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Journal of Parkinson’s Disease 12 (2022) 1727–1735
DOI 10.3233/JPD-223362
IOS Press
1727
Review
Parkinsonism-Hyperpyrexia Syndrome and
Dyskinesia-Hyperpyrexia Syndrome in
Parkinson’s Disease: Two Cases and
Literature Review
Jian-Yong Wanga, Jie-Fan Huanga, Shi-Guo Zhua, Shi-Shi Huanga, Rong-Pei Liua, Bei-Lei Hua,
Jian-Hong Zhub,∗and Xiong Zhanga,∗
aDepartment of Neurology, Institute of Geriatric Neurology, the Second Affiliated Hospital and Yuying Children’s
Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China
bDepartment of Preventive Medicine, Institute of Nutrition and Diseases, Wenzhou Medical University, Wenzhou,
Zhejiang, China
Accepted 20 June 2022
Pre-press 7 July 2022
Abstract. Parkinsonism-hyperpyrexia syndrome (PHS) and dyskinesia-hyperpyrexia syndrome (DHS) are rare but life-
threatening complications in Parkinson’s disease (PD). We herein presented two cases of PD patients and performed a
comprehensive and comparative literature review for these two syndromes. The first case was diagnosed as PHS with
cerebral salt wasting syndrome caused by abrupt withdrawal of antiparkinsonian medication. Her symptoms were gradually
remitted with reinstitution of the medication. The second one was an early-stage PD patient diagnosed as DHS in association
with abuse of antiparkinsonian drugs. Her symptoms were gradually remitted with reduced dosage of dopaminergic drugs.
Results of literature reviews revealed a total of 56 and 13 cases of PHS and DHS, respectively, and they were more likely to
occur in elderly and long-term PD patients. These two syndromes showed different female-to-male ratio, similar mortality,
and different recovery time. There were stark differences between PHS and DHS, including triggers (abrupt drug stoppage
versus drug abuse), symptoms (worsened tremor and rigidity versus continuous dyskinesia), and treatment (drug reinstitution
versus drug reduction). In summary, our reports and the review provide new insights into PHS and DHS in association with
PD and may facilitate rapid discrimination of the syndromes for timely and proper treatment to reduce mortality.
Keywords: Parkinsonism-hyperpyrexia syndrome, dyskinesia-hyperpyrexia syndrome, Parkinson’s disease, emergency, com-
plication
∗Corresponding authors: Xiong Zhang, M.D., Department of
Neurology, the Second Affiliated Hospital and Yuying Chil-
dren’s Hospital, Wenzhou Medical University, Wenzhou, Zhejiang
325027, China; E-mail: zhangxiong98@gmail.com and Jian-Hong
Zhu, Ph.D., Institute of Nutrition and Diseases, Wenzhou Medical
University, Biomedicine Research Building B305-B307, Wen-
zhou, Zhejiang 325035, China. E-mail: jhzhu@wmu.edu.cn.
BACKGROUND
Parkinson’s disease (PD) is a common neurode-
generative disease characterized by classical motor
features of parkinsonism and a progressive loss of
dopaminergic neurons in the substantia nigra pars
compacta. The clinical challenges of PD include dif-
ficulties to accurately diagnose at the earliest stage
ISSN 1877-7171 © 2022 – The authors. Published by IOS Press. This is an Open Access article distributed under the terms
of the Creative Commons Attribution-NonCommercial License (CC BY-NC 4.0).
1728 J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease
and to manage symptoms at later stages [1]. Acute
critical syndromes may occur in PD patients [2].
For instance, parkinsonism-hyperpyrexia syndrome
(PHS), also known as malignant syndrome or akinetic
crisis [3], is often caused by abrupt withdrawal of
dopaminergic drugs. Dyskinesia-hyperpyrexia syn-
drome (DHS), another acute complication of PD, was
first defined as an emergency in 2010 [4] and often
caused by antiparkinsonian drug abuse. Besides,
there are a number of other factors that provoke PHS
and DHS.
