J Rehabil Med 2014; 46: 475–478

Case Report

Recovery of an injured medial lemniscus pathway in a patient
with intracerebral haemorrhage
Jeong Pyo Seo and Sung Ho Jang
From the Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University,
Daegu, Republic of Korea

Objective: We describe here a patient with intracerebral
haemorrhage who showed recovery of an injured medial
lemniscus and its related thalamocortical pathway on followup diffusion tensor tractography.
Case report: A 48-year-old man presented with right hemiplegia following a spontaneous intracerebral haemorrhage
in the left corona radiata and basal ganglia. He underwent
conservative management for intracerebral haemorrhage
and comprehensive rehabilitative therapy.
Results: The kinesthetic sensation score (maximum score
24 points) of the Nottingham Sensory Assessment improved
from 6 points (at 2 weeks after injury) to 10 points (at 6
weeks) and to 18 points (at 12 weeks). For the left thalamocortical pathway, a discontinuation at the left midbrain below the haematoma was observed on the 2-week diffusion
tensor tractography. The 6-week diffusion tensor tracto­
graphy showed that the integrity of the left thalamocortical
pathway had been restored to the left primary motor cortex, and the 12-week diffusion tensor tractography showed
restoration to the left primary somatosensory cortex. The
fibre number of the left thalamocortical pathway showed an
increase (470 at 2 weeks after injury, 1,080 at 6 weeks, and
1,626 at 12 weeks).
Conclusion: This patient underwent recovery of an injured
thalamocortical pathway over a period of 10 weeks after the
second week following intracerebral haemorrhage, in terms
of restoration of discontinued integrity and increased fibre
number in the thalamocortical pathway.
Key words: diffusion tensor imaging; medial lemniscus; intracerebral haemorrhage; rehabilitation.
Correspondence address: Sung Ho Jang, Department of
Physical Medicine and Rehabilitation, College of Medicine,
Yeungnam University, 705-717 Daegu, Republic of Korea.
E-mail: strokerehab@hanmail.net
J Rehabil Med 2014; 46: 475–478
Accepted Jan 8, 2014; Epub ahead of print Apr 8, 2014
Introduction
Somatosensory dysfunction is common after stroke and can
lead to functional impairment; somatosensory function therefore has important implications for stroke patients (1, 2).
Elucidation of recovery mechanisms in stroke patients would

provide important guidance for rehabilitation. Many studies
have investigated the mechanisms of recovery of various
functions in stroke patients, focussing in particular on motor
function (3). However, relatively little is known about the
mechanism of recovery of somatosensory function (2, 4–9).
There are two main somatosensory tracts in the human brain:
the medial lemniscus and its related thalamocortical pathway
(ML), and the spinothalamic tract and its related thalamocortical pathway (STT). The ML is responsible for proprioception,
which results in the conscious awareness of body position in
space, and the STT is the neural tract responsible for pain and
body temperature. Many recent studies using diffusion tensor
tractography (DTT) have reported on the clinical usefulness of
DTT for the ML and STT, as well as methods used for identification of these tracts (10–12). However, little is known about
the mechanisms of recovery of these somatosensory tracts (8).
We report here on a patient who showed recovery of an
injured ML during a period of 3 months after an intracerebral
haemorrhage (ICH), as demonstrated by follow-up DTT.
Case report
A 48-year-old, right-handed man presented with right hemiplegia, which occurred at the onset of a spontaneous ICH. He
underwent conservative management for ICH at the department
of neurosurgery of a university hospital. Two weeks after onset
of ICH, he was transferred to the rehabilitation department of
the same university hospital in order to undergo rehabilitation.
Brain magnetic resonance images 2 weeks after onset showed
a haematoma in the left corona radiata and basal ganglia (Fig.
1A). The patient received comprehensive rehabilitative therapy, including neurotrophic drugs (ropinirole, levodopa, and
amantadine), movement therapy, somatosensory stimulation,
and procedures for spasticity control of the left finger flexors
(13, 14). Movement therapy and somatosensory stimulation
focused on improvement of sensori-motor function of the right
upper and lower extremities and was performed during the
physical and occupational therapy sessions, 5 times per week
(140 min/day). The subscale for kinesthetic sensation (maximum score 24 points) of the Nottingham Sensory Assessment
(NSA) was used for determination of somatosensory function
(15). The kinesthetic sensation score of the NSA improved
from 6 points (at 2 weeks after onset) to 10 points (at 6 weeks),

