Duane E. Haines - Neuroanatomy An Atlas of Structures, Sections, and Systems

The Diencephalon and Basal Nuclei With MRI 145

5-32 Coronal section of the forebrain through the ante- structures labeled in this figure can be easily identified in the 146 Internal Morphology of the Spinal Cord and Brain in Stained Sections rior nucleus of the thalamus and mammillary body. Many of the T1-weighted MRI. Cingulate gyrus Cingulum Corpus callosum, body Third ventricle Medial longitudinal stria Lateral ventricle, body Lateral longitudinal stria Choroid plexus of indusium griseum Stria medullaris thalami Fornix, body Dorsomedial nucleus of thalamus Caudate nucleus, body Stria terminalis Anterior nucleus External medullary lamina and thalamic reticular nucleusInternal capsule, Putamen Ventral lateral posterior limb nucleus Internal medullary laminaExtreme capsule lat. Thalamic fasciculus Claustrum Zona incerta Insula GlobusExternal capsule pallidus Lenticular fasciculus Optic tract med. Subthalamic nucleus Amygdaloid nuclear complexLateral ventricle, Mammillary body Mammillothalamic tract Alveus of hippocampus inferior horn Posterior hypothalamus Hippocampal formation Corticospinal fibers (somatomotor)

The Diencephalon and Basal Nuclei With MRI 147

Caudate Stria medullaris thalami 5-33 Slightly oblique section of the forebrain through the anterior 148 Internal Morphology of the Spinal Cord and Brain in Stained Sections nucleus, body Anterior nucleus nucleus of the thalamus and the subthalamic nucleus. The section also in- cludes the rostral portion of the midbrain tegmentum. Many of the struc- Stria terminalis tures labeled in this figure can be easily identified in the T1-weighted MRI adjacent to the photograph.Mammillothalamic Corpus callosum, tract body Fornix, body Choroid plexus Lateral ventricle, body Internal medullary laminaInternal capsule, External medullary posterior limb lamina and thalamic reticularExternal capsule nucleus Claustrum Putamen Dorsomedial Ventral lateral Globus pallidus, nucleus nucleus lateral segmentExtreme capsule VL to VA transition Thalamic fasciculus Third Red nucleus Cerebellorubral fibers and Lenticular ventricle cerebellothalamic fibers fasciculus Zona Lateral geniculate Subthalamic incerta nucleus nucleus Crus cerebri Corticonigral fibers Optic tract Substantia nigra Pallidonigral fibers Caudate Nigrostriatal fibers nucleus, tailLateral ventricle, inferior horn Hippocampus Oculomotor nerve

The Diencephalon and Basal Nuclei With MRI 149

5-34 Coronal section of the forebrain through the inter- thalamus. Many of the structures labeled in this figure can be 150 Internal Morphology of the Spinal Cord and Brain in Stained Sections ventricular foramen, genu of the internal capsule, rostral tip of the easily identified in the T1-weighted MRI adjacent to the pho- dorsal thalamus, and about the middle one-third of the hypo- tograph. Medial longitudinal stria Cingulate gyrus Lateral longitudinal stria Septum pellucidum of indusium griseum Fornix, column Caudate nucleus, head Corpus callosum, Choroid plexus body Interventricular foramen Lateral ventricle Claustrum Insula Internal capsule, Extreme capsule genu External capsule Putamen Anterior Stria terminalis nucleusGlobus pallidus: Lateral segment Third Ventral anterior nucleus Medial segment ventricle Lenticular fasciculus Fornix, column Ansa lenticularis Anterior commissure Basal nucleus of MeynertVentral amygdalofugal fibers Lateral hypothalamic area Supraoptic decussation Hypothalamic nuclei Optic tract Arcuate Amygdaloid nucleus (complex) Dorsomedial Ventromedial Supraoptic

The Diencephalon and Basal Nuclei With MRI 151

5-35 Coronal section of the forebrain through the anterior commis- 152 Internal Morphology of the Spinal Cord and Brain in Stained Sections sure and rostral aspects of the hypothalamus. Many of the structures la- beled in this figure can be easily identified in the T1-weighted MRI. Medial longitudinal stria Cingulate gyrus of indusium griseum Cingulum Lateral longitudinal stria Septum pellucidum Septal nuclei Corpus callosum, Fornix, column Caudate nucleus, head body Anterior commissure Stria terminalisInternal capsule, Lateral ventricle, anterior limb anterior horn ClaustrumExtreme capsule PutamenExternal capsule Globus pallidus, lateral segment Insula Diagonal band Basal nucleus of Meynert (of Broca) Supraoptic nucleusLateral olfactory stria Uncus Optic tract Preoptic area Anterior perforated Amygdaloid nucleus Third ventricle of hypothalamus substance Supraoptic decussation Infundibulum

The Diencephalon and Basal Nuclei With MRI 153

5-36 Coronal section of the forebrain through the head of the accumbens. Many of the structures labeled in this figure can be eas- 154 Internal Morphology of the Spinal Cord and Brain in Stained Sections caudate nucleus, rostral portions of the optic chiasm, and the nucleus ily identified in the T1-weighted MRI adjacent to the photograph. Anterior cerebral Cingulate gyrus arteries Cingulum Medial longitudinal stria Lateral longitudinal stria of indusium griseum Internal capsule, Corpus callosum, body anterior limb Lateral ventricle, anterior horn Caudate nucleus, head Septum pellucidum InsulaExtreme capsule PutamenExternal capsule Globus pallidus, Claustrum lateral segment Nucleus accumbens Optic chiasm Medial olfactory Lateral olfactory stria stria Middle cerebral artery Diagonal band (of Broca) Anterior cerebral artery Paraterminal gyrus

The Diencephalon and Basal Nuclei With MRI 155

Cingulate gyrus 5-37 Coronal section of forebrain through the head of the caudate 156 Internal Morphology of the Spinal Cord and Brain in Stained Sections Lateral longitudinal stria nucleus and the anterior horn of the lateral ventricle. Many of the structures labeled in this figure can be easily identified in the T1-weighted MRI Corpus callosum, rostrum adjacent to the photograph. Anterior cerebral arteries Cingulum Corpus callosum, body Medial longitudinal stria of indusium griseum Lateral ventricle, anterior horn External capsule Extreme capsule Septum Caudate nucleus, pellucidum headInternal capsule, Putamen anterior limb ClaustrumSubcallosal gyrus Olfactory sulcus Olfactory tract Orbital gyri Gyrus rectus (straight gyrus) Anterior cerebral arteries

The Diencephalon and Basal Nuclei With MRI 157

Vascular Syndromes or Lesions of the Forebrain 158 Internal Morphology of the Spinal Cord and Brain in Stained SectionsForebrain vascular lesions result in a wide range of and sensory losses in the contralateral foot, leg, and thigh one side of the body, but these signs usually spread to both sides withdeficits that include motor and sensory losses and a va- owing to damage to the anterior and posterior paracen- time. This is a neurodegenerative disease that has, in its later stages,riety of cognitive disorders. Forebrain vessels may be tral gyri (primary motor and sensory cortices for lower a dementia component.occluded by a thrombus. This is a structure (usually a extremity). Occlusion of distal branches of MCA resultsclot) formed by blood products and frequently attached in contralateral motor and sensory losses of the upper Transient Ischemic Attack: A transient ischemic attack, com-to the vessel wall. Deficits may appear slowly, or wax extremity, trunk, and face with sparing of the leg and monly called TIA, is a temporary (and frequently focal) neurologicand wane, as the blood flow is progressively restricted. foot, and a consensual deviation of the eyes to the ipsi- deficit that usually resolves within 10 to 30 minutes from the onset lateral side. This represents damage to the precentral of symptoms. The cause is temporary occlusion of a vessel or inade- Vessels may also be occluded by embolization. A for- and postcentral gyri and to the frontal eye fields. quate perfusion of a restricted vascular territory. TIA that last 60+eign body, or embolus (fat, air, piece of thrombus, piece minutes may result in some permanent deficits. This vascular eventof sclerotic plaque, clump of bacteria, etc.), is delivered Watershed Infarct: Sudden systemic hypoten- may take place anywhere in the central nervous system but is morefrom some distant site into the cerebral circulation where sion, hypoperfusion, or embolic showers may result in common in the cerebral hemisphere.it lodges in a vessel. Since this is a sudden event deficits infarcts at border zones between the territories servedusually appear quickly and progress rapidly. Interruption by the ACA, MCA, and posterior cerebral artery 5-38 Semidiagrammatic representation of the internal dis-of blood supply to a part of the forebrain will result in an (PCA). Anterior watershed infarcts (at the ACA–MCA tribution of arteries to the diencephalon, basal ganglia, and in-infarct of the area served by the occluded vessel. junction) result in a contralateral hemiparesis (mainly ternal capsule. Selected structures are labeled on the left side of leg) and expressive language or behavioral changes. Pos- each section; the general pattern of arterial distribution overlies Lesion in the Subthalamic Nucleus: Small vas- terior watershed infarcts (MCA–PCA interface) result in these structures on the right side. The general distribution pat-cular lesions occur in the subthalamic nucleus, resulting visual deficits and language problems. terns of arteries in the forebrain as shown here may vary fromin rapid and unpredictable flailing movements of the patient to patient. For example, the adjacent territories servedcontralateral extremities (hemiballismus). Movements Anterior Choroidal Artery Syndrome: Occlu- by neighboring vessels may overlap to varying degrees at theirare more obvious in the arm than in the leg. The clinical sion of this vessel may result from small emboli or small margins or the territory of a particular vessel may be larger orexpression of this lesion is through corticospinal fibers, vessel disease. This syndrome may also occur as a com- smaller than seen in the general pattern.therefore it is on the contralateral side of the body. plication of temporal lobectomy (removal of the tem- poral lobe to treat intractable epilepsy). The infarcted Abbreviations Occlusion of Lenticulostriate Branches to In- area usually includes the optic tract, lower portions of the basal nuclei, and lower aspects of the internal cap- APS Anterior perforated substanceternal Capsule: Damage to the internal capsule may sule. The patient experiences a contralateral hemiple- BCorCl Body of corpus callosumresult in contralateral hemiplegia (corticospinal fibers) and gia, hemihypethesia, and homonymous hemianopsia. These Crus cerebria loss, or diminution, of sensory perception (pain, ther- deficits are due to, respectively, involvement of corti- CC Centromedian nucleus of thalamusmal sense, proprioception) caused by damage to thalamo- cospinal fibers in the posterior limb of the internal cap- CM Dorsomedial nucleus of thalamuscortical fibers traversing the posterior limb to the overly- sule or possibly in the crus cerebri, involvement of DMNu Globus pallidusing sensory cortex. If the lesion extends into the genu of thalamocortical fibers in the posterior limb of the in- GP Hypothalamusthe capsule, a partial paralysis of facial muscles and tongue ternal capsule, and involvement of the fibers of the op- HyTh Pulvinar nuclear complexmovement may also occur contralaterally. tic tract. PulNu Putamen Put Splenium of the corpus callosum Infarction of Posterior Thalamic Nuclei: Oc- Parkinson Disease: Parkinson disease (paralysis SplCorCl Ventral anterior nucleus of thalamusclusion of vessels to posterior thalamic regions results in agitans) results from a loss of the dopamine-containing VA Ventral lateral nucleus of thalamuseither a complete sensory loss (pain/thermal sense, touch, cells in the substantia nigra. Although this part of the VLvibratory and position sense) on the contralateral side of brain is located in the midbrain, the terminals of thesethe body, or a dissociated sensory loss. In the latter case the nigrostriatal fibers are in the putamen and the caudatepatient may experience pain/thermal sensory losses but nucleus. The classic signs and symptoms of this diseasenot position/vibratory losses, or vice versa. As the le- are a stooped posture, resting tremor, rigidity, shuffling or fes-sion resolves the patient may experience intense persis- tinating gait, and difficulty initiating or maintainingtent pain, thalamic pain, or anesthesia dolorosa. movement (akinesia, hypokinesia, or bradykinesia). Ini- tially, the tremor and walking difficulty may appear on Occlusion of Distal Branches of the Anterior(ACA) or Middle (MCA) Cerebral Arteries: Oc-clusion of distal branches of the ACA results in motor

