A Schizophrenic Patient Who Developed Extreme Hypothermia after an Increase in the Dose of Haloperidol: A Case Report

Harada, Hiroyuki; Igarashi, Mikio; Sugae, S; Okamoto, Kenichi; Tsuji, Motohiro; Nakajima, Teruo

doi:10.1111/j.1440-1819.1994.tb03020.x

Cited by 14 publications

(10 citation statements)

References 7 publications

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“…However, anecdotal reports, caseseries studies and some small-sample, controlled animal studies (Adler and Geller, 1987 ;Boules et al, 2001 ;Catalina et al, 2002 ;Fjalland, 1979) and human studies (Eikenboom et al, 1997 ;Harada et al, 1994 ;Heh et al, 1988 ;Maeir et al, 1994 ;Shiloh et al, 2000 ;Yehuda, 1977) suggest that APDs can decrease body temperature, possibly via a direct effect on central (possibly hypothalamic) thermoregulatory effectors, or indirectly by reducing the levels of pyrogenic cytokines such as IL-1b, IL-6 and TNF-a (Kowalski et al, 2001 ;Monteleone et al, 1997). Since corneal temperature may correlate with core body temperature (Mapstone, 1968 ;Scott, 1988), our findings may further substantiate some of these previous reports which implied higher baseline core temperature in drug-free patients compared to APD-treated schizophrenia patients (Heh et al, 1988 ;Morgan and Cheadle, 1976 ;Shiloh et al, 2000Shiloh et al, , 2001.…”

Section: Discussionmentioning

confidence: 97%

“…However, neuroleptictreated schizophrenia patients may also exhibit hypothermia (Heh et al, 1988 ;Laborit, 1979 ;Maeir et al, 1994 ;Schwaninger et al, 1998), a within-normal range decrease , or increase Shiloh et al, 2001) in core body temperature as well as various hyperthermic syndromes such as febrile catatonia, neuroleptic malignant syndrome (NMS) (Lazarus et al, 1989) or neuroleptic-related heat stroke (Dixit et al, 1997). Nevertheless, accumulating data indicate that APDs may also lower baseline core body temperature (within normal range) (Harada et al, 1994 ;Heh et al, 1988 ;Maeir et al, 1994 ;Shiloh et al, 2000 ;Yehuda, 1977) and especially during the initial hours/days of administration (Clark, 1979 ;Shiloh et al, 2000). It was even anecdotally suggested that the therapeutic effect of APDs might correlate with a decrease in core body temperature of schizophrenia patients (Heh et al, 1988), and that typical APDs might differ from atypical APDs by their diverse effect on core body temperature (Bauer and Gaertner, 1983 ;Wahlbeck et al, 2000).…”

Section: Introductionmentioning

confidence: 93%

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Corneal temperature in schizophrenia patients

Shiloh

Munitz

Portuguese

et al. 2005

Int. J. Neuropsychopharm.

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Most data imply that dopaminergic transmission is essential for proper hypothalamic-mediated core temperature regulation. Altered central dopaminergic transmission is suggested to be involved in the pathophysiology of schizophrenia. Thus, hypothetically, schizophrenia patients might be at increased risk of developing thermoregulatory dysregulation manifested by alterations in core temperature, as well as in peripheral tissue, the temperature of which has been shown to correlate with core temperature (e.g. cornea). Previous small pilot studies of ours showed that schizophrenia patients may exhibit corneal temperature abnormalities. Hence, we assessed corneal temperature in a controlled sample of drug-free ( n =11) and medicated ( n =28) schizophrenia patients compared to healthy comparison subjects ( n =9), using a FLIR thermal imaging camera. Drug-free schizophrenia patients exhibited significantly higher corneal temperature compared to healthy subjects, typical antipsychotic drug (APD)-treated patients ( n =16) and atypical APD-treated patients ( n =12) (37.08+/-1.46 degrees C vs. 33.37+/-2.51 degrees C, 31.08+/-1.43 degrees C and 31.67+/-0.44 degrees C respectively, p <0.0001; p <0.001 vs. each group separately). The healthy comparison subjects and the atypical APD-treated patients exhibited comparable corneal temperatures and these two groups exhibited higher corneal temperatures compared to the typical APD-treated patients ( p <0.01 and p =0.051 respectively). In conclusion, this study indicates that drug-free schizophrenia patients exhibit substantially higher corneal temperature compared to healthy comparison subjects or medicated patients, and that APDs may decrease corneal temperature either to normal (atypical APD) or to subnormal (typical APD) values. The relevance of these phenomena to the pathophysiology of schizophrenia, the biological mechanism underlying drug-induced corneal temperature alterations, the possible role of temperature-lowering drugs (neuroleptics or non-neuroleptics) on schizophrenic psychosis as well as the role of corneal temperature as a tool to evaluate adherence to APD treatment merit further investigation via larger samples of both medicated and drug-free schizophrenia patients compared to matched controlled subjects.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 93%

Corneal temperature in schizophrenia patients

Shiloh

Munitz

Portuguese

et al. 2005

Int. J. Neuropsychopharm.

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“…The references cited in their communication are so important that they are listed again here. [6][7][8][9][10][11] According to his family, the patient presented here was not known to be taking any antipsychotic or neuroleptic drugs, and no pill bottles were found on his person or in his hotel room.…”

Section: Hypothermia Due To Neuroleptic Drugsmentioning

confidence: 99%

Osborn waves in the electrocardiogram, hypothermia not due to exposure, and death due to diabetic ketoacidosis

Sheikh

Hurst

2003

Clinical Cardiology

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Summary:Hypothermia usually occurs because a patient has been exposed to a cold environment; however, a number of nonenvironmental conditions may produce hypothermia. This report relates the clinical course of a patient whose hypothermia was due to severe diabetic ketoacidosis. In addition, we review the causes of hypothermia and Osborn waves beyond exposure to cold temperature. Hypothermia due to diabetic ketoacidosis is an uncommon complication of a common disease that carries with it clinically significant consequences. Accordingly, we believe that all clinicians should be aware of this potential complication of diabetic ketoacidosis and should be able to recognize the importance of the electrocardiogram in such patients.

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“…Festzuhalten ist, dass Hypothermien im Zusammenhang mit der Gabe verschiedenster Antipsychotika mit unterschiedlichen Rezeptorprofilen sowohl für typische als auch atypische Substanzen beschrieben wurden [15,32,37].…”

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Hypothermie unter Olanzapin

et al. 2011

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A review of the current literature reveals that thermoregulatory disturbances as sequelae of antipsychotic drug administration depend on individual disposition as well as various independent risk factors such as environmental temperature, somatic comorbidities, endocrinological abnormalities (e.g. hypothyroidism) and structural damage of the brain. A complex interaction of dopaminergic regulatory mechanisms in the ventral hypothalamus and peripheral vaso- and sudomotor adjustments seems to be causative. Hypothermia following antipsychotic drug administration represents a serious adverse drug reaction and a potentially life-threatening event.

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A Schizophrenic Patient Who Developed Extreme Hypothermia after an Increase in the Dose of Haloperidol: A Case Report

Cited by 14 publications

References 7 publications

Corneal temperature in schizophrenia patients

Corneal temperature in schizophrenia patients

Osborn waves in the electrocardiogram, hypothermia not due to exposure, and death due to diabetic ketoacidosis

Hypothermie unter Olanzapin

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