Auditory startle response in cervical dystonia

The at-risk population has been tested for geneticstatus, but these results are unknown to the author. Ab-normal sleep behaviors in MJD have been reported butonly a single case of RBD with polysomnogram confir-mation.6 One report7 described a patient with prolongedsleepwalking during NREM as well as REM sleep, as-sociated with prolonged confessional states. That patientalso exhibited periodic leg movements of sleep and ob-structive sleep apnea. Another report8 described 3 MJDpatients with progressive cognitive decline and episodesof delirium during sleep. Cognitive decline is not afeature of typical MJD, however.9 In another interestingcase, the offspring of a consanguineous marriage, withpsychotic behavior and dementia, had possible MJD withpossible RBD.10 His CAG repeat numbers were 60 & 60,which is higher than normal but smaller than required fora genetic diagnosis of MJD. The increased number ofnucleotide repeats in both alleles was thought to explainhis condition, which had features that were both typicaland atypical of MJD.

The pathology of RBD is unknown, but data suggesta correlation with dopamine deficiency11 and degen-eration in brainstem structures. MJD is a neurodegen-eration involving the substantia nigra, locus coeruleus,and other brainstem and cerebellar structures. Theseloci are often involved pathologically in the parkinso-nian disorders, which have been associated with RBD.Some have suggested that RBD is specifically associ-ated with alpha synuclein disorders.12 MJD involvesmany of the same brainstem centers affected by alphasynucleinopathies but has not been identified as hav-ing alpha synuclein pathologic findings. We believethat EDS and RBD-like behavior are increased inMJD, and other sleep disorders may be as well. Theseconditions may constitute one aspect of this disorderthat might be amenable to therapy.

Acknowledgments: We thank M. Silber, MD, C. Comella,MD, D. Dawson, MD, and M. Trieschmann, MD.

REFERENCES

1. Ferini-Strambi L, Zucconi M. REM Sleep behavior disorder. ClinNeurophysiol 2000;111(Suppl. 2):S136–S140.

2. Mahowald MW. Rapid eye movement sleep behavior disorder.Medlink Neurology. San Diego: Medlink 2002.

3. Friedman JH. Presumed rapid eye movement behavior disorder inMachado Joseph disease (spinocerebellar ataxia type 3). MovDisord 2002;17:1350–1353.

4. Boeve BF, Feraman TJ, Silber MH, Smith GE. Validation of aquestionnaire for the diagnosis of REM sleep behavior disorder.Neurology 2002;58(Suppl. 3):A509.

5. Nakano KK, Dawson DM, Spence A. Machado disease. A hered-itary ataxia in Portuguese emigrants to Massachusetts. Neurology1972;22:49–55.

6. Syed BH, Rye DB, Singh G. REM sleep behavior disorder andSCA-3 (Machado-Joseph disease). Neurology 2003;60:148.

7. Kushida CA, Clerk AA, Kirsch CM, et al. Prolonged confusionwith nocturnal wandering arising from NREM and REM sleep: acase report. Sleep 1995;18:757–764.

8. Fukutake T, Shinotoh H, Nishino H, et al. Homozygous Machado-Joseph disease presenting as REM sleep behavior disorder andprominent psychiatric symptoms. Eur J Neurol 2002;9:97–100.

9. Sudarsky LR, Coutinho P. Machado-Joseph Disease. Clin Neuro-sci 1995;3:17–22.

10. Fukutani Y, Katsukawa K, Matsubara R, et al. Delirium associatedwith Joseph disease. J Neurol Neurosurg Psychiatry 1993;56:1207–1212.

11. Eisensehr I, Lindeiner HV, Jager M, Noachter S. REM sleepbehavior disorder in sleep-disordered patients with versus withoutParkinson’s disease: is there a need for polysomnography? J Neu-rol Sci 2001;186:7–11.

12. Boeve BF, Silber MH, Ferman TI, et al. Association of REMbehavior disorder and neurodegenerative disease may reflect anunderlying synucleinopathy. Mov Disord 2001;16:622–630.

Auditory Startle Response inCervical Dystonia

Jorg Muller, MD,1 Markus Kofler, MD,2

Gregor K. Wenning, MD, PhD,1 Klaus Seppi, MD,1

Josep Valls-Sole, MD, PhD,3 andWerner Poewe, MD1*

1Department of Neurology, University HospitalInnsbruck, Austria; 2Department of Neurology, HospitalHochzirl, Austria; 3Department of Neurology, University

