Biomedical subjects
Publications and source records attributed to C R Bamford.
A case of tryptophan-associated eosinophilia, central nervous system complications, and multiple white matter lesions by magnetic resonance imaging is presented. Eosinophilia regardless of its cause should be included within the differential of patients exhibiting periventricular white matter lesions.
In the following communication we discuss evidence suggesting that an abnormal opioid-gonadotrophin interaction at the midbrain may be essential to the clinical expression of vocal tics in Tourette's Syndrome (TS). Data derived from animal studies and the striking similarity between the symptomatology of TS and encephalitis lethargica (EL) add further support to our hypothesis implicating an abnormal opioid-gonadotrophin interaction in the pathophysiology of TS.
During an eight year period 170 multiple sclerosis (MS) patients and 134 controls without physical impairment were followed closely to record all episodes of physical trauma and to measure their effect on exacerbation rate and progression of MS. There was a total of 1407 instances of trauma, which were sorted into various categories. Overall there was no significant correlation between all-traumas and disease activity. There was, however, a statistically significant negative correlation between traumatic episodes and exacerbations in 95 patients who had exacerbations during the programme, due primarily to less activity of the disease during a three month period following surgical procedures and fractures. Electrical injury had a significant positive association with exacerbation using a three month at-risk period, but there were no other significant positive correlations in any other category of trauma, including minor head injuries; there were no cases of head injury with prolonged unconsciousness. There was no linkage between the frequency of trauma and progression of disability. MS patients had two to three times more trauma than controls.
A case of L-tryptophan associated eosinophilia, myalgia, eosinophilic fasciitis, peripheral sensorimotor neuropathy, and multiple white matter lesions on MRI scan is reported. The various effects of eosinophilia on the nervous system are reviewed. The persistence of the neurological complications despite resolution of eosinophilia and steroid therapy is emphasized.
Two patients with similar clinical features are presented: both patients had chronic renal failure, on hemodialysis for many years but recently begun on a high-flux dialyzer; both had been receiving a carbidopa/levodopa preparation; and both had the onset of hallucinosis and recurrent seizures, which were refractory to anticonvulsants. The first patient died without a diagnosis; the second patient had a dramatic recovery following the administration of vitamin B6. Neither patient was considered to have a renal state sufficiently severe enough to explain their presentation.
The cortical potentials evoked by posterior tibial nerve stimulation were examined in a series of 141 hospital patients requiring extradural spinal surgery. One hundred and five patients were neurologically intact, while in 36 some deficit was present. In the intact subjects, the absolute latencies of the main medium-latency peaks (N30, P40, N50, P60) were found to vary with height and age. There were no additional gender-related differences. The latencies of the deficit group were longer than those of the intact group but only marginally useful as a clinical discriminator; their amplitudes were not significantly lower than those of the intact group. A model for variations in SEP latency is suggested.
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Gilles de la Tourette's syndrome (GTS) is a chronic neuropsychiatric disorder characterized by multiple involuntary motor and phonic tics associated with behavioural disturbances including obsessive-compulsive and aggressive behavior, depression and, rarely, psychosis. The relationship of GTS, presumed to be predominantly a dopaminergic disorder, and depression, presumed to be a noradrenergic-serotoninergic deficiency state, is currently poorly understood. The reports published to date on the effects of tricyclic antidepressants in GTS have been contradictory; while Messiha et al. (1976) used imipramine successfully in one GTS patient, Abuzzahab and Anderson (1973) and Fras (1978) on the other hand, found imipramine to exacerbate GTS symptoms and cautioned its usage in this syndrome. A more recent report suggested that imipramine is useful in GTS patients who exhibit symptoms of attention deficit disorder (Dillon et al., 1985). We report a patient with GTS whose depression and behaviour improved considerably when low-dose imipramine (Tofranil) was added to the regimen of anti-GTS medication. This report suggest that tricyclic antidepressants may be useful adjuncts in the management of GTS, and hints at norepinephrinergic and serotoninergic deficiencies as being components of the pathogenesis of the syndrome.
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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.
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.
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.
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