Viral meningoencephalitis: a review of diagnostic methods and guidelines for management.

BACKGROUND: Viral encephalitis is a medical emergency. The prognosis depends mainly on the pathogen and host immunologic state. Correct immediate diagnosis and introduction of symptomatic and specific therapy has a dramatic influence upon survival and reduces the extent of permanent brain injury. METHODS: We searched the literature from 1966 to 2009. Recommendations were reached by consensus. Where there was lack of evidence but consensus was clear, we have stated our opinion as good practice points. RECOMMENDATIONS: Diagnosis should be based on medical history and examination followed by CSF analysis for protein and glucose levels, cellular analysis, and identification of the pathogen by polymerase chain reaction amplification (recommendation level A) and serology (level B). Neuroimaging, preferably by MRI, is essential (level B). Lumbar puncture can follow neuroimaging when immediately available, but if this cannot be performed immediately, LP should be delayed only under unusual circumstances. Brain biopsy should be reserved only for unusual and diagnostically difficult cases. Patients must be hospitalized with easy access to intensive care units. Specific, evidence-based, antiviral therapy, acyclovir, is available for herpes encephalitis (level A) and may also be effective for varicella-zoster virus encephalitis. Ganciclovir and foscarnet can be given to treat cytomegalovirus encephalitis, and pleconaril for enterovirus encephalitis (IV class evidence). Corticosteroids as an adjunct treatment for acute viral encephalitis are not generally considered to be effective, and their use is controversial, but this important issue is currently being evaluated in a large clinical trial. Surgical decompression is indicated for impending uncal herniation or increased intracranial pressure refractory to medical management.

Silent brain infarcts and leukoaraiosis in young adults with first-ever ischemic stroke.

BACKGROUND: We recently observed that 13% of 1,008 consecutive adults aged 15-49 years with first-ever ischemic stroke had one or more silent brain infarcts (SBIs), and more than 5% presented with leukoaraiosis on CT or MRI. We sought to investigate the features of and risk factors for magnetic resonance (MR)-defined SBIs and leukoaraiosis in these patients. METHODS: We analyzed the radiologic features of SBIs and leukoaraiosis in MR-scanned patients (n = 669) blinded to clinical data and examined their relation with subtype of the overt stroke. We used logistic regression to identify factors predisposing to SBIs and leukoaraiosis. RESULTS: Of the 669 patients included, 86 (13%) had SBIs, 50 (7%) had leukoaraiosis, 17 (3%) had both, and 550 had no SBIs or leukoaraiosis and served as controls. The majority (54%) had a single SBI, 20% had two SBIs, and 27% had three or more SBIs. Most SBIs were located in basal ganglia (39%) or subcortical regions (21%), but cerebellar SBIs also were rather frequent (15%). Leukoaraiosis was mainly mild to moderate. Independent risk factors for SBIs were type 1 diabetes (odds ratio [OR] 5.78, 95% confidence interval 2.37-14.10), obesity (OR 2.12, 1.07-4.19), smoking (OR 1.69, 1.05-2.72), and increasing age (OR 1.08, 1.04-1.13). Risk factors for leukoaraiosis were type 1 diabetes (OR 9.75, 3.39-28.04), obesity (OR 2.42, 1.04-5.68), female sex (OR 2.25, 1.16-4.34), and increasing age (OR 1.19, 1.10-1.29). Small-vessel disease was the predominant cause of stroke in both those with SBIs (31%) and leukoaraiosis (44%). CONCLUSIONS: Silent brain infarcts and leukoaraiosis are not uncommon among young stroke patients--type 1 diabetes being the strongest risk factor.

Adult cervicocerebral artery dissection: a single-center study of 301 Finnish patients.

