Journal ofGerontology: MEDICAL SCIENCES Copyright 1999 by The Gerontological Society ofAmerica 1999, Val. 54A, No. 3, M129-M135

Postural Set for Balance Control is Normal inAlzheimer's but not in Parkinson's Disease

RaymondK.Y. Chong,' Christine L. Jones,? and Fay B. Horak- Downloaded from https://academic.oup.com/biomedgerontology/article/54/3/M129/564187 by guest on 27 September 2021 'Department ofPhysical Therapy, MedicalCollegeofGeorgia,Augusta. 2üregonHealthSeiences University, Neurological SeiencesInstitute, Portland.

Background. It has been suggested that patients with dementia of the Alzheimer type have abnorrnalities in the basal gan­ glia, and thus, may have similar sensorimotor problems as patients with basal ganglia degeneration from Parkinson's disease. Whether the sirnilarity extends to balance control is unknown. One distinguishing feature of balance disorder in Parkinson's disease is difficulty with changing postural set in terms of adapting the amplitude of leg muscle activity as a function of sup­ port condition. We, therefore, tested whether patients with Alzheimer's disease without extrapyramidal signs would showa sirnilar problem in changing postural set as patients with Parkinson's disease.

Methods. The ability to quickly change postural set was measured by comparing leg muscle activity under two conditions of support (free stance, versus grasping a frame, or sitting) during backward surface translations, during toes up surface rota­ tions, and during voluntary rise to toes. Results were compared among 12 healthy adults, 8 nondemented Parkinson's patients on their usual dose of medication, and 11 Alzheimer patients without extrapyrarnidal signs.

Results. Subjects with Alzheimer's, but not Parkinson's, disease performed sirnilarly to the healthy control subjects. They changed postural set immedfiately, by suppressing leg muscle activity to low levels when supported. Parkinson subjects did not change postural set irnmediately. They did not suppress the tibialis anterior in voluntary rise to toes when holding, nor the soleus in perturbed sitting as much as the healthy control and Alzheimer subjects in the first trial. Instead, the Parkinson sub­ jects changed set more slowly, over repeated and consecutive trials in both protocols. The onset latencies of soleus responses to backward surface translations and perturbed sitting, as weil as tibialis anterior responses to toes up rotations, were the same for aII three groups.

Conclusion. Alzheimer patients without extrapyrarnidal signs, unlike nondemented Parkinson's disease patients, have no difficulty in quickly changing postural set in response to altered support conditions. Our results, therefore, do not support the hypothesis that Parkinson's and uncomplicated Alzheimer's diseases share common postural set problems that may contribute to disordered balance control.

TI' is unclear whether patients with dementia of the Alzheimer surface translations or rotations as weil as preparatory muscle .1 type may have some similar balance control problems as pa­ activity associated with a voluntary task such as rising onto the tients with basal ganglia degeneration from Parkinson's disease toes (5,6). The amplitude of this preparatory leg muscle activa­ who do not have dementia. The incidence of falls is much tion can be modified by set-dependent neural mechanisms higher in both the Alzheimer and Parkinson population groups (7-9). Set is the process of adapting or changing the transmis­ than age-matched healthy individuals. Although many sion of neural pathways based on expectation, prior experience Alzheimer patients may show no clinically apparent movement or context. For example, healthy subjects show large responses disorders, including none associated with Parkinson's disease, if they expect a large perturbation, based on prior experience, pathological changes in the basal ganglia have been reported in even if the actual perturbation size is small (9). Similarly, these patients. For example, single photon emission tomography healthy subjects underrespond to a large perturbation if they technology reveal alterations in the function of D2 striatal recep­ had been exposed to a prior series of smaller perturbations. tors in Parkinson-free Alzheimer patients (1). Other ceilular ab­ Changes in the environmental context, such as support condi­ normalities, such as neurofibrillary tangles and neuritic plaques, tions, also require flexible adaptation of leg muscle activity, have also been found in the caudate and the putamen (2). These termed "postural set" (10). Postural set indicates how weil sub­ findings suggest that dysfunction of the basal ganglia may be jects use relevant environmental and sensory cues to prepare common in Alzheimer's disease. for or respond to an impending external threat to their balance. Simi1arly, reductions in cholinergic activity, typically associ­ One distinguishing balance disorder in patients with ated with Alzheimer's disease, have been observed in nonde­ Parkinson's disease is their difficulty in changing postural set mented Parkinson patients (3, see reference 4 for review). Given based on changes in support conditions. They fall to reduce tib­ these ceilular simi1arities between the two diseases, it is not clear ialis anterior activity like healthy individuals when lightly touch­ whether Alzheimer patients may have motor deficits affecting ing a stable frame during rotations of the support surface (11). balance control simi1arto Parkinson patients. Subtle differences Parkinson patients also do not suppress irrelevant leg muscle ac­ may exist which cannot be detected by casual observations. tivity as much as healthy individuals in response to translations Subtle and specific motor disorders of balance control can of the platform, when body position is changed from standing to be identified by quantifying automatic leg muscle responses to sitting on a stool with the feet dangling offthe ground (12).

