REVIEW

Neurology Series Editor, Wil[iam J. Mu[[atly, MD

Gait DisordersJessica M. Baker, MD

Deparlnrcnt of Neurologt, Brighatn and Women's Hospital, Boston, Mass.

6i)c'o.,tt"'t

ABSTRACI

Walking is an extraordinarily complex task requiring integration of the entire nervous system, making gaitsusceptible to a variety of underlying neurologic abnormalities. Gait disorders are particularly prevalent inthe elderly and increase fall risk. In this review we discuss an approach to the examination ofgait and high-light key features of common gait disorders and their underlying causes. We review gaits due to lesions ofmotor systems (spasticity and neuromuscular weakness), the cerebellum and sensory systems (ataxia), par-

kinsonism, and frontal lobes and discuss the remarkably diverse phenomenology of functional (psychogenic)

gait disorders. We offer a pragmatic approach to the diagnosis and management of neurologic gait disor-ders, because prompt recognition and intervention may improve quality of life in affected individuals.A 2U 8 Elsevier Inc. All rights reserved. . The American Jountal of Medicine (201 8) 1 31 , 602407

KEYW0RDS: Ataxia; Foot drop; Frontal gait; Functional movement disorder; Gait disorders; Parkinsonism;

Spasticiry

Gait disorders are common. contribute significantly to mor-bidity through falls,r and may yield clues to diseases occurringat all locations of the nervous system, making the examina-tion of gait one of the most complex and high-yieldcomponents of the neurologic examination. In this review we

offer a pragmatic approach to examining gait and discuss clin-ical features of common gait disorders and their underlyingetiologies. Abnormal gait is particularly prevalent in the elderly,

affecting approximately I in 3 community-dwelling indi-viduals older than 60 years. Gait disorders in this populationare associated with diminished quality of life2 and nursinghome placementr and may be an indicator of progression to

dementia in individuals with mild cognitive impairment.a Ahistory that includes weakness of the legs, imbalance, un-

steadiness on one's feet, or multiple falls may hint at an

underlying gait disorder. Prompt recognition, examination,and classification of gait disolders is therefore of para-mount importance.

Funding: None.

Conflict of Interestl None.Authorship: The author is solely responsiblc for the content of the manu-

script. JMB's current affiliaiion is: Department of Medicine, University ofWisconsin Hospital and Clinics. Madison.

Requests for reprints should be addresscd to Jessica M. Baker, MD, Uni-versity of Wisconsin Hospital and Clinics, Department of Medicine, I 111

Highland Avenue, WIMR 3rd floor, Madison, WI 53705.

E-mail address: jbaker3@uwhealth.org

0002-9343/5 - see liont matter O 2018 Elsevier Inc. All rights reserved.

https://doi.org/ 10. l0 I 6/j.am_imed.20l 7. I 1.0-5 1

PHYSIOLOGY AND THE GAIT CYCLE

Normal gait requires precise control of limb movements,posture, and muscle tone, an extraordinarily complex process

that involves the entire nervous system. Specialized groupsof neurons in the spinal cord and brainstem generate rhyth-mic activity and provide output to motor neurons, which inturn activate muscles in the limbs. The cerebral cortex inte-grates input from visual, vestibular, and proprioceptive systems;

additional input is received from the brainstem, basal ganglia,

cerebellum, and afferent neurons carrying proprioceptivesignals from muscle stretch receptors (as may be damagedin peripheral neuropathy). Together, these systems allow in-dividuals to walk not only in a straight, unencumbered linebut to adapt their gait to avoid obstacles and adjust posture

to maintain balance.5 Abnormalities of any portion of the

nervous system can therefore give rise to a gait disorder.The gait cycle (Figure 1) begins when one heel (illus-

trated here as right) strikes the ground. Supported by the stance

of the right leg, body weight shifts forward as the left leg flexes

at the hip and knees and swings forwards, eventually strik-ing the left heel on the ground. Weight then shifts forwardson the left leg, while the right leg swings forward and again

strikes the ground. Thus, while one leg is in srarce phase,

the opposite is in swing phase. Periods of double support,

during which both legs make contact with the ground, nor-

mally comprise approximately lOVo of the gait cycle6 butincrease as compensation for unsteadiness in many abnor-mal gaits.

Baker Gait Disorders 603

EXAMINATION OF GAITThe examination of gait begins with observing a patient as

he or she walks from the waiting a.rea to an examination room.

