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

Motor Pathways 197 Rubrospinal and Vestibulospinal Tracts Thigh Leg FootFace CorRu PTegDec Position of RuSp and VesSp RNu SC SVNu MVNu RuSp ML OCNu CC RNu PTegDec (TecSp) ATegDec (RuSp) LVNu FacNu MVNu InfVNu SpVNu LRNu MLF LVesSp RuSp RuSp MVesSp Py ML in MLF LCSp LVesSp RuSp to Laminae MVesSp V-VIII MVesSp to Laminae LVesSp VII and VIII LCSp RuSp LVesSp

198 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–14 Blank master drawing for motor pathways. This illustration is provided for self-evaluation of motor pathways understanding, for the instructor to expand on motor pathways not covered in this atlas, or both.

Motor Pathways 199

200 Synopsis of Functional Components, Tracts, Pathways, and Systems Cranial Nerve Efferents (III, IV, VI, XI-AccNu, XII)7–15 The origin and peripheral distribution of GSE fibers from the addition, the pupil may be unaffected (pupillary sparing) or dilated andoculomotor, trochlear, abducens, spinal accessory, and hypoglossal fixed. Lesions in the midbrain that involve the root of the IIIrd nervenuclei. Also shown are GVE fibers arising from the Edinger-Westphal and the crus cerebri give rise to a superior alternating (crossed) hemiplegia.nucleus and the distribution of postganglionic fibers from the ciliary This is a paralysis of most eye movement and possibly a dilated pupilganglion. Internuclear abducens neurons project, via the MLF, to con- on the ipsilateral side and a contralateral hemiplegia of the extremities.tralateral oculomotor neurons that innervate the medial rectus muscle(internuclear ophthalmoplegia pathway). Damage to the MLF (as in multiple sclerosis or small vessel occlusion) be- tween the VIth and IIIrd nuclei results in internuclear ophthalmoplegia; on Some authors specify the functional component of neurons in the attempted lateral gaze, the opposite medial rectus muscle will not adduct.accessory nucleus as special visceral efferent, some specify it as somatic A lesion of the IVth nerve (frequently caused by trauma) produces diplopiaefferent, and some are noncommittal. Because, in humans, the trapez- on downward and inward gaze (tilting the head may give some relief ), andius and sternocleidomastoid muscles originate from cervical somites the eye is slightly elevated when the patient looks straight ahead.located caudal to the last pharyngeal arch, the functional component isdesignated here as GSE. In addition, experiments in animals reveal that Diabetes mellitus, trauma, or pontine gliomas are some causes of VIthmotor neurons innervating the trapezius and sternocleidomastoid nerve dysfunction. In these patients, the affected eye is slightly ad-muscles are found in cervical cord levels C1 to approximately C6. ducted, and diplopia is pronounced on attempted gaze to the lesioned side. Damage in the caudal and medial pons may involve the fibers of Neurotransmitters: Acetylcholine (and probably calcitonin the VIth nerve and the adjacent corticospinal fibers in the basilar pons,gene-related peptide, CGRP) is found in the motor neurons of cranial giving rise to a middle alternating (crossed) hemiplegia. The deficits are annerve nuclei and in their peripheral endings. This substance is also ipsilateral paralysis of the lateral rectus muscle and a contralateralfound in cells of the Edinger-Westphal nucleus and the ciliary ganglion. hemiplegia of the extremities. The XIth nerve may be damaged cen- trally (as in syringobulbia or amyotrophic lateral sclerosis) or at the jugular Clinical Correlations: Myasthenia gravis (MG) is a disease caused foramen with resultant paralysis of the ipsilateral sternocleidomastoidby autoantibodies that may directly block nicotinic acetylcholine and upper parts of the trapezius muscle.receptors or damage the postsynaptic membrane (via complement me-diated lysis) thereby reducing the number of viable receptor sites. Oc- Central injury to the XIIth nucleus or fibers (as in the medialular movement disorders (diplopia, ptosis) are seen first in approxi- medullary syndrome or in syringobulbia) or to its peripheral parts (as inmately 50% of patients and are present in approximately 85% of all polyneuropathy or tumors) results in deviation of the tongue toward theMG patients. Movements of the neck and tongue may also be impaired, lesioned side on attempted protrusion. A lesion in the medial aspectswith the latter contributing to dysphagia and dysarthria. of the medulla will give rise to an inferior alternating (crossed) hemiplegia. This is characterized by a paralysis of the ipsilateral side of the tongue Lesions of the IIIrd nerve (as in the Weber syndrome or in carotid cav- (XIIth root damage) and contralateral hemiplegia of the extremitiesernous aneurysms) may result in 1) ptosis, 2) lateral and downward devi- (damage to corticospinal fibers in the pyramid).ation of the eye, and 3) diplopia (except on ipsilateral lateral gaze). In AbbreviationsAbdNr Abducens nerve OcNu Oculomotor nucleusAbdNu Abducens nucleus PO Principal olivary nucleus AccNr Accessory nerve Py PyramidAccNu Accessory nucleus (spinal accessory nu.) Red nucleus Basilar pons RNu Superior colliculus BP Crus cerebri SC Superior cerebellar peduncle, decussation CC Edinger-Westphal nucleus Trochlear decussation EWNu Facial colliculus SCP,Dec Trochlear nerveFacCol Hypoglossal nerve TroDec Trochlear nucleus HyNr Hypoglossal nucleus HyNu Medial lemniscus TroNr ML Medial longitudinal fasciculus TroNu MLF Oculomotor nerve OcNr Ganglion 1 Ciliary Review of Blood Supply to OcNu, TroNu, AbdNu and HyNu, and the Internal Course of their Fibers STRUCTURES ARTERIES OcNu and Fibers medial branches of posterior cerebral and posterior TroNu communicating (see Figure 5–27) AbdNu Abducens Fibers in BP paramedian branches of basilar bifurcation (see Figure 5–27) HyNu and Fibers long circumferential branches of basilar (see Figure 5–21) paramedian branches of basilar (see Figure 5–21) anterior spinal (see Figure 5–14)

Motor Pathways 201 Cranial Nerve Efferents (III, IV, VI, XI-AccNu, and XII)Position of Nucleusand InternalRoute of Fibers SC ML SNOcNu and EWNu OcNu EWNu RNu TroNu CC OcNr TroDec OcNr MLF TroNu 1 Muscles Innervated TroNr MLF Med. Rectus Ciliary; Sphincter of iris Inf. Oblique; Inf. and FacCol Exit of TroNr Med. recti AbdNu Sup. rectus TroDec TroNr Levator palpebrae MLF Sup. Oblique ML CC AbdNu BP SCP, Dec Lat. rectus AbdNr AbdNr HyNu HyNr Intrinsic tongue muscles, AccNr and styloglossus, hyoglossus, AccNu genioglossusHyNu Sternocleidomastoid MLF Trapezius ML PO Py HyNr

202 Synopsis of Functional Components, Tracts, Pathways, and Systems Cranial Nerve Efferents (V, VII, IX, and X)7–16 The origin and peripheral distribution of fibers arising from viates to the lesioned side when closed);, and 3) loss of the afferent limbthe SVE motor nuclei of the trigeminal, facial, and glossopharyngeal and of the corneal reflex. If especially large, a vestibular schwannoma mayvagus (via the nucleus ambiguus) nerves. Also shown are the origin of compress the trigeminal nerve root and result in a hemifacial sensoryGVE preganglionic parasympathetic fibers from the superior (to facial loss that may include the oral cavity. Trigeminal neuralgia (tic douloureux)nerve) and inferior (to glossopharyngeal nerve) salivatory nuclei and is an intense, sudden, intermittent pain emanating from the area of thefrom the dorsal motor vagal nucleus. Their respective ganglia are indi- cheek, oral cavity, or adjacent parts of the nose (distribution of V2 orcated as well as the structures innervated by postganglionic fibers aris- V3, see also Figure 7-7 on page 184).ing from each. The SVE functional component specifies cranial nervemotor nuclei that innervate head muscles that arose, embryologically, Tumors (such as chordoma or vestibular schwannoma), trauma, orfrom pharyngeal arches. Muscles innervated by the trigeminal nerve (V) meningitis may damage the VIIth nerve, resulting in 1) an ipsilateral fa-come from the 1st arch, those served by the facial nerve (VII) from the cial palsy (or Bell palsy); 2) loss of taste from the ipsilateral two-thirds2nd arch; the stylopharyngeal muscle originates from the 3rd arch and of the tongue; and (3) decreased secretion from the ipsilateral lacrimal,is innervated by the glossopharyngeal nerve (IX), and the muscles de- nasal, and sublingual and submandibular glands. Injury distal to therived from the 4th arch are served by the vagus nerve (X). chorda tympani produces only an ipsilateral facial palsy. A paralysis of the muscles on one side of the face with no paralysis of the extremities Neurotransmitters: The transmitter found in the cells of cra- is a facial hemiplegia. On the other hand, intermittent and involuntarynial nerve motor nuclei, and in their peripheral endings, is acetyl- contraction of the facial muscles is called hemifacial spasm. One cause ischoline; CGRP is also colocalized in these motor neurons. This compression of the facial root by an artery, most commonly a loop ofsubstance is also present in preganglionic and postganglionic para- the anterior inferior cerebellar artery or its branches. These patientssympathetic neurons. may also have deficits (vertigo, tinnitus, hearing loss) suggesting involve- ment of the adjacent vestibulocochlear nerve. Clinical Correlations: Patients with myasthenia gravis frequentlyhave oropharyngeal symptoms and complications that result in Because of their common origin from NuAm, adjacent exit from thedysarthria, and dysphagia. These individuals have difficulty chewing and medulla, and passage through the jugular foramen, the IXth and Xthswallowing, their jaw may hang open, and the mobility of facial mus- nerves may be damaged together (as in amyotrophic lateral sclerosis or incles is decreased. Imparied hearing (weakness of tensor tympani) and syringobulbia). The results are dysarthria, dysphagia, dyspnea, loss of tastehyperacusis (weakness of stapedius) may also be present. from the ipsilateral caudal tongue, and loss of the gag reflex, but no sig- nificant autonomic deficits. Bilateral lesions of the Xth nerve are life- Lesions of the Vth nerve (as in meningiomas or trauma) result in 1) loss threatening because of the resultant total paralysis (and closure) of theof pain, temperature, and touch on the ipsilateral face and in the oral muscles in the vocal folds (vocalis muscle).and nasal cavities; 2) paralysis of ipsilateral masticatory muscles ( jaw de- AbdNu Abducens nucleus Abbreviations ALS Anterolateral system BP Basilar pons SpTNu Spinal trigeminal nucleus Dorsal motor nucleus of vagus SpTTr Spinal trigeminal tractDVagNu Facial nerve SSNu Superior salivatory nucleus FacNr Facial nucleus TecSp Tectospinal tract FacNu Glossopharyngeal nerve TriMoNu Trigeminal motor nucleus GINr Hypoglossal nucleus TriNr Trigeminal nerve HyNu Inferior salivatory nucleus VagNr Vagus nerve ISNu Mesencephalic nucleus MesNu Medial lemniscus Ganglia ML Medial longitudinal fasciculus MLF Nucleus ambiguus 1 Pterygopalatine NuAm Principal (chief ) sensory nucleus 2 Submandibular PSNu 3 Otic 4 Terminal and/or intramural Review of Blood Supply to TriMoNu, FacNu, DMNu and NuAm, and the Internal Course of Their Fibers STRUCTURES ARTERIES TriMoNu and Trigeminal Root long circumferential branches of basilar (see Figure 5–21) FacNu and Internal Genu long circumferential branches of basilar (see Figure 5–21) DMNu and NuAm branches of vertebral and posterior inferior cerebellar (see Figure 5–14)