M129 M130 CHONGETAL.

The inability to guide behavior appropriately based on body cluded two new subjects, one healthy female elderly subject position in Parkinson's patients has been tenned an "egocentric (69 years) and one male Alzheimer subject (79 years, Mini­ localization" deficit (13). A similar problem may exist in pa­ Mental score 12) (Table 1). The Parkinson subjects were in tients with Alzheimer's disease. They have difficulties with stages m and IV on the Hoehn and Yahr scale. The protocol tasks related to spatial orientation such as localizing themselves was approved by the Human Subjects Review Board. in relation to objects (14) or sounds (15). Thus, although Alzheimer's disease afflicts widespread damage to cortical Protocol structures and the origin of Parkinson's disease is subcortical, The influence of changes in support conditions on postural

patients with Alzheimer's and Parkinson's diseases may share set were tested in all subjects in the following protocol se­ Downloaded from https://academic.oup.com/biomedgerontology/article/54/3/M129/564187 by guest on 27 September 2021 some common problems in balance control. quence: backward translations, toes up rotations, voluntary rise Because of the overlap of neurological and neurochemical to toes, and perturbed sitting. abnonnalities, without concomitant clinical manifestations of basal ganglia disease, we hypothesize that Alzheimer's disease Backward surface translation.-Backward translations of patients, even without extrapyramidal signs, may show balance the support surface for 3.2 cm at 13 cm/s were administered to control abnormalities simi1ar to those with Parkinson's disease. subjects while they stood quietly on a computer-operated plat­ To test this hypothesis, we compared adaptation of leg muscle form. This small perturbation size was chosen to maximize the activity in three groups of subjects (Alzheimer patients without potential influence of set and minimize peripheral sensory drive extrapyramidal signs, Parkinson patients without dementia, and (17). Five free stance and five holding trials were given in alter­ age-matched healthy controls) when postural set was influ­ nating order. In the free stance trials, subjects stood with the enced via changes in support conditions of holding or sitting. arms held across their chests. In the holding trials, the instruc­ Our results showed that uncomplicated Alzheimer patients, un­ tion was to hold with both hands firmly onto a horizontal, sta­ like those with Parkinson's disease, do not have difficulty in ble frame placed at the subject's waist level. Half of the sub­ changing postural set. These results suggest that Parkinson-like jects in each group started with the holding trial. To minimize postural set abnonnalities are unlikely to be a significant con­ extemal influences or constraints on the subjects' set, no special tributing factor to instability in this group of Alzheimer patients instructions were given to the subjects, other than to hold or not without extrapyramidal signs. However, they do not preclude to hold onto the support bar, and to try and maintain in-place the possibility of postural set abnormalities as a contributing balance during free stance perturbations, factor to falls in Alzheimer subjects with extrapyramidal signs. Toes up surface rotation.-Five holding and five free stance METHODS toes up rotations of the platfonn for 5° at 50°/s were given in altemating order. The instructions were the same as those used Subjects for the backward translation condition. Twelve healthy elderly adults (7 males and 5 females, age 62 ± 5 years, mean ± SD, range 59-80 years), 11 Alzheimer Voluntary rise to toes.-Subjects were asked to quickly rise patients (6 females, 5 males) (72 ± 10 years, range 53-83 onto their toes in three trials while holding, and then perform years), without extrapyramidal signs, postural instability or a another three trials of the same action without holding. history of falls and 8 nondemented Parkinson patients on their usual dose of medication (5 males and 3 females, age 60 ± 5 Perturbed sitting.-Five consecutive backward translations years, range 5D--67 years) gave their consent to be tested. These of the support surface for 3.2 cm at 13 cm/s were given while participants were the same subjects tested in the previous com­ subjects sat upright on a stool with their feet dangling off the panion study on sensory organization for balance (16), but in- ground.