The ideal setting for a formal gait examination is a long, un-

cluttered hallway, providing enough distance to reach a

comfortable walking speed with good arm swing. Hands

should be free except for neces-

sary assistive devices. Observeindividuals as they walk in a straight

Iine, but also note any difficultyrising from a chair. initiating gait.

or turning. The gait examinationprovides significant insight into an

individual's functional status, and

much will be missed if the assess-

ment is limited to the examinationroom! Make note of velctcity (dis-tance covered in a given time) and

cadence (steps per miwte). Stridelength meastres distance covered bythe gait cycle; step length mea-sures the distance covered duringthe swing phase of a single leg. Srep

width or ba.se is the distancebetween the left and right feet whilewalking (F'igure 2). Also make note

of posture, arm swing, the height ofeach step, leg stiffness, or side-to-

Gait disorders increase fa[L risk and often

resuLt from an undertying neurotogiccondition.

Specific features of abnormaI gaits resutt

from a combination of a deficit and at-tempts at compensation.

Many gait disorders are readity treat-able with specific therapies, such as

dopaminergic therapy for Parkinson's

disease, or cerebrospjnaI ftuid shunt-ing for normal pressure hydrocephaLus.

Physical therapy and assistive devices

may improve mobility and decrease fa[[risk.

Left Leg Left Heel

Swing Strike

CLINICAL FEATURES AND ETIOLOGY OF

GAIT DISORDERS

Gait disorders may be neurologic or nonneurologic in origin.

Common nonneurologic causes of abnomal gait include os-

teoarthritis of the hip and knee, orthopedic deformities, and

visual lossr; individuals may reduce

the stance time of the aff'ected lirnbto reduce pain, resulting in an asym-

metric cttttolgic gnil. Commonneurologic causes of abnr-rrmal gaits

are listed in the Tairle and are de-

scribed here irr fufther detail. Mildlyshortened step length, decreased ve-

locity, slightly widened base, and

increased double support time are

features ofnonnal agingT but are also

seen as a response to perceived in-stability, either intrinsic (eg,

disequilibrium) or extrinsic (eg,

walking on ice). Individuals may

walk with hands outstretched in an

attempt to steady themselves. Thiscoutictus gait is nonspecific but may

herald an underlying neurologic gait

disorder.

side lurching. Muscle strength and tone in the legs, sensation,

and reflexes rnay provide further clues as to the etiology ofan underlying gait disorder. The Romberg sign is tested by

asking patients to stand still with feet together and eyes closed

and is considered positive (abnormal) if eye closure pro-

vokes a fall. Test tandem gait by asking a patient to take at

Ieast 10 steps touching heel-to-toe, as if walking on a tight-rope. Heel or toe walking can unmask subtle distal weakness

that might be missed by direct confrontational testing.

Spastic GaitSpastic gaits are caused by lesions in the corticospinal tract

at any level and may be unilateral or bilateral. When unilat-eral, the affected Ieg is held in extension and plantar flexion;

the ipsilateral arm is often flexed. There is circumduction ofthe affected leg during the swing phase of each step. Common

causes include stroke or other unilateral lesions of the cere-

bral cortex. If bilateral, thc spastic gait may appear stifl--

legged or scissoring owing to increased tone in the adductor

muscles, such that the legs nearly touch with each step

RightToe Right Leg Right l-teel

Off Swing Strike

AIIAI IARight Heel LeftToe

Strike Off

Figure 1 The gait cycle. Right leg is shaded grey. The gait cycle is divided into stance and

swing phases. During stance, body weight shifts forward on the supporting leg, while the

opposite leg swings forward, eventually making contact with the ground via the heel. Shaded

blxes indicate periods of double support, during which both the left and right legs make

contact with the ground.

604 The American Journa[ of Medicine, VoL 131, No 6, June 2018

Gait cycle

6S,

often have difficulty rising from a chair without using theirarTns.

The steppage gair is caused by weakness of ankle dorsi-flexion, also known as afoot drop. Individuals with a steppagegait lift the swinging leg higher to compensate for the toes'inability to clear the ground with each step; the foot landingoften has a slapping quality. Weakness of ankle dorsiflexionmay be appreciated by direct testing on physical examina-tion, though more subtle weakness may be elicited when an

individual is asked to walk on his or her heels. Foot drop maybe bilateral, as can be seen in peripheral polyneuropathy, orunilateral. Common causes include an L5 radiculopathy orperoneal neuropathy, which can be differentiated from the

former by preservation of ankle inversion on physical exam-ination. Electromyography with nerve conduction studies mayaid in diagnosis. Individuals with foot drop may benefit fromankle foot orthoses, which stabilize the ankle in a neutralposition.

