Neurological Examination Research Articles

Left middle cerebral artery and sigmoid sinuses thrombosis in a female patient with Crohn's disease

Introduction: Neurologic manifestations in patients with inflammatory bowel disease (IBD) appear to be more common than in the past. However, vascular events in IBD are still a rare presentation and were reported in few cases. Case presentation: A 48-year-old female patient known case of Crohn’s disease presented with sudden onset aphasia, headache, blurring of vision, and decreased level of consciousness for 2 hours. The patient looked ill, confused, agitated, and aphasic. Neurologic examination shows dysarthria and 0/5 power of the right upper and lower extremity. A brain CT without contrast was ordered and showed acute ischemic stroke. The patient received tPA (alteplase) immediately in the intensive care unit and was under observation. On admission, brain CT angiography, MRI, and MRV were performed, which showed middle cerebral artery and sigmoid sinuses thrombosis. The patient has undergone cerebral catheterization, and an MCA stent was inserted. Post catheterization, the patient’s right-sided extremity power was improved to 3/5. She was discharged from the hospital after 13 days in good general condition except for her expressive aphasia. Conclusion: To the best of our knowledge, here we report the first case presented with both; cerebral venous sinus thrombosis and cerebral arteries thrombosis in a patient with IBD. Clinicians must be considered ischemic stroke in any patients with IBD presented with acute neurological manifestation, and an urgent interventional approach must be performed.

Endovascular treatment of direct carotid cavernous fistula resulting from rupture of intracavernous carotid aneurysm: A case report

BACKGROUND Direct carotid cavernous fistulas (CCFs) are typically the result of a severe traumatic brain injury. High-flow arteriovenous shunts secondary to rupture of an intracavernous aneurysm, resulting in direct CCFs, are rare. The use of a pipeline embolization device in conjunction with coils and Onyx glue for treatment of direct high-flow CCF resulting from ruptured cavernous carotid artery aneurysm in a clinical setting is not well documented. CASE SUMMARY A 58-year-old woman presented to our department with symptoms of blepharoptosis and intracranial bruits for 1 wk. During physical examination, there was right eye exophthalmos and ocular motor palsy. The rest of the neurological examination was clear. Notably, the patient had no history of head injury. The patient was treated with a pipeline embolization device in the ipsilateral internal carotid artery across the fistula. Coils and Onyx were placed through the femoral venous route, followed by placement of the pipeline embolization device with assistance from a balloon-coiling technique. No intraoperative or perioperative complications occurred. Preoperative symptoms of bulbar hyperemia and bruits subsided immediately after the operation. CONCLUSION Pipeline embolization device in conjunction with coiling and Onyx may be a safe and effective approach for direct CCFs.

Vessel wall imaging in the diagnosis of antiphospholipid syndrome presenting as Moyamoya syndrome-A case report.

Objectives: We describe a case of anti-phospholipid syndrome (APLS) vasculopathy presenting with Moyamoya syndrome (MMS) and show the associated intracranial vessel wall MRI (VWI) findings. Methods: A 37-year-old-woman presented with acute onset dizziness and left-sided weakness. Neurologic exam revealed a left facial droop and left hemiparesis. She underwent a comprehensive laboratory work-up for stroke. Neuroimaging included a CT head, CT angiogram, VWI, and digital subtraction angiography. Results: Work-up revealed a triple-positive APLS antibody profile. CT of the head showed an acute right basal ganglia infarction and right frontal subarachnoid hemorrhage. CT angiogram revealed severe stenosis of the right internal carotid artery terminus in a Moyamoya pattern. Intracranial VWI showed long-segment concentric vessel wall thickening and homogeneous vessel wall enhancement and T2-hyperintense wall edema of the stenotic right ICA terminus, M1 middle cerebral artery, and A1 anterior cerebral artery. She was treated with long-term anticoagulation with warfarin and a right superficial temporal artery to middle cerebral artery bypass. Discussion: We present intracranial VWI features of vessel wall pathology in a patient with primary APLS presenting with MMS.

