Brain abscess represents poorly or sharply delineated suppurative process of brain Substance, resulting from extension from adjacent foci or from hematogenous spread incidence. Despite the introduction of effective antibacterial therapy, the over-all incidence of brain abscess has not changed significantly over the past two decades (about 7 per 1000 neurosurgical operations). It is seen approximately one fifth as frequently as bacterial meningitis in a large general hospital.
Predisposing Factors.
Intracerebral infections are usually a consequence of .an adjacent primary focus of infection: middle ear, mastoid, paranasal sinuses, face or scalp and skull (osteomyelitis, compound fracture with wound contamination, or craniotomy wound infection). Bronchiectasis, lung abscess, empyema, skin infections, and acute bacterial endocarditis may be the source of hematogenous brain abscess; congenital heart disease with right-to-left shunt is an important predisposing factor. In approximately 10 per cent of brain abscesses an underlying cause cannot be determined.
Subacute and Chronic Middle Ear Infection and Mastoiditis
Over one-third of all brain abscesses stem from otitis infection. Infection usually spreads iicm the ear by either of two routes: direct extension to the roof of the tympanic cavity or mastoid bone (osteomyelitis) and then through the meningeal covering of the brain, or by extension along veins of the inner ear through diploic vessels of the skull and through intracranial venous channels into the substance of the brain. Thrombophlebitis of the pial vessels and dural sinuses, by impairing cerebral circulation, may cause infarction of brain tissue and facilitate development of local infection. The temporal lobe and cerebellum adjacent to the ear and mastoid, are the most common sites of otogenic abscess.Infections of the Face and Skull.
Infections of the Paranasal Sinuses.
Frontal and sphenoid sinuses are most frequently implicated in “neurogenic” brain abscess of the frontal and temporal lobes, respectively. Infection may erode the sinus wall and invade the brain directly or, as with otogenic infection, may spread by way of veins communicating with the cavernous sinus and brain.
Infections of the Face and Skull.
Intracranial spread of infection from the face or nose to the frontal lobe occurs by way of a septic thrombophlebitis. Compound fractures of the skull may result in brain abscess, particularly when the dura and brain are lacerated leaving a nidus of bone or foreign body in the devitalized tissue. Occasionally the original traumatic episode has seemed trivial and has been overlooked. Several cases of brain abscess due to a pencil point introduced through the orbit have been reported. Brain abscess may complicate stereotactic surgery and ventriculo vascular shunts.
You Must Know The Etiology And Pathogenesis of Brain Abscess (cerebral abscess)
A wide variety of microorganisms cause brain abscesses, and a careful attempt to establish a bacteriologic diagnosis should be made in every case. A Gram-stained smear of purulent material should be studied, at the time of surgery, and aerobic and anaerobic cultures, as well as cultures for fungi, should be obtained. In about 20 per cent of brain abscesses cultures are sterile. In about 25 per cent, most often when there is a contiguous extracerebral focus, two or more microbial species are isolated.
Staphylococcus aureus and various streptococci are the most frequently isolated organisms. Pneumococcus, formerly a leading cause of brain abscess, is only rarely incriminated today. Species of the Enterobacteriaceae (E. coli, Proteus, Klebsiella) are sometimes isolated, particularly from otogenic brain abscesses. Anaerobic bacteria (particularly streptococci and Bacteroides) may have a more prominent role in brain abscess than heretofore appreciated.
Rarely Actinomyces, Nocardia asteroides and other fungi may be recovered from an abscess cavity. Of interest is the frequent association of pulmonary alveolar proteinosis with pulmonary and occasionally cerebral nocardiosis. Hemophilus aphrophilus and the fungus Cladosporium trichoides rarely infect human beings, but when they do, they show a curious affinity for the central nervous system.
When Entamoeba histolytica causes brain abscess, there are associated lesions of the liver or lung in virtually every case. In Central and South America and parts of Europe and Asia cerebral cysticercosis (usually solitary cysts containing the larval form of the pork tapeworm Taenia solium) should be considered in patients presenting with symptoms of brain tumor. In the racemose form of disease, obstructive hydrocephalus results from the growth of cysts in the third or fourth ventricle. The clinical picture may suggest a diagnosis of pseudotumor cerebri. Very rarely the brain is the site of echinococcal cysts and the solitary or multiple granulomas of schistosomiasis.
Pathology.
Abscesses resulting from direct spread of infection are found in the brain adjacent to the primary extracerebral site; those resulting from retrograde venous propagation are often located at some distance from the primary focus in the distribution of the nearest venous sinus. Thus, for example, cerebellar abscess from otitis media is the result of spread of infection from the middle ear to its deep venous drainage into the transverse sinus, and thence medially into the veins draining the anterior superior portion of the ipsilateral cerebellar hemisphere. Metastatic abscesses are usually found in the distribution of the middle cerebral artery.
