Movement Disorders
Vol. 18, No. 12, 2003, pp. 1492–1498
© 2003 Movement Disorder Society

Dystonia in AIDS: Report of Four Cases
Stewart A. Factor, DO,1* Michelle Troche-Panetto, MD,2 and Susan A. Weaver, MD1
1

Albany Medical Center, Department of Neurology, Albany, New York, USA
Albany Medical Center, Department of Psychiatry, Albany, New York, USA

2

Abstract: Dystonia is a rare complication of acquired immune
deficiency syndrome (AIDS). We report four such cases related
to three different causes. Cases 1 and 2 both developed dystonia
secondary to biopsy-proven progressive multifocal leukoencephalopathy. One had left arm dystonia, whereas the other had
bilateral upper limb dystonia. One patient had associated akinesia and rigidity. Imaging demonstrated frontal and/or parietal
white matter lesions but no basal ganglia abnormalities. Case 3
developed hemidystonia and cervical dystonia from biopsyproven toxoplasmosis with a lesion in the thalamus. Case 4

suffered from AIDS dementia complex and developed cervical
dystonia while taking risperidone therapy. We also review
previously reported cases of dystonia in AIDS patients with the
same causes and discuss the issue of increased vulnerability of
the basal ganglia to HIV infection which, in turn, leads to
increased sensitivity to neuroleptics. When dystonia is seen in
AIDS patients, its pattern may be a clue to the ultimate cause.
© 2003 Movement Disorder Society
Key words: dystonia, AIDS, toxoplasmosis; progressive
multifocal leukoencephalopathy; neuroleptics

Neurological symptoms are common in patients with
acquired immunodeficiency syndrome (AIDS), although
less so than in the 1980s because of antiretroviral therapy. Small portions of these symptoms consist of movement disorders. The types of movement disorders commonly reported include hemiballism, chorea, tremor, and
parkinsonism, which may be associated with primary or
secondary (opportunistic) infection.1 Dystonia has only
rarely been reported. Here, we present four cases that
were seen at our institution over the past decade resulting
from three different causes.

ness and incoordination of his left arm followed by
episodes of numbness and “spasms” marching up the left
arm. A magnetic resonance imaging (MRI) scan revealed
a nonenhancing lesion in the right frontal premotor subcortical white matter (Fig. 1). A brain biopsy performed
in June 1995 revealed progressive multifocal leukoencephalopathy (PML). He received therapy for PML with
Ara-C and antiretroviral agents, and some improvement
in his symptoms was noted.
He was examined neurologically in April 1996, and
findings included increased tone in the left upper extremity associated with dystonic posturing. The fingers
and thumb were held flexed, and he had little control
of their movements. The fingers could be passively
opened, indicating a lack of contracture. His arm was
internally rotated. There also was mild weakness of
the left arm, hyperreflexia on the left side, but downgoing toes. Episodic clonic spasms of the left side with
elevation and external rotation of the left arm and
elevation of the left leg were observed (see Videotape,
Segment 1).
Dystonia was treated with baclofen, trihexyphenidyl,
and clonazepam but was unresponsive. Subsequently, the
spasms were diagnosed as left focal motor seizures,
documented by electroencephalogram. Follow-up exam-

CASE 1
The patient was a 34-year-old man diagnosed with
HIV infection in 1990. He was apparently well until
February 1995 when he developed Pneumocystis carinii
pneumonia. In March 1995, he noted the onset of weak-

A videotape accompanies this article.
*Correspondence to: Stewart A. Factor, DO, Parkinson’s Disease
and Movement Disorders Center of Albany Medical Center, 215 Washington Ave Ext, Albany, NY 12205. E-mail: factors@mail.amc.edu
Received 10 January 2003; Revised 22 April 2003; Accepted 10 June
2003
DOI 10.1002/mds.10602

