what drives progressive motor deficits in patients with acute pontine infarction?

Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be respon- sible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.

Millard-Gubler Syndrome in a Patient with Pontine Infarction: A Case Report

Millard-Gubler Syndrome is a rare neurological condition caused by damage to the sixth and seventh cranial nerves, as well as the corticospinal tract in the brainstem. It is characterized by the presence of ipsilateral facial paralysis and contralateral hemiplegia. We report a 55-year-old male patient who presented with sudden onset of left-sided weakness. Imaging revealed a pontine infarct. The patient therefore, was diagnosed with Millard-Gubler Syndrome also known as Ventral Pontine Syndrome based on his symptoms and imaging findings. He was treated with Aspirin and Atorvastatin and was referred to neurology for further consultation and to physiotherapy for his weakness. This case report highlights the importance of prompt recognition and diagnosis of Millard-Gubler Syndrome in patients with pontine infarction. Early identification especially with the use of high-resolution MRI can facilitate appropriate management and treatment, ultimately improving patient outcomes.

Restless legs syndrome secondary to pontine infarction:Clinical analysis of five cases

Objective: Pontine infarction is a common type of stroke in the cerebral deep structures, resulting from occlusion of small penetrating arteries, may manifest as hemi-paralysis, hemi-sensory deficit, ataxia, vertigo, and bulbar dysfunction, but patients presenting with restless legs syndrome (RLS) are extremely rare. Herein, we reported five cases with RLS as a major manifestation of pontine infarction.Methods: Five cases of pontine infarction related RLS were collected from July 2013 to February 2016. The diagnosis of RLS was made according to criteria established by the International RLS Study Group (IRLSSG) in 2003. Neurological functions were assessed according to the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS). Severity of RLS was based on the International RLS Rating Scale (IRLS-RS). Sleep quality was assessed by Epworth Rating Scale (ERS), and individual emotional and psychological states were assessed by Hamilton Depression Scale (HDS) and Hamilton Anxiety Scale (HAS).Results: The laboratory data at the onset including hemoglobin, serum concentration of homocysteine, blood urea nitrogen (BUN), creatinine, electrolytes, and thyroid hormones were normal. The electroencephalogram (EEG), lower-extremity somatosensory evoked potential (SEP), and nerve conduction velocity (NCV) in four limbs were normal. The average period of follow-up was 34.60 ± 12.76 months. The MRI examination showed acute or subacute pontine infarction lesions, 3 cases in the rostral inner side, 1 case in the rostral lateral and inner side, and 1 case in rostral lateral side. The neurological deficits included weakness in 4 cases, contralateral sensory deficit in 1 case, and ataxia in 2 cases. All 5 patients presented with symptom of RLS at or soon after the onset of infarction and 4 patients experienced uncomfortable sensations in the paralyzed limbs contralateral to the ischemic lesion. Their neurological deficits improved significantly 2 weeks later, but the symptoms of RLS did not resolve. Among them, 3/5 patients were treated with dopaminergic drugs. At the end of the follow-up, RLS symptom eventually resolved in 3 patients but persisted in two. The IRLS-RS, NIHSS and mRS scores were significantly lower at the onset than those at the last follow-up (P=0.035, 0.024 and 0.049, respectively). However, there was no significant difference in the ERS, HDS and HAS scores (P=0.477, 0.226 and 0.778, respectively).Conclusion: RLS can be an onset manifestation of pontine infarction, clinicians should be aware of this potential symptom. RLS usually occurs in the paralyzed limbs contralateral to the infarction lesion. The pathogenesis still needs further investigation.

Spared integrity of corticospinal tract within a pontine infarct A diffusion tensor tractography study

Integrity of the corticospinal tract is mandatory for good recovery of impaired motor function in patients who have suffered a stroke.A 67-year-old left hemiparetic female showed an infarct in the right pons.Three months after onset,motor function of the affected extremities recovered rapidly to a nearly complete state.Diffusion tensor tractography of both hemispheres showed that the corticospinal tract originated from the primary sensori-motor cortex and descended through the known corticospinal tract pathway.The tract of the affected（right）hemisphere descended through an area within the pontine infarct.The diffusion tensor tractography results suggest that from the onset,the integrity of the corticospinal tract appears to have been spared within the pontine infarct.

