Psychiatry - December 2008 - (Page 52)

[update on blood brain barrier] mechanisms of thermoregulation, altered calcium signalling, and neurotransmission potentially due to a compromised blood brain barrier (BBB) in the hypothalamus. THERMOREGULATION Hyperthermia is defined as a body temperature above 37˚C. There are several established causes of hyperthermia, including external (environmental), internal (metabolic), and central (chemical imbalances). Heat stress, heat fatigue, heat syncope, heat cramps, heat exhaustion, and heat stroke are a few commonly used terms. Heat exhaustion and heat stroke represent responses of the body to environmental challenges. Heat stroke is clearly an objective increase in body temperature above 40˚C, whereas other entities mentioned may or may not have detectable changes in body temperature. Hypothermia, although rare, can similarly result in response to internal, external, and central factors. Hypothermia is defined as a body temperature less than 35˚C, although 37˚C is the ideal body temperature. Temperatures dropping below 32˚C can have lethal consequences. However, unlike NMS, there is no known or well-established medical term associated with hypothermia. NMS and hypothermia, although rare, are considered life-threatening conditions generally potentiated by neuroleptics.1,2 Malignant hyperthermia (MH), on the other hand, while bearing striking clinical resemblence to NMS, is a genetically distinct, hypermetabolic syndrome3 associated commonly with anesthetics and not induced by neuroleptics. recently begun to take precedence in psychiatry over mechanisms exclusively involving neurotransmission.4 Calcium ions are the most important and widely used intracellular messengers5 in the brain. The proposed role of calcium dysregulation in the pathophysiology model of schizophrenia and calcium binding proteins in bipolar disorder 6,7 have been experimentally demonstrated. Effects of lithium in regulating calcium ions by interacting with calcium binding proteins, such as neuronal calcium sensor 1 (NCS-1), have been established.8 Importance of the regulatory role or signalling of intracellular calcium centrally in the development of NMS and MH has been thoroughly reviewed in another paper.9 serotonergic 5-HT2A receptors by risperidone. The authors, therefore, suggest ruling out hypothermia when a patient’s condition rapidly deteriorates following the initiation of antipsychotic medications. Conversely, blockage of D2 receptors could result in entirely opposite outcomes. Both hypo- and hyperthermia are associated with the use of antipsychotics and their individual mechanisms of action at the particular receptor site hypothetically by altering cellular calcium homeostasis (Figure 1). BBB Thermoregulation is a highly intercommunicative function12 involving internal, external, and central factors, which are greatly dependent on an intact BBB. A classic example of internal factors compromising the intactness of BBB would be menopausal women in whom hormonal disturbances result in hot flashes and night sweats as a response to compensatory thermoregulatory mechanisms. An example of central factors would be neuropsychiatric disorders or neurotransmitter dyregulation, which could lead to similar compensatory thermoregulatory mechanisms (e.g., tachycardia and sweating). On the other hand, extreme environmental variations or external factors also trigger compensatory thermoregulatory responses (e.g., sweating and altered heart rate). These thermoregulatory compensatory mechanisms are almost always associated with a psychological component. Therefore, to explore the role of thermoregulation in patients with compromised BBB, we first have to understand the basics of neurotransmission and calcium signalling centrally in the brain in response to either internal NEUROTRANSMISSION Involvement of neurotransmitters in maintaining thermoregulation is frequently mentioned in the literature. Although an association is suggested, there are no definitive data linking any particular neurotransmitter to hyper- or hypothermia. NMS is a rare, yet well-known, phenomenon induced either by initiating, abruptly stopping, or inappropriate dosing of antipsychotics.10 Some evidence points toward the genetic predisposition for this condition in some individuals in association with known triggers. Hypothermia, however, is less well described in the literature and is not a wellunderstood phenomenon. According to two reported cases,11 adjustments in antipsychotic dose resulted in severe hypothermia, not hyperthermia, leading to intensive care unit admissions. The postulated mechanism was thought to be stimulation of dopamine (D2) receptors and blockage of 12, DECEMBER] CALCIUM Consideration of altered calcium regulation or homeostasis has 52 Psychiatry 2008 [ V O L U M E 5, NUMBER

Table of Contents Feed for the Digital Edition of Psychiatry - December 2008

Psychiatry - December 2008 Editor’s Message Contents Editorial Advisory Board Antidepressant Prescribing by Specialty and Treatment of Premenstrual Dysmorphic Disorder Pain, Pain, Go Away: Antidepressants and Pain Management Why Psychotherapy Helps the Patient in Chronic Pain General Medical Drugs Associated with Depression Katatonia: A New Conceptual Understanding of Catatonia and a New Rating Scale Thermoregulation and the Role of Calcium Signalling in Neurotransmission Cognition and Schizophrenia: Is There a Role for Cognitive Assessments in Diagnosis and Treatment? Journal Watch Information for Authors

Psychiatry - December 2008

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