A case of herpes simplex encephalitis diagnosed by polymerase chain reaction]

A case of a 55-year-old male with herpes simplex encephalitis (HSE) was reported. He was admitted because of fever, headache and memory disturbance. T1 weighted MRI showed low signal intensity and T2 weighted imaging revealed high signal intensity in the medial portions of bilateral temporal lobes. Herpes simplex virus (HSV) antibody titer in cerebrospinal fluid (CSF) was not elevated. HSV DNA in CSF was amplified by polymerase chain reaction (PCR) and identified by the microplate hybridization method. The PCR technique would be useful for the diagnosis of HSE.     

Acyclovir resistance in herpes simplex virus type I encephalitis: a case report

Acyclovir resistance is rarely seen in herpes simplex virus (HSV) type I encephalitis. Prevalence rates vary between 0.5 % in immunocompetent patients (Christophers et al. 1998; Fife et al. 1994) and 3.5–10 % in immunocompromised patients (Stranska et al. 2005). We report a 45-year-old, immunocompetent (negative HIV antigen/antibody testing), female patient, without previous illness who developed—after a febrile prodromal stage—aphasia and psychomotor slowing. Cerebral magnetic resonance imaging (cMRI) showed right temporal and insular T2-hyperintense lesions with spreading to the contralateral temporal lobe. Cerebrospinal fluid (CSF) analysis yielded lymphocytic pleocytosis and elevated protein level. Polymerase chain reaction testing for HSV type I showed a positive result in repeat lumbar puncture. HSV type I encephalitis was diagnosed and intravenous acyclovir treatment was initiated (750 mg t.i.d.). Acyclovir treatment was intensified to 1000 mg t.i.d., due to clinical deterioration, ongoing pleocytosis and progression on cMRI 5 days after initiation of antiviral therapy. In parallel, acyclovir resistance testing showed mutation of thymidine kinase gene at position A156V prompting foscarnet therapy (60 mg t.i.d.). Patient’s condition improved dramatically over 2 weeks. Acyclovir resistance is rare but should be considered in case of clinical worsening of patient’s condition. To our knowledge, this is the first report of acyclovir resistance in HSV type I encephalitis of an immunocompetent and previously healthy patient in Austria.     

A case of herpes simplex encephalitis with noticeable findings of SPECT]

A 51-year-old man was admitted to our hospital because of fever, general fatigue and disturbance of consciousness. Neurological findings included disturbed consciousness, stiff neck and positive Kernig's sign. He was diagnosed as having herpes simplex encephalitis with HSV-DNA in the cerebrospinal fluid. MRI showed a lesion with low signal intensity in T1-weighted image and high signal intensity in T2-weighted image in the right temporal lobe. The single photon emission CT (SPECT) study showed discordance of 99mTc ethyl cysteinate dimer-SPECT (ECD-SPECT) and N-isopropyl-p-[123I]-iodoamphetamine-SPECT (IMP-SPECT). Decreased signal of ECD in the lesion where IMP uptake was increased could be due to decreased esterase activity. This report suggests that ECD-SPECT could fail to detect cerebral blood flow in the lesion with severe metabolic damage.     

Symmetrical brainstem encephalitis caused by herpes simplex virus

We describe a 53-year-old man with herpes simplex virus (HSV) brainstem encephalitis diagnosed based by positive HSV immunoglobulin M antibodies from cerebrospinal fluid. The MRI findings of this case had three unique features. First, the lesions were symmetrical. Second, the lesions may have been associated with reactivation of HSV infection in the region of the trigeminal nerve. Third, diffusion-weighted and apparent diffusion coefficient (ADC) imaging, conducted for the first time on an HSV brainstem encephalitis case, suggested that the lesions were associated with vasogenic edema.     

A case of brainstem encephalitis caused by herpes simplex virus type 1 with possible infection via trigeminal nerve]

A 24-year-old man was admitted to our hospital because of consciousness disturbance, a stiff neck and various brainstem symptoms including a right one-and-a-half syndrome and right peripheral facial palsy a week after an episode of pharyngitis and right facial herpes simplex. Magnetic resonance imaging of the brain on admission showed high-signal intensities in the right pontine tegmentum, right cerebellar peduncle and vermis on fluid-attenuated inversion recovery imaging. Examination of cerebrospinal fluid yielded mononuclear pleocytosis, elevated protein and increased IgM antibodies to herpes simplex virus (HSV) by enzyme immunoassay. HSV-1 specific antibodies also were detected in serum by neutralization test. We gave a diagnosis of brainstem encephalitis caused by HSV-1. The patient was successfully treated with high dose of acyclovir, steroid and intravenous immunoglobulin. He was discharged without any neurologic sequelae. We herein presented a case of atypical encephalitis due to HSV-1 involving mainly the brainstem with possible infection via right trigeminal nerve and summarized recent 35 cases with herpetic brainstem encephalitis since 1990.     

Acute hemorrhagic leukoencephalitis mimicking herpes simplex encephalitis: case report

Acute hemorrhagic leukoencephalitis (AHLE) is a more severe form of acute disseminated encephalomyelitis (ADEM) characterized by a fulminant clinical course and the presence of hemorrhagic necrosis of the white matter. We report the case of a 57-year-old woman who developed delirium following a respiratory infection. Magnetic resonance imaging of the brain disclosed signal abnormalities in the frontal and temporal lobes, usually found in herpes simplex encephalitis (HSE). Gram stain, India ink and acid-fast bacilli staining were all negative in CSF as was a polymerase chain reaction (PCR) for herpes simplex virus. A diagnosis of AHLE was made and the patient was treated with i.v. methylprednisolone 1g/day for 5 days. Despite treatment, the patient developed several neurological sequelae compatible with the severity of her illness.     

