The SLF is a large bundle of white matter in each cerebral hemisphere connecting the parietal, occipital, and temporal lobes with ipsilateral frontal cortices. Four subcomponents have been described. The superior horizontal fibers connect the superior parietal lobe to the frontal and opercular areas (SLF-I), the angular gyrus (SLF-II), the supramarginal gyrus (SLF-III), and the superior temporal gyrus (SLF-IV). SLF-IV is also called the arcuate fasciculus, the bundle that connects the superior temporal gyrus and the ventrolateral prefrontal cortex together [1]. A fifth SLF may connect the insular gyri and parietal lobes (a.k.a. temporoparietal SLF). The separate components are not completely identified in routine DTI acquisitions. Higher field strengths and high spatial resolution-based tractography is required to identify different components [2].

The SLF facilitates the formation of a bidirectional neural network that is necessary for cognitive processes such as attention, memory, emotions, and language. It connects higher- and lower-order auditory processing with frontal brain areas involved in the control of brain functions such as attention and working memory [3].

Functional deficits due to SLF damage depend on which part of the SLF is damaged. Damage to the left SLF causes language disorders such as impaired repetition, fluent aphasia, anomia, and speech arrest in neurosurgical procedures. Damage to the right SLF results in spatial-attention network deficits such as left hemi-spatial neglect [4]. Ideational apraxia—the inability to execute a sequence of actions in a complex learned motor acts despite understanding verbal commands—is thought to occur due to SLF damage in the region beneath the supramarginal gyrus of either parietal lobe [5]. Depressive disorder can result from SLF lesions in the insular region [6].

The ILF connects the temporal and occipital lobes. It is the more lateral of the white matter tracts in the temporoparietal region. The long fibers from the superior temporal, middle temporal, inferior frontal gyri, and fusiform gyri project to the cuneus, lingual gyrus, and lateral part of the occipital lobe forming the occipitotemporal connection. The short fibers connect parahippocampal gyrus and the uncus to the more posterior visual association areas. Short fibers also connect the primary, secondary, and association visual areas to the inferior parietal lobe and the intraparietal sulcus.

The right ILF has been implicated in the analysis of faces and plays an important role in visual memory and visually evoked emotions. The left ILF is important for the analysis of colors, forms, and shapes that allowing for object, word, and color recognition [7]. The ILF also plays an important role in language processing via the ventral language pathways including IFOF, UF, and EC [8].

Lesions in the ILF will disrupt information between visual areas and limbic and memory regions and may cause one or more of the following symptoms: prosopagnosia (disorder of face recognition, right greater than left hemisphere); visual object agnosia (left greater than right hemisphere); alexia (difficulty recognizing written words, seen in conjunction with additional splenial lesions); contralateral hemiachromatopsia (disorder of color recognition); impairment of recent visual memory; and deficits in visually evoked emotions (hypoemotionality). The ILF provides an indirect alternative route to ventral semantic processing and may be altered in patients with semantic dementia [9].

The middle longitudinal fasciculus is abbreviated MdLF to distinguish it from the medial longitudinal fasciculus which is in the brainstem (see Chaps. 7, 8, and 11). The MdLF connects the superior temporal gyrus to the parietal lobe. Dorsally the tract divides into two: one courses ventrolaterally toward the angular gyrus (MdLF-AG) and the other dorsomedially toward the superior parietal lobule (MdLF-SPL) [10]. These two fascicles are difficult to resolve using routine DTI, but it is important to know about the presence of this tract in correlating symptoms in patients with lesions in the anterior limb of the internal capsule.

The MdLF-AG plays a role in attention and language, while the MdLF-SPL is involved in visuospatial and integrative audiovisual functions. These tracts may be involved in neurodegenerative disorders such as primary progressive aphasia, posterior cortical atrophy, frontotemporal dementia, and Alzheimer’s disease [11].

The SFOF runs lateral to the ventricular ependyma below the corpus callosum. It is also known as the subcallosal fasciculus. It is not clear whether this is a cortico-cortical tract or a cortical-subcortical short bundle of fibers. The fibers likely contain corticostriate fibers connecting the cingulate gyrus, supplementary motor area, and the caudate nucleus [12]. It is of note that recent deterministic tractography and connectome studies performed on data from healthy subjects in the Human Connectome Project have challenged the existence of SFOF in humans and remain so at the time of the writing of this book [13].

The SFOF is responsible for the initiation and preparation of speech movement as well as the limbic aspects of speech. Damage to the SFOF leads to akinetic mutism (especially with lesions in the language dominant hemisphere) and transcortical motor aphasia. With the possible nonexistence of this tract, its functional implications require further investigation. Meola et al. [13] suggest that previous functions attributed to SFOF might be subserved by the more dominant IFOF as part of the ventral linguistic pathway.

The IFOF connects ventrolateral and dorsolateral prefrontal cortex (VLPFC and DLPFC, including the frontal eye fields) with posterior temporal cortex (middle and inferior gyri) and the occipital lobe (fusiform gyrus). It runs medial to the inferior longitudinal fasciculus. Both the frontal and parieto-occipital connections of the IFOF are complex as they fan out to reach different areas, and some authors further divide IFOF in five subcomponents (I, II, III, IV, and V), the descriptions of which are beyond the scope of this book [14]. Temporo-parieto-occipital cortex (TPO) is a multimodal region that includes portions of the parieto-occipital junction, intraparietal sulcus, angular gyrus, Wernicke’s area on the caudal superior temporal gyrus, superior temporal sulcus, and middle temporo-occipital gyrus. TPO cortex is connected to prefrontal cortex through the IFOF, providing reciprocal connections with multimodal association cortex, the frontal eye fields, and the PFC.

