The picture described is typical of a viral meningoencephalitis, more specifically VHZ, with significant tropism by the temporal lobe, causing febrile fever and in many cases aphasia, so the correct option would be 2, since the cerebrospinal fluid normally shows a moderate lymphocytic pleocytosis, with normal glycorrhachia. The rest are not correct because: The first one because it is not a bacterial meningitis that would present with more fever, the third one because limbic encephalitis usually presents afebrile with behavioral changes and the last one because the image they describe is not an abscess, well delimited.

The picture described is typical of a viral meningoencephalitis, more specifically VHZ, with significant tropism by the temporal lobe, causing febrile fever and in many cases aphasia, so [HIDDEN], since the cerebrospinal fluid normally shows a moderate lymphocytic pleocytosis, with normal glycorrhachia. The rest are [HIDDEN]: The first one because it is not a bacterial meningitis that would present with more fever, [HIDDEN] limbic encephalitis usually presents afebrile with behavioral changes and [HIDDEN] the image they describe is not an abscess, well delimited.

A 52-year-old man comes to the Emergency Department with headache and fever (37.8°C) of 2 days' evolution. In the last few hours, he also had difficulty in nomination and comprehension. The examination did not show nuchal rigidity, the most striking finding being the presence of a mixed aphasia. The cranial CT shows a faint hypodensity in the left temporal lobe without mass effect and without contrast uptake. Which of the following statements is correct?

Bacterial meningitis is the first diagnostic impression and treatment with 3rd generation cephalosporin should be initiated as soon as possible.

Most likely this patient's CSF shows a lymphocyte-predominant pleocytosis with normal glycorrhachia.

[An unusual presentation of herpetic encephalitis].

Herpetic encephalitis (HE) is the commonest cause of acute sporadic encephalitis in the United States and Europe. In 20% of cases, the clinical course is atypical and this may lead to delay in diagnosis and treatment. A 24 year old patient presented with aseptic meningitis, which had been present for the previous 10 days and which then became complicated by fever and aphasia. The cerebrospinal fluid (CSF) showed marked pleocytosis and increased protein. Cerebrospinal puncture was found to be positive for DNA of the herpes simplex virus. Magnetic resonance (MR) imaging showed a temporal lesion with intense uptake of contrast. Treatment was started with acyclovir and the patient improved over the days following this. At present the diagnosis of herpetic encephalitis is based on polymerase chain reaction (PCR) studies of the CSF and MR imaging. The correlation between patients with HE with cerebrospinal puncture showing positive for herpes and alterations on MR is 89%. In view of the 20% of atypical forms, a high degree of clinical suspicion is necessary to try to obtain early diagnosis and treatment.

Three cases of neoplastic meningitis initially diagnosed with infectious meningitis in emergency department.

Neoplastic meningitis (NM) is diagnosed by the presence of malignant cells in the cerebrospinal fluid (CSF). We report 3 patients with NM, who were misdiagnosed with infectious meningitis in emergency department (ED). Case 1. A 68-year-old man visited our ED with a 3-month history of headache. With MRI and CSF study, he was diagnosed with tuberculous meningitis. After 20 days, repeated CSF cytology showed malignant cells. His diagnosis was lung cancer with NM. Case 2. A 57-year-old man visited regional hospital ED with a 3-week history of headache and diplopia. Brain MRI was not contributory. With CSF examination, his diagnosis was aseptic meningitis. With worsening headache, he was referred to our ED. Repeated CSF showed malignant cells. His diagnosis was stomach cancer with NM. Case 3. A 75-year-old man visited a regional hospital with headache lasting for 4 months. His diagnosis was sinusitis. Persistent symptom brought him back, and he developed recurrent generalized seizures. Brain MRI showed diffuse leptomeningeal enhancement suggesting meningitis, and he was transferred to our ED. CSF exam showed malignant cells. His diagnosis was NM with unknown primary focus. When evaluating the patients with headache in ED, NM should be kept in mind as a differential diagnosis of meningitis.

InternalMed_Harrison

A brain abscess typically presents as an expanding intracranial mass lesion rather than as an infectious process. Although the evolution of signs and symptoms is extremely variable, ranging from hours to weeks or even months, most patients present to the hospital 11–12 days following onset of symptoms. The classic clinical triad of headache, fever, and a focal neurologic deficit is present in <50% of cases. The most common symptom in patients with a brain abscess is headache, occurring in >75% of patients. The headache is often characterized as a constant, dull, aching sensation, either hemicranial or generalized, and it becomes progressively more severe and refractory to therapy. Fever is present in only 50% of patients at the time of diagnosis, and its absence should not exclude the diagnosis. The new onset of focal or generalized seizure activity is a presenting sign in 15–35% of patients. Focal neurologic deficits including hemiparesis, aphasia, or visual field defects are part of

[Early diagnosis of herpes simplex virus encephalitis by single photon emission computed tomography (SPECT) in patients with normal MRI].

