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Biomedical subjects

N Quinn

Publications and source records attributed to N Quinn.

At least 109 records · Page 6Linked to original sources
PubMed1988

Blepharospasm: a review of 264 patients.

The natural history and response to different treatments have been evaluated in 264 patients with blepharospasm. The mean age of onset was 55.8 years and there was a female preponderance of 1.8 to 1. Dystonia elsewhere was found in 78% of patients, usually in the cranial-cervical region, and appeared to follow a somatotopic progression. A family history of blepharospasm or dystonia elsewhere was found in 9.5% of cases, which suggests a genetic predisposition. Ocular lesions preceded the onset of blepharospasm in 12.1% of cases. The response to drugs was inconsistent, although initial improvement was experienced by one fifth of patients treated with anticholinergics. Twenty-nine bilateral facial nerve avulsion operations were performed with benefit in 27 cases; but recurrences appeared in 22, on average one year after surgery. Botulinum toxin injections were performed in 151 patients. Significant improvement was achieved in 118 cases. Mean duration of benefit was 9.2 weeks. Transient ptosis and diplopia were the commonest side effects.

Adolescent↗
PubMed1987

Antiparkinsonian activity of a single oral dose of PHNO.

PHNO, a new D-2 agonist, was investigated in five patients with Parkinson's disease. In an acute, open, oral, dose-ranging study comparing benefit from single doses, 4 mg of PHNO was found to be equivalent to one tablet of Sinemet 25/250 mg. Adverse reactions were those anticipated for a dopaminomimetic agent. Because of its novel structure and apparent transcutaneous penetration, further studies on PHNO are desirable.

Administration, Oral↗
PubMed1987

Young onset Parkinson's disease.

We describe a personal series of 60 cases of parkinsonism with onset under the age of 40 years. Known causes for early onset of secondary parkinsonism, such as Wilson's disease or encephalitis, were excluded in every case. Two groups were identified: those with onset after the age of 21 in whom no hereditary factors could be ascertained (56 cases), and those with onset before 21 years all of whom had familial parkinsonism. In neither group have we found any association with prematurely grey hair, hypertension, diabetes, pernicious anaemia, or thyroid disorder. Among their families, we have not found any association with diabetes, pernicious anaemia, or thyroid disorder. We propose that cases of apparent idiopathic Parkinson's disease beginning between age 21-40 years should be called "young onset Parkinson's disease." Twenty percent of such patients in our series had at least one first- or second-degree relative in the same or antecedent generations with parkinsonism, but only 1.5% of their relatives at risk had parkinsonism, which is similar to the prevalence in the general population. Ten percent of these patients had at least one relative with essential tremor, but only 1.6% of their relatives at risk had tremor, which again was similar to the prevalence in the population in general. These patients with young onset Parkinson's disease responded well to levodopa therapy. However, dyskinesias and response fluctuations occurred early and frequently. The prevalence of dyskinesias and response fluctuations was strongly correlated with the duration of levodopa treatment, but not with the duration (or probably the severity) of the disease before levodopa therapy was commenced. The involuntary movements often were severe and frequently were diphasic. Despite long disease duration, the incidence of dementia in young onset patients aged less than 65 years was negligible. We believe that most, if not all, patients in this group have degenerative Lewy body idiopathic Parkinson's disease, representing the lower end of a skewed deviation for age of onset of this disease. We have so far failed to identify any additional environmental factor which may have accelerated disease onset in these patients. In contrast, cases of parkinsonism beginning before age 21 years were invariably familial. We proposed that they should be called "juvenile parkinsonism." All affected relatives with parkinsonism also had young disease onset, and all but one were siblings. None of four such patients seen by us has demented, and computed tomography (CT) scan has been normal in all four. We believe that most such patients have some form of genetically determined secondary parkinsonism.

Adult↗
PubMed1986

Ipsilateral blepharospasm and contralateral hemidystonia and parkinsonism in a patient with a unilateral rostral brainstem-thalamic lesion: structural and functional abnormalities studied with CT, MRI, and PET scanning.

A patient developed progressive right hemidystonia in childhood. Subsequently, left-sided blepharospasm, slurred and stuttering speech, and right-sided rigidity and bradykinesia, responsive to dopamine agonists, appeared. Investigation with computed tomography and magnetic resonance imaging (MRI) at age 43 years revealed a left-sided calcified rostral brainstem-thalamic lesion of uncertain aetiology. Although no structural lesion was seen in the striatal regions, L-[18F]-fluorodopa uptake was severely diminished in the left striatum but normal on the right. Dopamine receptor binding identified by [11C]-methylspiperone was in the normal range on both sides.

Adult↗
PubMed1986

Brain energy metabolism and dopaminergic function in Huntington's disease measured in vivo using positron emission tomography.

