Focal Cerebral Lesions Research Articles

Cognitive function after transapical aortic valve implantation: a single-centre study with 3-month follow-up

Reports on adverse neurological events following transcatheter aortic valve implantation (TAVI) have focused on strokes, while more subtle postoperative cognitive decline has not yet been systematically investigated. In this study, we prospectively examined neurological and cognitive outcomes in patients undergoing transapical (TA) and surgical aortic valve replacement (AVR). A total of 64 patients with severe symptomatic aortic stenosis were investigated between January 2008 and July 2009. Clinical neurological examination and comprehensive neuropsychological testing were performed before and after the procedure, at discharge and at 3-month follow-up. Diffusion-weighted magnetic resonance imaging (DW-MRI) was applied to detect morphological brain injury. TA-TAVI patients (n = 27) were older and at higher surgical risk compared with surgical AVR patients (n = 37; mean age 82.2 ± 4.7 vs 67.5 ± 8.9 years; log EuroSCORE 36.4 ± 13.2 vs 2.6 ± 8.5%, both P <0.001). There was one stroke in each group (3.7 vs 2.7%, P = 0.49), both classified as embolic based on imaging characteristics. After TA-TAVI, cognitive tests showed no decline during follow-up, while, after AVR, 7 of 11 tests showed a decline early after surgery. Similarly, with-in patient analysis showed that the rate of individuals with clinically relevant cognitive decline was increased early after AVR (TA-TAVI vs AVR: 18 vs 46% at discharge [P = 0.03]; 28 vs 6% at 3 months [P = 0.04]). New focal ischaemic cerebral lesions were detected on DW-MRI in 58% (7 of 12) of patients after TA-TAVI vs 34% (12 of 35) after AVR (P = 0.13). The number of brain lesions per patient and cumulative embolic load per patient were similar between groups. An association between postoperative cerebral ischaemia and cognitive dysfunction was not found (odds ratio 2.37, 95% confidence interval 0.05-113.75, P = 0.66). Cognitive function was only mildly impaired after TA-TAVI when compared with a marked, albeit transient, decline after surgical AVR. Focal embolic brain injury tended to occur more frequently after TA-TAVI, but this was not related to cognitive decline during the 3-month follow-up.

CRASH-2 (Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage) intracranial bleeding study: the effect of tranexamic acid in traumatic brain injury, a nested randomised, placebo-controlled trial.

Tranexamic acid (TXA) has been shown to reduce blood loss in surgical patients and the risk of death in patients with traumatic bleeding, with no apparent increase in vascular occlusive events. These findings raise the possibility that it might also be effective in traumatic brain injury (TBI). The Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage Intracranial Bleeding Study (CRASH-2 IBS) was conducted to quantify the effect of an early short course of TXA on intracranial haemorrhage and new focal cerebral ischaemic lesions in patients with TBI. CRASH-2 IBS was a prospective randomised controlled trial nested within the CRASH-2 trial. Randomisation was balanced by centre, with an allocation sequence based on a block size of eight. We used a local pack system that selected the lowest numbered treatment pack from a box containing eight numbered packs. Apart from the pack number, the treatment packs were identical. The pack number was recorded on the entry form, which was sent to the international trial co-ordinating centre in London, UK. Once the treatment pack number was recorded, the patient was included in the trial whether or not the treatment pack was opened or the allocated treatment started. All site investigators and trial co-ordinating centre staff were masked to treatment allocation. Ten hospitals: (India) Aditya Neuroscience Centre, Sanjivani Hospital, CARE Hospital, Christian Medical College, Medical Trust Hospital, Jeevan Jyoti Hospital and (Colombia) Hospital Universitario San Vicente de Paul, Hospital Pablo Tobón Uribe, Hospital Universitario San José de Popayán and Fundación Valle del Lili. The trial was conducted in a subset of 270 CRASH-2 trial participants. Patients eligible for inclusion in the CRASH-2 IBS fulfilled the inclusion criteria for the CRASH-2 trial, and also had TBI [Glasgow Coma Scale score of ≤ 14 and a brain computerised tomography (CT) scan compatible with TBI]. Pregnant women and patients for whom a second brain CT scan was not possible were excluded. Participants were randomly allocated to receive either a loading dose of 1 g of TXA infused over 10 minutes followed by an intravenous infusion of 1 g over 8 hours or matching placebo. The primary outcome was the increase in size of intracranial haemorrhage growth between a CT scan at hospital admission and a second scan 24-48 hours later. One hundred and thirty-three patients were allocated to TXA and 137 to placebo, of whom information on the primary (imaging) outcome was available for 123 (92%) and 126 (92%) respectively. The analysis suggested that TXA was likely to be associated with a reduction in haemorrhage growth [adjusted difference -3.8 ml, 95% credibility interval (CrI) -11.5 ml to 3.9 ml], fewer focal ischaemic lesions [adjusted odds ratio (OR) 0.54, 95% CrI 0.20 to 1.46] and fewer deaths (adjusted OR 0.49, 95% CrI 0.22 to 1.06). This was the first randomised controlled study to evaluate the effect of TXA in TBI patients and it found that neither moderate benefits nor moderate harmful effects can be excluded. However, although uncertainty remains, our analyses suggest that TXA administration might improve outcome in TBI patients and provide grounds for evaluating this hypothesis in future research. Current Controlled Trials ISRCTN86750102. This project was funded by the NIHR Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 16, No. 13. See the HTA programme website for further project information.

