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Biomedical subjects

M F Mazurek

Publications and source records attributed to M F Mazurek.

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

Circadian pattern of acute, neuroleptic-induced dystonic reactions.

OBJECTIVE: This study examined the timing of acute dystonic reactions in 200 patients taking neuroleptic medication for the first time. METHOD: Two hundred patients received a twice-daily regimen of low-dose neuroleptic. RESULTS: Over 80% of the episodes of acute dystonia occurred between 12:00 noon and 11:00 p.m. The observed circadian variation was not accounted for by sleep, fatigue, or time elapsed from the last dose of medication. CONCLUSIONS: The finding of a diurnal pattern in one of the recognized side effects of neuroleptic medication suggests that the therapeutic efficacy of neuroleptics might similarly vary over the course of the day.

Acute Disease↗
PubMed1995

Late-onset Tay-Sachs disease presenting as catatonic schizophrenia: diagnostic and treatment issues.

BACKGROUND: It is not commonly appreciated that patients with hexosaminidase A deficiency (Tay-Sachs disease) can first present in adulthood with psychiatric illness. METHOD: A 17-year-old non-Jewish male patient was referred with a history of treatment-resistant catatonic schizophrenia. We uncovered coexistent neurologic abnormalities and evidence of cognitive decline. Metabolic screening revealed a severe deficiency of beta-hexosaminidase A. We reviewed the literature on late-onset gangliosidosis with attention to (1) the nature of the associated psychiatric and neurologic abnormalities and (2) the treatment of psychosis in these patients. RESULTS: The patient's catatonia responded promptly to benzodiazepine therapy. Treatment with neuroleptic medication resulted in the rapid development of neuroleptic malignant syndrome. The patient was thereafter maintained on lorazepam with resolution of his acute psychiatric disturbances and unexpected improvement in his neurologic status. CONCLUSION: Patients with hexosaminidase deficiency may first present in adolescence or adulthood with psychiatric illness, particularly schizophrenic-like psychosis. The presence of speech disturbance, gait abnormalities, movement disorders, and cognitive decline may indicate an underlying metabolic disorder. The use of traditional neuroleptics to treat the psychosis in such individuals may produce an unacceptably high risk/benefit ratio. Benzodiazepines may ameliorate the psychiatric and neurologic abnormalities in these patients.

Adolescent↗
PubMed1994

Lorazepam treatment of acute and chronic catatonia in two mentally retarded brothers.

BACKGROUND: Acute catatonia of the retarded type responds rapidly to treatment with lorazepam. There is little information about (1) the efficacy of benzodiazepines in patients with longstanding catatonic syndrome; (2) the effect of longer-term lorazepam therapy in catatonic patients who do not respond to a brief trial of the medication; and (3) the development of catatonic syndromes in family members. METHOD: We gave lorazepam to two mentally retarded brothers with catatonia. One had become catatonic 2 weeks before starting treatment while the other had been hospitalized in a catatonic state for 5 years. RESULTS: The brother with acute catatonia recovered slowly but completely within 2 weeks of starting lorazepam. The brother with long-standing catatonia responded gradually during the first 5 months of treatment and required higher doses of lorazepam but did eventually recover and was discharged from the hospital on a regimen of lorazepam after 1 year of treatment. CONCLUSION: (1) Lorazepam may be effective even in patients who have been catatonic for years. (2) Catatonic patients who do not recover immediately with lorazepam may respond to a longer course or higher doses of the medication. (3) There may be a familial predisposition to developing catatonia in response to stressful situations.

Adult↗
PubMed1993

Reduced cerebral cortical but elevated striatal concentration of somatostatin-like immunoreactivity in dominantly inherited olivopontocerebellar atrophy.

Somatostatin-like immunoreactivity (SLI) was measured in the brains of nine patients with dominantly inherited olivopontocerebellar atrophy (OPCA), who all had a marked deficit of the cholinergic marker choline-acetyltransferase (ChAT) in the cerebral cortex and striatum. Mean concentrations of SLI in OPCA were significantly reduced by 42-58% in parietal and occipital cortices and frontal cortical eye fields, but were normal in other cortical areas, including two subdivisions of the temporal cortex which show marked depletions of both SLI and ChAT in Alzheimer's disease. This dissociation of SLI and ChAT indicates that a cortical cholinergic deficit does not invariably lead to reduction of somatostatin. In the caudate nucleus, the region of OPCA brain having the most severe ChAT deficit (-81%), SLI levels were significantly elevated by 46% and were negatively and significantly correlated with ChAT activities (r = -0.66). The SLI alterations could be due to abnormal somatostatin metabolism or release, or an increased number of somatostatin-containing neurons and could contribute to the brain dysfunction of OPCA.

Adult↗
PubMed1992

The cortical lesion of Huntington's disease: further neurochemical characterization, and reproduction of some of the histological and neurochemical features by N-methyl-D-aspartate lesions of rat cortex.

