Temporal Lobe Encephalitis Research Articles

A case of pseudotumorous lesion of the CNS caused by herpes simplex virus type 1 in a patient with secondary immunodeficiency

Pseudotumorcerebri is a general term for a number of non‑neoplastic CNS lesions of various origins that resemble neoplasia clinically and/or radiologically, often cause serious diagnostic mistakes and prescribing unreasonable treatment that may harm the patient. There are currently three types of pseudotumors of the brain, including inflammatory granulomatous lesions, idiopathic or symptomatic intracranial hypertension, and large demyelinating foci in the white matter of the cerebral hemispheres.This scientific publication describes the medical history of a patient with pseudotumor granulomatous temporal lobe encephalitis HSV‑1/2‑etiology, which developed against the background of secondary cellular immunodeficiency caused by long‑term use of methylprednisolone for rheumatoid arthritis. Initially, a misdiagnosis of brain glioma was made due to the similarity of clinical and radiological manifestations of encephalitis with brain tumor. Diagnostic error was identified only during neurosurgery to remove the probable tumor. Histological and immunohistochemical analysis of a brain tissue sample from a pseudotumorous lesion obtained by intraoperative biopsy showed signs of granulomatous macrophage inflammation with moderate microcystosis and a small amount of tissue detritus. The diagnosis of HSV‑1/2 neuroinfection was verified on the basis of PCR of cerebrospinal fluid obtained during neurosurgery. The patient was discontinued previously planned radiation therapy, which was categorically contraindicated in this case, and was prescribed treatment with acyclovir to inhibit the reproductive activity of the virus and dialysable extract of blood leukocytes to eliminate secondary immunodeficiency. Neurosurgical intervention was found to be unjustified. Methylprednisolone was discontinued, and the patient was transferred to an aminoquinolone series drug for the treatment of rheumatoid arthritis. Only after performing these interventions it was possible to achieve a significant improvement in the patient's condition.

1395. Comparison of Four Recommendations Guiding the Use of Neuroimaging in the Management of Bacterial Meningitis

BackgroundCurrently multiple sets of recommendations exist to guide the use of cranial imaging before lumbar puncture in adults with suspected meningitis. We aimed to compare the utility of the four main guidelines [Infectious Diseases Society of America (IDSA), European Society for Clinical Microbiology and Infectious Diseases (ESCMID), UK, and Swedish guidelines] in detecting major head CT scan findings that eventually impacted clinical management in adults with community-acquired bacterial meningitis.MethodsA retrospective observational study of 111 adults (age > 17 years) with community-acquired bacterial meningitis admitted to 10 tertiary care hospitals in Houston TX, between December 2004 and March 2016. Major and minor CT findings were stratified based on their inclusion status within the four separate guidelines.ResultsA total of 38 (34%) patients had minor head CT scans (small ischemic white matter changes, lacunar strokes) and 17 (15%) patients had major CT findings (hydrocephalus, subarachnoid hemorrhage or interventricular hemorrhage, cerebral edema, pneumocephalus, ventriculomegaly, septic embolus, hindbrain herniation, and temporal lobe encephalitis). Of those 17 with major CT findings, 6 patients had a change in clinical management [External Ventricular Drainage (EVD) placement] as a direct result of their CT findings. The IDSA set of guidelines was the only one that included all of the major CT scan findings and all the cases in which the findings of a brain CT resulted in a change in management (EVD placement).ConclusionThe IDSA was the most inclusive guideline in regards to (1) indications for cranial imaging that would have detected all major abnormal brain CT findings and 2) including cranial imaging that resulted in significant changes in clinical management in adults with community-acquired bacterial meningitis. Disclosures All authors: No reported disclosures.

Emergency Evaluation and Management of Encephalitis and Myelitis in Adults.

