Headache associated with intracranial infection …

Fu-Chi Yang MD PhD

Headache & Pain

Updated 04.15.2025
Released 09.20.1995
Expires For CME 04.15.2028

Headache associated with intracranial infection

Author: Fu-Chi Yang MD PhD

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Editor: Shuu-Jiun Wang MD

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Headache associated with intracranial infection

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Introduction

Overview

Headache is the most common symptom of intracranial infection; however, it only accounts for less than 1% of acute headache cases in the emergency department. In addition to headaches, encephalitis may present with fever, altered consciousness, focal neurologic deficits, and seizures (usually focal). Headaches may also occur in brain abscesses, for which otitis and mastoiditis are the most common predisposing conditions. Because the brain parenchyma lacks sensory receptors, headaches associated with encephalitis and brain abscesses likely result from meningeal inflammation fever, increased intracranial pressure, and traction on pain-sensitive intracranial structures.

Key points

	• No physical sign of meningeal irritation could accurately distinguish between patients with and without meningitis.
	• Headache is the most common symptom of bacterial meningitis (87%); bacterial meningitis accounts for less than 1% of acute headache cases in emergency settings (< 1%).
	• Headaches attributed to localized brain infection (code 9.1.4) include those due to brain abscess, subdural empyema, infectious granuloma, or other localized infective lesion; they typically present with fever, focal neurologic deficit(s), or altered mental state.
	• The prevalence of headache during acute SARS-CoV-2 infection (up to week 4) was approximately 50%, whereas persistent headache during the subacute phase was 31% in the first month and decreased to 16% at 9 months.

Historical note and terminology

Knowledge regarding intracranial infections has significantly evolved over the past two centuries. Bacterial meningitis was first described by Vieusseaux in 1805 as "epidemic cerebrospinal fever," with meningococcus later isolated from the cerebrospinal fluid (CSF) by Weichselbaum in 1887. Treatment advances were revolutionary, with the report of the effectivity of sulphonamides in 1932 (56) and penicillin in the 1940s, dramatically improving survival rates (54).

Diagnostic techniques advanced with the introduction of lumbar puncture by Quinke, enabling better characterization of both bacterial and viral infections. Later in 1925, Wallgren coined the term “aseptic meningitis” to describe self-limiting viral variants characterized by headache. Despite the growing evidence, the clinical examination for meningeal inflammation still relies on signs described by Kernig (1882) and Brudzinski (1909), which remain important elements of the neurologic evaluation for suspected cases.

Clinical manifestations

Presentation and course

	• The classical meningitis triad is fever, nuchal rigidity, and altered mental status; this triad occurs in 41% of acute bacterial meningitis cases and is more frequent in patients older than 60 years of age.
	• Headache, the most common symptom, is absent from the classical triad.
	• Aseptic meningitis may cause sudden-onset headaches.
	• Brain abscesses can manifest as headache, fever, mental status changes, and focal neurologic deficits.

Chapter nine (code 9.1) of the ICHD-III classifies headaches attributed to intracranial infection into four subtypes: 9.1.1 headache attributed to bacterial meningitis or meningoencephalitis; 9.1.2 headache attributed to viral meningitis or encephalitis; 9.1.3 intracranial fungal or other parasitic infections; and 9.1.4 headache attributed to localized brain infections.

Aseptic meningitis accounts for approximately 72% of cases, whereas bacterial and fungal meningitis comprises 8% (28). The classical triad is present in approximately 41% of patients with acute bacterial meningitis (04) and is more common in patients older than 60 years (66). However, its diagnostic sensitivity is poor (69). Lethargy, stupor, and seizure activity are highly suggestive of bacterial meningitis. Mental status changes are less common in viral compared to bacterial cases (73). Pneumococcal meningitis increases the likelihood of seizures, focal deficits, and reduced consciousness (70). Petechiae strongly indicates Neisseria meningitidis (20).

Encephalitis is characterized by headache, fever, altered consciousness, focal neurologic deficit, and seizures, sometimes with meningeal signs. A thunderclap headache may be its initial symptom (57).

Young children may not report headaches. Infants and neonates with acute bacterial meningitis often display lethargy, fussiness, sleepiness, jitteriness, anorexia, hypotonia, apnea, jaundice, diarrhea, or general weakness. Bulging anterior fontanels may occur, although neck stiffness is rare (17). Seizures occur before hospital admission in approximately 20% of cases.

Bacterial meningitis or meningoencephalitis. A Dutch study of 1268 adults with community-acquired bacterial meningitis reported that 83% of the patients had headaches, 74% had neck stiffness, 74% had fever, and 71% had impaired consciousness. Headache, often presenting as the first symptom, is typically holocranial acute and progressive and accompanied by nuchal rigidity and photo/phonophobia (46). A thunderclap headache may indicate acute bacterial meningitis. A persistent headache following bacterial meningitis or meningoencephalitis is typically diffuse and continuous, although migraine-like headaches have been reported (46). However, the Nord-Trøndelag Health Survey found a lower 1-year headache prevalence among individuals with prior intracranial infections (41). In the United Kingdom, encephalitis was associated with a 1.23-fold increase in new-onset headaches within a year (25).

Headaches in tuberculous meningitis occur in 50% to 100% of cases (53; 61). The headaches typically present as holocranial (60%) and throbbing (48.4%), with varying severity: mild (23.2%), moderate (23.2%), severe (36.8%), and intolerable (16.8%). Severe cases, particularly with tuberculous vasculitis, predict poorer outcomes (38). Seizures, CSF protein greater than 2.5 g/L, and basal exudates are significant predictors of headache severity (38).

Viral meningitis or encephalitis. Viral meningitis typically presents with a constellation of symptoms including fever, headache, neck stiffness, nausea, vomiting, photophobia, and sensitivity to bright light (35). The clinical manifestations vary by pathogen and individual factors.

Herpes simplex virus type 2 (HSV-2), the most common cause of viral meningitis, produces severe headaches in 96% to 100% of cases, accompanied by neck stiffness, nausea, vomiting, and photophobia are the most common symptoms (26). A notable HSV-2-infection variant is Mollaret meningitis, a rare recurrent aseptic lymphocytic meningitis with episodic headache, stiff neck, fever, and photophobia in a relapsing-remitting pattern (51).