Since treatment of herpes simplex virus encephalitis (HSVE) is most effective when started early, a sensitive and specific method for early diagnosis would be of great benefit. MRI and CT are commonly used for this purpose. In this study, we presented two patients who had serologically confirmed HSVE and had normal CT and MRI, but were diagnosed as having HSVE by means of SPECT in the early stage. Case 1 was a 56-year-old man who suddenly developed alexia. On admission, physical and neurological examination were unremarkable except for alexia, agraphia, acalculia, and left-right disorientation. Brain CT, MRI, and cerebral angiography were all normal. However, SPECT showed hyperaccumulation of 99m Tc-HM-PAO in the right temporal-occipital area. On the 5th hospital day, he became comatose. CSF study revealed marked pleocytosis. Even then, MRI including Gd-enhanced study was normal while SPECT continued to show hyperaccumulation. Detection of herpes simplex virus DNA in CSF by polymerase chain reaction was negative. Anti-HSV antibody titer in CSF and serum confirmed intrathecal production of the antibody on the 14th hospital day. Abnormal accumulation of tracer in SPECT returned to normal on the 31st day when he was alert but still had a mild Gerstman syndrome. Case 2 was a 61-year-old man with disturbance of consciousness, mental dysfunction, and generalized convulsion. He was diagnosed as having HSVE by means of CSF pleocytosis, detection of HSV DNA in CSF by polymerase chain reaction, and presence of anti-HSV antibody in the CSF. CT and MRI again revealed no abnormality while SPECT clearly showed hyperaccumulation in the left temporal lobe in an early stage. Hyperaccumulation of lipophilic tracer on SPECT study, especially in the temporal lobes, has been reported in the early stage of HSVE by previous investigators. Unlike MRI or enhanced CT, the increased tracer accumulation in SPECT does not reflect disruption of the blood-brain-barrier or inflammatory edema, but reflects hyperperfusion or some other HSVE related abnormality which is currently unknown. From these observations, we suggest that local hyperperfusion occurs before local inflammation, and that SPECT is the most useful scanning method for early diagnosis of HSVE when this disease is clinically suspected.

[Current therapeutic orientation in intracranial suppuration].

Changes in diagnosis and management of intracranial infections have been studied on a continuous series of 102 cases 1968 through 1980. Use of CT scan has not increased the number of patients diagnosed in acute phase (before the fifteenth day) but has increased the rate of case observed before the second day (37 p. cent with and 27 p. cent without the CT scan). However the neurological status and specially the state of consciousness has not changed. Four specific data of abscess diagnosis have been defined on 56 cases suspected to have an intracranial infection; 16 out of these cases have proven by surgery not to be infectious lesion. Evolution under treatment is best followed by CT. Final aspect on CT are not different after puncture or after excision. Average delay of disappearance of edema is 20 days and of abscess is 44 days. Importance of bacteriological study in the choice of antibiotics is underlined by comparison of bacteriological and clinical results. Since the introduction of a laboratory of bacteriology in the hospital in 1976, we observed a decrease of sterile cultures (11.5 p. cent and 56 p. cent before 1976), an increase of the number of germs identified in each case and specially anaerobic germs (40 p. cent after and 10 p. cent before 1976) and a decrease in mortality and sequelae (respectively 8,3 p. cent and 19.4 p. cent before 1976 and 11,5 p. cent and 33 p. cent before 1976). Use of CT scan and progress in bacteriological study have led us to simplify our surgical attitude in case of intracranial abscess: puncture as soon as the diagnosis is done on CT; antibiotics according to the bacteriological study and survey by CT in neurosurgical unit.

Paraneoplastic limbic encephalitis resembling acute herpetic encephalitis.

Introduction. Paraneoplastic limbic encephalitis (PLE) is a rare disorder that typically follows a chronic or subacute course of personality changes, memory loss, seizures, and hallucinations. Early diagnosis is difficult and characteristic symptoms can be mimicked by a variety of conditions. We present a case of PLE, initially presenting as acute herpetic encephalitis. Case Presentation. A 56-year-old male was admitted for evaluation of acute onset headache, fever, and confusion. On neurological examination he was confused with MMSE score of 15/30. CSF analysis revealed marked lymphocytic pleocytosis. A possible diagnosis of acute herpetic encephalitis was rendered and patient was treated with acyclovir. CSF PCR was negative. Cranial MRI revealed bilateral hyperintense lesions in medial temporal lobes with contrast enhancement. Despite treatment with acyclovir patient was deteriorated; thus, a paraneoplastic syndrome was suspected. Chest CT showed a right paratracheal lymph node mass, while a biopsy revealed neuroendocrine lung cancer. Auto antibodies to Hu were also detected. The patient was treated with steroids and chemotherapy. Six months later, he had complete tumour remission and marked neurological improvement. Discussion. PLE can rarely invade acutely, being indistinguishable from herpetic encephalitis. Inclusion of PLE in the differential diagnosis of acute encephalitis is of great clinical significance.

[Indication of neuro-imaging for the initial management and the follow-up of acute community-acquired bacterial meningitis].

Lumbar puncture is the best way to prove bacterial meningitis. It should be performed without any delay if the diagnosis is suspected. Herniation is a rare complication of LP. CT is normal in most cases of purulent meningitis, including those complicated by a subsequent herniation; normal CT results does not mean that performing a LP is safe. Three main clinical features can help determine which patient is at risk of herniation and should have a CT before LP. This risk has to be determined rapidly in the emergency ward while assessing anamnestic data, localization signs or symptoms, and level of consciousness. Cranial imaging (mainly MRI) is useful in the course of bacterial meningitis. Patients who do not respond well to treatment or with atypical presentation, persistence of fever, or new neurological signs should undergo brain imaging; MRI and CT may identify subdural effusions, brain abscesses, empyemas, hydrocephaly, or brain parenchymal changes (cerebritis, infarction, hemorrhage). CT and MRI are useful to screen for an ENT cause of bacterial meningitis, and mandatory in case of pneumococcal meningitis. Numerous MRI sequences are useful to identify bacterial meningitis complications: SE T1 without and with gadolinium injection, SE T2, FLAIR, gradient-echo T2, diffusion weighted imaging, MR angiography.

