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Cally Cause Arm Pain Distally;' They Rarely Parkinsonian Syndrome.' This Has Led to Occur Proximally Letters to the Editor 413 symptoms, becoming completely normal levodopa-induced chorea in 5 patients with iridis is generally thought to be that of failure J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.55.5.413-a on 1 May 1992. Downloaded from after 4 weeks. Fluoxetine was reintroduced at Parkinson's disease. The patients had a mean of pigment development rather than loss of the same dose and the depressive syndrome age of 54 (41-74) years, a mean duration of pigment that has already formed. Hypochro- disappeared without recurrence of toxic disease of 11 (7-21) years, mean duration of mia of the iris following acquired Horner's effects. levodopa therapy 9 (6-18) years and a mean syndrome has been reported but is rare. We A second case, a 57 year old woman, levodopa dose of 760 (450-1400) mg/day. report a case of this rare but interesting developed a generalised secondary partial All the patients were also receiving subcuta- manifestation of damage to the sympathetic epilepsy 3 months after an embolic cerebral neous apomorphine, 4 selegiline and 1 bro- nervous system to the eye. infarct. Phenytoin was introduced at 400 mg/ mocriptine. A 17 year old man was involved in a day. A year later the patient developed a The patients' dyskinesias were assessed motorcycle accident and suffered brachial depressive syndrome and fluoxetine was indi- over a one week baseline period on optimum plexus trauma, with loss of power and sensa- cated at a dose of 20 mg/day. Previously the anti-Parkinsonian therapy. They were then tion in the right arm followed by pain. phenytoin plasma level had been 11 5 ug/ml. given 2 Gm/day of GVG for one week and Examination 23 years later revealed partial Ten days later she developed vomiting, diffi- 3 Gm GVG for a second week. Assessment of C7 and complete C8 and TI paresis with culty with getting up and sitting and vertigo. dyskinesia severity was carried out using a corresponding sensory loss. He had post- The neurological examination showed trunk 4-point scale after a standard therapeutic traumatic brachial plexopathy pain for which ataxia, limb dysmetria, and multidirectional dose of sc apomorphine. he was seeking advice. Examination also nystagmus. Phenytoin plasma level was The patients also kept self-scoring diaries revealed a right Horner's syndrome with loss 47 ,ug/ml. for three days of each week to assess the of pigment in the right eye, his left being The fluoxetine was suspended and there number of hours "on" with and without coloured grey/green. was a progressive recovery of the signs and dyskinesias and the number of hours "off". Several mechanisms by which alteration in symptoms with a complete recovery in Baseline assessments showed that dyskinesias sympathetic activity may influence iris pig- approximately three weeks. Four weeks after were more severe later in the day in all mentation have been proposed.4 There may suspension of fluoxetine, the phenytoin plas- patients. On GVG no change in dyskinesia be failure of delivery of noradrenaline or ma level was 20 ,ug/ml for the same described severity occurred as judged by either the other melanin precursors to the melanocytes dose. apomorphine challenges or the self-scoring in the iris, perhaps mediated via cyclic In human studies an alteration of the diaries, but there was a mean increase in off adenosine monophosphate. There may be pharmacokinetics of fluoxetine was not hours from 3 to 4 hours. loss of activation of prostaglandins, or their found when administered simultaneously Four patients were unable to tolerate more precursors, or some melanotropic moiety, with other drugs (such as, ethanol, diazepam, than 2 Gm GVG due to increased severity of that are involved in melanin synthesis. Sev- chlorothiazide, tolbutamide and warfarin) Parkinsonian symptoms. The other patient eral cases of depigmentation of the iris' or and viceversa.3 In animal studies it was also noticed worsening of Parkinsonism on heterochromia iridis, with spots on the affec- shown that fluoxetine is a potent inhibitor of 3 Gm GVG. ted iris,6 have been reported following injury hepatic microsomal metabolism,2 this could Contradicting results with progabide, a to the sympathetic nervous system, but this be responsible for the increase of the pheny- gabaminergic agonist, have been reported in condition in the acquired state appears to be toin plasma level in these cases. The interval levodopa-induced dyskinesias in Parkinson's rare, although it may often be unrecog- between the first administration of fluoxetine disease.2 3 GVG was reported to aggravate nised. of the overdose Parkinsonism without improving tardive dys- P