Thalamic pathology in frontotemporal dementia: Predilection for specific nuclei, phenotype-specific signatures, clinical correlates, and practical relevance.

BACKGROUND: Frontotemporal dementia (FTD) phenotypes are classically associated with distinctive cortical atrophy patterns and regional hypometabolism. However, the spectrum of cognitive and behavioral manifestations in FTD arises from multisynaptic network dysfunction. The thalamus is a key hub of several corticobasal and corticocortical circuits. The main circuits relayed via the thalamic nuclei include the dorsolateral prefrontal circuit, the anterior cingulate circuit, and the orbitofrontal circuit. METHODS: In this paper, we have reviewed evidence for thalamic pathology in FTD based on radiological and postmortem studies. Original research papers were systematically reviewed for preferential involvement of specific thalamic regions, for phenotype-associated thalamic disease burden patterns, characteristic longitudinal changes, and genotype-associated thalamic signatures. Moreover, evidence for presymptomatic thalamic pathology was also reviewed. Identified papers were systematically scrutinized for imaging methods, cohort sizes, clinical profiles, clinicoradiological associations, and main anatomical findings. The findings of individual research papers were amalgamated for consensus observations and their study designs further evaluated for stereotyped shortcomings. Based on the limitations of existing studies and conflicting reports in low-incidence FTD variants, we sought to outline future research directions and pressing research priorities. RESULTS: FTD is associated with focal thalamic degeneration. Phenotype-specific thalamic traits mirror established cortical vulnerability patterns. Thalamic nuclei mediating behavioral and language functions are preferentially involved. Given the compelling evidence for considerable thalamic disease burden early in the course of most FTD subtypes, we also reflect on the practical relevance, diagnostic role, prognostic significance, and monitoring potential of thalamic metrics in FTD. CONCLUSIONS: Cardinal manifestations of FTD phenotypes are likely to stem from thalamocortical circuitry dysfunction and are not exclusively driven by focal cortical changes.

Unique Subtype of Microglia in Degenerative Thalamus After Cortical Stroke.

BACKGROUND AND PURPOSE: Stroke disrupts neuronal functions in both local and remotely connected regions, leading to network-wide deficits that can hinder recovery. The thalamus is particularly affected, with progressive development of neurodegeneration accompanied by inflammatory responses. However, the complexity of the involved inflammatory responses is poorly understood. Herein we investigated the spatiotemporal changes in the secondary degenerative thalamus after cortical stroke, using targeted transcriptome approach in conjunction with histology and flow cytometry. METHODS: Cortical ischemic stroke was generated by permanent occlusion of the left middle cerebral artery in male C57BL6J mice. Neurodegeneration, neuroinflammatory responses, and microglial activation were examined in naive and stroke mice at from poststroke days (PD) 1 to 84, in both ipsilesional somatosensory cortex and ipsilesional thalamus. NanoString neuropathology panel (780 genes) was used to examine transcriptome changes at PD7 and PD28. Fluorescence activated cell sorting was used to collect CD11c+ microglia from ipsilesional thalamus, and gene expressions were validated by quantitative real-time polymerase chain reaction. RESULTS: Neurodegeneration in the thalamus was detected at PD7 and progressively worsened by PD28. This was accompanied by rapid microglial activation detected as early as PD1, which preceded the neurodegenerative changes. Transcriptome analysis showed higher number of differentially expressed genes in ipsilesional thalamus at PD28. Notably, neuroinflammation was the top activated pathway, and microglia was the most enriched cell type. Itgax (CD11c) was the most significantly increased gene, and its expression was highly detected in microglia. Flow-sorted CD11c+ microglia from degenerative thalamus indicated molecular signatures similar to neurodegenerative disease-associated microglia; these included downregulated Tmem119 and CX3CR1 and upregulated ApoE, Axl, LpL, CSF1, and Cst7. CONCLUSIONS: Our findings demonstrate the dynamic changes of microglia after stroke and highlight the importance of investigating stroke network-wide deficits. Importantly, we report the existence of a unique subtype of microglia (CD11c+) with neurodegenerative disease-associated microglia features in the degenerative thalamus after stroke.

Robot-assisted stereotactic biopsy of pediatric brainstem and thalamic lesions.