Spinal Cord Medulloepithelioma in a Cat

A 13-month-old, neutered, male, domestic shorthair cat was referred with a history of progressive paraparesis, proprioceptive ataxia, and lumbar spinal pain. Neurological examination revealed non-ambulatory paraparesis consistent with L4-S1 myelopathy. Magnetic resonance of the thoracolumbar spinal cord identified a dorsal intradural extramedullary space-occupying lesion extending from L5 to L6. It was homogeneously hyperintense in T2-weighted imaging and isointense in T1-weighted imaging and exhibited marked and homogeneous contrast enhancement in the T1-weighted post-contrast imaging. The removed tissue was composed of neoplastic cells arranged as pseudostratified or multilayered trabecular and tubular structures, supported by internal and external limiting PAS-positive membranes. The neoplastic cells were immunoreactive for vimentin and NSE and negative for GFAP, Olig2, synaptophysin, PCK, S-100, NeuN, and nestin. The Ki-67 nuclear labeling index was up to 90%. The tumor was consistent with the diagnosis of medulloepithelioma, which is most frequently reported as an intraocular tumor. The morphological and immunohistochemical features of the tumor showed remarkable concordance with most human medulloepitheliomas. This is the first spinal cord medullopethelioma report in a cat, with the clinical, neuroradiological, histological, and immunohistochemical findings being described.

Equine neuroaxonal dystrophy/degenerative myeloencephalopathy in Gypsy Vanner horses.

Equine neuroaxonal dystrophy/degenerative myeloencephalopathy (eNAD/EDM) is a neurodegenerative disease that primarily affects young, genetically predisposed horses that are deficient in vitamin E. Equine NAD/EDM has not previously been documented in Gypsy Vanner horses (GVs). To evaluate: (1) the clinical phenotype, blood vitamin E concentrations before and after supplementation and pedigree in a cohort of GV horses with a high prevalence of neurologic disease suspicious for eNAD/EDM and (2) to confirm eNAD/EDM in GVs through postmortem evaluation. Twenty-six GVs from 1 farm in California and 2 cases from the Midwestern U.S. Prospective observational study on Californian horses; all 26 GVs underwent neurologic examination. Pre-supplementation blood vitamin E concentration was assessed in 17- GVs. Twenty-three were supplemented orally with 10 IU/kg of liquid RRR-alpha-tocopherol once daily for 28 days. Vitamin E concentration was measured in 23 GVs after supplementation, of which 15 (65%) had pre-supplementation measurements. Two clinically affected GVs from California and the 2 Midwestern cases had necropsy confirmation of eNAD/EDM. Pre-supplementation blood vitamin E concentration was ≤2.0 μg/mL in 16/17 (94%) of GVs from California. Post-supplementation concentration varied, with a median of 3.39 μg/mL (range, 1.23-13.87 μg/mL), but only 12/23 (52%) were normal (≥3.0 μg/mL). Normalization of vitamin E was significantly associated with increasing age (P = .02). Euthanized horses (n = 4) had eNAD/EDM confirmed at necropsy. GVs could have a genetic predisposition to eNAD/EDM. Vitamin E supplementation should be considered and monitored in young GVs.

Lenalidomide‐induced posterior reversible encephalopathy syndrome: A case report

AbstractPosterior reversible encephalopathy syndrome (PRES) is a disorder of cerebrovascular dysregulation. To our knowledge, we present the first case of lenalidomide‐induced PRES in English. A 59‐year‐old woman with history of multiple myeloma status post stem cell transplant and induction triple therapy 6 months ago with partial remission and subsequent high‐dose melphalan 1 month ago presented with progressive vision loss for 1 week. Her systolic blood pressure was >180 mmHg, and neurological examination demonstrated decreased vision bilaterally. Brain MRI revealed significant T2 hyperintensity restricted to temporal and occipital lobes and left occipital parenchymal hemorrhage and diffuse leptomeningeal enhancement. She had a witnessed generalized tonic–clonic seizure and EEG that captured an electrographic seizure originating from the occipital lobe. Her vision improved rapidly after discontinuing the lenalidomide. She was discharged to rehab with a normal neurological examination. We report the first English case of presumed lenalidomide induced PRES in a patient undergoing multiple myeloma treatment.

