Tropical Neurology - part 2 pptx

Acute meningococcal meningitis is usually seen in children and young adults,and only less than 10% cases are above 45 years of age.. Pneumococci are the commonest cause ofrecurrent menin

kyphus In active disease, intraoperative traction usually results in partial correction

of the deformity When the deformity exceeds 40˚ it may be wise to first instrumentposteriorly, achieve deformity correction and then debride and fuse anteriorly Pos-terior fixation is, however, not always necessary but if done helps in deformity cor-rection and graft consolidation in the desired position For high cervical levels, asubmandibular approach is used while the classical Southwick Robinson’s approachsuffices in other patients

Cervicothoracic junction: Surgical options in this region are transmanubrial

anterior decompression, transclavicular anterior decompression, and highcosto-transversectomy The transclavicular approach requires either dislocation orsurgical fracturing of the clavicle which is morbid In addition, access to the spine isalways anterolateral and oblique In comparison, the transmanubrial approach re-quires splitting of only the manubrium (which is easily rejoined and heals withoutnonunion), saves the thoracic duct from iatrogenic damage and, most importantly,allows direct anterior access to the spinal column for easy grafting and fixation

Management of Lumbosacral Tuberculosis

Backache is an important sequelae of the disease and is present in 54% of thecases bearing a direct relation to the number of vertebrae involved and the abnormallumbo-sacral angles.7 Any change in Lumbosacral angles to less than 10˚ will usuallyresult in accelerated degeneration and pain Hence, surgery may be aggressively ad-vocated in cases of acute deformity but no deficit

Role of thoracoscopic surgery: Thoracoscopic surgery is being used for drainage of

nonresolving abscesses and for the treatment of spinal tuberculosis with paraplegia;Fig 2.11 Illustration showing the various approaches used in decompression of tuber- culous spondylirtis.

although, its efficacy is yet to approach that of open surgery The main advantage ofthis technique lies in its minimal invasiveness and decreased morbidity

Management of kyphosis: Radical debridement and fusion is far superior to only

debridement in adults and children past their growth sensible age The changes indeformity in children are similar to those in adults, although some children have atendency toward spontaneous correction of the deformity Progression of deformity

in these cases is solely due to graft resorption, fracture or dislodgement with ary collapse.8

second-Management of Paraplegia

The general principle of management of paraplegia applies to Pott’s paraplegia

as well Besides antitubercular and surgical therapy, general care of the paraplegicpatient is very important such as—

Bladder care: if retention—clean, intermittent self-catheterization

Prevention of bedsores: frequent changes in position and water or air mattress.Prevention of deep vein thrombosis: low dose heparin and physiotherapy.Severe spasticity: baclofen, diazepam or tizanidine

Intraspinal Tuberculous Granuloma

Intraspinal tuberculous granuloma is usually associated with Pott’s spine although

it rarely can occur without vertebral involvement The spinal tuberculoma may beextradural, intradural extramedullary or intramedullary

Extradural spinal tuberculoma: Most extradural spinal tuberculomas are

second-ary to vertebral disease A number of patients have been reported in which dences of bony tuberculosis could not be detected These lesions are most likely due

evi-to hemaevi-togenous spread The patient may present with paraparesis or quadriparesisdepending on the site of the lesion The granuloma can be visualized on spinal MRIwhich can be confirmed at surgery Treatment consists of decompressive laminec-tomy or laminoplasty The anterior granuloma can be safely left if decompression isotherwise satisfactory Antitubercular therapy is continued at least for 18 months

Intradural spinal tuberculoma: Intradural extramedullary spinal tuberculoma is

rare and presents either as a round or oval hard mass adherent to the inner aspect ofthe dura and the spinal cord or as a granulomatous mass surrounding the spinalcord Clinically, patients present with extramedullary compressive myelopathy

Intramedullary spinal tuberculoma: Isolated intramedullary tuberculoma is rare.

The lesion is usually a single, hard, circumscribed mass of 7-10 mm in diameterassociated with localized arachnoiditis The majority of these patients have associ-ated pulmonary tuberculosis Neurological deficit in the form of paraplegia or quad-riplegia develops insidiously Spinal MRI or contrast CT scan show an enhancinglesion with or without associated perifocal edema Intramedullary tuberculoma can

be easily enucleated under the cover of antitubercular therapy

The primary spinal variety of tuberculous arachnoiditis constitutes 29% of allarachnoiditis It is believed that spinal arachnoiditis arises as a flare-up lesion offocal parenchymal lesion on the surface of the spinal cord similar to what happens incranial tubercular meningitis The meningeal reaction varies depending on the im-mune response of the host

Pathology

Gross examination of the spinal cord reveals a thick collar of exudate (Fig 2.12).The meninges are thick, opaque and lustreless Discrete and conglomerated tubercleswith a caseating center may be seen in the exudate There is spinal cord atrophy Onhistopathological examination four types of changes have been reported with spinalarachnoiditis which include borderzone rarefaction and spongification of the cord,central necrosis, ischemic myelopathy and associated intramedullary tuberculoma

Clinical Features

Subacute or chronic, single or multiple level and ascending or transverseradiculomyelopathy comprise the clinical picture of spinal arachnoiditis The sever-ity and extent of root or cord symptoms depend on the site of maximal involve-ment, such as a cauda equina lesion that presents as radiculopathy and higher lesions

as multifocal or single level radiculomyelopathy No age is exempt from spinal noiditis In the subacute form, the clinical symptoms develop on an average of twomonths although maximum severity is seen within 2-5 days following, during whichtime the course may be stationary The presentation consists of root pain, paresthe-sia, weakness, wasting and bladder dysfunction Root pain is lancinating in charac-ter, arising from single or multiple roots, or may be widespread Tingling numbnessfollows the root pain Vibration and joint position sense may be impaired in thelower limbs Paralysis of the limbs is mostly severe and produces paraplegia or quad-riplegia which is of upper or lower motor neuron type or a mixed variety dependingupon the extent of radiculomyelopathy Retention of urine may be an early or a latefeature The patient may have associated constitutional symptoms such as fever,anorexia and weight loss

arach-Chronic forms of adhesive spinal arachnoiditis progress over months or yearsand may be indistinguishable from spinal cord compression by a tumor It may besuspected if the root pain is scattered, persistent and upper motor neuron signs areassociated with lower motor neuron signs

Investigation

CSF: There is often partial or complete subarachnoid block which may result in

a dry tap The CSF is generally clear or xanthochromic depending on protein levelwhich is usually elevated There is CSF pleocytosis ranging from a few cells to a fewhundred cells CSF should be examined for AFB However CSF may be normal inlocalized or chronic arachnoiditis An extra CNS source of tuberculosis should also

be explored

Myelography: With the availability of water soluble contrast agents, myelography

is safe and commonly employed in the diagnosis of spinal arachnoiditis The graphic findings in spinal arachnoiditis include:

myelo-1 Slow movement of the dye column often with a filling defect and mentation of the column

frag-2 Total block appears as a ragged edge, or the dye column may extend liquely for two or more vertebral levels At times there may be a pitch fork

Fig 2.12 Dense adhesive arachnoiditis encasing the lumbar spinal cord The transverse section above shows exudate around the spinal cord (Courtesy Prof S.K Shankar).