Initially, the site is edematous and infiltrated with polymorphonuclear leukocytes. The lesion is poorly demarcated at this stage and represents a local suppurative encephalitis. Usually within two weeks of onset the center undergoes liquefaction necrosis. The surrounding zone of fibroblasts becomes progressively thicker and contains more collagen; this constitutes the wall of the abscess, and astrocytes proliferate in the adjacent cerebral tissue. Multiple satellite abscesses may develop and frequently communicate with the principal cavity.
Since abscess cavities usually spread through the central white matter, they often extend to and through the ventricular wall, producing the dire complications of ventricular empyema and meningitis. Brain abscess seldom, if ever, results from primary bacterial meningitis. Coincidental occurrence of brain abscess and meningitis is usually related to intraventricular leakage of the abscess. In support of this view, the three most common organisms in primary pyogenic meningitis occur only rarely as the cause of brain abscess.
Clinical Manifestations.
Age Incidence. Brain abscesses are most common in the second to fifth decades, but may occur at any age. They are rare in infancy, even in patients with congenital heart disease.
General Features.
A history of fever at the time of invasion of the brain by the infective agent may be elicited; but a third of patients will lack a history of fever and remain afebrile under observation. Blood cultures are usually sterile except in those with an underlying acute bacterial endocarditis.
Headache, the most frequent initial symptom of brain abscess, may develop suddenly or insidiously while the attention of the patient and physician is directed toward the primary infection of ear, sinus, or lung or to the congenital cyanotic heart disease. The headache may be localized to the side of the abscess, but it is often generalized and increases in severity as the infection progresses. Heightened intracranial pressure, manifested by nausea, vomiting, drowsiness, bradycardia, con fusion, and stupor, is common.
Papilledema is a relatively late finding that is recognized in a minority of cases. The increased intracranial pressure may result in signs of sixth- and, less often, in those of third-nerve palsy. They are often false localizing signs since the abscess may be remote from the cranial nerves. Although pathologically brain abscess progresses through several phases, there is no clear correlation with the clinical course of most patients. In some patients, usually those with metastatic brain abscesses, the illness runs a fulminating course, ending fatally in 5 to 15 days. In most, however, the course is considerably prolonged, and a diagnosis of cerebral neoplasm is often suspected.
Specific Neurologic Syndromes.
Temporal Lobe Abscess. Most temporal lobe abscesses are secondary to ear infection. Involvement of the dominant temporal lobe may produce a nominal (inability, to name objects) or Wernicke’s (inability to read, write, or understand spoken words) aphasia. Personality changes with bizarre psychotic behavior, including uncontrolled rage, may occur. Commonly, homonymous upper quadrantic field defect results from dysfunction of the inferior fibers of the optic radiation that course about the inferior horn of the lateral ventricle in the temporal lobe. Involvement of the pyramidal tracts is not common, and the only motor deficit may be a slight contralateral facio- brachial monoparesis. Herniation of the temporal lobe through the tentorium may develop precipitously and cause a homolateral third-nerve paralysis,. coma, and bilateral pyramidal tract signs.
Cerebellar Abscess.
Cerebellar abscesses are almost exclusively otogenic. Increased intracranial pressure, suboccipital headache, and stiff neck may be the only manifestations. The patient may stagger and veer to the side of the lesion. Impaired coordination of extremities on the same side, with poor performance of rapid, alternating movements and with intention tremor, may be present. Nystagmus is frequent and usually coarser when the gaze is directed to the side of the abscess. Associated diseases of the inner ear may contribute to the unsteady gait and nystagmus, and may produce vertigo. Seizures do not occur with abscesses restricted to the cerebellum.
Frontal Lobe Abscess.
Frontal lobe abscesses are most commonly associated with disease of the. frontal or, less frequently, the ethmoid’ sinuses. Drowsiness, inattention, disturbed judgment, and impaired intellectual functions are common; the findings may suggest a psychiatric diagnosis. Mutism and increased grasp, suck, and snout reflexes are often present. In about a fourth of cases focal or generalized convulsions occur; deviation of the head and eyes to the side opposite the lesion is a common pattern of seizure. When the abscess is large or in the posterior frontal region, a contralateral hemiparesis§ usually develops. Rarely, dysphagia results from a lesion on the dominant side.
Parietal Lobe Abscess.