BACKGROUND AND PURPOSE: There are only few small studies assessing potential risk factors, comorbidity, and prognostic factors in adult spontaneous cervicocerebral artery dissection (CAD). METHODS: We conducted a retrospective, hospital-based analysis on the prognostic factors and association of CAD with vascular risk factors in 301 consecutive Finnish patients, diagnosed from 1994 to 2007. RESULTS: Two thirds of the patients were men (68%). Women were younger than men. Migraine (36% of all patients), especially with visual aura (63% of all migraineurs), and smoking were more common in patients with CAD compared with the general Finnish population. At 3 months, 247 (83%) patients reached a favorable outcome. Occlusion of the dissected artery, internal carotid artery dissection (ICAD), and recent infection in infarction patients were associated with a poorer outcome. ICAD patients had less often brain infarction, but the strokes they had were more severe. Seven (2.3%) patients died during the follow-up (mean 4.0 years, 1186 patient years). Six (2%) patients had verified CAD recurrence. CONCLUSIONS: This study provides evidence for the association of CAD with male sex, and possible association with smoking and migraine. Occlusion of the dissected artery, ICAD, and infection appear to be associated with poorer outcome.

Viral encephalitis: a review of diagnostic methods and guidelines for management.

Viral encephalitis is a medical emergency. The spectrum of brain involvement and the prognosis are dependent mainly on the specific pathogen and the immunological state of the host. Although specific therapy is limited to only several viral agents, correct immediate diagnosis and introduction of symptomatic and specific therapy has a dramatic influence upon survival and reduces the extent of permanent brain injury in survivors. We searched MEDLINE (National Library of Medicine) for relevant literature from 1966 to May 2004. Review articles and book chapters were also included. Recommendations are based on this literature based on our judgment of the relevance of the references to the subject. Recommendations were reached by consensus. Where there was lack of evidence but consensus was clear we have stated our opinion as good practice points. Diagnosis should be based on medical history, examination followed by analysis of cerebrospinal fluid for protein and glucose contents, cellular analysis and identification of the pathogen by polymerase chain reaction (PCR) amplification (recommendation level A) and serology (recommendation level B). Neuroimaging, preferably by magnetic resonance imaging, is an essential aspect of evaluation (recommendation level B). Lumbar puncture can follow neuroimaging when immediately available, but if this cannot be obtained at the shortest span of time it should be delayed only in the presence of strict contraindications. Brain biopsy should be reserved only for unusual and diagnostically difficult cases. All encephalitis cases must be hospitalized with an access to intensive care units. Supportive therapy is an important basis of management. Specific, evidence-based, anti-viral therapy, acyclovir, is available for herpes encephalitis (recommendation level A). Acyclovir might also be effective for varicella-zoster virus encephalitis, gancyclovir and foscarnet for cytomegalovirus encephalitis and pleconaril for enterovirus encephalitis (IV class of evidence). Corticosteroids as an adjunct treatment for acute viral encephalitis are not generally considered to be effective and their use is controversial. Surgical decompression is indicated for impending uncal herniation or increased intracranial pressure refractory to medical management.

Electromagnetic function of polymicrogyric cortex in congenital bilateral perisylvian syndrome.

BACKGROUND: Congenital bilateral perisylvian syndrome (CBPS) is characterised by bilateral perisylvian polymicrogyria and suprabulbar paresis. Mild tetraparesis, cognitive impairment, and epilepsy are frequently associated. Sensory deficits are surprisingly rare, even though polymicrogyria often extends to auditory and sensorimotor cortex. OBJECTIVES: To study the sensorimotor and auditory cortex function and location in CBPS patients. METHODS: We mapped the sensory and motor cortex function onto brain magnetic resonance images in six CBPS patients and seven control subjects using sources of somatosensory and auditory evoked magnetic fields, and of rhythmic magnetoencephalographic (MEG) activity phase-locked to surface electromyogram (EMG) during voluntary hand muscle contraction. RESULTS: MEG-EMG coherence in CBPS patients varied from normal (if normal central sulcus anatomy) to absent, and could occur at abnormally low frequency. Coherent MEG activity was generated at the central sulcus or in the polymicrogyric frontoparietal cortex. Somatosensory and auditory evoked responses were preserved and also originated within the polymicrogyric cortex, but the locations of some source components could be grossly shifted. CONCLUSION: Plastic changes of sensory and motor cortex location suggest disturbed cortex organisation in CBPS patients. Because the polymicrogyric cortex of CBPS patients may embed normal functions in unexpected locations, functional mapping should be considered before brain surgery.

