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Rationale Todd paralysis (a stroke-like presentation in some patients with epilepsy) caused by limbic encephalitis (LE) is not easily distinguished from acute ischemic stroke by clinicians in the emergency room. Patient concerns We report a contactin-associated protein-like 2-antibody (CASPR2-Ab)-positive patient who presented with atypical LE. Diagnoses CASPR2-Ab-positive LE was the presumed diagnosis. Re-evaluation of cerebrospinal fluid (CSF) samples revealed autoantibodies targeting CASPR2 at an immunoglobulin G titer of 1:1. The clinical presentation of subacute onset seizures, abnormal electroencephalography, hypermetabolism on positron emission tomography, good immunotherapy response, and the presence of specific antibodies in serum supports a diagnosis of autoimmune LE. Intervention The patient received glucocorticoids (1 g for 3 days and 500 mg for 3 days), immunoglobulin (25 g for 3 days), sodium valproate (1 g for 3 days), and clonazepam (1 mg for 3 days). Outcomes Remission of temporal lobe epilepsy symptoms and cognitive dysfunction was observed. Follow-up analysis of CSF and serological examination were not approved by the patient. His Mini-Mental State Examination score improved to 21/30. Stable remission of symptoms was achieved throughout the follow-up period of 50 days. Lessons Autoimmune encephalitis (AE) should be considered in cases of late-onset epilepsy following meningioma peritumoral brain edema and resection. A diagnosis of AE should be considered in patients presenting with stroke-like symptoms if the magnetic resonance imaging abnormality does not match a known vascular territory. Early and correct diagnosis is crucial because immunotherapy is usually effective for this disease.

To study the change of enzymes and effect of garlicin treatment on the change in bronchoalveolar lavage fluid (BALF) of rats with Pneumocystis carinii pneumonia (PCP).Wistar rats were injected intramuscularly continually with dexamethasone to establish the rat model of PCP. The experimental rats (group A) were injected intramuscularly with garlicin at a dose of 10 mg/(kg x d) for 5 days in the 3rd, 6th and 9th week respectively, and SMZ/TMP therapy group (B), PCP infected group (C) and normal group (D) were established as controls. Three days after the last treatment, the rats of all groups were killed and BALF was collected without contamination and enzymes AST, ALF, CHE, ALP, LDH, CK, CKMB, HBDH, AFU, 5'NT, ADA were examined.The ALP level in group C [(573.41 +/- 350.63)U/L] was significantly higher than that in group D [(210.56 +/- 114.41) U/L] (q = 4.682, P0.01), group A [(392.07 +/- 217.57) U/L] (q = 3.851, P0.05), and group B [(325.21 +/- 180.65) U/L] (q = 4.380, P0.01); the level of CK, CKMB and 5'NT in group C [948.94 +/- 403.43, 489.47 +/- 254.46 and (6.76 +/- 3.11) U/L respectively] was higher than those in group D [426.22 +/- 319.00, 213.33 +/- 144.54 and (3.22 +/- 1.20) U/L] (q = 4.696, 3.784, 3.812, P0.05); there was no significant difference in the level of AST, ALT, CHE, LDH, HBDH, AFU and ADA among the four groups (F = 1.852, 0.958, 2.470, 1.423, 1.178, 1.342, 0.611, P0.05).The level of ALP, CK, CKMB but the ALP level decreases distinctly after the garlicin and 5'NT increases evidently in BALF of PCP infected rats, but the ALP level decreases distinctly after the garlicin treatment.

To explore the genetic model of cerebral infarction and to examine the relationship between cerebral infarction and genetic factor.A matched case-control study including 112 pairs pedigrees was carried out. Using the Li-Mantel-Gart method and the Falconer method to estimate the segregation ratio and the heritability of cerebral infarction.The prevalence rate of the first-degree and the second-degree relatives in cases was significantly higher than that in controls. The segregation ratio was 0.143 7 (0.113 0 - 0.174 4), significantly lower than 0.25, which showed that cerebral infarction did not possess the characteristics of monogenetic model. The results showed that the heritability of the first-degree and the second-degree relatives were 47.84% and 40.95% higher in male's than in female's.Cerebral infarction was a polygenetic disease, and the genetic factors played an important role in the occurrence of cerebral infarction, especially in males.