In those in whom both cisternal and lumbar myelograms are performed, theremay be filling defect extending over many segments which have irregular columnsabove and below the defect.

CT and MRI of spinal cord are preferred techniques because of the facility of theaxial section and because they are noninvasive Spinal cord pathology is clearly seen

CT and MRI show displacement of nerve roots of cauda equina and adherence ofroots particularly in clumps on the posterior dorsal sac Contrast MRI reveals en-hancement of the roots and meninges

The final confirmation of the diagnosis is achieved by biopsy of leptomeninges

A patient with adhesive arachnoiditis should be investigated for infective andnoninfective causes of arachnoiditis which are ennumerated in Table 2.4

Summary

In tuberculosis the spinal cord can be affected in vertebral involvement, loma and adhesive arachnoiditis in isolation or various combinations Spinal tuber-culosis is the commonest form of osteoarticular disease and accounts for 50% of allcases Vertebral destruction, spinal deformity and paraplegia are the main attributes

tubercu-of the disease Although paradiscal disease is the commonest type, atypical tions occur frequently in the form of extensive disease, multifocal infection, epidu-ral granuloma, intradural abscess and posterior element disease Diagnosis is based

presenta-on clinical features alpresenta-ong with radiological and laboratory evidence of tubercularinfection Despite modern imaging and laboratory techniques, tuberculous destruc-tion at times mimics malignancy and biopsy becomes necessary for cytological and

Table 2.4 Causes of spinal adhesive arachnoiditis

Infective Tubercular, syphilis, pyogenic, cryptococcus neoformans Noninfective Prolapsed intravertebral disc

Trauma Spondylotic radiculomyelopathy Intraspinal tumor, spinal angioma, secondaries Drugs-Penicillin, streptomycin, anaesthetics, myodil Idiopathic

histopathological diagnosis In addition to eradication of the disease, preventionand treatment of sequelae like paraplegia and deformity are the main aims of treat-ment Multi-drug chemotherapy is effective in the treatment of most cases of tuber-culous spondylitis Surgery is reserved for resistant cases, progressive deformity andsevere neurologic deficit Paraplegia in active disease responds much better to sur-gery than late onset paraplegia In all cases of paraplegia, surgery must aim at ad-equate neural recovery In children with significant residual spinal growth,surgery must aim at the preservation of the vertebral endplates In this regard, acombined anterior and posterior fusion corrects deformity and arrests its progres-sion The treatment of progressive kyphosis depends on the residual spinal growth,activity of the disease and neurologic status of the patient In general, deformitycorrection is safer and easier in active than in healed disease Implants may be used

to correct deformity and stabilize the spine

References

1 Tandon PN, Pathak SN Tuberculosis of central nervous system In: Spillaine JD

ed Tropical Neurology London: Oxford University Press, 1973:37-62

2 Rajasekaran, S., and Shanmugasundaram, T K Prediction of the angle of gibbusdeformity in tuberculosis of the spine J Bone Joint Surg 1987; 69-A:503-509

3 Kumar KA Clinical classification of Posterior spinal tuberculosis Int Orthop 1985;9:147-152

4 Lifeso R Atlanto-axial tuberculosis in adults J Bone Joint Surg 1987;69(2):183-187

5 Ninth Report of the Medical Research Council Working Party on Tuberculosis ofthe Spine: A 10-Year Assessment of Controlled Trials of Inpatient and OutpatientTreatment and of Plaster-of-Paris Jackets for Tuberculosis of the Spine in Children

on Standard Chemotherapy Studies in Masan and Pusan, Korea J Bone JointSurg 1985; 67-B (1):103-110

6 Tuli S Tuberculosis of the Skeletal System New Delhi: Jaypee Brothers, 1991:268

7 Pun WK, Chow SP, Luk KDK, Cheng CL, Hsu LCS, Leong JCY Tuberculosis ofthe lumbosacral junction Long-term follow-up of 26 cases J Bone Joint Surg1990; 72-B (4):675-678

8 Schulitz KP, John CY, Leong et al Growth changes of solidly fused kyphotic blockafter surgery for tuberculosis Spine 1997; 22:1150-1115

Tropical Neurology, edited by U K Misra, J Kalita and R A Shakir.

©2003 Landes Bioscience

Pyogenic Infections

of the Central Nervous System

Kameshwar Prasad, Sumit Singh, Shailesh Gaekwad and Chitra Sarkar

Pyogenic infections of the nervous system include acute bacterial meningitis,brain abscess, subdural empyema and epidural abscess Despite the availability ofeffective antibiotics, these disorders are still common and are an important cause ofmorbidity and mortality In this chapter, various pyogenic infections of the CNS arereviewed with special reference to the tropical countries

Acute Bacterial Meningitis

Acute bacterial meningitis (ABM) may be defined as an inflammation of thepia-arachnoid matter and the cerebrospinal fluid (CSF) of the subarachnoid spacedue to bacterial infection The subarachnoid space extends through the brain, spinalcord and sheaths of the optic nerves Any infection of this space involves all thespaces and is invariably associated with some ventriculitis

Epidemiology

Bacterial meningitis is widely prevalent throughout the world The incidence ofABM is difficult to estimate, particularly in the developing countries where a largenumber of patients remain unreported; however, it is probably more common indeveloping than in developed countries H influenzae type B (Hib) is the mostimportant cause of meningitis in children The majority of patients with Hib men-ingitis are seen in the months of June to September displaying a bimodal, seasonalvariation.1 Hib meningitis is common in children below five years of age, although

it is rare below the age of two months, probably due to transplacental transmission

of protective maternal antibodies The occurrence of Hib meningitis is inverselyproportional to the concentration of age-related and type-specific antibodies againstthe capsular antigens Susceptibility to Hib meningitis depends upon the presence

of H influenzae in the nasopharynx and the concentration of the type-specificanticapsular antibodies in the host N meningitidis is the commonest cause of epi-demic meningitis.2 It has a worldwide distribution The Sub-Saharan African regionhas a ‘meningitis belt’ which extends from 5-15˚ north of the equator and includesChad, Dahomey, Ghana, Mali, Niger, Nigeria and Sudan The annual incidence ofmeningococcal meningitis in this endemic belt is 70/100000 population, the peakincidence being in the months of April and May as opposed to winter and earlyspring in industrialized nations The reported cases and deaths due to meningitis inIndia are summarized in Table 3.1