Motor Pathways 203 Cranial Nerve Efferents (V, VII, IX, and X)Position of Nucleusand InternalRoute of FibersTriMotNu MesNu Motor root Structures Innervated PSNu of TriNr MLF Masticatory muscles and TecSp Motor root TriMotNu tensor tympani, of TriNr tensor veli palatini, ALS mylohyoid, ML digastric (ant. belly) BP Muscles of facial expression,SpTTr & AbdNu and stapedius, buccinator, SpTNu FacNu stylohyoid, platysma digastric (post. belly) MLF SSNu FacNr AbdNu ISNu GINr 1 SSNu NuAm Lacrimal gld.; mucous ML FacNr membranes of nose FacNu and mouth 2 Submandibular and sublingual glds.DVagNu VagNr HyNu DVagNu 3 MLF TecSp VagNr 4 Parotid gld. NuAm SpTTr and Stylopharyngeus ML SpTNu Striated mus. of pharynx, larynx, esophagus Thoracic and abdomnal viscera; smooth and cardiac muscle; glandular epithelium

204 Synopsis of Functional Components, Tracts, Pathways, and Systems Spinocerebellar Tracts7–17 The origin, course, and distribution pattern of fibers to the bellar fibers, in their mossy fiber terminals in the cerebellar cortex, andcerebellar cortex and nuclei from the spinal cord (posterior [dorsal] in their collateral branches that innervate the cerebellar nuclei.and anterior [ventral] spinocerebellar tracts, rostral spinocerebellarfibers) and from the external cuneate nucleus (cuneocerebellar Clinical Correlations: Lesions, or tumors, that selectively dam-fibers). Also illustrated is the somatotopy of those fibers originating age only spinocerebellar fibers are rarely, if ever, seen in humans. Thefrom the spinal cord. These fibers enter the cerebellum via the resti- ataxia one might expect to see in patients with a spinal cord hemisectionform body, the larger portion of the inferior cerebellar peduncle, or (as in the Brown-Sequard syndrome) is masked by the hemiplegia resultingin relationship to the superior cerebellar peduncle. After these fibers from the concomitant damage to lateral corticospinal (and other) fibers.enter the cerebellum, collaterals are given off to the cerebellar nucleiwhile the parent axons of spinocerebellar and cuneocerebellar fibers Friedreich ataxia (hereditary spinal ataxia) is an autosomal recessive dis-pass on to the cortex, where they end as mossy fibers in the graunular order the symptoms of which usually appear between 8 and 15 yearslayer. Although not shown here, there are important ascending spinal of age. There is degeneration of anterior and posterior spinocerebellarprojections to the medial and dorsal accessory nuclei of the inferior tracts plus the posterior columns and corticospinal tracts. Degenera-olivary complex (spino-olivary fibers). The accessory olivary nuclei tive changes are also seen in Purkinje cells in the cerebellum, in poste-(as well as the principal olivary nucleus) project to the cerebellar cor- rior root ganglion cells, in neurons of the Clarke column, and in sometex and send collaterals into the nuclei (see Figure 7-18 on page 206). nuclei of the pons and medulla. The axial and appendicular ataxia seen in these patients correlates partially with the spinocerebellar degener- Neurotransmitters: Glutamate (ϩ) is found in some spinocere- ation and also partially with proprioceptive losses via the degeneration of posterior column fibers. Abbreviations ACNu Accessory (external or lateral) cuneate PSCT Posterior (dorsal) spinocerebellar tract nucleus PSNu Principal (chief ) sensory nucleus of ALS Anterolateral system trigeminal nerve AMV Anterior medullary velum Py Pyramid ASCT Anterior (ventral) spinocerebellar tract RB Restiform body Cerebellum RSCF Rostral spinocerebellar fibers Cbl Cerebellar nuclei RuSp Rubrospinal tractCblNu Cuneocerebellar fibers Sacral representation CCblF Dorsal nucleus of Clarke S Spinal border cells DNuC Flocculonodular lobe SBC Superior cerebellar peduncle Intermediate zone SCP Spinal trigeminal nucleus FNL Lumbar representation SpTNu Spinal trigeminal tract IZ Mesencephalic nucleus SpTTr Thoracic representation L Medial lemniscus Trigeminal motor nucleus Posterior (dorsal) root ganglion T Vestibular nucleiMesNu TriMoNu ML PRG VesNu Review of Blood Supply to Spinal Cord Grey Matter, Spinocerebellar Tracts, RB, and SCP STRUCTURES ARTERIES Spinal Cord Grey PSCT and ASCT in Cord branches of central artery (see Figure 5–6) RB penetrating branches of arterial vasocorona (see Figure 5–6) SCP posterior inferior cerebellar (See Figure 5–14) long circumferential branches of basilar and superior Cerebellum cerebellar (see Figure 5–21) posterior and anterior inferior cerebellar and superior cerebellar

Cerebellum and Basal Nuclei (Ganglia) 205 Spinocerebellar TractsPosition of SCPASCT AMV SCP MesNu TriMoNu ML PSNu ASCT Lobules II-IV Lobules II-IV on SCPLobule V Lobule Ant. V Lobe Recrossing ASCT fibers in Cbl CblNu CblNu RB RB FNL CCblF Post. Lobe ACNu Lobule VIII PRG Lobule VIII PSCT RSCF DNuC Somatotopy Position Lamina VII PRG VesNu RB at C4-C8 Py ASCT SpTTr & Nu ASCT Intermediate zone (IZ) ALS + RuSp and \"spinal border\" cells (SBC) PSCT T DNuC ASCT L PSCT S L IZ T ASCT SBC

206 Synopsis of Functional Components, Tracts, Pathways, and SystemsPontocerebellar, Reticulocerebellar, Olivocerebellar, Ceruleocerebellar, Hypothalamocerebellar, and Raphecerebellar Fibers7–18 Afferent fibers to the cerebellum from selected brainstem ar- ticotropin (ϩ)-releasing factor are present in many olivocerebellareas and the organization of corticopontine fibers in the internal capsule fibers. Ceruleocerebellar fibers contain noradrenalin, histamine isand crus cerebri as shown here. The cerebellar peduncles are also indi- found in hypothalamocerebellar fibers, and some reticulocerebellarcated. Pontocerebellar axons are mainly crossed, reticulocerebellar fibers contain enkephalin. Serotonergic fibers to the cerebellum arisefibers may be bilateral (from RetTegNu) or mainly uncrossed (from from neurons found in medial areas of the reticular formation (openLRNu and PRNu), and olivocerebellar fibers (OCblF) are exclusively cell in Figure 7–18) and, most likely, from some cells in the adjacentcrossed. Raphecerebellar, hypothalamocerebellar, and ceruleocerebel- raphe nuclei.lar fibers are, to varying degrees, bilateral projections. Although all af-ferent fibers to the cerebellum give rise to collaterals to the cerebellar Clinical Correlations: Common symptoms seen in patients withnuclei, those from pontocerebellar axons are relatively small, having lesions involving nuclei and tracts that project to the cerebellum arecomparatively small diameters. Olivocerebellar axons end as climbing ataxia (of trunk or limbs), an ataxic gait, dysarthria, dysphagia, and dis-fibers, reticulocerebellar and pontocerebellar fibers as mossy fibers, and orders of eye movement such as nystagmus. These deficits are seen inhypothalamocerebellar and ceruleocerebellar axons end in all cortical some hereditary diseases (such as olivopontocerebellar degeneration, ataxialayers. These latter fibers have been called multilayered fibers in the lit- telangiectasia, or hereditary cerebellar ataxia), in tumors (brainstemerature because they branch in all layers of the cerebellar cortex. gliomas), in vascular diseases (lateral pontine syndrome), or in other con- ditions such as alcoholic cerebellar degeneration or pontine hemorrhages Neurotransmitters: Glutamate (ϩ) is found in corticopontine (see Figure 7-19 on page 208 for more information on cerebellar le-projections and in most pontocerebellar fibers. Aspartate (ϩ) and cor- sions). Abbreviations AntLb Anterior limb of internal capsule PonNu Pontine nuclei CblNu Cerebellar nuclei PO Principal olivary nucleusCerCblF Ceruleocerebellar fibers CPonF Cerebropontine fibers PPon Parietopontine fibers PRNu Paramedian reticular nuclei CSp Corticospinal fibers DAO Dorsal accessory olivary nucleus Py Pyramid FPon Frontopontine fibers RB Restiform body Hyth Hypothalamus RCblF Reticulocerebellar fibersHythCblF Hypothalamocerebellar fibers RetLenLb Retrolenticular limb of internal capsule RNu Red nucleus IC Internal capsule RetTegNu Reticulotegmental nucleus LoCer Nucleus (locus) ceruleus SCP Superior cerebellar peduncle LRNu Lateral reticular nucleus SubLenLb Sublenticular limb of internal capsule MAO Medial accessory olivary nucleus SN Substantia nigra MCP Middle cerebellar peduncle TPon Temporopontine fibers ML Medial lemniscus Number Key NuRa Raphe nuclei OCblF Olivocerebellar fibers 1 Nucleus raphe, pontis OPon Occipitopontine fibers 2 Nucleus raphe, magnus PCbIF Pontocerebellar fibers 3 Raphecerebellar fibers PostLb Posterior limb of internal capsuleReview of Blood Supply to Precerebellar Relay Nuclei in Pons and Medulla, MCP, and RB STRUCTURES ARTERIESPontine TegmemtumBasilar Pons long circumferential branches of basilar plus some from superiorMedulla RetF and IO cerebellar (see Figure 5–21)MCPRB paramedian and short circumferential branches of basilar (See Figure 5–21) branches of vertebral and posterior inferior cerebellar (see Figure 5–14) long circumferential branches of basilar and branches of anterior inferior and superior cerebellar (see Figure 5–21) posterior inferior cerebellar (see Figure 5–14)

