Author's Accepted Manuscript

Brain white matter tracts: Functional anatomy and clinical relevance AC Gerrish, AG Thomas, RA Dineen

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S0887-2171(14)00061-4 YSULT591

To appear in: Semin Ultrasound CT MRI

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Brain white matter tracts: Functional anatomy and clinical relevance

Gerrish AC1, Thomas AG1,2 and Dineen RA2,3

Author affiliations: 1

Imaging Department, Leicester Royal Infirmary, Leicester, UK


Department of Neuroradiology, Queens Medical Centre, Nottingham University Hospitals

NHS Trust, Nottingham, UK 3

Division of Clinical Neuroscience, University of Nottingham, Nottingham, UK

Corresponding author: Adam G Thomas E-mail: [email protected] Address: Imaging Department Leicester Royal Infirmary Infirmary Square, Leicester LE1 5WW Phone: (+44) (0)300 303 1573, Ext 6361 Abstract:

Diffusion tensor imaging (DTI) is increasingly available on clinical MR scanners and can be acquired in a relatively short time. There has been an explosion of applications in the research field but the use to the practising radiologist may seem obscure. This paper aims to highlight how DTI can be used to prompt a dedicated neuroanatomical search for white matter lesions in clinical presentations relating to motor, sensory, language and visuospatial deficits. The enhanced depiction of white matter tracts in the temporal stem is also highlighted; a region of importance in epilepsy surgery planning. Introduction Diffusion weighted imaging (DWI) has proven to be useful in many areas of neuroimaging and is routinely applied in clinical practise. Diffusion tensor imaging (DTI), whilst increasingly available, has yet to find routine clinical application outside of the research environment. After a brief description of DTI technique this review will focus on how DTI can aid in anatomical localisation of lesions and subsequently account for the clinical features that arise.

Diffusion tensor imaging In routine DWI, images sensitive to the diffusion of water in brain tissue are acquired with diffusion gradients applied in 3 orthogonal planes; the signal from the three separate images are av averaged to compensate for the effect that tissue ultrastructure has on water diffusion in any given direction. DTI allows characterisation of this underlying structure by the creation of the “diffusion tensor”. The tensor describes the 3D probability distribution of water diffusion (1). If diffusion is completely unrestricted (e.g. in cerebrospinal fluid, CSF) then this distribution will be spherical or isotropic – i.e. diffusion is equally likely in each

direction. In the white matter (WM), which comprises myelinated axons arranged into tracts, diffusion of water occurs relatively more easily along the course of a WM tract than directly perpendicular to it. The result is that for a WM voxel containing a single or dominant tract orientation, the diffusion distribution becomes anisotropic and is no longer spherical but ellipsoid, with a main axis parallel to the direction of the tract. The main axis of the ellipsoid is the principle eigenvector (e1), with second and third eigenvectors (e2 an1 e3) oriented perpendicular to e1 (fig 1). The amount of diffusion along each eigenvector is quantified as an eigenvalue (λ1-3 respectively). The average eigenvalue is the mean diffusivity (MD), a value analogous to the apparent diffusion coefficient derived by standard DWI). The tensor is calculated after probing the ease of diffusion in multiple directions; a minimum of six nonorthogonal, non-collinear directional experiments are required to calculate the tensor, but the more directions that are employed the more complete the characterisation of the tensor is. The penalty for increasing the number of directions is increased acquisition time; In clinical DTI 6-32 diffusion directions are typically used, but 60 + directions are often used in research settings. There are number of descriptors derived from the tensor that describe the degree of anisotropy of water diffusion, the most commonly used of which is Fractional Anisotropy (FA). In simple terms, this can be thought of a measure of how much ‘unlike’ a sphere, or how much directionality, the diffusion distribution has. An FA of 0 represents complete diffusion isotropy and an FA of 1 would represent a completely anisotropic tissue, although in practice this is not achieved.