© 2014 The Authors. doi: 10.2340/16501977-1796
Journal Compilation © 2014 Foundation of Rehabilitation Information. ISSN 1650-1977

J Rehabil Med 46

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J. P. Seo and S. H. Jang

Fig. 1. (A) T2-weighted images (2 weeks after injury) showing a haematoma and surrounding oedema in the left coronal radiata and basal ganglia.
(B) Results of diffusion tensor tractography (DTT). The right medial lemniscus and its related thalamocortical pathway (ML) originated from the right
cerebral cortex, including the primary somatosensory cortex, which passed along the known ML pathway. The 2-week DTT for the left ML showed a
discontinuation (green arrow) at the left midbrain below the haematoma. The 6-week DTT showed that the integrity of the left ML had been restored
to the left primary motor cortex. On the 12-week DTT, the trajectories of the left ML had increased and the integrity to the left primary somatosensory
cortex (blue arrow) had been restored. R: right; A: anterior.

then to 18 points (at 12 weeks). Weakness of the patient’s right
extremities improved from a Motricity Index of 9 points at 2
weeks to 49 points (at 6 weeks) and 56 points (at 12 weeks)
(16). As a result, the patient was able to walk independently
on an even floor at 6 weeks and ascend and descend stairs at
12 weeks after onset; however, due to severe injury of the left
corticospinal tract, he could not perform fine motor activities
with his right hand.
The patient provided signed, informed consent and the study
protocol was approved by our institutional review board.
Diffusion tensor TRACTOGRAPHY imaging
DTT images were acquired 3 times (at 2, 6, and 12 weeks
after onset) using a 6-channel head coil on a 1.5 T Philips
Gyroscan Intera (Philips Ltd, Best, The Netherlands) with
single-shot echo-planar imaging. For each of the 32 noncollinear diffusion sensitizing gradients, 70 contiguous slices
were acquired parallel to the anterior commissure-posterior
commissure line. Imaging parameters were as follows: acJ Rehabil Med 46

quisition matrix = 96 × 96, reconstructed to matrix = 192 × 192
matrix, field of view = 240 × 240 mm, repetition = 10,398 ms,
echo time = 72 ms, parallel imaging reduction factor (SENSE
factor) = 2, echo-planar imaging factor = 59 and b = 1000 s/
mm, number of excitations = 1, and a slice thickness of 2.5 mm
(acquired isotropic voxel size 2.5 × 2.5 × 2.5 mm). Removal of
eddy current-induced image distortions using affine multi-scale
2-dimensional registration was performed at the Oxford Centre
for Functional Magnetic Resonance Imaging of Brain Software
Library (FSL; www.fmrib.ox.ac.uk/fsl). Reconstruction of the
MLs was performed using DTI-Studio software (CMRM, Johns
Hopkins Medical Institute, Baltimore, MD, USA). MLs were
determined by selection of fibres passing through 2 regions
of interest (ROIs). The first ROI was located in accordance
with known anatomy at the level of the medulla (the portion
medio-posterior to the pyramid). The second ROI was at the
posterior part of the upper pons (blue colour) on the colour
map (12). Fibre tracking was started at any seed voxel with a
fractional anisotropy (FA) > 0.2 and ended at a voxel with a FA
of < 0.2 and a tract turning-angle of < 60º. The values of FA,

Recovery of injured medial lemniscus
Table I. Changes in clinical data and diffusion tensor tractography (DTT)
imaging parameters
Clinical data
NSA (1–24)
MI (1–100)
DTT imaging parameters
FA
ADC
FN

2 weeks

6 weeks

12 weeks

6
9

10
49

18
56

0.49
0.85
470

0.49
0.79
1,080

0.46
0.80
1,626

NSA: subscale for kinesthetic sensation of the Nottingham Sensory
Assessment; MI: Motricity Index; FA: fractional anisotropy; ADC:
apparent diffusion coefficient; FN: fibre number.