Brain diffusion changes in carotid occlusive disease treated with endarterectomy.

BACKGROUND: Patients with unilateral high-grade carotid stenosis or occlusion have been reported to have more leukoaraiosis and ischemic lesions in ipsilateral than in contralateral cerebral hemisphere. The lesions alter apparent diffusion coefficient (ADC) values in diffusion-weighted MRI (DWI). The overall effects of carotid endarterectomy on ADC values have not yet been explored. OBJECTIVE: S: To find out whether 1) average ADC (ADC(av)) values differed between hemispheres, 2) diffusion changes induced by carotid endarterectomy could be detected in brain tissue with serial DWI, and 3) patients with asymptomatic carotid stenosis differed from patients with a symptomatic stenosis. METHODS: Forty-five patients (22 with asymptomatic carotid stenosis and 23 with symptomatic carotid stenosis) with unilateral high-grade carotid stenosis underwent DWI before carotid endarterectomy and 3 and 100 days afterward, and 45 age- and sex-matched healthy control subjects were imaged once. We evaluated ADC(av) values in normal-appearing gray and white matter, watershed regions (WsR), and thalamus. RESULTS: ADC(av) values of ipsilateral white matter and WsR were higher than those of contralateral white matter and WsR, both being higher than in white matter and WsR of control subjects. After carotid endarterectomy, these differences were diminished, but the levels remained higher than in controls. ADC(av) values of gray matter and thalamus remained unaffected. Asymptomatic carotid stenosis and symptomatic carotid stenosis patient groups did not differ from each other. CONCLUSIONS: Carotid stenosis has an effect on diffusion in the white matter of the ipsilateral hemisphere, and it is partly reversible by carotid endarterectomy. The finding may be associated with leukoaraiotic development ("preleukoaraiosis").

Central nervous system aspergillosis in allogeneic stem cell transplant recipients.

Invasive aspergillosis (IA) is relatively common in allogeneic stem cell transplant (SCT) recipients. Although lungs are the most common site, central nervous system (CNS) involvement is also observed in this setting. We have retrospectively studied 14 cases of CNS aspergillosis found in a cohort of 455 allogeneic SCT recipients (incidence 3%). All patients, except one, had experienced acute graft-versus-host disease treated with high-dose methylprednisolone, and eight patients (57%) had also received ATG. The median time to the diagnosis of CNS aspergillosis was 124 days (range 49-347 days) from SCT. Pulmonary aspergillosis had been diagnosed earlier in four patients (29%). The most common initial symptoms of CNS aspergillosis were convulsions, hemiparesis, and mental alteration. Neuroradiological studies revealed single (two patients) or multiple (seven patients) focal lesions of 0.2-9 cm in diameter. Despite clinical suspicion in many patients, a confirmed diagnosis of CNS aspergillosis was made during life in only one patient. A total of 12 patients (86%) received amphotericin B. Despite therapy, all patients died 0-27 days (median seven days) after the initial CNS symptoms. CNS aspergillosis is not uncommon in allogeneic SCT recipients. Clinical manifestations are usually dramatic and progress quickly. Earlier and more effective treatment of IA is needed to prevent dissemination of infection into the CNS.

Effectiveness of operative treatment of internal orbital wall fracture with polydioxanone implant.

