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High-Yield FOURTH EDITION Professor Emeritus of Anatomy Huntington, West Virginia Jennifer K. Brueckner, PhD Associate Professor Assistant Dean for Student Affairs Department of Anatomy and Neurobiology Acquisitions Editor: Crystal Taylor This chapter on the cranial nerves is pivotal. It spawns more neuroanatomy examina- tion questions than any other chapter. Carefully study all of the Þgures and legends. The seventh cranial nerve deserves special consideration (see Figures 11-5 and 11-6). Understand the differ- This chapter describes the cortical localization of functional areas of the brain. How does the dominant hemisphere differ from the nondominant hemisphere? Figure 22-5 shows the effects of various major hemispheric lesions. What symptoms result from a lesion of the right infe- PREFACE This chapter describes apraxia, aphasia, and dysprosody. Be able to differentiate BrocaÕs aphasia from WernickeÕs aphasia. What is conduction aphasia? This is board-relevant material. While we have worked hard to ensure accuracy, we appreciate that some errors and omissions may have escaped our attention. We would welcome your comments and suggestions to improve this We wish you good luck. High-Yield FOURTH EDITION CHAPTER 1 Figure 1-2 Schematic diagram of peripheral nerve regeneration. CHAPTER 1 Conduction Velocity *Myelin sheath included if present. CLASSIFICATION OF NERVE FIBERS TABLE  derived from arachnoid cap cells and represent the second most common primary intracranial brain tumor after astrocytomas (15%)  are not invasive; they indent the brain; may produce hyperostosis  pathology: concentric whorls and calcified psammoma bodies  location: parasagittal and convexity  gender: f�emales men  associated with neurofibromatosis-2 (NF-2) Astrocytomas  represent 20% of the gliomas  historically benign  diffusely infiltrate the hemispheric white matter  most common glioma found in the posterior fossa of children Glioblastoma multiforme  represents 55% of gliomas  malignant; rapidly fatal astrocytic tumor  commonly found in the frontal and temporal lobes and basal nuclei  frequently crosses the midline via the corpus callosum (butterfly glioma)  most common primary brain tumor  histology: pseudopalisades, Figure 1-3 Supratentorial tumors of the central and peripheral nervous systems. In adults, 70% of tumors are supra- , cerebrospinal ßuid. CHAPTER 1 Free  Epidermi Dermi S Figure 1-5 Three important cutaneous receptors. Free nerve endings mediate pain and temperature sensation. Meiss- ate touch, pressure, and vibration sensation. Merkel disks mediate light touch. A 44-year-old woman with a complaint of dizziness and ringing and progressive hearing loss ¥Unilateral sensorineural hearing loss ¥Radiologic Þndings show a right cerebellopontine angle mass that involves the pons and cerebellum. ¥Neurologic workup shows discrimination impairment out of proportion to pure-tone thresholds. ¥Acoustic schwannomas are intracranial tumors that arise from the Schwann cells investing CN VIII (the vestibulocochlear nerve). They account for up to 90% of tumors found with- in the cerebellopontine angle. Cranial nerves V and VII are the next most common nerves CHAPTER 2 Figure 2-1 Development of the neural tube and crest. The alar plate gives rise to sensory neurons. The basal plate gives rise to motor neurons. The neural crest gives rise to the peripheral nervous system. Figure 2-2 The brain stem showing the cell columns derived from the alar and basal plates. The seven cranial nerve modalities are shown. general somatic afferent; general somatic efferent; GVA, general visceral afferent; general visceral efferent; special somatic afferent; SVA, special visceral afferent; special visceral efferent. (Adapted from Patten BM. Human Embryology, 3rd ed. New York: McGraw-Hill, 1969:298, with permission.) become functional. Myelination in the cerebral association cortex continues into the third A.MYELINATION OF THE CNS is accomplished by oligodendrocytes, which are not B Figure 2-5 Myelination in the pyramids and in the middle cerebellar peduncles. C.CRANIUM BIFIDUM results from a defect in the occipital bone through which meninges, cerebellar tissue, and the fourth ventricle may herniate. D.ARNOLD-CHIARI malformation (type 2) has a frequency of 1:1,000 (Figure 2-8). It results from elongation and herniation of cerebellar tonsils through foramen magnum, thereby blocking cerebrospinal ßuid ßow. E.DANDY-WALKER malformation has a frequency of 1:25,000. It may result from riboßavin inhibitors, posterior fossa trauma, or viral infection (Figure 2-9). F.HYDROCEPHALUS is most commonly caused by stenosis of the cerebral aqueduct during development. Excessive cerebrospinal ßuid accumulates in the ventricles and subarachnoid space. This condition may result from maternal infection (cytomegalovirus and toxoplasmosis). The frequency is 1:1,000. Figure 2-7 Midsagittal section through the brain stem and diencephalon. A craniopharyngioma ( lar in the midline. It compresses the optic chiasm and hypothalamus. This tumor is the most common supratentorial tumor that occurs in childhood and the most common cause of hypopituitarism in children. This is a T1-weighted mag- DEVELOPMENT OF THE NERVOUS SYSTEM Figure 2-9 Dandy-Walker malformation. Midsagittal section. An enormous dilation of the fourth ventricle results from failure of the foramina of Luschka and Magendie to open. This condition is associated with occipital meningocele, elevation of the conßuence of the sinuses (torcular Herophili), agenesis of the cerebellar vermis, and splenium of the corpus callosum. (Reprinted from Dudek RW, Fix JD. BRS Embryology . Baltimore: Williams & Wilkins, 1997:97, with per- Figure 2-8 Arnold-Chiari malformation. Midsagittal section. Normal cerebellum, fourth ventricle, and brain Abnormal cerebellum, fourth ventricle, and brain stem showing the common congenital anomalies: )beaking of the tectal plate, ( ) kinking and transforaminal herniation of the medulla into ) herniation and unrolling of the cerebellar vermis into the vertebral canal. An accompany- ing meningomyelocele is common. (Reprinted from Fix JD. . Baltimore: Williams & Wilkins, 1996:72, I.HYDRANENCEPHALY results from bilateral hemispheric infarction secondary to occlusion of the carotid arteries. The hemispheres are replaced by hugely dilated ven- A mother brings her newborn infant to the clinic because the infantÕs Òlegs donÕt seem to work right.Ó The infant was delivered at home without antenatal care. What is the most likely ¥Tufts of hair in the lumbosacral region ¥Clubfoot (Talipes equinovarus) ¥Chronic upper motor neuron signs, including spasticity, weakness, fatigability CHAPTER 3 Cingulate gyrus Superior frontal gyrus Anterior cerebral artery Crista galli Basilar artery Sphenoid sinus Nasopharynx Paracentral lobule Superior sagittal sinus Figure3-1 Midsagittal section of the brain and brain stem showing the structures surrounding the third and fourth Figure3-2 CROSS-SECTIONAL ANATOMY OF THE BRAIN Corpus callosum Fornix Lateral ventricle Anterior cerebral artery Hypophysis/infundibulum Mamillary body Cerebral aqueduct Thalamus Superior and inferior colliculi Fourth ventricle Cerebellar vermis Subarachnoid space Amy Hypophy terior commi Lateral ve tricle Corp Figure3-3 CHAPTER 3 Amy Hypophy Caver nus nus ophary Corp Lateral ve tricle Third ve tricle terior carotid artery Figure3-5 CROSS-SECTIONAL ANATOMY OF THE BRAIN Corp terped lar fo Pyramid of med Figure3-7 CHAPTER 3 Vel terpo perior nus d for Lateral ve tricle terior limb) tricle Tri e (of lateral tricle) Corp Optic radiatio al cortex terior limb) Corp Figure3-9 CROSS-SECTIONAL ANATOMY OF THE BRAIN al cerebral Optic tract Mamillary body Lateral ve tricle (tri perior collic terior cerebral artery adri Cerebellar vermi trai nus perior nus cerebri / amy Middle cerebral artery erve Optic tract Mamillary bodie Cerebral aq Cerebellar vermi perior nus erve Amy cerebri Lateral ve tricle (temporal hor Lateral ve tricle Figure3-11 CHAPTER 3 erve erve terior cerebral artery adri nus cerebri Cerebral aq Cerebellar vermi trai nus perior nus Figure3-13 CROSS-SECTIONAL ANATOMY OF THE BRAIN Figure3-16 Gross parasagittal section through the caudate nucleus, subthalamic nucleus, substantia nigra, and den- results in hemiballism. ParkinsonÕs disease results from a cell loss of the pigmented neurons in the substantia nigra. (Reprinted from M Roberts, J Hanaway, DK Morest, Febiger, 1987:79, with permission.) Figure3-15 Gross parasagittal section through the red nucleus, medial lemniscus, and inferior olivary nucleus. The corticospinal Þbers can be traced from the crus cerebri to the spinal cord. The abducent nerve (CN VI) is seen exiting from the pontonuclear sulcus. (Reprinted from M Roberts, J Hanaway, DK Morest, 2nd ed. Philadelphia: Lea & Febiger, 1987:81, with permission.) CHAPTER 3 Figure3-17 Coronal section through the anterior commissure, amygdala, septal nuclei, and optic chiasm. The septal nuclei have reciprocal connections with the hippocampal formation (subiculum). (Reprinted from M Roberts, J Hanaway, DK Morest, 2nd ed. Philadelphia: Lea & Febiger, 1987:9, with permission.) Figure3-18 Coronal section through the posterior limb of the internal capsule, mamillothalamic tract (MTT), mamil- lary body, and hippocampal formation. Note the MTT entering the anterior ventral nucleus. The optic tracts are visible bilaterally. (Reprinted from M Roberts, J Hanaway, DK Morest, phia: Lea & Febiger, 1987:19, with permission.) CROSS-SECTIONAL ANATOMY OF THE BRAIN Figure3-19 Coronal section through the thalamus, ventral posteromedial nucleus ( ), and ventral posterolateral ), posterior limb of the internal capsule, substantia nigra, and red nucleus. The optic tract lies dorsal to the temporal horn of the lateral ventricle. (Reprinted from M Roberts, J Hanaway, DK Morest, 2nd ed. Philadelphia: Lea & Febiger, 1987:23, with permission.) Figure3-20 Coronal section through the lateral and medial lemnisci, lateral and medial geniculate nuclei, and hip- pocampal formation. (Reprinted from M Roberts, J Hanaway, DK Morest, Philadelphia: Lea & Febiger, 1987:25, with permission.) CHAPTER 3 Figure3-21 Coronal section through the pulvinar nuclei, pineal gland (epiphysis), superior and inferior colliculi, and trochlear nerve (CN IV). (Reprinted from M Roberts, J Hanaway, DK Morest, ed. Philadelphia: Lea & Febiger, 1987:29, with permission.) Figure3-22 Axial section through the internal capsule, anterior commissure, and pulvinar nuclei. (Reprinted from M Roberts, J Hanaway, DK Morest, 2nd ed. Philadelphia: Lea & Febiger, 1987:51, with CROSS-SECTIONAL ANATOMY OF THE BRAIN Figure3-23 Axial section through the mamillary nuclei and the superior colliculi. (Reprinted from M Roberts, J Han- away, DK Morest, 2nd ed. Philadelphia: Lea & Febiger, 1987:57, with permission.) Figure3-24 Axial section through the mamillary nuclei, optic chiasm, and inferior colliculi. (Reprinted from M Roberts, J Hanaway, DK Morest, 2nd ed. Philadelphia: Lea & Febiger, 1987:59, with permis- 2.Subdural and epidural hematomas a.Subdural hematoma is caused by laceration of the superior cerebral (bridg- is caused by laceration of the middle meningeal artery. E.MENINGITIS is inßammation of the piaÐarachnoid area of the brain, the