Journal of Neurology, Neurosurgery, and Psychiatry, 1979, 42, 705-714

Abnormal head movementsMICHAEL A. GRESTY AND G. MICHAEL HALMAGYI

From the Medical Research Council Hearing and Balance Unit and Department ofNeuro-Ophthalmology, Institute of Neurology, National Hospital, London

S U M M A R Y Abnormal head movements have been studied in a variety of diseases using objec-tive recording techniques and the data analysed with respect to the frequency content of themovement. Flopping, nodding, tic, chorea, myoclonic jerks, and most head tremors involvefrequencies of approximately 2 and 4 Hz which correspond to the natural fundamental andsecond harmonic resonances of the head as determined by the mechanical properties of the head/neck system. These findings provide a basis for classification of abnormal head movements aswell as an explanation of the characteristics of those arising from hypotonia of the neck muscles.The similarities between tremor frequencies and natural resonances suggest that in the case ofthe head, tremor arises from disorders of neural mechanisms normally responsible for the finecontrol of voluntary head movement and for stabilisation of the head during disturbance ofposture. Head movements in cases of congenital nystagmus were found to be of two types. Somewere of bizarre waveform, in no way assisted vision, and were taken to be of primarily patho-logical origin and classified as tremors. Others were learned adaptive responses which assistedvision either by interrupting the nystagmus, as in the case of spasmus nutans, or by compensatingfor the nystagmus with an inverse waveform and were called nodding. A prerequisite for truecompensatory nodding is modified vestibulo-ocular reflex.

Head movements differ from movements of otherbody parts in two important ways. Firstly the headis responsible for the directional orientation ofthe special senses and its movements are influencedby the information these provide. It is, therefore,not unexpected that certain disorders of the specialsenses may lead to unusual head movements andthat disorders of head movement may forceunusual conditions upon the special senses.Secondly, the mechanical properties of the head/neck system, which normally influence head move-ments, also determine many of the characteristicsof abnormal head movements. In this study weexamine abnormal head movements and analysethem in terms of these mechanical properties andin terms of their interaction with the specialsenses.

Fundamental dynamics of head movement

Head movements have complicated trajectories be-

Address for reprint requests: Dr M. A. Gresty, MRC Hearing andBalance Unit, Institute of Neurology, The National Hospital, QueenSquare, London WCIN 3BG.Accepted 2 February 1979

cause the cervical spine, which is primarily respon-sible for head movement, is a jointed-rod systemwith alternative ways of achieving a given displace-ment (Fielding, 1957; Barnes and Rance, 1974;Viviani and Berthoz, 1975). This is illustrated inFig. 1 which shows the trajectories of a point oflight on the occiput of a normal human subjectduring head shaking and nodding at different fre-quencies. The path the light makes during thedown stroke of the head is not necessarily the sameas during the up stroke and during severe tremorsthese differences may become exaggerated. Formost of our purposes, however, it may be assumedthat the head makes fairly simple rotations aboutone universal joint.

Secondly, as a mechanical system with visco-elastic properties, the head/neck combination isassociated with certain natural resonant fre-quencies of movement.

Barnes and Rance (1974) have investigated theseresonances in normal subjects by oscillating thewhole body and observing the resulting un-controlled oscillations of the head. Their resultsshowed that there was a fundamental resonantfrequency at approximately 2 Hz and a second

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down

2 Hzstart

Up-a2d°

nodstart A

2 Hz

3 H z3 Hz

down

left A2 0°

A right200

Fig. 1 Loci of a point of light mounted on the occiput of a normal adult subject nodding andshaking his head at various frequencies while seated. During vertical movements the head isviewed from the side. During horizontal movements the head is viewed from above. Arrowsindicate the starting point of the head movement. The movement of the light sources weretransduced by means of a Schottky barrier photodetector mounted in the focal plane of a 35 mmcamera placed to view the head.

harmonic component at approximately 4 Hz whichresults from the geometry of head/neckarticulation.The same two frequencies can be identified dur-

ing voluntary head movements and are illustratedin Fig. 2. In A the recordings present a normalhead movement made to fixate a target in lateralgaze. The head moves in an S-shaped trajectory,the movements being a reasonable approximationto the response of a second order system withvisco-elastic properties which are slightly over-damped. Co-ordinated with the head movementthere is a stereotyped eye movement consisting ofa saccade towards the target (sac) followed bycompensatory, primarily vestibulo-ocular reflexmovements (VOR). The VOR maintains stablefixation during the head movement. The durationof the head movement is about 500 millisecondswhich suggests that the system should have anatural frequency of just above 2 Hz. Such apattern of co-ordination occurs in man (Crawford,1960; Bartz, 1966; Gresty, 1974) and animals(Collewijn, 1977).