1492

DYSTONIA IN AIDS

1493

2) and cerebellar white matter change was also seen. A
brain biopsy performed in February 1996 revealed PML.
Treatment for PML was started with Ara-C and antiretrovirals, but due to progressive dysphagia and aspiration,
it was discontinued. The dystonia persisted until his
death 6 months after diagnosis (July 1996).
CASE 3
The patient was a 44-year-old man diagnosed with
HIV infection in February 1988. He presented in February 1991 with a 3-day history of fever (40°C), gait
difficulty, mental status changes, and agitation followed
by unresponsiveness. A head computed tomography
(CT) scan performed 2 days earlier at another hospital
was reportedly negative. He also was anemic, had oral
thrush, and chronic hepatitis. In the past, he had been

FIG. 1. Magnetic resonance scan from Patient 1 demonstrates a nonenhancing lesion in the right frontal premotor subcortical white matter.

ination at 15 months revealed stable PML but continuing
seizures and dystonia.
CASE 2
The patient was a 43-year-old man diagnosed with
HIV infection in 1989. He developed thoracic herpes
zoster and oral candidiasis in May 1995. In December
1995, he was observed to have slurred speech, swallowing difficulties, incoordination of arm movements, and
unsteady gait.
Physical examination revealed masked, astonished facial expression, saccadic pursuits, and dysphagia. Speech
had qualities of dysarthria and pseudobulbar speech. His
neck was shifted anteriorly and held flexed. He had
bilateral upper limb dystonia, left worse than right. He
also manifested bilateral limb rigidity, moderate to severe bradykinesia, hyperreflexia, akinetic and ataxic gait,
stooping of his posture, and postural instability (see
Videotape, Segment 2).
MRI scan revealed bilateral nonenhancing lesions in
the deep frontal and parietal– occipital white matter (Fig.

FIG. 2. Magnetic resonance scan of Patient 2 demonstrates bilateral
nonenhancing lesions in the deep frontal and parietal– occipital white
matter.

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S.A. FACTOR ET AL.

treated with AZT and had no prior AIDS defining illnesses.
On physical examination he was in stupor, had right
CN-III palsy, papilledema, and nuchal and extremity
rigidity. CT scan revealed a nonenhancing mass lesion in
the right caudate nucleus, left thalamus, and left frontal
lobe (Fig. 3), initially with a midline shift. Treatment was
started with dexamethasone, pyrimethamine, and sulfadiazine.
Days 3 to 8 after admission, he started to open his eyes
and follow commands. On day 10, his muscle tone was
increased in all extremities and had bilateral Babinski
signs. The next day he showed upper extremity tremor at
rest. On day 12, a follow-up neurological exam demonstrated CN III palsy, myoclonus, right-turning cervical
dystonia with head tremor, and hypertrophy of the left
sternocleidomastoid, right hemidystonia, right hemiparesis, and increased tone bilaterally (see Videotape, Segment 3).
A brain biopsy of the right caudate on day 19 was
performed and revealed toxoplasmosis. Treatment with
the above-noted medications was continued with no improvement of the dystonia after approximately 1 month.
He was discharged after 1 month and not seen in followup.
CASE 4
The patient was a 40-year-old woman with an 8-year
history of HIV infection and a CD4 count of 81 in
August 1997. Her AIDS was associated with recent
AIDS dementia complex, hepatitis C, oral thrush, and
recurrent trichomonas infection. In addition, she had a
history of presumed cerebral toxoplasmosis, which led to
admission in June 1997 with complaints of headache,
nausea, and vomiting lasting 3 weeks followed by gait
difficulty. Examination at that time revealed a mild left
hemiparesis and wide-based gait. No involuntary movements were reported. A CT scan from the other hospital
demonstrated a right-sided mass lesion with surrounding
edema. She was treated with pyrimethamine, sulfadiazine, and dexamethasone with notable improvement. A
repeat CT scan before discharge demonstrated a 2-cm
lesion in the right basal ganglia with residual edema but
significant shrinkage of the mass and improvement of the
mass effect. Diagnosis of toxoplasmosis was presumed
based on the nature of the lesion in the imaging, response
to appropriate medications, and elevated toxo IgG. Other
past medical problems included bipolar disorder, anemia,
and cholestatic liver disease. Repeat MRI of the head 7
weeks later during another hospitalization showed no