Cerebellum and Basal Nuclei (Ganglia) 207 Pontocerebellar, Reticulocerebellar, Olivocerebellar, Ceruleocerebellar, Hypothalamocerebellar, and Raphecerebellar FibersPosition of Associated Tracts and Nuclei AntLb IC Hyth (FPon) PostLb (PPon)SubLenLb (TPon)RetLenLb (OPon) CPonF HythCblF LoCer RetTegNu CerCblF ML RNu SCP MCP SN PPon NuRa PonNu 1 OPon PCblF 2 TPon 3 CblNu FPon OCblF RBRetTegNu RCblF MCP DAO LRNu ML PCblF PRNu CPonF PO CSp PonNu PRNu MAO RBOCblF LRNu PO Py OCblF CerCblF PCblF

208 Synopsis of Functional Components, Tracts, Pathways, and SystemsCerebellar Cortioconuclear, Nucleocortical, and Corticovestibular Fibers7–19 Cerebellar corticonuclear fibers arise from all regions of the Lesions involving midline structures (vermal cortex, fastigial nu-cortex and terminate in an orderly (mediolateral and rostrocaudal) se- clei) and/or the flocculonodular lobe result in truncal ataxia (titubationquence in the ipsilateral cerebellar nuclei. For example, corticonuclear or tremor), nystagmus, and head tilting. These patients may also have afibers from the vermal cortex terminate in the fastigial nucleus, those wide-based (cerebellar) gait, are unable to walk in tandem (heel to toe),from the intermediate cortex terminate in the emboliform and globo- and may be unable to walk on their heels or on their toes. Generally,sus nuclei, and those from the lateral cortex terminate in the dentate nu- midline lesions result in bilateral motor deficits affecting axial andcleus. Also, cerebellar corticonuclear fibers from the anterior lobe typ- proximal limb musculature.ically terminate in more rostral regions of these nuclei while those fromthe posterior lobe terminate more caudally. Cerebellar corticovestibu- Damage to the intermediate and lateral cortices and the globose,lar fibers originate primarily from the vermis and flocculonodular lobe, emboliform, and dentate nuclei results in various combinations of theexit the cerebellum via the juxtarestiform body, and end in the ipsilat- following deficits: dysarthria, dysmetria (hypometria, hypermetria), dysdi-eral vestibular nuclei. These projections arise from Purkinje cells. adochokinesia, tremor (static, kinetic, intention), rebound phenomenon, un- steady and wide-based (cerebellar) gait, and nystagmus. One of the more Nucleocortical processes originate from cerebellar nuclear neurons commonly observed deficits in patients with cerebellar lesions is an in-and pass to the overlying cortex in a pattern that basically reciprocates tention tremor, which is best seen in the finger-nose test. The finger-to-fin-that of the corticonuclear projection; they end as mossy fibers. Some ger test is also used to demonstrate an intention tremor and to assessnucleocortical fibers are collaterals of cerebellar efferent axons. The cerebellar function. The heel-to-shin test will show dysmetria in the lowercerebellar cortex may influence the activity of lower motor neurons extremity. If the heel-to-shin test is normal in a patient with his/herthrough, for example, the cerebellovestibular-vestibulospinal route. eyes open, the cerebellum is intact. If this test is repeated in the same patient with eyes closed and is abnormal, this would suggest a lesion in Neurotransmitters: Gamma-aminobutyric acid (GABA) (Ϫ) is the posterior column-medial lemniscus system.found in Purkinje cells and is the principal transmitter substance pres-ent in cerebellar corticonuclear and corticovestibular projections. Cerebellar damage in intermittent and lateral areas (nuclei or cor-However, taurine (Ϫ) and motilin (Ϫ) are also found in some Purk- tex plus nuclei) causes movement disorders on the side of the lesioninje cells. GABA-ergic terminals are numerous in the cerebellar nuclei with ataxia and gait problems on that side; the patient may tend to falland vestibular complex. Some of the glutamate-containing mossy toward the side of the lesion. This is because the cerebellar nuclei pro-fibers in the cerebellar cortex represent the endings of nucleocortical ject to the contralateral thalamus, which projects to the motor cortexfibers that originate from cells in the cerebellar nuclei. on the same side, which projects to the contralateral side of the spinal cord via the corticospinal tract. Other circuits (cerebellorubal- Clinical Correlations: Numerous disease entities can result in rubospinal) and feedback loops (cerebelloolivary-olivocerebellar) fol-cerebellar dysfunction including viral infections (echovirus), hereditary low similar routes. Consequently, the motor expression of unilateraldiseases (see Figure 7–18), trauma, tumors (glioma, medulloblastoma), cerebellar damage is toward the lesioned side because of these doublyocclusion of cerebellar arteries (cerebellar stroke), arteriovenous malfor- crossed pathways.mation of cerebellar vessels, developmental errors (such as the Dandy-Walker syndrome or the Arnold-Chiari deformity), or the intake of toxins. Lesions of cerebellar efferent fibers, after they cross the midline inUsually, damage to only the cortex results in little or no dysfunction the decussation of the superior cerebellar peduncle, will give rise tounless the lesion is quite large or causes an increase in intracranial pres- motor deficits on the side of the body (excluding the head) contralat-sure. However, lesions involving both the cortex and nuclei, or only eral to the lesion. This is seen in midbrain lesions such as the Claude syn-the nuclei, will produce obvious cerebellar signs. drome. Abbreviations CorNu Corticonuclear fibers MVesSp Medial vestibulospinal tract CorVes Corticovestibular fibers MVNU Medial vestibular nucleus Flocculus NL, par Lateral cerebellar nucleus, parvocellular Flo Intermediate cortex region IC Inferior (spinal) vestibular nucleus NM, par Medial cerebellar nucleus,InfVesNu Juxtarestiform body parvocellular region JRB Lateral cortex NuCor Nucleocortical fibers LC Lateral vestibulospinal tract SVNu Superior vestibular nucleus LVesSp Lateral vestibular nucleus Vermal cortex LVNu Medial longitudinal fasciculus VC MLF Review of Blood Supply to Cerebellum and Vestibular Nuclei STRUCTURES ARTERIES Cerebellar Cortex branches of posterior and anterior inferior cerebellar and superior Cerebellar Nuclei cerebellar Vestibular Nuclei anterior inferior cerebellar and superior cerebellar posterior inferior cerebellar in medulla, long circumferential branches of basilar in pons

Cerebellum and Basal Nuclei (Ganglia) 209Cerebellar Corticonuclear, Nucleocortical, and Corticovestibular Fibers CorNu NuCor VCLC IC CorVes 4 NuCor 32 CorNu 1NL, par JRB NM, par Flo SVNu Nodulus LVNu MLF InfVNu MVNu LVesSp MVesSp Cerebellar Nuclei: 1= Medial (Fastigial) 2= Posterior Interposed (Globose) 3= Anterior Interposed (Emboliform) 4= Lateral (Dentate)

210 Synopsis of Functional Components, Tracts, Pathways, and Systems Cerebellar Efferent Fibers7–20 The origin, course, topography, and general distribution of belloreticular-reticulospinal, 3) cerebellothalamic-thalamocortical-fibers arising in the cerebellar nuclei. Cerebellofugal fibers project to corticospinal, and others. In addition, some direct cerebellospinalseveral thalamic areas (VL and VA), to intralaminar relay nuclei in ad- fibers arise in the fastigial nucleus as well as in the interposed nuclei.dition to the centromedian, and to a number of midbrain, pontine, andmedullary targets. Most of the latter nuclei project back to the cere- Neurotransmitters: Many cells in the cerebellar nuclei containbellum (e.g., reticulocerebellar, pontocerebellar), some in a highly or- glutamate (ϩ), aspartate (ϩ), or gamma-aminobutyric acid (Ϫ). Glu-ganized manner. For example, cerebello-olivary fibers from the den- tamate and aspartate are found in cerebellorubral and cerebellothala-tate nucleus (DNu) project to the principal olivary nucleus (PO), and mic fibers, whereas some GABA-containing cells give rise to cerebel-neurons of the PO send their axons back to the lateral cerebellar cor- lopontine and cerebello-olivary fibers. Some cerebelloreticulartex, with collaterals going to the DNu. projections may also contain GABA. The cerebellar nuclei can influence motor activity through, as ex- Clinical Correlations: Lesions of the cerebellar nuclei result in aamples, the following routes: 1) cerebellorubral-rubrospinal, 2) cere- range of motor deficits depending on the location of the injury. Many of these are described in Figure 7–19 on page 208. Abbreviations ALS Anterolateral system OcNu Oculomotor nucleus AMV Anterior medullary velum PO Principal olivary nucleus Basilar pons BP Cerebello-olivary fibers PonNu Pontine nuclei CblOl Cerebellothalamic fibers RetForm Reticular formation CblTh Cerebellorubral fibers CblRu Crus cerebri RNu Red nucleus Central grey (periaqueductal grey) RuSp Rubrospinal tract CC Centromedian nucleus of thalamus CeGy Corticospinal fibers SC Superior colliculus Dorsal accessory olivary nucleus SCP Superior cerebellar peduncle CM Dentate nucleus (lateral cerebellar nucleus) SCP, Dec Superior cerebellar peduncle, decussation CSp Emboliform nucleus (anterior interposed SN Substantia nigra DAO cerebellar nucleus) SVNu Superior vestibular nucleus DNu Edinger-Westphal nucleus ThCor Thalamocortical fibers ENu Fastigial nucleus (medial cerebellar nucleus) ThFas Thalamic fasciculus Globose nucleus (posterior interposed TriMoNu Trigeminal motor nucleus EWNu cerebellar nucleus) VL Ventral lateral nucleus of thalamus FNu Inferior colliculus VPL Ventral posterolateral nucleus of thalamus GNu Inferior (spinal) vestibular nucleus VSCT Ventral spinocerebellar tract Interstitial nucleus IC Lateral reticular nucleus ZI Zona incertaInfVNu Lateral vestibular nucleus Medial accessory olivary nucleus Number Key INu Medial lemniscus LRNu Medial longitudinal fasciculus 1 Ascending projections to superior LVNu Medial vestibular nucleus colliculus, and possibly ventral lateral and MAO Nucleus of Darkschewitsch ventromedial thalamic nuclei ML 2 Descending crossed fibers from superior MLF cerebellar peduncle MVNuNuDark 3 Uncinate fasciculus (of Russell) 4 Juxtarestiform body to vestibular nuclei 5 Reticular formation Review of Blood Supply to Cerebellar Nuclei and Their Principal Efferent Pathways STRUCTURES ARTERIES Cerebellar Nuclei SCP anterior inferior cerebellar and superior cerebellar long circumferential branches of basilar and superior cerebellar Midbrain Tegmemtum (RNu, CblTh, (see Figure 5–21) CblRu, OcNu) paramedian branches of basilar bifurcation, short circumferential VPL, CM, VL, VA branches of posterior cerebral, branches of superior cerebellar (see Figure 5–27) IC thalamogeniculate branches of posterior cerebral, thalamo- perforating branches of the posteromedial group of posterior cerebral (see Figure 5–38) lateral striate branches of middle cerebral (see Figure 5–38)