Diseases which degrade WM ultrastructure typically lead to

a reduction in the FA, and hence FA has been widely used in research settings to quantify WM damage. Other measurements derived from the tensor such as radial diffusivity and axial diffusivity are thought to reflect integrity of myelin and axonal integrity respectively,

and have been applied in research that attempts to identify different components of WM damage (2). In addition to representation of FA data as grayscale maps, the orientation of the diffusion ellipsoid within the voxel can be presented by use of color-coding of the voxel according to the principle eigenvector. The standard convention for color-coding is : red = where e1 is parallel to the x-axis of the image, , green = where e1 is parallel to the y-axis of the image, and blue = where e1 is parallel to the z-axis of the image. A number of different methods have been described to reconstruct WM tracts from DTI images, broadly referred to as tractography, but the methods by which this is done fall beyond the scope of this article. However, it is worth noting that the ‘tracts’ produced by such techniques are mathematically generated streamlines, derived from inherently limited imaging data; DTI voxels are orders of magnitude larger that the tissue ultrastructure that the technique aims to probe. Innovations such as Q-ball imaging can help to reduce uncertainties, for example at voxels containing crossing tracts (3). However, the streamline images generated by tractography should always be checked for plausibility against known neuroanatomy. .

Neuroanatomical correlation Standard clinical brain imaging combined with DWI is sensitive in detecting white matter pathology, but due to the poor visualisation of specific WM tracts by conventional imaging, does not always reveal the white matter structures that are affected by the pathology detected. The following section will review which WM structures should be assessed in various different clinical presentations and how DTI can help answer the frequent clinical question: “Does this lesion account for clinical presentation?”

Motor syndromes

The  corticospinal  tract  (CST)  conveys  efferent  white  matter projection  fibres  between  the  motor  cortex  and  the  spinal  cord,  enabling  voluntary  movement.  The  tract  predominantly  originates from the primary motor cortex (Brodmann area 4), but also includes fibres from  the pre‐motor and supplementary motor cortices (area 6), the somatosensory cortex (area  1,  2,  3a  &3b),  and  the  superior  parietal  lobule  (area  5)(4).  These  white  matter  fibres  converge  and  descend  through  the  corona  radiata,  the  posterior  limb  of  the  internal  capsule,  the  central  portion  of  the  cerebral  peduncle  and  the  ventral  aspect  of  the  pons,  before  decussating  in  the  medullary  pyramids  and  descending  within  the  spinal  cord  (5‐7)  (Figure 2).  Face, arm and leg weakness

The somatotopic arrangement of the primary motor cortex is preserved in the corticospinal  tract which conveys efferent white matter projection fibres between the motor cortex and  the  spinal  cord,  enabling  voluntary  movement.  Thus  the  motor  components  of  cortical  middle cerebral artery (MCA) or anterior cerebral artery (ACA) territory infarction (face, arm  or leg weakness,) can be reproduced by lesions at different points along its course.   Infarcts in the centrum semiovale may be large, presenting with all of the above MCA features but are more commonly lacunar with upper limb weakness (more than face/arm/leg) being the usual “pure motor” syndrome (8). Pure sensory syndromes have also been described. Sensory and motor fibres cannot be reliably distinguished within the centrum semiovale on color FA maps (Fig 2) but tractography has identified that the motor fibres are

situated more anteriorly (with face most anterior, leg most posterior) and sensory fibres more posterior but with opposite orientation (leg anterior, face posterior)(9-11). Ataxic hemiparesis/dysarthria-clumsy hand

This  presentation  should  prompt  evaluation  of  the  internal  capsule (but  also  thalamic  and  pontine lesions). As can be seen, the corticospinal tract runs primarily in the posterior limb  of  the  internal  capsule  (PLIC)  (Fig  2)  situated  in  its  posterior  third  quarter.  It  retains  the  somatotopic organisation seen in the corona radiata/centrum semiovale with the face fibres  most  anterior,  followed  by  the  arm,  trunk  and  leg  most  posterior.  The  corticobulbar  tract  runs  through  the  genu  of  the  internal  capsule  and  the  corticopontine  fibres  are  in  the  anterior limb (Fig 3). 

The  corticobulbar  tract  is  an  efferent  pathway  between  the  motor  cortex  and  the  motor  cranial nerve nuclei located within the brainstem. Like the corticospinal tract, the fibres of  this tract originate in the precentral (Brodmann area 4) and post‐central gyrus (area 3, 1 &  2),  however  there  is  also  contribution  from  the  frontal  eye  fields  (area  6  &  8)(4;6).  The  remainder  of  the  corticobulbar  tract  fibres  innervate  the  trigeminal,  facial,  glossopharyngeal, vagus, spinal accessory and hypoglossal nuclei, either directly or indirectly  via  interneurons  in  the  reticular  formation.  The  fibres  cross  in  the  brainstem  to  provide  bilateral innervation of the cranial nerve nuclei, with the exception of the lower facial nuclei,  which receive only contralateral projections(12). 

