Specific Lesion Patterns Research Articles

Retraction and replacement: Assessing the cortical microstructure in contralesional sensorimotor areas after stroke

Abstract Cortical thickness analyses have provided valuable insights into changes in cortical brain structure after stroke and their association with recovery. Across studies though, relationships between cortical structure and function show inconsistent results. Recent developments in diffusion-weighted imaging of the cortex have paved the way to uncover hidden aspects of stroke-related alterations in cortical microstructure, going beyond cortical thickness as a surrogate for cortical macrostructure. Animal data obtained in rats and monkeys have evidenced that contralesional motor areas undergo degenerative alterations in their microstructure which are accompanied by compensatory changes as well. We hypothesized that cortical diffusion imaging can detect similar changes in human stroke survivors. We re-analysed clinical and imaging data of 42 well-recovered chronic stroke patients from two independent cohorts (mean age 64 years, 4 left-handed, 71% male, 16 right-sided strokes) and 33 healthy controls of similar age and gender. Cortical fractional anisotropy, axial diffusivity, radial diffusivity and cortical thickness values were obtained for six key sensorimotor areas of the contralesional hemisphere. The regions included the primary motor cortex, dorsal and ventral premotor cortex, supplementary and pre-supplementary motor areas and primary somatosensory cortex. Linear models were estimated for group comparisons between patients and controls and for correlations between cortical fractional anisotropy, axial diffusivity, radial diffusivity and cortical thickness and clinical scores. Against our hypothesis, we did not find any significant alterations in contralesional cortical microstructure after stroke. Likewise, we did not detect any correlations between cortical microstructure and behavioural scores. Future analyses are warranted to investigate whether such alterations might occur in different populations, e.g. in later stages of recovery, in more severely impaired patients, or only in the ipsilesional hemisphere in patients with specific lesion patterns.

Vestibular assessment in sudden sensorineural hearing loss: Role in the prediction of hearing outcome and in the early detection of vascular and hydropic pathomechanisms.

Predicting hearing outcome in sudden sensorineural hearing loss (SSNHL) is challenging, as well as detecting the underlying pathomechanisms. SSNHL could be associated with vestibular damage since cochleo-vestibular structures share the same vascularization, along with being in close anatomical proximity. Whereas viral inflammations and autoimmune/vascular disorders most likely represent the involved aetiologies, early-stage Menière's disease (MD) can also present with SSNHL. Since an early treatment could beneficially influence hearing outcome, understanding the possible etiology plays a pivotal role in orienting the most appropriate treatment. We aimed to evaluate the extent of vestibular damage in patients presenting with SSNHL with or without vertigo, investigate the prognostic role of vestibular dysfunctions on hearing recovery and detect specific lesion patterns related to the underlying pathomechanisms. We prospectively evaluated 86 patients with SSNHL. Audio-vestibular investigation included pure-tone/speech/impedance audiometry, cervical/ocular-VEMPs, vHIT and video-Frenzel examination. White matter lesions (WML) were evaluated on brain-MRI. Patients were followed-up and divided into "SSNHL-no-vertigo," "SSNHL+vertigo" and "MD" subgroups. Hearing was more impaired in "SSNHL+vertigo" patients who exhibited either down-sloping or flat-type audiograms, and was less impaired in "MD" where low frequencies were mostly impaired (p < 0.001). Otolith receptors were more frequently involved than semicircular canals (SCs). Although the "SSNHL-no-vertigo" subgroup exhibited the lowest vestibular impairment (p < 0.001), 52% of patients developed otolith dysfunctions and 72% developed nystagmus. Only "MD" subjects showed anterior SC impairment and upbeating spontaneous/positional nystagmus. They more frequently exhibited cervical-VEMPs frequency tuning (p = 0.036) and ipsilesional spontaneous nystagmus (p < 0.001). "SSNHL+vertigo" subjects presented with more frequently impaired cervical-VEMPs and posterior SC and with higher number of impaired receptors (p < 0.001). They mainly exhibited contralesional spontaneous and vibration-induced nystagmus (p < 0.05) and only they showed the highest WML score and "vascular" lesion patterns (p < 0.001). Concerning the outcomes, hearing was better in "MD" and worse in "SSNHL+vertigo" (p < 0.001). Hearing recovery was mostly affected by cervical-VEMPs impairment and the number of involved receptors (p < 0.05). Patients with "vascular" lesion patterns presented with the highest HL degree and WML score (p ≤ 0.001), while none of them exhibited a complete hearing recovery (p = 0.026). Our data suggest that vestibular evaluation in SSNHL can provide useful information on hearing recovery and underlying aetiologies.