BYRNE and the beginning phenytoin C CLOUGH symptoms, also suggests a mechanism of the kinesias in psychotic patients on sustained Brook Hospital, Shooters Hill, metabolic alteration in the degradation of the neuroleptic therapy.4 GABA mimetic drugs London, UK anticonvulsant drug. therefore appear to have complex and contra- PATRICIO JALIL dictory actions in patients with movement Correspondence to: Mr Paul Byrne Servicio de Neurologia, Hospital Dr S6tero del Rio, disorders. This study is of interest in that UDA Neurologia, aggravation of Parkinsonism occurred with- 1 Hyodo T, Kare M, Shintomi Y Two cases of Pontificia Universidad Catdlica de Chile, out significant reduction in dyskinesias sug- congenital Horner's syndrome. Folia Ophthal- Santiago, Chile mol 1983;34:387-90. gesting that these two phenomena may not be 2 Ogle JW. On the influence of the cervical Correspondence to: Dr Jalil, Avda Salvador 2194, inextricable. portion of the sympathetic nerve and spinal Santiago, Chile N TURJANSKI cord upon the eye and it's appendages, A J LEES illustrated by clinical cases, with observations. Department of Neurology, Medicochiurgh Tran 1850;41:397-440. http://jnnp.bmj.com/ 1 Cooper GL. The safety offluoxetine. An update. The Middlesex Hospital, 3 Calhoun PF. Causes of heterochromia iridis BrJ Psychiatry 1988; 153-62. Mortimer Street, with special reference to paralysis of the 2 Fuller R, Rathbun R, Parli J. Inhibition of drug London WIN 8AA, UK cervical sympathetics. Am J Ophthalmol metabolism by fluoxetine. Res Commun Chem 1919;2:255-69. Pathol Pharmacol 1976;13:353-6. 4 Simon D, Austin J, Forslot L. Heterochromia 3 Lemberger L, Bergstrom R, Wolen R, et al. 1 Crossman AR. A hypothesis on the pathophy- pardus: implications of the spotted pale iris. Fluoxetine: Clinical Pharmacology and Phys- siological mechanisms that underlie levodopa Neuro-ophthalmology 1982;2:279-9 1. iologic Sisposition. J Clin Psychiatry 1985; or dopamine agonist-induced dyskinesia in 5 Mackley TA, Abbott K. Neurogenic hetero- 46:14-9. Parkinson's disease. Implications for future chromia: report of an interesting case. Am J 4 Stark P, Fuller R, Wong D. The pharmacologic strategies in treatment. Mov Disord Ophthalmol 1965;59:927-8. 1990;5: 100-8. 6 Miller NR. Disorders of pupillary function, profile of fluoxetine. J Clin Psychiatry on September 25, 2021 by guest. Protected copyright. 1985;46:7-13. 2 Bartholini G, Uloyd KG, Worms I, Constanti- accommodation and lacrimation. Walsh and 5 Steiner W, Fontaine R. Toxic reaction following nides J, Tisset R. GABA and GABAergic Hoyt's Clinical neuro-ophthalmology, 4th ed. the combined administration of fluoxetine medication relating to striatal dopamine func- Baltimore: Williams and Wilkins, 1982: and L-tryptophan: five case reports. Biological tion and Parkinsonism. In: Posner JL, et al, 500-7. 1986;21: 1067-71. eds. Adv Neurol, Vol 24, New York: Raven Psychiatry Press, 1979:253-9. 3 Bergmann KJ, Limongi JCP, LoweYH, Mendo- za MR, Yahr MD. Potentiation of the L-dopa effect in Parkinsonism by a direct GABA receptor agonist. Lancet 1984;i:559. Shoulder from tumour Gamma vinyl GABA in the treatment of 4 Gaio JM, Pollak P, Hommel M, et al. Clinical pain glomus Levodopa-induced dyskinesias in Par- and biochemical effects of gamma-vinyl gaba kinson's disease in tardive dyskinesia. J Neurol Neurosurg Psychiatry 1987;50: 1674-8. Localised pain in the shoulder often suggests a brachial plexus neuropathy or cervical In non-human primates blockade of the radiculopathy. Pain limited to a small area GABAergic inhibitory strio-pallidal pathways with sensory loss suggests a focal nerve lesion to the lateral segment of the globus pallidus Hypochromia iridis in acquired Hor- such as a neuroma. Glomus tumours typi- causes chorea, whereas stimulation causes a ner's syndrome cally cause arm pain distally;' they rarely Parkinsonian syndrome.' This has led to occur proximally. renewed interest in the potential value A 41 year old woman presented with point of gabaminergic agents in the treatment of The uncommon condition of congenital tenderness in the right posterior deltoid and Parkinson's disease and the complications of Homer's syndrome consists of ptosis, miosis, lateral suprascapular area. The tender area, levodopa therapy. facial anidrosis and hypochromia of the which had been present for several years, was We have investigated the irreversible inhib- affected iris.' This condition commonly less than 1 cm in diameter and located lateral itor of GABAtransaminase, gamma vinyl results from injury to the brachial plexus at to the spine of the right scapula. A friendly GABA (GVG) in the treatment of disabling birth.23 The mechanism of the hypochromia "touch on the shoulder" would cause an.
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