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Biomedical subjects

R Sandyk

Publications and source records attributed to R Sandyk.

At least 253 records · Page 14Linked to original sources
PubMed1988

Heightened cortisol response to administration of naloxone in Tourette's syndrome.

The release of corticotrophin-releasing factor (CRF) in the human has been shown to be under a direct inhibitory control derived from the locus coeruleus (LC). Opioids have been shown to inhibit CRF release. Based on our hypothesis of deranged opioid-noradrenergic activity in Tourette's syndrome (TS), we studied the effect of a naloxone challenge on plasma cortisol levels in 6 TS patients. In all patients naloxone produced a significant rise in cortisol secretion. These results support our hypothesis and suggest that in TS, noradrenergic LC receptors involved in CRF release are supersensitive as a result of chronic excessive endorphinergic activity.

Adolescent↗
PubMed1988

Opioid modulation of gonadotrophin release in Tourette's syndrome.

Currently the most prevailing hypothesis attempting to explain the pathophysiology of Tourette's syndrome (TS) suggests that the disease results from dopaminergic (DA) hyperactivity (Golden, 1986). Evidence for this hypothesis is indirect and includes the favorable response of these patients to haloperidol, exacerbation of symptoms with dopaminergic drugs (e.g., methylphenidate) and the findings of reduced DA metabolites in the CSF of some TS patients (Singer et al., 1982). We have recently suggested that deranged opioid functions may also be important in the pathophysiology of TS (Sandyk, 1985). Our hypothesis was based on the favorable response of a subgroup of patients to administration of opiate antagonists (e.g., naloxone, naltrexone) (Sandyk et al., 1986), and is also supported by a recent finding demonstrating depletion of striatal dynorphins in a subject with TS (Haber et al., 1986). Furthermore, based on several clinical features of the disease, we have recently suggested that the hypothalamus could be a site of dysfunction in the disease (Sandyk et al., 1986). To investigate the possible role of deranged opioid-mediated hypothalamic functions in TS further, we tested the effects of acute naloxone (Nx) challenge on plasma FSH and LH levels in 5 male TS patients (aged 11-16 years) and in 4 non-TS-diseased controls (narcoleptics). The plasma FSH and LH levels were drawn prior to and 30 min following the intramuscular administration of 1.2 mg of naloxone.

Adolescent↗
PubMed1988

The hypothalamus in dystonic movement disorders.

The term dystonia was introduced by Oppenheim and Vogt in 1911 to describe the relatively slow, sustained, frequently forceful contorting movements involving striatal muscles. Dystonia is characteristically seen in childhood ("primary dystonia"), but also occurs in a variety of other disorders of the CNS ("secondary dystonia"). In the case of childhood dystonia (dystonia musculorum deformans) symptoms usually occur in young patients in which case the illness is usually inherited as either autosomal dominant or recessive. In cases of adult onset dystonia, genetic factors are less likely (Eldrige, 1970). Although dystonic movement disorders have been presumed to originate from dysfunction of the basal ganglia, examination of the brains of patients who have died with idiopathic or hereditary dystonia musculorum deformans have revealed no consistent neuropathological or neurochemical abnormalities (Zeman, 1970). Furthermore, therapy of value in the treatment of other basal ganglia disorders, in these conditions, has not been helpful (Fahn, 1982). The following paper will discuss evidence implicating deranged hypothalamic neuropeptidergic functions in dystonia. We have developed a hypothesis, which reviews and incorporates published data, in which we discuss the role of deranged hypothalamic neuropeptidergic function in the pathnophysiology of idiopathic dystonia.

Adrenocorticotropic Hormone↗
PubMed1988

Elevated cerebrospinal fluid lactic acid levels in Creutzfeldt-Jakob disease.

The concentration of cerebrospinal fluid (CSF) lactic acid was determined in three patients with biopsy proven Creutzfeldt-Jacob disease (CJD). When compared with twenty demented patients diagnosed as having either Alzheimer's disease or multi-infarct dementia, the CSF lactic acid values of the CJD patients were significantly elevated (p less than .001). Elevated CSF lactic acid levels may be an important biochemical marker of CJD and useful in the differential diagnosis of dementia.

Aged↗
PubMed1988

Inhibitory effects of carbamazepine on clonidine-induced aggressive behavior in mice.

A behavioral study was made of the effect of carbamazepine (CBZ) on aggressive behavior evoked by high dose of clonidine in mice. This aggressive behavior has been reported to involve blockade of central adenosine receptors with which CBZ has been suggested to interact. After a single injection of clonidine (50 mg/kg i.p.), aggressive responses such as attacking and biting began within 5-10 min, were most marked at 20 min and usually ceased within 60 min. This behavior was attenuated by CBZ (45 mg/kg i.p.) but potentiated by caffeine (20 mg/kg i.p.). In addition, it was markedly inhibited by haloperidol (1.0 mg/kg i.p.), but unaffected by prazosin (1.5 mg/kg i.p.) and yohimbine (1.0 mg/kg i.p.). The inhibitory effect of CBZ on the aggressive behavior was dose-dependent at doses ranging from 15 to 60 mg/kg, while a high dose of CBZ alone induced sedation. The stimulatory effect of caffeine on the aggressive behavior was antagonized by pretreatment with CBZ (50 mg/kg i.p.). These results suggest that the receptor involved in clonidine-induced aggressive behavior was not mediated through the alpha-2 adrenoreceptor, but rather the adenosine receptor, and that the effect of carbamazepine on the adenosine receptor was agonistic in contrast with the effect of caffeine (an adenosine antagonist).