Neuroimaging observations in a cohort of elderly manifesting with new onset seizures: Experience from a university hospital

Background:The occurrence of epilepsy is higher among elderly patients. The clinical manifestations of seizures, causes of epilepsy, and choice of anti-epileptic drugs (AEDs) are different in elderly people with epilepsy compared to the young.Aim:To evaluate the imaging (CT/MRI) observations in elderly patients manifesting with new-onset seizures.Materials and Methods:Two hundred and one elderly patients with new onset seizures, >60 years (age: 68.0 ± 7.5 years; M:F = 1.8:1) from Jan’ 07 to Jan’ 09, were prospectively recruited. Observations of cranial CT scan (n = 201) and MR imaging (n = 43) were analyzed.Results:The type of seizures included: Simple partial (42%), generalized tonic-clonic (30.3%), and complex partial (27.4%). The pattern of epilepsy syndromes were acute symptomatic (42.3%), remote symptomatic (18.4%), cryptogenic (37.8%), and idiopathic (1.5%). Seizures were controlled with monotherapy in 85%. The CT scan (n = 201) revealed cerebral atrophy (139), mild (79), moderate (43), and severe (18); focal lesions (98), infarcts (45), hemorrhages (18), granuloma (16), tumor (15) and gliosis (4), and hemispheric atrophy (1), white matter changes (75) and diffuse edema (21). An MRI (n = 43) showed variable degree of cerebral atrophy (31); white matter changes (20); focal cerebral lesions (24); - infarct (7); intracranial hemorrhage (6); granuloma (5); tumor (6); gliosis (1); hemispheric atrophy (1); and prominent Virchow-Robin spaces (7); and UBOs (12). Patients with focal lesions in neuroimaging more often had partial seizures, symptomatic epilepsy, past stroke, focal deficit, absence of diffuse atrophy, focal EEG slowing, abnormal CSF, seizure recurrence at follow-up (P < 0.05).Conclusions:Brain imaging observations in elderly patients with new-onset seizures revealed underlying symptomatic nature, hence the etiology and thereby assisted in deciding the specific therapy.

Effect of tranexamic acid in traumatic brain injury: a nested randomised, placebo controlled trial (CRASH-2 Intracranial Bleeding Study)

Objective To assess the effect of tranexamic acid (which reduces bleeding in surgical patients and reduces mortality due to bleeding in trauma patients) on intracranial haemorrhage in patients with traumatic...