Column of fornix Head of caudate nucleus Septum pellucidum Rostral Anterior limb of internal capsule Body of fornix BCorCl Claustrum Body of caudate nucleus Insula Put Anterior nucleus of thalalmus GP Posterior limb of internal capsule APS HyTh Caudal Lateral dorsal nucleus Put VA-VL Arterial Patterns Within the Forebrain With Vascular Syndromes 159 Stria terminalis G DMNu P Optic tract Amygdaloid nuclear External capsule complex Red nucleusCrus of fornix Put VL DM Nu Hippocampal formation CM Hypothalamus CC Mammillary body Subthalamic nucleus Retrolenticular SplCorCl Medial posterior choroidal artery limb of PulNu Thalamogeniculate branches of posterior cerebral artery (branch of P2)internal capsule Anterior choroidal arteryLateral geniculate Optic tract Lateral striate branches (lenticulostriate arteries) of the middle nucleus Substantia nigra cerebral artery Tail of caudate nucleus Thalamoperforating branches of posterior cerebral artery (branch of P1) Medial geniculate Posteromedial branches of posterior cerebral artery (P1 segment) and nucleus Hippocampal formation branches of posterior communicating artery Anterolateral branches of middle and anterior cerebral artery Pineal Medial striate branch of anterior cerebral artery (branch of A2) Anteromedial branches of anterior cerebral artery and anterior communicating artery

CHAPTER 6 Internal Morphology of the Brain in StainedSections: Axial–Sagittal Correlations with MRIAlthough the general organization of Chapter 6 has been de- in this chapter gives the reader an opportunity to compare in-scribed in Chapter 1 (the reader may wish to refer back to this ternal brain anatomy, as seen in stained sections, with thosesection), it is appropriate to reiterate its unique features at this structures as visualized in clinical images generated in the samepoint. Each set of facing pages has photographs of an axial stained plane. Even a general comparison reveals that many features, assection (left-hand page) and a sagittal stained section (right-hand seen in the stained section, can be readily identified in the adja-page). In addition to individually labeled structures, a heavy line cent MRI.appears on each photograph. This prominent line on the axialsection represents the approximate plane of the sagittal section This chapter is also organized so that one can view structures inlocated on the facing page. On the sagittal section this line signi- either the axial or the sagittal plane only. Axial photographs appearfies the approximate plane of the corresponding axial section. on left-hand pages and are sequenced from dorsal to ventral (odd-The reader can identify features in each photograph and then, us- numbered Figures 6-1 through 6-9), while sagittal photographs areing this line as a reference point, visualize structures that are lo- on the right-hand pages and progress from medial to lateral (even-cated either above or below that plane (axial to sagittal compar- numbered Figures 6-2 through 6-10). Consequently, the user canison) or medial or lateral to that plane (sagittal to axial identify and follow structures through an axial series by simply flip-comparison). This method of presentation provides a format for ping through the left-hand pages or through a sagittal series by flip-reconstructing and understanding three-dimensional relation- ping through the right-hand pages. The inherent flexibility in thisships within the central nervous system. chapter should prove useful in a wide variety of instructional/ learning situations. The drawings shown in the following illustrate The magnetic resonance image (MRI) placed on every page the axial and sagittal planes of the photographs in this chapter. Fig. 6-6 Fig. 6-4 Fig. 6-8 Fig. 6-2 Fig. 6-10Axial Planes Fig. 6-1 Sagittal Planes Fig. 6-3 Fig. 6-5 Fig. 6-7 Fig. 6-9

162 Internal Morphology of the Brain in Stained SectionsCorCl Anterior horn of Sep lateral ventricle CaNu,H For PutAntNu VA Hab DMNu VL IntCap: AL CM G VPL Pl Cl Hip PulNu CP StTerCom Hip CaNu,T Hip,F OpRad Atrium of lateral ventricle6-1 Axial section through the head of the caudate nucleus and several shown in Figure 6-2 (facing page). Many of the structures labeled inkey thalamic nuclei (anterior, centromedian, pulvinar, habenular). The this photograph can be clearly identified in the adjacent T1-weightedheavy line represents the approximate plane of the sagittal section MRI. Abbreviations AntNu Anterior nucleus of thalamus HipCom Hippocampal commissure CaNu,H Caudate nucleus, head IntCap,AL Internal capsule, anterior limb CaNu,T Caudate nucleus, tail Internal capsule, genu Claustrum IntCap,G Internal capsule, posterior limb CI Centromedial nucleus of thalamus IntCap,PL Optic radiations CM Corpus callosum Pulvinar nuclear complex CorCI Choroid plexus OpRad Putamen CP Dorsomedial nucleus of thalamus PulNu Septum pellucidum DMNu Fornix, column Stria terminalis For Habenular nucleus Put Ventral anterior nucleus of thalamus Hab Hippocampal formation Sep Ventral lateral nucleus of thalamus Hip Hippocampus, fimbria StTer Ventral posterolateral nucleus Hip,F VA VL VPL

Axial–Sagittal Correlations 163 AntNu For,B LDNu CorCl,SplCorCl,G DMNuPrTecNu RNu SC SMT AC IC Hab PoCom For,Col HyTh MtTr TroNr MLF OpNr MB FNu OcNr AbdNu SCP,Dec NuGr BP ML Py PO HyNu LCSp6-2 Sagittal section through the column of the fornix, anterior thalamic represents the approximate plane of the axial section shown in Figurenucleus, red nucleus, and medial portions of the pons (abducens nucleus), 6-1 (facing page). Many of the structures labeled in this photograph cancerebellum (fastigial nucleus), and medulla (nucleus gracilis). The heavy line be clearly identified in the adjacent T1-weighted MRI. Abbreviations AbdNu Abducens nucleus MB Mammillary body AC Anterior commissure ML Medial lemniscus MLF Medial longitudinal fasciculus AntNu Anterior nucleus of thalamus MtTr Mammillothalamic tract BP Basilar pons NuGr Nucleus gracilis OcNr Oculomotor nerveCorCI,G Corpus callosum, genu OpNr Optic nerveCorCI,Spl Corpus callosum, splenium PO Principal olivary nucleus PoCom Posterior commissure DMNu Dorsomedial nucleus of thalamus PrTecNu Pretectal nuclei FNu Fastigial nucleus (medial cerebellar nucleus) Py Pyramid RNu Red nucleus For,B Fornix, body SC Superior colliculus For,Col Fornix, column SCP,Dec Superior cerebellar peduncle, decussation SMT Stria medullaris thalami Hab Habenular nuclei TroNr Trochlear nerve HyNu Hypoglossal nucleus HyTh Hypothalamus IC Inferior colliculus LCsp Lateral corticospinal tract LDNu Lateral dorsal nucleus

164 Internal Morphology of the Brain in Stained Sections Anterior horn of lateral ventricle Sep CaNu,H For,Col GPL MtTr InsHabCom Put SC,Br SC VA DMNu IntCap,AL Cl VL ExtCap InTCap,PL CM VPM VPL StTer MGNu CaNu, T PulNu OpRad Hip Tap6-3 Axial section through the head of the caudate nucleus, centrome- ure 6-4 (facing page). Many of the structures labeled in this photographdian nucleus, medial geniculate body, and superior colliculus. The heavy line can be clearly identified in the adjacent T2-weighted MRI.represents the approximate plane of the sagittal section shown in Fig- AbbreviationsCaNu,H Caudate nucleus, head MGNu Medial geniculate nucleus CaNu,T Caudate nucleus, tail MtTr Mammillothalamic tract Optic radiations Cl Claustrum OpRad Pulvinar nuclear complex CM Centromedian nucleus of thalamus PulNu Putamen DMNu Dorsomedial nucleus of thalamus Superior colliculus ExtCap External capsule Put Superior colliculus, brachium For,Col Fornix, column SC Stria terminalis Sep Septum pellucidum SC,Br Ventral anterior nucleus of thalamus GPL Globus pallidus, lateral segment StTer Ventral lateral nucleus of thalamusHab,Com Habenular commissure VA Ventral posterolateral nucleus of thalamus Hip Hippocampal formation VL Ventral posteromedial nucleus of thalamus Ins Insula VPL TapetumIntCap,AL Internal capsule, anterior limb VPMIntCap,PL Internal capsule, posterior limb Tap

Axial–Sagittal Correlations 165 LatVen,AH MtTr CorCl,B LDNu For,B CorCl, Spl AntNu PulNu DMNu CM VA AC H SC ThFas ICLenFas Hyth RNu AnLen SN OlfTr OpTr SCP ForVen CC ML BP NuGr FacNu PO SolNu & Tr NuCu6-4 Sagittal section through anterior and ventral anterior thalamic nu- sents the approximate plane of the axial section shown in Figure 6-3clei, red nucleus and central areas of the pons, cerebellum (and superior pe- (facing page). Many of the structures labeled in this photograph can beduncle), and medulla (solitary nuclei and tract). Note the position of the clearly identified in the adjacent T1-weighted MRI.facial motor nucleus at the pons-medulla junction. The heavy line repre- Abbreviations AC Anterior commissure LDNu Lateral dorsal nucleus AnLen Ansa lenticularis ML Medial lemniscus AntNu Anterior nucleus of thalamus Mammillothalamic tract Basilar pons MtTr Nucleus cuneatus BP Crus cerebri NuCu Nucleus gracilis CC Centromedian nucleus NuGr Olfactory tract CM Corpus callosum, body OlfTr Optic tractCorCl,B Corpus callosum, splenium OpTr Principal olivary nucleusCorCl, Spl Dorsomedial nucleus of thalamus Pulvinar nuclear complex DMNu Facial nucleus PO Red nucleus FacNu Fornix, body PulNu Superior colliculus For,B Fourth ventricle Superior cerebellar peduncle (brachium ForVen Prerubral field RNu conjunctivum) H Hypothalamus SC Substantia nigra HyTh Inferior colliculus Solitary nuclei and tract IC Lateral ventricle, anterior horn SCP Thalamic fasciculusLatVen,AH Lenticular fasciculus Ventral anterior nucleus of thalamus LenFas SN SolNu&Tr ThFas VA