In Fig. 2, trace B, the subject is asked to makea violent head movement sideways which he wouldnot normally do; as a result the head moves fasterand at the termination of the movement producesone cycle of oscillation at a frequency of about4 Hz. This, for convenience, we have referred toas the second harmonic resonance, but in truth itwill have active myogenic components mixed with

the passive response.During everyday activities the tendency of the

head/neck system to resonate is damped out. Whenone considers the high inertia of the head it isevident that the forces responsible for this must bequite powerful.

Subjects and methods

Patients with head movement disorders were sur-veyed prospectively over a 12 month period at theNational Hospital, Queen Square and the Hospitalfor Sick Children, Great Ormond Street, London.Head movements and movements of other bodyparts were examined by a photoelectric methodpreviously described (Gresty et al., 1976). In somepatients, eye movements were also recorded usingdirect coupled electro-oculography. In most casessupplementary use was made of closed circuitvideo recording.

Classification of abnormal head movements

The head may be affected by any of the five basictypes of dyskinesia in Marsden and Parkes' (1973)classification which lists tremor, tic, chorea,myoclonus, and dystonia. However, in addition,the head is subject to two dyskinesias which wecall "flopping" and "nodding."We have previously distinguished two types of

OF7,C) z

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A

sac- VOR

R

L0

Bsac VOR

sa\ey es

second/ harmonichead J resonance

c A central andoptokinet ic

sac compensation

/

f undamentalresonance

250 ms

Fig. 2 Patterns of co-ordination of the head and eyes in the horizontal planeduring voluntary movements to fixate targets in lateral gaze. (A) Normalstereotyped response consisting of an overdamped head movement, the onsetof which is synchronised with a voluntary saccade to the target (sac). Duringthe latter part of the movement the direction of the eyes in space isstabilised by predominately vestibular, "doll's head" reflexes (VOR). (B) Headand eye movements of a normal subject trying to move his head veryquickly. The head overshoots the final displacement and oscillates for onecycle which reflects the natural second harmonic resonance of headmovement although in reality the movement also contains active myogeniccomponents. The VOR cannot generate fast enough eye movements tocompensate for such a rapid head displacement and when the headovershoots the target a second saccade is made to acquire the targetposition. (C) Head and eye movements of a patient who had lost labyrinthinefunction one week before the recording as a result of gentamicin toxicity.Removal of labyrinthine control of the neck musculature reduced its tonewith the result that the head became underdamped, thus during active orpassive movement the head oscillated for several cycles at the fundamentalresonant frequency of 2 Hz.

head dyskinesia associated with congenitalnystagmus. One is essentially a learned movementwhich helps the child overcome his nystagmus andimprove vision (Gresty et al., 1976), and weclassify this as nodding. The other resembles thenystagmus in waveform, and is a true disorderedmovement probably generated by the same patho-logical mechanism (Gresty et al., 1978), and here itis classified as a tremor.

FLOPPINGFlopping is a passive, involuntary movementcharacterised by transient, exponentially decaying,pendular oscillations, occurring at the end of activehead movement or when head posture is disturbedby body movement.

