562 Matters arising J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.5.562-c on 1 November 1995. Downloaded from Davie et al reply: toxin (BTX-A) for limb spasticity. Our Dunne replies: We thank Ray Chaudhuri and colleagues for experience also suggests that botulinum Bhakta and his colleagues, in accord with their comments regarding our recent publi- toxin can be a safe and effective treatment our have treated cation in this Journal.I report, successfully patients They cite preliminary for spasticity in selected patients. We would, with chronic The mean duration results from a spectroscopic study localised spasticity. however, like to raise the following points: of spasticity for our patients was 10 (range to the putamen, carried out in a group of Not only does this treatment have a use in and the of benefit patients with 05-45) years, degree idiopathic Parkinson's disease.2 early spasticity but also where the limb is from botulinum toxin A treatment did not We have studied the published abstract of held in a flexed posture for many months or correlate with the duration of We their work and it would spasticity. seem that there even years. In these patients one might be agree that in some patients clinical differen- are significant methodological differences justified in thinking that immobility of a tiation between active and fixed or passive between their study and our own in terms of spastic limb is due to irreversible changes in contracture can be difficult. In this situation data acquisition, spectroscopic localisation, soft tissue and that inappropriate muscle we have found that needle EMG is and methods of measurement which make activity is no longer a relevant contributing extremely useful, as activation is direct comparison difficult. prominent factor. We have treated 15 such patients present if muscles are contributing substan- Ray Chaudhuri et al are correct to quote after hemiplegic stroke in whom severe to the abnormal We the the tially posture. grade recent paper by Holhouser et al.3 This is flexor spasticity of the forearm caused degree of motor unit potential activation the only large spectroscopic study of idio- difficulty with hand hygiene (in some cases with a five point ordinal scale (0 = no activa- pathic Parkinson's disease to date, in which fingernails traumatising the palmar skin). tion to 4 = full interference pattern), corre- spectra were collected from the basal ganglia These patients could be deemed to have lating this with limb posture and resistance in 151 patients with idiopathic Parkinson's major contractures, yet 80% responded to passive stretch. disease, 80-90% of the volume having been to botulinum toxin. This raises the interest- We agree that EMG localisation not localised to the striatum. They found no may sig- ing question of how to identify patients be required to achieve a satisfactory effect; nificant reduction in the NAA/creatine ratio in this category who might benefit from however, the optimal delivery technique is compared with controls. They noted a treatment. unknown and will randomised trials. decrease in the NAA/choline require ratio in the We note that needle EMG, was used to We find that EMG is a useful adjunct to older patients with idiopathic Parkinson's confirm the degree of spasticity in a muscle. physical examination by assisting in the disease. They concluded that their findings We are interested as to which EMG criteria accurate localisation of active muscle. may indicate a slight decrease in NAA or were used to assess spasticity? We have found a mean of alternatively increased improvement concentrations of In our experience of injecting biceps range of passive joint movement of 280 choline and creatine in this subgroup. brachii, flexor digitorum superficialis and (95% confidence intervals 21°-36°), and This highlights the difficulty of interpret- profundus, flexor carpi ulnaris, hamstrings, applying a threshold change of 100 or 150 ing the metabolite ratios as quoted by Ray hip adductors, and gastrocnemius, EMG does not alter our results. Chaudhuri et al,2 as it assumes that at least localisation is not required to achieve a satis- J W DUNNE one of these metabolites remains unchanged factory therapeutic effect. In vitro studies of Neurophysiology Laboratory, in concentration (a hypothesis Royal Perth Hospital, as yet rabbit longissimus dorsi have shown that dif- PO Box X2213 GPO Perth, unproved in idiopathic Parkinson's disease). fusion of botulinum toxin occurs up to Western Australia 6001, Australia In our recent study we have used a semi- 45 mm from the injection site and that the quantitative method to overcome this prob- toxin can cross fascial planes.2 In the light of lem. To date we have found a significant this we are interested in the authors' asser- reduction in apparent NAA concentration tion that needle electromyographic guidance Vascular ataxic