A 48-year-old man with typical Huntington's disease was investigated with computed tomography (CT) and positron emission tomography. Regional cerebral blood flow, oxygen extraction, oxygen and glucose utilisation, L-Dopa uptake, and dopamine (D2) receptor binding were measured using several positron-labelled tracers. CT showed slight atrophy of the head of caudate but no cortical atrophy, although distinct frontal lobe dysfunction was present on psychometric testing. Oxygen and glucose metabolism and cerebral blood flow were decreased in the striata and to a lesser extent in frontal cortex. Cerebral blood flow was in the low normal range throughout the remainder of the brain. A normal metabolic ratio was found in all regions, since the changes in glucose utilisation paralleled those in oxygen consumption. The capacity of the striatum to store dopamine as assessed by L-[18F]-fluorodopa uptake was normal, but dopamine (D2) receptor binding was decreased when compared to normal subjects.

Carbon Radioisotopes↗
PubMed1986

Brain dopamine metabolism in patients with Parkinson's disease measured with positron emission tomography.

L-[18F] fluorodopa was administered in trace amounts intravenously to healthy control subjects and to patients with Parkinson's disease. Striatal uptake of radioactivity was measured using positron emission tomography. The capacity of the striatum to retain tracer was severely impaired in patients compared to controls. This may reflect a reduction of striatal dopamine storage in Parkinson's disease. Patients showing the "on/off" phenomenon had an even greater decrease of striatal storage capacity.

Adult↗
PubMed1984

L-Dopa methyl ester--a candidate for chronic systemic delivery of L-Dopa in Parkinson's disease.

Continuous intravenous infusions of L-Dopa as a treatment for response swings in Parkinson's disease are limited by the insolubility and acidity of L-Dopa. Its methyl ester is a soluble neutral derivative that might be of benefit to these patients, and is examined in the present study in behavioural and biochemical animal models. On intraperitoneal or subcutaneous administration to mice L-Dopa methyl ester was equivalent to L-Dopa in reversing reserpine-induced akinesia and producing contraversive circling behaviour in rats with a 6-hydroxydopamine lesion of the medial forebrain bundle. On oral administration the methyl ester was more active. The administration of L-Dopa or the methyl ester produced equivalent changes in striatal and mesolimbic dopamine, homovanillic acid, and 3,4-dihydroxyphenylacetic acid metabolite levels. We suggest that systemic or subcutaneous infusion of L-Dopa methyl ester to patients who experience response fluctuations may provide a means of maintaining mobility.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

The treatment of severe dystonia in children and adults.

Twenty-three children (aged less than 18 years) and 17 adults with severe widespread dystonia were treated with high doses of benzhexol (up to 130 mg daily introduced slowly over many weeks). Children tolerated higher doses (median 30 mg/day) than adults (median 20 mg/day). 52% of the children gained useful benefit, many (43%) without unwanted side effects. Such an approach was less successful in adults; 41% gained benefit, but only 35% had no side effects. Twelve adults with severe axial dystonia, and two children with life-threatening generalised dystonia were treated with a combination of a low constant dose of tetrabenazine to which were added pimozide and benzhexol as necessary. The dose of tetrabenazine was aimed at 75 mg daily; pimozide was increased (6 to 25 mg/day) until the dystonia was relieved or Parkinsonism and other side-effects prevented further increments; if necessary benzhexol (6 to 30 mg/day) then was added to control side-effects and to provide additional benefit. 75% of the adults with severe axial dystonia, and one of the two children with life threatening generalised dystonia gained useful benefit from this regime. It is concluded that high dose benzhexol is the present first treatment of choice for children with severe dystonia, and is worth a try in adults but with less expectation of success. When benzhexol treatment alone fails in adults with severe disabling axial dystonia, or in children with life-threatening generalised dystonia, combined therapy with tetrabenazine, pimozide and benzhexol may give valuable symptomatic relief.

Adolescent↗
PubMed1984

Alterations in cognitive performance and affect-arousal state during fluctuations in motor function in Parkinson's disease.

Sixteen patients with idiopathic Parkinson's disease were selected who were all showing severe fluctuations in motor function ("on-off" phenomenon). Measures of cognitive function and of subjective affect/arousal state were taken on two occasions, once when "on" and once when "off". Twenty-five matched normal controls were also assessed on the same measures. Results revealed, on the average, a drop in cognitive function plus an adverse swing in affect/arousal state, in the patient group in the "off" condition, compared to the levels when "on". Analysis of the data suggested that the main factor associated with cognitive function when "off" was not the severity of disability but the level of affect/arousal. The fluctuations in cognitive function found tended to be mild relative to the severe changes in motor ability, and were present in only a proportion of patients.

Adult↗