Biomedical subjects
A Codina
Publications and source records attributed to A Codina.
Prolactin concentrations in serum unchanged in transient global amnesia.
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High density lipoprotein cholesterol in transient global amnesia.
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Painful ophthalmoplegia in systemic lupus erythematosus.
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Charcot-Marie-Tooth disease associated with 'essential tremor' and normal and/or slightly diminished motor conduction velocity. Report of 7 cases.
We present a study of 7 cases of Charcot-Marie-Tooth disease, associated with a dyskinesia clinically identical with essential tremor, in which motor conduction velocity in the upper limbs was normal or slightly diminished. An analysis of age of onset, sex distribution and clinical signs from cases in the literature is compared with the present series. A family with Charcot-Marie-Tooth disease in which affected members have widely different motor conduction velocity values is reported. Stress is laid upon the fact that categorization of this disease on electrophysiological studies in the upper limbs may present considerable difficulties.
[Involvment of the neural system in sarcoidosis].
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Letter: Methysergide and myoclonus.
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[Neurobrucellosis: a study of 41 cases].
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[Neurobrucellosis. Study of 41 cases].
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[Neurobrucellosis (study of 41 cases)].
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[Extrapyramidal syndrome caused by methochlopramide in patients with advanced renal insufficiency].
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[Familial hemiplegic migraine associated with nystagmus].
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[Melkersson-Rosenthal's syndrome].
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[Intracranial involvement in neurosarcoidosis: a report of 4 cases as initial manifestation of the disease].
INTRODUCTION: The incidence of sarcoidosis in our country is one of the lowest in Europe. Neurosarcoidosis affects only 5% on patients with sarcoidosis. Clinical cases. We describe four patients in which neurologic disfunction was the presenting finding. Initial neurological symptoms include status epilepticus, headache, fever and nerve cranial palsies. MRI showed a spectrum of protean central nervous abnormalities: 1. Hypotalamic infiltrating lesion; 2. Brain parenchyme enhanced masses; 3. Leptomeningeal enhancement, and 4. Focal white-matter lesions. Thoracic CT scan, bronchoscopy, Gallium scintigraphy and pulmonary biopsy yielded to diagnosis in three patients. Biopsy of the meninges was required in one patient because systemic involvement was not found. Histological examination of an intracranial mass was also performed in another patient to rule out tumoral lesions. ACE in serum was normal in all patients. CSF ACE was determine in only one patient and was also normal. Three patients started treatment with corticosteroids but one of them required adjuvant treatment with immunosuppressor. Cranial nerve palsy resolved spontaneously in the last patient. CONCLUSIONS: Clinical and radiological polymorphism explained the delay before diagnosis and the problems in ruling out other diseases. MRI is highly useful for the diagnosis and follow up treatment.
[Intraventricular hemorrhage due to the rupture of atherosclerotic dissecting aneurysm of the middle cerebral artery].
INTRODUCTION: We present a case of fusiform intracranial aneurysm where, apart from the unusual site, we draw attention to the form of clinical presentation, namely intraventricular haemorrhage. Clinical case. A 68 year-old-man with a history of smoking, hyperuricemia with seizures of gout treated with colchicine and allopurinol, and hypertension treated with captopril. Nine years previously he had a right capsulothalamic haematoma and presented (as a sequela of this) a left sensomotor deficit, with a good functional level. In December 1998 he was admitted for sudden onset of headache and deterioration of consciousness. He had right limb movements which were typical of decerebration and made intubation and mechanical ventilation necessary. Cerebral CT, with angiographic sequences, showed blood in the lateral ventricles and III ventricle, with ventricular dilation and a fusiform aneurysm of the left middle cerebral artery. In view of the neurological state of the patient, treatment of the aneurysm was postponed. After initial improvement, which permitted extubation, tetraparesia (predominantly right) and a pseudobulbar syndrome were seen. The patient had repeated respiratory infections and died from sepsis caused by Pseudomona aeruginosa (of respiratory origin) three months after admission. CONCLUSIONS: Fusiform intracranial aneurysms form 9% of all aneurysms. Localization to the middle cerebral artery is infrequent, the basilar trunk and internal carotid artery are commoner sites. In our case angio-CT was a useful non-invasive neuro-radiological technique.
[Vertebrobasilar abnormalities in patients with hemifacial spasm: MR-angiography findings].
INTRODUCTION: Hemifacial spasm (HFS) is a disorder characterized by a complex of symptoms with hyperactive motor dysfunction of the facial nerve. It is indicated that HFS in the majority of cases can be caused by a blood vessel compressing the nerve adjacent to the brainstem. PATIENTS AND METHODS: We studied and treated 44 patients with HFS. Magnetic resonance imaging (MR) and MR-angiography of the brain were performed in patients with HFS to asses the presence of an artery of the vertebrobasilar system compressing the root of the facial nerve. We evaluate the response to treatment with Botulinum toxin in these cases. 14 patients were excluded (6 patients presented HFS due to other lesions and in 8 patients the MR was not performed). The remaining 30 patients with idiopathic HFS underwent MR/MRA (3D-FISP) and it was also performed in 14 patients with synkineses after facial palsy to be used as controls. RESULTS: The MRA documented an abnormal position of the arteries surrounding the facial nerve (ipsilaterally to HFS) in 22 patients. The compressing artery was the PICA in 3 patients (10%), the AICA in 3 patients, the vertebral artery in 7 patients and the basilar artery in 8 patients, one patient showed a combined compression by AICA and PICA. The remaining 8 patients had a normal MRI. At the control group only one patient presented an abnormal AICA and the other had a normal MRI-MRA. Patients were followed-up for 22.4 months and after Botulinum toxin treatment patients kept 4.81 months free of symptoms. CONCLUSIONS: We recommend to perform MR studies in all HFS patients to rule out a secondary cause of the disease and MRA to evaluate the underlying vertebrobasilar abnormalities if surgery is planned. Botulinum toxin is a useful treatment in these patients and only after its failure, microvascular decompression will be considered.
[Determination of Doppler parameters in the study of basal cerebral veins: basal vein of Rosenthal and middle cerebral vein].
INTRODUCTION: To date, little attention has been paid to the study of the venous system by means of transcranial Doppler ultrasound. The objective of our study was to learn how to localize cerebral blood flow and find the normal values of different ultrasonographic parameters. PATIENTS AND METHODS: We studied 20 healthy persons in whom the arterial system of the circle of Willis had previously been shown to be normal. Transcranial Doppler scan was done with the person lying face upwards, using a transtemporal 2 MHz catheter. In the study we included persons in whom at least one of the two veins could be studied unilaterally. RESULTS: We studied twelve men and eight women aged between 25 and 78 years. The basal vein of Rosenthal, localized bilaterally in 70% of the cases, was identified as a wave of low pulsation between segments P1 and P2 of the posterior cerebral artery, going away from the catheter at a speed of about 11 cm/second. The middle cerebral vein was found bilaterally in only 35% of the cases as a wave near to the middle cerebral artery but in the opposite direction, at an average velocity of approximately 11.7 cm/second and of low pulsation. CONCLUSIONS: In spite of the technical problems, which can be solved using contrast agents, it is possible to study the cerebral venous system by means of transcranial Doppler. Our Unit is the first in Spain to show this. We therefore wish to promote the use of transcranial Doppler in cerebral venous disorders.