[Traumatic posterior atlantoaxial dislocation without fracture of the upper cervical spine in a female geriatric patient : Case report and literature search]. / Traumatische posteriore atlantoaxiale Dislokation ohne Fraktur der oberen Halswirbelsäule bei einer geriatrischen Patientin : Fallbericht und Literaturrecherche.

Traumatic posterior atlantoaxial dislocation (PAAD) without detection of a fracture of the upper cervical spine is a very rare injury that usually occurs in younger patients and in most cases leads to immediate death due to distraction of the spinal cord. In contrast, the present case describes this injury in a female geriatric patient at the age of 75 years. In the literature there are also clinical case reports, where traumatic PAAD without a fracture did not result in neurological deficits and where initially existing neurological deficits were completely reversible through closed or open reduction and internal fixation.

Protein kinase A regulates inflammatory pain sensitization by modulating HCN2 channel activity in nociceptive sensory neurons.

Several studies implicated cyclic adenosine monophosphate (cAMP) as an important second messenger for regulating nociceptor sensitization, but downstream targets of this signaling pathway which contribute to neuronal plasticity are not well understood. We used a Cre/loxP-based strategy to disable the function of either HCN2 or PKA selectively in a subset of peripheral nociceptive neurons and analyzed the nociceptive responses in both transgenic lines. A near-complete lack of sensitization was observed in both mutant strains when peripheral inflammation was induced by an intradermal injection of 8br-cAMP. The lack of HCN2 as well as the inhibition of PKA eliminated the cAMP-mediated increase of calcium transients in dorsal root ganglion neurons. Facilitation of Ih via cAMP, a hallmark of the Ih current, was abolished in neurons without PKA activity. Collectively, these results show a significant contribution of both genes to inflammatory pain and suggest that PKA-dependent activation of HCN2 underlies cAMP-triggered neuronal sensitization.