Acute meningococcal meningitis is usually seen in children and young adults,and only less than 10% cases are above 45 years of age In the United States, themajority of affected patients is under five years, whereas in the tropics the majority

of patients are between five and nine years.3 Epidemics usually occur due to group A

meningococcii every 8-12 year interval in the meningitis belt This trend of theinfection is probably due to the concentration of people who do not have immunityagainst the disease For the epidemic to occur there must be enough nonimmuneindividuals with the concerned pathogen Once an epidemic occurs, the herd im-munity of the population rises due to an increase in the nasopharyngeal carrier state.With the passage of time, the number of nonimmune individual increases and when

a critical mass is reached, an epidemic occurs An added factor may be a change inthe strain of the bacteria with increased virulence The meningococcal infectionspreads through droplets from the nasopharyngeal secretions of the carriers; there-fore, meningococcal meningitis is more common in overcrowded places such asschools and camps

Streptococcus pneumoniae is the commonest cause of meningitis in the adults Its

incidence in the tropical countries is not well known The average annual incidence

of this disease is between 1-2.3/100000 population in the United States with thepeak incidence between the months of December and May.4 Risk factors for pneu-mococcal meningitis are extremes of age, sickle cell disease, post-splenectomy state,lobar pneumonia and acute otitis media Pneumococci are the commonest cause ofrecurrent meningitis following CSF leak and meningitis in acquired or primaryimmunodeficiencies.5

Etiology

The etiology of acute bacterial meningitis depends on the setting in which itoccurs Community and hospital acquired meningitis differ widely in their bacte-riologic spectrum

Community Acquired Meningitis

H influenzae, S pneumoniae and N meningitidis together account for about75% of community acquired meningitis, and the remaining 25% are caused byGram-negative bacilli or other organisms There is a striking age-related predisposi-tion for different organisms to cause meningitis The Gram-negative bacilli and thegroup B streptococci are the commonest cause of meningitis in neonates, Hib andmeningococci in infants and young children, and pneumococci and Gram-negativebacilli in adults Gram-negative infections are common in infants and children indeveloping countries Klebsiella and Salmonella are also more common pathogens

in developing countries as opposed to the E coli in developed countries.6 Listeria

Table 3.1 Reported cases and deaths due to meningitis in India

monocytogenes meningitis has been increasingly reported from all over the world and

is an important cause of meningitis at the extremes of age It is more common inalcoholics, immunocompromised individuals and patients with hematological ma-lignancy Patients with immunodeficiency are also more prone to Gram-negativeand pneumococcal meningitis

Hospital Acquired Meningitis

Staphylococcus epidermidis is the commonest cause of meningitis associatedwith ventriculo-peritoneal shunts at all ages S aureus usually causes meningitisassociated with infective endocarditis and is a common cause of post-shunt menin-gitis, post-traumatic meningitis and infections following neurosurgical procedures.Anaerobic bacteria account for 1% of all cases of meningitis, being under-recog-nized, as the CSF is rarely cultured for anaerobic organisms Chronic otitis media,mastoiditis and sinusitis are the common predisposing conditions for anaerobic bac-terial meningitis

There is also a marked geographical variation in the pathogens causing tis Hib is the most common pathogen in the USA causing more than half of themeningitis In the UK, the meningococci and the pneumococci are more commonthan in the USA, but the most common cause is still Hib In the meningitis belt ofsub-Saharan Africa, the meningococcus is the most common pathogen

meningi-Pathogenesis

The capability of an organism to cause meningitis depends on its “pathogenicpotential.” To cause meningitis, the bacteria must enter the host, colonize at a par-ticular site, produce bacteremia and cross the blood brain barrier (BBB) to reach thesubarachnoid space where the organism easily proliferates The infection usuallybegins by colonization of the pathogen in the nasopharynx The bacterial factorsenhancing the colonization include presence of fimbriae, which play an importantrole in the adherence of meningococci to the nasopharyngeal mucosa H influenzaeadhere by their capsules and pneumococci by their lipopolysaccharide capsules Thehost prevents the adherence of the bacteria to the epithelium by the local secretion

of IgA Adherence of organisms followed by activation of local immune-mechanismscauses cytotoxicity mediated disruption of the tight junctions of the nasal epithe-lium; loss of cilia and ciliostasis; and finally the penetration of the organisms to thesubmucosa Once the bacteria enters the submucosal bloodstream, their polysac-charide capsules provide antiphagocytic activity The pneumococci activate the al-ternate complement pathway, which facilitates opsonization and subsequentphagocytosis of the bacteria Patients with defects in the alternative complementpathway are at a greater risk of pneumococcal infections e.g., patients with splenec-tomy and sickle cell disease

The mechanism of invasion of the subarachnoid space (SAS) by the bacteria isstill under speculation The dural venous sinuses, the thin dura over the cribriformplate, the choroid plexus, and the monocytes have all been implicated as the site ofinvasion by the organisms The bacteria may also enter the subarachnoid spacethrough the hematogenous route from a parameningeal suppurative focus or throughthe defects in the dura The normal CSF has almost undetectable levels of IgM,whereas IgG and IgA are barely detectable The low level of complement in the CSFaccounts for the impaired opsonization and phagocytosis in patients with meningitis.7

