The central sulcus separates which lobes of the cerebrum? What lobe does the lateral sulcus separate? What is it the buccal sulcus? What is inferior to the central sulcus? What is the gingiva that extends from the base of the sulcus to the mucogingival junction?
What region is superior to the lateral sulcus? The great cardiac vein and anterior interventricular artery can be found along the anterior what sulcus? What area is anterior to the central sulcus?
The area anterior to the central sulcus is the? What is a sulcus? The coronary sulcus is a groove that? What is the function of the atrioventricular sulcus? Study Guides. Trending Questions. What can you hold in your right hand but not in your left hand? Still have questions? Find more answers. Previously Viewed. Unanswered Questions. What characteristics of a tragic hero does Macbeth possess and banquo lack?
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In cases of subarachnoid hemorrhage, xanthochromia occurs within 2—4 h after the initial cerebral bleed; xanthochromia may develop in vitro if the CSF specimen contains increased numbers of red blood cells and is not centrifuged immediately upon arrival in the laboratory. The macroscopic appearance of CSF only enables a diagnostic path for purulent versus aseptic meningitis; however, appearance alone is not sufficient to make a specific diagnosis of bacterial or viral meningitis.
Because red cells may be present in spinal fluid as a result of subarachnoid hemorrhage or through a traumatic tap, it is important to note whether red tinged or bloody CSF clears as sequential specimen tubes of CSF are obtained. Such clearing suggests a traumatic tap and can be documented in the laboratory by counting the red cells in successive tubes.
CSF cells should be counted in the laboratory within 1—2 h of collection; further delays may result in a false low cell count because of cell lysis or adherence of cells to the walls of the specimen tube. Glucose enters the CSF by transport through the choroid plexus and capillary endothelium in the subarachnoid space.
When the barrier breaks down during meningitis, CSF protein tends to rise and increases with duration of disease prior to initiation of therapy. Elevation of CSF protein on its own, however, is not specific for any specific type of meningitis. Table It is important to recognize that a predominance of PMNs may occur early in viral meningitis, within the first 24—48 h, but this gradually shifts to a mononuclear predominance over the next 8 h if the lumbar puncture is repeated [ 45 , 46 ].
In patients with meningitis caused by L. Adapted with permission from Rand et al. Once CSF specimens are obtained, a gram stain should be performed immediately in patients with suspected bacterial meningitis followed by plating on solid culture media.
Centrifugation of CSF improves the yield for both gram stain smears and culture. With lower concentrations, there are simply too few organisms to detect by direct microscopy. Moreover, most children without bacterial meningitis have negative gram stain with a negative predictive value of Thus, CSF gram stain is useful in evaluating children for empiric therapy of bacterial meningitis [ 48 ].
In addition to gram stain, a number of other rapid diagnostic tests have been developed over the past 20 years for diagnosis of acute bacterial meningitis. In the s counter immunoelectrophoresis CIE was used for direct detection of bacterial polysaccharide antigens; this test is quite insensitive and is no longer in use.
Agglutination tests are commercially available for H. However, the sensitivity and specificity of these tests are no better than that of the gram stain, and they provide no additional diagnostic yield above and beyond the gram stain and the clinical picture and rarely influence the decision to treat empirically [ 49 , 50 ].
Therefore, they are not currently recommended in the diagnosis of acute bacterial meningitis upon initial presentation. The underlying problem with these tests is that they are not sensitive and specific enough to establish a diagnosis upon which to initiate appropriate therapy. For example, if a patient is sick enough to be admitted to the hospital, and found to have a low CSF glucose level and raised CSF white blood count, one would still initiate empiric antimicrobial and supportive therapy even if the agglutination tests are negative.
Extensive literature exists describing the application of real-time polymerase chain reaction PCR for detection and quantification of various bacterial and viral pathogens in CSF of patients with a putative diagnosis of bacterial meningitis.
Real-time PCR is faster and more sensitive than previous technologies. However, this technique is expensive and not readily available in most hospital laboratories. Moreover, in clinical practice, physicians are likely to initiate empirical antimicrobial therapy anyway after requesting testing by conventional methods, especially for patients with typical CNS symptoms and signs. In this case, rapid diagnostic testing using PCR assays is likely to not make a difference in the clinical the clinical decision making and medical management of the patient.