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

FIG. 3. Computed tomography scan of Patient 3 demonstrates initially
a nonenhancing mass lesion in the right caudate nucleus (a) and left
thalamus (a) and 10 days later left frontal lobe (b) with a hemorrhagic
mass in the right caudate nucleus c (the region that was ultimately
biopsied).

change in her old toxoplasmosis lesion but also showed
severe cerebral atrophy.
She was readmitted again 6 weeks later for gastrointestinal symptoms and worsening encephalopathy. Her

DYSTONIA IN AIDS
medications on admission included risperidone 2 mg
t.i.d. She had been on 3 mg t.i.d. as recently as a few
weeks before and had been on the drug “off and on” for
approximately 5 months for psychotic symptoms associated with AIDS dementia complex. There was a history
of noncompliance. Other medications included fluoxetine, bupropion, diazepam, and pyrimethamine maintenance. She was not on antiretroviral agents. In October,
she developed left neck pain and rotation of the head to
the right. Risperidone was reduced to 2 mg b.i.d. and
benztropine was added 2 mg b.i.d., but this treatment had
no effect. A repeat MRI imaging study was unchanged.
A neurology consultation was performed 3 days later.
Examination demonstrated a severely ill, cachectic
woman who had limited speech output but was not
aphasic. She was clearly encephalopathic. Regarding
cranial nerves, she had right central facial weakness,
moderate torticollis to the right with some laterocollis
left, and hypertrophy of the left sternocleidomastoid
muscle. She had limited range of motion with attempting
to turn to the left (see Videotape, Segment 4). On motor
examination she had a left hemiparesis and bilateral leg
muscle atrophy and weakness from a peripheral neuropathy. Her reflexes were absent in the lower extremities
but had bilateral clonus. Plantar reflexes were downgoing, and she had no apparent ataxia. She could not
walk. It was believed that the dystonia was neurolepticinduced, and the risperidone was discontinued. When
seen again in 3 days, there was no change in status.
Within the next few weeks, she developed orofacial
dyskinesia and died November 1997.
DISCUSSION
These cases indicate that, although dystonia is a rare
manifestation of AIDS, it can occur as the result of
several causes. Lesions in the putamen, caudate, or thalamus are usually implicated in the presentation of symptomatic dystonia.2 Keeping this in mind, one would
expect that toxoplasmosis would be the most likely cause
of this movement disorder, because it is common in
AIDS, occurring in approximately 30% of patients, and
because of its predilection for these deep brain regions.3
While we report such a case, it is clear that primary HIV
infection in conjunction with neuroleptic therapy and
PML are other possibilities. The dystonia seen in these
disorders has a different pattern, and this pattern might
represent a clue for the underlying diagnosis.
Patients 1 and 2 had biopsy-proven PML. PML is a
common opportunistic infection of JC virus and is seen
in approximately 5% of AIDS patients4 as well as others
with immune compromise.5 The infection attacks the

