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Biomedical subjects

D D Truong

Publications and source records attributed to D D Truong.

At least 37 records · Page 2Linked to original sources
PubMed1995

Diphenhydramine is effective in the treatment of idiopathic dystonia.

OBJECTIVE: To assess the effectiveness of diphenhydramine hydrochloride (Benadryl) in the treatment of patients with idiopathic truncal dystonia. DESIGN: Before-and-after trial. SETTING: University referral center. PATIENTS: Five consecutive patients with idiopathic truncal dystonia who were poorly treated with conventional pharmacotherapies. No patients were withdrawn from the trial for adverse side effects. INTERVENTIONS: Treatments with diphenhydramine hydrochloride (50 mg intravenously or up to 500 mg/kg orally). Follow-up for up to 20 months. MAIN OUTCOME MEASURE: Dystonia evaluation. RESULTS: Diphenhydramine therapy was associated with minimal side effects, and it was most effective in treating patients with dystonia who experienced lightning jerks. Treatment with intravenous diphenhydramine may have a predictive value on a future response to oral therapy. CONCLUSION: Diphenhydramine should be considered a therapeutic option for idiopathic truncal dystonia with lightning jerks.

Adult↗
PubMed1995

Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus.

Male Sprague-Dawley rats underwent cardiac arrest and resuscitation, subsequently exhibiting posthypoxic myoclonus. The audiogenic posthypoxic myoclonus in these animals could be attenuated with the following drugs: 5-hydroxytryptophan (5-HTP, serotonin [5-HT] precursor), N-(3-trifluoro-methylphenyl)piperazine hydrochloride (TFMPP, 5-HT1B/1C/2 agonist), (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrobromide (DOI, 5-HT2 agonist), and 1-(m-chlorophenyl)-biguanide hydrochloride (m-CPBG, 5-HT3 agonist). In contrast, the following drugs were ineffective: (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT, 5-HT1A agonist), buspirone hydrochloride (5-HT1A agonist), 7-trifluoromethyl-4(4-methyl-l-piperazinyl)-pyrrolo[1,2- a]quinoxaline maleate (CGS 12066B, 5-HT1B agonist), ketanserin tartrate (5-HT2 antagonist), methysergide maleate (5-HT2 antagonist), fluoxetine (5-HT uptake blocker), and saline (vehicle). The data suggest that enhancement of serotonergic activity, particularly through 5-HT2 and 5-HT3 receptors, have therapeutic potential for the treatment of posthypoxic myoclonus.

Animals↗
PubMed1995

Evidence for the involvement of histamine in the antidystonic effects of diphenhydramine.

Although diphenhydramine hydrochloride is known to eliminate or reduce the symptoms of dystonia in human patients with acute dystonic reactions and idiopathic torsion dystonia, its mechanism of action is still unclear. In the present study, we show that the antihistamine properties of diphenhydramine may contribute to its beneficial effects. Acute dystonic reactions were produced in rats with unilateral microinjection of haloperidol into the red nucleus as previously described. Similar to the pattern in humans, this effect could be attenuated by coadministration of diphenhydramine. Unilateral microinjection of histamine itself into the rat red nucleus produced dystonic postures (torticollis) in a dose-dependent manner, demonstrating that a histamine dysfunction could contribute to the pathophysiology of dystonia. The torticollis produced by histamine could be significantly attenuated with coadministration of the H1 antagonists diphenhydramine or pyrilamine or the H2 antagonist cimetidine. These effects are thought to be mediated through the red nucleus because significantly more torticollis was observed when histamine was injected into the red nucleus rather than surrounding mid-brain areas, the substantia nigra, or the lateral ventricle. The present data, taken together with studies in humans, suggest the involvement of histamine in some types of dystonia. Furthermore, the red nucleus and related motor pathways may have a more important role in dystonia than previously thought.

Animals↗
PubMed1995

Association between brain indole levels and severity of posthypoxic myoclonus in rats.