The meninges respond to the bacterial invasion by polymorphonuclear leukocytosis

The mechanism of entry of leukocytes into the SAS traversing the BBB is not knownalthough the role of a C5a complement has been suggested In the absence of aproper opsonic and bactericidal activity of neutrophils, there is a relentless multipli-cation of the pathogenic organisms in the SAS resulting in inflammation of thesubarachnoid space In meningitis, there is breakdown of the tight junctions of thecapillary endothelial cells and an increased pinocytosis across the cells This is due tothe lipopolysaccharide capsules of the bacteria, cytokines and interleukins The breach

of the blood brain barrier produces vasogenic cerebral edema resulting in increasedintracranial pressure (ICP) which adds to the cytotoxic and interstitial cerebral edema.The release of toxic substances from the bacteria or neutrophils results in cytotoxicedema and the released cells and/or molecules impair CSF flow leading to intersti-tial cerebral edema The inflammation of the meninges and the presence of an in-flammatory exudate in the subarachnoid space results in vasculitis of the large bloodvessels traversing this space This causes relative ischemia of the brain Associatedphlebitis of the cerebral veins may result in cortical venous thrombosis or duralsinus thrombosis which leads to focal deficits and seizures In meningitis, cerebralautoregulation is impaired and cerebral blood flow reduced Recently, the role offree radicals and reactive oxygen species in the neuronal injury in pyogenic meningi-tis has been suggested

Pathology

The response to bacterial invasion of the SAS is more marked over the ties of the cerebral cortex, imparting a yellowish-green color The exudate envelopsthe basal cisterns and extends to the spinal SAS mostly to the posterior surface of thespinal cord.8 Microscopically, exudate shows neutrophils and bacteria in the earlystage (Fig 3.1) As the opsonic activity of the neutrophils is impaired, live bacteriacan be demonstrated in the neutrophils There is subintimal inflammatory infiltratecomprising neutrophils and lymphocytes in the meningeal arteries which is unique

convexi-to pyogenic infections of the meninges The veins also share the inflammaconvexi-tory sponse and become distended Mural inflammation can result in cortical venousthrombosis with resultant cortical infarctions By the end of the first week in un-treated patients, the neutrophils are removed by macrophages and replaced by lym-phocytes Subtle changes such as edema of the subependymal and ependymal tissues,sloughing of the ependymal lining and swelling of the astrocytes and glial cells may

re-be visible in the brain parenchyma As the exudates increase, the SAS is reduced andCSF flow may be compromised Obstruction of the foramina of Luschka andMagendie results in noncommunicating hydrocephalus The inflammatory exudatealso blocks the arachnoid villi and further impedes CSF absorption, resulting inoozing of CSF in the periventricular white matter leading to interstitial edema Theexudate is very thick in Hib and is mostly localized to the basal cisterns, whereas it isthinner and more extensive on the cerebral convexities in pneumococcal infections.The SAS may be devoid of any inflammatory exudate in acute fulminant meningo-coccemia, whereas, the interstitial edema may be very significant These pathologi-cal features are usually seen in the untreated cases, and the pathology is markedlyaltered following antibiotic therapy

Clinical Manifestations

Patients with ABM usually present with a classical triad of fever, headache andaltered sensorium Almost all patients have fever and headache, but alteration in

sensorium usually develops later In the presence of these classical symptoms andsigns of meningeal irritation (neck rigidity and Kernig’s sign) it is easy to suspectABM In adults, the classical symptoms and signs of ABM are usually evident In astudy of 490 adult patients with ABM, fever was present in 95%, neck rigidity in88%, seizures in 29% and alteration in sensorium 78% (6% were deeply comatose).The most common organism isolated was S pneumoniae.9 Fever is of acute onset,continuous and high grade reaching up to 38-400 C Hyperpyrexia may occur, espe-cially in the terminal phase The pulse and respiratory rates rise with the progress ofthe disease Patients at extremes of age and in immunocompromised state may notmanifest with fever Headache may be bifrontal but is usually diffuse, associatedwith neck pain and stiffness Vomiting is often projectile and seen with increasingheadache Patients who present early in the course of the disease or those who arepartially treated may have a normal sensorium A history of acute otitis media, eardischarge, sore throat and pneumonia should be sought in all patients Skull trauma,CSF leak, an imunocompromised state, sickle cell anemia, diabetes, splenectomyand long term dialysis are frequently associated with pyogenic meningitis.Sometimes the classical features of meningitis may not be evident and a highindex of suspicion is needed Meningitis following head trauma may be immediate

or delayed and is usually associated with CSF rhinorrhea Such patients present withrecurrent episodes of meningitis In these patients fever may be absent and headache

or alteration in sensorium may be the only feature Bacterial meningitis may velop after neurosurgical operations In such patients, the pathogens are usuallyGram negative bacteria; however, the infections following ventriculo-peritoneal (VP)shunt are usually due to staphylococci The patients with shunt meningitis present

de-Fig 3.1 Photomicrograph of a patient with pyogenic meningitis showing thickened meninges with infiltration by inflammatory cells and congested blood vessels (H&E X 350).

with fever and worsening of symptoms of raised ICP Lumbar CSF may be normal,therefore, CSF examination, directly from the shunt reservoir, is preferable Dete-rioration in sensorium may be the only indicator of ABM

Meningitis in Children

In children the symptoms may not be typical and may manifest only with bility and lethargy The classical signs of neck stiffness may be absent in the earlyphase of the disease Children with meningitis have a weak, high-pitched cry, do notrespond to or stop crying on stimulation by the parents, are usually dehydrated andappear pale Features of raised ICP may be present in children with a fulminantinfection and include altered sensorium and poor pupillary reaction Infants mayhave bulging anterior fontanelle and older children may have papilledema Seizuresare more common in children with meningitis compared to the adults It is impor-tant to differentiate children with meningitis and seizures from those with febrileconvulsions Performing lumbar puncture in every child with febrile convulsions isnot useful in picking up extra cases of meningitis as compared to those with febrileconvulsions and signs of meningeal irritation However, it is advisable to perform aCSF study if the child develops meningeal signs after one to four hours of seizures,does not show rapid recovery or if doubt of meningitis persists

irrita-Meningitis in the Elderly

In the elderly, meningitis should be suspected if a febrile illness is associated withaltered sensorium The fever, though present, may not be high Alteration in senso-rium is reported in more than 90% of patients and neck rigidity in 50% The mor-tality is high, being about 40%

Diagnosis of Acute Bacterial Meningitis

The diagnosis ABM depends on clinical features and CSF analysis Presence ofmaculopopular skin rash, petechiae and hypotension due to adrenal failure(Waterhouse-Freidrichsen’s syndrome) suggest meningococcal meningitis A fulmi-nant course with focal neurological deficits and subdural empyema are common inpneumococcal meningitis Hemophilus influenzae meningitis affects young chil-dren and immunocompromised adults, and is commonly associated with subduraleffusion

