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PubMed1999

Crossed cerebellar diaschisis: the role of motor and premotor areas in functional connections.

The authors assessed the relationship between crossed cerebellar diaschisis (CCD) and cortico-pontine cerebellar pathway (CPCP) damage in 29 chronic supratentorial infarct patients to elucidate the role of motor and premotor areas for functional cerebro-cerebellar connections. The CCD rate was calculated from side-to-side cerebellar count differences on 123I-IMP single-photon emission computerized tomography images. Neuronal damage was estimated by the three scores of computed tomography density from equal to normal brain tissue (score 0) to equal to cerebrospinal fluid (score 2) in the 4 major regions on CPCP; frontal association, motor and premotor, sensory and parietal associations, and the posterior limb of the internal capsule. Two-factor factorial ANOVA by the score and the region revealed significant differences of the CCD rate in the score factor (score 0 or 1 vs. score 2, p = < 0.05) and the independency of these two factors. Categories determined by the scores in each region were analyzed by multiple stepwise regression analysis using the theory of quantification I, in which significant correlation only between CCD and the necrotic density (score 2) in motor and premotor areas were demonstrated (r = 0.515, p = < 0.05). The authors conclude that neuronal loss in motor and premotor areas seem to contribute significantly to functional cerebro-cerebellar disconnections.

Adult↗
PubMed1991

The G. L. Brown lecture. Adventures in anaesthesia.

The results presented in this lecture show that anaesthetic agents impede the transfer of information from the periphery to the cerebral cortex. This is shown both as a reduction in the amplitudes of the initial positive and negative waves of the cerebral cortical response evoked by simulation of the periphery and as an increase in the latency of this response. This effect is most probably a prime effect of anaesthesia since (a) it is common to all the anaesthetics used, (b) the potency of the anaesthetics is directly proportional to their lipid solubility, and (c) the effect is reversed by high ambient pressures. The major site at which information transfer is most susceptible to the action of anaesthetics is at the level of the ventrobasal thalamus, although the cells in cortical layer V also appear to have an enhanced susceptibility to anaesthetic action. This latter observation is seen both in whole animal and cortical slice preparations. None the less, the first site of synaptic transfer at which anaesthetics exert a profound effect is upon the monosynaptically generated responses of ventrobasal thalamic neurones to cuneothalamic input. A possible mechanism of action for anaesthetic agents acting at this site would be upon a hypothetical cortico-thalamic-reticular-thalamic loop with the theoretical ability to control the responsiveness of the ventrobasal thalamic cells. This action was proposed both from the activity of neurones in response to anaesthetic agents and the anatomical arrangement seen in the thalamus. The thalamic reticular nucleus is a curved sheath of cells situated between the internal capsule and the external medullary lamina, capping and bounding laterally the specific nuclei of the dorsal thalamus. There is both anatomical and physiological evidence that the thalamic reticular nucleus comprises part of the thalamic reticular formation: its cellular structure also resembles that of the brain stem regions of the reticular formation (Ramon-Moliner, 1975). Early degeneration and Golgi studies showed that ascending fibres from the medial parts of the pontine and mesencephalic components of the brain stem reticular formation innervated the thalamic reticular nucleus ventrally, by penetrating the zona incerta, and dorsally, via the intralaminar and dorsal thalamic nuclei (Scheibel & Scheibel, 1958). These observations have been confirmed and extended more recently and it appears that the major innervation of the thalamic reticular nucleus occurs via the ventral route which follows the entire course of the reticular nucleus. No fibres ascending from the dorsal column lemniscal system, the spino-cervico-lemniscal system or the spinothalamic tract have been observed to terminate within the thalamic reticular nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia↗
PubMed1969

Echo-location of bats after ablation of auditory cortex.

1. Echo-location of blinded Yuma bats (Myotis yumanensis) was studied after ablation of the auditory cortex (A.C.). A task of obstacle-avoidance was given to the bats. Hits and misses of strands were counted, and orientation sounds emitted by the bats during flight were recorded.2. After bilateral ablation of A.C., two bats out of six failed to avoid even large obstacles such as 3.7 mm strands and wall. These bats emitted orientation sounds at a rate of 10-15/sec during flight, but did not change that rate before crossing the obstacles and crashed into them. In these bats, other cortical areas in addition to A.C. were probably ablated.3. In three bats out of six, obstacle-avoidance performance was quite normal. These bats avoided even 0.2 mm strands with orientation sounds, the repetition rate of which was systematically increased before crossing the obstacles. In two of them, the dorsal half of the inferior colliculus (I.C.) was bilaterally ablated in addition to A.C. But ability to avoid the obstacles was not impaired at all. Their cerebral cortices did not show the normal positive-negative diphasic potential change in response to tonal stimuli, although the normal diphasic potential change was retained in A.C. of bats which could not echo-locate as a result of bilateral ablation of the main nucleus of I.C. A.C. appeared to be not essential for echo-location.4. Unilateral ablation of A.C. and the internal capsule had no effect on echo-location, but bilateral ablation of them usually resulted in death from operational trauma.5. It was suggested that A.C. was less important for sound localization in bats than in cats.

