Current pain and headache reports
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Curr Pain Headache Rep · Nov 2023
ReviewAnalgesic Techniques for Rib Fractures-A Comprehensive Review Article.
Rib fractures are a common traumatic injury that has been traditionally treated with systemic opioids and non-opioid analgesics. Due to the adverse effects of opioid analgesics, regional anesthesia techniques have become an increasingly promising alternative. This review article aims to explore the efficacy, safety, and constraints of medical management and regional anesthesia techniques in alleviating pain related to rib fractures. ⋯ Recently, opioid analgesia, thoracic epidural analgesia (TEA), and paravertebral block (PVB) have been favored options in the pain management of rib fractures. TEA has positive analgesic effects, and many studies vouch for its efficacy; however, it is contraindicated for many patients. PVB is a viable alternative to those with contraindications to TEA and exhibits promising outcomes compared to other regional anesthesia techniques; however, a failure rate of up to 10% and adverse complications challenge its administration in trauma settings. Serratus anterior plane blocks (SAPB) and erector spinae blocks (ESPB) serve as practical alternatives to TEA or PVB with lower incidences of adverse effects while exhibiting similar levels of analgesia. ESPB can be performed by trained emergency physicians, making it a feasible procedure to perform that is low-risk and efficient in pain management. Compared to the other techniques, intercostal nerve block (ICNB) had less analgesic impact and required concurrent intravenous medication to achieve comparable outcomes to the other blocks. The regional anesthesia techniques showed great success in improving pain scores and expediting recovery in many patients. However, choosing the optimal technique may not be so clear and will depend on the patient's case and the team's preferences. The peripheral nerve blocks have impressive potential in the future and may very well surpass neuraxial techniques; however, further research is needed to prove their efficacy and weaknesses.
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Curr Pain Headache Rep · Nov 2023
ReviewNeuromodulation for the Sphenopalatine Ganglion-a Narrative Review.
To provide an integrated overview of the current state of knowledge of neuromodulation for the sphenopalatine ganglion (SPG) by reviewing relevant and significant literature. ⋯ There are several case reports and clinical trials evaluating neuromodulation for the SPG. We identified two blinded, randomized clinical trials for patients with chronic cluster headache. The randomized trials and additional studies demonstrated the long-term safety, efficacy, and cost-effectiveness of neuromodulation for the SPG. Recent studies in Europe and the USA suggest that SPG neuromodulation is a novel modality with clinical importance for treating acute cluster headaches and reducing the frequency of attacks.
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Curr Pain Headache Rep · Nov 2023
ReviewDoes Physiologic Post-Concussion Disorder Cause Persistent Post-Traumatic Headache?
One system classifies patients with symptoms after concussion into physiologic, vestibulo-ocular, cervicogenic, and mood/cognition post-concussion disorders (PCD) based upon the preponderance of specific symptoms and physical impairments. This review discusses physiologic PCD and its potential relationship to the development of persistent post-traumatic headaches (PPTH). ⋯ Headache is the most reported symptom after a concussion. Headaches in physiologic PCD are suspected to be due to abnormal cellular metabolism, subclinical neuroinflammation, and dysfunction of the autonomic nervous system (ANS). These abnormalities have been linked to the development of migraine-like and neuralgia-related PPTH. Physiologic PCD is a potential cause of PPTH after a concussion. Future research should focus on how to prevent PPTH in patients with physiologic PCD.
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Curr Pain Headache Rep · Nov 2023
ReviewThe Spectrum of Headache in Leptomeningeal Metastases: A Comprehensive Review with Clinical Management Guidelines.
Headaches are a common, oftentimes debilitating symptom in patients with leptomeningeal metastases. ⋯ The third edition of the International Classification of Headache Disorders provides a useful diagnostic framework for headaches secondary to leptomeningeal metastases based on the temporal relationship of headache with disease onset, change in headache severity in correlation with leptomeningeal disease burden, and accompanying neurologic signs such as cranial nerve palsies and encephalopathy. However, headaches in patients with leptomeningeal metastases can be further defined by a wide range of varying cancer- and treatment-related pathophysiologies, each requiring a tailored approach. A thorough review of the literature and expert opinion on five observed headache sub-classifications in patients with leptomeningeal metastases is provided, with attention to necessary diagnostic testing, recommended first-line treatments, and prevention strategies.
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Curr Pain Headache Rep · Nov 2023
ReviewNeurovascular Compression-Induced Intracranial Allodynia May Be the True Nature of Migraine Headache: an Interpretative Review.
Surgical deactivation of migraine trigger sites by extracranial neurovascular decompression has produced encouraging results and challenged previous understanding of primary headaches. However, there is a lack of in-depth discussions on the pathophysiological basis of migraine surgery. This narrative review provides interpretation of relevant literature from the perspective of compressive neuropathic etiology, pathogenesis, and pathophysiology of migraine. ⋯ Vasodilation, which can be asymptomatic in healthy subjects, may produce compression of cranial nerves in migraineurs at both extracranial and intracranial entrapment-prone sites. This may be predetermined by inherited and acquired anatomical factors and may include double crush-type lesions. Neurovascular compression can lead to sensitization of the trigeminal pathways and resultant cephalic hypersensitivity. While descending (central) trigeminal activation is possible, symptomatic intracranial sensitization can probably only occur in subjects who develop neurovascular entrapment of cranial nerves, which can explain why migraine does not invariably afflict everyone. Nerve compression-induced focal neuroinflammation and sensitization of any cranial nerve may neurogenically spread to other cranial nerves, which can explain the clinical complexity of migraine. Trigger dose-dependent alternating intensity of sensitization and its synchrony with cyclic central neural activities, including asymmetric nasal vasomotor oscillations, may explain the laterality and phasic nature of migraine pain. Intracranial allodynia, i.e., pain sensation upon non-painful stimulation, may better explain migraine pain than merely nociceptive mechanisms, because migraine cannot be associated with considerable intracranial structural changes and consequent painful stimuli. Understanding migraine as an intracranial allodynia could stimulate research aimed at elucidating the possible neuropathic compressive etiology of migraine and other primary headaches.