Focal Cortical Atrophy Research Articles

Epileptic seizures in subcortical vascular encephalopathy

Cerebrovascular disease is one of the most common causes of epilepsy in the elderly. Most of the studies published relate to cortical infarction, subarachnoid, and intracranial hemorrhage, whereas the incidence of epilepsy from subcortical ischemia, i.e. deep lacunar infarctions and diffuse white matter lesions, is obscure. Therefore, we prospectively examined 18 patients with the precisely defined diagnosis of subcortical vascular encephalopathy (SVE), who were admitted to our hospital due to epileptic seizures (group A), and compared them to a similarly selected group matched for age, sex, risk factors, and neurological deficits with an equivalent severity of SVE but without seizures (group B). Subcortical lacunar infarctions were significantly more frequent in group A than group B ( 15 18 versus 4 18 , p < 0.001), whereas neither the extension, degree, distribution of periventricular white matter changes, nor the presence of internal hydrocephalus, focal or diffuse cortical atrophy showed any statistical significance. However, a temporal constant theta or delta EEG focus was present in 10 18 patients in group A but only in 1 18 patients from group B (p ⩽ 0.005). 10 18 patients developed epilepsy with further seizures during follow-up. The association of SVE, multiple subcortical lacunas, and temporal EEG abnormalities are suggestive for an increased risk for epileptic seizures, which is particularly important for the treatment of patients with SVE if uncertain paroxysmal episodes occur, e.g. transient ischemic attacks, seizures, or cardiac syncope.

Heterogeneity in progressive aphasia due to focal cortical atrophy. A clinical and PET study

Heterogeneity in progressive aphasia due to focal cortical atrophy. A clinical and PET study

MRI of the brain in chronic carbon monoxide poisoning.

We examined 13 patients with chronic carbon monoxide (CO) poisoning by magnetic resonance imaging (MRI); all of them had been in an explosion in a coal mine 25 years previously. Symmetrical globus pallidus lesions were observed in 12, as was degeneration of the white matter, with focal cortical atrophy. The temporal parietal and occipital lobes were usually affected, the parietooccipital region being the most frequently and extensively damaged. Of the 12 patients with white matter degeneration 7 had definitely asymmetrical cortical and subcortical lesions. There were 6 patients with dilated temporal horns, probably due to atrophy of the hippocampal gyri. A history of CO inhalation and an awareness of the typical distributions of lesions are important for recognition of the effects of CO poisoning, especially when patients are in the chronic stage.

The case of aphasia or neglect after striatocapsular infarction

The occurrence of aphasia or neglect was related to anatomo-structural (CT/MRI), functional [regional cerebral blood flow (rCBF)] and pathogenetic features [duration of middle cerebral artery (MCA) occlusion and degree of cortical leptomeningeal anastomoses] in 57 cases (26 with and 31 without aphasia or neglect) with strictly subcortical infarcts of one defined type, i.e. striatocapsular infarcts. No distinct pattern of language disturbances was found. Aphasic syndromes did not differ in the amount of involvement of the putamen, pallidum, head of caudate nucleus and white matter. Patients with aphasia or neglect had larger infarcts than those without. However, there was no specific involvement of the basal ganglia, the internal capsule or the deep white matter in patients with aphasia or neglect. Patients with aphasia or neglect had a significantly longer duration of MCA occlusion and mostly poor leptomeningeal collaterals. The cortical rCBF was significantly decreased in the cortical MCA territory in the patients with aphasia or neglect only. The rCBF remained low at follow-up after 1 year and corresponded to focal cortical atrophy on MRI, although neglect had subsided completely in all patients and aphasia had improved considerably in almost 75% of the cases. Aphasia or neglect after striatocapsular infarcts are most likely due to selective neuronal loss of the cerebral cortex due to prolonged MCA occlusion and insufficient collateral blood flow. Individual differences in recovery from aphasia after striatocapsular infarction can be explained in terms of the number of surviving cortical neurons.