[Multiple brain abscesses: a case report].

10 days before admission a 45-year old female experienced general weakness, and T 38 degrees C. During that period she had no cardio-respiratory nor neurological complaints, and the temperature varied between 37.5 degrees C and 38 degrees C. Her medical history was unremarkable, without immunodeficiency. The day before admission she presented with left arm paresis and during the next day it progressed to paralysis. She had no headache. On admission the following diagnostic procedures were performed: the cranial CT scan showed two lesions (possibly meta lesions). Chest X-ray was normal. WBC=15x10(9)/L, ESR=90/120. On the second day following admission brain MRI showed multiple abscesses in both hemispheres, mostly in the gray/white junction. High doses of IV metronidasol, cephtriaxon and cipfloxacin were administered without obtaining specimens for micro-biological diagnosis. In next two days she developed coma, respiratory insufficiency and septic temperature. Brain surgery was not performed due to severe involvement of the brain with multiple abscesses. Repeated chest X-ray revealed bilateral pneumonia. A lethal outcome occurred on the third day, regardless of all efforts. Autopsy showed multiple brain abscesses as well as on the lungs and liver. A beta-hemolytic streptococcal infection was established. Prevention includes treatment of the infection source. The classic triad of headache, fever and focal deficit occur in less than 50% of patients. Even in such cases brain abscess must be reconsidered CT appearance of brain abscess is similar to that of neoplastic and other infectious and non infectious diseases--especially in the stage of early cerebritis. If the CT findings are not clear, MRI should be performed.

[Fatal brain stem infarction due to rupture of a brain abscess: a case report].

We report a case of a brain abscess which initially presented with subcortical hematoma and ultimately resulted in fatal brain stem infarction due to its rupture into the subarachnoid space. A 50-year-old male was admitted to a nearby hospital with complaints of headache, fever, and sensory aphasia. He had ventricular septal defect found 15 years previously, sinusitis, and liver cirrhosis. Computerized tomographic (CT) scan revealed a left temporal subcortical hematoma. Gadolinium-DTPA enhanced magnetic resonance imaging (MRI) showed faint ring-like enhancement at the margin of the lesion. The left internal carotid angiogram demonstrated the vascular blush and early venous filling of the vein of Labbé. Administration of antibiotics and predonine resulted in resolution of fever within five days. MRI obtained 17 days after the onset showed typical ring-like enhancement. The mass was just adjacent to the lateral ventricle. The patient was transferred to our hospital for further examination and treatment 21 days after the onset. Fever had recurred 2 days before admission to our hospital. One day after admission, the patient began to vomit. About 15 hours following this symptom, he suddenly became comatose and tetraplegic. CT scan demonstrated a rupture of the abscess. Emergent drainage from the lateral ventricle and the abscess cavity was undertaken. Follow-up CT scan revealed multiple infarctions involving the upper brain stem and the bilateral thalamus. He died on the 29th day after the onset. The mechanisms of hemorrhage with a brain abscess and cerebral infarction after rupture of brain abscess are discussed. Hemorrhage with brain abscess is extremely rare. However, brain abscess should be considered as a possible etiology of an atypical hematoma. To avoid fatal rupture of the brain abscess, immediate treatment is essential. Once the rupture of the brain abscess occurs, its contents might cause vasospasm severe enough to cause cerebral infarction.

When time is short, and we are late!: A story of chronic meningitis.

We often face situations when the exact etiological diagnosis of meningitis is difficult. The reason behind this is that many pathogens have similar clinical, radiological, and laboratory pictures. The low yield of the pathogen in cerebrospinal fluid (CSF), non-availability of detail tests in all corners of the world, delay in availability of reliable results (like cultures), and difficulty in performing confirmatory tests like brain biopsy (in inconclusive cases) make the job of a clinician challenging. We report here a case where a late diagnosis of a disease owing to inconclusive results leads to dissemination. The complications following the introduction of the treatment based on presumption lead to further difficulty. We remained inclined to our diagnosis based on clinical judgement, acknowledged and managed the inflammatory changes secondary to the infection, and finally won the long battle. So, sometimes we need to make decisions based on clinical grounds. We need to depend on the fact that uncommon presentations of common diseases are commoner than a common presentation of uncommon diseases.

[COVID-19 and herpesvirus encephalitis].