166 Internal Morphology of the Brain in Stained SectionsAC CaNu,H LT GPL PutFor,Col GPMHyth MtTr VL SC IntCap,ALVPM CM VPL ClCeGy MGNu IntCap: SC PL PulNu RL Hip Hip,F ALV OpRad CP6-5 Axial section through the head of the caudate nucleus, ventral post- shown in Figure 6-6 (facing page). Many of the structures labeled ineromedial nucleus, medial geniculate body, and ventral parts of the pulvinar. this photograph can be clearly identified in the adjacent T1-weightedThe heavy line represents the approximate plane of the sagittal section MRI. Abbreviations AC Anterior commissure IntCap,AL Internal capsule, anterior limb ALV Atrium of lateral ventricle IntCap,Pl Internal capsule, posterior limb CaNu,H Caudate nucleus, head IntCap,RL Internal capsule, retrolenticular limb CeGy Central gray (periaqueductal gray) Lamina terminalis Claustrum LT Medial geniculate nucleus CI Centromedian nucleus of thalamus MGNu Mammillothalamic tract CM Choroid plexus Optic radiations CP Fornix, column MtTr Pulvinar nuclear complex For,Col Globus pallidus, lateral segment OpRad Putamen GPL Globus pallidus, medial segment PulNu Superior colliculus GPM Hippocampal formation Ventral lateral nucleus of thalamus Hip Hippocampus, fimbria Put Ventral posterolateral nucleus of thalamus Hip,F Hypothalamus SC Ventral posteromedial nucleus of thalamus HyTh VL VPL VPM

Axial–Sagittal Correlations 167 CorCl,G LDNu CorCl,Spl CaNu,H VL DMNu PulNu VA CM SC H IC RNuAC LL SN SCP ENu OpTr CC SOpNu CSNu AnLen LenFas ML TriMoNu FacNr OCblF NuCu6-6 Sagittal section through central regions of the diencephalon (cen- heavy line represents the approximate plane of the axial section showntromedian nucleus) and midbrain (red nucleus), and through lateral areas of in Figure 6-5 (facing page). Many of the structures labeled in this pho-the pons (trigeminal motor nucleus) and medulla (nucleus cuneatus). The tograph can be clearly identified in the adjacent T1-weighted MRI. Abbreviations AC Anterior commissure LL Lateral lemniscus AnLen Ansa lenticularis ML Medial lemniscus CaNu,H Caudate nucleus, head NuCu Nucleus cuneatus Crus cerebri OCblF Olivocerebellar fibers CC Centromedian nucleus of thalamus OpTr Optic tract CM Corpus callosum, genu PulNu Pulvinar nuclear complex CorCl,G Corpus callosum, splenium RNu Red nucleusCorCl,Spl Chief (prinicipal) sensory nucleus of trigeminal nerve SC Superior colliculus CSNu Dorsomedial nucleus of thalamus SCP Superior cerebellar peduncle (brachium con- DMNU Emboliform nucleus (anterior interposed cerebellar nucleus) junctivum) ENu Facial nerve SN Substantia nigra FacNr Field of Forel (prerubral field) SOpNu Supraoptic nucleus Inferior colliculus TriMoNu Trigeminal motor nucleus H Lenticular fasciculus Ventral anterior nucleus of thalamus IC Lateral dorsal nucleus of thalamus VA Ventral lateral nucleus of thalamus LenFas VL LDNu

168 Internal Morphology of the Brain in Stained Sections CaNu Ins LT HyTh LGNu Hip ForMtTrRNu AC ML OpTr CCIC,Br StTer CaNu,T IC MGNu OpRad6-7 Axial section through the hypothalamus, red nucleus, inferior col- the midbrain, represents a slightly oblique section through the mesen-liculus, and lateral geniculate body. The heavy line represents the ap- cephalon. The position of the lamina terminalis is indicated by the dou-proximate plane of the sagittal section shown in Figure 6-8 (facing ble-dashed lines. Many of the structures labeled in this photograph canpage). The axial plane through the hemisphere, when continued into be clearly identified in the adjacent T1-weighted MRI. Abbreviations AC Anterior commissure LGNu Lateral geniculate nucleus CaNu Caudate nucleus LT Lamina terminalisCaNu,T Caudate nucleus, tail Medial geniculate nucleus Crus cerebri MGNu Medial lemniscus CC Fornix ML Mammillothalamic tract For Hippocampal formation Optic radiation (geniculocalcarine fibers) Hip Hypothalamus MtTr Optic tract HyTh Inferior colliculus OpRad Red nucleus IC Inferior colliculus, brachium Stria terminalis IC,Br Insula OpTr Ins RNu StTer

Axial–Sagittal Correlations 169 AC ThFas Zl Lenfas VPM CaNu VL BrSC PulNu SThNu GPL GPM MGNu Put SN DNuOpTr Hip AmyNu CC MCP PCNu6-8 Sagittal section through the caudate nucleus, central parts of the proximate plane of the axial section shown in Figure 6-7 (facing page).diencephalon (ventral posteromedial nucleus), and lateral portions of the Many of the structures labeled in this photograph can be clearly iden-pons and cerebellum (dentate nucleus). The heavy line represents the ap- tified in the adjacent T1-weighted MRI. Abbreviations AC Anterior commissure MGNu Medial geniculate nucleusAmyNu Amygdaloid nucleus (complex) OpTr Optic tract Brachium of superior colliculus PCNu Posterior cochlear nucleus BrSC Caudate nucleus PulNu Pulvinar nuclear complex CaNu Crus cerebri Put Putamen Dentate nucleus (lateral cerebellar nucleus) SN Substantia nigra CC Globus pallidus, lateral segment Subthalamic nucleus DNu Globus pallidus, medial segment SThNu Thalamic fasciculus GPL Hippocampal formation ThFas Ventral lateral nucleus of thalamus GPM Lenticular fasciculus Ventral posteromedial nucleus of thalamus Hip Middle cerebellar peduncle (brachium pontis) VL Zona incerta LenFas VPM MCP ZI

170 Internal Morphology of the Brain in Stained Sections LT SN AmyNu CP SOR Hip CaNu,T OpTr FHip LatVen,IH IR DenGy HyTh OpRad MB CC MLSCP,Dec MLF LL SCP6-9 Axial section through ventral portions of the hypothalamus hemisphere, when continued into the midbrain, represents a slightly(supraoptic recess and mammillary body) and forebrain (amygdaloid nu- oblique section through the mesencephalon. Many of the structures la-cleus), and through the superior cerebellar peduncle decussation in the mid- beled in this photograph can be clearly identified in the adjacent T1-brain. The heavy line represents the approximate plane of the sagittal weighted MRI.section shown in Figure 6-10 (facing page). The axial plane through the Abbreviations AmyNu Amygdaloid nucleus (complex) LT Lamina terminalis CaNu,T Caudate nucleus, tail MB Mammillary body ML Medial lemniscus CC Crus cerebri MLF Medial longitudinal fasciculus CP Choroid plexus OpRad Optic radiations DenGy Dentate gyrus OpTr Optic tract FHip Fimbria of hippocampus SCP Superior cerebellar peduncle (brachium Hip Hippocampal formation conjunctivum) HyTh Hypothalamus SCP,Dec Superior cerebellar peduncle, decussation IR Infundibular recess of third ventricle SN Sustantia nigra LatVen,lH Lateral ventricle, inferior (temporal) horn Supraoptic recess of third ventricle LL Lateral lemniscus SOR

Axial–Sagittal Correlations 171 VL + VPL CaNu,B OpRad PulNu EML + ThRetNu OpTr AC CalSul ALV Hip GPL LGNu Put GPM CP FHip DenGy Hip DNu AmyNu LatVen,IH6-10 Sagittal section through the putamen, amygdaloid nucleus, and line represents the approximate plane of the axial section shown in Fig-hippocampus and through the most lateral portions of the diencephalon ure 6-9 (facing page). Many of the structures labeled in this photograph(external medullary lamina and ventral posterolateral nucleus). The heavy can be clearly identified in the adjacent T1-weighted MRI. Abbreviations AC Anterior commissure GPM Globus pallidus, medial segment ALV Atrium of lateral ventricle Hip Hippocampal formationAmyNu Amygdaloid nucleus (complex) LatVen,lH Lateral ventricle, inferior (temporal) horn CalSul Calcarine sulcus LGNu Lateral geniculate nucleusCaNu,B Caudate nucleus, body OpRad Optic radiations Choroid plexus OpTr Optic tract CP Dentate gyrus PulNu Pulvinar nuclear complexDenGy Dentate nucleus Put Putamen External medullary lamina ThRetNu Thalamic reticular nuclei DNu Fimbria of hippocampus Ventral lateral nucleus of thalamus EML Globus pallidus, lateral segment VL Ventral posterolateral nucleus of thalamus FHip VPL GPL

CHAPTER 7Synopsis of Functional Components, Tracts, Pathways, and SystemsThe study of regional neurobiology (brain structures in gross spec- the CD that comes with this atlas; these are taken from the cur-imens, in brain slices, in stained sections, and in MRI and CT) is rent edition of Stedman’s Medical Dictionary. In this respect, thethe basis for the study of systems neurobiology (tracts, pathways, full definitions are actually available in this book. Researching thecranial nerves and their functions), which, in turn, is the basis for full definition of a clinical term or phrase is a powerful and ef-understanding and diagnosing the neurologically impaired pa- fective learning tool. Also, each clinical term or phrase is avail-tient. Building on the concepts learned in earlier chapters on ex- able in any standard medical dictionary or comprehensive neu-ternal and internal brain anatomy in specimens and in MRI and rology text.CT, on brain vascular patterns, and on the relationships of cra-nial nerves with long tracts, this chapter explores systems neurobi- The layout of the drawings in this chapter clearly shows theology with a particular emphasis on clinical correlations. laterality of the tract/pathway. That is, the relationship between the location of the cell of origin and the termination of the fibers The format of each set of facing pages is designed to summa- making up a tract/pathway or the projections of cranial nerverize, accurately and consisely, the relationships of a given tract nuclei. This information is absolutely essential to understanding the po-or pathway. This includes, but is not limited to, 1) the location sition of a lesion and correlating this fact with the deficits seen in theof the cells of origin for a given tract/pathway, 2) its entire neurologically compromised patient. For example, is the deficit oncourse throughout the neuraxis and cerebrum, 3) the location of the same side as the lesion (ipsilateral), on the opposite side (con-the decussation of these fibers, if applicable, 4) the neurotrans- tralateral), or on both sides (bilateral)? The concept of lateralitymitters associated with the neurons comprising the tract/pathway, is usually expressed as “right,” “left,” or “bilateral” in reference5) a brief review of its blood supply, and 6) a summary of a num- to the side of the deficit(s) when written on the patient’s chart.ber of deficits seen as a result of lesions at various points in thetract/pathway. The structure of an atlas does not allow a detailed This chapter is designed to maximize the correlation betweendefinition of each clinical term on the printed page. However, structure and function, to provide a range of clinical examplesthe full definition of each clinical term or phrase is available on for each tract/pathway, and to help the user develop a knowl- edge base that can be easily integrated into the clinical setting.

