Biomedical subjects
Publications and source records attributed to A Codina.
We describe a postpartum 30-year-old woman who developed headaches, hypertension, and speech disturbances after bromocriptine treatment to suppress lactation. Brain MRI revealed intraparenchymal hematomas, and an angiographic study showed multiple arterial segmental narrowings compatible with postpartum cerebral angiopathy. We also comment on other cases of postpartum cerebral angiopathy.
Changes in the progression of disability is still the main variable measured in clinical trials involving patients with multiple sclerosis (EM). The amplified scale of the state of disability (EEDA) of Kurtzke continues to be the most widely used scale. One of the most important limitations of the EEDA is interobserver variability. The object of our study was to find the interobserver variability between members of our EM unit in patients with EEDA between 0 and 3.5 when applying functional systems (SF) and EEDA. Seven patients with recurrent remittent EM (EEDA 0-3.5), participating in a multicentric trial with natural beta-interferon, were assessed monthly for 12 months by two of four neurologists. The SF were assessed and the EEDA applied separately and without knowing the former. 80 paired examinations were made. Complete concordance of SF was only seen when a variation of 2 points was allowed, while it was very high for a variation of 0 and 1 points. Complete concordance for EEDA was seen in 36.6% of the cases and only in 11% was there discordance of 1 or 1.5 points. The average variability of EDSS was 0.39. There was greater variability when the two scores were at different levels of incapacity.
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INTRODUCTION: Asterixis is an uncommon sign in structural central nervous system disorders. When asterixis is present, one cannot rule out the possibility of a focal lesion, but it is almost always due to a metabolic encephalopathy. PATIENTS AND METHODS: In the last five years all patients with uni- or bilateral neurologic asterixis attended in our hospital have been studied. Cerebral computed tomogram or magnetic resonance imaging was performed in all patients with uni or bilateral asterixis. RESULTS: We describe 45 patients with different forms of structural cerebral pathology who presented unilateral (37 patients) or bilateral (8 patients) asterixis not associated to either toxic or metabolic disorder. Central nervous system ischemic or hemorrhagic disorders were found to be the most frequent causes of asterixis (95.5%) and the thalamus the most frequent localization for unilateral asterixis to result (54%). CONCLUSIONS: Bilateral asterixis is not always associated with toxic or metabolic disorders and it may be a sign of some structural neurologic alterations. A good correlation was found between the presence of unilateral asterixis and structural intracranial disease.
BACKGROUND AND PURPOSE: Delayed posttraumatic hemorrhage (DPTH) is one of the causes of intracerebral hemorrhage (ICH). Most of the published series were reported before the advent of CT. Clinical characteristics and CT findings are described. METHODS: Ten cases of CT-proven DPTH from a series of 216 patients (age range, 15 to 50 years) with ICH were evaluated. Previous CT scans performed in the first 6 hours after head injury were normal in all patients. Cerebral angiography showed no evidence of vascular disorders in any patient. RESULTS: DPTH was the fourth most common cause of ICH in our series. The symptom-free interval after head injury ranged from 1 to 15 days. Most hematomas were located deep in the hemisphere and were of small or medium size. Clinical course was good in the majority of cases; none of the patients died, and there was no recurrence. CONCLUSIONS: DPTH is a relatively frequent cause of ICH in young adults. There is no relationship with intensity of the previous head injury. The more frequent location deep in the hemisphere may be related to the younger age of our patients compared with those of other published series. The good outcome in our patients may be related to their youth and the absence of complications such as skull fracture, need for neurosurgery, or coagulation disorders.
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A 9-year-old boy presented with acute sensory neuronopathy, a condition generally associated with poor recovery. Although sensory nerve action potentials were abolished and sural nerve biopsy showed marked loss of myelinated fibers, he eventually made an almost complete clinical recovery.
Migraine in itself is a potential cause of cerebral infarct in young adults. However the mechanism of migrainous ictus is open to discussion. Some drugs (oral anticonceptives, ergotaminics) could favor its appearance. Three cases has described in the medical literature of migraine patients in whom betablockers administration has been related with onset of an ischemic ictus. We present two new cases of this association. Nonselective betablockers provoke an increase in platelet activity by stimulation of platelet alpha-2 receptors; this together with their vasoconstrictor effect could favor the apparition of cerebral infarction in patients with migraine. We suggest, following other authors, to include non selective betablockers in the group of drugs which have to be carefully managed in the patients with migraine, especially in those with the classical type (migraine with aura) in whom an initial vasoconstriction has been suggested.
Twenty-four patients with clinically defined multiple sclerosis were prospectively studied with the aim of establishing the frequency of retinal periphlebitis. In three cases (12.5%) retinal periphlebitis was observed. None of the patients with multiple sclerosis and retinal periphlebitis presented a severe form or progressive course of the disease; however, in one patient it caused complete unilateral amaurosis. Aggressive immunosuppressive treatment was effective in one case. Given the absence of myelin in the retina, the presence of retinal periphlebitis suggests the existence of a vascular mechanism in the pathogenesis of multiple sclerosis.
