Thalamic Lesions Research Articles

Brain magnetic resonance imaging is a predictor of bimanual performance and executive function in children with unilateral cerebral palsy.

To examine the association between brain magnetic resonance imaging (MRI) characteristics and executive function and bimanual performance in children with unilateral cerebral palsy (CP). Clinical MRI brain scans were classified as: (1) predominant pathological pattern (normal, white matter injury [WMI]; grey matter injury; focal vascular insults [FVI]; malformations; or miscellaneous); and (2) focal lesions (frontal, basal ganglia, and/or thalamus). Assessments included: (1) bimanual performance; (2) unimanual dexterity; and (3) executive function tasks (information processing, attention control, cognitive flexibility, and goal setting) and behavioural ratings (parent). From 131 recruited children, 60 were ineligible for analysis, leaving 71 children (47 males, 24 females) in the final sample (mean age 9y [SD 2y], 6y-12y 8mo). Brain MRIs were WMI (69%) and FVI (31%); and frontal (59%), thalamic (45%), basal ganglia (37%), and basal ganglia plus thalamic (21%). Bimanual performance was lower in FVI versus WMI (p<0.003), and with frontal (p=0.36), basal ganglia (p=0.032), and thalamic/basal ganglia lesions (p=0.013). Other than information processing, executive function tasks were not associated with predominant pattern. Frontal lesions predicted attention control (p=0.049) and cognitive flexibility (p=0.009) but not goal setting, information processing, or behavioural ratings. Clinical brain MRI predicts cognitive and motor outcomes when focal lesions and predominate lesion patterns are considered. What this paper adds Early brain magnetic resonance imaging (MRI) predicts bimanual performance and cognitive outcomes. Brain MRI may identify children requiring targeted interventions. Basal ganglia with/without thalamic lesions predicted bimanual performance. Frontal lesions were associated with attention control and cognitive flexibility. Brain MRI predominant patterns predicted motor, not cognitive outcomes, other than information processing.

MS optic neuritis-induced long-term structural changes within the visual pathway.

BackgroundThe visual pathway is commonly involved in multiple sclerosis (MS), even in its early stages, including clinical episodes of optic neuritis (ON). The long-term structural damage within the visual compartment in patients with ON, however, is yet to be elucidated.ObjectiveOur aim was to characterize visual system structure abnormalities using MRI along with optical coherence tomography (OCT) and pattern-reversal visual evoked potentials (VEPs) depending on a single history of ON.MethodsTwenty-eight patients with clinically definitive MS, either with a history of a single ON (HON) or without such history and normal VEP findings (NON), were included. OCT measures comprised OCT-derived peripapillary retinal nerve fiber layer (RNFL) and macular ganglion cell/inner plexiform layer (GCIPL) thickness. Cortical and global gray and white matter, thalamic, and T2 lesion volumes were assessed using structural MRI. Diffusion-weighted MRI-derived measures included fractional anisotropy (FA), mean (MD), radial (RD), and axial (AD) diffusivity within the optic radiation (OR).ResultsMean (SD) duration after ON was 8.3 (3.7) years. Compared with the NON group, HON patients showed significant RNFL (p = 0.01) and GCIPL thinning (p = 0.002). OR FA (p = 0.014), MD (p = 0.005), RD (p = 0.007), and AD (p = 0.004) were altered compared with NON. Global gray and white as well as other regional gray matter structures did not differ between the 2 groups.ConclusionA single history of ON induces long-term structural damage within the retina and OR suggestive of both retrograde and anterograde neuroaxonal degeneration.