Headaches commonly occur in people infected with the human immunodeficiency virus (HIV)/acquired immune deficiency syndrome, affecting 28% to 80% of adults with HIV infection in Africa (58; 40). Migraines occur in 5% of cases (58), but most headaches are dull and bilateral. Notably, headache severity correlates with disease progression (CD4 cell count, viral load) but not infection duration or antiretroviral use (34).

Headaches occur in approximately 50% of cases during the acute phase (≤4 weeks) of SARS-CoV-2 infection with persistent headaches affecting 31% within the first month, declining to 16% by 9 months (19). In younger individuals, these headaches are typically holocranial (63%), frontal (48%), pressing (75%), moderate in severity (median 7 out of 10), and often involve photophobia (58%) (22). Younger patients with a history of primary headaches are more prone to acute headaches, with approximately 50% reporting a greater severity than their typical migraines, whereas persistent subacute headaches occur more commonly in older individuals (19; 13).

A 2025 Bayesian change-point analysis identified distinct temporal patterns in headache and migraine dynamics during SARS-CoV-2 infection among patients with pre-existing migraine. Headache rates increased approximately 4 days before COVID-19 diagnosis and returned to baseline around 12 days after diagnosis, whereas migraine rates changed 2 days before diagnosis and normalized by day 11. Weekly headache days increased from 1.5±0.1 days pre-infection to 1.8±0.1 days during acute infection before recovering to 1.6±0.1 days post-infection. Similarly, weekly migraine days increased from 1.0±0.1 day to 1.3±0.1 days during infection, returning to 1.1±0.1 days afterward. These patterns were significantly more pronounced in females and patients older than 40 years of age, with minimal changes observed in male patients (75).

Post-COVID headaches can persist in up to 52% of cases, with 20.3% developing chronic daily headaches (CDHs). Risk factors include preexisting headaches, severe acute-phase headaches, and female sex. These chronic headaches are usually bilateral (84%), nonthrobbing, and associated with photophobia (76%) and phonophobia (84%). Although most cases respond to standard analgesics (94%), 45% who used analgesics within a median of 12 days/month develop medication overuse headaches (14). The trigeminovascular system may be implicated in the pathophysiology, particularly in mild cases (13).

SARS-CoV-2 variants demonstrate different headache persistence patterns, with the Delta variant showing higher post-COVID headache prevalence (12.9%) than the Wuhan (5.5%) or Alpha variants (3.8%). The Omicron variant has exhibited even higher persistence rates at 4 weeks post-infection (55).

Intracranial fungal or other parasitic infection. In the United States, acute Lyme neuroborreliosis typically presents with lymphocytic meningitis with episodic headaches and mild neck stiffness, cranial neuropathy (particularly facial palsy), and motor or sensory radiculoneuritis (60). In Europe, Borreliosis garinii infection causes (Bannwarth syndrome, a tick-borne meningopolyneuritis) that presents with painful radiculoneuritis and lymphocytic meningitis, often without headaches and can be followed by cranial neuropathy or paresis of the extremities (49).

Cryptococcus neoformans is a common cause of subacute aseptic meningitis presenting with headache and fever in over 75% of cases, typically developing over 2 to 4 weeks (71). Coccidioidomycosis meningitis, also manifests as headache and fever, but the clinical symptoms of which are highly variable (63).

Localized brain infection. Brain abscesses present with headache, mental status changes, focal neurologic deficits, and fever. A Danish cohort study reported headaches in Denmark, 66% of cases, fever in 54%, cognitive impairment in 46%, nausea and vomiting in 38%, seizures in 25%, cranial nerve palsy in 24%, neurologic deficits in 48%, and other motor and sensory nerve deficits in 42% (06). The classic triad of headache, fever, and neurologic deficit occurred in only 20% of patients. Symptoms vary by abscess location, size, host immune status, and pathogen virulence. Intravenous or nasal substance use increases abscess risk in children and adolescents, particularly in those with patent foramen ovale (07).

Prognosis and complications

Headaches typically resolve with infection remission but may persist for months in some cases. A minority experiences headaches lasting over 3 months post-infection (29).

A 10-year retrospective study found that meningitis is responsible for only 6.3% of fetal headaches (44). Bacterial meningitis is associated with significant morbidity and mortality, varying by geography, age, and pathogen (28). Mortality for adults ranges from 6% in Germany to 54% in Malawi, and from 10% to 58% in neonates in developed and developing countries, respectively (28). Early complications include cerebral edema, obstructive hydrocephalus, septic shock, and seizures, whereas long-term sequelae include focal neurologic deficits, hearing loss, cognitive impairments, and epilepsy (43). Risk factors for poor outcomes, include older age, hypotension, seizures, delayed antibiotic use, concomitant pneumonia, purpuric rash, tachycardia, lower Glasgow Coma Scale (GCS) scores, focal neurologic deficits, low CSF white blood cell (WBC) count, positive blood cultures, and high serum C-reactive protein levels (28).

Viral meningitis generally has an excellent prognosis, with full recovery in most cases. However, some patients develop persistent neurologic symptoms. In contrast, encephalitis is associated with significant mortality and morbidity, with herpes simplex virus encephalitis mortality ranging from 5% to 20% (01). Poor outcomes correlate with age, pre-existing illness, fever on admission, prolonged fever post-treatment, and lower Glasgow Coma Scores or higher acute physiology and chronic health evaluation scores on admission (01).

Brain abscess mortality has drastically improved with advances in antimicrobials, imaging, and surgical techniques. A Danish nationwide cohort study reported 6% in-hospital mortality, rising to 12% at 6 months post-discharge, and the death rate increased to 12%. Favorable outcomes increased from 24% at discharge to 57% after 6 months (06).

The prevalence of post-COVID headache decreases over 2 months before stabilizing. Among patients who developed chronic daily headaches, 72% reported persistent headaches at a median follow-up of 804 days, although 57% noted gradual improvement. Higher initial headache intensity and pre-existing primary headache disorders are linked to headache persistence (14).

