Clinical Presentation and Causes of Non-traumatic Spinal Cord Injury: An Observational Study in Emergency Patients

Introduction: Diagnosing non-traumatic spinal cord injury (NTSCI) is often challenging. However, clear discrimination from non-spinal pathologies, e.g., “myelopathy-mimics” (MMs), is critical in preventing long-term disability and death. In this retrospective study we (1) investigated causes of NTSCI, (2) identified clinical markers associated with NTSCI and (3) discuss implications for NTSCI management.Methods: Our sample consisted of 5.913 consecutive neurological and neurosurgical patients who were treated in our emergency department during a one-year period. Patients with a new or worsened bilateral sensorimotor deficit were defined as possible NTSCI. We then compared clinical and imaging findings and allocated patients into NTSCIs and MMs.Results: Of ninety-three included cases, thirty-six (38.7%) were diagnosed with NTSCI. Fifty-two patients (55.9%) were classified as MMs. In five patients (5.4%) the underlying pathology remained unclear. Predominant causes of NTSCI were spinal metastases (33.3%), inflammatory disorders (22.2%) and degenerative pathologies (19.4%). 58.6% of NTSCI patients required emergency treatment. Presence of a sensory level (p = <0.001) and sphincter dysfunction (p = 0.02) were the only significant discriminators between NTSCI and MMs.Conclusion: In our study, one-third of patients presenting with a new bilateral sensorimotor deficit had NTSCI. Of these, the majority required emergency treatment. Since there is a significant clinical overlap with non-spinal disorders, a standardized diagnostic work-up including routine spinal MRI is recommended for NTSCI management, rather than an approach that is mainly based on clinical findings.

An elderly woman presents with a “Transient Ischemic Attack”: A curable cause

We report a 78-year-old female who presented to the Emergency department after a 10-minute episode of transient ischemic attack (TIA)-like symptoms of right side sensorimotor deficit, presumably due to a left carotid artery ischemia syndrome, only to be found surprisingly to have bilateral multifocal acute infarcts of cardioembolic pattern by brain magnetic resonance imaging, and, even more surprisingly, to have a rare, but curable embolic source from a large left atrial myxoma. This case report emphasizes the importance of following existing guidelines to timely and thoroughly investigate the potential management-changing causes for all TIA patients. Rare but curable causes of stroke or TIA in young adults such as cardiac myxoma can also occur in the elderly patient population.

Atrophy of spared subcortical nuclei relates to worse post-stroke sensorimotor outcomes across 28 cohorts worldwide

ABSTRACTObjectiveTo identify associations between atrophy of spared subcortical nuclei and sensorimotor behavior at different timepoints after stroke.MethodsWe pooled high-resolution T1-weighted MRI brain scans and behavioral data in 828 individuals with unilateral stroke from 28 cohorts worldwide. Cross-sectional analyses using linear mixed-effects models related post-stroke sensorimotor behavior to non-lesioned subcortical volumes. We analyzed subacute (≤90 days) and chronic (≥180 days) stroke; sub-analyses in chronic stroke were performed on class of sensorimotor deficit (impairment, activity limitations) and side of lesioned hemisphere, with exploratory analyses in early stroke (≤21 days) and across all time (Bonferroni-corrected, p<0.004).ResultsWorse sensorimotor behavior was associated with a smaller ipsilesional thalamic volume in both early (n=179; d=0.68) and subacute (n=274, d=0.46) stroke. In chronic stroke (n=404), worse sensorimotor behavior was associated with smaller ipsilesional putamen (d=0.52) and nucleus accumbens (d=0.39) volumes, and a larger ipsilesional lateral ventricle (d=−0.42). Worse chronic sensorimotor impairment specifically (measured by the Fugl-Meyer Assessment; n=256) was associated with smaller ipsilesional putamen (d=0.72) and larger lateral ventricle (d=−0.41) volumes, while several measures of activity limitations (n=116) showed no significant relationships. In the full cohort (n=828), sensorimotor behavior was associated with the volumes of the ipsilesional nucleus accumbens (d=0.23), putamen (d=0.33), thalamus (d=0.33), and lateral ventricle (d=−0.23).ConclusionsWe demonstrate significant relationships between post-stroke sensorimotor behavior and reduced volumes of subcortical gray matter structures that were spared by stroke, which differ by time and class of sensorimotor measure. These findings may provide new targets for improving post-stroke sensorimotor outcomes.

Dynamic Relationship between Sense of Agency and Post-Stroke Sensorimotor Deficits: A Longitudinal Case Study

Post-stroke sensorimotor deficits impair voluntary movements. This impairment may alter a person’s sense of agency, which is the awareness of controlling one’s actions. A previous study showed that post-stroke patients incorrectly aligned themselves with others’ movements and proposed that their misattributions might be associated with their sensorimotor deficits. To investigate this hypothesis, the present study compared the agency dynamics in a post-stroke patient A (PA) with sensorimotor deficits, who rarely used her paretic upper limbs in her daily life to patient B (PB), who had a paretic upper limb with almost normal functions and activity. At the second, fourth, and eighth weeks following their strokes, PA and PB completed experiments where they performed horizontal movements while receiving visual feedback, and analyzed if the visual feedback represented their own or another’s movements. Consequently, PB made no misattributions each week; whereas, PA made incorrect self-attributions of other’s movements at the fourth week. Interestingly, this misattribution noticeably decreased at the eighth week, where PA, with an improved paretic upper limb, used her limb almost as much as before her stroke. These results suggest that the sense of agency alters according to the sensorimotor deficit severity and paretic upper limb activity.