Parkinsonian GaitThe parkinsonian gait is among the most common gait dis-orders in the elderly. The classic "shuffling" appearance is

StepfwidthJ

(Figure 3B). Common causes of bilateral spastic gait (spasticparaparesis) include cerebral palsy, cervical spondylotic my-elopathy, and multiple sclerosis, among many others, and are

often accompanied by signs of myelopathy, such as boweland bladder dysfunction, increased reflexes, and Babinski sigrs.Antispasticity agents such as baclofen or tizanidine are vari-ably effective in improving gait but may reduce painful spasms.

Botulinum toxin injections may be useful in cases of focalspasticity.

Neuromuscular GaitsWeakness of muscles of the lower extremities may manifestas a gait disorder. The waddling gait can be seen in cases ofproximal muscle weakness, such as myopathy. In normal gaitthe gluteal muscles serve to stabilize the pelvis, elevating thenon-weight-bearing side with each step. With weakness ofthese muscles, and particularly the gluteus medius, instabil-ity of the weight-bearing hip instead causes the non-weight-bearing side to drop (Trendelenburg's sign). This leads toexcessive side-to-side trunk motion, giving the gait a wad-dling appearance.E Individuals with proximal muscle weakness

Table Prevatence of Neurotogic Gait Disorders in L17 Community-Dwetting Adutts

. (\-,'?-=SteP length ----.-':s Q<F

Stride length

Figure 2 Terminology describing the gait cycle. Reproduced with permission from Pirkerand Katzenschlager.6

Neurotogic Gait Disorder (GD) Number (Percentage)* TotaI Numberl Causes (Number)

Sing[e neurotogic GD

5ensory ataxicParki nsonian

FrontaI

Cerebeltar ataxic

Cautious

Pa retic/hypoto ni c

Spastic0ther

Muttipte neurotogic GD

TotaI

81 (6e.2)22 (18)te (76.2)

e (7.7)

7 (6,0)

7 (6.0)6 (5.1)6 (5.1)5 (4.3)

36 (30.8)1,77

46

34

PeripheraI sensory neuropathy (46)Parkinson's disease (18), drug-induced parkinsonism (8),

other (4)Vascutar disease (20), normaL pressure hydrocephdtus (1),

dementia (7), other (3)Stroke (3), multipLe scterosis (1), essentiaI tremor (3), chronic

atcohoI abuse (1), other (2)Idiopathic (7)Lumbar spinal stenosis (7), peripherat nerve injury (5). other (3)

Ischemic stroke (3), intracerebraI hemorrhage (3), congenitat (1)Vestibutar disease (6), dyskinetic (4)

31

10

7

1,4

7

10

Modified and used with permission from Mahtknecht P., Kiecht S., Btoem 8.R., Wittei J., Scherfter C., Gasperi A., Rungger G., Poewe W., Seppi K. Prev-

alence a nd burden of gait disorders in etderly men and women aged 90-97 yea rs: a population-based study. PLoS 0NE. 2o13;82e69627 .

*Percentage represents individuats with a singte gait disorder as a proportion of the entire study population.tTotal number of individuats with each gait disorder, includes individuats with muttiple causes of gait disorders, For examp[e, 22 of 777 individuats

had an isolated sensory ataxic gait disorder, 24 individuals had sensory ataxia and an addjtional neurologic gait disorder.

Baker Gait Disorders 605

-J.\L(_,.--\la

A. Normal

4- ,4

E. Frontal

Figure 3 Graphic representation ofclassical gait disorders. (A)Normal step length and width. See text for details. Reproducedwith permission from Pirker and Katzenschlager.6

caused by a decrease in both step length and height; postureis stooped, arm swing is reduced, and the base is narrow tonornal (Figure 3D). Parkinsonian turns are characterizedbysimultaneous rotation of the head, trunk, and pelvis, the so-

called en bloc turn: in normal individuals. the head rotatesfirst, followed by the trunk then pelvis.e Parkinson's diseaseis typically asymmetric at onset, so arrn swing and step lengthare diminished more on the affected side. Asymmetric shuf-fling can often be heard as scuffing of one foot more thanthe other. A parkinsonian (resting) tremor may activate duringwalking. Step length, velocity, arm swing, and turning speed

