[Cerebral infarction as first manifestation of thrombocytopenia caused by pentosan polysulfate].
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Biomedical subjects
Publications and source records attributed to A Gironell.
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We report a patient who developed severe thrombocytopenia and ischemic stroke following pentosan polysulfate treatment. An ELISA test employed in type-II heparin-induced thrombocytopenia was highly positive. To our knowledge, this is the first case in which this test has been performed in a pentosan polysulfate-induced thrombocytopenia (PIT). Our data suggest that the antibody against pentosan polysulfate-platelet complex also cross-reacts with heparin-platelet factor 4 complex. Due to its greater sensitivity and wider availability, this ELISA test should be used in cases where PIT is suspected.
The contribution of dopaminergic systems to cognitive defects in Parkinson's disease and the cognitive effects of levodopa remain controversial. The levodopa plasma levels and the neuropsychological performance of 10 parkinsonian patients with a stable motor response to the drug and 10 matched parkinsonian patients with a 'wearing-off' phenomenon were studied 12 h after levodopa was withdrawn (time zero), and at 1 h and 4 h after an oral dose of levodopa (i.e. at '+1H' and '+4H'), to investigate whether discrete cognitive domains are more sensitive to levodopa in parkinsonian patients with the wearing-off phenomenon. Considering the 20 patients as a whole, levodopa significantly diminished the response time in verbal and visuospatial memory tests, the extradimensional matching test and the Wisconsin card sorting test (WCST), without significantly improving or worsening the patient's accuracy. A significant group-by-time effect was only evident in the WCST; while in stable patients levodopa produced no changes, wearing-off patients significantly reduced the number of categories achieved and had more perseverative errors at +1H, recovering at +4H. These results confirm previous findings of selective adverse effects of levodopa on highly demanding executive tasks in Parkinson's disease and additionally suggest that some previous discrepancies between studies may be accounted for by lack of differentiation between stable and wearing-off conditions. 'Frontal' disturbances on neuropsychological tests with levodopa may become evident only after massive degeneration of the dopamine systems has occurred.
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The authors describe 9 patients with bipolar affective disorder associated with cerebrovascular lesions. Eight had negative family histories of affective disorders and late age at onset (after age 40) of manic-depressive symptoms. Only one, with positive family history of affective disorders, developed mood swings before age 40. Clinical subtypes of bipolar disorder and patterns of affective cycling in these stroke patients resembled those previously reported in functional bipolar disorder. Five patients had concurrent hyperkinetic movement disorders, and one depressed patient presented with unilateral left-sided parkinsonism that disappeared during a manic switch. In most patients, bipolar affective disorder was associated with right hemisphere lesions that involved subcortical and midline structures. Findings suggest that damage to frontal-basal ganglia-thalamocortical circuits by subcortical vascular lesions may simultaneously provoke disorders of movement and mood regulation.
We studied the behavioral, cognitive, and neuroimaging characteristics of obsessive-compulsive disorder (OCD) in 13 patients with focal brain lesions (acquired OCD) and compared their clinical features and the severity of obsessive and compulsive (OC) symptoms with patients with idiopathic OCD. Both OCD groups were further compared with matched normal controls on a series of neuropsychological tests. Patients with acquired OCD had a negative familial history and later age at onset of OCD symptoms than patients with idiopathic OCD. The two OCD groups showed relatively similar clinical phenomenology, severity of OC symptoms, and profile of neuropsychological deficits. Compared with normal control subjects, both OCD groups showed cognitive deficits affecting attention, intellectual function, memory, word retrieval, and motor and executive functions. Eight of the 13 patients with acquired OCD had abnormal neurologic examinations, whereas only 3 of the 13 patients with idiopathic OCD had abnormal neurologic examinations. Neuroimaging in the acquired OCD group disclosed a variety of lesions involving exclusively the cerebral cortex (frontal, temporal, or cingulate regions), the basal ganglia, or both. These results suggest that acquired and idiopathic OCDs may share a common pathophysiologic mechanism, and that structural damage to specific frontal-limbic-subcortical circuits plays an important role in the pathogenesis of acquired OCD.
We carried out a retrospective analysis into the possible uses of thrombotic drugs on 190 consecutive patients with ischaemic stroke who had been admitted to the Neurological Service of the Barcelona 'Hospital de la Santa Creu i Sant Pau' in accordance with exclusion criteria commonly accepted for the use of this type of medication. We thus analyzed the initial symptoms, type of instauration, etiological diagnosis and topographical diagnosis. In those patients who could be possible candidates for such treatment with these drugs we assessed their disability variations (on the Rankin scale) at the end of two weeks using currently available therapeutic means. 70% of patients would subsequently be excluded from our study. Among reasons for exclusion were especially minor neurological deficiencies, age and latency time. As for patients included, most predominant factors were immediate instauration, cardioembolic etiological mechanism and severe onset symptomatology (motor disorder, awareness and language abnormalities). We observed a substantial spontaneous improvement in 7% of patients. This fact is especially clear in cardioemboligenic etiology patients. Bearing the spontaneous improvement cases in mind, we concluded that some 23% of patients with ischaemic cerebrovascular pathology could benefit from thrombotic drugs in our milieu.