Huntington's disease is a progressive neurodegenerative disease in which the basal ganglia are preferentially affected. Recent evidence, however, suggests involvement of the cerebral cortex as well, with sparing of neurochemically defined subsets of gamma-aminobutyric acid (GABA)-ergic interneurons. In the present study, we examined changes in concentrations of the amino acid neurotransmitters GABA, glutamate, and aspartate in nine cortical regions from 23 patients with advanced Huntington's disease and 12 control brains. GABA concentrations were significantly increased in eight of the nine regions, consistent with a sparing of GABAergic local circuit neurons in the context of progressive cortical atrophy. Small but significant increases in glutamate were found in six of the nine regions, while aspartate levels were generally unaffected. Striate cortex (Brodmann's area 17) showed the most profound increases in GABA and glutamate. We also investigated the effects of powdering the excitotoxins N-methyl-D-aspartate (NMDA) or kainic acid onto the dura of rats. The resulting lesions were examined at 1 week and 6 months. The NMDA-induced lesions showed striking sparing of parvalbumin-positive neurons (a subset of GABAergic interneurons), and this sparing was reflected in neurochemical measurements of GABA; kainic acid lesions failed to display this selectivity. Somatostatin, cholecystokinin, and vasoactive intestinal polypeptide concentrations were spared by the NMDA-induced lesions, and substance P levels were significantly increased. These results provide evidence that NMDA excitotoxic lesions of cerebral cortex can produce a selective pattern of neuronal damage similar to that which occurs in Huntington's disease.

Age Factors↗
PubMed1991

Serum iron and neuroleptic malignant syndrome.

Neuroleptic malignant syndrome (NMS) is a fulminant, life-threatening reaction to neuroleptic medications. The only consistently described biochemical abnormalities are increased creatine kinase and leucocytosis. Because of a possible association between NMS and dopaminergic function and between serum iron and dopaminergic function, we prospectively measured serum iron in 26 episodes of NMS in twenty-three patients. In 25 episodes (96%) serum iron concentration was 10 mumol/l or lower--more than 2 SD below the mean normal value. Serum iron in 11 episodes (36%) was 4 mumol/l or lower. In each episode for which data are available, serum iron returned to normal upon resolution of the NMS. Serum iron may be a helpful adjunct for the diagnosis of the disorder. The pronounced reduction in serum iron suggests that the acute phase reaction may have a role in NMS.

Acute Disease↗
PubMed1991

MPTP-induced neurotoxicity and the quest for a preventative therapy for Parkinson's disease.

Less than 10 years have passed since the discovery that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is capable of producing parkinsonism in both humans and non-human primates. In that time, there has been considerable interest in the possibility that the pathogenesis of idiopathic Parkinson's disease (PD) might involve a process analogous to that of MPTP toxicity. One hypothesis holds that PD might arise, at least in part, from exposure to an MPTP-like environmental toxin. Rapid progress has been made towards elucidating the precise mechanism by which MPTP exerts toxicity, and clarifying the relationship of MPTP toxicity to idiopathic PD. The goal of these efforts is to develop a therapy that inhibits the underlying disease process in PD.

Environmental Pollutants↗
PubMed1991

The treatment of neuroleptic malignant syndrome. Are dantrolene and bromocriptine useful adjuncts to supportive care?

In a prospective study of 20 patients with NMS, those who received dantrolene (2 patients) or bromocriptine (2 patients) or both (4 patients) tended to have a more prolonged course of illness and a greater incidence of sequelae than those treated with supportive care alone. These results do not indicate a useful role for dantrolene or bromocriptine in the treatment of NMS.

Adult↗
PubMed1991

Cholecystokinin and somatostatin in Alzheimer's disease postmortem cerebral cortex.

The neuropeptides cholecystokinin (CCK) and somatostatin are synthesized in separate, but morphologically similar, populations of locally projecting neurons in cerebral cortex. Concentrations of somatostatin are markedly diminished in Alzheimer's disease (AD), suggesting possible dysfunction of the intrinsic cortical neurons in which it is produced. We determined whether cortical levels of CCK might be similarly affected in AD by dissecting postmortem brain samples from 14 histologically confirmed cases of AD and 17 age-matched controls and measuring CCK and somatostatin by radioimmunoassay. CCK-like immunoreactivity was significantly reduced in the AD brains by 24 to 38% in five of the 11 cortical areas examined but was normal in the remaining regions. Somatostatin concentrations measured in the same tissue extracts were consistently decreased by 45 to 65%. These results indicate that (1) CCK-immunoreactive neurons in cortex are affected by the AD process, and (2) the changes in levels of CCK are less dramatic than the reductions of somatostatin immunoreactivity.

Alzheimer Disease↗
PubMed1991

Neurochemical characterization of excitotoxin lesions in the cerebral cortex.