Spatial Coding in the Subiculum Requires Anterior Thalamic Inputs

Hippocampal function relies on the anterior thalamic nuclei, yet the reasons remain poorly understood. While anterior thalamic lesions disrupt parahippocampal spatial signalling, their impact on the subiculum is unknown, despite the importance of this area for hippocampal networks. We recorded subiculum cells in rats with either permanent (N-methyl-D-aspartic acid) or reversible (muscimol) anterior thalamic lesions. The diverse spatial signals normally found in the subiculum, including place cells, disappeared following permanent thalamic lesions and showed marked disruption during transient lesions. Meanwhile, permanent anterior thalamic lesions had no discernible impact on CA1 place fields. Thalamic lesions reduced spatial alternation performance (permanently or reversibly) to chance levels, while leaving a non-spatial recognition memory task unaffected. These findings, which help to explain why anterior thalamic damage is so deleterious for spatial memory, cast a new spotlight on the importance of subiculum function, and reveal its dependence on anterior thalamic signalling.

Discrepancies in Hearing Thresholds between Pure-Tone Audiometry and Auditory Steady-State Response in Non-Malingerers.

To evaluate discrepancies between pure-tone audiometry (PTA) and auditory steady state response (ASSR) tests in non-malingerers and investigate brain lesions that may explain the discrepancies, especially in cases where the PTA threshold was worse than the estimated ASSR threshold. PTA, speech audiometry, auditory brainstem response, ASSR, and neuroimaging tests were carried out on individuals selected from 995 cases of hearing impairment. Among these, medical records of 25 subjects (19 males, 6 females; mean age = 46.5 ± 16.0 years) with significant discrepancy between PTA and estimated ASSR thresholds were analyzed retrospectively. To define acceptable levels of discrepancy in PTA and ASSR hearing thresholds, 56 patients (27 males, 29 females; mean age = 53.0 ± 13.6 years) were selected for the control group. Magnetic resonance images, magnetic resonance angiograms, and positron emission tomograms were reviewed to identify any neurologic abnormalities. Pathologic brain lesions were found in 20 cases (80%) in the study group, all of which showed a significant discrepancy in hearing threshold between PTA and ASSR. Temporal lobe lesions were found in 14 cases (70%), frontal lobe lesions in 12 (60%), and thalamic lesions without the frontal or temporal lobe in 2 cases (10%). On repeated PTA and ASSR tests a few months later, the discrepancy between ASSR and behavioral hearing thresholds was reduced or resolved in 6 cases (85.7%). Temporal lobe lesions were found in all 3 cases in which the estimated ASSR threshold worsened with unchanged PTA threshold, and frontal lobe lesions were found in all 3 cases in which the PTA threshold improved but the estimated ASSR threshold was unchanged. No neurological lesions were found in 5 cases (20%) of patients with a discrepancy between ASSR and behavioral hearing thresholds. Clinicians should not rely exclusively on ASSR, especially in cases of central nervous system including temporal, frontal lobe, or thalamus lesions. If no lesions are found in a neuroimaging study of a patient with a discrepancy between PTA thresholds and estimated ASSR thresholds, further functional studies of the brain may be needed. If clinicians encounter patients with a discrepancy between PTA thresholds and estimated ASSR thresholds, an evaluation of brain lesions and repeat audiologic tests are recommended in lieu of relying solely on ASSR.

Acute Demyelinating Encephalomyelitis(ADEM) Presenting With Dystonia

Introduction: Acute disseminated encephalomyelitis (ADEM) is a monophasic autoimmune inflammatory demyelinating disease of the central nervous system that predominantly involves the white matter of the brain and spinal cord(1). It is a rare disease affecting both children and adults (2). In the majority of cases ADEM usually appears after vaccinations or viral/bacterial infections Methods: This was a case study of two patients with ADEM presenting with dystonia. The study was conducted at King Khalid Hospital in Hail, Saudi Arabia. Results: MRI studies showed subcortical white matter lesion in the right frontal region in patient 1, and a right thalamic lesion in patient 2. Conclusion: We conclude that the lesions detected by the MRI were responsible for the limb dystonia. We believe that the lesions seriously disrupted the cortical-striatal pathways in the right cerebral hemisphere, leading to hemi-dystonia.

