Nigerian Journal of surgical Research Vol 8 No 1-2 ,2006 ,1 - 18

Review Article

Neurosurgical

B. B. Shehu, M. R. Mahmud and N. J. Ismail,

Neurosurgery unit, Department of Surgery Usmanu Danfodio university Teaching Hospital Sokoto, Sokoto state, Nigeria Requests for reprints to DR. B. B. SHEHU Neurosurgery Unit, Department Of Surgery Usmanu Danfodio University Teaching Hospital Sokoto, Sokoto State, Nigeria E-Mail: [email protected]

Abstract

The central is a very delicate and vulnerable organ which enjoys protection by layers of coverings. It is described as an immunological vacuum, and when afflicted by infections the outcome is most often devastating. Factors leading to compromise of the host defense play a major role in establishing neurosurgical infections. A number of such factors can either be avoided or minimized. Over the past decades, these infections have been fatal. However, more recently, the advent of newer more effective antibiotics, improved bacteriological studies, advanced imaging facilities, and meticulous surgical techniques have turned around the outcomes. This article will review infections of the central nervous system of neurosurgical significance. Keywords: Neurosurgical; Infections; Bacterial; Fungal; Viral; Parasitic

Introduction

The practice of medicine has been greatly advanced The immunologic response to invasion by microbes by the technological improvements of the last century. involves three components: humoral response, The treatment of neurosurgical infections has cellular response, and complement system. These particularly improved dramatically. The development mechanisms are normally absent in the central of newer antibiotics ,advances in bacteriology and nervous system (CNS) in the absence of microbial imaging, and precision in surgical procedures have provocation. The CNS has in fact been considered an transformed diseases that were previously associated immunologic vacuum that is slow in the recruitment with high mortality into entities that routinely have of systemic host defenses in confronting any complete cures. Two main factors, among others, microbial penetration. This characteristic permits a have significantly influenced the natural history of small number of organisms the ability to invade, neurosurgical infections. These factors are the host multiply quickly , and harm the host with an attendant defenses and the antibiotic characteristics. higher mortality compared to infections in other parts of the body. It is documented that there is no evidence Host Defenses of antibacterial activity in the (CSF) as would be found elsewhere in the body 1, 2 In the central nervous system, host defenses comprise and the immunoglobulin levels in the CNS are two main categories: the anatomical barrier and the characteristically low. The 1gG and 1gA CNS levels immunologic response to microbial invasion. are 0.5% of serum, and 1gM levels are less than 0.1% The anatomical barriers include skin, subcutaneous 3. In purulent the levels of tissue, bones of the skull , spinal column and the immunoglobulins are low and rise slowly. meninges, guard against microbial penetration. In the normal state, usually there are no When any of these protective barriers is breached by polymorphonuclear leukocytes circulating in the CSF surgery , trauma and congenital defects, the risk of and there are no phagocytes seen on antigen rises significantly.

2 Neurosurgical infections Shehu BB et al presentation. Phagocytic cells migrate into the CSF in response to infection or injury, but they are inefficient in the absence of opsonizing antibodies. It is known the absence of meningeal . Some drugs that infected CSF is chemotactic for with lower lipid solubility that are usually highly polymorphonuclear leukocytes but the beneficial ionized at physiological pH e.g. most β-lactam effect of leukocytes in CSF is still unclear. Two penetrate the BBB poorly in the absence of meningeal studies describing the role of leucocytes in CSF inflammation. Molecules with high serum protein present conflicting results: in one study bacterial binding (> 90%) enter the CSF with difficulty as only meningitis with low CSF leukocyte was associated the free molecules can enter the CSF with significant with high mortality , and in another study there was ease. Finally, some antibiotics may be removed from high CSF leucocytes and bacterial proliferation CSF to the blood by an active transport “pump” progressed unhindered . The later point is explained mechanism in the choroid plexus (e.g. penicillins, by the lack of complement and opsonizing antibodies cephalosporins),. This mechanism is energy necessary to enhance opsonophagocytic activity and dependent and is inhibited by conditions such as bacterial killing. Worthy of note o is the fact that meningitis and uraemia.4, 5 polymorphonuclear leukocyte diapedesis(migration) is sluggish (14 – 16 hours), giving room for the initial Scalp infections invading bacteria to proliferate unhindered. Infection may establish itself due to the low levels of The scalp is a common site for infection. The danger Complement concentrations in normal CSF. This of its infection stems from its closeness to the skull localized complement deficiency is further worsened and brain, and the possibility of spreading disease. by the presence of leukocyte proteases, released Scalp anatomy has an important bearing on during meningitis and will lead to degradation of understanding the outcome of scalp infections. Of its complement components. Further deficiency of five layers (skin, connective tissue, galea complement components in the CSF is influenced by aponeurotica, loose connective tissue, and the variable permeability of the blood-brain barrier pericranium), the first three move as a unit. Access of (BBB), enhanced clearance from CSF, and decreased bacteria to the subgaleal space may permit extensive production within the CNS. spread of infection and may produce osteomyelitis, Infection of the CNS may be due to some host factors. epidural or subdural infection, or via the These factors include acquired diploic or emissary veins of the skull. syndromes, other T-cell defects, asplenia, The vascular supply of the scalp is abundant, hypogammaglobulinaemia, and leukopaenia, conferring a natural resistance to infection, but also providing a potential route for haematogenous seeding Antibiotics and the central nervous system from other locations. Also the extensive anastomosis of vessels of the scalp, face and neck allow retrograde The blood-brain barrier (BBB) separates the extension of scalp infection. Lymphatic channels form intravascular compartment from the CSF, thereby a rich network in the neighbourhood of the vertex. restricting efflux of substances, including antibiotics Enlargement and tenderness of the lymph nodes may into the CSF. The BBB is commonly divided into indicate an unrecognized scalp infection. blood-brain and blood-CSF barriers.4 Most antibiotics penetrate the BBB poorly. However, Spontaneous scalp infections permeability increases significantly in the presence of bacterial meningitis by disrupting tight junctions Spontaneous scalp infections are rare, produced by between endothelial cells and increasing the number almost any type of pyogenic bacterium, virus and of pinocytic vesicles. Consequently, antibiotic fungus. Non healing ulcers and chronic sinus tracts penetration into CSF increases significantly. Besides should be suspected of harbouring infection. the BBB, a number of characteristics of the drug Alopecia or scalp thickening may precede frank scalp molecule are among important factors affecting CSF infection.6 Therefore, preoperative evaluation of a antibiotic concentration. These include molecular craniotomy patient should include scalp examination. weight, lipid solubility, degree of ionization, serum Any evidence of infection should delay the procedure protein binding, and the mode of removal of the drug as possible. from CSF. Since most antibiotics penetrate the CSF by passive Carbuncle: diffusion across the BBB, small molecules with Many patients present with a carbuncle which is a simple structure and low molecular weight achieve type of a simple staphylococcal folliculitis. It a higher CSF levels than do large, complex molecules. deeply infiltrating lesion situated in the thick, Lipophilic drugs (e.g. chloramphenicol, sulfonamides, inelastic skin such as in the region of the occiput.7 It and rifampicin) will penetrate well into CSF even in begins as a very tender nodule that enlarges over 5