apparent diffusion coefficients (ADC) and fibre number (FN)
were measured.
The right ML originated from the right cerebral cortex, including the primary somatosensory cortex (S1), which passed
along the known ML pathway (Fig. 1B). The 2-week DTT for
the left ML showed a discontinuation at the left midbrain below
the haematoma. The 6-week DTT showed that the integrity of
the left ML had been restored to the left primary motor cortex;
however, it was not connected to the left S1. On the 12-week
DTT, the trajectories of the left ML were increased and the
integrity to the left S1 was restored (Fig. 1B). Although the
FA and ADC values of the DTTs for the left ML were similar,
the FNs were increased (470 at 2 weeks, 1,080 at 6 weeks, and
1,626 at 12 weeks) (Table I).
Discussion
This patient underwent a process of recovery of an injured
ML during a period of 10 weeks after the second week following ICH, in terms of restoration of discontinued integrity
and increased FN of the injured ML, and clinical recovery of
proprioception on the affected side. Regarding the integrity of
the injured ML, the left ML appeared to be severely injured,
as shown by 2-week DTT, in terms of a discontinuation at the
midbrain level below the haematoma. On follow-up DTTs, the
integrity of the discontinued left ML was shown to be restored
to the left primary motor cortex at 6 weeks after symptom
onset, and to the left S1, which is the main origin of the ML,
at 12 weeks after onset. The FN of the left ML showed an
increase over time at 2 weeks (470), 6 weeks (1,080), and 12
weeks (1,626), with no significant changes in the FA and ADC
values. The FA value represents the degree of directionality of
microstructures such as axon and myelin, and the ADC value
indicates the magnitude of water diffusion (17). The FN reflects
the total number of fibres in a neural tract (17). Therefore, the
increment of FN of the left ML suggests the increment of FN
of the injured left ML. In addition, clinical recovery of proprioception on the NSA subscale for the right side (a score of 6 at 2
weeks, 10 at 6 weeks, and 18 at 12 weeks) appears to provide
additional evidence of the recovery of the injured left ML.
The mechanisms of recovery of somatosensory function in
stroke patients are classified as follows: recovery of an injured

477

somatosensory pathway, peri-lesional reorganization, contribution of the unaffected somatosensory cortex, contribution of
the secondary somatosensory cortex, and recovery mechanisms
in patients with thalamic lesion (2, 4–9). There have been few
studies of the recovery of an injured somatosensory pathway
in patients with stroke (8). In 2010, Hong & Jang (8) reported
the recovery of somatosensory function in a patient with a
spontaneous ICH in the right cortex and corona radiata. The
patient presented with severe somatosensory dysfunction on
the left side at onset, and the kinesthetic sensation score of the
NSA (maximum score 24 points) improved from 12 points at 3
weeks to 18 points at 7 weeks. On the 3- and 7-week functional
MRI, the ipsilesional cortex centred on the S1 was activated
during proprioceptive input of the affected hand. Activation
of ipsilesional S1 showed an increase on the 7-week fMRI,
compared with that of the 3-week fMRI. The injured ML was
not reconstructed on the 3-week DTT; however, the injured
ML was reconstructed through the medial side of the lesion to
the S1. By contrast, the patient described in this study showed
more severe deficit of proprioception at initial evaluation and
showed a different course of recovery (longer and poorer). In
addition, the patient described in the previous study showed
restoration to the ipsilesional S1 at 7 weeks after onset; in
contrast, this patient showed restoration to the ipsilesional
primary motor cortex at 6 weeks and then to the ipsilesional
S1 at 12 weeks after onset (18).
In conclusion, we report here a patient who showed recovery
of a severely injured ML after ICH in terms of clinical recovery and recovery of the integrity and FN of DTT. Because this
case report demonstrated the process of recovery of a severely
injured ML during the early phase following ICH, this provides
information about recovery of somatosensory dysfunction,
which is useful for stroke rehabilitation. Detailed knowledge
about recovery mechanisms in stroke would provide the basis
for establishment of scientific rehabilitation strategies. However, this study is limited as it is a single case report. Further
complementary studies with larger numbers of patients are
warranted. In addition, research is required into the effects of
the rehabilitative modalities employed with this patient, including the neurotrophic drugs (which are known to be effective in
motor recovery of stroke patients (13, 14)) on the recovery of
an injured ML. The clinical significance of this kind of recovery
of the ML also requires clarification. However, the limitations
of DTT imaging, which may underestimate or overestimate of
fibres of a neural tract should be taken into account (19).
AcknowledgeMENTs
This work was supported by the DGIST R&D Program of the Ministry of
Education, Science and Technology of Korea (14-BD-0401).