Neuronal degeneration that occurs in both ischemia and degenerative neurologic illnesses may involve excitotoxic mechanisms. In the present study, we examined whether cortical lesions with agonists acting at subtypes of glutamate receptors result in selective patterns of neuronal death. Injections of quinolinic acid, NMDA, homocysteic acid, kainic acid (KA), and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) were made at 2 sites in the dorsolateral frontoparietal cortex in rats. After 1 week, the cerebral cortex was either dissected for neurochemical studies, or animals were perfused for histologic evaluation. Concentrations of somatostatin (SS), neuropeptide Y (NPY), substance P (SP), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay, while amino acids and catecholamines were measured by high-performance liquid chromatography (HPLC) with electrochemical detection. NMDA agonists (quinolinic acid, homocysteic acid, and NMDA itself) resulted in dose-dependent reductions in glutamate and GABA, while SS, NPY, SP, CCK, and VIP were either unchanged or significantly increased in concentration. KA and AMPA at doses that resulted in comparable GABA depletions caused significant reductions in SS concentrations. Markers of cortical afferents were spared. All excitotoxins resulted in dose-dependent marked increases in uric acid concentrations. Histologic examination verified that lesions with NMDA agonists produced relative sparing of NADPH-diaphorase, SS, VIP, and CCK neurons. These results show that NMDA excitotoxin lesions result in a pattern of selective neuronal damage in the cerebral cortex that is similar to that which occurs in both ischemia and Huntington's disease.

Animals↗
PubMed1990

Catatonic syndrome in a general psychiatric inpatient population: frequency, clinical presentation, and response to lorazepam.

In a prospective open trial conducted on a general psychiatric ward, the authors diagnosed catatonic syndrome 15 times in 12 patients over a 1-year period. These 12 patients represented 9% of all admissions. The following signs were present in two thirds or more of the episodes studied: immobility (100%), staring (92%), mutism (85%), withdrawal/refusal to eat (78%), posturing/grimacing (73%), and rigidity (66%). Other signs of catatonia were seen less frequently. Lorazepam 1 to 2 mg was administered in every case, and patients were evaluated at hourly intervals. Of the 15 episodes, 12 responded completely and dramatically to lorazepam treatment within 2 hours, 1 responded partially, and 2 had no response. Adverse effects were infrequent. A CNS abnormality or dysfunction was evident in 8 of the 12 responders, suggesting that a beneficial response to lorazepam is not limited to patients with pure psychogenic catatonia. The prompt recognition and treatment of catatonia may reduce morbidity in and length of stay for hospitalized psychiatric patients.

Adolescent↗
PubMed1989

Neurochemical characteristics of aluminum-induced neurofibrillary degeneration in rabbits.

Aluminum-induced neurofibrillary degeneration in rabbits is known to affect particular populations of neurons. The neurotransmitter alterations which accompany aluminum neurofibrillary degeneration were examined in order to assess how closely they mimic those of Alzheimer's disease. There was a significant reduction in choline acetyltransferase activity in entorhinal cortex and hippocampus as well as significant reductions in cortical concentrations of serotonin and norepinephrine in the aluminum-treated rabbits. Significant reductions in glutamate, aspartate and taurine were found in frontoparietal and posterior parietal cortex. Concentrations of GABA were unchanged in cerebral cortex. Both substance P and cholecystokinin immunoreactivity were significantly reduced in entorhinal cortex but there were no significant changes in somatostatin, neuropeptide Y and vasoactive intestinal polypeptide. The five neuropeptides were unaffected in striatum, thalamus, cerebellum and brainstem. Neurochemical changes were found in the regions with the most neurofibrillary degeneration while regions with little or no neurofibrillary degeneration were unaffected. The reductions in choline acetyltransferase activity, serotinin and noradrenaline suggest that some neuronal populations preferentially affected in Alzheimer's disease are also affected by aluminum-induced neurofibrillary degeneration; however, the cortical somatostatin deficit which is a feature of Alzheimer's disease is not replicated in the aluminum model.

Aluminum↗
PubMed1988

Cerebrospinal fluid somatostatin and neuropeptide Y. Concentrations in aging and in dementia of the Alzheimer type with and without extrapyramidal signs.

Cerebrospinal fluid somatostatin and neuropeptide Y concentrations were measured in 26 healthy normal subjects, 27 patients with dementia of the Alzheimer type (DAT), and seven patients with DAT with extrapyramidal signs (EDAT). In healthy normal subjects, there was no significant correlation between age and either somatostatin or neuropeptide Y concentration. However, the concentrations of both peptides correlated significantly with each other. In patients with DAT and EDAT, the concentrations of somatostatin (17.5 +/- 5.0 and 16.4 +/- 5.0 pg/mL, respectively) were significantly reduced relative to age-matched control subjects (23.1 +/- 8.2 pg/mL) but were unrelated to dementia severity and did not change significantly during the progression of the disease. Neuropeptide Y concentrations did not differ significantly between the age-matched control, DAT, and EDAT groups (38.2 +/- 12.8, 37.0 +/- 12.3, and 30.3 +/- 7.8 pg/mL, respectively). These results suggest that in DAT, dysfunction of cortical somatostatin but not neuropeptide Y transmitter systems is reflected by reduced cerebrospinal fluid concentrations.

Adult↗