Table 1.Alzheimer(A) and Parkinson(B) subjectcharacteristics.

Alzheimer Parkinson Subject M-M Age (year) Subject H&Y Age (year) Duration (year) Levodopa (mg/day) PHo 27 72 MO III 49 5 200 PL 23 70 JF III 59 12 500 WT 23 77 PT III 62 7 400 HB 22 69 JR IV 55 8 525 HS 22 77 WH IV 61 6 300 MM 20 77 DN IV 61 17 1125 RB 19 55 WL IV 63 31 200 EK 18 78 VN IV 67 15 700 PHa 12 53 ER 12 79 FL 8 83

M-M, Mini-Mental State Exarnination score: H & Y,Hoehn & Yahr severity scale. CHANGING POSTURAL SET IN ALZHEIMER'SAND PARKINSON'S DISEASES M131

DataAnalyses to toes up surfacerotations, did not differamong the groups (p The firstplatfonn shear artifactwas measuredas the onset of > .05). Onset latency of responses was different for the proto­ platform movement. Surface electromyography (EMG) of cols, F(2,52) =61.6,p < .001.The latencyofthe shortenedtib­ soleus activity was analyzed for the standing and sitting back­ ialis anterior responses to toes up surfacerotations was longer ward translation conditions. Tibialis anterior activity was ana­ than soleus responses to pertubed sittingand backwardsurface lyzed for the toes up rotation and voluntary rise to toes condi­ translations (p < .01).The onset latency of soleus responses to tions. All individual EMG traces were band-pass filtered at perturbedsitting was longerthan backwardsurfacetranslations 70-200 Hz, fuIl-wave rectified, and low-passfiltered at 100 Hz (p< .05). prior to sampling at 480 Hz and storage for off-line analyses. Downloaded from https://academic.oup.com/biomedgerontology/article/54/3/M129/564187 by guest on 27 September 2021 The onset latency of the muscle response was identified from TibalisAnterior Responses to Toes Up Surface Rotations: individual trials of rectified surface EMG traces (4 ms/pixel Holding Versus FreeStance monitor resolution) as the earliest time that EMG activity ex­ The Alzheimergroup did not differfrom the healthycontrol ceededbaselineleveland remainedhigh for at least 25 ms. The group in the reduction of tibialisanterioractivity when holding integrated EMG (IEMG) over the first 75-ms window from during toes up surface rotations. In contrast, the Parkinson onsetlatency was obtainedaftersubtracting quiet stanceEMG. group did not reduce tibialis activity as much as the healthy The influence of postural set on musclepattern of activity was control group when holding. Figure 1 shows a roster of 10 tib­ quantified by expressing the magnitude of muscle activity ialis anterior EMG traces from a representative subjectin each (lEMG) in the holding and perturbed sitting conditions as a per­ of the three groups. Odd number trials are from the free stance centage of the mean IEMG obtained durlng freestanceperturba­ condition, and even number ones are from the holding condi­ tions(11). There was no difference between subjects who started tion.The healthycontrolgroup reduced tibialis anterioractivity withthe holding trialversus subjects who beganwith free stance. while holding to 25% ± 18% of free stance values and the There was also no difference in the effect of holding and free Alzheimergroupto 28% ± 25%. However, the Parkinsongroup stance in theearlyandlaterpartsof thetrials. Therefore, themean reduced to only 56% ± 25% of free stance values, F(2,27) = of the five holding and free stance trials were computed for each 4.9,p < .05 comparedto healthy controls(Figure2A). One 83 subject, To test the hypothesis that Alzheimer's and Parkinson's years old Alzheimer subject, with a Mini-Mental score of 8, diseases sharecommonproblems withchanging postural set,the showedonly a 10%reduction of the tibialisanterior. mean percentage change in