Hospital Barcelona, Barcelona, Spain

Abstract: The excitability of brainstem neurons is abnor-mally enhanced in patients with cervical dystonia (CD), butthe extend of such abnormality is not known. We examinedwhether patients with CD showed abnormalities in theauditory startle response (ASR), a brainstem reflex elicitedby an unexpected loud stimulus. Thirteen patients with CDwere investigated 3 months after botulinum toxin treat-ment. Thirteen healthy volunteers served as controls. ASRswere elicited by binaural high-intensity auditory stimuli.Reflex electromyographic (EMG) activity was recorded si-multaneously with surface electrodes bilaterally from mas-seter, orbicularis oculi, sternocleidomastoid, and bicepsbrachii muscles. We found that ASR onset latencies weresimilar for patients and controls. CD patients had signifi-cantly lower ASR probabilities than controls (P � 0.007).ASR area under the curve was significantly smaller in CD

*Correspondence to: Prof. Dr. Werner Poewe, Department of Neu-rology, University Hospital Innsbruck, Austria, Anichstr. 35, A-6020Innsbruck, Austria. E-mail: [email protected]

Received 5 February 2003; Revised 21 May 2003; Accepted 16 June2003

DOI 10.1002/mds.10609

1522 J. MULLER ET AL.

Movement Disorders, Vol. 18, No. 12, 2003

patients (P � 0.017). Similar to controls, patients showed asignificant habituation of ASR (P < 0.001, each); however,CD patients showed a prolonged tonic or phasic EMGactivity after the initial ASR that was not observed incontrols. Normal latencies and recruitment pattern indicatea preserved organization of intrinsic neural pathways me-diating ASR in CD. Reduced ASR probability and magni-tude as well as prolonged EMG activity after the properstartle response corroborate and extend previous findingson brainstem dysfunction in CD. © 2003 Movement Disor-der Society

Key words: auditory startle response; cervical dystonia;brainstem reflex; pedunculopontine nucleus (PPN)

Primary cervical dystonia (CD) is a disorder of basalganglia function. Previous studies on blink reflex recov-ery curves have indicated increased brainstem interneu-ronal excitability in patients with CD.1–3 Loss of inhibi-tion of brainstem reflexes in dystonia likely reflectsalterations in descending projections to inhibitory neu-rons, which are modulated indirectly by the pallido-thalamo-cortical motor circuit.4 The auditory startle re-flex (ASR) is a brainstem reflex in response to anunexpected loud stimulus. The initial reaction involveseye closure, facial grimacing, neck flexion, and abduc-tion or flexion of the arms; the response habituates rap-idly with repeated presentation of the same stimulus.ASR is used for neurophysiological research and hasbeen applied in studies of different movement disor-ders.5–10 Evidence from animal studies11,12 and observa-tions in patients13 suggest strongly that the ASR is me-diated via brainstem structures and that the basal gangliaand thalamus are implicated in modulation and plasticityof the startle reflex.14–16 The present study was carriedout to elucidate ASR properties and to extend previousfindings on brainstem pathophysiology in patients withprimary CD.

PATIENTS AND METHODS

ASRs were recorded in 13 consecutive patients withprimary CD (4 men, 9 women; median age �54 years;age range �35–69 years; median disease duration, 6years; disease duration range � 3–18). Secondary causesof dystonia such as basal ganglia lesions and drug expo-sure had been excluded in all patients through cerebralmagnetic resonance imaging (MRI), history, and labora-tory investigations. Genetic testing for DYT-1 was neg-ative in all patients with CD. Patients were recruitedfrom the outpatient movement disorders clinic of theInnsbruck University Hospital. All patients were on reg-ular therapy with botulinum toxin type A (BtxA) for atleast 1 year and none received anticholinergic drugs.ASRs were investigated 3 months after the previous

BtxA therapy in all patients. The median severity of CDassessed by the Tsui score was 7.0 (severity range �4–13).17 Thirteen healthy age- and gender-matched vol-unteers (4 men, 9 women; median age � 54 years; agerange � 35–63 years) served as controls. Most controlsubjects were physicians and staff members and wereaccustomed to the laboratory setting. Patients andhealthy volunteers were studied in the supine position ina quiet semi-darkened room,10 and were asked to stayawake and relaxed. Care was taken to avoid potentialvisual or auditory prepulse stimuli.18 After normal bilat-eral hearing thresholds were ascertained, ASRs wereelicited by 8 binaurally presented tone bursts that dif-fered randomly in tonal frequency and intensity (250 Hz,90 dB; 500 Hz, 105 dB; 750 Hz, 110 dB; 1,000 Hz, 110dB nHL) to enhance the novelty of the stimulus.10 Con-secutive stimuli were given at intervals of 2 to 3 minutes.Non-rectified surface electromyographic (EMG) record-ings were obtained simultaneously after each stimulusfrom masseter, orbicularis oculi, sternocleidomastoid,and biceps brachii muscles bilaterally. With the excep-tion of the sternocleidomastoid muscle, none of thesemuscles had received previous BtxA injections. Silver-silver chloride cup electrodes were attached over musclebelly and tendon where applicable. Single sweeps of 500msec including 20 msec prestimulus delay were recordedwith filters set at 10 and 10,000 Hz and traces containingbackground activity with a mean amplitude exceeding 50�V were rejected from further analysis. ASRs wereaccepted in traces without background activity whenEMG activity of at least 30 �V occurred at onset laten-cies defined according to minimum latencies for individ-ual muscles reported previously (23 msec in masseter, 17msec in orbicularis oculi, 23 msec in sternocleidomas-toid, and 60 msec in biceps brachii muscles).5,6,10,13,19

