CASE REPORT

Heatstroke in patients with Parkinson’s disease

Satoshi Yamashita • Yuji Uchida • Sachi Kojima •

Hideya Sakaguchi • En Kimura • Yasushi Maeda •

Makoto Uchino

Received: 16 October 2010 / Accepted: 28 October 2011 / Published online: 6 November 2011

� Springer-Verlag 2011

Abstract We present two Parkinson’s disease (PD)

patients, who experienced heatstroke. Both patients mani-

fested central nervous system dysfunction with elevated

core temperature. Despite adequate lowering of the body

temperature, multiorgan-dysfunction syndrome including

encephalopathy, rhabdomyolysis, acute renal failure, acute

respiratory failure, and disseminated intravascular coagu-

lopathy was noted in one patient, leading to permanent

neurologic damage. Because the ensuing multiorgan

dysfunction could determine the functional prognosis in

heatstroke patients, it is important to provide information

about the prevention of heatstroke to patients, who are

isolated or are severely disabled in the advanced stages

of PD.

Keywords Heatstroke � Parkinson’s disease �Dyshidrosis � Thermoregulatory failure �Heat-shock proteins

Introduction

Heatstroke is characterized by elevated core temperature

(above 40�C) and CNS dysfunctions such as delirium,

convulsions, or coma [1]. Heatstroke is often fatal, and

survivors may sustain permanent neurologic damage

despite adequate lowering of the body temperature [2]. We

present two PD patients, who experienced heatstroke.

Case reports

Patient 1

A 75-year-old woman had a 10-year history of PD with

dementia, treated with 150 mg/day levodopa alone because

of hallucination, with Hoehn and Yahr (H/Y) [3] stage 5 in

on and off states. She presented with appetite loss on 26 July

2008, during environmental heat wave. Although she had

medicine the previous day, on the morning of 29 July, her

family found her unconscious in a room with no air-con-

ditioning. On admission, she was comatose (Glasgow Coma

Scale 7 [GCS; eye response (E), 2; verbal response (V), 1;

motor response (M), 4]), with severe bradykinesia, usual

level of rigidity, and H/Y stage of 5. Blood pressure was

150/100 mmHg; heart rate, 170–180 beats/min; and rectal

temperature, 40.1�C. Laboratory tests revealed no inflam-

mation with hemoconcentration (hemoglobin, 16.7 g/dl;

hematocrit, 49.4%). Serum levels of creatinine, blood urea

nitrogen, and sodium ion were elevated at 1.14 mg/dl,

37.2 mg/dl, and 155 mEq/l, respectively. After rapid cold

saline infusion with ice pack application, core temperature

decreased to approximately 36�C at 4 h after treatment. The

usual dose of levodopa was administered through a naso-

gastric tube after hospitalization. Despite prompt cooling,

she did not regain consciousness. She was then intubated,

underwent iced gastric lavage, and transported to the

intensive care unit (ICU). Hypernatremia and prerenal

failure were stabilized by continuous saline infusion on the

second day. After extubation, the respiratory and circula-

tory systems were normal, but the patient remained coma-

tose with bradykinesia and H/Y stage of 5. Myocardial

imaging with 123I-metaiodobenzylguanidine (MIBG)

revealed a markedly reduced uptake, suggestive of cardiac

sympathetic denervation.

S. Yamashita (&) � Y. Uchida � S. Kojima � H. Sakaguchi �E. Kimura � Y. Maeda � M. Uchino

Department of Neurology, Faculty of Life Sciences,

Kumamoto University, 1-1-1 Honjo,

Kumamoto 860-8556, Japan

e-mail: y-stsh@kumamoto-u.ac.jp

123

Neurol Sci (2012) 33:685–687

DOI 10.1007/s10072-011-0842-7

Patient 2

A 60-year-old man had a 23-year history of PD, treated with

300 mg/day levodopa, 200 mg/day amantadine, 5 mg/day

selegiline, 150 lg/day pergolide, and 100 mg/day quetia-

pine, with H/Y stage of 4 in on and off states. Since May

2006, with his wife’s assistance, he had food and medicines.

His living environment was hot with no air-conditioning.

He had slight fever since 3 August 2006, during environ-

mental heat wave. Six days later, he was found febrile and

unconscious. On admission, the patient was comatose [GCS

6 (E, 1; V, 1; M, 4)] with high rectal temperature (42�C),

and respiratory and cardiovascular failure (blood pressure,

58/32 mmHg; heart rate, 160 beats/min) was noted. His

muscle tonus was hypotonic, but Babinski and Chaddock

signs were positive bilaterally. He was immediately intu-

bated, mechanically ventilated, and transported to the ICU.