Distinct cognitive components and their neural substrates underlying praxis and language deficits following left hemisphere stroke

Apraxia is characterised by multiple deficits of higher motor functions, primarily caused by left hemisphere (LH) lesions to parietal-frontal praxis networks. While previous neuropsychological and lesion studies tried to relate the various apraxic deficits to specific lesion sites, a comprehensive analysis of the different apraxia profiles and the related (impaired) motor–cognitive processes as well as their differential neural substrates in LH stroke is lacking.To reveal the cognitive mechanisms that underlie the different patterns of praxis and (related) language deficits, we applied principal component analysis (PCA) to the scores of sub-acute LH stroke patients (n = 91) in several tests of apraxia and aphasia. Voxel-based lesion-symptom mapping (VLSM) analyses were then used to investigate the neural substrates of the identified components.The PCA yielded a first component related to language functions and three components related to praxis functions, with each component associated with specific lesion patterns. Regarding praxis functions, performance in imitating arm/hand gestures was accounted for by a second component related to the left precentral gyrus and the inferior parietal lobule. Imitating finger configurations, pantomiming the use of objects related to the face, and actually using objects loaded on component 3, related to the left anterior intraparietal sulcus and angular gyrus. The last component represented the imitation of bucco-facial gestures and was linked to the basal ganglia and LH white matter tracts. The results further revealed that pantomime of (limb-related) object use depended on both the component 2 and 3, which were shared with gesture imitation and actual object use.Data support and extend the notion that apraxia represents a multi-componential syndrome comprising different (impaired) motor–cognitive processes, which dissociate – at least partially – from language processes. The distinct components might be disturbed to a varying degree following LH stroke since they are associated with specific lesion patterns within the LH.

Association of clinical headache features with stroke location: An MRI voxel-based symptom lesion mapping study.

Background We have recently shown that the presence of headache in ischemic stroke is associated with lesions of the insular cortex. The aim of this post-hoc subgroup analysis was to investigate the association of specific headache features with stroke location in patients with acute ischemic stroke. Methods In this observational study, patients (mean age: 61.5, 58% males) with ischemic stroke and acute headache (n = 49) were investigated. Infarcts were manually outlined on 3D diffusion weighted magnetic resonance imaging (MRI) scans and transformed into standard stereotaxic space; lesions of the left hemisphere were mirrored in the x-axis to allow a voxel-wise group analysis of all patients. We analyzed the association of lesion location and the following phenotypical characteristics by voxel-based symptom lesion mapping: Headache intensity, different qualities of headache (pulsating, tension-type like and stabbing), and the presence of nausea, of cranial autonomic symptoms and of light or noise sensitivity. Results Headache intensity was associated with lesions of the posterior insula, the operculum and the cerebellum. "Pulsating" headache occurred with widespread cortical and subcortical strokes. The presence of "tension-like" and "stabbing" headache was not related to specific lesion patterns. Nausea was associated with lesions in the posterior circulation territory. Cranial-autonomic symptoms were related to lesions of the parietal lobe, the somatosensory cortex (SI) and the middle temporal cortex. The presence of noise sensitivity was associated with cerebellar lesions, whereas light sensitivity was not related to specific lesions in our sample. Conclusion Headache phenotype in ischemic stroke appears to be related to specific ischemic lesion patterns.