Neuroimaging plays little role in the diagnosis of acute bacterial meningitis except as indicated earlier to rule out the presence of mass lesions and raised ICP, which might increase the risk of herniation when lumbar puncture is performed. The major value of CT and MRI scans in patients with acute bacterial meningitis is in the investigation of complications, such as cerebral infarction, vasculitis, abscess, or hydrocephalus.
In some cases this may progress to a subdural empyema, which may account for the prolonged fever Fig. Cortical infarction is a common complication of bacterial meningitis and usually results from vasospasm of cerebral vasculature or vasculitis associated with the meningitis itself. Cerebritis is an early complication that may occur during the first 4 days Fig. Early necrotic regions filled with polymorphonuclear cells, lymphocytes, and plasma cells and with ill-defined parenchymal swelling characterize cerebritis.
In late cerebritis 4—8 days , central necrosis increases, there is vascular proliferation and more inflammatory cells, and suppurative foci begin to breakdown and become encapsulated. Findings in acute meningitis are frequently subtle especially viral meningitis. A presents normal CSF within the ventricles and sulci as hypointense dark relative to brain.
With pial inflammation there is leak of proteinaceous fluid into the subpial and subdural spaces. This highly proteinaceous fluid is hyperintense bright relative to brain and thus becomes visualized on fluid-sensitive MRI sequences. Serous subdural effusions are often present as well, which are imaged as high-intensity fluid outside the brain, as in this case, but without contrast enhancement along their surfaces. These types of fluid collections are considered noninfective and they typically clear spontaneously after medical treatment.
The contrasted MRI b demonstrates pial hyperemia along the right lateral cerebral convexity compare to left side. On the left there is thickening of the pia probably early subpial empyema. When the distribution of the inflammatory process involves mainly the upper brain stem, as in this instance, it is described as rhombencephalitis. Rhombencephalitis is uncommon but is one the manifestations of Listeria-based meningitis, as in this case.
Note there is relatively little abnormal enhancement in this case of Listeria infection. If there is thick obvious enhancement in a similar distribution, findings would be more consistent with a granulomatous infection, as in fungal or tuberculous meningitis. Similar findings can also be part of noninfectious granulomatous pial disease, as in neurosarcoidosis and non-Langerhans histiocytosis; thus, tissue confirmation is usually necessary.
Active meningitis and secondary subdural effusions. This FLAIR sequence, which emphasizes tissue edema, but deemphasizes bulk CSF signal, shows increased signal along the trigones of the lateral ventricular surfaces indicative of ependymitis, plus increased signal along the pial surfaces indicative of meningitis, plus minimal ventriculomegaly. All of these findings commonly occur in acute meningitis.
Additionally, there are small bifrontal extra axial fluid collections without any signal along their margins which are consistent with likely sterile subdural effusions. The fluid signal is minimally higher than CSF within the lateral ventricles indicating elevated CSF protein, a feature common to reactive subdural effusions.
Acute frontal sinusitis with secondary subdural empyema; images include contiguous post-contrast mid-convexity axial MRI sections. This case illustrates the spread pattern of subdural empyema. The source of the infection is the frontal sinus. Once the infection accesses the subdural space it can spread widely within the intracranial compartment. In this instance, it continues all the way to the occipital region.
These multicentric pockets of subdural empyema are often sequestered requiring multiple surgical drains. Thus, it is imperative that the full extent of the subdural empyema is appreciated. Acute left frontal lobe bacterial cerebritis; images include pre and post-contrast CT sections sagittal projection lower thoracic area. The early phase of brain infection early cerebritis demonstrates nonspecific cerebral edema and poorly defined contrast enhancement. There is frequently reactive pial hyperemia.
In later stages the cerebritis will organize into early then mature stages of brain abscess. The pathophysiology of the blood—brain barrier is of critical importance in determining the choice of antimicrobials for the treatment of acute bacterial meningitis. The penetration of the blood—brain barrier is a function of both the properties e.
For example, chloramphenicol, which is highly lipid soluble, will readily penetrate uninflamed meninges. Fortunately, in inflamed meninges therapeutic concentrations of penicillins, cephalosporins, and vancomycin can be achieved for treatment of the vast majority of cases of bacterial meningitis. Because only the free, unbound portion of an antimicrobial agent is capable of crossing the blood—brain barrier, the degree of protein binding of the antimicrobial in the patient serum is critical in determining how much of the agent eventually gets through to the CSF.