Lumbar Puncture and CSF Analysis

Acute bacterial meningitis results in raised intracranial pressure and may be ciated with brain abscess, subdural empyma or epidural abscess Lumbar puncture

asso-in the presence of raised asso-intracranial pressure may precipitate braasso-in herniation, whichmay be fatal However, the risk of brain herniation should be balanced against theneed to establish the diagnosis early and this decision is sometimes difficult Inpatients with fever, headache and any history of otitis media, pain in the ear, recenthead injury, facial infection, cranial osteomyelitis, focal neurologic deficit, papille-dema and cyanotic congenital heart disease, CT scan should be carried out toexclude space occupying lesions, but antibiotics should be administered while wait-ing for the results of the CT scan Before starting empirical antibiotic therapy, bloodcultures, cultures from ear, nose, throat discharges or skin rashes, if any, should besent Instituting antibiotic therapy 1-2 hours before the lumbar puncture will notdecrease the diagnostic sensitivity if the culture of the CSF is done in conjunctionwith testing of CSF antigens and blood culture Samples for blood sugar should be

withdrawn simultaneously with the CSF The CSF is examined for cell count, tein, sugar, Gram’s stain, culture and sensitivity The characteristic CSF findings inpyogenic meningitis include a turbid appearance, polymorphonuclear pleocytosis,low sugar and high protein It is important to examine the CSF as early as possiblebecause the WBCs tend to disintegrate after 90 minutes In the case of a traumaticlumbar puncture, the correction factor for WBC count is 700 RBCs for each WBC

pro-If the peripheral RBC and WBC counts are deranged then the following formulamay be used

True WBC (CSF) = Actual WBC (CSF) – WBC (Blood) x RBC (CSF)/RBC (Blood)

In a traumatic lumbar puncture, a correction of 1 mg of protein/dl should bemade for every 1000 RBC and the glucose estimation should be done as early aspossible in the supernatant after centrifugation of the CSF sample Any delay canlead to an erroneously low glucose report due to utilization of the glucose by thecells The CSF and blood glucose ratio is usually 0.6 Hyperglycemia may mask alow CSF sugar In the very early phase of meningitis and severe infection, the CSFmay be normocellular, but this does not exclude meningitis.10 In such cases a repeatCSF examination may reveal a purulent CSF after 12-24 hours The CSF culture indeveloped countries is positive in about 80% of cases, but the yield is lower in thedeveloping countries Plating the CSF directly on to the culture plates improves thepositivity Gram’s stain may be positive even if the CSF is normal The staining can

be done from the whole CSF directly if the CSF is turbid and from the centrifugedsediment if the CSF is clear Acridine orange staining may be positive when Gram’sstaining is negative; it imparts a bright red color to the bacteria However, it offers

no special advantage if the Gram’s stain is positive In patients where Gram’s stainand CSF culture are negative, blood culture may still be positive in 50% of the cases.Partially treated pyogenic meningitis offers difficulties in interpretation of the CSFreports The Gram’s stain or culture is usually sterile after 24 hours of antibiotictherapy The CSF glucose rises by the third day The CSF protein and cells arerelatively resistant and remain elevated, usually for ten days, though to a lower level

In patients with partially treated meningitis, a negative CSF Gram’s stain and aninconclusive CSF cytobiochemical analysis, the newer tests for rapid diagnosis, whichare described below, may be helpful

Latex Agglutination and Counterimmunoelectrophoresis Tests

These tests depend on the demonstration of bacterial antigens in the CSF usingserum or antisera directed against the specific antigen and are sensitive and specificfor detection of Hib Sensitivity and specificity of these tests are relatively low fordetection of other pathogens As the tests do not require viable organisms in theCSF, the number of false positives may be high In 27 consecutive cases of acutebacterial meningitis subjected to the latex agglutination test, we could detect theantigen in only seven cases It may be due to higher pathogenicity of bacteria in oursettings, thus causing meningitis at a lower antigenic load or our subjects may not

be mounting the level of immune response necessary for the test to be positive

Limulus Amebocyte Lysate Test

This test can detect minimal quantities of Gram-negative pathogens and holdssome promise in meningitis following neurosurgical procedures, where Gram-negativeorganisms are common The sensitivity varies between 70% and 100%

Polymerase Chain Reaction (PCR)

PCR detects the bacterial DNA Sensitivity and specificity of 91% has beenreported False positives and lack of availability are the obvious limitations of PCR

Neuroimaging

In ABM, contrast CT scan may show some enhancement of the ependyma andthe meninges In a patient suspected of meningitis, CT scanning is indicated if thepatient has papilloedema or a focal neurological deficit to exclude a space occupyinglesion In a patient with confirmed meningitis CT scanning is indicated if the pa-tient develops seizures or a focal neurological deficit Prolonged coma or fever is also

an indication for a CT scan MRI scan can detect meningeal enhancement, focalcerebritis, infarctions, cortical venous thrombosis and subdural effusions much bet-ter and earlier than the CT scan, however; it is more expensive and difficult to carryout in a semiconscious patient

Differential Diagnosis

Viral Meningitis

In 20-25% patients with viral meningitis in the initial stage, CSF shows morphonuclear pleocytosis Mumps, enteroviruses, herpes simplex virus and lym-phocytic choriomeningitis reveal a low CSF glucose level However, a repeat CSFexamination 8 to 24 hrs later shows a significant reduction of polymorphs in 90%

poly-of patients with viral meningitis

spi-in diagnosis

Tuberculous Meningitis (TBM)

The diagnosis of TBM is relatively easy when there is a history of six weeksduration or more and the CSF shows lymphocytic pleocytosis, raised protein anddecreased glucose Partially treated pyogenic meningitis is difficult to distinguishfrom tuberculous meningitis A helpful point is the time between onset of the firstsymptom and the onset of alteration of the sensorium If this gap is more than oneweek it favors the diagnosis of TBM, and if it is only a few days it favors pyogenicmeningitis However, if it is between a few days to one week, extra cranial evidence

of tuberculosis or pyogenic infection should be sought; if no clue is available, it isworthwhile to treat for both ABM and TBM If the response is dramatic, antituber-cular therapy should be discontinued and the patient to be kept under observation

If the patient does not show remarkable improvement within the first few days,antitubercular therapy is continued

Fungal Meningitis

Cryptococcal and candidial meningitis may also mimic bacterial meningitis and

in immunocompromised individuals may present acutely with polymorphonuclearpleocytosis in CSF CSF from immunocompromised individuals, therefore, should

be routinely subjected to fungal smear and culture

Chemical Meningitis

Chemical meningitis caused by hemorrhage, spinal anesthesia, contrast mediaand keratin from dermoid tumors may rarely produce a purulent CSF with a poly-morphonuclear pleocytosis History and CT scanning, however, resolve the issue.Acute hemorrhagic leukoencephalitis and cerebral malaria have been reported toproduce a similar CSF profile and should be kept in mind Unusual diseases likeSLE cerebritis, Beçhet’s syndrome and CNS angiitis may produce a similar illnesswith a purulent CSF

