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Biomedical subjects

E Melamed

Publications and source records attributed to E Melamed.

At least 145 records · Page 8Linked to original sources
PubMed1989

[Syringomyelic form of leprosy].

A 60-year-old man suffered from recurrent painless burns. During his first neurological work-up, ulcers with trophic changes were noted on the dorsum of both hands. Temperature and pain sensation were decreased over the upper extremities, but touch, vibration and position sense were normal. Syringomyelia was considered, but neuroradiologic evaluation was negative. A year later he was readmitted and was found to have patchy anesthesia involving all extremities, but no distal muscle weakness or wasting; tendon reflexes were normal. Leprosy was diagnosed and confirmed by skin and nerve biopsies. This syringomyelic form of leprosy is difficult to diagnose as it often mimics intraspinal space-occupying lesions. In Israel, where leprosy is still endemic, unusual sensory disturbances, such as patchy dysesthesia, should suggest its possibility.

Diagnosis, Differential↗
PubMed1988

Early and delayed neurotoxicity of mitoxantrone and doxorubicin following subarachnoid injection.

Doxorubicin (DXR) and Mitoxantrone (MXN) were administered into the subarachnoid space of mice or the ventricular system of rats. The maximal non-toxic systemic single dose (zero mortality = LDo) of DXR or MXN was used as reference for planning drug doses for CSF administration. LDo in mice were: 8 mg/kg DXR and 6 mg/kg MXN; in rats: 6 mg/kg DXR and 4.5 mg/kg MXN. Signs of neurotoxicity were remarkably similar in DXR or MXN treatment animals and included: head tremor, atactic-dystonic posture and circling behavior. The toxicity was dose dependent. Doses of greater than or equal to 10% the LDo caused early appearance of clinical signs: a dose of 10% LDo caused neurotoxicity in 90% of DXR treated mice and in only 15% of MXN-treated animals. Treatment with 25% LDo MXN caused neurotoxicity in 30% of treated animals. Doses of less than or equal to 5% the LDo caused a delayed onset of DXR neurotoxicity in one third of treated mice (after 60-90 days). In rats, neurotoxicity was of an early onset and augmented severity following doses of greater than or equal to 5% LDo. Abnormal histopathological findings were detected only in symptomatic animals with early toxicity and were usually restricted to superficial cortical layers in mice or the basal surface of the brainstem in rats. Brains of mice with delayed toxicity were unremarkable. The levels of monoamine neurotransmitters and their metabolites (DA, DOPAC, HVA, NE, 5HT) in the striatum, cortex and cerebellum of mice with early and delayed DXR neurotoxicity did not differ from normal brains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Involvement of ventral noradrenergic bundle in corticosterone secretion following neural stimuli.

In view of the involvement of noradrenaline (NA) in the regulation of adrenocortical secretion, its role in the rise of plasma corticosterone following neural stimuli was evaluated in rats. The injection of the catecholamine neurotoxin 6-hydroxydopamine (6-OHDA) into the ventral noradrenergic bundle in the brain stem, which projects to the hypothalamus, caused an average depletion of NA of 72% and 78% in the mediobasal hypothalamus and the paraventricular nuclei respectively, when compared to the rats injected with vehicle. In the animals injected with 6-OHDA, the basal level of corticosterone in plasma and the response to stress induced with ether were not affected. However, the adrenocortical discharge was very significantly inhibited following photic, acoustic and sciatic nerve stimulation. The present experiments support the results of previous studies on the stimulatory effect of NA on adrenocortical secretion.

Acoustic Stimulation↗
PubMed1988

Hypothalamic norepinephrine mediates limbic effects on adrenocortical secretion.

The purpose of this study was to elucidate the role of norepinephrine (NE) in the mediation of adrenocortical responses following limbic stimuli. The effects of stimulation of the dorsal and ventral hippocampus and the midbrain reticular formation on the plasma corticosterone (CS) levels was studied in rats with vehicle or 6-hydroxydopamine (6-OHDA) injected bilaterally into the paraventricular nucleus of the hypothalamus (PVN). The injection of 6-OHDA caused a very significant reduction in the concentration of PVN NE and blocked the rise in plasma CS following the stimulation of the above three limbic structures. The basal CS level and the response to ether stress were not affected. The present study supports previous observations on the stimulatory role of NE on CS secretion and that the modulatory effects of extrahypothalamic limbic structures on the adrenocortical activity depend on the presence of NE in the PVN.