The  corticopontine  tract  consists  of  fibres  which  originate  from  the  frontal,  temporal,  parietal  and  occipital  lobe  cortices  and  terminates  in  the  pontine  nuclei.  There  are  two  divisions – the frontopontine fibres run in an anteroposterior direction in the anterior limb 

of  the  internal  capsule  (green  on  color  FA  maps)  whereas  the  temporo‐occipito‐parietal  division  runs  in  a  superoinferior  direction  (blue  on  color  FA)  through  the  retrolenticular  portion(4;6;13). After termination of the corticopontine tract in the pontine nuclei, afferent  fibres  are  conveyed  to  the  cerebellum  via  the  transverse  pontine  fibres  and  ipsilateral  middle  cerebellar  peduncle,  completing  the  cortico‐pontine‐cerebellar  pathway.  This  enables cerebellar modulation of planned movement (Fig 4)(4;12).  

Ataxic  hemiparesis  results  when  there  is  damage  to  both  corticospinal  tracts  and  cortico‐ ponto‐cerebellar tracts within the posterior limb/genu of the internal capsule (the vascular  territory  of  the  anterior  choroidal  artery).  Pure  dysarthria  is  usually  seen  with  cortical  lesions  but  the  association  of  clumsy  hand  may  be  seen  in  patients  with  lesions  of  the  genu/PLIC (14). 

Hemiparesis with oculomotor abnormalities 

The association of crossed hemiplegia with third nerve palsy is known as Weber’s syndrome.  The  proximity  of  the  third  nucleus  to  the  corticospinal  tract  in  the  cerebral  peduncle  accounts for the association usually encountered in paramedian midbrain infarcts from P1  posterior  cerebral  artery  (PCA)  occlusion.  The  corticospinal  fibres  are  located  centrally  within  the  cerebral  crus  with  face  fibres  found  medially  and  leg  laterally  (15).  The  CST  is  surrounded  by  the  corticopontine  fibres  with  frontopontine  fibres  medially  and  temporo‐ occipito‐parietal fibres laterally.  Infarcts may involve the cortico‐ponto‐cerebellar fibres in  the cerebral peduncle causing third nerve palsy with cerebellar signs (Claude’s syndrome) or  also the adjacent red nucleus, causing third nerve palsy with chorea (Benedikt’s syndrome)  (16;17). 

Crossed hemiparesis and facial symptoms 

This association is found in lesions affecting the pontine tegmentum. The involvement of the  CST  causes  the  contralateral  hemiparesis  but  involvement  of  the  trigeminal  nerve  nuclei  (motor  and  sensory)  causes  ipsilateral  (hence  crossed)  facial  motor  weakness/numbness.  The somatotopic  organization  of  the  CST  in  the  pons  is  of  facial  fibres anteromedially  and  foot fibres posterolaterally (18). Other cranial nerve nuclei may be affected by lesions in the  pons;  the  association  of  hemiplegia  with  contralateral  VIth/VIIth  nerve  palsies  locates  the  lesion to the hemipons on the side of the cranial nerve palsies (Millard‐Gubler syndrome).  Dysarthria‐clumsy hand syndrome may also be caused by lesions of the basis pontis due to  combined  damage  to  the  corticospinal  tract  and  trigeminal  motor/facial  nerve  nuclei.  Extensive damage to the pons can involve the pontine reticular formation and present with  reduced consciousness. If the pontine reticular formation is spared but there is still bilateral  damage  to  the  corticospinal  and  corticobulbar  tracts  then  a  “locked‐in”  syndrome  occurs  with quadriparesis and aphonia but preservation of consciousness. 

Hemiparesis with crossed tongue weakness 

This  combination  occurs  in  anterior/medial  medullary  syndromes.  Due  to  the  associated  sensory involvement, it is discussed below. 

Sensory syndromes 

Sensory pathways ascend from the spinal cord through the brainstem to the thalamus in a  variety  of  tracts,  each  carrying  different  modalities  of  sensory  perception.  The  tract  most  identifiable on DTI is the medial lemniscus; relaying proprioception and fine touch sensation 