Chinese expert consensus on diagnosis and management of split cord malformation

Split cord malformation (SCM) is a neural tube defect that the spinal cord is longitudinally separated into two hemicords with individual functions, which causes severe spinal cord impairment and sensorimotor deficit. As a kind of myelodysplasia and a special type of tethered cord syndrome, SCM is not widely understood, and common issues in the diagnosis and treatment of SCM should be clarified. In this paper, the Chinese Split Cord Malformation Working Group made a consensus for SCM on embryopathogenesis and types, clinical presentations, neuroimaging assessment, indications and principle of the surgery, surgical techniques and nuances, and prognosis and follow up.

Modification of both functional neurological symptoms and neuroimaging patterns with a good anatomoclinical concordance: a case report

Background In the nineteenth century, Jean Martin Charcot explained functional neurological disorder (formerly called conversion disorder) as a “psychodynamic” lesion. Numerous advances in neuroimaging have permitted identification of the neural underpinnings of this disorder. Case presentation Herein we describe a case of functional neurological disorder (FND) with initial left sensorimotor deficit, in-coordinated limb movements, neglect, clouded consciousness, slurred speech and a semiology of visual impairment. A single photon emission computed tomography (SPECT) showed a right thalamic hypoperfusion, which is rather concordant with the initial semiology. Later, the semiology changed, presenting with a predominantly neurovisual complex presentation. The second SPECT showed no more thalamic abnormalities but an hypoperfusion in the right temporo-occipital junction, right inferior parietal lobe and left superior frontal lobe, which is also rather concordant with the changing semiology. Conclusions This case illustrates the evolving neuroimaging patterns of FND but also the concordance between semiology and neuroimaging findings in FND supporting Charcot's theory of “dynamic lesion”.

Assessing the Effects of Cytoprotectants on Selective Neuronal Loss, Sensorimotor Deficit and Microglial Activation after Temporary Middle Cerebral Occlusion

Although early reperfusion after stroke salvages the still-viable ischemic tissue, peri-infarct selective neuronal loss (SNL) can cause sensorimotor deficits (SMD). We designed a longitudinal protocol to assess the effects of cytoprotectants on SMD, microglial activation (MA) and SNL, and specifically tested whether the KCa3.1-blocker TRAM-34 would prevent SNL. Spontaneously hypertensive rats underwent 15 min middle-cerebral artery occlusion and were randomized into control or treatment group, which received TRAM-34 intraperitoneally for 4 weeks starting 12 h after reperfusion. SMD was assessed longitudinally using the sticky-label test. MA was quantified at day 14 using in vivo [11C]-PK111195 positron emission tomography (PET), and again across the same regions-of-interest template by immunofluorescence together with SNL at day 28. SMD recovered significantly faster in the treated group (p = 0.004). On PET, MA was present in 5/6 rats in each group, with no significant between-group difference. On immunofluorescence, both SNL and MA were present in 5/6 control rats and 4/6 TRAM-34 rats, with a non-significantly lower degree of MA but a significantly (p = 0.009) lower degree of SNL in the treated group. These findings document the utility of our longitudinal protocol and suggest that TRAM-34 reduces SNL and hastens behavioural recovery without marked MA blocking at the assessed time-points.

Dissecting the impact of depression on decision-making

BackgroundCognitive deficits in depressed adults may reflect impaired decision-making. To investigate this possibility, we analyzed data from unmedicated adults with Major Depressive Disorder (MDD) and healthy controls as they performed a probabilistic reward task. The Hierarchical Drift Diffusion Model (HDDM) was used to quantify decision-making mechanisms recruited by the task, to determine if any such mechanism was disrupted by depression.MethodsData came from two samples (Study 1: 258 MDD, 36 controls; Study 2: 23 MDD, 25 controls). On each trial, participants indicated which of two similar stimuli was presented; correct identifications were rewarded. Quantile-probability plots and the HDDM quantified the impact of MDD on response times (RT), speed of evidence accumulation (drift rate), and the width of decision thresholds, among other parameters.ResultsRTs were more positively skewed in depressed v. healthy adults, and the HDDM revealed that drift rates were reduced—and decision thresholds were wider—in the MDD groups. This pattern suggests that depressed adults accumulated the evidence needed to make decisions more slowly than controls did.ConclusionsDepressed adults responded slower than controls in both studies, and poorer performance led the MDD group to receive fewer rewards than controls in Study 1. These results did not reflect a sensorimotor deficit but were instead due to sluggish evidence accumulation. Thus, slowed decision-making—not slowed perception or response execution—caused the performance deficit in MDD. If these results generalize to other tasks, they may help explain the broad cognitive deficits seen in depression.