Neurosurgical Infections Shehu BB et al 3 days after which it discharges pus. Central ulceration Osteomyelitis Of The Skull develops to involve the full thickness of the scalp. Treatment consists of surgical drainage and culture of Osteomyelitis of the skull is a relatively rare disease. drained pus. A broad spectrum antibiotics should be However, the proximity of the brain and the commenced before culture results are obtained. propensity to formation of epidural abscess necessitates prompt diagnosis and definitive early Atypical organisms may be the cause and so cultures treatment. The skull infection originates from three for aerobic and anaerobic bacteria and fungi, as well key sources : (a) Paranasal sinusitis, mastoiditis, or as biopsy of the adjacent scalp should be obtained otitis; by direct spread (b) haematogenous spread following debridement.8 secondary to bacteraemia or fungaemia; (c) penetrating trauma or craniotomy. Necrotizing fascitis War wounds tend to be more extensive and It is a rapidly progressive, highly destructive contaminated than civilian wounds, but principles of rapidly,fatal bacterial invasion of the subcutaneous treatment are same . and subgaleal spaces. Spread is limited by the scalp attachments: the supra orbital ridges anteriorly, and Pain and swelling at the wound site should subside the occipital protuberance posteriorly. It commonly within a few days of closure. Clinical manifestation occurs spontaneously, following minor trauma, and of traumatic wound infection may become apparent may present following craniotomy. There is a diffuse within days to months after closure.When an infected patch or erythema and progresses and rapidly scalp wound is suspected, treatment should be undermines the scalp with widespread necrosis and immediate.9 The wound is opened, all purulent usually, associated with severe toxaemia. There is material evacuated and suture materials removed, and sloughing and ulceration due to vascular thrombosis devitalized tissue excised. To ensure satisfactory in the subcutaneous tissue and deep dermis . The recovery of the exposed skull, the wound should be entire calvaria may be denuded as the pericranium closed loosely over a drain, which should be removed becomes incorporated into a layer of thick fibrous within 24 to 48 hours. A single layered closure with tissue. Bacteriology shows multiple organisms, often an inert suture material, followed by a gentle staphylococcus epidermidis, staphylococcus aureus, compressive dressing to obliterate any dead space, are and streptococcus spp. Immediate generous applied9. débridement, with copious antibiotic irrigation of the Staphylococcus species are the commonest culprits, subgaleal space is advocated. Multiple postoperative and appropriate systemic antibiotics should be started inspections and débridement are usually necessary before culture result is obtained. Persistence of with a planned second-look operation after the first 24 infection after adequate treatment should suggest hours. Split skin grafting can then be applied after subgaleal spread, underlying osteomyelitis, or two weeks. Systemic toxicity must be treated erroneous identification of the offending organism. aggressively. Mortality may be from multiple organ Signs of meningeal irritation, , new focal failure but commonly there is septic shock , cardiac neurologic deficits, or a decreased level of failure and respiratory failure . Hyperbaric oxygen consciousness may signal penetration of the infection may help in the treatment of necrotising fascitis. beyond the galea, which warrants a lumbar puncture and a further investigation including a contrast Infection in Scalp Lacerations enhanced CT scan and MRI.

Most scalp wounds heal satisfactorily, even those that Craniotomy infections are grossly contaminated at the time of closure. Any delay in débridement increases the risk of infection. Most recent studies report risk of infection of 1 to 3%, Unfortunately, minor scalp wounds are usually although re-operation on glioma patients is associated ignored, and these may result in serious infections9. with rates as high as 11%.10 This increased risk may be attributed to reopening of surgical wounds and Certain principles are to be followed. The entire scalp prior irradiation of the scalp. Other factors must be inspected thoroughly and cleansed to remove contributing to the risk of infection after craniotomy debris. The depth of the would must be checked for include long duration of surgery, multiple incisions, skull penetration. Any CSF leak should be noted and a placement of a drain , foreign body, the presence of a skull fracture with dural tear suspected. Because the CSF leak, and immunosuppression of the patient.11 scalp is highly mobile, a skull fracture may be Treatment consists of systemic antibiotics and beyond the limits of the wound. The wound must be surgical débridement. The risk of spreading thoroughly cleaned with a sterile solution and foreign superficial infection to the deeper layers after material and devitalized tissue removed. craniotomy is sufficiently serious to warrant antibiotic Lacerations that do not sever the aponeurotic layer do administration even before cultures are obtained. not gape, and can easily be re-approximated. Early detection of a craniotomy flap infection is Lacerations through the galea result in a wide important by looking out for the local and systemic separation and require suturing of the galea as well as signs of infection. Once infection is identified, the the skin. Tetanus prophylaxis should be administered. wound must be opened. All purulent material and 4 Neurosurgical infections Shehu BB et al visible sutures should be removed, followed by that of small cystic areas of skull destruction with a mechanical débridement and irrigation. Dura should significant risk of meningeal spread. Extensive bone not be violated unless subdural infection is suspected. debridement is successful in the treatment of The standard technique is removal of an infected bone disseminated coccidiodomycosis by decreasing the flap to prevent it being a nidus for chronic infection. antigen load in the immunosuppressed patient.13 A subsequent cranioplasty is then done later. Postoperative Osteomyelitis of the Skull. Contiguous spread Osteomyelitis may follow craniotomy or trauma . The contiguous spread of infection from frontal The presence of a compound fracture significantly sinusitis is the most frequent source of skull increases the risk of osteomyelitis as does inadequate osteomyelitis. Invasion of the skull by the direct initial treatment.14 spread of infective organisms occurs via the diploic Craniofacial reconstruction, is considered a clean veins. The diploic space communicates freely with the procedure, may presents a significant risk of valveless veins of the mucous membranes of the osteomyelitis because there may be ; violation of frontal sinuses, so septic emboli can translocate easily mucosal barriers so opening the oronasal cavity to the to the dura. The arterial blood supply to the inner cranium and bone grafting is often required. Risk of table of the skull is diminished and retrograde infection can be minimized by the use of staged thrombosis can occur, creating an avascular outer procedures. Incisions and bone grafts should be table. When the pericranium is elevated from the limited whenever possible14 underlying bone by a process of necrosis and . suppuration, swelling and oedema occur, commonly referred to as pott’s puffy tumour. Other symptoms of Diagnosis of skull Osteomyelitis. osteomyelitis include pain, erythema, and fever. Patients with intracranial extension may present with Diagnosis of osteomyelitis is mainly clinical, seizures, neurological deficits or persistent manifesting as pain, swelling, and fluctuance. X-ray .12 and radionuclide imaging may help to confirm or Staphylococcus is the single most important pathogen localize the infection. Radiographic evidence is seen in osteomyelitis of the skull. 12 Systemic antibiotics only after 30 to 50% of bone is demineralised, and have not eliminated the need for surgery in the thus may be absent in the acute phase of treatment of osteomyelitis associated with sinusitis. A osteomyelitis.15 The pattern is that of a moth-eaten wide craniectomy of all necrotic bone to the freely appearance due to avascular necrosis. Chronic bleeding bone edge must be ensured. Involved osteomyelitis is identified by the presence of sinuses and associated empyema should be drained radiopaque sequestra (calcified necrotic bone). CT and frontal sinuses exenterated when they scan has the same lag phase behind the acute communicate with the intracranial space. The dura osteolytic changes (Fig. 1) but is still superior to x- should be left intact whenever possible.11,12 rays in imaging skull base and identifying intracranial empyema or abscess. Haematogenous Skull Osteomyelitis Radionuclide scans using technetium – 99m and Gallium – 67 are more sensitive than x-ray and CT Reports of osteomyelitis of haematogenous origin are scan.15 Other diagnostic studies such as leukocyte rare. Syphilitic and typhoid osteomyelitis are extinct count, and erythrocyte sedimentation rate, are normal in most developed countries, but very occasionally too often to be of diagnostic value. However, when occur in developing countries. Disseminated elevated, they may be useful indicators of treatment coccidiodomycosis, a fungus, frequently involves efficacy, if followed serially. bone by haematogenous spread.13 The presentation is

Neurosurgical Infections Shehu BB et al 5

(a) (b) (Fig. 1) Bone window (a) and plain (b) CT images demonstrating moth eaten appearance of chronic osteomyelitis on the frontal bone with overlying soft tissue swelling- Pott’s Puffy tumour. See spear

Antibiotics in the treatment of Osteomyelitis of the patients with bacterial meningitis. The table below Skull. gives a summary.