(Fig  5).  First  order  sensory  neurones  ascend  the  spinal  cord  within  the  dorsal  columns,  terminating  in  the  dorsal  column  nuclei  within  the  medulla;  nucleus  gracilis  and  nucleus  cuneatus. Here they synapse with second order sensory neurones, which project superiorly  as the internal arcuate fibres and decussate, before ascending into the brain as the medial  lemnisci. The medial lemniscus is found in a paramedian position as it ascends through the  medulla and pons. Its fibres are somatotopically organised, with those from the arm, trunk  and leg located posterior to anterior within the tract. As the tract ascends, it rotates laterally  and becomes more peripheral. In the midbrain, the arm, trunk and leg fibres are positioned  medial to lateral within the tract. The medial lemniscus passes dorsal and lateral to the red  nucleus  and  substantia  nigra,  before  terminating  in  the  ventral  posteriolateral  nucleus  of  the  thalamus.  Here,  the second  order  neurones synapse  with  third  order  neurones,  which  ascend to the primary somatosensory cortex(4;12;19). Facial sensation is conveyed via the  sensory  nucleus  of  trigeminal  nerve  which  spans  the  brainstem.  Second  order  neurones  form  the  trigeminal  leminiscus,  just  medial  to  the  medial  leminscus  in  the  pons  and  terminate  in  the  ventral  postero‐medial  (VPM)  nucleus  of  the  thalamus.  Pain  and  temperature sensation from the body run in the spinothalamic tracts which decussate at (or  within 1‐2 levels of) entry to the spinal cord. These are found  laterally within the medulla  and pons and come to lie just posterior to the medial lemniscus in the midbrain before also  terminating  in  the  thalamic  sensory  nuclei.  The  corresponding  spinal  nucleus  of  the  trigeminal  nerve  conveying  facial  pain/temperature  sensation  is  located  more  posterolaterally, near the nucleus ambiguus in the medulla. 

Sensory disturbance with lower cranial nerve palsies. 

Medullary lesions (particularly infarcts) may be centered anteriorly, in which case the medial  lemniscus and hypoglossal nerve may be affected leading to clinical features of contralateral  decrease  in  proprioception/vibration  (the  medial  lemnisi  are  already  crossed),  ipsilateral  weakness  of  intrinsic  muscles  of  the  tongue  (and  hence  unopposed  action  of  the  normal  tongue muscles, pushing the tongue to the side of the lesion) and contralateral hemiplegia  due  to  involvement  of  the  CST  in  the  medullary  pyramids  above  the  level  of  decussation.  Posterolateral lesions give rise to the Wallenberg syndrome where there is a combination of  eighth – tenth nerve palsies (vertigo, hoarseness, deviated uvula (away from side of lesion),  ataxia  (involvement  of  inferior  cerebellar  peduncle)  and  crossed  facial  and  body  sensory  deficits in pain and temperature. The facial involvement is ipsilateral due to involvement of  the spinal trigeminal nucleus/tract whereas the body involvement is contralateral due to the  (already crossed) spinothalamic tract (17).  

Isolated Hemibody numbness 

Anatomically  this  can  only  be  explained  by  a  thalamic  lesion  or  a  lesion  in  the  pontine  tegmentum  where  the  (crossed)  medial  lemnisci  and  spinothalamic  tracts  run  in  close  proximity.  


Combined sensorimotor stroke 

Other than cortical infarcts affecting the pre and post central gyri, the combination of both  face/arm  weakness  with  same‐side  multimodal  sensory  disturbance  should  prompt  inspection  of  the  posterior  aspect  of  the  corona  radiata  where  the  superior  thalamic 

radiations  from  the  VPM/VPL  (ventral  posterolateral)  thalamic  nuclei  are  found  in  close  proximity to the corticospinal tract. 



Disorders of language 

Assessment of cortical damage to the inferior frontal gyrus/frontal operculum (Broca’s area)  and  posterosuperior  temporal  gyrus/angular  gyrus  (Wernicke’s  area)  are  of  prime  importance in patients presenting with dysphasia/aphasia. However, the white matter tracts  connecting  these  areas  and  other  regions  of  the  brain  are  now  recognised  to  represent  a  putative ‘language network’ and as such should also be assessed in this clinical scenario. The  role of the arcuate fasciculus is covered extensively in the paper by Smits et al in this issue.  

The arcuate fasciculus is the arched portion of the superior longitudinal fasciculus, thought  to connect Broca’s area, within the pars opercularis of the frontal lobe, and Wernicke’s area,  within the posterior temporal lobe. It projects posteriorly from the anterior frontal region,  running along the superior margin of the claustrum towards the occipital region, and then  curves  inferiorly  and  anteriorly  into  the  temporal  lobe  to  reach  the  middle  and  inferior  temporal  gyri  (Fig  6)(4‐6).  The  connections  of  the  other  components  of  the  superior  longitudinal fasciculus include the angular and supramarginal gyri of the parietal lobe, and  the pre and post‐central gyri of the frontal lobe(20;21). 