The SARS-CoV-2 virus, which causes COVID-19, could give rise to damage the nervous system. Many studies have been conducted on this topic, but few have focused specifically on encephalitis. The effect of SARS-CoV-2 on the clinical expression of other neurotropic viruses, such as Herpesviridae, is unknown. We describe the cases of two young men (39 and 18 years old) in whom SARS-CoV-2 had been detected -reverse transcription polymerase chain reaction (RT-PCR)-, and with a clinical diagnosis and cerebrospinal fluid (CSF) analysis consistent with encephalitis. The first patient had a positive PCR for varicella zoster virus in CSF, while the second had a positive PCR for herpes simplex virus types 1 and 2. The first patient, who was recently diagnosed with human immunodeficiency virus, presented with fever, headache, vomiting, cough, inappropriate behaviour and epileptic seizures; the second was seen to have fever, headache, myalgia and exanthema. Both offered the same laboratory findings (lymphopenia and high interleukin 6). CSF showed pleocytosis with a predominance of monomorphonuclear cells, hyperproteinorrachia and normal glycorrhachia. A cranial CT scan showed only mild diffuse cerebral oedema in the first case. Both cases were treated with corticosteroids, antibiotics and acyclovir. The second progressed favourably, while the first did not. Little is known about co-infection of SARS-CoV-2 with neurotropic viruses, such as Herpesviridae, and we have only limited evidence of direct neurological involvement of SARS-CoV-2, due to the technical difficulty of detecting it in the nervous system, thus making it important to take co-infection into account in order to be able to establish an early diagnosis and treatment to improve prognosis.

[Initial patient assessment of infectious diseases and diagnostic steps with fever].

The initial assessment of patients with infectious diseases is challenging because of the extremely broad differential diagnosis as well as different host pathogen interactions influenced by a different immune status. The formal initial assessment, including the present and past medical history, thorough physical examination, clinical first impressions as well as routine laboratory analyses, is the basis of every preliminary diagnosis. Specific chief complaints have to be recognized in order to narrow down the differential diagnosis. In cases of life-threatening illnesses, such as septicemia, endocarditis, bacterial meningitis and severe pneumonia, the first diagnostic and therapeutic steps should be performed in a rapid sequence: bacterial blood samples, sputum and/or liquor samples are required and the initial antibiotic therapy has to be chosen empirically as the relevant bacterial spectrum related to the suspected illness must be covered. In less urgent cases it is recommended that a multi-step diagnostic approach be carried out which takes the differential diagnosis into account and prioritizes the probabilities. In the latter situation antibiotic treatment should be delayed to diagnose the infection correctly. Importantly, atypical courses must necessitate careful and critical reassessment of the diagnosis.

Tuberculosis meningo-encephalitis with positive csf for KB and slowly favourable evolution. Case report.

Meningoencephalitis produce by Koch bacillus is a disease including various symptoms, with often atypical onset and evolution, and with an etiological diagnosis being rarely established. It therefore remains a disease with severe prognosis, despite adequate treatment. a 47 years old male from Neamt County, with chronic otitis in his recent medical history, comes to the emergency room for fever, severe headache, confusion, equilibrium disorders, influenced health status, and meningeal irritation signs. Given his otitis and antibiotic therapy received in recent medical history, the patient was initially diagnosed and treated for beheaded bacterial meningitis (348 elements/mm3, 89% lymphocytes, 5% granulocytes, proteinorrhachia 1.54 g/l). Clinical and paraclinical evolution was poor with persistent fever and headache, impaired mental state, and the spinal puncture showed increased pleocytosis (725 elements/mm3), lymphocytosis (78%), increased proteinorrhachia (2.12 g/l), and low levels of glycorrhachia and chlorurorrhachia. Tuberculosis meningoencephalytis was suspected (confirmed after 3 weeks through cultures on Lowenstein-Jensen medium: positive for Mycobacterium tuberculosis), and a tuberculostatic treatment associating four drugs and intravenous Ciprofloxacin was started. Although the treatment included substances against cerebral edema and neurotrophic agent, his evolution showed persistent headache syndrome. We noticed very slow decrease in CSF pleocytosis (after a month) of treatment the patient still had 240 elements/mm3, 85% lymphocytesand 15% granulocytes. Moreover, due to hepatic toxicity a reduction of the tuberculostatic doses was needed. The beginning of the tuberculosis infection symptoms is often surprising, with clinical signs regarding secondary determinations (meningoencephalitis) association with another infection (otitis--wrong diagnosis). as well as persistent yet slowly favorably evolving symptoms, both clinically and paraclinically (CSF parameters). The etiological agent is extremely rarely isolated, due to a very slow growth of the Koch bacillus on special culture mediums and also because such diagnosis is not often considered before starting the treatment.

A contribution to the rapid diagnosis of subdural empyema.

The authors report their experience with CT scanning ina series of 4 cases of subdural empyema, over a period of 10 months; all the patients were male, aged 16 to 25 years. A review of the literature shows that this disease, in spite of the large variety and efficacy of the available antibiotics, is marked by a significant mortality and morbidity rate if the diagnosis is delayed. Study of the cases reported here, as well as those in the literature, attests that CT scanning of the brain is nowadays the method of choice for early diagnosis of these lesions, and for timing of appropriate intervention according to variations in the development stage of the suppuration. From the study of this series of cases, it is clear that in the future, CT scanning of the brain will certainly allow the hope of a greater survival rate and an appreciable decrease in morbidity in cases of subdural empyema.

