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PubMed1994

Inhibitory actions of motor cortex following unilateral brain lesions as studied by magnetic brain stimulation.

Noninvasive transcranial magnetic stimulation (TMS) of the motor cortex not only induces short-latency, motor-evoked potentials (MEP) in contralateral muscles, but also inhibitory phenomena. One type of inhibitory action appears directly after the MEP in contralateral muscles and can be visualized by blockade of tonic, voluntary electromyographic (EMG) activity (postexcitatory inhibition, PI). Evidence for a cortical origin of PI, especially in its later part, was derived from double cortical stimulation in previous studies and is further supported by examination of PI in patients with focal hemispheric unilateral brain lesions in the present study. Thirty patients with different sites of vascular or tumour lesions were studied by TMS. In 6 patients with circumscribed lesions of the primary sensorimotor cortex a significant shortening of PI to contralateral muscles was observed. In 7 patients with focal lesions of the thalamus or internal capsule, in 6 patients with lesions of the premotor cortex and in 5 patients with lesions restricted to the parietal or temporal lobe, a significant prolongation of PI to the contralateral muscles was detected. Six patients with transient ischemic attacks showed either prolongation or shortening of PI. We conclude that PI is predominantly generated in the primary motor cortex, correspondingly its damage causes shortening of PI. In contrast, damage to brain areas that project to the primary motor cortex is followed by prolongation of PI. This remote effect on the primary motor cortex may result from disinhibition of cortical interneurones.

Adult↗
PubMed1985

Few cortical cholecystokinin immunoreactive neurons have long projections.

Cholecystokinin (CCK)-like immunoreactive neurons have been reported to be widely distributed throughout both the neo- and allocortices. In the present study, we were interested in determining whether these cortical CCK neurons have long projections using the double-labeling technique of fluorescence retrograde tracing combined with immunofluorescence for CCK. The distribution of CCK immunoreactive perikarya and fibers was plotted throughout the rostro-caudal extent of the cerebral cortex in both untreated and colchicine-treated albino rats. In the double-labeling experiments, the animals received injections of fluorescent retrograde tracers into cortical, limbic, striatal or thalamic structures, followed one to two days later by colchicine treatment. Brains were subsequently processed for indirect immunofluorescence for CCK-octapeptide and fluorescent dye localization. It was found that 1) a small number of prefrontal cortical CCK neurons were double-labeled with both fluorescent dye and immunofluorescence for CCK after dye injection into midline thalamus, 2) only rarely were cortical CCK neurons double-labeled with injection of tracers into cortex, striatum, or other subcortical structures, 3) numerous midbrain CCK neurons were double-labeled after dye injection into prefrontal cortex and anterior cingulate cortex. and 4) colchicine or cannula injection damage to cortical forebrain tracts (corpus callosum, internal capsule, external capsule, anterior commissure) resulted in the appearance of numerous CCK immunoreactive fibers not normally seen in the undamaged tracts. Although the possibility remains that cortical CCK neurons may be refractory to transport of retrograde tracers, these results suggest that CCK-like immunoreactive neurons of the rat cerebral cortex are predominantly local circuit neurons and that only minor cortico-cortical and cortico-subcortical CCK-containing projections exist.

Animals↗
PubMed1988

Striatal influences on paravermal cerebellar activity.

Units were recorded extracellularly in paravermal cortex (lobule VI) of the cerebellum of chloralose anesthetized cats. Electrical stimulation of the striatum evoked excitation followed by inhibition in these neurons. In addition, the somatosensory properties of these cells were also affected by the striatum. A conditioning-test paradigm (C-T) was used in which conditioning stimulation was applied to the striatum. Test responses were evoked in cerebellar neurons by facial stimulation. As a function of the C-T interval, striatal stimulation could either enhance or suppress the test facial responses. In another procedure, a moveable electrode was used to map the thresholds for affecting the cerebellum from different points in the striatum. The lowest mean threshold was in the putamen followed respectively by the internal capsule and caudate nucleus. Control experiments suggested that striatal effects on the cerebellum were due neither to extra-striatal current spread nor antidromic activation of corticostriatal fibers. These data were discussed with regard to models of striatal motor functioning that indicate a role in postural control and sensory gating.