hemiparesis: a re- collected from a spectroscopic volume for BTX-A injection "enhances the accuracy evaluation localised to the putamen and globus pallidus of injections" and wondered whether EMG in only one of nine patients with idiopathic was used only to locate deep muscles, or was Prompted by the unexpectedly high rate of a Parkinson's disease.4 Whereas we agree that it also used to define the injection site within potential embolic source in patients with the our findings do not exclude the possibility of a given muscle. clinical syndrome of ataxic in neuronal loss hemiparesis or dysfunction occurring We appreciate that change in range of the recent study by Moulin et within the putamen al,l alone in idiopathic motion of joints after treatment may be we studied the frequency of a potential Parkinson's disease, this needs to be con- relatively large but we would suggest a cardioembolic source, and internal carotid firmed by the demonstration of an absolute higher threshold be used for difference in artery stenosis > 50% ipsilateral to a pre- reduction of NAA from this structure. goniometer measurements as an indicator sumed hemispheric infarct, in patients C A DAVIE for real http://jnnp.bmj.com/ D H MILLER change. Although a change of 50 has presenting with the syndrome of ataxic G J BARKER previously been suggested as a criterion of hemiparesis (AH) or dysarthria-clumsy hand A J LEES improvement,3 we agree with the opinion of syndrome (DCHS). Patients had been regis- Gajdosik and Bohannon4 that this threshold tered as described in an earlier report.2 1 Davie CA, Pirtosek Z, Barker GJ, Kingsley is too low. Even in healthy subjects, within Among our first 859 patients we registered DPE, Miller DH, Lees AJ. Magnetic reso- observer errors to 5% have nance spectroscopic study of parkinsonism up been reported 47 (5%) cases of AH/DCHS; 27 had a related to boxing. J Neurol Neurosurg for hip goniometry.5 lacunar infarct on CT, two a territorial Psychiatry 1995;58:688-91. BIPIN B BHAKTA infarct, whereas 16 had no CT 2 J ALASTAIR COZENS specific Ray Chaudhuri K, Lemmens G, Williams S, lesion. There were no with other Ellis C, Leigh PN. Proton magnetic reso- M ANNE CHAMBERLAIN patients on September 27, 2021 by guest. Protected copyright. nance spectroscopy study of striatal changes Rheumatology and Rehabilitation Research Unit, specific lesions on CT, such as haemor- in Parkinson's disease. J Neurol 1995;242 University ofLeeds, UK rhage. the chance of a JOHN M BAMFORD Obviously, specific (suppl 2):S 15. lesion other than a small infarct was 3 Holshouser BA, Komu Moller Department ofNeurology, deep M, HE, low in our a Zijlmans J, Kolem H, Hinshaw Jr DB, et al. St James University Hospital, series. In prior analysis of the Localised proton NMR spectroscopy in the Leeds, UK first 350 patients AH/DCHS was a more striatum of patients with idiopathic accurate predictor of a small deep infarct Parkinson's disease: a multicentre pilot than motor study. Magn Reson Med 1995;33:589-94. pure syndrome or sensory motor 4 Davie CA, Wenning GK, Barker GJ, Tofts PS, syndrome.2 Twenty four (51%) of our cases Kendall BE, Quinn N, et al. Differentiation 1 Dunne JW, Heye N, Dunne SL. Treatment had whereas six had a of chronic limb spasticity with botulinum hypertension, (13%) of multiple system atrophy from idiopathic potential cardioembolic stroke source. Four Parkinson's disease using proton magnetic toxin A. J Neurol Neurosurg Psychiatry resonance spectroscopy. Ann Neurol 1995; 1995;58:232-5. of 35 (11%) patients who had carotid ultra- 37:204-10. 2 Borodic GE, Pearce LB, Ferrante R. Thera- sound studies had an ipsilateral stenosis peutic botulinum toxin: histologic effects and > 50%. diffusion properties. In: DasGupta BR, ed. Percentages were similar for patients Botulinum and tetanus neurotoxins. New York: with or without lesions on CT. Considered Plenum Press, 1993:623-45. separately, the frequency of these two 3 Boone DC, Azen SP, Lin C-M, Spence C, sources of potential embolism are Baron C, Lee L. Reliability of goniometric rather measurements. Phys Ther 1978;58: 1355-60. low; however, almost a quarter of our Treatment of chronic limb spasticity 4 47 cases had either of these two features. with Gajdosik RL, Bohannon RW. Clinical mea- botulinum toxin A surement of range of motion. Review of Our data, therefore, concur with those goniometry emphasising reliability and valid- of Moulin et al,I in that We read with interest the ity. Phys Ther 1987;67:1867-72. among patients short report by 5 Ellis presenting with a syndrome of "cerebellar Dunne et al' the use of MI, Stowe J. The hip. Clin Rheum Dis regarding botulinum 1982;8:655-75. type" ataxia the number with a potential Matters arising 563 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.59.5.562-c on 1 November 1995. Downloaded from source of embolism is substantial. How- Do musical hallucinations