DWI Lesion Patterns Predict Outcome in Stroke Patients with Thrombolysis

Background: Lesion patterns may predict prognosis after acute ischemic stroke within the middle cerebral artery (MCA) territory; yet it remains unclear whether such imaging prognostic factors are related to patient outcome after intravenous thrombolysis. Aims: The aim of this study is to investigate the clinical outcome after intravenous thrombolysis in acute MCA ischemic strokes with respect to diffusion-weighted imaging (DWI) lesion patterns. Methods: Consecutive acute ischemic stroke cases of the MCA territory treated over a 7-year period were retrospectively analyzed. All acute MCA stroke patients underwent a MRI scan before intravenous thrombolytic therapy was included. DWI lesions were divided into 6 patterns (territorial, other cortical, small superficial, internal border zone, small deep, and other deep infarcts). Lesion volumes were measured by dedicated imaging processing software. Favorable outcome was defined as modified Rankin scale (mRS) of 0-2 at 90 days. Results: Among the 172 patients included in our study, 75 (43.6%) were observed to have territorial infarct patterns or other deep infarct patterns. These patients also had higher baseline NIHSS score (p < 0.001), a higher proportion of large cerebral artery occlusions (p < 0.001) and larger infarct volume (p < 0.001). Favorable outcome (mRS 0-2) was achieved in 89 patients (51.7%). After multivariable analysis, groups with specific lesion patterns, including territorial infarct and other deep infarct pattern, were independently associated with favorable outcome (OR 0.40; 95% CI 0.16-0.99; p = 0.047). Conclusions: Specific lesion patterns predict differential outcome after intravenous thrombolysis therapy in acute MCA stroke patients.

Lesion Pattern in Patients With Erectile Dysfunction of Suspected Arterial Origin

Purpose: To determine the specific lesion pattern of supplying arteries in patients with cardiovascular risk factors suffering from treatment-refractory erectile dysfunction (ED). Methods: From May 2012 to August 2013, 26 men (median age 55 years) poorly responsive to phosphodiesterase-5 inhibitor therapy were evaluated for a possible vascular cause for their ED. The men were examined with penile duplex sonography and digital subtraction angiography (DSA). Arterial lesions in the common and internal iliac arteries and the internal pudendal arteries considered amenable to endovascular therapy were treated with angioplasty ± stents. Retrospectively, 2 blinded investigators independently evaluated the DSA images and categorized the vascular patterns of the erection-related arteries as normal, macroangiopathy (occlusive lesions of the internal pudendal arteries), or microangiopathy (smaller caliber arteries distal to the internal pudendal circulation with no distal arterial reconstitution). Results: Seventeen macroangiopathic lesions were successfully treated by angioplasty in 11 patients. The treated arterial lesions were mainly located in the internal (n=10) and common iliac arteries (n=2), whereas the internal pudendal artery were involved in 5 cases. Microangiopathic lesions lacking distal reconstitution were present in 7 patients, and the remaining 8 patients had normal vessels supplying the penis. Patients with macroangiopathy undergoing angioplasty had a higher prevalence of peripheral artery disease (63.6% vs 6.7%, p=0.003). Conclusion: In this preliminary series of ED patients with cardiovascular risk factors and pathologic duplex sonographic flow parameters, roughly 40% exhibited arterial lesions amenable to endovascular revascularization. In the patients with macroangiopathy, vessels upstream of the internal pudendal artery were most commonly affected. More studies are warranted to define the role of endovascular procedures in this ED subpopulation.

