Basilar Artery Tortuosity May Be Associated with Early Neurological Deterioration in Patients with Pontine Infarction.

BACKGROUND: Early neurological deterioration (END) occurs in patients with pontine infarction that is adversely associated with a long-term functional outcome. As basilar artery (BA) tortuosity may alter hemodynamics, we investigated whether factors including BA tortuosity are associated with END and poor outcome at 3 months. METHODS: We reviewed patients with acute (<7 days from stroke onset) unilateral pontine infarction mainly involving the pontine base and/or tegmental regions from January 2017 through April 2021. END was defined as increase of ≥2 in total National Institutes of Health Stroke Scale (NIHSS) score or ≥1 in motor NIHSS score within first 72 h. A poor clinical outcome was defined as modified Rankin Scale (mRS) 3-6 at 3 months. The BA tortuosity index (TI) was measured: ([actual/straight length -1] x 100). To assess interobserver agreement, TI measurements were obtained by 2 independent raters. RESULTS: The study included 245 patients; END occurred in 72 (29.3%) and 35 (14.2%) showed poor outcome at 3 months. Old age (odds ratio [OR] = 1.03, 95% confidence interval [CI] 1.004-1.062; p = 0.027), previous stroke history (OR = 2.36, 95% CI: 1.176-4.717; p = 0.016), lower initial NIHSS (OR = 0.72, 95% CI: 0.628-0.827; p < 0.001), and high BA TI (OR = 1.17, 95% CI: 1.062-1.295; p = 0.002) were associated with END. On the other hand, old age (OR = 1.04, 95% CI: 1.002-1.073; p = 0.037) and END (OR = 3.03, 95% CI: 1.429-6.403; p = 0.004) were associated with poor outcome at 3 months. CONCLUSIONS: High BA tortuosity may be a factor associated with END in patients with pontine infarction. As END was related to unfavorable clinical outcome, this risk may have to be carefully considered in patients with high BA tortuosity.

How I do it: Subtemporal transtentorial approach for cavernous malformation of the pons.

BACKGROUND: Removal of a pontine cavernous malformation requires sufficient exposure since any restriction on surgical freedom may lead to suboptimal visualization of the lesion, injury to the brainstem, and neurological catastrophe. METHODS: We describe and demonstrate the subtemporal transtentorial approach to a cavernous malformation of the upper pons, with emphasis on adequate surgical exposure while avoiding the need for extensive bone removal of the skull base. CONCLUSIONS: The meticulous technique is paramount to the successful removal of any brainstem cavernous malformation. Along with the surgical exposure, delicate handling of the malformation is demonstrated in the accompanying operative video.

Intravenous thrombolysis for pure pontine infarcts caused by cardiac myxoma: a case report and literature review.

Purpose: Cardiac myxoma (CM) is a rare but important cause of ischemic stroke, and typically involves the middle cerebral artery and rarely affects the brainstem only. The safety and efficacy of intravenous thrombolysis (IVT) for CM-related acute cerebral embolism are not clear.Methods: We report a case of a 55-year-old woman who suffered a CM-related acute cerebral embolism presented with pure pontine infarcts and achieved a favorable prognosis by IVT with urokinase. We summarized the clinical data of this entity and performed a literature review of 21 previous reports of patients with CM-related acute cerebral embolism who were treated with IVT.Results: In combination with previous reports, we found that the majority of patients (81.8%) obtained improvements in symptoms after IVT, including 63.6% in remarkable clinical improvement. The total rate of IVT-induced intracerebral hemorrhage was 22.7% and all occurred within 36 h, including hemorrhagic infarction type 1 (4.5%) and parenchymal hematoma type 2 (18.2%). Most of the cases had relatively good outcomes and no case died due to IVT.Conclusion: Taken together, our findings support the use of IVT as an effective and safe tool for the ultra-early treatment of CM-related acute phase ischemic stroke.

Clinical Characteristics and Clinical Course of Body Lateropulsion in 47 Patients with Brainstem Infarctions.

