PubMed Health⌕ Search

Biomedical subjects

M Guttman

Publications and source records attributed to M Guttman.

63 records · Page 4Linked to original sources
PubMed1987

Regional cerebral glucose metabolism in SLE chorea: further evidence that striatal hypometabolism is not a correlate of chorea.

The pathophysiology of chorea in systemic lupus erythematosus (SLE) is uncertain. Pathologic examination has not identified a specific location for the causative lesion(s) and immunologic mechanisms have been suggested in its etiology. In other choreic disorders, such as Huntington's disease and benign hereditary chorea, glucose hypometabolism in the striatum has been demonstrated by positron computed tomography (PCT) using [18F]deoxyglucose. With this technique we have studied four patients with chorea secondary to SLE. In these patients the regional distribution of cerebral glucose metabolism was normal. In particular, striatal glucose metabolism was within the normal range, even though the ratio of striatal to cortical glucose metabolism was increased. Our results show that striatal hypometabolism, as seen in other disorders manifesting chorea, is not the PCT correlate of the dyskinesia.

Adult↗
PubMed1987

Receptors in the basal ganglia.

The study of neurotransmitter receptors aids in the understanding of the normal anatomy, pharmacology, therapeutics and pathophysiology of disease processes involving the basal ganglia. Receptors may be studied in vitro by homogenate binding experiments, enzyme analysis or quantitative autoradiography and in vivo with positron emission tomography. In the substantia nigra (SN), receptors have been identified for somatostatin, neurotensin, substance P, glycine, benzodiazepine and GABA, opiates, dopamine, angiotensin converting enzyme (ACE) and serotonin. The striatum has receptors for dopamine, GABA and benzodiazepines, acetylcholine, opiates, substance P, glutamate and cholecystokinin. GABA and benzodiazepine receptors are also located in the globus pallidus. In Parkinson's disease, striatal dopamine D-2 receptors are elevated in patients that have not received L-DOPA therapy. This supersensitivity is reversed with agonist therapy. Muscarinic binding to cholinergic receptors seems to correlate with dopamine receptors. Delta opiate receptors are increased in the caudate and mu binding is reduced in the striatum. In the SN of patients with Parkinson's disease, there is reduced binding of somatostatin, neurotensin, mu and kappa opiates, benzodiazepine and GABA and glycine. In Huntington's disease, there is reduced binding of GABA and benzodiazepines, dopamine, acetylcholine, glutamate and CCK. There is increased binding of GABA in both the SN and globus pallidus. Glycine binding is increased in the substantia nigra and ACE is reduced.

Animals↗
PubMed1986

Dopamine D2 receptor density remains constant in treated Parkinson's disease.

D2 dopamine receptor densities were measured in postmortem samples of the caudate nucleus and putamen from 36 parkinsonian patients. The relationship between the age of the patient, duration of the disease, and duration of L-dopa therapy versus density of brain D2 dopamine receptors was examined using [3H]spiperone. Receptor density in parkinsonian tissues was constant over the age range of 56 to 90 years, as was the case for control tissues. Density did not change with duration of disease up to 24 years. Treatment with L-dopa did not cause progressive reduction in receptor density. The diminished clinical response in the final stages of Parkinson's disease is not due to receptor dropout, and must depend on other factors.

Age Factors↗
PubMed1985

L-dopa reverses the elevated density of D2 dopamine receptors in Parkinson's diseased striatum.

Striatal dopamine receptors were studied using [3H]-spiperone in postmortem tissues of thirty-six patients with Parkinson's Disease. Each tissue was analyzed by the receptor saturation method. In non-treated patients, the D2 dopamine receptor density was elevated in the caudate nucleus and putamen compared to controls. The dissociation constant for [3H]-spiperone was similar in all groups. The elevated density of D2 receptors in non-treated patients may indicate dopaminergic supersensitivity in this disease. The elevated density was reversed with dopamine agonist therapy, but the density was not lower than control tissues.

Adult↗
PubMed1985

Studies on the utility of urinary 3,4-dihydroxyphenylethylene-glycol (DHPG) measurement.

The utility of urinary DHPG measurement as an index of NE function was evaluated in an animal model by determining its excretion following pharmacological manipulations that are known to alter noradrenergic activity. Acute desipramine (DMI) administration (10 mg/kg, i.p., b.i.d.) significantly reduced urinary DHPG (-26%) but not MHPG (-18%) excretion. Acute yohimbine administration (5 mg/kg, i.p., b.i.d.) significantly increased urinary DHPG and MHPG levels to a similar extent (+46%). These findings suggest that urinary DHPG levels also provide a sensitive indicator reflecting changes in NE neuronal activity. Further, DHPG may be a better measure of NE metabolism than MHPG to assess the efficiency of the NE neuronal uptake system.

Animals↗
PubMed1984

Visual loss secondary to a giant aneurysm in a patient with tuberous sclerosis.

We report a fifty three year old man who presented with progressive visual loss. Investigation disclosed a giant aneurysm with optic nerve compression, which was successfully treated surgically. The patient had typical skin lesions of tuberous sclerosis, but did not suffer from a seizure disorder or mental retardation. In the past he had had an enucleation for glaucoma secondary to a retinal phakoma. Cerebral aneurysms are discussed in relation to the tuberous sclerosis disease process. After review of the literature, we propose that the aneurysms are secondary to dysplastic change in the vessel walls, this is in keeping with the abnormal tissue proliferations in this disease.

Carotid Artery Diseases↗