Uraemic brainstem encephalopathy mimicking ocular myasthenia: a case report

BackgroundUraemia causes a generalised encephalopathy as its most common neurological complication. Isolated brainstem uraemic encephalopathy is rare. We report a case of fatigable ptosis and complex ophthalmoplegia in brainstem uraemic encephalopathy.Case presentationA 22-year-old Sri Lankan man with end stage renal failure presented with acute onset diplopia and drooping of eyelids progressively worsening over one week. The patient had not complied with the prescribed renal replacement therapy which was planned to be initiated 5 months previously. On examination, his Glasgow coma scale score was 15/15, He had a fatigable asymmetrical bilateral ptosis. The ice-pack test was negative. There was a complex ophthalmoplegia with bilateral abduction failure and elevation failure of the right eye. The diplopia did not worsen with prolonged stare. The rest of the neurological examination was normal. Serum creatinine on admission was 21.81 mg/dl. The repetitive nerve stimulation did not show a decremental pattern. Magnetic resonance imaging (MRI) of the brain demonstrated diffuse midbrain and pontine oedema with T2 weighted/FLAIR hyperintensities. The patient was haemodialyzed on alternate days and his neurological deficits completely resolved by the end of the second week of dialysis. The follow up brain MRI done two weeks later demonstrated marked improvement of the brainstem oedema with residual T2 weighted/FLAIR hyperintensities in the midbrain.ConclusionsUraemia may rarely cause an isolated brainstem encephalopathy mimicking ocular myasthenia, which resolves with correction of the uraemia.

Evaluation of the diagnostic value of transcranial electrical stimulation (TES) to assess neuronal functional integrity in horses

Medical imaging allows for the visualization of spinal cord compression sites; however, it is impossible to assess the impact of visible stenotic sites on neuronal functioning, which is crucial information to formulate a correct prognosis and install targeted therapy. It is hypothesized that with the transcranial electrical stimulation (TES) technique, neurological impairment can be reliably diagnosed.ObjectiveTo evaluate the ability of the TES technique to assess neuronal functional integrity in ataxic horses by recording TES-induced muscular evoked potentials (MEPs) in three different muscles and to structurally involve multiple ancillary diagnostic techniques, such as clinical neurological examination, plain radiography (RX) with ratio assessment, contrast myelography, and post-mortem gross and histopathological examination.MethodsNine ataxic horses, showing combined fore and hindlimb ataxia (grades 2–4), were involved, together with 12 healthy horses. TES-induced MEPs were recorded bilaterally at the level of the trapezius (TR), the extensor carpi radialis (ECR), and tibialis cranialis (TC) muscles. Two Board-certified radiologists evaluated intra- and inter-sagittal diameter ratios on RX, reductions of dorsal contrast columns, and dural diameters (range skull-T1). Post-mortem gross pathological and segmental histopathological examination was also performed by a Board-certified pathologist.ResultsTES-MEP latencies were significantly prolonged in both ECR and TC in all ataxic horses as opposed to the healthy horses. The TR showed a mixed pattern of normal and prolonged latency times. TES-MEP amplitudes were the least discriminative between healthy and ataxic horses. Youden’s cutoff latencies for ataxic horses were 24.6 ms for the ECR and 45.5 ms for the TC (sensitivity and specificity of 100%). For healthy horses, maximum latency values were 22 and 37 ms, respectively. RX revealed spinal cord compression in 8 out of 9 involved ataxic horses with positive predictive values of 0–100%. All ataxic horses showed multi-segmental Wallerian degeneration. All pathological changes recorded in the white matter of the spinal cord were widely dispersed across all cervical segments, whereas gray matter damage was more localized at the specific segmental level.ConclusionTES-MEP latencies are highly sensitive to detect impairment of spinal cord motor functions for mild-to-severe ataxia (grades 2–4).