improve with dopaminergic treatment. t0

Freezing of gait and festinatior are features of more ad-

vanced Parkinson's disease. Freezing is defined as "an episodicinability (lasting seconds) to generate effective stepping"despite the intention to walk.rr Affected individuals feel as

if their feet are stuck to the floor. often associated with al-ternating trembling of the legs. Freezing is commonly seen

while initiating gait, tuming, or approaching a destination butcan also be provoked by features ofone's environment, such

as narrow hallways, doorways, or even large crowds. tz Freez-ing is a major contributor to fall risk.13 Freezing may improvewith optimization of dopaminergic medications. If freezingpersists despite medication adjustment, symptoms may improve

with visual or auditory cueing. For example, individuals may

avoid or overcome freezing by consciously stepping over aline on the floor, or marching to the beat of a metronome. Alaser line produced by an attachment to a cane or walker may

be a particularly effective intervention.ra't5 Festination de-

scribes a phenomenon in which steps become increasinglyrapid and short, so that gait takes on the appearance ofrunning.The center of gravity moves forward. Festination may precede

freezing but also occurs independently and further contrib-utes to fall risk.t6

Cerebeltar Ataxic Gaitlrsions of the cerebellum cause irregular, uncoordinated move-ments called ataxia. Ataxia of the limbs (appendicular ataxia,as might be assessed with finger-nose-finger testing) is typ-ically caused by lesions of the cerebellar hemispheres, whereasataxia ofgait (truncal ataxia) is caused by midline lesions ofthe cerebellar vermis.rT In its mildest form the cerebellar ataxicgait may manifest only as difflculty with tandem gait; indi-viduals may sway or fall when asked to walk heel-to-toe. Inmore severe form the gait is wide-based (to compensate forinstability), step length is variable, turns are unsteady, andthere is frequent side-to-side lurching or deviation (Figure 3C).Symptoms do not clearly worsen with eye closure. Assistivedevices such as a walker may decrease the risk of injury dueto falls. The broad differential diagnosis of cerebellar gait ataxiamay be narrowed by time course of symptom onset; strokeis a common cause of acute ataxia. autoimmune or other in-flammatory disorders are often subacute, and neurodegenerative

conditions or alcohol may cause chronic cerebellar ataxia.Imaging of the brain is typically warranted.

Sensory Ataxic GaitIndividuals with deflcits of proprioception (limb and joint po-sition sense) are unable to sense the position of their feetrelative to the ground, resulting in an unsteady gait. The stance

is wide-based, with a shortened step length and stompingquality as the foot hits the ground. Visual cues may partial-ly compensate for proprioceptive deficits, so affectedindividuals often look down at their feet while walking. Gaittherefore worsens dramatically in the dark or with eyes closed,

a feature useful for differentiating sensory from cerebellarataxia. Romberg's sign is present. Sensory ataxic gaits are

commonly caused by lesions of peripheral nerves or the dorsalcolumns of the spinal cord, such as with syphilis or vitaminB12 deficiency. Joint position and vibratory sense are dimin-ished in the lower extremities; loss of reflexes suggests thepresence of a peripheral neuropathy. Many patients improvewith physical therapy.ls

FrontaI GaitHigher-level gait disorders encompass a class of gaits notcaused by lesions ofthe corticospinal tract, basal ganglia, cer-

ebellum, or neuromuscular systems.'' Among the mostcorrmon of higher-level gait disorders is the frontal gait, typ-ically caused by Iesions of the frontal lobes (Figure 3E).Impaired balance is a core feature, and like cerebellar and

sensory ataxia, step width is also widened. Step length is de-

creased and variable, and step height is diminished. Failureto initiate gait is a prominent feature, feet may appear gluedto the floor when an individual attempts to begin walking, a

feature that may also occur in isolation.re Freezing with turnsis common. These features lead to the classic description ofthis gait as "magnetic." Common causes include microvas-

a\ -rS-!--- q#

B. Spastic

-4 .* 4ud*- *4€

c=-&.^lE *6_#qf\G*<# \<FX#,oar=4"C. Cerebellar Ataxic

444c41 ,44qjF q:r7.s a:r7-s- q# q#D- Parklnsonian

606 The American Journal of Medicine, Vot 131, No 6, June 2018

cular white matter disease, vascular or neurodegenerativedementias, and normal pressure hydrocephalus (NPH), the

latter of which may be accompanied by cognitive decline and

urinary incontinence and should be excluded by imaging. Only

a small proportion of individuals with NPH present with the

complete triad, so suspicion should be high in the setting ofenlarged ventricles and a compatible gait disorder. Gait ab-

normalities are an early feature of NPH and are also the most

likely to respond to cerebrospinal fluid shunting.20 For indi-viduals with frontal gaits from disorders other than NPH,physical therapy and assistive devices may improve ambulation

and decrease fall risk.