Infection of the central nervous system is often a life-threatening emergency. In many cases, the clinician faces an unknown pathogen and must rely upon clinical acumen and a thorough, systematic diagnostic investigation to establish a diagnosis and initiate appropriate treatment. Because patients typically present with a syndrome, such as temporal lobe encephalitis, rather than a known pathogen (e.g., herpes simplex virus 1 encephalitis), we describe diagnostic considerations in the context of their neuroanatomic tropisms and patterns of disease. This paradigm reflects the challenges clinicians face; however, tropisms are not absolute, patterns of disease are not specific, and this approach does not obviate the need for empirical treatment while a systematic diagnostic investigation is underway. Specific treatment is available for many infectious agents, including bacterial, fungal, and parasitic pathogens, as well as the herpesviruses. In cases with no specific treatment, clinicians must strive to establish the diagnosis (and thereby spare unneeded treatment), anticipate and recognize complications and pitfalls, and initiate appropriate supportive care, all of which are best achieved with a well-prepared multidisciplinary team.

Herpesvirus Infections of the Nervous System.

This article reviews the spectrum of neurologic disease associated with human herpesvirus infections. As more patients are becoming therapeutically immunosuppressed, human herpesvirus infections are increasingly common. Historically, infections with human herpesviruses were described as temporal lobe encephalitis caused by herpes simplex virus type 1 or type 2. More recently, however, additional pathogens, such as varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6 have been identified to cause serious neurologic infections. As literature emerges, clinical presentations of herpesvirus infections have taken on many new forms, becoming heterogeneous and involving nearly every location along the neuraxis. Advanced diagnostic methods are now available for each specific pathogen in the herpesvirus family. As data emerge on viral resistance to conventional therapies, newer antiviral medications must be considered. Infections from the herpesvirus family can have devastating neurologic outcomes without prompt and appropriate treatment. Clinical recognition of symptoms and appropriate advanced testing are necessary to correctly identify the infectious etiology. Knowledge of secondary neurologic complications of disease is equally important to prevent additional morbidity and mortality. This article discusses infections of the central and peripheral nervous systems caused by herpes simplex virus type 1 and type 2, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6. The pathophysiology, epidemiology, clinical presentations of disease, diagnostic investigations, imaging characteristics, and treatment for each infectious etiology are discussed in detail.

P 82 Case presentation – haemorrhagic encephalitis by HSV with organic psychosyndrome with slowing, personality change, memory disturbance/word-finding disturbance and moderate neurological abnormalities [severe headache, hyperaesthesia in the face, pathological reflexes

The 16-year-old patient J.P. was ill for five days with fever (maximum 38.9 °C, 38.2 °C on the day before), bipolar headache, nausea, and vomiting twice. No further signs of infection, pretreatment with paracetamol and ibuprofen. J.P. had hardly eaten, but still drunken enough. On admission, J.P. cmplained of bifrontal headache and nausea, but was well-oriented. Motor movement and sensitivity normal, muscles normoton. No meningitic signs, no ataxia, proper reflexes of the muscles triggerable identically on both sides. Temp. 36.4 °C, RR 112/67 mmHg, Hf 69 beats/min, oxygen saturation 96%. Laboratory chemistry: no relevant increased inflammation parameters. No meningism in multiple examination by pediatric consultants in the following one and a half days. An increase in headaches, an unclear change in the personality of the patient, retarded reactions (“always very reserved and sparing of words”), an MRI of the head was performed, showing a typical encephalitis picture with haemorrhagic temporal lobe encephalitis, as is often observed in HSV encephalitis. After lumbar puncture, we immediately began acyclovir therapy. At times very severe headaches were treated parenterally with metamizole and piritramide. The personality changes increased in the first few days. The patient was initially only limited oriented (knew, for example, that we had the first day of the week, but not that this is the Monday, knew that his sisters had visited him on the previous day and could distinguish them by telling the place of their residence, but did not know their names) and was significantly slowed down. The symptoms slowly decreased somewhat from the 6th day of treatment onwards. After 11 days there was still pronounced memory and word-finding disorder, slight disorientation and attention deficits. An inpatient early rehabilitation was organized, but by J.P. rejected it after extensive discussions. With the consent of his parents he wished a long-term outpatient rehabilitation, which was organized in co-operation with the health insurance, the parents and the therapists working in the county. In addition to pediatric support, this included physiotherapy on a neurophysiological basis, speech therapy and occupational therapy. In the further course the general condition improved, the personality disorder regressed and the word-finding disturbances also improved. The thorough neuropsychological assessment before dismissal showed disturbances in the area of memory, attention, visual perception and executive functions, in spite of the overall improvement. After 3 1/2 weeks, J.P. In good general condition and subjectively free of complaints in the further outpatient rehabilitation. Parallel to this J.P. attended his previous school class, and after a few months in the following summer he passed the final exams of the school (Fachoberschulreife/Realschulabschluss). The diagnostic measures are presented in the clinical context: MRI at the beginning, after 4 weeks, after 3 and 7 months EEG Neuropsychological testing before rehabilitation and after 6 months.

