Anatomical routes where infection can spread to the brain

Infectious agents may reach the nervous system through several routes of entry:
-

Hematogenous spread by way of the arterial blood supply is the most common
means of entry. There can also be retrograde venous spread, through the anastomoses
between veins of the face and the venous sinuses of the skull.
Direct implantation of microorganisms is almost invariably due to traumatic
introduction of foreign material. In rare cases it can be iatrogenic, as when microbes
are introduced with a lumbar puncture needle.
Local extension can occur with infections of the skull or spine. Sources include air
sinuses, most often the mastoid or frontal; infected teeth; cranial or spinal
osteomyelitis; and congenital malformations, such as meningomyelocele.
Peripheral nerves also may serve as paths of entry for a few pathogensin
particular, viruses such as the rabies and herpes zoster viruses.

Epidural and Subdural infection

-

Direct or local spread

Epidural abscess
o From adjacent focus of infection sinusitis or osteomyelitis
o In spinal epidural abscess spinal cord compression neurosurgical
emergency
Subdural empyema
o Spread of infection into subdural space from skull or air sinuses
o Underlying arachnoid and subarachnoid spaces are unaffected
o Large subdural empyema mass effect
o Thrombophlebitis spread to bridging veins cross subdural space
venous occlusion and infarction of brain

Hematogenous spread (Most common)

-

From nasopharynx blood stream subarachnoid space through complex

interactions with endothelial cells.
Porous structure of choroid plexus capillaries facilitates their spillage into the CSF.
o The CSF is an ideal medium for the spread of bacteria because it provides
enough nutrients for their multiplication and has few phagocytic cells, and low
levels of antibodies and complement
o Initially, bacteria multiply uninhibited and can be identified in smears,
cultures, or by ELISA detection of their antigens before there is any
inflammation.
Bacterial toxins cause neuronal apoptosis and cell wall lipopolysaccharide, released
from bacteria, damages the blood brain barrier (BBB).
Increased vascular permeability from BBB damage, in turn, causes cerebral edema,
increased intracranial pressure, decreased cerebral perfusion, hypoxia, and neuronal
necrosis.
Cells of the innate immune system of the brain, located in the BBB, choroid plexus,
and ependyma, detect bacteria and secrete cytokines, chemokines, and complement,
which attract circulating neutrophils into the CSF. Neutrophils have powerful

lysosomal enzymes and free radicals, which they use to kill bacteria, but have a short
life span.
o Lysis of the immune cells damage brain tissue, nerves, and blood vessels.
o Vasculitis and clotting cause cerebral infarcts.
o Brain damage in bacterial meningitis is caused in part by the direct action of
bacteria and in part by the antibacterial inflammatory response.
o The brain has elaborate mechanisms for controlling inflammation but, in some
cases, unbalanced defence reactions can cause severe injury.
Sinus spread
Infection from the face may reach the cavernous sinus through its many anastomotic
connections, with severe consequences. The cavernous sinus drains by two larger channels,
the superior and inferior petrosal sinuses, ultimately into the internal jugular vein via the
sigmoid sinus, also draining with emissary vein to pterygoid plexus.
-

Spread of infection to pterygoid plexus can spread to brain via the connection
between the pterygoid plexus and the cavernous sinus

Regulation of ICP
-

Monroe-Kellie Doctrine
The pressure-volume relationship between ICP, volume of CSF, blood, and brain
tissue, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie doctrine
or the Monro-Kellie hypothesis.
The Monro-Kellie hypothesis states that the cranial compartment is incompressible,
and the volume inside the cranium is a fixed volume. The cranium and its constituents
(blood, CSF, and brain tissue) create a state of volume equilibrium, such that any
increase in volume of one of the cranial constituents must be compensated by a
decrease in volume of another
The principal buffers for increased volumes include CSF and, to a lesser extent, blood
volume. These buffers respond to increases in volume of the remaining intracranial
constituents. For example, an increase in lesion volume (e.g. epidural hematoma) will
be compensated by the downward displacement of CSF and venous blood. These
compensatory mechanisms are able to maintain a normal ICP for any change in
volume less than approximately 100120 mL

Cushing reflex
-

Hypertension, bradycardia, irregular respirations (Cheyne-Stokes breathing)

Signs of ICP
-

Headache when you wake up

Papilledema
Projectile vomiting
Bradycardia
HTN