Neurology_Adams

The infection may take the form of a brainstem encephalitis, or “rhombencephalitis,” specifically with several days of headache, fever, nausea, and vomiting followed by asymmetrical cranial-nerve palsies, signs of cerebellar dysfunction, hemiparesis, quadriparesis, or sensory loss. Respiratory failure has been reported. Of 62 cases of Listeria brainstem encephalitis reported 25 years ago by Armstrong and Fung 8 percent were in immunosuppressed patients, however, in the current era 20 percent or fewer of affected patients are immunocompetent. In the elderly, no additional cause of immune disorder appears to be necessary. Meningeal signs were present in the only half the patients in the above mentioned series, and the spinal fluid often showed misleadingly mild abnormalities. CSF cultures yielded Listeria in only 40 percent of cases (blood cultures were even more often normal). Consistent with our experience, the early CT scan was often normal; MRI, however, has revealed abnormal

Neurology_Adams

Diagnosis The CSF findings are much the same as in aseptic meningitis (lymphocytic pleocytosis, mild protein elevation, normal glucose values). Occasionally, early sampling of CSF may show few or no cells and subsequent tests may be more typical of an inflammatory disorder. Recovery of virus from blood or CSF is usually not possible and PCR testing is routinely only applied during local epidemics and for the detection of herpes viruses. Recently, it has been possible to use next generation sequencing to identify obscure causes of encephalitis. However, antiviral immunoglobulin (Ig) M antibody is present in the serum and CSF within the first days of symptomatic disease and can be detected and quantified by means of ELISA, making it preferable to other testing serologic for specific diagnosis. Some patients have not developed antibodies by the time of admission to the hospital and the test may have to be repeated in several days. The MRI may be normal or show signal changes and edema in

Neurocysticercosis in a 23-year-old Chinese man.

Male, 23 FINAL DIAGNOSIS: Neurocysticerosis Symptoms: Diplopia • fever • headache • insomnia • neck stiffness • vomiting Albendazole Clinical Procedure: - Specialty: Neurology. Challenging differential diagnosis. Neurocysticercosis is a brain infection caused by the larval stage of the tapeworm Taenia (T.) solium. It is the most important parasitic disease of the human central nervous system and represents the most common cause of acquired epilepsy in developing countries. Here, we report the case of a 23-year-old Chinese man who presented to the emergency department with a 7-day history of helmet headache radiating to the nuchal region and associated with vomiting, confusion, and fever. Cerebrospinal fluid (CSF) was clear, with increased pressure, lymphocytic pleocytosis, decreased glucose, and increased protein levels. Bacterial antigen detection test on CSF was negative, as were CSF bacterial and fungal cultures. Despite broad-spectrum antibiotic and antiviral therapy, the patient still complained of insomnia, diplopia, headache, neck stiffness, and pain in the sacral region. A second LP was performed and CSF had the same characteristics as the first LP. A brain and spinal cord MRI revealed widespread arachnoiditis and small septated cysts with CSF-like signal in the cisterna magna, within the fourth ventricle, and at the level of L3-L4. Cysticercus-specific immunoglobin G antibodies were detected by ELISA in the CSF. The patient received albendazole (15 mg/kg/day) and dexamethasone (5 mg/day) for 4 weeks, with progressive resolution of neurological symptoms. This case shows that, even if rare, neurocysticercosis may be responsible for meningeal symptoms and should be included in the differential diagnosis, especially in patients from endemic countries.

Fifteen-year review of the mortality of brain abscess.

Ninety consecutive cases of brain abscess admitted to this center between 1964 and 1978 have been reviewed. The overall mortality has fallen in three consecutive 5-year periods from 42 to 21 to 9.7%. A number of factors seem to be responsible for this. Early surgical intervention was associated with the reduction in mortality between the first and second 5-year periods. Recognition of the significance and extent of cerebral edema, confirmed since computed tomographic (CT) scans have been available, led to a greater use of steroids during the last 5-year period, but the number of patients thus treated was too small to permit an assessment of any effect on mortality. There is no evidence to suggest a change in the natural history of the disease, and surgical management has not altered significantly. Experience with CT scanning in this center in the diagnosis of brain abscess is limited. It is therefore not possible no assess whether any improvement in mortality may have arisen from the early and accurate diagnosis obtainable with this technique. Improvement in culture technique has been of major importance, leading to a better understanding of the bacteriology of brain abscesses. This has allowed a more rational antibiotic program to be instituted, in particular the use of agents active against obligate anaerobes.

Traumatic pseudoaneurysm of the middle meningeal artery: possible indicators for early diagnosis in the computed tomography era.

Traumatic pseudoaneurysms of the middle meningeal artery, which are associated with high mortality, are difficult to detect early by CT. We provide serial CT scans to show the steps of their formation and suggest characteristics that could be useful in the detection. A 25-year-old man was initially in deep coma had an anisocoric pupil after a traffic accident. Brain CT showed basal skull fracture and traumatic subarachnoid hemorrhage with severe brain swelling. Emergent decompressive craniectomy was performed, and 2 days later, an EDH appeared at the left temporal fossa. Careful examination of the image revealed a hypodense nodule inside the acute hematoma. He underwent craniotomy to remove the hematoma. Serial CT of the residual hematoma showed the gradual development of an organized hematoma around the hypodense nodule. The nodule had low density, which was strongly enhanced on CT after injection of contrast medium. The nodule was highly suspected to be a vascular lesion. A middle meningeal artery pseudoaneurysm was discovered through a 3-dimensional computed tomographic angiography. He underwent another craniotomy to remove the pseudoaneurysm. The diagnostic approach was CT, 3-dimensional CT, and craniotomies. Four CT findings may be useful for early diagnosis: (1) basal skull fracture in the temporal region; (2) hypodense nodule within an acute hematoma; (3) hypodense nodule within an organized and encapsulated hematoma; and (4) strong and homogenous enhancement of the hypodense nodule within an organized and encapsulated hematoma. Three-dimensional computed tomographic angiography is an effective and noninvasive tool to confirm this diagnosis.