BACKGROUND: In patients with lower lateral medullary infarction (LMI) located under the vestibular nucleus, proprioceptive impairment due to dorsal spinocerebellar tract (DSCT) is considered a pathological condition for body lateropulsion. In patients with brainstem infarction located at or above the level of the vestibular nucleus, other pathways, such as the crossed vestibulothalamic tract (CVTT), are considered responsible. RESEARCH QUESTION: The clinical course of body lateropulsion between each anatomical level of infarction remains unclear. Further, whether body lateropulsion refers to a static or a dynamic symptom also remains unclear. METHODS: We examined 47 patients who exhibited body lateropulsion and categorized them into four groups: lower LMI under the vestibular nucleus, LMI at the level of the vestibular nucleus, pontine infarction, and midbrain infarction. The patients' time to acquire static upright standing position and gait in a straight line were statistically analyzed by a log-rank test using the Kaplan-Meier method. RESULTS: Body lateropulsion in the static upright position was less frequent in the lower LMI group than in the other groups. SIGNIFICANCE: Lower LMI primarily affected body lateropulsion in gait. DSCT damage could affect ipsilateral hip joint or leg coordination, causing body lateropulsion in dynamic situation.

Recurrent Pontine Strokes in a Young Male.

A 34-year-old patient presented to the emergency department with recurrent neurologic symptoms of sudden onset. MRI showed white matter hyperintensities consistent with small vessel disease, predominantly in the pons. There were no known cardiovascular risk factors (CVRF) and extensive workup for vasculitis was negative. The preliminary diagnosis was small vessel primary central nervous system vasculitis, but immunosuppressive treatment did not stop a progression of the disease over 6 months. Repeated negative diagnostic workup for vasculitis, lack of response to therapy, young age, and predominant involvement of the pons were compatible with pontine autosomal dominant microangiopathy and leukoencephalopathy (PADMAL), which is a very rare monogenic cause of cerebral small vessel disease due to upregulation of collagen type-IV. Correspondingly, a COL4A1 mutation was found. Therapy was immediately stopped in favour of more strict adjustment of the CVRF including lowering of LDL < 70 mg/dl and extensive monitoring of blood-pressure.

Prognostic evaluation of branch atheromatous disease in the pons using carotid artery ultrasonography.

BACKGROUND: Branch atheromatous disease is an ischemic stroke, involving occlusion or severe stenosis of the perforating artery, causing neurologic symptoms and serious sequelae. We aimed to investigate initial morphometric and hemodynamic characteristics of the vertebral artery immediately post-onset to predict lesion expanding. METHODS: This case-control study collected demographic, historical, and physical examination data from 44 patients with branch atheromatous disease in the pons at admission. The maximum ischemic pons area and stenosis rate in the basilar artery were calculated using magnetic resonance images. Diameter, velocity, and flow volume of the vertebral arteries were measured using carotid artery ultrasonography. Correlations between ischemic lesion extent and these parameters were investigated. RESULTS: Patients were assigned to groups of less (Group 1) or more (Group 2) than the median maximum ischemic area in the pons, calculated from magnetic resonance images (121.6 mm2). Modified Rankin scale scores were significantly worse in Group 2. Blood pressure and blood findings were similar between groups. Group 2 showed significantly higher basilar artery stenosis rates. Flow volume, velocity, peak systolic velocity, and end-diastolic velocity in the vertebral artery on both sides were significantly decreased in Group 2. CONCLUSIONS: Deteriorated vertebral artery hemodynamics caused a more extensive ischemic lesion in branch atheromatous disease in the pons. Evaluation of the vertebral using carotid artery ultrasonography in the acute phase may be useful for predicting disease progression.

Effects of injuries to descending motor pathways on restoration of gait in patients with pontine hemorrhage.