P174. Effects of left and right brain damage on anticipatory motor behavior during grasping and lifting with the ipsilesional hand

Behavioral studies in patients with left and right brain damage revealed the specialized function of both hemispheres in motor control. Recently, we investigated anticipatory grip force control in patients with stroke affecting the left or the right hemisphere during object lifting with the ipsilesional non-paretic hand. We found imprecise anticipation of grip force to the weight of everyday objects (like a carton with milk or a package of paper tissues) in patients with left brain damage while patients with right brain damage performed closer to normal. This finding suggests a particular role of the motor-dominant left brain in predicting object properties based on knowledge about the object identity. By contrast, we found no deficit of anticipatory grip force control in stroke patients when the initial weight information was provided by the size of the object. Also the perceptual size-weight-illusion was the same in patients and control subject. In the present study we tested material as the critical variable determining object weight. We hypothesized that the anticipation of material information as well as the so-called material-weight illusion may be reduced in patients with left brain damage, as material information about object characteristics may be a less direct cue to weight compared to size. Twelve patients with left brain damage (LBD), ten patients with right brain damage (RBD) and fourteen control subjects (CTR) lifted two pairs of identically-weighted objects which differed in size in the size-weight-illusion paradigm and in apparent material (polystyrene and aluminum) in the material-weight-illusion paradigm. In an additional control pair, the size and weight of two wooden blocks differed in the natural way. Participants’ grip forces and the lift forces were measured with a sensor (170 g) attached to the objects’ top surfaces. Subjects had to indicate which object in a pair is felt heavier before and after 6 lifts of each cube in a pair. Participants of all three groups experienced the size–weight–illusion. The material–weight–illusion was perceived less clearly without a clear difference between patients and control subjects. During the first lift of each object, the steepness of the grip force increase (quantified as the peak grip force rate) reflected the objects’ apparent weight as indicated by size. However variability was substantial in both patients groups. Different materials induced less clear differences in grip force rate. In particular, patients with left brain damage failed to scale their grip force profile according to the material. Also for the wooden object pair, data of LBD patients revealed a weaker anticipation of object properties than observed in the other groups. Our results confirm the normal processing of object size information for the scaling of grip forces and for the perception of the size-weight illusion in patients with brain damage, indicating that size processing is resistant to a wide range of brain damage. LBD patients in particular showed no consistent scaling of grip forces according to variations in material properties. Performance variability was however large in patients, suggesting that deficits depend on the specific lesion pattern which varied a lot across patients. In conclusion, the motor-dominant left hemisphere seems to play a prominent role in the processing of material information for object manipulation. However the responsibility seems to be less selective than when information is derived from object identity.

Lesion correlates of patholinguistic profiles in chronic aphasia: comparisons of syndrome-, modality- and symptom-level assessment

One way to investigate the neuronal underpinnings of language competence is to correlate patholinguistic profiles of aphasic patients to corresponding lesion sites. Constituting the beginnings of aphasiology and neurolinguistics over a century ago, this approach has been revived and refined in the past decade by statistical approaches mapping continuous variables (providing metrics that are not simply categorical) on voxel-wise lesion information (voxel-based lesion-symptom mapping). Here we investigate whether and how voxel-based lesion-symptom mapping allows us to delineate specific lesion patterns for differentially fine-grained clinical classifications. The latter encompass 'classical' syndrome-based approaches (e.g. Broca's aphasia), more symptom-oriented descriptions (e.g. agrammatism) and further refinement to linguistic sub-functions (e.g. lexico-semantic deficits for inanimate versus animate items). From a large database of patients treated for aphasia of different aetiologies (n = 1167) a carefully selected group of 102 first ever ischaemic stroke patients with chronic aphasia (∅ 12 months) were included in a VLSM analysis. Specifically, we investigated how performance in the Aachen Aphasia Test-the standard clinical test battery for chronic aphasia in German-relates to distinct brain lesions. The Aachen Aphasia Test evaluates aphasia on different levels: a non-parametric discriminant procedure yields probabilities for the allocation to one of the four 'standard' syndromes (Broca, Wernicke, global and amnestic aphasia), whereas standardized subtests target linguistic modalities (e.g. repetition), or even more specific symptoms (e.g. phoneme repetition). Because some subtests of the Aachen Aphasia Test (e.g. for the linguistic level of lexico-semantics) rely on rather coarse and heterogeneous test items we complemented the analysis with a number of more detailed clinically used tests in selected mostly mildly affected subgroups of patients. Our results indicate that: (i) Aachen Aphasia Test-based syndrome allocation allows for an unexpectedly concise differentiation between 'Broca's' and 'Wernicke's' aphasia corresponding to non-overlapping anterior and posterior lesion sites; whereas (ii) analyses for modalities and specific symptoms yielded more circumscribed but partially overlapping lesion foci, often cutting across the above syndrome territories; and (iii) especially for lexico-semantic capacities more specialized clinical test-batteries are required to delineate precise lesion patterns at this linguistic level. In sum this is the first report on a successful lesion-delineation of syndrome-based aphasia classification highlighting the relevance of vascular distribution for the syndrome level while confirming and extending a number of more linguistically motivated differentiations, based on clinically used tests. We consider such a comprehensive view reaching from the syndrome to a fine-grained symptom-oriented assessment mandatory to converge neurolinguistic, patholinguistic and clinical-therapeutic knowledge on language-competence and impairment.