have a neu- These hallucinations could be checked by ever, a potential cardioembolic source, large rological cause? having a light on after dark and by opening vessel disease, or even the absence of hyper- her eyes. Her balance was very poor. She tension do not exclude the presence of small Wodarz et all present a case of musical hal- had brief Menieriform attacks comprising vessel disease as the cause of a lacunar lucinations attributed to basal ganglia calcifi- nausea, a whirring vibration in her head like infarct presenting with AH/DCHS. Patients cations. The patient, however, satisfies only an egg beater, deafness, and mental confu- could have more than one type of vascular one of the four criteria for determining a sion. She could tolerate the cramps and disease, one of which becomes symptomatic neurological as opposed to epileptic or oto- other symptoms, but most of all she was in first. The fact that most silent brain infarcts logical cause for musical hallucinations.2 terror of these vibrations, later described as in patients with a cardioembolic territorial There was no evidence for epileptic activity, loud buzzing, roaring in the ears, noises in infarct are small lesions also point at this but there was deafness and tinnitus. The the head, or pulsations. The auditory sensa- possibility.3 I wonder whether Moulin et al' patient had "cerebellar" ataxia, but no other tion depended on the rapidity of the vibra- would recommend carotid endarterectomy cerebellar symptoms, with apparently no tion. in patients with AH/DCHS with a small check if this ataxia was partly or wholly of It only needs a couple of cases with con- deep hemispheric infarct on brain imaging vestibular origin. She had chronic sistent neurological lesions but no deafness and a > 70% ipsilateral internal carotid hypoparathyroidism, yet no mention was to completely sink the otogenic theory23 and artery stenosis? I know neurologists who, made of any drugs she was taking. so reduce the causal possibilities for musical considering a carotid lesion a coincidental These criteria2 were set up on the general hallucinations. My previous appeal2 for such feature, don't even perform carotid ultra- scientific principle that if most cases of a a case has been unsuccessful, so it is reason- sound in patients with lacurnar stroke. phenomenon are caused by a known factor able to assume that there is no case in the J LODDER (in this case ear disease), one should be very medical literature. Wodarz et all state that Department ofNeurology, University Hospital Maastricht, cautious before concluding that the remain- musical hallucinations can occur with brain- PO Box 5800, ing cases are due to a second, quite different stem lesions, but give no reference. Please NL-6202 AZ Maasnicht, factor (brain disease), rather than being vari- could they cite one which includes patients The Netherlands ants of the first cause. without cochlear or neural deafness? I 1 Moulin Th, Bogousslavsky J, Chopard JL, Wodarz et all offer a simplistic version of appeal again to neurologists to publish new Ghika J, Crepin-Leblond Th, Martin V, the otogenic theory, which, not surprisingly, non-deaf cases of musical hallucinations. Maeder P. Vascular ataxic hemiparesis: a they then dismiss. It is clear that hearing loss A G GORDON re-evaluation. J Neurol Neurosurg Psychiatry 32 Love Walk, 1995;58:422-7. itself is not a sufficient factor, and indeed London SE5 8AD, UK 2 Lodder J, Bamford J, Kappelle J, Boiten J. drugs can induce musical hallucinations in What causes false clinical prediction of small people with normal hearing.3 It seems that 1 Wodarz N, Becker T, Deckert J. Musical hallu- deep infarcts? Stroke 1994;25:86-91. is an 3 Boon A, Lodder J, Heuts-van Raak L, Kessels the extra factor endolymphatic cinations associated with post-thyroidectomy hydrops, as seen in incipient Meniere's dis- hypoparathyroidism and symmetric basal F. Silent brain infarcts in 755 consecutive ganglia calcifications. J Neurol Neurosurg patients with a first-ever supratentorial ease. This can cause fluctuating or progres- Psychiatry 1995;58:763-4. ischemic stroke. Relationship with index- sive hearing loss, hyperacusis, or no deafness stroke subtype, vascular risk factors, and 2 Gordon AG. Musical hallucinations. Neurology mortality. Stroke 1994;25:23-84. but with audiosensitivity, or tinnitus, or ver- 1994;44:986-7. This seems to be the mechanism 3 Gordon AG. Benzodiazepines and the ear- tigo. tinnitus, hallucinations and schizophrenia. whereby a wide range of drugs induce musi- Can J Psychiatry 1993;38:156-7. cal hallucinations in normal subjects; deaf 4 Ikeda K, Kobiyashi T, Kusakari J, Takasaka T, ears are even more susceptible to drugs.2 In Yumita S, Furukawa Y. Sensorineural hear- Moulin and Bogousslavsky reply: ing loss associated with hypoparathyroidism. We are delighted that the data from their own case Wodarz et all