Both PHS and DHS are rare but life-threatening
complications of PD. Compared with PHS, DHS
is even rarer. Hyperthermia occurs in both PHS
and DHS. Although hyperthermia is believed to be
resulted from massive dyskinetic movements [4], it
is also considered to be attributed to dysfunction
of central thermoregulation [5]. Many pathological
processes in PD may result in abnormal thermoregu-
lation. Autonomic dysfunction, a common non-motor
symptom, may lead to abnormal sweating and skin
cooling in high temperature [6, 7]. Hypothalamic
dopamine release, which is disturbed in PD patients,
may increase when temperature rises [8]. Indeed,
autonomic dysfunction and altered metal status are
often observed in patients with PHS and DHS. How-
ever, pathological mechanisms by which PHS and
DHS occur in PD remain unclear.
Herein, we reported two cases of PD patients
who were diagnosed with PHS and DHS, as well as
performed a comprehensive literature review and a
comparative analysis of these two syndromes.
CASE DESCRIPTION
Case 1: PD with PHS
The patient was a 57-year-old woman with a
6-year history of PD. She had regular follow-up
visits to the Second Affiliated Hospital of Wen-
zhou Medical University. The patient has been
treated with pramipexole (0.75 mg/day) and madopar
(625 mg/day) since the age of 56. Her medical history
was unremarkable. The patient was transported to the
emergency department because she developed a con-
fusional state, fever, diaphoresis, and severe tremor.
Six days before, she discontinued the antiparkin-
sonian prescription drugs herself because of slight
dyskinesia.
In the emergency department with a confusional
state, her body temperature was 38.6◦C and heart
rate was 102 beats per minute. Neurological exam-
inations showed that she developed severe tremor
and rigidity on her four limbs, dysphagia, and
diaphoresis. Meningeal and other neurological signs
were unremarkable. Blood tests showed high crea-
tinine kinase level (465 IU/L), low serum sodium
level (119.7 mmol/L), and low serum uric acid level
(61 mol/L). Leukocyte number (5.08 ×109/L) was
within the normal range. Urinalysis showed nor-
mal urine specific gravity (1.024), high urine sodium
level (415.2 mmol per 24 h), and high urine chloride
level (415.7 mmol per 24 h). Bacteriological culture
of blood was negative.
We diagnosed the patient as PHS. The diagno-
sis of cerebral salt wasting syndrome (CSWS) was
based on low serum levels of sodium and uric acid,
normal urine specific gravity, and high urine levels
of sodium and chloride. For PHS, she was treated
with madopar (250 mg; thrice daily) via a nasogas-
tric feeding tube and sedated with benzodiazepines.
For CSWS, she was given intravenous fluids and
sodium supplementation. During the hospitalization,
the patient developed pulmonary infection and uri-
nary tract infection such that antibiotics were also
administered. Her clinical conditions were worsened
in the first few days but were then gradually improved.
Her body temperature returned to 37.0◦C on day
22 after the hospitalization. The leukocyte number
rose in the first three days and returned to normal
on day 4. The rise and recovery might be caused by
the infection and the use of antibiotics, respectively.
Creatinine kinase and serum sodium levels became
normal on day 7 and day 18, respectively. As a note,
serum sodium level was declined from day 2 to day
4 even with sodium supplementation. Because her
tremor was remitted on day 4, we prescribed the
patient with madopar (625 mg/day) and pramipexole
(0.75 mg/day). Since then, her rigidity and mental
state were improved steadily. On day 23, she was
able to follow instructions and perform rehabilita-
tion training. She has been taking antiparkinsonian
medication as prescribed and returning for follow-
up visits regularly since being discharged from the
hospital.
Case 2: PD with DHS
The patient aged 74 when she visited the Second
Affiliated Hospital of Wenzhou Medical University
and was diagnosed as PD. We treated the patient with
piribedil (150 mg/day) and selegiline (10 mg/day)
and she did not show symptoms of motor fluctuation.
J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease 1729
She had displayed bradykinesia and resting tremor in
her left limbs in the past 4 years. Her medical history
included hypertension, diabetes, and osteoporosis.
In a September afternoon, the patient was transported
to the emergency department due to severe chor-
eiform dyskinesia, hyperthermia, and hallucination
in the past 9 hours. Prior to the emergency visit,
the patient disregarded doctor’s prescription and took
madopar (1500 mg/day; prescribed from another hos-
pital) and selegiline (30 mg/day) by her own decision
for 3 consecutive days.
In the emergency department, she was in a confu-
sional state with hallucination. Her body temperature
was 39.7◦C and heart rate was 123 beats per minute.