With increased concentrations of protein in the CSF, protein binding becomes a significant factor in the effectiveness those antimicrobials that are highly protein bound. The penetration of aminoglycosides is generally so poor that they are of little value in the treatment of acute meningitis when given intravenously, although they may be useful intrathecally.
The penetration of the third-generation cephalosporins e. Quinolones, tetracyclines, and macrolides do not penetrate the blood—brain barrier sufficiently to be useful first-line agents in the treatment of meningitis, whereas sulfa agents e. Treatment regimens for acute bacterial meningitis in children above the age of 3 months and in adults up to the age of 50 is geared to treating the most common pathogens: N.
The prevalence of penicillin-resistant S. By definition, fully susceptible pneumococci are susceptible to penicillin at less than 0. Once a clinical diagnosis of acute bacterial meningitis is suspected or made, institution of antimicrobial therapy should be immediate. If clinical evaluation raises a suspicion of raised intracranial pressure, or if the patient manifests signs of papilledema or focal neurological deficits, blood should be drawn for culture and baseline testing e.
Choice of empirical antimicrobial therapy is dictated by the age of the patient, vaccine status, and whether bacterial meningitis was acquired in the community or within the healthcare setting. For community-associated meningitis, the microorganisms most commonly implicated are S.
Initial empirical therapy for community-acquired meningitis: for adult and children 3 months—50 years, ceftriaxone or cefotaxime can be given, especially if risk factors e. If the patient is very sick or if gram-positive cocci are seen on CSF microscopy, vancomycin should be added to the therapeutic regimen to cover for penicillin-resistant S.
In adults more than 60 years of age, patients with chronic alcoholism, immunosuppression, or other debilitating conditions, the possibility of L. Empirical therapy to cover L. Therapy may need to be broadened depending on the results of the gram stain. In cases where gram-negative diplococci are seen, it is probably prudent to wait until culture results confirm N. Treatment of the most common etiologic agents of acute bacterial meningitis is summarized in Table The utility of adjunctive therapy with dexamethasone in the treatment of acute bacterial meningitis remains controversial.
The use of dexamethasone as an adjunct to therapy in acute bacterial meningitis is complex. It has been shown clearly in animal models and in patient studies that dexamethasone reduces the level of inflammation and reduces the levels of the inflammatory cytokines IL1 beta and tumor necrosis factor alpha [ 56 ].
Animals that received a higher dose had therapeutic peaks maintained despite steroid use, suggesting that the anti-inflammatory effect of the steroids, which reduce entry of antibiotics into the CSF, may be overcome to some extent by increasing the dose [ 57 ]. In animal studies of experimental pneumococcal meningitis, an antibiotic-induced secondary inflammatory response in the CSF was demonstrated only in animals with high initial CSF bacterial concentrations; these effects were modulated by dexamethasone therapy [ 58 ].
Human studies of the use of dexamethasone have clearly shown that there is a reduction in severe hearing loss in patients who have H. In children with meningitis due to S.
In summary, dexamethasone probably should be used as an adjunct in children at a dose of 0. A more recent study has shown that adjunctive dexamethasone in the treatment of acute bacterial meningitis in adults does not appear to significantly reduce death or neurological disability and concludes that the benefit of adjunctive dexamethasone for all or any subgroup of patients with bacterial meningitis remains unproven [ 60 ].
The duration of treatment of bacterial meningitis is based on empiric observation. In general, the minimum duration treatment is 7 days as long as the patient is afebrile for the last 4—5 days. Treatment of S. Meningitis following trauma and neurosurgical procedures is discussed elsewhere.
Elevated ICP is a result of cerebral edema due to acute bacterial meningitis and should be anticipated. Clinical manifestations of raised ICP include bradycardia, hypertension, altered mental status, drowsiness, obtundation and coma, third cranial nerve palsies, including unilateral or bilateral dilated, poorly reactive or nonreactive pupils, abnormal ocular movement, abnormal respiration, or decerebrate posturing.
