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PubMed1982

[Cerebellar atrophies].

The concept of cerebellar atrophy was first introduced by Pierre Marie in 1893 in his description of hereditary cerebellar ataxia. Subsequent criticism of this notion was refuted by the report of new clinicopathological entities which are compatible with it. The contributions of the Clinic for Diseases of the Nervous System are discussed in this paper. Etiological classification is difficult, in spite of progress made in the genetic, epidemiologic, and biochemical approaches to cerebellar atrophies. Pathologic findings appear to supply the most secure basis for presentation of these affections. Predominantly cortical atrophies may be localized to the vermis. This is the case in the familial cerebello-olivary atrophy of Holmes (1907), in tardive cortical atrophy (Pierre Marie, Foix and Alajouanine, 1922), and in the cerebellar atrophy of alcoholics (Alajouanine, Castaigne, Contamin and Lebourges, 1959; Victor, Adams and Mancall, 1959), in which the lesions are similar. The frequent intrication of the various etiological factors: age, deficiencies, alcohol, heredity, suggests the role of a sometimes primary, sometimes latent genetic predisposition, revealed during various pathological conditions. Cortical cerebellar atrophy may be of the diffuse type, as in paraneoplastic cerebellar atrophy (Brouwer and Biemond, 1938), which is closely related to subacute polioencephalomyelitis in cancer patients (Dubas et al., 1982), and in congenital atrophy of the granular layer (Norman, 1940), which is more a dysgenesis than a true degenerative affection. Lesions affecting mainly the efferent or afferent cerebellar pathways include olivopontocerebellar atrophy (Dejerine and André Thomas, 1900) which should be included in the larger overall concept of multiple system atrophy (Oppenheimer, 1976), and dentorubric atrophy (Ramsay Hunt, 1921) which themselves should be integrated in the group of spinocerebellar atrophies. Finally, olivorubrocerebellar atrophy (Lejonne and Lhermitte, 1909) and crossed cerebellar atrophy, traditionally studied together with cerebellar atrophies, are only the result of a pre-existing lesion.

Atrophy↗

PubMed2006

Atrophy and defects detection of the external anal sphincter: comparison between three-dimensional anal endosonography and endoanal magnetic resonance imaging.

PURPOSE: Using endoanal magnetic resonance imaging, atrophy of the external anal sphincter can be established. This aspect has not been thoroughly investigated using three-dimensional anal endosonography. The purpose of this study was to compare prospectively three-dimensional anal endosonography to magnetic resonance imaging in the detection of atrophy and defects of the external anal sphincter in patients with fecal incontinence. In addition, we compared both techniques for anal sphincter thickness and length measurements. MATERIALS AND METHODS: Patients with fecal incontinence underwent three-dimensional anal endosonography and magnetic resonance imaging. Images of both endoluminal techniques were evaluated for atrophy and defects of the external anal sphincter. External anal sphincter atrophy scoring with three-dimensional anal endosonography depended on the distinction of the external anal sphincter and its reflectivity. External anal sphincter atrophy scoring with magnetic resonance imaging depended on the amount of muscle and the presence of fat replacement. Atrophy score was defined as none, moderate, and severe. A defect was defined at anal endosonography by a hypoechogenic zone and at magnetic resonance imaging as a discontinuity of the sphincteric ring and/or scar tissue. Differences between three-dimensional anal endosonography and magnetic resonance imaging for the detection of external anal sphincter atrophy and defects were calculated. In addition, we compared external anal sphincter thickness and length measurements in three-dimensional anal endosonography and magnetic resonance imaging. RESULTS: Eighteen patients were included (median age, 58 years; range, 27-80; 15 women). Three-dimensional anal endosonography and magnetic resonance imaging did not significantly differ for the detection of external anal sphincter atrophy (P = 0.25) and defects (P = 0.38). Three-dimensional anal endosonography demonstrated atrophy in 16 patients, magnetic resonance imaging detected atrophy in 13 patients. Three-dimensional anal endosonography agreed with magnetic resonance imaging in 15 of 18 patients for the detection of external anal sphincter atrophy. Using the grading system, 8 of the 18 patients scored the same grade. Three-dimensional anal endosonography detected seven external anal sphincter defects and magnetic resonance imaging detected ten. Three-dimensional anal endosonography and magnetic resonance imaging agreed on the detection of external anal sphincter defects in 13 of 18 patients. Comparison between three-dimensional anal endosonography and magnetic resonance imaging for sphincter thickness and length measurements showed no statistically significant concordance and had no correlation with external anal sphincter atrophy. CONCLUSION: This is the first study that shows that three-dimensional anal endosonography can be used for detecting external anal sphincter atrophy. Both endoanal techniques are comparable in detecting atrophy and defects of the external anal sphincter, although there is a substantial difference in grading of external anal sphincter atrophy. Correlation between three-dimensional anal endosonography and magnetic resonance imaging for thickness and length measurements is poor. Inconsistency between the two methods needs to be evaluated further.