Neurological examinations revealed continuous
dyskinesia over her head, trunk, and four limbs, with
her skin being sweaty. Meningeal and other neuro-
logical signs were unremarkable. Blood tests showed
high levels of creatinine kinase (821 IU/L), myohe-
moglobin (1937 ng/mL), and leukocytes (13.36 ×
109/L). Aspertate aminotransferase and creatinine
levels were slightly elevated (49 U/L and 101 mol/
L, respectively). Chest computerized tomography
and cranial magnetic resonance imaging were neg-
ative. Bacteriological culture of blood was negative.
We diagnosed the patient as DHS. She was sedated
with intravenous midazolam infusion and hydrated
with normal saline. Oral antiparkinsonian drugs
were suspended on day 0. In an attempt to pre-
vent from being rebounded to PHS, we monitored
the patient’s condition and gave her a small dose of
madopar (62.5 mg) when mild parkinsonism symp-
toms appeared. Physical antipyretic measures were
administered to lower her body temperature. Since
then, her clinical condition had gradually improved.
The hallucination disappeared on day 2. On day
4, her body temperature (37.2◦C) and leukocyte
number (7.79 ×109/L) were back to normal. Her
dyskinesia was remitted completely on day 5. Cre-
atinine kinase and myohemoglobin levels became
normal on day 14 (207 IU/L and 165 ng/mL, respec-
tively). Before she was discharged from the hospital,
we prescribed her with a low dose of madopar
(250 mg/day). Since then, the patient has been
taking antiparkinsonian medication as prescribed
and showing stable conditions in the telephone
follow-ups.
The study was approved by the Ethics Commit-
tee of the Second Affiliated Hospital and Yuying
Children’s Hospital, Wenzhou Medical University.
Written informed consents for publication were
obtained from the patients.
LITERATURE REVIEW AND DISCUSSION
PD patients may experience life-threatening com-
plications such as PHS and DHS. These two
syndromes share significant similarities but also show
major differences in several aspects including causes,
clinical manifestations, and treatments. As summa-
rized in Fig. 1, we herein present two cases of patients
who developed PHS or DHS. We then review all
known up-to-date cases of PHS and DHS in PD and
provide a comparative analysis of these two syn-
dromes.
Literature related to PHS and DHS in PD were
searched in Medline via PubMed up to May 1, 2022.
The searching term for PHS was “(((((neuroleptic
malignant-like syndrome) OR (Neuroleptic-like
Malignant Syndrome)) OR (Parkinson hyperpyrexia
syndrome)) OR (Parkinsonism hyperpyrexia syn-
drome)) OR ((((Parkinson’s Disease[Title/Abstract])
OR (Parkinson Disease[Title/Abstract])) OR
(Parkinsonism[Title/Abstract])) AND (((((Fever)
OR (Hyperpyrexia)) OR (Pyrexia)) OR (Pyrex-
ias)) OR (malignant syndrome))))”. The searching
term for DHS was “(((((fever[Title/Abstract]) OR
(hyperpyrexia[Title/Abstract])) OR (pyrexia[Title/
Abstract])) OR (pyrexias[Title/Abstract])) AND
(((dyskinesia[Title/Abstract]) OR (dyskinesias[Title/
Abstract])) OR (hyperkinetic[Title/Abstract])))”.
To increase search hits, the “Parkinson”-associated
terms were not included for the DHS search. As a
result, 688 and 141 literatures on PHS and DHS
were obtained, respectively. After additional title
and abstract screening, we eventually retrieved 48
articles for PHS and 9 for DHS (Supplementary
Tables 1 and 2).
PHS was first described as a neuroleptic malignant
syndrome-like syndrome in a PD patient after discon-
tinuation of his antiparkinsonian medication [9]. As
summarized in Table 1 and Supplementary Table 1
including our case, 56 such cases have been reported
since 1981 and twenty-four of them are women
[10–56]. The onset of PHS ranges from 43 to 79 years
of age with PD duration between 1 to 25 years. Seven
of the reports with 10 patients recorded the onset of
PHS in summertime [10, 11, 16, 17, 23, 26, 50]. The
most common cause of PHS is determined to be the
reduction or withdrawal of antiparkinsonian medica-
tion (26 cases), followed by battery depletion of deep
brain stimulation (DBS) impulse generator (7 cases).
