Ipsilateral Thalamus Research Articles

Cerebrolysin reduces amyloid-β deposits, apoptosis and autophagy in the thalamus and improves functional recovery after cortical infarction

Focal cerebral infarction causes amyloid-β (Aβ) deposits and secondary thalamic neuronal degeneration. The present study aimed to determine the protective effects of Cerebrolysin on Aβ deposits and secondary neuronal damage in thalamus after cerebral infarction. At 24h after distal middle cerebral artery occlusion (MCAO), Cerebrolysin (5ml/kg) or saline as control was once daily administered for consecutive 13days by intraperitoneal injection. Sensory function and secondary thalamic damage were assessed with adhesive-removal test, Nissl staining and immunofluorescence at 14days after MCAO. Aβ deposits, activity of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1), apoptosis and autophagy were determined by TUNEL staining, immunofluorescence and immunoblot. The results showed that Cerebrolysin significantly improved sensory deficit compared to controls (p<0.05). Aβ deposits and BACE1 were obviously reduced by Cerebrolysin, which was accompanied by decreases in neuronal loss and astroglial activation compared to controls (all p<0.05). Coincidently, Cerebrolysin markedly inhibited cleaved caspase-3, conversion of LC3-II, downregulation of Bcl-2 and upregulation of Bax in the ipsilateral thalamus compared to controls (all p<0.05). These findings suggest that Cerebrolysin reduces Aβ deposits, apoptosis and autophagy in the ipsilateral thalamus, which may be associated with amelioration of secondary thalamic damage and functional recovery after cerebral infarction.

Reorganization of sensory pathways after neonatal hemidecortication in rats

We investigated ascending somatosensory pathways in neonatally hemidecorticated rats. Injection of an anterograde tracer, biotinylated dextran amine (BDA), into the contralesional dorsal root ganglions revealed ipsilateral projections to the dorsal column nuclei (DCN) in hemidecorticated rats as well as in normal rats. Injection of BDA into the DCN on the same side revealed that while most axons projected to the contralateral thalamus, some axons were detected in the ipsilateral thalamus in hemidecorticated rats while such projections were rarely detected in normal rats. The results suggest that aberrant ipsilateral projections of DCN neurons contralateral to the lesion developed after the hemidecortication.

Hyperphosphorylation of tau protein in the ipsilateral thalamus after focal cortical infarction in rats

Hyperphosphorylation of tau has been considered as an important risk factor for neurodegenerative diseases. It has been found also in the cortex after focal cerebral ischemia. The present study is aimed at investigating changes of tau protein expression in the ipsilateral thalamus remote from the primary ischemic lesion site after distal middle cerebral artery occlusion (MCAO). The number of neurons in the ventroposterior thalamic nucleus (VPN) was evaluated using Nissl staining and neuronal nuclei (NeuN) immunostaining. Total tau and phosphorylated tau at threonine 231 (p-T231-tau) and serine 199 (p-S199-tau) levels, respectively, in the thalamus were measured using immunostaining and immunoblotting. Moreover, apoptosis was detected with terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling (TUNEL) assay. It was found that the numbers of intact neurons and NeuN+ cells within the ipsilateral VPN were reduced significantly compared with the sham-operated group, but the levels of p-T231-tau and p-S199-tau in the ipsilateral thalamus were increased significantly in rats subjected to ischemia for 3 days, 7 days and 28 days. Furthermore, the number of TUNEL-positive cells was increased in the ipsilateral VPN at 7 days and 28 days after MCAO. Thus, hyperphosphorylated tau protein is observed in ipsilateral thalamus after focal cerebral infarction in this study. Our findings suggest that the expression of hyperphosphorylated tau protein induced by ischemia may be associated with the secondary thalamic damage after focal cortical infarction via an apoptotic pathway.

Brainstem arteriovenous malformation presenting with dyspraxic handwriting in a young girl

We report the case of a 11-year-old girl who developed an isolated hand-writing disorder with dysgraphia at the beginning of the school year in the sixth grade. A brain magnetic resonance angiography showed a round arteriovenous malformation sited in the left side of the midbrain extending to the ipsilateral medio-basal thalamus. Child neurologists should never neglect a thorough neurological evaluation in case of isolated worsening of handwriting, to rule out possible underlying organic causes.