Adult↗

PubMed1998

Partial atrophy in prostate needle cores: another diagnostic pitfall for the surgical pathologist.

We have seen in consultation a variant of atrophy, which is frequently confused with well-differentiated adenocarcinoma of the prostate. We have designated this entity as partial atrophy to distinguish it from its more common counterpart of fully developed atrophy. Partial atrophy is defined as benign prostate glands with relatively scant cytoplasm, yet the glands are not fully atrophic in that they do not appear basophilic at low magnification. Fifty-one cases of partial atrophy were identified (4 from Johns Hopkins Hospital, 47 from consultation). Within the partial atrophy focus, irregular (crinkled) nuclei were frequent in 23.5% and occasionally present in 33.3% of cases. Visible nucleoli were frequent in 25.4% of cases. Basal cells were not identifiable in 27.4% of cases or were hard to identify in 35.3% of cases. No intraluminal crystalloids or blue-tinged mucinous secretion was identified in partial atrophy. Adenocarcinoma or glands suspicious for cancer were present in other cores in 15.6% of cases. More fully developed atrophy was present in simultaneously obtained needle cores in 35.3% of cases. In the cases in which regular atrophy was the only coexisting condition, it was present within one 10x field from the partial atrophy in 22.2%, farther than one 10x field from the partial atrophy in 11.1%, and present in the same gland as the partial atrophy in 66.7%. Partial atrophy may be confused with low-grade adenocarcinoma because of the focus of crowded glands, irregular nuclei, and visible nucleoli. Clues for recognizing partial atrophy include relatively scant cytoplasm, distinct crinkled nuclei, pale cytoplasm similar to adjacent, more recognizably benign glands, and association with more fully developed benign atrophy.

Adenocarcinoma↗

PubMed2006

A working group classification of focal prostate atrophy lesions.

Focal atrophy is extremely common in prostate specimens. Although there are distinct histologic variants, the terminology is currently nonstandardized and no formal classification has been tested for interobserver reliability. This lack of standardization hampers the ability to study the biologic and clinical significance of these lesions. After informal and formal meetings by a number of the authors, focal atrophy lesions were categorized into 4 distinct subtypes as follows: (i) simple atrophy, (ii) simple atrophy with cyst formation, (iii) postatrophic hyperplasia, and (iv) partial atrophy. In phase 1 of the study, pathologists with varying levels of experience in prostate pathology were invited to view via the Internet a set of "training" images with associated descriptions of lesions considered typical of each subtype. In phase 2 of the study, each participant provided diagnoses on a series of 140 distinct "test" images that were viewed over the Internet. These test images consisted of the 4 subtypes of atrophy and images of normal epithelium, high grade prostatic intraepithelial neoplasia, and carcinoma. The diagnoses for each image from each pathologist were compared with a set of "standard" diagnoses and the kappa statistic was computed. Thirty-four pathologists completed both phases of the study. The interobserver reliability (median kappa) for classification of lesions as normal, cancer, prostatic intraepithelial neoplasia, or focal atrophy was 0.97. The median kappa for the classification of atrophy lesions into the 4 subtypes was 0.80. The median percent agreement with the standard diagnosis for the atrophy subtypes were: simple 60.6%, simple with cyst formation 100%; postatrophic hyperplasia 87.5%; partial atrophy 93.9%. The lower percentage for simple atrophy reflected a propensity to diagnose some of these as simple atrophy with cyst formation. Seven pathologists completed the phase 2 analysis a second time, and their intraobserver reproducibility was excellent. Three of 4 pathologists with low agreement with the standard diagnosis for simple atrophy improved their scores after repeating the analysis after re-examination of the "training set" of images. In conclusion, these criteria for variants of focal prostate atrophy may facilitate studies to examine the relation between various patterns of prostate atrophy and prostate cancer.