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Pathogenesis of neuropsychiatric manifestations of systemic lupus erythematosus (SLE) has not been clearly defined, and the search for pathogenic mechanisms has focused on the importance of several autoantibodies. There is increasing evidence that antibodies against gangliosides may have a pathogenic role in some neurological disorders. The aim of the present study was to examine the association between antibodies against gangliosides and neuropsychiatric SLE. We found anti-type II ganglioside antibodies in two out of 32 patients with multiple sclerosis (6.25%) and in 10 out of 60 patients with SLE (16.6%); five of 17 patients with neurological abnormalities also had high levels of these antibodies (29.4%). Five of the 10 patients with SLE and positive antiganglioside antibody had only IgM antibodies, three had IgG antibodies and two had both isotypes. By chi-square analysis, the incidence of anti-type II ganglioside antibodies was not significantly higher in patients with symptoms related to the nervous system than in SLE patients without neurological involvement (P > 0.2). No clear correlation was found between antibodies against gangliosides and cardiolipin.
Pituitary apoplexy (PA) is currently considered as one of the causes of empty sella (ES). However, in most reported cases the diagnosis of PA was based on anamnesis. A prospective study of three patients diagnosed during the PA episode was carried out. Periodical evaluations of hormone concentrations and cerebral computed tomography images were carried out. Initially, the three patients had a global anterior pituitary developed ES within 6 and 18 months. Surgical therapy was not undertaken in any case. Owing to the rarity of the disease definitive conclusions are difficult to obtain; however, the present study suggests that after an episode of PA global anterior pituitary failure develops, with subsequent ES. Early medical therapy with glucocorticoids can avoid surgical therapy.
Somatostatin levels were measured in cerebrospinal fluid of patients with Alzheimer's disease, multi-infarct dementia and normal pressure hydrocephalus and compared with levels from a normal control group. All pathological groups showed a statistically significant decrease of somatostatin with respect to the control group, but no significant differences were found amongst them. A negative correlation was found between the Mini Mental State Test and the somatostatin levels in Alzheimer's disease patients but not in the other groups. Our results confirm that the lower levels of somatostatin in cerebrospinal fluid are not specific to Alzheimer's disease and indicate that the decrease found in all the groups is probably the result of neuronal destruction or damage in the diseases examined.
Fifty-four shunt-responsive patients were selected from a prospective protocol directed to study patients with suspected normal pressure hydrocephalus (NPH). Patients with gait disturbances, dementia, non-responsive L-Dopa Parkinsonism, urinary or faecal incontinence and an Evans ratio greater or equal to 0.30 on the CT scan were included in the study. As a part of their work-up all patients underwent intracranial pressure monitoring and hydrodynamic studies using Marmarou's bolus test. According to mean intracranial pressure (ICP) and the percentage of high amplitude B-waves, patients were subdivided in the following categories: 1) Active hydrocephalus (mean ICP above 15 mmHg), which is in fact no tone normal pressure hydrocephalus; 2) Compensated unstable hydrocephalus, when mean ICP was below 15 mmHg and B-waves were present in more than 25% of the total recording time and 3) Compensated stable hydrocephalus when ICP was lower or equal to 15 mmHg and beta waves were present in less than 25% of the total recording time. The majority of the patients in this study (70%) presented continuous high or intermittently raised ICP (active or unstable compensated hydrocephalus group). Mean resistance to outflow of CSF (Rout) was 38.8 mm Hg/ml/min in active hydrocephalus and 23.5 mm Hg/ml/min in the compensated group (Students t-test, p less than 0.05). Higher resistance to outflow was found in patients with obliterated cortical sulci and obliterated Sylvian cisterns in the CT scan. No statistically significant correlation was found when plotting the percentage of beta waves against pressure volume index (PVI), compliance or Rout. An exponential correlation was found when plotting beta waves against the sum of conductance to outflow and compliance calculated by PVI method (r = 0.79). Patients with the so-called normal pressure hydrocephalus syndrome have different ICP and CSF dynamic profiles. Additional studies taking into consideration these differences are necessary before defining the sensitivity, specificity and predictive value of ICP monitoring and CSF studies in selecting appropriate candidates for shunting.
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In a 2-year prospective study of 146 patients with cerebral ischemia, we compared vascular risk factors for stroke with clinical and laboratory findings, particularly antiphospholipid antibodies. Ten patients (6.8%) were positive for at least one antiphospholipid antibody; one patient had systemic lupus erythematosus, one had rheumatoid arthritis, and the remaining eight fulfilled criteria for the diagnosis of primary antiphospholipid syndrome. These patients were predominantly male, not necessarily young, and 50% of them did not have any other vascular risk factors; there were no significant clinical or paraclinical differences between these patients and those without antiphospholipid antibodies. Outcome in the 10 patients was good, and platelet antiaggregating drugs proved to be useful in preventing further cerebrovascular ischemic events in our patients.