In the normal subject the tendency for the headto resonate is well controlled by damping due toneck muscle tone and by control signals whichcorrect for external disturbances. However, whenmuscle tone is reduced or the braking signal whicharrests movement is inadequate, the head/necksystem becomes underdamped and tends tooscillate both at the termination of voluntarymovement and when head posture is passivelydisturbed by other body movements. This produces

the appearance of a "floppy head." The head mayoscillate in the horizontal or vertical planes; how-ever, gravity contributes to the disturbance in thevertical plane. Sudden loss of labyrinthine functionproduces a transient reduction of neck muscletone. Figure 2, C shows the effect of such hypo-tonia on the voluntary head movements of apatient who had lost all labyrinthine function as aresult of gentamicin toxicity one week before therecording. At the end of the voluntary displace-ment the head tends to swing from side to side atthe fundamental resonant frequency of about2 Hz. Several cycles of oscillation occur beforethe motion comes under control. Such passiveoscillations of the head are particularly causedby unexpected movements which "jar" the wholebody. Flopping occurs in any disorder whichcauses neck hypotonia: neurogenic or myogenicmuscle atrophy, cerebellar syndromes, cervicaldeafferentation, and absent labyrinthine function.

Cerebellar syndromes, especially in multiplesclerosis, may be associated with both head flop-ping and head tremor. In such cases frequencyanalysis will clearly distinguish the 4 Hz tremorcomponents of the dyskinesia from the 2 Hz headflopping (see below).

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TIC AND NODDINGThese are acquired behavioural patterns, sub-stantially under voluntary control and not thedirect result of some basic pathology but rather, anadaptive response to a pathological condition. Atic is a single, rapid, stereotyped movement,occurring intermittently and on appearances diffi-cult to distinguish from chorea or myoclonus.Nodding is an active, regular, sustained, usuallypendular oscillation consisting of 2 and 4 Hzfrequency components. Several tics occurring insequence take on the appearance of nodding.Nodding is a sustained rhythmic movement whichon waveform alone is indistinguishable from atremor. Nodding and tic are in some sense volun-tary, as each may be suppressed or imitated bythe patient, and each tends to occur when thepatient's attention is drawn to it. Two conditionsin which these occur are:1. Tic and nodding of neurotic origin Thesemovements appear to have no direct biologicalvalue and to have no organic pathological cause.Nodding usually takes a 4 Hz sinusoidal waveformand may be accompanied by synchronised gentlerocking of the torso. The reader may prove tohimself how easy it is to produce continual noddingat this frequency by shaking his head from sideto side as fast as comfortably possible. It becomesevident that there is a natural rhythm (of 4 Hz)which is comfortable and can be sustained.2. Congenital nystagmus with head noddingCertain patients with congenital nystagmus reportan improvement in vision when they shake theirheads. These head movements are presumably anadaptive behavioural strategy and classified hereas head nodding.During normal visual fixation on a target, the

direction of visual fixation is the simple sum ofthe position of the eyes in the head and thedirection in which the head is pointing. The com-pensatory "doll's head" reflex, which consist of acombination of vestibular and optokonetic reflexes,normally works to preserve the direction of fixationby producing movements of the eyes which areequal in magnitude yet opposite in direction tohead movements. The two thus cancel leaving thedirection of fixation undisturbed.The problem of a patient with congenital

nystagmus is that his eyes are moving relative tothe object of fixation, producing image movementacross the retina, thus degrading vision. Firstly,one may consider the effect of head movement onsomeone with nystagmus who has normal doll'shead, and in particular vestibulo-ocular reflexes.As before, the direction of visual fixation is deter-mined by the sum of the position of the eyes in

Michael A. Gresty and G. Michael Halmagyi

the head and the direction of the head itself. Inthis case the sum consists of the head movementless the compensatory eye movement plus the on-going nystagmus. The normal compensatory eyemovements, of course, cancel with the headmovement leaving the actual direction of fixationstill determined by the nystagmus. Therefore, apatient who possesses normal compensatory eyemovement reflexes cannot ordinarily use his headto overcome the visual deficiency produced by hisnystagmus.From this analysis it follows that for head

nodding to improve vision, as patients testify, thenodding must either (a) diminish the nystagmus bysome means, or (b) during the nodding the com-pensatory reflexes must be radically altered, sothat the combination of nystagmus and noddingprovides periods of relatively stable visual fixation.The cases below illustrate these two ways in

which head nodding can improve visual fixation.The traces in Fig. 3 are from a child thought tohave spasmus nutans. With the head still there wasa high frequency, convergent, pendular nystagmusin the horizontal plane. When looking attentivelythe patient would shake his head from side to side,and during this time there would be normal,compensatory eye movements without anynystagmus. This child could apparently "switchoff" his nystagmus by some unknown mechanismassociated with head movement and perhaps re-lated to vestibular function.A second child demonstrates the effect of

modified vestibulo-ocular reflexes on nystagmus.He presented with a gross nystagmus with highand low amplitude components. When concentrat-ing on a visual task he would shake his head in an