Action Potentials↗
PubMed1994

Globoid cell leukodystrophy: comparison of neuropathology with magnetic resonance imaging.

Previous imaging studies in infants with globoid cell leukodystrophy (GLD) using computed tomography have demonstrated a reduction in cerebral white matter and increased density symmetrically in the regions of the thalami, periventricular white matter, and the internal capsules. Correlation of these findings with morphologic studies at necropsy has not been made. In particular, deposition of calcium has not been described. We have evaluated two children with GLD confirmed by the absence of leukocyte galactosylceramide beta-galactosidase activity using repeated magnetic resonance (MR) scans in each and correlated the imaging results with post-mortem analyses in one. Neuropathologic examination revealed abnormalities typical for GLD. In addition to the absence of normal myelination throughout cerebral and cerebellar white matter, MR images demonstrated the presence of a paramagnetic effect in the regions of the thalami, corona radiata, and centra semiovale. We have observed in histologic preparations from these areas a dense accumulation of globoid cells and some calcium, which we suggest may be responsible for producing the paramagnetic effect.

Brain↗
PubMed1995

Acquired hepatocerebral degeneration in a liver transplant recipient.

A 47-year-old-man lapsed into coma 12 h after liver transplantation, and remained comatose until death 38 days later. Prior to transplantation he had repeated episodes of hepatic encephalopathy, but no fixed neurological signs. Autopsy revealed typical features of acquired hepatocerebral degeneration with diffuse but patchy pseudolaminar cortical necrosis, variable amount of neuronal loss in the cerebral cortex, basal ganglia and other areas, and proliferation of Alzheimer type II glia. In addition, there was central pontine and extensive extrapontine myelinolysis involving the lateral and medical geniculate bodies, the thalamus, internal capsule, fornix, mamillothalamic tract, white matter bundles in the caudate and pallidum, the oculomotor nuclei and the foliar white matter of the cerebellum. The distinction between myelinolytic lesions and lesions due to hepatocerebral degeneration was not always clear. Although neurological complications and brain lesions are rather common after liver transplantation, there have been no reports of acquired hepatocerebral degeneration in liver transplant recipients. Our data lend support to the idea that a single prolonged comatose episode, due to hepatic dysfunction, may induce permanent parenchymal brain damage.

Autopsy↗
PubMed1995

Intracerebral vascular occlusion in familial erythrophagocytic lymphohistiocytosis: a case report of two siblings.

Neuropathological findings in two siblings with familial erythrophagocytic lymphohistiocytosis (FEL) are reported. Case 1 showed the typical neuropathological findings of FEL with lymphohistiocytic infiltration of the leptomeninges and perivascular spaces. A characteristic erythrophagocytosis was detected in inguinal lymph nodes, lung and bone marrow. Case 2 revealed calcification and necrotic lesions in the brain. In the necrotic areas, parenchymal calcification, vascular medial calcification, and occlusion of many vessels due to subendothelial fibrosis were detected. The areas of necrosis correlated with the distribution of occluded vessels. These changes were most prominent in putamen, internal capsule, thalamus and dentate nucleus. Hypercytokinemia is suspected to be the underlying mechanism for the clinical and laboratory findings in patients with FEL, although the relationship to the vascular pathology is unclear.

Arterial Occlusive Diseases↗
PubMed1990

Prominent white matter lesions develop in Mongolian gerbils treated with 100% normobaric oxygen after global brain ischemia.