[The characteristics of the present-day clinical course of tuberculous meningitis].

Clinical patterns of tuberculous meningitis have been analyzed for 32 admissions to the bacterial meningitis department of the 2nd Moscow Infection Hospital in 1983-1991. Early diagnosis of tuberculous meningitis caused great difficulties because of rare cases of tuberculous history, atypical symptoms (an acute onset, in particular), an obscure meningeal syndrome, rare neurological symptoms, atypical liquor characteristics (frequent neutrophil pleocytosis, a small protein rise, normal glucose). Secondary bacterial meningitides presented most serious difficulties for differential diagnosis. So did cerebral abscesses and viral meningitis. Antituberculous therapy should be started at first sings of tuberculous nature of meningitis as the disease outcomes are determined to a large extent by early administration of proper treatment.

Two cases of dengue meningitis: a rare first presentation.

Dengue, a mosquito-borne disease caused by a flavivirus, is recognized in over 120 countries with 3.6 billion people living in areas at risk. Neurological manifestations are infrequently reported as clinical consequences of dengue infection. Though severe dengue may be associated with meningoencephalitis, meningitis is a rare initial presentation of otherwise uncomplicated dengue fever. We report two adult patients who presented with fever, headache, and nuchal rigidity without the typical symptoms of dengue infection. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis in one and slight neutrophilic pleocytosis in the other with a normal glucose value and negative bacterial cultures. Dengue was suspected because thrombocytopenia was symptomatic in one patient and documented during the hospital course, and was confirmed by demonstration of IgM antibody in the cerebrospinal fluid samples specific for dengue in both cases. Our report demonstrates that meningitis with or without encephalitis can be the first manifestation of dengue infection. In endemic areas, dengue infection should be considered as a probable etiological agent of meningitis. Regular monitoring of platelet count can be an invaluable diagnostic screening tool. In appropriate clinical settings detection of anti-dengue IgM both in serum and in CSF may lead to correct diagnosis.

[Meningitis (II)--acute bacterial meningitis].

Acute meningitis is a medical emergency, particularly in patients with rapidly progressing disease, mental status changes or neurological deficits. The majority of cases of bacterial meningitis are caused by a limited number of species, i.e. Streptococcus pneumoniae, Neisseria meningitis, Listeria monocytogenes, group B Streptococci (Streptococcus agalactiae), Haemophilus influenzae and Enterobacteriaceae. Many other pathogens can occasionally cause bacterial meningitis, often under special clinical circumstances. Treatment of meningitis includes two main goals: Eradication of the infecting organism, and management of CNS and systemic complications. Empiric therapy should be initiated without delay, as the prognosis of the disease depends on the time when therapy is started. One or two blood cultures should be obtained before administering the first antibiotic. Empiric therapy is primarily based on the age of the patient, with modifications if there are positive findings on CSF gram stain or if the patient presents with special risk factors. It is safer to choose regimens with broad coverage, as they can usually be modified within 24-48 hours, when antibiotic sensitivities of the infecting organism become available. Adjunctive therapy with dexamethasone is also administered in severely ill patients concomitantly with the first antibiotic dose. In patients who are clinically stable and are unlikely to be adversely affected if antibiotics are not administered immediately, including those with suspected viral or chronic meningitis, a lumbar puncture represents the first step, unless there is clinical suspicion of an intracerebral mass lesion. Findings in the CSF and on CT scan, if performed, will guide the further diagnostic work-up and therapy in all patients.

First_Aid_Step2

MRI may demonstrate a contrast-enhancing lesion in the temporal lobe (in HSV). HSV encephalitis requires immediate IV acyclovir. CMV encephalitis is treated with IV ganciclovir +/– foscarnet. Give doxycycline for suspected Rocky Mountain spotted fever, Lyme disease, or ehrlichiosis. A focal, suppurative infection of the brain parenchyma, usually with a “ringenhancing” appearance due to fbrous capsule. The most common infective organisms are streptococci, staphylococci, and anaerobes; multiple organisms are often implicated (80–90% of cases are polymicrobial). Nonbacterial Although other medications may be used, rifampin is the frequently tested prophylaxis of choice for close contacts of patients with meningococcal meningitis. The presence of RBCs in CSF without a history of trauma indicates HSV encephalitis. HSV encephalitis is associated with high morbidity. PCR is highly sensitive and specific. A full course of IV acyclovir is mandatory.

Parafalcine empyema, a tricky infectious cause of headache: a case report.

