because motor weakness is one of the most serious disabling sequelae of stroke , so it is important to elucidate the motor recovery mechanism for successful rehabilitation . many studies have attempted to elucidate the motor recovery mechanism of stroke and several motor recovery mechanisms have been suggested . however , the majority of these studies focus on cerebral infarct and relatively little is known about the motor recovery mechanism of intracerebral hemorrhage ( ich ) . diffusion tensor imaging ( dti ) can help to investigate the motor recovery mechanism of ich by enabling the direct visualization and estimation of the corticospinal tract ( cst ) . , we report on a patient with ich who showed a change in the origin of an injured cst from the premotor cortex ( pmc ) to the primary motor cortex ( m1 ) . an 86-year - old woman presented with complete paralysis of the right upper and lower extremities , which occurred at the onset of spontaneous ich ( motricity index ( mi ) : 0 ( full mark : 100 ) ) ( table 1 ) . longitudinal changes in motor function t2-weighted mr images showed a hematoma in the left fronto - parietal lobe , including m1 , at 1 month after onset , that resolved at 5 months after onset ( figure 1a ) . from 1 month to 5 months after onset , she received comprehensive rehabilitative management , which included the administration of neurotrophic drugs ( ropinirole , bromocriptine , levodopa , and amantadine ) , movement therapy , and neuromuscular electrical stimulation of the affected finger extensors and ankle dorsiflexors . movement therapy focused on improving the motor functions of the right upper and lower extremities and included physical and occupational therapy sessions five times per week . weakness of her left extremities improved from an mi score of 0 point at 1 month to 27 points at 2 months and to 52 points ( 5 months after ich onset ) after 4 months of rehabilitation . as a result , she was able to extend the affected fingers against gravity and to walk independently on even ground . brain magnetic resonance images , diffusion tensor imaging ( dti ) and transcranial magnetic stimulation results of an 86-year - old female patient with a hematoma in the left fronto - parietal lobe . ( a ) t2-weighted magnetic resonance images showed a hematoma in the left fronto - parietal lobe including the primary motor cortex at 1 month after onset , which was resolved at 5 months after onset . dti results showed that at 1month and 5 months after intracerebral hemorrhage , the right csts originated from the cerebral cortex , including the primary motor cortex , and then passed through the known cst pathway . in the left ( affected ) hemisphere , the csts originated from the left premotor cortex at 1 month after onset , and from the left primary motor cortex and premotor cortex at 5 months after onset . a motor evoked potential of low amplitude ( 100 v ) was obtained from right abductor pollicis brevis muscle by the affected ( left ) hemisphere stimulation at 1 month after onset . however , motor evoked potential amplitude was increased to the normal range ( 3.8 mv ) at 5 months after onset . ich volume was measured on ct image and t2-weighted mri images through picture archived communication system ( pacs , marotech , korea ) . the maximum width ( x ) , length ( y ) and height ( z ) of lesion at the level where a hematoma was clearly seen were measured . the ich volume was calculated according to the formula : the volume of ich was 37.19 mv on the ct images at the ich onset and 26.71 mv on the mr images at 1 month after onset . diffusion tensor images were acquired using a synergy - l sensitivity encoding ( sense ) head coil on a 1.5-t philips gyroscan intera system ( hoffman - laroche , mijdrecht , the netherlands ) using a single - shot echo planar imaging with a navigator echo . for each of the 32 noncollinear diffusion - sensitizing gradients , 60 contiguous slices ( matrix = 192  192 , field of vision = 240 mm , repetition time / echo time = 10 726/76 ms , b = 600 mm / s , number of excitations = 1 , thickness = 2.5 mm ) were acquired . three - dimensional reconstructions of fiber tracts were obtained using the dti task card software ( philips extended mr work space 2.6.3 ) ( threshold fractional anisotropy ( fa ) = 0.15 , angle = 45 ) . fiber tracts passing through both region of interests ( cst portion of the anterior mid - pons and low - pons on the color map ) were designated final tracts of interest . at 1 month and 5 months after ich onset , dti results showed that in the right ( non - affected ) hemisphere , the right cst originated from the cerebral cortex ( including m1 ) and passed through the known cst pathway . however , in the left ( affected ) hemisphere , the cst originated from the left pmc at 1 month and from the left m1 and pmc at 5 months ( figure 1b ) . tms was performed using a magstim novametrix 200 magnetic stimulator equipped with a 9-cm mean diameter circular coil ( novametrix medical systems inc , wallingford , ct , usa ) . the left hemisphere was stimulated by a counterclockwise current and the right hemisphere was stimulated by a clockwise current . motor - evoked potentials ( meps ) were obtained from both abductor pollicis brevis muscles in a relaxed state . excitatory threshold ( et ) was defined as the minimum stimulus required to elicit an mep with a peak - to - peak amplitude of 50 v or greater during two of four attempts . each site was stimulated three times with inter - stimulus intervals of  10 seconds , and shortest latency and average peak to peak amplitude were estimated . mep ( latency : 23.5 ms ; amplitude : 100 v ; et : 100% ) was evoked from the affected ( left ) hemisphere during the tms study conducted at 1 month after ich onset , but the amplitude increased to the normal range at 5 months after ich onset ( latency : 19.7 ms ; amplitude : 3.8 mv ; et : 70% ) ( figure 1c ) . ich volume was measured on ct image and t2-weighted mri images through picture archived communication system ( pacs , marotech , korea ) . the maximum width ( x ) , length ( y ) and height ( z ) of lesion at the level where a hematoma was clearly seen were measured . the ich volume was calculated according to the formula : the volume of ich was 37.19 mv on the ct images at the ich onset and 26.71 mv on the mr images at 1 month after onset . diffusion tensor images were acquired