Postcraniotomy Headache

Etiology

PCH is often multifactorial. The risk factors for this condition are the following:[3][4]

• Age: younger than 45 years
• Gender: women
• Approaches: skull base surgeries involving suboccipital and subtemporal approaches due to considerable dissection of major muscles
• Postsurgical cerebrospinal fluid (CSF) leakage: orthostatic in nature and decreases with recumbency
• Neurosurgical duration: greater than 4 hours
• Type of tumor: higher incidence in individuals with astrocytomas and metastatic brain tumors
• Size of tumor: increased incidence of chronic PCH in patients with small-sized tumors
• Location of tumor: increased incidence in individuals with intraventricular and infratentorial tumors
• Direct closure of dura: increases the risk of pain compared to duraplasty
• Type of anesthesia: inhalational agents are associated with higher pain scores than total intravenous anesthesia
• Craniotomy vs craniectomy: Craniectomy is associated with a higher incidence of PCH [5]
• Comorbidities present: Preoperative headache, presence of uncontrolled anxiety or depression [6]

Factors that reduce PCH occurrence include bone dust removal and preoperative steroid administration.[7]

Epidemiology

The true incidence of PCH is unknown owing to methodological differences, case definition inconsistencies, and multiple surgical approaches used by retrospective reviews regarding this condition. However, looking broadly, most studies report that more than 30% of craniotomy patients develop acute PCH.[8] Chronic PCH, commonly seen after acoustic neuroma excision, has an incidence of 28.4% at 3 years postoperation.[9]

Pathophysiology

The pathophysiology of chronic pain is still unclear at the molecular level. Some of the possible factors responsible include:

• Sensitization of central neurologic pain perception
• Structural changes in neurons in the central nervous system
• Hyperstimulation of γ-aminobutyric acid (GABA) receptors in the raphe nuclei
• Changes in the serotonergic and hemodynamic system
• Role of catecholaminergic nerves

However, the most straightforward mechanism that can explain the evolution of this condition is direct trauma from the surgical procedure itself. Injury to the soft tissue, musculature, bone, or meninges results in peripheral nociceptor activation, leading to abnormal action potential transmission along afferent A-δ and C fibers and, subsequently, somatic pain.

Factors that may aggravate PCH include nerve injury, meningeal and internal tissue irritation from bone dust, muscle adherence to the dura, surgical scar neuroma formation, central sensitization, and aberrant nerve regeneration.[10]

History and Physical

On history, patients may report a continuous, pulsatile, or pounding pain of variable intensity, similar to a tension headache, that appears within 7 days of the surgery. The pain is typically ipsilateral to the surgical site, though generalized headaches have also been reported. The pain increases in frequency in the first few days but becomes less frequent over time. New sensory or motor deficits usually do not accompany PCH, and pathology must be suspected if new focal neurologic signs are observed. Patients may also report nausea, photophobia, anxiety, temporomandibular disorders, and depression in association with PCH. Response to analgesics and migraine medications varies.

Some individuals may have residual neurologic deficits even after a successful craniotomy. These patients' most recent neurologic examination results can serve as a baseline before performing a new one. Pathology must be ruled out in the presence of new focal neurologic signs.

Head and neck examination may reveal the presence of scar neuromas. Palpating this scar can reproduce the pain in patients with chronic PCH.[11]

Evaluation

PCH is a clinical diagnosis. However, when the diagnosis is doubtful, a non-contrast head computed tomography (CT) scan is recommended as the initial imaging modality to rule out a suspected intracranial pathology.

The current criteria for diagnosing PCH according to the International Classification of Headache Disorders 3 (ICHD-3) are summarized in the following table:

Table. Criteria for Diagnosing Postcraniotomy Headache

About a quarter of patients who experience acute PCH later develop persistent or chronic PCH. When a headache following craniotomy becomes persistent, the possibility of a medication-overuse headache should be considered.[12]

Chronic postcraniotomy pain can be divided into 4 grades based on severity[13]:

Grade-1: Patients have a minor annoyance

Grade-2: Headaches are present nearly every day

Grade-3: Patients require medicines every day

Grade-4: Patients feel incapacitated. 

Patients can grade chronic headaches using the McGill Pain Questionnaire and Brief Pain Inventory scoring system.

Treatment / Management

Investigations about the best PCH management strategies are ongoing. Meanwhile, medications for headaches with similar phenotypes are widely used in current practice. However, care must be taken when prescribing drugs that may obscure the ability to monitor neurologic responses. Opioids are an example, which have additional risks like addiction and respiratory depression.[14] 

For acute PCH, multimodal analgesia is recommended. Pharmacologic options include the following:

• Opioids: Codein, tramadol, morphine, fentanyl, and remifentanil
• Nonopioids: Paracetamol, nonsteroidal anti-inflammatory drugs (NSAIDs), dexmedetomidine, gabapentinoids, dexamethasone, transdermal patches

Combining opioids and nonopioids reduces the risk of developing adverse events.[21] Some combinations successfully used in past studies are fentanyl-ketorolac and tramadol-diclofenac.