The IFOF facilitates higher visual processing via the ventral processing stream which connects the more lateral and ventral occipitotemporal areas with the frontal areas to facilitate recognition of objects, places, colors, faces, and words. It is also associated with ventral language semantic pathways [15].

Isolated lesions of the IFOF are rare. Associated lesions in the occipitoparietal (dorsal stream) and the occipitotemporal lobe (ventral stream) may cause deficits in visuospatial processing including oculomotor apraxia (loss of volitional saccades, usually accompanied by lesions in the posterior parietal lobe); optic ataxia (inaccurate reaching to objects using vision input, e.g., Balint syndrome); impaired spatial relations related to difficulty in the perception of depth, size, orientation, and shape; and akinetopsia, the inability to recognize motion. Visual agnosia and poor visual memory are usually associated with ventral occipitotemporal stream lesions, including topographagnosia, the inability to remember places and previous routes. Lesions in the right IFOF are also associated with nonverbal semantic deficits, although the integrity of both right and left IFOF is important in the ventral semantic processing [16]. Left IFOF damage has been reported in aphasia [17].

The UF connects the anterior tip of the temporal lobes with orbitofrontal cortex. In the inferolateral frontal lobe, it is located inferior to the IFOF and “hooks” around and into the anterior pole of the temporal lobe providing fibers to the parahippocampal gyrus, the uncus, and the amygdala [18, 19].

The UF is involved with retrieval of past information, both semantic and episodic memory. It is also important in encoding and storage of social and emotional concepts [18]. Damage to the right UF results in impaired retrieval of episodic memory including autobiographical and event-related memories, while damage to the left UF results in impaired retrieval of semantic memory including knowledge of concepts and facts. Right UF damage also disrupts emotional empathy making patients apathic and indifferent to how other people feel [20].

The cingulum bundle is a “C”-shaped fiber bundle that lies immediately beneath the cingulate gyrus, draping over the corpus callosum. It connects the septal area to the uncus. The cingulum is distinguished histologically into an anterior and a posterior cingulum. The anterior cingulum is agranular and links motor cortex with strong connections to parts of the limbic system (amygdala, medial dorsal thalamus) and DLPFC. The posterior cingulum is granular, relaying sensory information to the largely interconnecting multimodal TPO cortex. Recent DTI studies have identified three different subdivisions: parahippocampal, retrosplenial, and subgenual subdivisions. The parahippocampal cingulum brings inputs from the posterior cingulate cortex and parietal areas to the medial temporal lobe. The retrosplenial part connects the prefrontal cortex, anterior cingulate cortex, and posterior cingulate cortex. The subgenual subdivision is likely to connect the anterior cingulate region to limbic areas such as the amygdala, the insula, and the uncus [21].

The anterior cingulum carries information that is important in attention and volitional control of cognitive and motor functions. It mirrors frontal lobe functions, is important in self-awareness, and subserves functions such as error recognition, conflict detection, and problem solving. The more ventral part is involved in emotion and visceral function, while the more dorsal portion is involved in cognition and higher-order motor function. It is the site of internally driven eye movements. The posterior cingulum carries information that plays an integrative role in visuospatial processing.

Damage to the anterior cingulum (including cingulotomy) causes several different emotional and/or behavioral deficits, including lack of affective response to pain, decreased anxiety, executive dysfunction, reduced spontaneous behavior, akinetic mutism, reduced intentional saccades, and depression. Right side damage may lead to paranoia, dysphoria, and a feeling of being frightening, whereas a left side damage leaves one with a feeling of chill without anxiety. Ventral lesions may cause intense fear and are related to phobia, post-traumatic stress disorder, and obsessive-compulsive disorder; dorsal lesions may cause a feeling of anticipation of movement. Anterior cingulotomy may be an effective surgical treatment for intractable pain and severe refractory obsessive-compulsive disorder [22, 23].

Damage to the posterior cingulum is associated with retrosplenial amnesia (anterograde and retrograde components of memory), topographical disorientation, and loss of verbal memory and metamorphopsia (blurring of the right sides of the objects).

The external capsule (ExC) lies lateral to the putamen and medial to the claustrum. It is a thin sheet of association fibers connecting the cerebral cortex to the striatum, largely covered by the insular folds. Fibers in the medial aspect are derived from the IFOF and cross over the foot of the corona radiate [24]. The UF provides fibers to the anterior portion of the ExC and reaches the rostral end of the corpus striatum. The posterior fibers form the bulk of the ExC and are largely derived from the ILF. Some fibers from the frontal lobe enter the ExC and reach the nuclei in the tegmentum of the mesencephalon and the substantia nigra. The ExC is a route for cholinergic fibers from the basal forebrain to the cerebral cortex

The extreme capsule (EC) lies between the claustrum medially and the insula laterally. It spans from the inferior frontal cortex (Broca’s area) through the middle part of the superior temporal gyrus into the inferior parietal lobule (angular gyrus/Geschwind’s territory) adjacent to the middle longitudinal fascicle [25]. The EC is important in language processing, specifically language expression.

Isolated lesions of the ExC and EC are rare. Strokes involving the external capsule and the extreme capsule can cause transient partial motor symptoms, transient speech arrest, and/or dysarthria [26]. Language impairment most frequent in left-sided lesions. Mild-to-moderate contralateral hemiparesis may develop. Sensory deficits usually do not with ExC or EC damage. Anterograde and retrograde axonal degeneration may involve the striatum due to ExC hemorrhage [27, 28].

The IC is classically subdivided into five anatomical divisions: the anterior limb (ALIC), genu, posterior limb (PLIC), and retrolenticular and sublenticular divisions. Five major types of fiber projections pass through the various divisions of the IC thalamocortical, corticothalamic, corticopontine, corticobulbar, and corticospinal [29, 30].