174 Synopsis of Functional Components, Tracts, Pathways, and Systems SL SSA SL G G S SG S G SVA S V V VV S S G GVA E E E AA A A G V G S E S E A S V E posteriorGSA GVA medial lateralSL GVEGSE anterior GSA GG GG SV VS GVA EE AA GVE GSE SL7–1 A semidiagrammatic summary of the positions of functional In the brainstem, however, there is a slight transposition of the SVEcomponents as seen in the developing neural tube (left) and in the and GSA functional components. Embryologically, SVE cell groups ap-spinal cord and brainstem of the adult (right). In the neural tube, the pear between those associated with GSE and GVE components. As de-alar plate and its associated GSA and GVA components are posterior velopment progresses, however, SVE cell groups migrate (open ar-(dorsal) to the sulcus limitans (SL) while the basal plate and its related row) to anterolateral areas of the tegmentum. Cell groups associatedGVE and GSE components are anterior (ventral) to the SL. In the adult with the GSA functional component are displaced from their postero-spinal cord, this general posterior/anterior relationship is maintained, lateral position in the developing brainstem by the newly acquired cellalthough the neural canal (as central canal) is reduced and/or absent. groups having SSA components (as well as other structures). Conse- quently, structures associated with the GSA component are located Two major changes occur in the transition from spinal cord to brain- (open arrow) in more anterolateral and lateral areas of the brainstem.stem in the adult. First, as the central canal of the cervical cord enlarges The approximate border between motor and sensory regions of theinto the fourth ventricle and the cerebellum develops, the posterior brainstem is represented by an oblique line drawn through the brain-portion of the neural tube is rotated laterally. Consequently, in the stem beginning at the SL. The medial (from midline) to lateral posi-adult, the sulcus limitans is present in the brainstem with motor com- tions of the various functional components, as shown on the far rightponents (adult derivatives of the basal plate) medial to it, and sensory of this figure, are taken from their representative diagrams of brain-components (adult derivatives of the alar plate) are located laterally. stem and cord and are directly translatable to Figure 7–2 (facing page).Second, in the brainstem, special functional components (SVE to mus- The color-coding of the components on this figure correlate with thatcles of pharyngeal arch origin; SVA taste and olfaction; SSA vestibular, in Figure 7–2 on the facing page.auditory, and visual systems) are intermingled with the rostral contin-uation of the general functional components as found in the spinal cord.GSA General somatic afferent AbbreviationsGSE General somatic efferentGVA General visceral afferent SSA Special somatic afferentGVE General visceral efferent SVA Special visceral afferent SVE Special visceral efferent SL Sulcus limitans

Cranial nerves Components of Cranial and Spinal Nerves 175 GG S SG SG Midbrain SV V VV SS EE E AA AA 1. Oculomotor nuc. (GSE) 2. Edinger-Westphal nuc. (GVE) 2 3. Trochlear nuc. (GSE) 1 4. Mesencephalic nuc. & tr. 4 of V (GSA) 3 7 SL 9 Pons 56 10 5. Abducens nuc. (GSE) S 6. Sup. salivatory nuc. (GVE) 7. Motor trigeminal nuc. (SVE) L 8. Motor facial nuc. (SVE) 9. Principle sensory nuc of V (GSA) 10. Spinal trigeminal nuc. (GSA) (pars oralis) 8 a 17 Medulla oblongata 13 M 11. Hypoglossal nuc. (GSE) SP 12. Dorsal motor nuc. of vagus (GVE) 14 13. Inf. salivatory nuc. (GVE) 14. Nuc. ambiguus (SVE) 15 15. Solitary nuc. and tr. 15a: gustatory nuc. (SVA) 11 18 15b: cardiorespiratory nuc (GVA) 12 b 16. Vestibular nuclei (SSA) SL 16 S = Sup; L = Lat; M = Med; Sp. = Spinal 17. Cochlear nuc. (SSA) 18. Spinal trigeminal nuc. (GSA) (pars interpolaris, pars caudalis)Cervical 20 24 Spinal cord cord SL 19. Medial motor cell column (GSE)Thoracic 21 cord 20. Accessory nuc. (GSE) 21. Lateral motor cell columns (GSE) 22. Intermediolateral cell column (GVE) 23. Visceral afferent receptive areas (GVA) 19 22 24. Substantia gelatinosa, nucleus proprious and associated GSA receptive areas 23 25. Sacral parasympathetics (GVE)Lumbosacral 21 cord 25 GG GG SV VS EE AA Spinal nerves continuous cell groups) from one division of the brainstem to the next or from brainstem to spinal cord. The nucleus ambiguus is a7–2 The medial to lateral positions of brainstem cranial nerve column of cells composed of distinct cell clusters interspersed withand spinal cord nuclei as shown here are the same as in Figure 7–1. more diffusely arranged cells, much like a string of beads. Nuclei as-This diagrammatic posterior (dorsal) view shows 1) the relative po- sociated with cranial nerves I (olfaction, SVA) and II (optic, SSA) aresitions and names of specific cell groups and their associated func- not shown. The color-coding used on this figure correlates with thattional components, 2) the approximate location of particular nuclei on Figure 7–1 (facing page).in their specific division of brainstem and/or spinal cord, and 3) therostrocaudal continuity of cell columns (either as continuous or dis-

176 Synopsis of Functional Components, Tracts, Pathways, and Systems7–3 Orientation drawing for pathways. The trajectory of most cospinal fibers are found in the internal capsule, crus cerebri, basilarpathways illustrated in Chapter 7 appears on individualized versions of pons, pyramid, and lateral corticospinal tract). Third, the location of ter-this representation of the central nervous system (CNS). Although minals containing specific neurotransmitters is indicated by the site(s) ofslight changes are made in each drawing, so as to more clearly diagram termination of each tract (glutaminergic terminals of corticospinal fibersa specific pathway, the basic configuration of the CNS is as represented are located in the spinal cord gray matter). In addition, the action of mosthere. This allows the user to move from pathway to pathway without neuroactive substances is indicated as excitatory (ϩ) or inhibitory (Ϫ).being required to learn a different representation or drawing for each This level of neurotransmitter information, as explained here for gluta-pathway; also, laterality of the pathway, a feature essential to diagno- minergic corticospinal fibers, is repeated for each pathway drawing.sis (see introduction), is inherently evident in each illustration. Clinical Correlations: The clinical correlations are designed to The forebrain (telencephalon and diencephalon) is shown in the give the user an overview of specific deficits (i.e., hemiplegia, athetosis)coronal plane, and the midbrain, pons, medulla, and spinal cord are seen in lesions of each pathway and to provide examples of some syn-represented through their longitudinal axes. The internal capsule is dromes or diseases (i.e., Brown-Sequard syndrome, Wilson disease) inrepresented in the axial plane in an effort to show the rostrocaudal dis- which these deficits are seen. Although purposefully brief, these cor-tribution of fibers located therein. relations highlight examples of deficits for each pathway and provide a built-in mechanism for expanded study. For example, the words in The reader should become familiar with the structures and regions italics in each correlation are clinical terms and phrases that are definedas shown here because their locations and relationships are easily trans- on the CD (from Stedman’s) included with this atlas or can be foundferable to subsequent illustrations. It may also be helpful to refer back in standard medical dictionaries and clinical neuroscience textbooks.to this illustration when using subsequent sections of this chapter. Consulting these sources, especially the CD available in this atlas, will significantly enhance understanding of the deficits seen in the neuro- Neurotransmitters: Three important facts are self-evident in the logically compromised patient. Expanded information, based on thedescriptions of neurotransmitters that accompany each pathway draw- deficits mentioned in this chapter, is integrated into some of the ques-ing. These are illustrated by noting, as an example, that glutamate is tions for chapter 7. Referring to such sources will allow the user tofound in corticospinal fibers (see Figure 7–10). First, the location of neu- glean important clinical points that correlate with the pathway underronal cell bodies containing a specific transmitter is indicated (glutamate- consideration, and enlarge his or her knowledge and understanding bycontaining cell bodies are found in cortical areas that project to the spinal researching the italicized words and phrases.cord). Second, the trajectory of fibers containing a particular neurotrans-mitter is obvious from the route taken by the tract (glutaminergic corti- Abbreviations CE Cervical enlargement of spinal cord IntCap,PL Internal capsule, posterior limb Cer Cervical levels of spinal cord LatSul Lateral sulcus (Sylvian sulcus) CinSul Cingulate sulcus LatVen Lateral ventricle CaNu Caudate nucleus (ϩ Put ϭ neostriatum) LSE Lumbosacral enlargement of spinal cord CM Centromedian (and intralaminar) nuclei Lumbosacral level of spinal cord CorCI Corpus callosum LumSac Lateral and ventral thalamic nuclei Dien Diencephalon L-VTh excluding VPM and VPL DMNu Dorsomedial nucleus of thalamus Mesencephalon For Fornix Mes Metencephalon GP Globus pallidus (paleostriatum) Met Myelencephalon GPl Globus pallidus, lateral segment Myelen Putamen (ϩ CaNu ϭ neostriatum) GPm Globus pallidus, medial segment Put Subthalamic nucleus HyTh Hypothalamic area SThNu Telencephalon Internal capsule Telen Thoracic levels of spinal cord IC Internal capsule, anterior limb Thor Ventral posterolateral nucleus of thalamusIntCap,AL Internal capsule, genu VPL Ventral posteromedial nucleus of thalamus VPM IntCap,G

Orientation 177 Midline Cerebral cortex CinSul LatVen Basal ganglia CorCl CaNu For L-VTh DMNu Telen & DienLatSul CM IC IC GPl VPL GPm PutInternal Capsule CaNu Rostral VPM HyTh SThNu Mes IntCap, G Midbrain IntCap, AL Met Dien Caudal Pons & Cerebellum Put GP IntCap, PL Medulla Myelen Cer Spinal Cord CE Thor LSE LumSac Midline

