These infections reach the intracranial structures by one of two pathways, either by hematogenous spread (emboli of bacteria or infected thrombi) or by extension from cranial structures adjacent to the brain (ears, paranasal sinuses, osteomyelitic foci in the skull, penetrating cranial or congenital sinus tracts) (see Durand et al and Thigpen et al for summaries of this subject). In a number of cases, infection is iatrogenic, being introduced in the course of cerebral or spinal surgery, the placement of a ventriculoperitoneal shunt or, rarely, by a lumbar puncture needle. Increasingly, craniospinal infections are nosocomial, that is, acquired in-hospital; in urban hospitals, nosocomial meningitis is now as frequent as the non–hospital-acquired variety as noted in the review by van der Beek and colleagues.
Surprisingly little is known about the mechanisms of hematogenous spread and animal experiments involving the injection of virulent bacteria into the bloodstream have yielded somewhat contradictory results. In most instances of bacteremia or septicemia, the nervous system seems not to be infected; yet sometimes a bacteremia caused by pneumonia or endocarditis is the only apparent predecessor to meningitis. With respect to the formation of brain abscess, cerebral tissue has a notable resistance to infection. Direct injection of virulent bacteria into the brain of an animal seldom results in abscess formation. In fact, this condition has been produced consistently only by injecting culture medium along with the bacteria or by causing necrosis of the tissue at the time bacteria are inoculated. In humans, infarction of brain tissue because of arterial occlusion (thrombosis or embolism) or venous occlusion (thrombophlebitis) may be a common and perhaps necessary antecedent by way of causing of a necrotic nidus.
The mechanism of meningitis and brain abscess from infection of the middle ear and paranasal sinuses is easier to understand. The cranial epidural and subdural spaces are practically never the sites of blood-borne infections, in contrast to the spinal epidural space, where such infections are either by hemtogenous spread or from contiguous osteomyelitis. Furthermore, the cranial bones and the dura mater (which essentially constitutes the inner periosteum of the skull) protect the cranial cavity against the ingress of bacteria. This protective mechanism may fail if suppuration occurs in the middle ear, mastoid cells, or frontal, ethmoid, and sphenoid sinuses. Two pathways from these sources have been demonstrated: infected thrombi may form in diploic veins and spread along these vessels into the dural sinuses (into which the diploic veins flow), and from there, in retrograde fashion, along the meningeal veins into the brain, and an osteomyelitic focus may erode the inner table of bone and invade of the dura, subdural space, pia-arachnoid, and even brain. Each of these pathways has been observed by the authors in fatal cases of epidural abscess, subdural empyema, meningitis, cranial venous sinusitis with meningeal thrombophlebitis, and brain abscess. However, in many cases coming to autopsy, the pathway of infection cannot be determined.