infarction is the most common event resulting in wallerian degeneration ( wd ) in the central nervous system ( cns ) . we report a case showing symmetrical restricted diffusion in middle cerebellar peduncles ( mcps ) after 21 days of the onset of symptoms , which was interpreted as wd . further , magnetic resonance imaging ( mri ) after 12 weeks revealed high signal on diffusion - weighted images ( dwi ) and apparent diffusion coefficient ( adc ) maps . transient signal abnormalities in mcps on dwi following brain stem infarction may be seen and should not be mistaken for a new ischemic event . 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 . upon admission , 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 mri at this time [ figure 1 ] 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 [ figure 2 ] , 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 . 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 . 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 . initial mri of brain on admission : axial diffusion - weighted images ( a , b ) new tiny hyperintense signal foci in ventral and paramedian pons on both sides ( arrows ) suggestive of acute infarcts . the central paramedian pons reveals lesser hyperintensity due to subacute infarct . at this time , mcps were normal ( c ) axial t2w image ( a ) hyperintense signal in paramedian midbrain and pons with contrast enhancement ( b ) suggestive of subacute infarct . coronal mra image ( c ) no flow in intracranial right vertebral and basilar arteries mri [ figure 3 ] 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 100 mg daily was considered . twelfth day follow - up mri : axial t2w images ( a ) shows symmetrical hyperintense signal in both the mcps ( arrow ) . few hyperintense foci are also seen in pons . diffusion - weighted image ( b ) corresponding adc map ( c ) reveals reduced signal suggestive of restricted diffusion last follow - up mri [ figure 4 ] was done 12 weeks after the onset showed gliosis in midbrain and ventral pons . 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 . twelve weeks follow - up mri shows persistent hyperintense signal in both the mcps ( arrows ) on axial t2w . note the gliotic change in tegmentum of pons on the right side ( a ) both mcps reveal mild hyperintense signal on diffusion image ( b ) and adc maps ( c ) with decreased fractional anisotropy ( d ) 2d diffusion tensor image ( dti ) superimposed on t1 post - contrast images shows paucity of fibers in mcp ( e ) and also of transverse pontine fibers ( f ) wd has been extensively described as affecting the corticospinal tract ( cst ) in association with pathologies of the cerebrum and internal capsule . kuhn et al . , described four stages of wd in the cerebrum and they can be observed after 4 weeks on t2w images , however , as early as 12 days with dwi on cst . castillo et al . , found increased signal on dwi suggestive of wd of cst within 72 h after the symptoms in 20% of cases . neuroanatomically , the brachium pontis , or mcps are a large bundle of fibers that connect the pons with the cerebellum . the pontine nuclei receive input from the cerebral cortex via the corticopontine tract and project almost exclusively to the contralateral cerebellum via the transverse pontine fibers and mcps , which constitute the pontocerebellar tract . the pontocerebellar fibers cross at an upper pontine level ; hence , in unilateral pontine infarction , there is damage to local pontine nuclei resulting in ipsilesional involvement of the mcp , and to axons of more lateral neurons which will have to cross midline to reach contralateral mcp [ figure 5 ] . unilateral pontine lesions damage the local pontine neurons , thus affecting ipsilateral mcp after its fibers have crossed , and also damage the ipsilateral lateral fibers which have to cross the midline to form opposite mcp most of the papers report t2-hyperintense signal in mcps due to unilateral pontine infarction at or after 3 months of the onset of symptoms . in our patient , there were bilateral small paramedian pontine infarctions due to basilar artery thrombosis , resulting in increased signal in both mcps . these mcps revealed restricted diffusion as early as 21 days from the onset of symptoms , suggesting acute wd and facilitated diffusion with paucity of fibers at 12 weeks follow - up . to the best of our knowledge , no case report showing sequential evolution of wd in mcps due to basilar artery thrombosis has been described . this may be due to poor clinical outcome of patients with basilar artery thrombosis leading to bilateral brainstem infarcts . similar signal abnormalities are also seen in central pontine myelinosis , in neurodegenerative disorders like olivopontocerebellar atrophy , spinocerebellar ataxia , adrenoleukodystropy , alcoholic liver disease , wilson disease , hypoglycemic coma , or progressive multifocal leukoencephalopathy ( pml ) . presence of restricted diffusion in brainstem with no flow in basilar artery suggests the primarily vascular etiology , rather than a metabolic abnormality . mri and mra help in assessing the extent of brainstem infarction and the length of the occluded artery . patients with no or only relatively small dwi lesions may have a favorable outcome , if reperfusion is achieved with intra - arterial or intravenous thrombolysis . the common etiological factors are local thrombosis in basilar artery which also commonly affects vertebral artery origin , artery - to - artery thromboembolism , cardiac emboli , and vertebral artery dissections . in an acute event , basilar thrombolysis with stenting of vertebral artery due to atheromatous vertebrobasilar stenosis may be considered . for high - grade symptomatic basilar artery stenosis refractory to medical therapy ( warfarin or aspirin ) , in conclusion , restricted diffusion of the mcps following pontine infarction is transient and when imaged during that duration ; it may mimic a new infarction focus . knowledge of sequential evolution of wd of both mcps following pontine infarction / basilar artery thrombosis helps to avoid this misdiagnosis .
wallerian degeneration ( wd ) is the process of demyelination and disintegration of the distal axonal segment following the interruption of the axonal integrity or damage to the neuron . 
 we report a patient having wd of middle cerebellar peduncles due to pontine infarction caused by basilar artery thrombosis . 
 we review the anatomy and discuss the pathogenesis of this condition .