Deformidades estriatales en PD

Review
Striatal deformities of the hand and foot in Parkinson’s
disease
Ramsey Ashour, Ron Tintner, Joseph Jankovic
Striatal deformities of the hand and foot are abnormal postures that are common in patients with advanced
Parkinson’s disease (PD); they can present in the early stages of PD and in other parkinsonian disorders. Over a
century ago, Charcot and Purves-Stewart recognised these deformities, which cause substantial functional disability
and discomfort. The term striatal is used because pathology in the neostriatum (putamen and caudate) has been
suggested to cause the deformities, but the pathogenesis is unknown. Misdiagnosis of the deformities is common—
particularly when they occur early and in the absence of cardinal parkinsonian signs, such as tremor, bradykinesia,
and rigidity—because the hand deformities are similar to those in rheumatoid arthritis, equinovarus foot deformity
typically suggests an orthopaedic problem, and toe extension may be thought to be the Babinski sign of upper-motorneuron syndromes. Here we review the background and clinical features of these deformities to highlight these
commonly unrecognised and poorly understood parkinsonian signs.
Introduction
Various abnormal postures and movements have been
associated with pathology in the neostriatum, a
combination of putamen and caudate.1 The terms
“striatal hand” and “striatal foot” were originally used by
Charcot2 and Purves-Stewart3 to report the distal limb
deformities typically associated with Parkinson’s disease
(PD). Striatal limb deformities might not be easily
differentiated from dystonia, a well-recognised
movement disorder in patients with PD and other
parkinsonian disorders.1 By contrast with fixed striatal
hand and foot deformity, dystonia commonly begins
during activity and can be associated with dystonic
tremor. In patients with PD who are treated with
levodopa and have motor fluctuations, dystonia, such as
painful fixed inversion of the foot and flexion of the toes,
can be part of the wearing-off process.4 If untreated,
dystonia can develop into a fixed contracture, although
the fixed posture is generally different from that of
striatal hand or foot. Fixed deformity is rarely isolated,
except for complex regional pain syndrome, particularly
after trauma.5 Although striatal deformities have been
reported in 10% of patients with untreated, advanced
PD,1 prevalence has not been systematically studied.
Because the deformities are commonly wrongly
diagnosed—eg, rheumatoid arthritis, Dupuytren’s
contractures,6,7 flexor tendon entrapment of the digits
(also referred to as trigger finger and trigger thumb or de
Quervain’s tenosynovitis8), Babinski sign, and other
pseudodystonic disorders—we discuss the clinical
associations of striatal deformities. The primary aim of
this review is to draw attention to these commonly
unrecognised signs and to consider possible
pathogenetic mechanisms and treatment.
Striatal hand
In the late 19th century, Charcot described a “digital
deformation simulating that of primitive chronic
articular rheumatism” in which fingers were “alternately
flexed and extended at their several articulations”.2 He
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noted that the deformities in his “paralysis agitans”
patients were “neither the articular tumefaction and
stiffness, nor the osseous deposits and cracking sounds
of nodose rheumatism”. Indeed, unlike rheumatoid
arthritis, local signs of joint involvement, such as pain,
tenderness, heat, and swelling, are absent in striatal
hand. Also, rheumatoid arthritis tends to occur
bilaterally, whereas focal dystonia before PD tends to be
unilateral, with tremor, rigidity, and bradykinesia
developing on the ipsilateral side (table 1).1,9
In the “paralysis agitans” section of his Manual of
Diseases of the Nervous System, Gowers10 included
illustrations of striatal hand accompanied by a
description of the abnormal posture: “. . .[the fingers] are
flexed at the metacarpophalangeal joints and extended at
the others. . .the digits deviate toward the ulnar side, as
in chronic rheumatoid arthritis”. Purves-Stewart also
briefly mentioned the “interosseal attitude” of the hands
in his patients.3 Many years later, Gortvai11 expanded on
the early observations, describing four stages of hand
deformity in PD—progression from moderate
metacarpophalangeal flexion and interphalangeal
extension to severe proximal interphalangeal
Lancet Neurol 2005; 4: 423–31
Parkinson’s Disease Center and
Movement Disorders Clinic,
Department of Neurology,
Baylor College of Medicine,
Houston, TX, USA (R Ashour BS,
R Tintner MD, J Jankovic MD)
Correspondence to:
Prof Joseph Jankovic, Director of
Parkinson’s Disease Center and
Movement Disorders Clinic,
Department of Neurology, Baylor
College of Medicine, Suite 1801,
