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. 2014 Jun 20;137(8):2178–2192. doi: 10.1093/brain/awu142

Table 3.

Clinical investigations of GlyR antibody patients referred from 2008–12

Total number of patients 45
Investigations (number performed) Results Number of abnormal results/number tested
Brain MRI (n = 36) n = 3 with white matter lesions; n = 1 atrophy; n = 2 temporal lobe inflammation; n = 2 other FLAIR lesions; n = 2 small vessel disease; n = 26 normal 10/36
Spinal cord MRI (n = 23) n = 4 short or patchy lesions; n = 1 longitudinally-extensive lesion; n = 18 normal  5/23
EMG (n = 29) n = 8 continuous motor unit activity; n = 6 spontaneous or stimulus-induced activity; n = 2 sensory neuropathy; n = 1 neuromyotonic discharges; n = 12 normal 17/29
EEG (n = 21) n = 11 slow activity; n = 3 focal epileptic; n = 1 cortical disturbance; 6 normal 15/21
CSF (n = 30) Any abnormality: n = 18 18/30
n = 13 pleocytosis; n = 4 prot (>1 g/l); n = 6 OCB; normal n = 12
GAD antibodies (n = 43) 4 >1000 U/ml (∼25 000 IU/ml); 1 100 U/ml; 40 negative  4/45
Chest CT/whole body PET scan (n = 20) n = 3 thymoma; n = 1 abdominal lymph nodes; n = 1 breast metastases; n = 15 normal  5/20
Other autoantibodies n = 4 high GAD (>1000 U/ml); n = 1 high VGKC (2248 pM); n = 2 low VGKC (<200 pM); n = 3 low NMDAR; n = 6 thyroid; n = 1 ANA; n = 1 Sjogrens Syndrome; 15 normal; no paraneoplastic antibodies reported 13/28

Onconeural antibodies were reported negative by the referring neurologists and were not retested in this study.

ANA = antinuclear antibodies; OCB = oligoclonal bands.