178 Synopsis of Functional Components, Tracts, Pathways, and Systems Posterior (Dorsal) Column-Medial Lemniscus System7–4 The origin, course, and distribution of fibers composing the used to describe deficits seen in lesions of the parietal cortex. Bilateralposterior (dorsal) column (PC)-medial lemniscus (ML) system. This il- damage (as in tabes dorsalis or subacute combined degeneration of the spinallustration shows the longitudinal extent, the positions in representa- cord) produces bilateral losses. Although ataxia is the most common fea-tive cross-sections of brainstem and spinal cord, and the somatotopy of ture in patients with tabes dorsalis, they also have a loss of deep tendonfibers in the PC and ML. The ML undergoes positional changes as it reflexes, severe lancinating pain over the body below the head (more com-courses from the myelencephalon (medulla) rostrally toward the mes- mon in the lower extremity), and bladder dysfunction. The ataxia thatencephalic-diencephalic junction. In the medulla, ML and ALS fibers may be seen in patients with posterior column lesions (sensory ataxia) isare widely separated and receive different blood supplies, whereas in due to a lack of proprioceptive input and position sense. These individ-the midbrain, they are served by a common arterial source. As the ML uals tend to forcibly place their feet to the floor in an attempt to stimu-makes positional changes, the somatotopy therein follows accordingly. late such sensory input. A patient with mild ataxia due to posterior col-Fibers of the postsynaptic posterior column system (shown in green) umn disease may compensate for the motor deficit by using visual cues.are considered in detail in Figure 7–6 on page 182. Patients with subacute combined degeneration (SCD) of the spinal cord first have signs and symptoms of posterior column involvement, fol- Neurotransmitters: Acetylcholine and the excitatory amino lowed later by signs of corticospinal tract damage (spastic weakness of legs,acids glutamate and aspartate are associated with some of the large- increased deep tendon reflexes, Babinski sign).diameter, heavily myelinated fibers of the posterior horn and posteriorcolumns. Rostral to the sensory decussation, medial lemniscus lesions result in contralateral losses that include the entire body excluding the head. Clinical Correlations: Damage to posterior column fibers on one Brainstem lesions involving medial lemniscus fibers usually include ad-side of the spinal cord (as in the Brown-Sequard syndrome) results in an ip- jacent structures, result in motor and additional sensory losses, andsilateral loss of vibratory sensation, position sense, and discriminative may reflect the distribution patterns of vessels (as in medial medullary ortouch (astereognosis, stereoagnosis) below the level of the lesion. The term medial pontine syndromes). Large lesions in the forebrain may result in astereoanesthesia is frequently used to specify a lesion of peripheral nerves complete contralateral loss of modalities carried in the posteriorthat results in an inability to perceive proprioceptive and tactile sensa- columns and anterolateral systems, or may produce pain (as in the thal-tions. The term tactile agnosia is sometimes considered to be synony- amic syndrome).mous with these preceding three terms. However, tactile agnosia is also Abbreviations ALS Anterolateral system NuGr Gracile nucleus BP Basilar pons PC Posterior column CC Crus cerebri PO Principal olivary nucleus CTT Central tegmental tract Postcentral gyrus FCu Cuneate fasciculus PoCGy Posterior paracentral gyrus FGr Gracile fasciculus PPGy Posterior (dorsal) root ganglia IAF Internal arcuate fibers PRG Pyramid IC Internal capsule Py Restiform body ML Medial lemniscus RB Red nucleus MLF Medial longitudinal fasciculus RNu Substantia nigraNuCu Cuneate nucleus SN Ventral posterolateral nucleus of thalamus VPL Somatotopy of Body AreasA Fibers conveying input from upper extremity S5 Fibers from approximately the fifth sacral L Fibers conveying input from lower extremity levelN Fibers conveying input from neck T Fibers conveying input from trunk T5 Fibers from approximately the fifth thoracicC2 Fibers from approximately the second level cervical level Review of Blood Supply to DC-ML System STRUCTURES ARTERIES PC in Spinal Cord ML in Medulla penetrating branches of arterial vasocorona (see Figure 5–6) ML in Pons anterior spinal (see Figure 5–14) overlap of paramedian and long circumferential branches of basilar ML in Midbrain (see Figure 5–21) VPL short circumferential branches of posterior cerebral and superior Posterior Limb of IC cerebellar (see Figure 5–27) thalamogeniculate branches of posterior cerebral (see Figure 5–38) lateral striate branches of middle cerebral (see Figure 5–38)

Sensory Pathways 179 Posterior Column-Medial Lemniscus System PoCGy Trunk Thigh Uexptpreemr ity Leg PPGy Somatosensory cortex Somatotopy in PC and ML Foot Post. limb, ICFace A T L Position of ML L A ALS L VPL ML T ML A CC RNu ML BP SN LTA ALS MLF CTT ML ML RB MLF A IAF ALS T NuGr NuCu PO ML L Py FGr FCu S5 T5 ML NuGr C2 NuCu PRG, T6 IAF L TA N PRG, T6 Py FGr FCu Laminae III-V

180 Synopsis of Functional Components, Tracts, Pathways, and Systems Anterolateral System7–5 The longitudinal extent and somatotopy of fibers composing the fibers or projection neurons, conveying nociceptive (pain) informa-anterolateral system (ALS). The ALS is a composite bundle containing tion.ascending fibers that terminate in the reticular formation (spinoreticu-lar fibers), the mesencephalon (spinotectal fibers to deep layers of the Clinical Correlations: Spinal lesions involving the anterolateralsuperior colliculus, spinoperiaqueductal fibers to the periaqueductal system (as in the Brown-Sequard syndrome) result in a loss of pain andgrey), the hypothalamus (spinohypothalamic fibers), and the sensory re- temperature sensations on the contralateral side of the body beginninglay nuclei of the dorsal thalamus (spinothalamic fibers). Other fibers in one to two levels caudal to the lesion. Syringomyelia produces bilateralthe ALS include spinoolivary projections to the accessory olivary nuclei. sensory losses restricted to adjacent dermatomes because of damage toSpinothalamic fibers terminate primarily in the VPL and reticulothala- the anterior (ventral) white commissure. Vascular lesions in the spinalmic fibers terminate in some intralaminar nuclei, and in medial areas of cord (such as acute central cervical cord syndrome) may result in a bilateralthe posterior thalamic complex. and splotchy loss of pain and thermal sense below the lesion because the ALS has a dual vascular supply. Fibers from the PAG and nucleus raphe dorsalis enter the nucleusraphe magnus and adjacent reticular area. These latter sites, in turn, Vascular lesions in the lateral medulla (posterior inferior cerebellar arteryproject to laminae I, II, and V of the spinal cord via raphespinal and syndrome) or lateral pons (anterior inferior cerebellar artery occlusion)reticulospinal fibers that participate in the modulation of pain trans- result in a loss of pain and thermal sensations over the entire contralat-mission in the spinal cord. eral side of the body (ALS) as well as on the ipsilateral face (spinal trigeminal tract and nucleus), coupled with other motor and/or sensory Neurotransmitters: Glutamate (ϩ), calcitonin gene-related deficits based on damage to structures these vessels serve. Note that thepeptide, and substance P(ϩ)-containing posterior (dorsal) root gan- ALS and PC-ML systems are separated in the medulla (in different vas-glion cells project into laminae I, II (heavy), V (moderate), and III, IV cular territories) but are adjacent to each other in the midbrain (basi-(sparse). Some spinoreticular and spinothalamic fibers contain cally in the same vascular territory). Consequently, medullary lesionsenkephalin (Ϫ), somatostatin (Ϫ), and cholecystokinin (ϩ). In addi- will not result in deficits related to both pathways, while a lesion in thetion to enkephalin and somatostatin, some spinomesencephalic fibers midbrain may result in a contralateral loss of pain, thermal, vibratory,contain vasoactive intestinal polypeptide (ϩ). Neurons in the PAG and and discriminative touch sensations on the body, excluding the head.nucleus raphe dorsalis containing serotonin and neurotensin projectinto the nuclei raphe magnus and adjacent reticular formation. Cells in Profound loss of posterior column and anterolateral system modali-these latter centers that contain serotonin and enkephalin send ties, or intractable pain and/or paresthesias (as in the thalamic syndrome),processes to spinal cord laminae I, II, and V. Serotonergic raphespinal may result from vascular lesions in the posterolateral thalamus. So-or enkephalinergic reticulospinal fibers may inhibit primary sensory called thalamic pain may also be experienced by patients who have brainstem lesions. Abbreviations A Input from upper extremity regions PRG Posterior (dorsal) root ganglion ALS Anterolateral system Py PyramidAWCom Anterior (ventral) white commissure Raphespinal fibers CC Crus cerebri RaSp Restiform body Internal capsule RB Reticular formation (of midbrain) IC Input from lower extremity regions Reticulothalamic fibers L Middle cerebellar peduncle RetF Red nucleus MCP Medial lemniscus RetTh Input from sacral regions ML Medial longitudinal fasciculus Superior colliculus MLF Nuclei RNu Spinoreticular fibers Nu Nucleus of Darkschewitsch S Spinotectal fibersNuDark Nucleus raphe, dorsalis Spinothalamic fibers NuRa,d Nucleus raphe, magnus SC Input from thoracic regionsNuRa,m Periaqueductal gray SpRet Ventral posterolateral nucleus of thalamus PAG Postcentral gyrus SpTec Laminae I-VIII of Rexed PoCGy Posterior paracentral gyrus SpTh PPGy T VPL I-VIII STRUCTURES Review of Blood Supply to ALS ALS in Spinal Cord ARTERIES ALS in Medulla penetrating branches of arterial vasocorona and branches of central ALS in Pons (see Figures 5–6 and 5–14) ALS in Midbrain caudal third, vertebral; rostral two-thirds, posterior inferior cerebellar VPL (see Figure 5–14) Posterior Limb of IC long circumferential branches of basilar (see Figure 5–21) short circumferential branches of posterior cerebral, superior cerebellar (see Figure 5–27) thalamogeniculate branches of posterior cerebral (see Figure 5–38) lateral striate branches of middle cerebral (see Figure 5–38)

Sensory Pathways 181 Anterolateral System PoCGy Trunk eUxptrpeemr ity Thigh Somatosensory cortex Leg Post. limb, IC PPGy Foot Somatotopy of ALS fibersFace Intralaminar Nu A T Position of ALS fibers L VPL SC, RetF, PAG SpTec SC LTA NuDark CC ALS PAG LTA SpRet PAG, NuRa,d SpTh ALS ML ALS RNu AWCom RetTh MLF ALS ML NuRa,m BP RaSp RB MLF S ALS A ML T Py L RaSp Laminae I-VIII PRG PRG S AWCom RaSp to Laminae L I, II, V T A ALS

182 Synopsis of Functional Components, Tracts, Pathways, and SystemsPostsynaptic-Posterior (Dorsal) Column System and the Spinocervicothalamic Pathway7–6 The origin, course, and distribution of fibers composing the cal nucleus and the dorsal column nuclei, glutamate (and substance P)postsynaptic-posterior column system (upper) and the spinocervi- may also be present in some postsynaptic dorsal column fibers.cothalamic pathway (lower). Postsynaptic-posterior column fibersoriginate primarily from cells in lamina IV (some cells in laminae III and Clinical Correlations: The postsynaptic-posterior column andV-II also contribute), ascend in the ipsilateral dorsal fasciculi, and end spinocervicothalamic pathways are not known to be major circuits inin their respective nuclei in the caudal medulla. Moderate-to-sparse the human nervous system. However, the occurrence of these fiberscollaterals project to a few other medullary targets. may explain a well known clinical observation. Patients that have re- ceived an anterolateral cordotomy (this lesion is placed just ventral to the Fibers of the spinocervical part of the spinocervicothalamic pathway denticulate ligament) for intractable pain may experience complete oralso originate from cells in lamina IV (less so from III and V). The axons partial relief, or there may be a recurrence of pain perception withinof these cells ascend in the posterior part of the lateral funiculus (this is days or weeks. Although the cordotomy transects fibers of the antero-sometimes called the dorsolateral funiculus) and end in a topographic lateral system (the main pain pathway), this lesion spares the posteriorfashion in the lateral cervical nucleus: lumbosacral projections termi- horn, posterior columns, and spinocervical fibers. Consequently, thenate posterolaterally and cervical projections anteromedially. Cells of recurrence of pain perception (or even the partial relief of pain) inthe posterior column nuclei and the lateral cervical nucleus convey in- these patients may be explained by these postsynaptic-dorsal columnformation to the contralateral thalamus via the medial lemniscus. and spinocervicothalamic projections. Through these connections, some nociceptive (pain) information may be transmitted to the ventral Neurotransmitters: Glutamate (ϩ) and possibly substance P posterolateral nucleus and on to the sensory cortex, via circuits that by-(ϩ) are present in some spinocervical projections. Because some cells pass the anterolateral system and are spared in a cordotomy.in laminae III-V have axons that collateralize to both the lateral cervi- Abbreviations ALS Anterolateral system AWCom Anterior (ventral) white commissure Cuneate fasciculus FCu Gracile fasciculus FGr Internal arcuate fibers IAF Lateral cervical nucleus LCerNu Medial lemniscus ML Cuneate nucleus NuCu Gracile nucleus NuGr Posterior (dorsal) root ganglion PRGReview of Blood Supply to Dorsal Horn, FGr, FCu, LCerNuSTRUCTURES ARTERIESFGr, FCu in Spinal Cord penetrating branches of arterial vasocorona and some branchesLCerNu from central (sulcal) (see Figure 5–6)NuGr NuCu penetrating branches of arterial vasocorona and branches from central (see Figure 5–6) posterior spinal (see Figure 5–14)