Many implants, some made from teflon or silicone, have been used for internal orbital wall reconstruction. Late complications relating to use of such implants have been reported. In this prospective study a polydioxanone (PDS) implant absorbable in vivo was used for internal orbital wall reconstruction. Follow-up involved clinical examination, magnetic resonance imaging (MRI) and computerized tomography (CT). Clinical examinations were undertaken before operation and up to 36 weeks postoperatively. Sixteen consecutive patients (10 pure blow-out fractures, six with associated zygomatic fracture) took part in the study. Prevalences of diplopia, proptosis and enophthalmus were recorded during each follow-up examination. This study revealed no muscle entrapment within the fracture line. Although CT results confirmed bone growth in the internal orbital wall, shape was unsatisfactory, and orbital volume was not reduced. MRI revealed thick scar formations in six cases (37.5%), fibrotic sinuses filled with air or gas in three cases (19%) and a fibrotic sinus with fluid around the PDS in one case (6%). Our results suggest that use of PDS in reconstructing the internal orbital wall is inadvisable.

CNS manifestations of Nasu-Hakola disease: a frontal dementia with bone cysts.

BACKGROUND: Nasu-Hakola disease or polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL) is a genetically heterogeneous disease characterized by a combination of systemic bone cysts and dementia. OBJECTIVE: The authors present a neurologic, neuroradiologic, and neuropathologic analysis of a series of PLOSL patients in which the diagnosis has been confirmed by molecular genetic methods. METHODS: Clinical, neurophysiologic, and imaging follow-up data on eight patients as well as autopsy samples of three patients were analyzed in this study. All eight patients were homozygous for a loss-of-function mutation in the DAP12 gene. RESULTS: In most patients, the disease debuted with pain in ankles and wrists after strain during the third decade, followed by fractures caused by cystic lesions in the bones of the extremities. Frontal lobe syndrome and dementia began to develop by age 30, leading to death by age 40. Neuroimaging disclosed abnormally high and progressively increasing bicaudate ratios and calcifications in the basal ganglia as well as increased signal intensities of the white matter on T2-weighted MR images even before the appearance of clinical neurologic symptoms. Three patients who had undergone autopsies showed an advanced sclerosing leukoencephalopathy with frontal accentuation, widespread activation of microglia, and microvascular changes. CONCLUSIONS: Although PLOSL in most patients manifests by bone fractures, some patients do not show any osseous symptoms and signs before the onset of neurologic manifestations. Consequently, patients with frontal-type dementia of unknown origin should be investigated by x-ray of ankles and wrists. The current results suggest early basal ganglia involvement in PLOSL.

MR imaging after aneurysmal subarachnoid hemorrhage and surgery: a long-term follow-up study.

BACKGROUND AND PURPOSE: We assumed that patients with surgically treated aneurysmal subarachnoid hemorrhage (SAH) might have more lesions than those revealed by CT that could be visible on MR images. METHODS: We conducted a retrospective study of a series of 147 patients with aneurysmal SAH who were treated surgically within 3 days of the onset of SAH. One hundred four patients (mean age, 48.8 years) underwent MR imaging studies 2.1 to 5.6 years (mean, 3.3 years) postoperatively. RESULTS: Eighty-four (81%) patients presented a total of 152 areas of increased signal intensity on T2-weighted images, consistent with infarction; 48% of the patients had lesions in the frontal lobes. CT performed 3 months postoperatively revealed hypodense areas on the scans of only 57% of the patients and showed lesions in the frontal lobes of only 16% of the patients. CONCLUSION: Patients who undergo early surgery for aneurysmal SAH have more lesions than are revealed by CT. The difference is remarkable, especially in the frontal lobes.

Adverse long-term effects of brain radiotherapy in adult low-grade glioma patients.