Other triggers include experiencing the “Off” state,
premenstrual period, diabetic coma, heatwave, ces-
sation of fava bean intake, hyponatremia, infection,
1730 J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease
Fig. 1. Summary of the symptoms and treatments for these two cases. Day 0, the day of hospitalization; dashed arrow line, taken when
needed; solid arrow line, taken daily; dark patterns, reduced severity with lower height.
constipation, diarrhea, and drinking too little fluids. In
recent years, the DBS surgery number for PD patients
has been increasing dramatically. Thus, it should be
brought into attention as to the likelihood of PHS due
to perioperative antiparkinsonian drug discontinua-
tion and DBS stimulator battery depletion. Given the
relatively long operation time of DBS, anesthesia,
surgery, and stress may become potential triggers for
PHS. It may be important to maintain a certain dose
of antiparkinsonian medication during the periopera-
tive period. Compared with traditional drug therapy,
the efficacy of DBS is more effective and stable to
control parkinsonism. As a result, follow-up visits of
such patients may become irregular. Therefore, clini-
cians should remind patients to have follow-up visits
regularly as well as to warn them of potentially severe
outcomes if the battery power is depleted.
The main clinical manifestations of PHS are
hyperthermia, worsened tremor and rigidity, altered
mental status, autonomic dysfunction, and diaphore-
sis (Table 1 and Supplementary Table 1). Other less
common symptoms include dysphagia, myoclonus,
J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease 1731
Table 1
Comparative analysis of PHS and DHS in PD patients
PHS DHS
Subject, n 56 13
Gender, F/M 24/32 10/3
Age, y (mean ±SD) 63.2 ±9.2 71.3 ±6.0
PD duration, y (mean ±SD) 12.0 ±5.8 17.1 ±8.2
Mortality, n (%) 12 (21.4) 2 (15.4)
Recovery ratio, n (%) 44 (78.6) 11 (84.6)
Recovery time, days (IR)a13 (5–22) 4 (3.5–6)
Triggers (%)bReduction/withdrawal of antiparkinsonian
medication (46.4)
Antiparkinsonian drug change/abuse (38.5)
Battery depletion of DBS impulse generator (12.5) Heatwave (38.5)
Heatwave (5.4) Infection (23.1)
Constipation/diarrhea (5.4) Trauma (15.4)
Infection (3.6) Gastrointestinal dysmotility (7.7)
Premenstrual period (1.8)
Diabetic coma (1.8)
Experience of the “Off” state (1.8)
Hyponatremia (1.8)
Without common trigger (16.1)
Manifestations (%)bHyperthermia (98.2) Hyperthermia (100)
Worsened tremor and rigidity (94.6) Continuous dyskinesia (100)
Altered mental status (73.2) Altered mental status (76.9)
Autonomic dysfunction (76.8) Autonomic dysfunction (46.2)
Diaphoresis (48.2) Diaphoresis (23.1)
Myoclonus (7.1) Dehydration (15.4)
Rhabdomyolysis (5.4) Rhabdomyolysis (15.4)
Dystonia (3.6)
Dehydration (3.6)
Treatments Reinstitution of antiparkinsonian medication, vital
function support, intravenous fluids, antipyretic
drugs, and physical antipyretic measures
Reduction of dopaminergic drugs, vital function
support, intravenous fluids, antipyretic drugs, and
physical antipyretic measures
aThe recovery time with an exact number is included for calculation. bThe percentage numbers are calculated in relation to the total subjects.
DBS, deep brain stimulation; DHS, dyskinesia-hyperpyrexia syndrome; F, female; IR, interquartile range; M, male; PHS, parkinsonism-
hyperpyrexia syndrome; SD, standard deviation.
rhabdomyolysis, dystonia, and dehydration. Our
patient is additionally diagnosed with CSWS. Hypo-
natremia has been reported in another case and con-
sidered as a cause of PHS [28]. We believe that
hyponatremia is an outcome of CSWS resulting
from PHS because serum sodium level continues to
decline within the first four days even with sodium
supplementation to the patient. The treatment of
PHS includes vital function support, reinstitution
of antiparkinsonian medication, intravenous flu-
ids, empiric antibiotics, benzodiazepines, antipyretic
drugs, and physical antipyretic measures. Among the
56 cases, 12 patients died shortly or in a few days
and 44 patients were recovered from the symptoms
within 2–32 days.