Journal Article↗
PubMed1990

Corticospinal volleys evoked by anodal and cathodal stimulation of the human motor cortex.

1. In fifteen neurologically normal subjects, corticospinal volleys evoked by transcranial stimulation of the motor cortex were recorded from the spinal cord using epidural electrodes in the high-thoracic and low-thoracic regions during surgery to correct scoliosis. 2. Anodal stimulation at the vertex produced complex corticospinal volleys that could be recorded at both sites, with multiple waves analogous to the D and I waves documented in animal experiments. These volleys were of higher amplitude when the cathode was 7 cm lateral to the vertex rather than 7 cm anterior. There were no differences in conduction time between the two recording sites for D and I waves, when these waves could be identified at the low-thoracic site. 3. Anodal stimuli of 150 V commonly produced a descending volley containing a single peak at both recording sites. Modest increases in stimulus intensity to 225-375 V produced a peak 0.8 ms in advance of the wave of lowest threshold in thirteen subjects and, in seven subjects, further increases produced an additional peak 1.7 ms in advance of the first-recruited wave. The early peaks increased in size with stimulus intensity, replacing the first-recruited wave. These results suggest that the site of impulse initiation with electrical stimulation of the motor cortex shifts from superficial cortex to deep structures, approximately 5 and 10-11 cm below the cortex. These sites are probably the internal capsule and the cerebral peduncle. 4. With cathode at the vertex and anode over the 'hand area' the response of lowest threshold occurred at the latency of the anodal D wave but could not be recorded at the low-thoracic site, suggesting that it was generated by the anode over the 'hand area'. Slightly higher intensities induced a 'cathodal D wave' and still higher intensities produced late peaks at latencies of anodal I waves. These cathodal D and I waves involved axons innervating lumbar segments. There was no evidence that cathodal stimulation preferentially produced I waves. Cathodal stimulation at the vertex with the anode 7 cm anteriorly produced similar results: D waves were produced at relatively low intensities, but I waves appeared at relatively high stimulus intensities if at all.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1991

Membrane properties and synaptic responses of rat striatal neurones in vitro.

1. A tissue slice containing a section of striatum was cut obliquely from rat brain so as to preserve adjacent cortex and pallidum. Intracellular recordings were made from 368 neurones, using either conventional or tight-seal configurations. 2. Two types of neurone were distinguished electrophysiologically. Principal cells (96%) had very negative resting potentials (-89 mV) and a low input resistance at the resting membrane potential (39 M omega): membrane conductance (10 nS at -65 mV) increased within tens of milliseconds after the onset of hyperpolarization (99 nS at -120 mV). Secondary cells (4%) had less negative resting potentials (-60 mV) and a higher input resistance (117 m omega at the resting potential): hyperpolarization caused an inward current to develop over hundreds of milliseconds that had the properties of H-current. 3. Most principal cells were activated antidromically by electrical stimulation of the globus pallidus or internal capsule. Intracellular labelling with biocytin showed that principal cells had a medium sized soma (10-18 microns), extensive dendritic trees densely studded with spines and, in some cases, a main axon which extended towards the globus pallidus. 4. Electrical stimulation of the corpus callosum or external capsule evoked a depolarizing postsynaptic potential. This synaptic potential was reversibly blocked by a combination of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) and DL-2-amino-5-phosphonovaleric acid (APV, 30 microM), but was unaffected by bicuculline (30 microM) and picrotoxin (100 microM). The underlying synaptic current had a fast component (time to peak about 4 ms), the amplitude of which was linearly related to membrane potential and which was blocked by CNQX; in CNQX the synaptic current had a slower component (time to peak about 10 ms) which showed voltage dependence typical of N-methyl-D-aspartate (NMDA) receptors. Both currents reversed at -5 mV. 5. Focal electrical stimulation within the striatum (100-300 microns from the site of intracellular recording) evoked a synaptic potential that was partially blocked (45-95%) by CNQX and APV: the remaining synaptic potential was blocked by bicuculline (30 microM). The bicuculline-sensitive synaptic current reversed at the chloride equilibrium potential. 6. The findings confirm that the majority of neostriatal neurones (principal cells, medium spiny neurones) project to the pallidum and receive synaptic inputs from cerebral cortex mediated by an excitatory amino acid acting through NMDA and non-NMDA receptors. These cells also receive synaptic inputs from intrinsic striatal neurones mediated by GABA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Inhibitory synaptic potentials in guinea-pig substantia nigra dopamine neurones in vitro.