Carotid arteries were occluded bilaterally for 15 min in two groups of Mongolian gerbils. The first group received 100% oxygen during the first 3 h of reperfusion. During that period, room air was given to the second group. After 3 h, both groups received room air. Brains of gerbils that died within 14 days after occlusion were removed, fixed in formalin and embedded in paraffin. Gerbils that survived 15-28 days were perfused with formalin before their brains were removed and embedded in paraffin. Adjacent, serially cut sections were stained with luxol fast blue (LFB)-H&E, cresyl violet, according to the Bodian method, or immunocytochemically with antisera raised against myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP). In brain sections of gerbils receiving 3 h of 100% oxygen, there were circumscribed white matter lesions in the corpus striatum, lateral thalamus, mesencephalon and posterior limb of the internal capsule. Myelin sheaths were swollen, fragmented and were less intensely stained by MBP antiserum. MBP and LFB-stained myelin fragments were present extracellularly and in macrophages. Many axons in these areas appeared undamaged. Previously described ischemic changes were found in gray matter and some areas of white matter in both groups. However, neurons in the deeper laminae of the cerebral cortex appeared to be better preserved in gerbils given oxygen. The results suggest that hyperoxia, if present immediately after transient brain ischemia, may damage myelin more severely than other cellular elements.

Animals↗
PubMed1990

Axonal swellings in the corticospinal tracts in amyotrophic lateral sclerosis.

In 2 of 16 cases with sporadic amyotrophic lateral sclerosis (ALS) large numbers of axonal swellings were observed in the corticospinal tracts over a region extending from the posterior limbs of internal capsules to the bulbar pyramids. On electron microscopy, these axonal swellings were seen to consist of accumulations of neurofilaments and altered neuronal organelles (mitochondria and secondary lysosomes). Their morphology differed from the spheroids seen in the anterior horn in ALS.

Amyotrophic Lateral Sclerosis↗
PubMed1990

Magnetic resonance imaging in motor neuron disease.

Magnetic resonance imaging (MRI) of the brain was evaluated in 20 patients with motor neuron disease (MND) and in a control group of 11 healthy people. Bilateral increased signal areas of various sizes in the centrum semiovale, corona radiata, internal capsule, pedunculi of midbrain, pons, medulla and even in the frontal lobe, topographically related with the corticospinal tract, were found in 8 out of 20 patients. Three out of 4 patients with progressive bulbar paralysis and 5 out of 11 cases of amyotrophic lateral sclerosis had abnormal MRI. Such MRI abnormalities have neither been found in patients with progressive muscular atrophy nor in controls, suggesting that they may be the hallmark of pyramidal tract degeneration in motor neuron disease.

Adult↗
PubMed1991

Distribution of aromatase-immunoreactive cells in the mouse forebrain.

The distribution of aromatase-immunoreactive cells was studied by immunocytochemistry in the mouse forebrain using a purified polyclonal antibody raised against human placental aromatase. Labeled perikarya were found in the dorso-lateral parts of the medial and tuberal hypothalamus. Positive cells filled an area extending between the subincertal nucleus in the dorsal part, the ventromedial hypothalamic nucleus in the ventral part, and the internal capsule and the magnocellular nucleus of the lateral hypothalamus in the lateral part. The same distribution was seen in the two strains of mice that were studied (Jackson and Swiss), and the number of immunoreactive perikarya did not seem to be affected by castration or testosterone treatment. No immunoreactivity could be detected in the medial regions of the preoptic area and hypothalamus; these were expected to contain the enzyme based on assays of aromatase activity performed in rats and on indirect autoradiographic evidence in mice. Our data raise questions concerning the distribution of aromatase in the brain and the mode of action of the centrally produced estrogens.

Animals↗
PubMed1991

Striatopallidonigral degeneration in Pick's disease: a clinicopathological study of 41 cases.