Clinical vignette

Case 1. A 44-year-old man was admitted to the hospital with a 4-day history of persistent pain in the bilateral occipital and temporal regions. The nonthrobbing headache was not associated with nausea, vomiting, photophobia, or phonophobia. Although the headache was initially tolerable, it persisted despite ibuprofen administration. He later visited the emergency room due to excruciating pain. His temperature was 38.6°C, and he had no history of recent trauma, symptoms of upper respiratory infections, sore throat, rashes, or mucosal lesions.

On examination, the patient’s temperature was 36.9°C, and other vital signs were normal. He was moaning and refused to sit upright. No skin or genital lesions were present. Although he maintained neck flexion, meningismus was absent. The neurologic examination revealed unremarkable findings.

Laboratory tests showed an elevated C-reactive protein level (2.18 mg/dL). CSF analysis revealed 432 WBC/mm3 (97% lymphocytes, 1% monocytes), seven erythrocytes per mm3, 49 mg/dL glucose, and 156.7 mg/dL protein. CSF cultures were negative, but polymerase chain reaction detected varicella-zoster virus. Magnetic resonance imaging showed diffuse meningeal enhancement without focal lesions.

Intravenous acyclovir was administered for 5 days but was switched to valaciclovir due to phlebitis. The headaches improved significantly without recurrence.

Comment. Varicella-zoster virus reactivation-related meningitis is more common than previously assumed, accounting for 5% to 29% of viral meningitis cases (36; 21). Although most sporadic encephalitis is caused by herpes simplex virus-1, viral meningitis in immunocompetent adults is typically due to herpes simplex virus-2.

PCR analysis is crucial for diagnosing aseptic meningitis. The optimal treatment remains uncertain, but guidelines issued by the Infectious Diseases Society of America recommend the intravenous administration of acyclovir (10 to 15 mg/kg every 8 hours) for varicella zoster virus encephalitis (64). The Association of British Neurologists and British Infection Association National Guidelines suggest intravenous acyclovir (10 mg/kg) three times daily (59).

Case 2. A 12-year-old boy presented to the Emergency Department with a week-long headache, and body temperature elevation was noted 1 day before admission. The headache was holocranial, dull, and achy and accompanied by nausea, vomiting, photophobia, and phonophobia. His temperature was 38°C, and his pulse was 100 bpm. Fundoscopic findings were normal, but slight neck resistance was noted. Kernig and Brudzinski signs were negative. Neurologic examination was normal.

Laboratory studies revealed a white blood cell count of 12,000 cells/mm with a normal differential count. CSF analysis revealed an opening pressure of 18 cm of H2O, closing pressure of 16 cm of H2O WBC count of 12 mm3 (83% monocytes, 17% polymorphonuclear cells), and glucose and protein levels of 60 dL; each staining was negative, leading to a viral meningitis diagnosis.

Despite treatment, fever and headaches persisted. The following day, CSF WBC count increased to 80/mm3, and the protein level rose to 70 mg/dL. A computed tomography (CT) scan on day 3 revealed a frontal lobe abscess, with sinus imaging confirming frontal sinus osteomyelitis. The patient underwent surgery and antibiotic therapy, recovering without sequelae.

Comment. The classic triad of headache, fever, and focal neurologic deficit appears in only 20% of brain abscess cases. The prolonged headache should have prompted earlier brain imaging as enteroviral meningitis symptoms are usually brief.

Biological basis

	• Streptococcus pneumoniae is the most common cause of bacterial meningitis.
	• Herpes simplex virus is the leading cause of aseptic meningitis.
	• Brain abscesses are most frequently caused by microorganisms belonging to the Streptococcus and Staphylococcus species.
	• Headache attributed to intracranial infection may result from meningeal inflammation, increased intracranial pressure, or a mass that exerts traction on pain-sensitive intracranial structures.

Etiology and pathogenesis

Streptococcus pneumoniae accounts for approximately 72% of bacterial meningitis cases, whereas Neisseria meningitidis is responsible for approximately 11% of cases in patients older than 16 years of age. In early-onset neonatal meningitis, approximately 35% of cases are caused by Escherichia coli and Streptococcus agalactiae (28). Mycobacterium tuberculosis causes subacute and chronic meningitis, whereas cryptococcus, nocardia, candida, histoplasma, and coccidiomycosis are common causes of chronic meningitis.

Viruses are implicated in 20% to 50% of aseptic meningitis cases (65), with herpes simplex virus accounting for 50% to 75% of identified cases. Varicella zoster virus, enteroviruses, and arboviruses account for the most of the remaining cases (65).

Brain abscesses commonly contain multiple organisms reflecting their source, with Streptococcus and Staphylococcus species being the most frequently identified causative microorganisms (08). The most common predisposing conditions are contiguous infections, such as otitis or mastoiditis (33%), sinusitis (10%), meningitis (6%), and odontogenic foci (5%) (08).

Headaches in intracranial infection cases primarily result from three mechanisms: meningeal inflammation, increased intracranial pressure, and traction on pain-sensitive intracranial structures. Pathogens trigger inflammatory cascades that release proinflammatory cytokines, disrupt the blood-brain barrier, and induce vascular dysregulation, contributing to vasogenic brain edema and loss of cerebrovascular autoregulation (47; 33).

Because the brain parenchyma lacks sensory receptors, headaches associated with encephalitis and brain abscesses likely result from secondary meningeal involvement or increased intracranial pressure. The characteristics of headaches differ by underlying pathophysiology: direct meningeal involvement typically provokes nuchal rigidity, photophobia, and phonophobia, whereas increased intracranial pressure causes headaches that worsen with coughing, bending, or lying down, with greater severity in the morning.

The trigeminal nerve, which innervates the meninges, plays a critical role in pain generation through the trigeminovascular system. Inflammatory stimuli activate unmyelinated sensory C-fibers to release vasoactive neuropeptides, including substance P and calcitonin gene-related peptides, further propagating the inflammatory response and pain signaling.

Differential diagnosis

A headache indicates a significant organic disease if it (1) is new or changes in pattern, (2) occurs after the age of 50, (3) is exertional or positional, (4) is thunderclap in nature, (5) is posttraumatic, (6) presents with meningismus or fever, (7) is accompanied by focal neurologic signs, or (8) presents with significant comorbidities (23).