1. The properties of stimulus-evoked and spontaneous inhibitory synaptic potentials were examined in guinea-pig substantia nigra dopamine neurones in sagittal and coronal midbrain slices in the presence of glutamate receptor antagonists. 2. Focal electrical stimulation within the substantia nigra, cerebral peduncle, internal capsule or the striatum evoked a biphasic IPSP consisting of a fast and a slow component, with peak latencies of about 30 and 250 ms, respectively. The fast component was sensitive to chloride injection, reversed polarity at -79.4 +/- 1.1 mV and was blocked by the GABAA receptor antagonists picrotoxin and bicuculline. The slow IPSP reversed at -99.3 +/- 5.4 mV and was blocked by the GABAB receptor antagonists 2-hydroxysaclofen and CGP 35348. 3. Spontaneous IPSPs were observed in many neurones. These events reversed polarity at -77.5 +/- 2.6 mV and were completely blocked by bicuculline and/or picrotoxin. In the presence of TTX, small spontaneous events remained which probably represent miniature IPSPs. In coronal slices, application of 4-aminopyridine raised the frequency of spontaneous IPSPs, presumably by activating nigral interneurones, but failed to reveal spontaneous biphasic IPSPs or spontaneous pure slow IPSPs. 4. The amplitude of the fast IPSPs fluctuated from trial to trial. Amplitude histograms of minimal fast IPSPs displayed evenly spaced peaks, suggesting that synaptic transmission is quantal at these synapses. The measured peak spacing depended on the driving force for Cl-. 5. The fast IPSP showed little or no paired-pulse depression, and in the presence of 2-hydroxysaclofen (400-600 microM) showed paired-pulse facilitation. The GABAB agonist baclofen inhibited the fast IPSP via a presynaptic mechanism. The pharmacologically isolated slow IPSP showed marked paired-pulse facilitation. 6. It is concluded that synaptic inhibition in the substantia nigra is mediated by GABA, is relatively resistant to frequency-dependent depression and is regulated by presynaptic GABAB autoreceptors. Striatonigral and pallidonigral fibres activate both GABAA and GABAB receptors, while intranigral pathways appear to activate predominantly GABAA receptors.

Animals↗
PubMed2004

Ethanol suppression of ventral tegmental area GABA neuron electrical transmission involves N-methyl-D-aspartate receptors.

Ventral tegmental area (VTA) GABA neurons are critical substrates modulating the mesocorticolimbic dopamine system implicated in natural and drug reward. The aim of this study was to evaluate the effects of ethanol on glutamatergic and GABAergic modulation of VTA GABA neuron electrical synaptic transmission. We evaluated the effects of systemic ethanol (0.05-2.0 g/kg i.p.), the N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine (MK-801; 0.05-0.2 mg/kg i.v.), the connexin-36 gap junction blocker quinidine (5-20 mg/kg i.v.), the fast-acting barbiturate methohexital (Brevital; 5-10 mg/kg i.v.), and the benzodiazepine chlordiazepoxide (Librium; 5-10 mg/kg i.v.), as well as in situ VTA administration of NMDA and the GABA(A) receptor agonist muscimol, on VTA GABA neuron spontaneous activity and internal capsule stimulus-induced poststimulus spike discharges (ICPSDs). Systemic ethanol, quinidine, and dizocilpine reduced, whereas local NMDA enhanced, and the systemic and local GABA(A) receptor modulators did not significantly alter VTA GABA neuron ICPSDs. Ethanol potentiated dizocilpine inhibition of VTA GABA neuron ICPSDs, but not quinidine inhibition. In situ microelectrophoretic application of dopamine markedly enhanced VTA GABA neuron firing rate (131%), spike duration (124%), and spike coupling, which were blocked by systemic quinidine. These findings indicate that VTA GABA neurons are coupled electrically via gap junctions and that the inhibitory effect of ethanol on electrical transmission is primarily via inhibition of NMDA receptor-mediated excitation, not via enhancement of GABA receptor-mediated inhibition. Thus, the rewarding properties of ethanol may result from inhibitory effects on excitatory glutamatergic neurotransmission between electrically coupled networks of midbrain GABA neurons.