He underwent continuous cold saline infusion and ice pack

application. The usual dose of anti-parkinsonian medicine

was administered via a nasogastric tube. On the second day,

core temperature decreased to 36.5�C and blood pressure

normalized. However, he did not regain consciousness, and

disseminated intravascular coagulopathy and rhabdomyol-

ysis were noted. An intensive medical treatment including

platelet transfusions and continuous hemodiafiltration was

initiated. He underwent tracheostomy, following which the

respiratory and circulatory systems gradually recovered. On

the 13th day, he remained comatose with brainstem

reflexes, with severe bradykinesia and H/Y stage of 5. EEG

revealed diffuse, low-amplitude, slow waves, although

brain MRI revealed mild atrophy of the bilateral fronto-

temporal lobe. Two years after the onset of heatstroke, the

patient remained comatose. At this point, EEG still showed

diffuse, low-amplitude, slow waves.

Discussion

We present two PD patients, who suffered from heatstroke.

It has been reported previously that many patients with PD

tolerate extremes of temperature poorly. PD patients with

fatal heatstroke were described shortly in several reports

[4]. In the pathophysiology of heatstroke, thermoregulatory

failure, exaggeration of the acute phase response, and

alteration in the expression of heat-shock proteins has been

suggested to contribute to the progression from heat stress

to heat stroke. Thus, we may explain the vulnerability of

PD patients to heatstroke by several possibilities: PD

patients especially with severe locomotive disability or

cognitive decline tend to be unable to avoid heat stress.

Anti-cholinergic agents such as trihexyphenidyl could

interfere with salt and water balance by impairing sweat-

ing. An altered expression of heat-shock proteins might be

present in PD patients because of chaperoning some mis-

folded proteins.

Furthermore, we speculated that hyperthermia could be

initially induced by heat retention caused by dyshidrosis

associated with PD in these two cases. Many reports show

that 30–50% of PD patients experience sweating distur-

bances such as hyperhidrosis and hypohidrosis [5]. Some

studies using a hydrograph showed that a decrease in

sweating of the lower limb was associated with the severity

of motor impairment associated with PD [6]. There is

evidence indicating that the origin of dyshidrosis was CNS

including the hypothalamus, the dorsal vagal nucleus, and

the intermediolateral cell column [7]. However, others [8]

imply that the hypohidrosis might be postganglionic, and

this may be explained by the reduced uptake of myocardial

MIBG in patient 1. Therefore, PD may be a risk factor for

thermoregulatory failure, especially in the advanced stages.

We should rule out the diagnoses of malignant syn-

drome and acute akinesia: the most prominent thermoreg-

ulatory abnormality on PD patients. Takubo et al. [9]

defined malignant syndrome as a condition affected by

severe worsening of parkinsonian symptoms, akinesia, and

fever as a consequence of treatment withdrawal. In their

report, 55% of the episodes appeared to have been induced

by inadequate drug intake, whereas the rest of events were

triggered by intercurrent infections, anorexia, reduced food

intake, and even hot weather alone. Onofrj et al. [10]

reported that acute akinesia is a syndrome characterized by

sudden onset, extreme akinesia with aphagia, rise of tem-

perature, duration of several days and fatal outcome if no

infusion therapy is initiated. In their paper, the patients

were divided into two groups because of the different

precipitating factors: the group who presented acute

akinesia which could not be attributed to drug absorption

alterations, and the other group whose akinesia could

hypothetically be dependent on insufficient drug avail-

ability. Thus, both the malignant syndrome and acute

akinesia are likely to be heterogeneous condition, which

could be overlapped with heatstroke with regard to the

pathophysiology. Although the present patients showed

severe loss of consciousness without increased rigidity at

the onset, which would be rarely seen in patients with

malignant syndrome [9], it may be impossible to exclude

the possibility of coexisting malignant syndrome fully.

So far, few studies have focused on the susceptibility of

PD patients to heatstroke. We should note that the ensuing

multiorgan dysfunction could determine the functional

prognosis in heatstroke patients. Because normalizing body

temperature does not prevent inflammation, coagulation, and

progression to multiorgan dysfunction after the onset of

heatstroke [1], use of immunomodulators or agents that

activate heat-shock proteins should be considered, especially

when critical condition is likely to be attributable to release

686 Neurol Sci (2012) 33:685–687

123

of cytokines accompanied by inflammatory reactions. The

incidence of heatstroke in PD patients might increase with

the rise in temperatures due to global warming. Therefore, it

is important to provide information about the prevention of

heatstroke to patients, who are isolated or are severely

disabled in the advanced stages of PD.

Acknowledgments This work was partly supported by Grants-in-

Aid from the Research Committee of CNS Degenerative Disease, the

Ministry of Health, Labour and Welfare of Japan.

Conflict of interest The authors certify that there is no current or

potential conflict of interest in relation to this article.

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