Faculty Bibliography
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36
Rapid Number Naming and Quantitative Eye Movements May Reflect Contact Sport Exposure in a Collegiate Ice Hockey Cohort
BACKGROUND: The King-Devick (K-D) test of rapid number naming is a reliable visual performance measure that is a sensitive sideline indicator of concussion when time scores worsen (lengthen) from preseason baseline. Within cohorts of youth athletes <18 years old, baseline K-D times become faster with increasing age. We determined the relation of rapid number-naming time scores on the K-D test to electronic measurements of saccade performance during preseason baseline assessments in a collegiate ice hockey team cohort. Within this group of young adult athletes, we also sought to examine the potential role for player age in determining baseline scores. METHODS: Athletes from a collegiate ice hockey team received preseason baseline testing as part of an ongoing study of rapid rink-side performance measures for concussion. These included the K-D test (spiral-bound cards and tablet computer versions). Participants also performed a laboratory-based version of the K-D test with simultaneous infrared-based video-oculographic recordings using an EyeLink 1000+. This allowed measurement of the temporal and spatial characteristics of eye movements, including saccadic velocity, duration, and intersaccadic interval (ISI). RESULTS: Among 13 male athletes, aged 18-23 years (mean 20.5 +/- 1.6 years), prolongation of the ISI (a combined measure of saccade latency and fixation duration) was the measure most associated with slower baseline time scores for the EyeLink-paired K-D (mean 38.2 +/- 6.2 seconds, r = 0.88 [95% CI 0.63-0.96], P = 0.0001), the K-D spiral-bound cards (36.6 +/- 5.9 seconds, r = 0.60 [95% CI 0.08-0.87], P = 0.03), and K-D computerized tablet version (39.1 +/- 5.4 seconds, r = 0.79 [95% CI 0.42-0.93], P = 0.001). In this cohort, older age was a predictor of longer (worse) K-D baseline time performance (age vs EyeLink-paired K-D: r = 0.70 [95% CI 0.24-0.90], P = 0.008; age vs K-D spiral-bound cards: r = 0.57 [95% CI 0.03-0.85], P = 0.04; age vs K-D tablet version: r = 0.59 [95% CI 0.06-0.86], P = 0.03) as well as prolonged ISI (r = 0.62 [95% CI 0.11-0.87], P = 0.02). Slower baseline K-D times were not associated with greater numbers of reported prior concussions. CONCLUSIONS: Rapid number-naming performance using the K-D at preseason baseline in this small cohort of collegiate ice hockey players is best correlated with ISI among eye movement-recording measures. Baseline K-D scores notably worsened with increasing age, but not with numbers of prior concussions in this small cohort. While these findings require further investigation by larger studies of contact and noncontact sports athletes, they suggest that duration of contact sports exposure may influence preseason test performance.
PMCID:6022287
PMID: 28746058
ISSN: 1536-5166
CID: 2654292
Type 1 Diabetes, Celiac Disease, and Neuropathy-A Nationwide Cohort Study
OBJECTIVE: Both type 1 diabetes (T1D) and celiac disease (CD) have been linked to an increased risk of neuropathy. This study examined the risk of neuropathy in patients with T1D compared with patients with both T1D and CD. METHODS: In a nationwide population-based cohort, T1D was defined as having a diagnosis of diabetes between 1964 and 2009 recorded in the Swedish National Patient Register in individuals
PMID: 28827484
ISSN: 1537-1611
CID: 2676242
Isoniazid induced cerebellar neurotoxicity in a 45-year-old-woman with Sjogren's disease, chronic renal insufficiency, and extrapulmonary tuberculosis: A case report [Meeting Abstract]
Objective: Though peripheral neuropathy is widely known as an adverse effect from isoniazid, very rarely have cerebellar deficits been identified as neurologic sequelae from isoniazid for treatment of tuberculosis. Background: We report a patient with Sjogren's disease, chronic kidney disease and recently diagnosed extrapulmonary tuberculosis having completed 5 days of rifampin, isoniazid, pyrazinamide, ethambutol, and pyridoxine therapy, presenting to the emergency department with 2 days of acute onset dysarthria and difficulty walking. Less than a handful of cases involving isoniazid induced cerebellar neurotoxicity have been reported worldwide thus far, predominately in South Asia. Design/Methods: A 45-year-old Bangladeshi woman with medical history as stated above, was admitted to a general medicine service with sudden onset of gait ataxia and dysarthria. Inpatient neurology service was consulted thenceforth. Results: Upon presentation, vitals and basic