OBJECTIVE: To study the long-term effects of radiotherapy on cognitive function in adult patients operated on for low-grade glioma. METHODS: A cohort of 160 patients who underwent surgery for low-grade gliomas of cerebral hemisphere between 1980 and 1992 in a single institution serving a defined population was studied. At a mean follow-up time of 7 years, 28 of the 101 patients who had postoperative irradiation (and no second surgery or chemotherapy) were still alive and eligible for MRI and neuropsychological study. Twenty-three of 59 patients who did not have radiotherapy, second surgery, or chemotherapy were alive and eligible at a mean of 10 years. RESULTS: The group that had postoperative irradiation performed significantly worse than the group that did not in cognitive tests. This difference was not accounted for by histologic diagnosis; location, extent of removal, or progression of the tumor; or any patient factor. Leukoencephalopathy was more severe in the group that had postoperative irradiation than in the group without radiotherapy, and correlated to poor memory performances only in the postoperative radiotherapy group. Average Karnofsky performance scale score was significantly lower in the group that had postoperative irradiation than in the group that did not. CONCLUSION: In adults with low-grade glioma, postoperative radiotherapy poses a significant risk of long-term leukoencephalopathy and cognitive impairment.

Three-dimensional integration of brain anatomy and function to facilitate intraoperative navigation around the sensorimotor strip.

We studied 12 patients with brain tumors in the vicinity of the sensorimotor region to provide a preoperative three-dimensional visualization of the functional anatomy of the rolandic cortex. We also evaluated the role of cortex-muscle coherence analysis and anatomical landmarks in identifying the sensorimotor cortex. The functional landmarks were based on neuromagnetic recordings with a whole-scalp magnetometer, coregistred with magnetic resonance images. Evoked fields to median and tibial nerve and lip stimuli were recorded to identify hand, foot and face representations in the somatosensory cortex. Oscillatory cortical activity, coherent with surface electromyogram during isometric muscle contraction, was analyzed to reveal the hand and foot representations in the precentral motor cortex. The central sulcus was identified also by available anatomical landmarks. The source locations, calculated from the neuromagnetic data, were displayed on 3-D surface reconstructions of the individual brains, including the veins. The preoperative data were verified during awake craniotomy by cortical stimulation in 7 patients and by cortical somatosensory evoked potentials in 5 patients. Sources of somatosensory evoked fields identified correctly the postcentral gyrus in all patients. Useful corroborative information was obtained from anatomical landmarks in 11 patients and from cortex-muscle correlograms in 8 patients. The preoperative visualization of the functional anatomy of the sensorimotor strip assisted in designing the operational strategy, facilitated orientation of the neurosurgeon during the operation, and speeded up the selection of sites for intraoperative stimulation or mapping, thereby helping to prevent damage of eloquent brain areas during surgery.

Basal brain injury in aneurysm surgery.

OBJECTIVE: The goal of this study was to determine the frequency of lesions in the basal frontotemporal area that were related to surgical damage to the brain tissue. METHODS: A prospective series of 101 patients with ruptured intracranial aneurysms were examined with high-field magnetic resonance imaging, 2 to 6 years (mean, 3.3 yr) after early surgery. RESULTS: Lesions in the basal frontotemporal region, on the side of the pterional approach, were observed for 36 patients. These lesions were not visible in computed tomographic scans obtained pre- or postoperatively or 3 months after subarachnoid hemorrhage. Patients with ruptured aneurysms in the anterior communicating artery exhibited fewer of these lesions than did patients with aneurysms in the internal carotid artery or middle cerebral artery; this difference was not statistically significant. The age of the patient, the duration and depth of hypotension, the amount of blood or ventricular enlargement in pre- and postoperative computed tomographic scans, and the incidence and severity of angiographic vasospasm in pre- and postoperative angiograms did not predict the existence of these lesions. The clinical conditions of the patients, as assessed using the Glasgow Outcome Scale, at 3 months after surgery and at the time of magnetic resonance imaging did not predict the existence of these lesions. Nine of the 10 patients who underwent surgical treatment of unruptured aneurysms on the contralateral side exhibited no signs of tissue damage. CONCLUSION: Surgical treatment of ruptured intracranial aneurysms seems to cause damage in the basal frontotemporal region in one-third of patients. The significance of these lesions remains unclear.