Abstract 66: Ischemic Lesion Evolution and Hemorrhagic Transformation After Thrombolysis with Neuroprotection in FAST-MAG

Background: The frequency and range of early infarct signs in acute cerebral ischemia patients have been described in several 6-24 hour cohorts, but are incompletely characterized among under 2 hour presenting patients who actually proceed to receive IV tissue plasminogen activator (tPA). Prompt treatment with tPA improves outcomes after acute ischemic stroke, providing a platform to test promising neuroprotective strategies. We analyzed baseline and 24-hour imaging studies in an initial cohort of thrombolysis cases in the FAST-MAG trial of prehospital initiation of neuroprotection. Methods: Baseline and 24-hour CT/MRI studies acquired in 100 consecutive patients enrolled in FAST-MAG and treated with intravenous tPA were rated by two imaging experts for the presence of early ischemic changes (EIC), hyperdense vessel signs (HVS), ASPECTS score, white matter hyperintensities, prior infarction, lesion pattern and hemorrhagic transformation (HT), blind to all other data in the trial. Results: Among the 100 patients, mean age was 72±13 years; 44% were women; and median NIHSS was 14 (IQR 8-20). Initial imaging was obtained a mean of 91±29 minutes after last known well and routine post-thrombolysis imaging was obtained a mean of 23±13 hours later. Modality for initial scans was CT in 92% and MRI in 8%, and for follow-up scans CT in 63% and MRI in 37%. EIC were noted in 44%, including insular ribbon sign in 35%, lenticular obscuration in 28% and cortical effacement in 10%. HVS was visualized in 50%. Initial ASPECTS was median 9 (IQR 8-10) and 7 (IQR 4-9) at 24 hours. 24-hour lesion patterns were characterized as predominantly cortical in 50%, subcortical in 19%, scattered in 23% and no lesion in 8%. At 24 hours, ASPECTS correlated with NIHSS (R=-0.409, p&lt;0.001) whereas specific lesion patterns did not (p=NS). Cortical lesion patterns at 24 hours were predicted by cortical effacement on initial CT (23% vs. 0%, p=0.011). HT occurred in 26%, including 15% HI1, 3% HI2, 4% PH1, 3% PH2 and 1% IVH. Factors associated with HT were lower baseline ASPECTS (7.5 vs. 8.7, p=0.002) and more severe baseline NIHSS (18 vs. 13, p=0.021). Conclusions: Among patients imaged a mean of 1.5 hours after onset and then treated with thrombolysis, hyperdense vessel signs are present in one-half and early signs of ischemic parenchymal injury are present in nearly half, but are generally mild. Observed rates of HT were low. Serial imaging of patients treated with field neuroprotective therapies followed by post-arrival thrombolysis is often informative at initial and follow-up time points and has potential as biomarkers to interrogate treatment effects in prehospital neuroprotection studies.

