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Biomedical subjects

M Mintz

Publications and source records attributed to M Mintz.

At least 37 records · Page 2Linked to original sources
PubMed1996

Neurological and developmental problems in pediatric HIV infection.

Human immunodeficiency virus type-1 (HIV-1)-associated neurologic disease, known as "HIV-1-associated progressive encephalopathy" (PE), is a common concomitant in the progression towards AIDS. PE, characterized by a triad of symptoms including impaired brain growth, progressive motor dysfunction, and loss or plateau of developmental milestones, is believed to result from both direct and indirect effects of HIV-1 infection on the central nervous system (CNS). Consequent to the hallmark systemic immune deficiency of HIV infection, the CNS becomes susceptible to opportunistic infections which add further morbidity and mortality, and may contribute either directly or indirectly to neurologic symptoms which can often mimic PE. Static encephalopathies (SE) represent fixed, nonprogressive neurologic or neurodevelopmental deficits in HIV-infected children. SE may or may not be caused by HIV infection but are often associated with such identifiable insults as prematurity, in utero exposure to toxins or infectious agents, or head trauma. Additional neurological manifestations of HIV infection are seizures, cerebrovascular complications (i.e., stroke), myelopathies, neuromuscular syndromes, and CNS complications of opportunistic infections. Neurobehavioral aberrations have also been observed in pediatric HIV infection. In addition to the neuropathogenesis, theories regarding the timing and detection of the neurological problems associated with pediatric HIV infection are discussed along with a presentation of current treatment paradigms and their rationales. The importance of identifying the numerous environmental factors, including nutritional status, that may confound the ability to discriminate between a primary or secondary role of HIV infection in the various neurological problems of HIV infection is discussed.

AIDS Dementia Complex↗
PubMed1996

Epidural hematoma of a cauda equina in a child with hemophilia A.

PURPOSE: The presenting signs, treatment, and outcome of an epidural hematoma of the cauda equina in a child with severe hemophilia are reported for the first time. PATIENTS AND METHODS: A 20-month-old boy with severe hemophilia A (factor VIII <0.01 U/ml) presented with a 12-day history of refusal to stand and constipation of 5-7 days duration. He had normal deep tendon reflexes with normal sensation and withdrawal to pinprick of his lower extremities bilaterally. He stood on his right leg, but had inversion of his left foot and refused to bear weight on his left leg. MRI revealed an epidural hematoma of the cauda equina and a distended bladder. Factor VIII replacement therapy and lumbosacral laminectomy with evacuation of the hematoma resulted in recovery of a normal gait, but bladder dysfunction persisted for 11 months. Clean intermittent catheterization (CIC) was required until bladder function returned. RESULTS: Complete neurologic recovery occurred 11 months after presentation CONCLUSION: This case demonstrates the following points: (a) an epidural hematoma of the cauda equina in a child with severe hemophilia can present with neurologic findings that are as subtle as those seen in normal children; (b) CIC can be performed safely over an extended period without factor VIII replacement; and (c) complete recovery is possible, despite prolonged bladder dysfunction and a 12-day interval between the onset of symptoms and treatment.

Cauda Equina↗
PubMed1996

Levodopa therapy improves motor function in HIV-infected children with extrapyramidal syndromes.

Five children with human immunodeficiency virus type-1 (HIV-1) infection, aged 4 to 13 years, manifested extrapyramidal dysfunction characterized by rigidity/stiffness, ambulation difficulties/shuffling gait, dysarthria/drooling/swallowing dysfunction, hypomimetic/inexpressive facies, and bradykinesia. Levodopa therapy caused an initial improvement in all symptoms, and the effect was sustained in most patients. Levodopa is a useful adjunctive therapy in HIV-1-infected children with extrapyramidal syndromes, by enhancing motor function and improving their quality of life.

Child, Preschool↗
PubMed1995

First month of neuroleptic treatment in schizophrenia: only partial normalization of the late positive components of visual ERP.