Cerebellum and Basal Nuclei (Ganglia) 211 Cerebellar Efferent Fibers CSp VL ThCor CM VPL ThFas Position of SCP, Zl CblTh, and CblRuSCP NuDark, INu, 1 CeGy SC OcNu, EWNu RNu RetForm ML RNu PonNu CblTh & CeGy SVNu CblRu CC SN 2 CblOl 43 LRNu DAODNu FNu PO VSCT IC 5 MAO MLF ENu GNu 5 Cerebellospinal ML 5 fibers SN LVNu SCP, Dec InfVNu AMV MVNu SCP TriMoNu 5 ALS & RuSp ML BP

212 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–21 Blank master drawing for pathways projecting to the cere- bellar cortex, and for efferent projections of cerebellar nuclei. This il- lustration is provided for self-evaluation of understanding of pathways to the cerebellar cortex and from the cerebellar nuclei, for the in- structor to expand on cerebellar afferent/efferent pathways not cov- ered in the atlas, or both.

Cerebellum and Basal Nuclei (Ganglia) 213

214 Synopsis of Functional Components, Tracts, Pathways, and Systems Striatal Connections7–22 The origin, course, and distribution of afferent fibers to, and enkephalinergic cells in the neostriatum (primarily the caudate) andefferent projections from, the neostriatum. These projections are ex- cell loss in the cerebral cortex. Loss of neostriatal cell terminals in thetensive, complex, and in large part, topographically organized; only lateral and medial segments of the globus pallidus correlate, respec-their general patterns are summarized here. Afferents to the caudate tively, with the development of choreiform movements and later withand putamen originate from the cerebral cortex (corticostriate fibers), rigidity and dystonia. Loss of cortical neurons correlate, respectively,from several of the intralaminar thalamic nuclei (thalamostriate), from with personality changes and eventual dementia. Huntington chorea isthe substantia nigra-pars compacta (nigrostriate), and from some of the rapid, unpredictable, and may affect muscles of the extremities, face,raphe nuclei. Neostriatal cells send axons into the globus pallidus (pa- and trunk; abnormal movements seem to flow through the body. Pa-leostriatum) as striopallidal fibers and into the substantia nigra pars tients commonly attempt to mask the abnormal movement by tryingreticulata as a strionigral projection. to make it appear to be part of an intended movement (parakinesia). Neurotransmitters: Glutamate (ϩ) is found in corticostriate Symptoms in Wilson disease (hepatolenticular degeneration) appear infibers, and serotonin is found in raphestriatal fibers from the nucleus persons between 10 to 20 years of age. Copper accumulates in the basalraphe dorsalis. Four neuroactive substances are associated with striatal nuclei (ganglia) and the frontal cortex, with resultant spongy degener-efferent fibers, these being gamma-aminobutyric acid (GABA)(Ϫ), ation in the putamen and cortex. These patients may show athetoiddynorphin, enkephalin(Ϫ), and substance P(ϩ). Enkephalinergic and movements, rigidity and spasticity, dysarthria, dysphagia, contractures, andGABA-ergic striopallidal projections are numerous to the lateral pal- tremor. A unique movement of the hand and/or upper extremity inlidum (origin of pallidosubthalamic fibers), while dynorphin-contain- these patients is called a flapping tremor (asterixis) sometimes describeding terminals are more concentrated in its medial segment (source of as a wing-beating tremor. Copper can also be seen in the corneapallidothalamic fibers). Enkephalin and GABA are also present in stri- (Kayser-Fleischer ring) in these patients.onigral projections to the pars reticulata. Because substance P andGABA are found in striopallidal and strionigral fibers, some of the for- In Parkinson disease (onset at 50 to 60 years of age), there is a pro-mer may be collaterals of the latter. Dopamine is present in nigrostri- gressive loss of dopaminergic cells in the substantia nigra-pars com-atal projection neurons and in their terminals in the neostriatum. pacta, of their terminals in the caudate and putamen, and of their den- drites that extend into the substantia nigra-pars reticulata. Patients Clinical Correlations: Degenerative changes and neuron loss in with Parkinson disease characteristically show a resting tremor (pill-the caudate nucleus and putamen result in movement disorders. Ex- rolling), rigidity (cog wheel or lead pipe), and bradykinesia or hypokinesia.amples are seen in Sydenham chorea (rheumatic chorea), Huntington disease The slowness of movement may also be expressed in speech (dysarthria,(a dominantly inherited disease), and Wilson disease (a genetic error in hypophonia, tachyphonia) and in writing (micrographia). These patientsthe patient’s ability to metabolize copper). In persons with Parkinson have a distinct stooped flexed posture and a festinating gait. Behavioraldisease, a loss of the dopamine-containing cells in the pars compacta of changes are also seen. Parkinson disease and Huntington disease arethe substantia nigra and of their nigrostriatal terminals in the caudate progressive neurodegenerative disorders.nucleus and putamen occurs. Dystonia, a movement disorder seen in some patients with basal nu- Sydenham chorea is a disease usually seen in children between 5 and clei disease, is characterized by increased/sustained muscle contrac-15 years of age, resulting from infection with hemolytic streptococcus. tions that cause twisting of the trunk or extremities resulting in abnor-The choreiform movements are brisk and flowing, irregular, and may in- mal posture. These patients may also have unusual and repetitivevolve muscles of the limbs, face, oral cavity, and trunk. Dystonia may movements of the extremities or of the neck (cervical dystonia or spas-be seen; muscle weakness is common. In most patients, the disease re- modic torticollis). Dystonia may be an inherited progressive disease orsolves following successful treatment of the infection. have other causes and may be seen in children or young adults. The symptoms may initially appear during movements or when talking but Huntington disease is a progressive genetic disorder the symptoms of in later stages may be present at rest.which appear at 35 to 45 years of age. There is loss of GABA-ergic and AbbreviationsCaNu Caudate nucleus SNpc Substantia nigra, pars compactaCorSt Corticostriate fibers SNpr Substantia nigra, pars reticulata Globus pallidus, lateral segment StNig Striatonigral fibers GPL Globus pallidus, medial segment StPal Striatopallidal fibersGPM Nigrostriatal fibers SThNu Subthalamic nucleusNigSt Putamen ThSt Thalamostriatal fibers Raphe nuclei Zona incerta Put Raphestriatal fibers ZIRaNu RaSt Review of Blood Supply to Caudate, Putamen, SN, CC, and IC STRUCTURES ARTERIES Caudate, Putamen and IC medial striate a. for head of caudate and lateral striate SN and CC branches of middle cerebral for Put and IC (see Figure 5–38) paramedian branches of basilar bifurcation, short circumferential branches of posterior cerebral and some from superior cerebellar (see Figure 5–27)

Cerebellum and Basal Nuclei (Ganglia) 215 Striatal Connections Cerebral cortex CorSt CorSt Ca,Nu StPal ThSt NigSt PutIntralaminar StNig StPal CorSt nuclei RaSt GPL NigSt GPM Zl SThNu SNpc SNpr RaNu