IEMG activity while holding were In the free stance condition, three Parkinson and two compared amongthe groups for: (i) soleus responses to backward Alzheimer subjects lost their balance in the first trial. One surface translation, (ii) tibialis anterior responses to toesup surface Parkinson and one Alzheimer subject, both showed coactiva­ rotation, (iii) tibialis anterior activity in the first trialof riseto toes tion in the ankle muscles, lost balance in all five trials. Tibialis while holding, and (iv) soleus responses to the first trial of per­ anterioronset latencyin responseto toes up surface rotationoc­ turbed sitting. Thesepercent changeIEMGdatawereentered into curred between 147-171 ms, and did not differ among the a 3 (Group) X 4 (Protocol) ANOVA, with repeated measures on groups (p > .05). protocol (p < .05).A significant effect was followed by simple maineffects analyses usingDunnett's test(p < .05)tocompare leg Soleus Responses to Backward Surface Translations: Holding IEMG between the healthy control versus the Parkinson and Versus FreeStance Alzheimer groups. Contrast comparisons (p < .05) between the Except for one subject (Mini-Mental score of 18), the first and subsequent trials for boththe voluntary riseto toeswhile Alzheimergroup did not differfrom the healthycontrol group. holding and perturbed sitting protocol werealsoperfonnedwithin They both reducedsoleusactivitywhen holdingto 41% ± 18% each group. Data sets with unequal variance were first trans­ and 44% ± 22% of free stance values,respectively. In contrast, formed to logarithrn values priorto simple main effects analyses only two out of eight (25%) Parkinsonsubjects showednormal to obtain comparable between-group variance. The same statisti­ soleus reduction (25% and 35%) of free stance values when cal procedure was perfonnedon the onsetlatencies of muscle re­ holding. These resultsare consistentwith the finding of normal sponses to backward translation (soleus), toes up rotation (tibialis reductionin 23% (7 out of 31) of Parkinson subjects in another anterior), and perturbed sitting (soleus). A Pearson correlation study(11). Soleusresponses to backwardsurfacetranslations in analysis (p < .05)was alsoconducted to testthe positive relation­ the Parkinson group when holding was 56% ± 20% of free shipbetween the postural set performance of the Alzheimer sub­ stance,which differed from the healthycontrols, F(2, 26) =8.8, jects andtheirMini-Mental Statescores. Alldataareexpressed as p< .01 (Figure2B).There was no difference in soleusonset la­ mean± standard error(SE). tencies between the holding and free stance trials within each group nor among the groups (p > .05). One Alzheimersubject REsULTS (70 years old, Mini-Mental score 23) showed a mean latency responseof 129ms, which was three standarddeviations larger Summary than that of the healthycontrol group (100 ± 10 ms). Onset la­ The extent of decrease in leg muscle activity in the holding tency of soleus musclein responseto backwardsurfacetransla­ and sitting conditions depended on the Group and Protocol. tionsrangedbetween98 and 115 ms in all the othersubjects. IEMG analyses revealeda main effectof Group, F(2,20) = 8.6, p< .01, a main effect of Protocol, F(3,60) = 5.9, p < .01, and a TibialisAnterior Activity During Voluntary Rise to Toes Group X Protocol interaction effect, F(6,60) = 2.9, p < .02. When Holding Onset latencyof soleus responses to backward surfacetransla­ Tibialis anterior was activated to move the body center of tions and perturbedsitting,as weIlas tibialisanteriorresponses mass forward in preparation for a voluntary rise to toes. When M132 CHONGETAL.

