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PubMed2005

Subacute spongiform encephalopathies.

Subacute spongiform encephalopathies are rare fatal diseases that affect the central nervous system, which is thought to be caused by prions, characterized clinically by a rapid progressive dementing course, along with generalized myoclonus. The prototype of these conditions in humans is Creutzfeldt-Jakob Disease (CJD). Although the final diagnosis depends on neuropathological examination, the presence of periodic sharp wave complexes on EEG and of the neuron-specific enolase, tau protein, S-100, and of the 14-3-3 protein in the cerebrospinal fluid, make the diagnosis of probable CJD. However, as these criteria are not completely accurate and the early diagnosis is extremely difficult, much interest has been focused recently on imaging methods. With the advent of diffusion-weighted imaging, MRI has shown high sensitivity and specificity, therefore being considered a useful method for the early diagnosis of this entity.

Creutzfeldt-Jakob Syndrome↗
PubMed2005

Agrypnia excitata in a patient with progeroid short stature and pigmented Nevi (Mulvihill-Smith syndrome).

We report the video-polysomnographic sleep characteristics of a 25-year-old woman with the Mulvihill-Smith syndrome, a rare clinical condition characterized by progeria-like aspect, peculiar multiple pigmented nevi, low stature, and cognitive impairment. Among the various exams, two overnight video-polysomnographic recordings were carried out; moreover, cerebral MRI and molecular analysis of the prion protein gene (PRNP) were also performed. The video-polysomnographic recordings showed the absence of clear sleep episodes but the presence of periods during which the patient had poor contact with the environment, stereotyped afinalistic movements of the upper limbs and hands, irregular or periodic breathing (with central apnea episodes), heart rate arrhythmia, and rapid eye movements. Cerebral MRI showed only diffuse mild enlargement of the cortical sulci and the molecular genetics analysis of the PRNP was normal. Our clinical and neurophysiological study seems to indicate that a particular condition of severe sleep disruption, similar to some extent to that reported in the fatal familial insomnia and in the Morvan fibrillary chorea, which has been indicated as Agrypnia Excitata in recent literature, might be associated with the Mulvihill-Smith syndrome. The inclusion of a detailed study on the sleep characteristics of eventual additional patients will certainly help our understanding of this rare condition.

Adult↗
PubMed2006

Cerebral cortical and deep venous thrombosis without sinus thrombosis: clinical MRI correlates.

BACKGROUND: Cortical and/or deep vein thrombosis (CDVT) without dural sinus involvement is uncommon and presents diagnostic difficulty for many reasons. Our aim is to determine the relationship between magnetic resonance imaging (MRI) findings and clinical findings in patients with CDVT. METHODS: Forty-six patients with venous stroke proved on MRI included in our Registry, corresponding to 0.1% of 4650 patients with stroke, were studied. Magnetic resonance angiography (MRA) was performed in all patients, and 18 of them had follow-up MRA. Outcome was evaluated by using the Glasgow Outcome Scale at the time of discharge and during follow-up. RESULTS: Thirty-two patients presented cortical venous stroke; 21 of them had involvement of the dorsomedial venous system, six had a defect in the posteroinferior venous group, and five had a defect in the anteroinferior venous group. Thirteen patients presented simultaneous involvement of the superficial and deep venous system; seven with a defect in the parietal and internal cerebral veins (three with involvement of vein of Gallen), four with a defect in the temporooccipital (vein of Labbé) and basal vein of Rosenthal, two with a deficit in the anterior frontotemporal and uncal-pterygoid venous system. One patient had deep venous thrombosis primarily localized to the thalami bilaterally and the basal ganglia on the right because of occlusion of the thalamostriate veins. The main presenting symptoms of CDVT were headache, focal neurologic signs, partial complex or secondary generalized seizures, and consciousness disturbances in those with deep venous thrombosis, presented alone or in combination at onset. CDVT was more than twofold more frequent in women than in men. Pregnancy, puerperium, oral contraceptive use, and infections were the most common predisposing factors. CONCLUSION: Computerized tomography, conventional MRI and diffusion-weighted imaging showing ischemic and/or hemorrhagic lesion that does not follow the boundary of classical arterial boundaries without signs of sinus thrombosis, and partial or generalized seizures followed by focal neurologic signs may predict CDVT. The outcome of patients with cortical venous stroke was good, but not in those with cortical plus deep venous infarction.

Adult↗
PubMed1997

Congenital muscular torticollis: magnetic resonance imaging and ultrasound diagnosis.