Traditionally  it  was  believed  that  lesions  of  the  arcuate  fasciculus  interrupted  the  connection  between  Broca’s  and  Wernicke’s  areas,  causing  conductive  aphasia.  More 

recently, this has been disputed, and it has been suggested that the arcuate fasciculus plays  a  more  complex  role  in  language  and  in  speech  formation,  via  connections  with  the  pre‐ motor and motor cortex(22;23).  

More specific disorders of naming objects – e.g. in ability to name famous faces or objects  should  prompt  assessment  of  the  uncinate  fasciculus  ‐  a  tract  passing  from  the  middle  temporal  gyrus  which  crosses  the  anterior  portion  of  the  temporal  stem  and  curves  superiorly and anteriorly towards the frontal operculum. The fibres pass through the inferior  portions of the external and extreme capsules, where they lie beneath those of the inferior  occipitofrontal  fasciculus.  Passing  forwards  into  the  fronto‐orbital  white  matter  in  close  proximity  to  the  inferior  occipitofrontal  fasciculus,  the  fibres  fan  out  horizontally  towards  the  gyrus  rectus  (area  11),  medial  retro‐orbital  cortex  (area  12)  and  the  subcallosal  area  (area 25)(5;6;24;25) (Fig 7). 

Disorders of attention/visuospatial orientation 

DTI  is  revealing  the  relevance  of  the  white  matter  structures  beneath  the  typical  cortical  locations involved in attention – usually the non‐dominant parietal lobe. Visual and tactile  hemineglect is usually attributed to damage to the inferior parietal lobule, particularly the  temporo‐parieto‐occipital  association  cortex.  However,  these  broad  cortical  areas  share  intimate  subcortical  white  matter  connections  with  the  underlying  superior  longitudinal  fasciculus  (SLF)  which  is  described  as  having  four  subdivisions;  SLF  I,  SLF  II,  SLF  III  and  the  arcuate fasciculus (see above) (Fig 8)(20;22).  SLF II in particular is thought to play a role in  visuo‐spatial  awareness.  Damage  to  the  tract,  along  with  other  grey  and  white  matter  structures, has been implicated in studies of stroke patients with spatial neglect(26‐30). 

There is asymmetry in the functions of SLFII/parietal cortex between hemispheres. The right  (usually  non‐dominant)  hemisphere  has  a  role  in  visuospatial  attention  for  both  hemispheres  whereas  the  left  inferior  parietal  lobule  subserves  a  variety  of  functions  as  revealed  by  the  clinical  features  of  Gerstmann  syndrome(17).  This  syndrome  represents  a  tetrad  of  right‐left  disorientation,  finger  agnosia (inability  to  name/identify  fingers  in  each  hand),  agraphia  (inability  to  write)  and  acalculia  (inability  to  perform  mathematical  calculations). Traditionally this was attributed to lesions of the non‐dominant angular gyrus  but  debate  has  long  continued  as  to  whether  such  a  diverse  set  of  functions  could  be  performed  by  such  a  small  region  of  cortex.  Recent  DTI  studies  however  have  mapped  lesions  to  the  subcortical  white  matter  (SLF  II)  and  provide  evidence  that  findings  may  be  explained  by  a  disconnection  syndrome(31).  Ideomotor  or  orofacial  apraxias  (inability  to  execute skilful or learned movements) have also linked to SLF damage (32) 

Callosal disconnection syndromes 

The anatomical arrangement of fibres within the corpus callosum gives rise to its functional  organisation.  Transfer  of  motor  and  somatosensory  information  occurs  within  the  body,  auditory  information  within  the  isthmus  and  visual  information  within  the  splenium.  Somatotopic  organisation  of  the  callosal  motor  fibres  within  the  body  of  the  corpus  callosum  has  been  demonstrated  using  a  combination  of  functional  magnetic  resonance  imaging (fMRI) and diffusion tensor imaging (DTI). (1) Despite being the largest white matter  tract  in  the  brain  (Fig  9),  lesions  of  the  corpus  callosum  may  have  very  subtle  clinical  presentations. However, lesion studies do reveal fascinating insights into the distribution of  function between the hemispheres. 