216 Synopsis of Functional Components, Tracts, Pathways, and Systems Pallidal Efferents and Nigral Connections7–23 The origin, course, and distribution of efferent projections rons, which give rise to nigrostriatal, nigroamygdaloid, and severalof the globus pallidus (upper illustration), and connections of the sub- other projections; GABA in pars reticulata cells, which give rise to ni-stantia nigra (lower drawing) that were not shown in relation to the grocollicular and nigrothalamic fibers; and glycine in some local circuitpallidum or in Figure 7–22 on page 215. The ansa lenticularis (dashed nigral neurons. Glutamate (ϩ) is found in corticonigral fibers, andline) arches around the internal capsule and passes caudally to join in serotonin (Ϫ) is associated with raphenigral fibers; these latter fibersthe formation of the thalamic fasciculus. Pallidosubthalamic fibers orig- originate primarily from the nucleus raphe dorsalis.inate primarily from the lateral pallidal segment, but pallidothalamicprojections, via the ansa lenticularis and lenticular fasciculus, arise The dopaminergic projections to the frontal cortex, shown here asmainly from its medial segment. The substantia nigra has extensive arising only from SNpc, originates from this cell group as well as fromconnections, the clinically most important being the dopaminergic ni- the immediately adjacent ventral tegmental area. Excessive activity ingrostriatal fibers. The globus pallidus influences motor activity by way neurons comprising this projection may play a partial role in schizo-of pallidothalamic-thalamocortical-corticospinal (and corticonuclear phrenia.[corticobulbar]) pathways. Clinical Correlation: Movement disorders associated with le- Neurotransmitters: Gamma-aminobutyric acid (Ϫ)-containing sions in the neostriatum and substantia nigra are reviewed in Figurecells in the globus pallidus give rise to pallidonigral projections, which 7–22 on page 214. Hemorrhage into, the occlusion of vessels servingend primarily in the substantia nigra-pars reticulata. Although GABA or a tumor within, the subthalamic nucleus will result in violent flail-is also found in some subthalamopallidal axons, this latter projection ing movements of the extremities, a condition called hemiballismus.contains many glutaminergic (ϩ) fibers. Dopamine-containing, GABA Hemiballistic movements are seen contralateral to the lesion because(Ϫ)-containing, and glycine (Ϫ)-containing cells are present in the the motor expression of this lesion is through the corticospinal tract.substantia nigra. Of these, dopamine is found in pars compacta neu- Lesions confined to the globus pallidus, as in hemorrhage of lenticu- lostriate arteries, may result in hypokinesia and rigidity without tremor. AbbreviationsAmyNig Amygdalonigral fibers PedPonNu Pedunculopontine nucleusAmyNu Amygdaloid nucleus (complex) Put PutamenAnLent Ansa lenticularis Raphe nuclei Caudate nucleus RaNu Superior colliculus CaNu Centromedian nucleus of thalamus SC Substantia nigra, pars compacta CM Corticonigral fibers Substantia nigra, pars reticulata Corticospinal fibers SNpc Subthalamic fasciculus CorNig Globus pallidus, lateral segment SNpr Subthalamonigral fibers CSp Globus pallidus, medial segment SThFas Subthalamic nucleus GPL Lenticular fasciculus (H2) SThNig Thalamocortical fibers GPM Nigroamygdaloid fibers SthNu Thalamic fasciculus (H1) Nigrocollicular fibers ThCor Ventral anterior nucleus of thalamus LenFas Nigrotectal fibers ThFas Ventral lateral nucleus of thalamusNigAmy Nigrosubthalamic fibers Ventromedial nucleus of thalamus NigCol Nigrothalamic fibers VA Zona incerta NigTec Pallidonigral fibers VL NigSTh VM ZI NigTh PalNig Review of Blood Supply to Pallidum, Subthalamic Area, and SN STRUCTURES ARTERIES GPM/GPL lateral striate branches of middle cerebral and branches of anterior choroidal (see Figure 5–38) SThNu posteromedial branches of posterior cerebral and posterior communicating (see Figure 5–38) SN branches of basilar bifurcation, medial branches of posterior cerebral and posterior communicating, short circumferential branches of posterior cerebral (see Figure 5–27)

Cerebellum and Basal Nuclei (Ganglia) 217Pallidal Efferents and Nigral Connections Motor cortex ThCor Intralaminar CaNu Put nuclei VA VL ThFas LenFas CSp GPL ZlForel's Field H GPM SThNu SThFas SThNig and AnLent Nig Sth PalNig SNpr SNpc PedPonNu CorNig Nigral efferents Ca,Nu to frontal cortex NigTh VM GPL Zl VL Put GPM SthNu SC NigAmy and AmyNig Nigral efferents to SNpr olfactory tubercle SNpc and bed nucleus ofNigCol the stria terminalis RaNu AmyNu

218 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–24 Blank master drawing for connections of the basal ganglia. This illustration is provided for self-evaluation of understanding of basal ganglia connections, for the instructor to expand on basal nuclei pathways not covered in this atlas, or both.

Cerebellum and Basal Nuclei (Ganglia) 219

220 Synopsis of Functional Components, Tracts, Pathways, and Systems Pupillary Pathways7–25 The origin, course, and distribution of fibers involved in the ducing a bitemporal hemianopsia) or the uncrossed fibers in the right (orpathway for the pupillary light reflex. In addition, the pathway for sym- left) side of the optic chiasm. These lateral lesions produce a right (orpathetic innervation of the dilator muscle of the iris is also depicted. The left) nasal hemianopsia.pathway from the midbrain reticular formation to the intermediolateralcell column may also have a multisynaptic component, with relay sta- Optic (geniculocalcarine) radiations (see Figures 7–26 and 7–27 ontions in the pontine and medullary reticular formations. Postganglionic pages 222 and 223) may pass directly caudal to the upper lip (cuneus)sympathetic fibers to the head originate from the superior cervical gan- of the calcarine sulcus or follow an arching route (the Meyer, or Meyer-glion. Although not shown, descending projections to the intermedio- Archambault loop) through the temporal lobe to the lower bank (linguallateral cell column also originate from various hypothalamic areas and gyrus) of the calcarine sulcus. Temporal lobe lesions involving thenuclei (hypothalamospinal fibers), some of which receive retinal input. Meyer-Archambault loop, or involving fibers entering the lingual gyrus, can produce a homonymous superior quadrantanopia. A homonymous Neurotransmitters: Acetylcholine is the transmitter found in inferior quandrantanopia is seen in patients with damage to upper (pari-the preganglionic and postganglionic autonomic fibers shown in this il- etal) parts of the geniculocalcarine radiations or to these fibers as theylustration. In addition, N-acetylaspartylglutamate is present in some enter the cuneus.retinal ganglion cells (retinogeniculate projections). Damage to the visual cortex adjacent to the calcarine sulcus (distal Clinical Correlations: Total or partial blindness in one or both posterior cerebral artery occlusion) results in a right (or left) homony-eyes may result from a variety of causes (such as gliomas, meningiomas, mous hemianopsia. With the exception of macular sparing, this deficit isstrokes, aneurysms, infections, and demyelinating diseases); lesions may the same as that seen in optic tract lesions.occur at any locus along the visual pathway. A complete lesion (for ex-ample, a transection) of the optic nerve will result in blindness and loss Vascular lesions (as in the lateral medullary syndrome), tumors (suchof the pupillary light reflex (direct response) in the eye on the injured as brainstem gliomas), or syringobulbia may interrupt the descending pro-side and a loss of the pupillary light reflex (consensual response) in the jections from hypothalamus (hypothalamospinal fibers) and midbrainopposite eye when shining a light in the blind eye. On the other hand, shin- to the intermediolateral cell column at upper thoracic levels. This maying a light in the normal eye will result in a pupillary light reflex (direct result in a Horner syndrome (ptosis, miosis, and anhidrosis) on the ipsilat-response) in that eye and a consensual response in the blind eye. A pi- eral side. The enophthalmos (a slight sinking of the eyeball into the or-tuitary adenoma may damage the crossing fibers in the optic chiasm (pro- bit) frequently mentioned in relation to Horner syndrome is not really very apparent in afflicted patients. Abbreviations CC Crus cerebri PoCom Posterior commissureCilGang Ciliary ganglion PrTecNu Pretectal nucleus Edinger-Westphal nucleus Pulvinar nuclear complex EWNu Intermediolateral cell column PulNu Reticular formation ILCC Lateral geniculate nucleus RetF Red nucleus LGNu Medial geniculate nucleus RNu Superior colliculus Medial lemniscus SC Superior colliculus, brachium MGNu Oculomotor nerve SC,Br Superior cervical ganglion ML Optic chiasm Substantia nigra Optic nerve SCerGang White ramus communicans OcNr Optic tract SN OpCh OpNr WRCom OpTr Review of Blood Supply to OpTr, MGB, LGB, SC, and Midbrain Tegementum, Including PrTecNu STRUCTURES ARTERIES OpTr MGNu, LGNu anterior choroidal (see Figure 5–38) SC and PrTecNu thalamogeniculate branches of posterior cerebral (see Figure 5–38) long circumferential branches (quadrigeminal) of posterior cerebral, Midbrain Tegmentum posterior choroidal, and some from superior cerebellar (to SC) (see Figures 5–27 and 5–38) paramedian branches of basilar bifurcation, medial branches of posterior cerebral and posterior communicating, short circumferential branches of posterior cerebral (see Figure 5–27)

Optic, Auditory, and Vestibular Systems 221 Pupillary Pathways Dilator muscles of iris Sphincter mus. of iris Sphincter mus. of ciliary body Ganglion cells of retinaCilGang OpNr OpCh OcNr OpTr OcNr Midbrain CC Via blood RetF vessels RNu LGNu ML SN SCerGangLGNu MGNu MGNu SC,Br SC SC,Br PulNu PulNu PrTecNu PoCom HySpF EWNu ILCC Spinal nerve WRCom Thoracic cord T1-T3 Anterior root

222 Synopsis of Functional Components, Tracts, Pathways, and Systems Visual Pathways Visual fields Retinae Ganglion cells of retina LGNu Laminae mc 1 Optic nerve 2 Optic chiasm 3 Optic tract Substantia nigra pc 4 5 Medial lemniscus Meyer's Loop 6 Red nucleus Crus cerebri MGNu MGNu LGNu SC,Br SC,Br Optic radiations PulNu PulNu (in retrolenticular Sup. colliculus Oculomotor Nu. limb of internal Pretectal Nu. Edinger-Westphal Nu. capsule) Cuneus Lingual gyrus CalSul7–26 The origin, course, and distribution of the visual pathway are Neurotransmitters: Cholecystokinin (ϩ) is present in someshown. Uncrossed retinogeniculate fibers terminate in laminae 2, 3, geniculocalcarine fibers. N-acetylaspartylglutamate is found in someand 5, while crossed fibers end in laminae 1, 4, and 6. Geniculocal- retinogeniculate fibers, and in some lateral geniculate and visual cor-carine fibers arise from laminae 3 through 6. Retinogeniculate and tex neurons.geniculocalcarine pathways are retinotopically organized (see facing Clinical Correlations: Deficits seen following lesions of variouspage). parts of visual pathways are described in Figure 7-25 on p. 220. Abbreviations CalSul Calcarine sulcus MGNu Medial geniculate nucleus LGNu Lateral geniculate nucleus PulNu Pulvinar nuclear complex Magnocellular SC,Br Superior colliculus, brachium mc Parvocellular pc

Optic, Auditory, and Vestibular Systems 223 Visual Pathways LEFT RIGHT B' A' Visual fields C' BA D' Orientation fo all Levels overlapped for M Except Visual Cortex both eyes CD Dor Dor Lat Med Lat B' A' Ven Ven BA BA MVisual fields for M individuaol eyes CD D' C D C' DC C' D' C M B' DRetinae AB M A B A' DC C' D' C M B' DOptic nerves AB M A B A' Optic chiasm A Optic B M tracts M C B' A' D Lateral D' geniculate C' MD nuclei CM A D' C' B C' A' B' C D' D Optic radiations MM B B' A A' D' Primary visual cortex C'MD CM CuneusMA Calcarine sulcus BM A' B' Lingual gyrus7–27 Semidiagrammatic representation of the retinographic Clinical Correlations: Deficits seen following lesions of various parts of the visual pathway are described in Figure 7-25 on p. 220.arrangement of visual and retinal fields, and the subsequent topogra-phy of these projections throughout the visual system. Upper-case let-ters identify the binocular visual fields (A, B, C, D), the macula (M),and the monocular visual fields (AЈ, BЈ, CЈ, DЈ).