Lesion patterns in patients with cryptogenic stroke with and without right‐to‐left‐shunt

Despite numerous studies, the role of patent foramen ovale (PFO) as a risk factor for stroke due to paradoxical embolism is still controversial. On the assumption that specific lesion patterns, in particular multiple acute ischaemic lesions on diffusion-weighted magnetic resonance imaging, indicate a cardioembolic origin, we compared the MRI findings in stroke patients with right-to-left shunt (RLS) and those without. The records of 486 patients with diagnosis of cerebral ischaemia were reviewed. For detection of RLS, contrast-enhanced transcranial Doppler (c-TCD) was carried out in all patients. An MRI scan of the brain was performed in all patients. Affected vascular territories were divided into anterior cerebral artery, middle cerebral artery, vertebrobasilar artery system including posterior cerebral artery, brain stem and cerebellar stroke, and strokes occurring in more than one territory. We did not find a specific difference in neuroradiological lesion patterns in patients with RLS compared with patients without RLS. In particular, 23 of 165 patients (13.9%) with RLS showed multiple ischaemic lesions on MRI in comparison with 45 of 321 patients (14.0%) without RLS (P = 0.98). These findings also applied for the subgroup of cryptogenic strokes with and without RLS. We found no association between an ischaemic lesion pattern that is considered as being typical for stroke due to cardiac embolism and the existence of PFO. Therefore, our findings do not provide any support for the common theory of paradoxical embolism as a major cause of stroke in PFO carriers.

Alcohol abuse and acute behavioural disturbances in a 24-year-old patient

MBD was named after two Italian pathologists who described acute demyelination of the corpus callosum at necropsy in 3 South-Italian male red-wine drinkers. Etiology is unknown. The main pathological features range from demyelination with preserved axon structure, to extensive necrosis with cystic formation and microbleedings. Clinical features are highly variable and include reduced consciousness, unsteady gait, behavioural disturbances, motor defects, seizures and, rarely, interhemispheric disconnection syndromes. Most of these can be seen in much more frequent alcohol-related disorders like Wernicke’s encephalopathy or central pontine myelinolysis, which may not have distinct ocular findings. Recent brain-imaging methods, particularly MRI, disclosed highly specific lesion patterns which, combined with the clinical features, were used to divide MBD in 2 subtypes: type A, characterized by consciousness impairment, extensive T2-weighted hyperintense swelling of the corpus callosum, and bad prognosis; and type B, characterized by behavioural and gait disturbances, restricted ‘‘sandwich-like” T2-weighted hyperintense lesions in the corpus callosum genu or splenium, and a better outcome. MRI also assumes a pivotal role in distinguishing MBD from other diseases, as the lesions affect the central layers of the corpus callosum and

Brain-derived proteins in the CSF, do they correlate with brain pathology in CJD?

BackgroundBrain derived proteins such as 14-3-3, neuron-specific enolase (NSE), S 100b, tau, phosphorylated tau and Aβ1–42 were found to be altered in the cerebrospinal fluid (CSF) in Creutzfeldt-Jakob disease (CJD) patients. The pathogenic mechanisms leading to these abnormalities are not known, but a relation to rapid neuronal damage is assumed. No systematic analysis on brain-derived proteins in the CSF and neuropathological lesion profiles has been performed.MethodsCSF protein levels of brain-derived proteins and the degree of spongiform changes, neuronal loss and gliosis in various brain areas were analyzed in 57 CJD patients.ResultsWe observed three different patterns of CSF alteration associated with the degree of cortical and subcortical changes. NSE levels increased with lesion severity of subcortical areas. Tau and 14-3-3 levels increased with minor pathological changes, a negative correlation was observed with severity of cortical lesions. Levels of the physiological form of the prion protein (PrPc) and Aβ1–42 levels correlated negatively with cortical pathology, most clearly with temporal and occipital lesions.ConclusionOur results indicate that the alteration of levels of brain-derived proteins in the CSF does not only reflect the degree of neuronal damage, but it is also modified by the localization on the brain pathology. Brain specific lesion patterns have to be considered when analyzing CSF neuronal proteins.