using a synergy - l sensitivity encoding ( sense ) head coil on a 1.5-t philips gyroscan intera system ( hoffman - laroche , mijdrecht , the netherlands ) using a single - shot echo planar imaging with a navigator echo . for each of the 32 noncollinear diffusion - sensitizing gradients , 60 contiguous slices ( matrix = 192  192 , field of vision = 240 mm , repetition time / echo time = 10 726/76 ms , b = 600 mm / s , number of excitations = 1 , thickness = 2.5 mm ) were acquired . three - dimensional reconstructions of fiber tracts were obtained using the dti task card software ( philips extended mr work space 2.6.3 ) ( threshold fractional anisotropy ( fa ) = 0.15 , angle = 45 ) . fiber tracts passing through both region of interests ( cst portion of the anterior mid - pons and low - pons on the color map ) were designated final tracts of interest . at 1 month and 5 months after ich onset , dti results showed that in the right ( non - affected ) hemisphere , the right cst originated from the cerebral cortex ( including m1 ) and passed through the known cst pathway . however , in the left ( affected ) hemisphere , the cst originated from the left pmc at 1 month and from the left m1 and pmc at 5 months ( figure 1b ) . tms was performed using a magstim novametrix 200 magnetic stimulator equipped with a 9-cm mean diameter circular coil ( novametrix medical systems inc , wallingford , ct , usa ) . the left hemisphere was stimulated by a counterclockwise current and the right hemisphere was stimulated by a clockwise current . motor - evoked potentials ( meps ) were obtained from both abductor pollicis brevis muscles in a relaxed state . excitatory threshold ( et ) was defined as the minimum stimulus required to elicit an mep with a peak - to - peak amplitude of 50 v or greater during two of four attempts . each site was stimulated three times with inter - stimulus intervals of  10 seconds , and shortest latency and average peak to peak amplitude were estimated . mep ( latency : 23.5 ms ; amplitude : 100 v ; et : 100% ) was evoked from the affected ( left ) hemisphere during the tms study conducted at 1 month after ich onset , but the amplitude increased to the normal range at 5 months after ich onset ( latency : 19.7 ms ; amplitude : 3.8 mv ; et : 70% ) ( figure 1c ) . in this patient , we investigated changes of the injured left cst and found that the injured cst seemed to recover as detected by dti , tms and clinical observation . at 1 month after ich onset , the left cst originated from the pmc by dti , and the mep obtained at the right hand showed low amplitude and a latency compatible with that of the cst . by contrast , 5-month results revealed that the left cst originated from the left m1 by dti and that mep amplitude had improved to the normal range by tms . the m1 is the major origin of the cst , although the cst is known to originate from the extensive cerebral cortex , including the pmc , the primary somatosensory cortex , and the prefrontal cortex . on the other hand , consequently , the dti and tms results of this patient suggest that the severely injured left cst had recovered over 4 months in terms of its origin and fiber number . furthermore , clinically , the finding that the patient was able to flex and extend against gravity at 5 months after ich onset provides additional evidence of left cst recovery . as a result , right extremity motor functions seemed to have been recovered due to reorganization of the injured left cst originating from the left pmc to left m1 . it is also possible that compression of the cst into the left pmc recovered in concert with hematoma resolution . for the motor recovery mechanism in ich , several dti based studies have described recovery of an injured cst or the contribution made to recovery by the contralateral unaffected cst . during the last 5 years , a number of serial dti studies have described the recovery of injured cst after ich . jang et al demonstrated the recovery process of an injured cst in a patient with a subcortical ich by serial dti . the patient presented with complete paralysis of right extremities at onset , but over 16 months , motor functions of affected extremities slowly recovered to nearly normal . furthermore , dtt showed that the origin of the cst had changed from the posterior parietal cortex at 1 month to the primary somatosensory cortex at 4 months and m1 at 16 months . the authors suggested that recovery of the origin of the damaged cst was due to a process of normalization from the parietal cortex to m1 . by contrast , our patient showed a change in the origin of the injured cst from the pmc to m1 . this study described changes of an injured cst that occurred in concert with motor recovery in a patient with ich . to the best of our knowledge , this is the first longitudinal study to demonstrate a change in the origin of an injured cst from the pmc to m1 in ich . results from this study suggest a motor recovery mechanism of ich and the important implications regarding brain plasticity and brain rehabilitation after ich . however , this study is obviously limited by case numbers , and further complementary studies involving larger case numbers are warranted .
many studies have attempted to elucidate the motor recovery mechanism of stroke , but the majority of these studies focus on cerebral infarct and relatively little is known about the motor recovery mechanism of intracerebral hemorrhage . in this study , we report on a patient with intracerebral hemorrhage who displayed a change in injured corticospinal tract originating from the premotor cortex to the primary motor cortex on diffusion tensor imaging . an 86-year - old woman presented with complete paralysis of the right extremities following spontaneous intracerebral hemorrhage in the left frontoparietal cortex . 
 the patient showed motor recovery , to the extent of being able to extend affected fingers against gravity and to walk independently on even ground at 5 months after onset . 
 diffusion tensor imaging showed that the left corticospinal tract originated from the premotor cortex at 1 month after intracerebral hemorrhage and from the left primary motor cortex and premotor cortex at 5 months after intracerebral hemorrhage . 
 the change of injured corticospinal tract originating from the premotor cortex to the primary motor cortex suggests motor recovery of intracerebral hemorrhage .