Cribriform Plate Infection

Syndromes

■ Localization

CNS infection may involve the leptomeninges and CSF spaces (meningitis), the ventricular system (ventriculitis), the gray and white matter of the brain (encephalitis), or the spinal cord (myelitis). A focus of bacterial infection of the brain is called a brain abscess, or cerebritis in the early stage before a frank abscess is formed. Pus located between the dura mater and the arachnoid membrane is called a subdural empy-ema, while pus outside the dura is called an epidural abscess.

The clinical manifestations may be acute (purulent meningitis, CNS listeriosis, herpes simplex encephalitis), subacute (cerebral abscess, focal encephalitis, neuroborreliosis, neurosyphilis, tuberculous meningitis, actinomyco-sis, nocardiosis, rickettsiosis, neurobrucellosis), or chronic (tuberculous meningitis, neurosyphilis, neuroborreliosis, Whipple encephalitis, Creutzfeldt-Jakob disease). The epidemiological pattern of infection may be sporadic, endemic or epidemic, depending on the pathogen.

■ Clinical Manifestations

Meningitis and encephalitis rarely occur as entirely distinct syndromes; they usually present in mixed form (meningoencephalitis, en-cephalomyelitis). CSF examination establishes the diagnosis.

These disorders may present in specific ways in certain patient groups. Neonates and children commonly manifest failure to thrive, fever or hypothermia, restlessness, breathing disorders, epileptic seizures, and a bulging fontanelle. The elderly may lack fever but frequently have behavioral abnormalities, confusion, epileptic seizures, generalized weakness, and impairment of consciousness ranging to coma. Im-munodeficient patients commonly have fever, headache, stiff neck, and drowsiness in addition to the manifestations of their primary illness. Meningitic syndrome is characterized by fever, severe, intractable headache and backache, photophobia and phonophobia, nausea, vomiting, impairment of consciousness, stiff neck, and hy-perextended posture, with opisthotonus or neck pain on flexion. Kernigs sign (resistance to passive raising of leg with extended knee) and Brudzinski's sign (involuntary leg flexion on passive flexion of the neck) are signs of meningeal involvement. Painful neck stiffness is due to (lepto)meningeal irritation by infectious meningitis, septicemia, subarachnoid hemorrhage, neoplastic meningitis, or other causes. Isolated neck stiffness not caused by meningitis (meningism) may be due to cervical disorders such as arthrosis, fracture, intervertebral disk herniation, tumor, or extrapyramidal rigidity. Papilledema is usually absent; when present, it indicates intracranial hypertension (p. 158). Encephalitic syndrome is characterized by headache and fever, sometimes accompanied by epileptic seizures (often focal), focal signs (cranial nerves deficits, especially of CN III, IV, VI, and VII; aphasia, hemiparesis, hemianopsia, ataxia, choreoathetosis), behavioral changes, and impairment of consciousness (restlessness, irritability, confusion, lethargy, drowsiness, coma). The neurological signs may be preceded by limb pain (myalgia, arthralgia), a slight increase in body temperature, and malaise. For acute cerebellitis (^ ataxia), see p. 276. Brain stem encephalitis produces ophthalmoplegia, facial paresis, dysarthria, dysphagia, ataxia, and hearing loss.

Myelitic syndrome. Myelitis presents with severe local pain, paraparesis, paresthesiae, or some combination of these. Incomplete or complete paraplegia or quadriplegia (p. 48) develops within a few hours (acute) or days (subacute). The differential diagnosis may be difficult.

Subdural empyema, abscess

Osteomyelitis

Epidural abscess

Neck stiffness

Brain stem encephalitis

Myelitis, spinal abscess -

Meningitis

Subdural empyema, abscess

Osteomyelitis

Neck stiffness

Subdural Empyema Pathogenesis

Epidural abscess

Encephalitis, focal encephalitis (cerebritis), abscess

Brain stem encephalitis

Myelitis, spinal abscess -

Meningitis

Ventriculitis

Cerebellitis, cerebellar abscess

Encephalitis, focal encephalitis (cerebritis), abscess

Ventriculitis

Cerebellitis, cerebellar abscess

Sites of CNS infection

Pathogenesis

Pathogens usually reach the CNS by local extension from a nearby infectious focus (e. g. sinusitis, mastoiditis) or by hematogenous spread from a distant focus. The ability of pathogens to spread by way of the bloodstream depends on their virulence and on the immune status of the host. They use special mechanisms to cross or circumvent the blood-brain barrier (p. 8). Some pathogens enter the CNS by centripetal travel along peripheral nerves (herpes simplexvirus type I, variE cella-zoster virus, rabies virus), others by en-•S docytosis (Neisseria meningitidis), intracellular ^ transport (Plasmodium falciparum via erythro-1« cytes, Toxoplasma gondii via macrophages), or in-O tracellular invasion (Haemophilus influenzae). u Those that enter the subarachnoid space probably g do so by way of the choroid plexus, venous "3 sinuses, or cribriform plate (p. 76). Having •fa entered the CSF spaces, pathogens trigger an in-(<u flammatory response characterized by the release of complement factors and cytokines, the influx of leukocytes and macrophages, and the activation of microglia and astrocytes. Disruption of the blood-brain barrier results in an influx of fluids and proteins across the vascular en-dothelium and into the CNS, causing vasogenic cerebral edema (p. 162), which is accompanied by both cytotoxic cellular edema and interstitial edema due to impaired CSF circulation. Cerebral edema causes intracranial hypertension. These processes, in conjunction with vasculitis, impairment of vascular autoregulatory mechanisms, and/or fluctuations of systemic blood pressure, lead to the development of ischemic, metabolic, and hypoxic cerebral lesions (focal necrosis, territorial infarction).

porting (as specified by local law), prevention of exposure (isolation of sources of infection, disinfection, sterilization), and prophylaxis in persons at risk (active and passive immunization, chemoprophylaxis).

Treatment. Patients with bacterial or viral meningoencephalitis must be treated at once. The treatment strategy is initially based on the clinical and additional findings. Antimicrobial therapy is first given empirically in a broad-spectrum combination, then specifically tailored in accordance with the species and drug sensitivity pattern of the pathogen(s) identified. Causative organisms may be found in the CSF, blood, or other bodily fluids (e. g., throat smear, urine or stool samples, bronchial secretions, gastric juice, abscess aspirate).

Treatment (Table 28, p. 375)

The immune system is generally no longer able to hold pathogens in check once they have spread to the CNS, as the immune response in the subarachnoid space and the neural tissue itself is less effective than elsewhere in the body. Having gained access to the CNS, pathogens meet with favorable conditions for further spread within it.

Prophylaxis. The occurrence and spread of CNS infection can be prevented by mandatory re-

Venous sinus -

Otitis media, mastoiditis

Venous sinus -

Otitis media, mastoiditis

Cribriform Plate Infection

Sinusitis (frontal sinus)

Nasal route of infection (cribriform plate)

Hematogenous spread of endocarditis infection Routes of CNS infection

Sinusitis (frontal sinus)

Nasal route of infection (cribriform plate)

infection Routes of CNS infection

CSF space

(subarachnoid space)

Macrophage

Endothelial cell

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Responses

  • Iines
    Where is the cribriform plate located?
    6 years ago
  • iiro
    How encephalitis is spread in the brain?
    5 years ago
  • lodovica bellucci
    How to treat an infection of the cribriform plate?
    1 year ago

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