Plaques of Nonstenotic Basilar Arteries with Isolated Pontine Infarction on Three-dimensional High Isotropic Resolution Magnetic Resonance Imaging

Background： There are few studies for evaluating plaque characteristics of nonstenotic basilar arteries （BA）. Our aim was to determine entire BA plaques with a three-dimensional volumetric isotropic turbo spin-echo acquisition （VISTA） and investigate the differences between the patients with and without isolated pontine infarction （IPI）. Methods： Twenty-four consecutive symptomatic patients with nonstenotic BA on time of flight magnetic resonance angiography （TOF MRA） were enrolled from China-Japan Friendship Hospital between January 2014 and December 2014. BA was classified as ＂normal＂ or ＂irregular＂ based on TOF MRA, and ＂normal wall＂, ＂slight wall-thickening＂, and ＂plaque＂ based on three-dimensional VISTA images. Outcomes from MRA and VISTA were compared. Patients were categorized as IPI and non-lPl groups based on the diffusion-weighted imaging. Clinical and plaque characteristics were compared between the two groups. Results： A total of 1024 image slices including 311 （30.37%） plaque slices, 427 （41.70%） slight wall-thickening slices, and 286 （27.93%） normal wall slices for the entire BA from 23 patients were finally included for analysis. VISTA images detected plaques in all the 9 （100%） irregular MRA patients and 7 of 14 （50%） normal MRA patients. IPl was found in 11 （47.83%） patients. Compared to non-IPI group, the IPI group had a higher percentage of plaque slices （P = 0.001 ） and lower percentage of normal wall slices （P = 0.014） than non-IPl group. Conclusions： Three-dimensional V1STA images enable detection of BA plaques not visualized by MRA. BA plaques could be found in both the IPl and non-IPl group. However, IPI group showed plaques more extensively in BA than the non-IPI group.

Clinical and Radiological Features of Wallerian Degeneration of the Middle Cerebellar Peduncles Secondary to Pontine Infarction

Background： Wallerian degeneration （WD） of bilateral middle cerebellar its characteristics have not yet been clarified because of the low incidence peduncles （MCPs） can occur following pontine infarction, but Thus, the present study discussed the clinical and radiological features to improve the awareness of this disease. Methods： Clinical and radiological information from consecutive individuals diagnosed with WD of bilateral MCPs following pontine infarction in three hospitals over the past 4 years between October 2012 and October 2016 were retrospectively investigated and compared with a control group （patients with pontine infarction had no secondary WD）. Results： This study involved 30 patients with WD of MCPs, with a detection rate of only 4.9%. The primary infarctions （χ2 -24.791, P = 0.001, vs. control group） were located in the paramedian pons in 21 cases （70.0%）, and ventrolateral pons in nine cases （30.0%）. WD of the MCPs was detected 8-24 weeks after pons infarction using conventional magnetic resonance imaging （M RI）; all secondary WDs were asymptomatic and detected incidentally. All WD lesions exhibited bilateral, symmetrical, and boundary blurring on MRI. The signal features were hypointense on Tl-weighted imaging, hyperintense on T2-weighted imaging and fluid-attenuated inversion recovery, and slightly hyperintense or isointense on diffusion-weighted imaging and apparent diffusion coefficient maps. Secondary brainstem atrophy was found in six （20.0%） cases. A Modified Rankin Scale score 0-2 was found in 10 （33.3%） cases and score 〉2 in 20 （66.7%） cases at 90 days after discharge, and the short-term prognosis was worse than that in control group （χ2 =12.814, P - 0.001 ）. Conclusions： Despite the rarity of bilateral and symmetrical lesions of MCPs, secondary WD should be highly suspected if these lesions occur within 6 months after pontine infarction, particularly parainedian ports. Conventional MRI appears to be a relatively sensitive method for detecting WD of MCPs, which might affect the short-term prognosis.