6550 Fannin, Houston,
TX 77030, USA
josephj@bcm.tmc.edu
Features
Rheumatoid arthritis
Striatal abnormalities
Pathophysiological
features
Joints
Radiographic changes
Proliferative synovitis, autoimmunity,
microbial initiator
Swollen, warm, painful, pannus formation
Joint effusions, juxta-articular osteopenia
with erosions, narrowed joint space with
loss of cartilage
Morning stiffness, decreased range of
motion (active and passive)
Generally symmetrical joint involvement,
polyarticular
Association with HLA DR4 or DR1
Non-inflammatory, dystonic features,
soft-tissue elastic changes
Painful, contractures
Normal
Mobility
Distribution
Genetics
Extra-articular features
Cutaneous and visceral rheumatoid
nodules, increased serum rheumatoid
factor, synovial cysts, vasculitis, episcleritis
Fixed deformity, may respond to levodopa
or botulinum toxin
In most cases develops on one side with
ipsilateral emergence of cardinal PD signs
Seems to be more common in
juvenile-onset PD
Rigidity, bradykinesia, tremor
Table 1: Striatal deformity and rheumatoid arthritis9
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Review
hyperextension with distal phalangeal subluxation,
leading to distal interphalangeal flexion. Clinical and
radiological findings prompted Gortvai to comment that
the hand joints of his patients with PD were healthy,
even after many years of deformed posture.11 He showed
the role of small muscle contraction in the production of
the deformities, observing that ulnar-nerve block with a
local anaesthetic stopped the deformity in patients
whereas ulnar-nerve stimulation produced the abnormal
posture in healthy people. Since Gortvai’s research,
several reports have described many “typical” hand
deformities associated with parkinsonism with different
patterns of flexion or extension at the various digital
articulations.12–18 The most typical deformity associated
with striatal hand is characterised by flexion of the
metacarpophalangeal joints, extension of the proximal
interphalangeal joints, flexion of the distal
interphalangeal joints, and ulnar deviation (figure 1).19
Some features of striatal hand in patients with
untreated PD are common to other well-described forms
of dystonia. Striatal hand must be differentiated from:
dystonia in primary dystonic states; dystonia
contributing to a differential phenotypic expression of
the same disease, as in dystonia-parkinsonism
syndromes; dystonia as a complication of pharmacotherapy;4,20–22 and dystonia associated with an ablative
lesion or high-frequency, deep-brain stimulation.23–25
In addition, striatal hand must be differentiated from
entrapment neuropathies and cervical myelopathies.26
Although striatal hand (metacarpophalangeal flexion,
interphalangeal extension, ulnar deviation) is similar to
the swan-neck deformities that occur in some arthritic
disorders, other postures have been described that more
closely parallel the opposite boutonnière deformity
(metacarpophalangeal extension, proximal interphalangeal flexion, distal interphalangeal extension).
Postures with features intermediate between these two
prototypical positions also occur and are common in
advanced disease.12,13,15,17 A claw-hand deformity has also
been described in PD.13 Whereas metacarpophalangeal
flexion and interphalangeal extension, due to
contraction of the lumbricals and interossei respectively,
seem to be the earliest signs of striatal hand,
hyperextension and subluxation of the terminal
phalanges are thought to be signs of more advanced
deformity.11 In addition to disfigurement, striatal hand
can cause pain or discomfort and can affect daily
activities such as writing, eating, and buttoning. Severe
Figure 1: Striatal hand in a patient with typical PD
424
flexion of the fingers can lead to pressing of fingernails
into the palm of the hand, causing abrasion and
secondary infection (figure 2). Such contractures are
typical in advanced PD and other parkinsonian
disorders, but they can occur even in early stages and
also secondary to reactive fibrosis resulting from
treatment with an ergot dopamine agonist (eg,
bromocriptine, pergolide),14 which can also cause
fibrosis in the lungs, heart, and other tissues.27
Although hand deformities are accepted as a
common complication in patients with advanced,
treated PD, less attention has been given to the
frequency of striatal hand as an early sign in patients
who have not been treated.18 We have seen a mild
flexion of the metacarpophalangeal joint in the hands
of many patients with early PD, even before other
parkinsonian features present. This flexion is typically
on the side initially affected by tremor, rigidity,
or bradykinesia. Although prospective studies
must validate this observation, clinicians should
search for this sign as evidence of the side of the
initial presentation.