The pattern of evolution and associated features are key to differential diagnosis. Thunderclap headaches warrant urgent evaluation for acute neurologic disorders, whereas exertion-related headaches may suggest aneurysm rupture but can also occur in benign headache disorders. Cognitive changes suggest an intracranial process but may also occur in migraines. A headache resembling prior episodes is less concerning, although acute central nervous system (CNS) events can trigger migraines. First-time headaches in older patients are less likely to be migraines (23).

Distinguishing a severe migraine from meningitis, encephalitis, or subarachnoid hemorrhage can be challenging, particularly with thunderclap headaches. Aneurysmal subarachnoid hemorrhage typically presents with a sudden severe headache, stiff neck, photophobia, nausea, vomiting, and possibly obtundation or coma. A preceding minor hemorrhage can signal the likelihood of a major rupture within hours to weeks, but may be difficult to diagnose. In minor leaks, headache, nausea, or vomiting are common, whereas loss of consciousness is less frequent (67).

Reversible cerebral vasoconstriction syndrome (RCVS), characterized by “recurrent thunderclap headaches” and “reversible cerebral vasoconstrictions,” are more prevalent than previously recognized and should be differentiated from aneurysmal subarachnoid hemorrhage (15). RCVS complications include ischemic stroke over the watershed zones, cortical subarachnoid hemorrhage, and intracerebral hemorrhage. Any patient with a sudden severe, sudden-onset headache should undergo neuroimaging and lumbar puncture (74).

The syndrome of transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL), also known as pseudomigraine with neurologic symptoms and lymphocytic pleocytosis syndrome, is a rare, self-limiting disorder (02). Patients, more often men, experience migraine episodes with lymphocytic pleocytosis, typically between the ages of 14 and 39 years. One-quarter of patients report prodromal, viral-like illnesses. The clinical picture comprises at least one neurologic deficit lasting over 4 hours, including hemiparesthesia, dysphagia, or hemiparalysis accompanied by mild-to-moderate bilateral throbbing headache and, occasionally, fever. CSF analysis reveals lymphocytic pleocytosis (> 15 cells/uL) with elevated CSF protein. CT and MRI findings are normal, whereas electroencephalography often shows focal slowing. The etiopathogenesis remains unclear, although post-infectious or inflammatory mechanisms involving autoantibodies have been proposed (02).

Spontaneous intracranial hypotension can mimic aseptic meningitis. Notably, orthostatic headache and diffuse pachymeningeal enhancement on contrast MRI help differentiate it from viral meningitis (03).

Viral encephalitis is caused by neurotropic viruses but can be mimicked by brain abscess, tumor, postinfectious encephalomyelitis, or toxic encephalopathy. Clues for differentiation include symptom onset speed, prodrome history, infectious exposure, travel history, suspected or known toxic ingestion, and medical history. A new headache persisting for days or weeks may indicate a primary neurologic disorder requiring full evaluation.

Drug-induced aseptic meningitis should be recognized, with most patients presenting with headache, fever, meningismus, and mental status changes (48). Four classes of medications—nonsteroidal anti-inflammatory drugs, antibiotics, immunosuppressive-immunomodulatory drugs, and antiepileptic drugs account for 26% to 35% of cases. Onset varies from minutes to 5 months after exposure, and systemic disorders, particularly systemic lupus erythematosus are commonly observed. CSF findings include neutrophilic pleocytosis, normal-to-low glucose and elevated protein, with normal neuroimaging. Symptoms typically resolve within days after drug discontinuation.

Distinguishing infectious from autoimmune encephalitis is challenging. Although both conditions differ in headache presence, fever, epileptic seizures, and CSF cell counts, clinical algorithms have shown low sensitivity (58%) and specificity (8%) for diagnosing autoimmune encephalitis. Notably, headaches are less common in autoimmune encephalitis (68).

Diagnostic workup

	• Kernig and Brudzinski signs are unreliable for diagnosis.
	• Polymerase chain reaction testing has high sensitivity and specificity enabling more accurate infection diagnosis.
	• Lumbar puncture is contraindicated in patients with a brain abscess.

For over a century, clinicians have relied on physical examination findings such as neck stiffness, as well as Kernig and Brudzinski signs to diagnose meningitis. However, these signs have limited diagnostic accuracy, with sensitivities of only 5% for Kernig and Brudzinski signs 30% for nuchal rigidity (28). The jolt accentuation test, which exacerbates headache with horizontal neck rotation, demonstrates modest utility with pooled sensitivity and specificity of 65.3% and 70.4%, respectively (30).

Current guidelines from American, British, and European infection societies recommend immediate lumbar puncture neuroimaging delays in immunocompetent adults with suspected bacterial meningitis who present with a Glasgow Coma Scale score greater than or equal to 12 and no seizures (69). The following CSF profile typically helps differentiate infection types:

	• Bacterial meningitis: Neutrophilic pleocytosis) (> 1000/μL), hypoglycorrhachia (< 30 mg/dL), elevated protein >level (> 100 mg/dL) (66).
	• Viral meningitis: Mild pleocytosis, (< 1000 cells/mm³), initial polymorphonuclear predominance shifting to lymphocytic normal or slightly elevated, protein level, normal slightly reduced glucose level (73)
	• Fungal meningitis: Mononuclear pleocytosis (20 to 500 cells/mm³), elevated protein level, variable glucose concentrations (24)
	• Tuberculous meningitis: Lymphocytic pleocytosis, reduced glucose level (35 to 45 mg/dL) (45)

CSF lactate, when measured before antibiotic treatment, effectively differentiates bacterial from viral meningitis, with 93% sensitivity and 96% specificity. The advantage of CSF lactate lies on being unaffected by serum concentration, unlike glucose.