OBJECTIVE: Biopsies of tumors located in deep midline structures require highly accurate stereotaxy to safely obtain lesional tissue suitable for molecular and histological analysis. Versatile platforms are needed to meet a broad range of technical requirements and surgeon preferences. The authors present their institutional experience with the robotic stereotactic assistance (ROSA) system in a series of robot-assisted biopsies of pediatric brainstem and thalamic tumors. METHODS: A retrospective analysis was performed of 22 consecutive patients who underwent 23 stereotactic biopsies of brainstem or thalamic lesions using the ROSA platform at Rady Children's Hospital in San Diego between December 2015 and January 2020. RESULTS: The ROSA platform enabled rapid acquisition of lesional tissue across various combinations of approaches, registration techniques, and positioning. No permanent deficits, major adverse outcomes, or deaths were encountered. One patient experienced temporary cranial neuropathy, and 3 developed small asymptomatic hematomas. The diagnostic success rate of the ROSA system was 91.3%. CONCLUSIONS: Robot-assisted stereotactic biopsy of these lesions may be safely performed using the ROSA platform. This experience comprises the largest clinical series to date dedicated to robot-assisted biopsies of brainstem and diencephalic tumors.

Osteopontin Attenuates Secondary Neurodegeneration in the Thalamus after Experimental Stroke.

Cortical cerebral ischemia elicits neuroinflammation as well as secondary neuronal degeneration in remote areas. Locally distinct and specific secondary neurodegeneration affecting thalamic nuclei connected to cortical areas highlights such processes. Osteopontin (OPN) is a cytokine-like glycoprotein that is excreted in high amounts after cerebral ischemia and exerts various immunomodulatory functions. We here examined putative protective effects of OPN in secondary thalamic degeneration. We subjected male Wistar rats to photothrombosis and subsequently injected OPN or placebo intracerebroventricularly. Immunohistochemical and fluorescence staining was used to detect the extent of neuronal degeneration and microglia activation. Ex vivo autoradiography with radiotracers available for human in vivo PET studies, i.e., CIS-4-[18F]Fluor-D-Proline (D-cis-[18F]FPRO), and [6-3H]thymidine ([3H]thymidine), confirmed degeneration and proliferation, respectively. We found secondary neurodegeneration in the thalamus characterized by microglial activation and neuronal loss. Neuronal loss was restricted to areas of microglial infiltration. Treatment with OPN significantly decreased neurodegeneration, inflammation and microglial proliferation. Microglia displayed morphological signs of activation without expressing markers of M1 or M2 polarization. D-CIS-[18F]FPRO-uptake mirrored attenuated degeneration in OPN-treated animals. Notably, [3H]thymidine and BrdU-staining revealed increased stem cell proliferation after treatment with OPN. The data suggest that OPN is able to ameliorate secondary neurodegeneration in thalamic nuclei. These effects can be visualized by radiotracers D-CIS-[18F]FPRO and [3H]thymidine, opening new vistas for translational studies. Graphical Abstract Intracerebroventricular injection of osteopontin attenuates thalamic degeneration after cortical ischemia (pink area). Disruption of thalamocortical connections (blue) and degeneration of thalamic nuclei (encircled) leads to microglia activation. Osteopontin protects from both neurodegeneration and microglia activation as assessed by histological analysis and autoradiograpic studies.

Delayed-onset central poststroke pain due to degeneration of the spinothalamic tract following thalamic hemorrhage: A case report.

RATIONALE: Recent studies have used diffusion tensor tractography (DTT) to demonstrate that central poststroke pain (CPSP) was related to spinothalamic tract (STT) injury in patients with stroke. However, few studies have been reported about delayed-onset CPSP due to degeneration of the STT following a stroke. PATIENT'S CONCERNS: A 57-year-old female patient presented with right hemiparesis after stroke. Two weeks after onset, she did not report any pain. At approximately 6 months after onset, she reported pain in the right arm and leg, and the pain slowly intensified with the passage of time. At 14 months after onset, the characteristics and severity of her pain were assessed to be continuous pain without allodynia or hyperalgesia; tingling and cold-sensational pain in her right whole arm and leg (visual analog scale score: 5). DIAGNOSES: The patient was diagnosed as the right hemiparesis due to spontaneous thalamic hemorrhage. INTERVENTIONS: Clinical assessment and diffusion tensor imaging (DTI) were performed 2 weeks and 14 months after onset. OUTCOMES: She suffered continuous pain in her right whole arm and leg (visual analog scale score: 5). On DTT of the 2-week postonset DTI scans, the configuration of the STT was well-preserved in both hemispheres. However, in contrast to those 2-week postonset results, the 14-month postonset DTT results showed partial tearing and thinning in the left STT. Regardless, both the 2-week and 14-month postonset DTT showed that the left STT passed through the vicinity of the thalamic lesion. LESSONS: Diagnostic importance of performing a DTT-based evaluation of the STT in patients exhibiting delayed-onset CPSP following intracerebral hemorrhage.