Functiona[ (Psychogenic) Gait DisorderFunctional gait disorders, formerly referred to as "psycho-genic," frequently co-occur with other functional neurologicdisorders and are common in clinical practice. Though theirpresentation is heterogeneous, functional gait disorders are

typically abrupt in onset, fluctuate over time, and are bothsuggestible and easily distractible. Common patterns includeexcessive slowing of gait or buckling of the knees, usuallywithout falls.2r Abnormal twisting or muscle contractions may

superficially resemble dystonia. Astasia-abasia describes an

inability to stand or walk without support, despite ability to

otherwise use the legs normally. Bizarre, inefflcient pos-

tures that appear unsteady yet do not result in falls are another

feature of functional gait disorders.22 Mood disorders are

present in a substantial number of patients but are not re-quired for diagnosis.2l

The diagnosis of a functional gait disorder should be made

not purely by exclusion of organic disease but by positive iden-

tification of internal inconsistencies or distractibility. Forexample, functional gait disorders or postural instability may

normalize when an individual is asked to walk while talkingon the phone. Sharing these inconsistent features with thepatient highlights their potential reversibility and may be ther-

apeutic. Communicating the diagnosis should focus more onpositive features than diseases that have been excluded and

emphasize mechanism over etiology. The metaphor of "aproblem with the software, not the hardware" may be par-

ticularly effective.2r Treatment often involves a

multidisciplinary team of neurologists and psychiatrists;

consensus-based guidelines for physical therapy have been

published.2a

CONCLUSIONSGait disorders are a major source of disability, morbidity, and

mortality in the elderly and may be neurologic ornonneurologic in origin. When neurologic in origin, gait dis-

orders may arise from lesions in any part of the nervous

system. This review has provided an overview of the clini-cal features of various gait disorders, emphasizing clinicalfeatures allowing for prompt recognition, offering an oPpor-

tunity fbr effective intervention and improvement in qualityof life.

ACKNOWLEDGMENTSI thank Dr. Lewis Sudarsky for insightful comments on an

early draft of this review.

Referencesl. Guideline for the prevention of falls in older persons. American Geri-

atrics Society. British Geriatrics Society, and American Academy ofOnhopaedic Surgeons Panel on Falls Prevention. J Am Geriatr Soc.

2001 :49(5):664-672. doi: I 0. 10461j.1532-5415.2001.49 I 15.x.

2. Mahlknecht P, Kiechl S, Bloem BR, et al. Prevalence and burden ofgait disorders in elderly men and women aged 60-97 years: a population-

based study. P Lo S O N E. 2013 :8(7 ):e69627. doi: I 0. I 37 l/journal.pone.0069627.

3. Verghese J, LeValley A, Hall CB, Katz MJ, Ambrose AF, Lipton RB.Epidemiology of gait disorders in community-residing older adults. JA m G e r i a r r S o c, 2006;54(2) :255-261. doi : I 0. I I I I I j.l 532- 54 I 5.2005

.00580.x.4. Montero-Odasso MM, Sarquis-Adamson Y, Speechley M, et al. Asso-

ciation of dual-task gait with incident dementia in mild cognitiveimpairment: results from the gait and brain study. JAMA Neurol.2017',7 4(7 ):857 -865. doi : I 0. I 00 I /jamaneurol.20 I 7.0643.

5. Takakusaki K. Neurophysiology of gait: from the spinal cord to the

frontal lobe. Mov Disord. 2013:.28(ll):1483-1491. doi:10.1002/mds.25669.

6. Pirker W, Katzenschlager R. Gait disorders in adults and the elderly: a

clinical guide. Wien KI in Wochenschr. 2016:129:8|-95. doi: I 0. I007/s00508-016-1096-4.

7. Aboutorabi A. Arazpour M, Balramizadeh M, Hutchins SW, FadayevaLm

R. The effect of aging on gait parameters in able-bodied older sub-jects: a literature review. Aging Clin Exp Res.2016:28(3):393-405.doi: I 0. I 007/s40520-01 5-0420-6.