Molecular and serological testing has revolutionized diagnosis. PCR assays demonstrate greater than 90% sensitivity and specificity for detecting common bacterial and viral pathogens, although the sensitivity decreases to less than 50% when performed 1 week after symptom onset (47; 73; 52). Pathogen-specific tests include cryptococcal antigen detection (97% sensitivity, 86% to 100% specificity), GeneXpert MTB/RIF for tuberculosis, and galactomannan antigen for aspergillosis. Metagenomic next-generation sequencing of CSF aids diagnosis when conventional testing is inconclusive, with 57.5% sensitivity and 87.4% specificity in patients exhibiting headache, increased CSF WBC count, or reduced glucose level (18).

For brain abscess evaluation, MRI with diffusion-weighted/T1-weighted imaging with and without gadolinium is recommended with contrast-enhanced CT as an alternative (05).

Importantly, lumbar puncture is contraindicated in patients with brain abscesses due to herniation risk (15% to 30%) unless the information is deemed essential (31).

If no pathogen is detected despite thorough investigation, alternative diagnoses such as epilepsy, cerebrovascular disease, autoimmune encephalitis, or non-neurologic conditions should be considered (18).

Management

	• Timing of corticosteroid administration does not affect overall outcomes, although postantibiotic administration may slightly improve hearing loss.
	• The European Society of Clinical Microbiology and Infectious Diseases recommends corticosteroids for brain abscesses with severe symptoms due to perifocal edema or impending herniation.

The treatment for bacterial meningitis consists of supportive care, prompt antibiotic administration, and measures to lower intracranial pressure. (62). Broad-spectrum antibiotics should be initiated, with subsequent adjustments based on culture results (62).

A 2015 Cochrane review reported that corticosteroids significantly reduce hearing loss and neurologic sequelae (09). Adjunctive corticosteroid therapy has been shown to reduce morbidity and mortality in all but late-stage disease for patients with tuberculosis meningitis (39).

For Lyme disease with erythema migrans, amoxicillin, cefuroxime, or doxycycline should be prescribed as first-line agents (37). Oral doxycycline is effective for neuroborreliosis in adults with meningitis, cranial neuritis, and radiculitis, whereas the parenteral route is recommended for cases. Viral meningitis and encephalitis are managed with supportive care, including measures to lower intracranial pressure. Notably, empirical acyclovir treatment is recommended for suspected herpes simplex virus encephalitis.

Brain abscess management requires either surgical drainage or excision alongside antibiotic therapy. Stereotactic aspiration is recommended for diagnosis and decompression unless contraindicated due to the suspected organism type or the patient’s clinical condition (10). Lesions exceeding greater than 2.5 cm in diameter or causing a mass effect typically necessitate aspiration or excision. Empirical antibiotics for immunocompetent patients include vancomycin, metronidazole, and cefotaxime (12), whereas patients with immunosuppression require tailored treatment based on their immune defect. It is not always practical to drain the abscess; therefore, open excision is often performed initially or after unsuccessful aspiration (11). Nonsurgical treatment is indicated for patients with multiple abscesses, abscesses smaller than 2 cm in diameter, or abscesses in surgically inaccessible regions or in the cerebritis stage, and those with a normal level of consciousness without clinical deterioration (11). In such patients, measures to lower intracranial pressure may be required.

In the absence of clear evidence of harm, the European Society of Clinical Microbiology and Infectious Diseases strongly recommends corticosteroid administration for patients with brain abscesses who have severe symptoms due to perifocal edema or impending herniation. For aspirated or conservatively treated brain abscesses, intravenous antimicrobial treatment for 6 to 8 weeks is recommended, although expert opinion suggests shorter durations, such as 4 weeks, for patients undergoing abscess excision (05).

Headaches associated with intracranial infections should resolve with treatment of the underlying condition. Non-opioid analgesics can be used, whereas opioids may be used for severe cases, although their use may obscure neurologic assessments such as level of consciousness and pupillary size. Persistent headaches after the resolution of the infection and complications require an evaluation and possible treatment for chronic headaches. Neuroimaging should be performed to rule out the sequelae such as hydrocephalus, residual cerebral edema, or mass effect. Once these entities are excluded, lumbar puncture may be necessary to assess intracranial pressure, even in the absence of papilledema.

Triptans may help control headaches in patients with bacterial meningitis, but further studies are needed to confirm their efficacy.

The 2010 IDSA and 2022 WHO guidelines emphasize the importance of CSF drainage to control intracranial hypertension in patients with cryptococcal meningitis. Clinical CSF drainage methods include lumbar puncture, lumbar drainage, Ommaya reservoir implantation, and ventriculoperitoneal shunting. Repeated lumbar punctures are recommended in patients with CSF pressure greater than or equal to 250 mmH2O until the opening pressure is reduced by 50% or reaches normal levels (50; 32; 42). Lumbar drainage is an option for patients needing daily lumbar punctures, whereas Ommaya reservoirs or ventriculoperitoneal shunting may be required in refractory cases despite infection risks, particularly in patients with HIV (42).

In COVID-19-related headaches, 93% of patients required acute treatment. The most common medications were paracetamol (46%), ibuprofen (44%), triptans (28%), and metamizole (26%). The highest pain-free response rates at 2 hours were achieved with dexketoprofen (58.8%), triptans (57.7%), and ibuprofen (54.3%). Preventive treatment was needed in 75% of patients, with amitriptyline (66%) being the most commonly prescribed, followed by anesthetic nerve blocks (18%) and onabotulinumtoxin A (11%). Response rates were the highest for amitriptyline (50%) and nerve blocks (38.9%), with onabotulinumtoxin A showing the best 75% responder rate (18.2%). Preventive efficacy was greater in patients with a migraine history (22).

Regarding potential modifiers of headache patterns during SARS-CoV-2 infection, a 2025 study found no significant impact of COVID-19 vaccination on headache frequency during acute infection, regardless of vaccine type, dose, or the interval between vaccination and COVID-19 diagnosis (75).

A structured approach is crucial for managing postinfectious chronic daily headache, particularly post-COVID headaches. Key considerations include acute pain control and preventing medication overuse. Studies have shown that 96% of patients with post-COVID chronic daily headaches use acute pain medications, with 45% meeting the criteria for medication overuse. Early identification of chronicity risk factors, such as history of primary headache, high headache intensity, and female sex, is essential. Medication use should be monitored, as the median analgesic use reaches 12 days per month in this population (14).