Compensatory Mechanism for Face Perception Suggested by a SPECT Activation Study

Background The bilateral temporo-occipital lobes are the usual site of pathology in patients with prosopagnosia. However, the mechanisms leading to this disorder are not fully understood. We investigated the neural mechanism of compensation for prosopagnosia in a patient with focal right posterior temporal lobe encephalitis without prosopagnosia. Methods A single-photon emission computed tomography (SPECT) scan was performed using a brain-dedicated 32-phototube SPECT scanner and technetium-99m hexamethyl-propylene amine oxime to measure regional cerebral blood flow (rCBF). A SPECT activation study was performed in each of two conditions: the familial faces retrieval task and a control task. Results The SPECT activation study revealed a significant increase in rCBF in the contralateral temporal lobe (from 72 during control conditions to 99 mL/100 g/min during the activation paradigm). Conclusions This finding suggests that the region contralateral to the brain lesion compensates for the function of face perception. Our result may explain the reason why prosopagnosia rarely occurs with single, well-circumscribed lesions. The activation pattern seen in this study may be helpful for understanding the neural mechanism of compensation for prosopagnosia.

Temporal Lobe Encephalitis Need not Always be Herpes Simplex Encephalitis: Think of Tuberculosis

Historically, temporal lobe encephalitis is considered as a pathognomonic feature of Herpes simplex encephalitis. This rule may not always be true and we believe that clinicians should keep their differential open. We here report once such. Case of a 36-year-old Indian male who developed altered sensorium following a prodrome of headache and fever. Examination and imaging suggested Temporal Lobe Encephalitis (TLE). Herpes encephalitis was considered and he was started on anti-virals awaiting lumbar puncture reports. Cerebrospinal fluid (CSF) analysis for Herpes Polymerase Chain Reaction (PCR) turned out to be negative. Later, to our surprise PCR for tuberculosis (TB) was positive. CSF was 100% lymphocytic and Adenosine deaminase was 12. He was started on 5 drug anti-tuberculosis regimen following which he showed a significant clinical improvement. Given the prevalence of tuberculosis in the sub-continent, clinicians must be aware of this diagnostic possibility when a patient with TLE does not respond to anti-virals. Apart from disease specific therapy, multi-disciplinary approach involving speech therapy is warranted. An early aetiological characterization of TLE has both diagnostic and prognostic implications, failing which patient may succumb.

Use of clinical and neuroimaging characteristics to distinguish temporal lobe herpes simplex encephalitis from its mimics.