1495

oligodendroglia, causing white matter lesions with intact
axons. The clinical symptoms depend on the location of
the lesion but most commonly include cognitive symptoms, focal, segmental or hemiweakness, and visual deficits due to the parieto-occipital lesions that occur. Extrapyramidal disease, including parkinsonism and
dystonia, do occur but are rare. Whereas a figure of 1 to
2% exists for parkinsonism,6,7 there are no estimates for
dystonia. The prognosis despite symptomatic treatment
is poor, with greater than 80% of patients dying within 1
year.4 Diagnosis requires brain biopsy.
One of our patients with PML had bilateral upper limb
dystonia combined with akinetic rigid symptoms and the
other had unilateral limb dystonia. Similar phenomena
have been described in several previous case reports.
Singer and colleagues8 reported a 13-year-old girl with
AIDS and PML who had a rapidly progressive akinetic
rigid syndrome, including postural instability, associated
with dystonic facial grimacing. She died after 10 months.
de Toffol and coworkers9 described a 31-year-old man
who presented with an akinetic rigid syndrome and, after
7 months, developed upper limb dystonia (bilateral and
asymmetric), myoclonus, and apraxia (unilateral). This
finding was followed by postural instability and alien
limb, and he ultimately died after 13 months. Two other
cases of dystonia without akinesia have also been reported. One case developed left hemiparesis and foot
dystonia,10 and the other case demonstrated right hyperreflexia and intermittent hemidystonia.11 These patients
died after 6 and 12 weeks, respectively. There have been
three other cases of PML-related dystonia in patients
who did not have AIDS. One patient had leukemia and
was immune-suppressed from his chemotherapy. He presented with upper limb hypokinesia but no rigidity and
progressed over 10 months to have unilateral rest tremor,
head tremor, bilateral hypokinesia, apraxia, freezing gait,
and facial and right arm dystonia.7 The other 2 patients
were not immune-suppressed (so-called primary PML).
One had a 5-year history of parkinsonism with all the
cardinal features, including freezing gait and memory
impairment before developing dystonia of the left foot.
With progression, she developed cognitive decline, including psychosis, apraxia, and generalized dystonia and
died after 10 years of illness (unusual for the length of
survival for PML).6 The last case was a 24-year-old
woman who presented with myoclonic jerks and several
months later developed tremor and dystonia of the left
hand. Weakness came 4 months later, and she died after
1 year of further progression.5 In some cases, the movement disorder was the presenting feature of PML,5,7,8
whereas others had the symptoms come on later. The

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S.A. FACTOR ET AL.

combination of parkinsonism, dystonia, myoclonus, and
apraxia are reminiscent of corticobasal ganglionic degeneration, and the diagnosis was entertained in some, but
the course is generally too fast. However, that combination of features should make one consider the diagnosis
of PML.
The dystonia occurred in some of these patients because of basal ganglia infiltration of the JC virus, and this
infiltration was demonstrated by MRI and postmortem
evaluation.4,8,10,11 However, several cases demonstrated
no lesions in this region by pathological examination,6,9
indicating that this finding is not required but makes it
difficult to explain the presence of dystonia. One had
parietal lesions and the other had frontal, temporal, and
occipital lesions, including the cortical gray matter. Our
patients did not have basal ganglia involvement by MRI
scan; however, they did have extensive white matter
lesions in the frontal, parietal, temporal, and occipital
regions. Without confirmation by postmortem examination, we will not know definitively if the JC virus spread
to the deep gray matter, but dystonia apparently can
occur in either case.
Our third patient had right-turning cervical dystonia
and right hemidystonia secondary to biopsy proven toxoplasmosis. This finding was probably secondary to the
left thalamic lesion, but he also had left frontal and right
caudate nucleus lesions on CT scan. Toxoplasmosis is
the most common central nervous system opportunistic
infection.3 The clinical features are protean with focal or
generalized or mixed neurological syndromes, depending
on the number, size, and location of the encephalitic
regions.3 The symptoms are not only the result of encephalitis but also edema, vasculitis, and hemorrhage.
The onset can be insidious, subacute, or acute in nature.
Our patient presented initially with the generalized findings of lethargy and stupor but then developed focal
findings. The movement disorder most commonly associated with toxoplasmosis is hemichorea/hemiballism,
which has been reported in several cases.12 It is usually
associated with an abscess in the subthalamic nucleus.
Other syndromes reported include parkinsonism from
bilateral basal ganglia disease, chorea, rubral tremor, and
akathisia.10,12 Dystonia is rare. We are aware of one other
case, reported by Tolge and Factor in 1991.13 That patient had a presumed diagnosis based on an elevated
toxoplasmosis titer, presence of multifocal subcortical
lesions, and response of those lesions to typical toxoplasmosis therapy. The patient had a focal arm and hand
dystonia secondary to lenticular nucleus and thalamic
abscesses. It was irreversible, despite appropriate therapy.