spinal cord, 1.Bacterial meningitis is characterized clinically by fever, headache, nuchal rigidity, and KernigÕs sign. (With the patient supine, the examiner ßexes the patientÕs hip but Figure 4-1 The subarachnoid spaces and cisterns of the brain and spinal cord. Cerebrospinal ßuid is produced in the choroid plexuses of the ventricles. It exits the fourth ventricle, circulates in the subarachnoid space, and enters the supe- rior sagittal sinus through the arachnoid granulations. Note that the conus medullaris terminates at L-1. The lumbar cis- tern ends at S-2. (Reprinted from CR Noback, NL Strominger, R Demarest, The human nervous system, more: Williams & Wilkins, 1991:68, with permission.) MENINGES, VENTRICLES, AND CEREBROSPINAL FLUID 2 1 7 8 7 6 5 4 Figure 4-3 Axial section through the midbrain and the herniating parahippocampal gyrus. The left oculomotor nerve B C D E Figure 4-4 CHAPTER 4 B C D Figure 4-5 Computed tomography axial section showing an intraparenchymal hemorrhage in the left frontal lobe. ) Intraparenchymal hemorrhage; ( ) internal capsule; ( ) calciÞed glomus in the trigone region of B C D Figure 4-6 Computed tomography axial section showing an epidural hematoma and a skull fracture. ( ) skull fracture; ( ) calciÞed glomus in the trigone region of the lateral ventricle. MENINGES, VENTRICLES, AND CEREBROSPINAL FLUID B Figure 4-7 Computed tomography (CT) axial section showing a skull fracture ( ) underlies the fracture. The CT scan shows a bone window. The patient is a 68-year-old man with alcoholic cirrhosis. He fell 4 weeks ago. He has a his- tory of progressive weakness on the right side. What is the most likely diagnosis? ¥Hemiparesis BLOOD SUPPLY Figure 5-1 Arteries of the base of the brain and brain stem, including the arterial circle of Willis. Figure 5-2 Cortical territories of the three cerebral arteries. Lateral aspect of the hemisphere. Most of the lateral convexity is supplied by the middle cerebral artery. Medial and inferior aspects of the hemisphere. The anterior cere- bral artery supplies the medial surface of the hemisphere from the lamina terminalis to the cuneus. The posterior cere- bral artery supplies the visual cortex and the posterior inferior surface of the temporal lobe. (ModiÞed from Tšndury, as presented in J Sobotta, CHAPTER 5 Superior sagittal sinus Anterior cerebral artery Cavernous part of ICA Figure 5-4 Figure 5-5A: Carotid angiogram, lateral projection. Carotid angiogram, anteroposterior projection. Vertebral angiogram, lateral projection. Vertebral angiogram, anteroposterior projection. CHAPTER 5 Figure 5-7 Figure 5-8 Carotid angiogram, venous phase, showing the cerebral veins and venous sinuses. BLOOD SUPPLY Pericallo al artery of ACA Fro topolar bra of ACA Ophthalmic artery Cervical ICA ACA Cortical bra of MCA Lateral triate bra pracli oid part of ICA Figure 5-9 Carotid angiogram, lateral projection. Identify the cortical branches of the anterior cerebral artery ( and middle cerebral artery ( ). Follow the course of the internal carotid artery ( ) may result in third-nerve palsy. The paracentral lobule is irrigated by the callosomarginal artery. Figure 5-10 Carotid angiogram, anteroposterior projection. Identify the anterior cerebral artery ( ), middle cere- ), and internal carotid artery ( internal capsule. anterior communicating artery. CHAPTER 5 terior choroidal arterie perior cerebellar artery ilar artery Vertebral artery Thalamoperforati arterie Figure 5-11 Calcari e artery of PCA Temporal bra of PCA Vertebral artery PCA perior cerebellar artery ilar artery PICA Figure 5-12 Vertebral angiogram, anteroposterior projection. Which artery supplies the visual cortex? The calcarine artery, a branch of the posterior cerebral artery ( ). Occlusion of the PCA (calcarine artery) results in a contralateral posterior inferior cerebellar artery. BLOOD SUPPLY ter table Perio er table) Arach Figure 5-13 An epidural hematoma results from laceration of the middle meningeal artery. Arterial bleeding into the epidural space forms a biconvex clot. The classic Òlucid intervalÓ is seen in 50% of cases. Skull fractures are usually found. Epidural hematomas rarely cross sutural lines. (Reprinted from AG Osburn, KA Tong, . St. Louis: Mosby, 1996:191, with permission.) Figure 5-14 A subdural hematoma (SDH) results from lacerated bridging veins. SDHs are frequently accompanied by superior cerebral veins. The SDH extends over the crest of the convexity into the interhemispheric Þssure but does not cross the dural attachment of the falx cerebri. The clot can be crescent-shaped, biconvex, or multiloculated. SDHs are more common than epidural hematomas and always cause brain damage. (Reprinted from AG Osburn, KA Tong, . St. Louis: Mosby, 1996:192, with permission.) CHAPTER 5 A 62-year-old man comes to the clinic complaining of problems with his vision and a horrible headache that began earlier in the day. He reports bumping into objects and not being able to SPINAL CORD Segment C1 Segment C4 Segment C8 Segment T2 Segment T12 Segment L4 Segment S3 Lateral horn (intermediolateral cell column) Figure 6-2 Spinal cord segments. Cervical segments are the largest segments. The thoracic and sacral segments are relatively small. Note the presence of an intermediolateral cell column in the thoracic and sacral segments. (Reprinted from A Siegel, HN Sapru, . Baltimore: Lippincott Williams & Wilkins, 2006:142, with permission.) CHAPTER 6 A 46-year-old man was admitted with complaints of lower back pain that radiated down to his foot over the last 2 months. The pain was not relieved with medical therapy. What is your ¥Absent right ankle jerk ¥Weakness of dorsißexion and plantar ßexion ¥Decreased pinprick over the dorsum of the foot ¥An anteroposterior myelogram demonstrated compressionof the Þrst sacral nerve root on the left at the level of theL5-S1 vertebrae. ¥Lumbar intervertebral disc herniation CHAPTER 7 Figure 7-1 AUTONOMIC NERVOUS SYSTEM Figure 7-2 CHAPTER 8 Thalamus Internal capsule Lentiform nucleus Trigeminal nerve Nucleus gracilis Internal arcuate fibers Cuneate fasciculus Pacinian corpuscle Postcentral gyrus Pons Cervical spinal cord Lumbosacral spinal cord Trunk area Arm area Face area Ventral posterolateral nucleus of thalamus Spinal trigeminal nucleus Gracile fasciculus Meissner’s corpuscle Gracile fasciculus Cuneate fasciculus Figure 8-2 The dorsal columnÐmedial lemniscus pathway. Impulses conducted by this pathway mediate discrimina- TRACTS OF THE SPINAL CORD Figure 8-3 CHAPTER 8 Figure 8-4 volitional motor activity. The cells of origin are located in the premotor, the motor, and the sensory cortices. nerve. (Adapted from MB Carpenter, J Sutin, . Baltimore: Williams & Wilkins, 1983:285, with per- B.CLINICAL FEATURES. Interruption of this tract at any level results in HornerÕs syn- drome (i.e., miosis, ptosis, hemianhidrosis, and apparent enophthalmos). The signs are Figure 8-5 A 17-year-old man complained of pain on the left side of his chest and progressive weakness of his left lower limb for 2 months before coming to the clinic. What is the most likely diag- ¥Neurologic evaluation revealed weakness in the left lower limb; spasticity and hyper- reßexia at the knee and ankle were also observed. ¥On the left side, a loss of two-point discrimination, vibratory sense, and proprioception below the hip was observed. A loss of pain and temperature sensation below the T7 der- matome was observed on the right side. ¥Brown-SŽquard syndrome, resulting from an upper motor neuron lesion (tumor) at T5-T6 Damage results in ipsilateral spastic paresis with Damage results in contralateral loss of pain and temperature sensation one segment below the lesion. hypothalamospinal tract at T-1 and above. Damage results in ipsilateral HornerÕs syndrome (i.e., miosis, ptosis, hemianhidrosis, and apparent enophthalmos). ventral (anterior) horn. Damage results in ipsilateral ßaccid paralysis of inner- B.VENTRAL SPINAL ARTERY OCCLUSION (Figure 9-2F) causes infarction of the ante- rior two-thirds of the spinal cord but spares the dorsal columns and horns. It results in damage to the following structures: Damage results in bilateral spastic paresis with Damage results in bilateral loss of pain and tem- perature sensation below the lesion. hypothalamospinal tract at T-2 and above. Damage results in bilateral HornerÕs syndrome. ventral (anterior) horns. Damage results in bilateral ßaccid paralysis of the innervated muscles. Figure 9-1 Transverse section of the cervical spinal cord. The clinically important ascending and descending path- ways are shown on the left. Clinical deÞcits that result from the interruption of these pathways are shown on the right Destructive lesions of the posterior (dorsal) horns result in anesthesia and areßexia. Destruction of the ventral white commissure interrupts the central transmission of pain and temperature impulses bilaterally through the lateral spinothal- C.SUBACUTE COMBINED DEGENERATION (VITAMIN B NEUROPATHY) (Figure 9-2G) is caused by pernicious (megaloblastic) anemia. It results from damage to the following structures: Damage results in bilateral Damage results in bilateral spastic paresis with spinocerebellar tracts. Damage results in bilateral arm and leg dystaxia. Figure 9-2 Classic lesions of the spinal cord. Poliomyelitis and progressive infantile muscular atrophy (Werdnig- Hoffmann disease). Multiple sclerosis. Amyotrophic lateral sclerosis. Hemisection of the spinal cord (Brown-SŽquard syndrome). BRAIN STEM Figure 10-1 The dorsal surface of the brain stem. The three cerebellar peduncles have been removed to expose the rhomboid fossa. The trochlear nerve is the only nerve to exit the brain stem from the dorsal surface. The facial colliculus Figure 10-2 Corticospinal tract (in the base of the pons) B.LATERAL STRUCTURES Facial (intraaxial) nerve Þbers Spinal nucleus and tract of trigeminal nerve (CN V) CRANIAL NERVES Figure 11-2 movements. Tilting the chin to the right side results in compensatory intorsion of the left eye and extorsion of the right Paralysis of the right superior oblique muscle results in extorsion of the right eye, causing diplopia. Tilting the chin to the right side results in compensatory intorsion of the left eye, thus permitting binocular alignment. (Reprinted from JD Fix. , 3rd ed. Baltimore: Williams & Wilkins, 1996:220, with permission.) Figure 11-3 Tertiary neuron Facial nucleus corneal reflex fiber To orbicular oculi muscle From cornea Trigeminothalamic Secondary neuron Primary neuron V-1 V-2 V-3 V-3 (motor) Principal sensory of nucleus (CN V) Afferent limb of corneal reflex Efferent limb of corneal reflex Figure 11-4 The corneal reßex pathway showing the three neurons and decussation. This reßex is consensual, like the pupillary light reßex. Second-order pain neurons are found in the caudal division of the spinal nucleus of trigeminal nerve. Second-order corneal reßex neurons are found at more rostral levels. GSA, SVA, and GVE Þbers. All Þrst-order sensory neurons are found in the geniculate 1.Anatomy. The facial nerve exits the brain stem in the cerebellopontine angle. It enters the internal auditory meatus and the facial canal. It then exits the facial canal and skull through the stylomastoid foramen. 