Vestibular hemispatial neglect: patterns and possible mechanism

Recent reports have suggested that hemispatial neglect may be a vestibular disorder at the cortical level, based on the similarities of symptoms and neural correlates between the two phenomena. If this is the case, peripheral vestibulopathy may lead to hemispatial neglect. However, the etiology of hemispatial neglect in patients with unilateral peripheral vestibulopathy remains unclear. The aims of the present study were to investigate the following: (1) if unilateral peripheral vestibulopathy might cause hemispatial neglect, and if so, (2) whether hemispatial neglect in unilateral peripheral vestibulopathy might be induced by horizontal bias for eye position and body orientation or whether it is secondary to vestibular cortical dysfunction following unilateral peripheral vestibulopathy. Twenty-five consecutive patients with acute vestibular neuritis were recruited at the Dizziness Clinic of Pusan National University Hospital. All participants underwent neglect testing and measurements of horizontal bias for eye position and head and body orientation. Hemispatial neglect occurred in 32 % of patients with unilateral peripheral vestibulopathy. The frequency of contralesional neglect was equal to that of ipsilesional neglect. All patients with hemispatial neglect showed abnormal performance in bisection tasks. The incidence and severity of the horizontal bias of eye position and head and body orientation did not differ between patients with or without hemispatial neglect. Our study demonstrates that hemispatial neglect can develop after acute unilateral peripheral vestibulopathy. Hemispatial neglect after acute unilateral peripheral vestibulopathy may be attributed to damaged vestibular subnuclei, which receive afferents from both peripheral vestibular end organs and the vestibulocerebellum and project to the ipsilateral or contralateral thalamus and vestibular cortex.

Lack of secondary pathology in the thalamus after focal cerebral ischemia in nonhuman primates

Remote regions such as the thalamus undergo secondary degeneration after cerebral ischemia. In rodents, the pathology in the thalamus is characterized by a robust inflammatory reaction, β-amyloid (Aβ) accumulation and calcification. Here we studied whether nonhuman primates subjected to middle cerebral artery occlusion (MCAO) display a similar pathology. Common marmosets (n=4) were subjected to transient MCAO for 3h. Two sham-operated animals served as controls. All animals underwent MRI examination (T2) on postoperative day 7 to assess the location of the infarct. After a 45-day follow-up period, the animals were perfused for histology to evaluate β-amyloid and calcium load in the peri-infarct regions and the thalamus. There was no Aβ or calcium staining in the sham-operated marmosets. The contralateral hemisphere was devoid of Aβ and calcium staining in MCAO animals, except calcium staining in one animal. In the ipsilateral cortex, patchy groups of Aβ-positive cells were observed. Occasional calcium staining was observed in the peri-infarct regions, lesion core, and remote regions such as the substantia nigra. The most important, the thalamus was devoid of any sign of Aβ and calcium aggregation in MCAO animals. Staining for glial fibrillary acidic protein (GFAP) showed marked astrogliosis in the ipsilateral cortex and thalamus. In conclusion, our preliminary study in marmosets did not identify Aβ and calcium pathology in the thalamus following cerebral ischemia as shown in rodents.

Spinal cord stimulation modulates cerebral neurobiology: a proton magnetic resonance spectroscopy study

Although spinal cord stimulation (SCS) is a widely used treatment for chronic neuropathic pain secondary to spinal surgery, little is known about the underlying physiological mechanisms. The primary aim of this study is to investigate the neural substrate underlying short-term SCS by means of (1)H MR spectroscopy with short echo time, in 20 patients with failed back surgery syndrome. Marked increase of γ-aminobutyric acid (GABA) and decrease in glucose in the ipsilateral thalamus were found between baseline situation without SCS and after 9' of SCS, indicating the key role of the ipsilateral thalamus as a mediator of chronic neuropathic pain. In addition, this study also showed a progressive decrease in glucose in the ipsilateral thalamus over time, which is in line with the findings of previous studies reporting deactivation in the ipsilateral thalamic region. The observation of GABA increase and glucose decrease over time in the ipsilateral thalamus may be the causal mechanism of the pain relief due to SCS or an epiphenomenon.