R eyeright

L eye ]l1left

head

250ms 500 ms

Fig. 3 Nystagmus of a child with spa,mus nutans.The nystagmus consists of high frequency, convergentoscillations of the eyes with the phase relationshipindicated by the vertical arrow (right hand traces).Whenever the head moved the nystagmus ceased; thus,in the left hand traces the head is shaken from sideto side and normal compensatory doll's head eyemovements are evoked. The implication in this case isthat the head shaking is not pathological but a learnedresponse used by the child to "switch off" thenystagmus.

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irregular fashion as illustrated in Fig. 4. Duringthis manoeuvre, however, there was little changein the pattern of his nystagmus which clearly indi-cated that the head shaking was not eliciting avestibulo-ocular reflex. If a vestibulo-ocular reflexhad been evoked it would have added to thenystagmus and modified the eye movement waveform. In fact the head shaking took the samepattern as the nystagmus but was executed in theopposite direction, thus cancelling the eye move-ments and providing a period of relatively stablevisual fixation. Although the vestibulo-ocularreflex was absent during the nodding, the presenceof responses to impulsive rotational testing indarkness demonstrated that under other circum-stances vestibulo-ocular reflexes were present.These findings are consistent with those of

Forssman (1964) who demonstrated the apparentabsence of vestibulo-ocular reflexes in nearly halfhis patients with congenital nystagmus. He attri-buted his findings to central adaptive processesrather than to a pathological state. Similar volun-tary nonvisual modification of vestibulo-ocular

reflexes has been demonstrated previously (Barret al., 1976) in normal subjects. These two casesshow that the types of nodding which are fre-quently referred to as congenital in origin, whenexamined objectively, can be shown to be learnedbehaviour patterns of adaptive value.

CHOREAChorea is an active, wholly involuntary, singlemovement which resembles a fragment of normalvoluntary movement but is random and inappro-priate in timing and often exaggerated incharacter. Its basic frequency of 2 Hz is the sameas the basic frequency of normal voluntary move-ment and for these reasons it is attributed to theabnormal triggering of a single movement routinefrom the normal repertoire of head movements(Fig. 5).Although Marsden and Parkes (1973) classify

athetosis with the dystonias, we have chosen notto include dystonia or torticollis in the presentdiscussion of head dyskinesias but will considerathetosis alone.

head a

500msFig. 4 Raw data records of head and eye movementsduring readings of a visual display by a 10 year oldchild with congenital nystagmus and nodding. In theabsence of nodding the nystagmus was irregular.When nodding occurred the nystagmus took the formindicated in the Fig.-an overall slow drift from leftto right with occasional saccadic movements to theleft upon which were superimposed oscillatorymovements at a frequency of 4 Hz. The pattern ofhead movement was more or less a mirror image ofthe eye movement and thus was able to compensatesuccessfully for the nystagmus, maintaining relativelystable direction of vision. The arrows indicate thesuccessful phase locking between head and eyemovement. As discussed in the text the ability toproduce compensatory head movement such as thisis possible only in the absence of labyrinthine function.The scaling of the traces is accurate to within 25%.

ATHETOSISAthetotic movements of the head resemble certainvoluntary movements which have low frequencycontent, and a typical athetotic writhing of thehead contains frequencies below 1.0 Hz. It alsomay be an elementary part of normal behaviourwhich is released inappropriately. Normal volun-tary movement contains slow components and"optimally timed" faster ones. Thus, for example,the head can be moved either in a slow, smoothfashion or if a refixation is made, quickly, in atime period determined by the resonant frequency,with optimal speed and accuracy. Chorea and

]30b

1 sFig. 5 Normal voluntary and choreic head movementsin the horizontal plane recorded from a patient withParkinson's disease and drug-induced chorea. In theleft hand traces the patient was required to turn hishead from side to side while looking at the examineras if to test doll's head reflexes. Being a naive subjectit is presumed that he made a fairly normalunselfconscious movement. The right hand traceswere recorded during an episode of chorea. The tracesare indistinguishable in terms of velocity or frequencycontent of the movement.