We have previously reported the presence of posthypoxic, audiogenic myoclonus in rats after cardiac arrest and the ability of the 5-HT precursor, 5-HTP, to attenuate these muscle jerks. In addition, we have recently shown that 5-HT2 and 5-HT3 agonists can reduce the severity of myoclonus in these animals, suggesting a deficiency in serotonergic neurotransmission. In the present study, the levels of 5-HTP, 5-HT, and 5-HIAA were measured in seven regions of the brain in myoclonic and normal rats to identify the areas of the brain in which a serotonergic dysfunction resides. Similar to previous studies, we observed pronounced posthypoxic, audiogenic myoclonus 3 and 14 days after resuscitation from cardiac arrest, with a resolution of the abnormal movements by 45 days postarrest. HPLC measurements revealed significant changes in indole levels in the following areas of the brain: cortical 5-HIAA, striatal 5-HT, striatal 5-HIAA, hippocampal 5-HT, mesencephalic 5-HIAA, myelencephalic 5-HT, myelencephalic 5-HIAA, cerebellar 5-HTP, and cerebellar 5-HT. The changes in striatal 5-HT, cortical 5-HIAA, and mesencephalic 5-HIAA appear most relevant to the pathophysiology of posthypoxic myoclonus because regression analyses showed significant correlations between the myoclonus scores of the animals and the levels of these indoles. Based on the observed pattern of results, we postulate a dysfunction in serotonergic lateral (cortical) and far lateral (extrapyramidal) ascending pathways in posthypoxic myoclonus.

5-Hydroxytryptophan↗
PubMed1995

Chronic treatments with 5-HT1A agonists attenuate posthypoxic myoclonus in rats.

Following 10 min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. This phenomenon peaked at 14 days and disappeared by 60 days after cardiac arrest. From previous results, the 5-hydroxytryptamine (5-HT) system was implicated in the pathogenesis of the disease. In the present study, we investigated the involvement of 5-HT1A receptors in posthypoxic myoclonus in rats. Single injections of 5-HT1A agonists, buspirone (5 and 10 mg/kg body wt.) or 8-OH-DPAT (1, 2, and 4 mg/kg), had no effect on either the intensity or time course of the disease. In contrast, multiple injections (twice a day for 7 or more days) of buspirone (10 mg/kg) or 8-OH-DPAT (4 mg/kg) significantly attenuated the myoclonus scores of animals (p < 0.05). The results indicate that chronic stimulation of 5-HT1A receptors in the brain may accelerate endogenous compensatory mechanisms and shorten the time course of the disease.

Animals↗
PubMed1995

Regulation of tyrosine protein kinase receptor Trk-B and motor function in rats following cardiac arrest.

Following 10 min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. Sixty days later, the motor function of the animals was restored. In the present study, we investigated brain levels of tyrosine protein kinase receptor Trk-B with quantitative immunoblot analysis at various time points following cardiac arrest. In the frontal cortex, a significant reduction of Trk-B was found in rats 3 days (53%) after cardiac arrest, whereas significant increases were detected in rats 14 (124%) and an average 60 days (98%) after cardiac arrest. In the striatum, significant increases were found in rats 3 (389%), 14 (483%), and 60 days (521%) after resuscitation. In contrast, significant reductions of Trk-B were detected in the cerebellum of rats 3 (46%), 14 (22%), and 60 days (18%) after cardiac arrest. The results indicate that regulation of Trk-B may vary in different brain regions and have important roles in recovery processes following hypoxic-ischemic insults to the brain.

Animals↗
PubMed1995

Astrocyte-derived growth factor (S100 beta) and motor function in rats following cardiac arrest.

Following 10-min cardiac arrest and resuscitation, the central serotonergic system and motor function of rats were found to be affected and later on restored. Astrocyte-derived growth factor (S100 beta) is known to promote survival and neurite outgrowth of serotonergic neurons. In the present study, brain levels of S100 beta were investigated with quantitative immunoblot analysis at various time points following cardiac arrest. Significant reductions of S100 beta were found in the cerebral cortex (30%), midbrain (35%), and cerebellum (46%) of rats 3 days postcardiac arrest. In contrast, at 14 and > 45 days, significant increases of S100 beta were detected in the cerebral cortex (57%; 81%), midbrain (70%; 97%), and cerebellum (84%; 157%). The results indicate that reactive astrocytosis and elevated levels of S100 beta may participate in the recovery processes following hypoxic-ischemic insults to the brain.