Papilledema is relatively uncommon and as such is an unreliable sign of raised ICP as it may take several hours to develop after the ICP has increased. Signs of herniation may supersede those of increased pressure and include unequal, dilated, or nonreactive pupils, dysconjugate eye movements, decorticate and decerebrate posturing, and bradycardia with abnormal respiratory patterns.
Patients who are awake and alert can be monitored closely. Patients who are obtunded or comatose, or who manifest other signs of increased ICP may well benefit from ICP monitoring. Pressures exceeding 20 mmHg should be treated and some studies suggest that even pressures greater than 15 mmHg may benefit from treatment [ 61 ].
When these waves develop on a background of already increased ICP, herniation and irreversible brain stem injury may ensue [ 61 , 62 ]. Plateau waves: characterized by a sudden rapid elevation of intracranial pressure to 50— mmHg for 5—20 min. After a sustained period of elevation, the termination of the wave is characterized by a rapid decrease of ICP.
These waves are thought to be caused by changes in cerebral blood flow. Hypertonic osmotic agents, such as mannitol or hypertonic saline infusions, play a vital role in the reduction of elevated intracranial pressure and treatment of cerebral edema in patients with CNS infections [ 63 — 68 ]. Both mannitol and hypertonic saline reduce cerebral edema in many clinical syndromes [ 63 — 67 ]. However, recent data suggest that hypertonic saline appears to achieve a greater reduction in ICP than other osmotic agents [ 63 , 65 ].
The object in using osmotic agents is to achieve a sustained reduction in intracranial pressure by modifying the modes and rates of administration of the respective osmotic agent [ 63 — 67 ]. Phenobarbital therapy may be considered if raised ICP remains uncontrolled by the foregoing interventions. Caution is advised in the use of hyperventilation to lower arterial PaCO 2 concentrations because overly vigorous treatment may cause these values to fall below 25 mmHg, running the risk of further reductions in cerebral blood flow causing cerebral ischemia.
The dose of mannitol in children is 0. Mannitol and hypertonic saline act as hyperosmolar agents and remain almost entirely within the intravascular space, producing an osmotic gradient that shifts intracranial fluid into this space. Dexamethasone has been used to reduce intracranial swelling in other settings primarily because of its effectiveness in vasogenic cerebral edema. Various clinical studies support the use of adjunctive dexamethasone in infants or children with H.
High-dose barbiturates may be helpful when other methods have failed to control increased ICP. Barbiturates decrease the CNS metabolic demand for oxygen thereby decreasing cerebral blood flow which, in turn, causes a fall in ICP. Such therapies require regular ICP measurements and monitoring of cerebral electrical activity with electroencephalography. Pentobarbital is preferred because of its relatively short half-life 24 h versus phenobarbital with a relatively longer half-life.
Side effects of high-dose barbiturate therapy include cardiac depression with arrhythmias and hypotension, thus mandating invasive hemodynamic monitoring in these patients. If not treated, seizures may progress to status epilepticus, which in turn can lead to anoxic damage of the temporal lobe, cerebellum, and thalamus.
The principles of therapy are to control seizure activity quickly and definitively. To initiate therapy, short-acting anticonvulsants, such as lorazepam or diazepam, are administered followed by a long-acting agent like phenytoin.
Lorazepam is given IV in doses of 1—4 mg in adults, and 0. The rate should be decreased if signs of toxicity, such as hypotension or a prolonged QT interval, develop. If phenytoin is not successful in controlling seizure activity, intubation and treatment with IV phenobarbital may be necessary.
Patients must be watched and monitored carefully for signs of toxicity, such as hypotension and respiratory depression. Should these measures fail to control seizures, general anesthesia and additional phenobarbital therapy may have to be considered. However, since , meningococcal disease incidence has decreased and incidence for serogroups C and Y, which represent the majority of cases of vaccine-preventable meningococcal disease, is at historic lows.
In , a quadrivalent meningococcal polysaccharide-protein conjugate vaccine MCV4 was licensed for use among persons aged 11—55 years, and during the same year, the Advisory Committee on Immunization Practices ACIP recommended routine vaccination with 1 dose of MCV4 for persons aged 11—12 years, persons entering high school i.
In , ACIP approved updated recommendations for the use of quadrivalent serogroups A, C, Y, and W meningococcal conjugate vaccines in adolescents and persons at high risk for meningococcal disease [ 75 , 76 ].