Alien hand syndrome (in which patients are unable to control usually their left hand which  appears  to  have  a  life  of  its  own)  usually  results  from  lesions  affecting  the  genu/anterior  body of the corpus callosum. Motor planning for the left hand occurs in both right and left  premotor/supplementary  motor  cortices,  whereas  the  right  supplementary  motor  area  (SMA)/premotor cortex only controls the left hand; thus the left hemisphere is dominant in  motor control. With callosal damage the usual ‘conscious’ control of the left hand from the  left pre‐motor cortex cannot reach the right side of the brain. As such the left hand is only  controlled by the right ‘subconscious’ pre‐motor cortex(33).  

Alexia without agraphia is an example of the functional disconnection of the splenium. This  usually  occurs  in  a  left  PCA  territory  infarct  where  the  splenium  of  the  corpus  callosum  is  also  involved.  In  addition  to  the  homonymous  hemianopia  that  this  produces,  there  is  failure of transfer of visual information from the functioning right occipital cortex, across the  splenium  to  the  left  (dominant)  angular  gyrus  where  comprehension  of  written  language  occurs. However, the angular gyrus is still connected to Broca’s and Wernicke’s areas and as  such can still generate language in both spoken and written form (17).  

Other, rare manifestations of callosal disconnection include unilateral left hand apraxia and  agraphia  (inability  to  perform  complex  tasks/writing)  –  the  instruction  is  understood  but  unable to be transmitted to the right hemisphere to generate the motor plan. 

Other commissural tracts 

The anterior commissure (Fig 10) is a compact fibre bundle which crosses the midline at the  superior  aspect  of  the  lamina  terminalis,  just  anterior  to  the  columns  of  the  fornix.  Internally, the commissure comprises of two limbs; the smaller anterior limb, whose 

fibres extend within the anterior perforating substance to connect the olfactory bulbs and  nuclei,  and  the  main  posterior  limb,  which  projects  laterally  beneath  the  caudate  and  lentiform  nuclei  to  reach  the  middle  and  inferior  temporal  gyri,  as  well  as  the  parahippocampal  gyrus,  amygdala,  bed  nucleus  of  stria  terminalis  and  the  nucleus  accumbens(4;6;7;34).  

The role of the anterior commissure has not been fully established, but it is thought to be  involved  in  olfactory  and  non‐visual  communication(35;36).  In  cases  of  corpus  callosal  agenesis  or  callosotomy,  it  may  be  able  to  partially  compensate  for  the  loss  of  interhemispheric transfer(37‐40). 

A  disconnection  syndrome  arising  from  damage  to  the  anterior  commissure  is  verbal  anosmia for the right nostril where patients are unable to describe smells presented to the  right  nostril. Whilst  the right olfactory cortex is intact, information cannot be conveyed to  the language centers in the left hemisphere for ‘naming’ to take place (17).    


Frontal lobe behavioural syndromes 

Clinical presentation with akinetic mutism, abulia (lack of initiative/motivation) is frequently  encountered  in  patients  with  damage  to  the  medial  frontal  lobes  (usually  ACA  territory  infarction  or  post  traumatic)  and  heads  of  the  caudate  nuclei.  However  the  fact  that  very  similar  clinical  syndromes  may  be  produced  by  paramedian  anterior  thalamic  infarcts  suggests  important  connections  between  these  two  structures  via  the  anterior  thalamic  radiations  (Fig  11)(41).  These  have  extensive  connections  to  the  dorsolateral  prefrontal 

cortex via the anterior limb of the internal capsule. The anterior thalamic nuclei are part of  the Papez circuit and involved in memory formation – this is explored further by Lovblad et  al in this issue. 



Psychiatric disorders 

The anterior thalamic radiations and medial forebrain bundles along with the cingulum (see  below)  have  been  an  area  of  intense  interest  for  those  attempting  to  find  anatomical  correlates of both schizophrenia and depression (42) 

Urinary incontinence and pain 

Lesions  of  the  anterior  cingulate  cortex  are  well  known  to  be  affect  bladder  control  but  recent  white  matter  distribution  studies  have  identified  damage  to  the  cingulum  (Fig  12)  and  superior  occipitofrontal  fasciculus  (Fig  13)  to  be  associated  with  type  and  severity  of  urinary  incontinence  (43).  The  cingulum  is  readily  identifiable  on  color  FA  maps  with  the  largest component running anteroposteriorly in the paramedian subcortical white matter of  the cingulate gyrus.  The superior occipitofrontal fasciculus runs alongside the body of the  lateral  ventricle  and  the  dorsal  aspect  of  the  caudate  nucleus,  connecting  the  parietal  (Brodmann  area  7  &  39)  and  occipital  lobes  (area  19)  with  the  frontal  lobe  (area  8  &  6),  paralleling the more laterally located superior longitudinal fasciculus in parts(4‐6;20). Due to  its proximity to the anterior thalamic radiations/anterior limb of the internal capsule there  has been some interest in the role of this tract in schizophrenia (44). 