The major effect of antibiotics has been on the Table 1 - Common bacteria causing meningitis adequate treatment of sinus infection, with resultant decrease in the risk of osteomyelitis. Staph. spp and Organisms Ages possibly methicillin – resistant staph spp must be a b c d taken into account. Immunosuppression may lead to Str agalctiae (grp +++ + - - Bacilli -ve +++ + + + fungal involvement. Salmonella is common with L monocytogenes ++ + + + haemoglobinopathies; pseudomonas in drug addicts H influenzae ++++ + + and diabetic patients; Escherichia coli, in neonates. Str pneumoniae + + + +++ +++ The antibiotics are adjusted when culture results are N Meningitidis - +++ ++ ++ S aureus + + + + available. Generally, 1 to 2 weeks of intravenous S. epidermidis + + + + antibiotic therapy followed by 6 to 12 weeks of oral A=0-1mo b= 1mo-4yr c=4-30yr d=>30Yr therapy is recommended. Resolution of infection can be documented by a serial gallium nucleotide scans (where available), and a normal ESR value Infections following neurosurgical procedures, are quite different from those found in other situations..16 Bacterial Meningitis Staphylococcus aureus may be involved in postoperative meningitis but gram-negative bacilli are Most cases of meningitis are caused by bacterial or also regularly encountered in these patients. viral infection of the leptomeninges and CSF, but the Escherichia coli, Klebsiella pneumoniae, list of other causes is extensive. This disease is Pseudomonas aeruginosa, Proteus spp., Enterobacter associated with significant morbidity and mortality, spp, and Acinetobacter spp are regularly isolated. but currently there is improved survival of patients When a CSF leak is present, Streptococcus with bacterial meningitis, owing to major advances in pneumoniae is the commonest organism. When a antimicrobial therapy. ventricular shunt is present, staphylococcus Atypical and new bacterial forms causing meningitis epidermidis is the leading cause of infection, followed are encountered in patients with infection following by diphtheroids such as propionibacterium acnes. This craniotomy , shunt placemnent and in unique distribution of causative organisms requires an immunosuppressive conditions These present new approach to therapy that is quite different from that challenges in management and the outcome is less 10,16 1,2,3 used in non-neurosurgical patients. predictable..

Causative organisms Pathology

The incidence of the leading causes of bacterial Grossly, post mortem brain specimen is frequently meningitis varies strikingly with age of the patient. swollen, sometimes with evidence of herniation. The This relationship is so important that it must always sulci may be obliterated following cortical oedema. be taken into account when planning the therapy of 6 Neurosurgical infections Shehu BB et al

Pus may be found in sulci and major fissures, often in The patient is acutely ill, with fever often above 39ºc. contact with veins and venous sinuses. Exudates may There may be petechial rash. There may be evidence surround the base of the brain or the cerebellum and of portal of entry such as otitis media, sinusitis, dorsum of the . mastoiditis, orbital cellulitis, and bacterial endocarditis. Signs of meningeal inflammation Associated findings may include subdural effusions, (kernig’s and Brudzinski’s) are present. Cranial nerve subdural empyema, venous sinus thromboses, cortical abnormalities occur in 10% of cases, mainly transient infarctions and secondary . Small CrN VI palsy. Papilloedema is not common. In perivascular collections of inflammatory cells may advanced cases with raised the occur within the brain itself. pupillary signs of tentorial herniation may be present. Microscopy reveals purulent inflammation of the In premature infants and neonates the manifestation leptomeninges with dilated thrombosed veins and a may be atypical with absent neck stiffness and low or variable amount of haemorrhage. The superficial normal temperature. layers of the cerebral cortex may be inflamed, and The post neurosurgical patient with bacterial perivascular collections of leukocytes may be found meningitis may also have atypical features. Nuchal deeper in the brain. Organisms, often in large rigidity, , and altered consciousness are less numbers, may be identified by special stains. In viral reliable as diagnostic features because they may also meningitis frank pus does not form and the be caused by the recent operation. Body temperature inflammatory cells are primarily mononuclear. In of above 38% in the post operative period should cases of chronic meningitis from tuberculosis or suggest the possibility of meningitis. cryptococcosis, the exudate is also primarily mononuclear, sometimes with granulomas.17 Diagnosis

Clinical features The diagnosis of meningitis is based mainly on examination of the CSF. The more important tests are Bacterial meningitis may be preceded by symptoms of summarized below. upper respiratory tract infection. The typical manifestations include high fever, severe headache, Table 2 - Diagnostic tests on CSF sample for acute photophobia, neck stiffness, nausea, vomiting, and bacterial meningitis. anorexia. Back pain, myalgia and altered consciousness are frequent. Tests Findings

Standard tests

Cell count usually >500 cells/mm3, with predominance of polymorphonuclear leukocytes.

Protein level usually >100 mg/ell

Glucose level usually < 40mg/dl; CSF: serum ratio usually < 0.4

Gram’s stain For common pathogens, positive in 70 – 80%; for gram- negative bacilli positive in 50%.

Counterimmuno Positive in 70-80% of cases; helpful in patients taking electrophoresis or antibiotics and for early identification of organisms. Coagglutination

Supplementary Tests Lactic acid level usually ≥ 35 mg/dl Limulus lysate assay +ve in meningitis caused by gram-negative bacilli. Complications India ink preparation : positive for cryt. neoformans Bacterial meningitis is associated with many Slide agglutination +ve for cryptococcal antigen complications some of which may be life threatening Wet mount “ for by themselves. These include ,