Sensory Pathways 183 Postsynaptic-Posterior (Dorsal) Column System and the Spinocervicothalamic Pathway FGrML Other FCu brainstem targets IAF NuCu PRG FCuNuGr Laminae IV FGr (III-VII) PRG ALS FGr FGr Laminae IV (III-VII) ALS ML LCerNu FGrAWCom PRG FCu Laminae IV (III-VII) PRG Dorsolateral region of lateral funiculus ALS

184 Synopsis of Functional Components, Tracts, Pathways, and Systems Trigeminal Pathways7–7 The distribution of general sensory (GSA) information origi- tile sensation from the ipsilateral face, oral cavity, and teeth; 2) ipsilat-nating on cranial nerves V (trigeminal), VII (facial), IX (glossopharyn- eral paralysis of masticatory muscles; and 3) ipsilateral loss of thegeal), and X (vagus). Some of these primary sensory fibers end in the corneal reflex. Damage to peripheral portions of the trigeminal nervechief sensory nucleus, but most form the spinal trigeminal tract and may be traumatic (skull fracture, especially of supraorbital and infraor-end in the spinal trigeminal nucleus. bital branch), inflammatory (as in herpes zoster), or result from tumor growth. The deficit would reflect the peripheral portion of the trigem- Neurons in the spinal trigeminal nucleus and in ventral parts of the inal nerve damaged.chief sensory nucleus give rise to crossed anterior (ventral) trigeminothal-amic fibers. Collaterals of these ascending fibers influence the hy- Trigeminal neuralgia (tic douloureux) is a severe burning pain restrictedpoglossal, facial (corneal reflex, supraorbital, or trigeminofacial reflex), and to the peripheral distribution of the trigeminal nerve, usually its V2trigeminal motor nuclei; mesencephalic collaterals are involved in the (maxillary) division. This pain may be initiated by any contact to areasjaw reflex, also called the jaw-jerk reflex. Collaterals also enter the dorsal of the face such as the corner of the mouth, nose, lips, or cheek (e.g.,motor vagal nucleus (vomiting reflex), the superior salivatory nucleus shaving, putting make-up on, chewing, or even smiling). The attacks(tearing/lacrimal reflex), and the nucleus ambiguus and adjacent reticular frequently occur without warning, may happen only a few times aformation (sneezing reflex). Uncrossed posterior (dorsal) trigeminothal- month to many times in a single day, and are usually seen in patientsamic fibers arise from posterior regions of the chief sensory nucleus. 40 years of age or older. One probable cause of trigeminal neuralgia is compression of the trigeminal root by aberrant vessels, most com- Neurotransmitters: Substance P (ϩ)-containing and cholecys- monly a loop of the superior cerebellar artery (see page 41). Othertokinin (ϩ)-containing trigeminal ganglion cells project to the spinal causes may include tumor, multiple sclerosis, and ephaptic transmissiontrigeminal nucleus, especially its caudal part (pars caudalis). Glutamate (ephapse) in the trigeminal ganglion. This is the most common type of(ϩ) is found in many trigeminothalamic fibers arising from the chief sen- neuralgia.sory nucleus and the pars interpolaris of the spinal nucleus. It is presentin fewer trigeminothalamic fibers from the pars caudalis and in almost In the medulla, fibers of the spinal trigeminal tract and ALS arenone from the pars oralis. The locus ceruleus (noradrenergic fibers) and served by the posterior inferior cerebellar artery (PICA). Conse-the raphe nuclei (serotonergic fibers) also project to the spinal nucleus. quently, an alternating hemianesthesia is one characteristic feature of theEnkephalin (Ϫ)-containing cells are present in caudal regions of the PICA syndrome. This is a loss of pain and thermal sensations on one sidespinal nucleus, and enkephalinergic fibers are found in the nucleus am- of the body and the opposite side of the face. Pontine gliomas may pro-biguus and in the hypoglossal, facial, and trigeminal motor nuclei. duce a paralysis of masticatory muscles (motor trigeminal damage) and some loss of tactile input (chief sensory nucleus damage), as well as Clinical Correlations: Lesions of the trigeminal ganglion or nerve other deficits based on what adjacent structures may be involved.proximal to the ganglion result in 1) a loss of pain, temperature, and tac- Abbreviations ALS Anterolateral system MesNu Mesencephalic nucleus VPM Ventral posteromedial nucleus CC Crus cerebri ML Medial lemniscus VTTr of thalamus CSNu Chief (principal) sensory Ophthalmic division of Ventral trigeminothalamic nucleus OpthV trigeminal nerve tract DTTr Dorsal trigeminothalamic tract Restiform bodyFacNu Facial nucleus RB Reticular formation Ganglia General somatic afferent RetF Red nucleus GSA Hypoglossal nucleus RNu Spinal trigeminal nucleus 1 Trigeminal ganglionHyNu Internal capsule SpTNu Spinal trigeminal tract 2 Geniculate ganglion Mandibular division of SpTTr Trigeminal motor nucleus 3 Superior of glossopharyngeal IC trigeminal nerve TriMoNu Temporomandibular joint 4 Superior of vagusManV Maxillary division of trigeminal TMJ Ventral posterolateral nucleus nerve VPL of thalamusMaxV Review of Blood Supply to SpTT, SpTNu, and Trigeminothalamic Tracts STRUCTURES ARTERIES SpTTr and SpTNu caudal third, vertebral; rostral two-thirds, posterior in Medulla inferior cerebellar (see Figure 5–14) SpTTr and SpTNu in Pons long circumferential branches of basilar (see Figure 5–21) Trigeminothalamic Fibers short circumferential branches of posterior cerebral and in Midbrain superior cerebellar (see Figure 5–27) VPM thalamogeniculate branches of posterior cerebral Posterior Limb of IC (see Figure 5–38) lateral striate branches of middle cerebral (see Figure 5–38)

Sensory Pathways 185 Trigeminal Pathways TrunkSomatosensory Uexptpreemr ity Thigh cortex Leg Foot FacePosterior VPM limb, IC DTTr VTTr MesNuPosition of Trigeminal tracts CSNu Origin of SA Data 1 GSA, skin of face, forehead MesNu and part of scalp; mem-ALS branes of nose and of nasal, maxillary and frontal DTTr TriMoNu sinuses; oral cavity, teeth; ant. 2/3 of tongue; musclesVTTr RNu TriMoNu of mastication, TMJ; corneaML SpTTr and conjunctiva; dura of FacNu SpTNu mid. and ant. cranial fossae CC 2 GSA, external auditory meatus, 3 med. and lat. surfaces RetF 4 of ear (conchae) SpTTr VTTr GSA, small area on ear SpTNuSomatotopy in SpTTr and SpTNu GSA, med. and lat. surfaces of ear (conchae); post.Input from 7,9,10 RB HyNu wall and floor of external SpTTr auditory meatus; tympanic Man. V membrane; dura of post. Max. V SpTNu cranial fossa Opth. V ALS SpTTr SpTNu

186 Synopsis of Functional Components, Tracts, Pathways, and Systems Solitary Pathways7–8 Visceral afferent input (SVA-taste; GVA general visceral sen- adjacent dorsal motor vagal nucleus. Cholecystokinin (ϩ), somato-sation) on cranial nerves VII (facial), IX (glossopharyngeal), and X (va- statin (Ϫ), and enkephalin (Ϫ) are present in solitary neurons, in cellsgus) enters the solitary nuclei via the solitary tract. What we com- of the parabrachial nuclei, and in some thalamic neurons that projectmonly call the solitary “nucleus” is actually a series of small nuclei that to taste, and other visceral areas, of the cortex.collectively form this rostrocaudal-oriented cell column. Clinical Correlations: Lesions of the geniculate ganglion, or fa- Solitary cells project to the salivatory, hypoglossal, and dorsal mo- cial nerve proximal to the ganglion, result in 1) ipsilateral loss of tastetor vagal nuclei and the nucleus ambiguus. Solitary projections to the (ageusia) from the anterior two-thirds of the tongue and 2) an ipsilateralnucleus ambiguus are largely bilateral and are the intermediate neurons facial (Bell) palsy. Although a glossopharyngeal nerve lesion will result inin the pathway for the gag reflex. The afferent limb of the gag-reflex is ageusia from the posterior third of the tongue on the ipsilateral side, thiscarried on the glossopharyngeal nerve, and the efferent limb originates loss is difficult to test. On the other hand, glossopharyngeal neuralgia is anfrom the nucleus ambiguus. In this respect, the efferent limb travels on idiopathic pain localized to the peripheral sensory branches of the IXthboth the glossopharyngeal and vagus nerves. Although not routinely nerve in the posterior pharynx, posterior tongue, and tonsillar area. Al-tested, the gag-reflex should be evaluated in patients with dysarthria, dys- though comparatively rare, glossopharyngeal neuralgia may be aggra-phagia, or hoarnessness. Solitariospinal fibers are bilateral with a con- vated by talking or even swallowing. Occlusion of the posterior inferiortralateral preponderance and project to the phrenic nucleus, the inter- cerebellar artery (as in the posterior inferior cerebellar artery or lateralmediolateral cell column, and the ventral horn. The VPM is the medullary syndrome), in addition to producing an alternate hemianesthesia,thalamic center through which visceral afferent information is relayed will also result in ageusia from the ipsilateral side of the tongue becauseonto the cerebral cortex. the posterior inferior cerebellar artery serves the solitary tract and nu- clei in the medulla. Neurotransmitters: Substance P (ϩ)-containing and cholecys-tokinin (ϩ)-containing cells in the geniculate ganglion (facial nerve) Interestingly, lesions of the olfactory nerves or tract (anosmia, lossand in the inferior ganglia of the glossopharyngeal and vagus nerves of olfactory sensation; dysosmia, distorted olfactory sense) may affectproject to the solitary nucleus. Enkephalin (Ϫ), neurotensin, and how the patient perceives taste. Witness the fact that the nasal conges-GABA (ϩ) are present in some solitary neurons that project into the tion accompanying a severe cold will markedly affect the sense of taste. Abbreviations AmyNu Amygdaloid nucleus (complex) SalNu Salivatory nucleiCardResp Cardiorespiratory portion (caudal) of SolTr & Nu Solitary tract and nuclei solitary nucleus Special visceral afferent GustNu Gustatory nucleus (rostral portion of SVA Tract solitary nucleus) Tr Visceral afferent GVA General visceral afferent VA Ventral posteromedial nucleus of HyNu Hypoglossal nucleus thalamus HyTh Hypothalamus VPM Inf VNu Inferior (or spinal) vestibular nucleus MVNu Medial vestibular nucleus Number Key NuAm Nucleus ambiguus PBNu Parabrachial nuclei 1 Geniculate ganglion of facial Restiform body 2 Inferior ganglion of glossopharyngeal RB 3 Inferior ganglion of vagus 4 Dorsal motor vagal nucleus Review of Blood Supply to SolNu and SolTr STRUCTURES ARTERIES SolNu and Tr in caudal medulla, anterior spinal; rostral medulla, posterior inferior inferior cerebellar cerebellar (See Figure 5–14) Ascending Fibers long circumferential branches of basilar and branches of superior in Pons cerebellar (see Figure 5–21) VPM thalamogeniculate branches of posterior cerebral (see Figure 5–38) Posterior Limb of IC lateral striate branches of middle cerebral (see Figure 5–38)

Sensory Pathways 187 Solitary Pathways Thigh Trunk extUrepmpietyr Leg Foot Face HyTh AmyNu VPM PBNu to HyNu, Origin of VA data SalNu SVA, taste, ant. 2/3 of tongue 1 GVA, submand., subling., lac. glds. SVA 2 SVA, taste, post. 1/3 of tongue (GustNu)SolTr and Nu 4 GVA, parotid gld.; mucosa of GVA (CardResp) 3 pharynx; tonsillar sinus; post. 1/3 of tongue; carotid body NuAm SVA, taste buds at root of tongue and on epiglottis GVA, pharynx; larynx; aortic bodies; thoracic and abdominal visceraSolitariospinal Tr Position of SolTr & Nu MVNu InfVNu RB SolTr and Nu

188 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–9 Blank master drawing for sensory pathways. This illustration is provided for self-evaluation of sensory pathway understanding, for the instructor to expand on sensory pathways not covered in the atlas, or both.