The cingulate cortex is also thought to have a prime role in the emotional content of pain  perception  (45);  a  recent  study  of  patients  with  trigeminal  neuralgia  found  altered  microstructure of white matter in the cingulum amongst other regions of the brain thought  to be involved in pain processing (corpus callosum, posterior cingulum, SLF)(46) 

Surgical considerations: The temporal stem 

The white matter core connecting the temporal lobe with the frontal lobe is known as the  temporal stem (Fig 14). It contains a number of important association fibre tracts, and plays  a significant role in the reciprocal spread of tumour, infection and seizure activity between  the temporal lobe and the rest of the brain(7;24;25). 

The  precise  definition,  anatomical  boundaries  and  contents  of  the  temporal  stem  vary  slightly  between  authors;  however  the  most  frequently  used  description  is  that  of  Ebeling  and Cramon(25). They define the temporal stem on the coronal plane as the band of white  matter  situated  between  the  lower  circular  sulcus  of  the  insula  and  the  lateral  superior  margin  of  the  temporal  horn,  containing  the  anterior  commissure,  uncinate  fasciculus,  inferior occipitofrontal fasciculus, Meyer’s loop of the optic radiation, ventral amygdalofugal  fibres and inferior thalamic fibre tracts (see Swienton and Thomas and Lovblad et al in this  issue for further consideration of these tracts).  

Standard diffusion tensor imaging and tractography methods have not been as successful in  imaging the temporal stem as in other white matter tracts of the brain, due to the fact that  it  contains  multiple,  intermingled  tracts  running  in  different  directions(7;24).  An  anatomic  dissection tractography study by Kier et al(24) combined progressive dissection of the tracts  with  3D  MR  imaging  in  order  to  define  the  individual  white  matter  tracts  of  the  temporal 

stem.  They  used  the  coronal  landmarks  described  by  Ebeling  and  Cramon,  with  the  amygdala  and  lateral  geniculate  body  defined  as  the  anterior  and  posterior  boundaries  of  the  stem.  They  demonstrated  the  uncinate  fasciculus  crossing  the  anterior  portion  of  the  temporal  stem,  with  the  inferior  occipitofrontal  fasciculus  and  Meyer’s  loop  located  more  posteriorly,  traversing  the  temporal  stem  for  the  majority  of  its  length.  The  inferior  occipitofrontal  fasciculus  was  located  superior  to  Meyer’s  loop  throughout  most  of  its  course.  

Detailed  understanding  of  the  internal  anatomy  of  the  temporal  stem  is  especially  important  when  performing  surgical  procedures  involving  the  temporal  lobe,  as  its  disruption may result in deficits of learning, spatial, visual and verbal function.  


Whilst an exhaustive list of potential lesion locations is beyond the scope of this article it is  clear that DTI allows identification of many important white matter tracts. Knowledge of the  location  of  these  tracts  and  their  respective  functions  should  help  the  reader  identify  the  clinical relevance of neuroradiological findings and perform directed searches for lesions in  the clinical scenarios described. 









Figure Legends: 

Figure  1:  The  diffusion  tensor  ellipsoid.  Isotropic  diffusion  (a)  takes  the  form  of  a  sphere  where  the  magnitude  of  diffusion  is  equal  in  all  directions  such  as  in  CSF  or  cortical  grey  matter. Anistropic diffusion tensor represented by ellipsoid (b) – the tensor is characterised  by  3  eigenvectors  which  have  an  eigenvalue/magnitude  (length  of  arrow)  and  orientation  (axis). The eigenvalue (λ1) of e1 represents the principle axis of the tensor and is thought to  be a measure of axonal integrity  Figure 2: The corticospinal tract. Paired color FA maps (left) with superimposed tractography of the right corticospinal tract (pink) with standard axial T1 gradient echo volume. The red stars indicate the location of the corticospinal tract as identified by the tractography. In a) the contribution from both pre and post central gyri can be appreciated, the relative posterior position in the centrum semiovale is seen in c); the location in the posterior half of the PLIC is seen in d); the anterior paramedian location within the pons is appreciated in g) and h) along with the anterolateral position in the medullary pyramid in i). Figure 3: The internal capsule. Axial color FA map (a) and MPRAGE anatomical study (b) at the level of the internal capsule. The anterior limb of the internal capsule (1) is seen between the head of the caudate (C) and putamen (P). It is green with anteroposterior fiber orientation

