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Causality of pediatric brainstem infarction and basilar artery fenestration?

Pediatric arterial thromboembolic stroke is an uncommon condition and rarely is reported to be associated with a cerebral artery fenestration. This clinical report discusses the case of a child with brainstem infarction and basilar artery fenestration. A cardiac source of thromboembolic events could be excluded; however, detailed coagulation analysis revealed in addition an apoliopoprotein(a) size polymorphism. Because we assume that the two concurrent pathologies in combination caused the arterial thromboembolic stroke, the evaluation of all potential triggers including vascular anomalies and coagulation disorders should be considered in unexplained pediatric infarction.

Basilar Artery↗

Recurrent pontine base infarction: a controlled study.

OBJECTIVES: To assess the clinical features of and risk factors for recurrent pontine base infarction. METHODS: This study includes 5 patients with unilateral pontine base infarction who developed another infarction on the opposite side and, for comparison, 10 follow-up period-matched patients with unilateral pontine base infarction who did not develop recurrent pontine infarction. MRI and angiogram studies were performed in all cases. The two groups were compared. RESULTS: The patients with recurrent pontine base infarction developed quadriparesis, dysarthria and dysphagia. MRI showed bilateral infarcts abutting on the basal surface of the pons. Angiogram studies revealed diseased basilar artery in 3 patients. There were no differences regarding age, gender, angiogram findings and frequency of hypertension, diabetes mellitus, cigarette smoking and hypercholesterolemia between the patients with recurrent stroke and those without. However, the former had a significantly higher number of risk factors for atherosclerosis (p < 0.05) and higher frequency of coronary heart disease (p < 0.05) than the latter. CONCLUSIONS: The number of risk factors for atherosclerosis and a concomitant presence of coronary heart disease may be factors related to recurrent pontine base infarction in patients with unilateral pontine infarction. The main pathogenesis of recurrent pontine base infarction seems to be basilar artery branch atherothrombosis.

Adult↗

Pathological laughter as a symptom of midbrain infarction.

Pathological laughter is an uncommon symptom usually caused by bilateral, diffuse cerebral lesions. It has rarely been reported in association with isolated cerebral lesions. Midbrain involvement causing pathological laughter is extremely unusual. We describe three patients who developed pathological laughter after midbrain and pontine-midbrain infarction. In two patients a small infarction in the left paramedian midbrain was detected, whereas the third one sustained a massive bilateral pontine infarction extending to the midbrain. Laughter heralded stroke by one day in one patient and occurred as a delayed phenomenon three months after stroke in another. Pathological laughter ceased within a few days in two patients and was still present at a two year follow-up in the patient with delayed-onset laughter. Pathological laughter can herald midbrain infarction or follow stroke either shortly after onset of symptoms or as a delayed phenomenon. Furthermore, small unilateral midbrain infarctions can cause this rare complication.

Brain Stem Infarctions↗

Massive pontine hemorrhagic infarction associated with embolic basilar artery occlusion.

We report here an autopsy case of massive pontine hemorrhagic infarction secondary to embolic basilar artery occlusion. A large embolus appeared to have traversed the vertebral artery into the basilar artery as a result of basilarization of the vertebral artery due to severe stenosis of the contralateral vertebral artery. Extensive ischemia due to embolic occlusion of the entire length of the basilar artery, and migration of the embolus are assumed to have resulted in a massive pontine hemorrhagic infarction.

Aged↗

Spectrum of medial medullary infarction: clinical and magnetic resonance imaging findings.

Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1% of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction.

Adult↗

Isolated medial medullary infarction due to vertebral artery dissection.

A 54-year-old man developed left hemiparesis and tactile and deep sensory disturbance following onset of rightside cervical pain. These symptoms resulted from an isolated infarct in the right medial area of the upper medulla oblongata and intracranial vertebral artery (VA) dissection. Atherosclerotic disease of the VA is the most common cause of medial medullary infarction. In past reports of isolated medial medullary infarction, only a few cases involved VA dissection.

Angiography↗

Autonomic consequences of brainstem infarction.

OBJECTIVE: It is well known that patients with brainstem infarctions sometimes experience dizziness, vertigo and falls, although the exact mechanism is not clear. Therefore, we designed a study to quantify autonomic function in patients with brainstem infarction. PATIENTS AND METHODS: We examined autonomic function in 15 patients with brainstem infarctions, who had a history of vertigo, nausea, floating sensation and/or general fatigue during standing, and 31 age-matched controls using the composite autonomic scoring scale (CASS), which was used to grade autonomic function. The patients underwent initial autonomic assessment and then were subjected to aniracetam therapy. The drug was given orally (dose of 600 mg/day) for a duration of 56 days. Upon completion of aniracetam administration, the CASS was again tested. RESULTS: Upon initial assessment, the patients had mild reductions in mean blood pressure (MBP) and lack of an increasing heart rate (HR) within 5 min of head up-tilt, an impairment in BP correction during late phase II and reduced phase IV beat-to-beat BP response to the Valsalva maneuver, and reduced heart rate response to deep breathing (HRdb). CASS indicated mild autonomic dysfunction. After 8 weeks of treatment with aniracetam, the patients' symptoms improved and the autonomic tests showed improvement in autonomic function. CONCLUSION: Part of the pathogenesis of recurrent vertigo or dizziness with brainstem infarction might be due to mild autonomic dysfunction. Aniracetam, which activates the cholinergic system in brain, might correct the cardiovagal system in these patients. The CASS may be a sensitive tool for assessing mild autonomic dysfunction in patients with brainstem infarction.

Aged↗

Trigeminal neuralgia due to pontine infarction.

Trigeminal neuralgia (TN) is most commonly caused by vascular compression of the trigeminal nerve root entry zone. Secondary trigeminal neuralgia due to ischemic lesion of the pons is very rare. Here we report a patient with a pontine infarct transecting the central trigeminal pathways resulting with trigeminal neuralgia.

Aged↗

[Central neurogenic hyperventilation associated with a pontine infarction].

Central neurogenic hyperventilation in patients with a normal level of consciousness is uncommon. This condition occurs in bilateral pontine tegmental lesions, particularly tumors such as CNS lymphomas and glioma, as well as traumatic lesions. The physiopathological mechanisms are unknown and no there is no effective treatment for this entity. We report a case of central neurogenic hyperventilation associated to a unilateral basal pontine infarction.

Brain Stem Infarctions↗