Atrophy↗

PubMed1999

Clinical patterns of patients with temporal lobe epilepsy and pure amygdalar atrophy.

PURPOSE: MRI volumetric measurements (MRIvol) have been proven reliable in determining mesial temporal atrophy in patients with TLE. We attempted to correlate the clinical features with different patterns of hippocampal formation (HF) and amygdala (AM) atrophy in patients with TLE without foreign tissue lesion. METHODS: We studied 65 patients with refractory TLE. They were divided into five groups according to MRIvol results: pure AM atrophy (n = 11, 10 unilateral and one bilateral), unilateral HF atrophy (n = 16), bilateral HF atrophy (n = 12), unilateral AM + HF atrophy (n = 13), and patients with normal volumes of AM and HF (n = 13). MRIvol of AM and HF were performed by using a protocol previously described by Watson et al. (Neurology 1992;42:1743-50). RESULTS: Patients with AM atrophy had later onset of seizures compared with those with unilateral HF atrophy (p < 0.01). History of febrile convulsions (p < 0.0001) and frequent secondarily generalized tonic-clonic seizures (GTCSs) were more often found in patients with HF atrophy compared with those with pure AM atrophy and those with normal volumes (p = 0.04). Prolonged postictal confusion was more often found with AM atrophy (p = 0.05). Memory impairment was more severe in patients with HF atrophy than in those with AM atrophy only or in those with normal volumes (p = 0.03). There were no significant differences among the five groups in the following parameters: age, duration of epilepsy, seizure frequency, and presence and type of aura. CONCLUSIONS: Prolonged postictal confusion appeared to be related to AM atrophy, in keeping with previous clinical observations. These patients also had a lower incidence of early febrile convulsions, older age at epilepsy onset, lower frequency of secondary GTCS, and lesser memory dysfunction compared with patients with hippocampal atrophy.

Adolescent↗

PubMed2001

Comparison of precancerous conditions: atrophy and intestinal metaplasia in Helicobacter pylori gastritis among Chinese and Dutch patients.

AIM-Atrophy and intestinal metaplasia (IM) as precancerous conditions consistently begin in the antrum and are most severe along the lesser curvature. The aim of this study was to investigate discrepancies in the prevalence, the severity of atrophy, and IM in antral mucosa of Helicobacter pylori infected gastritis and difference in age of onset among Chinese and Dutch patients. METHODS-Two hundred and sixty five Chinese patients and 261 Dutch patients with H pylori infection were enrolled. The degrees of atrophy and IM were graded according to the updated Sydney system. RESULTS-The overall prevalences of atrophy and IM were lower in Dutch patients (42% and 26%, respectively) than in Chinese patients (52% and 32%, respectively). Only the difference in atrophy reached significance (p = 0.028). However, in both Chinese and Dutch patients, the degrees of atrophy and IM were low and severe degrees were rare. The mean ages of Chinese and Dutch patients with atrophy and IM were higher than those without atrophy and IM (with atrophy (Chinese patients): mean, 42.12; SD, 9.80; with IM (Chinese patients): mean, 42.56; SD, 9.96; with atrophy (Dutch patients): mean, 55.16; SD, 12.20; with IM (Dutch patients): mean, 57.79; SD, 11.13; without atrophy (Chinese patients): mean, 39.71; SD, 10.16; without IM (Chinese patients): mean, 40.19; SD, 9.99; without atrophy (Dutch patients): mean, 45.70; SD, 12.44; without IM (Dutch patients): mean, 46.89; SD, 12.68). Atrophy and IM occurred earlier and were more severe in Chinese patients, with both reaching a peak value in patients over 60 years. CONCLUSIONS-There are geographical differences in the prevalence and severity of H pylori infected gastritis, in particular with respect to atrophy and IM, which suggests that infection with H pylori occurs earlier in life and has a higher prevalence in CHINA:

Adolescent↗

PubMed1998

Clinical course of newly developed or progressive patchy chorioretinal atrophy in pathological myopia.