Adrenal Cortex↗
PubMed1988

Brain grafting may reverse loss of responsiveness to levodopa therapy in Parkinson's disease.

Loss of efficacy and response fluctuations develop in many patients with Parkinson's disease after long-term levodopa therapy. This may be due in part to near-total degeneration of the surviving nigrostriatal dopaminergic neurons during disease progression, with massive decreases in the capacity of the striatum to form and store dopamine from exogenous levodopa. It was recently suggested that intracerebral grafting of fetal nigral or adrenal chromaffin cells may be beneficial in advanced Parkinson's disease by reestablishing spontaneous dopaminergic neurotransmission or by secretion of trophic factors that promote sprouting of residual dopaminergic nerve-terminals. It is now hypothesized that intrastriatal transplantation of such cellular elements that contain the enzyme dopa decarboxylase and dopamine storage sites may significantly increase synthesis, storage, and release of dopamine from exogenous levodopa. It may therefore reverse loss of responsiveness and restore the initial smooth and stable beneficial effect of levodopa therapy.

Adrenal Glands↗
PubMed1987

Effect of intrastriatal and intranigral administration of synthetic neuromelanin on the dopaminergic neurotoxicity of MPTP in rodents.

Previous studies showed that the neurotoxin MPTP and its toxic metabolites bind with high affinity to neuromelanin (NM). Therefore, the presence of NM in human and primate but not in rodent substantia nigra, theoretically may be responsible for the species-selective dopaminergic (DA) toxicity of MPTP. We measured DA levels in rodent striatum 7 days after an acute single challenge with MPTP (40 mg/kg, s.c.) given alone or 24 h following unilateral intrastriatal injections of synthetic DA-NM in mice and intrastriatal or intranigral pigment administration in rats. Ipsilateral striatal DA levels were unaffected in control rodents treated with unilateral intrastriatal or intranigral DA-NM. In mice, systemic MPTP produced marked striatal DA depletions which were mildly increased in the striata given prior DA-NM injections. In rats, a species resistant to MPTP, administration of toxin did not affect striatal DA levels. However, after pretreatment with unilateral intrastriatal DA-NM, MPTP induced mild DA falls in ipsilateral striata. By contrast, intranigral administration of DA-NM followed by MPTP, did not alter ipsilateral striatal DA in rats. The findings suggest that intrastriatal DA-NM in mice and rats may augment or initiate, respectively. MPTP-induced damage to sensitive DA-nerve-terminals perhaps by its action as a depot for binding and protracted release and action of the toxin. Lack of effect of intranigral DA-NM which is retained extraneuronally suggests that role of NM in the toxicity of MPTP may depend on its location within DA cell bodies in the nigra.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

The neurotoxin MPTP does not affect striatal superoxide dismutase activity in mice.

Intraneuronal superoxide generation may be a possible mechanism of the dopaminergic (DA) neurotoxicity of MPTP. In such case, MPTP might theoretically affect superoxide dismutase (SOD) activity. We determined SOD activity and DA levels in striata of mice at 0.5, 1, 4, 16, 24 h or 7 days after an acute single injection of MPTP (40 mg/kg, s.c.). MPTP produced marked striatal DA depletions from 4 h post-treatment but SOD activity remained unaltered and similar to controls at all time points. Intrastriatal injections of purified SOD 15 min prior to systemic administration of MPTP did not attenuate the MPTP-induced striatal DA depletions in mice at 7 days post-treatment. Combined administration of MPTP with the SOD inhibitor diethyldithiocarbamate markedly enhanced striatal DA decreases produced by MPTP alone. Findings suggest that MPTP does not act via inhibition of SOD. Therefore, potentiation of MPTP toxicity by diethyldithiocarbamate may be due to interference with other enzymatic systems.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Regional brain superoxide dismutase activity is altered differently by heat in warm and cool mice.

The significant regional variation in brain superoxide dismutase (SOD) activity was similar in mice from both warm and cool cohorts. Mice in the cool cohort generally had higher SOD activity, which varied significantly with body temperature in striatum and in preoptic area of the hypothalamus. Changes in SOD activity following heating were revealed only when warm and cool cohorts were analysed separately. SOD activity decreased significantly in striatum, hypothalamus, and hippocampus of the cool cohort only. The decline was to levels consistent with those of the warm cohort. Body temperature of cool mice increased more than that of warm mice following each increment of heating so resultant body temperatures became similar. The role of SOD as part of a differential defense against heat stress in warm and cool mice is presented.