and contains the frontal corticopontine fibres and anterior thalamic radiations. 2 and 3 are the posterior limb of the internal capsule between the thalamus (T) and globus pallidus (GP). 2 represents the genu where corticobulbar fibres are found, 3 is the location of the corticospinal tract. 4 represents the retrolenticular portion, containing the supero-inferiorly orientated temporo-parietal fibers of the corticopontine tract and also the superior thalamic radiations carrying sensory fibres from the thalamus to sensory cortex. Figure 4: The corticopontocerebellar tract. Coronal (a and b) and axial (c and d) color FA maps with superimposed tractography of the corticospinal tract (green, (a)) and corticopontine tracts (pink, b and d) showing fibres crossing the pons (red tract, arrows, c) to the left cerebellar hemisphere (arrow, b) via the middle cerebellar peduncle (arrow, d) Figure 5: The medial lemniscus. Tractography of the medial lemiscus/central tegmental tracts (green) superimposed on sagittal (a) and axial (b) color FA maps. The supero-inferior tracts are situated posteriorly in the pons and colored blue. C) Axial T2 weighted images with position of the medial lemnisci (blue) highlighted. Figure 6: The arcuate fasiculus. Tractography of the arcuate fasiculus superimposed on fused color FA map/MPRAGE volume in a) – c). The horizontal portions in the parietal lobes (d) and temporal lobes (f) are colored green due to anteroposterior orientation where the vertical segment (e) is colored blue on color FA maps. Figure 7: The uncinate fasciculus. Tractography of the uncinate fasculus (green, a), b)) superimposed on sagittal a) and axial (b) fused color FA map/MPRAGE. The course through the external capsule/subinsular white matter in to the frontal lobes is shown by solid arrows (c, d), along with its close proximity to the inferior fronto-occipital fasciculus (dashed arrows, d).

Figure 8: The superior longitudinal fasciculus. Axial (a) and coronal (b) color FA maps showing the course of SLF 1 (arrows), connecting frontal and parietal lobes, medial to the corona radiate (blue); axial (c) and coronal (d) color FA maps showing SLF II (arrows) in the inferior parietal lobule; axial (e) and coronal (f) color FA maps showing how SLF III (arrows) is only just appreciable as a anteroposterior tract running in the parietal operculum; sagittal (g) and coronal (h) color FA maps of the arcuate fasciculus (arrows) – note how the posterosuperior aspect of the arcuate fasciculus is in close proximity to SLF II in the inferior parietal lobe. Figure 9: The corpus callosum. Sagittal (a), coronal (b) and axial (d) color FA maps and color-encoded tractography (c) of the corpus callosum. Arrows show the red right-left components. Figure 10: The anterior commissure. Axial and sagittal (a and c) fused color FA maps/MPRAGE and axial (b) and coronal (d) FA maps showing position of the anterior commissure (arrows). This white matter tract predominantly connects the anterior temporal lobes. Figure 11: The anterior thalamic radiations. Color FA map (a) with superimposed tractography of the anterior thalamic radiation. The tract can be seen originating from the medial thalamus (dashed arrow) and passing through the anterior limb of the internal capsule (solid arrow). Equivalent locations are shown on axial MPRAGE (b). Figure 12: The cingulum. Axial (a) and coronal (b) color FA maps showing position of the horizontal portion of the cingulum (arrows); tractography of the cingulum (orange) superimposed on axial (c) and sagittal (d) color FA map/MPRAGE fusion images.

Figure 13: The superior occipitofrontal fasciculus. Axial (a) and coronal (b) color FA maps showing position of the superior occipitofrontal fasciculus (arrows) along with corresponding location on anatomical axial MPRAGE image (c). As can be seen, the tract more accurately runs between parietal (not occipital) and frontal lobes. Figure 14: The temporal stem. Coronal color FA map (a), MPRAGE (b) and T2 weighted image of the temporal stem. The position of the temporal stem is indicated by the dashed red line in b and c. The positions of the white matter tracts are shown: inferior occipitofrontal fasiculus (white arrow), isthmus of uncinate fasciculus (dashed white arrow), anterior commissure (yellow arrow), Meyer’s loop (red arrow).

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Brain white matter tracts: functional anatomy and clinical relevance.

Diffusion tensor imaging is increasingly available on clinical magnetic resonance scanners and can be acquired in a relatively short time. There has b...
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