Erfan Bashar
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Meningitis

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Educational scope notice: This is a study note for medical students, not medical advice, diagnosis, or treatment guidance. Clinical management should follow local protocols and current guidelines. Drug dosing below is intentionally omitted; exact regimens follow local protocols.

Meningitis is inflammation of the pia and arachnoid mater, the membranes covering the brain and spinal cord. It is a neurological emergency because delay in empiric antibiotics increases death and permanent disability. Pain sensitivity within the skull resides in the dura mater, the dural and meningeal vessels, and the large cerebral vessels. The pia and arachnoid themselves are largely insensitive. Inflammation that stretches these pain-sensitive meningeal and vascular structures produces neck pain with resistance to flexion.

The three bedside signs share one mechanism: stretching inflamed meninges causes pain. Passive neck flexion pulls on cervical meninges and meets reflex resistance (nuchal rigidity). The same flexion triggering hip and knee bending is the Brudzinski sign. Pain on knee extension with the hip flexed is the Kernig sign. These signs are insensitive, so their absence never excludes meningitis. They accompany any meningeal irritation, including subarachnoid blood and carcinomatous spread, not only infection. A hyperacute stiff neck favours subarachnoid haemorrhage. A progressive one favours meningitis.

The classic triad of fever, neck stiffness, and altered mental status is present in only 41% of bacterial cases. Most patients show at least one feature, so the absence of the full triad never excludes the disease. Headache is nearly universal. Cranial nerve involvement occurs in a minority. Deafness is the most common lasting cranial complication of pneumococcal disease, affecting roughly 1 in 7 survivors, which is why hearing follow-up matters after pneumococcal meningitis.

Cerebrospinal fluid profiles

Lumbar puncture is the central investigation. Opening pressure is recorded at the tap. Glucose must always be read against simultaneous serum glucose. The usual pattern is:

  • Bacterial: cloudy or purulent fluid, white cells often above 1,000 per microlitre with neutrophil predominance, protein high, glucose low (below about 40% of serum).
  • Viral: clear fluid, usually fewer than 200 white cells per microlitre with lymphocytic predominance, normal glucose, mildly raised protein.
  • Tuberculous: clear or slightly cloudy fluid with lymphocytic predominance, high protein, and low glucose; the full subacute course, workup, and treatment live in the companion note on tuberculous meningitis (/notes/neurology/tuberculous-meningitis/).

No single cutoff confirms bacterial meningitis on its own. Many bacterial cases never show every typical extreme of low glucose and glucose ratio with high protein and cell counts, so falling short of them does not exclude bacterial disease.

Cause follows age and setting

Community-acquired adult meningitis is most often pneumococcal, with meningococcus second and concentrated in young adults. Pneumococcus carries the worse prognosis. Hospital-acquired disease after neurosurgery more often involves staphylococci and gram-negative bacilli. Listeria matters past age 50 and in immunocompromised patients. Listeria is not covered by ceftriaxone alone, which is why ampicillin joins the regimen there.

Empiric treatment starts on suspicion

Antibiotics begin immediately when bacterial meningitis is suspected, without waiting for imaging or lumbar puncture results. The standard adult structure is a third-generation cephalosporin plus vancomycin below age 50. Above 50, or with impaired cellular immunity, ampicillin is added to cover Listeria. Local resistance patterns may modify this backbone, so exact regimens follow local guidelines. Dexamethasone, begun before or with the first antibiotic dose, improves survival in pneumococcal disease; exact dosing follows local protocols. That survival benefit is pneumococcus-specific and must not be generalised to all pathogens. Cultures then narrow therapy. Durations run about 10 to 14 days for pneumococcus and longer for Listeria.

Close contacts of meningococcal cases receive prophylactic antibiotics as soon as possible, ideally within 24 hours of identifying the index patient. Rifampin, ciprofloxacin, and ceftriaxone each clear nasopharyngeal carriage in 90 to 95% and are all acceptable agents. Prophylaxis covers household, childcare, and oral-secretion contacts. The exact agent follows local public health protocols.

Complications and the milder forms

The main complications are:

  • Swelling within the rigid skull can herniate and kill.
  • Inflamed basal vessels can occlude and infarct.
  • Cortical irritation provokes seizures.
  • Blocked reabsorption produces hydrocephalus, acutely or as a late normal-pressure picture.

Viral meningitis, most often enteroviral, is typically self-limiting over about two weeks with supportive care. Culture-negative (aseptic) meningitis spans viral, tuberculous, fungal, Lyme, and carcinomatous causes.

Non-infectious meningitis occurs in systemic disease such as Behcet disease, lupus, vasculitis, and sarcoidosis. It tends to mimic viral fluid findings, so the systemic context guides diagnosis.

Evidence anchors

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