Complications

Cerebral Infarction

Venous or arterial infarctions may result as a consequence of thrombophlebitis

or arteritis Focal seizures, focal deficits or increasing intracranial pressure may nal its development

com-Hydrocephalus

Communicating or obstructive hydrocephalus is seen in about 15–20% of cases.Obstructive symptoms, delayed or in acute phase usually do not require shunting

Subdural Effusion or Subdural Empyema

Subdural effusion is almost confined to children less than two years of age and isreported in as high as 50% of cases Subdural empyema, on the other hand, is veryuncommon Both of these conditions are easily diagnosed by CT scan or MRI.Subdural effusion is almost always self-limiting, but subdural empyema usually re-quires craniotomy

Cerebral Edema and Herniation

Cerebral edema and herniation may be a prominent feature in some patientswith ABM The pathogenic effects include cytotoxic, interstitial and vasogenic edema.The resulting raised intracranial pressure may cause cerebral herniation or reducedcerebral blood flow

Cranial Nerve Palsy

In ABM the third, sixth, seventh and eighth cranial nerves are commonly fected The third, sixth and seventh cranial nerves usually recover spontaneously,but deafness is a well-known sequelae of ABM, especially in children

Treatment

Acute bacterial meningitis is a neurological emergency and is fatal if left treated Antibiotic therapy should be started immediately whenever the diagnosis issuspected Blood culture and CSF studies should be done as soon as possible

un-Choice of Antibiotics

For an antibiotic to be effective in ABM, it should be able to cross the BBB, act

in a purulent CSF and maintain a bactericidal level in the CSF long enough to killthe bacteria Factors which determine the level of antibiotics in the CSF are lipidsolubility, size of the molecules and protein binding Low protein binding, smallmolecular size and high lipid solubility increase the CSF availability of the drug InCSF the efficacy of an antibiotic depends on its metabolism The metabolites of adrug may or may not be as effective as the parent drugs The concentrations of theantibiotics in the CSF should exceed the in vitro MIC by 20-fold for optimal efficacy

Specific Therapy for Pathogenic Bacteria

Once the reports of the culture and sensitivity are available, the antibiotics areprescribed according to the culture reports If culture is negative empiric therapy iscontinued depending on the clinical response (Tables 3.2 and 3.3)

H influenzae Type b (Hib) Meningitis

About one third of the strains of Hib are resistant to ampicillin, therefore a thirdgeneration cephalosporin instead of a combination of ampicillin and chloramphemicol

is recommended by the American Academy of Pediatrics.11 Cefotaxime andceftriaxone are both equally effective but the latter has the benefit of a twice-dailyregimen Cefuroxime has been found to be less effective than cefotaxime Gram’sstain and CSF culture obtained after treatment with cefuroxime were found to bepositive in various trials Cefotaxime causes an earlier sterilization of the CSF, andhas fewer complications when compared to cefuroxime for treatment of H.influenzaemeningitis.12

Nisseria meningitidis

Strains of N meningitidis are still sensitive to penicillin, hence, it is the drug ofchoice Partial resistance to penicillin has been reported, but still, resistance due toproduction of β lactamase is extremely rare In case of resistance or allergy to peni-cillins, a third generation cephalosporin can be used instead

Streptococcus pneumoniae

The incidence of drug resistance against S pneumoniae is 20-58% cocci resistant to penicillin G at even higher MIC has been reported Strains resis-tant to cephalosporins have also been reported Under such circumstances penicillin

Pneumo-G cannot be relied upon for the empirical treatment of pneumococcal meningitis

In patients with mild resistance to penicillin, third generation cephalosporin should

be started and those with severe infection, a combination of vancomycin and a thirdgeneration cephalosporin should be used Intrathecal administration of antibiotics

is generally not required but can be considered in patients with infection due to ahighly resistant strain of pneumococcus Newer agents like imipenem have beenused in the past, but is not used now because of it’s seizurogenic activities Meropenem,

a carbapenem, however, is safer and holds some promise in the management of thesecases Third generation cephalosporins (cefpirome, fluroquinolones like trovalfloxacin,

Gram-Negative Bacilli

Third generation cephalosporins are the drug of choice for Gram negative ganisms Traditional combinations with aminoglycosides and penicillin have a curerate of 40-90% as compared to the cephalosporins like ceftazidime, cefotaxime andceftriaxone, which cure 78-94% cases In case of suspicion of Pseudomonasareuoginosa, ceftazidime is preferred Fluroquinolones like pefloxacin have been used

or-in patients with suspected Gram negative menor-ingitis but should be reserved formulti-resistant cases

Table 3.2 Common pathogens and empiric therapeutic recommendations based

on age of patients with bacterial meningitis

Age of Patient Common Bacterial Empiric Antimicrobial

Pathogens Therapy*

1-4 weeks Streptococcus agalactiae, Ampicillin plus cefotaxime,

Escherichia coli, Listeria or ampicillin plus an monocytogenes, Klebsiella aminoglycoside pneumoniae, Enterococcus

species 4-12 weeks S.agalactiae, E.coli, L Ampicillin plus a third

monocytogenes, H generation cephalosporin influenzae, Streptococcus

pneumoniae, Neisseria meningitislis

3 months-18 years H influenzae, N Third generation

cepha-meningitidis, S losporin, or ampicillin plus

18-50 years S pneumoniae, N Third generation

cepha-meningitidis losporin or benzylpenicillin* More than 50 years S pneumoniae, N Ampicillin plus a third

meningitidis, L generation cephalosporin monocytogenes, anaerobic

Chloramphenicol with its activity against bacteroides and penicillin with its tivity against most other anaerobes can be used for anaerobic meningitis Metron-idazole has excellent activity against most anaerobes and should be used with penicillinfor anaerobic meningitis

ac-Post-Traumatic Meningitis

With the most likely organism being pneumococcus, a third generation losporin is the therapy of choice

cepha-Meningitis Following Neurosurgical Procedures

For procedures other than ventriculoperitoneal shunt, Gram negative organismsare the most common pathogens To provide cover for pseudomonas, a combina-tion of ceftazidime with an aminoglycoside is the preferred regimen Staphylococcicause most post-VP shunt meningitis and should be managed with vancomycinwith or without rifampicin Intrashunt and intraventricular vancomycin may betried in nonresponders