Persistent anterograde amnesia due to the artery of Percheron occlusion: a case report.

Bilateral thalamic infarction involving the artery of Percheron (AOP) can cause diagnostic difficulties due to the varying clinical presentations. AOP infarcts presented with isolated memory impairment are not common and the factors affecting the persistence of memory disorders are still unknown. A 41-year-old male patient was hospitalized with acute unconsciousness. MRI disclosed bilateral paramedian thalamic infarction The patient had isolated memory deficit and his anterograde amnesia continued without any change in the past decade. More cases might answer the questions concerning the intra- and extra-thalamic structures responsible for the amnesic syndrome and the factors affecting the persistence of the symptoms.

Clinical and Neuroimaging Findings in Thalamic Territory Infarctions: A Review.

The thalamus is a part of the diencephalon, containing numerous connections between the forebrain and subcortical structures. It serves an important function as a relay center between the cerebral cortex and the subcortical regions, particularly with sensory information. The thalamus also plays a major role in regulating arousal and the levels of awareness. Distinct vascular distribution of the thalamus give rises to different syndromic presentation of thalamic nuclei infarcts. The clinical records and available imaging studies of patients with confirmed thalamic territory infarcts on magnetic resonance imaging (MRI) at the University Hospital of Rochester were reviewed and analyzed. This analysis was then used to provide an effective summary of thalamic vascular anatomy, the clinical symptoms, and syndromes associated with strokes in the affected territories. Specifically, we review the syndromes associated with classic vascular territories, including the anterior, paramedian, inferolateral, and posterior thalamic nuclei, that are supplied by the polar (tuberothalamic), paramedian, inferolateral (thalamogeniculate), and posterior choroidal arteries, respectively. In addition, we will also review the variant thalamic territories and associated infarction syndromes of the anteromedian, central, and posterolateral territories. This review article is aimed to better the clinical and radiologic understanding as well as the diagnosis of classic and variant thalamic territory infarcts. This article will also briefly touch on the recovery of function after thalamic infarcts.

Degeneration of paramedian nuclei in the thalamus induces Holmes tremor in a case of artery of Percheron infarction.

RATIONALE: Holmes' tremor is an uncommon neurologic disorder following brain insults, and its pathogenesis is undefined. The interruption of the dento-rubro-thalamic tract and secondary deterioration of the nigrostriatal pathway are both required to initiate Holmes' tremor. We used nuclear medicine imaging tools to analyze a patient with concurrent infarction in different zones of each side of the thalamus. Finding whether the paramedian nuclear groups of the thalamus were injured was a decisive element for developing Holmes' tremor. PATIENT CONCERNS: A 36-year-old woman was admitted to our department due to a bilateral paramedian thalamic infarction. Seven months after the stroke, a unilaterally involuntary trembling with irregularly wavering motions occurring in both her left hand and forearm. DIAGNOSIS: Based on the distinct features of the unilateral coarse tremor and the locations of the lesions on the magnetic resonance imaging (MRI), the patient was diagnosed with bilateral paramedian thalamic infarction complicated with a unilateral Holmes' tremor. INTERVENTIONS: The patient refused our recommendation of pharmacological treatment with levodopa and other dopamine agonists based on personal reasons and was only willing to accept physical and occupational training programs at our outpatient clinic. OUTCOMES: We utilized serial anatomic and functional neuroimaging of the brain to survey the neurologic deficit. A brain magnetic resonance imaging showed unequal recovery on each side of the thalamus. The residual lesion appeared larger in the right-side thalamus and had gathered in the paramedian area. A brain perfusion single-photon emission computed tomography (SPECT) revealed that the post-stroke hypometabolic changes were not only in the right-side thalamus but also in the right basal ganglion, which was anatomically intact. Furthermore, the brain Technetium-99m-labeled tropanes as a dopamine transporter imaging agents scan ( Tc-TRODAT-1) displayed a secondary reduction of dopamine transporters in the right nigrostriatal pathway which had resulted from the damage on the paramedian nuclear groups of the right-side thalamus. LESSONS: Based on the functional images, we illustrated that a retrograde degeneration originating from the thalamic paramedian nuclear groups, and extending forward along the direct innervating fibers of the mesothalamic pathway, played an essential role towards initiating Holmes' tremor.