224 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–28 Blank master drawing of visual pathways. This illustration is provided for self-evaluation of visual pathway understanding, for the instructor to expand on aspects of the visual pathways not covered in the atlas, or both.

Optic, Auditory, and Vestibular Systems 225

226 Synopsis of Functional Components, Tracts, Pathways, and Systems Auditory Pathways7–29 The origin, course, and distribution of the fibers collectively hearing loss and conduction hearing loss, and to lateralize the deficit. Incomposing the auditory pathway. Central to the cochlear nerve and the Weber test, a tuning fork (512 Hz) is applied to the midline of the fore-dorsal and ventral cochlear nuclei this system is, in a general sense, bi- head or apex of the skull. In the normal patient, the sound (conductedlateral and multisynaptic, as input is relayed through brainstem nuclei through the bones of the skull) is heard the same in each year. In the caseen route to the auditory cortex. Synapse and crossing (or re-crossing) of nerve deafness (lesions of the cochlea or cochlear nerve), the sound is bestof information can occur at several levels in the neuraxis. Conse- heard in the normal ear, while in conductive deafness, the sound is best heardquently, central lesions rarely result in a total unilateral hearing loss. in the abnormal ear. In the Rinne test, a tuning fork (512 Hz) is placedThe medial geniculate body is the thalamic station for the relay of au- against the mastoid process. When the sound is no longer perceived, theditory information to the temporal cortex. prongs are moved close to the external acoustic meatus, where the sound is again heard; this is the situation in a normal individual (positive Rinne Neurotransmitters: Glutamate (ϩ) and aspartate (ϩ) are found in test). In middle ear disease, the sound is not heard at the external meatussome spiral ganglion cells and in their central terminations in the cochlear after it has disappeared from touching the mastoid bone (abnormal or neg-nuclei. Dynorphin-containing and histamine-containing fibers are also ative Rinne test). Therefore, a negative Rinne test signifies conductivepresent in the cochlear nuclei; the latter arises from the hypothalamus. A hearing loss in the ear tested. In mild nerve deafness (cochlea or cochlearnoradrenergic projection to the cochlear nuclei and to the inferior col- nerve lesions), the sound is heard by application of the tuning fork to theliculus originates from the nucleus locus ceruleus. Cells in the superior mastoid and movement to the ear (the Rinne test is positive). In severeolive that contain cholecystokinin and cells in the nuclei of the lateral lem- nerve deafness, the sound may not be heard at either position.niscus that contain dynorphin project to the inferior colliculus. Althoughthe olivocochlear bundle is not shown, it is noteworthy that enkephalin is In addition to hearing loss and tinnitus, large vestibular schwannomasfound in some of the cells that contribute to this projection. may result in other signs and symptoms. These include nausea, vomiting and ataxia/unsteady gait (vestibular root involvement), weakness of fa- Clinical Correlations: There are three categories of deafness. cial muscles (facial root involvement), and altered sensation from theConductive deafness is due to problems of the external ear (obstruction face and a diminished corneal reflex (trigeminal root involvement).of the canal, wax build-up) or disorders of the middle ear (otitis media, There may also be general signs associated with increased intracranialotosclerosis). Nerve deafness (sensorineural hearing loss) results from diseases pressure (lethargy, headache, and vomiting).involving the cochlea or the cochlear portion of the vestibulocochlearnerve. Central deafness results from damage to the cochlear nuclei or Central lesions (as in gliomas or vascular occlusions) rarely producepossibly their central connections. unilateral or bilateral hearing losses that can be detected, the possible exception being pontine lesions that damage the trapezoid body and Hearing loss may result from trauma (such as fracture of the petrous nuclei. Injury to central auditory pathways and/or primary auditorybone), demyelinating diseases, tumors, certain medications (strepto- cortex may diminish auditory acuity, decrease the ability to hear cer-mycin), or occlusion of the labyrinthine artery. Damage to the cochlear tain tones, or make it difficult to precisely localize sounds in space. Pa-part of the VIIIth nerve (as in vestibular schwannoma) results in tinnitus tients with damage to secondary auditory cortex in the temporal lobeand/or deafness (partial or total) in the ipsilateral ear. High-frequency experience difficulty in understanding and/or interpreting sounds (au-hearing losses are most common. ditory agnosia). The Weber test and Rinne test are used to differentiate between neural AbbreviationsAbdNu Abducens nucleus MLF Medial longitudinal fasciculus ACNu Anterior (ventral) cochlear nucleus PCNu Posterior (dorsal) cochlear nucleus ALS Anterolateral system PulNu Pulvinar nuclear complex CC Crus cerebri Restiform body FacNu Facial nucleus RB Reticular formation IC Inferior colliculus RetF Superior colliculus IC,Br Inferior colliculus, brachium Superior cerebellar peduncle, decussation Inferior colliculus, commissure SC Superior oliveIC,Com Internal capsule, sublenticular limb SCP,Dec Spiral ganglion IC,SL Lateral geniculate nucleus Spinal trigeminal tract LGNu Lateral lemniscus SO Trapezoid body LL Lateral lemniscus, nucleus SpGang Trapezoid nucleus LL,Nu Medial geniculate nucleus Transverse temporal gyrus Medial lemniscus SpTTr MGNu TrapB ML TrapNu TTGy Review of Blood Supply to Cochlear Nuclei, LL (and associated structures), Pontine Tegmentum, IC, and MGB STRUCTURES ARTERIES Cochlear Nuclei LL, SO in Pons anterior inferior cerebellar (see Figure 5–14) IC long circumferential branches of basilar (see Figure 5–21) long circumferential branches (quadrigeminal branches) of basilar, MGB superior cerebellar (see Figure 5–27) thalamogeniculate branches of posterior cerebral (see Figure 5–38)

Optic, Auditory, and Vestibular Systems 227 Auditory Pathways PulNu LGNu MGNuTTGY IC,SL IC,Br Positions of LL and Related Structures SC IC,Com IC,Com IC IC LL ALS LL,Nu LL LL CC ML FacNu PCNu SCP,Dec SO RetF FacNu SpTTr LL ALS SO ML TrapNu TrapB RetF ACNu SpGang PCNu ACNu Hair cells in organ of corti LL RB LL SO ML TrapB

228 Synopsis of Functional Components, Tracts, Pathways, and Systems Vestibular Pathways7–30 The origin, course, and distribution of the main afferent and Clinical Correlations: The vestibular part of the VIIIth nerve canefferent connections of the vestibular nuclei (see also Figures 7–13, be damaged by many of the same insults that affect the cochlear nerve7–19, and 7–20). Primary vestibular afferent fibers may end in the (see Figure 7–29). Damage to vestibular receptors of the vestibular nervevestibular nuclei or pass to cerebellar structures via the juxtarestiform commonly results in vertigo. The patient may feel that his or her body isbody. Secondary vestibulocerebellar axons originate from the vestibu- moving (subjective vertigo) or that objects in the environment are movinglar nuclei and follow a similar path to the cerebellum. Efferent projec- (objective vertigo). They have equilibrium problems, an unsteady (ataxic)tions from the vestibular nuclei also course to the spinal cord through gait, and a tendency to fall to the lesioned side. Deficits seen in nerve le-vestibulospinal tracts (see Figure 7–13), as well as to the motor nuclei sions—or in brainstem lesions involving the vestibular nuclei, includeof the oculomotor, trochlear, and abducens nerves via the MLF. Cere- nystagmus, nausea, and vomiting, along with vertigo and gait problems. Abellar structures most extensively interconnected with the vestibular facial palsy may also appear in concert with VIIIth nerve damage in pa-nuclei include the lateral regions of the vermal cortex of anterior and tients who have a vestibular schwannoma. These vestibular deficits, alongposterior lobes, the flocculonodular lobe, and the fastigial (medial) with partial or complete deafness, are seen in Ménière disease.cerebellar nucleus. Lesions of those parts of the cerebellum with which the vestibular Neurotransmitters: Gamma-aminobutyric (Ϫ) is the transmit- nerve and nuclei are most intimately connected (flocculonodular lobe andter associated with many cerebellar corticovestibular fibers and their fastigial nucleus) result in nystagmus, truncal ataxia, ataxic gait, and aterminals in the vestibular complex; this substance is also seen in cere- propensity to fall to the injured side. The nystagmus seen in patients withbellar corticonuclear axons. The medial vestibular nucleus also has vestibular lesions and the internuclear ophthalmoplegia seen in some patientsfibers that are dynorphin-positive and histamine-positive; the latter with multiple sclerosis are signs that correlate with the interruption ofarise from cells in the hypothalamus. vestibular projections to the motor nuclei of III, IV, and VI via the MLF. Abbreviations AbdNu Abducens nucleus PAG Periaqueductal gray ALS Anterolateral system Py Pyramid Cbl Cerebellar RB Restiform body Cerebellar corticovestibular fibers Red nucleusCbl-CoVes Cerebellar nuclei RNu Superior colliculus CblNu Hypoglossal nucleus SC Superior cerebellar peduncle, HyNu Inferior colliculus decussation IC Inferior (spinal) vestibular nucleus SCP,Dec Substantia nigra InfVNu Juxtarestiform body Solitary nucleus JRB Lateral vestibulospinal tract SN Solitary tract LVesSp Lateral vestibular nucleus SolNu Spinal trigeminal tract LVNu Mesencephalic nucleus SolTr Superior vestibular nucleus MesNu Medial lemniscus SpTTr Trochlear nucleus ML Medial longitudinal fasciculus SVNu Vestibular ganglion MLF Medial vestibulospinal tract TroNu Vestibulocerebellar fibers, primary Medial vestibular nucleus VesGang Vestibulocerebellar fibers, secondary MVesSp Oculomotor nucleus VesCbl,Prim MVNu VesCbl,Sec OcNu Review of Blood Supply to Vestibular Nuclei, TroNu, and OcNu STRUCTURES ARTERIES Vestibular Nuclei posterior inferior cerebellar in medulla (see Figure 5–14), long TroNu and OcNu circumferential branches of basilar in pons (see Figure 5–21) paramedian branches of basilar bifurcation, medial branches of posterior cerebral and posterior communicating, short circumferential branches of posterior cerebral (see Figure 5–27)