2.The GSA component vates the posterior surface of the external ear through the posterior auricular branch of CN VII. It projects centrally to the spinal tract and nucleus of trigemi- nal nerve. 3.The GVA component has no clinical signiÞcance. The cell bodies are located in the geniculate ganglion. Fibers innervate the soft palate and the adjacent pharyn- Figure 11-6 CN] VII) nucleus. An upper motor neuron ) lesion (e.g., stroke involving the internal capsule) results in contralateral weakness of the lower face, with spar- ing of the upper face. A lower motor neuron ( ) lesion (e.g., BellÕs palsy) results in paralysis of the facial muscles in both the upper and lower face. (Redrawn from WE DeMyer, Technique of the neurological examination: A programmed 4th ed. New York: McGraw-Hill, 1994:177, with permission.) 4.The SVA component (taste) projects centrally to the solitary tract and nucleus. It innervates the taste buds from the anterior two-thirds of the tongue through: intermediate nerve. tympanic membrane and malleus. It contains the SVA and GVE (parasympa- GVA component innervates structures that are derived from the endoderm (e.g., pharynx). It innervates of the posterior one-third of the tongue, tonsil, upper pharynx, tympanic cavity, and auditory tube. It also innervates carotid sinus (baroreceptors) and carotid body (chemoreceptors) Motor cortex Decussation CN X (vagal nerve) Levator veli palatini UMN lesion Pyramid Figure 11-7 Innervation of the palatal arches and uvula. Sensory innervation is mediated by the glossopharyngeal (CN) IX]. Motor innervation of the palatal arches and uvula is mediated by the vagus nerve (CN X). A patient with an upper motor neuron ( (left) and a lower motor neuron ( ) lesion (right). When this patient says ÒAh,Ó the palatal arches sag. The uvula deviates toward the intact (left) side. (ModiÞed from WE DeMyer, Technique of the neurological examination: a pro- , 4th ed. New York: McGraw-Hill, 1994:191, with permission.) CHAPTER 11 Motor cortex Corticobulbar tract Hypoglossal nerve Corticobulbar tract (spastic paralysis) (flaccid paralysis) nucleus Pyramid Genioglossus muscle Figure 11-9 Motor innervation of the tongue. Corticonuclear Þbers project predominantly to the contralateral hypoglossal nucleus. An upper motor neuron ( ) lesion causes deviation of the protruded tongue to the weak (con- tralateral) side. A lower motor neuron ( ) lesion causes deviation of the protruded tongue to the weak (ipsilateral) Tongue with UMN and LMN lesions. (ModiÞed from WE DeMyer, Technique of the neuro- 4th ed. New York: McGraw-Hill, 1994:195, with permission.) cranial division (accessory portion), which arises from the nucleus ambiguus of the medulla. It exits the medulla from the postolivary sulcus and joins the vagal nerve (CN X). It exits the skull through the jugular foramen with CN IX and CN innervates larynx through the inferior (recur- rent) laryngeal nerve, with the exception of the cricothyroid muscle. which arises from the ventral horn of cervi- 1.First-order neurons are located in the trigeminal (gasserian) ganglion. They give rise to axons that descend in the spinal tract of trigeminal nerve and synapse with second-order neurons in the spinal nucleus of trigeminal nerve. 2.Second-order neurons are located in the spinal trigeminal nucleus. They give rise to decussating axons that terminate in the contralateral ventral posteromedial 3.Third-order neurons are located in the VPM nucleus of the thalamus. They pro- ject through the posterior limb of the internal capsule to the face area of the somatosensory cortex (BrodmannÕs areas 3, 1, and 2). mediates tactile discrimination and pressure sen- sation from the face and oral cavity. It receives input from MeissnerÕs and Pacinian cor- 1.First-order neurons are located in the trigeminal (gasserian) ganglion. They synapse in the principal sensory nucleus of CN V. Superior cerebellar peduncle Motor nucleus CN V Corticospinal tract Motor cortex 4th ventricle Pons Lateral pterygoid muscle Figure 12-1 Function and innervation of the lateral pterygoid muscles (LPMs). The LPM receives its innervation from the motor nucleus of the trigeminal nerve found in the rostral pons. Bilateral innervation of the LPMs results in protru- sion of the tip of the mandible in the midline. The LPMs also open the jaw. Denervation of one LPM results in deviation of the mandible to the ipsilateral or weak side. The trigeminal motor nucleus receives bilateral corticonuclear input. , lower motor neuron; , upper motor neuron. (ModiÞed from WE DeMyer, Technique of the , 4th ed. New York: McGraw-Hill, 1994:174, with permission.) tearing (lacrimal) reßex occurs as a result of corneal or conjunctival irritation. oculocardiac reßex occurs when pressure on the globe results in B.CLINICAL CORRELATION. TrigeminalNeuralgia(tic douloureux) is characterized by recurrent paroxysms of sharp, stabbing pain in one or more branches of the trigeminal nerve on one side of the face. It usually occurs in people older than 50 years, and it is more common in women than in men. Afferent Limb Efferent Limb Corneal reßex Ophthalmic nerve (CN V-1) Mandibular nerve (CN V-3) Mandibular nerve (CN V-3) Tearing (lacrimal) reßex Ophthalmic nerve (CN V-1) Oculocardiac reßex Ophthalmic nerve (CN V-1) Vagal nerve (CN X) The cell bodies are found in the mesencephalic nucleus of CN V. TABLE Ma Pri ory al tri V-3 with primary dary Figure 12-3 receives input from the contralateral cochlear nuclei and supe- rior olivary nuclei. receives input from the lateral lemniscus. It projects through the brachium of the inferior colliculus to the medial geniculate body. receives input from the nucleus of the inferior colliculus. It projects through the internal capsule as the auditory radiation to the primary audi- tory cortex, the transverse temporal gyri of Heschl. Figure 13-1 Peripheral and central connections of the auditory system. This system arises from the hair cells of the ized by the bilaterality of projections and the tonotopic localization of pitch at all levels. For example, high pitch (20,000 is localized at the base of the cochlea and in the posteromedial part of the transverse temporal gyri. B.BRAIN STEM AUDITORY EVOKED POTENTIALS (BAEPS) A 45-year-old woman presents with a 10-year history of auditory decline in her left ear. The problem began after her Þrst pregnancy. There is no history of otologic infection or trauma. ¥The external auditory meatus and tympanic membrane were benign bilaterally. ¥The Weber test lateralized to the left side at 512 Hz, and the Rinne test was negative at ¥Otosclerosis CHAPTER 14 Figure 14-1 Peripheral connections of the vestibular system. The hair cells of the cristae ampullares and the maculae of the utricle and saccule project through the vestibular nerve to the vestibular nuclei of the medulla and pons and the ßocculonodular lobe of the cerebellum (vestibulocerebellum). Figure 14-2 The major central connections of the vestibular system. Vestibular nuclei project through the ascending ) to the ocular motor nuclei and subserve vestibuloocular reßexes. Vestibular nuclei also project through the descending MLF and lateral vestibulospinal tracts to the ventral horn motor neurons of the spinal cord and mediate postural reßexes. When the brain stem is intact, there is deviation of the eyes to the side of the cold With bilateral MLF transaction in unconscious subjects, there is deviation of the With lower brain stem damage to the vestibular nuclei, there is no deviation of the A 60-year-old woman came to the clinic with complaints of progressive hearing loss, facial weakness, and headaches on the right side. She also said that she had become more unsteady ¥Reduced pain and touch sensation in right face ¥Right facial weakness ¥Absent right corneal reßex ¥Hearing loss on right side ¥No response to caloric test stimulation on right side ¥Bilateral papilledema ¥Acoustic neuroma is a six-layered nucleus. Layers 1, 4, and 6 receive crossed Þbers; layers 2, 3, and 5 receive uncrossed Þbers. The lateral geniculate body receives input from layer VI of the striate cortex (BrodmannÕs area 17). It also receives Þbers from the Figure 15-1 visual cortex (BrodmannÕs area 17) sure. The with macular sparing. The visual cortex has a Figure 15-2 CHAPTER 15 Figure 15-3 and calcarine sulcus. Transection of the upper division results in right lower homonymous quadrantanopia. Transec- results in right upper homonymous quadrantanopia. (Reprinted from JD Fix, roanatomy. Baltimore: Williams & Wilkins, 1997:261, with permission.) Figure 15-4 The pupillary light pathway. Light shined into one eye causes both pupils to constrict. The response in direct pupillary light reßex . The response in the opposite eye is called the pupillary light reßex C.ARGYLL ROBERTSON PUPIL reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodationÐconvergence). It occurs in A 40-year-old man comes to the clinic with a severe unilateral headache on the left side with a drooping left upper eyelid. He experienced mild head trauma 1 week ago. He does not com- plain of blurred or double vision. What is the most likely diagnosis? ¥The right pupil is 4 mm and normally reactive, and the left pupil is 2 mm and normally reactive. ¥The left pupil dilates poorly. ¥There is 2- to 3-mm ptosis of the left upper eyelid. ¥HornerÕs syndrome. receives input from the cerebellum (dentate nucleus), globus pallidus, and substantia nigra. It projects to the motor cortex (BrodmannÕs area 4) and the supplementary motor cortex (BrodmannÕs area 6). (ventrobasal complex) is the nucleus of termina- tion of general somatic afferent (touch, pain, and temperature) and special visceral afferent (taste) Þbers. It has two subnuclei. ventral posterolateral nucleus receives the spinothalamic tracts and the Figure 17-1 Major afferent and efferent connections. The anterior limb A 90-year-old woman complains of an intense burning sensation on the left side of her neck HYPOTHALAMUS Paraventricular and supraoptic nuclei  regulate water balance  produce ADH and oxytocin Anterior nucleus  thermal regulation (dissipation of heat) Figure 18-1 mamillary nucleus receives input from the hippocampal formation through the postcommissural fornix. It projects to the anterior nucleus of the thalamus through the mamillothalamic tract (part of the Papez circuit). Patients with Wer- nickeÕs encephalopathy, which is a thiamine (vitamin B ) deÞciency, have lesions in the mamillary nucleus. Lesions are also associated with alcoholism. plays a role in thermal regulation (i.e., con- servation and increased production of heat). Lesions result in poikilothermia inability to thermoregulate). anorexia starvation. C.MAJOR FIBER SYSTEMS OF THE HYPOTHALAMUS fornix is the largest projection to the hypothalamus. It projects from the hip- and septal area. The fornix then projects from the septal area to the hippocampal medial forebrain bundle traverses the entire lateral hypothalamic area. It inter- connects the orbitofrontal cortex, septal area, hypothalamus, and midbrain. projects from the mamillary nuclei to the anterior nucleus of the thalamus (part of the Papez circuit). stria terminalis is the major pathway from the amygdala. It interconnects the septal area, hypothalamus, and amygdala. conducts Þbers from the supraoptic and par- aventricular nuclei to the neurohypophysis, which is the release site for ADH and tuberohypophysial (tuberoinfundibular) tract conducts Þbers from the arcu- ate nucleus to the hypophyseal portal system (see Figure 18-2). contains direct descending autonomic fibers. CHAPTER 18 D.FOOD INTAKE REGULATION. Two hypothalamic nuclei play a role in the control of Figure 18-3 Coronal section through the hypothalamus at the level of the dorsomedial, ventromedial, and lateral hypo- thalamic nuclei. Lesions or stimulation of these nuclei result in obesity, cachexia, and rage. The column of the fornix separates the medial from the lateral hypothalamic zones. A lesion of the optic tract results in a contralateral hemi- , fornix; ventral posterior nucleus of thalamus. (Reprinted from JD Fix, , 3rd ed. Baltimore: Williams & Wilkins, hippocampal formation Figure 19-1 Major connections of the amygdaloid nucleus. This nucleus receives input from three major sources: the olfactory system, sensory association and limbic cortices, and hypothalamus. Major output is through two channels: The stria terminalis projects to the hypothalamus and the septal area, and the ventral amygdalofugal pathway ( VAFP ) pro- jects to the hypothalamus, brain stem, and spinal cord. A smaller efferent bundle, the diagonal band of Broca, projects to the septal area. Afferent Þbers from the hypothalamus and brain stem enter the amygdaloid nucleus through the and anterior choroidal arteries of the internal carotid arteries). It causes anterograde Figure 19-3 Midsagittal section through the brain stem and diencephalon showing the distribution of lesions in WernickeÕs encephalopathy. ( ) Periventricular area. ) Inferior colliculus. Lesions in the mamillary nuclei are associated with WernickeÕs encephalopathy and thiamine (vitamin B ) deÞciency. LIMBIC SYSTEM Figure 19-4 Major connections of the hippocampal formation. The hippocampal formation (HF) consists of three parts: hippocampus, dentate gyrus, and subiculum. The two major hypothalamic output pathways are (1) granule cell via mossy Þber to pyramidal cell via precommissural fornix to septal nuclei and (2) subicular neuron via postcommissural fornix to the medial mamillary nucleus. The HF plays an important role in learning and memory, and lesions of the HF result in short-term memory defects. In AlzheimerÕs disease, loss of cells in the HF and entorhinal cortex leads to loss of , cornu ammonis. The sector CA1 is very sensitive to hypoxia (cardiac arrest or stroke). (Reprinted from JD Fix, , 3rd ed. Baltimore: Williams & Wilkins, 1996:332, with permission.) A 15-year-old boy was knocked out after several rounds of boxing with friends. Computed tomography scanning showed acute subdural hematoma associated with the right cerebral hemisphere. After regaining consciousness, the boy no longer experienced normal fear and complained of being very hungry all the time. What is the most likely diagnosis? CEREBELLUM Normal cerebellum Cerebellar-olivary atrophy Diffuse paraneoplastic atrophy Congenital atrophy of granular layer Figure 20-2 Various forms of cerebellar atrophy. , middle cerebellar peduncle; , inferior cerebellar peduncle; , superior cerebellar peduncle. (Reprinted from J Poirier, F Gray, R Escourolle, Manual of basic neuropathology, 3rded. 3.Ependymomas constitute 15% of all brain tumors in children. They occur most frequently in the fourth ventricle. They usually obstruct the passage of CSF and cause hydrocephalus. Olivopontocerebellar atrophy Dentatorubral atrophy Figure 20-2 A 50-year-old woman presented with a history of poor coordination of hands, speech, and eye Figure 21-2 A parasagittal section through the caudate nucleus ( ), internal capsule ( ). (ModiÞed from TA Woolsey, J Hanaway, MH Gado, brain atlas: a visual guide to the human central nervous system , 2nd ed. Hoboken: John Wiley & Sons, 2003:128, with 2.Glutamate (GLU) excitotoxicity results when GLU is released in the striatum and binds to its receptors on striatal neurons, culminating in an action poten- tal. GLU is removed from the extracellular space by astrocytes. In Hunting- tonÕs disease, GLU is bound to the Figure 21-3 An axial (horizontal) section through the anterior commissure ( iÞed from TA Woolsey, J Hanaway, MH Gado, The brain atlas: a visual guide to the human central nervous system ed. Hoboken: John Wiley & Sons, 2003:100, with permission.) with neuronal death most likely occurs in cerebrovascular accidents (e.g., stroke). 3.Clinical signs include choreiform movements, hypotonia, and progressive dementia. D.OTHER CHOREIFORM DYSKINESIAS 1.SydenhamÕs chorea (St. VitusÕ dance) is the most common cause of chorea over- all. It occurs primarily in girls, typically after a bout of rheumatic fever. BASAL NUCLEI (GANGLIA) AND STRIATAL MOTOR SYSTEM Figure 21-4 A coronal section through the lentiform nucleus and the amygdaloid nucleus ( )and the globus pallidus ( ); the amygdaloid nucleus appears as a circular proÞle below the uncus. (ModiÞed from TA Woolsey, J Hanaway, MH Gado, The brain atlas: a visual guide to the human central nervous , 2nd ed. Hoboken: John Wiley & Sons, 2003:60, with permission.) CHAPTER 21 Figure 21-5 Major afferent and efferent connections of the striatal system. The striatum receives major input from three sources: the thalamus, neocortex, and substantia nigra. The striatum projects to the globus pallidus and substan- tia nigra. The globus pallidus is the effector nucleus of the striatal system; it projects to the thalamus and subthalamic nucleus. The substantia nigra also projects to the thalamus. The striatal motor system is expressed through the corti- , centromedian nucleus; Figure 21-6 Major neurotransmitters of the striatal motor system. Within the striatum, globus pallidus, and pars 2.Chorea gravidarum usually occurs during the second trimester of pregnancy. Many patients have a history of SydenhamÕs chorea. E.HEMIBALLISM that usually results from a vascular lesion of tic) movements of one or both extremities. F.HEPATOLENTICULAR DEGENERATION (WILSONÕS DISEASE) recessive disorder A 30-year-old man presents with dysarthria, dysphagia, stiffness, and slow ataxic gait. There is no history of schizophrenia or depression and no family history of any neurodegenerative ¥The patient scored a 20/26 on the mini-mental status exam. The patient showed increased tone in all extremities, with normal strength. ¥A generalized cerebral and cerebellar atrophy and a very small caudate nucleus were CEREBRAL CORTEX Figure 22-1 Neurocortical circuits. cell. Loops show synaptic junctions. (Reprinted from A Parent, CarpenterÕs human neuroanatomy , 9th ed. Baltimore: Williams & Wilkins, 1996:868, with permission.) of these areas of the frontal lobe causes contralateral spastic paresis. Contralat- eral pronator drift is associated with frontal lobe lesions of the corticospinal 2.Frontal eye Þeld (BrodmannÕs area 8). Destruction causes deviation of the eyes to 3.BrocaÕs speech area (BrodmannÕs areas 44 and 45). This is located in the poste- rior part of the inferior frontal gyrus in the dominant hemisphere (Figure 22-4). Destruction results in expressive, nonßuent aphasia (BrocaÕs aphasia). The patient understands both written and spoken language but cannot articulate speech or write normally. BrocaÕs aphasia is usually associated with contralateral facial and 4.Prefrontal cortex (BrodmannÕs areas 9Ð12 and 46Ð47). Destruction of the ante- rior two-thirds of the frontal lobe convexity results in deÞcits in concentration, orientation, abstracting ability, judgment, and problem-solving ability. Other frontal lobe deÞcits include loss of initiative, inappropriate behavior, release of sucking and grasping reßexes, gait apraxia, and sphincteric incontinence. Destruc- tion of the orbital (frontal) lobe results in inappropriate social behavior (e.g., use of obscene language, urinating in public). Perseveration is associated with frontal CHAPTER 22 Parahippocampal cortex (5, 7) Visual association (9, 10, 11, 12) Figure 22-2 Some motor and sensory areas of the cerebral cortex. Lateral convex surface of the hemisphere. Medial surface of the hemisphere. The numbers refer to the Brodmann brain map (BrodmannÕs areas). CEREBRAL CORTEX Figure 22-3 Sensory representation in the postcentral gyrus. Motor rep- resentation in the precentral gyrus. (Reprinted from W PenÞeld, T Rasmussen, New York: Hafner, 1968:44, 57, with permission.) Figure 22-4 Cortical areas of the dominant hemisphere that play an important role in language production. The visual image of a word is projected from the visual cortex (BrodmannÕs area 17) to the visual association cortices (Brod- mannÕs areas 18 and 19) and then to the angular gyrus (BrodmannÕs area 39). Further processing occurs in WernickeÕs speech area (BrodmannÕs area 22), where the auditory form of the word is recalled. Through the arcuate fasciculus, this information reaches BrocaÕs speech area (BrodmannÕs areas 44 and 45), where motor speech programs control the vocal- ization mechanisms of the precentral gyrus. Lesions of BrocaÕs speech area, WernickeÕs speech area, or the arcuate fas- ciculus result in dysphasia. (Reprinted from JD Fix, , 3rd ed. Baltimore: Lippincott Williams & Wilkins, c.Dysgraphia and dyslexia. d.Dyscalculia. e.Contralateral hemianopia or lower quadrantanopia. ABC Figure 22-5 Testing for construction apraxia. The patient was asked to copy a cross. These drawings show contralateral CEREBRAL CORTEX Figure 22-6 Focal destructive hemispheric lesions and the resulting symptoms. dominant left hemisphere. Lateral convex surface of the nondominant right hemisphere. nondominant hemisphere. CHAPTER 22 Figure 22-8 Chimeric (hybrid) Þgure of a face used to examine the hemispheric function of commissurotomized or she sees the face of a man, the left hemisphere predominates in vocal tasks. If he or she is asked to point to the face and points to the woman, the right hemisphere predominates in pointing tasks. A 50-year-old woman was referred to neurology with a year-long history of poor memory and speech difÞculties. She noted an inability to remember the names of common household CHAPTER 23 Figure 23-1 Certain antidepressants increase 5-HT availability by reducing its reuptake. 5-HT have antidepressant proper- Figure 23-4 Distribution of norepinephrine-containing neurons and their projections. The locus ceruleus (located in the pons and midbrain) is the chief source of noradrenergic Þbers. The locus ceruleus projects to all parts of the central Figure 23-3 Distribution of dopamine-containing neurons and their projections. Two major ascending dopamine pathways arise in the midbrain: the nigrostriatal tract from the substantia nigra and the mesolimbic tract from the ven- tral tegmental area. In patients with ParkinsonÕs disease, loss of dopaminergic neurons occurs in the substantia nigra and the ventral tegmental area. Dopaminergic neurons from the arcuate nucleus of the hypothalamus project to the portal vessels of the infundibulum. Dopaminergic neurons inhibit prolactin. 