Pathophysiological aspects of transient ischemic attacks

Current views of the pathophysiology of transient ischemic attacks (TIA) are based on the concept of focal cerebral ischemic brain lesions [1‐6]. Many aspects of transient focal cerebral ischemia have been studied both in carefully controlled experimental conditions and in clinical studies. At the same time, detailed pathophysiological characterization of reversible focal ischemic brain lesions represents a very complex problem. In clinical studies on patients, this is restricted by a multitude of factors which are difficult to control: the difficulty of identifying accurately the time of onset of ischemia, the heterogeneity of patients in terms of age, gender, and genetic differences, etc. Serious difficulties occur on comparison of clinical and experimental data because of anatomical, pathophysiological, genetic, and other differences between people and laboratory animals [3, 5, 7‐10]. One major point in the concept of focal cerebral ischemic brain lesions is the “ischemic cascade,” which is a chain of complex molecular genetic and biochemical derangements in brain cells occurring in response to decreases in local cerebral blood flow (CBF) which, in certain conditions, ends with irreversible structural brain damage [1, 3, 5, 11]. The sequence of steps in the “ischemic cascade” has been established: 1) a decrease in brain blood flow; 2) glutamate excitotoxicity; 3) intracellular accumulation of calcium; 4) activation of intracellular enzymes; 5) increases in nitric oxide synthesis and development of oxidant stress; 6) expression of early response genes; 7) the long-term effects of ischemia (local inflammatory reactions, microvascular lesions, damage to the blood-brain barrier); 8) apoptosis [1, 11]. The time framework of the occurrence of the steps in the “ischemic cycle” have been identified: energy deficiency in ischemic tissue occurs in the first three hours, glutamate excitotoxity occurs at 3‐6 h, and impairments to calcium homeostasis and lactate acidosis occur at one day. The long-term effects of ischemia start 2‐3 h from the onset of ischemia and reach a maximum at 12‐36 h (oxidative stress, local inflammation) and 2‐3 days (apoptosis), but persist for long periods (several months) [1, 11].

564 A Comparison of Electrographic Seizure Characteristics in Term Neonates with Hypoxic-Ischaemic Encephalopathy and Focal Cerebral Lesions

Background and aims: In term neonates with seizures, it is important to distinguish between hypoxic-ischaemic encephalopathy (HIE) and focal cerebral lesions as soon as possible to aid clinical intervention. We compared seizure onset, duration and morphology in term neonates with HIE and focal cerebral lesions.Methods: Term neonates with perinatal distress or abnormal neurology were recruited. Continuous multichannel video-EEG recording within 72 hours of birth was performed.Results: In 26 term neonates recruited, 13 had EEG seizures [HIE(n=5); focal arterial infarction(n=3); focal intraparenchymal haemorrhage(n=2); unknown pathology(n=3)]. EEG recordings commenced at a median age(range) of 6.0(1.8-59.2) hours. The median recording duration was 61.4(24.0-122.1) hours.The median seizure onset occurred earlier in HIE than in focal cerebral lesions [13.4(8.3-42.2) hours vs 38.6(18.0-59.7) hours]. The median total seizure burden per neonate with HIE was higher than in focal cerebral lesions [212.4(55.2-640.2) minutes vs 112.9(12.9-189.1) minutes]. Seizures were more frequent in HIE than in focal cerebral lesions (577 vs 113 events). Two neonates with severe HIE also had status epilepticus.Electrographic seizures in neonates with focal cerebral lesions originated from the site of injury displayed a characteristic spike wave focal morphology with minimal frequency change. Variable seizure morphologies and frequencies were seen in HIE. The background EEG activity in focal cerebral lesions was well preserved, though asymmetries were evident. The background EEG activity in HIE showed global abnormalities.Conclusions: The contrasting seizure characteristics in neonates with HIE and focal cerebral lesions may prove useful for automated seizure detection systems and guide appropriate management strategies.

Prognostic Significance of Interictal Epileptiform Discharges in Newly Diagnosed Seizure Disorders

EEGs performed for new-onset seizures show epileptiform discharge in approximately 18% to 56% of children and 12% to 50% of adults. An EEG after sleep deprivation improves detection of epileptiform abnormalities, showing discharge in 13% to 35% of patients whose standard EEG findings were normal. Some studies have also shown a higher yield with EEG performed within 24 hours after the seizure. The EEG is a useful diagnostic study in this clinical setting for a number of reasons. First, specific EEG abnormalities help characterize the seizure type and epilepsy syndrome, which allows more informed decisions regarding therapy and more accurate prediction of seizure control and ultimate remission. Second, in certain cases, the EEG may detect more subtle seizures, including absence, myoclonic, or partial seizures. Third, specific EEG patterns may alert the clinician to the presence of a focal cerebral lesion. Fourth, most studies have shown that an epileptiform discharge is predictive of seizure recurrence, particularly in patients with idiopathic epilepsy. In the presence of epileptiform discharge, the recurrence risk is approximately double what would be predicted after a normal EEG. The predictive value of nonepileptiform abnormalities is not clearly established.