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

Cervical dystonia is rarely the result of focal lesions.
Meltzer14 reported another case of AIDS and cervical
dystonia but the CT scan was normal. A small number of
cases with various diagnoses causing focal lesions such
as stroke, arteriovenous malformation, traumatic infarction, and traumatic cerebral hemorrhage2,15–18 have been
implicated in symptomatic cervical dystonia. Usually,
the lesion is in the striatum contralateral to the direction
of turning. For our patient, the largest lesion was in the
ipsilateral striatum (caudate nucleus) but contralateral
thalamic or frontal lobe lesions may have played a role.
The fourth patient had AIDS dementia complex (also
referred to as HIV-associated dementia, or HAD) and
cervical dystonia presumed to be secondary to antipsychotic therapy. Evidence suggesting that included
chronic treatment with a neuroleptic for the previous 5
months, the occurrence of associated orofacial dyskinesia after withdrawal, and the occurrence of the toxoplasma lesion on the incorrect side (indicating noncausality). There are two key issues that relate to this patient.
First is the notion that HIV patients have an increased
susceptibility to extrapyramidal symptoms from neuroleptics. Second is that this patient developed dystonia
while being treated with an atypical antipsychotic.
There have been numerous case reports of acute-onset
parkinsonism and dystonia from dopamine antagonist
agents in AIDS.10,19 –24 In these cases, the doses of neuroleptics used were at a low or standard level, onset of
the movement disorder was often abrupt and progression
was rapid. The clinical features were often severe, some
were even life-threatening.22,23 They typically improved
with drug withdrawal; however, rechallenge led to recurrence, and in some cases, the disorder was persistent.
These cases suggested that there was an increased risk
for extrapyramidal symptoms in HAD patients treated
with dopamine-blocking agents, and this suggestion was
confirmed later by Hriso and colleagues.25 They retrospectively reviewed the medical records of 31 AIDS
patients and 32 non-AIDS psychiatric patients, all of
whom were treated with neuroleptics. The AIDS patients
had an estimated 2.4 times higher likelihood of experiencing parkinsonism or dystonia. This rate occurred despite the use of lower doses in the AIDS group.
There is increasing evidence supporting the notion that
this increased susceptibility is more than just an increased sensitivity to drug actions but is actually due to
selective vulnerability of the basal ganglia and, in particular, the dopaminergic system to the HIV infection.22,26 –28 That evidence is demonstrated by clinical,
neuroimaging, and neuropathology studies. Clinically,
approximately 15% of patients presenting with HAD are