Non-Selective Calcium Channel Blocker Bepridil Decreases Secondary Pathology in Mice after Photothrombotic Cortical Lesion

Experimental studies have identified a complex link between neurodegeneration, β-amyloid (Aβ) and calcium homeostasis. Here we asked whether early phase β-amyloid pathology in transgenic hAPPSL mice exaggerates the ischemic lesion and remote secondary pathology in the thalamus, and whether a non-selective calcium channel blocker reduces these pathologies. Transgenic hAPPSL (n = 33) and non-transgenic (n = 30) male mice (4–5 months) were subjected to unilateral cortical photothrombosis and treated with the non-selective calcium channel blocker bepridil (50 mg/kg, p.o., once a day) or vehicle for 28 days, starting administration 2 days after the operation. Animals were then perfused for histological analysis of infarct size, Aβ and calcium accumulation in the thalamus. Cortical photothrombosis resulted in a small infarct, which was associated with atypical Aβ and calcium accumulation in the ipsilateral thalamus. Transgenic mice had significantly smaller infarct volumes than non-transgenic littermates (P<0.05) and ischemia-induced rodent Aβ accumulation in the thalamus was lower in transgenic mice compared to non-transgenic mice (P<0.01). Bepridil decreased calcium load in the thalamus (P<0.01). The present data suggest less pronounced primary and secondary pathology in hAPPSL transgenic mice after ischemic cortical injury. Bepridil particularly decreased calcium pathology in the thalamus following ischemia.

Detection of remote neuronal reactions in the Thalamus and Hippocampus induced by rat glioma using the PET tracer cis-4-[¹⁸F]fluoro-D-proline.

After cerebral ischemia or trauma, secondary neurodegeneration may occur in brain regions remote from the lesion. Little is known about the capacity of cerebral gliomas to induce secondary neurodegeneration. A previous study showed that cis-4-[(18)F]fluoro-D-proline (D-cis-[(18)F]FPro) detects secondary reactions of thalamic nuclei after cortical infarction with high sensitivity. Here we investigated the potential of D-cis-[(18)F]FPro to detect neuronal reactions in remote brain areas in the F98 rat glioma model using ex vivo autoradiography. Although the tumor tissue of F98 gliomas showed no significant D-cis-[(18)F]FPro uptake, we observed prominent tracer uptake in 7 of 10 animals in the nuclei of the ipsilateral thalamus, which varied with the specific connectivity with the cortical areas affected by the tumor. In addition, strong D-cis-[(18)F]FPro accumulation was noted in the hippocampal area CA1 in two animals with ipsilateral F98 gliomas involving hippocampal subarea CA3 rostral to that area. Furthermore, focal D-cis-[(18)F]FPro uptake was present in the necrotic center of the tumors. Cis-4-[(18)F]fluoro-D-proline uptake was accompanied by microglial activation in the thalamus, in the hippocampus, and in the necrotic center of the tumors. The data suggest that brain tumors induce secondary neuronal reactions in remote brain areas, which may be detected by positron emission tomography (PET) using D-cis-[(18)F]FPro.

Cortical modulation of thalamic function during cortical spreading depression- Unraveling a new central mechanism involved in migraine aura"

The thalamus is a key structure in migraine pathophysiology[1]. Direct cortico-thalamic connections provide important interactions on both cortical and thalamic structures[2]. Cortical spreading depression (CSD), believed to underlie the pathophysiology of migraine aura[3], would be expected to influence sensory responses of thalamic neurons, through such corticothalamic interactions. To investigate this, a CSD was induced while recording neuronal activity from ipsilateral thalamic neurons responding to electrical stimulation of dural vessels. CSD induced a transient increase of spontaneous activity for 30-150s. Following this activity, in 43% of the studied neurons, spontaneous neuronal activity, as well as, Aδ- and C-fiber activity in response to dural vessel stimulation, was significantly enhanced for 15-90min by 94±17%, 27±6% and 109±33%, respectively. In 38% of neurons, spontaneous neuronal firing, Aδ- and C-fiber activity were significantly decreased following CSD by a maximum of 44±3%. Interestingly, none of the short or long-lasting effects of a single CSD within the thalamus were altered following trigeminal ablation. In a different experimental group, multiple waves of K+-induced CSDs significantly inhibited neuronal activity, compared to a single CSD. Thalamic recordings during a single CSD were further compared to CSD-evoked responses in the ipsilateral and contralateral trigeminocervical complex (TCC). CSD induced both inhibitory and excitatory responses on ipsilateral and contralateral second order neurons, through different mechanisms of action, as previously described[4],5. In comparison, CSD induced a higher degree of neuronal activation within the ipsilateral sensory thalamus, compared to the facilitatory evoked-activity of CSD within the TCC (ipsilateral spontaneous activity:94±17% vs 27±11%; C-fiber activity:109±33% vs 36±5%). The data demonstrate that CSD markedly alters neuronal firing of ipsilateral third order thalamic neurons, independent of peripheral trigeminal inputs. This provides a new mechanism by which CSD may indeed induce central head pain via cortico-thalamic circuits and may shed more light on the relationship between aura and headache.