Clinical studies on renovascular hypertension with bilateral renal artery stenosis

Clinical studies were performed on 7 renovascular hypertensive patients (3 male and 4 female, mean age 50.6 +/- 18.6) with bilateral renal artery stenosis. Duration of hypertension ranged from 2 months to 24 years (mean 6.1 +/- 8.2 years) before evaluation. All had stenosis or occlusion of both main renal arteries or these branches shown by arteriography. In 4 of the 7 patients atheromatous stenosis or occlusion was present; the remaining two had aortitis syndrome and one had fibromuscular hyperplasia. Of the 7 patients operated, two who had both negative renal renin study and ureteric catheterization study; one was failure after bilateral percutaneous transluminal angioplasty (PTA), and another one was improved after axillo-femoral bypass operation. In one patient with positive results of both studies an area of focal cortical atrophy was present in upper part of the left kidney. The patient, therefore, underwent partial nephrectomy the left kidney but failed to have decrease of blood pressure and was subsequently treated with antihypertensive medications. In the remaining four patients operated, two who had both positive renin and catheterization studies preoperatively were cured or improved after PTA in negative side and nephrectomy of positive side kidney. Other two patients with contradictory results of renin and catheterization studies underwent, PTA of the renal artery of the kidney with the highest renin levels. But their hypertension was maintained despite sufficient dilatation of the renal artery and PRA from the contralateral kidney was noted to be markedly increased after PTA. Therefore, nephrectomy of the contralateral nonfunctioning contracted kidney was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

CT-scanning and magnetic resonance imaging in idiopathic spasmodic torticollis.

Twenty-five consecutive patients with idiopathic spasmodic torticollis (IST) were investigated with computerized tomography (CT) or magnetic resonance imaging (MRI) of the brain. In only six patients (24%) did CT or MRI reveal brain pathology (focal cortical atrophy and lacunary infarcts). No consistent pathological pattern was detected. Consequently, CT and MRI of the brain provides little diagnostic information in this disorder.

The role of apoptosis in the development of renal cortical tubular atrophy associated with healed experimental renal papillary necrosis

An animal model of chronic analgesic nephropathy, in which renal papillary necrosis was induced by the administration of a single injection of bromoethylamine 2-hydrobromide in male Sprague-Dawley rats, was used to investigate the pathogenesis of the atrophy of tubules that leads to cortical atrophy or 'scarring' in analgesic nephropathy. One of the major objectives was documentation of the participation of apoptosis, a distinctive mode of cell death, in the process of cortical tubular atrophy. Control and treated groups of animals were studied at 2 wks, and at subsequent monthly intervals up to 4 mths. At each time, light microscopy and ultrastructure were used to relate changes in cellular pathology to alterations in renal mass. Apoptosis was quantitated in paraffin sections, and autoradiographic identification of cells showing tritiated thymidine uptake was used as an indication of cell proliferation. In animals with total renal papillary necrosis (RPN), focal or diffuse cortical atrophy developed, the extent of which appeared to be proportional to the extent of the RPN. Renal mass was reduced only in those kidneys that developed extensive, diffuse lesions. Compensatory renal growth occurred in the areas of healthy tissue adjacent to the foci of atrophy, with both cellular hyperplasia and hypertrophy playing roles in its development. One of the prominent cellular events was the appearance of apoptotic cells and bodies, with invading intraepithelial macrophages involved in their phagocytosis and degradation. We propose that this form of cell death plays an important role in the pathogenesis of cortical atrophy. Current descriptions of the cortical lesions that occur in analgesic nephropathy refer to the changes as 'scars'. Although the focal lesions have a macroscopic appearance that resembles scars, the results of the present study indicate that usage of this terminology may be misleading, since scarring is often described after severe tissue injury or necrosis, which was not identified in the present study.

Abstracts

An animal model of chronic analgesic nephropathy, in which renal papillary necrosis was induced by the administration of a single injection of bromoethylamine 2-hydrobromide in male Sprague-Dawley rats, was used to investigate the pathogenesis of the atrophy of tubules that leads to cortical atrophy or 'scarring' in analgesic nephropathy. One of the major objectives was documentation of the participation of apoptosis, a distinctive mode of cell death, in the process of cortical tubular atrophy. Control and treated groups of animals were studied at 2 wks, and at subsequent monthly intervals up to 4 mths. At each time, light microscopy and ultrastructure were used to relate changes in cellular pathology to alterations in renal mass. Apoptosis was quantitated in paraffin sections, and autoradiographic identification of cells showing tritiated thymidine uptake was used as an indication of cell proliferation. In animals with total renal papillary necrosis (RPN), focal or diffuse cortical atrophy developed, the extent of which appeared to be proportional to the extent of the RPN. Renal mass was reduced only in those kidneys that developed extensive, diffuse lesions. Compensatory renal growth occurred in the areas of healthy tissue adjacent to the foci of atrophy, with both cellular hyperplasia and hypertrophy playing roles in its development. One of the prominent cellular events was the appearance of apoptotic cells and bodies, with invading intraepithelial macrophages involved in their phagocytosis and degradation. We propose that this form of cell death plays an important role in the pathogenesis of cortical atrophy. Current descriptions of the cortical lesions that occur in analgesic nephropathy refer to the changes as 'scars'. Although the focal lesions have a macroscopic appearance that resembles scars, the results of the present study indicate that usage of this terminology may be misleading, since scarring is often described after severe tissue injury or necrosis, which was not identified in the present study.