In a previous study we recorded visual event-related potentials (ERP) in drug-naive schizophrenics during passive-attention and active-attention tasks. Patients, compared to normal controls, had much lower late positive components (LPC) in both sessions, but nearly normal LPC increase from passive to active task. The present sample consisted of drug-naive and drug-free patients who were tested before and during the first month of neuroleptic treatment. Neuroleptics initiated gradual amelioration of psychiatric symptoms expressed by reduced Brief Psychiatric Rating Scale (BPRS) scores. Schizophrenics compared to controls showed a session-related increase in LPC amplitude, but this process of LPC recovery was too minor to fully normalize the low LPC amplitudes in patients. Furthermore, the treatment either did not improve or even reduce the LPC reaction to the active-attention task. These findings indicate that normalization of low LPC in schizophrenia might require a long period of treatment, and that patients' reduced LPC reactivity to the task might be contributed, rather than treated, by neuroleptics.

Adult↗
PubMed1995

Activation of the subthalamic nucleus and pedunculopontine tegmentum: does it affect dopamine levels in the substantia nigra, nucleus accumbens and striatum?

Parkinson's disease is a neurodegenerative disorder, of which the most prominent morphological feature is the progressive loss of dopaminergic nigrostriatal neurons. Increased glutamatergic transmission in the basal ganglia has been implicated in the pathophysiology of Parkinson's disease (PD). This study investigated whether death of substantia nigra (SN) dopaminergic neurons could be caused by the hyperactivity of afferent pathways resulting in the release of a toxic dose of excitatory amino acids in the SN. Twice-daily unilateral stimulation of the subthalamic nucleus (STN) for 21 days, using two different pulse frequencies and current strengths, significantly increased amphetamine-induced rotation, whereas sham stimulated rats showed significantly reduced rotation. Striatal and SN dopamine (DA) levels were unaffected when compared to naïve and sham stimulated rats. However, levels of the DA metabolite, homovanillic acid (HVA), were significantly higher in the ipsilateral anterior striata of rats that had been stimulated at high frequency (100 Hz) and low current (100 microA) as compared to sham treated animals. Stimulation of the pedunculopontine tegmentum (PPT), using a single kainic acid injection, did not affect DA concentration in the ipsilateral striatum and nucleus accumbens when compared to sham-treated rats. DA levels in the contralateral striatum and nucleus accumbens of lesioned rats were significantly higher than ipsilateral levels. DOPAC/DA ratios were lower in the contralateral striatum and nucleus accumbens, suggesting decreased DA turnover. Glutamic acid decarboxylase activity was significantly higher in the ipsilateral than the contralateral SN. The physical manifestations of PD require a large reduction in caudate and putamen DA levels and no such depletion was measured in this study.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1995

Long-term effects of amygdaloid kindling on striatal dopaminergic terminals.

The present study assessed the effects of kindling on striatal DA terminals. Kindled and control rats were tested for DA transporter density using [3H]GBR-12935 binding to striatal membranes and for amphetamine and KCl-induced [3H]DA release from striatal slices. Kindling decreased the maximal number of [3H]GBR-12935 binding sites in the dorsal striatum of rats sacrificed either 2 h or 4 weeks after the last seizure but had no effect on stimulated fractional [3H]DA release. These findings suggest a minor damage to DA terminals in the dorsal striatum. At the same postseizure time points, kindling augmented the hyperlocomotion associated with novel environment. Explanation of this effect requires in vivo measures of striatal DA functioning.

Amygdala↗
PubMed1995

Carnitine in human immunodeficiency virus type 1 infection/acquired immune deficiency syndrome.

There is an increasing body of evidence that subgroups of patients infected with human immunodeficiency virus type 1 possess carnitine deficiency. Secondary carnitine deficiencies in these individuals may result from nutritional deficiencies, gastrointestinal disturbances, renal losses, or shifts in metabolic pathways. However, tissue depletion precipitated by drug toxicities, particularly zidovudine, is a major etiology and concern. Carnitine deficiency may impact on energy and lipid metabolism, causing mitochondrial and immune dysfunction. There are convincing laboratory data showing the in vitro ameliorative effects of L-carnitine supplementation of zidovudine-induced myopathies and lymphocyte function. Studies measuring the impact of L-carnitine supplementation on clinical characteristics are ongoing.

Carnitine↗
PubMed1994

The effect of repeated amphetamine treatment on striatal DA transporter and rotation in rats.

The effect of repeated amphetamine treatment on the involvement of the striatal DA transporters in rotation behavior was tested in rats. Repeated amphetamine treatment had no effect on [3H]DA uptake or [3H]GBR-12935 binding density. However, unlike the naive rats who rotated away from the striatum with a lower density of DA transporters, rats sensitized to amphetamine rotated toward the striatum with a lower density of DA transporters. These findings imply that repeated amphetamine augments the subcortical involvement in behavioral output.