BACKGROUND AND PURPOSE: Gait disturbance due to injuries of the descending motor pathway, including corticospinal tract (CST), corticoreticular pathway (CRP), and medial and lateral vestibulospinal tracts (VSTs), are commonly encountered disabling sequelae of pontine hemorrhage. We investigated relations between changes in the CST, CRP, and medial and lateral VST and corresponding changes in gait function in patients with pontine hemorrhage. METHOD: Nine consecutive stroke patients with pontine hemorrhage, and 6 age-matched normal subjects were recruited. Four patients were allocated to group A (can't walk independently) and 5 to group B (can walk independently). Diffusion tensor imaging (DTI) data were acquired twice at acute to subacute stage and chronic stage after stroke onset. Diffusion tensor tractography (DTT) was used to reconstruct CST, CRP, medial and lateral VST. RESULT: The CRP shows a significantly different between groups A and B in both initial and follow up DTT (p > 0.05). In contrast, CST, medial VST and lateral VST did not show a significant difference (p > 0.05). Regarding DTI parameters of CRPs in group A, percentages of patients with fractional anisotropy (FA) and mean diffusivity (MD) values more than two standard deviation from normal were higher by follow up DTI than by initial DTI, however, the CRPs in group B only showed increased abnormal range of MD. CONCLUSIONS: The CST does not play an essential role in recovery of independent walking and vestibulospinal tracts may not crucially affect recovery of independent walking in patients with pontine hemorrhage. In contrast, and intact CRP or changes of the CRP integrity appear to be related to the recovery of gait function.

"Basilar Web" Causing Basilar Branch Infarction.

We present a young patient with no vascular risk factors with a basilar branch infarction secondary to a shelf-like filling defect of the basilar artery. This defect was present and unchanged on repeat imaging and determined to be most consistent with a basilar web. Similar to carotid webs, a basilar web is believed to be an area of focal intimal fibroplasia that increases the risk of brainstem infarction. Focal fibroplasia of the posterior circulation should be considered when evaluating young adults with posterior circulation strokes of otherwise undetermined cause.

Response of Cerebral Blood Flow and Blood Pressure to Dynamic Exercise: A Study Using PET.

Dynamic exercise elicits fluctuations in blood pressure (BP) and cerebral blood flow (CBF). This study investigated responses in BP and CBF during cycling exercise and post-exercise hypotension (PEH) using positron emission tomography (PET). CBF was measured using oxygen-15-labeled water (H215O) and PET in 11 human subjects at rest (Rest), at the onset of exercise (Ex1), later in the exercise (Ex2), and during PEH. Global CBF significantly increased by 13% at Ex1 compared with Rest, but was unchanged at Ex2 and during PEH. Compared with at Rest, regional CBF (rCBF) increased at Ex1 (20~42%) in the cerebellar vermis, sensorimotor cortex for the bilateral legs (M1Leg and S1Leg), insular cortex and brain stem, but increased at Ex2 (28~31%) only in the vermis and M1Leg and S1Leg. During PEH, rCBF decreased compared with Rest (8~13%) in the cerebellum, temporal gyrus, piriform lobe, thalamus and pons. The areas showing correlations between rCBF and mean BP during exercise and PEH were consistent with the central autonomic network, including the brain stem, cerebellum, and hypothalamus (R2=0.25-0.64). The present study suggests that higher brain regions are coordinated through reflex centers in the brain stem in order to regulate the cardiovascular response to exercise.

Vertebrobasilar Artery Stroke as the Heralding Sign of Systemic Lupus Erythematosus.