Sensory Pathways 189

190 Synopsis of Functional Components, Tracts, Pathways, and Systems Corticospinal Tracts7–10 The longitudinal extent of corticospinal fibers and their posi- is a hallmark of this disease. Ocular muscles are usually affected firsttion and somatotopy at representative levels within the neuraxis. The (diplopia, ptosis), and in approximately 50% of patients, facial andsomatotopy of corticospinal fibers in the basilar pons is less obvious than oropharyngeal muscles are commonly affected ( facial weakness, dys-in the internal capsule, crus cerebri, pyramid, or spinal cord. In the de- phagia, dysarthria). Weakness may also be seen in limb muscles but al-cussation of the pyramids, fibers originating from upper extremity ar- most always in combination with facial/oral weaknesses.eas of the cerebral cortex cross rostral to those that arise from lower ex-tremity areas. In addition to fibers arising from the somatomotor area Injury to corticospinal fibers on one side of the cervical spinal cordof the cerebral cortex (area 4), a significant contingent also originate (as in the Brown-Sequard syndrome) results in weakness (hemiparesis) orfrom the postcentral gyrus (areas 3, 1, 2); the former terminate pri- paralysis (hemiplegia) of the ipsilateral upper and lower extremities. Inmarily in laminae VI-IX, while the latter end mainly in laminae IV and addition, and with time, these patients may exhibit features of an upperV. Prefrontal regions, especially area 6, and parietal areas 5 and 7 also motor neuron lesion (hyperreflexia, spasticity, loss of superficial abdominalcontribute to the corticospinal tract. reflexes, and the Babinski sign). Bilateral cervical spinal cord damage above C4–C5 may result in paralysis of all four extremities (quadriple- Neurotransmitters: Acetylcholine, gamma-aminobutyric acid gia). Unilateral spinal cord lesions in thoracic levels may result in paral-(Ϫ), and substance P (ϩ, plus other peptides) are found in small cor- ysis of the ipsilateral lower extremity (monoplegia). If the thoracic spinaltical neurons presumed to function as local circuit cells or in cortico- cord damage is bilateral both lower extremities may be paralyzed (para-cortical connections. Glutamate (ϩ) is present in cortical efferent plegia). Small lesions within the decussation of the pyramids may resultfibers that project to the spinal cord. Glutaminergic corticospinal fibers in a bilateral paresis of the upper extremities (lesion in rostral portions)and terminals are found in all spinal levels but are especially concen- or a bilateral paresis of the lower extremities (lesion in caudal portions)trated in cervical and lumbosacral enlargements. This correlates with based on the crossing patterns of fibers within the decussation.the fact that approximately 55% of all corticospinal fibers terminate incervical levels of the spinal cord, approximately 20% in thoracic lev- Rostral to the pyramidal decussation, vascular lesions in the medullaels, and approximately 25% in lumbosacral levels. Some corticospinal (the medial medullary syndrome), pons (the Millard-Gubler or Foville syn-fibers may branch and terminate at multiple spinal levels. Lower mo- dromes), or midbrain (the Weber syndrome) all produce alternatingtor neurons are influenced by corticospinal fibers either directly or in- (crossed) hemiplegias. These present as a contralateral hemiplegia of thedirectly via interneurons. Acetylcholine and calcitonin gene-related upper and lower extremities, coupled with an ipsilateral paralysis ofpeptides are present in these large motor cells and in their endings in the tongue (medulla), facial muscles or lateral rectus muscle (pons),skeletal muscle. and most eye movements (midbrain). Sensory deficits are frequently seen as part of these syndromes. Lesions in the internal capsule (lacu- Clinical Correlations: Myasthenia gravis, a disease characterized nar strokes) produce contralateral hemiparesis sometimes coupled withby moderate to profound weakness of skeletal muscles, is caused by various cranial nerve signs due to corticonuclear (corticobulbar) fibercirculating antibodies that react with postsynaptic nicotinic acetyl- involvement. Bilateral weakness, indicative of corticospinal involve-choline receptors. Progressive muscle fatigability throughout the day ment, is also present in amyotrophic lateral sclerosis. AbbreviationsACSp Anterior corticospinal tract LCSp Lateral corticospinal tract Somatotopy of CSp Fibers ALS Anterolateral system ML Medial lemniscus Anterior paracentral gyrus MLF Medial longitudinal fasciculus A Position of fibers coursing toAPGy Basilar pons PO Principal olivary nucleus upper extremity regions of BP Crus cerebri Precentral gyrus spinal cord CC Corticonuclear (corticobulbar) PrCGy Pyramid fibers Py Restiform body L Position of fibers coursing to CNu Corticospinal fibers RB Red nucleus lower extremity regions of Internal capsule Substantia nigra spinal cord CSp RNu IC SN T Position of fibers coursing to thoracic regions of spinal cord Review of Blood Supply to Corticospinal Fibers STRUCTURES ARTERIES Posterior Limb of IC lateral striate branches of middle cerebral (see Crus Cerebri in Figure 5–38) Midbrain paramedian and short circumferential CSp in BP branches of basilar and posterior Py in Medulla communicating (see Figure 5–27) LCSp in Spinal Cord paramedian branches of basilar (see Figure 5–21) anterior spinal (see Figure 5–14) penetrating branches of arterial vasocorona (leg fibers), branches of central artery (arm fibers) (See Figure 5–6)

Motor Pathways 191 Corticospinal Tracts PrCGeUyxptrpeemr ity Trunk Thigh CSp fibers in CC Leg APGy Somatomotor cortex CSp fibers in BP Foot Somatotopy of CSpFace Post. limb, IC Position of CSp A T ALS L ML LT RNu A SN CC VesNu Face ALS (CNu Fibers) MLF ML L TA BP CSp CSp fibers in Py RB MLF LTA Pyramidal (motor) decussation ALS ML ACSp PO Py LCSp LCSp L T A Laminae IV-IX ALS ACSp

192 Synopsis of Functional Components, Tracts, Pathways, and Systems Corticonuclear (Corticobulbar) Fibers7–11 The origin, course, and distribution of corticonuclear (corti- may produce a transient gaze palsy in which the eyes deviate toward thecobulbar) fibers to brainstem motor nuclei. These fibers influence—ei- lesioned side and away from the side of the hemiplegia. In addition tother directly or through neurons in the immediately adjacent reticular a contralateral hemiplegia, common cranial nerve findings in capsular le-formation—the motor nuclei of oculomotor, trochlear, trigeminal, ab- sions may include 1) deviation of the tongue toward the side of theducens, facial, glossopharyngeal and vagus (both via nucleus ambiguus), weakness and away from the side of the lesion when protruded and 2)spinal accessory, and hypoglossal nerves. paralysis of facial muscles on the contralateral lower half of the face (central facial palsy). This reflects the fact that corticonuclear (cortico- Corticonuclear (corticobulbar) fibers arise in the frontal eye fields (ar- bulbar) fibers to genioglossus motor neurons and to facial motor neu-eas 6 and 8 in caudal portions of the middle frontal gyrus), the precen- rons serving the lower face are primarily crossed. Interruption of cor-tral gyrus (somatomotor cortex, area 4), and some originate from the ticonuclear fibers to the nucleus ambiguus may result in weakness ofpostcentral gyrus (areas 3,1, 2). Fibers from area 4 occupy the genu of palatal muscles contralateral to the lesion; the uvula will deviate to-the internal capsule, but those from the frontal eye fields (areas 8,6) may wards the ipsilateral (lesioned) side on attempted phonation. In addi-traverse caudal portions of the anterior limb, and some (from areas tion, a lesion involving corticonuclear fibers to the accessory nucleus3,1,2), may occupy the most rostral portions of the posterior limb. may result in drooping of the ipsilateral shoulder (or an inability to el-Fibers that arise in areas 8 and 6 terminate in the rostral interstitial nucleus evate the shoulder against resistance) due to trapezius weakness, andof the medial longitudinal fasciculus (vertical gaze center) and in the parame- difficulty in turning the head (against resistance) to the contralateraldian pontine reticular formation (horizontal gaze center); these areas, in turn, side due to weakness of the sternocleidomastoid muscle. In contrast toproject respectively to the IIIrd and IVth, and to the VIth nuclei. Fibers the alternating hemiplegia seen in some brainstem lesions, hemispherefrom area 4 terminate in, or adjacent to, cranial nerve motor nuclei ex- lesions result in spinal and cranial nerve deficits that are generally, butcluding those of III, IV, and VI. not exclusively, contralateral to the cerebral injury. Although not illustrated here, the superior colliculus receives cor- Brainstem lesions, especially in the midbrain or pons, may result intical input from area 8 and from the parietal eye field (area 7) and also the following: 1) vertical gaze palsies (midbrain), 2) the Parinaud syn-projects to the riMLF and PPRF. In addition, it is important to note drome—paralysis of upward gaze (tumors in area of pineal), 3) internu-that descending cortical fibers (many arising in areas 3, 1, 2) project to clear ophthalmoplegia (lesion in MLF between motor nuclei of III andsensory relay nuclei of some cranial nerves and to other sensory relay VI), 4) horizontal gaze palsies (lesion in PPRF), or 5) the one-and-a-halfnuclei in the brainstem, such as those of the posterior column system. syndrome. In the latter case, the lesion is adjacent to the midline and in- volves the abducens nucleus and adjacent PPRF, internuclear fibers Neurotransmitters: Glutamate (ϩ) is found in many corticofu- from the ipsilateral abducens that are crossing to enter the contralat-gal axons that directly innervate cranial nerve motor nuclei and in eral MLF, and internuclear fibers from the contralateral abducens nu-those fibers that terminate near (indirect), but not in, the various mo- cleus that cross to enter the MLF on the ipsilateral (lesioned) side. Thetor nuclei. result is a loss of ipsilateral abduction (lateral rectus) and adduction (medial rectus, the “one”) and a contralateral loss of adduction (medial Clinical Correlations: Lesions involving the motor cortex (as in rectus, the “half ”); the only remaining horizontal movement is con-cerebral artery occlusion) or the internal capsule (as in lacunar strokes tralateral abduction via the intact abducens motor neurons.or occlusion of lenticulostriate branches of M1) give rise to a con-tralateral hemiplegia of the arm and leg (corticospinal fiber involve-ment) coupled with certain cranial nerve signs. Strictly cortical lesions AbbreviationsAbdNu Abducens nucleus OcNu Oculomotor nucleusAccNu Accessory nucleus (spinal accessory nu.) PPRF Paramedian pontine reticular formation FacNu Facial nucleus riMLF Rostral interstitial nucleus of the medial HyNu Hypoglossal nucleus Internal capsule longitudinal fasciculus IC Nucleus ambiguus TriMoNu Trigeminal motor nucleusNuAm TroNu Trochlear nucleus Review of Blood Supply to Cranial Nerve Motor Nuclei STRUCTURES ARTERIES OcNu and EWNu paramedian branches of basilar bifurcation and medial branches TriMoNu of posterior cerebral and posterior communicating (see Figure AbdNu and FacNu 5–27) NuAm HyNu long circumferential branches of basilar (see Figure 5–21) long circumferential branches of basilar (see Figure 5–21) posterior inferior cerebellar (see Figure 5–14) anterior spinal (see Figure 5–14)