We describe the spectrum of etiologies associated with temporal lobe (TL) encephalitis and identify clinical and radiologic features that distinguish herpes simplex encephalitis (HSE) from its mimics. We reviewed all adult cases of encephalitis with TL abnormalities on magnetic resonance imaging (MRI) from the California Encephalitis Project. We evaluated the association between specific clinical and MRI characteristics and HSE compared with other causes of TL encephalitis and used multivariate logistic modeling to identify radiologic predictors of HSE. Of 251 cases of TL encephalitis, 43% had an infectious etiology compared with 16% with a noninfectious etiology. Of infectious etiologies, herpes simplex virus was the most commonly identified agent (n = 60), followed by tuberculosis (n = 8) and varicella zoster virus (n = 7). Of noninfectious etiologies, more than half (n = 21) were due to autoimmune disease. Patients with HSE were older (56.8 vs 50.2 years; P = .012), more likely to be white (53% vs 35%; P = .013), more likely to present acutely (88% vs 64%; P = .001) and with a fever (80% vs 49%; P < .001), and less likely to present with a rash (2% vs 15%; P = .010). In a multivariate model, bilateral TL involvement (odds ratio [OR], 0.38; 95% confidence interval [CI], .18-.79; P = .010) and lesions outside the TL, insula, or cingulate (OR, 0.37; 95% CI, .18-.74; P = .005) were associated with lower odds of HSE. In addition to HSE, other infectious and noninfectious etiologies should be considered in the differential diagnosis for TL encephalitis, depending on the presentation. Specific clinical and imaging features may aid in distinguishing HSE from non-HSE causes of TL encephalitis.

Intracerebral hematoma complicating herpes simplex encephalitis

ObjectivesTo describe two patients who developed an intracranial hematoma as a complication of temporal lobe encephalitis due to herpes simplex type 1 virus, and to review the literature. Patients and methodsThe first patient, a 45-year-old woman developed a brain hematoma in the location of the encephalitic lesion on day 9 after the onset of herpes simplex encephalitis (HSE) that required surgical evacuation. The second patient, a 53-year-old woman was being treated for HSE; on day 8 after admission a temporal lobe hematoma with midline shift was disclosed due to persistent headache. Both patients survived but were left with sequelae. We conducted a PubMed/MEDLINE search from 1986 to April 2013 on this topic. ResultsWe have found 20 additional cases reported in the literature and review their characteristics. Hemorrhage was present on admission in 35% of pooled patients, and consistently involved the area of encephalitis. Clinical presentation of intracranial hemorrhage overlapped the encephalitic symptoms in two-thirds of the patients. Half of patients underwent surgery. Overall, mortality rate was low (5.2%), and half of patients fully recovered. ConclusionsIntracranial bleeding, although infrequent, can complicate the evolution of herpes simplex encephalitis and should be borne in mind since its presence may require neurosurgery. Although its presentation may overlap the encephalitic features, the lack of improvement or the worsening of initial symptoms, particularly during the second week of admission, should lead to this suspicion and to perform a neuroimaging study.

Herpes encephalitis preceded by ipsilateral vestibular neuronitis

A 74-year-old woman developed vertigo and jerk nystagmus to the left with normal cerebral imaging. Three days later she developed fever, altered mental state and left medial temporal lobe hypodensity, confirmed on lumbar puncture to be due to herpes simplex type 1 encephalitis. We propose that the patient had vestibular neuronitis caused by HSV-1 that progressed to ipsilateral temporal lobe encephalitis.

Murine gammaherpesvirus‐68 infection of mice: A new model for human cerebral Epstein–Barr virus infection

Epstein-Barr virus infection may cause severe neurological complications that are not mirrored by animal models. Here, we show that nasal inoculation of newborn BALB/c wild-type mice with MHV-68, a murine gammaherpesvirus, causes cerebral infection with inflammation in 50% of the animals. The inflammatory patterns are strikingly similar to those known from Epstein-Barr virus, including hydrocephalus, meningitis, cerebellitis, focal or diffuse encephalitis, and temporal lobe encephalitis. This offers a new powerful tool to study the virological and immunological characteristics of cerebral gammaherpesvirus infections.

Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis

Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis

Isolated retrograde amnesia for autobiographical material associated with acute left temporal lobe encephalitis

Retrograde amnesia for autobiographical material in the absence of anterograde amnesia or other memory disturbances was found in a patient with acute viral encephalitis. Memory loss showed a temporal gradient, but new learning was spared. Both brain perfusion imaging with 99mTc-HMPAO SPECT, and EEG localized the lesion in the left temporal lobe while CT and MRI were normal. This observation supports the anatomical differentiation between the different memory functions. The uncommon combination of isolated retrograde amnesia without other neuropsychological findings may raise the doubt of psychogenic aetiology, which in this case was refuted.