The magnetic resonance imaging (MRI) and sonographic appearances of congenital muscular torticollis were studied in a 6-week-old female infant who presented with a firm mass in the right sternocleidomastoid muscle and clinical signs of torticollis. MRI and ultrasound were performed to exclude neoplasm. MRI showed a diffusely enlarged, right sternocleidomastoid muscle that was isointense to normal muscle on T1-weighted conventional spin-echo images. The muscle became progressively brighter and more heterogeneous in signal intensity on proton density- and T2-weighted conventional spin-echo sequences. A thin rim of bright signal intensity on the T2-weighted images surrounded most of the muscle. Ultrasound demonstrated fusi-form enlargement with patchy inhomogeneous areas of increased echogenicity. At 14 weeks there were signs of clinical improvement, with softening of the mass and decreased torticollis.

Female↗
PubMed1994

Adult Toxocara canis encephalitis.

A 48-year-old patient with Toxocara canis infection developed severe ataxia, rigor and neuropsychological disturbances. An aetiology was proven by an indirect immunofluorescence test. CT and MRI revealed both diffuse and circumscribed white matter lesions. Angiography showed multiple occlusion of branches of the middle cerebral artery. Anthelminthic treatment was beneficial in the initial stage of the disease, but had no effect on progression of CNS symptoms. Immunosuppressive therapy with prednisolone and azathioprine yielded partial recovery and stabilisation of the patient.

Animals↗
PubMed1995

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a clinicopathological and genetic study of a Swiss family.

This paper reports a Swiss family affected by a cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) linked to chromosome 19q12. In three generations several members of this family had recurrent stroke-like episodes and, some developed subcortical dementia, migraine-like headaches, and depression. The clinically affected family members had multiple subcortical infarcts and diffuse leukoencephalopathy on MRI. Necropsy of one patient showed a distinctive non-amyloid and non-atherosclerotic angiopathy of small cerebral and leptomeningeal arteries with concentric depositions of a basophilic granular material replacing the smooth muscle cells of the media. Linkage analysis with five chromosome 19 markers spanning the estimated CADASIL interval showed the absence of any recombinant and positive Lod scores, highly suggestive of linkage of this condition to the CADASIL locus. CADASIL might be an underestimated cause of familial stroke and should be considered in the differential diagnosis of hereditary stroke.

Adult↗
PubMed1998

Dominantly inherited proximal myotonic myopathy and leukoencephalopathy in a family with an incidental CLCN1 mutation.

A two generation family of Greek origin with mild myotonia, predominantly proximal muscle weakness, and cataracts compatible with the syndrome of proximal myotonic myopathy, is reported. In addition, brain MRI showed a diffuse leukoencephalopathy in the propositus. Molecular genetic studies showed the R894X mutation in exon 23 of the muscle chloride channel gene in the propositus but in only one of her two clinically affected offspring, indicating that it is not the mutation causing disease in this family.

Abnormalities, Multiple↗
PubMed1998

An unusual course of progressive multifocal leukoencephalopathy in a patient with idiopathic CD4+ T lymphocytopenia.

A case is reported of idiopathic CD4+T lymphocytopenia with progressive multifocal leukoencephalopathy and cervical lymph node tuberculosis. A 57 year old Japanese man presented with cervical lymphadenopathy and progressive neurological deficits, and six months later he developed akinetic mutism. He had a persistent severely depressed number of circulating CD4+T lymphocytes in the absence of human immunodeficiency virus infection. T1 weighted MRI showed a diffuse decreased signal intensity limited to the white matter without mass effect. A brain biopsy specimen had a morphology similar to that of progressive multifocal leukoencephalopathy. Polyomavirus antigen was detected in the brain lesion, and viral DNA was identified in nucleated blood cells and urine. Unusually this serious medical condition has lasted for more than three years without remission. To our knowledge this is the first patient with CD4+T lymphocytopenia with progressive multifocal leukoencephalopathy, suggesting that similar opportunistic infections should be considered even in previously normal people.

Antigens, Viral↗
PubMed2002

Visual and spectral analysis of sleep EEG in acute hemispheric stroke.