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athetosis are similarly related in that the trajec-tories of the movements in each resemble thoseof voluntary movements. They are dissimilar inthat the chorea is time optimised.

MYOCLONUSMyoclonus occurs in two forms (Halliday, 1975)."Jerk" myoclonus consists of rapid, shock-like, attimes violent contractions involving one body partat a time and responsive, sometimes excessivelyso, to sensory input. Figure 6B shows recordingsfrom such a case, a 7 year old girl with a cerebellarand myoclonic syndrome from a degenerativedisorder, perhaps a lipidosis. Brief, 4 Hz crescendo-decrescendo sinusoidal oscillations occur in re-sponse to a loud noise. Jerk myoclonus may bedistinguished from flopping of the head in terms offrequency components and response to arousingstimuli (compare traces A and B of Fig. 6)."Rhythmical" myoclonus when affecting the

head, closely resembles tremor and is discussedbelow.

TREMORHead tremor is an active, wholly involuntary,sustained pendular oscillation that is related torest, posture, action, and intention in the sameway as limb tremor and occurs in the samediseases.The Table gives details of 18 patients with head

tremor prospectively surveyed and examined in12 months. The most common causes of headtremor were cerebellar syndromes, essentialtremor, and Parkinson's disease. Figure 7 shows

A

forcestep

1 s

u p

20d

idown

right

B _ 50

A eftnoise 1 s

Fig. 6 (A) Head displacement in the vertical plane ofa patient with bilateral loss of labyrinthine function as

a result of gentamicin toxicity. The patient pressesdown on a lever loaded with 2 kg, the lever issuddenly released, and the patient attempts tomaintain his head posture. The head oscillates at thefundamental resonant frequency of 2 Hz after theforce step input. (B) Myoclonic jerk respon Fe consistingof horizontal oscillations of the head at a frequency of4 Hz in a 7 year old boy. The myoclonus was inducedby a loud noise.

Michael A. Gresty and G. Michael Halmagyi

the distribution of tremor frequencies and fromthis it is evident that there is a modal frequencyof 4 Hz with lesser peaks at 2.5 and 6 Hz. Thetremors occurring at 6 Hz are within the rangeof physiological tremor and may originate in adifferent neural mechanism. In some cases thereis synchronisation between head tremor and tremorof other parts, in other cases there is none. Thetwo lower frequencies of head tremor coincidewith the fundamental and second harmonicresonances of the head/neck system, and thereforeit is possible that some head tremors at least resultfrom derangements of the neural mechanismsresponsible for damping and fine control of headmovement and for maintenance of head postureduring body movement.

Deterioration of head tremorThe postural head tremor of case 3 was observedto deteriorate over a year, and the findings arepresented in Fig. 8. Trace B shows that the tremorwas particularly evident with head posture to theleft and as in trace A, was sinusoidal in naturewhen the patient was first examined. The tremorwas absent when the patient was lying down. Oneyear later the tremor was no longer a simplesinusoidal movement (trace C) but appeared to bea mixture of frequencies over a wider band, itsamplitude had increased slightly and it was presentwith the head straight. With the head turned tothe left the tremor decreased in amplitude con-siderably and became of very high frequency,with an irregular waveform. The high frequencyof the tremor was within the range of the"physiological" variety (Halliday and Redfearn,1956). It is likely that the tremor represented inFig. 8 C is the result of progressive deteriorationand that the frequencies contained within reflectthe variability in tremor frequencies found in ourpatients. It was felt that the high frequencytremor of trace D was a newly appearing pheno-menon unrelated to the lower frequency tremorand perhaps involving the mechanisms ofphysiological tremor.

