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M A Pagano

Publications and source records attributed to M A Pagano.

24 records · Page 2Linked to original sources
PubMedDate not supplied

[Cerebral haematoma in the course of herpes simplex encephalitis].

INTRODUCTION: Herpes simplex encephalitis (HSE) is the most common cause of infectious encephalitis at all ages. The usual presentation includes a high temperature, headache and confusion associated with convulsions and signs of a focal neurological deficiency. The typical findings shown by magnetic resonance imaging (MRI) consist of hyperintense lesions, in T2 and FLAIR sequences, especially in the medial and inferior temporal lobe. AIMS. The aim of this paper is to report a case of HSE that associated a cerebral haematoma (CH) in its clinical course. CASE REPORT: A 69 year old female patient who was admitted to hospital because of a syndrome of high temperature, confusion and urinary infection. Studies of the cerebrospinal fluid showed only a slight pleocytosis, and a polymerase chain reaction (PCR) for the herpes simplex virus (HSV) was required. Initial MRI scanning showed an image that was compatible with cerebritis in the left parieto occipital lobe. A later RMI scan revealed a cerebral haematoma in the left parieto occipital lobe, together with new haemorrhagic foci in the bifrontal and in the right temporal lobes. The haematoma was drained surgically and empirical therapy was begun with acyclovir, and later a positive HSV PCR was received. The patient responded favourably to the therapy and was discharged from hospital. DISCUSSION: A variety of atypical presentations in HSE have been reported. Our case presented scant pleocytosis, infrequent lesion topography and coursed with CH. Only a few cases of this last occurrence have been reported in the literature. CONCLUSION: The presence of infrequent features, such as CH, within the framework of the clinical features of encephalopathy cannot exclude the possible existence of HSE.

Aged↗
PubMedDate not supplied

[Electrophysiological evaluation of a case of sensory-motor multifocal acquired demyelinating neuropathy. The effects of immunoglobulin therapy].

INTRODUCTION: Sensory motor multifocal acquired demyelinating neuropathy (SMMADN) is a variant of the chronic multifocal neuropathies. Several reports have been published about the clinical and electrophysiological progression in motor multifocal neuropathy (MMN) prior to and following immunoglobulin (Ig) therapy, but we have found no reports that deal with SMMADN. AIMS: We describe a case of SMMADN in which we conducted a clinical and electrophysiological evaluation before and after therapy with Ig UNC Hemoderivados. CASE REPORT: Female, 40 years of age, who presented asymmetrical weakness in all four limbs which she had been suffering for 12 years. We observed distal muscular atrophies, notable weakness and paresthesias in the four limbs. Electrophysiological studies revealed demyelinating neuropathy with secondary axonal involvement. Intravenous Ig was indicated. We observed a clear improvement in muscular strength, and changes in motor and sensory conduction speeds, but not in the amplitudes of the respective potentials. CONCLUSION: SMMADN is a chronic sensory motor multiple mononeuropathy that begins in the upper limbs and progresses asymmetrically down towards the lower members. The most usual sensory disorders are distal paresthesias. Electrophysiology presents conduction blockages, temporal dispersion, prolongation of the distal latencies, diminished conduction speeds, absence or prolongation of the F wave in one or more motor nerves, and abnormal sensory conduction speed. Accepted treatment is with Ig and, in some cases, with corticoids. In our case, the variations that were obtained could be explained by myelin reconstitution following the immunomodulatory effect of Ig and the axonal involvement that existed due to the secondary sequelae of the inflammatory process.

Adult↗
PubMedDate not supplied

[Posterior reversible encephalopathy syndrome: some case reports].

INTRODUCTION: In 1996, Hinchey et al described a clinico-radiological picture they called posterior reversible leukoencephalopathy syndrome (PRLS), which is characterized by visual disorders, seizures, altered mental states and changes in the subcortical white matter of the temporoparietooccipital lobes that are shown up in the neuroimages. These clinical manifestations are associated with arterial hypertension. Later, other triggering elements, such as cytostatic drugs, were described without being linked to hypertension. Other authors have suggested the name of posterior reversible encephalopathy, since magnetic resonance imaging (MRI) reveals a high percentage of cortical compromise. CASE REPORTS: We present three cases of posterior reversible encephalopathy with different origins. Two of the cases involved females, one of whom was a 19-year-old hypertensive with lupus nephropathy and the other was a 33-year-old with eclampsia. The third case was an 11-year-old male child with post streptococcal glomerulonephritis and hypertension. The most relevant signs and symptoms included seizures, visual disorders, arterial hypertension and sensory deterioration. MR played a decisive role in diagnosis and it revealed an alteration of the signal in the supra and infratentorial white matter of the cortex and the subcortex, which was predominant in the posterior areas of the encephalon. The three cases presented a significant radiological and clinical improvement in a short time. CONCLUSION: Failure of the self regulation of cerebral vascular circulation, with development of oedema, is the most widely accepted hypothesis to explain the pathophysiological mechanism at work in this entity.

Adult↗
PubMedDate not supplied

[Peripheral neuropathy in Anderson-Fabry disease: its physiology, evaluation and treatment].

AIMS: The purpose of this study was to review the peripheral neurological aspects of Anderson-Fabry disease (AFD). DEVELOPMENT: AFD is a disease caused by lysosomal deposits that was first reported in 1898. This entity has begun to attract renewed interest in recent years because of the progress made in diagnostic techniques and the appearance of enzyme replacement therapy. This pathological condition is transmitted by recessive inheritance linked to the X chromosome and results from a deficiency of the enzyme alpha-galactosidase A, which leads to the accumulation of glycosphingolipids in endothelial and perithelial cells, as well as those of the smooth muscles in blood vessels, the dorsal root ganglia and other structures in the central and peripheral nervous systems. Symptoms during childhood include: neuropathic pain that is predominantly distal in the four limbs (and expresses itself as severe attacks that are often linked to changes in temperature and exercise that interfere with daily activities), hypohidrosis and angiokeratomas. The most serious complications appear during adulthood and include: kidney failure, heart failure and strokes. CONCLUSION: The arrival of enzyme replacement therapy is the first part of a chain in the treatment of AFD, where gene therapy and substrate inhibition therapy are beginning to emerge as real therapeutic alternatives. In spite of all this, at present, the management of painful symptoms is not at all satisfactory for patients and therefore further study and a deeper understanding of the mechanisms involved will allow more specific and effective therapeutic measures to be developed with which to provide patients with greater relief.

Diagnosis, Differential↗