowing the development of preventive measures. This study analyzed the incidence and timing of stroke, the topography and mechanisms of cerebral lesions, independent predictors, and late outcome after the occurrence of this complication in patients undergoing CABG. We retrospectively analyzed prospectively collected data from 2985 patients (2064 men [67%]), with a mean age of 66 +/- 11 years, who underwent CABG between January 1998 and December 2006. Stroke was defined as any new permanent focal neurologic deficit (early stroke, < or = 24 hours; delayed, > 24 hours postoperatively). The incidence of stroke was 1.6% (n = 48) and similar between conventional CABG (1.6%) and off-pump CABG (1.4%). Early stroke occurred in 25 patients (52%). Brain imaging was obtained in 44 patients (92%): 44 had computed tomography, 3 had magnetic resonance imaging. Results were positive in 33 of 44 patients (75%), showing large embolic stroke in 25 (76%), watershed in 5 (15%), and mixed pattern in 3 (9%). Chronic ischemic changes were found in 17 patients. Multivariate analysis revealed extensive aortic calcification (odds ratio [OR], 4.2), previous stroke (OR, 2.2), female sex (OR, 1.9), and congestive heart failure (OR, 2.6) as predictors of stroke. The hospital mortality rate after stroke was 16.7% (n = 8) compared with 1.5% (n = 44) in those without (p < 0.001). The mortality rate was higher in early stroke at 24% (6 of 25) compared with 9% (2 of 23) in late stroke. Survival of stroke patients was 87% at 1 year and 62% at 5 years and was significantly reduced compared with 96% and 85%, respectively, in patients without stroke (p<0.001). Most strokes after CABG occurred early after surgery. This complication is associated with an increased hospital mortality and morbidity and reduced long-term survival. The infarction type had no impact on early and late outcome. Preoperative computed tomography scan seems warranted in patients at risk and without any previous history of stroke.

Memantine in Major Depression with Catatonic Features

Memantine in Major Depression with Catatonic Features

Bilateral restricted diffusion in optic nerves as an indicator of traumatic optic neuropathy

A 20-year-old man suffered from a severe polytrauma and resultant bilateral traumatic optic neuropathy. CT imaging did not show any intraparenchymal injury affecting the visual system. MR examination performed 2 weeks after trauma showed a severe reduction of apparent diffusion coefficient (ADC), suggesting optic nerve ischemia. The patient was discharged with permanent bilateral blindness as post-traumatic sequela. Follow-up MRI 16 months following injury demonstrated bilateral optic nerve atrophy and increased ADC compatible with chronic ischemic changes. This case shows that diffusion-weighted imaging in traumatic optic neuropathies may be of importance for diagnosis and therapeutic intervention.

Is Right Coronary Artery Hypoplasia and Sudden Death an Underdiagnosed Association?

Determining whether hypoplasia of a coronary artery has caused or contributed to death is often complicated by an absence of histologic evidence of myocardial ischemia in the area of the heart supplied by the affected artery and also by the lack of data for assessing coronary artery size at autopsy. A 45-year-old woman is reported who collapsed and died and who was found at autopsy to have a dominant, small-caliber, right coronary artery, with acute and chronic ischemic changes in the posterior interventricular septum supplied by the diminutive vessel. This case provides evidence that small-caliber coronary arteries may be associated with a lethal outcome. Given the difficulties that may occur in determining whether there is a causal link between small coronary artery caliber and death, it is possible that this may be an underdiagnosed cause of sudden cardiac death, rather than a coincidental finding of minimal significance.