Lesion pattern in patients with multiple sclerosis and depression.

To assess if a specific lesion pattern or changes of the basal limbic system as seen in primary depression and depression associated with neurodegenerative disorders might be identified in depressive multiple sclerosis (MS) patients, we submitted 78 MS patients to a MRI examination consisting of a quantitative measurement of lesions and of hyperintense signals from the pontomesencephalic midline (raphe). Furthermore relaxometry of the pontomesencephalic midline, a transcranial ultrasound examination rating its echogenicity semiquantitatively and a standardized neurological, neuropsychiatric and neuropsychological assessment were obtained. Thirty-one patients fulfilled the DSM-IV criteria for depression. Depressed MS patients had a significantly larger temporal lesion load than non-depressed MS patients, especially on the right side. A trend of difference was detected for lesions of the right parietal lobe, the right frontal lobe, the cerebellum and the total lesion load. Neither hyperintense signals or relaxometry nor echogenicity of the region at the level of the pontomesencephalic midline were significantly different between the groups. We conclude that depression in MS patients is not associated with an alteration of the basal limbic system at the brainstem as seen in Parkinson's disease or unipolar depression but with an increased lesion load of the projection areas of the basal limbic system.

Catheter ablation approach on the right side only for paroxysmal atrial fibrillation therapy: long-term results.

We report the long-term follow-up of a right side only catheter ablation approach for paroxysmal AF. Eighteen patients with AF refractory to drugs entered the study. Ablation was attempted in the right atrium only by creating linear lesions based on a specific design including from two to four linear lesions. Induction of AF was attempted before ablation and after placement of the lesions. A septal lesion was performed in nine patients. In ten patients atrial defibrillation thresholds (ADFTs) before ablation and following creation of the linear lesions were compared. After a mean follow-up of 22 +/- 11 months, seven patients had recurrence of AF, and another nine patients experienced atrial flutter or atrial tachycardia. Five patients remained in sinus rhythm without medications and four required the use of drugs. Three patients had sporadic AF and six were in chronic AF. The recurrence rate was similar in patients with and without the septal lesion. However, a cure with right side ablation appeared to be predicted by the presence of disorganized and earlier activity in the high right atrium and crista terminalis. Linear lesions in the right atrium were associated with a lower ADFT (pre 2.6 +/- 04 J vs post 1.7 +/- 0.6 J). In conclusion, in a small number of patients, control of AF can be obtained with a right side only approach. Certain activation patterns may identify patients suitable to this approach. No specific lesion pattern appeared more effective. Right atrial linear lesions resulted in lower ADFT.

Neuropathology of Movement Disorders

This article reviews the cytoskeletal abnormalities, morphologic lesion patterns, and resulting pathophysiology of the most frequent neurodegenerative movement disorders caused by dysfunction of the basal ganglia and related neuronal loops. The following topics are discussed: Among the akinetic-rigid Lewy body disorders is idiopathic Parkinson’s disease, which reveals specific lesion patterns of pathophysiologic and therapeutic relevance. Dementia with Lewy bodies characterized by cortical Lewy bodies appears intermediate between Parkinson’s and Alzheimer’s diseases. Tau pathologic disorders may show some clinical and morphologic overlap. Multiple system atrophy has ubiquitous oligodendroglial inclusions as a cytopathologic hallmark. Secondary parkinsonism includes drug-related, toxic, and other symptomatic disorders. Hyperkinetic disorders include CAG-related inherited diseases, showing specific genetic defects and morphologic lesions. Dystonia syndromes show inconsistent pathologic findings, and myoclonus maybe related to a variety of disorders. Consensus data on clinical and neuropathologic criteria already existing for some disorders, together with molecular genetic and biochemical data will provide further insight into the complex pathophysiology and pathogenesis of movement disorders.