Effects of age on negative BOLD signal changes in the primary somatosensory cortex

In addition to a contralateral activation of the primary and secondary somatosensory cortices, peripheral sensory stimulation has been shown to elicit responses in the ipsilateral primary somatosensory cortex (SI). In particular, evidence is accumulating that processes of interhemispheric inhibition as depicted by negative blood oxygenation level dependent (BOLD) signal changes are part of somatosensory processes. The aim of the study was to analyze age-related differences in patterns of cerebral activation in the somatosensory system in general and processes of interhemispheric inhibition in particular. For this, a functional magnetic resonance imaging (fMRI) study was performed including 14 younger (mean age 23.3±0.9years) and 13 healthy older participants (mean age 73.2±8.3years). All subjects were scanned during peripheral electrical median nerve stimulation (40Hz) to obtain BOLD responses in the somatosensory system. Moreover, the individual current perception threshold (CPT) as a quantitative measure of sensory function was determined in a separate psychophysical testing. Significant increases in BOLD signal across the entire group could be measured within the contralateral SI, in the bilateral secondary somatosensory cortex (SII), the contralateral supplementary motor area and the insula. Negative BOLD signal changes were delineated in ipsilateral SI/MI as well as in the ipsilateral thalamus and basal ganglia. After comparing the two groups, only the cortical deactivation in ipsilateral SI in the early stimulation phase as well as the activation in contralateral SI and SII in the late stimulation block remained as statistically significant differences between the two groups. The psychophysical experiments yielded a significant age-dependent effect of CPT change with less difference in the older group which is in line with the significantly smaller alterations in maximal BOLD signal change in the contra- and ipsilateral SI found between the two groups. Healthy aging seems to be associated with a decrease in intracerebral inhibition as reflected by smaller negative BOLD signal changes during fMRI tasks. This finding could constitute an important link between age-related neurophysiological changes and behavioral alterations in humans.

Age-dependent alterations in cAMP signaling contribute to synaptic plasticity deficits following traumatic brain injury

The elderly have comparatively worse cognitive impairments from traumatic brain injury (TBI) relative to younger adults, but the molecular mechanisms that underlie this exacerbation of cognitive deficits are unknown. Experimental models of TBI have demonstrated that the cyclic AMP-protein kinase A (cAMP-PKA) signaling pathway is downregulated after brain trauma. Since the cAMP-PKA signaling pathway is a key mediator of long-term memory formation, we investigated whether the TBI-induced decrease in cAMP levels is exacerbated in aged animals. Aged (19months) and young adult (3months) male Fischer 344 rats received sham surgery or mild (1.4–1.6 atmospheres, atm) or moderate (1.7–2.1atm) parasagittal fluid-percussion brain injury. At various time points after surgery, the ipsilateral parietal cortex, hippocampus, and thalamus were assayed for cAMP levels. Mild TBI lowered cAMP levels in the hippocampus of aged, but not young adult animals. Moderate TBI lowered cAMP levels in the hippocampus and parietal cortex of both age groups. In the thalamus, cAMP levels were significantly lowered after moderate, but not mild TBI. To determine if the TBI-induced decreases in cAMP had physiological consequences in aged animals, hippocampal long-term potentiation (LTP) in the Schaffer collateral pathway of the CA1 region was assessed. LTP was significantly decreased in both young adult and aged animals after mild and moderate TBI as compared to sham surgery animals. Rolipram rescued the LTP deficits after mild TBI for young adult animals and caused a partial recovery for aged animals. However, rolipram did not rescue LTP deficits after moderate TBI in either young adult or aged animals. These results indicate that the exacerbation of cognitive impairments in aged animals with TBI may be due to decreased cAMP levels and deficits in hippocampal LTP.