Motor Pathways 193 Corticonuclear (Corticobulbar) Fibers Motor cortex, Frontal eye fieldsprecentral gyrusGenu of IC riMLF OcNuBilateral for upper face TroNu = Direct to motor TriMoNu neurons of nucleus PPRF = Indirect to motor AbdNu neurons via adjacent reticular formation FacNu = Bilateral projections Crossed for lower face = Primarily crossed NuAm projections Crossed for uvula (soft palate) Crossed for genioglossus muscle HyNu AccNu

194 Synopsis of Functional Components, Tracts, Pathways, and SystemsTectospinal and Reticulospinal Tracts7–12 The origin, course, position in representative cross-sections ing system that modulates pain transmission at the spinal level. Manyof brainstem and spinal cord, and the general distribution of tectospinal reticulospinal fibers influence the activity of lower motor neurons.and reticulospinal tracts. Tectospinal fibers originate from deeper lay-ers of the superior colliculus, cross in the posterior (dorsal) tegmental Clinical Correlations: Isolated lesions of only tectospinal anddecussation, and distribute to cervical cord levels. Several regions of reticulospinal fibers are essentially never seen. Tectospinal fibers pro-cerebral cortex (e.g., frontal, parietal, temporal) project to the tec- ject to upper cervical levels where they influence reflex movement oftum, but the most highly organized corticotectal projections arise from the head and neck. Such movements may be diminished or slowed inthe visual cortex. Pontoreticulospinal fibers (medial reticulospinal) patients with damage to these fibers. Pontoreticulospinal (medial retic-tend to be uncrossed, while those from the medulla (bulboreticu- ulospinal) fibers are excitatory to extensor motor neurons and to neu-lospinal or lateral reticulospinal) are bilateral but with a pronounced rons innervating axial musculature; some of these fibers may also in-ipsilateral preponderance. Corticoreticular fibers are bilateral with a hibit flexor motor neurons. In contrast, some bulboreticulospinalslight contralateral preponderance and originate from several cortical (lateral reticulospinal) fibers are primarily inhibitory to extensor mo-areas. tor neurons and to neurons innervating muscles of the neck and back; these fibers may also excite flexor motor neurons via interneurons. Neurotransmitters: Corticotectal projections, especially those Reticulospinal (and vestibulospinal) fibers contribute to the spasticityfrom the visual cortex, utilize glutamate (ϩ). This substance is also that develops in patients having lesions of corticospinal fibers. Thesepresent in most corticoreticular fibers. Some neurons of the giganto- reticulospinal and vestibulospinal fibers (see Figure 7-13 on page 196)cellular reticular nucleus that send their axons to the spinal cord, as also contribute to the tonic extension of the arms and legs seen in de-reticulospinal projections, contain enkephalin (Ϫ) and substance P cerebrate rigidity when spinal motor neurons are released from de-(ϩ). Enkephalinergic reticulospinal fibers may be part of the descend- scending cortical control. Abbreviations ALS Anterolateral system PO Principal olivary nucleusATegDec Anterior tegmental decussation PTegDec Posterior tegmental decussation (tectospinal fibers) (rubrospinal fibers) Py Pyramid BP Basilar pons RB Restiform body CC Crus cerebri RetNu Reticular nuclei CRet Corticoreticular fibers RetSp Reticulospinal tract(s) CTec Corticotectal fibers RNu Red nucleusGigRetNu Gigantocellular reticular nucleus RuSp Rubrospinal tract LCSp Lateral corticospinal tract SC Superior colliculus ML Medial lemniscus SN Substantia nigra MLF Medial longitudinal fasciculus SpVNu Spinal (or inferior) vestibular nucleus MVNu Medial vestibular nucleus TecSp Tectospinal tract OcNu Oculomotor nucleusReview of Blood Supply to SC, Reticular Formation of Pons and Medulla, and TecSp and RetSp Tracts in Cord STRUCTURES ARTERIESSC long circumferential branches (quadrigeminal branch) of posteriorPontine Reticular cerebral plus some from superior cerebellar and posterior Formation choroidal (see Figure 5–27)Medullary Recticular long circumferential branches of basilar plus branches of superior Formation cerebellar in rostral pons (see Figure 5–21)TecSp and RetSp branches of vertebral plus paramedian branches of basilar at medulla-pons junction (see Figure 5–14) branches of central artery (TecSp and Medullary RetSp); Tracts penetrating branches of arterial vasocorona (Pontine RetSp) (see Figures 5–14 and 5–6)

Motor Pathways 195 Tectospinal and Reticulospinal Tracts CRetCTec Postition of TecSp and RetSp SC CTec SC PTegDec CRet TecSp SN ML CRet CC RNu PTegDec (TecSp)Pontine RetNu: ATegDec (RuSp) oralis MLF caudalis TecSp RetNu of Pons ALS ML Pontine RetSp InfVNu BP GigRetNu RB Pontine RetSp MVNu ALS MLF Medullary RetSp PO TecSp GigRetNu TecSp ML Py LCSp Medullary RetSp ALS to Laminae VII (VI,VII, IX) TecSp to Laminae VI, VII (VIII) Pontine RetSp of cervical levels to Laminae VIII (VII,IX)

196 Synopsis of Functional Components, Tracts, Pathways, and SystemsRubrospinal and Vestibulospinal Tracts7–13 The origin, course, and position in representative cross-sec- Clinical Correlations: Isolated injury to rubrospinal and vestibu-tions of brainstem and spinal cord, and the general distribution of lospinal fibers is really not seen in humans. Deficits in fine distal limbrubrospinal and vestibulospinal tracts. Rubrospinal fibers cross in the an- movements seen in monkeys following experimental rubrospinal le-terior (ventral) tegmental decussation and distribute to all spinal levels sions may be present in humans. However, these deficits are over-although projections to cervical levels clearly predominate. Cells in dor- shadowed by the hemiplegia associated with injury to the adjacent cor-somedial regions of the red nucleus receive input from upper extremity ticospinal fibers. The contralateral tremor seen in patients with theareas of the motor cortex and project to cervical cord, but those in ven- Claude syndrome (a lesion of the medial midbrain) is partially related totrolateral areas of the nucleus receive some fibers from lower extremity damage to the red nucleus as well as to the adjacent cerebellothalamicareas of the motor cortex and may project in sparse numbers to lum- fibers. These patients may also have a paucity of most eye movementbosacral levels. The red nucleus also projects, via the central tegmental on the ipsilateral side and a dilated pupil (mydriasis) due to concurrenttract, to the ipsilateral inferior olivary complex (rubroolivary fibers). damage to exiting rootlets of the oculomotor nerve. Medial and lateral vestibular nuclei give rise to the medial and lateral Medial vestibulospinal fibers primarily inhibit motor neurons inner-vestibulospinal tracts, respectively. The former tract is primarily ipsi- vating extensors and neurons serving muscles of the back and neck. Lat-lateral, projects to upper spinal levels, and is considered a component eral vestibulospinal fibers may inhibit some flexor motor neurons, butof the medial longitudinal fasciculus in the spinal cord. The latter tract they mainly facilitate spinal reflexes via their excitatory influence on spinalis ipsilateral and somatotopically organized; fibers to lumbosacral levels motor neurons innervating extensors. Vestibulospinal and reticulospinaloriginate from dorsal and caudal regions of the lateral nucleus, while (see Figure 7-12 on page 194) fibers contribute to the spasticity seen in pa-those to cervical levels arise from its rostral and more ventral areas. tients with damage to corticospinal fibers or to the tonic extension of the extremities in patients with decerebrate rigidity. In the case of decerebrate Neurotransmitters: Glutamate (ϩ) is present in corticorubral rigidity, the descending influences on spinal flexor motor neurons (corti-fibers. Some lateral vestibulospinal fibers contain aspartate (ϩ), cospinal, rubrospinal) is removed; the descending brainstem influence onwhereas glycine (Ϫ) is present in a portion of the medial vestibu- spinal extensor motor neurons predominates; this is augmented by exci-lospinal projection. There are numerous gamma-aminobutyric acid tatory spinoreticular input (via ALS) to some of the centers giving rise to(Ϫ)-containing fibers in the vestibular complex; these represent the reticulospinal fibers (see also Figure 7-12 on page 194).endings of cerebellar corticovestibular fibers. AbbreviationsATegDec Anterior tegmental decussation MVessp Medial vestibulospinal tract (rubrospinal fibers) MVNu Medial vestibular nucleus OcNu Oculomotor nucleus CC Crus cerebri Posterior tegmental decussation (tectospinal CorRu Corticorubral fibers PTegDec fibers) FacNu Facial nucleus Pyramid InfVNu Inferior (or spinal) vestibular nucleus Py Red nucleus RNu Rubrospinal tract LCSp Lateral corticospinal tract RuSp Superior colliculus LRNu Lateral reticular nucleus Superior vestibular nucleus LVNu Lateral vestibular nucleus SC Tectospinal tract LVesSp Lateral vestibulospinal tract SVNu Vestibulospinal tracts TecSp ML Medial lemniscus VesSp MLF Medial longitudinal fasciculusReview of Blood Supply to RNu, Vestibular Nuclei, MFL and RuSp, and Vestibulospinal Tracts in Cords STRUCTURES ARTERIESRNu medial branches of posterior cerebral and posterior communicatingVestibular Nuclei plus some from short circumferential branches of posterior cerebralMLF (see Figure 5–27)MVesSpLVesSp and RuSp posterior inferior cerebellar in medulla (see Figure 5–14) and long circumferential branches in pons (see Figure 5–21) long circumferential branches of basilar in pons (see Figure 5–21) and anterior spinal in medulla (see Figure 5–14) branches of central artery (see Figures 5–6 and 5–14) penetrating branches of arterial vasocorona plus terminal branches of central artery (see Figure 5–6)