Neurosurgical Infections Shehu BB et al 7 seizures, venous thrombosis, brain abscess, subdural or the temporal lobe. A single abscess is usually effusion, subdural empyema, shock and persistent or formed, located superficially in the brain near the site recurrent fever. of the primary infection. Frontal sinusitis can result in a brain abscess in the anterior or inferior portions of Treatment the frontal lobe; sphenoid sinusitis, an abscess in either the frontal or the temporal lobe; maxillary The principles of treatment are, to provide adequate sinusitis, an abscess in the temporal lobe; and supportive care through the critical period of illness, ethmoidal sinusitis, an abscess on the frontal lobe. and to eradicate the organism with appropriate Dehiscence of the posterior table of the frontal sinus, antibiotic therapy. either from trauma or osteitis, provides an important Supportive measures include prevention of shock and avenue for direct extension of infection into the cellular oedema by strict fluid input and output, brain.18 adequate control of respiration, control of seizures and Metastatic brain abscesses arise by haematogenous control of raised intracranial pressure. dissemination of infection from a primary site that is With regards to specific antibacterial therapy, the remote from the brain. The abscesses that form are ideal antibiotic for this serious infection should have frequently multiple and occur at the junction of white the characteristics of good CSF penetration, and gray matter. The incidence of matastatic brain bactericidal activity in the CSF, and proven efficacy abscess in each part of the brain is proportional to its in clinical practice. Because there is no room for regional blood flow, therefore, most common in the error in the early period of treatment, high dose distribution of the middle cerebral artery (primarily parenteral antibiotic therapy should be used in all the parietal lobe) but can also be found in more cases. unusual locations such as the cerebellum and brain stem.18 Brain Abscess Apart from 20-37% of patients whose primary site is unknown,19 the commoner sites include skin pustules, A brain abscess is a localized suppurative process dental or tonsilar abscesses, chronic pulmonary within the brain parenchyma caused by a wide variety infections, osteomyelitis, septicaemia, and bacterial of bacteria, fungi, and protozoa. Despite advances in endocarditis. Craniocerebral trauma is a well known diagnosis and antibiotic therapy, the incidence of predisposing factor to brain abscess, especially if brain abscess does not appear to be changing and may there are retained foreign bodies such as bone in fact be increasing. Computerized tomography (CT) fragments or an overlying wound infection. Brain has become indispensable in determining the location, abscesses seldom occur from bullet injuries, because size and pattern of contrast enhancement of the lesion. the clinging debris is often sterilized by the heat of the In the past few decades, there has been a steep rise in metal. Additionally, basal skull fractures with CSF the number of immunosuppressed patients and a leak can predispose to meningitis and brain abscess. concomitant rise in brain abscess caused by Previous craniotomy and shunt catheters are also a opportunistic organisms, which present diagnostic and known cause. therapeutic challenges.18 The incidence of brain abscess is increased many folds in immunocompromised patients, who include Pathogenesis those with diabetes, tuberculosis, sarcoidosis, those on anticancer chemotherapy, organ transplant recipients, Predisposing factors and sources those on prolonged broad spectrum antibiotic therapy, and patients with acquired immunodeficiency Majority of brain abscesses arise by direct spread syndrome. They usually suffer opportunistic from paranasal sinuses, middle ear, or mastoid infections that are of low virulence and pathogenicity infections. Infection can spread from the paranasal to humans such as fungi, parasites and unusual sinuses by way of retrograde thrombophlebitis bacteria.18,19 through the valveless diploic veins to either the frontal

Histogenesis

The CNS is vulnerable to destruction by infectious important histological changes take place. Oedema processes and is incapable of mounting a significant reaches its maximum with the increase in size of the defense by itself. A gliotic zone develops slowly necrotic center and the formation of pus. A reticulin around a site of infection and does little to limit the network is set down around the periphery of the zone spread of infection. Early cerebritis (days 1 to 3) of inflammation by fibroblasts that serves as the demonstrate a local inflammatory response precursor to the collagen capsule. Early capsule surrounding the adventitia of blood vessels. The formation (days 10 to 13) occurs when the collagen cerebritis is associated with the development of network is consolidated and the necrotic center is oedema and the beginning of a central necrotic region. isolated from the adjacent parenchyma. This process In the late cerebritis stage (days 4 to 9) the most is the most crucial in order to protect the surrounding 8 Neurosurgical infections Shehu BB et al tissue from injury. In the late capsule formation (day The raised ICP when accompanied by mass effect 14 and later) the abscess has five distinct regions: (1) can cause an alteration in level of consciousness, an a necrotic center, (2) a peripheral zone of important prognostic factor. Focal neurologic deficits inflammatory cells and fibroblasts, (3) Collagen are location dependent and include hemiparesis, capsule, (4) zone of neovascularity, and (5) zone of aphasia, visual field cuts, nystagmus, and ataxia. reactive gliosis with oedema18 Seizures present in about half the cases Various factors influence the rate and extent of preoperatively. Fever is usually low grade. capsular formation, which include the causative Menigismus and papilloedema are not very organism, the origin of infection, the host’s immune uncommon features. Sudden deterioration may competence, and use of antibiotics and suggest uncal or tonsilar herniation, or even corticosteroids.19 subarachnoid or intraventricular rupture. Laboratory analysis is of little value in the diagnosis. Clinical features Lumbar puncture is contraindicated. CSF and haematologic findings are nonspecific. The clinical presentation of patients with brain abscess can be protean and depends on the location, Radiologic evaluation size, number of the lesions, virulence of the causative organism, host immune status, associated oedema, Computed tomography is the most important factor in and degree of intracranial hypertension. Abscesses, improving the prognosis of brain abscess, along with being acute inflammatory processes, usually present development of antibiotics. CT classically shows a with a short clinical course. The short history is the smooth thin regular contrast enhanced wall with a main clinical deference with other intracranial mass central region of hypodensity (fig. 2). The ventricular lesions. Symptoms present within 2 weeks. side of the wall is usually thinner. MRI is still being The main symptom is headache that is constant and evaluated in the diagnosis of cerebral abscess, but it recalcitrant. When associated with raised intracranial gives images similar to CT pressure (ICP) there will be nausea and vomiting. . .

(a) (b)

(c) (d)

Neurosurgical Infections Shehu BB et al 9

Fig. 2. CT scan images showing smooth, thin, regular contrast enhanced wall with a hypodense centre, surrounded by oedema. Cerebral abscess of the frontal (a and b) and parietal (c) lobes. Note the aerocoele in (b), depicting the previous aspiration site, and the multiple cerebral abscesses in (d).

Management Of Cerebral Abscess 1. If multiple ring enhancing lesions are found, Non-operative treatment emergent surgery for all abscesses greater than 2.5cm in diameter or for those causing marked The choice of antibiotics for any bacterial abscess mass effect should be undertaken either by depends on the causative organism, penetration of the excision or preferably by stereotaxic aspiration. antibiotic into the abscess cavity, its bactericidal or 2. If all abscesses are less than 2.5cm and are not bacteristatic capacity, and its bacteriological causing mass effect, then the largest abscess spectrum. The size of the abscess cavity is also should be aspirated for microbiological important. Abscesses greater than 2.5cm in diameter identification. seldom respond to antibiotic therapy. Once tissue has 3. Antibiotics should be withheld until pathological been obtained empirical antibiotics are initiated, and material is obtained for culture. directed at the most likely organisms even before 4. Broad-spectrum antibiotics should be used until definitive culture results are available. It is advocated culture results are available and the antibiotics that because of the existence of stereotaxic operative can be adequately tailored to these results. techniques, rarely should lesions be treated with Afterwards, antibiotics are continued for antibiotics before cerebral tissue is obtained, except in minimum of 6 to 8 weeks and in the the presence of uncontrollable bleeding diathesis or a immunocompromised often more than 1 year. lesion smaller than 1.5cm in a neurologically intact 5. Post operatively, CT scan or MRI should be patient with a clear source of infection. In the case of performed weekly or at any sign of deterioration. multiple abscesses, antibiotics can be used as sole Repeated surgical drainage should be undertaken treatment for lesions smaller than 2.5cm if cultures if; from one of the abscesses have yielded a causative organism. (a) there is an enlargement of an abscess after 2 weeks of treatment or after clinical Operative treatment deterioration or (b) there is failure of an abscess to diminish in The operative management of cerebral abscesses is size after 4 weeks of antibiotic therapy. based on two separate procedures: aspiration with the help of stereotaxic guidance or complete Use of Corticosteroids excision.18,19,20 Aspiration has produced excellent result as it allows The use of corticosteroids in the treatment of cerebral for precise localization and decompression of abscess abscess is disputed. Most surgeons believe that its cavity with minimal tissue damage. This is of great use should be primarily in clinical situations when the advantage when dealing with deeply seated lesions, cerebral oedema and the mass effect created by it are with those in eloquent areas, or with multiple significantly debilitating or pose imminent danger to abscesses. It can be done under local anaesthesia, the patient’s survival. hence reducing the surgical risk.20 In the cerebritis stage when an open procedure may cause significant Follow up neurological deficit, a needle biopsy can retrieve tissue for culture. Antibiotic use alone is often It is paramount for all patients with cerebral abscess curative at this stage. to undergo serial radiography to evaluate the Excision is indicated in certain circumstances. Post resolution of the initial process. Weekly studies traumatic abscesses associated with retained foreign should be done during the course of antibiotic bodies can only be approached in this fashion because therapy, and 1 week afterwards then followed 1 a cure can be effected only after complete removal of month later, then every 2 months until the process has foreign material. In an abscess following a CSF leak, resolved. MRI has not shown any significant abscess excision combined with leak repair is advantage over CT scan, and it is only logical to use mandated. Fungal abscesses are often only cured the same modality throughout the course of any given through total excision. Cerebellar abscesses should be patient. explored through craniectomy, because any failure of treatment can be rapidly fatal. Complications