Analysis of Variance↗
PubMed1995

Expression of Bcl-2 and Bax in the frontoparietal cortex of the rat following cardiac arrest.

Following 10-min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. This phenomenon peaked at 14 days and disappeared by 45 days after cardiac arrest. The mechanisms for the initial dysfunction and later restoration of motor function are not completely known. In the present study, involvement of Bcl-2 and Bax in these phenomena was investigated. In the frontoparietal cortex, both bcl-2 and bax mRNA levels were significantly increased 1, 3, 7, 14, and 28 days postresuscitation. bax mRNA levels continued to be high 45 days postcardiac arrest, whereas bcl-2 mRNA levels were returned to control levels. The apoptotic cells were found in layers IV to VI of the frontoparietal cortex of rats 3 days postcardiac arrest. These results indicate that after cardiac arrest, the initial rise of Bax levels may mediate apoptosis and neurodegeneration in the rat brain. At later time points, increased levels of Bcl-2 may contribute to recovery of motor function in posthypoxic rats.

Animals↗
PubMed1995

Alterations of brain levels of phosphoinositidase-C-linked Gq alpha/G11 alpha proteins and motor function in rats after cardiac arrest.

BACKGROUND AND PURPOSE: Phosphoinositidase-C-linked Gq alpha and G11 alpha proteins have only recently been characterized. Second messenger systems are known to be affected by hypoxia-ischemia. However, the effects of hypoxia-ischemia on the brain levels of Gq alpha and G11 alpha proteins are not known. Therefore, in the present studies, the effects of hypoxia-ischemia on Gq alpha and G11 alpha proteins in rats were investigated with quantitative immunoblot analysis. METHODS: Cardiac arrest was induced in male Sprague-Dawley rats by an intracardial injection of KCl. Resuscitation began 10 minutes afterwards. At various time points after resuscitation, animals were killed and the cerebral cortex, striatum, and cerebellum were dissected. Levels of Gq alpha and G11 alpha proteins were investigated by quantitative immunoblot analysis. RESULTS: At 1, 2, 4, and 6 hours after resuscitation, Gq alpha and G11 alpha protein levels remained unaltered. However, a significant reduction of these proteins was seen in the cerebral cortex and cerebellum of rats 3 and 14 days after cardiac arrest, with partial recovery by an average of 60 days. In contrast, no significant change was detected in the striatum. CONCLUSIONS: These observations indicate that phosphoinositidase-C-linked signal transduction pathways may be attenuated after hypoxic-ischemic insults to the brain, and that this phenomenon, together with many other factors, may contribute to the expression of motor dysfunction in rats after cardiac arrest.

Analysis of Variance↗
PubMed1994

Novel rat cardiac arrest model of posthypoxic myoclonus.

We describe the time course of and pharmacology associated with auditory-induced muscle jerks following cardiac arrest in rats. The data indicate that several key features of this model mimic those of human posthypoxic myoclonus. Similar to the human form, the muscle jerks appear in the rats following an acute hypoxic episode (cardiac arrest). Initially, it is known that both spontaneous and auditory-induced myoclonus are present in these animals; some cardiac-arrested rats also exhibit seizures. Over the first few days after the arrest, episodes of both the seizure activity and spontaneous myoclonus disappear. The auditory-induced myoclonus continues to worsen, reaches a peak about 2 weeks after the arrest, then declines over time to subnormal levels. The auditory-induced muscle jerks exhibited by the cardiac arrested animals are attenuated by the typical antimyoclonic drugs 5-hydroxytryptophan, valproic acid, and clonazepam. In addition, the novel anticonvulsant felbamate was found to have antimyoclonic properties. The data suggest that this rat cardiac arrest model may be a valuable tool for investigating the pathophysiologic mechanisms of posthypoxic myoclonus and for developing new therapeutic strategies for treating the disorder.