Outcomes

Approximately 30% of bacterial meningitis survivors report persistent, diffuse, and continuous headaches, often with dizziness or cognitive impairments such as difficulty concentrating or memory issues. Post-infection headache syndromes have been documented in isolated case reports, but no robust evidence supports lasting headaches following other types of infections. Prospective studies are needed to better characterize post-infection headaches and their effects on pre-existing primary headache disorders (52).

References

01: Abbuehl LS, Hofmann E, Hakim A, Dietmann A. Can we forecast poor outcome in herpes simplex and varicella zoster encephalitis? A narrative review. Front Neurol 2023;14:1130090. PMID 37435162
02: Babi MA, Applebee A, Shapiro R, Waheed W. Syndrome of transient headache and neurologic deficits with cerebrospinal fluid lymphocytosis presenting as acute neurological emergencies. Cephalalgia 2017;37(3):284-9. PMID 27036641
03: Balkan II, Albayram S, Ozaras R, et al. Spontaneous intracranial hypotension syndrome may mimic aseptic meningitis. Scand J Infect Dis 2012;44(7):481-8. PMID 22404365
04: Bijlsma MW, Brouwer MC, Kasanmoentalib ES, et al. Community-acquired bacterial meningitis in adults in the Netherlands, 2006-14: a prospective cohort study. Lancet Infect Dis 2016;16(3):339-47. PMID 26652862
05: Bodilsen J, D'Alessandris QG, Humphreys H, et al. European society of Clinical Microbiology and Infectious Diseases guidelines on diagnosis and treatment of brain abscess in children and adults. Clin Microbiol Infect 2024;30(1):66-89.** PMID 37648062
06: Bodilsen J, Duerlund LS, Mariager T, et al. Clinical features and prognostic factors in adults with brain abscess. Brain 2023;146(4):1637-47. PMID 36037264
07: Bonfield CM, Sharma J, Dobson S. Pediatric intracranial abscesses. J Infect 2015;71 Suppl 1:42-6.** PMID 25917804
08: Brouwer MC, Coutinho JM, van de Beek D. Clinical characteristics and outcome of brain abscess: systematic review and meta-analysis. Neurology 2014a;82(9):806-13.** PMID 24477107
09: Brouwer MC, McIntyre P, Prasad K, van de Beek D. Corticosteroids for acute bacterial meningitis. Cochrane Database Syst Rev 2015;2015(9):CD004405. PMID 26362566
10: Brouwer MC, Tunkel AR, McKhann GM, van de Beek D. Brain abscess. N Engl J Med 2014b;371(5):447-56.** PMID 25075836
11: Brouwer MC, van de Beek D. Epidemiology, diagnosis, and treatment of brain abscesses. Curr Opin Infect Dis 2017;30(1):129-34.** PMID 27828809
12: Calfee DP, Wispelwey B. Brain abscess. Semin Neurol 2000;20(3):353-60. PMID 11051299
13: Caronna E, van den Hoek TC, Bolay H, et al. Headache attributed to SARS-CoV-2 infection, vaccination and the impact on primary headache disorders of the COVID-19 pandemic: a comprehensive review. Cephalalgia 2023;43(1):3331024221131337.** PMID 36606562
14: Carvalho LCLS, Silva PAD, Rocha-Filho PAS. Persistent headache and chronic daily headache after COVID-19: a prospective cohort study. Korean J Pain 2024;37(3):247-55. PMID 38881283
15: Chen SP, Fuh JL, Wang SJ. Reversible cerebral vasoconstriction syndrome: an under-recognized clinical emergency. The Adv Neurol Disord 2010;3(3):161-71.** PMID 21179608
16: Chu KH, Howell TE, Keijzers G, et al. Acute headache presentations to the emergency department: A state‐wide cross‐sectional study. Acad Emerg Med 2017;24(1):53-62.** PMID 27473746
17: Davis LE. Acute bacterial meningitis. Continuum (Minneap Minn) 2018;24(5, Neuroinfectious Disease):1264-83.** PMID 30273239
18: Deng J, Chen X, Bu Y, Zhang J, Han J. Exploring the appropriate situation of performing CSF mNGS in patients with proposed intracranial infections. BMC Neurol 2024;24(1):429. PMID 39501184
19: Fernandez-de-Las-Penas C, Gómez-Mayordomo V, Cuadrado ML, et al. The presence of headache at onset in SARS-CoV-2 infection is associated with long-term post-COVID headache and fatigue: A case-control study. Cephalalgia 2021;41(13):1332-41. PMID 34134526
20: Flægstad T. Meningococcal meningitis. In: Hakan Dogan K, editor. Disorders of consciousness-a review of important issues. IntechOpen 2020.
21: Frantzidou F, Kamaria F, Dumaidi K, Skoura L, Antoniadis A, Papa A. Aseptic meningitis and encephalitis because of herpesviruses and enteroviruses in an immunocompetent adult population. Eur J Neurol 2008;15(9):995-7. PMID 18637823
22: García-Azorín D, García-Ruiz C, Sierra-Mencía Á, et al. Acute and preventive treatment of COVID-19-related headache: A series of 100 patients. Life (Basel) 2024;14(7):910. PMID 39063663
23: Giamberardino MA, Affaitati G, Costantini R, Guglielmetti M, Martelletti P. Acute headache management in emergency department. A narrative review. Intern Emerg Med 2020;15(1):109-17.** PMID 31893348
24: Gottfredsson M, Perfect J. Fungal meningitis. Semin Neurol 2000;20(3):307-22. PMID 11051295
25: Granerod J, Davies NWS, Ramanuj PP, Easton A, Brown DWG, Thomas SL. Increased rates of sequelae post-encephalitis in individuals attending primary care practices in the United Kingdom: a population-based retrospective cohort study. J Neurol 2017;264(2):407-15. PMID 27766471
26: Gundamraj V, Hasbun R. Viral meningitis and encephalitis: an update. Curr Opin Infect Dis 2023;36(3):177-85. PMID 37093042
27: Handschin N, Oppliger M, Brehm A, et al. Nontraumatic headache in adult emergency patients: prevalence, etiologies, and radiological findings. J Clin Med 2020;9(8):2621.** PMID 32806717
28: Hasbun R. Progress and challenges in bacterial meningitis: a review. JAMA 2022;328(21):2147-54.** PMID 36472590
29: Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia 2018;38(1):1-211.** PMID 29368949
30: Iguchi M, Noguchi Y, Yamamoto S, Tanaka Y, Tsujimoto H. Diagnostic test accuracy of jolt accentuation for headache in acute meningitis in the emergency setting. Cochrane Database Syst Rev 2020;6(6):CD012824.** PMID 32524581
31: Jain R, Chang WW. Emergency department approach to the patient with suspected central nervous system infection. Emerg Med Clin North Am 2018;36(4):711-22.** PMID 30297000
32: Jjunju S, Nuwagira E, Meya DB, Muzoora C. Persistently elevated intracranial pressure in cryptococcal meningitis- 76 therapeutic lumbar punctures. Med Mycol Case Rep 2023;40:50-3. PMID 37283716
33: Kim KS. Investigating bacterial penetration of the blood-brain barrier for the pathogenesis, prevention, and therapy of bacterial meningitis. ACS Infect Dis 2020;6(1):34-42. PMID 31805229
34: Kirkland KE, Kirkland K, Many WJ Jr, Smitherman TA. Headache among patients with HIV disease: prevalence, characteristics, and associations. Headache 2012;52(3):455-66. PMID 22077887