Immunocompromised Hosts

Patients with impaired cell mediated immunity are susceptible to Listeria tion and those with impaired humoral immunity to encapsulated organisms likepneumococus, Hib and P aeruginosa The treatment should include antibiotics cov-ering both Gram positive and Gram negative bacteria, particularly pseudomonas

infec-Duration of Therapy

The duration of therapy depends on the suspected or isolated organism Thepatients with meningococcal and Hib meningitis usually recover with seven and tendays therapy, respectively Those with pneumococcus do so in two weeks TheGram-negative organisms need to be treated for three to six weeks It may be noted

Table 3.3 Antibiotics dose schedule to be used in pyogenic meningitis

Penicillin G 20-24 million U/day intravenously (divided doses every 4 h) Ampicillin 12 g/day intravenously (every 4 h)

Ceftriaxone 2-4 g/day intravenously (every 12 h)

Cefotaxime 8 g/day intravenously (every 4 h)

Ceftazidime 6 g/day intravenously (every 8 h)

Nafcillin 8-12 g/day intravenously (every 4 h)

Oxacillin 9-12 g/day intravenously (every 4 h)

Vancomycin 2 g/day intravenously (every 6 h)

Seizures are common in children with meningitis and adults with pneumococcalmeningitis The seizures may be due to electrolyte imbalance following poor oralintake or a syndrome of inappropriate antidiuretic hormone (SIADH); cortical venousthrombosis or cerebral infarction To terminate a seizure, a short acting benzodiaz-epine may be required followed by loading and maintenance dose of phenytoin orphenobarbitone Children develop SIADH sooner than adults In adults it is man-aged by restriction of fluids and water and by increase in sodium intake In children,fluid restriction can cause dehydration, particularly if fever is present A daily re-quirement of 1200 ml/m2 is mandatory with 20-40 meq K+/m2 body surface area

Steroids

Corticosteroids reduce cytokine-mediated inflammation Dexamethasone is themost studied corticosteroid in this condition and at least 10 clinical trials have beenreported Moreover, meta-analyses of the clinical trials suggest that dexamethasone

in children in a dose of 0.15 mg/kg body weight every six hours for four days givenjust before antibiotics may be beneficial.15-16 For adults, the benefit is doubtful

Adjuvant Therapy

The role of nonsteroidal anti-inflammatory drugs in the therapy of experimentalmeningitis has been evaluated These drugs are associated with the prevention ofinflux of leukocytes in the CSF and a reduced incidence of cerebral edema, neuro-logical sequelae and mortality Their clinical efficacy remains to be proven Mono-clonal antibodies and pentoxyphylline have also been tried as an adjunct to theusual regimens of antibiotics without proven benefit

Mortality

The overall mortality in ABM varies between 15-25% It depends on a largenumber of factors, namely age, duration of illness, level of consciousness, time lagbetween the onset of disease and institution of therapy and the organism respon-sible The mortality is higher at the extremes of age Neonates and infants have thehighest mortality Patients with Gram negative meningitis and those with alteration

in sensorium at the time of presentation have a higher mortality

Prevention and Prophylaxis

Vaccination is the most effective means of preventing bacterial meningitis inchildren H influenzae type b conjugate vaccine has decreased the incidence of Hibmeningitis in children in developed countries A polyvalent vaccine containing thepolysaccharide capsule of groups A,C,Y and w 135 is currently available and is rec-ommended for high risk children over two years of age

Pneumococcal vaccine is derived from the capsular polysaccharide antigen from

23 serotypes of the pneumococci and is recommended only for use in high riskchildren above two years of age Conjugate vaccines against the meningococci group

A and C are currently available The vaccine is derived from the polysaccharidecapsule of meningococci and has been responsible for the reduction of the occur-rence of major epidemics of meningococcal group A meningitis in the developedcountries Phase II trials with meningococcal group C vaccine have been completed,and it holds promise for the prevention of the disease Phase III trials are pending,and the long term benefits of the vaccine are yet to be established.17

Prophylaxis with rifampicin is recommended for all intimate contacts of patientswith meningococcal meningitis Health workers in intimate contact with the in-fected patients should also use this prophylaxis Rifampicin is given in a dose of 10mg/kg or a maximum of 600 mg/day for two days in children up to two years of ageand adults respectively Alternatively, a single intramuscular injection of ceftriaxonemay be given if rifampicin is contraindicated,.as in pregnancy.18 The householdcontacts of patients with Hib meningitis should be put on a prophylactic treatmentwith rifampicin, if there is at least one contact with age less than four years

in men then in women with peak incidence at 30-45 years of age

Etiology

The introduction of newer antibiotics has changed the spectrum of the gens causing brain abscess Staphylococcus aureus was the most common cause ofbrain abscess in the preantibiotic era but enterobacteriacae have replaced S aureus.Bacteroides and other anaerobes, particularly streptococci, are also important causes

patho-of brain abscess Patients with chronic frontal or ethmoidal sinusitis tend to have afrontal lobe abscess and streptococcus is the most common organism The temporallobe abscesses are usually associated with ear infections and are due to mixed patho-gens Gram negative organisms and the bacteroides are common, particularly if thebrain abscess is associated with chronic otitis media and cholesteatoma The inter-medius group of organisms have a striking preponderance to cause focal suppurativelesions of the brain Though S pneumoniae causes bacterial meningitis frequently,

it is an uncommon cause of brain abscess except in immunocompromised states

Staphylococci are the most common pathogens in post-traumatic abscesses obes commonly cause brain abscess and the pathogens include clostridium, bacteroi-des and actinomycetes The pathogenic flora for the brain abscess has changedsignificantly due to an increase in the number of immumocompromised subjectswhere abscesses due to Nocardia20 are common In immunocompromised patientsaspergillus and other dimorphic fungi are also common and account for a very highmortality Though cryptococcus usually causes fungal meningitis, it is known tocause focal suppuration of the brain as well In patients with AIDS, toxoplasma and

Anaer-Entamoeba histolytica can also cause brain abscess The prognosis in such cases is

extremely poor The immune status of the patient can indicate the likely pathogenicorganism Patients with T lymphocyte defects, for example AIDS patients, are mostlyaffected by toxoplasma, nocardia, cryptococcus or Listeria, whereas neutropenic pa-tients by pseudomonas or other Gram negative organisms These patients also have

a predisposition for fungal abscess, particularly if they are on broad spectrumantibiotics

