Hypnic headache and caffeine.

Hypnic headache (HH) is a rare primary headache disorder primarily affecting patients over the age of 50 years. This headache entity occurs exclusively at night almost always at the same time. Imaging data as well as the strict circadian rhythm of headache attacks suggest a hypothalamic involvement in the underlying pathophysiology of this headache disorder. One interesting clinical feature about HH is its therapeutic response to caffeine as an acute as well as prophylactic agent. This review addresses the efficacy of caffeine in HH as well as in other headache disorders, and attempts to give insight into the analgesic properties of this substance. In addition, it depicts possible problems of caffeine consumption with regard to headache.

Cluster headache and the hypothalamus: causal relationship or epiphenomenon?

Typical clinical features of cluster headache (CH) include circadian/circannual rhythmicity and ipisilateral cranial autonomic features. This presentation has led to the assumption that the hypothalamus plays a pivotal role in this primary headache disorder. Several studies using neuroimaging techniques or measuring hormone levels supported the hypothesis of a hypothalamic involvement in the underlying pathophysiology of CH. Animal studies added further evidence to this hypothesis. Based on previous data, even invasive treatment methods, such as hypothalamic deep brain stimulation, are used for therapy. However, the principal question of whether these alterations are pathognomonic for CH or whether they might be detected in trigeminal pain disorders in general, in terms of an epiphenomenon, is still unsolved. This article summarizes studies on hypothalamic involvement in CH pathophysiology, demonstrates the involvement of the hypothalamus in other diseases and tries to illuminate the role of the hypothalamus based on this synopsis.

Hypothalamic gray matter volume loss in hypnic headache.

OBJECTIVE: Hypnic headache (HH) is a rare primary headache disorder characterized by strictly nocturnal headache attacks that mostly occur at the same time at night. The pathophysiology of this disease is poorly understood, but hypothalamic involvement was suspected as the hypothalamus represents the cerebral management center of sleep regulation and pain control. METHODS: Fourteen patients with HH and 14 age-matched and gender-matched healthy controls were investigated using magnetic resonance imaging-based voxel-based morphometry. RESULTS: We detected gray matter volume decrease in the posterior hypothalamus of HH patients. Additional gray matter decrease was observed in brain areas known to be associated with cerebral pain processing, including the cingulate cortex, operculum, and frontal lobe, as well as in the temporal lobe. INTERPRETATION: Our data confirm the hypothesized involvement of the posterior hypothalamus in the pathophysiology of HH and emphasize the importance of this structure for sleep regulation and pain control.

The hypothalamus: specific or nonspecific role in the pathophysiology of trigeminal autonomic cephalalgias?

The clinical features of trigeminal autonomic cephalalgias (TACs), such as trigeminal distribution of pain, circadian/circannual rhythmicity, and ipsilateral cranial autonomic features, suggest a crucial role of the hypothalamus in the underlying pathophysiology of these primary headache disorders. Hypothalamic involvement is supported by several neuroimaging, neuroendocrine, genetic, experimental pain, and animal studies. Unfortunately, these different studies were unable to resolve the paramount question of whether the detected hypothalamic alterations are pathognomonic for TACs or whether they merely represent an epiphenomenon of different pain conditions in general. This review summarizes studies on hypothalamic involvement in TAC pathophysiology, demonstrates hypothalamic activation in other painful diseases, and evaluates the role of the hypothalamus in the pathophysiologic mechanisms associated with these different conditions.

Gray matter changes related to chronic posttraumatic headache.

BACKGROUND: Although up to 15% of patients with whiplash injury develop chronic headache, the basis and mechanisms of this posttraumatic headache are not well understood. METHODS: Thirty-two patients with posttraumatic headache following whiplash injury were investigated within 14 days after the accident and again after 3 months using magnetic resonance-based voxel-based morphometry. Twelve patients developed chronic headache lasting longer than 3 months and were studied a third time after 1 year. RESULTS: Patients who developed chronic headache revealed decreases in gray matter in the anterior cingulate and dorsolateral prefrontal cortex after 3 months. These changes resolved after 1 year, in parallel to the cessation of headache. The same patients who developed chronic headache showed an increase of gray matter in antinociceptive brainstem centers, thalamus, and cerebellum 1 year after the accident. CONCLUSION: We demonstrate adaptive gray matter changes of pain processing structures in patients with chronic posttraumatic headache in regard to neuronal plasticity, thus providing a biologically plausible basis for this common, disabling problem.