Regional chorioretinal atrophy in the posterior fundus (patchy chorioretinal atrophy) in pathological myopia impairs vision severely when it covers the macula. The aim of this study was to assess the course of development and progression of patchy chorioretinal atrophy in pathological myopia. The location and progression of patchy chorioretinal atrophy that was either newly developed or had progressed during the follow-up period (mean 5.25 years) were analyzed. A total of 41 lesions of patchy atrophy were newly developed in 30 eyes of 25 patients. These lesions were more likely to occur in marginal regions of a posterior staphyloma but frequency per unit area was highest in the macula. There were 138 lesions of patchy chorioretinal atrophy that progressed in 75 eyes of 53 patients. Sixty percent of the lesions of patchy chorioretinal atrophy in marginal regions of a posterior staphyloma spread toward the center. Seventy percent of the lesions of patchy chorioretinal atrophy in the macula spread in all directions. Fluorescein angiography of newly developed patchy chorioretinal atrophy showed hyperfluorescence in 50% and hypofluorescence in 27%. Fluorescein angiography of progressive lesions of patchy chorioretinal atrophy showed hypofluorescence in 69%. Fluorescein angiography of some progressive areas of patchy chorioretinal atrophy, which showed a change from hyperfluorescence to hypofluorescence within several years, suggested that damage to the retinal pigment epithelium preceded the progression of the patchy chorioretinal atrophy. In conclusion, the patchy chorioretinal atrophy is most likely to occur in the macula and to enlarge in all directions. And it is suggested that the patchy chorioretinal atrophy which shows hyperfluorescence by fluorescein angiography should be kept under observation because our data suggest that this finding indicates progression in the future.

Adult↗

PubMed2002

Eight-year follow-up study of brain atrophy in patients with MS.

OBJECTIVE: To characterize whole-brain atrophy in relapsing-remitting MS (RRMS) patients over an 8-year period. The specific goals of this study were to determine if brain atrophy is related to subsequent disability status and to identify MRI correlates of atrophy progression. METHODS: A follow-up study was conducted to reassess patients from a phase III trial of interferon beta-1a (IFNbeta-1a) 8 years after randomization. Clinical and MRI data from 172 patients followed over 2 years in the original trial were used as baseline data. Follow-up data were obtained on 160 patients, including 134 patients with follow-up MRI examinations. Brain atrophy was estimated by automated calculation of brain parenchymal fraction. The relation between atrophy during the original trial and disability status at follow-up was determined. Correlations were also determined between lesion measurements from the original trial and the brain parenchymal fraction at follow-up. RESULTS: Brain atrophy was correlated with subsequent disability status. Atrophy rate during the original trial was the most significant MRI predictor of disability status at follow-up. Brain atrophy at follow-up was related to lesion volumes measured during the original trial. CONCLUSIONS: The relation between atrophy progression and subsequent neurologic disability status suggests that atrophy progression during RRMS is clinically relevant. Therefore, atrophy progression may be a useful marker for disease progression in clinical trials. The relation between lesions and subsequent atrophy indicates that brain atrophy may be related to focal tissue damage at earlier points in time, but important predisposing or other factors contributing to atrophy remain undefined.

Adjuvants, Immunologic↗

PubMed2000

[Dose-dependent relationship of chronic use of phenytoin and cerebellar atrophy in patients with epilepsy].

The chronic treatment with phenytoin or the acute intoxication by this drug may cause permanent cerebellar injury with atrophy of cerebellum vermis and hemispheres, which can be detected by neuroimaging studies. The aim of the present study was to investigate the correlation between the dosage and duration of treatment with phenytoin and the occurrence of cerebellar atrophy. Sixty-six patients were studied and had their tomographies analyzed for cerebellar atrophy. Of the 66 patients studied, 18 had moderate/severe atrophy, 15 had mild atrophy and 33 were considered to be normal. The patients with moderate/severe atrophy were those with higher exposure to phenytoin (longer duration of treatment and higher total dosage) showing statistically significant difference when compared to patients with mild atrophy or without atrophy (p=0. 02). Further, the patients with moderate/severe atrophy had serum levels of phenytoin statistically higher than those of patients with mild atrophy or without atrophy (p = 0.008). There was no association between other antiepileptic drugs dosage or duration of treatment and degree of cerebellar atrophy. We also found that older patients had cerebellar atrophy more frequently, indicating that age or duration of the seizure disorder may also be important in the determination of cerebellar degeneration in these patients. We conclude that although there is a possibility that repeated seizures contribute to cerebellar damage, long term exposure to phenytoin, particularly in high doses and toxic serum levels, cause cerebellar atrophy.