Free stance Holding SoleusResponses to Perturbation DuringSitting With FeetDangling Leg activity was irrelevant for regaining balance during Contra} subject seated platform translations because subjects' feet were dan­ gling off the ground. Both the healthy control and Alzheimer groups reduced soleus activity to 6% ± 3% and 8% ± 4%, re­ Tri~ spectively, of free stance perturbation values. In contrast, the Parkinson subjects changed postural set more slowly (Figure 4; Tri~ indicated by arrow). They showed a larger soleus response in Downloaded from https://academic.oup.com/biomedgerontology/article/54/3/M129/564187 by guest on 27 September 2021 TrialS Tri~~ the first sitting trial, 26% ± 8% of free stance values. Similar to the reduction of tibialis anterior activity with repeated trials T~ Trial~ during voluntary rise to toes, Parkinson subjects also reduced soleus activation with repeated trials in perturbed sitting, Tri~ ~ F(4,20) = 3.1, p < .05. Onset latency of response ranged be­ Trial 10 "",. " tween 104 and 134 ms for all groups. There was no correlation between the postural set perfor­ ~~r~on mance of the Alzheimer subjects and their Mini-Mental State .., subject scores (p > 05). rn~ rn~ DISCUSSION Trial~ T~ Alzheimer subjects without extrapyramidal signs did not have the same type of balance control problems as the Parkinson sub­ Tri~ Tri~ jects. Unlike the Parkinson subjects, the Alzheimer subjects did not have difficulty in changing postural set. They reduced leg Trial~ Tri~ muscle activity when holding or sitting. Postural set problems in the Parkinson, but not the Alzheimer, subjects suggests that the Tri~ Tri~ influence of postural set on motor coordination operatesmainly at the subcorticallevel. Set-dependent changes in the amplitude of muscle activ­ Alzheimer subject ity due to changes in support conditions were observed in automatie responses to backward surface translations and Tri~IIfoj""__"'__ toes up surface rotations, as weIl as in preparatory muscle activity associated with a voluntary action (rise to toes), Tri~ with no changes in onset latencies. Parkinson subjects had difficulty quickly changing set in all these types of different Trial...... 6 ,&,.....l4...... _ postural set tasks, suggesting a general, rather than a task­ dependent, deficit in changing postural set. The normal Tri~ft6J""'.,.. _ onset latency of responses in the legs of Parkinson subjects is consistent with previous studies (12,17). The onset la­ Tri~...... ,_ tency of responses in the Alzheimer subjects were also not different from the other groups, although delayed motor and _500ms sensory nerve conduction velocities have been reported (19). Figure 1. Raster of 10 consecutive tibialis anterior EMG traees during toes Even the four most demented subjects in our study had nor­ up surface rotations for a representative subject in each of the three groups. mal response latencies compared to the healthy control Odd number trials were free stance condition; even number trials were holding group. condition. Healthy control and Alzheimer subjects changed postural set imme­ diately by increasing and decreasing muscle response as a function of support. The relatively normal adaptive motor behavior in the Parkinson subjects could not change set immediately, and showed little adjust­ Alzheimer subjects supports the suggestion from other studies ments. Note the reversal in response amplitude between trials 7 and 8. that coordination is relatively unscathed in Alzheimer patients without extrapyramidal signs, even in the late stages of their disease (2). They even retain anormal capacity to learn new holding, healthy control and Alzheimer subjects reduced tibialis motor tasks (20). Only the oldest Alzheimer subject (age 83 anterior activity in the first trial to 44% ± 9% and 32% ± 14% with Mini-Mental score of 8) showed little reduction of tibialis of free stance conditions, respectively. Parkinson subjects, on anterior activity in toes up rotations. During neurological the other hand, reduced to only 75% ± 9%, F(2,20) = 3.5, p < screening, this subject was slow to perform and maintain some .05 compared to healthy controls (Figure 2C). They changed of the motor tasks such as finger tapping. This reflected a com­ postural set more slowly over trials, before they performed sim­ bination of a cognitive problem and bradykinesia, but not ex­ ilarly to the healthy control and Alzheimer subjects. Figure 3 il­ trapyramidal signs associated with Parkinson's disease, such as lustrates the immediate reduction of tibialis anterior activity in a tremor and rigidity. representative control and Alzheimer subject, but not in a We specifically tested Alzheimer patients who did not have Parkinson subject (indicated by arrows). extrapyramidal signs. Alzheimer patients who do have these CHANGING POSTURAL SET IN ALZHEIMER'SAND PARKINSON'S DISEASES MI33