attribute deaf- Laryngoscope 1987;97: 1075-9. Maastricht confirm our study-that is, that ness to presbyacusis. This is an overused 5 Schoelly ML, Heuscher JE. Contribution a potential sources of embolism to the brain default diagnosis, which should be confined l'etude des psychoses tetaniques. Monatsschrift to with smooth tone fur Psychiatrie und Neurologie 1950;119: are not uncommon in patients with acute patients high symmetric 141-55. stroke presenting as ataxic hemiparesis. losses. Their patient had mild pancochlear 6 Dda CF. Psychological states resulting from We also agree with the point that the perceptive hearing loss, worse on the left, far parathyroid deficiency. Journal of Abnornal exact aetiology of brain infarct is presumed more consistent with at least some hydrops and Social Psychology 1939;34:481-96. rather than proven in most instances, but component. A third of patients with hypo- it may be presented also from another per- parathyroidism4 had inner ear hearing loss, spective: the presence of a small deep infarct not presbyacusis but suggestive of cochlear is commonly compatible with underlying hydrops (slight or unilateral or asymmetric http://jnnp.bmj.com/ small vessel disease, although there is no test or low tone losses, pancochlear losses, etc). which can show this in vivo; however, this Other factors which could trigger an acute assumption does not rule out the possibility hydrops in a deaf or normal ear include Wodarz et al reply: that it may also be embolic, especially if a anything likely to reduce perilymphatic Gordon's interesting comments and the source of embolism is indeed shown. The pressure, such as dehydration, hypotension, additional three patients with postsurgical argument of the coexistence of cardioem- weight loss,3 or, as in this case,' electrolyte hypoparathyroidism and associated psy- bolic territorial infarct with silent small deep imbalance. chosis are very much appreciated. The musi- infarcts' (Lodder's ref3), could also be pre- Wodarz et al' claim that musical halluci- cal hallucinations in these patients, however, sented the other way around to support the nations have not been reported before in were associated with various other psychi- on September 27, 2021 by guest. Protected copyright. concept that small deep infarcts may often postsurgical hypoparathyroidism. There is, atric symptoms such as delirious state, be embolic in origin. however, a case5 distinguished by the rich- epileptic seizures, and paranoid ideation. On The answer to the question asked by ness and intensity of hallucinations, which is the contrary, our patient, in terms of psy- Lodder about the performance of carotid very instructive as necropsy showed chopathological syndromes, presented with endarterectomy in patients with deep small absolutely no brain pathology. (There are isolated musical hallucinosis. As in his previ- infarct and ipsilateral > 70% carotid stenosis many other reports that I have not checked.) ous comments to other papers Gordon seems to lie in the randomised trials of She' heard music and bells ringing and attributes musical hallucinations to a periph- carotid endarterectomy, in which these talked of composing a symphony! In other eral = otogenic mechanism.' His support for patients were included and contributed to hallucinations she felt herself being thrown this hypothesis in our patient is, however, the global superiority of surgery over med- through the air or down a hole. Her sight based on some misunderstandings.2 ical treatment alone. Thus the neurologists was very poor and she had vivid visions (1) We did, in fact, report the drugs given mentioned by Lodder are not following the thought to have been of retinal origin. In to our patient during inpatient treatment. In scientific data, which showed the usefulness another patient the main hallucinations were the six months preceding the hallucinosis of carotid surgery in symptomatic patients a feeling of flying through the air and oscilla- she received the equivalent of 2-3 mmol with >70% carotid stenosis. tions in the head. No mention was made of Ca2+ intravenously only when symptoms of otological examinations. An autobiographi- tetany occurred (once or twice per month). 1 Boon A, Lodder J, Heuts-van Raak L, Kessels cal account, however, by a social worker6 This might well result in an acute ear F. Silent brain infarcts in 755 consecutive confirms that vestibular and auditory hallu- hydrops, as suggested by Gordon. As the patients with a first-ever supratentorial ischemic stroke. Relationship with index- cinations are prominent features of psy- musical hallucinosis disappeared, however, stroke subtype, vascular risk factors, and chosis. She felt herself suspended in mid-air after addition of oral dihydrotachysterol plus mortality. Stroke 1994;25:23-84. or upside down, or suddenly being moved. oral and intravenous Ca2+, a drug induced