P629 An uncommon cause for a frequent problem

Abstract Introduction Libman-Sacks endocarditis is the most characteristic cardiac manifestation of the autoimmune disease systemic lupus erythematosus. Embolic phenomena, although uncommon, can also complicate valvular abnormalities and can cause neurologic and systemic complications. Case Report Man, 52 years old. Active smoker and with previous peptic ulcer history. Admitted to our emergency department due to sudden onset of confusion and incoherent speech. The physical examination showed only a Glasgow Coma Scale of 9 and the presence of expressive aphasia. Normal pulmonary and cardiac auscultation, without any other pathological findings on physical examination. Investigations showed a normal EKG, chest X-Ray and arterial-blood gas test. Blood test showed only the presence of thrombocytopenia, leucocytosis and renal disfunction. Brain CT revealed left-sided thalamic lacunar lesion. We assumed an ischemic stroke and admitted the patient in our emergency department. Neurological deterioration in the first 24h. A new brain CT was performed and showed multiple lesions in the middle cerebral artery territory. The echocardiogram was performed and showed the presence of multiples vegetations in both mitral leaflets with moderate to severe mitral regurgitation associated. We assume an ischemic stroke in the context of possible infective endocarditis. Medical therapy was optimized and empirical antimicrobial therapy was started (ampicillin + gentamicin + flucoxacillin). The patient never had fever during hospital stay. Duke criteria with only 1 major criteria. Persistent negative microbiological cultures with decreasing inflammatory parameters. Blood tests revealed a progressive increase level of INR (2-4) and renal function deterioration. Patient began with massive episodes of diarrhea and sudden decrease of haemoglobin level (sudden reduction of 3g/dl). Endoscopic studies were performed and multiple ischemic lesions of embolic etiology and small vessel disease had been described. Serology test revealed a positive IgG for Mycoplasma pneumoniae. Autoimmune lab tests showed positivity for lupus anticoagulant, anticardiolipin and anti–beta-2 glycoprotein I. We discussed the clinical case with our autoimmune experts team and the diagnosis of Systemic Lupus Erythematosus + Antiphospholipid Syndrome + Libman-Sacks Endocarditis was assumed. The patient started immunosuppressive therapy (Azathioprine + Mycophenolate Mofetil + Prednisolone). Despite the used therapy the size of vegetation persisted and mitral regurgitation didn’t improve. In this context, the patient was presented to our cardiac surgery team and underwent surgical intervention (vegetation removal + mitral valve repair). Evaluation one year after surgery revealed progressive functional and echocardiographic improvement. Conclusion The authors presented a didactic clinical case where valvular surgery was required thanks to a hemodynamically significant valvular dysfunction and embolic events.

Evaluation of Improvement of Tissue Contrast and Reduction of Imaging Time by Shortening TR in Brain T&lt;sub&gt;2&lt;/sub&gt; FLAIR Using MTC Pulse

T2 fluid-attenuated inversion recovery (FLAIR) using inversion recovery pulse to suppress cerebrospinal fluid signal needs adequate T1 recovery time after data acquisition, otherwise, the T2-weighted contrast in brain tissue will get lower. Over 10000 ms of repetition time (TR) is recommended for the 1.5 T MR scanner, so it is difficult to shorten the imaging time. We verified whether T2 FLAIR combined with the magnetization transfer contrast (MTC) pulse shows better gray-to-white matter (GM/WM) and lesion-to-normal tissue contrasts even when the TR is shortened compared to the conventional T2 FLAIR. Optimal parameters of the MTC pulse were determined with a self-produced phantom, which modeled on cerebral cortical gray and white matters. GM/WM contrasts of the phantom were measured in T2 FLAIR with the MTC pulse while decreasing TR gradually from 10000 ms to 6500 ms. Although GM/WM contrast of the phantom in T2 FLAIR with the MTC pulse gradually decreased as the TR got shortened, the T2 FLAIR with the MTC pulse of 6500 ms of TR still showed 27% higher contrast than the conventional T2 FLAIR (TR 10000 ms). GM/WM contrast in T2 FLAIR with the MTC pulse was improved also in healthy volunteers, but improvement in thalamo-medullary contrast was less than that of cerebral cortico-medullary and putamino-medullary contrasts. It seems to be because thalamus, which is a deep gray matter, shows a higher MTC effect than other gray matters. Thus, it is necessary to note that the tissue contrast might differ between T2 FLAIR with the MTC pulse and the conventional T2 FLAIR. Because general lesions with an elongated T2 value show lower MTC effect compared to the normal brain tissue, a clinical case with thalamic lesion showed that the lesion-to-normal tissue contrast improved in T2 FLAIR with the MTC pulse of 6500 ms of TR. Although it is necessary to note the difference in contrast between some tissues, T2 FLAIR with the MTC pulse improves GM/WM and lesion-to-normal tissue contrasts even when the TR is shortened compared to the conventional T2 FLAIR, and it enables to shorten the imaging time.