ASR probability was calculated by dividing the numberof all accepted reflex responses by the total number ofrecorded traces and multiplying by 100; ASR latencieswere measured from stimulus onset to ASR onset. ASRarea under the curve was calculated during the first 100msec after response onset20 to avoid possible contami-nation with voluntary muscle activation. ASR habitua-tion was assessed by comparing the number of musclesshowing startle responses to stimuli 1�2 with the num-ber of responses to stimuli 7�8. Numbers are given asmedian values throughout and statistical analyses (Fisherexact test, Mann-Whitney U Test, Wilcoxon test) wereapplied as appropriate.

RESULTS

ASRs were elicited less frequently in patients with CD(68%) compared with normal controls (76%, P � 0.007).

AUDITORY STARTLE RESPONSE IN CERVICAL DYSTONIA 1523


Patients with CD had lower ASR probabilities in themasseter (70 vs. 89%; P � 0.001) and sternocleidomas-toid muscles (69 vs. 85%; P � 0.004) compared withcontrols. ASR probability did not differ between patientsand controls in the orbicularis oculi (99 vs. 100%; notsignificant [n.s.]) and biceps brachii muscles (33 vs.30%; n.s.).

ASR onset latencies did not differ significantly be-tween patients with CD and controls (P � 0.2), and thesame pattern of muscle activation occurred in bothgroups. In both patients and controls, ASR latencies wereshortest in orbicularis oculi (36 vs. 33 msec) and longestin biceps brachii (110 vs. 143 msec), with intermediatelatencies in sternocleidomastoid (60 vs. 66 msec) andmasseter muscles (63 vs. 67 msec).

The ASR area under the curve measured for all mus-cles during the first 100 msec after response onset wassignificantly smaller in patients with CD compared withcontrols (P � 0.017). In all individual muscles, themedian ASR magnitude was smaller in patients com-pared with controls: orbicularis oculi (�45%), bicepsbrachii (�38%), masseter (�20%), and sternocleido-mastoid muscles (�19%).

In CD patients, no significant side-to-side differencewith respect to the dominant head deviation was ob-served for ASR probability (P � 0.2), latency (P � 0.3),and area under the curve (P � 0.8).

Patients with CD showed a significant habituation ofthe ASR when all muscles were analyzed together (P �

0.001). ASR probability decreased with successive stim-uli by 81% in biceps brachii, 47% in sternocleidomas-toid, and by 46% in masseter muscles (P � 0.001 foreach). No habituation occurred in the orbicularis oculimuscle.

An unexpected finding was a prolonged increase inEMG activity that was separated occasionally from theinitial (proper) ASR in CD patients (see Fig. 1A–C).EMG activity measured as area under the curve duringthe last 200 msec of the total 500 msec recording periodwas therefore significantly larger (P � 0.001) in patientswith CD. Prolonged EMG activity occurred most often inorbicularis oculi and sternocleidomastoid muscles, fol-lowed by masseter muscles with only few late responsesin biceps brachii muscles. This prolonged EMG activitywas phasic in 3 patients (Fig. 1B) and showed a contin-uous activation pattern (Fig. 1A) in the remaining pa-tients, irrespective of the presence or absence of headtremor on clinical examination.

In 2 patients (1 with tonic and 1 with phasic prolongedEMG activity), we determined whether the prolongedEMG activity burst was part of the startle response byapplying a prepulse stimulus.21 Prepulse stimulation wasachieved by weak electrical stimuli (three times sensorythreshold) delivered to the right index finger through ringelectrodes 150 msec before the startling stimulus.22 Fourconditioned and four unconditioned test responses wererecorded randomly. Prepulse alone did not elicit anystartle response. Similar to healthy controls, prepulse

FIG. 1. Representative examples of auditory startle responses in a patient with a prolonged continuous activation pattern (A), in a patient with aprolonged burst-like pattern (B), and in a normal control subject (C). The arrow and vertical lines indicate the auditory stimulus. CD, cervical dystonia;MSS, masseter muscle; OrOc, orbicularis oculi muscle; SCM, sternocleidomastoid muscle; BB, biceps brachii muscle; L, left; R, right.



inhibition (PPI) reduced the ASR magnitude in CD by atleast 30% in all cranial nerve supplied muscles; however,the prepulse did not affect the magnitude of the pro-longed EMG activity in both patients with CD.

