Author's Accepted Manuscript
Brain white matter tracts: Functional anatomy and clinical relevance AC Gerrish, AG Thomas, RA Dineen
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Cite this article as: AC Gerrish, AG Thomas, RA Dineen, Brain white matter tracts: Functional anatomy and clinical relevance, Semin Ultrasound CT MRI , http://dx.doi.org/10.1053/j.sult.2014.06.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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?”
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 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.
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 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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