Relationship Between Olfactory Disturbance After Acute Ischemic Stroke and Latent Thalamic Hypoperfusion.

Odor detection, recognition, and identification were assessed in 19 acute ischemic stroke patients who had no magnetic resonance imaging-detectable thalamic lesions but in whom technetium-99m ethyl cysteinate dimer single photon emission tomography revealed thalamic hypoperfusion. Although these patients were unaware of reduced olfactory function, they exhibited significantly lower scores in tests for odor identification and recognition threshold as compared with 9 ischemic stroke controls that had normal thalamic hypoperfusion. However, absolute odor detection thresholds were similar in the 2 groups. These results demonstrate the usefulness of cerebral perfusion scintigraphy in assessing sensory loss after ischemic stroke and provide further evidence for the role of the thalamus in olfaction.

7T MRI cerebral leptomeningeal enhancement is common in relapsing-remitting multiple sclerosis and is associated with cortical and thalamic lesions

Background: Meningeal inflammation may contribute to gray matter (GM) involvement in multiple sclerosis (MS) and is proposed to manifest as magnetic resonance imaging (MRI) leptomeningeal enhancement (LME). Objective: To investigate how LME relates to GM lesions in relapsing-remitting multiple sclerosis (RRMS) at 7T. Methods: A total of 30 RRMS subjects (age (mean ± standard deviation (SD)): 44.0 ± 11.3 years, 93% on disease-modifying treatment) and 15 controls underwent gadolinium-enhanced three-dimensional (3D) MP2RAGE (magnetization-prepared 2 rapid gradient-echo) and fluid-attenuated inversion recovery (FLAIR) MRI. LME, cortical lesions (CLs), thalamic lesions (TLs), and white matter (WM) lesions were expert-quantified. Wilcoxon rank-sum, two-sample t-tests, Spearman correlations, and regression models were employed. Results: Two-thirds (20/30) of MS subjects and 1/15 controls (6.7%) had LME. LME+ MS subjects had 2.7 ± 1.5 foci, longer disease duration (14.9 ± 10.4 vs. 8.1 ± 5.7 years, p = 0.028), increased CL number (21.5 ± 12.6 vs. 5.5 ± 5.0, p < 0.001) and volume (0.80 ± 1.13 vs. 0.13 ± 0.13 mL, p = 0.002), and increased TL number (3.95 ± 2.11 vs. 0.70 ± 1.34, p < 0.001) and volume (0.106 ± 0.09 vs. 0.007 ± 0.01 mL, p < 0.001) versus LME– subjects. LME focus number correlated more highly with CL (rs = 0.50, p = 0.01) and TL (rs = 0.81, p < 0.001) than WM lesion (rs = 0.34, p > 0.05) volume. Similar LME–CL number associations were observed in unadjusted and WM lesion–adjusted comparisons (both p < 0.001). Conclusion: Cerebral LME is common in RRMS at 7T and is independently associated with GM injury. We hypothesize that cerebrospinal fluid (CSF)-related inflammation links cortical and thalamic injury.