Evaluation of peripheral and autonomic nervous systems dysfunctions in patients with Parkinson’s disease

BackgroundPeripheral neuropathy (PN) is increasingly recognized in Parkinson’s disease (PD). This study aimed to evaluate peripheral nerve and autonomic nervous system dysfunction in PD. Forty patients with PD (20 drug-naïve, 20 on treatment) and 20 controls underwent neurological examination, Toronto Clinical Neuropathy Score (TCNS), nerve conduction studies, autonomic function tests including (heart rate variability, Blood pressure changes with standing and sustained handgrip, and sudomotor pathways. The Ewing classification system scored each test to quantify autonomic failure severity). Laboratory tests (B12, homocysteine, methylmalonic acid).ResultsTreated patients with PD had higher MDS-UPDRS scores than drug-naïve (p = 0.001). TCNS indicated mild PN in some drug-naïve patients, and mild–moderate PN in treated patients. Nerve conduction studies showed significant sensory and motor neuropathy in treated versus drug-naïve PD and controls. Treated patients had lower B12, higher homocysteine/methylmalonic acid than other groups. Across autonomic tests, controls had the most normal results, followed by drug-naïve patients, with treated patients being most abnormal. Autonomic dysfunction correlated with disease duration, severity, L-dopa dose. Lower B12, higher homocysteine/methylmalonic acid levels were associated with greater neuropathy and disease severity.ConclusionPatients with PD show evidence of PN and autonomic dysfunction, which is milder in drug-naïve patients but worsens with disease progression and treatment. Peripheral nervous system assessments may help diagnose and monitor PD neuropathy and effects of interventions.

Successful Treatment of Cerebral Tuberculoma in Acquired Immune Deficiency Syndrome Patient a Case Report

Introduction: Tuberculosis (TB) remains a leading problem in developing and endemic countries. Cerebral tuberculosis is a rare but dangerous complication of tuberculosis infection in the central nervous system. The immunosuppressive condition in human immunodeficiency virus infection is a risk factor for severe tuberculosis. Case Report: An Indonesian man, 32 years old, married, came with complaints of headaches, dizziness, delirium, nausea and vomiting since 1 month before the examination. He had a history of TB treatment 1 year before the examination. The results of the neurological examination were within normal limits, the HIV test was reactive and there was a decrease in CD4. Head MRI examination with contrast showed multiple solid nodules in the thalamus with the largest size 2.3×2.7 cm, indicating cerebral tuberculoma. Chest x-ray was normal, GeneXpert MTB sputum was not detected. Next, primary treatment is given with anti-tuberculosis drugs, Highly Active Antiretroviral Therapy (HAART), co-trimoxazole, and dexamethasone. There was clinical, laboratory and radiological improvement after 12 months of treatment. Viral load is undetectable, CD4 is elevated. A head CT scan did not show tuberculoma. He became healthy and was able to return to work Discussion: Cerebral tuberculoma is a condition characterized by the presence of intracranial tuberculoma. The clinical manifestations are non-specific, such as headaches or seizures. This is caused by space occupying lesions and increase intracranial pressure. In this case, the diagnosis of cerebral tuberculoma was made through head MRI with contrast. TB therapy and co-trimoxazole are given as soon as the diagnosis is made, while antiretrovirals are given 2 weeks after he has tolerated the TB medication. The minimum duration of therapy for cerebral tuberculosis is 12 months. He require lifelong antiretroviral medication. Conclusion: Tuberculoma should be considered as differential diagnosis of space-occupying lesions in patients HIV/AIDS. Early diagnosis, adequate therapy, patient adherence and family support can cure severe tuberculosis.

9 “Don’ts” for the Neurological Exam: A Novel Method to Improve Medical Student Neurological Exam Confidence (P1-7.007)

9 “Don’ts” for the Neurological Exam: A Novel Method to Improve Medical Student Neurological Exam Confidence (P1-7.007)

The Neurological Examination: Overcoming Language Barriers to Increase Access to Patient-directed Neurologic Care (P1-4.013)

The Neurological Examination: Overcoming Language Barriers to Increase Access to Patient-directed Neurologic Care (P1-4.013)

Subarachnoid Hemorrhage Depletes Calcitonin Gene-Related Peptide Levels of Trigeminal Neurons in Rat Dura Mater