Head tremor associated with congenital nystagmusFigure 9 shows the head and eye movementrecords of a woman with congenital nystagmuswhich was of the sawtooth variety when passive,but changed to the complex waveform shownduring reading. Head shaking occurred only whenher attention was engrossed in a visual task orwhen she was tired. It was of relatively smallamplitude compared to the eye movements butconsisted of a complex waveform which resembledthe eye movement waveform in its periodicity. The

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Table Patients with head tremors

Case Sex Age Head tremors Other tremors Diagnosis(yr)

Plane Frequency Otherfeatures Body part Frequency Otherfeatures(Hz) (Hz)

I F 21 H and V 5-5.6 - - - - Multiple sclerosis withpyramidal and cerebellardeficits

2 M 25 H 4.2 2.2 Hz flopping Upper limb 3.7 Postural tremor Kearns-Sayre syndromewith cerebellar signs

3 M 51 H 3-4 2.0 Hz flopping - - - Spinocerebellar degeneration4 M 56 0 2.5-5.4 ? two - - - Brainstem stroke

frequencies, onejust above andone just below4 Hz

5 M 81 H and V 4.0-4.6 - Upper limbs - - Essential tremor6 F 21 H 4.0 - - - - Multiple sclerosis with

pyramidal and cerebellardeficits

7 F 32 H 4.3 - Limbs ? Intention tremor Multiple sclerosis8 F 28 H 2.4 - Upper limbs 3.5 Postural tremor Cerebellar degeneration9 F 38 H 2.4 Flopping at 2 Hz - - - Multiple sclerosis10 M 68 H 6.7 - Limbs/trunk 6.7/8.0 Postural tremor Progressive muscular atrophy

and tremor ? cause11 F 51 H 4.0 Head tremor - - - Idiopathic head tremor and

only when turned dystoniato the right

12 F 59 H 5.5-6.5 Maximal with - - - Idiopathic head tremor andhead turned to dystoniathe left

13 M 40 H 3.4 Head to the left Upper limbs 3.3 Postural tremor Cerebellar degeneration14 F 54 H 3.4 - Palate and 3.4 Synchrony of head, Syndrome of palatal

larynx, finger 2.6 palate and larynx myoclonusand eyes (invertical plane)

15 M 24 H 2.7-3.5 - Palate and - Variable usually in Palatal myoclonuslarynx, upper lip, phase with headeyes (verticalplane)

16 F 62 H 3.4 - Upper limbs 6.0 Resting tremor Parkinson's disease: onLevodopa

17 M 58 H and V 2.4 Irregular tremor Footand 4.0 Resting tremor Parkinson's disease: onor chorea finger Levodopa

18 F 56 H 3.8 - Upper limbs 4 and 18 Postural tremor ? Essential tremor

Abbreviations: H =horizontal, V = vertical, 0 = oblique.

head tremorsn=18

3 4 5 6 Hz

head movement appeared to modify thenystagmus. In this patient it is quite clear that thehead movement did not switch off the nystagmusbut did change its waveform. We interpret thesefindings as indicating that the head movementelicited a normal compensatory doll's head reflexwhich combined with the nystagmus and did notassist in stabilising vision. The similarity betweenthe head and eye waveforms and the preservationof the VOR suggest that both the head and eyemovement abnormalities were the result of acommon basic pathology. For these reasons wehave called this abnormal head movement atremor.

Mechanisms of head tremorBecause of the similarity between the frequenciesof head tremor and the natural resonant fre-

7

6

5

4

3

2

Fig. 7 Histogram of the frequencies of head tremorin the 18 patients documented in the Table. Thehistogram frequency resolution is 0.5 Hz.

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May 1977

A C

right

I,d300[

I vo untarylB movement

left

is

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Fig. 8 Tremor of the head in the horizontal plane of a patient withspinocerebellar degeneration (case 3). The patient was observed for a year.Trace A shows the sinusoidal tremor present in the head with eccentricpositions to the left. B shows how the tremor varied with head position.One year later the tremor was present in the primary head position (C) andhad assumed an irregular waveform. When the head was turned to the farleft a high frequency irregular tremor appeared (D).

eyes ] 20°

head /350

1 sFig. 9 Example of a type of congenital nystagmuswith nodding. The recording is taken from a womanwith congenital nystagmus and nodding whose headmovement waveform reflects certain characteristics ofthe eye movements. The pattern of head movement isnot compensatory but is pathological in its own right.(v)=vertical eye movement.

quencies of the head and neck, it is tempting tospeculate that the two are connected in some way,and our approach to understanding the link is tobegin by considering the basic physical require-ments for movement. Most limb movements (withthe possible exception of ocular movements) re-quire a distinct sequence of muscle contractions toinitiate, continue, and finally stop the movement.An optimally efficient movement is made withrespect to the natural resonant frequency of thelimb. Movement of a limb at its resonant fre-quency, however, risks the limb becoming un-stable and oscillating, which means that at thetermination of the movement the muscles have tostop the limb and counter any tendency to

resonate. Should the stopping action be weak ortimed incorrectly the limb will overshoot, pro-ducing dysmetria. Should the activity responsiblefor countering resonance be insufficient or wronglytimed, the limb will oscillate.