Headache caused by subdural empyema is usually associated with fever and symptoms and/or clinical signs of meningeal irritation and increased intracranial pressure. We describe a patient with headache with absence of these signs or symptoms of meningeal irritation or intracranial pressure, who turned out to have a parafalcine subduralempyema. A 28-year-old man had headache for 2 weeks, which had started with visual symptoms with duration of 5 minutes. Two days later, he developed fever. During these 2 weeks, he had recurrence of visual symptoms for 4 times, with duration of several minutes.Neurologic examination at presentation on the emergency department showed no meningeal irritation or papilledema. However, on closer examination, a limited homonymous hemianopsia on the left side and a drift of the left leg were found. Magnetic resonance imaging showed parafalcine subdural empyema on the right side of the falx and a small brain abscess right occipitally. Neuronavigated craniotomy was performed, which confirmed the presence of empyema and allowed culture of the specimens. Streptococcus milleri group was cultured,which allowed narrowing of the antibiotic therapy to Benzylpenicillin12 million entities per 24 hours. Headache and subdural empyema diminished during treatment, and at follow-up 12 weeks after start of treatment, patient had no remaining complaints. Parafalcine-located subdural empyema can present without presence of clear localizing symptoms or signs like meningeal irritation and increased intracranial pressure. When headache is accompanied with fever, one should extensively question neurologic symptoms, and a thorough neurologic examination should be done.

[Brain abscesses. Value of computed tomography. A review of seven cases (author's transl)].

Based on a series of seven cases of subtentorial abscess, the authors analyze the results of different methods of exploration. Though in certain clinical conditions (intracranial hypertension and meningeal infections) the etiology is of no consequence, in most cases of definite diagnosis can be made of a space-occupying lesion by the use of EEG, arteriography, and scintigraphy examinations, without establishing the precise nature of the affection. As expected, computed tomography appears to be the most reliable examination. Diagnosis was confirmed by this method in 6 of the 7 cases, and it also enabled the number, size, and location of the lesions to be determined. Typical appearances after injection of an iodized contrast medium revealed the development of an abscess following the intracerebral infection, and determined the time for surgical intervention. In spite of intensive care and antibiotic therapy, an abscess remains a "delayed-action bomb", with poor prognosis, requiring drainage or surgical excision as soon as conditions are appropriate. The mortality and morbidity of this rare, and therefore poorly recognized, affection should improve with systematic use of the scanner during meningeal infections.

Paraneoplastic limbic encephalitis with associated hypothalamitis mimicking a hyperdense hypothalamic tumor: a case report.

Paraneoplastic limbic encephalitis is an uncommon association of common malignancies such as small cell lung carcinoma, testicular teratoma, and breast carcinoma. The nonspecific nature of the clinical presentation, lack of freely available diagnostic markers, and requirement for advanced imaging techniques pose a great challenge in the diagnosis of this disease in resource-poor settings. A 64-year-old previously healthy Sri Lankan man was admitted to the general medical unit with subacute memory impairment regarding recent events that had occurred during the previous 3 weeks. Initial noncontrast computed tomography of the brain revealed a hyperdensity in the hypothalamic region surrounded by hypodensities extending toward the bilateral temporal lobes; these findings were consistent with a possible hypothalamic tumor with perilesional edema. The patient later developed cranial diabetes insipidus, which was further suggestive of hypothalamic disease. Interestingly, gadolinium-enhanced magnetic resonance imaging of the brain showed no such lesions; instead, it showed prominent T2-weighted signals in the inner mesial region, characteristic of encephalitis. The possibility of tuberculosis and viral encephalitis was excluded based on cerebrospinal fluid analysis results. Limbic encephalitis with predominant hypothalamitis was suspected based on the radiological pattern. Subsequent screening for underlying malignancy revealed a mass lesion in the right hilum on chest radiographs. Histological examination of the lesion showed small cell lung cancer of the "oat cell" variety. We suggest that the initial appearance of a hyperdensity in the hypothalamus region on noncontrast computed tomography is probably due to hyperemia caused by hypothalamitis. If hypothalamitis is predominant in a patient with paraneoplastic limbic encephalitis, magnetic resonance imaging will help to differentiate it from a hypothalamic secondary deposit. Limbic encephalitis should be considered in a patient with computed tomographic evidence of a central hyperdensity surrounded by bitemporal hypodensities. This pattern of identification will be useful for early diagnosis in resource-poor settings.

[Not Available].

In spite of modern antibiotic treatment, bacterial meningitis still has a dubious prognosis. Secondary complications are responsible for death or permanent neurologic deficits. The indication for imaging is 2-fold. Beside the search for a source of infection, an early detection of secondary complications is attempted.We report about a patient with hematogenous pneumococcal meningitis, who developed a subdural empyema and vascular stenoses of the basal cerebral arteries. These changes as well as the resulting infarctions were detected with MRI in an early state. Thus, an adequate therapy could be initiated. Especially FLAIR images, diffusion-weighted sequences and a time of flight MRA proved to be valuable in this setting.

Pearls and oy-sters: tuberculous meningitis: not a diagnosis of exclusion.