Cerebral ischemia because of vertebrobasilar insufficiency (VBI) rarely presents as an initial sign within the systemic lupus erythematosus (SLE) population, and there are very few case reports supporting this manifestation. This report details 3 different patients with SLE who experienced VBI as an initial manifestation. Patient 1 was a 24-year-old female who developed a bilateral pontine lesion as a consequence of basilar artery stenosis. Patient 2 was a 34-year-old male with an acute ischemic lesion on the right side of his cerebellum and pons because of significant stenosis in the distal segment of the right vertebral artery. Patient 3 was a 37-year-old female, previously diagnosed with multiple sclerosis, with multiple lesions in her cerebellum and pons bilaterally. Further investigations within this case revealed severe stenosis of the left vertebral artery. The diagnosis of SLE was based on clinical presentations such as myalgia, skin rashes, ulcers, and fatigue along with relevant laboratory findings including positive anti ds-DNA antibody and depressed levels of complement C3 and C4 proteins. In young patients with multifocal ischemic lesions or infarcts in the posterior cerebral circulation system, physicians should investigate for less common etiologies such as SLE.

Twenty-Four Syndrome: An Untold Presentation of Pontine Hemorrhage.

Pontine hemorrhages are relatively uncommon. Various atypical manifestations of pontine stroke like eight-and-a-half syndrome, fifteen-and-a-half syndrome, and sixteen syndrome have been described in the past. We came across a case of pontine bleed that presented with bilateral facial palsy, bilateral horizontal gaze palsy, and contralateral sensorineural hearing loss accounting to the hitherto not described "twenty-four syndrome" with Horner's syndrome and left hemiparesis.

Varicella zoster virus reactivation antedating ipsilateral brainstem stroke.

itor Title: Varicella zoster virus reactivation antedating ipsilateral brainstem stroke Authors: Giuliana Galassi1, Maurilio Genovese2, Marisa Meacci3, Marcella Malagoli2 Affiliations: 1Department of Biomedical, Metabolic, Neural Sciences, University Hospital of Modena, Italy, 2Neuroradiology Service, University Hospital of Modena, Italy, 3Department of Laboratory Medicine and Patholgy, Microbiology and Virology Unit, University Hospital of Modena, Italy Corresponding Author: Giuliana Galassi, MD, Department of Biomedical, Metabolic, Neural Sciences, University Hospital of Modena, Via P. Giardini 1455, Modena, Italy, Tel: 39-3497325802, Email: giulianagalassi46@gmail.com Abstract: Varicella zoster virus (VZV) infection and reactivation are associated with a number of neurologic conditions. Unifocal large vessel infarcts may follow zoster in the trigeminal or cervical distribution as a result of transaxonal transport of virus from trigeminal or cervical afferent fibers that innervate vessels. Ophthalmic zoster (HZO) might cause ophthalmoplegic syndromes, with secondary optic neuritis. Mechanisms include local orbital muscle inflammation and, viral spread from the ophthalmic branch of the fifth nerve with associated vasculopathy. A 72-year-old man developed a vesicular rash in the territory of C5-T5-6. Within four weeks, the patient developed headache, dysphagia, left facial and extremity ataxic weakness. Magnetic resonance imaging (MRI) revealed a right pontine infarction. A 66-year-old woman presented with right-sided painfull HZO. One week later she developed complete external ophthalmoplegia and blurred vision. MRI showed ill-defined signal alteration in the retrobulbar tissue. Three weeks later, the patient was admitted because of dysarthria, deviated tongue, left-sided limb weakness, and tactile hypoesthesia. Spinal fluid contained 23 lymphocytes/mm3 and increased protein. The serum contained antibodies to VZV IgG and IgM in both cases. The patients received intravenously acyclovir with improvement. This report confirms unusual occurrence of ipsilateral brainstem stroke after VZV reactivation in immunocompetent subjects.

"Salt and Pepper" Pontine Infarct.

A paramedian pontine stroke may herald the unique symptom of "salt and pepper" eye pain, in which patients describe the sensation of pepper rubbed into the eye. While localization of the lesion is a common thread among published cases, the mechanism for the sensation of eye pain is still a matter of conjecture. It is important for clinicians to be aware of this unique symptom because strokes rarely present with eye pain and failure to establish this diagnosis might lead to a poor clinical outcome.

Selective Unidirectional Horizontal Saccadic Paralysis From Acute Ipsilateral Pontine Stroke.

