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Physical Examination

The classic triad of meningitis consists of fever, nuchal rigidity, and altered mental status, but not all
patients have all 3, and almost all patients have headache. Altered mental status can range from irritability
to somnolence, delirium, and coma. The examination reveals no focal neurologic deficits in the majority of
cases. Furthermore, the majority of patients with bacterial meningitis have a stiff neck, but the meningeal
signs are insensitive for diagnosis of meningitis.[13]
Acute bacterial meningitis in otherwise healthy patients who are not at the extremes of age presents in a
clinically obvious fashion. In contrast, most patients with subacute bacterial meningitis pose a diagnostic
challenge. Systemic examination occasionally reveals a pulmonary or otitis media coinfection.
Systemic findings can also be present. Extracranial infection (eg, sinusitis, otitis media, mastoiditis,
pneumonia, or urinary tract infection [UTI]) may be noted. Endotoxic shock with vascular collapse is
characteristic of severe N meningitidis(meningococcal) infection.
General physical findings in viral meningitis are common to all causative agents, but some viruses
produce unique clinical manifestations that help focus the diagnostic approach. Enteroviral infection is
suggested by the presence of the following:

Exanthemas
Symptoms of pericarditis, myocarditis, or conjunctivitis
Syndromes of pleurodynia, herpangina, and hand-foot-and-mouth disease
Increased blood pressure with bradycardia can also be present. Vomiting occurs in 35% of patients.
Nonblanching petechiae and cutaneous hemorrhages may be present in meningitis caused by N
meningitidis (50%), H influenzae, S pneumoniae, or S aureus.[14] Arthritis is seen with meningococcal
infection and with M pneumoniaeinfection but is less common with other bacterial species.

Infants
Infants may have the following:

Bulging fontanelle (if euvolemic)


Paradoxic irritability (ie, remaining quiet when stationary and crying when held)
High-pitched cry
Hypotonia
In infants, the clinicians should examine the skin over the entire spine for dimples, sinuses, nevi, or tufts
of hair. These may indicate a congenital anomaly communicating with the subarachnoid space.

Focal neurologic signs


Focal neurologic signs include isolated cranial nerve abnormalities (principally of cranial nerves III, IV, VI,
and VII), which are present in 10-20% of patients. These result from increased intracranial pressure (ICP)
or the presence of exudates encasing the nerve roots. Focal cerebral signs are present in 10-20% of
patients and may develop as a result of ischemia from vascular inflammation and thrombosis.
Papilledema is a rare finding (< 1% of patients) that also indicates increased ICP, but it is neither sensitive
nor specific: it occurs in only one third of meningitis patients with increased ICP and is present not only in
meningitis but also in brain abscess and other disorders.

Signs of meningeal irritation


For more than 100 years, clinicians have relied on meningeal signs (nuchal rigidity, Kernig sign, and
Brudzinski sign) to evaluate patients with suspected meningitis and help determine who should undergo a
lumbar puncture (LP). However, a prospective study of 297 adults with suspected meningitis documented
very low sensitivities for these signs: 5% for the Kernig sign, 5% for the Brudzinski sign, and 30% for
nuchal rigidity.[13] Thus, the absence of the meningeal signs should not defer the performance of the LP.

Systemic and extracranial findings


Systemic findings on physical examination may provide clues to the etiology of a patients meningitis.
Morbilliform rash with pharyngitis and adenopathy may suggest a viral etiology (eg, Epstein-Barr virus
[EBV], cytomegalovirus [CMV], adenovirus, or HIV). Macules and petechiae that rapidly evolve into
purpura suggest meningococcemia (with or without meningitis). Vesicular lesions in a dermatomal
distribution suggest VZV. Genital vesicles suggest HSV-2 meningitis.
Sinusitis or otitis suggests direct extension into the meninges, usually with S pneumoniae or, less often, H
influenzae. Rhinorrhea or otorrhea suggests a cerebrospinal fluid (CSF) leak from a basilar skull fracture,
with meningitis most commonly caused by S pneumoniae.
Hepatosplenomegaly and lymphadenopathy suggest a systemic disease, including viral (eg,
mononucleosislike syndrome in EBV, CMV, and HIV) and fungal (eg, disseminated histoplasmosis). The
presence of a heart murmur suggests infective endocarditis with secondary bacterial seeding of the
meninges.