BACKGROUND: Reports on the effects of focal hemispheric damage on sleep EEG are rare and contradictory. PATIENTS AND METHODS: Twenty patients (mean age +/- SD 53 +/- 14 years) with a first acute hemispheric stroke and no sleep apnea were studied. Stroke severity [National Institute of Health Stroke Scale (NIHSS)], volume (diffusion-weighted brain MRI), and short-term outcome (Rankin score) were assessed. Within the first 8 days after stroke onset, 1-3 sleep EEG recordings per patient were performed. Sleep scoring and spectral analysis were based on the central derivation of the healthy hemisphere. Data were compared with those of 10 age-matched and gender-matched hospitalized controls with no brain damage and no sleep apnea. RESULTS: Stroke patients had higher amounts of wakefulness after sleep onset (112 +/- 53 min vs. 60 +/- 38 min, p < 0.05) and a lower sleep efficiency (76 +/- 10% vs. 86 +/- 8%, p < 0.05) than controls. Time spent in slow-wave sleep (SWS) and rapid eye movement (REM) sleep and total sleep time were lower in stroke patients, but differences were not significant. A positive correlation was found between the amount of SWS and stroke volume (r = 0.79). The slow-wave activity (SWA) ratio NREM sleep/wakefulness was lower in patients than in controls (p < 0.05), and correlated with NIHSS (r = -0.47). CONCLUSION: Acute hemispheric stroke is accompanied by alterations of sleep EEG over the healthy hemisphere that correlate with stroke volume and outcome. The increased SWA during wakefulness and SWS over the healthy hemisphere contralaterally to large strokes may reflect neuronal hypometabolism induced transhemispherically (diaschisis).

Electroencephalography↗
PubMed2005

Amyotrophic lateral sclerosis: new developments in diagnostic markers.

There is an intensive search for diagnostic markers in amyotrophic lateral sclerosis (ALS). Protein analysis (proteomics) of the cerebrospinal fluid (CSF) appears particularly promising using mass spectrometry and 2-D gel electrophoresis to detect low and high molecular weight proteins, respectively. It is open whether protein changes specific for ALS will be found. This also holds true for inflammatory proteins such as the cytokine monocyte chemoattractant protein-1 which has been detected in CSF in ALS and for other cytokines such as interleukin-1beta. Increases of the protein Nogo A and B in muscle tissue and decreases of the growth factor vascular endothelial growth factor in blood may also be useful for monitoring the course of ALS. Clinical neurophysiology provides markers for upper and lower motor neuron damage. A very sensitive method to detect early upper motor neuron involvement is the transcranial magnetic stimulation modification 'triple stimulation technique' which can show significant changes in patients without clinical upper motor neuron signs. The loss of lower motor neurons can be closely monitored by MUNE techniques (motor unit number estimate). In modern imaging, the MRI technique DTI (diffusion tensor imaging) has the greatest diagnostic potential for ALS. It can separate between normal and ALS in group comparisons and may be improved to be diagnostic in individual patients. Voxel-based morphometry can reliably demonstrate regional cortical atrophy in motor areas and beyond although it is not appropriate for use in individual patients.

Amyotrophic Lateral Sclerosis↗
PubMed2004

Angiogenesis in symptomatic intracranial atherosclerosis: predominance of the inhibitor endostatin is related to a greater extent and risk of recurrence.

BACKGROUND AND PURPOSE: Angiogenesis may be beneficial in chronic myocardial and limb ischemia, but its role in intracranial atherosclerosis remains unknown. We aimed to investigate the relationship between the pro-angiogenic vascular endothelial growth factor (VEGF) and the anti-angiogenic endostatin, and the extent and risk of recurrence of symptomatic intracranial atherosclerosis. METHODS: Of a total of 94 consecutive patients with symptomatic intracranial stenoses, 40 fulfilled all inclusion criteria. Intracranial stenoses were confirmed by magnetic resonance angiography. Magnetic resonance imaging (MRI) including diffusion-weighted sequences was conducted. Plasmatic VEGF and endostatin were determined from blood samples obtained 3 months after stroke onset, and patients were followed-up thereafter. RESULTS: A total of 144 intracranial stenoses were confirmed (median number per patient=3). Endostatin/VEGF ratio gradually augmented with the increasing number of intracranial stenoses (r=0.35, P=0.02). Diabetes mellitus (OR, 6.04; CI, 1.1 to 32.2; P=0.03) and a higher endostatin/VEGF ratio (OR, 15.7; CI, 2.2 to 112.3; P=0.006) were independently associated with a greater extent of intracranial atherosclerosis. During a median follow-up of 13 months, 8 patients (20%) experienced a new cerebral ischemic event. A higher baseline endostatin concentration was an independent predictor of new events (hazard ratio, 7.24; CI, 1.6 to 33.8; P=0.011) in a Cox regression model after adjustment for age, sex, number of stenotic vessels, and risk factors. Patients with a higher endostatin level had a lower survival free of new events (P=0.01, log-rank test). CONCLUSIONS: A predominance of the inhibitor endostatin within the endogenous angiogenic response is associated with a greater extent and risk of recurrence of symptomatic intracranial atherosclerosis, suggesting that angiogenesis may be beneficial in this condition.

