Cold stimulus headache is defined as a transient headache triggered by exposure to cold stimuli applied externally to the head, ingested, or inhaled. It is categorized into three subtypes in the International Classification of Headache Disorders. Subtype 4.5.2, commonly known as “brain freeze” or “ice cream headache”, presents as sudden, short-lasting pain induced by the consumption of cold foods or beverages. This condition is usually benign and non-disabling, occurs in susceptible individuals, and provides insight into the activation of the trigeminovascular pathway and the role of cold in the pathogenesis of migraine. This chapter discusses the clinical, diagnostic, and therapeutic aspects of headaches induced by the ingestion or inhalation of cold stimuli. A case-based approach illustrates two volunteers who developed migraine-like headaches after stimulation with ice. These findings expand the understanding of this headache subtype, offering practical insights into its pathophysiology and treatment. Cold-stimulus headache (CSH) is a transient pain induced by exposure to cold stimuli applied externally to the head, ingested, or inhaled. According to the International Classification of Headache Disorders (ICHD-3), subtype 4.5.2, commonly known as “brain freeze” or “ice cream headache”, is characterized by short-lasting pain triggered by cold foods or beverages. Although benign and non-disabling, CSH provides valuable insight into the activation of the trigeminovascular system and the role of cold in headache pathophysiology. This chapter discusses the clinical, diagnostic, and therapeutic aspects of headaches attributed to ingestion or inhalation of cold stimuli, using a case-based approach. Two volunteers developed migraine-like headaches after an ice stimulus applied to the oral cavity. The cold exposure triggered both immediate pain consistent with CSH and delayed migraine attacks occurring one to three hours later, suggesting that ice-induced headache can act as a migraine trigger. These findings highlight the interaction between cold-induced pain and migraine mechanisms. Neuronal hyperexcitability, activation of the trigeminovascular pathway, and the potential involvement of the TRPM8 receptor, a cold-sensitive ion channel, appear central to this process. Activation of this receptor and the subsequent release of calcitonin generelated peptide (CGRP) may sensitize trigeminal neurons and precipitate migraine in susceptible individuals. Understanding these mechanisms not only refines clinical management and patient education but also contributes to broader insights into primary headache pathophysiology and pain modulation.

Cold-Stimulus Headache

章节
发表日期：

2026年

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Daniella Araújo de Oliveira,
Marcelo Valença

摘要

Cold stimulus headache is defined as a transient headache triggered by exposure to cold stimuli applied externally to the head, ingested, or inhaled. It is categorized into three subtypes in the International Classification of Headache Disorders. Subtype 4.5.2, commonly known as “brain freeze” or “ice cream headache”, presents as sudden, short-lasting pain induced by the consumption of cold foods or beverages. This condition is usually benign and non-disabling, occurs in susceptible individuals, and provides insight into the activation of the trigeminovascular pathway and the role of cold in the pathogenesis of migraine. This chapter discusses the clinical, diagnostic, and therapeutic aspects of headaches induced by the ingestion or inhalation of cold stimuli. A case-based approach illustrates two volunteers who developed migraine-like headaches after stimulation with ice. These findings expand the understanding of this headache subtype, offering practical insights into its pathophysiology and treatment. Cold-stimulus headache (CSH) is a transient pain induced by exposure to cold stimuli applied externally to the head, ingested, or inhaled. According to the International Classification of Headache Disorders (ICHD-3), subtype 4.5.2, commonly known as “brain freeze” or “ice cream headache”, is characterized by short-lasting pain triggered by cold foods or beverages. Although benign and non-disabling, CSH provides valuable insight into the activation of the trigeminovascular system and the role of cold in headache pathophysiology. This chapter discusses the clinical, diagnostic, and therapeutic aspects of headaches attributed to ingestion or inhalation of cold stimuli, using a case-based approach. Two volunteers developed migraine-like headaches after an ice stimulus applied to the oral cavity. The cold exposure triggered both immediate pain consistent with CSH and delayed migraine attacks occurring one to three hours later, suggesting that ice-induced headache can act as a migraine trigger. These findings highlight the interaction between cold-induced pain and migraine mechanisms. Neuronal hyperexcitability, activation of the trigeminovascular pathway, and the potential involvement of the TRPM8 receptor, a cold-sensitive ion channel, appear central to this process. Activation of this receptor and the subsequent release of calcitonin generelated peptide (CGRP) may sensitize trigeminal neurons and precipitate migraine in susceptible individuals. Understanding these mechanisms not only refines clinical management and patient education but also contributes to broader insights into primary headache pathophysiology and pain modulation.