Brain activity changes in a monkey model of central post-stroke pain

Central post-stroke pain (CPSP) can occur after stroke in the somatosensory pathway that includes the posterolateral region of the thalamus. Tactile allodynia, in which innocuous tactile stimuli are perceived as painful, is common in patients with CPSP. Previous brain imaging studies have reported plastic changes in brain activity in patients with tactile allodynia after stroke, but a causal relationship between such changes and the symptoms has not been established. We recently developed a non-human primate (macaque) model of CPSP based on thalamic lesions, in which the animals show behavioral changes consistent with the occurrence of tactile allodynia. Here we performed functional magnetic resonance imaging under propofol anesthesia to investigate the changes in brain activation associated with the allodynia in this CPSP model. Before the lesion, innocuous tactile stimuli significantly activated the contralateral sensorimotor cortex. When behavioral changes were observed after the thalamic lesion, equivalent stimuli significantly activated pain-related brain areas, including the posterior insular cortex (PIC), secondary somatosensory cortex (SII), anterior cingulate cortex (ACC), and amygdala. Moreover, when either PIC/SII or ACC was pharmacologically inactivated, the signs of tactile allodynia were dampened. Our results show that increased cortical activity plays a role in CPSP-induced allodynia.

Patient-Reported Prevalence of Non-motor Symptoms Is Low in Adult Patients Suffering From 5q Spinal Muscular Atrophy.

Background: 5q spinal muscular atrophy (SMA) is an autosomal recessive lower motoneuron disease caused by deletion or mutations in the survival motor neuron 1 gene (SMN1) which results in reduced expression of full-length SMN protein. The main symptoms are caused by spinal motor neuron demise leading to muscle atrophy, and medical care mostly refers to motor symptoms. However, new insights of recent studies in severe SMA type I revealed disease involvement of several non-motor regions, for example cardiac, vascular, sensory nerve involvement, and thalamic lesions. Non-motor symptoms (NMS) were previously described in many neurodegenerative diseases i.e., Parkinson's disease and, importantly, also amyotrophic lateral sclerosis.Methods: We screened for NMS in 70 adult patients with SMA type II (SMAII) and type III (SMAIII) and 59 age/sex-matched healthy controls (controls) in a multicenter cross-sectional study including 5 different centers with specialized expertise in medical health care of motoneuron diseases. We used a self-rating questionnaire including 30 different items of gastrointestinal, autonomic, neuropsychiatric, and sleep complaints [NMS questionnaire (NMSQuest)], which is a validated tool in Parkinson's disease.Results: Total NMS burden was low in adult SMA (median: 3 items) and not significantly different compared to controls (median: 2 items). Total NMS of SMA patients did not correlate with disease severity scores. However, the items “swallowing difficulties,” “falling,” and particularly “swelling legs” were significantly more frequently reported in SMA. Neuropsychiatric symptoms were reported in a frequency comparable to controls and were not significantly increased in SMA.Conclusion: Patient-reported prevalence of NMS in adult SMA was low, which does not argue for a clinically relevant multisystemic disorder in SMAII/III. Importantly, adult SMA patients do not seem to suffer more frequently from symptoms of depression or adaptive disorders compared to controls. Our results yield novel information on previously underreported symptoms and will help to improve the medical guidance of these patients.

Uncus Herniation Presenting as Immediate Onset Postoperative Hemichorea

AbstractChorea is defined as a state of excessive spontaneous movements, irregularly timed, nonrepetitive, randomly distributed, and abrupt in character. Thalamic and subthalamic lesions are commonly known to cause hemichorea. Here, we describe a patient with hydrocephalus due to aqueductal stenosis that caused hemichorea in the immediate postoperative period due to subthalamic infarct of uncus herniation. Considering that hydrocephalus symmetrically affects the central nervous system, the asymmetric presentation of chorea in the immediate postoperative period after wakening up from anesthesia could be confusing if a possibility of uncus herniation is not considered.