The vaccine contains immunogenic polysaccharide capsular material from serogroups A, C, Y, and W The vaccine has few side effects and is believed to be protective for at least 3—5 years.
Persons at increased risk for severe pneumococcal disease include those who are immunocompromised, asplenic or splenectomized, or patients with chronic illness such as chronic cardiovascular disease e.
Viral CNS infections may be classified as exogenous due to infection with a viral agent acquired outside the host or endogenous due to reactivation of viruses that have remained latent in the host. HSV encephalitis is unique in that it may occur as part of the primary infection or be seen in patients in whom the infection has been latent for many years. Meningitis and meningoencephalitis are the most common viral CNS infections encountered in the United States.
The overwhelming majority of these infections are caused by enteroviruses, which produce disease in outbreaks occurring mainly during the summer months, but may occur during May to October in warmer parts of the United States. While virtually all of the various serotypes of echovirus and Coxsackie virus can produce meningitis and meningoencephalitis, in addition to other syndromes, the 15 most commonly noted enteroviruses in the United States during — accounted for CSF was the most common specimen type.
The epidemiologic pattern is one in which certain strains, such as echovirus 30 or echovirus 9, cause disease endemically, while other strains occur in sporadic outbreaks varying from year to year in different regions. Enteroviruses are transmitted from person to person by the fecal-oral route and their activity tends to be increased in areas of overcrowding, poverty, and generally poor hygienic conditions. Arboviruses account for the majority of epidemic cases of encephalitis.
Their occurrence follows an identical seasonal distribution to that of viral meningitis and meningoencephalitis associated with enteroviruses. However, the mode of transmission is completely different. Arboviruses are spread by the bite of infected mosquitoes, which are part of a complex cycle of enzootic transmission between birds, mosquitoes, and small mammals. The epidemiology of these diseases may be affected in part by prevention efforts from the public health authorities.
For example, many states maintain surveillance systems that include testing of mosquitoes for the presence of virus, as well as sentinel chicken flocks to determine arbovirus activity. Such efforts lead to early recognition of an outbreak and warnings by public health authorities for the population to take precautions such as insect repellants, wearing long sleeve shirts, and avoiding outdoor activity in the early evening hours when transmission is most likely to occur.
In addition, mosquito control activities may contribute to reduction in rates of infection. In August of , an outbreak of encephalitis was detected in the borough of Queens, New York City: 62 patients were confirmed infected with an agent identified as the arbovirus West Nile virus WNV ; seven eventually died.
This followed a massive die-off among birds, particularly crows that had been observed during the month before the outbreak. Most of those affected with serious illness were elderly, although one patient was 29 years old [ 79 — 81 ]. During the ensuing decade, WNV occurrence started to spread westward across the continental United States, and by the end of approximately 1 in blood donors were thought to be infected with WNV CDC data.
Although rabies is rare among humans in the United States, potential exposures to rabid animals lead to between 16, and 39, persons receiving post rabies exposure prophylaxis each year [ 82 ]. Since the s, the incidence of rabies in domestic animals has declined dramatically because of immunization of dogs and other domestic animals. Unlike the situation in developing countries, wild animals are the most important potential source of rabies for both humans and domestic animals in the United States; most reported cases of rabies occur among raccoons, skunks, and foxes and various species of bats [ 82 ].
Viral infection of the CNS occurs via two distinct routes: hematogenous and neuronal. Because viruses must replicate intracellularly, the ability to cause disease is largely determined by whether viral surface proteins can attach to specific receptors on specific cells in affected tissues—i.
Cells that do not express this receptor generally do not become infected with HIV [ 84 ]. Enteroviruses are transmitted in human populations largely through fecal-oral transmission. These viruses survive stomach acid, replicate in the intestine, and an initial viremia leads to infection of multiple organs within the body.
A secondary viremia from these sources can lead to CNS involvement. The prompt production of antibody disrupts this second viremia and prevents invasion of the CNS. In the case of arboviruses, humans typically become infected when an infectious mosquito pierces the host epidermis to take a blood meal, depositing virus principally in the extravascular tissue although direct inoculation into the bloodstream can occur.
Local replication is followed by viremia, and brain involvement is probably determined by viral tropism and the rapidity of the host immune response. For CNS infections that occur following a viremia, invasion of the brain involves attachment of the virus to the endothelial cells, presumably via specific receptors.
