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J C Garcia-Monco

Publications and source records attributed to J C Garcia-Monco.

At least 19 recordsLinked to original sources
PubMed2005

EFNS guideline on the diagnosis and management of alcohol-related seizures: report of an EFNS task force.

Despite being a considerable problem in neurological practice and responsible for one-third of seizure-related admissions, there is little consensus as to the optimal investigation and management of alcohol-related seizures. The final literature search was undertaken in September 2004. Consensus recommendations are given graded according to the EFNS guidance regulations. To support the history taking, use of a structured questionnaire is recommended. When the drinking history is inconclusive, elevated values of carbohydrate-deficient transferrin and/or gammaglutamyl transferase can support a clinical suspicion. A first epileptic seizure should prompt neuroimaging (CT or MRI). Before starting any carbohydrate containing fluids or food, patients presenting with suspected alcohol overuse should be given prophylactic thiamine parenterally. After an alcohol withdrawal seizure (AWS), the patient should be observed in hospital for at least 24 h and the severity of withdrawal symptoms needs to be followed. For patients with no history of withdrawal seizures and mild to moderate withdrawal symptoms, routine seizure preventive treatment is not necessary. Generally, benzodiazepines are efficacious and safe for primary and secondary seizure prevention; diazepam or, if available, lorazepam, is recommended. The efficacy of other drugs is insufficiently documented. Concerning long-term recommendations for non-alcohol dependent patients with partial epilepsy and controlled seizures, small amounts of alcohol may be safe. Alcohol-related seizures require particular attention both in the diagnostic work-up and treatment. Benzodiazepines should be chosen for the treatment and prevention of recurrent AWS.

Alcohol Withdrawal Seizures↗
PubMed2005

Recurrent stroke associated with cannabis use.

Drug misuse represents a risk factor for cerebrovascular disease, especially among young people. Despite the fact that cannabis is the most widely used illicit drug, there are only a few reports associating its use with cerebrovascular disease. We describe a patient who suffered three ischaemic strokes immediately after cannabis consumption. Other stroke aetiologies were ruled out, and neuroimaging revealed infarcts in different arterial areas as well as evidence of non-atherosclerotic arterial disease, which suggests an underlying vasculopathy of uncertain (toxic or inflammatory) origin. Cannabis use may be associated with ischaemic stroke in young patients, but its mechanism is unclear.

Adult↗
PubMed2003

Quality of life in migraine patients: a qualitative study.

The impact of migraine on quality of life has been traditionally evaluated by quantitative analysis, but diverse aspects remain insufficiently assessed, so a complementary qualitative approach may have advantages. The aim of this study was to assess the impact of migraine on the quality of life of migraineurs through the perception of patients and their relatives, and healthcare professionals. Qualitative methods were used, including six focus groups and nine personal interviews with 33 migraine patients under physician-directed treatment, five self-medicated patients, five relatives of migraine patients and seven healthcare professionals. Migraine has a negative affect on the quality of life, including physical, emotional and social aspects of daily life such as family, work and social relationships. Family environment and psychological well-being of patients were the aspects most affected according to patients and relatives. Health professionals emphasized work impairment and focused on pharmacological management and on the need for adequate information about migraine for non-medicated patients and patients' relatives. Qualitative methods, such as focus groups and interviews, are a valuable resource for assessing quality of life and well-being of migraine patients. These techniques open up new areas for further research.

Adult↗
PubMed1999

The challenge of drug-induced aseptic meningitis.

Several drugs can induce the development of aseptic meningitis. Drug-induced aseptic meningitis (DIAM) can mimic an infectious process as well as meningitides that are secondary to systemic disorders for which these drugs are used. Thus, DIAM constitutes a diagnostic and patient management challenge. Cases of DIAM were reviewed through a MEDLINE literature search (up to June 1998) to identify possible clinical and laboratory characteristics that would be helpful in distinguishing DIAM from other forms of meningitis or in identifying a specific drug as the culprit of DIAM. Our review showed that nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, intravenous immunoglobulins, and OKT3 antibodies (monoclonal antibodies against the T3 receptor) are the most frequent cause of DIAM. Resolution occurs several days after drug discontinuation and the clinical and cerebrospinal fluid profile (neutrophilic pleocytosis) do not allow DIAM to be distinguished from infectious meningitis. Nor are there any specific characteristics associated with a specific drug. Systemic lupus erythematosus seems to predispose to NSAID-related meningitis. We conclude that a thorough history on prior drug intake must be conducted in every case of meningitis, with special focus on those aforementioned drugs. If there is a suspicion of DIAM, a third-generation cephalosporin seems a reasonable treatment option until cerebrospinal fluid cultures are available.

Anti-Bacterial Agents↗
PubMed1999

Procedural learning is impaired in patients with prefrontal lesions.

