A Contemporary Perspective on the Management of Post-Craniotomy Headache and Pain

Abstract

There is a dearth of evidence-based practice regarding the differential diagnosis, natural history, and management of post-craniotomy headache. The etiology of post-craniotomy headache is typically multifactorial, with patients' medical history, type of craniotomy, and perioperative management all playing a role. Post-craniotomy headaches are often undertreated, yet available evidence supports a multimodal approach for both prophylaxis and management. Many therapeutic techniques that aim to treat or prevent post-craniotomy headache require more robust validation than clinical evidence currently imparts. Pre- and intraoperative locoregional anesthesia should be the mainstay of prophylaxis; the role of opiates co-administered with analgesics, corticosteroids, and antiepileptic therapy in the acute perioperative phase is of paramount importance. Treatment of chronic PCH is less well-defined but should involve trials of analgesic, antineuropathic, and antiepileptic medications before enlisting experimental treatments. Comorbid psychiatric, musculoskeletal, or seizure disorders should be managed distinctly from post-craniotomy headaches. In patients failing all extant therapies, experimental approaches should be considered. These include subanesthetic ketamine infusion or surgical site injection with local anesthetics, corticosteroids, or botulinum toxin. Post-craniotomy headache is a complex phenomenon with many underutilized treatment options available, and many more under investigation. Nonetheless, further research is required to differentiate the efficacy of contemporary treatment strategies and to elucidate the applicability of novel therapies.

Analgesia in the Neurosurgical Intensive Care Unit

“…Acute pain after craniotomy is considered moderate to severe during the first two postoperative days. It is often underrated and hard to estimate, potentially becoming chronic (8,9). No analgesic regimen for post-craniotomy pain was proven as efficient for all patients (1,10), although opioids provided superior acute pain relief compared to other drugs in small clinical studies (11).…”

Secondary Headache: Current Update

“…The scalp receives neural supply from branches of the cervical plexus and trigeminal nerve, whereas the dura is innervated by the meningeal branches of the trigeminal and vagus nerve. Fibrous adhesions between the dura, overlying scalp, and musculature have been suspected as a potential cause of PCH 4 . Patients undergoing suboccipital craniectomy have a significantly greater incidence of headaches than craniotomy at the same site 5,6 .…”

“…The quality of pain is usually described as pulsating or pounding with a resemblance to that of either migraine or tension-type headaches. 1 Typically, the pain is maximal at the site of the craniotomy.…”

“…Primary headaches are classified in the third edition of the International Classification of Headache Disorders, 3rd edition (ICHD-3) into 4 major classes: migraine, tension-type headache, trigeminal autonomic cephalalgias, and other primary headache disorders. 1 In the ICHD-3, secondary headaches are classified into 8 major headache classes, and within these classes, they are further subclassified. Using specific suclasses, the following secondary headache classes will be discussed in this paper: headache attributed to trauma or injury to the head and/or neck, headache attributed to cranial or cervical vascular disorder, headache attributed to non-vascular intracranial disorder, headache attributed to a substance or its withdrawal, headache attributed to infection, headache attributed to disorder of homeostasis, and headache or facial pain attributed to disorder of the cranium, neck, eye, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure.…”

El papel del anestesiólogo en cirugía de epilepsia

“…[39][40][41] La lidocaína es el único anestésico local intravenoso con propiedades anticonvulsivas y efectos mínimos en la ECoG a dosis adecuadas; sin embargo, con concentraciones plasmáticas mayores a 9 μg/mL, se han observado convulsiones por toxicidad, por lo que conviene tener presentes las dosis máximas y la vía de administración. 2,42 Elección de la técnica anestésica…”