Adult↗

PubMed2005

Regional lobar atrophy predicts memory impairment in multiple sclerosis.

BACKGROUND AND PURPOSE: In recent studies, measures of whole brain atrophy were strongly correlated with neuropsychological testing, explaining more variance than measures of lesion burden in patients with multiple sclerosis. The relationship between regional lobar atrophy and cognitive impairment is yet to be examined. We endeavored to assess the clinical significance of regional lobar atrophy in multiple sclerosis. METHODS: In a cross-sectional study, we evaluated 31 patients with multiple sclerosis with brain MR imaging and neuropsychological testing. Impairment was determined by comparison with demographically matched healthy controls. MR imaging generated measures of lesion burden (fluid-attenuated inversion recovery hyperintense volume), general atrophy (brain parenchymal fraction), central atrophy (lateral ventricle volume), and lobar atrophy (regional brain parenchymal fraction of frontal, temporal, parietal, and occipital lobes in each hemisphere). Neuropsychological testing emphasized measures of processing speed and memory, because these are commonly affected in multiple sclerosis. RESULTS: Patients with multiple sclerosis showed significant atrophy and impairment on all neuropsychological tests. Regional atrophy accounted for the most variance in all regression models predicting memory performance. Left temporal atrophy was the primary predictor of auditory/verbal memory (partial r's = 0.55-0.61), and both left and right temporal atrophy predicted visual/spatial memory performance (partial r's = 0.51-0.67). Models predicting learning consistency retained frontal lobe atrophy measures (partial r's = 0.44-0.68). Central and general atrophy measures were the primary predictors in modeling processing speed (partial r's = 0.42-0.64). CONCLUSION: Regional atrophy accounts for more variance than lesion burden, whole brain atrophy, or lateral ventricle volume in predicting multiple sclerosis-associated memory dysfunction.

Adult↗

PubMed2003

Significance of fornix atrophy in temporal lobe epilepsy surgery outcome.

BACKGROUND: Previous magnetic resonance imaging (MRI) studies have shown concurrent fornix atrophy in a large proportion of patients with hippocampal atrophy. The contribution of the fornix as an independent preoperative determinant of surgical outcome is unknown. OBJECTIVE: To evaluate the contribution of the fornix as a determinant of surgical outcome in patients with preoperatively determined temporal lobe epilepsy. METHODS: We selected 78 patients who had undergone anterior temporal lobectomy for intractable temporal lobe epilepsy at the University of Alabama at Birmingham Epilepsy Center during a 24-month period. All patients underwent standard presurgical investigations and intracranial investigations when needed. Magnetic resonance imaging volumetric studies were performed prior to surgery using previously published techniques. Patients were assessed regularly for postoperative seizure control. Outcome after at least 3 years was evaluated using Engel's classification for epilepsy. The chi2 test was used to compare categorical data. RESULTS: Seventy-eight patients were included in this study. Eight patients were excluded because of inadequate follow-up. Thirty-five patients (44.9%) had unilateral isolated hippocampal atrophy exclusively on MRI volumetry, 29 (37.2%) had unilateral hippocampal atrophy with ipsilateral fornix atrophy, and 6 (7.7%) had isolated fornix atrophy without hippocampal atrophy. Twenty-eight patients (80%) in the unilateral hippocampal atrophy group were seizure free (ie, Engel class 1: patients who are completely seizure free with no aura and who do not receive antiepileptic drugs) compared with 21 patients (73%) in the fornix and hippocampal atrophy group (P =.57). All 6 patients with isolated fornix atrophy achieved an Engel's class 1 outcome. CONCLUSIONS: These findings suggest that identification of fornix atrophy with or without associated hippocampal atrophy is not an important preoperative determinant of surgical outcome. However, in the presence of a normal hippocampus, fornix atrophy may be valuable in predicting seizure-free outcome.

Adolescent↗

PubMed2001

Cerebral atrophy related to corticotherapy in systemic lupus erythematosus (SLE).