A total of 13 PD patients with DHS has been
reported including our case [4, 5, 57–63] (Table 1 and
Supplementary Table 2). The onset of DHS ranges
from 62 to 80 years of age, and 10 of them are women.
According to 4 reports, 6 patients developed the syn-
drome in summer [5, 59–61]. Two cases including
ours occurred in early autumn when the ambient tem-
perature might still be relatively high [57]. Indeed,
heatwave is one of the common triggers of DHS. It has
been conceived that DHS usually occurs in advanced
PD patients [64], with disease duration ranging from
10 to 34 years. Nonetheless, our case suggests that
DHS may also occur in early-stage PD patients.
Two most common provocation factors for DHS
are antiparkinsonian drug change or abuse and heat-
wave (5 cases each; Table 1 and Supplementary
Table 2). Excessive dopaminergic stimulation is
destructive given that PD patients are defective in
the maintenance of dopamine status. Other DHS trig-
gers include infection, trauma, and gastrointestinal
dysmotility. Clinical manifestations of DHS include
hyperthermia, continuous dyskinesia, altered mental
status, and to a less extent, autonomic dysfunc-
tion, diaphoresis, dehydration, and rhabdomyolysis.
The treatment of DHS includes vital function sup-
port, reduction of dopaminergic drugs, intravenous
infusions, antipyretic drugs, and physical antipyretic
1732 J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease
Box 1. Suggested diagnostic criteria and management schemes for PHS
Diagnosis
1. Clear triggers before the onset. These include reduction/withdrawal of antiparkinsonian medication, battery
depletion of DBS impulse generator, and heatwave. Of note, a small percentage of patients may lack any of
such triggers.
2. Core clinical manifestations are required. These include hyperthermia, worsened parkinsonism, and elevated
creatinine kinase.
3. At least two of the following clinical manifestations are required. These include altered mental status,
autonomic dysfunction, diaphoresis, myoclonus, rhabdomyolysis, dystonia, and dehydration.
4. The following conditions should be excluded: neuroleptic malignant syndrome, serotonin syndrome,
dyskinesia-hyperpyrexia syndrome, heat stroke, intracranial infection, autoimmune encephalitis, septicemic
shock, drug intoxication, and thyroid crisis.
5. An alternative syndrome should be considered if the expert physician, based on full clinical manifestations
and auxiliary assessments, feels that an alternative condition is more likely than PHS.
Management
1. Treat the underlying triggers immediately.
2. Provide adequate supportive treatments including vital function support, intravenous fluids, antipyretic
drugs, and antipyretic measures.
3. Antibiotics treatment is not necessary, but spectrum antibiotics should be applied immediately if the patient
is infected.
4. Oral or nasogastric dopaminergic drugs should be used immediately when the diagnosis of PHS is confirmed.
5. Delirium in patients should be treated with intravenous benzodiazepines infusion (Taken when needed).
6. If the patient develops multiple organ failure, intensive care unit treatment and multidisciplinary care should
be initiated immediately.
measures. Among the 13 cases, 2 patients died in a
few days due to pneumonia and renal failure or acute
pulmonary edema [60]. The remaining 11 patients
were recovered within 2–10 days.
Both PHS and DHS are prone to occur in elderly
PD patients with long disease duration (Table 1).
Although DHS mainly occurs in females, PHS is pre-
dominantly found in males. The recovery rate for both
syndromes is about 80% despite a faster recovery in
DHS than in PHS patients. Clinical manifestations of
PHS and DHS are mostly similar, including raised
creatinine kinase. The raised kinase level may occur
in rhabdomyolysis, myositis, myocardial infarction,
muscular dystrophy, etc. Diagnosis of rhabdomyoly-
sis requires not only high creatinine kinase but also
elevated myohemoglobin in blood and urine. Thus,
raised creatinine kinase alone does not mean the
occurrence of rhabdomyolysis, which is only present
in a small percentage of PHS and DHS cases. How-
ever, a stark difference between these two syndromes
is that worsened tremor and rigidity is dominated in
PHS, but continuous dyskinesia is exclusively found
in DHS patients. PHS may be induced by abrupt
stoppage in the antiparkinsonian treatment such
as drug withdrawal or DBS stimulator power loss
whereas DHS is plausibly induced by the abuse
of antiparkinsonian drugs. Accordingly, the primary
treatment for PHS is drug reinstitution and for DHS
is drug reduction. Other auxiliary treatments are basi-
cally alike. Therefore, careful inquiry of medication
history and appropriate neurological examinations
are indispensable for rapid recognition and treatment
of the syndromes. No diagnostic criteria are available
for these two conditions to the best of our knowl-
edge. We herein suggest diagnosis criteria for PHS
(Box 1) and DHS (Box 2) based on the reported cases
and our aforementioned rationales. Structured sug-
gestions are also provided toward the management
of PHS (Box 1) and DHS (Box 2) for the reference
of clinicians.