Animals↗
PubMed1989

Subplate neurons pioneer the first axon pathway from the cerebral cortex.

During the development of the nervous system, growing axons must traverse considerable distances to find their targets. In insects, this problem is solved in part by pioneer neurons, which lay down the first axonal pathways when distances are at a minimum. Here the existence of a similar kind of neuron in the developing mammalian telencephalon is described. These are the subplate cells, the first postmitotic neurons of the cerebral cortex. Axons from subplate neurons traverse the internal capsule and invade the thalamus early in fetal life, even before the neurons of cortical layers 5 and 6, which will form the adult subcortical projections, are generated. During postnatal life, after the adult pattern of axonal projections is firmly established, most subplate neurons disappear. These observations raise the possibility that the early axonal scaffold formed by subplate cells may prove essential for the establishment of permanent subcortical projections.

Animals↗
PubMed1979

Stimulation of human periaqueductal gray for pain relief increases immunoreactive beta-endorphin in ventricular fluid.

Immunoreactive beta-endorphin was measured in the ventricular fluid of six patients with chronic pain. Stimulation of the periaqueductal gray matter in three patients with pain of peripheral origin resulted in significant increases (50 to 300 percent) in the concentration of ventricular immunoreactive beta-endorphin. In three other patients suffering deafferentation dysesthesia, stimulation of the posterior limb of the internal capsule did not alter the concentration of this peptide. These results provide evidence of the release of human immunoreactive beta-endorphin in vivo and suggest that naloxone-reversible pain relief achieved by stimulation of the periaqueductal gray matter may be in part mediated by the activation of beta-endorphin-rich diencephalic areas.

Aged↗
PubMed1977

Striatal efferent fibers play a role in maintaining rotational behavior in the rat.

Rats in which ascending dopamine-containing neurons have been unilaterally destroyed by injections of 6-hydroxydopamine are known to rotate after being injected with apomorphine or L-dopa. The rotation is markedly reduced by either (i) ipsilateral electrocoagulations of the caudate-putamen or internal capsule or (ii) ipsilateral coronal knife cuts immediately rostral to the substantia nigra. Neostriatal efferent fibers, in particular the strionigral projection, appear to be required for the expression of this dopamine-dependent behavior.

Animals↗
PubMed1997

Neurologic disease induced by polytropic murine retroviruses: neurovirulence determined by efficiency of spread to microglial cells.

Several murine leukemia viruses (MuLV) induce neurologic disease in susceptible mice. To identify features of central nervous system (CNS) infection that correlate with neurovirulence, we compared two neurovirulent MuLV, Fr98 and Fr98/SE, with a nonneurovirulent MuLV, Fr54. All three viruses utilize the polytropic receptor and are coisogenic, each containing a different envelope gene within a common genetic background. Both Fr98 and Fr98/SE induce a clinical neurologic disease characterized by hyperexcitability and ataxia yet differ in incubation period, 16 to 30 and 30 to 60 days, respectively. Fr54 infects the CNS but fails to induce clinical signs of neurologic disease. In this study, we compared the histopathology, regional virus distribution, and cell tropism in the brain, as well as the relative CNS viral burdens. All three viruses induced similar histopathologic effects, characterized by intense reactive astrogliosis and microglial activation associated with minimal vacuolar degeneration. The infected target cells for each virus consisted primarily of endothelial and microglial cells, with rare oligodendrocytes. Infection localized predominantly in white matter tracts of the cerebellum, internal capsule, and corpus callosum. The only feature that correlated with relative neurovirulence was viral burden as measured by both viral CA protein expression in cerebellar homogenates and quantification of infected cells. Interestingly, Fr54 (nonneurovirulent) and Fr98/SE (slow disease) had similar viral burdens at 3 weeks postinoculation, suggesting that they entered the brain with comparable efficiencies. However, spread of Fr98/SE within the brain thereafter exceeded that of Fr54, reaching levels of viral burden comparable to that seen for Fr98 (rapid disease) at 3 weeks. These results suggest that the determinants of neurovirulence in the envelope gene may influence the efficiency of virus spread within the brain and that a critical number of infected cells may be required for induction of clinical neurologic disease.

Animals↗
PubMed1983

Lacunar infarcts in polycythaemia with raised packed cell volumes.