labs were unremarkable, aside from creatinine of 3.9 from a baseline of 3.2 due to underlying renal disease. Neurological exam was notable for dysmetria, markedly wide based gait, and difficulty with tandem. MRI brain without contrast revealed symmetric T2/FLAIR signal abnormality affecting the bilateral cerebellar dentate nuclei without associated restricted diffusion. Upon cessation of isoniazid, the patient reported nearly complete resolution of symptoms 48 hours after admission. Conclusions: Due to the frequency of isoniazid use as a treatment for tuberculosis coupled with the prevalence of chronic kidney disease, it is critical that physicians are aware of isoniazid's ability to cause cerebellar deficits especially since discontinuation of the medication led to rapid resolution of the symptoms. This case also brings into question whether toxicity is not only induced by concomitant chronic kidney disease, but also by acute kidney injury
EMBASE:616549884
ISSN: 1526-632x
CID: 2608942
The evaluation of small fiber neuropathy: A survey of American Academy of Neurology members [Meeting Abstract]
Objective: To determine how neurologists evaluate and test for small fiber neuropathy. Background: Small fiber neuropathy (SFN) affects the thinly myelinated and unmyelinated sensory and autonomic nerve fibers. Symptoms of SFN can be difficult for practitioners to recognize. There is clinical and etiological heterogeneity, and sometimes SFN overlaps with the more commonly recognized distal symmetric large fiber polyneuropathy. Clinical practice in the evaluation of distal symmetric polyneuropathy has been demonstrated to differ amongst neurologists, neuromuscular specialists and internists. Design/Methods: We surveyed 798 neurologists who are members of the American Academy of Neurology (AAN) including 400 members randomly selected from a pool of neurologists who, according to internal AAN records, had indicated neuromuscular medicine to be either a primary or secondary subspecialty. The second half of the sample consisted of randomly selected members who had indicated neuromuscular medicine to neither be a primary nor a secondary specialty. Respondents answered a survey instrument with a list of serum tests and procedures for different neuropathy clinical scenarios. Results: The survey response rate was 29.3% (234/798), with 67.9% of respondents identified as specializing in neuromuscular medicine. When asked which tests they would order given a clinical scenario of distal symmetric SFN, neuromuscular specialists were more likely to order electromyography/nerve conduction studies, skin biopsy for SFN, anti-nuclear antibodies, oral glucose tolerance tests, and serum immunofixation compared to nonneuromuscular neurologists who were more likely to order a serum folate level. Conclusions: Our findings reveal that neuromuscular neurologists are more likely to order as part of their initial evaluation of SFN serum tests recommended in the AAN practice parameter for distal symmetric polyneuropathy and skin biopsies for pathological confirmation of SFN. The development of an AAN practice parameter for SFN may help promote consistent practice amongst neurologists of all subspecialties
EMBASE:616550323
ISSN: 1526-632x
CID: 2608872
Epilepsy monitoring unit length of stay
With an increasing focus on quality metrics, hospital length of stay (LOS) in the U.S. has garnered significant scrutiny. To help establish evidence-based benchmarks for epilepsy monitoring unit (EMU) metrics, we evaluated the impact of multiple variables on LOS through a retrospective analysis of 905 consecutive inpatient adult EMU admissions. The most common reasons for admission were event characterization (n=494), medication adjustment (n=189), and presurgical evaluation (n=96). Presurgical evaluations experienced a longer average LOS (aLOS) of 7.1days versus patients admitted for other indications (p<0.001). Patients with symptomatic generalized epilepsy (n=22) had a longer aLOS (6.9days) than patients with other types of epilepsy/events (p<0.001). Patients admitted on two or fewer antiepileptic drugs (AEDs) had a shorter aLOS than patients admitted on three or more AEDs (4.3days vs 6.3days, respectively; p<0.001). A history of previous invasive epilepsy management was associated with a longer aLOS than those without (6.2days vs 4.7days, respectively; p<0.0001). Epilepsy monitoring unit aLOS is influenced by admission indication, epilepsy classification, medication burden, and having had prior invasive management. Multiple variables should be considered when analyzing LOS EMU metrics, arguing against a "one size fits all" approach.