A case of nonalcoholic Wernicke’s encephalopathy due to an extreme diet based on magnetic resonance imaging features

Wernicke’s encephalopathy is a rare occurrence in Indonesia because alcohol consumption is very low. However, in Indonesia, Wernicke’s encephalopathy could be triggered by an inadequate intake of thiamine (vitamin B1) due to an extreme diet for several months. It is a case of a 31-year-old male, who presented to the emergency room with a decreased level of consciousness. According to the family, for the last few weeks, he has become less responsive and less attentive. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) revealed a unique picture with symmetrical lesions in the bilateral medial thalamus, mammillary bodies, periaqueductal gray matter, and the dorsal surface of the medulla oblongata. Clinically, there is no neck stiffness and no fever. The laboratory results from the blood and cerebrospinal fluid have ruled out meningitis. Treatment with thiamine 200 mg t.i.d. has shown an excellent response and significant clinical improvement. The earlier thiamine substitution treatment is started, the better the outcome because thiamine will prevent further injury to the brain and enhance recovery.

Primary diffuse leptomeningeal gliomatosis with parenhycmal infiltration: A clinico- radio-pathological correlation

Primary Diffuse Leptomeningeal Gliomatosis (PDLG), as first described by Moore (1954), is a very rare form of cancer resulting from the meningeal heterotopic astrocytes that convert into malignancies and possibly causing obstruction on the Virchow spaces leading to cystic parenchymal infiltration. This case, 4th documented case of atypical parenchymal infiltration, is a 45 -year old male with gradually progressive headache, difficulty sleeping and profound anxiety, left-sided numbness and seizures. Cranial CT- Scan showed right thalamic lesion without hydrocephalus. A possible thalamic infarct or cavernoma was considered. Subsequent MRI showed the same thalamic lesion but now with focal leptomeningeal enhancement probably secondary to glioma versus tuberculosis. He was given anti-Koch’s medications and steroids. Leptomeningeal biopsy confirmed this malignancy. Post- mortem autopsy revealed thickened leptomeninges, right thalamic mass involving the centromedial and posterolateral portion and small cystic lesions all over the surface. Histopathology showed Virchow -robin space infiltration proving the parenchymal involvement through the pial vessels. This case highlighted the possibility of parenchymal involvement which challenged the traditional diagnostic criteria and may now serve as a basis for a revised diagnostic criteria . In this case, imaging also showed an underestimation of the extent of atypical brain parenchymal infiltration. Hence, headache coupled by leptomeningeal enhancement should always warrant close imaging surveillance and possibly repeated biopsies to rule out this exceptional condition.

Bilateral Hearing Loss in Wernicke Encephalopathy

Wernicke encephalopathy is a syndrome caused by thiamine deficiency whose three typical symptoms are ophthalomoplegia, ataxia, and confusion. There are also rare reports of bilateral hearing loss, which can be caused by damage to the bilateral inferior colliculus or thalamic lesions, or by energy failure of the cochlea. This case suggests that thiamine should be administered based on the possibility of Wernicke encephalopathy occurring in malnourished or alcoholic patients with sudden bilateral hearing loss. Key Words: Wernicke encephalopathy, Thiamine, Hearing loss, bilateral

Clinical characteristics and magnetic resonance imaging findings in nine patients with nonalcoholic Wernicke's encephalopathy: a retrospective study.