Management of Multiple Abscesses. The first most dreaded complication of cerebral abscess is herniation secondary to mass effect. This The following are recommendations by Manelak and is avoided by identifying such patients before they Resenblum21 as regards the management of multiple have deep changes in their mentation. If these abscesses. changes do occur, drainage of the abscess cavity 10 Neurosurgical infections Shehu BB et al should promptly reduce the mass effect. Also use of Most commonly, intracranial epidural abscesses corticosteroids is indicated here. develop secondary to foreign body implantation by The second most dreaded complication is abscess trauma, adjacent osteomyelitis or post operative rupture into the ventricle and subarachnoid space, a neurosurgical or otolaryngological complications, or condition that in the past was considered universally sequel to sinusitis or mastoiditis. Other less common fatal. It is now treated with ventricular drainage and factors include orbital suppurations, congenital dermal systemic and intraventricular antibiotics. It remains a sinuses, and sagittal sinus phlebitis. Abscesses curable but serious complication. following sinusitis are caused by streptococci whereas S. aureus and S. epidermidis follow trauma. Other unusual organisms have also been associated with abscesses, such as Actinomyces and Arachnia Prognosis propionica.

The single most important factor affecting outcome is Clinical features and Diagnosis the preoperative neurological findings. The mortality ranges from 0-21% in alert patients to 60% in those A preceding history of trauma, paranasal sinusitis, with signs of herniation, and to 89% in those with mastoiditis, or otolaryngological or neurosurgical coma. But recently with introduction of CT scan, procedure is usually obtained. There may be improved bacteriological techniques, more versatile headache at the overlying area of infection, antibiotics, and stereotaxic surgery most major centers periorbital swelling or a chronic draining sinus along report a mortality of less than 10%. an incision line. A patient with a suspected epidural The morbidities are mainly focal neurologic deficit, empyema who develops progressive deterioration in cognitive impairment, and seizures. These are also on level of consciousness, a focal neurological deficit, the decline because of the above mentioned factors. and/ or should be evaluated urgently for an associated subdural empyema (a more dreaded complication of epidural abscess). Intracranial Epidural Abscess Treatment Aetiopathogenesis of Intracranial Epidural Abscess The hallmark of treatment are prompt recognition of the features, early evacuation of abscess, and Intracranial epidural abscesses are rarely encountered resection of potentially infected bone. Broad in neurosurgical practice. They mostly occur as spectrum antibiotics are given empirically pending complications of sinusitis. Septic thrombophlebitis, bacteriological diagnosis. Prophylactic or direct infection to the epidural space, may occur anticonvulsants and corticosteroids may not be secondary to sinusitis, leading to an epidural abscess. necessary unless in the presence of a subdural The abscess is limited by the dural attachment at empyema. suture lines along the base of the skull and the inferior The dura must not be violated except with radiologic sagittal sinus.22 evidence of an associated subdural empyema, as seen in 20% of cases.22, 23

Prognosis The most life threatening subdural empyema is the spontaneous or acute variety. It is commonly related Intracranial epidural abscesses unassociated with to paranasal sinusitis, ear infection and subdural empyema or intracerebral infections carry an haematogenous disease. excellent prognosis, particularly when detected early Subacute subdural empyema uncommonly follows and radical resection of the purulent material has been trauma, and caused by staphylococcus, serratia and performed. diphtheroids. It is generally walled off and responds well to appropriate treatment. Subdural Empyema Chronic subdural empyema, or infected subdural effusion has been seen mainly in infants. Hemophilus Subdural empyema connotes diffusion of pus over the Influenza is the common offending organism. cerebral convexity, subfrontal space, sylvian fissure, and interhemispheric region. This spread often leads Clinical Presentation to bilateral infection.