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Introduction: Progesterone (PROG) is well-studied in animal models of adult traumatic brain injury (TBI), and has advanced to clinical trials in adults. However, there are no animal studies of PROG in pediatric TBI. Hypothesis: We hypothesized that PROG would be neuroprotective in a rat model of pediatric TBI. Methods: Immature male and female rats underwent controlled cortical impact (CCI) to the left parietal cortex at 2 ages (PND 9-11, 17-22). Rats received either PROG (10 mg/kg at 1h i.p., 6h s.c., Q24h s.c.) or vehicle (22.5% cyclohexdrin). Control rats were na?, age-matched littermates given vehicle. Brain mitochondria were isolated from the ipsilateral hemisphere at 24h after CCI. Active (State 3) and resting (State 4) respiration were measured, and respiratory control ratio (RCR, State III/State IV) was determined. Mitochondrial glutathione (GSH) content was measured using a fluorescence assay. Microglial activation (Iba-1, CD11b) was evaluated at 3d and 7d after CCI. Lesion volume was measured at 7d after CCI. Results: In PND 17-22 male rats, TBI significantly reduced mitochondrial RCR by ~25% ipsilateral to injury, and post-injury PROG treatment preserved mitochondrial RCR (p<0.05 TBI+PROG vs TBI+vehicle). In PND 17-22 female rats, there was a trend toward preserved mitochondrial RCR (p=0.1). Mitochondrial GSH levels were higher in uninjured female rats (p<0.001 vs. male rats). TBI reduced mitochondrial GSH levels by ~16% in male rats and ~40% in female rats, which was prevented by PROG treatment in male rats only. Activated microglia were seen throughout the brain at 3d and 7d after TBI in both ages studied. PROG decreased the density of Iba-1 staining, and appeared to change the morphology of microglia to a more ramified “quiescent” form. The density of CD11b+ microglia in the ipsilateral thalamus at 7d after injury was reduced by PROG. Lesion volume was reduced in progesterone treated PND 17-22 male rats at 7d after CCI. Conclusions: PROG prevents mitochondrial dysfunction, reduces neuroinflammation and decreases lesion volume after TBI in immature rats. Future studies will assess correlation with neurologic outcomes. These studies provide valuable information for planning future clinical trials of PROG in pediatric TBI.

Adversive seizures associated with periodic lateralised epileptiform discharges (PLEDs) after left orbital contusion

We report a patient who presented with adversive seizures associated with periodic lateralised epileptiform discharges (PLEDs), a month after head trauma. The PLEDs predominantly involving the left frontal contacts became more frequent at the onset of adversive seizures during EEG. Brain MRI demonstrated a contusion scar in the left orbital cortex with reduced diffusion, not only around this orbital lesion but also in the ipsilateral anteromedial thalamus. Single photon emission computed tomography revealed focal cerebral hyperperfusion in the left medial orbitofrontal region, basal ganglia, and thalamus. The abnormal metabolism involving the thalamus and striatum could be associated with the ipsilateral orbital contusion and might have been caused by cortical-subcortical, trans-synaptic hyperactivity. Further studies are warranted to determine the role of subcortical structures in the generation of PLEDs and adversive seizures. [Published with video sequences].

Thalamic medial dorsal nucleus atrophy in medial temporal lobe epilepsy: A VBM meta-analysis