Striatal foot
In a lecture on the symptoms of “paralysis agitans” in
1877, Charcot gave an account of two patients whose feet
were “stiff, extended, and turned in, simulating the
malformation known as talipes equines (varus)
clubfoot”.2 Claw-like “extension of the first and
concomitant flexion of the second phalanges” were seen
in both patients. Gowers10 also noted in his discussion of
“paralysis agitans” that “[rigidity] may extend to the feet,
and even cause talipes equinovarus, and distortion of the
toes—extension of the first, and flexion of the other
phalanges so as to cause a claw-like deformity”. Similar
posturing (hallucal hyperextension, flexion of the other
toes, ankle inversion) was described 10 years later in five
of 28 patients with “paralysis agitans” who were
observed for 2 years.3 This “toe curling” symptom with
pain and cramps was unpredictably associated with
walking and preceded all other symptoms by up to
2 years in three of the five patients.
Several studies done before the era of levodopa
treatment attributed foot and other deformities to PD.11,12
In 1972, Duvoisin and colleagues28 noted that “this
dystonic phenomenon is an intrinsic feature of PD”. By
use of the term “striatal foot”, they described the typical
features, including big-toe extension, flexion of the other
toes, equinovarus foot positioning, and pain.28 Striatal
foot deformity can cause pain and impair the ability to
stand, walk, and wear shoes. If untreated, skin
ulceration and bone erosion can happen (figure 3).
Equinovarus foot positioning produces inadequate
support, hinders early and mid-stance dorsiflexion, and
prevents the tibia from moving over the stationary
foot.29,30 Thus, the stance phase of gait is shortened, and
push-off propulsion and forward propulsion are
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Review
Figure 2: Typical striatal hand deformity and severe flexion contracture
Left and middle: typical striatal hand deformity in the right hand. Right: marked flexion of fingers resulting in severe flexion-contracture in the left hand.
hindered.31 Early swing-phase limb advancement and
foot clearance are also affected. Pressure is increased
over the lateral aspect of the foot and ankle instability
occurs.29,31
Over the years, different terms have been used to
describe the striatal foot deformity, including the
dystonic foot response of parkinsonism,32 dystonic
claudication,33 striatal toe,34,35 hitchhiker’s great toe,29
pseudo-rheumatoid deformity,36 and pseudo-Babinski.35
The all-encompassing term foot dystonia is commonly
used to describe dystonic posturing of the legs and feet
that happens in various clinical settings including PD
and
other
Parkinson-plus
syndromes.19,33,37–43
Furthermore, striatal toe and equinovarus foot are used
to describe clinical patterns of motor dysfunction, such
as upper-motor-neuron syndrome, that are visually
similar or identical to but aetiologically distinct from
striatal foot in PD.29 As with striatal hand, striatal foot
must be differentiated from other well-described forms
of dystonia commonly attributed to dopaminergic
therapy, such as off-period and biphasic dystonia.4
Striatal foot in PD is part of the primary disease process
and can be one of the earliest signs in untreated
patients.1,3,19,28,32,33,36–45
When striatal foot is a secondary (symptomatic)
dystonia in patients with PD, it might be mistaken for a
primary dystonic state (sporadic or familial), particularly
when the classic parkinsonian signs are absent. Primary
adult-onset dystonia rarely involves the feet, and thus the
possibility of PD should be considered in all adults who
present with isolated foot dystonia.1
Striatal toe is a type of striatal foot, but without the
equinovarus foot. Electromyographic analyses have
shown a different pattern of muscle contraction in
striatal foot from that in the Babinski response;28
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however, the exact differences need further study.