Neurosurgical Infections Shehu BB et al 11

Acute subdural empyema presents with headache, Chronic subdural empyema is managed through burr altered sensorium, focal neurological deficit, seizures, hole evacuation, copious antibiotic irrigation and the pyrexia, nausea and vomiting. A history of paranasal use of drain.23 sinusitis and ear suppuration may be evident. Once a focal deficit or altered sensorium develops, the Granulomatous Disorders Of The Central Nervous neurological deterioration rapidly progresses to a System devastating outcome if the empyema is not treated radically. Chronic granulomatous disorders of the CNS are Subacute subdural empyema commonly follows a relatively uncommon and hence usually present burr hole infection. It may also follow an infected diagnostic difficulties especially to the unwary. craniotomy or trauma. The incision usually shows evidence of infection. There may be low-grade fever Tuberculosis and meningismus. A focal neurologic deficit, a significant alteration of mental state, and seizures are Over the past 50 years, vigorous public health control less likely. The empyema is commonly walled off by measures and the availability of anti tuberculosis adhesions and is limited to the surgical site. This has chemotherapy have reduced greatly the prevalence of a good prognosis. pulmonary tuberculosis world wide, especially in the Chronic subdural empyema presents with pyrexia, developed world. Incidence rates vary widely irritability, and lethargy in infants. Seizures, a full or between countries in inverse relation to tense anterior fontanelle, and a progressive increase in socioeconomic conditions. However, the advent of head circumference are common. Past history of HIV has worsened the incidence recently, especially meningitis is commonly obtained in these children. in HIV endemic areas. Although the incidence of pulmonary tuberculosis Diagnosis (TB) has declined in the US, the number of extrapulmonary TB cases, including TB infections of CT and MRI are now the ‘gold standard’ in diagnosis the CNS has remained constant at approximately 4000 of subdural empyema. CSF examination and skull x- new cases per year. TB meningitis accounts for rays are often of limited value. approximately 15% of extrapulmonary cases or about CT usually demonstrates paranasal sinusitis, an 0.7 % of all clinical TB in the US.24 epidural collection, and skull changes of CNS TB comprises three clinical categories: osteomyelitis. The subdural empyema appears as a , intracranial tuberculoma, and hypodense and diffuse collection which may be spinal tuberculous arachnoiditis (Pott’s disease). Each associated with mass effect and surrounding category has its variable manifestation. parenchymal oedema. T1- weighted MRI images demonstrate diffuse low Diagnosis. signal extradural collections and a relative high signal on T2-weighted images. Enhanced T1-weighted axial The patient with TB meningoencephalitis usually images reveal a peripheral ring enhancement. presents with malaise, lassitude, low-grade fever, intermittent headache, and often a personality change. Initial Treatment This may progress to meningismus, vomiting, A satisfying outcome in subdural empyema depends confusion, cranial nerve palsies, and signs of upper on prompt intervention. It is fatal, with a mortality of motor neuron lesion. In untreated cases death may 42% in comatose patients, and 6 to 14% in awake to ensue in 5 – 7 weeks. moderately lethargic patients. Once diagnosis is The clinical diagnosis of TB meningitis begins with established, administration of anticonvulsants is high index of suspicion. Delay in diagnosis and recommended due to high likelihood of seizures. treatment negatively influences the prospect for Antibiotics are instituted empirically pending culture recovery with minimal neurological sequelae. results. A positive tuberculin skin test may be of some diagnostic importance. However, a negative is of no Surgical Management significance as false negative results are seen in a variety of situations. Mild anaemia may be present. It is recommended to approach a subdural empyema Full blood count and even Erythrocyte sedimentation via an appropriate craniotomy, coupled with gentle rate are usually normal. suction and copious antibiotic irrigation. Dura should Blood chemistry is usually normal except in the be meticulously closed and the bone flap replaced presence of syndrome of inappropriate ADH after thorough cleaning. Serial follow-up CT scans secretion, which has been observed in a minority of are recommended for early identification of residual cases of miliary tuberculosis complicated by or recurrent collections. Parenteral antibiotics are meningitis. continued for 4 to 12 weeks, depending on response. The classic CSF findings are elevated protein levels, a Subacute subdural empyema is managed by re- decreased glucose concentration, and lymphocytosis. exploration of surgical site, antibiotic irrigation and Repeated (serial) CSF examinations give better excision of loculating membranes. results. Cultures of CSF will be positive in 80% of cases, but if the patient is to survive, therapeutic 12 Neurosurgical infections Shehu BB et al decisions will have to be made long before the results The intense fibrosis that occurs in TB meningitis may of the culture are available. lead to obliteration of the subarachnoid space and subsequent hydrocephalus. Neuroradiological Findings Treatment and outcome CT scan or MRI are the current imaging modalities of choice in the diagnosis and treatment of TB of the The most important principle of therapy is that it CNS. They allow the assessment of the developments should be initiated on the basis of strong suspicion in the clinical course, evaluation of hydrocephalus and and not delayed until proof has been obtained. The ventriculomegaly associated with basilar meningitis outcome is usually good when therapy is initiated of CNS Tuberculosis. Enhanced CT or MRI in cases before development of focal neurological deficit or of miliary TB with no clinical meningitis have significant alteration of consciousness. revealed multiple small lesions compatible with tuberculoma.25 Tuberculoma, tuberculous brain Medical Therapy abscess, and focal tuberculosis meningoencephalitis are either closely related processes or different stages The medical treatment requires a multidrug therapy, of the same process. consisting of 3 to 4 anti tuberculous drugs. Isoniazid remains the cornerstone of treatment as it has good Pathology of Tuberculosis CSF penetration even without meningeal inflammation. Current recommended regimens for At autopsy, the brains of patients dying with TB treatment employ the use of drugs such as isoniazid, meningitis reveal thickening and fibrosis of the rifampicin, ethambutol and pyrazinamide.24 arachnoid, especially over the base of the brain. Corticosteroids administration may give dramatic Small tubercles may be seen. In pyogenic meningitis, response in patients with rapidly deteriorating mental cerebral infarction may be seen due to intraluminal status, increased intracranial pressure, cerebral thrombosis of major cerebral vessels. oedema, focal neurologic signs, spinal block, On microscopy, the meninges show caseating hydrocephalus, and basilar optochiasmatic granuloma, and partial destruction of cranial nerves. pachymeningitis. The decision to employ Typical tubercles consisting of a central area of corticosteroids should rest on a strong presumptive or caseous necrosis surrounded by epithelioid positive diagnosis. Their use in uncertain cases can macrophages and lymphocytes with prominent be especially devastating if the patient has fungal langhan’s giant cells are seen in active TB meningitis. meningitis, and the benefits of steroids must be judged against this possibility.24

Surgical Treatment Following inhalation of the organism primary pulmonary infection and subsequent dissemination Surgical decompression of the ventricular system in may occur if the host defenses allow. On cases of hydrocephalus with raised intracranial dissemination, C neoformans invades multiple organ pressure, should not be delayed in patients with systems, with a predilection for the CNS. progressive neurological impairment. Decompression Cryptococcosis of the CNS manifests as one or more is achieved readily by ventriculostomy or ventricular of the following syndromes: Chronic meningitis, shunting. Laminectomy and abscess drainage, on the , or cryptococcomas. Immunosuppressive other hand, can be done to decompress spinal lesion. therapies and diseases act as predisposing factors.26

Cryptococcosis Cryptococcomas are not very common and present as focal neurologic abnormalities including hemiparesis, Cryptococcosis is a systemic fungal disease of man hemianopsia, and focal seizures. If spinal cord is and animals caused by Cryptococcus neoformans. involved, there may be quadriparesis or paraparesis. CNS infection commonly manifests as meningitis. Headache (75%) and mental status changes (50%) are While modern treatment has improved the prognosis the commonest presentations in cases of meningitis considerably, CNS cryptococcosis is increasing due to and meningoencephalitis. Nausea, vomiting, pain and the ever rising population of immunocompromised nuchal rigidity also occur. As many as 15% have no subjects. C. neoformans has a world wide distribution symptoms referable to the nervous system and yet and, at present, four subtypes designated A to D are have infection. As a result it is important to perform a recognized. All the serotypes are believed to be lumbar puncture in suspected cases.26 equally virulent.26

Neurosurgical Infections Shehu BB et al 13

Clinical Diagnosis amphotericin B is reserved for cases of relapse or the critically ill. With the exception of isolated cryptococcoma without meningeal involvement C. neoformans of the CNS is Surgical treatment diagnosed by CSF examination. However, lumbar puncture should not be done in the presence of Craniotomy and resection of the granulomatous mass features of raised intracranial pressure until the is the ideal in patients with mass effect. presence of an intracranial mass is ruled out, Hydrocephalus may also require surgical intervention. preferably by CT scan. Neurosurgical assistance may also be required to Lumbar Puncture reveals elevated intracranial insert ventricular access device (Ommaya reservoir) pressure, lymphocytic pleocytosis, elevated protein to instill antifungal drugs and obtain CSF for repeated level and reduced CSF glucose. India stain is positive analysis. in 75% of cases of meningitis and CSF culture Other granulomatous CNS disorders include positive in 90% of cases. Other tests include Aspergilosis, blastomycosis, Histoplasmosis, cryptococcal antigen titre, which may be elevated.26 Sarcoidosis, Brucellosis, sporotrichosis, and Leprosy. The radiologic findings in CNS cryptococcosis are non specific. All patients should undergo CT or MRI Fungal Infections Of The Central Nervous System to diagnose cryptococcomas as well as detect hydrocephalus. On CT cryptococcomas appear as Most fungal infections of the CNS of utmost homogeneously enhanced lesion, that are isodense or neurosurgical importance have been mentioned under lucent before contrast infusion. CT findings may granulomatous CNS disorders. However, other show no abnormalities in meningoencephalitis.18 fungal infections worthy of mention are candidiasis, Histoplasmosis, Coccidiodomycosis, blastomycosis Pathology and narcodiosis.