Animals↗
PubMed1994

Bilateral imbalance in striatal DA-uptake controls rotation behavior.

We tested the relation between bilateral imbalance in striatal DA uptake and asymmetric rotation behavior. Rats were screened for either spontaneous or amphetamine-induced preferred direction of rotation and the presynaptic DA transporter in the ipsi- and contralateral striatum was characterized in vitro by measuring [3H]DA uptake or [3H]GBR-12935 binding. DA uptake was lower in the striatum contralateral to either the spontaneous or amphetamine-induced preferred direction of rotation. Similar imbalance in the density of the transporter was confirmed by the binding experiments. These results support the hypothesis that striatal imbalance in DA uptake produces asymmetric behavior during spontaneous rotation. Further studies are required to assess the involvement of DA transporter imbalance in amphetamine-induced behavioral asymmetry.

Amphetamine↗
PubMed1994

Effect of amygdaloid kindling on rat striatal dopamine D1- and D2-receptors.

The effect of kindling on dopaminergic (DA) neurotransmission was assessed by measuring dopamine D1- and D2-receptor binding in the dorsal and ventral striatum of rats either 2 hours (short-term) or 3-4 weeks (long-term) after the last kindled seizure. Kindling did not have any significant long-term effect on DA D2-receptor Kd or Bmax values in the dorsal or ventral striatum or on DA D1-receptor parameters in the dorsal striatum. The short-term effect of kindled seizures was to abolish the asymmetry in DA D2-receptor density observed in the dorsal striatum of control rats. DA D1-receptor density was also increased in the dorsal striatum contralateral to the kindled amygdala of short-term rats. The short-term effects support the notion that limbic seizures can modify the lateral imbalance of DA activity in the striatum.

Amphetamine↗
PubMed1994

Unilateral inferior olive NMDA lesion leads to unilateral deficit in acquisition and retention of eyelid classical conditioning.

New Zealand White rabbits (Oryctolagus cuniculus) were trained for acquisition (N = 21) or retention (N = 10) of classical eyelid conditioning with unilateral or bilateral N-methyl-DL-aspartate chemical lesions of the rostromedial dorsal accessory inferior olive (rmDAO; multiple injections totaling 76 to 342 nmol). In all instances, subjects were unable to learn or retain conditioning on the side contralateral to the lesion. Learning rates were comparable for lesions outside of the rmDAO and sham operates. These findings demonstrate a specific unilateral deficit whereas in previous research the answer to this question was ambiguous since electrolytic lesions effectively cause bilateral olivary lesions. This research agrees with the concept that the inferior olive projects essential information about the unconditioned stimulus to a cerebellar locus of learning and memory for classical conditioning.

Animals↗
PubMed1994

Clinical comparison of adult and pediatric NeuroAIDS.

Human Immunodeficiency Virus type-1 (HIV-1)-associated neurologic disease occurs as the initial presenting clinical manifestation of acquired immunodeficiency syndrome (AIDS) in 3-7% of infected patients, but in up to 18% of children and adolescents (Janssen, 1992; Janssen et al., 1992; Scott et al., 1989; Mintz et al., 1989a; Epstein et al., 1986). The overall prevalence of dementia in adult AIDS patients is 7.3-11.3% (Janssen, 1992), but up to 30-60% of children with AIDS manifest an analogous progressive encephalopathy (Epstein et al., 1986; Belman et al., 1988; Mintz, 1992; The European Collaborative Study, 1990). As a result of both direct and indirect effects of HIV-1 infection of the central nervous system (CNS), a distinct clinical and pathologic picture has emerged of insidious and severe neurologic deterioration, termed "AIDS Dementia Complex" (ADC) in adults, and "HIV-1-associated Progressive Encephalopathy" (PE) in children (Working Group, 1991) (see Table 1). In the severe manifestations of this pariah, there is little dispute as to the necessity of CNS HIV-1 infection for precipitating the cascade of adverse neurologic symptoms, although the pathogenic mechanisms of neurologic dysfunction and destruction--whether a result of direct cellular infection of HIV, secondarily produced and upregulated cytotoxic cytokines, or co-infection with opportunistic pathogens--remains an area of active research (Epstein and Gendelman, 1993; Fiala et al., 1993; Wiley and Nelson, 1988; Saito et al., 1994; Koenig et al., 1986; Sharer, 1992). Furthermore, the existence of systemic immune deficiency renders the CNS susceptible to opportunistic infection (OI), particularly in adult patients, adding further to morbidity and mortality (Clifford and Campbell, 1992). With the introduction of antiretroviral nucleoside analogues, there have been reports of a decreasing incidence of ADC (Portegies et al., 1989; Day et al., 1992), and amelioration--at least temporarily--of PE in children (Pizzo et al., 1988; Mintz and Epstein, 1992; Brouwers et al., 1990; Mintz et al., 1990). This appends further evidence to the central precipitating role of CNS HIV-1 infection.