Modified activation of somatosensory cortical network in patients with right-hemisphere stroke.

To study the effects of parietal lesions on activation of the human somatosensory cortical network, we measured somatosensory evoked fields to electric median nerve stimuli, using a whole-scalp 122-channel neuromagnetometer, from six patients with cortical right-hemisphere stroke and from seven healthy control subjects. In the control subjects, unilateral stimuli elicited responses which were satisfactorily accounted for by modelled sources in the contralateral primary (SI) and bilateral secondary (SII) somatosensory cortices. In all patients, stimulation of the right median nerve also activated the SI and SII cortices of the healthy left hemisphere. However, the activation pattern was altered, suggesting diminished interhemispheric inhibition via callosal connections after right-sided stroke. Responses to left median nerve stimuli showed large interindividual variability due to the different extents of the lesions. The strength of the 20-ms response, originating in the SI cortex, roughly reflected the severity of the tactile impairment. Right SII responses were absent in patients with abnormal right SI responses, whereas the left SII was active in all patients, regardless of the responsiveness of the right SI and/or SII. Our results suggest that the human SI and SII cortices may be sequentially activated within one hemisphere, whereas SII ipsilateral to the stimulation may receive direct input from the periphery, at least when normal input from SI is interrupted.

MRI enhancement and microvascular density in gliomas. Correlation with tumor cell proliferation.

RATIONALE AND OBJECTIVES: Angiogenesis and proliferation activity are important indicators of tumor behavior in human gliomas. The authors studied how tumor enhancement in MR imaging and intratumoral vascular density were correlated with cell proliferation in cerebral gliomas. METHODS: The authors studied retrospectively 62 cerebral gliomas. Patients were examined before surgery with contrast-enhanced MR imaging. Microvessel density and the cell proliferation rate of tumor specimens were measured immunohistochemically using factor VIII and MIB-1 antibodies. Contrast enhancement of the tumors was evaluated by two radiologists. RESULTS: Contrast enhancement was observed in 45 tumors and was correlated with histologic cell proliferation (P = 0.0007) and microvessel density (P = 0.01). There was also a correlation between tumor vascular density and the cell proliferation rate (r = 0.51, P < 0.0001). Histologic tumor grade was associated with vascular density (P = 0.001). CONCLUSIONS: Lesion enhancement on preoperative contrast-enhanced MR imaging correlates with vascularity and proliferation activity of gliomas. The additional correlation between tumor vascularity and proliferation suggests that intratumoral microvessel density could be useful in estimating tumor proliferation.

Gelsolin-related spinal and cerebral amyloid angiopathy.

Gelsolin-related amyloidosis (familial amyloidosis, Finnish type) is a rare disorder, reported worldwide in kindreds carrying a G654A or G654T gelsolin gene mutation. Facial palsy, mild peripheral neuropathy, and corneal lattice dystrophy are characteristic, but atrophic bulbar palsy, ataxia of gait, and minor cognitive impairment may occur. In histological and immunohistochemical studies of the central nervous system in 4 patients with a G654A gelsolin mutation, we found widespread spinal, cerebral, and meningeal amyloid angiopathy, with deposition of gelsolin-related amyloid (AGel). Marked extravascular deposits occurred in the dura, spinal nerve roots, and sensory ganglia. The amyloid deposits were also variably immunoreactive for apolipoprotein E (ApoE), alpha1-antichymotrypsin (alpha1-ACT), and cystatin C (Cys C). Cerebral perivascular fibrinogen immunoreactivity was occasionally noted. The patients showed posterior column degeneration and diffuse loss of myelin in the centrum semiovale with perivascular accentuation. Postmortem magnetic resonance imaging, performed on 1 patient, showed white matter lesions, colocalizing with the histological abnormalities. Our study shows that deposition of AGel in the spinal and cerebral blood vessel walls, meninges, as well as spinal nerve roots and sensory ganglia is an essential feature of this form of systemic amyloidosis and may contribute to the central nervous system symptoms.