DControl []I Parkinson ~ Alzheimer

A. B. C. 90 90

ec 80 .6 :g ..8 70 Downloaded from https://academic.oup.com/biomedgerontology/article/54/3/M129/564187 by guest on 27 September 2021 -o o#.=- 60 ~--§ 50 +:l • '.-4 ~ ~ 8 § 40 o u = 30 ~ -~ 20 10 10 o o Tibialis anterior: Soleus: Tibialis anterior: Toes up rotation Backward translation Voluntary Rise to toes

Figure 2. Decrease in muscle activity when holding, nonnalized to free stance values. Data are expressed as group mean ± SE. A, TIbialis anterior responses to toes up surface rotations. B, Soleus responses to backward surface translations. C, TIbialis anterior activity during voluntary rise to toes (first triaI). *p< .05 com­ pared to the healthy control group.

Control subject Parkinson subject Alzheimer subject

Trial 1 Trial 1

Trial 2 Trial 2 Trial 2 J~ ~

Trial 3

Figure 3. TIbialis anterior and soleus EMG activity during three consecutive trials of voluntary rise to toes when holding, in a representative subject from each of the three groups. Unlike healthy control and Alzheimer subjects, Parkinson subjects changed set more slowly (indicated by arrows). M134 CHONGETAL.

6 30 i ,.. ..e -o-Control 25 fcu c, -o-Alzheimer fj -Ir-Parkinson ij 20 '1ii- ~~ Downloaded from https://academic.oup.com/biomedgerontology/article/54/3/M129/564187 by guest on 27 September 2021 ..t:l 6 .9:= 15 "t:S"'d ~. 0~ u 10 8 0 t: o 5 ::s~

(I) -g 0 0 -(/) 1 2 3 4 5 Trial number Figure 4. Mean ± SE bars showing soleus responses to backwardtranslationswhile sitting upright on a stool with feet dangling. Healthycontrol and Alzheimer sub­ jects changed set immediatelyby reducingsoleus activityto low levelsin the firsttrial.Parkinsonsubjectschanged set more slowly,overtrials.*p< .05, trial I versus5.