Following invasion, an acute inflammatory reaction occurs with a perivascular distribution within the brain parenchyma and varying degrees of involvement of the meninges, depending on the infecting viral agent. The perivascular inflammatory response is predominately mononuclear although polymorphonuclear leukocytes may be seen.
Infection of neural cells results in degenerative changes and phagocytosis by tissue macrophages or microglial cells. Some pathologic features are unique to certain viruses: for example, cerebral atrophy and production of multinucleated giant cells and multiple nodules of infected microglia are seen in the white matter in patients with HIV encephalitis Fig.
In the case of rabies, histopathologic evidence of rabies encephalomyelitis inflammation in brain tissue and meninges includes mononuclear infiltration, perivascular cuffing of lymphocytes or polymorphonuclear cells, lymphocytic foci, Babes nodules consisting of glial cells, and the pathognomonic Negri body—an intracytoplasmic inclusion body within which the virus can be identified Fig.
The pathology specimen is from the brain of a year-old male with recently diagnosed HIV. The patient developed pneumonia and died of respiratory failure. Herpes encephalitis autopsy case: year-old male patient with end-stage AIDS. Figure shows herpesvirus-infected neurons with marginated chromatin and glassy, smudged nuclei. The T2-w image a illustrates cytogenic edema distributed not only within the anterior and mesial right temporal lobe but also within the frontotemporal association bundle and basifrontal cortex.
It involves gray and white matter. There is less obvious change on the left. This pattern, in the right clinical context, is typical of HSV-1 cerebritis. It has a differential of tumoral gliomatosis, but the latter typically has a more prolonged presenting clinical course. The post-contrast T1-w image b demonstrates pial and perivascular enhancement.
HSV-1 is an angiophilic organism which can produce a necrotizing intrinsic angiitis which can cause subarachnoid hemorrhage, although not in this case. Note the perivascular cuffing due to the perivascular accumulation of inflammatory cell infiltrates i. In the case of HSV, the distribution involves the medial part of the temporal lobe bilaterally with one temporal lobe generally much more involved than the other.
Autopsy studies carried out on patients who died during active HSV encephalitis show the presence of virus in the olfactory bulbs, olfactory tracts, and the tracts of the limbic system which end in the hippocampus, amygdala, insula, cingulate gyrus, and olfactory cortex [ 86 ]. Thus, the virus appears to gain access to the CNS from the nasal mucosa to the olfactory bulbs and olfactory tracts, although the mechanism by which the virus does this remains unknown.
About two-thirds of cases of HSV encephalitis in adults and older children occur in patients who have antibody to the virus at the time of infection. Many of these patients have a history of cold sores dating back 20—30 years.
In the other one-third of patients, antibody to HSV is lacking at the time of onset of symptoms indicating that the encephalitis is likely part of the primary infection. Infection of the CNS in neonates generally follows systemic viremic spread; however, there is no temporal lobe localization.
Rabies infection may result from contact with saliva or other secretions from infected animals as well as the animal bite itself. Rabies replicates initially at the local site of inoculation, and for this reason emergency preventive measures, such as thorough cleansing of the wound and infiltration with human rabies immunoglobulin, can be effective in preventing infection with this viral agent.
In the process of local replication, the rabies virus invades the nerve sheaths and is transported via nerve cells to the CNS. Thus, bites on the lower extremities may take months to produce symptoms in the CNS, whereas bites in the face may reach the CNS within weeks. It is also important to recognize that the initial incident may be forgotten because of the length of time of the onset of CNS symptoms after the initial infecting event or because the inoculation may be unapparent as has been reported for bats [ 87 ].
Therefore, a high index of suspicion for rabies is essential when managing patients with encephalitis of unknown cause, especially in patients who exhibit signs of hyperirritability. Viral meningitis is an acute illness characterized by fever, headache, stiff neck, photophobia, and varying degrees of nonspecific symptoms such as malaise, myalgia, nausea, vomiting, abdominal pain, or diarrhea.