Optic, Auditory, and Vestibular Systems 229 Vestibular Pathways Position of Vestibular Nuclei, MLF, and Related Structures PAG SC MesNu OcNu ML RNu SN OcNu TroNu IC TroNu ALS AbdNu MLF ML SCP,Dec CblNu MLF Cbl-CoVes SVNu LVNu JRBVesCbl, Sec AbdNu SVNu Cbl cortex JRB VesCbl, Prim MLF SpTTr LVNu ALS ML VesGang MVNu HyNu InfVNu MVNu andCrista ampullaris InfVNu Macula utriculi MVesSp in MLF RB Macula sacculi SpTTr LVesSp MLF SolTr and Nu ML Py

230 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–31 Blank master drawing for auditory or vestibular pathway. This illustration is provided for self-evaluation of auditory or vestibu- lar pathway understanding, for the instructor to expand on aspects of these pathways not covered in the atlas, or both.

Optic, Auditory, and Vestibular Systems 231

232 Synopsis of Functional Components, Tracts, Pathways, and Systems Hippocampal Connections7–32 Selected afferent and efferent connections of the hippocam- to the dentate gyrus, Ammon’s horn, and subiculum; and serotonin-pus (upper) and the mammillary body (lower) with emphasis on the ergic fibers arise from the rostral raphe nuclei.circuit of Papez. The hippocampus receives input from, and projectsto, diencephalic nuclei (especially the mammillary body via the post- Clinical Correlations: Dysfunction associated with damage tocommissural fornix), the septal region, and amygdala. The hippocam- the hippocampus is seen in patients with trauma to the temporal lobe,pus receives cortical input from the superior and middle frontal gyri, as a sequel to alcoholism, and as a result of neurodegenerative changessuperior temporal and cingulate gyri, precuneus, lateral occipital cor- seen in the dementing diseases (such as Alzheimer disease and Pick disease).tex, occipitotemporal gyri, and subcallosal cortical areas. The mam- Bilateral injury to the hippocampus results in loss of recent memorymillary body is connected with the dorsal and ventral tegmental nuclei, (remote memory is unaffected), impaired ability to remember recentanterior thalamic nucleus (via the mammillothalamic tract), septal nu- (new) events, and difficulty in turning a new experience (somethingclei, and through the mammillotegmental tract, to the tegmental pon- just done or experienced) into a longer-term memory that can be re-tine and reticulotegmental nuclei. trieved at a later time. Also, memory that depends on visual, tactile, or auditory discrimination is noticeably affected. These represent visual Neurotransmitters: Glutamate (ϩ)-containing cells in the agnosia, tactile agnosia, and auditory agnosia, respectively.subiculum and Ammon’s horn project to the mammillary body, otherhypothalamic centers, and the lateral septal nucleus through the fornix. In the Korsakoff syndrome (amnestic confabulatory syndrome) there is mem-Cholecystokinin (ϩ) and somatostatin (Ϫ) are also found in hip- ory loss, dementia, amnesia, and a tendency to give confabulated re-pocampal cells that project to septal nuclei and hypothalamic struc- sponses. This type of response is fluent but consists of a string of unrelated,tures. The septal nuclei and the nucleus of the diagonal band give rise or even made up, “memories” that never actually occurred or make noto cholinergic afferents to the hippocampus that travel in the fornix. In sense. This may lead to an incorrect conclusion that the patient is suffer-addition, a gamma-aminobutyric acid (Ϫ) septohippocampal projec- ing from dementia. In addition to lesions in the hippocampus in these pa-tion originates from the medial septal nucleus. Enkephalin and gluta- tients, the mammillary bodies and dorsomedial nucleus of the thalamusmate containing hippocampal afferent fibers arise from the adjacent en- are noticeably affected. The Korsakoff syndrome (see also the Wernicke-torhinal cortex; the locus ceruleus gives origin to noradrenergic fibers Korsakoff syndrome) as seen in chronic alcoholics is largely owing to thi- amine deficiency and can be treated with therapeutic doses of this vitamin. AC Anterior commissure AbbreviationsAmHrn Ammon’s horn Amygdaloid nucleus (complex) LT Lamina terminalis Amy Anterior nucleus of thalamus MB Mammillary body AntNu Corpus callosum, genu MedFCtx Medial frontal cortex CC, G Corpus callosum, splenium MedTh Medial thalamus CC,Spl Cingulum MTegTr Mammillotegmental tract Cingulate gyrus MtTr Mammillothalamic tract Cing Corticohippocampal fibers NuAcc Nucleus accumbensCingGy Dentate gyrus OpCh Optic chiasmCorHip Entorhinal cortexDenGy Fornix Pi Pineal Gyrus rectus RSplCtx Retrosplenial cortex EnCtx Hippocampus For Hypothalamus SepNu Septal nuclei Internal capsule, genu SMNu Supramammillary nucleus GyRec Hip Sub Subiculum TegNu Tegmental nuclei Hyth VmNu Ventromedial hypothalamic nucleus IC,G Review of Blood Supply to Hip, MB, Hyth, and CingGy STRUCTURES ARTERIES Hip anterior choroidal (see Figure 5–38) MB, Hyth branches of circle of Willis (see Figure 2–21) AntNu thalamoperforating (see Figure 5–38) CingGy branches of anterior cerebral

Limbic System 233 Hippocampal Connections CingGy Cing IC,G For AntNuCC,G CC,Spl RSplCtx For CorHip MedTh Pi AC SepNu Amy EnCtx LT DenGy GyRec Hip AmHrn NuAcc Sub VmNu OpCh MB CingGy Cing IC,G For MTTr AntNu MTegTr For AC TegNu SepNu Hyth LT OpCh DenGy Hip AmHrn Sub EnCtx Amy MB

234 Synopsis of Functional Components, Tracts, Pathways, and Systems Amygdaloid Connections7–33 The origin, course, and distribution of selected afferent and complex. Acetylcholine is present in afferents to the amygdala from theefferent connections of the amygdaloid nuclear complex in sagittal (up- substantia innominata, as well as from the septal area. In patients withper) and coronal (lower) planes. The amygdala receives input from, Alzheimer disease and the associated dementia, there is a marked lossand projects to, brainstem and forebrain centers via the stria terminalis of acetylcholine-containing neurons in the basal nucleus of the sub-and the ventral amygdalofugal pathway. Corticoamygdaloid and amyg- stantia innominata, in the cortex, and in the hippocampus.dalocortical fibers interconnect the basal and lateral amygdaloid nucleiwith select cortical areas. Clinical Correlations: Dysfunctions related to damage to the amygdaloid complex are seen in patients with trauma to the temporal Neurotransmitters: Cells in the amygdaloid complex contain lobes, herpes simplex encephalitis, bilateral temporal lobe surgery to treatvasoactive intestinal polypeptide (VIP, ϩ), neurotensin (NT), so- intractable epileptic activity, and in some CNS degenerative disordersmatostatin (SOM,Ϫ), enkephalin (ENK,Ϫ), and substance P (SP, ϩ). (such as Alzheimer disease and Pick disease). The behavioral changes seenThese neurons project, via the stria terminalis or the ventral amyg- in individuals with amygdala lesions collectively form the Klüver-Bucydalofugal path, to the septal nuclei (VIP, NT), the bed nucleus of the syndrome. In humans these changes/deficits are 1) hyperorality; 2) visual,stria terminalis (NT, ENK, SP), the hypothalamus (VIP, SOM, SP), the tactile, and auditory agnosia; 3) placidity; 4) hyperphagia or other dietarynucleus accumbens septi, and the caudate and putamen (NT). Sero- manifestations; 5) an intense desire to explore the immediate environ-tonergic amygdaloid fibers originate from the nucleus raphe dorsalis ment (hypermetamorphosis), and 6) what is commonly called hypersexual-and the superior central nucleus, dopaminergic axons from the ventral ity. These changes in sexual attitudes are usually in the form of com-tegmental area and the substantia nigra-pars compacta, and noradren- ments, suggestions, and attempts to make a sexual contact (such asalin-containing fibers from the locus ceruleus. Glutamate (ϩ) is found touching) rather than in actual intercourse or masturbation. These pa-in olfactory projections to the prepiriform cortex and the amygdaloid tients may also show aphasia, dementia, and amnesia. Abbreviations AC Anterior commissure NuRa,d Nucleus raphe, dorsalis Amy Amygdaloid nuclear complex NuRa,m Nucleus raphe, magnus AmyCor Amygdalocortical fibers NuRa,o Nucleus raphe, obscurusAmyFugPath Amygdalofugal pathway NuRa,p Nucleus raphe, pallidus AntHyth Anterior hypothalamus NuStTer Nucleus of the stria terminalis Ba-LatNu Basal and lateral nuclei Olfactory bulb CaNu Caudate nucleus OlfB Optic chiasmCen-MedNu Central, cortical and medial nuclei OpCh Periaqueductal (central) gray CorAmy Corticoamygdaloid fibers Parabrachial nuclei DVagNu Dorsal motor vagal nucleus PAG Parafascicular nucleus EnCtx Entorhinal cortex PBrNu Pineal Fornix Preoptic nucleus For Globus pallidus PfNu Prepiriform cortex GP Hypothalamus Pi Putamen Hyth Lamina terminalis Septal nuclei LT Lateral hypothalamic area POpNu Substantia nigra, pars compacta LHAr Medial thalamic nuclei PPriCtx Solitary nucleus MedThNu Medial geniculate nucleus Stria terminalis MGNu Midline thalamic nuclei Put Subiculum MidTh Nucleus accumbens SepNu Substantia innominata NuAcc Nucleus centralis, superior Ventral tegmental area NuCen,s Nucleus ceruleus SNpc Ventromedial hypothalamic nucleus NuCer SolNu StTer Sub Subln VenTegAr VmNu Review of Blood Supply to Amy and Related CentersSTRUCTURES ARTERIESAmy anterior choroidal (see Figure 5–38)Hyth branches of circle of Willis (see Figure 5–38)Brainstem (see Figures 5–14, 5–21, and 5–27)Thalamus thalamoperforating, thalamogeniculate (see Figure 5–38)