DISCUSSION

The present study demonstrates alterations of ASR inpatients with primary CD compared with ASR in healthycontrols. Normal recruitment pattern together with nor-mal ASR latencies suggest that there is no organizationaldisturbance of intrinsic neural pathways mediating thisbrainstem reflex. Contradictory findings, however, oflower ASR probability and magnitude on the one hand,and the excitatory phenomenon of prolonged EMG ac-tivity after initial ASR on the other hand, indicate acomplex disturbance in the control of this brainstemreflex in CD.

The ASR is mediated by a pathway comprising thecochlear nucleus and the nucleus reticularis pontis cau-dalis (NRPC), which projects to cranial and spinal motorneurons.11,23,24 The NRPC is a key element of the path-way that mediates ASR and receives inhibitory cholin-ergic projections from the pedunculopontine tegmentalnucleus (PPN).25 This pathway modulates prepulse inhi-bition and reduces baseline startle.25 The PPN receivesdense and predominantly inhibitory basal ganglia input,mainly from the globus pallidus and substantia nigra parsreticulata.26,27 Intraoperative microelectrode recordingsin patients with primary dystonia demonstrate reducedpallidal activity at rest and during movement.4,27 Accord-ing to these observations, reduced pallidal inhibition ofthe PPN would be expected to reduce startle probabilityand magnitude, which was indeed shown for CD patientsin the present study.

Similar to healthy controls, CD patients exhibited sig-nificant habituation of ASR probability with successivestimuli. Habituation is a characteristic feature ofpolysynaptic reflexes and ASR habituation is thought toresult from synaptic depression of brainstem interneu-rons localized in the pontine reticular formation.6 Withrepeated stimuli, the number of reflex responses de-creased significantly except for that in the orbicularisoculi muscle, where no habituation was observed, inagreement with previous studies indicating that an audi-tory stimulus also elicits the acoustic blink reflex in thismuscle.10,11,13

Despite normal habituation with repetitive stimulation,single auditory stimuli elicited prolonged EMG activityafter the initial ASR in CD patients (Fig. 1A,B), a featurethat has not yet been described in any basal ganglia disor-der. The prolonged EMG activity was distinguishable fre-quently from the proper startle response and was not af-

fected by ASR modulation through PPI. The excitatoryphenomenon of prolonged EMG activity after the properASR apparently conflicts with findings of reduced ASRprobability and magnitude in the present study. Voluntaryor dystonic muscle activity could have contributed to thisfinding; however, this pattern of recurrent EMG activitywas not observed in healthy controls. In addition, dystoniawas confined to the cervical region whereas the recurrentEMG activity was also observed in masseter, sternocleido-mastoid, and biceps brachii muscles of CD patients.

Very short absolute refractory periods of startle-medi-ating substrates28 may indeed allow for a rapidly reoc-curring EMG activity after a single tone burst underpathological conditions. This impaired ASR circuit inhi-bition might be mediated by either disinhibition fromafferent projections or threshold changes of the reflexcircuit itself. Accordingly, a loss of inhibition for variousbrainstem reflexes has been reported in patients withCD.1–3,29–31 In particular, reports of an enhancement ofthe blink reflex recovery curve, despite normal latencyand duration of the blink reflex itself, are consistent withour results.1–3,29–31 Both findings suggest an increasedbrainstem interneuronal excitability in patients with CD.

A brainstem structure that participates in modulation ofthe startle reflex is the vestibular nucleus via the vestibu-lospinal tracts.32 Stimulation of the vestibular nucleus innormal rats evoke bilateral, startle-like responses with shortrefractory periods, and combined vestibular nucleus andacoustic stimulation enhance these startle-like responseswith cross-modal summation without collision effects.32

This model is of particular interest, because previous re-search indicates a vestibular involvement in the pathophys-iology of primary CD.33,34 Alternatively, reduced pallidalinhibition of the PPN with increased cholinergic projectionfrom the PPN to the NRPC might account for the appar-ently contradictory findings of reduced ASR probability andimpaired ASR circuit inhibition in CD. Anatomical tracingstudies indicate that these cholinergic projections releaseexcitatory as well as predominantly inhibitory effects inacoustically responsive NRPC neurons that are likely toresult in differential modulation of ASR.25

In summary, the present study demonstrated: (1) pre-served organization of intrinsic neural pathways mediat-ing the startle response in CD; (2) reduction of thebaseline startle; and (3) an excitatory phenomenon ofprolonged EMG activity after the initial ASR. ProlongedEMG activity may indicate impaired ASR circuit inhibi-tion in CD corresponding to findings of enhancement ofthe blink reflex recovery curve. The underlying patho-physiology of a reduced baseline startle is unclear andindicates the need for further studies.

AUDITORY STARTLE RESPONSE IN CERVICAL DYSTONIA 1525


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Auditory startle response in cervical dystonia