Modification of neuromagnetic cortical signals by thalamic infarctions.

Auditory evoked responses and spontaneous cortical activity were recorded with a whole-scalp 122-channel neuromagnetometer from 7 patients, who had small thalamic infarctions in the region of the left anterior tuberothalamic artery and associated memory defects. In contrast to healthy control subjects, with dominant rhythmic activity at 10.6 +/- 0.6 Hz in the parieto-occipital region, the spectral maximum in the patients was at 8.9 +/- 0.4 Hz. Abnormal acceleration of rhythmic activity was also observed bilaterally in rolandic areas. Our findings imply that lesions of non-specific thalamic nuclei may disturb human brain rhythms in widespread cortical areas. 'Mismatch responses' to deviant tones (1.1 kHz) among standards (1.0 kHz), suggested to reflect sensory auditory memory in healthy subjects, were absent in 2 patients, markedly decreased in 3, and normal in 2, implying that pathways passing through the anteromedial thalamus contribute to modulation of these responses. We conclude that local unilateral lesions in the anteromedial thalamus may cause extensive, bilateral alterations in the brain's electric activity.

Three hands: fragmentation of human bodily awareness.

We describe patient E.P. who occasionally perceives a 'ghost' hand which copies the previous positions of the left hand with a 0.5-1 min time lag, but follows the movement patterns of the right hand. The symptoms started after an operation of a ruptured aneurysm, followed by an infarction of the right frontal lobe; E.P. also has a previously lesioned corpus callosum. Neuromagnetic recordings revealed that activity of the left secondary somatosensory cortex was strongly suppressed during the ghost arm percept, thereby providing an objective correlate for E.P.'s sensations. We conclude that simultaneous mental contents about body scheme may be based on neural information extracted at considerably different times, resulting in fragmentation of bodily awareness.

Unilateral hyperfusion in brain-perfusion SPECT predicts poor prognosis in acute encephalitis.

We studied 88 patients with acute encephalitis using hexamethylpropyleneamine oxime and single photon emission computed tomography (SPECT). All patients had been initially treated with intravenous acyclovir. The etiology could be disclosed in 37 patients (42%), which included 15 patients with herpes simplex encephalitis, 7 with varicella-zoster encephalitis, and 29 with other encephalitides (Mycoplasma, adenovirus, influenza, rotavirus, rubella, Epstein-Barr, arbovirus, syphilis, and tuberculosis). Unilateral hyperperfusion in SPECT was an independent predictor of poor prognosis, whereas neither clinical outcome variables, such as seizures, state of consciousness, and focal neurologic findings, nor CSF or EEG findings were not. Focal unilateral hyperperfusion is an indicator of severe inflammation of the brain tissue and predicts a poor outcome as assessed in terms of activities of daily living after recovery.

Spin-echo MRI of chronic intracerebral haematomas.

Our purpose was to characterise the MRI appearances of clinically non-neoplastic chronic intracerebral haematomas (ICH). We examined 25 patients with a history of clinically non-neoplastic 0.5-to 1.5-year-old ICH who underwent prospective follow-up 1.0-T spin-echo MRI of the brain. On T1-weighted images most lesions gave lower signal than white matter and were isointense with cerebrospinal fluid (CSF). On T2-weighted images most were either totally low-signal and slit-like, or had a high-signal centre and a low-signal margin. The low-signal (haemosiderin) rim showed areas of discontinuity in 7 cases. Of 24 lesions, 4 showed small enhancing areas on contrast-enhanced images. In 10 cases the brain parenchyma surrounding the lesion showed high-signal on T2- and low signal on T1-weighted images, probably representing encephalomalacia. In 20 cases enlargement of a nearby CSF space was observed, and 14 cases showed atrophy of the brain stem ipsilateral to the lesion. We thus found more variation on MRI of clinically non-neoplastic chronic ICH than previously described.