Molecular diagnosis of cerebral toxoplasmosis: comparing markers that determine Toxoplasma gondii by PCR in peripheral blood from HIV-infected patients

As cerebral toxoplasmosis is the most common cerebral focal lesion in AIDS patients, this study evaluated three PCR markers for diagnosis, since some limitations remain present, such as low parasite levels in some clinical samples. The molecular markers were B22-B23 and Tg1-Tg2 (based on the B1 gene) and Tox4-Tox5 (non-coding fragment, repeated 200-300-fold). DNA samples from 102 AIDS patients with previously known diagnosis were analyzed. The cerebral toxoplasmosis group was constituted of DNA extracted from the blood of 66 AIDS patients, which was collected before or until the third day of the therapy for toxoplasmosis. DNA from the blood of 36 AIDS patients with other neurologic opportunistic infections was used as control group. Sensitivities of B22-B23, Tg1-Tg2, and Tox4-Tox5 markers were of 95.5%, 93.9%, and 89.3%, respectively. In the control group, the specificities were of 97.2% (B22-B23), 88.9% (Tg1-Tg2), and 91.7% (Tox4-Tox5). The association of at least two markers increased the PCR sensitivity and specificity. The concordance index between two markers varied from 83.3% to 93.1%. These data demonstrated that all markers evaluated here were highly sensitive for T. gondii determination, although B22-B23 has been shown to be the best. The association of two markers increases PCR sensitivity, but the procedure was more expensive and time-consuming.

Molecular diagnosis of cerebral toxoplasmosis: comparing markers that determine Toxoplasma gondii by PCR in peripheral blood from HIV-infected patients

As cerebral toxoplasmosis is the most common cerebral focal lesion in AIDS patients, this study evaluated three PCR markers for diagnosis, since some limitations remain present, such as low parasite levels in some clinical samples. The molecular markers were B22-B23 and Tg1-Tg2 (based on the B1 gene) and Tox4-Tox5 (non-coding fragment, repeated 200-300-fold). DNA samples from 102 AIDS patients with previously known diagnosis were analyzed. The cerebral toxoplasmosis group was constituted of DNA extracted from the blood of 66 AIDS patients, which was collected before or until the third day of the therapy for toxoplasmosis. DNA from the blood of 36 AIDS patients with other neurologic opportunistic infections was used as control group. Sensitivities of B22-B23, Tg1-Tg2, and Tox4-Tox5 markers were of 95.5%, 93.9%, and 89.3%, respectively. In the control group, the specificities were of 97.2% (B22-B23), 88.9% (Tg1-Tg2), and 91.7% (Tox4-Tox5). The association of at least two markers increased the PCR sensitivity and specificity. The concordance index between two markers varied from 83.3% to 93.1%. These data demonstrated that all markers evaluated here were highly sensitive for T. gondii determination, although B22-B23 has been shown to be the best. The association of two markers increases PCR sensitivity, but the procedure was more expensive and time-consuming.

Axillary artery cannulation reduces neurologic complications and clinically unapparent focal cerebral lesions

Axillary artery cannulation reduces neurologic complications and clinically unapparent focal cerebral lesions

Controlling the Volume of the Focal Cerebral Ischemic Lesion through Photothrombosis

Stroke is the third leading cause of human death. Various models have been used to study the mechanisms of tissue damage and neuronal protection. Each model has its advantages and disadvantages. Middle cerebral artery occlusion (MCAo), has been widely used, but produces large ischemic lesions of varying size, which is a disadvantage in the study of neuronal protective mechanisms. Photothrombosis provides an alternative model that can produce consistent lesion size. In this model, ischemia is induced by photo-activation of rose bengal in blood flow by green light illumination. Because ischemia can be induced while animals are kept in a stereotaxic device or on the stage of a microscope, this model has become widely used for in vivo study of cellular structure and function. In this study, photothrombosis was generated by using a wide-field epi-fluorescent microscope equipped with a metal halide lamp and ischemia was confirmed by blood flow reduction monitored by laser Doppler flowmetry. We demonstrated, by adjusting the intensity of output light and the size of irradiated area in the cortex, that the photothrombosis model can, with high reproducibility, be used to generate ischemic infarction of various sizes in mouse brains. Using immunostaining and histochemistry of brain sections, our data showed that photothrombosis induced neuronal death and that brain infarct volume was correlated with the power output and the size of irradiated area of the cortex.