35: Kohil A, Jemmieh S, Smatti MK, Yassine HM. Viral meningitis: an overview. Arch Virol 2021;166(2):335-45. PMID 33392820
36: Koskiniemi M, Rantalaiho T, Piiparinen H, et al. Infections of the central nervous system of suspected viral origin: a collaborative study from Finland. J Neurovirol 2001:7(5):400-8. PMID 11582512
37: Kullberg BJ, Vrijmoeth HD, van de Schoor F, Hovius JW. Lyme borreliosis: diagnosis and management. BMJ 2020;369:m1041. PMID 32457042
38: Kumar S, Verma R, Garg RK, Malhotra HS, Sharma PK. Prevalence and outcome of headache in tuberculous meningitis. Neurosciences (Riyadh) 2016;21(2):138-44. PMID 27094524
39: Leonard JM. Central nervous system tuberculosis. Microbiol Spectr 2017;5(2). PMID 28281443
40: Leone M, Giani L, Phaka M, et al. Burden of headache in a HIV-positive population of sub-Saharan Africa. Cephalalgia 2022;42(9):918-25. PMID 36472590
41: Linde M, Langnes HA, Hagen K, Bergh K, Stovner LJ. No increase in headache after previous intracranial infections: a historical cohort study (HUNT). Eur J Neurol 2012;19(2):324-31. PMID 21951375
42: Liu MZ, Dai XH, Zeng MT, Chen EQ. Clinical treatment of cryptococcal meningitis: an evidence-based review on the emerging clinical data. J Neurol 2024;271(6):2960-79. PMID 38289535
43: Lucas MJ, Brouwer MC, van de Beek D. Neurological sequelae of bacterial meningitis. J Infect 2016;73(1):18-27. PMID 27105658
44: Lynch KM, Brett F. Headaches that kill: A retrospective study of incidence, etiology and clinical features in cases of sudden death. Cephalalgia 2012;32(13):972-8. PMID 22875877
45: Mai NT, Thwaites GE. Recent advances in the diagnosis and management of tuberculous meningitis. Curr Opin Infect Dis 2017;30(1):123-8.** PMID 27798497
46: Marchioni E, Minoli L. Headache attributed to infections nosography and differential diagnosis. Handb Clin Neurol 2010;97:601-26. PMID 20816458
47: McGill F, Heyderman RS, Panagiotou S, Tunkel AR, Solomon T. Acute bacterial meningitis in adults. Lancet 2016;388(10063):3036-47. PMID 27265346
48: Morís G, Garcia-Monco JC. The challenge of drug-induced aseptic meningitis revisited. JAMA Intern Med 2014;174(9):1511-2. PMID 25003798
49: Ogrinc K, Lusa L, Lotrič-Furlan S, et al. Course and outcome of early European Lyme neuroborreliosis (Bannwarth syndrome): clinical and laboratory findings. Clin Infect Dis 2016;63(3):346-53. PMID 27161773
50: Perfect JR, Dismukes WE, Dromer F, et al. Clinical practice guidelines for the management of cryptococcal disease: 2010 update by the infectious diseases society of America. Clin Infect Dis 2010;50(3):291-322. PMID 20047480
51: Petersen PT, Bodilsen J, Jepsen MPG, et al. Benign recurrent lymphocytic meningitis (Mollaret’s meningitis) in Denmark: a nationwide cohort study. Eur J Neurol 2024;31(1):e16081. PMID 37797296
52: Ramesh R, Ranganathan LN. Headache in infections. Curr Opin Neurol 202538(3):281-7. PMID 39878050
53: Raut T, Garg RK, Jain A, et al. Hydrocephalus in tuberculous meningitis: Incidence, its predictive factors and impact on the prognosis. J Infect 2013;66(4):330-7. PMID 23291048
54: Rosenberg DH, Arling PA. Landmark article Aug 12, 1944: Penicillin in the treatment of meningitis. JAMA 1984;251(14):1870-6. PMID 6366279
55: Sampaio Rocha-Filho PA. Headache associated with Coronavirus disease 2019. Neurol Clin 2024;42(2):507-20. PMID 38575263
56: Scheld WM, Mandell GL. Landmark perspective. Sulfonamides and meningitis. JAMA 1984;251(6):791-4. PMID 6363730
57: Silberstein SD. Evaluation and emergency treatment of headache. Headache 1992;32(8):396-407. PMID 1399562
58: Sohail S, Nakigozi G, Anok A, et al. Headache prevalence and its functional impact among HIV-infected adults in rural Rakai District, Uganda. J Neurovirol 2019;25(2):248-53. PMID 30607892
59: Solomon T, Michael BD, Smith PE, et al. Management of suspected viral encephalitis in adults — Association of British Neurologists and British Infection Association National Guidelines. J Infect 2012;64(4):347-73.** PMID 22120595
60: Steere AC, Strle F, Wormser GP, et al. Lyme borreliosis. Nat Rev Dis Primers 2016;2:16090.** PMID 27976670
61: Synmon B, Kayal AK, Goswami M, et al. Clinical and radiological spectrum of intracranial tuberculosis. A hospital based study in Northeast India. Indian J Tuberc 2017;64(2):109-18. PMID 28410693
62: Tan YC, Gill AK, Kim KS. Treatment strategies for central nervous system infections: an update. Expert Opin Pharmacother 2015;16(2):187-203. PMID 25328149
63: Thakur KT, Wilson MR. Chronic meningitis. Continuum (Minneapolis Minn) 2018;24(5):1298-326.** PMID 30273241
64: Tunkel AR, Glaser CA, Bloch C, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2008;47(3):303–27. PMID 18582201
65: Tyler KL. Acute viral encephalitis. N Engl J Med 2018;379(6):557-66.** PMID 30089069
66: van de Beek D, Brouwer MC, Koedel U, Wall EC. Community-acquired bacterial meningitis. Lancet 2021;398(10306):1171-83. PMID 34303412
67: Viarasilpa T, Ghosh P, Gidwani S, et al. Prognostic significance of sentinel headache preceding aneurysmal subarachnoid hemorrhage. World Neurosurg 2020;139:e672-6. PMID 32339738
68: Wagner JN, Kalev O, Sonnberger M, Krehan I, von Oertzen TJ. Evaluation of clinical and paraclinical findings for the differential diagnosis of autoimmune and infectious encephalitis. Front Neurol 2018;9:434. PMID 29951031
69: Wall EC, Chan JM, Gil E, Heyderman RS. Acute bacterial meningitis. Curr Opin Neurol 2021;34(3):386-95. PMID 33767093
70: Weisfelt M, van de Beek D, Spanjaard L, Reitsma JB, de Gans J. Clinical features, complications, and outcome in adults with pneumococcal meningitis: a prospective case series. Lancet Neurol 2006;5(2):123-9.** PMID 16426988
71: Williamson PR, Jarvis JN, Panackal AA, et al. Cryptococcal meningitis: epidemiology, immunology, diagnosis and therapy. Nat Rev Neurol 2017;13(1):13-24.** PMID 27886201
72: World Health Organization. Defeating bacterial meningitis by 2030. Available at: https://www.who.int/initiatives/defeating-meningitis-by-2030. Accessed November 2021.
73: Wright WF, Pinto CN, Palisoc K, Baghli S. Viral (aseptic) meningitis: a review. J Neurol Sci 2019a;398:176-83.** PMID 30731305
74: Yang CW, Fuh JL. Thunderclap headache: an update. Expert Rev Neurother 2018;18(12):915-24.** PMID 30334463
75: Yeh JT, Wang YF, Tzeng YS, Chen SP, Pan LH, Wang SJ. Exploring the impact of acute SARS-CoV-2 infection on headache pattern in patients with migraine: A novel Bayesian analysis. Headache 2025;65(5):745-55. PMID 39927465