The mortality rates of the reported cases are 21.4%
and 15.4% for PHS and DHS, respectively (Table 1).
Among the 14 deceased patient cases (Supplemen-
tary Tables 1 and 2), there are a total of 12 aged 50
or older and 12 with more than 9 years of PD dura-
tion, respectively. The causes of death and number are
J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease 1733
Box 2. Suggested diagnostic criteria and management schemes for DHS
Diagnosis
1. Clear triggers before the onset. These include antiparkinsonian drug change/abuse, heatwave, infection,
trauma, and gastrointestinal dysmotility. Of note, a small percentage of patients may lack any of such
triggers.
2. Core clinical manifestations are required. These include hyperthermia, continuous dyskinesia, and elevated
creatinine kinase.
3. At least one of the following clinical manifestations are required. These include altered mental status,
autonomic dysfunction, diaphoresis, dehydration, and rhabdomyolysis.
4. The following conditions should be excluded: neuroleptic malignant syndrome, serotonin syndrome,
parkinsonism-hyperpyrexia syndrome, heat stroke, intracranial infection, autoimmune encephalitis, septice-
mic shock, drug intoxication, and thyroid crisis.
5. An alternative syndrome should be considered if the expert physician, based on full clinical manifestations
and auxiliary assessments, feels that an alternative condition is more likely than DHS.
Management
1. Treat the underlying triggers immediately.
2. Provide adequate supportive treatments including vital function support, intravenous fluids, antipyretic
drugs, and antipyretic measures.
3. Antibiotics treatment is not necessary, but spectrum antibiotics should be applied immediately if the patient
is infected.
4. Carefully reduce antiparkinsonian drugs while avoiding rebound to PHS.
5. Delirium in patients should be treated with intravenous benzodiazepines infusion (Taken when needed).
6. If the patient develops multiple organ failure, intensive care unit treatment and multidisciplinary care should
be initiated immediately.
hyperthermic coma (3), respiratory failure (10), renal
failure (7), heart failure (3), disseminated intravascu-
lar coagulation (2), and septicemic shock (1). These
data suggest that patients of older age and longer dis-
ease duration may be more susceptible to develop
multisystem organ failure and malignant outcome.
Because some cases may have died before being diag-
nosed as PHS or DHS and some may be reluctant to
get the death endpoint to be published, the mortality
is likely to be underreported. Patients may be treated
on general wards in general. But with the mortality
rate as high as it is, we recommend treating the under-
lying triggers immediately with adequate supportive
treatments. Those with multiple organ failure should
be immediately initiated for intensive care unit treat-
ment and multidisciplinary care in monitored settings
to reduce potential mortality (Boxes 1 and 2).
In summary, we herein present two cases of PD
patients with hyperpyrexia. One was PHS coupled
with CSWS caused by abrupt withdrawal of the
antiparkinsonian medication, and the other was drug
abuse-induced DHS occurred in early-stage PD. Our
reports and the comparative review provide new and
updated insights into PHS and DHS in PD and may
facilitate rapid discrimination of the syndromes for
timely and proper treatment to reduce mortality.
ACKNOWLEDGMENTS
The authors are grateful to hospital personnel
who took care of the patients. The study was
supported in part by fundings from Wenzhou Munic-
ipal Science and Technology Bureau (Y2020065,
and Y20180136), Fundamental Research Funds for
Wenzhou Medical University (KYYW202030), and
Novel Technology Program of the Second Affiliated
Hospital and Yuying Children’s Hospital (2022014).
CONFLICT OF INTEREST
The authors declare that there is no potential con-
flict of interest.
SUPPLEMENTARY MATERIAL
The supplementary material is available in the
electronic version of this article: https://dx.doi.org/
10.3233/JPD-223362.
1734 J.-Y. Wang et al. / PHS and DHS in Parkinson’s Disease
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