2.Enkephalins are the most widely distributed and abundant opiate peptides. They are found in the highest concentration in the globus pallidus. Enkephalins coexist Figure 23-5 Distribution of 5-hydroxytryptamine (serotonin)-containing neurons and their projections. Serotonin- containing neurons are found in the nuclei of the raphe. They project widely to the forebrain, cerebellum, and spinal cord. The (1)GABA-ergic striatal neurons project to the globulus pallidus and sub- (2)GABA-ergic pallidal neurons project to the thalamus. (3)GABA-ergic nigral neurons project to the thalamus. (4)GABA receptors (GABA-A and GABA-B) are intimately associated with benzodiazepine-binding sites. Benzodiazepines enhance GABA activity. (a)GABA-A receptors (b)GABA-B receptors are found on the terminals of neurons that use another transmitter (i.e., norepinephrine, dopamine, serotonin). Acti- vation of GABA-B receptors decreases the release of the other trans- mitter. b.Glycine is the major inhibitory neurotransmitter of the spinal cord. It is used by the Renshaw cells of the spinal cord. 2.Excitatory amino acid transmitters a.Glutamate (Figure 23-7). GLU is the major excitatory transmitter of the Neocortical glutamatergic neurons project to the striatum, subthalamic GLU is the transmitter of the cerebellar granule cells. GLU is also the transmitter of nonnociceptive, large, primary afferent Þbers that enter the spinal cord and brain stem. GLU is the transmitter of the corticobulbar and corticospinal tracts. b.Aspartate. A major excitatory transmitter of the brain, aspartate is the trans- mitter of the climbing Þbers of the cerebellum. Neurons of climbing Þbers are found in the inferior olivary nucleus. c.Behavioral correlation. GLU, through its Figure 23-6 )-containing neurons and their projections. GABA-ergic neu- rons are the major inhibitory cells of the central nervous system. GABA local circuit neurons are found in the neocortex, hippocampal formation, and cerebellar cortex (Purkinje cells). Striatal GABA-ergic neurons project to the thalamus and D.MYASTHENIA GRAVIS A 60-year-old man presents with progressive stiffness accompanied by difÞculty in walking and going down stairs. He has an expressionless face and a vacant, staring gaze. Examina- tion revealed limited ocular motility in all directions. What is the most likely symptomatic ¥Tremor at rest, with pill-rolling motion of the hand ¥Rigidity observed when the patientÕs relaxed wrist is ßexed and extended ¥Bradykinesia ¥ParkinsonÕs disease is a progressive neurodegenerative disorder associated with a loss of dopaminergic nigrostriatal neurons. Often, patients are given levodopa combined with carbidopa. Nerve cells use levodopa to make dopamine to compensate for the loss of nigro- striatal neurons, whereas carbidopa delays the conversion of levodopa into dopamine until it reaches the brain. Effortful speech Dysarthric speech Telegraphic speech Transcortical sensory Transcortical Wernicke’s Mixed transcortical Figure 24-1 The Òaphasia squareÓ makes it easy to differentiate the six most common Ònational boardÓ aphasias. BrocaÕs, APRAXIA, APHASIA, AND DYSPROSODY A 7-year-old boy presents with difÞculty in articulating words, though he can hear words and understand their meaning. His mother noted he had difÞculty in breast-feeding during infancy. ¥Limited ability to produce speech sounds ¥Groping for correct placement of the tongue, lips, and jaw during speech ¥Omission of words in sentences ¥Atypical facial expressions ¥Apraxia results when sounds do not easily form into words. A complex coordination of lips, tongue, and throat muscles is required to articulate words. TABLE OF CRANIAL NERVES TypeOrigin TypeOrigin XÐVagal SVA, special visceral afferent; SSA, special somatic afferent; GVE, general visceral efferent; GSE, general somatic efferent; SVE, spe- cial visceral efferent; GSA, general somatic afferent; GVA, general visceral afferent; CN, cranial nerve. APPENDIX II Characteristics Literally means Òto dance;Ó patients cannot maintain a sustained posture; demonstrate ÒmilkmaidÕs gripÓ and ÒharlequinÕs tongueÓ Disintegration of Nissl substance in a neuronal cell body following damage Characterized by both upper and lower motor neuron signs, including back and leg pain, paresthesias and weakness, perineal or saddle anesthesia, and urorectal dysfunction; often results from acute disc herniation Congenital malformation characterized by underdevelopment of the cere- terior cranial fossa; developmental delays, enlarged head circumference, and symptoms of hydrocephalus may be observed Small punctate hemorrhages of the midbrain and pons resulting from arteri- TABLE OF COMMON NEUROLOGICAL DISEASE STATES Characteristics APPENDIX II Characteristics Tabes dorsalis Tic douloureux Wallerian degeneration Watershed infarct WilsonÕs disease WeberÕs syndrome Wernicke-Korsakoff syndrome tissue in the cord; results in pain, weakness, and stiffness in the trunk and Slow degeneration of the neurons in the dorsal columns of the spinal cord; results in abnormal proprioceptive signals Also known as trigeminal neuralgia; unilateral, severe, stabbing pain of the face, particularly jaw, cheek, or lip Process of degeneration of the axons distal to a site of transection amyotrophic lateral sclerosis (ALS) nonhereditary motor neuron disease affecting both upper and lower motor neurons; charac- electromyography. There are no sensory Lou GehrigÕs amyotrophy Muscle wasting or atrophy. Failure of the cerebral and cere- bellar hemispheres to develop; results from failure of the anterior neuropore to close. Circumscribed dilation of an artery (e.g., berry aneurysm). anhidrosis Horner syndrome. Pupils that are unequal in size; found in a third-nerve palsy and HornerÕs syn- drome. name objects; may result from a lesion of the Ignorance of the presence of Anton syndrome (visual anosognosia) of awareness of being cortically blind; bilateral occipital lesions affecting the visual association cortex. Impaired or absent communication apparent enophthalmos HornerÕs syndrome that makes the eye appear Disorder of voluntary movement; the the inability to properly use an object (e.g., a aprosodia (aprosody) pitch, rhythm, and the variation of stress in area postrema Chemoreceptor zone in the to recognize parts of the body; seen with pari- and ßinging of the contralateral extremities. gives rise to lower motor neurons (LMNs). BellÕs palsy Idiopathic facial nerve paralysis. BenediktÕs syndrome by a lesion of the midbrain affecting the intraaxial oculomotor Þbers, medial and cerebellothalamic Þbers. cerebral artery; ruptured berry aneurysms are arachnoid hemorrhage. blepharospasm Involuntary recurrent spasm of both eyelids; effective tr Tight junctions (zonulae occludentes) of the capillary endothelial cells. bloodÐcerebrospinal ßuid (CSF) barrier Tight choroid plexus. Extreme slowness in movement; seen in ParkinsonÕs disease. BrocaÕs aphasia DifÞculty in articulating or inferior frontal gyrus; also called expressive Progressive bulbar palsy; a lower motor neuron (LMN) paralysis affecting prototypic disease is amyotrophic lateral scle- rosis (ALS), characterized by dysphagia, dysarthria, and dysphonia. irrigating the external auditory meatus with either cold or warm water; remember COWS Sensory and motor nerve has relatively normal comprehension and Inability to perform and pronation); seen in cerebellar disease. disagreeable sensation produced by normal Movement disorders attributed to dal) system. Movements are generally charac- terized as insuppressible, stereotyped, and Inability to perform facial Visible twitching of muscle Þbers seen in lower motor neuron (LMN) disease. Acceleration of a shufßing gait seen in ParkinsonÕs disease. cle Þbers found in lower motor neuron GerstmannÕs syndrome dysgraphia, and dyscalculia; results from a contralateral extremities. hemiparesis Slight paralysis affecting one side of the body; seen in stroke involving the inter- Paralysis of one side of the body. herniation Pressure-induced protrusion of brain tissue into an adjacent compartment; Disorder charac- (memory), and seizures; the most common cause of encephalitis in the central nervous system. The temporal lobes are preferentially a complex multistep act (e.g., patient cannot of the brain stem just under the fourth ventri- which mediate vestibuloocular reßexes (e.g., nystagmus). Severance of this tract results in Transverse lines on Þngernails and Large brain weighing more Protrusion of the meninges of the brain or spinal cord through an osseous defect in the skull or vertebral canal. Protrusion of the meninges and the brain through a defect in meroanencephaly Less severe form of anen- cephaly in which the brain is present in rudi- microencephaly (micrencephaly) brain weighs approximately 1400 g. micrographia ParkinsonÕs disease. microgyria (polymicrogyria) Small gyri; corti- Arnold-Chiari syndrome. Millard-Gubler syndrome abducent and facial hemiparesis; an ipsilateral sixth and seventh nerve palsy and a contralat- eral hemiparesis. produce the myelin sheath in the peripheral nervous system (PNS). neuroÞbrillary tangles cal structures found in the neurons of AlzheimerÕs patients. neuroÞbromatosis(von Recklinghausen A neurocutaneous disorder. NeuroÞ- bromatosis type 1 consists predominantly of roÞbromas, Lish nodules, schwannomas), whereas type 2 consists primarily of intracra- neurohypophysis pituitary gland; derived from the downward neuropathy Disorder of the nervous system. porencephaly Cerebral cavitation caused by localized agenesis of the cortical mantle; the presbycusis(presbyacusia)I perceive or discriminate sounds as part of the aging process; due to atrophy of the organ of Corti. progressive supranuclear palsy downgaze paresis followed by paresis of other eye movements. As the disease progresses, the remainder of the motor cranial nerves proprioception ing from muscles, tendons, and other internal tissues. Conscious proprioception is mediated prosopagnosia DifÞculty in recognizing protopathic sensation Pain, temperature, and pseudobulbar palsy(pseudobulbar supranu- Upper motor neuron (UMN) syn- drome resulting from bilateral lesions that interrupt the corticobulbar tracts. Symptoms include difÞculties with articulation, mastica- tion, and deglutition; results from repeated Type of visual agnosia seen in the KlŸver-Bucy syndrome. Severe mental thought disorder. Drooping of the upper eyelid; seen in HornerÕs syndrome and oculomotor nerve Voluntary motor system consisting of upper motor neurons (UMNs) in the corticobulbar and corticospinal Hiccups; frequently seen in the pos- terior inferior cerebellar artery (PICA) syndrome. somatesthesia(somesthesia) perature. Increased muscle tone (hypertonia) Central gustatory pathway, 79 Central nervous system (CNS) regeneration in, 3 Centromedian nucleus, 116 Cerebellar artery, superior, 41, 42 Cerebellar astrocytomas, 7 Cerebellar cortex, 130 Cerebellar neurons, 130Ð131 Cerebellar peduncles, 130 Cerebellar tumors, 132Ð134 Cerebellar veins, superior, 41 Cerebellopontine angle, 115 Cerebellum cerebellar pathway, 131Ð132, 131 syndromes and tumors of, 132Ð134, 133 Cerebral aqueduct, 32 Cerebral artery anterior, 38, 39 posterior, 39 Cerebral cortex, 142Ð150 functional areas of, 142Ð148, 144 split-brain syndrome, 148, 149 Cerebral veins, 43, 44 great, 41, 43, 44 superior, 43, 44 Cerebrospinal ßuid (CSF), 3, 33Ð34, 33 Chorda tympani, 81 Chorea, 166 Chorea gravidarum, 141 Choroid Þssure, 13 Choroid plexus, 32Ð33 Choroid plexus papillomas, 7 ChromafÞn cells, 9 Chromatolysis, 3, 166 Ciliary ganglion, 53, 105 Cingulectomy, 128, 129 Central nervous system Cochlear nerve, 82, 93, 94 acoustic neuroma, 112 Communicating rami, of autonomic