PurposeWernicke’s encephalopathy (WE) is a severe neurological disorder caused by thiamine deficiency. The most common cause of WE is alcoholism. However, there is a significant paucity of information in the existing literature relating to nonalcoholic WE. In this study, we investigated the clinical characteristics and neuroimaging findings of nine patients with nonalcoholic WE.Patients and methodsWe retrospectively collated clinical data from nine patients who had been diagnosed with WE in accordance with established criteria including age, gender, risk factors and clinical manifestations. We also collated initial hematological and neuroimaging findings.ResultsThe mean age of the nine patients was 54.0±17.1 years; four of these patients (44.4%) were male. All nine patients had a history of fasting (range, 5–47 days) prior to WE. Four of the nine patients (44.4%) exhibited the classical triad, and eight (88.9%) showed alterations in mental status. Magnetic resonance imaging (MRI) scans showed that all nine patients had symmetric lesions of the medial thalamus. MRI also revealed other WE-related lesions in mammillary bodies (22.2%), the periaqueductal region (55.6%), the tectal plate of the midbrain (77.8%), cranial nerve nuclei (77.8%) and in the symmetric subcortical white matter (11.1%).ConclusionOur analysis showed that fasting is a common cause of WE in nonalcoholic patients and that MRI is a useful tool for the diagnosis of WE. The most common MRI findings were symmetrical lesions of the medial thalamus lesions, followed by the tectal plate of the midbrain and cranial nerve nuclei.

B-01 Cognitive Deficits Following Hemorrhagic Stroke in Reversible Cerebral Vasoconstriction Syndrome: A Case Study

Abstract Objective Reversible cerebral vasoconstriction syndrome (RCVS), a relatively rare condition presenting as severe thunderclap headache with or without neurological deficits, is characterized by vasoconstriction of cerebral arteries which often resolves within three months and may be associated with stroke. Previous case reports examining neuropsychological profiles of RCVS patients demonstrated stroke-specific and/or diffuse global impairments that often exceed impairment expected post-acute phase of clinical stroke and possibly suggest residual deficits related to RCVS alone (Perdices &amp; Herkes, 2018). Method The present case is a 36-year-old right-handed African-American male who sustained a left thalamic hemorrhage with extension into the ventricular system following marijuana use. Cerebral angiogram was suggestive of RCVS. The Montreal Cognitive Assessment (MoCA), Western Aphasia Battery (WAB), Repeatable Battery for the Assessment of Neuropsychological Status- Update (RBANS), and Peabody Picture Vocabulary Teat- 4th edition (PPVT-4) were administered at bedside. Results Neuropsychological testing was abnormal with severe global impairments on tasks requiring attention and processing speed, visuospatial abilities, immediate and delayed memory, and executive functioning. The patient’s expressive speech was characterized by fluent output with pronounced provoked and unprovoked phonemic and semantic paraphasias. Additionally, he evidenced confabulatory responses during memory testing and lost mental set during tasks requiring simultaneous attention. Conclusions Considering the patients clear sensorium at the time of the evaluation, these deficits extend beyond what would be expected by a single thalamic lesion and implicate more generalized cerebral dysfunction secondary to his RCVS. Consistent with previous case studies, this case demonstrates how RCVS may confound and contribute to neurocognitive deficits even after hemorrhagic stroke.

Psychiatric Symptoms and Benzodiazepine Use Mask a Patent Foramen Ovale-Related Stroke: A Cautionary Tale.

Neurological and psychiatric diseases often present with overlapping features. Patients are sometimes seen by internal medicine, neurology and psychiatry clinicians and time can be important for determining whether a condition is organic or not.The authors present the case of a 31-year-old woman admitted to the emergency department with altered mental status and incomprehensible speech. She had a previous history of anxiety and smoking and was under therapy with benzodiazepines and combined hormonal contraceptives.After an acute neurological disorder was ruled out, the patient was transferred to the psychiatry department, where she was re-evaluated after 12 hours of observation and benzodiazepine washout. As speech impairment and confusion were still present, she was transferred to the Stroke Unit. A bilateral thalamic lesion containing a small focal haemorrhage and a moderate grade right-to-left shunt were identified. A patent foramen ovale was confirmed leading to the final diagnosis of acute ischaemic infarction secondary to a paradoxical embolism.Medical therapy was preferred over percutaneous closure. Risk factors were removed (smoking and hormonal contraceptives), and after the patient recovered completely acetylsalicylic acid 100 mg daily was initiated.LEARNING POINTSPsychiatric symptoms and medication often mask organic conditions, so observation and re-evaluation are key.There are new guidelines for the treatment of patent foramen ovale-related strokes, but not all patients fit the guidelines.A relationship between stroke in the young adult, smoking and hormonal contraceptives should always be considered.