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We describe three adults who had hemorrhagic strokes during the acute phase of bacterial meningitis (BM). We also report the results of a literature review and a review of the charts of 296 adults treated at our hospital for acute BM. The diagnosis of hemorrhagic stroke was made based on the results of cerebral computed tomography (CT) for two of 92 patients with BM who had CT performed and by means of lumbar puncture and a postmortem study in one other case. Two patients died of cerebral bleeding. Although the frequency of hemorrhagic stroke was only 2.1% among adults with acute BM, it is a major determinant of prognosis for such patients.
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BACKGROUND: The origin of weight gain after functional surgery for Parkinson's disease (PD) is incompletely known. We have done a prospective study to determine the possible causes of weight gain after pallidal and subthalamic surgery. PATIENTS AND METHOD: Twenty-seven patients were studied (9 unilateral pallidotomy, 9 bilateral deep brain stimulation (DBS) of palidum, and 9 bilateral DBS of suthalamic nucleus) with a follow-up of 12 months. The relationship between weight gain and changes in motor situation, levodopa dosage, dyskinesias, dysphagia and mood state were analyzed. The patients filled a questionnaire about the severity and etiology of weight gain. RESULTS: Weight gain was noted in 26 patients (mean of 4.7 kg at 12 months). It was found a significant correlation between weight gain and improvement of dyskinesias (AIMS) (r = 0.461; p = 0.023), the scores of the UPDRS part III, (r = 0.479; p = 0.028), and a significant inverse correlation with the pre-operative weight of the patient (r = 0.399; p = 0.050). Weight gain was most pronounced with bilateral than unilateral pallidal surgery (p = 0.021). The majority of patients referred weight gain as an slight adverse event and secondary to the improvement of dyskinesias. CONCLUSION: Functional surgery for PD, independently of the surgical target, provokes weight gain which is benign in the majority of cases. Reduction of energy expenditure with respect to the pre-operative situation would be the responsible of that phenomenon.
INTRODUCTION: Deterioration of attention in the preclinical phase of dementia of Alzheimer s type (DAT) is not very well known neither available studies are conclusive. OBJECTIVE: We outline if would be possible to identify a deficit of sustained attention in preclinical phase of DAT and if this attentional dysfunction could help to identify those patients, referred by subjective memory complaints (SMC), who will progress in a few years to DAT. PATIENTS AND METHODS: We compared basal exploration in a task of sustained attention (CPT) of 70 patients referred by SMC and followed longitudinally for 2 years. Twenty seven patients developed probable DAT and forty three remained clinically stable. RESULTS: Patients who will be diagnosed 2 years later with DAT performed significantly more poorly than patients who did not develop DAT. Patients who will be diagnosed 2 years later with DAT made a higher number of omission errors and obtained a lower number of correct responses. CONCLUSION: CPT paradigm is a vigilance task that detects deterioration of sustained attention in the preclinical phase of DAT and could be an objective indicator of the cognitive decline in the preclinical phase of Alzheimer s disease.
INTRODUCTION: The cognitive evoked potential N400 permits an objective assessment of the verbal semantic processing. It has been suspected to be clinically useful in cognitive abnormalities and a correlation with attentional and memory functions has been found. The present study tries to validate the translation and adaptation of the English paradigm to the Catalan and Spanish languages. METHOD: The study was performed on 16 healthy volunteers with Catalan native language and 16 volunteers with Spanish native language. Three blocks of 50 sentences (4-9 words) were administered using headphones. The last word of 50 % of the sentences was incongruent. The beginning of this word was the trigger for the EEG average. EEG leads used were: Fz, Cz, Pz, C3, C4, T3, T4 with biauricular reference. The measures were amplitude and latency of the potential obtained after the subtraction of the EEG average of congruent and incongruent sentences. A t-test for one sample (the original potential) was applied. RESULTS: Amplitude and latency of the potential obtained by the Catalan and Spanish languages were not result statistically different from the original potential. The major amplitude was obtained in Cz. Mean amplitudes: Catalan language: 5.3 2.3 V (95 % CI for the difference: 0.39 2.12 V); Spanish language: 5.2 2.3 V (95 % CI for the difference: 0.43 2.32 V). CONCLUSIONS: The Catalan and Spanish version of the N400 evoked potential offer the possibility to use an objective instrument for the study of language in neuroscience.
A nuclear oculomotor nerve syndrome is rarely caused by mesencephalic lesions. We describe 5 patients, 4 with unilateral syndrome (3 due to ischemia and 1 to mesencephalic hemorrhage) and 1 with bilateral nuclear ischemia of the third cranial nerve. These patients represent 0.2% of those admitted with cerebral vascular pathology over the last 12 years. Symptoms are consistent with descriptions of the anatomic organization of this nucleus, with peripheral paralysis of the contralateral superior rectus and possible bilateral involvement of the eyelid elevator and the pupillary constrictor muscles. A noteworthy symptom seen in these cases is supranuclear paralysis of the upward gaze on the side of the lesion, with ocular elevation achieved in response to oculocephalic stimuli in 2 cases and with Bell's synkinesis in 4. We analyze the nature of 22 published cases of unilateral nuclear damage and of 14 published cases of bilateral nuclear damage. Unilateral damage may or may not lead to ipsilateral pupillary involvement, uni- or bilateral eyelid ptosis, contralateral ocular hypotropia, and possible horizontal paresis of the contralateral gaze. Associated deficits are hemiparesis or crossed hemiataxia. Unresponsive pupils and bilateral ptosis associated with tetraparesis, bilateral ataxia and altered states of consciousness were seen with bilateral nuclear lesions. Infarction is the main cause (in 32 out of 41) and recovery of full ocular movement is uncommon.