BACKGROUND: Impairment of unidirectional horizontal saccades with sparing of smooth pursuit has been described in human lesions in the dorsomedial pons. They have been too large to allow localization to the pontine paramedian reticular formation (PPRF). METHODS: Single case report. RESULTS: A patient with impaired rightward saccades but spared rightward pursuit eye movements had a brain MRI showing a discrete area of restricted diffusion in the region corresponding to the PPRF. CONCLUSIONS: This case provides support for the concept that PPRF lesions in humans may selectively impair unidirectional horizontal saccades.

Clinical Study of Seven Patients with Infarction in Territories of the Anterior Inferior Cerebellar Artery.

BACKGROUND: The prominent features of anterior inferior cerebellar artery (AICA) infarction are vertigo, cerebellar ataxia, and impaired hearing. The present study investigated neurological characteristics associated with AICA infarction. MATERIALS AND METHODS: The locations of infarcts in 7 patients (age, 32-72 years) with AICA infarction were divided into the lower lateral pons, the middle cerebellar peduncle (MCP), and the cerebellum. RESULTS: Ischemic lesions were located in the MCP in 6 patients, spread to the lower lateral pons in 3, and involved the cerebellum in 4 patients. Standing posture and gait were impaired in all patients. Five and 4 patients had impaired hearing and vertigo, respectively. Two patients had only symptoms of labyrinthine disease, and 1 had these symptoms accompanied by impaired hearing. The symptoms in 2 patients with the lesion in the lateral pons were consistent with those in Gasperini syndrome. Two of 3 patients without vertigo had ataxia of the extremities. Stenosis of the vertebral artery or basilar artery in 5 patients indicated that the etiology was branch atheromatous disease. CONCLUSIONS: The most prominent symptom of truncal and gait ataxia and the frequent association between vertigo and impaired hearing were consistent with the characteristics of AICA infarction. Two patients without vertigo had ataxia of the trunk and extremities that might have been due to involvement of the dorsal spinocerebellar tract in the inferior cerebellar peduncle.

Severe White Matter Hyperintensity Is Associated with Early Neurological Deterioration in Patients with Isolated Pontine Infarction.

OBJECTIVE: Pontine infarction is a common type of brain stem infarction and early neurological deterioration (END). We evaluated the possibility of severe white matter hyperintensity (WMH) as a predictor of END in isolated pontine infarction. METHODS: We recruited 2 types of patients with isolated pontine infarction within 24 h from symptom onset. END was defined as an increase of ≥1 point on the motor National Institutes of Health Stroke Scale (NIHSS) or ≥2 points on the total NIHSS score within 72 h from admission. We graded WMH using Fazekas scale, which is dichotomized into mild (grades 0-1) and moderate to severe (grades 2-3) on fluid-attenuated inversion recovery images. RESULTS: A total of 82 patients with an isolated pontine infarction were selected. END was detected in 23 patients (28%). Severe periventricular and subcortical WMH (PVWMH and SCWMH, respectively) were more frequent in deteriorating patients (p = 0.001 and p = 0.019, respectively). A logistic regression analysis revealed that both severe PVWMH (OR 6.17; 95% CI 1.93-19.75, p = 0.002) and SCWMH (OR 3.19; 95% CI 1.10-9.23, p = 0.032) remained independent predictors of END. CONCLUSIONS: Both severe PVWMH and SCWMH were useful to predict END in patients with isolated pontine infarction.

Stroke Subtypes and Topographic Locations Associated with Neurological Deterioration in Acute Isolated Pontine Infarction.