A 21-year-old man presented to his local emergency department with 5 days of headache, which was dull, occipital, bilateral, nonthrobbing, and progressively worsening. It was associated with mild fever, photophobia, and neck pain and stiffness. He had no history of headache, chronic illness, recent vaccinations, cutaneous rash, cough, diarrhea, arthralgia, or myalgia. He was from Ecuador and had been living in the United States for less than 1 year. He had been incarcerated while in Ecuador. Sublingual temperature on admission was 102.6°F. Other vital signs were within normal limits. On physical examination, he appeared thin but not cachectic. He had meningismus and photophobia, but no papilledema and his mental status was alert and attentive. There were no focal neurologic deficits. CSF contained red blood cells: 24 × 10(3)/μL; white blood cells: 85/μL (lymphocytic predominant); protein: 128 mg/dL; and glucose: 48 mg/dL (CSF/serum glucose ratio = 0.53). CSF Gram stain and cultures, PPD test, and blood and urine cultures were all negative. CT scan of the head on day of admission was entirely normal. MRI without gadolinium contrast showed a single punctate T2 hyperintensity in the left frontal periventricular white matter. Chest radiograph was clear. He received empiric vancomycin, ceftriaxone, and acyclovir. Corticosteroids were not given. The patient did not improve with antibiotics and continued to be intermittently febrile. On day 5, he became abruptly more somnolent, then comatose, opening eyes only to pain, his pupils were 5 mm and reactive, he had intact brainstem reflexes, withdrawing both arms and legs. Emergent head CT showed development of hydrocephalus and a ventriculoperitoneal shunt was emergently placed. The neurologic examination did not improve after shunt placement, and repeat head CT showed increased hydrocephalus with bilateral cerebral infarcts. On day 11, he was transferred to Columbia University Medical Center for intensive care. He was febrile and comatose. He did not open his eyes to pain, pupils were 7 mm minimally reactive, brainstem reflexes were intact, and he exhibited extensor posturing to pain. Mannitol was given, corticosteroid therapy was started, and an extraventricular drain was placed. The next day, his right pupil was 8 mm and nonreactive. MRI showed diffuse contrast enhancement of the arachnoid, extensive infarction of basal ganglia, midbrain, and pons, and small ring-enhancing lesions in the cerebellum (figure 1, A-D). Repeat lumbar puncture showed red blood cells: 550 × 10(3)/μL; white blood cells: 250/μL (14% neutrophils, 80% lymphocytes, 6% monocytes); protein: 65 mg/dL; and glucose: <10 mg/dL (CSF/serum glucose ratio = 0.08). CSF testing for Cryptococcus and toxoplasmosis was negative. CSF acid fast bacilli (AFB) smear was negative ×2, and CSF nucleic acid amplification test was also negative for tuberculosis. Serum HIV test was negative. Not until 14 days after initial presentation and 3 days after transfer to the intensive care unit was antituberculosis therapy finally started, because the pattern of infarcts on the MRI suggested basilar meningitis and he had not improved on broad-spectrum antibiotics. That same day, the first sputum AFB smear was positive, as were all succeeding daily sputum AFB smears. Tuberculosis nucleic acid amplification was positive from the sputum, but persistently negative from the CSF. Daily portable chest radiographs had been normal (read as likely atelectasis), but chest CT showed dense consolidations in the left lung and diffuse micronodular opacities throughout both lungs. Two days later, only 21 days after the onset of his headache, the patient died of cardiopulmonary arrest secondary to transtentorial cerebral herniation. Thirteen days later, the CSF culture became positive for Mycobacterium tuberculosis sensitive to streptomycin, isoniazid, ethambutol, rifampin, and pyrazinamide.

First_Aid_Step2

CT or MRI to rule out other diagnoses. CBC may reveal leukocytosis; CSF fndings vary (see Table 2.8-4). TAB LE 2.8-3. Causes of Meningitisa,b GBS E. coli/GNRs Listeria S. pneumoniae Neisseria meningitidis H. inﬂ uenzae type b Enteroviruses N. meningitidis Enteroviruses S. pneumoniae HSV S. pneumoniae GNRs Listeria N. meningitidis a Causes in HIV include Cryptococcus, CMV, HSV, VZV, TB, toxoplasmosis (brain abscess), and JC virus (PML). b Note: The incidence of H. inﬂ uenzae meningitis has ↓ greatly with the introduction of the H. inﬂ uenzae vaccine in the last 10–15 years. TABLE 2.8-4. CSF Prof les

[A 64-year-old woman with progressive gait disturbance and dementia for one year].

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been

[Fever without a source. Diagnostic difficulties in invasive bacterial diseases in children observed on bacterial meningitis model].

Acute infection of the central nervous system is the most common cause of fever associated with signs and symptoms of CNS disease in children. Unfortunately most of these symptoms are non-specific. Specific signs appear very often late in the course of illness. 761 cases of bacterial meningitis in children above 1 month of life were investigated. Only 46.1% of cases were correctly diagnosed during the first doctor's exam. We found that correct diagnosis depends on time between the first symptoms of illness and the first physician visit. If this period of time is below 16 hours the risk of wrong diagnosis is very high due to lack of specific signs of CNS infection. In many cases only fever is present then.

Headache

One recommended diagnostic approach is as follows. If any urgent red flags are present such as visual loss, new seizures, new weakness, new confusion, further workup with imaging and possibly a lumbar puncture should be done (see red flags section for more details). If the headache is sudden onset (thunderclap headache), a computed tomography test to look for a brain bleed (subarachnoid hemorrhage) should be done. If the CT scan does not show a bleed, a lumbar puncture should be done to look for blood in the CSF, as the CT scan can be falsely negative and subarachnoid hemorrhages can be fatal. If there are signs of infection such as fever, rash, or stiff neck, a lumbar puncture to look for meningitis should be considered. If there is jaw claudication and scalp tenderness in an older person, a temporal artery biopsy to look for temporal arteritis should be performed and immediate treatment should be started. Neuroimaging