A case report on 1-year follow-up of bilateral thalamic glioma.

Bilateral thalamic glioma is one of the rarest tumor occurrences, representing a small fraction of thalamic gliomas, which only accounts for 1-1.5% of all brain tumors. It is usually a diffuse, low-grade astrocytoma (WHO grade II), seen mainly in adults, with approximately 25% of them involving children under the age of 15. Radiotherapy is the main mode of treatment since surgical intervention is limited to a role of biopsy and management of secondary effects, due to the deep brain location of the lesion and the complexity of the involved structures. We report a 1-year follow-up of a 55-year-old female patient with bilateral WHO grade II thalamic astrocytoma. Following histological and neuroradiological consensus regarding the diagnosis, the patient was referred for radiotherapy. The effectiveness of available therapy and long-term neuroradiological follow-up is not reliably established due to rapid fatal evolution following diagnosis. Contrary to the norm, our patient showed stable disease with radiotherapy for a 1-year period.

Repeated head trauma is associated with smaller thalamic volumes and slower processing speed: the Professional Fighters' Brain Health Study.

OBJECTIVES: Cumulative head trauma may alter brain structure and function. We explored the relationship between exposure variables, cognition and MRI brain structural measures in a cohort of professional combatants. METHODS: 224 fighters (131 mixed martial arts fighters and 93 boxers) participating in the Professional Fighters Brain Health Study, a longitudinal cohort study of licensed professional combatants, were recruited, as were 22 controls. Each participant underwent computerised cognitive testing and volumetric brain MRI. Fighting history including years of fighting and fights per year was obtained from self-report and published records. Statistical analyses of the baseline evaluations were applied cross-sectionally to determine the relationship between fight exposure variables and volumes of the hippocampus, amygdala, thalamus, caudate, putamen. Moreover, the relationship between exposure and brain volumes with cognitive function was assessed. RESULTS: Increasing exposure to repetitive head trauma measured by number of professional fights, years of fighting, or a Fight Exposure Score (FES) was associated with lower brain volumes, particularly the thalamus and caudate. In addition, speed of processing decreased with decreased thalamic volumes and with increasing fight exposure. Higher scores on a FES used to reflect exposure to repetitive head trauma were associated with greater likelihood of having cognitive impairment. CONCLUSIONS: Greater exposure to repetitive head trauma is associated with lower brain volumes and lower processing speed in active professional fighters.

Thalamic lesions: a radiological review.

BACKGROUND: Thalamic lesions are seen in a multitude of disorders including vascular diseases, metabolic disorders, inflammatory diseases, trauma, tumours, and infections. In some diseases, thalamic involvement is typical and sometimes isolated, while in other diseases thalamic lesions are observed only occasionally (often in the presence of other typical extrathalamic lesions). SUMMARY: In this review, we will mainly discuss the MRI characteristics of thalamic lesions. Identification of the origin of the thalamic lesion depends on the exact localisation inside the thalamus, the presence of extrathalamic lesions, the signal changes on different MRI sequences, the evolution of the radiological abnormalities over time, the history and clinical state of the patient, and other radiological and nonradiological examinations.

Multiple thalamo-cortical disconnections in anterior thalamic infarction: implications for thalamic mechanisms of memory and language.