Aged↗
PubMed2000

Serial MRI after transient focal cerebral ischemia in rats: dynamics of tissue injury, blood-brain barrier damage, and edema formation.

BACKGROUND AND PURPOSE: With the advent of thrombolytic therapy for acute stroke, reperfusion-associated mechanisms of tissue injury have assumed greater importance. In this experimental study, we used several MRI techniques to monitor the dynamics of secondary ischemic damage, blood-brain barrier (BBB) disturbances, and the development of vasogenic edema during the reperfusion phase after focal cerebral ischemia in rats. METHODS: Nineteen Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion of 30 minutes, 60 minutes, or 2.5 hours with the suture occlusion model. MRI, including diffusion-weighted imaging (DWI), T2-weighted imaging, perfusion-weighted imaging, and T1-weighted imaging, was performed 5 to 15 minutes before reperfusion, as well as 0.5, 1.5, and 2.5 hours and 1, 2, and 7 days after withdrawal of the suture. Final infarct size was determined histologically at 7 days. RESULTS: In the 30-minute ischemia group (and partially also after 60 minutes), DWI abnormalities reversed transiently during the early reperfusion period but recurred after 1 day, probably due to secondary ischemic damage. After 2.5 hours of ischemia, DWI abnormalities no longer reversed, and signal intensity on both DWI and T2-weighted images increased rapidly in the previously ischemic region due to BBB damage (enhancement on postcontrast T1-weighted images) and edema formation. Early BBB damage during reperfusion was found to be predictive of relatively pronounced edema at subacute time points and was probably related to the increased mortality rates in this experimental group (3 of 7). CONCLUSIONS: Reperfusion after short periods of ischemia (30 to 60 minutes) appears to be mainly complicated by secondary ischemic damage as shown by the delayed recurrence of the DWI lesions, whereas BBB damage associated with vasogenic edema becomes a dominant factor with longer occlusion times (2.5 hours).

Animals↗
PubMed1989

Autosomal recessive cerebellar hypoplasia.

Cerebellar hypoplasia is found in association with a variety of neurologic and systemic disorders. It is the primary finding in the uncommonly reported condition of autosomal recessive cerebellar hypoplasia. We describe two siblings with cerebellar hypoplasia documented in both by magnetic resonance imaging (MRI) and review the clinical features of previously reported cases of autosomal recessive cerebellar hypoplasia. The most common findings in this disorder are nonprogressive ataxia, strabismus, mental retardation, and speech delay with dysarthria. Previously reported cases have been confirmed by autopsy, pneumoencephalography, or computed tomographic (CT) scans. MRI clearly documents diffuse cerebellar hypoplasia and aids in distinguishing autosomal recessive cerebellar hypoplasia from other disorders. The pathophysiology of this disorder is uncertain, however, studies of the weaver mutant mouse (an animal model of autosomal recessive cerebellar hypoplasia) suggest that an abnormality of the Bergmann glia may lead to the observed granule cell layer deficiency in these patients. This diagnosis should be considered for children with nonprogressive ataxia and families should be made aware of the 25% recurrence risk.

Cerebellar Diseases↗
PubMed1996

Transient encephalopathy after paclitaxel (Taxol) infusion.

Paclitaxel (Taxol) is a novel antineoplastic agent that acts by promoting microtubule polymerization. Although myelosuppression and peripheral neurotoxicity are well known and dose limiting, there have been no reports of CNS toxicity apart from two patients with seizures. This may reflect that paclitaxel has little or no blood-brain barrier penetration. We report two women treated with paclitaxel who developed a clinical state characterized by confusion, word-finding difficulty, and behavioral changes. One had bilateral extensor plantar responses. These symptoms appeared 1 week after paclitaxel infusion and resolved spontaneously. Subsequent infusions were associated with a similar self-resolving encephalopathy in one patient and recurrent headache and ataxia in the other. Neuroimaging (including enhanced MRI), LP, and laboratory investigations did not reveal other causes. Electroencephalography showed diffuse nonspecific slowing. One MRI had prominent but nonspecific high signal intensity abnormalities in the deep white matter of the cerebral hemispheres. Based on temporal association, diagnostic exclusion, and repeated episodes with subsequent challenges, we believe these patients may have experienced CNS toxicity from paclitaxel. The mechanism for this self-resolving encephalopathic process is unclear.

Adenocarcinoma↗
PubMed1998

Phenotypic variation in leukoencephalopathy with vanishing white matter.