Subarachnoid hemorrhage (SAH) remains a major cause of cerebrovascular morbidity, eliciting severe headaches and vasospasms that have been shown to inversely correlate with vasodilator calcitonin gene-related peptide (CGRP) levels. Although dura mater trigeminal afferents are an important source of intracranial CGRP, little is known about the effects of SAH on these neurons in preclinical models. The present study evaluated changes in CGRP levels and expression in trigeminal primary afferents innervating the dura mater 72 h after experimentally induced SAH in adult rats. SAH, eliciting marked damage revealed by neurological examination, significantly reduced the density of CGRP-immunoreactive nerve fibers both in the dura mater and the trigeminal caudal nucleus in the medulla but did not affect the total dural nerve fiber density. SAH attenuated ex vivo dural CGRP release by ~40% and in the trigeminal ganglion, reduced both CGRP mRNA levels and the number of highly CGRP-immunoreactive cell bodies. In summary, we provide novel complementary evidence that SAH negatively affects the integrity of the CGRP-expressing rat trigeminal neurons. Reduced CGRP levels suggest likely impaired meningeal neurovascular functions contributing to SAH complications. Further studies are to be performed to reveal the importance of impaired CGRP synthesis and its consequences in central sensory processing.

Long-term course of a case with a novel homozygous kyphoscoliosis peptidase variant.

We herein report a case with a novel homozygous variant in the kyphoscoliosis peptidase (KY) gene. A 58-year-old Japanese female was referred to our hospital with a gait disturbance that gradually worsened after the age of 50. She had bilateral equinus foot deformity since early childhood. Neurological examination revealed moderate weakness of the neck, trunk, femoral, and brachial muscles, mild respiratory failure, and areflexia. Whole-exome sequencing revealed a novel homozygous frameshift variant of the KY gene, NM_178554.6:c.824del p.(Glu275Glyfs*53). Our case demonstrated that KY-associated neuromuscular disease can present with extremely slow progressive muscle weakness and respiratory failure over a long natural course.

Primary CNS vasculitis: insights into clinical, neuropathological, and neuroradiological characteristics

Background and objectivesPrimary CNS vasculitis (PCNSV) is a rare inflammatory disorder that affects the blood vessels of the central nervous system (CNS). We aimed to analyze the neurological presentations, clinical follow-up, and long-term outcomes of patients with primary central nervous system vasculitis.MethodsWe conducted a retrospective analysis of medical records to assess the neurological presentation, rate of remission, and functional status at the last follow-up in patients with primary central nervous system vasculitis seen in our center in the last 13 years (2010–2023).ResultsWe identified five patients, whose median age at symptom onset was 31 years (range: 15–41 years), including four male individuals (80%) from Muslim Arab (n = 4) and Ashkenazi Jewish (n = 1) backgrounds. Symptoms persisted for a median of 36 weeks (range: 3 weeks to 4 years) before diagnosis, with one case exceeding 3 years. Follow-up lasted a median of 56 months (range: 20–161 months). Clinical symptoms varied, presenting unilateral weaknesses (n = 2), cognitive and gait abnormality (n = 1), headaches (n = 1), and epileptic seizures (n = 1). MRI scans revealed abnormalities in the basal ganglia, corona radiata, parietal, and frontal lobes, showing hemorrhage, vasogenic edema, restricted diffusion, and enhancement post-gadolinium. All patients reported progressive holocephalic headaches and cognitive changes with overall progressive symptoms. Initial neurological examinations revealed abnormalities in all patients and included one or more of the following: cognitive or visual impairment (n = 2), seizures (n = 1), and unilateral UMN signs (n = 2) at the initial neurological examination, all but one patient required walking aids including (cane 2, wheelchair, bedridden 1). Patients were stable (n = 2), deteriorated (n = 1), or improved (n = 2). Following treatment, two patients still required ambulatory aids, with one using a cane and the other using a wheelchair, while the remaining three did not require any ambulatory aids.DiscussionThe study on PCNSV highlights varied symptoms and diagnostic challenges, including delayed diagnosis and a spectrum of neurological issues from cognitive impairments to seizures. Brain biopsies showed lymphocytic infiltration, thrombi, and necrosis. Immunotherapy significantly improved clinical and radiological outcomes. Over 56 months of follow-up, outcomes varied from stability and deterioration to improvement.