Lacunar (small deep cerebral infarcts) infarction is described in association with raised packed cell volumes. Two patients had polycythaemia vera, one stress polycythaemia. They presented with transient ischaemic episodes and were shown by computed tomography to have lacunes deep in the basal ganglia and internal capsule. Such lesions may be caused by small vessel occlusions related to increased viscosity and impaired oxygen consumption by adjacent tissues. Finding a raised packed cell volume in patients with lacunes and transient ischaemic attacks offers a further possibility of treatment.

Aged↗
PubMed2005

Diffusion tensor imaging and voxel based morphometry study in early progressive supranuclear palsy.

BACKGROUND: A comprehensive characterisation of grey and white matter changes in progressive supranuclear palsy (PSP), the second most common extrapyramidal syndrome after Parkinson disease, is still not available. OBJECTIVE: To evaluate grey and white matter changes in mild PSP patients by voxel based morphometry (VBM) and diffusion tensor imaging (DTI), respectively. METHODS: 14 mild PSP patients and 14 healthy controls entered the study and underwent a clinical and neuropsychological evaluation according with a standardised assessment. Each subject had a structural magnetic resonance imaging (MRI) study. Processing analysis of MRI data was carried out according to optimised VBM and fractional anisotropy was determined. RESULTS: Compared with the controls, in PSP patients VBM analysis showed a significant clusters of reduced grey matter in premotor cortex, frontal operculum, anterior insula, hippocampus, and parahippocampal gyrus, bilaterally. With regard to subcortical brain regions, the pulvinar, dorsomedial and anterior nuclei of the thalamus, and superior and inferior culliculum were affected bilaterally. A bilateral decrease in fractional anisotropy in superior longitudinal fasciculus, anterior part of corpus callosum, arcuate fascicolus, posterior thalamic radiations, and internal capsule, probably involving the cortico-bulbar tracts, was present in PSP patients. CONCLUSIONS: These data provide evidence for both grey and white matter degeneration in PSP from the early disease stage. These structural changes suggest that atrophy of cortical and subcortical structures and neurodegeneration of specific fibre tracts contribute to neurological deficits in PSP.

Aged↗
PubMed1983

Dystonia caused by putamino-capsulo-caudate vascular lesions.

Three cases of unilateral dystonia of vascular origin are presented and compared with those in the literature. Damage in the region of the lenticulostriate arteries accounted for ischaemic lesions of the putamino-capsulo-caudate region, the external pallidum probably also being involved. This syndrome appears if the ischaemic accident took place during childhood. The functions of each of these structures and the possible role of the anterior limb of the internal capsule are discussed.

Adolescent↗
PubMed1984

Isolated facial palsy: a new lacunar syndrome.

Three cases of sudden isolated upper motor neuron facial palsy and two with associated pseudobulbar palsy have been seen. All were without significant limb weakness. Computed tomography demonstrated small deep infarcts in the internal capsular/corona radiata regions. Pure upper motor neuron facial palsy may be another lacunar syndrome, due to a lesion in the internal capsule or corona radiata.

Basal Ganglia Diseases↗
PubMed1984

Clinico-anatomical correlations in uncomplicated stroke.

A method for making clinico-anatomical correlations by computer superimposition of brain maps derived from CT scan images, described in a companion paper, was tested in 19 patients with an uncomplicated left hemiparesis due to acute stroke. Eight patients with an isolated left hemiparesis had small lesions in the most rostral part of the right internal capsule. The composite lesion maps of 11 patients whose left hemiparesis was complicated only by spinothalamic sensory loss showed a larger area of damage more caudally in the posterior part of the posterior limb of the capsule, abutting the thalamus. The close correlation between the results obtained by this method and those obtained in previous clinico-pathological studies of patients with uncomplicated strokes, confirms the validity of this mapping technique.

Basal Ganglia↗
PubMed1984

Hemi-dystonia secondary to localised basal ganglia tumour.

An 8-year-old boy with an 18 month history of left limb hemi-dystonia due to a right lenticular nucleus astrocytoma originating in the putamen is reported. Subsequent neuropathological study demonstrated that the tumour was mainly localised to the right lenticular nucleus, with cystic necrosis in the infero-lateral putamen. Solid tumour also infiltrated the right hypothalamus, the anterior commisure and the optic chiasm, and there was perivascular spread into the globus pallidus, internal capsule and roof of the right lateral ventricle. This case, and the few other published reports of symptomatic dystonia due to focal brain lesions verified pathologically, indicate that damage to the lenticular nucleus, and to the putamen in particular, can cause limb dystonia in man.

Astrocytoma↗