Pathogenesis and Pathology

The most common predisposing condition for brain abscess is ear infection.Otogenic brain abscesses are usually located in the temporal lobes or the cerebellum

In contrast to chronic otitis media, acute infections seldom cause brain abscesses.Brain abscesses secondary to sinusitis are becoming increasingly rare, and the frontallobe is almost exclusively involved in these cases Abscesses of dental origin are lo-cated in the frontal or temporal lobes Brain abscess is a rare complication of pyo-genic meningitis except in cases of neonates with Gram negative bacterial infection

It is uncommon to have brain abscess following trauma or brain surgery ing brain injuries and transsphenoidal pituitary surgery may result in brain abscesses.Lung abscess and bronchiectasis are common causes of multiple brain abscesses due

Penetrat-to hemaPenetrat-togenous spread, mostly in the middle cerebral artery terriPenetrat-tory Congenitalcyanotic heart disease and infective endocarditis are other sources for hematogenousbrain abscesses accounting for 1-5% of cases

Animal experiments have revealed that it is extremely difficult for a brain abscess

to develop in normal brain tissue Some degree of damage to the brain is necessaryalong with a source of bacteria The spread of infection from a nearby source to thebrain tissue is either direct, through a hematogenous route or through emissaryveins, which undergo retrograde thrombophlebitis Patients with congenital cyan-otic heart disease are prone to cerebral microinfarctions due to polycythemia anddecreased blood flow as a result of increased viscosity of the blood Colonization ofbacteria in these damaged areas is followed by formation of the brain abscess.Brain abscess evolves through four stages Early cerebritis is characterized by aninflammatory exudate of polymorphonuclear leukocytes,which tends to localize tothe perivascular region with the development of a necrotic center This area is sur-rounded by cerebral edema This state usually lasts for one to three days Late cerebritisusually extends from the fourth to ninth day The necrotic center of the abscessincreases in size with neovascularization at the periphery The capillaries are newlyformed and are surrounded by early reactive astrocytosis There is an accumulation

of fibroblasts in the periphery which form the capsule at a later stage Early capsuleformation extends from days 10-13 The necrotic center decreases in size and thefibroblasts increase in number along with further neovascularization (Fig 3.2) Latecapsule formation is the last stage after two weeks A mature capsule is formed and

Clinical Features

Fifty percent of patients with brain abscess present with a triad of fever, headacheand focal neurological deficit which is usually subacute, though a fulminant presen-tation may rarely be seen Focal or generalized headache of moderate to severe de-gree is the dominant symptom Headache may be accompanied with nausea andvomiting Seizures occur in 25-40% of cases, mostly in frontal lobe abscesses Papil-loedema and other features of raised ICP may ensue Focal neurological deficitsoccur in 50% of patients and include hemiparesis, visual field defects or cranialnerve deficits Patients may have varying degrees of alteration of sensorium Neuro-logical signs depend upon the location of the abscess, for example, temporal ab-scesses present with aphasia, hemiparesis and field defects The signs of associatedpredisposing conditions such as ear infections, sinusitis, chest infections and con-genital cyanotic heart disease may also be present

Diagnosis

Lumbar puncture is contraindicated in a patient with suspected brain abscessbecause of risk of herniation The CSF picture is almost similar to pyogenic menin-gitis; sugar is low with moderate rise of proteins and polymorphonuclear leukocytes

In 10% of patients CSF may be normal The CT scan with contrast enhancementremains the radiological investigation of choice for the brain abscess In CT scan,abscess appears as an area of hypodensity surrounded by a uniform ring enhance-

ment and perifocal edema (Fig 3.4-3.6) Cranial CT scan has a sensitivity of 95-99%

and a specificity of 70% Resolving hematoma, subacute infarct, inflammatory loma and metastasis or primary neoplasia can show similar CT scan findings Thepresence of intraventricular hyperdensities and ependymal enhancement indicatesventriculitis MRI can provide better delineation of the brain abscess in the stage ofearly cerebritis and also displays the perifocal edema better MRI remains the inves-tigation of choice for posterior fossa abscesses Newer investigative modalities likeindium-III labeled leukocyte scintigraphy, 99-Tc-hexamethylpropylenamineoximescintigraphy and thallium-201 SPECT are currently under evaluation for the diag-nosis of brain abscess in early stage

granu-Treatment

The local milieu of the abscess, the blood brain barrier and the bacterial flora ofthe brain abscess, determine the response to antibiotics The capsule of the brainabscess impairs drug penetration, therefore, longer duration of treatment is needed.There are no trials to support the use of a particular antibiotic regimen Most regi-mens include penicillin because of its excellent efficacy against streptococci As analternative to penicillin, cefotaxime can be used Due to isolation of anaerobes inmost cultures from brain abscesses, metronidazole is used Abscesses secondary totrauma or neurosurgical procedures should be treated with vancomycin A common

pathogen after otitic infection is Pseudomonas aeruginosa, therefore, ceftazidime is

Fig 3.2 Photomicrograph of a brain abscess showing thick fibrous capsule externally (➔) with the polymorphonuclear cell debris in the center (H & E X 350).

Fig 3.3 High powered view of a chronic abscess showing predominant infiltration by lymphocytes and plasma cells (H & E X 750).

included in their regimens Only a small proportion of patients with brain abscessrespond favorably to medical treatment alone The surgical procedures currentlyused are aspiration and excision of the abscess There are no reports of randomizedtrials comparing aspiration with excision The choice of the method depends on thesite, size, capsule thickness of the abscess as well as the choice of the surgeon Thecurrent consensus is that all brain abscesses should be given a trial of aspiration withantibiotics and surgery should be reserved for larger abscesses, failed aspiration orfor posterior fossa abscess The antibiotics should begin before surgery and continue

Fig 3.4 Axial contrast enhanced CT scan showing a well-defined rounded lesion in the left temporal lobe There is peripheral ring enhancement of uniform thickness and the central core is hypodense with perilesional edema which is suggestive of brain abscess.

Subdural Empyema

Subdural empyema is defined as an infection of the subdural space i.e., the spacebetween the dura and the arachnoid matter Though the disease has been known formany decades, improvement in diagnostic and therapeutic measures have contrib-uted to better outcome than what it was about 25 years ago

Fig 3.6 Postoperative CT scan, axial section showing diffuse, thickened and intensely enhancing ependyma of both lateral ventricles The enhancement is more marked along the trigone Findings are suggestive of ventriculitis following rupture of the abscess into the ventricles.