References
1. Bogousslavsky J, Caplan LR. Stroke syndromes. 2nd ed. Cambridge: Cambridge University Press; 2001.
2. Jang SH. Recovery mechanisms of somatosensory function in
J Rehabil Med 46

478

J. P. Seo and S. H. Jang

stroke patients: implications of brain imaging studies. Neurosci
Bull 2013; 29: 366–372.
3. Calautti C, Baron JC. Functional neuroimaging studies of motor recovery after stroke in adults: a review. Stroke 2003; 34: 1553–1566.
4. Rossini PM, Tecchio F, Pizzella V, Lupoi D, Cassetta E, Pasqualetti P, et al. On the reorganization of sensory hand areas after
mono-hemispheric lesion: a functional (MEG)/anatomical (MRI)
integrative study. Brain Res 1998; 782: 153–166.
5. Forss N, Hietanen M, Salonen O, Hari R. Modified activation of
somatosensory cortical network in patients with right-hemisphere
stroke. Brain 1999; 122: 1889–1899.
6. Ohara S, Lenz FA. Reorganization of somatic sensory function in
the human thalamus after stroke. Ann Neurol 2001; 50: 800–803.
7. Staines WR, Black SE, Graham SJ, McIlroy WE. Somatosensory
gating and recovery from stroke involving the thalamus. Stroke
2002; 33: 2642–2651.
8. Hong JH, Jang SH. Is combined functional magnetic resonance
imaging and diffusion tensor tractography a useful tool for evaluation of somatosensory dysfunction recovery after intracerebral
hemorrhage? Neural Regen Res 2010; 5: 1109–1112.
9. Jang SH. Contra-lesional somatosensory cortex activity and
somatosensory recovery in two stroke patients. J Rehabil Med
2011; 43: 268–270.
10. Wakana S, Jiang H, Nagae-Poetscher LM, van Zijl PC, Mori S.
Fiber tract-based atlas of human white matter anatomy. Radiology
2004; 230: 77–87.
11. Yamada K, Nagakane Y, Yoshikawa K, Kizu O, Ito H, Kubota T, et

J Rehabil Med 46

al. Somatotopic organization of thalamocortical projection fibers
as assessed with MR tractography. Radiology 2007; 242: 840–845.
12. Yang DS, Hong JH, Byun WM, Kwak SY, Ahn SH, Lee H, et al.
Identification of the medial lemniscus in the human brain: combined study of functional MRI and diffusion tensor tractography.
Neurosci Lett 2009; 459: 19–24.
13. Molina-Luna K, Pekanovic A, Rohrich S, Hertler B, SchubringGiese M, Rioult-Pedotti MS, et al. Dopamine in motor cortex is
necessary for skill learning and synaptic plasticity. PLoS One
2009; 4: e7082.
14. Kwon HG, Jang SH. Significance of rehabilitative management
during the critical period for motor recovery in intracerebral hemorrhage: a case report. J Rehabil Med 2012; 44: 280–284.
15. Lincoln NB, Jackson JM, Adams SA. Reliability and revision of
the Nottingham Sensory Assessment for stroke patients. Physio­
therapy 1998; 84: 358–365.
16. Demeurisse G, Demol O, Robaye E. Motor evaluation in vascular
hemiplegia. Eur Neurol 1980; 19: 382–389.
17. Assaf Y, Pasternak O. Diffusion tensor imaging (DTI)-based
white matter mapping in brain research: a review. J Mol Neurosci
2008; 34: 51–61.
18. Fujii Y, Nakada T. Cortical reorganization in patients with subcortical hemiparesis: neural mechanisms of functional recovery and
prognostic implication. J Neurosurg 2003; 98: 64–73.
19. Yamada K, Sakai K, Akazawa K, Yuen S, Nishimura T. MR tractography: a review of its clinical applications. Magn Reson Med
Sci 2009; 8: 165–174.