nervous system, 53, 56 Corneal reßex, 90, 91 Cortical centers for ocular motility, 106Ð107, Corticonuclear Þbers, 73, 78 Corticospinal tracts, diseases of, 65, 66 Cowdry type A inclusion bodies, 5 Cranial nerves, 74Ð87 abducent nerve, 79, 163 accessory nerve, 85Ð87, 85 facial nerve, 79Ð81, 79 glossopharyngeal nerve, 82Ð84, 83 hypoglossal nerve, 86 oculomotor nerve, 75Ð76, 162 olfactory, 74, 75 optic nerve, 13, 74, 101, 103 Dorsal midbrain syndrome, 111, 112 Dura mater, 30, 31 Facial colliculus syndrome, 111 Facial nerve, 79Ð81, 79 acoustic neuroma, 113 Fast anterograde axonal transport, 2 Lateral geniculate body, 102 Lateral inferior pontine syndrome, 110, 111 Lateral medullary syndrome, 109, 167 Lateral striate arteries, 40Ð41, 40 Papez circuit of, 127, 127 Lingual nerve, 81 Lower motor neuron ÒLocked-inÓ syndrome, 114, 167 Lou GehrigÕs disease. Amyotrophic lateral sclerosis Lower motor neuron (LMN), lesions of, 65, 66 Macroglia, 3 Mamillary bodies axial image through, 17, 22 coronal section through, 17, 20 Mamillary nucleus, 122 Mandibular nerve, 88, 89 Marcus Gunn. Relative afferent pupil Maxillary artery, 43, 47 Maxillary nerve, 88, 89 Medial geniculate body, 94, 94 Medial inferior pontine syndrome, 110 Medial longitudinal fasciculus (MLF) syndrome, 111, 111 Medial medullary syndrome, 109 Medial midbrain syndrome, 112, 112 Medial preoptic nucleus, 120, 121 Medial striate arteries, 39 Memory loss, 128 olfactory groove, 146 Palsy. Papez circuit, 127, 127 Paramedian midbrain syndrome, 111Ð112, 112 Superior cerebellar artery, 41, 42 Superior cerebellar veins, 41 Superior cerebral vein, 43, 44 Superior cervical ganglion, 106 Superior olivary nucleus, 93, 94 SVA. Special visceral afferent Special visceral efferent SydenhamÕs chorea, 139 Tabes dorsalis, 167 Tanycytes, 3 Tardive dyskinesia, 141 Taste, 81Ð82, 84 Tearing reßex, 91, 91 Tegmentum, 72 Temperature regulation, 122 Temporal lobe, 146Ð148 Tensor tympani paralysis, 78 Tentorial incisure, transtentorial herniation, 34, 34 Terminal ganglion, 53 axial image through, 17, 21 Third-nerve palsy, 38, 105 Tic douloureux, 167 Tinnitus, 82 Tongue, 86 ÒTop of the basilarÓ syndrome, 115 Tracts corticospinal, 65, 66 lateral corticospinal, 62 posterior column-medial lemniscus pathway, 58Ð59, 60 Transcortical mixed aphasia, 159 Transcortical motor aphasia, 159 Transcortical sensory aphasia, 159 Transforaminal herniation, 34, 34 Transtentorial herniation, 34, 34 Transverse temporal gyri of Heschl, 94 Trapezius muscle paralysis, 87 Trapezoid body, 93, 94 Trigeminal ganglion, 88, 89 Trigeminal nerve, 76Ð78, 77 Trigeminal neuralgia, 78, 91 Trigeminal reßexes, 90Ð91, 91 Trigeminal system, 88Ð92 Trigeminothalamic pathways, 88Ð90, 90 Trochlear nerve, 76, 77 Tumors cerebellar, 132Ð134 glomus jugulare, 113 Tuning fork tests, 95, 95 Upper motor neuron Transtentorial herniation Upper motor neuron (UMN), lesions of, 65, 66 Vagal nerve, 83 jugular foramen syndrome, 113 Vasoactive intestinal polypeptide (VIP), 57 Veins, of brain, 41 Venous dural sinuses, 41, 42 Ventral spinal artery occlusion, 66, 67 Ventral tegmental area, 126 Ventricular system, 32Ð33 Ventromedial nucleus, 120 Vertebral angiography, 41, 42 Vertebral artery, 40, 42 Vertebrobasilar system, 39 Vertical diplopia, trochlear nerve and, 76 Vertigo, 82 Vestibular nerve, 82, 98 acoustic neuroma, 112 Vestibular nuclei, 70, 72 Vestibular nystagmus, 99 Vestibular pathways, 97Ð99, 98 Vestibular system, 97Ð100 Vestibulocochlear nerve, 82, 94 acoustic neuroma, 112Ð113, 113 Vestibuloocular reßexes, 99Ð100, 99 VIP. Vasoactive intestinal polypeptide Viral meningitis, 31Ð32 Visual cortex, 103 Visual pathway, 101Ð103, 102 Visual system, 101Ð108 cortical and subcortical centers for ocular motility, 106Ð107, near reßex and accommodation pathway, 106 pupillary dilation pathway, 105Ð106, 105 pupillary light reßex pathway, 104 visual pathway, 101Ð103, 102 Wada test, 148 Wallenberg. Lateral medullary syndrome Wallerian degeneration, 2, 167 Water balance regulation, 122 Watershed infarcts, 160, 167 WeberÕs syndrome, 167. Medial midbrain syndrome Wernicke-Korsakoff syndrome, 116, 167 WernickeÕs aphasia, 159, 159 WernickeÕs encephalopathy, 128, 128 WernickeÕs speech area, 146 WilsonÕs disease, 167. High-Yield FOURTH EDITION Based on your feedback on previous editions of this text, the fourth edition has been reorganized and updated signiÞcantly. New features include chapter reorganization, terminology updates con- Terminologica Anatomica , addition of a table of common neurologic disease states, and an online ancillary of board-style review questions. To make the most effective use of this book, The authors applaud all of the individuals at Lippincott Williams & Wilkins involved in this revision, including Crystal Taylor, Kelley Squazzo, Jennifer Verbiar, and Wendy Druck, Aptara Project Man- ager. Without their hard work, dedication, cooperation, and understanding, our vision for this new edition would not have been realized. Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .v Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .ix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1 I.Neurons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1 II.Nissl substance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1 III.Axonal transport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1 IV.Wallerian degeneration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2 V.Chromatolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3 VI.Regeneration of nerve cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3 VII.Glial cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . VIII.The bloodÐbrain barrier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5 IX.The bloodÐCSF barrier . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . X.Pigments and inclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5 XI.The classiÞcation of nerve Þbers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5 XII.Tumors of the CNS and PNS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .5 XIII.Cutaneous receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .7 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9 I.The neural tube . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9 II.The neural crest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9 III.The anterior neuropore . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11 IV. The posterior neuropore . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11 V.Microglia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11 VI.Myelination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11 VII.Positional changes of the spinal cord . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13 The optic nerve and chiasm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13 IX.The hypophysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13 X.Congenital malformations of the CNS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .13 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17 II.Midsagittal section . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17 III.Coronal section through the optic chiasm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17 IV.Coronal section through the mamillary bodies . . . . . . . . . . . . . . . . . . . . . . . . . . . .17 V.Axial image through the thalamus and internal capsule . . . . . . . . . . . . . . . . . . . . .17 VI.Axial image through the midbrain, mamillary bodies, and optic tract . . . . . . . . . . .17 VII.Atlas of the brain and brain stem . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .17 CONTENTS Meninges, Ventricles, and Cerebrospinal Fluid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .30 I.Meninges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .30 II.Ventricular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .32 III.Cerebrospinal ßuid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .33 IV.Herniation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .34 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .38 I.The spinal cord and lower brain stem . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .38 II.The internal carotid system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .38 III.The vertebrobasilar system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .40 IV.The blood supply of the internal capsule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .41 V.Veins of the brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .41 VI.Venous dural sinuses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .41 VII.Angiography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .41 VIII.The middle meningeal artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .43 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .49 I.Gray and white rami communicans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .49 II.Termination of the conus medullaris . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .49 III.Location of the major motor and sensory nuclei of the spinal cord . . . . . . . . . . . . .49 IV.The cauda equina . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .50 V.The myotatic reßex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .50 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .53 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .53 CONTENTS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .70 I.Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .70 II.Cross section through the medulla . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .70 III.Cross section through the pons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .70 IV.Cross section through the rostral midbrain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .72 V.Corticonuclear Þbers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .73 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .74 I.The olfactory nerve (CN I) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .74 II.The optic nerve (CN II) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .74 III.The oculomotor nerve (CN III) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .75 IV.The trochlear nerve (CN IV) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .76 V.The trigeminal nerve (CN V) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .76 VI.The abducent nerve (CN VI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .79 VII.The facial nerve (CN VII) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .79 VIII.The vestibulocochlear nerve (CN VIII) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . IX.The glossopharyngeal nerve (CN IX) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .82 X.The vagal nerve (CN X) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . XI.The accessory nerve (CN XI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .85 XII.The hypoglossal nerve (CN XII) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .87 Trigeminal System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .88 I.Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .88 II.The trigeminal ganglion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .88 III.Trigeminothalamic pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .88 IV.Trigeminal reßexes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .90 V.The cavernous sinus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .92 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93 I.Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93 II.The auditory pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93 III.Hearing defects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .95 IV.Auditory tests . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .95 Vestibular System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97 I.Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97 II.The labyrinth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97 III.The vestibular pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97 IV.Vestibuloocular reßexes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .99 Visual System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .101 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .101 II.The visual pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .101 III.The pupillary light reßex pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .105 .The pupillary dilation pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .105 CONTENTS V.The near reßex and accommodation pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . .106 VI.Cortical and subcortical centers for ocular motility . . . . . . . . . . . . . . . . . . . . . . .106 VII.Clinical correlation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .107 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .109 I.Lesions of the medulla . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .109 II.Lesions of the pons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .110 III.Lesions of the midbrain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .111 IV.Acoustic neuroma (schwannoma) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .112 V.Jugular foramen syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .113 VI.ÒLocked-inÓ syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .114 VII.Central pontine myelinolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .114 VIII. ÒTop of the basilarÓ syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .115 IX.Subclavian steal syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .115 X.The cerebellopontine angle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .115 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .116 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .116 II.Major thalamic nuclei and their connections . . . . . . . . . . . . . . . . . . . . . . . . . . . .116 III.Blood supply . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .118 IV.The internal capsule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .118 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .120 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .120 II.Functions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .122 III.Clinical correlation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .124 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .125 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .125 II.Major components and connections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .125 III.The Papez circuit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .127 IV.Clinical correlation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .127 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .130 I.Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .130 II.Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .130 III.The major cerebellar pathway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .131 IV.Cerebellar dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .132 V.Cer ebellar syndromes and tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .132 . . . . . . . . . . . . . . . . . . . . . . . . . .135 I.Basal nuclei (ganglia) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .135 II.The striatal (extrapyramidal) motor system . . . . . . . . . . . . . . . . . . . . . . . . . . . . .135 III.Clinical correlation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .136 CONTENTS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .142 I.Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .142 II.The six-layered neocortex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .142 III.Functional areas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .142 IV.Focal destructive hemispheric lesions and symptoms . . . . . . . . . . . . . . . . . . . . . .148 V.Cerebral dominance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .148 VI.Split-brain syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .148 VII.Other lesions of the corpus callosum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .149 VIII.Brain and spinal cord tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .149 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .151 I.Important transmitters and their pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .151 II.Functional and clinical considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .156 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .158 I.Apraxia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .158 II.Aphasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .158 III.Dysprosody . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .160 Appendix I. Table of Cranial Nerves . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .162 Appendix II. Table of Common Neurologic Disease States . . . . . . . . . . . . . . . . . . . . . .165 Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .181 are classiÞed by the number of processes (Figure 1-1). A.PSEUDOUNIPOLAR NEURONS are located in the spinal (dorsal root) ganglia and sen- sory ganglia of cranial nerves (CN) V, VII, IX, and X. B.BIPOLAR NEURONS are found in the cochlear and vestibular ganglia of CN VIII, in NISSL SUBSTANCE AXONAL TRANSPORT A.FAST ANTEROGRADE AXONAL TRANSPORT is responsible for transporting all newly synthesized membranous organelles (vesicles) and precursors of neurotransmit- ters. This process occurs at the rate of 200 to 400 mm/day. It is mediated by neuro- (Fast transport is neurotubule-dependent.) B.SLOW ANTEROGRADE TRANSPORT is responsible for transporting Þbrillar WALLERIAN DEGENERATION is anterograde degeneration characterized by the disap- pearance of axons and myelin sheaths and the secondary proliferation of Schwann cells. It occurs in the central nervous system (CNS) and the peripheral nervous system (PNS). CHAPTER 1 Figure 1-1 Types of nerve cells. Olfactory neurons are bipolar and unmyelinated. Auditory neurons are bipolar and myelinated. Spinal (dorsal root) ganglion cells (cutaneous) are pseudounipolar and myelinated. Motor neurons are mul- indicate input through the axons of other neurons. Nerve cells are characterized by the CHROMATOLYSIS REGENERATION OF NERVE CELLS A.CNS. Effective regeneration does not occur in the CNS. For example, there is no regeneration of the optic nerve, which is a tract of the diencephalon. There are no basement membranes or endoneural investments surrounding the axons of theCNS. B.PNS. Regeneration does occur in the PNS. The proximal tip of a severed axon grows endoneurium. The axon sprout grows at the rate of 3 mm/day (Figure 1-2). are the nonneural cells of the nervous system. A.MACROGLIA astrocytes and oligodendrocytes 1.Astrocytes perform the following functions: They project foot processes that envelop the basement membrane of capillar- ies, neurons, and synapses. NEUROHISTOLOGY endothelial cells; some authorities include the astrocytic foot processes. Infarction of brain destroys the tight junctions of endothelial cells and results in A.LIPOFUSCIN GRANULES are pigmented cytoplasmic inclusions that commonly accumulate with aging. They are considered residual bodies that are derived from B.MELANIN (NEUROMELANIN) stantia nigra and locus coeruleus. It disappears from nigral neurons in patients who have ParkinsonÕs disease. C.LEWY BODIES are neuronal inclusions that are characteristic of ParkinsonÕs dis- D.NEGRI BODIES are intracytoplasmic inclusions that are pathognomonic of rabies. They are found in the pyramidal cells of the hippocampus and the Purkinje cells of the cere- E.HIRANO BODIES are intraneuronal, eosinophilic, rodlike inclusions that are found in the hippocampus of patients with AlzheimerÕs disease. F.NEUROFIBRILLARY TANGLES consist of intracytoplasmic degenerated neuroÞla- ments. They are seen in patients with AlzheimerÕs disease. G.COWDRY TYPE A INCLUSION BODIES are intranuclear inclusions that are found in neurons and glia in herpes simplex encephalitis. THE CLASSIFICATION OF NERVE FIBERS is shown in Table 1-1. are shown in Figures 1-3 and 1-4. NEUROHISTOLOGY According to national board questions, the Þve most common brain tumors are 1.Glioblastoma multiforme, 2.Meningioma, hemisphere. 3.Schwannoma, a benign peripheral tumor derived from Schwann cells. 4.Ependymoma, cord gliomas. 5.Medulloblastoma, CUTANEOUS RECEPTORS (Figure 1-5) are divided into two large groups: free nerve Free nerve endings are nociceptors (pain) and thermoreceptors (cold and heat). Encapsulated endings are touch receptors (MeissnerÕs corpuscles) and pressure and vibration receptors (Pacinian corpuscles). Merkel disks are unencapsulated light touch receptors. NEUROHISTOLOGY Choroid plexus papillomas  historically benign  represent 2% of the gliomas  one of the most common brain tumors in patients 2 years of age  occur in decreasing frequency: fourth, lateral, and third ventricle  CSF overproduction may cause hydrocephalus Craniopharyngiomas  represent 3% of primary brain tumors  derived from epithelial remnants of Rathke’s pouch  location: suprasellar and inferior to the optic chiasma  cause bitemporal hemianopia and hypopituitarism  calcification is common Pituitary adenomas (PA)  most common tumors of the pituitary gland  prolactinoma is the most common (PA)  derived from the stomodeum (Rathke’s pouch)  represent 8% of primary brain tumors  may cause hypopituitarism, visual field defects (bitemporal hemianopia and cranial nerve palsies CNN III, IV, VI, V-1 and V-2, and postganglionic Hemangioblastomas  characterized by abundant capillary blood vessels and foamy cells; most often found in the cerebellum Figure 1-4 children, 70% of tumors are infratentorial. (Figure 2-1) gives rise to the central nervous system (CNS) brain and spinal cord). and spinal cord have sensory neurons. motor neurons (Figure 2-2). three primary vesicles, ary vesicles (Figure 2-3). (see Figure 2-1) gives rise to peripheral nervous system (PNS) (i.e., peripheral nerves and sensory and auto- 1.Pseudounipolar ganglion cells of the spinal and cranial nerve 2.Schwann cells 3.Multipolar ganglion cells 4.Leptomeninges (the pia-arachnoid), which envelop the brain and spinal cord 5.ChromafÞn cells of the suprarenal medulla (which elaborate epinephrine). 6.Pigment cells 7.Odontoblasts (which elaborate predentin) 8.Aorticopulmonary septum 9.Parafollicular cells (calcitonin-producing C-cells) 1)Be familiar with neural crest derivatives. 