Striatal toe has been differentiated from the Babinski
sign according to toe fanning and flexion synergy of
other muscles in the same leg, which are both features
of the Babinski response.35 Other disorders with limb
abnormalities similar to striatal foot include peripheral
vascular disease, lumbar canal stenosis, familial
paroxysmal exercise-induced dystonia, and exerciseinduced hypocalcaemic-tetanic spasms.43
Classification and diagnosis
Although the term striatal is used to describe these
deformities, it is inaccurate because it implies a nonspecific lesion in the striatum (eg, neostriatum,
paleostriatum, and corpus striatum) even though there
Figure 3: Striatal foot with severe skin ulceration and bone erosion
425
Review
is little evidence that a striatal lesion is needed to
produce the posture. Furthermore, traumatic, vascular,
or other lesions in the striatum rarely produce striatal
deformities.46 Moreover, the term does not adequately
account for the range of extrastriatal lesions that could
lead to these postural deformities. We suggest use of the
terms striatal hand and striatal foot to help with
recognition of the clinical entity of distal limb deformity
in parkinsonism.
Although in this review we focus on striatal hand and
striatal foot associated with PD, there are many other
parkinsonian disorders in which striatal hand occurs,
including multiple system atrophy,40,47,48 corticobasal
degeneration,49 progressive supranuclear palsy,50–52 NBIA
(neurodegeneration of the brain with iron
accumulation),53 and parkinsonism-dementia seen in
western Pacific regions.54
The relation between parkinsonism and coexistent
abnormal postures, such as striatal hand, striatal foot,
bent spine, scoliosis, and camptocormia, is not well
understood. Camptocormia—a disorder characterised
by pronounced flexion of the thoracolumbar spine,
which is most prominent on standing and walking and
relieved in the supine position—is associated with
various musculoskeletal and neurological causes,
including parkinsonism, dystonia, and other
neurological and non-neurological disorders.55 In
patients with idiopathic PD, camptocormia is
increasingly identified and should not be confused with
bent spine syndrome seen in axial myopathies.1,55–59
Camptocormia associated with active contraction of the
rectus abdominus can be treated with injection of
botulinum toxin into that muscle.60 Scoliosis is a lateral
curvature of the spine accompanied by vertebral rotation
that results in asymmetrical deformity of the trunk.
Scoliosis is more common in patients with PD61–63 than
in elderly people of similar age to those with PD.63–65
Epidemiology
Striatal hand and foot deformities might present in up
to 10% of untreated patients with advanced PD;1
however, neither the true prevalence nor the relation of
these deformities with age and sex has been
systematically studied. Although many reports support
the high prevalence of dystonia in patients with
idiopathic, untreated PD,1,19,20,37,66 few have questioned
the relation, some even noting a similar prevalence of
focal dystonia in untreated PD and the general
population.38 Patients who develop dystonia before or
with PD tend to be younger than the general population
of patients with PD.1 Similarly, patients with early-onset
PD, particularly those with PARKIN mutations, are
more likely to have dystonia.67
Foot dystonia develops in 20–40% of patients
with PD receiving sustained levodopa treatment,42 and
some studies have found that striatal foot precedes
treatment in 2·4–8·0% of patients.32,68 In a series of
426
86 parkinsonian patients, which was done before
levodopa treatment was available, 34 (~40%) had some
deformity of the hands, including 14 (~24%) of
58 patients with PD.12 By contrast with this finding,
only three cases of hand deformity in patients with PD
were recorded during 12 months in a “busy” neurology
department; however, a formal epidemiological study
was not done.15
Pathophysiology
Early reports attributed the characteristic postural
deformities in PD to muscular rigidity.2,3 Later studies
on striatal foot suggested an extrapyramidal origin,
differentiating the deformity from similar but
unrelated frontal release, such as the “grasp”, and
proprioceptively mediated flexion synergy in mesial
frontal-lobe lesions.32,69
Various lesions disrupting striatopallidothalamic
projections produce focal dystonia in human
beings;20,46,70–72 research with animal models has given
insights as well. For example, foot dystonia similar to
that seen in early PD has been reported in studies of
parkinsonism in monkeys induced by 1-methyl-4phenyl-1,2,3,6-tetrahydropyridine (MPTP).73 Also, the
abnormal posture and compulsive circling behaviour in
dogs74 and cats75,76 after unilateral ablation of the caudate
nucleus77 suggest that asymmetrical degenerative
changes in the caudate—through disruption of its tonic
effect on posture and locomotion—contribute to
the development of scoliosis in patients with PD and
in patients with postencephalitic parkinsonism.