Q fever mimicking herpetic encephalitis

We describe a patient with temporal lobe encephalitis associated with primary Coxiella burnetii infection who presented with CT and MRI findings suggestive of herpes simplex encephalitis and an initial improvement during treatment with acyclovir. Q fever should be considered in the differential diagnosis of patients whose manifestations suggest herpes encephalitis.

Autopsy neuropathological findings in 'burnt out' herpes simplex encephalitis and use of the polymerase chain reaction to detect viral DNA.

We have conducted an autopsy study of the brains of three patients with 'burnt out' temporal and frontal lobe encephalitis, thought to be due to previous herpes simplex virus infection. The brains showed marked atrophy and yellow-brown discolouration predominantly involving the anterior part of both temporal lobes. Histology revealed destruction of grey and white matter, perivascular and leptomeningeal aggregates of lymphocytes and macrophages, and severe gliosis. Immunohistochemistry for herpesvirus antigens was negative but, by use of the polymerase chain reaction, a segment of the thymidine kinase gene of herpes simplex virus type 1 was detected in sections of temporal lobe from all three brains. These findings support the hypothesis that herpes simplex virus may persist within the central nervous system after acute herpes encephalitis, to cause latent or low-grade productive infection.

Transient Global Amnesia–A Review of 213 Cases from the Literature

TGA is a clearly recognisable clinical syndrome with many and varied aetiologies, the most ubiquitous being transient cerebral ischaemia. This entity is probably much more common than the literature suggests, many patients not coming to the attention of a physician due to the transient nature of the isolated memory defect and the risk of recurrence being low, it is of interest that many of the original patients described tended to be the more prominent members of the community, e.g. physicians and relatives of physicians, perhaps suggesting that the occurrence of TGA in such a person is less likely to pass unnoticed. In the differential diagnosis one should include the following: transient cerebral ischaemia, epilepsy, migraine, temporal lobe encephalitis, psychogenic fugues, post-traumatic, and rarely cerebral neoplasms.

Transient Global Amnesia—A Review of 213 Cases from the Literature

Summary: Transient global amnesia–A review of 213 cases from the literature. R D. Rollinson, Aust. N.Z. J. Med., 1978, 8, pp. 547–549. TGA is a clearly recognisable clinical syndrome with many and varied aetiologies, the most ubiquitous being transient cerebral ischaemia. This entity is probably much more common than the literature suggests, many patients not coming to the attention of a physician due to the transient nature of the isolated memory defect and the risk of recurrence being low. It is of interest that many of the original patients described tended to be the more prominent members of the community, e.g. physicians and relatives of physicians, perhaps suggesting that the occurrence of TGA in such a person is less likely to pass unnoticed. In the differential diagnosis one should include the following: transient cerebral ischaemia, epilepsy, migraine, temporal lobe encephalitis, psychogenic fugues, post-traumatic, and rarely cerebral neoplasms.

Incongruous oral and written naming: Evidence for a subdivision of the syndrome of Wernicke's aphasia

A 28-year-old man developed the fluent paraphasic speech characteristic of Wernicke's aphasia after an episode of necrotizing temporal lobe encephalitis. He exhibited an unexpected, and heretofore unreported, superiority of written naming over oral naming. His reading comprehension was modestly superior to his auditory comprehension as well. These findings are at variance with the traditional view of Wernicke's aphasia as an undissociable syndrome of defective reading, writing, and speech. They suggest that an appropriately placed lesion can partially spare reading and writing while still producing fluent paraphasic speech.

Differential diagnosis of transient amnesia.

In a group of 39 consecutive patients attending neurological clinics with transient amnesia patients with transient global amnesia formed the largest group; others suffered from epilepsy, migraine, temporal lobe encephalitis, or psychogenic fugues. In most cases the clinical features suggested the aetiology, but an electroencephalogram recorded as soon after the attack as possible may help in distinguishing amnesia due to temporal lobe epilepsy.