The meninges are thickened. Small cysts are located Parasitic Infections Of The Central Nervous within the cortex and deeper. There is little or no System surrounding inflammatory reaction or gliosis. In areas of inflammation there are lymphocytes, plasma cells, The parasites that most commonly cause human eosinophils, and multinucleated giant cells. India ink disease are nematodes and protozoa. They are usually demonstrates the capsule clearly. localized in certain organs of the body, but in the present of background malnutrition or Medical Treatment immunosuppression they become disseminated disease, with some having special predilection to the Combination therapy of Amphotericin B with 5- CNS. flurocytosine gives a favourable response. Intrathecal

Cerebral Echinococcosis, or hydatid disease is caused by the , a motile histotoxic protozoon, tape worm Echinococcus granulosus and is endemic is the causative agent of cerebral amoebiasis, which in the Mediterranean area, South Africa and parts of primarily afflicts young men. It is a relatively rare South America. Canines, the definitive hosts, harbour complication of intestinal amoebiasis, which is the adult warm in their small intestine. Humans, endemic in Africa, Latin America, South East Asia intermediate hosts, ingest the egg via faecooral route, and Mexico. CNS infection is thought to result from which hatch, releasing the larvae (oncosphere). These haematogenous spread from the gastrointestinal tract. penetrate the gut wall and spread primarily to the liver It results in multiple, poorly demarcated necrotic and lungs. lesions located at the gray-white mater junction. CNS involvement occurs in less than 2% of cases. Occasionally, amoebae can be identified within these The larvae forms a primary cyst which enlarges at a lesions. They present with focal neurological deficits, rate of 1 to 5 cm per year. Primary cysts of the brain raised intracranial pressure, seizures, and are usually single, but occasionally multiple. meningismus. Most patients have liver abscesses. CNS hydatid disease manifests depending on the Diagnosis is established by recovering the organism location and size of the cyst and include raised from the gastrointestinal tract or liver, or with intracranial pressure, seizures, and focal neurological serological tests. deficit. CT images of the brain show focal hypodense lesions Diagnosis is usually established by consistent with cerebritis early in the disease and one serological tests. ELISA is sensitive but not specific. or more ring enhancing lesions with surrounding The double-diffusion test in agar, using arc-5 antigen oedema later.27 Treatment is with metronidazole and from sheep hydatid fluid, is more specific. On CT, aspiration of large cerebral abscesses. hydatid cysts may be unilocular or multilocular. Unilocular cysts are usually large, spherical and no Echinococcosis surrounding oedema. They often lie adjacent to the 14 Neurosurgical infections Shehu BB et al inner table of the skull, with density similar to that of but immunocompromised patients show no CSF. The cyst wall does not enhance, though enhancement. MRI is more sensitive. calcified in 20 to 40% of cases. Multiloculated cysts Biopsy of an intracranial lesion may be required to may be clustered or scattered and often associated establish a diagnosis. The treatment include a with oedema and contrast enhancement of the cyst combination of folate antagonists pyrimethamine and wall. The finding of multiple small low density, sulfadiazine. Response to therapy can be monitored secondary cysts within a primary cyst is with serial MRIs, which should show a decrease in pathognomonic of cerebral hydatid disease. MRI oedema, mass effect, and the number and size of shows the primary cyst as a well defined lesion with enhancing lesions within 2 to 4 weeks of therapy.28 signal intensity similar to that of CSF in both T1, and Other parasites of neurosurgical importance include T2 weighted images. cysticercosis, schistosomiasis, Trypanosomiasis, The primary treatment of CNS hydatid cyst is surgical Trichinosis, and Plasmodium spp(cerebral malaria). excision of the intact cyst. Care must be taken not to spill the contents into the surgical field. If the cyst Viral Infections Of The Central Nervous System cannot be removed injection of 20% saline, formalin, cetrimide, or silver nitrate kills the protoscoleces. Human Immunodeficiency Virus Type 1 Long term therapy with albendazole is also effective. Over 50% of patients infected with Human Toxoplasmosis Immunodeficiency virus type 1 (HIV-1), the agent of the acquired immunodeficiency syndrome (AIDS), Toxoplasmosis is caused by Toxoplasma gondii, an will develop symptomatic neurological disease. In obligate intracellular pathogen. It has a worldwide some autopsy series, neuropathologies are found in distribution especially in areas where cats are used as over 90% of cases. pets, or where improperly cooked meat is consumed. The spectrum of neurological disorders that Infection can also follow transfusion with complicate HIV-1 infection is extremely wide. The contaminated blood products. The organism can illnesses can be classified as those due to the survive up to 50 days in refrigerated anticoagulated infection, and those that arise as a consequence of blood. Fetal infection can occur from acute material immunosuppression. The precise mechanism by infection especially during first trimester. which the virus produces the primary neurologic T. gondi exists in three forms: trophozoites, tissue disorders has not been fully understood. The common cysts, and oocysts. Lymphnodes, skeletal muscle, disorders include , , myocardium, retina, placenta, and brain are the usual peripheral neuropathy, and inflammatory myopathy. target organs. Secondary neurologic diseases include cerebral CNS infection is accompanied by mononuclear cell toxoplasmosis and cryptococcal meningitis infiltrate and microglial module formation. It can be particularly, and neoplasms such as primary CNS associated with focal or diffuse necrotizing lymphoma.29 encephalitis, meningitis, or abscesses. In the immunocompromised, lesions tend to develop in the Primary HIV 1 Related Neurological Disease. basal ganglia, white matter, or gray-white interface. CNS involvement is rare, and usually seen in the HIV-1 Meningitis. immunocompromised patient. It is the commonest cause of encephalitis and brain abscesses in AIDS Meningitis is frequently associated with HIV-1 patients, and manifests as headache, altered infection. Since clinical features are nonspecific, consciousness, seizures and focal neurological careful microbiological and cytological studies of the deficits. CSF are required to establish the diagnosis. When Congenital toxoplasmosis produces widespread evidenced only by CSF pleocytosis, HIV-1 itself is inflammation and necrosis. Necrotic areas are most perhaps the commonest cause of meningitis in prevalent in periventricular and periaqueductal infected patients. Other common causes of meningitis regions. Other manifestations include cortical include Cryptococcosis, tuberculosis, syphilis, and atrophy, ventriculomegaly, and intracranial lymphoma. calcifications. Victims suffer seizures, severe developmental delays and cerebral palsy. HIV-1 Encephalopathy. Toxoplasmosis is best diagnosed using one of several serological tests, including Sabin-Feldman dye test, The incidence of HIV-1 encephalopathy has been indirect fluorescent dye test for IgG, and DS-1gM- about 16-30%. An apparent decline may be the result ELISA. On CT there may be one or more rounded of effective antiretroviral therapy. However, the isodense or hypodense lesions with ring enhancement,

Neurosurgical Infections Shehu BB et al 15 incidence at autopsy is also varied between 17% and oligodendrocytes containing large abnormal nuclei. 70%. CT reveals nonenhancing hypodense white matter The pathology is characterized by brain atrophy with lesion without mass effect in the centrum semiovale, sulcal widening, ventricular dilatation, meningeal usually in the parieto-occipital region, and the fibrosis, white matter pallor, diffuse astrocytosis, and cerebellum. MRI is very sensitive. CSF studies may multinucleate giant cells. not be very helpful. Brain biopsy may be employed to confirm diagnosis. The encephalopathy typically sets in during moments Zidovudine, cytosine arabinoside and interferon-alpha of advanced immunosuppression and intercurrent have been proposed as therapies. Survival time systemic disease. It manifests with disturbance in ranges 0.3 to 18 months. intellect, fatigue, malaise, forgetfulness, incoordination and gait disturbance. Cytomegalovirus.