Amnesia and linguistic deficits that are associated with thalamic damage have attracted the attention of researchers interested in identifying the neural networks involved in memory and language. The Papez circuit, which is composed of the hippocampus, mammillary body and anterior thalamic nuclei, was first proposed to be critical for memory. However, subsequently, the roles of the neural circuit consisting of the rhinal/parahippocampal cortices and the mediodorsal thalamic nuclei became evident. The ventral lateral nuclei or its adjacent structures have been found to be involved in semantic processing, but the specific neural circuits dedicated to language functions have not been identified. Anterior thalamic infarcts, which affect very circumscribed regions of the ventral anterior portion of the thalamus, often cause paradoxically prominent memory and language deficits. We conducted tractography analyses in 6 patients with left anterior thalamic infarcts to identify neural connections or circuits in which disruptions are associated with memory and language deficits in this condition. The current study demonstrated that the mammillothalamic tract, which connects the mammillary body with the anterior thalamic nuclei, and the anterior and inferior thalamic peduncles, which contain neural fibers that extend from several thalamic nuclei to the anterior temporal, medial temporal and frontal cortices, are disrupted in anterior thalamic infarction. These extensive thalamo-cortical disconnections appear to be due to the dissection of the neural fibers that penetrate the ventral anterior nucleus of the thalamus. Our results suggest the following: (1) amnesia that is associated with anterior thalamic infarction is best interpreted in the context of dual/multiple-system theories of memory/amnesia that posit that multiple neural circuits connecting the anterior and mediodorsal thalamic nuclei with the hippocampus and rhinal/parahippocampal cortices work in concert to support memory function; and (2) the semantic deficits observed in this syndrome may be associated with thalamo-anterior temporal and thalamo-lateral frontal disconnections.

Connectivity-based parcellation of the thalamus explains specific cognitive and behavioural symptoms in patients with bilateral thalamic infarct.

A novel approach based on diffusion tractography was used here to characterise the cortico-thalamic connectivity in two patients, both presenting with an isolated bilateral infarct in the thalamus, but exhibiting partially different cognitive and behavioural profiles. Both patients (G.P. and R.F.) had a pervasive deficit in episodic memory, but only one of them (R.F.) suffered also from a dysexecutive syndrome. Both patients had an MRI scan at 3T, including a T1-weighted volume. Their lesions were manually segmented. T1-volumes were normalised to standard space, and the same transformations were applied to the lesion masks. Nineteen healthy controls underwent a diffusion-tensor imaging (DTI) scan. Their DTI data were normalised to standard space and averaged. An atlas of Brodmann areas was used to parcellate the prefrontal cortex. Probabilistic tractography was used to assess the probability of connection between each voxel of the thalamus and a set of prefrontal areas. The resulting map of corticothalamic connections was superimposed onto the patients' lesion masks, to assess whether the location of the thalamic lesions in R.F. (but not in G. P.) implied connections with prefrontal areas involved in dysexecutive syndromes. In G.P., the lesion fell within areas of the thalamus poorly connected with prefrontal areas, showing only a modest probability of connection with the anterior cingulate cortex (ACC). Conversely, R.F.'s lesion fell within thalamic areas extensively connected with the ACC bilaterally, with the right dorsolateral prefrontal cortex, and with the left supplementary motor area. Despite a similar, bilateral involvement of the thalamus, the use of connectivity-based segmentation clarified that R.F.'s lesions only were located within nuclei highly connected with the prefrontal cortical areas, thus explaining the patient's frontal syndrome. This study confirms that DTI tractography is a useful tool to examine in vivo the effect of focal lesions on interconnectivity brain patterns.

Bilateral central pain sensitization in rats following a unilateral thalamic lesion may be treated with high doses of ketamine.

BACKGROUND: Central post-stroke pain is a neuropathic pain condition caused by a vascular lesion, of either ischemic or hemorrhagic origin, in the central nervous system and more precisely involving the spinothalamocortical pathway responsible for the transmission of painful sensations. Few animal models have been developed to study this problem. The objectives of this study were to evaluate different modalities of pain in a central neuropathic pain rat model and to assess the effects of ketamine administered at different doses. Animals were evaluated on the rotarod, Hargreaves, Von Frey and acetone tests. A very small hemorrhage was created by injecting a collagenase solution in the right ventral posterolateral thalamic nucleus. Following the establishment of the neuropathy, ketamine was evaluated as a therapeutic drug for this condition. RESULTS: Histopathological observations showed a well localized lesion with neuronal necrosis and astrocytosis following the collagenase injection that was localized within the VPL. No significant change in motor coordination was observed following surgery in either the saline or collagensae groups. In the collagenase group, a significant decrease in mechanical allodynia threshold was observed. A sporadic and transient cold allodynia was also noted. No thermal hyperalgesia was seen following the collagenase injection. Ketamine was then tested as a potential therapeutic drug. A significant decrease in motor coordination was seen only following the administration of 25 mg/kg of ketamine in both groups. An alleviation of mechanical allodynia was achieved only with the high ketamine dose. The minimal effective ketamine serum concentration (150 ng/mL) was only achieved in animals that received 25 mg/kg. CONCLUSIONS: An intrathalamic hemorrhage induced a bilateral mechanical allodynia in rats. Cold hyperalgesia was observed in 60% of these animals. Mechanical allodynia was alleviated with high doses of ketamine which corresponded with therapeutic plasmatic concentrations.