PurposeMedial temporal lobe epilepsy (MTLE) is associated with MTLE network pathology within and beyond the hippocampus. The purpose of this meta-analysis was to identify consistent MTLE structural change to guide subsequent targeted analyses of these areas.MethodsWe performed an anatomic likelihood estimation (ALE) meta-analysis of 22 whole-brain voxel-based morphometry experiments from 11 published studies. We grouped these experiments in three ways. We then constructed a meta-analytic connectivity model (MACM) for regions of consistent MTLE structural change as reported by the ALE analysis.Key findingsALE reported spatially consistent structural change across VBM studies only in the epileptogenic hippocampus and the bilateral thalamus; within the thalamus, the medial dorsal nucleus of the thalamus (MDN thalamus) represented the greatest convergence (P < 0.05 corrected for multiple comparisons). The subsequent MACM for the hippocampus and ipsilateral MDN thalamus demonstrated that the hippocampus and ipsilateral MDN thalamus functionally co-activate and are nodes within the same network, suggesting that MDN thalamic damage could result from MTLE network excitotoxicity.SignificanceNotwithstanding our large sample of studies, these findings are more restrictive than previous reports and demonstrate the utility of our inclusion filters and of recently modified meta-analytic methods in approximating clinical relevance. Thalamic pathology is commonly observed in animal and human studies, suggesting it could be a clinically useful indicator. Thalamus-specific research as a clinical marker awaits further investigation.

Bepridil decreases Aβ and calcium levels in the thalamus after middle cerebral artery occlusion in rats.

Alzheimer's disease (AD) and cerebral ischaemia share similar features in terms of altered amyloid precursor protein (APP) processing and β-amyloid (Aβ) accumulation. We have previously shown that Aβ and calcium deposition, and β-secretase activity, are robustly increased in the ipsilateral thalamus after transient middle cerebral artery occlusion (MCAO) in rats. Here, we investigated whether the non-selective calcium channel blocker bepridil, which also inhibits β-secretase cleavage of APP, affects thalamic accumulation of Aβ and calcium and in turn influences functional recovery in rats subjected to MCAO. A 27-day bepridil treatment (50 mg/kg, p.o.) initiated 2 days after MCAO significantly decreased the levels of soluble Aβ40, Aβ42 and calcium in the ipsilateral thalamus, as compared with vehicle-treated MCAO rats. Expression of seladin-1/DHCR24 protein, which is a potential protective factor against neuronal damage, was decreased at both mRNA and protein levels in the ipsilateral thalamus of MCAO rats. Conversely, bepridil treatment restored seladin-1/DHCR24 expression in the ipsilateral thalamus. Bepridil treatment did not significantly affect heme oxygenase-1- or NAD(P)H quinone oxidoreductase-1-mediated oxidative stress or inflammatory responses in the ipsilateral thalamus of MCAO rats. Finally, bepridil treatment mitigated MCAO-induced alterations in APP processing in the ipsilateral thalamus and improved contralateral forelimb use in MCAO rats. These findings suggest that bepridil is a plausible therapeutic candidate in AD or stroke owing to its multifunctional role in key cellular events that are relevant for the pathogenesis of these diseases.

P.4.e.003 Brain structural correlates of dysfunctional beliefs in obsessive-compulsive disorder: role of the temporal pole

To investigate cerebral grey matter (GM) volumetric abnormalities in temporal lobe epilepsy (TLE) patients who develop de novo depression following TLE surgery using voxel-based morphometry (VBM).We retrospectively examined pre-surgical grey matter (GM) volumes in 30 patients with TLE due to unilateral left-sided hippocampal sclerosis using 1.5-T MRI scan, which were segmented with optimised VBM parameters and normalised to a sample template using DARTEL, with SPM8 software. Voxel-wise GM differences between patients that developed de novo post-surgical depression (n = 5) were compared with patients with no pre- or postoperative psychiatric diagnoses (n = 25), using independent samples t-tests with age, gender and secondary generalised tonic–clonic seizures (SGTCS) as covariates (p < .001, unc).Reduced preoperative bilateral GM in orbitofrontal cortices (OFC) and ipsilateral cingulate gyrus and thalamus were significantly associated with the development of de novo depression within 4 years postoperatively. Further analyses revealed no differences in seizure freedom (ILAE 1 vs 2–6) or postoperative memory decline between the groups.Although the development of postoperative de novo depression following TLE surgery is likely to be multi-factorial, our results suggest that bilateral OFC and ipsilateral cingulate gyrus and thalamic atrophy in left-sided TLE patients may play a modulatory role. Abnormalities in these areas have also been implicated in primary mood disorders. Prospective neuroimaging studies with larger cohorts are warranted to replicate these results, and further elucidate the neural correlates of de novo depression.