OBJECTIVE: This study investigated predictors of neurological deterioration (ND) in acute isolated pontine infarction. METHODS: Two hundred fifty-nine patients with acute isolated pontine infarctions identified using diffusion-weighted imaging were retrospectively analyzed. The patients were divided according to the presence/absence of ND, defined as increased (≥2 units) National Institutes of Health Stroke Scale scores 5 days after onset. Pontine infarctions comprised 3 stroke subtypes: vertebrobasilar large-artery disease, basilar artery branch disease (BABD), and small-artery disease (SAD), according to basilar artery atherosclerosis severity and lesion extent of the transverse axial plane. Topographic locations of longitudinal pontine infarctions in the axial plane were divided into upper, middle, lower, and whole. RESULTS: Of the 259 patients (male : female = 136:123, 68.84 ± 10.24), only 27.4% exhibited ND. The prevalence was significantly increased in females, whereas smoking was significantly decreased in patients with ND. BABD and lower pontine infarctions were significantly more frequent in patients with ND (70.4% and 43.7%, respectively) than in patients without ND (51.6% and 30.3%, respectively). SAD and upper pontine infarctions were significantly less frequent in patients with ND (16.9% and 7.0%, respectively) than in patients without ND (30.3% and 23.4%, respectively). BABD and lower pontine infarctions were positively related to ND. CONCLUSIONS: This is the first study to demonstrate that BABD and lower pons lesions are predictors of ND in acute isolated pontine infarction. These findings indicate the potential importance of early identification of stroke subtypes and topographic locations in the prevention of ND in patients with suspected pontine infarction.

A Novel Brainstem Hemorrhage Model by Autologous Blood Infusion in Rat: White Matter Injury, Magnetic Resonance Imaging, and Neurobehavioral Features.

BACKGROUND: Primary brainstem hemorrhage (BSH) has the highest mortality and morbidity as a subtype of intracerebral hemorrhage. A major limitation of BSH research is the lack of a corresponding animal model. The purpose of this study was to establish a novel rat model of BSH and to characterize the resulting brain injury, especially focusing on white matter injury. METHODS: BSH was produced by stereotactically injecting autologous whole blood into the pons. Time course of hematoma resolution was observed by 7-T magnetic resonance imaging. White matter injury was evaluated in detail by multiple parameters including diffuse tensor imaging (DTI), demyelination, axonal injury, oligodendrocyte degeneration, and oligodendrocyte precursor cell proliferation. Brain water content and neurobehavior were also evaluated. RESULTS: Blood infusion (30 µL) led to a stable, reproducible hematoma in the right basotegmental pons. The hematoma absorption started, became obvious, and was nearly completed at 7, 14, and 30 days, respectively. Hematoma caused obvious brain edema at 3 days. White mater injury was observed pathologically, which was in line with decreased fractional anisotropy (FA) in DTI in the pons. FA reduction was also noticed in the cerebral peduncle and medulla. Behavioral abnormality persisted for at least 14 days and neurofunction was recovered within 1 month. CONCLUSIONS: This novel model can produce a stable hematoma resulting in brain edema, white matter injury, and neurofunctional deficits, which could be useful for future investigation of pathophysiological mechanisms and new treatment evaluation after BSH.

Recurrent Hemorrhagic Venous Infarctions Caused by Thrombosis of a Pontine Developmental Venous Anomaly and Protein S Mutation.

A 34-year-old man presented with an acute onset of upbeat nystagmus, slurred speech, and limb and truncal ataxias. The patient had a history of limb ataxia and gait disturbance previously treated as brainstem encephalitis with corticosteroids 3 years previously. Brain magnetic resonance imaging showed pontine developmental venous anomaly (DVA) and hemorrhagic infarction within the drainage territory of the DVA. Three months later, the patient exhibited recurrent limb ataxia, double vision, and numbness of the left side of the body. The brain magnetic resonance imaging revealed recurrent hemorrhagic venous infarction within the same territory of the pontine DVA. Laboratory tests disclosed a hypercoagulable state owing to a decrease of protein S activity despite the normal antigen level. Genetic testing indicated that the patient was a homozygous carrier of protein S Tokushima. The patient's severe disability remained unchanged in spite of treatment with anticoagulation therapy using warfarin. We propose that further research on hereditary coagulopathy be carried out in patients with recurrent episodes of DVA-related infarction.