Simultaneous two-voxel localized 1H-observed 13C-edited spectroscopy for in vivo MRS on rat brain at 9.4 T: Application to the investigation of excitotoxic lesions

13C spectroscopy combined with the injection of 13C-labeled substrates is a powerful method for the study of brain metabolism in vivo. Since highly localized measurements are required in a heterogeneous organ such as the brain, it is of interest to augment the sensitivity of 13C spectroscopy by proton acquisition. Furthermore, as focal cerebral lesions are often encountered in animal models of disorders in which the two brain hemispheres are compared, we wished to develop a bi-voxel localized sequence for the simultaneous bilateral investigation of rat brain metabolism, with no need for external additional references. Two sequences were developed at 9.4 T: a bi-voxel 1H–( 13C) STEAM-POCE (Proton Observed Carbon Edited) sequence and a bi-voxel 1H–( 13C) PRESS-POCE adiabatically decoupled sequence with Hadamard encoding. Hadamard encoding allows both voxels to be recorded simultaneously, with the same acquisition time as that required for a single voxel. The method was validated in a biological investigation into the neuronal damage and the effect on the Tri Carboxylic Acid cycle in localized excitotoxic lesions. Following an excitotoxic quinolinate-induced localized lesion in the rat cortex and the infusion of U– 13C glucose, two 1H–( 13C) spectra of distinct (4 × 4 × 4 mm 3) voxels, one centred on the injured hemisphere and the other on the contralateral hemisphere, were recorded simultaneously. Two 1H bi-voxel spectra were also recorded and showed a significant decrease in N-acetyl aspartate, and an accumulation of lactate in the ipsilateral hemisphere. The 1H–( 13C) spectra could be recorded dynamically as a function of time, and showed a fall in the glutamate/glutamine ratio and the presence of a stable glutamine pool, with a permanent increase of lactate in the ipsilateral hemisphere. This bi-voxel 1H–( 13C) method can be used to investigate simultaneously both brain hemispheres, and to perform dynamic studies. We report here the neuronal damage and the effect on the Tri Carboxylic Acid cycle in localized excitotoxic lesions.

Pearls &amp; Oy-sters: Selective postictal aphasia

Ictal and postictal language dysfunction is common and strongly predictive of language laterality in monolingual patients. For bilingual patients, selective dysfunction has been reported for a single language with focal cerebral lesions, electrical brain stimulation, and intracarotid sodium amytal. Two right-handed Ukrainian-English bilingual patients with left perisylvian structural lesions, late onset complex-partial seizures, and postictal aphasia for English are presented and discussed with regard to mechanisms of selective aphasia and factors contributory to language lateralization in bilingual patients. Ukrainian was the native language of both patients with English acquired after 7 years of age. Regular/video-EEG showed left temporal epileptogenesis. A 56-year-old man, who had a left hemorrhagic stroke at age 50 and had not spoken Ukrainian for 40 years, was unable to speak English for approximately 20 minutes postictally but had global preservation of Ukrainian. A 71-year-old woman, who had a left temporal epidermoid cyst and had not spoken Ukrainian since childhood, had 10- to 15-minute postictal expressive aphasia in English but not Ukrainian and preservation of comprehension in both languages. These cases are instructive and consistent with the literature on cerebral organization of language in bilingual individuals. For both patients, postictal aphasia with preservation of Ukrainian is consistent with findings from clinical and experimental studies indicating that later age of second language acquisition (>6 years) rather than language proficiency is a primary factor in language laterality. Second, global aphasia in the man with a late lesion vs expressive aphasia with preservation of comprehension of English in the woman with a prenatal/early lesion is consistent with the atypical language laterality described for individuals with left-sided lesions sustained prior to age 5. Although neither Wada test nor fMRI was done to assure left hemisphere laterality of spoken Ukrainian and English, this is probable, and the selective postictal aphasia observed for both patients is consistent with the differential intrahemispheric organization reported for the two languages of bilingual individuals. Possible mechanisms of selective postictal aphasia, e.g., active inhibition, and differences in language networks in bilingual patients are discussed.

