Serial Brain Imaging Research Articles

Reversible cerebral atrophy: a case report and literature review

Reversible cerebral atrophy is not a typically considered phenomenon in the clinical setting although it may be responsible for a variety of symptoms, from mild cognitive difficulty to dementia. We describe a patient with schizophrenia who was found to have reversible brain atrophy during an episode of delirium of multiple etiologies, which resolved after the delirium was treated. According to our PubMed search, these brain changes may be more common (as against popular belief) in clinical scenarios such as alcohol use [1], endogenous or exogenous steroid alterations, malnutrition—particularly in anorexia nervosa [2] and kwashiorkor [3], valproic acid use [4–6] and normal pressure hydrocephalus when treated with cerebrospinal fluid (CSF) shunting [7]. Reversible cerebral atrophy is likely underrecognized due to the fact that serial brain imaging is rarely obtained in any given patient. If a patient develops cognitive decline in the above scenarios, it may be worthwhile considering that it is due to reversible brain atrophy, especially since the treatment can be as simple as correcting the implicated etiology. Reversible cerebral atrophy has been hypothesized to be caused by fluid loss followed by fluid intake [8], dehydration [9], reversible white matter loss [10] and gray matter structural changes.

Commentary on “Diagnosis of Alzheimer’s disease: Two decades of progress.” Perspectives on “Perspectives”

t m The article by Dr. Zaven Khachaturian is a superb, conise summary of the development of our understanding of ementias in general and of Alzheimer’s disease (AD) in articular. It documents that good leadership from the Fedral Government can be part of the solution. It also provides ound counsel on what needs to be done now. As indicated in that article, improvement in the diagnosis f AD or other dementia in the clinical setting is not now a ressing problem. Dementia can be recognized with confience on the basis of medical history (anamenusis) and europsychological testing. Treatable conditions that conribute to cognitive disability can be detected by the nowtandardized dementia workup, given reasonable clinical cumen on the part of the examiner. Serial brain imaging tudies can indicate whether there is evidence of accelerated trophy even before symptoms become debilitating, in time or people to make appropriate practical arrangements. The iagnosis of AD can be made with more than 90% confience on the basis of a careful evaluation, as documented by number of studies in which patients were followed up until utopsy. The course of AD is hard to predict in any indiidual patient, except for the generalization that worse illess tends to progress more rapidly, ie, that the best availble predictor of the future is the past. However, there is no urrent clinical reason to make the diagnosis in the earliest tages of the disease. People in the age range at risk for AD re also at risk for other debilitating illnesses, such as trokes. They should make sound financial and personal lans including a living will and a health care proxy regardess of whether they might be in the early stages of AD. More pressing problems are scientific:

Meningiomas may be a component tumor of multiple endocrine neoplasia type 1.

Recently, an increased incidence of some nonendocrine tumors are reported in patients with multiple endocrine neoplasia type 1 (MEN 1). There are rare reports of meningiomas and other central nervous system tumors in these patients, but it is unknown if they are more frequent or if allelic loss of the MEN1 gene is important in their pathogenesis. The aim of this study was to address these two latter questions. Results from a prospective study of 74 MEN 1 patients with suspected/proven pancreatic endocrine tumors (PETs) were analyzed, as well as molecular studies performed on a resected meningioma. All patients had serial brain imaging studies (computed tomography, magnetic resonance imaging, and octreoscanning since 1994) and yearly studies evaluating MEN 1 involvement with a mean follow-up of 7.2 years. Results were compared with 185 patients with sporadic Zollinger-Ellison syndrome. Six patients (8%) had meningiomas. Meningiomas were single and found late in the MEN 1 course (mean age = 51 years). Magnetic resonance imaging/computed tomography were more sensitive than octreoscanning. Their diagnosis averaged 18 years after the onset of hyperparathyroidism, 10-15 years after pituitary disease or PETs. Meningiomas were 11 times more frequent in patients with PETs with MEN 1 than without MEN 1 (P = 0.017). No clinical, laboratory, or MEN 1 feature distinguished patients with meningiomas. Meningiomas were asymptomatic and 60% showed no growth. A resected meningioma showed loss of heterozygosity at 11q13 and 1p, including at p73 and ARHI/NOEY2 locus, but not at the neurofibromatosis 2 gene locus. These results show meningiomas are not an infrequent occurrence in MEN 1, and loss of the function of the MEN1 gene product plays a role in their pathogenesis in these patients.

An “eye” out for trauma

Retinal hemorrhages have long been recognized as a clue to the presence of inflicted head injury in children. The precise mechanism by which this occurs has not been totally understood. A step in this direction is reported in this issue of The Journal by Gilles and associates from Children's Hospital in Los Angeles. These workers used a database containing serial fundus photographs and brain imaging in 14 children with inflicted head injury, 10 of whom had retinal hemorrhages. In most cases, there was good correlation between the laterality of the initial fundus findings and the localization of injury on computed tomography (CT) imaging. In some cases, it was a matter of time before the lateralization became evident on CT, although it could be predicted by the initial appearance of the fundus. This observation supports the hypothesis that retinal findings in children with inflicted head injury are consequent to the transmission of intracranial pressure gradients to the retinal sheath and vessels. In addition to providing the practitioner with a nice review of the effects of these injuries in children, the paper is an example of the use of careful clinical examinations in testing complex physiologic hypotheses.