8. RopperAH, Samuels MA, Klein JP. Chapter7. Disorders of stance and

gait. In: Ropper AH, Samuels MA, Klein JP, erJs. Principles of Neu-

robg.'-. I}tb ed. New York, NY: McGaw-Hill; 2011:ll5-126.9. Hong M. Perlmutter JS, Earhart GM. A kinematic and electromyo-

graphic analysis of turning in people with Parkinson disease. Neurorehabil

Neural Repair. 2009;23(2):166- I 76. doi: 10. I 177 /1545968308320639.

10. Smulders K, Dale ML, Carlson-Kuhta P, Nutt JG, Horak FB.Pharmacological treatment in Parkitrson's disease: eft'ects on gait. Pur-

kinsonism Re lat D isord. 20 t 613 I :3- I 3. doi: I 0. I 0 I 6/j.parkreldis.20 16

.07.006.

I l. Giladi N, Nieuwboer A. Understanding and treating freezing of gait inparkinsonism, proposed working definition, and setting the stage. Mov

Di so t d. 2O08 :23(suppl 2):5423-5425. doi: I 0. I 002 I mds.2 I 927 .

12. Nutt JG, Bloem BR, Giladi N, Hallett M, Horak FB, Nieuwboer A.Freezing of gait: moving tbrward on a mysterious clinical phenome-

non. L.tncet Neurol. 2011;10(8):734-744. doi:10.1016/51474-4422(11)7Ot43-0.

13. Kerr GK, Worringham CJ, Cole MH, Lacherez PF, Wood JM, Silburn

PA. Predictors of future falls in Parkinson disease. Neurology.2010;7 5(2): I I 6-124. doi:10.1212/!VNL.0b0 I 3e3 I 8 I e7b688.

14. McCandless PJ. Evans BJ. Janssen J. Selfe J, Churchill A, Richards J.

Effect of three cueing devices for people with Parkinson's disease withgait initiation difficulties. G o i t Post ure. 20 I 6:44:7 - | I . doi: I 0. 10 t 6/j.gaitpost.20 I 5. I 1.006.

15. Donovan S, Lim C, Diaz N, et al. Laserlight cues for gait freezing in

Parkinson's disease: an open-label sludy. Purkinsortism Relat Disotd.

20ll',17 (4):240-245. doi: 10.101 6/j.parkreldis.20l 0.08.01 0.

16. Ebersbach G, Moreau C, Gandor F, Defebvre L, Devos D. Clinical syn-

dromes: Parkinsonian gait. Mov Disord. 2O13;28(l 1):1552-1559.

doi : I 0. 1002/mds.25675.

17. Timmann D, Brandauer B, Hermsdijrfer J, et al. l-esion-symptom mapping

of the h urnan cerebel lu m. C e re b e I I u m. 2tJ08l'7 (4) :602-606. doi : I 0. I 007/

sl23ll-008-0066-4.I 8. Baker JM, Sudarsky L. Gait disorders, balance and falls. In: Jameson

JL, Fauci AS. Kasper DL, Hauser SL, Longo DL, Loscalzo J, eds.

Baker Gait Disorders 607

Harrisons Principks of Internal Medicine.20th ed. New York NY:McGraw-Hill; 2017:l-20,2018. [Chapter 23]. In press.

19. Nuft JG, Marsden CD, Thompson PD. Human walking and higherJevelgait disoders, particularly in the elderly. Neurulogy. 1993;43Q):268-279.

20. Klassen BT, Ahlskog JE. Normal pressure hydrocephalus: how oftendoes the diagnosis hold water? Ne urolo gy. 2011 ;77 (12):1119- 1125.

doi : I 0. 1 2 I 2AIINL .Ofi 13 e3 I 822tu2f5.21. Baik JS, Lang AE. Gait abnormalities in psychogenic movement dis-

orders. Mov Disord. 200'l :22(3):395-399. doi: 10.1002:/mds.21283.

22. l-nmpert T, Brandt T, Dieterich M, Huppert D. How to identify psy-

chogenic disorders of stance and gait. A video study in 37 patients. .I

N eurol. l99l ;238(3): 140- 146.

23. Stone J. Functional neurological disorders: the neurological assess-

ment as treatment. Neurophysiol Clin. 2016;16(l):7 -17. doi:.10.11361

practneurol-20 I 5 -00l24l .

24. Nielsen G, Stone J, Matthews A, et al. Physiotherapy for functionalmotor disorders: a consensus recommendation. J Neurol NeurosurgPsychiatry. 2015;86(10):1113-ll 19. doi:10.1136/jnnp-2014-309255.