to NMDA Receptors in Cerebral and Spinal Cord Infarctions


Fig. 1

T2-weighed MRI for: (a) a 83-year-old female, multiple lesions in white matter seen on MRI, (b) a 76-year-old male with recurrent ischemic stroke and lesions with hemorrhagic transformation in left frontal parietal area, (c) a 55-year-old female with chronic ischemic stroke in right middle cerebral artery area



A total of 119 subjects were included in the study with demographic data summarized in Table 1. Patients with SC infarction (n = 27, age of 56.8 ± 3.3) of non-traumatic origin comprised subgroup Ia. Patients with post-traumatic myelopathy (PTM) composed subgroup Ib (n = 25, age of 46.7 ± 2.1). The average duration of myelopathy within 15–26 months is estimated.


Table 1

Enrolled subject demographic characteristics

























































Group


Age, mean ± SD


Male


Female


N


%


N


%


SC infarction


56.8 ± 3.3


17


63.0


10


37.0


Posttraumatic myelopathy (PTM)


46.7 ± 2.1


15


60.0


10


40.0


Radiculopathy (Rad)


57.0 ± 1.7


18


56.3


14


43.7


Ischemic stroke (IS)


56.6 ± 1.5


17


56.7


13


43.3


Healthy subjects


50.2 ± 3.6


8


53.3


7


46.7


Comparison of the SC subgroups revealed no significant difference in neurological manifestations between subgroups Ia and Ib (p ˃ 0.05). Most patients in both groups (90%) are characterized by central lower paraparesis or paraplegia, with a gradient of motor and sensory loss involving the lower extremities more than the upper extremities. The neurological status of patients was significantly more severe in patients with PTM than in patients with SC infarction (p < 0.05). The course of myelopathy in the main subgroups is shown in Fig. 2.

../images/459789_1_En_12_Chapter/459789_1_En_12_Fig2_HTML.jpg

Fig. 2

Spinal cord MRI sequences (left-to-right): (a) thoracic spine area: T2 (1, 3) and STIR (2) of a 47-year-old female with spinal stroke in the ASA territory and Factor V Leiden thrombophilia (arrows indicate prolong hyperintensities on level of T7–L1). (b) cervical spine area T1 (1), T2 (2), and STIR (3) of a 56-year-old male patient with ischemic myelopathy due to protrusion on the C3–C4 (arrow indicates hyperintensity of lesion and edema on level C4)


Among the main causes of SC infarction (Ia subgroup), herniated intervertebral discs in 12 (44.4%) cases, arteriovenous malformations in 6 (22.2%) patients, and thrombotic coagulopathies in 3 (11.1%) cases were diagnosed. In 6 (22.2%) patients, the cause of SC infarction could not be established at the time of the study. The isolated lesion of cervical segments in 10 (37%), thoracic segments in 6 (22.2%), and lumbosacral in 2 (7.4%) were defined by MRI. There were observed lesions spread within cervical/thoracic areas (n = 3, 11.1%) and thoracolumbar region (n = 6, 22.2%).


In the PTM subgroup Ib, spinal cord injury was more common in the form of household trauma in 13 (52%) cases, motor vehicle accidents in 7 (28%) cases, acts of violence in 3 (12%) patients, and sport-related injuries in 2 (8%) cases.


Spinal cord injuries by compression (66%), compression/fractures of vertebral bodies (13%), and dislocations and fracture-dislocations (21%) were characterized. In 8 (32%) patients with PTM, cervical and spinal cord injuries were diagnosed, 7 (28%) had thoracic and 5 (20%) lumbosacral injuries. The injuries of the thoracic and lumbosacral areas are diagnosed in 5 (20%) patients. The analysis of MRI scans showed that in both main subgroups, T2 and short tau inversion recovery (STIR) sequence hyperintensity foci along the spinal cord length of 60–80 mm (Table 2, Fig. 2).


Table 2

Lesion volumes in patients with SC infarction and PTM defined by MRI


















































Lesion volume, mL


SC infarction (n = 27)


PTM (n = 20a)


N


%


N


%


<1.0


5


18.5


2


10


1–3


6


22.2


4


20


3–5


4


14.8


6


30


6–8


7


25.9


6


30


>8


5


18.5


2


10



aNumber of patients with brain and spinal MRI


3.2.2 NR2 Antibody Results


The NR2 Ab values ​​in groups of healthy subjects (range, 0.5–2.22 ng/mL) and radiculopathy (range, 0.57–2.58 ng/mL) did not differ (Fig. 2a). At the same time, NR2 Ab amounts in serum from IS patient (range, 0.61–9.37 ng/mL) and patients with SC infarction/PTM were significantly increased compared to that for patients with radiculopathy (p = 0.0001) and healthy subjects (p = 0.013). There was no difference in NR2 Ab levels between IS patients and those with SC infarction (Table 3, Fig. 2a).


Table 3

Evaluation of NR2 antibodies in serum of patients







































































Group


N


Gender


NR2 Ab ng/mL


p a


M


F


Median [Q25; Q75]


Average


Maximum


SC infarction


27


17


10


1.92 [1.60; 2.45]


2.30


8.12



PTM


25


15


10


1.51 [1.29; 1.98]


1.63


3.50


0.45


IS


30


17


13


1.46 [0.99; 2.42]


1.96


9.37


0.18


Rad


32


18


14


1.25 [0.87; 1.59]


1.29


2.58


0.0001


Healthy subjects


15


8


7


1.30 [1.01; 1.53]


1.31


2.22


0.013



aKruskal–Wallis criteria in comparison with group SC infarction


A comparison of NR2 Ab distributions shown in Fig. 2b for patients with PTM (range, 0.27–3.50 ng/mL) and SC infarction (range, 0.84–8.12 ng/mL) showed a significant difference (p = 0.008). In SC infarction group, a positive moderate correlation between the concentration of NR2 Ab and the size of lesions in spinal cord defined by MRI (r = 0.49, p < 0.05) was found. The latter might indicate an increased permeability of the vessels located in the area of SC ischemic injury and release into the bloodstream (Fig. 3).

../images/459789_1_En_12_Chapter/459789_1_En_12_Fig3_HTML.png

Fig. 3

NR2 Ab levels in serum of subject (a) healthy (C), radiculopathy (Rad), IS, SC infarction, and post-traumatic myelopathy (PTM), Kruskal–Wallis and post hoc tests, Mann–Whitney U test, median [25; 75], (b) patients with traumatic myelopathy (1) and SC infarction (2), Mann–Whitney U test

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Nov 7, 2020 | Posted by in Uncategorized | Comments Off on to NMDA Receptors in Cerebral and Spinal Cord Infarctions

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