OBJECTIVES: To 1) determine the effect of prefrontal cortex lesions on procedural learning (PL), measured by a serial reaction-time task (SRTT); 2) confirm whether visuomotor PL is lateralized to one hemisphere; and 3) clarify the relation between visuomotor sequence learning and verbal sequence learning, working memory, and executive functions. BACKGROUND: Previous cognitive neuroscience research has implicated the prefrontal cortex in visuomotor PL but there is a lack of studies examining patients with prefrontal cortex lesions. METHODS: We studied 22 patients with strictly unilateral prefrontal cortex lesions (traumatic, ischemic, hemorrhagic, or tumors) and 52 cognitively intact controls matched for age, sex, and educational level. We administered to subjects long (10-item sequence) and short (4-item sequence) versions of the SRTT. With the long version, each hand was evaluated separately. Learning was indicated by the shortening of response times (RT) and decrease in errors across the sequential blocks and, most importantly, the rebound increase in RTs and errors when comparing the last sequence block with the next random block. Frontal lobe functions and verbal sequence learning were also assessed. RESULTS: Patients with unilateral prefrontal cortex lesions show PL impairment that involves both hands, although more errors were observed when the hand contralateral to the lesion was performing. Only those patients whose lesions were >2 cm in diameter were impaired. Neuropsychologic evaluation indicated impaired verbal sequence learning and executive function deficits. Patients with poorer working memory and verbal sequence learning were also more impaired in visuomotor sequence learning. CONCLUSIONS: The prefrontal cortex has a role in PL and is part of the neural circuit that mediates this type of learning.

Adult↗
PubMed1999

Central nervous system tuberculosis.

Involvement of the central nervous system (CNS) by Mycobacterium tuberculosis, particularly meningitis, is the most severe form of tuberculous infection. Parenchymal CNS involvement can occur in the form of tuberculoma or, more rarely, abscess. Although surgery was initially advocated as the mainstay of therapy, more recent evidence suggests that parenchymal forms of CNS tuberculosis can be cured with medical treatment alone. Also, damage of the spinal cord, roots, and spine can occur in the form of spinal meningitis, radiculomyelitis, spondylitis, or spinal cord infarction.

Humans↗
PubMed1998

Disparity between serological reactivity to Borrelia burgdorferi and evidence of past disease in a high-risk group.

A prevalence study of past Lyme borreliosis in persons with outdoor occupations was done. Consenting individuals (n = 302) were administered a questionnaire eliciting demographic and occupational data and a clinical history, and were asked to donate a serum specimen for detection of antibodies to Borrelia burgdorferi by enzyme-linked immunosorbent assay (ELISA), immunoblotting, and borrelia inhibition assays, and for detection of potentially cross-reactive antibodies. Of 302 individuals, 77 (25%) had reactive antibodies detected by ELISA. Of these 302 individuals, 44 (15%) met the criteria of the Centers for Disease Control and Prevention for serological reactivity as evidenced by immunoblotting, and 70 (23%) had inhibitory activity. Through the clinical criteria employed, only 11 individuals with serological reactivity had prior illness compatible with Lyme borreliosis. Higher ELISA absorbances were positively correlated with age and duration of outdoor occupation. The results from three serological assays and the lack of reactivity to potentially cross-reactive infectious agents indicate that serological reactivity was due to exposure to B. burgdorferi. The disparity between serological reactivity and the clinical evidence of Lyme borreliosis suggests cumulative exposure to a nonpathogenic form of B. burgdorferi.

Adult↗
PubMed1997

Mechanisms of injury in Lyme neuroborreliosis.

Neurologic injury in infection with Borrelia burgdorferi can be due to the direct action of the spirochetes and spirochetal products on neural cells. There is in vitro evidence for the adherence of this organism to neurons, to glia, and to Schwann cells. Adhesion was found to be associated with galactocerebroside, a glycolipid component of myelin, and could act as a receptor for B. burgdorferi in oligodendroglia and in Schwann cells. Another pathway for neurologic injury could be through amplification of the inflammatory response by newly invading organisms (acute) and persisting (chronic) organisms. There is experimental evidence for production of IL-6, TNF-alpha, and nitric oxide by neural cells exposed to B. burgdorferi. Similar findings have been obtained from neuroborreliosis patients. Although less likely, there is the possibility that autoreactive mechanisms could have a role in the development of some manifestations of neuroborreliosis.

Humans↗
PubMed1997

A mouse model of Borrelia meningitis after intradermal injection.

Both young and adult C3H/HeN mice developed meningitis within 3 weeks of intradermal inoculation with a newly identified uncultivable Borrelia species, an agent of human relapsing fever. Meningoencephalitis with perivascular infiltrates and plexitis developed at approximately 25 days after inoculation. Infiltrates were composed of B and plasma cells and monocytes. This model recreated the meningitis associated with spirochetal infections through an intradermal route of infection.

