1.Posterior Surgery for Cervical Myelopathy: Laminectomy, Laminectomy with Fusion, and Laminoplasty.
Asian Spine Journal 2008;2(2):114-126
No abstract available.
Laminectomy
2.Physical Signs and Clinical Features of Cervical Myelopathy in Elderly Patients, Especially 80 Years or Older: Comparison of 100 Consecutive Operative Cases across Three Age Groups
Takahiko HAMASAKI ; Toshio NAKAMAE ; Naosuke KAMEI ; Yasushi FUJIWARA ; John M. RHEE ; Nobuhiro TANAKA ; Yoshinori FUJIMOTO ; Nobuo ADACHI ; Shoji SHIMOSE
Asian Spine Journal 2023;17(5):916-921
Methods:
We evaluated 100 consecutive surgical patients with CM and divided them into the following groups: 80s (34 patients; mean age, 83.9 years), 70s (33 patients; mean age, 73.9 years), and 69 or younger (33 patients; mean age, 60.9 years). The clinical symptoms and physical signs were evaluated and recorded.
Results:
Although the recovery rate decreased with increasing age, all groups demonstrated a significant improvement in clinical symptoms relative to preoperative values. The Hoffman sign and hyperreflexia of the triceps tendon were, respectively, present in 82% and 88% of patients in the 80s group, 74% and 64% of those in the 70s group, and 69% and 82% of those in the 69 or younger group, with no significant difference among the groups. In contrast, the rates of hyperreflexia of the patellar and Achilles tendons were, respectively, 59% and 32% in the 80s group, 85% and 48% in the 70s group, and 91% and 70% in the 69 or younger group, with significant differences.
Conclusions
The positivity rate of the lower extremity hyperreflexia decreased significantly with increasing age in patients with CM. The absence of hyperreflexia, particularly lower extremity, is not uncommon in elderly patients with suspected CM.
3.A Comparison of Computed Tomography Measures for Diagnosing Cervical Spinal Stenosis Associated with Myelopathy: A Case-Control Study.
Brett A FREEDMAN ; C Edward HOFFLER ; Brian M CAMERON ; John M RHEE ; Maneesh BAWA ; David G MALONE ; Melissa BENT ; Tim S YOON
Asian Spine Journal 2015;9(1):22-29
STUDY DESIGN: Retrospective comparative study. PURPOSE: To assess differences in computed tomography (CT) imaging parameters between patients with cervical myelopathy and controls. OVERVIEW OF LITERATURE: There is a lack of information regarding the best predictor of symptomatic stenosis based on osseous canal dimensions. We postulate that smaller osseous canal dimensions increase the risk of symptomatic central stenosis. METHODS: CT images and medical records of patients with cervical myelopathy (19 patients, 8 males; average age, 64.4+/-13.4 years) and controls (18 patients, 14 males; average age, 60.4+/-11.0 years) were collected. A new measure called the laminar roof pitch angle (=angle between the lamina) was conducted along with linear measures, ratios and surrogates of canal perimeter and area at each level C2-C7 (222 levels). Receiver-operator curves were used to assess the diagnostic value of each. Rater reliability was assessed for the measures. RESULTS: The medial-lateral (ML) diameter (at mid-pedicle level) and calculated canal area (=anterior-posterior. x ML diameters) were the most accurate and highly reliable. ML diameter below 23.5 mm and calculated canal area below 300 mm2 generated 82% to 84% sensitivity and 67% to 68% sensitivity. No significant correlations were identified between age, height, weight, body mass in dex and gender for each of the CT measures. CONCLUSIONS: CT measures including ML dimensions were most predictive. This study is the first to identify an important role for the ML dimension in cases of slowly progressive compressive myelopathy. A ML reserve may be protective when the canal is progressively compromised in the anterior-posterior dimension.
Body Weight
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Case-Control Studies*
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Constriction, Pathologic
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Humans
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Male
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Medical Records
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Retrospective Studies
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Spinal Cord Compression
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Spinal Cord Diseases*
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Spinal Stenosis*
4.Circadian Polymorphisms in Night Owls, in Bipolars, and in Non-24-Hour Sleep Cycles.
Daniel F KRIPKE ; Walter T KLIMECKI ; Caroline M NIEVERGELT ; Katharine M REX ; Sarah S MURRAY ; Tatyana SHEKHTMAN ; Gregory J TRANAH ; Richard T LOVING ; Heon Jeong LEE ; Min Kyu RHEE ; Farhad F SHADAN ; J Steven POCETA ; Shazia M JAMIL ; Lawrence E KLINE ; John R KELSOE
Psychiatry Investigation 2014;11(4):345-362
People called night owls habitually have late bedtimes and late times of arising, sometimes suffering a heritable circadian disturbance called delayed sleep phase syndrome (DSPS). Those with DSPS, those with more severe progressively-late non-24-hour sleep-wake cycles, and those with bipolar disorder may share genetic tendencies for slowed or delayed circadian cycles. We searched for polymorphisms associated with DSPS in a case-control study of DSPS research participants and a separate study of Sleep Center patients undergoing polysomnography. In 45 participants, we resequenced portions of 15 circadian genes to identify unknown polymorphisms that might be associated with DSPS, non-24-hour rhythms, or bipolar comorbidities. We then genotyped single nucleotide polymorphisms (SNPs) in both larger samples, using Illumina Golden Gate assays. Associations of SNPs with the DSPS phenotype and with the morningness-eveningness parametric phenotype were computed for both samples, then combined for meta-analyses. Delayed sleep and "eveningness" were inversely associated with loci in circadian genes NFIL3 (rs2482705) and RORC (rs3828057). A group of haplotypes overlapping BHLHE40 was associated with non-24-hour sleep-wake cycles, and less robustly, with delayed sleep and bipolar disorder (e.g., rs34883305, rs34870629, rs74439275, and rs3750275 were associated with n=37, p=4.58E-09, Bonferroni p=2.95E-06). Bright light and melatonin can palliate circadian disorders, and genetics may clarify the underlying circadian photoperiodic mechanisms. After further replication and identification of the causal polymorphisms, these findings may point to future treatments for DSPS, non-24-hour rhythms, and possibly bipolar disorder or depression.
Bipolar Disorder
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Case-Control Studies
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Comorbidity
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Depression
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Genetics
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Haplotypes
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Humans
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Melatonin
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Phenotype
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Photoperiod
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Polymorphism, Single Nucleotide
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Polysomnography
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Sleep Wake Disorders, Circadian Rhythm
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Strigiformes*