Furthermore, rats with hemiparkinsonism, induced by
unilateral injection of 6-hydroxydopamine into the left
ventralis tegmenti, showed strong ipsilateral deviation;78
the severity of scoliosis was closely related to the
decrease in extracellular striatal dopamine and to the
development of postsynaptic dopamine receptor
supersensitivity. A similar mouse model showed the
development of dyskinesias and abnormal posture after
6-OHDA injection into the sensorimotor striatum.79
Of the basal ganglia, the lentiform nucleus (putamen
and globus pallidus) is commonly involved when
dystonia and parkinsonism coexist.1 Lenticular
lesions are also associated with the development
of camptocormia.55,59 Thalamic relay nuclei have
been associated with contralateral symptomatic
hemidystonia,20,69 and lesions in the posterior and
posteriolateral thalamus, red nucleus, and subthalamic
nucleus have been reported to cause various
dystonias.1,23–25,46,50–52,70–72
Dystonia in PD includes a range of focal dystonias—
eg, cervical dystonia, limb dystonia, blepharospasm and
other cranial dystonias, and hemidystonia.1,19–21,37,38,80,81
Although striatal hand and foot overlap with other forms
of dystonia, comparison of the clinical features of these
deformities with those in primary (idiopathic) dystonia
shows substantial differences (table 2).19,38,80
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Why some patients with PD develop striatal deformity
and others do not is not clear, and there is no predictor
of striatal deformity in patients with PD. In one study,12
the frequency of striatal hand was associated with the
amount of generalised rigidity but not with the amount
or duration of tremor. Severe rigidity has also been
suggested to contribute.15 Study of limb contractures in
patients with PD by use of transcranial magnetic
stimulation found that central motor conduction time is
lower in the limb that is more severely affected; shorter
central motor conduction time reflects decreased
excitability in cortical-inhibitory circuits and has been
suggested to contribute to overactive and inappropriate
muscle contraction in the hand.17
Qualitative research findings that striatal hand is more
common in women than in men could be explained by
more ligament laxity in women than in men—ie, by an
interaction between a central tone disturbance and
a peripheral, predisposing state.16 Epidemiological
studies82–84 reporting much higher rates of anterior cruciate
ligament injury in females than males participating in the
same sports have prompted investigation of non-contact
mechanisms and risk factors to explain the difference.85–87
The effects of female hormones on connective-tissue
structure have been studied,82,83,88,89 and some have shown
that collagen structure and tensile properties vary with
hormonal fluctuations in women.90,91 Similarly, studies
have identified transcripts for oestrogen and progesterone
receptors in normal connective tissue in women.90,92 In
rats, oestrogen increases elastin in connective tissue93–95
and decreases collagen in tendons and fascias.88 The
cyclically released hormone relaxin changes collagen
metabolism through an effect on the secretion of
procollagenases by tissue fibroblasts.96,97 Although these
findings provide clues to the sex-specific factors that
predispose or perhaps contribute to joint and soft-tissue
pathology, particularly for sports-related trauma, their role
in the development of striatal-limb deformities in PD is
speculative. Observations that these deformities are
associated with sex must be substantiated by formal
epidemiological studies; the deformities could be caused
by many factors with anatomical, sociological, and
hormonal differences modifying the course of disease in
individual patients.