Revolutionizing Neonatal Care: A Comprehensive Assessment of Neuromotor Development in At-Risk Infants Using the Novel Neonatal Infant Motor Assessment Scale (NIMAS) Test Battery

We developed a new neonatal neuromotor test battery, the Neonatal Infant Motor Assessment Scale (NIMAS), to perform a detailed neuromotor and holistic assessment of at-risk infants in the neonatal period. Methods: A total of 68 infants (28–41 Gestational weeks) hospitalised in the Neonatal Intensive Care Unit were included in the study. The NIMAS is a scale consisting of Automatic Motor Area, Functional Motor Area and sociodemographic form. The Dubowitz Neurological Examination and the Amiel-Tison Neurological Assessment Tests were also applied to evaluate the construct validity of the test. Results: The mean gestational age at birth was 34.62 ± 3.07 weeks and birth weight was 2305.66 ± 738.95. Fifty-one (75%) of the babies were premature and 17 (25%) were term babies. The KMO value to test the adequacy of the distribution for factor analysis was found to be at a very good level. Barlett’s test result was 2198.389 (p < 0.05). The amount of variance obtained as 44.76% in the study was at a sufficient level. The factor loads of the questions in the automatic motor domain dimension varied between 0.523 and 0.694 and the factor loads of the questions in the functional motor domain dimension varied between 0.619 and 0.772. Since Cronbach’s alpha was above 0.70, the reliability was adequate. Inter-rater scale agreement in the automatic motor domain was 81.1%; scale agreement in the functional motor domFain was 92.9%; and the NIMAS total score agreement was 93.4%. These agreements were statistically significant (p < 0.05). Total correlation above 0.20 indicates that the item is important for the question. According to the results obtained, total correlation values were between 0.258 and 0.720. Conclusions: The NIMAS is the first test battery to assess the “Functional Motor Area” and this questionnaire, based on the results of the analyses, is a valid, reliable and clinically usable measurement tool for the infant at-risk at the neonatal period.

Streptococcus intermedius causing primary bacterial ventriculitis in a patient with severe periodontitis - a case report

BackgroundStreptococcus intermedius is a member of the S. anginosus group and is part of the normal oral microbiota. It can cause pyogenic infections in various organs, primarily in the head and neck area, including brain abscesses and meningitis. However, ventriculitis due to periodontitis has not been reported previously.Case presentationA 64-year-old male was admitted to the hospital with a headache, fever and later imbalance, blurred vision, and general slowness. Neurological examination revealed nuchal rigidity and general clumsiness. Meningitis was suspected, and the patient was treated with dexamethasone, ceftriaxone and acyclovir. A brain computer tomography (CT) scan was normal, and cerebrospinal fluid (CSF) Gram staining and bacterial cultures remained negative, so the antibacterial treatment was discontinued. Nine days after admission, the patient’s condition deteriorated. The antibacterial treatment was restarted, and a brain magnetic resonance imaging revealed ventriculitis. A subsequent CT scan showed hydrocephalus, so a ventriculostomy was performed. In CSF Gram staining, chains of gram-positive cocci were observed. Bacterial cultures remained negative, but a bacterial PCR detected Streptococcus intermedius. An orthopantomography revealed advanced periodontal destruction in several teeth and periapical abscesses, which were subsequently operated on. The patient was discharged in good condition after one month.ConclusionsPoor dental health can lead to life-threatening infections in the central nervous system, even in a completely healthy individual. Primary bacterial ventriculitis is a diagnostic challenge, which may result in delayed treatment and increased mortality.

Impact of Upper Limb Motor Recovery on Functional Independence After Traumatic Low Cervical Spinal Cord Injury.