Thalamic astrocytic hamartoma and associated meningoangiomatosis in a German shepherd dog.

The present paper describes an astrocytic thalamic hamartoma associated with tectal meningoangiomatosis in a 3-month-old female German shepherd dog showing strabismus, opistotonus, circling, and fore limb hypermetria. MR images of the brain showed a well-defined intra-axial mass in the tectal region. The mass was hypointense to gray matter on T2-weighted images and hyperintense to gray matter on precontrast T1-weighted images. Histologically, glial cells arranged in a multinodular pattern characterized the mass. More caudally the lesion merged with subpial abnormal newly formed plaque-like shaped tissue characterized by thick branching bundles of spindle-shaped cells surrounding a central vessel. In the nodules, GFAP and vimentin were diffusely expressed. In the vascular proliferation Factor VIII-positive reaction was limited to endothelial cells while the remaining spindle-shaped cells were diffusely SMA-positive. The glial nodules did not express lysozyme and MAC387, nor neurofilaments and nestin.

Clinical properties of regional thalamic hemorrhages.

BACKGROUND: Thalamic hemorrhage constitutes 6% to 25% of intracerebral hemorrhages. Vascular lesions affecting the thalamus may cause a variety of clinical symptoms. This retrospective study aims to evaluate localization of hemorrhage and clinical symptoms in patients with thalamic hemorrhage. METHODS: One hundred and one patients with thalamic hemorrhage were examined retrospectively in our department. Hemorrhages were classified into 5 groups according to computed tomography: medial (thalamoperforate), anterolateral (tuberothalamic), posterolateral (thalamogeniculate), dorsal (posterior choroidal), and global. The relation between volume, localization, and penetration to adjacent structures/ventricles of hemorrhage and risk factors, clinical features, and prognosis were evaluated. RESULTS: The study group included 101 patients. Eighty-two percent of the patients had hypertension, 19.8% had diabetes mellitus, 14.9% had cardiac disease, and 5.9% had chronic renal failure. Mean blood pressure was 173/101 mm Hg. Decreased Glasgow coma scale was significantly higher in the global hemorrhage group than in all regional groups (Chi-square, 10.54; P = .002). Medial group hemorrhages had a significantly higher rate than anterolateral, posterolateral, and dorsal intraventricular expansion. Out of speech disorders, 49% of patients had a right thalamic lesion (especially dysarthria) and 51% of patients had a left thalamic lesion (mostly aphasia). CONCLUSIONS: In the study, we detected that the most important risk factor in thalamic hemorrhage is hypertension. The prognosis is worse in global and medial group hemorrhages, especially those which rupture to the ventricle, than the other groups. Thalamic lesions cause a variety of symptoms, including forms of aphasia, such as crossed dextral aphasia.

Minimally invasive procedures reduced the damages to motor function in patients with thalamic hematoma: observed by motor evoked potential and diffusion tensor imaging.

BACKGROUND: The purpose of this study was to observe changes in motor function using diffusion tensor imaging (DTI) and motor-evoked potential (MEP) in patients with thalamic hematoma treated by minimally invasive procedures. METHODS: Forty-three patients with thalamic hematoma were randomized to either a minimally invasive group (MI group) or a medical treatment group (MT group). The patients in the MI group underwent whole-brain DTI and MEP measurements both before and 2 weeks after the thalamic hematoma was evacuated by minimally invasive procedures. The fractional anisotropy (FA) values of the corticospinal tract (CST) in the internal capsule and MEP ipsilateral to the hematoma side and the contralateral side were determined and then compared with the MT group. RESULTS: DTI showed that fibers in the internal capsule ipsilateral to the hematoma decreased either in number or were interrupted because of hematoma-induced damages, and in both groups, the CST FA values on admission were significantly lower (0.428 ± 0.032 and 0.415 ± 0.048 for the MI and MT groups, respectively) than the control values. Two weeks after the hematoma was evacuated, the number of fibers and the FA values of the CST in the internal capsule had both increased significantly relative to the values on admission. MEP was recorded simultaneously in all patients who were treated with minimally invasive procedures, and the latency of MEP decreased compared with the MT group. As FA values of the CST in internal capsule increased and MEP appeared with its latency decreased, the modified National Institutes of Health Stroke Scale score decreased after the surgery. CONCLUSIONS: Minimally invasive procedures for thalamic hematoma evacuation could effectively reduce the degree of injury to the function as observed by a combination of DTI and MEP measurements.