A pathophysiological model for parkinsonism and
dystonia, such as observed in levodopa-related, offperiod dystonic processes, has been proposed to involve
dopaminergic hypofunction with concurrent or
compensatory cholinergic hyperfunction.42 Improvement in patients treated with baclofen has led some to
posit a contributory role for other neurotransmitter
systems (specifically glutamate and GABA) in dystonia
as well.32 Furthermore, a hypothesised rostrocaudal
gradient of decreased dopaminergic and increased
GABA-ergic function across a somatotopically organised
striatum42 might underlie the dystonic complications in
the feet of patients with PD.
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Distinguishing
features*
Striatal deformities
Primary idiopathic dystonia
Fixed or mobile
Pain
Relatively fixed
Typically painless
When present
Typically
present at rest
Concomitant parkinsonism
signs and symptoms
(tremor, rigidity, bradykinesia)
Typically affects the hands,
but can also affect the feet
and other parts of the body
Typically persists during sleep
Mobile, but can evolve into contractures if left untreated
Typically painless, but some dystonias (eg, cervical) are
associated with local pain
Commonly induced by action
Other symptoms
Anatomy
Sleep association
Commonly other dystonic features are present
Dystonia affecting legs and feet is very rare at onset in adults; if
present, dystonia is commonly associated with parkinsonism
Not present during sleep, except when associated with
contractures
*These features are not absolute and are given as a guide.
Table 2: Striatal deformities and primary idiopathic dystonia19,38,80
Progression of striatal-limb deformities from
abnormal contraction to fixed contracture results in
further functional disability in patients already coping
with PD symptoms. Particularly distressing is the rapid,
unpredictable development of contractures in levodoparesponsive patients. In previous studies on hand
contractures in PD, the progression of deformity to fixed
contracture happened over periods of 2 weeks,14
2 months,15 2 weeks to 2 months,17 and 6 months.98 In
most of the patients with PD in these studies,
contractures developed after several years of disease
with a strong (but not fully understood) female
preponderance.
The combination of long-lasting, fixed posture, and
sustained muscle contraction associated with hypertonia
reduces the number of sarcomeres in the affected
muscle groups.99 Furthermore, torque measurements
during imposed constant-velocity muscle-contraction
cycles have been used to show secondary changes in the
mechanical properties of affected muscles and their
surrounding tissues in patients with long-standing
spasticity.100 In particular, alterations in soft-tissue
plasticity and viscoelasticity are thought to cause atrophy
and fibrosis in both muscle and connective tissue98–100
and could thus compound the effect of sarcomere-loss
and muscle shortening in the overall progression of
deformity to fixed contracture. Although contracture
development has been well characterised in patients
with long-standing spasticity, similar changes seem
possible in patients with PD—electromyographic
analyses show excessive, involuntary motor-unit
recruitment in rigid muscles apparently at rest that is
not suppressible, and the average area of surface
electromyographic readings relates to clinical
assessment of rigidity.101
The rapid development of limb contractures in patients
with PD taking the ergot dopamine agonist bromocriptine
mesilate14 suggests drug-induced reactive fibrosis as a
pathogenetic mechanism of contracture. Indeed, in most
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Search strategy and selection criteria
References for this review were identified from searches of
MEDLINE up to March 1, 2005. The keywords “Parkinson’s
disease”, “parkinsonism”, “dystonia”, “primary”, “secondary”,
“focal”, “hand deformity”, “foot deformity”, “musculoskeletal
deformity”, “striatum”, “contractures”, “dyskinesias”, and
“levodopa” were entered in various combinations with the
inclusion of all subheadings. The references of each paper
were studied for pertinent papers for follow-up, and many
additional searches were done up to April 15, 2005. No limits
were placed on the dates of publication. Only articles
published in English were consulted in the initial review.