Flow-dependent versus spreading-like impairment of brain tissue integrity during focal cerebral ischemia and its consequences for neuroprotective strategies

Focal cerebral ischemic lesions demonstrate a gradual reduction of blood flow from the rim to the core. Flow reduction induces irreversible damage in the core region, whereas more peripheral tissue, i.e. penumbral tissue, is applicable to therapeutic interventions. Secondary mechanisms for lesion growth involve excitotoxicity, extracellular ion shifts, lactate generation, tissue acidosis, inflammation, spreading depolarization and many other processes. These toxic mediators accumulate in the ischemic core and endanger the still viable rim by diffusion or other spreading-like mechanisms, probably in part largely independent from blood flow. A substantial proportion of hemodynamic penumbral tissue could be demonstrated both in experimental settings and in clinical practice, whereas the precise spatial and temporary contribution of secondary mechanisms is much more difficult to investigate in our patients. Diffusion or spreading-mediated neurotoxicity will affect a small rim around the necrotic lesion. Due to the third power of volumetric analysis this would contribute to a large amount in small experimental lesions, but to a negligible amount of tissue in large clinical lesions and could therefore explain the difference in efficacy of neuroprotective strategies between experimental and clinical setups. Therefore, we discuss the likelihood of direct flow-dependent versus diffusion- or spreading-mediated impairment of endangered tissue in focal cerebral ischemia.

Significance of Neurologic Complications in the Modern Era of Cardiac Transplantation

Severe neurologic complications after cardiac transplantation are devastating outcomes of this life-saving procedure. Incidence, risk factors, and morbidity of neurologic events in the modern era of cardiac transplantation are yet to be defined. Between 1996 and 2005, 200 patients (64% men; mean age, 49 +/- 12 years) underwent heart transplantation at our institution. Overall, 46 patients (23%) showed a wide spectra of early neurologic complications. Cause of ischemic complications was stroke in 11 patients (7 had concomitant epileptic seizures) and transient ischemic attack (TIA) in 7. Encephalopathy (n = 10), epileptic seizures unrelated to focal cerebral lesions (n = 7), severe headache (n = 6), cerebral infection (n = 3), and peripheral nervous system injuries (n = 2) completed the spectra of adverse neurologic outcomes. Multivariate analysis identified advanced age (p = 0.03), preoperative left ventricular assist device support (p = 0.02), preoperative intraaortic balloon pump support (p < 0.001), prolonged cardiopulmonary bypass time (p < 0.001), and postoperative hepatic failure (p = 0.04) as independent predictors of early neurologic complications. Postoperative morbidities associated with neurologic complications included longer ventilation time (p < 0.001), longer stay in the intensive care unit (p < 0.001), and higher incidence of pneumonia (p < 0.001) and sepsis (p = 0.01) compared with patients without neurologic events. There was a trend toward higher in-hospital mortality (15% versus 6%, p = 0.07), but there was no difference in long-term survival (65% versus 78%, p = 0.15). Despite rigorous pretransplantation screening, neurologic complications were common after cardiac transplantation. Most frequently, these complications were not the actual cause of death, but they significantly contributed to increased morbidity. Preoperative mechanical circulatory support requirement was the strongest predictor for adverse neurologic outcome.

Periodic Lateralized Epileptiform Discharges in Neurosyphilis

We report two patients of neurosyphilis with periodic lateralized epileptiform discharges (PLEDs) in the EEG. Patient 1, a 32-yr-old man manifested with rapidly progressive cognitive decline and abnormal behavior and recurrent generalized tonic-clonic seizures. EEG revealed periodic epileptiform discharges arising from the anterior temporal and frontal region, predominantly from the right. Diffusion weighted MRI of brain did not show any focal restricted diffusion. Patient 2, a 33-yr-old woman presented with 2-year history of behavioral abnormalities, generalized tonic-clonic seizures and unconcerned urinary incontinence. EEG revealed PLEDS arising from the left anterior temporal region. Her CT scan showed gross cerebral atrophy. Both the patients improved partially with treatment and PLEDs resolved completely. PLEDs may be recorded in EEG of patients with neurosyphilis without imageological evidence of focal cerebral lesion.