HETEROGENEITY IN PROGRESSIVE APHASIA DUE TO FOCAL CORTICAL ATROPHY

Six patients with a slowly progressive aphasic disorder due to degenerative cortical disease are reported. The length of history varied from 18 months to 6 years. In 5 patients, there was a naming deficit, associated in 4 of these with some abnormalities in comprehension. One patient had a progressive history of reduced speech output, which was associated with an orofacial dyspraxia. All patients were studied neuropsychologically, and in addition regional cerebral metabolism was measured using position emission tomography. A localized left hemisphere deficit was found in all patients except 1, who had the longest history and the most profound clinical deficit, and who also had right hemisphere hypometabolism. The major brunt of the deficit was in the anterior portion of the left temporal lobe in all but 1 case, the patient with poor speech output who had a more severe left posterior frontal deficit. These findings suggest that in progressive aphasia due to focal cortical atrophy there is heterogeneity in the clinical presentation and anatomical site of the deficit, with possible implications for the underlying aetiology.

Potassium reduction of lithium-induced histological changes of the rat kidney

The effects of a high potassium content in the diet on the development of lithium-induced histological and functional changes of the kidneys were studied in rats. Lithium was administered with the food for periods varying from 3 to 12 weeks in two dose levels leading to serum lithium concentrations of 0.5–0.8 and 0.9–1.3 mmol/liter, respectively. Histological changes were assessed by light microscopy and functional disturbances by determination of water intake and the intake of a 0.46 m NaCl solution. Lithium administration led to flattening of the tubular epithelium and widening of the tubular lumens in the distal convoluted tubules and collecting ducts. Focal cortical nephron atrophy and early stages of interstitial fibrosis developed in some rats given lithium for 9 to 12 weeks. Administration of a potassium-rich diet reduced the morphological changes in the distal parts of the nephron significantly, most pronounced in the kidneys of rats given the lowest lithium dosage. Potassium also diminished lithium-induced polyuria and the requirement for sodium. The results suggest a general preventive effect of potassium against lithium-induced functional and morphological changes of the kidney.

Electroencephalography and computerized transaxial tomography in patients with temporal lobe epilepsy.

Computerized transaxial tomography was carried out on 112 patients with partial seizures with complex symptomatology. Structural abnormalities were defined in 33% of their studies: tumors in 8 patients, diffuse cerebral atrophy in 2, focal cortical atrophy in 27 and vascular abnormality in 1 case.

Computerized transaxial tomography in the evaluation of patients with focal epilepsy.

Computerized transaxial tomography was carried out on 50 consecutive unselected patients referred to a neurologic practice for evaluation of focal epilepsy. Structural abnormalities were defined in 35.3 percent of these studies: porencephalic cysts in six patients, diffuse cerebral atrophy in five, cerebral hemiatrophy in three, focal cortical atrophy in two, neoplasms in two, hydrocephalus in one patient, and cerebeller hypoplasia in one. Computerized transaxial tomography is a useful outpatient procedure for evaluation and follow-up of patients with focal seizure disorders.

RADIUM AND CANCER

<h3>OBJECTIVE</h3> To describe the clinical, neurophysiological, and MRI findings in 10 patients with primary lateral sclerosis (PLS). <h3>RESULTS</h3> The course of the disease was very slowly progressive. Spasticity due to upper motor neuron dysfunction was the most prominent sign, but EMG showed slight lower motor neuron signs, such as a mixed pattern on maximal voluntary contraction and enlarged motor unit potentials. One patient had clinically mild lower motor neuron involvement. Central motor conduction times (CMCT) were more prolonged in PLS than is the case in ALS. Minor sensory signs were found on neurophysiological examination, comparable with those in ALS. In four patients serum creatine kinase activity was raised. On MRI cortical atrophy was seen, most pronounced in the precentral gyrus and expanding into the parietal-occipital region. <h3>CONCLUSIONS</h3> PLS is a distinct clinical syndrome, part of the range of motor neuron diseases. Besides pronounced upper motor neuron symptoms, mild lower motor neuron symptoms can also be found, as well as (subclinical) sensory symptoms. PLS can be distinguished from ALS by its slow clinical course, a severely prolonged MEP, and a more extensive focal cortical atrophy.