Cognitive decline and hypersomnolence: thalamic manifestations of a tentorial dural arteriovenous fistula (dAVF).

BACKGROUND: Intracranial dural arteriovenous fistulas (dAVFs) often present with pulsatile tinnitus, orbital congestion, and headache. Occasionally, they present with focal neurologic deficits, a dementia-like syndrome, hemorrhage, or ischemic infarction. METHODS: This study is based on the case of a 71-year-old gentleman who presented with 6 months of progressive forgetfulness, inattention, and hypersomnolence. Four weeks prior to presentation, he developed symptoms of left-sided pain, numbness, and worsening weakness. Neurologic examination demonstrated hypersomnolence, a score of 30/38 on the Kokmen Short Test of Mental Status, and left hemiparesis. MRI brain revealed bilateral thalamic T2 hyperintensities with associated enhancement. MR venogram (MRV) showed a vascular malformation in the posterior fossa and occlusion of the straight sinus. Conventional cerebral angiogram confirmed a tentorial dAVF. The dAVF was definitively treated with transarterial embolization, followed by clip ligation of the arterialized draining vein. Twelve weeks later, there was clinical resolution of left hemiparesis and improvement in cognitive status. MRI revealed complete resolution of the thalamic hyperintensities. MRV demonstrated recanalization of the straight sinus. RESULTS: Intracranial dAVFs are uncommon but potentially life-threatening acquired vascular malformations. The initiating factor is venous hypertension, causing retrograde flow, venous congestion, ischemia, and sometimes infarction. The spectrum of clinical manifestations in dAVFs reflects the degree of venous congestion present. If retrograde venous flow is surgically obliterated, then venous hypertension may be reversible. Bilateral thalamic venous congestion can present as a thalamic dementia. CONCLUSION: We conclude that intracranial dAVFs with thalamic venous congestion should be considered in the diagnostic differential for patients who present with subacute cognitive decline and T2 hyperintense thalamic signal change.

Thalamic sensory strokes with and without pain: differences in lesion patterns in the ventral posterior thalamus.

OBJECTIVE: Vascular lesions of the posterolateral thalamus typically result in a somatosensory syndrome in which some patients develop central neuropathic post-stroke pain (CPSP). Damage to the spinothalamic tract terminus is assumed to be a prerequisite for thalamic CPSP. At the nuclear level, it remains a matter of debate whether the ventral posterolateral nucleus (VPL) or the posterior portion of the ventral medial nucleus (VMpo) constitutes the decisive lesion site. The hypothesis of the study was that lesion location in thalamic CPSP patients differs from that in thalamic stroke patients without pain, and the aim was to identify whether this difference comprises the VPL and/or the VMpo. DESIGN: 30 patients with chronic thalamic stroke and a persistent contralateral somatosensory syndrome were examined. CPSP patients (n=18) were compared with non-pain control patients. By coregistration of a digitised thalamic atlas with T1 weighted MR images, lesion clusters were allocated to the thalamic nuclei. RESULTS: VPL was affected in both groups, but CPSP lesion clusters comprised the more posterior, inferior and lateral parts of the VPL compared with controls. Additional partial involvement of the VMpo was seen in only three pain patients. In three other pain patients, lesions involved neither the VPL nor the VMpo, but mainly affected the anterior pulvinar. CONCLUSION: This study specifies the role of the VPL in thalamic CPSP and shows that the posterolateratal and inferior parts in particular are critically lesioned in pain patients. In this thalamic subregion, afferents of the spinothalamic tract are known to terminate. In contrast, the data do not support a pivotal impact of the VMpo on thalamic CPSP.