The frequency and degree of stiatopallidonigral (SPN) degeneration were examined in 41 autopsy cases of Pick's disease. Based on the degree of SPN degeneration, these cases were arranged into four groups: 1) group I (severely degenerate; 19.5%), 2) group II (moderately degenerate; 22.0%), 3) group III (mildly degenerate; 36.5%), and 4) group IV (non-degenerate; 22.0%). 17 of the 41 cases had a definite (moderate to severe) SPN degeneration. The striatum, especially the caudate nucleus, was most frequently and most severely affected, while the internal segment of the globus pallidus was least frequently and least severely affected. In general, the oral portions of the SPN nuclei were more severely involved. In addition, in the putamen and globus pallidus the dorsomedial portions adjacent to the internal capsule were apt to be affected more markedly than the other portions. In the substantia nigra the degeneration tended to be more predominant in the pars reticulata than in the pars compacta, although both were usually involved. In addition, the medial to central portions of the substantia nigra were more vulnerable. In comparing the severely and moderately degenerate groups (groups I and II) with the mildly and non degenerate groups (groups III and IV), the former had more female cases, longer duration of illness, and more third-stage cases. In addition, the former contained more cases with lower brain weight and (predominant) frontal atrophy type, and more atypical cases without Pick bodies, or with symmetrical pyramidal tract degeneration or with combined traumatic lesions. It is notable that in all cases with definite SPN degeneration no extrapyramidal involuntary movements had been detected.

Adult↗
PubMed1988

LCBF values decline while L lambda values increase during normal human aging measured by stable xenon-enhanced computed tomography.

Results of measurements of LCBF and L lambda values utilizing optimal CT-CBF methods under resting conditions are reported among thirty-two neurologically normal volunteers aged between 20 and 88 years. Measurements were made during inhalation of 26-30% stable xenon gas for 8 min and serial scanning utilizing a state-of the-art CT scanner with both eyes closed and ears unplugged. LCBF values for cortical gray matter were lowest in occipital cortex and highest in frontal cortex. Gray matter flow values were also high in subcortical structures with highest values measured in the thalamus. For white matter, highest flow values were measured in the internal capsule. Changes in LCBF and L lambda values were analyzed with respect to advancing age. Significant age-related declines in LCBF values were observed in occipital cortex and frontal white matter. Significant age-related increases in L lambda values were measured in frontal and temporal cortex, caudate nucleus and thalamus. Possible explanations are offered for these age-related increases in L lambda values for gray matter, such as accumulation of lipofuscin in neurons and relative compacting of gray matter with advancing age. The latter increases the numbers of nerve cells sampled per volume of gray matter measured.

Administration, Inhalation↗
PubMed1981

Thalamic bleeding: diagnosis, course and prognosis.

Isolated thalamic bleeding without involvement of the internal capsule or other neighboring structures is extremely rare. Thalamic hemorrhage often leads to bleeding into the ventricular system. The extent of the bleeding is not a valid criterion for prognosis. The chance of survival was found to be poorest in initially comatose patients. CT is eminently suitable for determining the size and position of the hemorrhage and also for the followup of thalamic bleeding. No significant correlation was found between the clinical and CT outcome.

Adolescent↗
PubMed1980

[Clinical, endocrinological, and computerized tomography scans for symmetrical calcification of the basal ganglia (author's transl)].

Symmetrical calcification of the basal ganglia was found in 2% of 8000 computerized tomography (CT) scans. Of 19 cases, only 2 were detectable on conventional skull films. The less prominent calcifications were most often found in the region of the pallidum, the knee of the internal capsule. Also, the lesions were generally symmetrical. Thus these factors must be considered basic morphological characteristics of the pathophysiological process. Additional neurological disorders were present in 6 patients. Neurological symptoms in the remaining 13, when present, depended on the extent of the lesion. The most common finding was tremor, although disturbances of fine motor control, transient lateralizing signs, and seizures were also noted. No particular constellation of symptoms or signs permitted accurate clinical localization of the lesions. The patients could be divided into three groups on the basis of clinical findings: (1) young people with marked cerebral calcinosis ('idiopathic' calcification of basal ganglia), (2) patients with hypoparathyroidism, and (3) older patients with relatively little calcification. Most patients with calcific lesions will be included in the third group. Any calcification of basal ganglia detected by CT scans demands careful evaluation of calcium metabolism.

Adult↗
PubMed1975

[Delayed initiation of voluntary movements after pyramidal lesions in man (author's transl)].