Migrainous Headache and Gliotic Thalamic Lesion after Treated Neuroblastoma in Childhood

Migrainous Headache and Gliotic Thalamic Lesion after Treated Neuroblastoma in Childhood

PB1774 ACUTE PROMYELOCYTIC LEUKEMIA PRESENTING AS VERTEBROBASILAR ISCHEMIC STROKE IN A YOUNG WOMAN

Background:Acute Promyelocytic Leukemia (APL) carries a high risk of early death due to coagulopathy triggered by the leukemic cells, which initiate a cascade of disseminated intravascular coagulation and hyperfibrinolysis. Patients are at risk for hemorrhagic and thrombotic events, but bleeding dominates the clinical picture and is responsible for most of the early deaths.Arterial thrombosis is rare in APL, and its mortality is extremely high. The best management strategy when occurring in APL is unknown, since anticoagulants or fibrinolytics may aggravate the CID but without them the thrombosis may be fatal.Aims:We present a rare case of APL presenting as a vertebrobasilar ischemic stroke, which evolved favorably with treatment of the subjacent leukemia alone, without use of anticoagulation or antiaggregation.Methods:Case report.Results:A 36‐year old previously healthy woman presented with sudden onset aphasia and right‐sided hemiparesis with central facial paralysis, vertical gaze palsy and loss of horizontal gaze to the left.Blood work showed anemia (Hb 6.6 g/dL), a white blood cell (WBC) count of 7900x109/L of which 62% were atypical promyelocytes, and 19,000 x109/L platelets (Figure 1‐A). A concomitant disseminated intravascular coagulation was diagnosed based on thrombocytopenia, hypofibrinogenemia (100 mg/dL), prolonged prothrombin time (&gt; seconds) and elevated D‐dimers (10,98 μg/mL). These findings raised the suspicion of Acute Promyelocytic Leukemia, an entity usually associated with bleeding but also rarely with thrombosis.Emergent head CT and angio‐CT scan showed no lesions. Based on the neurological findings, a presumptive diagnosis of vertebrobasilar ischemic stroke was established, and thrombolysis with alteplase was indicated. However, the risks of aggravating the bleeding predisposition of the patient and precipitating hemorrhagic transformation of the stroke outweighed the benefits, and both alteplase and anticoagulants were withheld.Instead, management focused on treating the leukemia. Oral all‐trans retinoic acid was immediately initiated, and idarrubicin was added after confirming major infiltration of the bone marrow with atypical promyelocytes. Surprisingly, the hallmark translocation t(15;17) was not detected by fluorescence in‐situ hybridization (FISH), but the fusion transcript PML‐RARα was identified by reverse transcription with polymerase chain reaction (RT‐PCR), thus confirming a diagnosis of cryptic APL.A magnetic resonance of the head performed 24 hours later showed hyperintense lesions in the left thalamus, caudate and midbrain, and right parietal operculum (Figure 1).The patient achieved hematologic complete remission after induction therapy and recovered to a mild right hemiplegia after intensive physical rehabilitation. She is currently in molecular complete remission and is undergoing maintenance treatment in the outpatient setting, medicated with dipyridamole as secondary stroke prevention.Summary/Conclusion:The management of thrombotic events in APL is a challenge, since the increased bleeding risk associated with anticoagulation must be weighed against the potential lethality of the thrombosis if it is left untreated. Central nervous system arterial thrombosis has a particularly poor prognosis.imageWe present a case that illustrates the importance of early APL treatment with ATRA and supportive measures in reverting the coagulopathy of the disease.