New-onset acute symptomatic seizure in a neurological intensive care unit

New-onset acute symptomatic seizures can be the presenting feature of acute neurological diseases. The etiological spectrum of new-onset acute symptomatic seizures and outcome may be different in developing countries when compared to developed countries. To study the clinical profile of new-onset acute symptomatic seizures as the first presenting event in patients with acute neurological illness in a neurological intensive care unit (NICU) in a developing country. Prospective study in a NICU in a tertiary care hospital. Consecutive patients with acute symptomatic new-onset seizure admitted to NICU in a tertiary care hospital over a period of 28 months. The etiology was determined by neuroimaging and appropriate investigations including cerebrospinal fluid examination. Of the 3,151 admissions, 66 (2.1%) were related to new-onset acute symptomatic seizures as the first presentation. The mean age was 49.07 + 20.20 years. Tonic-clonic, generalized tonic-clonic or partial seizure with or without secondary generalization were the seizure type. At presentation 52 (79%) patients had single seizure, 10 (15%) patients had seizure clusters and four (6%) patients presented with status epilepticus (SE). The major etiological risk factors were central nervous system (CNS) infections (32%), metabolic disorders (32%) and cerebrovascular diseases (21%). In the NICU 10 (15%) patients had early seizure recurrence and three (4.5%) developed SE. Of these 13 patients, in nine (69%) patients the pathology was infection-related and the other commonality was involvement of cortical gray matter. Factors associated with seizure recurrence or SE were focal cerebral lesions involving cortical gray matter or diffuse cerebral pathology, meningoencephalitis. In 69% of these patients the pathology was infection-related. There were only two deaths, both in patients with SE and related to the underlying etiology. The risk of seizure recurrence and SE after the first acute symptomatic seizure is likely to be high in patients with acute focal cerebral lesions and diffuse CNS infections. The commonality in both the pathologies is cortical gray matter involvement.

Thalamo-cortical connectivity in children born preterm mapped using probabilistic magnetic resonance tractography

Our aim was to investigate the feasibility of studying white matter tracts and connections between the thalamus and the cortex in 2-year-old infants who were born preterm by probabilistic magnetic resonance (MR) tractography. Using this approach, we were able to visualize and quantify connectivity distributions in a number of white matter tracts, including the corticospinal tracts, optic radiations, fibers of the genu and splenium of the corpus callosum, superior longitudinal fasciculus and inferior fronto-occipital fasciculus, and to map the distribution within thalamus of fibers connecting to specific cortical regions. In eleven infants with no MR evidence of focal cerebral lesions and appropriate neurodevelopment as shown by general quotient (GQ) scores above 100, we mapped cortical connections to the thalamus that appeared similar to those reported in adults. However, in a proof-of-principle experiment, we examined one further child with marked white matter abnormalities and found that the volume and pattern of thalamo-cortical connections were severely disrupted. This technique promises to be a useful tool for assessing connectivity in the developing brain and in infants with lesions.

Patients with West syndrome whose ictal SPECT showed focal cortical hyperperfusion

To clarify the mechanism of clustered spasms in West syndrome (WS), we examined ictal SPECT and EEG, as well as those during the interictal period, in three patients with symptomatic WS who had apparent focal cerebral lesions. For ictal SPECT and EEG, we monitored the patients with EEG, and as soon as we noticed the occurrence of clustered spasms clinically and electroencephalographically, [ 99mTc]ECD was injected intravenously and flushed thoroughly with saline. In these three patients, regional cerebral blood flow (rCBF) increased during ictus and decreased during the interictal period in the area that coincided with the focal cerebral lesion recognized by CT/MRI. The ictal hyperperfusion of bilateral basal ganglia was also detected in two of the three patients. The ictal EEG showed a diffuse slow wave complex corresponding to a clinical spasm. The sharp waves that preceded the diffuse slow wave complex and the spasm appeared in the same area in which rCBF increased during ictus. None of the patients showed partial seizure before or after clustered spasms clinically or electroencephalographically during the ictal SPECT study. Secondary generalization from a cerebral focus may explain the mechanism of spasms in these patients with WS: focal cortical discharge may primarily generate clustered spasms and trigger the brainstem and basal ganglia structures to produce spasms.

Neurological examination identified 61% of patients with focal cerebral hemisphere lesions but without obvious focal signs

Anderson NE, Mason DF, Fink JN, et al . Detection of focal cerebral hemisphere lesions using the neurological examination. J Neurol Neurosurg Psychiatry 2005;76:545–9. [OpenUrl][1][Abstract/FREE Full Text][2] Q In patients...