5-Hydroxytryptophan↗
PubMed1994

Involvement of 5-HT2 receptors in posthypoxic stimulus-sensitive myoclonus in rats.

We have previously reported that rats exhibited audiogenic myoclonus at 3 days after cardiac arrest. This phenomenon peaked at 14 days, gradually tapered off at older ages, and disappeared in most rats by 60 days following cardiac arrest. Because treatment with the 5-HT2-selective agonist, (+/-)-1-2,5-dimethoxy-4-iodophenyl-2-aminopropane (DOI) significantly attenuated audiogenic myoclonus in these postcardiac-arrest rats, the involvement of 5-HT2 receptors in posthypoxic stimulus-sensitive myoclonus was suggested. In the current study, we, therefore, examined the binding properties of 5-HT2 receptors in the rat bain at various time points following cardiac arrest. The affinity constant of [3H]ketanserin binding to 5-HT2 receptors in cortical membranes of rats did not change. In contrast, Bmax values were found to be reduced at 3 and 14 days after cardiac arrest with some recovery after 60 days. Taken together with previous results, these results indicate that hypoactivity of central 5-HT2 neurotransmission may underlie the development of posthypoxic stimulus-sensitive myoclonus in rats.

Acoustic Stimulation↗
PubMed1991

Posttraumatic torticollis.

We report six cases of torticollis precipitated by neck trauma. The dystonia began 1 to 4 days after the trauma and differed clinically from idiopathic torticollis by marked limitation of range of motion, lack of improvement after sleep ("honeymoon period"), and absence of geste antagonistique. Worsening with action was not present; nor was there improvement with support as seen with idiopathic torticollis. Onset of pain immediately after the trauma and marked spasms of the paracervical muscles were other predominant features. Anticholinergic therapy was without benefit; however, some improvement occurred with botulinum toxin injection. It is concluded that torticollis can be caused by peripheral trauma and that it has unique clinical characteristics.

Adult↗
PubMed1991

A method for the treatment of abductor spasmodic dysphonia with botulinum toxin injections: a preliminary report.

A preliminary technical report of the effective treatment of abductor spasmodic dysphonia with botulinum toxin is presented. Our technique attempts to place the toxin close to the posterior cricoarytenoid muscle to allow diffusion of the material to the PCA. Our pilot study demonstrates that botulinum toxin is an effective approach for reducing or eliminating the abductor glottal spasms during phonation and, thereby, providing functional speech communication.

Adult↗
PubMed1991

Treatment of oromandibular dystonia with botulinum toxin.

Botulinum toxin produces muscle weakness by inhibition of acetylcholine release at the neuromuscular junction. The toxin has been used successfully for symptomatic treatment of focal dystonias. Our experience in the use of botulinum toxin for the treatment of oromandibular dystonia in five patients is reported. Improvement following treatment was reported as marked by 1 patient, moderate by 1 patient, and mild by 3 patients. Similar improvement was noted by the examiners. One patient with mild cosmetic improvement developed significant dysphagia requiring feeding by a nasogastric tube for a 3-month period.

Botulinum Toxins↗
PubMed1990

Movement disorders in mitochondrial myopathies. A study of nine cases with two autopsy studies.

Of 85 consecutive patients with mitochondrial myopathy, 29 had clinically significant central nervous system involvement. Nine of these had movement disorders that included dystonia, chorea, parkinsonism, and myoclonus. Autopsy studies of one patient with ataxia, dementia, and parkinsonism followed by dystonia showed the features of olivopontocerebellar atrophy with additional degenerative changes in the basal ganglia. Postmortem in a further case with myoclonus, deafness, muscle weakness, retinopathy, and ataxia showed symmetrical mineralisation of the striatopallidodentatal system.

Adult↗