The aim of this study was to evaluate the frequency and intensity of cerebral atrophy using CT scanning and the possible relation to corticosteroid therapy or disease in systemic lupus erythematosus (SLE) and to analyse the relationships between cerebral atrophy and activity disease and neuropsychiatric manifestations in lupus patients. We studied 107 consecutive SLE patients (American Rheumatology Association 1982 criteria) who were taking steroid drugs at the time and not selected for any particular manifestation (group 1). A complete clinical, neurological and laboratory evaluation was performed. The American College of Rheumatology's classification for neuropsychiatric manifestations and SLE disease activity index for activity were employed. Group 2 comprised 39 non-SLE patients with oral chronic steroid use (1 mg/k/day for more than 3 consecutive months); 50 normal individuals were the controls (group 3). There were no demographic differences between the groups. Brain CT was performed in all individuals and the frequency and the intensity (minimal, moderate and severe) of atrophy analysed, through well-defined measures and indices, by two neuroradiologists. Cerebral atrophy was significantly more frequent in groups 1 and 2 than in group 3, but with no significant difference between groups 1 and 2. The severity of cerebral atrophy was significantly higher in SLE patients (p<0.05), independent of steroid dose or duration of disease. In both groups no patient presented severe atrophy. Lupus patients with and without cerebral atrophy presented neuropsychiatric manifestations and activity disease in a similar proportion. The more frequent neuropsychiatric manifestation in lupus patients with cerebral atrophy was seizures (p<0.05). Chronic glucocorticoid therapy was responsible for cerebral atrophy, with a comparable incidence in both lupus and non-lupus patients compared to age and gender-matched normal subjects untreated with glucocorticoids. The disease activity was not related to cerebral atrophy in group 1 and seizures were the neurologic manifestation related to cerebral atrophy. The severity of the cerebral atrophy was independent of steroid dose, or duration of treatment. Moreover, the disease itself contributes to the severity of this process, but not to the development of cerebral atrophy.

Adrenal Cortex Hormones↗

PubMed2006

Relationship between external anal sphincter atrophy at endoanal magnetic resonance imaging and clinical, functional, and anatomic characteristics in patients with fecal incontinence.

PURPOSE: External anal sphincter atrophy at endoanal magnetic resonance imaging has been associated with poor outcome of anal sphincter repair. We studied the relationship between external anal sphincter atrophy on endoanal magnetic resonance imaging and clinical, functional, and anatomic characteristics in patients with fecal incontinence. METHODS: In 200 patients (mean Vaizey score, 18 (+/-2.9 standard deviation)) magnetic resonance images were evaluated for external anal sphincter atrophy (none, mild, or severe) by radiologists blinded to anorectal functional test results and details from medical history. Subgroups of patients with and without atrophy were compared for medical history, anal manometry, pudendal nerve latency testing, anal sensitivity testing, external anal sphincter thickness, and external anal sphincter defects. Whenever significant differences were detected, we tested for differences between patients with mild and severe atrophy. RESULTS: External anal sphincter atrophy was demonstrated in 123 patients (62 percent): graded as mild in 79 (40 percent), and severe in 44 patients (22 percent). Patients with atrophy were more often female (P < 0.001) and older (P = 0.003). They had a lower maximal squeeze (P = 0.01) and squeeze increment pressure (P < 0.001). Patients with severe atrophy had a lower maximal squeeze (P = 0.003) and squeeze increment pressure (P < 0.001) than patients with mild atrophy. These effects were not attenuated by potential confounding variables. Patients with atrophy could not be identified a priori by other characteristics. CONCLUSIONS: External anal sphincter atrophy at endoanal magnetic resonance imaging was depicted in 62 percent of patients, varying from mild to severe. Because increasing levels of atrophy were associated with impaired squeeze function, further studies are needed to evaluate whether grading atrophy is clinically valuable in selecting patients for anal sphincter repair.

Age Factors↗

PubMed2006

Is hippocampal atrophy a future drug target?