symptoms may form a subtype of Alzheimer's disease. This difficulty quickly taking advantage of the stability afforded by groupof patientsmay showproblemswith changing posturalset the ambnlatory devices when conditions change. For example, similarto Parkinson patients. Studiesshouldbe conducted to test properlychangingthe placement of the walker or changing the this hypothesis. Ifthe hypothesis is confinned, then the frequent hand-grip force on a rail are necessary to navigate safely falling experienced by theseAlzheimerpatientsmay be due to a throughor aroundthe environment. Undercertainprecarioussit­ combination of difficulty dealing with visual distraction or sen­ uations, the inability to change set quicklycould still result in a soryincongruency (16),as weIl as to difficulty withchanging set fall in Parkinson's patients. quickly, relatedto basalgangliadegeneration. Our studies are consistent with previous work showing that set-changing difficulty in Parkinsonindividuals is task-indepcn­ ClinicalImplications dent. For example, Parkinsonpatientsmake more errors in card­ By asking our subjects to hold onto a frame, we provided sortingtasks when required to change set by switchingto a new both an externalcue for orientation, as weIlas a mechanical sup­ sorting rule (21-23). In key-press reaction time studies, they port for equilibrium. We allowed them to grip firmly onto the make more errors when required to switch between sequences stable support frame, unlikeother studies which requested their (24). Finally, Parkinsonpatientstakelongerto respond when in­ subjectsto maintainlightcontact(11). Despite thisexternalcue, structed to switch set as quickly as possible, between either our Parkin-son subjectsdid not change set quickly, by decreas­ color-shape dimensions or betweenkey-press sequences(25). ing or suppressing leg muscleactivity when theyweresupported In conclusion, Alzheimer patients without extrapyramidal by holding or sitting. Their difficulty with changing set quickly signs, unlike Parkinsonpatients, have normal postural set func­ was evident when the supported-unsupported tasks were given tion in regardsto balancecontrol.Our resultsdo not support the alternately, requiring subjects to change set every trial. They hypothesis that Parkinson's disease and uncornplicated changed set more slowly, as shown in the voluntary rise-to-toes Alzheimer's disease share common postural set abnormalities action, as weIl as in the backwardsurfacetranslations while sit­ that may lead to falls. Gur results are consistent with the notion ting with feet dangling. In these blocked,rather than alternating that association cortex and hippocampal structures, which are\ trials, repeated set-change was not required. This allowed the compromised in uncomplicatedAlzheimer's disease,do not sig­ Parkinson subjects to gradually change their muscle pattern. nificantly contribute to the prefrontal/basal ganglia circuitry Thus, their ability to change set in the blocked conditions sug­ thoughtto be essentialto the regulation of posturalset. gests that Parkinson individuals were slower in changing set, and thereforewere unableto adapt in the alternating conditions ACKNOWLEDGMENTS in which they had to change set immediately. The slowness to Supported by grants from the National Institute on Aging AG-06457 and change set based on changes in support conditions in our study Alzheimer Center Grant AG-08017. suggests that although support from walkers, handrail, or the We thank J. Nutt, MD, for referring Parkinson patients, 1. Kaye, MD, for re­ caregiver's arm could enhance their stability, they would have ferring Alzheimer patients, and C. Shupert, PhD, and 1. Frank, PhD, for testing subjects and collecting data. CHANGING POSTURAL SET IN ALZHEIMER'S AND PARKINSON'S DISEASES M135

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Endowed Chalr In Geropsychlatry

The Department of Psychiatry at the University of Califor­ nia, San Francisco, is seeking applications from basic or clinical scientists for the new position of Director of Gero­ psychiatry. Appointment will be at the Associate or Full Professor level. Candidates must be psychiatrists with clinical and teaching interests in the area of geropsychia­ try and have arecord of outstanding achievement in a relevant scientific area. Substantial resources will be de­ voted to the position including the leon Epstein Chair in Geropsychiatry. The successful candidate will be ex­ pected to develop a program in geropsychiatry in close cooperation with the Departments of Neurology and Medicine. Interested applicants should send curriculum vitae and a letter of interest to Nelson B. Freimer, MD, Chair, Search Committee, c/o Natasha Page Carroll, UCSF, Department of Psychiatry, 401 Parnassus Avenue, Box NGl-0984, San Francisco, CA 94143-0984. This po­ sition will remain open until filled. UCSF is an affirmative acnon/equal opportunity employer. The University under­ takes affirmative action to assure equal employment op­ portunity for underutilized minorities and women, for per­ sons with disabilities and for Vietnam-era veterans and special disabled veterans.