OBJECTIVE: The objective of this study is to describe milder and later onset variants of a recently described leukoencephalopathy with vanishing white matter. BACKGROUND: The diagnostic criteria used currently for this disease include an early-childhood onset of neurologic deterioration. METHODS: Clinical, MRI, and spectroscopic findings of five patients were reviewed who fulfilled all inclusion criteria for the disease of vanishing white matter, apart from the age at onset. In one patient histopathologic findings were documented. RESULTS: Onset of the disease was in late childhood or adolescence in four patients, and one patient was still presymptomatic in his early twenties. The course of the disease tended to be milder than in the patients with early-childhood onset. MRI revealed a diffuse cerebral hemispheric leukoencephalopathy with evidence of white matter rarefaction. MRS of the abnormal white matter showed a serious decrease but not complete disappearance of all "normal" signals and, in some patients, the presence of extra signals from lactate and glucose. Changes in relative spectral peak heights were compatible with axonal damage or loss, but not with active demyelination or substantial gliosis. Autopsy in one patient confirmed the extensive rarefaction of the cerebral white matter. There was a commensurate loss of axons and myelin sheaths. Within the brainstem, pontine lesions were present, also involving the central tegmental tracts--a phenomenon previously described in early-onset patients. CONCLUSION: Later onset does occur in the disease of vanishing white matter, and both MRS and histopathology are compatible with a primary axonopathy rather than primary demyelination.

Adolescent↗
PubMed2000

Memory deficits after bilateral anterior fornix infarction.

The authors report a patient who suddenly developed memory loss without any other focal neurologic deficits. Neuropsychological testing showed severe anterograde verbal and visual memory deficits that improved gradually over several months, but not to the point of the premorbid state. Brain MRI with diffusion-weighted imaging performed 3 days after onset revealed acute infarction involving the bilateral fornices and the right genu of the corpus callosum. The authors suggest that acute fornix infarction may cause anterograde memory deficits.

Cerebral Infarction↗
PubMed1994

Neuroimaging and neuropathologic findings in AIDS patient with cytomegalovirus infection.

This 21-year-old male with hemophilia A developed cytomegalovirus (CMV) retinitis associated with acquired immunodeficiency syndrome (AIDS). He had a history of numerous blood transfusions. Serum antibody titers became positive for human immunodeficiency virus (HIV), when the patient was 18 years of age. Three years later, he developed CMV retinitis due to his immunosuppression. Ganciclovir (DENOSINE, TANABE SEIYAKU CO., LTD., Osaka, Japan) therapy given for 4 weeks produced a marked improvement in the ocular fundal findings, but the neurologic signs and symptoms, including headache, hypoesthesia, disorientation, and dementia became worse. T2-weighted magnetic resonance imaging (MRI) demonstrated a diffuse high intensity area in the periventricular white matter and small focal or patchy lesions in the hippocampus, basal ganglia, midbrain, medulla oblongata and the nucleus dentatus. The patient died of HIV encephalopathy and CMV infection. Characteristic CMV intranuclear inclusion bodies were observed histologically in most sites of the brain including the hippocampus, white matter, basal ganglia, midbrain, medulla oblongata, nucleus dentatus and the retina. Infiltration by monocyte-macrophage and multinucleated giant cells, which are characteristic of HIV encephalopathy, were observed in the periventricular white matter and the hippocampus. In this patient, the neuroimaging findings were compatible with the neuropathologic observations. MR imaging proved useful in detecting the central nervous system (CNS) lesions of AIDS and CMV infection.

AIDS Dementia Complex↗
PubMed2003

Mechanical impacts to the skulls of rats produce specific deficits in maze performance and weight loss: evidence for apoptosis of cortical neurons and implications for clinical neuropsychology.

The purpose of this experiment was to induce closed head injuries that might be applicable to clinical neuropsychology. Six adult female albino rats were struck over the right dorsal skull by a 200-gm weight that fell through a 0.9-m tube while another six rats served as controls. The rats that received the impact to the skulls displayed significantly more weight loss and fewer completions of the maze during the subsequent two to four days (effect size about 40%) while their open field behaviors, response latencies to thermal stimulation of the feet, and immobility within a conditioned fear setting did not differ significantly from those of controls. Histological analyses of the brains about 35 days after the impact indicated striking alterations in the morphology of cerebral cortical neurons, strongly suggestive of an apoptotic-like process, within the dorsal cerebral cortices below the likely impact site. Distributions of clusters of these aberrant-looking cells were also evident opposite to the impact site within the ventral cerebrum. Because apoptosis is involved with minimal inflammation and edema, detection of diffuse apoptosis by MRI and CT would be unlikely even though the influence on adaptability would be significant.

Animals↗