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Fu-Chi Yang MD PhD

Dr. Yang of National Defense Medical Center in Taiwan has no relevant financial relationships to disclose.
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Editor

Shuu-Jiun Wang MD

Dr. Wang of National Yang-Ming University and Taipei Veterans General Hospital received research grants from AbbVie, Lundbeck, Pfizer, Novartis, and Orient Europharma as principal investigator. He received speaker honorariums from AbbVie, Biogen, Eli Lilly, Hava Biopharma, and Pfizer.
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Former Authors

Stephen D Silberstein MD
Debra Ann Pollack MD
Paula M Mendes MD
Madhavi Gupta MD
Jong-Ling Fuh MD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: No sex preponderance
Heredity: none
Population groups selectively affected: No population group selectively affected
Occupation groups selectively affected: None selectively affected

ICD & OMIM codes

ICD-10: Encephalitis: G05

Intracranial abscess: G06.0

Non-arthropod-borne viral disease of CNS: A89

Meningitis, unspecified: G03.9

Viral meningitis, unspecified: A87.9
ICD-11: Encephalitis, not elsewhere classified: 8E48

Viral encephalitis, not elsewhere classified: 1C80

Viral meningitis, unspecified: 1C8E.Z

Infectious meningitis, unspecified: 1D01.Z

Intracranial abscess: 1D03.3

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Headache associated with intracranial infection

Associated Disorders

Bacterial meningitis
Lyme disease

Differential Diagnosis

migraine
thunderclap headache
ruptured aneurysm
aneurysmal subarachnoid hemorrhage
nonbacterial meningitis
- meningoencephalitis
- lymphocytic pleocytosis
- acute purulent sinusitis
- CNS lymphoma
- neurotropic viruses
- lupus
- sarcoidosis
- carcinomatous meningitis
- subdural empyema
- epidural abscess
- cerebral neoplasm
- cerebrovascular accident
- encephalitis
- brain tumor
- postinfectious encephalomyelitis
- toxic encephalopathy
- drug-induced aseptic meningitis
- cerebral infarction
- subdural hematoma

Also Relevant

Arboviral encephalitis
Brain abscess
Cryptococcal meningitis
Diagnosis of CNS infections
Gram-negative bacillary meningitis
- Headache associated with HIV and AIDS
- Herpes simplex encephalitis
- Recurrent meningitis
- Viral meningitis

Clinical Categories

Headache & Pain

Headache associated with intracranial infection …

Headache associated with intracranial infection

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

Special considerations

Anesthesia

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Suzetrigine

Atogepant

Headache associated with HIV and AIDS

Primary exercise headache

Chiropractic manipulation: neurologic complications

Myofascial pain syndrome

Femoral neuropathy

Primary headache associated with sexual activity

Headache associated with intracranial infection

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Outcomes

Special considerations

Anesthesia

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Suzetrigine

Atogepant

Headache associated with HIV and AIDS

Primary exercise headache

Chiropractic manipulation: neurologic complications

Myofascial pain syndrome

Femoral neuropathy

Primary headache associated with sexual activity

This is an article preview.
Start a Free Account
to access the full version.