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Biomedical subjects

J L Muñoz-Blanco

Publications and source records attributed to J L Muñoz-Blanco.

10 recordsLinked to original sources

[Prolonged acute renal failure and severe polyradiculopathy in ethylene glycol intoxication].

Ethylene glycol intoxication involves acute renal failure and severe metabolic acidosis. Prolonged renal insufficiency can occur but terminal chronic renal failure has been reported in very few cases. We describe a patient who after ingestion of 920 ml of ethylene glycol developed prolonged acute renal failure needing hemodialysis for 37 days and then he partly recovered renal function. The patient developed a severe sensitive-motor and autonomic polyradiculopathy.

Acute Kidney Injury↗

[Neurological complications of Mediterranean boutonneuse fever. Presentation of a case of acute encephalomeningomyelitis and review of the literature].

Mediterranean spotted fever is an infectious disease due to Rickettsia conorii usually considered as benign; however, 10% of cases may have severe complications. We report a patient with celiac disease who developed encephalomeningomyelitis secondary to Mediterranean spotted fever. Meningoencephalitic involvement occurred during the acute phase, with myelitis appearing early during convalescence, as acute onset paraplegia involving the lumbosacral spinal cord. A magnetic resonance study showed multifocal white matter disturbances, with no lesions in the spinal cord. One month following onset, R. conorii antibodies serum level was 1/640. A cutaneous biopsy performed during the acute phase revealed endothelial hyperplasia, intraluminal thrombosis and lymphocytic perivascular infiltrate. Several immunological disturbances were found (circulating immune complexes, antinuclear antibodies, IgG paraproteinemia). The development of a systemic vasculitis is the major pathogenetic factor in the origin of systemic complications of Mediterranean spotted fever. We review the neurological syndromes reported in association with R. conorii infection. Our case is the second described as acute myelopathy complicating Mediterranean spotted fever.

Acute Disease↗

[Lipidic myopathies].

The lipid storage myopathies are produced by a biochemical defect that directly or indirectly interferes with the metabolism of fatty acids in the muscle fiber. The oxidation of fatty acids is performed by enzymes lying in the mitochondrial membranes and matrix. The phenotype is very similar between the different biochemical defects, presenting with two large groups: One with early-onset, metabolic crisis and multisystemic failure, and one with late-onset, predominant myopathy and myoglobinuria. The diagnosis of these disorders has advanced significatively in the last ten years, permitting their classification at molecular level according to the biochemical and genetic defect.

Carnitine↗

Neuroleptic malignant syndrome related to tetrabenazine introduction and haloperidol discontinuation in Huntington's disease.

We describe the second reported case of neuroleptic malignant syndrome (NMS) related to tetrabenazine therapy in Huntington's disease. In the previously reported case, factors capable of potentiating NMS included a high dosage of tetrabenazine exceeding the accepted therapeutic range, and co-medication with the dopamine-synthesis inhibitor alpha-methylparatyrosine, while in the present case abrupt introduction of the drug and discontinuation of concomitant neuroleptics may have contributed to this important adverse reaction. Uneventful recovery occurred in both cases without the need for drugs specifically enhancing dopaminergic transmission, while rechallenge by tetrabenazine with conventional doses and slow upward titration was not followed by recurrence of the NMS. Tetrabenazine has proved to be a safe and frequently useful drug in the long-term treatment of approximately 400 dyskinetic patients. We believe that NMS related to this drug is rare, provided that it is properly administered.

Female↗

Interference of pentobarbital and thiopental with the vascular contraction and noradrenaline release in human cerebral arteries.

Thiopental and pentobarbital induced dose-dependent vasodilations in human cerebral arteries previously contracted with noradrenaline (NA), serotonin (5-HT) and KCl. Preincubation with both barbiturates decreased the contractions evoked by the three agents. Pentobarbital and thiopental reduced the Ca2+-induced contractile effects in K+-depolarized arteries and 5-HT-Ca2+ and NA-Ca2+ contractions dose-dependently. The tritium release evoked by K+ from these vessels prelabelled with [3H]NA was significantly reduced by both barbiturates at 10(-3) M and by Ca2+ removal. These results indicate that pentobarbital and thiopental essentially produce a similar interference with Ca2+ influx inhibiting the contractile responses induced by the three vasoactive agents and the exocytotic NA release evoked by K+.

Cerebral Arteries↗

[Giant cell arteritis, bilateral anterior ischemic optic neuropathy and anticardiolipin antibodies].

CLINICAL CASE: We report a case of giant cell arteritis (GCA) that developed acute bilateral amaurosis secondary to anterior ischemic optic neuropathy (AION), without other symptoms and with a normal erythrocyte sedimentation rate (ESR). Physical examination revealed painless and pulseless temporal arteries, ophthalmoscopic findings were blurring of margins, hyperaemia and elevation of both optic discs. Visual acuity was limited to hand motion perception and light-darkness discrimination. Six months before of this syndrome, the patient was diagnosed of polymyalgia rheumatica and was maintained asymptomatic with 6 mg/day of deflazacort. Temporal artery biopsy was diagnostic. An elevated IgG type anticardiolipin antibodies (ACA) rate was detected in serum. The remaining laboratory studies were normal. CONCLUSIONS: In old people with uni or bilateral acute visual loss, even with normal erythrocyte sedimentation rate and without other symptoms associated, it is necessary to have a high index of suspicion in order to detect giant cell arteritis. This can facilitate an early diagnosis and immediate initiation of treatment with high doses of corticosteroids. An elevated level of IgG type anticardiolipin antibodies may be a risk factor to thrombotic complications, as anterior ischemic optic neuropathy, in patients with giant cell arteritis.

Acute Disease↗

[Segmental motor paralysis caused by the varicella zoster virus. Clinical study and functional prognosis].

INTRODUCTION: Segmental motor paralysis of the limbs (SMP) complicates 2-3% of the cases of cutaneous herpes zoster. Viral invasion and inflammation of the motor neurons of the anterior horn cells by the varicella-zoster virus (VVZ) causes clinical weakness at the same time and site as the cutaneous eruption. OBJECTIVES: To analyze the clinical findings, complementary investigations and functional prognosis of patients with SMP at brachial plexus and lumbosacral levels. PATIENTS AND METHODS: We made a retrospective study of 10 patients with SMP admitted to the Hospital Universitario Gregorio Maranon de Madrid during 1989-1999, aged between 38 and 84 years (6 women, 4 men). Neurological examination was done, including muscle balance, complementary studies including microbiology (serum and CSF serology, viral PCR-ADN), neurophysiology using MNR of the spine and plexuses and functional prognosis on the NDS, NSS and RANKIN scales. RESULTS: There is a close relationship between dermatome and myotome involvement (90%). The brachial and lumbosacral plexuses were equally affected (50%). Plasma and CSF VVZ serology was positive in 50% of the cases, permitting diagnosis of a patient with no cutaneous lesions (zoster sine herpete). Denervation of the myotomes involved and the paraspinal muscles was shown on neurophysiological studies. In most cases there was functional improvement, with complete functional recovery in 80% of the cases after 12 months. CONCLUSIONS: VVZ should be considered amongst the aetiologies of SMP, even in the absence of cutaneous lesions (zoster sine herpete). The SMP coincides in time and place with the dermatome lesions. In most patients there is complete functional recovery within 12 months.

Adult↗