Limbic System 235 Amygdaloid Connections MedThNu MidTh, PfNu, MGNu StTerPut, CaNu NuAcc StTer VmNu, LHAr NuStTer AC PAG LT SNpc, VenTegAr NuRa,d AntHyth OpCh POpNU NuCerOlfB PBrNu AmyFugPath Amy Cen-MedNu NuCen,s Ba-LatNu PPriCtx Sub NuRa,m EnCtx SolNu NuRa,p NuRa,o DVagNu Prefrontal cortex Cingulate gyrus CaNu Insula Put GP NuStTer Temporal StTer NuAcc lobe SepNu AmyCor For CorAmy Hyth Parahippocampal gyrus POpNu to StTer SubIn AmyFugPath Cen-MedNu Amy Ba-LatNu

236 Synopsis of Functional Components, Tracts, Pathways, and Systems 7–34 Blank master drawing for limbic pathways. This illustration is provided for self-evaluation of limbic pathways or connections, for the instructor to expand on aspects of these pathways not covered in the atlas, or both.

Limbic System 237

CHAPTER 8 Anatomical–Clinical Correlations:Cerebral Angiogram, MRA, and MRV

240 Anatomical–Clinical Correlations Parietal branches (of MCA) A Angular branch Callosomarginal branch (of MCA) (of ACA) Middle cerebral artery Pericallosal branch (MCA) (of ACA) Anterior cerebral artery (ACA) Internal carotid artery BOphthalmic artery Internal carotid artery (petrous part) Internal carotid artery (cavernous part) Internal carotid artery (cerebral part)8-1 Internal carotid angiogram (left lateral projection, arterial an important source of blood supply to the retina. Occlusion of thephase) showing the general patterns of the internal carotid, middle, ophthalamic artery may result in blindness in the eye on that side. Theand anterior cerebral arteries (A, B) and an image with especially good terminal branches of the ophthalamic artery will anastomose with su-filling of the ophthalmic artery (B). The ophthalmic artery leaves the perficial vessels around the orbit. Compare with Figures 2-12 (page 19)cerebral part of the internal carotid and enters the orbit via the optic and 2-25 (page 27).canal. This vessel gives rise to the central artery of the retina, which is

A Cerebral Angiogram, MRA, and MRV 241 Inferior sagittal sinus Superior sagittal sinus Thalamostriate veinInternal cerebral vein Superior cerebral veins Venous angle Straight sinusInferior cerebral veins Transverse sinus Superficial middle Great cerebral vein (of Galen) cerebral vein Sigmoid sinus Inferior anastomotic vein B (of Labbé) Basal vein Superior cerebral (of Rosenthal) veins Superior anastomotic vein Superficial middle (of Trolard) cerebral vein Straight sinus Inferior anastomotic vein (of Labbé)8-2 Two internal carotid angiograms (left lateral projection, ve- bral vein is called the venous angle (A). The interventricular foramennous phase). Superficial and deep venous structures are clear in A, but is located immediately rostral to this point.Compare these images withB shows a particularly obvious vein of Trolard. The thalamostriate vein the drawings of veins and sinuses in Figures 2-13 (page 19) and 2-28(A) at this location can also be called the superior thalamostriate vein. (page 29).The junction of the superior thalamostriate vein with the internal cere-

242 Anatomical–Clinical Correlations Middle cerebral artery (M4–cortical branches)Anterior cerebral artery (A4, A5) Middle cerebral artery (M2–insular branches)Anterior cerebral artery Lenticulostriate branches (A3) (of M1) (A2) Middle cerebral artery (A1) (M1) Internal carotid artery Internal carotid artery (cerebral part) (cavernous part) Internal carotid artery (petrous part)8-3 Internal carotid angiogram (anterior–posterior projection, (supracallosal) and A5 (postcallosal) segments are located superiorarterial phase). Note general distribution patterns of anterior and (above) the corpus callosum.middle cerebral arteries and the location of lenticulostriatebranches. The A1 segment of the anterior cerebral artery is located The M1 segment of the middle cerebral artery is located betweenbetween the internal carotid bifurcation and the anterior communi- the internal carotid bifurcation and the point at which this vesselcating artery. The distal portion of the anterior cerebral artery branches into superior and inferior trunks on the insular cortex. As(ACA) immediately rostral to the anterior communicating artery branches of the middle cerebral artery pass over the insular cortex theyand inferior to the rostrum of the corpus callosum is the A2 segment are designated as M2, as M3 when these branches are located on the in-(infracallosal). The portion of the ACA arching around the genu of ner surface of the frontal, parietal, and temporal opercula, and as M4the corpus callosum is the A3 segment (precallosal) and the A4 where they exit the lateral sulcus and fan out over the lateral aspect of the cerebral hemisphere. Compare with Figure 2-21 on page 25.

Cerebral Angiogram, MRA, and MRV 243 Arachnoid villi Superior cerebral veinsSuperior sagittal sinus Superior sagittal Inferior sagittal sinus sinusConfluence of sinuses Transverse Transverse sinus sinus Sigmoid sinus 8-4 Internal carotid angiogram (anterior–posterior projection, ve- nous phase). The patient’s head is tilted slightly; this shows the arch- ing shapes of the superior and inferior sagittal sinuses to full advantage. Note the other venous structures in this image and compare with the arterial phase shown in Figure 8-3 on page 242 and the images in Fig- ures 8-5 and 8-6 on pages 244 and 245. Also compare with Figure 2- 28 on page 29.

244 Anatomical–Clinical Correlations A Superior sagittal sinus Superficial cerebral veinsB Superior sagittal sinus Confluence of sinuses Transverse sinusSigmoid sinus Jugular bold Internal jugular vein8-5 Digital subtraction image of an internal carotid angiogram (an- in the jugular fossa at the point where the sigmoid sinus is continu-terior–posterior projection, venous phase). Image A is early in the ve- ous with the IJV; this continuity is through the jugular foramen. Thenous phase (greater filling of cortical veins), whereas image B is later jugular foramen also contains the roots of cranial nerves IX, X, andin the venous phase (greater filling of the sinuses and jugular vein). Both XI, the continuation of inferior petrosal sinus with the IJV and sev-images are of the same patient. eral small arteries. Compare with Figures 2-16 (page 21) and 2-19 (page 23). The jugular bulb is a dilated portion of internal jugular vein (IJV)

Cerebral Angiogram, MRA, and MRV 245 B ACA PCAA SSS MCA TS SCA CS ICA BA AICA VA Anterior cerebral artery (ACA) Anterior communicating artery Posterior cerebral artery (PCA)C A2 segment Superior cerebellar artery (SCA) A1 segment Superior sagittal sinus (SSS)Middle cerebral artery (MCA) Internal carotid artery (ICA): M2 segment M1 segment Cerebral part Cavernous partSigmoid sinus Petrous partTransverse sinus (TS)Confluence of sinuses (CS) Anterior inferior cerebellar artery (AICA) Vertebral artery (VA) Basilar artery (BA)8-6 Magnetic resonance angiography (MRA) is a noninvasive terior to posterior. C shows the relative position of the major vesselsmethod for imaging cerebral arteries, veins, and sinuses simultane- and dural sinuses as imaged in A and B. The superior sagittal sinus, asously. A 3-D phase contrast MRA (A) and an inverted video image seen in A and B, is usually continuous with the right transverse sinus atwindow (B) of the same view show major vessels and sinuses from an- the confluence of sinuses.

246 Anatomical–Clinical Correlations AThalamogeniculate arteries Parieto-occipitialPosterior choroidal arteries branches (of PCA) Posterior cerebral arteries Calcarine branch (PCA) (of PCA) Thalamoperforating Posterior inferior arteries cerebellar artery (PICA) Basilar bifurcation Vertebral artery (VA) Posterior communicating artery Superior cerebellar artery (SCA) Basilar artery (BA) B Parieto-occipital branches Calcarine branch PCA Basilar bifurcation SCA BA Anterior inferior cerebellar artery8-7 A vertebral artery angiogram (left lateral PICAprojection, arterial phase) is shown in A, and thesame view, but in a different patient, is shown in B, VAusing digital subtraction methods. Note the charac-teristic orientation of the major vessels. Comparewith Figure 2-21 on page 25.

Cerebral Angiogram, MRA, and MRV 247 PCA PCA, Cortical branches SCA AICA Thalamoperforating arteries B Basilar artery (BA)Posterior cerebral arteries Vertebral artery (VA) (PCA) Posterior cerebral artery,Superior cerebellar artery Cortical branches (SCA) BA Thalamoperforating arteries AICA (of the basilar bifurcation) PICA SCA Anterior inferior cerebellar artery (AICA) Posterior inferior cerebellar artery (PICA) VA8-8 A vertebral artery angiogram (anterior–posterior projection, The root of the oculomotor (IIIrd) nerve, after exiting the inferiorarterial phase) is shown in A; the same view, but in a different patient, aspect of the midbrain, characteristically passes through the interpe-is shown in B, using digital subtraction methods. Even though the in- duncular cistern and between the superior cerebellar and posteriorjection is into the left vertebral, there is bilateral filling of the vertebral cerebral arteries en route to its exit from the skull through the supe-arteries and of branches of the basilar artery. The thalamoperforating rior orbital fissure. In this position the IIIrd nerve may be damaged byarteries are important branches of P1 that generally serve rostral por- large aneurysms that impinge on the nerve root. Compare with Figurestions of the diencephalon. 2-40 (page 39) and 2-41 (page 40).