Hippocampus is the brain structure, vital for episodic and declarative memory. Atrophy of the human hippocampus is seen in a variety of psychiatric and neurological disorders e.g. recurrent depression, schizophrenia, bipolar disorder, post-traumatic stress disorder, epilepsy, head injury, and Alzheimer's disease (AD). Importantly, aging hippocampus also undergoes atrophy. In many instances, for example, AD, the atrophy precedes the development of symptoms while in others, there is a temporal relationship between atrophy and symptomatology. The presence of atrophied hippocampus is one of the most consistent features of many common psychiatric disorders. Several factors contribute to this atrophy. Stress is one of the most profound factors implicated and the mechanisms involve glucocorticoids, serotonin, excitatory amino acids etc. Hippocampal formation as a whole can undergo atrophy or its individual structural components e.g. apical dendrities can exhibit atrophy. Several drugs of unrelated classes have been shown to prevent atrophy indicating heterogenous manner in which hippocampal atrophy is produced. These include, tianeptine (affects structural plasticity in hippocampus and is an effective antidepressant); phenytoin (antiseizure and neuroprotective); fluoxetine (downregulates neurodegenerative enzyme and increases neuroprotective hippocampal S100 beta); lithium (neuroprotective and antiapoptotic); tricyclic antidepressants (increase hippocampal neurogenesis); antipsychotics (reduce hippocampal neuronal suppression); sodium valproate (increases neurogenesis) and mifepristone (antioxidant, neuroprotective and anti-glucocorticoid). Now the most important question is: to what extent does the hippocampal atrophy play a role in the genesis of symptoms of diseases or their progression? And if it does, can we achieve the same degree of prevention or reversal seen in experimental animals, in humans also. An even more important question is: whether the prevention of atrophy would be clinically useful in affecting disease, viz slowing its progression, reducing morbidity, complications or positively affecting the outcome of one or more of its clinically important aspects. If the answer to this is yes, we would have to know at what stage of the disease we use the drugs, dose, duration, follow-up and efficacy. The use of these drugs in the above mentioned conditions can not only test the potential of atrophy as a future drug target, but could also help in learning more about the hippocampus in both health and diseases.

Atrophy↗

PubMed2005

The diagnostic yield of the evaluation for isolated unexplained optic atrophy.

PURPOSE: To report the diagnostic yield for the evaluation of isolated and unexplained optic atrophy. SETTING: Two tertiary care academic neuroophthalmology clinics. DESIGN: Retrospective case series. PARTICIPANTS: Patients with optic atrophy. METHODS: Retrospective review of all charts with the diagnosis of optic atrophy. Included patients were adults with isolated, but unexplained, optic atrophy. Patients were excluded if they were children, had incomplete or inadequate documentation of the findings, had nonneurologically isolated optic atrophy (e.g., other localizing findings), or had a history (e.g., prior neuroimaging study showed a compressive lesion, prior ischemic optic neuropathy) or examination (e.g., central retinal artery occlusion) evidence for an etiology for the optic atrophy. MAIN OUTCOME MEASURE: Results of diagnostic evaluation. RESULTS: A total of 1110 charts with the diagnosis of optic atrophy were reviewed from the 2 participating institutions (368 from the University of Cincinnati and 742 from the University of Iowa). Of these 1110 charts, 91 (8%) with isolated unexplained optic atrophy were included, and 1019 charts (92%) were excluded. Of 91 included patients, 18 (20%) had a compressive lesion causing optic atrophy, and 73 (80%) cases had no etiology for the optic atrophy on neuroimaging. Of the 18 patients with abnormal imaging (e.g., meningioma, pituitary adenoma, craniopharyngioma) studies, 11 had bilateral and 7 had unilateral optic atrophy. Five of the 18 patients had progressive visual loss, 3 had hemianopic visual field loss, and 11 were younger than 50 years old. CONCLUSIONS: Patients with optic atrophy in our study typically had historical or examination findings that led to an etiologic diagnosis. Neuroimaging showed an etiology in 20% of patients. Other laboratory testing did not produce an etiologic diagnosis in the absence of a suggestive history or examination. On the basis of our results, we recommend neuroimaging for all patients with unexplained optic atrophy and consideration for directed laboratory studies only.

Brain Neoplasms↗

PubMed1996

Significance of mesial temporal atrophy in relation to intracranial ictal and interictal stereo EEG abnormalities.