PMID: 27064830
ISSN: 1525-5069
CID: 2078262
Amifampridine phosphate (Firdapse(®)) is effective and safe in a phase 3 clinical trial in LEMS
OBJECTIVE:We evaluated the efficacy and safety of amifampridine phosphate (Firdapse(®)) for symptomatic treatment in Lambert-Eaton myasthenic syndrome (LEMS). METHODS:Phase 3, randomized, double-blind, study. Patients were treated initially with amifampridine phosphate for 7-91 days, followed by randomization to continue amifampridine phosphate for 14 days or placebo (7-day taper, 7-day placebo). The primary efficacy endpoints were changes from baseline at day 14 in Quantitative Myasthenia Gravis and Subject Global Impression scores. RESULTS:The coprimary efficacy end points and 1 of the secondary efficacy end points were met, showing a significant benefit of aminfampridine phosphate over placebo at Day 14. All 5 primary, secondary, and tertiary endpoints achieved statistical significance at Day 8. Amifampridine phosphate was well tolerated; the most common adverse events were oral and digital paresthesias, nausea, and headache. CONCLUSIONS:This study provides Class I evidence of efficacy of amifampridine phosphate as a symptomatic treatment for LEMS.
PMID: 26852139
ISSN: 1097-4598
CID: 5806592
Neuropathy and Celiac Disease-Reply
PMID: 26457636
ISSN: 2168-6157
CID: 1823242
Brachioplasty-associated multiple mononeuropathies [Letter]
PMID: 25703458
ISSN: 1097-4598
CID: 1823272
Risk of Neuropathy Among 28,232 Patients With Biopsy-Verified Celiac Disease
IMPORTANCE: Earlier research on celiac disease (CD) and neuropathy has been hampered by the use of inpatient data, low study power, and lack of neuropathic characteristics. OBJECTIVE: To examine the relative risk and absolute risk of developing neuropathy in a nationwide population-based sample of patients with biopsy-verified CD. DESIGN, SETTING, AND PARTICIPANTS: Between October 27, 2006, and February 12, 2008, we collected data on small-intestinal biopsies performed at Sweden's 28 pathology departments between June 16, 1969, and February 4, 2008. We compared the risk of neuropathy in 28,232 patients with CD (villous atrophy, Marsh 3) with that of 139,473 age- and sex-matched controls. Cox proportional hazards regression estimated hazard ratios (HRs) and 95% CIs for neuropathy defined according to relevant International Classification of Diseases codes in the Swedish National Patient Register (consisting of both inpatient and outpatient data). MAIN OUTCOMES AND MEASURES: Neuropathy in patients with biopsy-verified CD. RESULTS: Celiac disease was associated with a 2.5-fold increased risk of later neuropathy (95% CI, 2.1-3.0; P < .001). We also found an increased risk (with results reported as HRs [95% CIs]) of chronic inflammatory demyelinating neuropathy (2.8; 1.6-5.1; P = .001), autonomic neuropathy (4.2; 1.4-12.3; P = .009), and mononeuritis multiplex (7.6; 1.8-32.4; P = .006), but no association between CD and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68). CONCLUSIONS AND RELEVANCE: We found an increased risk of neuropathy in patients with CD. This statistically significant association in a population-based sample suggests that CD screening should be completed in patients with neuropathy.
PMID: 25962148
ISSN: 2168-6157
CID: 1823262
Bortezomib-associated demyelinating neuropathy--clinical and pathologic features
OBJECTIVES: Bortezomib is a proteasome inhibitor that is frequently used for multiple myeloma and lymphoma. A sensory predominant axonal neuropathy is associated with bortezomib treatment but a demyelinating neuropathy is also described primarily based on electrodiagnostic findings. We report a series of patients treated with bortezomib who developed peripheral neuropathy and were found to have demyelinating features on electrodiagnostic testing. METHODS: Four patients who developed a bortezomib-induced peripheral neuropathy underwent electrophysiological testing, and 1 patient had a nerve biopsy. RESULTS: The four patients with bortezomib-induced peripheral neuropathy had demyelinating features on their electrophysiological testing. The nerve biopsy performed in 1 patient demonstrated a demyelinating component in a background of axonal degeneration. CONCLUSIONS: Although most toxic neuropathies are symmetrical axonal neuropathies, bortezomib is part of a small list of agents that may cause a demyelinating polyneuropathy and axonal degeneration. These findings have been confirmed by nerve biopsy.
PMID: 25996966
ISSN: 1537-1611
CID: 1823252