Animals↗
PubMed1987

Regional cerebral blood flow in Down's syndrome.

Regional cerebral blood flow was measured in 14 patients with Down's syndrome, in 46 patients with Alzheimer's disease and senile dementia of the Alzheimer type, and in 114 age-matched controls, using the xenon 133 inhalation technique. Cerebral blood flow was reduced in 13 of 14 Down's patients by a mean of 16.8 +/- 2.5% from expected age-matched normal values. Degrees of regional cerebral blood flow reduction did not differ among the frontal, temporal, parietal, and occipital regions in both cerebral hemispheres. The regional cerebral blood flow decreases were similar in magnitude and pattern to those in Alzheimer patients. These findings constitute an additional similarity between the two disorders.

Adolescent↗
PubMed1987

Paraventricular nucleus serotonin mediates neurally stimulated adrenocortical secretion.

The purpose of this study was to further elucidate the role of serotonin (5-HT) in adrenocortical regulation. The effects of stimulating the frontal cortex and extrahypothalamic limbic structures, on plasma corticosterone (CS) responses, were studied in rats with vehicle or 5,7-dihydroxytryptamine (5,7-DHT) injection into the midbrain raphe nuclei. In another group of rats the neurotoxin was injected locally into the paraventricular nucleus (PVN) in view of its importance in adrenocortical regulation, and the effects of photic and dorsal hippocampal stimulation on plasma CS were studied. 5,7-DHT caused a significant depletion of hypothalamic 5-HT and blocked the rise in plasma CS following the stimulation of the above neural modalities. These studies suggest that the PVN 5-HT mediates the adrenocortical responses following afferent neural stimuli.

5,7-Dihydroxytryptamine↗
PubMed1987

The regional cerebral blood flow in patients under chronic hemodialytic treatment.

Regional cerebral blood flow (rCBF) was measured by the xenon-133 inhalation method in an unselected group of nine chronic hemodialysis patients before and after a single hemodialytic treatment. All patients underwent neurological, neuropsychological, and biochemical evaluations on the same occasions. Predialysis rCBF values did not differ from those obtained in age-matched normal controls. Following hemodialysis, there was a mild reduction in the rCBF by a mean of 7 +/- 2.6% (p = 0.02). The posthemodialysis rCBF reduction was not associated with any neurological or cognitive dysfunction. The causes of hemodialysis-induced rCBF decreases are unknown, but increased blood viscosity and biochemical changes, such as urea reduction and blood alkalinization, may play a role.

Adult↗
PubMed1987

Late-onset progressive radiculomyelopathy in patients with cervical athetoid-dystonic cerebral palsy.

Three patients with severe athetoid-dystonic type of cerebral palsy involving the neck musculature developed in their fourth to fifth decade progressive cervical radiculomyelopathy associated with vertebral spondylarthrotic compressive lesions in addition to their long-standing neurological syndrome. It is likely that the late-onset myelopathy is linked to continuous torsion, compression and 'wear and tear' of the cervical spinal cord, induced by the involuntary movements. In 2 patients decompressive cervical spinal surgery was ineffective, suggesting irreversible damage.

Adult↗
PubMed1987

Forms of dystonia in patients with Parkinson's disease.

We studied various forms of dystonia associated with Parkinson's disease (PD) in 207 patients who were on levodopa therapy for more than 1 year. Dystonia, sometimes more than one type, occurred in 63 (30%). In five patients, dystonia preceded initiation of treatment. Fifteen patients had peak-dose dystonia, 33 had early-morning dystonia, and 20 had "off-period" dystonia. The different clinical features of the dystonias are presented and compared. Findings indicate that dystonia is a frequent feature of levodopa-treated PD patients.

Adult↗
PubMed1986

Effect of serotonergic, corticostriatal and kainic acid lesions on the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) in mice.

In mice, prior destruction of striatal 5-hydroxytryptamine (5-HT) neurons by intrastriatal or intraventricular injections of 5,7-dihydroxytryptamine did not abolish or attenuate DA depletions produced in striatum by 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). This suggests that although they contain monoamine oxidase type B, the oxidative conversion of MPTP to 1-methyl-4-phenyl-pyridinium ion (MPP+) does not take place in 5-HT neurons. Likewise, decortication and kainic acid lesions did not prevent or enhance striatal MPTP-induced DA decrements suggesting that corticostriatal projections and striatal neurons are not involved in the mechanisms of MPTP neurotoxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