Chronic meningitis
It is essential to perform careful general, systemic, and neurologic examinations, looking especially for the
following:

Lymphadenopathy
Papilledema and tuberculomas during funduscopy
Meningismus
Cranial nerve palsies
Tuberculous meningitis
The presentation of chronic tuberculous meningitis may be acute, but the classic presentation is subacute
and spans weeks. Patients generally have a prodrome consisting of fever of varying degrees, malaise,
and intermittent headaches. Cranial nerve palsies (III, IV, V, VI, and VII) often develop, suggesting basilar
meningeal involvement.
Clinical staging of tuberculous meningitis is based on neurologic status, as follows:

Stage 1 - No change in mental function, with no deficits and no hydrocephalus


Stage 2 - Confusion and evidence of neurologic deficit
Stage 3 - Stupor and lethargy
Syphilitic meningitis
The median incubation period before the appearance of symptoms in chronic syphilitic meningitis is 21
days (range, 3-90 days), during which time spirochetemia develops. Syphilitic meningitis usually occurs
during the primary or secondary stage of syphilis, complicating 0.3-2.4% of primary infections during the
first 2 years. Its presentation is similar to those of other types of aseptic meningitis, including headache,
nausea, vomiting, and meningismus.
Meningovascular syphilis occurs later in the course of untreated syphilis, and the symptoms are
dominated by focal syphilitic arteritis (ie, focal neurologic symptoms associated with signs of meningeal
irritation) that spans weeks to months and results in stroke and irreversible damage if left untreated.
Patients with concomitant HIV infection have an increased risk of accelerated progression.
Lyme meningitis
Although rare during stage 1 of Lyme disease, central nervous system (CNS) involvement with meningitis
may occur in Lyme diseaseassociated chronic meningitis and is characterized by the concurrent
appearance of erythema migrans at the site of the tick bite. More commonly, aseptic meningitis syndrome
occurs 2-10 weeks after the erythema migrans rash. This represents stage 2 of Lyme disease, or the
borrelial hematogenous dissemination stage.

Headache is the most common symptom of Lyme diseaseassociated chronic meningitis, with
photophobia, nausea, and neck stiffness occurring less frequently. Somnolence, emotional lability, and
impaired memory and concentration may occur. Facial nerve palsy is the most common cranial nerve
deficit. These symptoms of meningitis usually fluctuate and may last for months if left untreated.
Fungal meningitis
Meningitis from C neoformans usually develops in patients with defective cell-mediated immunity
(see CNS Cryptococcosis in HIV). It is characterized by the gradual onset of symptoms, the most
common of which is headache.
Coccidioidal meningitis is the most serious form of disseminatedcoccidioidomycosis; it usually is fatal if
left untreated. These patients may present with headache, vomiting, and altered mental function
associated with pleocytosis, elevated protein levels, and decreased glucose levels. Eosinophils may be a
prominent finding on CSF analysis.
Patients infected with B dermatitidis may present with an abscess or fulminant meningitis. Patients
infected with H capsulatum may present with headache, cranial nerve deficits, or changes in mental
status months before diagnosis.

Helminthic eosinophilic meningitis


After ingestion of A cantonensis larvae, which are found in raw or undercooked mollusks, most patients
with symptomatic disease present with nonspecific and self-limited abdominal pain caused by larval
migration into the bowel wall. On rare occasions, the larvae can migrate into the CNS and cause
eosinophilic meningitis. Although A cantonensis is prevalent in Southeast Asia and tropical Pacific islands,
infestations from this parasitic nematode have been reported in the United States and the Caribbean. [15]

Aseptic meningitis
In contrast to patients with bacterial meningitis, patients with aseptic meningitis syndrome usually appear
clinically nontoxic, with no vascular instability. (SeeAseptic Meningitis.) In many cases, a cause for
meningitis is not apparent after initial evaluation, and the condition is therefore classified as aseptic
meningitis. These patients characteristically have an acute onset of meningeal symptoms, fever, and CSF
pleocytosis that is usually prominently lymphocytic.
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