A 53-year-old man with essential hypertension abruptly developed rightward body lateropulsion (BL), and mild dysesthesia in the right upper extremity. No other neurologic abnormalities were observed. Cranial magnetic resonance imaging demonstrated a small infarct lesion in the middle pontine tegmentum on the left side. Under antiplatelet agent, the patient became asymptomatic within 7 days. BL is defined as irresistible falling to one side without motor weakness. Damage to the ascending graviceptive pathway (GP) may cause BL. GP from the vestibular nuclei to the Cajal interstitial nucleus crosses the midline in the caudal pons. Based on previous reports, the location of GP was speculated in the rostral pons. However, its precise location remains unreported in the middle pons. This is a second reported case of BL due to a middle pontine tegmentum infarction. In addition, findings of neurologic and magnetic resonance imaging in our patient suggest that GP may run in the dorsal region to the medial lemniscus in the middle pons.
Patient 1 developed leftward body lateropulsion (BL), right internuclear ophthalmoplegia, and hypalgesia and thermohypoesthesia in the territory of the left trigeminal nerve due to an infarction in the right rostral ponine tegmentum. Patient 2 developed rightward BL and left non-paralytic pontine exotropia without alternating exotropia due to an infarction in the left rostral pontine tegmentum. Although impairment of the ascending graviceptive pathway (GP) causes BL, its precise location remains uncertain. Neurologic findings in our patients suggest that GP may run in the vicinity of the medial longitudinal fasciculus, ventral trigemino-thalamic tract and paramedian pontine reticular formation in the rostral pons.
An 80-year-old Japanese woman with paroxysmal atrial fibrillation suddenly developed sensory aphasia, with moderate weakness restricted to the right shoulder with normal muscle strength in the elbow, wrist and fingers. There were no other neurological abnormalities. Diffusion-weighted cranial magnetic resonance imaging demonstrated scattered infarct lesions in the territory of the left middle cerebral artery (MCA), probably due to cardiogenic embolism. Right-sided shoulder palsy might have been caused by a localized infarct lesion in the precentral gyrus on the left side, and resolved within 10 days. Because the area corresponding to the shoulder is small in the primary motor cortex, isolated shoulder palsy due to cortical infarction is very rare. Its etiology remains controversial, but borderzone ischemia between the anterior cerebral artery and MCA, and atherothrombosis of the cortical branch of MCA are proposed. Our case shows that the area corresponding to the shoulder receives blood from the cortical branch of MCA.
A 47-year-old man with dyslipidemia abruptly developed pain and temperature sensation disturbance on the left-sided face and rightsided body and extremities, and left-sided peripheral facial palsy. There were not any other neurological symptoms. Cranial magnetic resonance imaging demonstrated a localized infarct lesion in the left lateral inferior pons. The left anterior inferior cerebellar artery (AICA) was demonstrated by magnetic resonance angiography. Consequently, infarction of the left caudomedial branch of AICA might involve spinothalamic tract, spinal trigeminal nucleus and facial nerve. Here, we emphasize that combination of crossed pain and temperature sensation disturbance with peripheral facial palsy is an indicating sign of a localized lateral inferior pontine lesion.
A 49-year-old woman without contributory medical history presented with zoster in the left-sided second cervical dermatome, and underwent oral valaciclovir at 3000 mg/day. Five days later, bitemporal hemianopia developed. Corrected visual acuities were spared, and funduscopic fi ndings demonstrated no abnormalities in both eyes. Varicella-zoster virus (VZV) viremia was proved by the polymerase chain reaction test. Cerebrospinal fl uid examination fi ndings were normal. Cranial and orbital magnetic resonance imaging demonstrated no abnormalities. Thereafter, under 7 days of intravenous aciclovir at 1500 mg/day, bitemporal hemianopia gradually improved. This is a fi rst reported case of isolated optic chiasmal neuritis secondary to VZV infection.
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