Effect of apomorphine on human sleep.
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Biomedical subjects
Publications and source records attributed to C Cianchetti.
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Four patients affected by Huntington's chorea (HC) with a well defined family history of the disease were injected intramuscularly with apomorphine hydrochloride in nonemetic doses, ranging from 1 to 4 mg. Soon after treatment, all patients showed a marked decrease in abnormal involuntary movements. Pretreatment with haloperidol (2 mg intramuscularly) or sulpiride (100 mg intramuscularly) 30 minutes prior to apomorphine treatment, prevented the therapeutic effect of this compound. It is suggested that apomorphine-induced improvement in Huntington's Chorea is mediated by the stimulation of a special kind of dopamine receptor, leading to inhibition of the activity of dopaminergic neurons.
This report describes a child, offspring of a first cousin marriage, with a severe and progressive disorder of bone and cartilage growth associated with a myotonia-like syndrome. Clinical manifestations of this disease began at birth with marked generalized muscle hypertrophy, stiffness, myotonia and multiple skeletal deformities. Successively severe dwarfism and mental retardation were observed. Neurophysiological studies showed continuous high frequently low voltage activity at rest and myotonic discharges which did not wax and wane. These abnormalities persisted after complete curarization. Muscle biopsy showed mild dystrophic changes. Polymeric glycosaminoglycans and degradation product excretion was normal. These findings are similar to those described in Schwartz-Jampel syndrome, but since the clinical picture was fully expressed at birth and was unusually severe, it is suggested that the patient's condition may have represented a severe variant of this syndrome.
Surface markers of cerebrospinal fluid (CSF) cells have been studied in comparison with those of peripheral blood lymphocytes. The great majority (about 95%) of CSF cells bear surface markers of thymus-dependent lymphocytes (E rosettes with uncoated sheep red blood cells), while being devoid of bone-marrow derived cell markers (EAC rosettes with complement-coated red blood cells). In contrast with lymphocytes from peripheral blood, CSF cells form predominantly 'early' and 'sphere'-shaped E rosettes, and bear receptors for the complement-fixing segment of immunoglobulins G. Treatment with concentrated CSF does not affect rosette forming ability of peripheral blood lymphocytes.
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A sibship consisting of three siblings, one male and two females with unrelated parents, showed a clinical syndrome including: infantile spasms with hypsarrhythmia, microcephaly, severe mental retardation and spastic quadriplegia. The pneumoencephalogram performed in two sibs showed agenesis of the corpus callosum and aqueductal stenosis with tri-ventricular dilatation. The disorder did not show a progressive course with deterioration of mental and neurologic functions. No biochemical or cytogenetic defect could be identified. Complement fixation for cytomegalovirus was negative. This syndrome complex is probably inherited as an autosomal recessive trait. The clinical and the genetic aspects of the syndrome are discussed.
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In healthy volunteers the emetic effect of apomorphine (5-10 mg, i.m.) was prevented by haloperidol (2 mg), metoclopramide (10 mg) and sulpiride (100 mg), injected intramuscularly. In parkinsonian patients, apomorphine (1 mg) given alone ameliorated the neurological symptoms (30% improvement in the disability score), but the improvement was accompanied by nausea, vomiting, sedation or sleepiness. Haloperidol (2 mg) prevented not only the emetic effect of apomorphine (10 mg), but also its therapeutic efficacy in parkinsonism. Indeed, the disability score was worsened by the drug combination in some patients. Moreover, after haloperidol, apomorphine produced deep sedation and sleep. By contrast, in parkinsonian patients pretreated with metoclopramide (10 mg) or sulpiride (100 mg), apomorphine (10 mg) markedly diminished tremor and rigidity and failed to produce nausea, vomiting and sleepiness.
The toxic polyneuropathy observed in a group of shoe-industry workers in Italy was clinically characterised by a symmetrical prevalently distal motor deficit, with occasional marked weakness of pelvic girdle muscles, and frequently by only subjective sensory symptoms; non-specific disturbances usually preceded neurological signs. Subclinical cases of 'minimal' chronic neuropathy, characterised by alterations of a neurogenic type in the EMG without a reduction of motor nerve conduction velocity, were also observed. Worsening of the clinical picture, with further lowering of nerve conduction velocity, was noted in some cases up to four months after removal from the toxic environment. In the most severe cases clinical recovery took up to three years. The electromyographic and electroneurographic features were consistent with a mixed axonal neuropathy, with clear prevalence of the damage in the distal part of the nerve (dying-back neuropathy). Volatile substances, such as n-hexane and other low boiling point hydrocarbons found in high percentage in solvents and glues, are suggested as the causative agent.
Since 1957, when the first cases of the so-called shoe-makers' toxic polyneuropathy were reported, nearly 400 cases have been described in the Italian literature. The substance that was considered to be responsible for the disease was triorthocresylphosphate (TOCP) contained in glues, artificial leathers, and some types of paints. However numerous chemical analyses of glues and leathers taken from factories where cases of the disease occurred have shown that in almost all instances little or no TOCP was present. In addition the disease manifests itself more frequently during winter and spring and this is not consistent with the absorption of the causative agent through the skin and/or gastrointestinal tract. In order to clarify the aetiology of the disease 122 workers in the shoe industry affected by toxic polymeuropathy during the period 1971-74 were studied. Workplaces where cases of polyneuropathy had occurred were visited and samples of glues and solvents were taken for chemical analysis. The polyneuropathy chiefly affects workers engaged in glueing and in the cleaning process, but it also affects those who do not have direct contact with glues or solvents. The disease is more common in women (68%) than in men (32%) and, in its more severe form begins with overwhelming prevalence during winter and early spring regardless of the job performed. No direct relationship has been found between the severity of the disease and the number of years of work in the shoe industry or of specific exposure (that is the number of years of work in the activity performed at the onset of the disease). The polyneuropathy is found almost exclusively among workers of the artisam type in small shoe factories, where standards of hygiene are low. Chemical analysis of glues and cleaning fluids collected from five different factories, where 20 cases of polyneuropathy occurred, showed the presence of paraffin hydrocarbons with a low boiling point (pentane, 2-methyl-pentane, 3-methyl-pentane, n-hexane, etc.) in concentrations of more than 80% by weight.
The diagnosis of ocular myopathy associated with a primary retinal pigment epitheliopathy in a 20-year-old man was based on the integrity of the retinal functions, despite progressive worsening of muscular activity in the systems affected by the disease, and on the results of retinal fluorescein angiography. Although the changes in the pigment epithelium were not prominent ophthalmoscopically, they were clearly visible angiograpically. Atypical forms of retinal pigment dystrophy occurring during the course of ocular myopathy appear to be clinical expressions of a unique genetic defect confined to the pigment epithelial layer. We assume that the gene is capable of inducing a pleiotropic effect.
The influence of electric activation of the peroneal nerve (i.e., of anterior leg muscles) on the ipsilateral soleus H response was studied in normal, parkinsonian, hemiplegic and spastic spinal paraplegic subjects. The anterior muscles were held in a forced extended position to obtain their maximal stretch during isometric contraction. The stimulus evoking soleus H reflex was delivered after a conditioning stimulus to the peroneal nerve at different intervals, between 10 and 500 msec. The excitability curve of the soleus H reflex obtained in this way showed a rather constant pattern in normal subjects, which significantly differed from that of the parkinsonians. "Pyramidal" patients showed a pattern not significantly disimilar from normals. Parkinsonians were characterized by clear facilitation of the soleus H response for intervals (about 100-150 msce) corresponding to the maximum tension increase on the anterior muscles.
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