Cervical spinal cord injury (SCI) causes devastating loss of upper limb function and independence. Restoration of upper limb function can have a profound impact on independence and quality of life. In low-cervical SCI (level C5-C8), upper limb function can be restored via reinnervation strategies such as nerve transfer surgery. The translation of recovered upper limb motor function into functional independence in activities of daily living (ADLs), however, remains unknown in low cervical SCI (i.e., tetraplegia). The objective of this study was to evaluate the association of patterns in upper limb motor recovery with functional independence in ADLs. This will then inform prioritization of reinnervation strategies focused to maximize function in patients with tetraplegia. This retrospective study performed a secondary analysis of patients with low cervical (C5-C8) enrolled in the SCI Model Systems (SCIMS) database. Baseline neurological examinations and their association with functional independence in major ADLs-i.e., eating, bladder management, and transfers (bed/wheelchair/chair)-were evaluated. Motor functional recovery was defined as achieving motor strength, in modified research council (MRC) grade, of ≥ 3 /5 at one year from ≤ 2/5 at baseline. The association of motor function recovery with functional independence at one-year follow-up was compared in patients with recovered elbow flexion (C5), wrist extension (C6), elbow extension (C7), and finger flexion (C8). A multi-variable logistic regression analysis, adjusting for known factors influencing recovery after SCI, was performed to evaluate the impact of motor function at one year on a composite outcome of functional independence in major ADLs. Composite outcome was defined as functional independence measure score of 6 or higher (complete independence) in at least two domains among eating, bladder management, and transfers. Between 1992 and 2016, 1090 patients with low cervical SCI and complete neurological/functional measures were included. At baseline, 67% of patients had complete SCI and 33% had incomplete SCI. The majority of patients were dependent in eating, bladder management, and transfers. At one-year follow-up, the largest proportion of patients who recovered motor function in finger flexion (C8) and elbow extension (C7) gained independence in eating, bladder management, and transfers. In multi-variable analysis, patients who had recovered finger flexion (C8) or elbow extension (C7) had higher odds of gaining independence in a composite of major ADLs (odds ratio [OR] = 3.13 and OR = 2.87, respectively, p < 0.001). Age 60 years (OR = 0.44, p = 0.01), and complete SCI (OR = 0.43, p = 0.002) were associated with reduced odds of gaining independence in ADLs. After cervical SCI, finger flexion (C8) and elbow extension (C7) recovery translate into greater independence in eating, bladder management, and transfers. These results can be used to design individualized reinnervation plans to reanimate upper limb function and maximize independence in patients with low cervical SCI.

Fibrocartilaginous embolism: a rare cause of cervical spine infarction

Introduction and importance: One of the uncommon causes of ischaemic myelopathy is fibrocartilaginous embolisation, which results from the intersomatic disc nucleus pulposus becoming embolised into the spinal vasculature during Valsalva-like manoeuvres. Case presentation: A 29-year-old female patient presented to the authors’ emergency department with general weakness, dizziness, and an inability to move her right hand after a minor trauma. These symptoms deteriorated suddenly until the patient became quadriplegic. The clinical picture and MRI led to a diagnosis of fibrocartilaginous embolism. Clinical discussion: Fibrocartilaginous embolism is a rare cause of spine infarction. There is still little understanding of the underlying cause of FCE. Most cases occur sporadically in people without a family history of the disease, such as the authors’ case, and diagnosis is based on imaging of the spinal cord and ruling out other causes of a blockage in the vascular system within the spinal cord, infectious and inflammatory causes. Conclusion: When a practitioner suspects that a patient may have fibrocartilaginous embolism (FCE), they should take the patient’s history and do a neurological examination. An MRI is required since it is thought to be the most accurate method of diagnosing FCE.

Neuroimaging-guided diagnosis of possible FTLD-FUS pathology: a case report

BackgroundThis case report presents a patient with progressive memory loss and choreiform movements.Case presentationNeuropsychological tests indicated multi-domain amnestic mild cognitive impairment (aMCI), and neurological examination revealed asymmetrical involuntary hyperkinetic movements. Imaging studies showed severe left-sided atrophy and hypometabolism in the left frontal and temporoparietal cortex. [18F]Flortaucipir PET exhibited moderately increased tracer uptake in hypometabolic areas. The diagnosis initially considered Alzheimer’s disease (AD), frontotemporal degeneration (FTD), and corticobasal degeneration (CBD), cerebral hemiatrophy syndrome, but imaging and cerebrospinal fluid analysis excluded AD and suggested fused-in-sarcoma-associated FTD (FTLD-FUS), a subtype of the behavioural variant of FTD.ConclusionsOur case highlights that despite the lack of specific FUS biomarkers the combination of clinical features and neuroimaging biomarkers can guide choosing the most likely differential diagnosis in a complex neurological case. Imaging in particular allowed an accurate measure of the topography and severity of neurodegeneration and the exclusion of AD-related pathology.