Walsh & Hoyt: Empyema

Empyema (from the Greek word meaning ""suppuration"") is pus that collects in a preformed space that is not confined by a capsule. Intracranial empyemas usually occur in the subdural or epidural spaces where the wide extent of these potential spaces and the relative avascularity of the dura are such that pus, once formed, normally spreads too rapidly for effective adhesions to develop. An epidural empyema is a relatively uncommon lesion; however, cranial subdural empyemas are the second most common cause of localized intracranial infection after brain abscesses. Subdural empyemas are much more common in men than in women, perhaps reflecting a higher incidence of frontal sinus disease and trauma in men than in women. Kaufman et al. suggested that young men have rapid growth of the frontal sinus, resulting in thinning of the sinus walls and an incomplete barrier to infection

Walsh & Hoyt: Mucoceles and Pyoceles

A mucocele is formed when drainage of mucus from one of the paranasal sinuses becomes blocked by obstruction of its ostium. If the contents of a mucocele become secondarily infected, the resulting mass is called a pyocele or mucopyocele. A mucocele or pyocele may develop in any of the paranasal sinuses, and any of these sinuses may become primarily infected

Walsh & Hoyt: Mucoceles, Pyoceles, and Sinusitis

Although mucoceles, pyoceles, and sinusitis are not infections of neural tissue, they not infrequently produce neuro-ophthalmologic symptoms and signs through their effects on adjacent neural and vascular structures. In most cases, damage is caused by compression by an expanding mass; however, in some cases, the infection itself produces visual or neurologic complications

Walsh & Hoyt: Edema

A common response of the brain to a variety of insults is edema. Infections and inflammations of the CNS produce several types of edema: vasogenic, cytotoxic, interstitial, and hypo-osmotic. Some of these types can be distinguished by MR imaging. A variety of organisms produce toxins that can cause vasogenic cerebral edema. Bacteria are the most common organisms that produce such toxins. Clostridium botulinum, Clostridium tetani, and Corynebacterium diphtheriae all produce toxins capable of causing vasogenic cerebral edema. Other similar toxins include streptolysin O, the staphylococcal alpha-toxin, and the toxins produced by Shigella dysenteriae, Bacillus anthracis, Haemophilus pertussis, H. influenzae, and Escherichia coli. Release of cell wall fragments from Streptococcus pneumoniae also may produce vasogenic cerebral edema

Walsh & Hoyt: Lesions Produced by Infection

A variety of lesion types may be produced by infections and inflammations. These include abscesses, aneurysms, areas of demyelination, cerebral edema, empyemas, encephalitis, granulomas, meningitis, mucoceles and pyoceles, neuritis, and vasculitis. In this section, we consider the origin, pathologic features, clinical manifestations, and treatment of these lesions

Walsh & Hoyt: Encephalitis (Meningoencephalitis)

Encephalitis is inflammation confined to the brain; meningoencephalitis is inflammation of both the brain and the leptomeninges. Both encephalitis and meningoencephalitis are characterized by infection and destruction of neurons and glial cells. They are primarily diseases of children, with the youngest children being the most devastated by their effects. Nevertheless, they can occur in adults of all ages. These disorders almost always are caused by a virus that has gained access to the CNS by one of two routes, hematogenous or neuronal

Walsh & Hoyt: Neuritis

Neuritis is a generic term indicating inflammation of a nerve. The inflammation may result from the direct effects of an organism, from its antigenic effects on the immune system, or from mechanisms unrelated to current or previous infection or insult. Organisms capable of producing neuritis by direct infection of cranial or peripheral nerves include Neisseria gonorrhoeae, Mycobacterium leprae, Histoplasma capsulatum, Cryptococcus neoformans, trypanosomes, HIV, CMV, and Borrelia burgdorferi. In addition, both herpes simplex virus and varicella-zoster virus can infect sensory ganglia and thus can cause both peripheral and cranial neuropathies

Walsh & Hoyt: Vasculitis

Intracranial arteries and veins may become infected by a variety of organisms. The infection may be a primary process within the vascular system itself or may result from the effects of an acute, subacute, or chronic contiguous process that penetrates the vessel. The inflammatory response varies greatly depending on the blood vessels affected, the type of organism responsible, the mode of spread, and the stage of the infectious disease. The principal types of reactions are: (a) the suppurative inflammation produced mainly by pyogenic bacteria; (b) the nonsuppurative or proliferative response seen in typhoid fever and scarlet fever; (c) the hemorrhagic response seen in anthrax, glanders, and some viral infections; and (d) the histiocytic and granulomatous response seen in syphilis, leprosy, and tuberculosis. The sequelae of infectious angiitis also are variable. There may be little or no structural damage. Extensive fibrosis with calcification and luminal stenosis may occur. The vessel may become thrombosed but later recanalize. The vessel may rupture, producing subarachnoid or intracerebral hemorrhage. Finally, the vessel wall may weaken and dilate, resulting in formation of a mycotic aneurysm or pseudoaneurysm. Clinically important infectious angiitis in humans may be caused by a number of different organisms, including pyogenic bacteria, viruses, spirochetes, fungi, and rickettsiae