Acute Wallerian degeneration of middle cerebellar peduncles due to basilar artery thrombosis
A 59-year-old male patient with known arterial hypertension, hypercholesterolemia, and diabetes mellitus came to our hospital with accentuated dysarthria, skew deviation, double vision, and right hemisyndrome since 2 days. Before that the patient had acute vertigo for 9 days as the initial symptom and he went to a local hospital where MRI of the brain was performed, which showed acute tegmental infarction of left paramedian pons.\nUpon admission, the patient was drowsy and markedly dysarthric. Neurological examination showed abnormal horizontal movements of the extraocular muscles and spontaneous nystagmus; however, vertical gaze was maintained. Left facial palsy as well as weakness in the upper and lower extremities on both sides was noted. The total National Institute Health Stroke Scale (NIHSS) score was 8/42.\nMRI at this time [] revealed small bilateral foci of restricted diffusion in the ventral pons. The central paramedian pons and the midbrain showed lesser hyperintense signal on DWI and contrast enhancement suggestive of subacute infarct. MR angiography (MRA) revealed no flow void in intracranial right vertebral artery and basilar artery [], suggesting thrombosis. Consensus decision was taken to avoid catheter cerebral angiography and thrombolysis, as the patient had history of bleeding per rectum 1 month prior. Intravenous unfractionated heparin was administered. Extensive work-up to rule out any cause of vasculitis was done; however, these were normal. Four days later, he was in full control of his spaciotemporal orientation; however, he developed new ataxia on the left side. The oculomotor and motoric deficits were unchanged. Intravenous heparin was continued and the patient was managed conservatively. On day 12, he further developed diminished facial sensation in trigeminal distribution, dysmetria, and dysdiadokinesia of the lower left extremity and the NIHSS score was 5/42.\nMRI [] performed at this time (day 12) revealed restricted diffusion in both the MCPs with hyperintense signal on fluid-attenuated inversion recovery (FLAIR) images symmetrically. The new lesions were interpreted as WD due to bilateral paramedian pontine infarction following the basilar artery thrombosis. No new focus of acute infarct was seen. At this time, intravenous heparin was stopped and prophylactic aspirin 100mg daily was considered. Patient was transferred to neurorehabilitation clinic and gradually regained power in extremities.\nLast follow-up MRI [] was done 12 weeks after the onset showed gliosis in midbrain and ventral pons. Persistent T2-hyperintense signal was noted in both the MCPs with decreased fractional anisotropy. Paucity of fibers of MCP and transverse pontine fibers was also seen. Presently, the patient has persistent mild dysarthria, dysmetria, and inability to converge eyes, but otherwise there are no motor or sensory defects.