Other references followed up were reviewed in English only;
papers written in other languages in this category were
allowed only if an English translation was available.
reports of patients with PD who rapidly developed
contractures, the patients were being treated with ergot
dopamine agonists14,17 or ergolines.98 Furthermore, digital
vasospasm,102,103 pleuropulmonary fibrosis,27,104–107 and
retroperitoneal fibrosis107–110 have all been reported in
patients treated with bromocriptine mesilate as well as
other ergot compounds. An interaction between ergot
compounds and serotonin receptors could explain the
production of tissue fibrosis,14,111–114 and both
bromocriptine mesilate and methylsergide are known to
interact with 5-HT1 and 5-HT2 receptors.114,115 Serotoninsecreting carcinoid tumours have been linked to
endocardial and pulmonary fibrosis.114,116,117 Other
fibroblast-modulating substances have been researched,
including tachykinins (eg, substance P and substance K)118
and growth factors, including platelet-derived growth
factor,119,120 insulin-like growth factors,121 and the
transforming growth factor family.117,122
Treatment
Dystonia responds variably to treatment with systemic
drugs in parkinsonism. The response to antiparkinsonian drugs is less predictable in striatal hand
and foot than in primary dystonia, although levodopa
and anticholinergic agents have improved dystonia in
some cases.32,33,35,36,42–44 We have observed cases in which a
complete resolution of striatal-hand dystonia was
achieved with levodopa treatment. Anticholinergics,
baclofen, and benzodiazepines have also been variously
successful in treating foot dystonia in parkinsonism,
including striatal foot in PD.123,124
Botulinum-toxin injection is a treatment option. In
combination with systemic drugs, botulinum toxin is the
preferred treatment for focal dystonias and has been used
in the treatment of striatal toes.34,60 The dose injected is
guided by electromyographic activity in the affected
muscles. Botulinum-toxin injection into the lumbricals
and short adductors of the thumb has led to functional
improvement and pain relief in patients with PD who
428
have striatal hand with varying amounts of contracture.98
However, the large muscle groups contributing to
dystonia in the foot as well as the associated contracture
can make botulinum-toxin injections less effective
in striatal deformities than in more mobile forms
of dystonia.123 Also, chemodenervation of extensor
hallucis longus for striatal toe might unmask
co-contraction of flexor hallucis longus29 and therefore
necessitate further treatment.
If conventional, non-operative treatments are
unsuccessful, orthopaedic surgical interventions can be
attempted. Split anterior tibial-tendon transfer with
extrinsic toe-flexor release and percutaneous achillestendon lengthening has been reported to result in
substantial functional improvement and plantigrade foot
in patients with idiopathic foot dystonia.123
Z-lengthening procedures and capsulotomy have also
been used in the treatment of hand deformities in PD.13
Neurosurgical treatments that have been assessed for
the treatment of PD and dystonia include stereotactic
pallidotomy, thalamotomy, and deep-brain stimulation.1,11,25,125–128 Cooper125–127 described improvement and
even complete resolution of striatal hand and foot
deformities after occlusion of the anterior choroidal
artery and stereotactic thalamotomy in patients with PD.
Patients with PD who had combined thalamic lesion in
the ventralis intermedius and ventralis oralis nuclei
(selective Vim-Vo thalamotomy) for the treatment of
dyskinesias showed improvement in limb dystonia.128
Nevertheless, the role of neurosurgery in the treatment
of striatal hand and foot requires further study; surgery
is generally reserved for patients with other severe
symptoms refractory to non-surgical treatments.
Conclusion
Investigation of the temporal relation between the early
development of striatal hand and foot deformities,
initially shown with slight flexion of the
metacarpophalangeal joint, and the natural history of PD
might give insight into the pathogenesis of this sign and
its relation to underlying pathology. Future studies
should assess whether there are predictors for the
development of deformity and whether the deformities
are associated with disease severity and progression,
symptom laterality, age, sex, and other clinical markers.
Acknowledgments
We thank the staff at the Mary Moody Medical Library in Galveston,
TX, USA, for providing copies of papers published before 1975 for
this review. We also thank the National Parkinson Foundation for
their support.
Authors’ contributions
All authors contributed equally to this review.
Conflicts of interest
We have no conflicts of interest.
Role of the funding source
No funding source had a role in the preparation of this paper or in the
decision to submit it for publication.
http://neurology.thelancet.com Vol 4 July 2005
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