Acute seizures after intracerebral hemorrhage: a factor in progressive midline shift and outcome.

To determine whether early seizures that occur frequently after intracerebral hemorrhage (ICH) lead to increased brain edema as manifested by increased midline shift. A total of 109 patients with ischemic stroke (n = 46) and intraparenchymal hemorrhage (n = 63) prospectively underwent continuous EEG monitoring after admission. The incidence, timing, and factors associated with seizures were defined. Serial CT brain imaging was conducted at admission, 24 hours, and 48 to 72 hours after hemorrhage and assessed for hemorrhage volume and midline shift. Outcome at time of discharge was assessed using the Glasgow Outcome Scale score. Electrographic seizures occurred in 18 of 63 (28%) patients with ICH, compared with 3 of 46 (6%) patients with ischemic stroke (OR = 5.7, 95% CI 1.4 to 26.5, p < 0.004) during the initial 72 hours after admission. Seizures were most often focal with secondary generalization. Seizures were more common in lobar hemorrhages but occurred in 21% of subcortical hemorrhages. Posthemorrhagic seizures were associated with neurologic worsening on the NIH Stroke Scale (14.8 vs 18.6, p < 0.05) and with an increase in midline shift (+ 2.7 mm vs -2.4 mm, p < 0.03). There was a trend toward increased poor outcome (p < 0.06) in patients with posthemorrhagic seizures. On multivariate analysis, age and initial NIH Stroke Scale score were independent predictors of outcome. Seizures occur commonly after ICH and may be nonconvulsive. Seizures are independently associated with increased midline shift after intraparenchymal hemorrhage.

Transient ischaemic attacks are associated with increased rates of global cerebral atrophy

Objectives: To determine whether patients presenting with a first transient ischaemic attack (TIA) subsequently show increased rates of brain atrophy compared with age matched controls; and to assess potential risk...

Costello syndrome in two Brazilian children.

The increasing number of children with Costello syndrome described world wide has helped in delineating further the characteristic features of this condition. We report here two children, seen in the...

Patterns of recurrence of glioblastoma multiforme after external irradiation followed by implant boost

Purpose : To study patterns of recurrence in patients with focal primary glioblastoma treated on Northern California Oncology Group protocol 6G-82-2 including surgery, focal external beam radiotherapy (59.4–60 Gy) with oral hydroxyurea followed by temporary brain implant with high-activity iodine-125 sources (50 Gy), and six cycles of chemotherapy with procarbazine, lomustine, and vincristine. Methods and Materials : Serial brain imaging scans were available for review in 25 of 34 patients with glioblastoma who underwent brain implant boost. Of 381 scans performed between the date of diagnosis and the date of death or last follow-up, 362 (95%) were re-reviewed. Disease progression was scored as local (within 2 cm of the implant site), separate within the brain parenchyma (⩾ 2 cm from the implant site), subependymal, or systemic. Both initial and subsequent failures were scored. Results : Three patients are 5-year survivors, without evidence of disease, at 267, 292, and 308 weeks. Of the 22 initial sites of failure, 17 (77%) were local, three (14%) were separate brain lesions (one of which was due in retrospect to multicentric disease at diagnosis), one (5%) subependymal, and one (5%) systemic. Five patients with local failure later had other sites of failure, including a separate brain lesion in 1, subependymal spread in 3, and both in 1. One patient with separate brain failure later had local progression and then subependymal spread. Conclusion : Although there was a significant risk of separate brain lesions or subependymal spread over time, local tumor progression was the predominant pattern of failure.

A case of chronic epileptic encephalopathy of neonatal onset: A probable concern of human cytomegalovirus

A 10-year-old male patient, who had suffered from intractable convulsions from the neonatal period, is presented. Serial brain images suggested slow, gradual destruction of neural elements. Human cytomegalovirus (HCMV) DNA was detected in his cerebrospinal fluid (CSF) by means of the polymerase chain reaction. Intrathecal interferon had a favorable effect on his seizures. We assume a close relationship between HCMV and some chronic types of epileptic encephalitis/encephalopathy.

Chronic progressive multiple sclerosis: serial magnetic resonance brain imaging over six months.

Eight patients in the chronic progressive stage of multiple sclerosis were studied prospectively with magnetic resonance imaging of the head and neurological examination every 2 weeks for 6 months. There were no clinical relapses and disability ratings did not change between the start and completion of the study. Despite the clinical inactivity, a total of 86 active events (new, reappearing, or enlarging lesions) were identified by magnetic resonance imaging over the 6 months, with 50 (51%) of 98 follow-up scans showing evidence of one or more active lesions. New and changing lesions were indistinguishable in appearance, distribution, and temporal pattern from those previously seen in patients who had relapsing and remitting multiple sclerosis. However, as noted previously, the patients in the chronic progressive stage had many more confluent lesions than did the group in relapse. These results strongly suggest that the frequently observed clinical evolution of multiple sclerosis into a chronic progressive course is not accompanied by a fundamental change in the disease process. In fact the chronic progressive stage seems associated with more active changes demonstrated by scans than does relapsing and remitting multiple sclerosis. This study also confirms our previous experience that serial magnetic resonance imaging is much more sensitive than clinical examination in detecting disease activity in multiple sclerosis.