Spinal cord stimulation modulates cerebral function: an fMRI study

Although spinal cord stimulation (SCS) is widely used for chronic neuropathic pain after failed spinal surgery, little is known about the underlying physiological mechanisms. This study aims to investigate the neural substrate underlying short-term (30s) SCS by means of functional magnetic resonance imaging in 20 patients with failed back surgery syndrome (FBSS). Twenty patients with FBSS, treated with externalized SCS, participated in a blocked functional magnetic resonance imaging design with stimulation and rest phases of 30s each, repeated eight times in a row. During scanning, patients rated pain intensity over time using an 11-point numerical rating scale with verbal anchors (0 = no pain at all to 10 = worst pain imaginable) by pushing buttons (left hand, lesser pain; right hand, more pain). This scale was back projected to the patients on a flat screen allowing them to manually direct the pain indicator. To increase the signal-to-noise ratio, the 8-min block measurements were repeated three times. Marked deactivation of the bilateral medial thalamus and its connections to the rostral and caudal cingulate cortex and the insula was found; the study also showed immediate pain relief obtained by short-term SCS correlated negatively with activity in the inferior olivary nucleus, the cerebellum, and the rostral anterior cingulate cortex. Results indicate the key role of the medial thalamus as a mediator and the involvement of a corticocerebellar network implicating the modulation and regulation of averse and negative affect related to pain. The observation of a deactivation of the ipsilateral antero-medial thalamus might be used as a region of interest for further response SCS studies.

Differential retinal origins of separate anatomical channels for pattern and motion vision in rabbit

The most conspicuous feature of the rabbit retina is the visual streak that extends along the horizontal azimuth from the nasal margin to the temporal limit of the retina. We believe the streak processes movement vision and that the temporal region (area centralis) is responsible for pattern perception. Both anatomical and behavioural experiments were used to test this hypothesis. Behavioural measures of pattern vision in normal and chiasma-sectioned rabbits revealed both to have the same visual acuity. Using OKN as a measure of movement vision, normal rabbits showed both a directional and velocity-tuned response. The chiasma-sectioned rabbits, with only uncrossed fibre projections remaining, showed a total loss of movement detection. The injection of HRP into the vitreal chamber of one eye in normal rabbits revealed extensive uptake throughout the contralateral thalamus. In the ipsilateral thalamus, there was uptake solely from the ipsilateral retinal projection to a restricted wafer of the lateral geniculate nucleus (LGN). The chiasma cut rabbits showed a very different distribution of HRP in the thalamus. The uptake was restricted to a thin wafer of the LGN, with no contralateral uptake. Thus, the thalamic projections from the retinal area centralis were strictly segregated from the thalamic target areas for the visual streak without any overlap. These findings provide strong evidence for separate retinal origins with anatomically separate pathways for pattern and movement vision in the rabbit.

Postoperative Transient Reduced Diffusion in the Ipsilateral Striatum and Thalamus

Restriction of diffusion has been reported in the early phase of secondary neuronal degeneration, such as wallerian degeneration. The purpose of this study was to investigate postoperative transient reduced diffusion in the ipsilateral striatum and thalamus as a remote effect of surgery. Six hundred two postoperative MR imaging examinations in 125 patients after cerebral surgery were retrospectively reviewed, focusing on the presence of reduced diffusion in the striatum and/or thalamus. The distribution of reduced diffusion in the striatum was classified into 3 groups: anterior, central, and posterior. Reduced diffusion in the thalamus was also classified on the basis of the anatomic locations of the thalamic nuclei. Further follow-up MRI was available in all patients with postoperative reduced diffusion, and acute infarctions were excluded. The patient medical records were reviewed to evaluate neurologic status. Restriction of diffusion was observed in the striatum and/or thalamus ipsilateral to the surgical site in 17 patients (13.6%). The distribution of signal abnormality correlated with the location of the operation, in concordance with the architecture of the striatocortical and thalamocortical connections. Reduced diffusion was observed from days 7 to 46 after the operation, especially during days 8-21. The signal abnormalities completely resolved on follow-up examinations. The median follow-up period was 202 days (interquartile range, 76-487 days). Postoperative transient reduced diffusion in the ipsilateral striatum and/or thalamus likely represents an early phase of secondary neuronal degeneration based on its characteristic distribution and time course. Clinically, this reduced diffusion should not be mistaken for postoperative ischemic injury.