CSF studies show mononuclear pleocytosis with a Human cytomegalovirus (CMV) is a ubiquitous, low count and elevated protein. The main value of enveloped, DNA – containing herpes virus that infects brain imaging is to rule out other neurological leukocytes during primary infection of healthy young disorders. CT and MRI show . There adults. It then remains latent and reactivated only may be diffuse, patchy or punctate white matter during periods of immunosuppression. A single disorders. patient may harbour multiple strains of the virus. Microscopic lesions include microglial nodules and Zidovudine has been confirmed to be beneficial in the inclusions in the brain tissues. Guancyclovir is shown treatment of HIV-1 encephalopathy.29, 30 to be effective in the treatment of disseminated CMV, but it is associated with neutropaenia.30 HIV-1 Associated Myelopathy Fungal, Protozoal, and Bacterial infections HIV-1 associated myelopathy is a unique degeneration of the spinal cord seen at autopsy in Fungal infections associated with HIV-1 infection more than 20% of cases. It begins insidiously and is include cryptococcal meningitis, candidiasis, characterized by leg weakness, gait impairment, coccidiodomycosis and histoplasmosis. paraesthesia, vague leg discomfort, and bladder and Toxoplasmosis is a common protozoa associated with bowel incontinence. The disorder typically occurs HIV-1 infection. Common secondary bacterial with advanced immunosuppression. Patients have infections include mycobacterial infections, spastic paraparesis, lower extremity hypereflexi neurosyphylis, Listeria monocytogenes, and Norcadia (except when diminished as a result of concomitant astroides infections. peripheral neuropathy), gait ataxia, and impaired sensation. Usually, the lower extremities, are Neoplasms associated with HIV-1 infection. symmetrically involved. Other HIV-1 related afflictions of the spinal cord include acute The advent of HIV-1 infection has increased the myelopathy, spinal , and a relapsing incidence of CNS lymphomas dramatically. Systemic remitting myelopathy. lymphoma metastatic to the CNS, and primary CNS Histology reveals loss of myelin and spongy lymphoma are the commonest neoplasms associated degeneration, particularly in the dorsal and lateral with HIV-1 infection. columns. Microglial nodules and HIV-1 The role of the neurosurgeon include shunting for multinucleate giant cells are also seen. hydrocephalus, implantation of reservoirs for No treatment has been demonstrated unequivocally to intrathecal chemotherapy decompression procedures be of value in vacuolar myelopathy. for intraspinal neoplasms, and also brain biopsy to establish definitive diagnosis.29, 30 Secondary (Opportunistic) HIV-1 Related Neurological Diseases. Other Viral Infections Of The Central Nervous System Viral Infections Herpes Simplex Virus Progressive multifocal leukoencephalopathy This is caused by JC virus, a papovirus. It stays latent This is one of the herpes viruses. Herpes simplex in the reticuloendothelial system in 75% of the virus type 1 (HSV-1) is a ubiquitous agent against population, and is reactivated at the time of which approximately 90% of adult population have immunosuppression. Once the infection is established developed antibodies. It is usually acquired through in the brain, oligodendrocytes and astrocytes become nonsexual activity. This is in contrast to the Herpes infected. . Limb weakness, cognitive dysfunction, simplex virus type 2 (HSV-2) acquired through sexual visual loss, gait disturbance, speech and language activity. Infection of herpes simplex virus is through defects, and headache are the presenting symptoms. intimate, personal contacts, and acquired from virus Histology reveals demyelination, giant astrocytes with shed at a mucosal surface or another peripheral site. pleomorphic hyperchromatic nuclei, and Following viral replication at the primary site, it is 16 Neurosurgical infections Shehu BB et al transmitted by retrograde axonal flow via the indicative of poor prognosis , which is characterized peripheral nerves to sensory ganglia where latency is by areas of haemorrhage in the temporal or frontal established. The virus may be reactivated by region. MRI is most sensitive for early diagnosis, mechanical trauma, exposure to cold, sunlight, wind, showing selective temporal lobe gray matter oedema menstruation or emotional stress. Once reactivated and thickening, and in the later stage, haemorrhages, the virus travels along dermatomes to produce lesion and encephalomalacia. CSF studies show non on ocular, genital or cutaneous sites. It becomes specific changes. localized and heals in the immunocompetent, and may become disseminated in the immunocompromised With the advent of relatively nontoxic and effective patient.30 antiviral agent to treat HSV encephalitis, the trend is now to treat empirically with acylovir rather than Herpes simplex virus Type 1 – Encephalitis perform brain biopsy. However, there may be indications for intracranial pressure monitoring in Herpes simplex virus encephalitis is caused by type 1 patients with severe encephalitis. virus in 95% of adult cases. It is an acute haemorrhagic necrotizing encephalitis associated with Herpes Simplex Virus Type 2 severe morbidity. The disease is mainly localized to the subfrontal and medial temporal lobes, explained Aseptic meningitis caused primarily by HSV-2 has by entry of the virus via the olfactory mucosa, and been associated with genital herpes virus infection in spread along the olfactory bulb and nerve. It is immunocompetent patients. It presents with a self characterized by acute onset headache, behavioural limited meningeal irritation, fever, headache, changes, focal neurologic signs, seizures, and coma. vomiting, photophobia, and nuchal rigidity. Signs of 70% of untreated cases die and survivors often have encephalitic illness are rarely present. CSF findings severe neurological sequelae. include elevated intracranial pressure, lymphocytic pleocytosis, elevated protein content, and moderate There are usually electroencephalographic changes. hypoglycorrhachia. Infectious virus can be isolated CT is normal in the initial stage, and abnormalities are from CSF.

Creutzfeldt – Jakob Disease. seconds) in a patient with and myoclonus, give the presumptive diagnosis of CJD. CT and MRI Creuztfeldt-Jakob disease (CJD) is one of the diseases images are nonspecific.30, 31 caused by the “unconventional” viruses. It has three Brain biopsy could help provide the classic distinct manifestations; the sporadic cases, the histological picture of all spongiform familial cases, and those from iatrogenic transmission. : loss of neurons, neuronal The incidence for sporadic cases is 1 per million. The vacuolation, astrogliosis, and absence of familial type is linked to gene mutation on inflammatory response. Although brain biopsy chromosome 20. Direct inoculation is the only proven remains the best diagnostic tool for most atypical way of disease transmission. The initial rise in , including CJD, this approach merits very incidence of the disease following the use of growth careful consideration because there is no known hormone extracted from cadaveric pituitary gland has treatment for CJD, and decontamination of surgical been reduced since introduction of a recombinant instruments requires special protocols. source. Corneal transplant, placement of deep electroencephalogram electrodes into the brain, use of infected neurosurgical instruments, and dural grafts Conclusion have all been implicated in disease transmission. Neurosurgical infections are caused by a variety of The patients present with higher cortical dysfunction, organisms ranging from bacterial, fungal, viral to dementia, behavioural and sleep disturbance, parasitic. The modes of presentation in most of these intellectual decline, and myoclonic jerks. Following infections are similar, but yet each has its subtle accidental transmission incubation period is 4 months distinct fingerprint, which requires knowledge, to 2 years, but up to 30 years has been reported. Once diligence, and meticulousness to diagnose. Prompt symptoms and signs appear, most patients live 6 to 12 diagnosis and active early treatment are the hallmarks months. No treatment is known. of a satisfactory outcome. Electroencephalogic changes (repetitive, high-voltage, triphasic-sharp discharges with a periodicity of 1 to 2

Neurosurgical Infections Shehu BB et al 17

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