Aging↗
PubMed1995

Lyme neuroborreliosis.

Neuroborreliosis, an infection of the nervous system caused by spirochetes of the genus Borrelia, has achieved worldwide attention in the last decade as part of the clinical spectrum of Lyme disease. This disorder, caused by Borrelia burgdorferi, has increased in incidence to become the most frequent arthropod-borne infection in North America and Europe. As a result of this rapid rise in incidence and of its protean neurological manifestations, this disease has created an important challenge to modern neurology. The diverse manifestations of neuroborreliosis require that it be included in the differential diagnosis of many neurological disorders. This review takes a chronological approach to clinical neuroborreliosis to summarize its most important aspects. The limitations as well as the benefits of laboratory diagnosis are also considered, with the aim of providing assistance in this area. Recent advances in neuroimmunology regarding the pathogenesis of neuroborreliosis that may elucidate its protean clinical spectrum are summarized.

Europe↗
PubMed1995

Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides.

Patients with neuroborreliosis produce antibodies, mostly of the immunoglobulin M (IgM) class, to gangliosides, particularly to those with Gal(beta 1-3)GalNac terminal sequences. Lewis rats were immunized with a nonpathogenic strain of Borrelia burgdorferi and with a chloroform-methanol extract (nonprotein) of this organism (CM) to determine whether antibodies to B. burgdorferi also recognized gangliosides. Rats were also immunized with asialo-GM1 to determine whether the elicited antibodies recognized antigens in B. burgdorferi. Rats immunized with B. burgdorferi produced low levels of IgM antibodies that cross-reacted with asialo-GM1 and GM1. Rats immunized with CM had marked IgM reactivity to asialo-GM1 and GM1. Immunization with asialo-GM1 resulted in antibodies that cross-reacted with B. burgdorferi antigens. Although antibodies to B. burgdorferi were of both the IgM and IgG classes, those to CM and to asialo-GM1 and GM1 were predominantly in the IgM fraction. Reactivity of the IgM antibodies decreased after adsorption with the heterologous and the homologous antigens, indicating bidirectional cross-reactivity between CM, asialo-GM1, and GM1 and that immunization with one produces antibodies to the other. There was no in vivo deposition of Ig in peripheral nerves, nor was there nerve pathology as a result of immunizations, but IgM antibodies to asialo-GM1 and CM recognized homologous antigens in the nodes of Ranvier of peripheral nerves from nonimmunized rats. This immunization model suggests that antibodies to gangliosides in Lyme disease have a microbial origin and are potentially relevant in pathogenesis.

Animals↗
PubMed1995

[Pathomechanisms of neuroborreliosis].

Lyme neuroborreliosis has a protean clinical spectrum and a complex and still obscure pathogenesis. Central and peripheral nervous system involvement may occur, with several different mechanisms acting together or separately. Invasion of the nervous system by Borrelia burgdorferi occurs early in the course of the infection. Direct interaction of the spirochete with neural cells may result in neurological damage, as may the immune response elicited against the organism. Both T- and B-cell autoreactivity against endogenous neural structures is present and there seems to be a crossreaction between neural antigens and the flagellin of Borrelia burgdorferi. Meningitis is probably due, at least in part, to inflammatory mechanisms elicited by the presence of spirochetes in the CSF. Inflammatory and angiopathic peripheral nerve changes may lead to axonal damage resulting in peripheral neuropathy. The elaboration of proinflammatory mediators provides another possible pathway for nerve cell injury. There is still a lack of a suitable animal model to recreate the neurological manifestations paralleling human disease. However, rat and mouse models and, more recently, nonhuman primates have so far provided important information on the pathogenesis of this infection and hopefully will provide the opportunity to elucidate many still unclear mechanisms.

Animals↗
PubMed1991

Cytotoxicity of Borrelia burgdorferi for cultured rat glial cells.

A cytotoxic effect, as measured by 51Cr release, was detected after a 6-h incubation with two strains of Borrelia burgdorferi with neonatal rat primary brain cultures and with astroglial enriched cultures derived from the primary rat brain cells. A low-passage strain, J31, induced a significantly greater cytotoxic effect than did strain B31 in long-term in vitro culture. Live spirochetes and sonicates of both strains induced cytotoxicity, whereas heat-killed organisms did not. The degree of injury was greater in the primary brain than in the astroglial enriched cultures. Scanning electron microscopy revealed marked contraction of the membrane sheets and bleb production by the oligodendroglia of primary brain cultures after incubation with B. burgdorferi. The astroglial layer appeared unharmed.

Animals↗