Chronic PCH may be managed depending on the cause. The usual management modalities include the following:

• Analgesics: Paracetamol, codeine, NSAIDS, tricyclic antidepressants, amitriptyline
• Anticonvulsants: Carbamezepine, sodium valproate, gabapentin, lamotrigine
• Sodium channel blockers: Lignocaine
• Sumatriptan
• Trigger-point injections
• Topical Capsaicin
• Botulinum toxin type A
• Surgical techniques: C2 gangliotomy, C2 ganglionectomy, C2 to C3 rhizotomy, C2 to C3 root decompression, distal neurectomy
• Neurolysis
• Occipital nerve stimulation
• Botulinum toxin-A
• Radiofrequency nerve ablation
• Cryoablation
• Manual neck traction

Alternative modalities may also be considered for patients with chronic PCH. Some options are physical therapy, stress management, neck collars, acupuncture, transcutaneous electrical nerve stimulation, hot and cold packs, massage, and biobehavioral interventions. However, more research is required to support the use of alternative treatments for PCH.

Preventive strategies also comprise an important part of PCH management. Reducing the risk of this condition also minimizes exposure to potentially addictive treatments. The various PCH-preventive modalities include the following:

• Modification of surgical techniques, such as:
  • Choosing craniotomy over craniectomy
  • Closing the wound by applying methyl methacrylate between the dura and cervical muscles
  • Using extradural abdominal fat graft for closure during retrosigmoid craniotomy instead of standard wound closure techniques
  • Performing a duraplasty instead of direct dural closure
• Preemptive analgesia by scalp infiltration, scalp block, and preemptive NSAIDs

The dural and scalp nerves mentioned previously may be anesthetized with a ring block from the nasion to the external occipital protuberance or blocking the individual nerves. Meanwhile, nerves commonly targeted during a scalp block for PCH prevention include the following (see Image. Sensory Areas of the Head):

• Supraorbital nerve
• Supratrochlear nerve
• Zygomaticotemporal nerve
• Auriculotemporal nerve
• Lesser occipital nerve
• Greater occipital nerve
• Greater auricular nerve

Single-time wound instillation of ropivacaine (12 ml of 0.25%) through a surgical (subgaleal) drain during wound closure has proven beneficial to neurosurgical patients undergoing supratentorial craniotomy in a recent clinical trial. This treatment reduces postoperative pain, analgesic consumption, and early emergence in these individuals.[15]

Other treatments that have shown potential in preventing PCH in early studies are the following:

• Intravenous acetaminophen [16][17]
• Levetiracetam [18]
• Preoperative diclofenac
(A1)

The following modalities are currently being studied:

• Preincisional infiltration with dexamethasone palmitate emulsion
• Local infiltration of flurbiprofen axetil [19][20]
(A1)

Evidence is lacking regarding effective PCH preventive treatments 48 hours after surgery.

Differential Diagnosis

The differential diagnosis of PCH includes the following:

• Postsurgical cerebrospinal fluid leak
• Hydrocephalus
• Intracranial hemorrhage
• Other headache types, such as cervicogenic, tension, cluster, and migraine
• Medication-overuse headache
• Meningitis or intracranial other infection
• Temporomandibular joint disorder

A thorough clinical evaluation and appropriate imaging studies can differentiate these conditions from PCH.

Prognosis

PCH improves over time as the patient recovers from the surgical procedure. However, the prognosis may be influenced by the following factors:

• Underlying cause: headaches associated with severe inflammation can take longer to resolve.

• Management: patients respond variably to PCH treatment modalities.

• Patient-specific factors: individual patient characteristics, such as pain tolerance, overall health, and the presence of preexisting medical conditions, can influence the course of postcraniotomy headaches.

• Complications: postoperative complications like infections and CSF leaks can impact the prognosis. 

• Treatment compliance: patient adherence to postoperative care instructions impacts recovery from the procedure and, thus, PCH resolution.

• Psychosocial factors: stress, anxiety, and other psychosocial factors can influence the perception and persistence of postcraniotomy headaches. 

Patients experiencing postcraniotomy headaches should communicate any changes in symptoms or concerns to their healthcare team. Regular follow-up appointments allow for ongoing assessment and adjustments to the treatment plan as needed, ultimately contributing to a more favorable prognosis.

Complications

Acute PCH can evolve into the chronic type. Both acute and chronic PCH can cause stress and anxiety and reduce patients' functional levels and quality of life. Patients may also experience rebound headaches and adverse medication effects while treating the condition. Serious disorders like life-threatening intracranial pressure changes and meningitis must be ruled out if patients report changes in pain quality.