Chronic herpes simplex virus encephalitis in childhood

Although herpes simplex virus is a major cause of acute encephalitis in childhood, chronic herpes simplex virus encephalitis has only rarely been reported. This report presents a case of chronic herpes simplex virus encephalitis in a 6-year-old female. Diagnosis was based on the detection of herpes simplex virus deoxyribonucleic acid by polymerase chain reaction in combination with the cerebrospinal fluid/serum ratio of herpes simplex virus-specific immunoglobulin G, the presence of herpes simplex virus-specific oligoclonal immunoglobulin G bands in cerebrospinal fluid, and calcifications in the temporal regions found on cerebral computed tomographic scan. Prolonged antiviral therapy was beneficial to later mental development.     

Amnesia following herpes simplex encephalitis]

We describe three patients presenting themselves with amnesia following herpes simplex encephalitis. All three patients showed anterograde amnesia. Moreover, one patient showed retrograde amnesia extending about fifty years prior to the onset of the illness. Two patients revealed semantic memory disorder, disinhibitory behaviors and confabulations, which suggested the existence of frontal lobe dysfunction. MRI of all three patients disclosed uni- or bilateral temporal lesions. SPECT images showed decreased uptake not only in the temporal lobes but also in the frontal lobes. Amnesia following herpes simplex encephalitis has been thought to be caused by the temporal lobe disorder. However, we postulate that the frontal lobe dysfunction might contribute to the appearance of amnesia.     

Virus reactivation after immunotherapy of anti-NMDAR encephalitis secondary to herpes simplex encephalitis: A case report

Herpes simplex encephalitis is the most common cause of sporadic fatal encephalitis. More than half of patients with herpes simplex encephalitis will die and the vast majority of survivors have severe neurologic sequelae without effective antiviral therapy. Some people experience relapses such as secondary anti-N-methyl-d-aspartate receptor encephalitis despite appropriate antiviral treatment. It is rare that virus reactivation after immunotherapy of anti-N-methyl-d-aspartate receptor encephalitis after herpes simplex encephalitis. In the present study, we retrospectively review one patient who showed this rare situation.     

Atypical brainstem encephalitis caused by herpes simplex virus 2

BACKGROUND: Herpes simplex encephalitis is one of the most common and serious sporadic encephalitides of immunocompetent adults. Herpes simplex virus 2 (HSV-2) infections of the central nervous system usually manifest as subacute encephalitis, recurrent meningitis, myelitis, and forms resembling psychiatric syndromes. OBJECTIVES: To report and discuss magnetic resonance imaging (MRI) findings and clinical features in atypical brainstem encephalitis and facial palsy associated with HSV-2. SETTING: Neurology department of a tertiary referral center. PATIENT: A 37-year-old woman was admitted to the hospital with fever, diplopia, left hemiparesis, sensory change in the face and limbs, personality changes, frontal dysexecutive syndrome, and a stiff neck. Brain MRI showed multifocal high-signal intensities in the pons, midbrain, and frontal lobe white matter on T2-weighted and fluid-attenuated inversion recovery images. Cerebrospinal fluid (CSF) polymerase chain reaction (PCR) amplification analysis was positive for HSV-2. Acyclovir therapy was started, and the encephalitic symptoms disappeared with a negative conversion of HSV-2 PCR in the CSF. However, after the discontinuation of acyclovir therapy, peripheral facial palsy occurred on the left side. A possible relapse or delayed manifestation of the HSV-2 infection was suspected, and the acyclovir therapy was restarted. A complete remission was achieved 3 days after the treatment. She was discharged without any neurologic sequelae. CONCLUSIONS: We describe a patient who developed atypical encephalitis due to HSV-2 and peripheral facial palsy, which could also be related to the HSV-2. This case suggests that HSV-2 should be considered among the possible causes of atypical or brainstem encephalitis and that the PCR amplification method of the CSF can help reveal the possible cause of HSV-2.     

Syndrome of inappropriate secretion of anti-diuretic hormone associated with limbic encephalitis due to herpes simplex virus infection--a case report]

We report a case of syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) associated with limbic encephalitis. A 79-year-old woman was admitted with a complaint of fever, disturbance of consciousness and generalized seizure. Her conscious level was E1V2M4 by Glasgow coma scale. Physical examination showed generalized seizure, neck stiffness, hyperreflexia and flaccid paralysis in her all extremities, and pathological reflexes. Blood analysis revealed hyponatremia, decrease of plasma osmolarity, spared secretion of urine sodium and increase of ADH, leading to the diagnosis of SIADH. Cerebrosponal fluid examination showed mild pleocytosis, elevated protein, and normal glucose level. Although herpes simplex virus (HSV) DNA was not detected by the polymerase chain reaction method, titers of anti-HSV IgG antibody elevated chronologically. Brain MRI revealed abnormal T2 and FLAIR high intensities in the cingulate gyrus and hippocampus bilaterally. An EEG revealed periodic synchronous discharges predominantly in the frontal areas. Based on the clinical course, laboratory data, MRI and EEG findings, we diagnosed as SIADH associated with acute limbic encephalitis caused by HSV infection. After the fluid restriction and sodium supply, plasma sodium was normalized. Administration of acyclovir and steroid was not so effective, however her condition improved gradually. Several cases of SIADH associated with limbic encephalitis have been reported; however, the pathophysiology is to be clarified. We thought that in the presented case, SIADH was caused by disturbance of the hormonal control at the hypothalamus on the pituitary gland due to the spreading of inflammation from limbic system to these areas.