AIDS Dementia Complex↗
PubMed1994

Overexpression of nef as a marker for restricted HIV-1 infection of astrocytes in postmortem pediatric central nervous tissues.

In previous studies, using polymerase chain reaction amplification of HIV-1 genes directly from pathologic tissues of children who died with AIDS encephalopathy, we showed that the reading frame of the HIV-1 regulatory nef gene is open, suggesting that the nef protein was expressed. We now show, using immunocytochemistry and in situ hybridization with nef-specific probes in postmortem pediatric CNS tissues, that nef mRNA and protein are present in up to 20% of astrocytes in tissue sections selected for extensive histopathology. By contrast, HIV-1 structural proteins such as gag and their coding mRNAs are present in multinucleated giant cells that harbor productive infection and are the hallmark of HIV-1 infection in the CNS. These findings are consistent with the nonproductive infection of glial cells observed in vitro, and imply that HIV-1 infection of astrocytes is restricted to early regulatory gene products, of which nef is the best target as it is expressed at high levels and is membrane-anchored. In developing central nervous tissues of children, restricted and latent HIV-1 infection of astrocytes may be extensive and contribute significantly to HIV-1 neuropathogenesis.

Aged↗
PubMed1994

[Diagnostic and therapeutic value of laparoscopic needle biopsies of persistent para-uterine cysts: absence of recurrences and consecutive pregnancies. In view of ultrasonography-guided biopsies].

In the presence of a persistent para-uterine cyst, the actual tendency is to operate by laparotomy or most frequently by laparoscopic surgery. This leads to ablation of 20% of the so called "Functional cysts". A 30 years experience of laparoscopic puncture of 745 persistent para-uterine cysts, among which 321 were preserved and controlled, shows that 69% of them, of various origin or nature do not recur, whereas many pregnancies happen to come at short notice: 59% of 117 patients who wished to be pregnant had 73 known living children. Young, nulliparous or sterile patients, could at a first step, under strict conditions, get the benefit of a sonographic-guided diagnostic and therapeutic puncture, avoiding a useless endoscopy or ablation.

Adolescent↗
PubMed1993

Effect of nootropic Solcoseryl on kainic acid-induced excitotoxic brain injury.

Solcoseryl (S) has been shown to provide significant cytoprotection in a variety of models of cerebral hypoxia. In the present study, we quantified the epileptiform effects caused by kainic acid administered into the pontine reticular formation of rats and their response to S pretreatment. Compared to saline, the agent appeared to significantly reduce the mortality of rats in the course of status epilepticus. However, S-pretreated rats manifested an increased incidence of behavioral seizures. This untoward effect is attributed to the fact that S improves the functional potential of injured tissue and retards the period of metabolic exhaustion at a time when neuronal activity should be minimized.

Actihaemyl↗
PubMed1993

Effect of an adenosine A1 agonist injected into substantia nigra on kindling of epileptic seizures and convulsion duration.

The substantia nigra pars reticulata (SNr) has been reported to be critically involved in the development and propagation of epileptic seizures, while extracellular adenosine appears to be important for making seizures stop. In the present study, an adenosine A1 receptor agonist [N6-cyclohexyladenosine (CHA); 2.0 nmol/side, or vehicle] was injected bilaterally into the SNr shortly before each of the first five of a series of daily kindling stimuli delivered to the rat amygdala. Injections did not affect the acquisition of kindled afterdischarges or the rate at which seizures developed over subsequent kindling sessions, but convulsions occurring 48-72 h after treatment were significantly shortened. Thus, purinergic mechanisms in the SNr do not appear to be specifically involved in the acquisition of kindled seizures but may contribute to a postictal inhibitory process that shortens the convulsive component.

Adenosine↗