DYSTONIA IN AIDS
parkinsonian.26 With regard to neuroimaging, MRI volumetric studies demonstrate reduction of the basal ganglia
volume out of proportion to generalized atrophy. Fluorodopa positron emission tomography demonstrates hypermetabolism of basal ganglia early in the course and
hypometabolism late when compared to cortical regions.
Proton MRI spectroscopy demonstrates decreased NAA/
choline ratio in the lenticular nucleus.26,28
Pathological studies demonstrate that basal ganglia
bear the brunt of infection with the findings of multinucleated giant cells, microglial nodules, and HIV-infected
microglia and macrophages being most prominent in the
caudate nucleus and putamen.26 –28 In addition, there is a
greater neuronal loss in the globus pallidus23 and substantia nigra.26 Immunohistochemistry studies have demonstrated high concentrations of certain structural envelope proteins (gp41 and gp120) and core proteins (p24
and Tat) of the HIV in the globus pallidus, striatum,
midbrain, thalamus, and dentate nucleus of the cerebellum.26 –28 Neurochemical studies have shown a decrease
in dopamine and homovanillic acid levels in the cerebrospinal fluid and striatum with normal levels of monoamines such as serotonin.26,28 Finally, it has been shown
that HIV RNA is not distributed uniformly in the brain in
patients with HAD. The basal ganglia represent one
region that is selectively infected by the HIV virus.29
Thus, the increased susceptibility to neuroleptics likely
relates to neuronal dysfunction and loss in the basal
ganglia, including substantia nigra, which causes an increased reaction to the dopamine receptor blockade
caused by the drugs.
The mechanism of neuronal death in these regions
remains an active area of investigation. The virus does
not infect the neurons directly, so the injury is likely
precipitated by indirect means. Several cellular toxins
released by infected macrophages, astrocytes, and microglia have been implicated, including cytokines (tumor
necrosis factor-a, interleukin-6), arachidonic acids,
quinolinic acid, and nitric oxide. In addition, several
structural and regulatory proteins of the HIV virus (gp41,
gp120, Tat, and Rev) have neurotoxic properties, which
could work independently or in tandem with the cellular
toxins. The evidence thus far points to a final common
pathway of excitotoxicity and possibly apoptosis as the
mechanisms of cell death.26,27
Our Patient 4 developed cervical dystonia while taking
the atypical antipsychotic risperidone. Previous cases of
drug-induced rigidity or dystonia were treated with standard neuroleptics or metoclopramide.10,19 –24 It would be
expected that atypical agents would be less likely to
cause this problem. However, in the case of risperidone,

1497

that may not be true. Although often considered atypical
because of its high affinity for 5HT receptors compared
to D2, it behaves pharmacologically like a typical
agent.30 Its propensity to worsen motor features of Parkinson’s disease supports this finding.31 There are no
data on olanzapine and quetiapine to this point in AIDS
patients. Because olanzapine worsens motor features of
PD in a manner similar to risperidone,31,32 it probably
should be avoided. Quetiapine may hold some promise
because it is relatively well tolerated in PD; however,
one must be cautious because it is suggested to worsen
parkinsonism in PD patients with dementia.33 One small
study of clozapine has demonstrated that patients can
tolerate it without developing parkinsonism, but we must
exercise caution because of its propensity to lower white
blood cell count, especially in a group already immunesuppressed.34
In conclusion, dystonia can occur as the result of
several causes in AIDS patients. The pattern of dystonia
seen may be a clue to the cause. With PML, dystonia
occurs in association with parkinsonism, myoclonus,
apraxia, and pyramidal tract signs reminiscent of corticobasal ganglionic degeneration. When toxoplasmosis is
the cause, the more common presentation is segmental or
hemidystonia most commonly affecting the limbs. And
with neuroleptics, one is more likely to see focal or
generalized dystonia.
LEGENDS TO THE VIDEO
Segment 1. Patient 1 is a 34-year-old man with dystonia of the left arm and hand. The fingers and thumb are
flexed. He has difficulty opening and closing the left fist
and performing other dexterous maneuvers and has increased tone. His left arm is internally rotated and has no
arm swing seen with walking.
Segment 2. Patient 2 is a 43-year-old man with
masked, astonished facial expression, bradykinesia, and
rigidity of the upper limbs and neck. His neck is anteriorly shifted. He has bilateral arm and hand dystonia,
worse on the left.
Segment 3. Patient 3 is a 44-year-old man with a right
CN III palsy, bilateral increased tone, right hemiparesis,
and myoclonus. He has cervical dystonia with rightturning torticollis and limited range of motion. Note the
hypertrophied left sternocleidomastoid. He also has right
hemidystonia.
Segment 4. Patient 4 is a 40-year-old woman with
late-stage AIDS dementia complex who developed cervical dystonia from risperidone. The videotaped examination demonstrates moderate torticollis and laterocollis

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S.A. FACTOR ET AL.

to the right, hypertrophy of the left sternocleidomastoid
muscle, and decreased range of motion.
Acknowledgments: This work was supported by the Albany
Medical Center Parkinson’s Research Fund and the Riley Family Chair of Parkinson’s Disease (S.A.F.).

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