The reaction times for rapid movements in muscles of arm and leg were measured in 20 patients with unilateral lesions of the motor cortex and the internal capsule. Rapid unilateral and bilateral movements after an acoustic signal (click) on the pyramidally paretic side were compared with the normal side. In these patients and in 10 normal subjects, electromyographic and mechanical recordings from symmetrical muscles of both sides were compared. 2. All patients with pyramidal lesions showed in the case of unilateral movements a marked prolongation of motor latency in the affected muscles: compared to the normal side, the movement started 30-160 msec later in muscles contralateral to the lesion of the motor cortex. In contrast, normal subjects showed equal latencies on both sides with maximal differences of 10-20 msec. 3. When movements were executed bilaterally the latency prolongation in the pyramidally paretic muscles was markedly diminished or disappeared in later stages. In most patients the bilateral movements started simultaneously in the normal and the paretic muscles, except in 5 recent lesions of the contralateral motor cortex. 4. The significance of the findings is discussed in terms of the function of the human motor cortex in starting and controlling voluntary movements. It is assumed that the disappearance of latency prolongation when movements are executed bilaterally in patients with unilateral pyramidal lesions can be best explained by homolateral projections of uncrossed pyramidal fibres to the motoneurones. 5. These results, and other observations, suggest that the motor cortex starts and controls voluntary movements via rapidly conducting pyramidal fibres to the motoneurones. This occurs after a preprogramming and a readiness posture is established by other cerebral structures. The prolongation of motor latencies after motor cortex lesions is probably due to a disturbance in the rapidly conducting cortico-spinal projections to spinal motoneurones and interneurones.

Adult↗
PubMed1988

Comparison of brain ribonucleases of rabbit, guinea pig, rat, mouse and gerbil.

The brain ribonucleases of rabbit, guinea pig, rat, mouse and gerbil were investigated by histochemical and biochemical methods. For the localization, the ribonucleases were electrophoretically transferred from cryostat sections to polyacrylamide gels. Elevated ribonuclease activities were found in the cortex, the basal ganglia, the hippocampal formation and the ventricles, whereas the corpus callosum and the internal capsule exhibited lower activities. The total RNA degrading activities of the brain extracts of the different species varied in a wide range. However, a pre-requisite for the measurement of acid soluble degradation products in the test system was the inactivation of endogeneous ribonuclease inhibitors, present in all extracts. Molecular weight analysis by means of SDS-polyacrylamide gel electrophoresis revealed a characteristic set of ribonucleases for each species, consisting of enzymes with different pH-optima.

Animals↗
PubMed1991

Capsular and thalamic infarction caused by tentorial herniation subsequent to head trauma.

Five patients (4 male and 1 female) were observed to have capsular and thalamic infarction ascribed to descending transtentorial herniation (DTH) caused by head injury. A lucid interval immediately after the trauma and the presence of an epidural hematoma (EDH) characterized all five cases. At the time of hospitalization consciousness was seriously impaired and signs of cerebral herniation were apparent. Two to four days after the trauma, low attenuation in the computed tomography (CT) images pinpointed intracerebral damage in the anterolateral part of the thalamus and in the internal capsule on the same side as that of the EDH in three patients, and in the other two patients bilateral thalamic and capsular damage was noted. The low attenuation implicated the perforating arteries, that is the anterior thalamoperforating and anterior choroidal arteries, suggesting infarcted regions caused by occlusion of these arteries. Findings in the present study suggest that arterial occlusion in closed head injury may result from DTH. Moreover, infarction may be attributed to the delayed effects of injury.

Adult↗
PubMed1991

Reversible MRI and CT findings in uremic encephalopathy.

In this 35-year-old woman with chronic glomerulonephritis and uremic encephalopathy, the basal ganglia bilaterally, internal capsules and periventricular white matter showed hypodensity on CT, low signal intensity on T1-weighted MRI and high signal intensity on T2-weighted MRI. Following a series of dialyses, her clinical symptoms and blood chemistry improved. The CT and MRI returned to normal. These reversible abnormalities may be caused by reversible ischemic change, but disorders of cerebral metabolism and uremic toxins may contribute.

Adult↗