In addition, there are important passivemechanical influences on the head created in-directly by body movement which have frequenciesclose to 2 Hz. Thus Cavagna et al. (1976) haveshown that during walking and running the fre-quency of oscillation of the centre of gravity ofthe entire body tends towards 2 Hz as the paceincreases. Without effective measures to counterresonance, activities such as running would setoff uncontrolled oscillations of the head at theresonant frequencies.During body movements it is obvious that the

head is not held rigidly on the trunk to preventit from swaying out of control. Quite the opposite.The head is suspended "fluidly," stabilised inspace, and moving with respect to the body tocounter mechanical disturbances. Therefore, themechanism responsible for countering unwantedmovement and resonance must have access toprecise timing signals and because of the highinertia of the head, be quite powerful. It is quiteconceivable that when such a mechanism breaksdown in some way it will produce involuntaryoscillations of the head. Furthermore, the oscilla-tion would tend to be at the natural resonantfrequencies which the mechanism was designed toovercome. There is then the possibility that tremorin some central nervous diseases is the result ofthe breakdown of mechanisms normally respon-sible for countering unwanted movements.Head tremor may be phase locked to tremor of

D

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other parts of the body such as the palate andthe larynx (case 15). There are two possible inter-pretations of this finding. The first is that sincethese body parts do not have the same naturalfrequencies of movement, the tremor is related tosome function of the nervous system other thancontrol of unwanted movement. The second viewis that since body movement is organised har-moniously with use of a few basic rhythms (trywalking while swinging the arms twice as quicklyas the legs), most limbs do have similar naturalfrequencies of movement and some body partsmay simply use certain dominant rhythms to timetheir functions.A common explanation of the mechanism of

some cerebellar tremors (Marshall, 1968) is thatthey arise from the hypotonia which is char-acteristic of cerebellar disease. During posture,through loss of tone the limb is insufficientlysupported and tends to fall away. A correctiveadjustment is made which leads into a furthercycle of oscillation and so forth. This view of theorigin of the tremor is incomplete, for spectralanalysis of the movement wave form (Gresty andHalmagyi, in preparation) reveals two principalfrequencies of movement, one due to hypotonicpostural swaying at about 3 Hz, and a second at4-5 Hz which is apparently an active component.The two combine to give the "ragged" appearanceof many cerebellar tremors. The origin of cere-bellar tremor iies in hypotonia compounded withdeficits in the mechanism responsible for the scal-ing and timing of neuromuscular signals whichbrake movement and convert movement toposture. By implication of the clinical context thecerebellum is concerned with these functions.

Conclusions

We have shown that in a variety of diseases thefrequency characteristics of head dyskinesias areclosely related to the mechanical properties of thehead/neck system. A classification of headdyskinesias is elaborated, emphasising thisrelationship. In particular, distinctions are madebetween passive dyskinesias caused by neckhypotonia, adaptive dyskinesias sometimes theresult of abnormal eye movements, and dyskinesiassuch as tremor and chorea.Movement of the head/neck system is of im-

portance to the organisation of whole body move-ment. We know, for example, that if the neck isdeafferented orientation in space is lost althoughthe special senses are intact (Cohen, 1961).Furthermore. there is the consideration that the

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head is the platform which carries the specialsenses and orients them directionally, and to thisend much of body movement is subservient. Theseconsiderations suggest that a clue to under-standing body movement is via examination oftheir relationship to the static and dynamicrequirements of the head.

We would like to thank Mr David Taylor, con-sultant ophthalmologist to the Hospital for SickChildren, Great Ormond Street, London, forallowing us to see his patients. Dr Halmagyi heldan Alexander Piggott Wehrner fellowship throughthe Medical Research Council and a grant fromthe Mason Medical Research Foundation.

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