We studied 31 consecutive patients with temporal and extratemporal epilepsy who underwent presurgical evaluation with stereotaxic depth EEG (SEEG) to assess the relationships between amygdalo-hippocampal (AM-HF) atrophy and the location of SEEG seizure onset and SEEG interictal abnormalities. Scalp EEG recordings with sphenoidal electrodes had shown bitemporal ictal or interictal epileptic abnormalities in all. Patients underwent high quality MRI scans, including MRI volumetric measurements of mesial temporal structures. None had foreign tissue lesions. The final conclusions of the SEEG investigation coincided with the lateralization obtained by MRI volumetric measurements in the eight patients who had significant unilateral atrophy of the amygdala, hippocampus or both (> 2 SD below the mean of controls). In these patients with unilateral atrophy, all or > 75% of clinical seizures originated from the atrophic side. The seven patients with bilateral, but significantly asymmetrical, mesial atrophy had bilateral seizure onsets with > 70% originating from the more atrophic side in four, from the less atrophic side in two, and without predominance in one. The one patient with severe bilateral symmetrical atrophy had seizures originating equally from both sides. Five patients had no atrophy on MRI, but depth electrodes revealed predominant unilateral ictal temporal onsets in four of them. There was no significant correlation between the frequency of SEEG interictal spikes and the amount of AM-HF atrophy. However, we found a significant correlation between the severity of SEEG background disturbance in AM and HF and the degree of atrophy of these structures. Patients with unilateral atrophy were more frequently free of seizures after surgery than those with bilateral or no atrophy (P < 0.05). We conclude that unilateral mesial atrophy predicts ipsilateral mesial SEEG seizure onset despite bitemporal extracranial EEG foci. However, in patients with significant bilateral mesial atrophy, SEEG seizures may originate from either side, even in the presence of significant asymmetry. Finally, the identification of unilateral mesial atrophy has prognostic importance.

Adult↗

PubMed2001

Rates of global and regional cerebral atrophy in AD and frontotemporal dementia.

OBJECTIVE: Serial registered MRI provides a reproducible technique for detecting progressive cerebral atrophy in vivo and was used to determine if there were differences between the rates of cerebral atrophy in AD and frontotemporal dementia (FTD). METHODS: Eighty-four patients with dementia (54 AD and 30 FTD) and 27 age-matched control subjects each had at least two volumetric MR scans. Serial scans were positionally matched (registered), and brain volume loss was determined by calculation of the brain boundary shift integral. RESULTS: There was a difference between the rates of whole-brain atrophy in patients (mean annual volume loss 2.7% of total brain volume) and in control subjects (mean annual volume loss 0.5%). AD and FTD were associated with different rates of atrophy (mean annual losses 2.4 and 3.2%). The range of atrophy rates in the FTD group (0.3 to 8.0%) greatly exceeded that in the AD group (0.5 to 4.7%). Frontal-variant FTD was associated with a wider range of atrophy rates than temporal-variant FTD. Analysis of regional brain atrophy rates revealed that there was widespread symmetrically distributed cerebral volume loss in AD, whereas in frontal FTD there was greater atrophy anteriorly and in temporal FTD the atrophy rate was greatest in the left anterior cerebral cortex. CONCLUSIONS: Both AD and FTD patients had increased rates of brain atrophy. Whereas the patients with AD were associated with a relatively restricted spread of atrophy rates, the greater spread of rates observed in the patients with FTD may reflect the heterogeneity of disease in FTD, with differences observed between frontal and temporal FTD. Increased rates of whole-brain atrophy did not discriminate AD from FTD, but analysis of regional atrophy rates revealed marked differences between patient groups.

Aged↗

PubMed1989

[Relationship between condylar atrophy and tooth loss in stomatognathic dysfunction].

In our previous study, we concluded normal subjects did not present an abnormal morphology of condyle, while 30% of stomatognathic dysfunction patients revealed abnormality, and especially about 20% presented atrophy. In this study, we selected 146 patients with stomatognathic dysfunction and analysed patients with atrophy in condyle comparing patients without atrophy. We obtained following results. 1. 37 patients (25%) with dysfunction showed atrophy in condyle. Among them, 15 patients showed bilateral atrophy, and 22 showed unilaterally. 2. Among 22 patients with unilateral atrophy in condyle, 15 patients (68%) showed correspondence between symptomatic side and atrophy side. 3. Among 37 patients with atrophy in condyles, 30 patients (81%) showed organic changes in TMJ components. 4. Mean age of atrophy (+) group was significantly younger than that of atrophy (-) group. 5. No significant relationship was observed between the distinction of sex and atrophy existence in condyle. 6. Significant relationship was observed between loss of lower first molar and atrophy existence in condyle. Most of the patients of atrophy (+) group lost their lower first molars in growth period of TMJ components from mixed dentition through puberty and left them without restoration.

Atrophy↗