Generally, neither disturbance of mental status nor abnormal neurological signs are characteristic of viral meningitis. The presence of obtundation, disorientation, seizures, or localized neurologic signs should suggest brain parenchymal involvement and a diagnosis of encephalitis or meningoencephalitis. Neck stiffness is generally less severe compared with bacterial meningitis. Clinical clues to an enteroviral etiology include presence of a viral exanthem, pleuropericarditis, pleurodynia, painful oropharyngeal ulcers, or peripheral vesicular lesions suggestive of hand, foot, and mouth disease.
A parameningeal infectious focus e. Thus, a patient with an epidural abscess or a brain abscess could present with mild headache, fever, and a CSF picture identical to that of viral meningitis.
Some cases of sphenoid or frontal sinusitis may feature a CSF pleocytosis. Patients with fungal and tuberculous meningitis may also present with headache, fever, and stiff neck, but in general the clinical course is longer than an acute viral meningitis.
The CSF in patients with cryptococcal meningitis may be completely normal. Viruses other than enteroviruses can also produce aseptic meningitis. For example, HSV type II produces very typical aseptic meningitis with low-grade fever, headache, stiff neck, and photophobia as part of primary genital herpes infection.
Therefore, it is important to question the sexually active patient about a history of genital herpetic lesions and to perform a pelvic examination in women where indicated. Aseptic meningitis can also be seen as part of the syndrome of primary HIV infection.
Certain strains of leptospirosis will typically present with aseptic meningitis; however, most cases present in conjunction with systemic disease and severe involvement of other organs such as lung, liver, and kidney. Lymphocytic choriomeningitis virus LCMV belongs to the family Arenavirus and is found globally [ 88 ]. LCMV meningitis is typically associated with exposure to rodents, such as common house mouse Mus musculus and M.
Transmission occurs by inhalation aerosol and droplet , fomites, or direct contact with excreta or blood from infected rodents. The incubation period is 1—2 weeks; symptoms are nonspecific and include fever, chills, myalgia, headache, photophobia, anorexia, pharyngitis, and cough. CNS invasion is seen only in a few patients either after an initial febrile illness.
During the neurologic phase, patients acquire aseptic meningitis and peripheral leukocytosis. The laboratory diagnosis of viral meningitis is generally one of exclusion. Viral cultures of CSF that yield growth of enteroviruses are diagnostic.
PCR has become available for the diagnosis of enteroviral meningitis and these PCR platforms correlate very well with the results of viral culture. Unfortunately, PCR testing may not be routinely available at clinical microbiology laboratories for various reasons, including cost cutting measures and lack of trained personnel.
For aseptic meningitis associated with systemic infections, such as leptospirosis, syphilis, or ehrlichiosis, diagnosis can be confirmed through standard serologic testing generally available at state public health laboratories or reference laboratories. Because there are over 75 different enterovirus serotypes, testing is only possible for a subset of these. In addition there is tremendous overlap in the serologic response between the different serotypes such that seroconversion to one or more enterovirus serotype can occur.
Moreover, since there is no specific therapy, expensive laboratory testing is unlikely to affect patient outcome. For these reasons, serologic studies for the diagnosis of enterovirus infections are generally not indicated.
A common diagnostic misconception is the usefulness of CSF antibodies. The great cardiac vein and anteriorinterventricularartery can be found along what sulcus? What marks the boundary between the ventricles? Where do bacteria grow on teeth? What is minimal blunting of the left costophrenic sulcus?
The central sulcus separates which lobes of the cerebrum? What lobe does the lateral sulcus separate? What is it the buccal sulcus? What is inferior to the central sulcus? What is the gingiva that extends from the base of the sulcus to the mucogingival junction?
What region is superior to the lateral sulcus? The great cardiac vein and anterior interventricular artery can be found along the anterior what sulcus? What area is anterior to the central sulcus? The area anterior to the central sulcus is the? What is a sulcus?
The coronary sulcus is a groove that? What is the function of the atrioventricular sulcus? Study Guides. Trending Questions. What can you hold in your right hand but not in your left hand? Still have questions? Find more answers. Previously Viewed. What happens if bacteria gets trapped in the median sulcus? Unanswered Questions. What characteristics of a tragic hero does Macbeth possess and banquo lack? What could result if a 30 year old lawyer continued to eat as he did as a 17 years old football player?
What is the function of resorcinol in the seliwanoff's test? How do you maximally develop the intelligence quotient of a child? Get the Answers App.
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