Adenosine↗
PubMed1988

Gonadotropin deficiency in Tourette's syndrome: a preliminary communication.

Plasma baseline levels of gonadotropins and sex steroids were measured in 17 patients with Tourette's Syndrome (TS). In addition, a Gonadotropin Stimulation test, using a synthetic Gonadotropin releasing factor analogue (GnRH, 100 micrograms, i.v.), was performed in 7 patients. Plasma levels of Luteinizing Hormone (LH) were uniformly low in all patients, while those of Follicle Stimulating hormone (FSH) and sex steroids were less depressed in some patients and in the normal range in others. In all patients, stimulation with GnRH analogue produced a marked rise in LH levels, but the FSH responses were much less dramatic and did not significantly exceed that of normal controls. Our findings indicate reduced gonadotropin release in patients with TS, and support the hypothesis of hypothalamic involvement in the disease.

Adolescent↗
PubMed1988

L-tryptophan in neuroleptic-induced tardive dyskinesia.

Administration of the serotonin precursor L-tryptophan in a patient with neuroleptic-induced tardive dyskinesia, produced a dramatic reduction in the severity of the abnormal movements within 24 hours. This report supports our hypothesis that alterations in the function of serotoninergic neurotransmission are implicated in the pathophysiology of neuroleptic-induced tardive dyskinesia.

Antipsychotic Agents↗
PubMed1988

Dopamine and insulin interact to modulate in vitro glucose transport in rat adipocytes.

The in vitro effects of dopamine (DA) and insulin on -14C glucose oxidation (transport) in isolated rat adipocytes was studied. Low to intermediate concentrations of DA combined with low concentrations of insulin tended to stimulate glucose transport whilst high concentrations of DA combined with high concentrations of insulin produced inhibition of insulin stimulated glucose transport. The effect of DA on glucose transport was mediated via beta-adrenergic receptors, since propranolol, but not haloperidol or phentolamine, antagonised these effects of dopamine. These effects of dopamine on glucose transport may be relevant to the pathophysiology of Parkinson's disease and other neuropsychiatric conditions in which abnormalities of dopaminergic functions are thought to be of major pathogenic importance.

Adipose Tissue↗
PubMed1988

Naltrexone suppresses abnormal sexual behavior in Tourette's syndrome.

Abnormal sexual behavior occurs in 30-40% of patients with Tourette's syndrome (TS). Two patients with TS who exhibited distressing abnormal sexual behavior experienced amelioration of symptoms with administration of the oral opiate receptor antagonist naltrexone (TrexanR). Conventional anti-TS drugs including haloperidol and clonidine were ineffective. Abnormal sexual behavior may be another feature of the disease responding to opiate blockers.

Adolescent↗
PubMed1988

Interictal temporal lobe epileptiform discharges and their relationship to secondarily generalized epilepsy.

In a previous study of epileptic phenomena in 19 patients with partial complex seizures, it was noted that seizures of left temporal lobe origin had a higher incidence of secondary generalization. To evaluate this observation further, we retrospectively reviewed reports of EEGs for evidence of focal interictal epileptiform discharges (FIED) of temporal lobe origin and correlated this finding with seizure type. Of 3,276 EEG reports reviewed, 195 showed FIED. The medical records of these patients were reviewed and 79 had sufficient information therein to enable seizure classification. Of 79 patients, 61 had secondary generalized seizures, 45 with left temporal FIED, 16 with right FIED. Of 79 patients, 18 had partial seizures, 13 with right temporal FIED, 5 with left FIED (p less than 0.001). These findings suggest that seizures of left temporal lobe origin may have a higher incidence of secondary generalization. The significance of this observation and its relevance to medical and surgical treatment of complex partial seizures is discussed.

Adolescent↗
PubMed1988

A case of Tourette's syndrome with midbrain involvement.

Several hypotheses have attempted to incriminate a particular anatomical region responsible for the complex symptomatology of Tourette's syndrome (TS). Recently, Devinsky speculated that damage to the peri-aqueductal gray matter (PAG) and midbrain tegmentum may represent the major anatomical site of dysfunction in TS. A patient with TS in whom radiological evidence indicated midbrain involvement may support Devinsky's hypothesis. A 7-year-old boy exhibited motor and vocal tics since the age of four. These were associated with hyperactive behavior, stereotype body movements, abnormal sexual behavior and coprolalia. At the age of five he was placed on methylphenidate for hyperactive behavior which resulted in marked exacerbation of the tics. Family history was unremarkable. Neurological examination was normal with the exception of the tics. Endocrine evaluation, including plasma cortisol, growth hormone, prolactin and TSH were normal with the exception of reduced FSH, LH and testosterone levels. Sexual maturation was normal. MRI head scan was normal with the exception of an asymmetry of the cerebral peduncles with the left larger than the right. CSF examination was normal. While the nature of this patient's radiological abnormalities is not clear, our findings of asymmetric cerebral peduncles associated with TS may support a role for the midbrain in the pathophysiology of TS. The likelihood of the latter assumption seems to be further confirmed by a recent report in which peri-third ventricular and PAG calcifications were detected by CT scan of the head in an adult patient with TS. Further MRI investigations in other cases of TS may clarify the anatomical relationship of the midbrain to the symptomatology of TS.

Child↗