Parietal lobe abscesses are usually hematogenous but large otogenic temporal lobe abscesses may extend to the parietal lobe. Impaired position sense, two-point discrimination, and stereognosis are characteristic signs of an anterior parietal lobe abscess. Focal sensory and motor seizures occur. Homonymous hemianopia, visual inattention (often demonstrated by bilateral simultaneous stimulation of visual fields), and impaired optokinetic nystagmus are encountered with more posterior and deep lesions. Dysphasia is a feature of inferior parietal lobe abscess on the dominant side. When the posterior parieto-temporo-occipital region is affected, there may be impaired recognition of fingers, difficulty in differentiating left from right, acalculia, and agraphia (Gerstmann’s syndrome).
Brain Abscess Presenting as Acute Meningitis.
Occasionally patients’ with brain abscess present signs of meningitis, including fever, headache, stiff neck, and pleocytosis; focal neurologic signs are’ usually in evidence also. The syndrome is most often due to leaking of the abscess into the lateral ventricle. Massive rupture into the ventricle is a catastrophic event, with high fever, shock, and coma, and should be easily recognized. Pleocytosis with cell counts of more than 30,000 per cubic millimeter and reduced sugar concentrations are usual.
Bacteria can often be seen on Gram stain and can. be grown on culture.In some patients with a similar clinical picture organisms are not found, and the syndrome may represent the phase of “bacterial encephalitis.” The important point to be stressed is that one should be alert to the possibility of a brain abscess in any patients with chronic ear or sinus disease who develop meningitis. – These patients often improve on treatment of the meningitis only to develop evidence of an intracranial mass lesion one or two weeks later as encapsulation of the abscess progresses.
Laboratory Diagnosis.
Cerebrospinal fluid pressure is commonly 200 to 300 mm. H20, but may be Considerably higher, particularly in the presence of intraventricular rupture. The cell count varies from a few to several hundred, with lymphocytes predominating. In cases of intraventricular rupture of the abscess, cell counts may be in excess of 50,000 or 100,000 (mainly neutrophils). Also, cell counts of several thousand, with neutrophils predominating, may occur during the early phase of brain abscess (“bacterial encephalitis”). The sugar level is not reduced unless there is a simultaneous suppurative meningitis.
The protein may be increased up to several hundred milligrams per 100 ml.Roentgenograms of the chest, mastoid, and sinuses may identify the .original focus. Displacement of the pineal or, very rarely, an air-fluid level in the lesion will be demonstrated by roentgenograms of the skull. A focus of high-voltage slow- wave activity on the side of the abscess, and maximal over the area of the lesion, characterizes the typical electroencephalogram. Localization of the abscess may also be obtained by scanning the brain after intravenous injection of an isotope, by arteriography, or by pneumography.
Treatment of Brain Abscess
Early diagnosis and prompt antimicrobial treatment are crucial. Surgery is employed once acute cerebral inflammation and edema are brought under control, and consists of initial aspiration of the abscess cavity,- followed in some cases by excision at a later time, or primary total excision of the abscess. The method employed depends, to some extent, on the site of the lesion, but whenever feasible, primary excision is probably preferable.
Since in brain abscesses penicillin-susceptible organisms predominate, 10 million to 20 million units of penicillin per day intravenously should be started prior to operation. If there is.reason to suspect an organism not susceptible to. penicillin, e.g., gram-negative bacilli from a chronic ear infection, then chloramphenicol or similar drugs should be given concurrently. One of the semisynthetic penicillins, e.g., oxacillin, should be used if a penicillin-resistant Staphylococcus is suspected. The antimicrobial therapy should be modified as necessary at the time of operation, based on examination of a Gram-stained smear and culture of the abscess.
Sure, here’s a concise tabular format for “Brain Abscess: Causes, Symptoms, Treatment”:
| Aspect | Details |
|---|---|
| Causes | – Bacterial or fungal infection |
| – Spread from nearby infection (e.g., ear, sinuses) | |
| – After head injury or surgery | |
| Symptoms | – Headache |
| – Fever | |
| – Nausea and vomiting | |
| – Changes in mental status (confusion, drowsiness) | |
| – Neurological symptoms (weakness, speech difficulties, seizures) | |
| Treatment | – Antibiotics or antifungal medications |
| – Steroids to reduce swelling | |
| – Surgical drainage or removal if necessary | |
| – Long-term rehabilitation may be needed |
This table summarizes the key points related to brain abscesses. The causes range from infections to injuries, symptoms vary from headaches to neurological issues, and treatments include medications and possibly surgery.
Conclusion:
Brain abscess is a serious medical condition that requires immediate attention. Understanding the causes, symptoms, and treatment options can help individuals seek prompt medical care and improve outcomes. If you or someone you know is experiencing symptoms of a brain abscess, seek medical attention immediately. Your health and well-being depend on it.