2)Recognizes the dual origin of the pituitary gland. The closure of the anterior neuropore gives rise to the Failure to close results in anencephaly (i.e., failure of the brain to Failure to close results in spina biÞda (Figure 2-4). arise from the monocytes. MYELINATION begins in the fourth month of gestation. Myelination of the corti- DEVELOPMENT OF THE NERVOUS SYSTEM Figure 2-3 The brain vesicles indicating the adult derivatives of their walls and cavities. (Reprinted from Moore KL. The Developing Human:Clinically Orienting Embryology, Figure 2-4 The various types of spina biÞda. (Reprinted from Sadler TW. LangmanÕs Medical Embryology, Baltimore: Williams & Wilkins, 1990:363, with permission.) DEVELOPMENT OF THE NERVOUS SYSTEM newborn, the conus medullaris ends at the third lumbar vertebra (L-3). THE OPTIC NERVE AND CHIASMA are derived from the diencephalon. The optic nerve Þbers occupy the choroid Þssure . Failure of this Þssure to close results in (pituitary gland) is derived from two embryologic substrata (Figures 2-6 and 2-7). A.ADENOHYPOPHYSIS (anterior lobe)is derived from an ectodermal diverticulum of RathkeÕs pouch nants of RathkeÕs pouch may give rise to a congenital cystic tumor, a craniopharyn- B.NEUROHYPOPHYSIS (posterior lobe)develops from a ventral evagination of the hypothalamus (neuroectoderm of the neural tube). CONGENITAL MALFORMATIONS OF THE CNS A.ANENCEPHALY (MEROANENCEPHALY) results from failure of the anterior neuro- pore to close. As a result, the brain does not develop. The frequency of this condition B.SPINA BIFIDA results from failure of the posterior neuropore to form. The defect usu- ally occurs in the sacrolumbar region. The frequency of spina biÞda occulta is 10%. Third ventricle Pars tuberalis of adenohypophysis Adenohypophysis (anterior lobe) Craniopharyngeal canal Remnant of Rathke’s pouch Infundibulum of hypothalamus Diaphragma sellae Pars intermedia of anterior lobe Neurohypophysis (posterior lobe) Dura Figure 2-6 Midsagittal section through the hypophysis and sella turcica. The adenohypophysis, including the pars tuberalis and pars intermedia, is derived from RathkeÕs pouch (oroectoderm). The neurohypophysis arises from the infundibulum of the hypothalamus (neuroectoderm). The illustrations in this chapter are accompanied by corresponding MIDSAGITTAL SECTION (Figures 3-1 through 3-3). The location of the structures shown in the Þgures should be known. (Figures 3-4 and 3-5). The location of the structures shown in the Þgures should be known. CORONAL SECTION THROUGH THE MAMILLARY BODIES (Figures 3-6 and 3-7). The location of the structures shown in the Þgures should be known. (Figures 3-8 and 3-9). The location of the structures shown in the Þgures should be known. AXIAL IMAGE THROUGH THE MIDBRAIN, MAMILLARY BODIES, AND (Figures 3-10 through 3-13). The location of the structures shown in the Þgures should be known. ATLAS OF THE BRAIN AND BRAIN STEM (Figures 3-14 through 3-24). Included are midsagittal, parasagittal, coronal, and axial sections of thick, stained brain slices. The mini-atlas provides you with the essential examination structures labeled on computed Meninges, Ventricles, are three that surround the spinal cord and brain. pia mater,arachnoid mater, dura mater. covers the surface of the brain and spinal cord. Cerebrospinal ßuid is produced by the choroid plexus and absorbed by the arachnoid villi that protrude into the venous sinuses. Cerebrospinal ßuid pathways are well demonstrated in Figure 4-1. (Remember: Kernig More than 70% of cases occur in children younger than 5 years. The disease may cause cranial nerve palsies and hydrocephalus. a.Common causes newborns(younger than 1 month) , bacterial meningitis is most fre- group B streptococci (Streptococcus agalactiae), older infants and young children(1 through 23 months) Streptococcus pneumoniae young adults (2 through 18 years) , it is most frequently caused by , it is most frequently caused by Strep- has signiÞcantly reduced b.CSF Þndings Numerous polymorphonuclear leukocytes Decreased glucose levels Increased protein levels 2.Viral meningitis by fever, headache, nuchal rigidity, and KernigÕs sign. a.Common causes. Many viruses are associated with viral meningitis, includ- b.CSF Þndings Numerous lymphocytes Moderately increased protein levels choroid plexus is a specialized structure that projects into the lateral, third, and fourth ventricles of the brain. It consists of infoldings of blood vessels of the pia mater CHAPTER 4 1.Noncommunicating hydrocephalus results from obstruction within the ventri- 2.Communicating hydrocephalus results from blockage within the subarachnoid 3.Normal-pressure hydrocephalus arachnoid villi. It may occur secondary to posttraumatic meningeal hemorrhage. Clinically, it is characterized by the triad of progressive dementia, ataxic gait, and urinary incontinence. is a colorless acellular ßuid. It ßows through the ventricles A.FUNCTION 1.CSF supports the central nervous system (CNS) and protects it sive injury. transports hormones and hormone-releasing factors. MENINGES, VENTRICLES, AND CEREBROSPINAL FLUID Cerebrospinal Subarachnoid Bacterial Viral Clear, cloudy 5 lymphocytesRed blood cells 1,000 polymorphonuclear 25Ð500 present Protein 45 mg/dLNormal to Elevated, 45 mg/dLNormal BACTERIAL MENINGITIS, AND VIRAL ENCEPHALITIS TABLE 4.Total protein levels HERNIATION (Figures 4-2 through 4-7) A.TRANSTENTORIAL (UNCAL) HERNIATION is protrusion of the brain through the tentorial incisure. This may result in oculomotor paresis and contralateral hemiplegia. B.TRANSFORAMINAL (TONSILLAR) HERNIATION is protrusion of the brain stem and cerebellum through the foramen magnum. Clinical complications include obtundation C.SUBFALCINE (CINGULATE) HERNIATION is herniation below the falx cerebri. This condition does not necessarily result in severe clinical symptoms. It can present as headache. Compression of the anterior cerebral artery may result in contralateral leg CHAPTER 4 5 6 2 Tumor Figure 4-2 Coronal section of a tumor in the supratentorial compartment. ( ) Anterior cerebral artery; ( herniation; ( ) posterior cerebral artery (compression results in contralateral hemi- ) uncal (transtentorial) herniation; ( ) KernohanÕs notch (contralateral cerebral peduncle), with damaged cor- ) tentorium cerebelli; ( )tonsillar (transforaminal) herniation, which damages vital medullary centers. (Adapted with permission from Leech RW, Shumann RM: Neuropathology. New York, Harper & Row, 1982, p. 16.) are supplied with blood through anterior spinal artery (Figure 5-1). The anterior spinal artery supplies the the anterior spinal artery supplies the pyramid, medial lemniscus, and root Þbers of cranial nerve (CN) XII. (see Figure 5-1) consists of the internal carotid artery ophthalmic artery enters the orbit with the optic nerve (CN II). The central artery 1)The essential arteries supplying the brain and spinal cord and the functional areas that 2)The carotid and vertebral angiograms and the epidural and subdural hematomas in CHAPTER 5 Figure 5-3 Coronal section through the cerebral hemisphere at the level of the internal capsule and thalamus, show- THE VERTIBROBASILAR SYSTEM See Figure 5-1. vertebral artery is a branch of the subclavian artery. It gives rise to the spinal artery posterior inferior cerebellar artery (PICA), ambiguus (CN IX, X, and XI) and the inferior surface of the cerebellum. basilar artery is formed by the two vertebral arteries. It gives rise to the following arteries: which includes the corticospinal Þbers and the exiting root Þbers of the abducent nerve (CN VI). labyrinthine artery arises from the basilar artery in 15% of people. It arises from the anterior inferior cerebellar artery in 85% of people. anterior inferior cerebellar artery (AICA) tegmentum, including CN VII, the spinal trigeminal tract of CN V, and the inferior surface of the cerebellum. superior cerebellar artery supplies the dorsolateral tegmentum of the rostral pons (i.e., rostral to the motor nucleus of CN V), the superior cerebellar pedun- cle, the superior surface of the cerebellum and cerebellar nuclei, and the cochlear posterior cerebral artery (see Figures 5-1 through 5-3) is connected to the carotid artery through the posterior communicating artery. It provides the geniculate bodies, and occipital lobe (which includes the visual cortex and the infe- rior surface of the temporal lobe, including the hippocampal formation). of this artery results in a THE BLOOD SUPPLY OF THE INTERNAL CAPSULE comes primarily from the of the middle cerebral artery and the anterior choroidal artery superior cerebral (ÒbridgingÓ) veins ation results in a great cerebral vein (of Galen)drains the deep cerebral veins into the receives blood from the bridging veins and emissary veins (a potential route for transmission of extracranial infection into brain). The superior sagittal sinus also receives cerebrospinal ßuid (CSF) through the arachnoid villi. cavernous sinus contains CN III, IV, V-1 and V-2, and VI and the postganglionic A.CAROTID ANGIOGRAPHY. Figures 5-5A and B show the internal carotid artery, ante- rior cerebral artery, and middle cerebral artery. B.VERTEBRAL ANGIOGRAPHY. Figures 5-5Cand D show the vertebral artery, PICA and AICA, basilar artery, superior cerebellar artery, and posterior cerebral artery (Figures 5-6 and 5-7). BLOOD SUPPLY BLOOD SUPPLY AC Figure 5-6 See Figures 5-9 through 5-12. THE MIDDLE MENINGEAL ARTERY, maxillary artery, nium through the portion. Laceration results in (hematoma) (Figures 5-13 and 5-14). GRAY AND WHITE RAMI COMMUNICANS (Figure 6-1) TERMINATION OF THE CONUS MEDULLARIS (see Figure 4-1) occurs in the new- born at the level of the body of the third lumbar vertebra (L-3). In the adult, it occurs at the level of the lower border of the Þrst lumbar vertebra (L-1). This is clinically relevant in LOCATION OF THE MAJOR MOTOR AND SENSORY NUCLEI OF THE SPINAL (Figure 6-2) 1)The adult spinal cord terminates (conus terminalis) at the lower border of the Þrst lum- bar vertebra. 2)The newbornÕs spinal cord extends to the third lumbar vertebra. In adults, the cauda equina extends from vertebral level L-2 to coccygeal vertebra (Co). nucleus of the accessory nerve, from C-1 to C-6 phrenic nucleus, from C-3 to C-6 Motor and sensory roots that are found in the subarachnoid space below the conus medullaris form the cauda equina. They exit the vertebral canal through the lumbar intervertebral and sacral foramina. THE MYOTATIC REFLEX (see Figure 6-1) is a monosynaptic and ipsilateral CHAPTER 6 TABLE Figure 6-1 The four functional components of the thoracic spinal nerve: general visceral afferent ( GVA somatic afferent ( ), general somatic efferent ( ), and general visceral efferent ( ). Proprioceptive, cutaneous, The autonomic nervous system (ANS) is a general visceral efferent controls and regulates smooth muscle,cardiac muscle,andglands. projection neurons: 1.Preganglionic neurons. 2.Postganglionic neurons. A.CN III (ciliary ganglion). B.CN VII C.CN IX D.CN X COMMUNICATING RAMI A.WHITE RAMI COMMUNICANTES, CHAPTER 7 Structure Note erection versus ejaculation: Remember hoot, where TABLE B.GRAY RAMI COMMUNICANTES, which are found at all spinal levels and are C.DOPAMINE, which is the neurotransmitter of the small, intensely ßuorescent (SIF) CLINICAL CORRELATION A.MEGACOLON (HIRSCHSPRUNGÕS DISEASE, CONGENITAL AGANGLIONIC is characterized by extreme dilation and hypertrophy of the colon, with AUTONOMIC NERVOUS SYSTEM Tracts of the Spinal Cord Figure 8-1 shows the ascending and descending tracts of the spinal cord. This chapter covers four of the major tracts. POSTERIOR (DORSAL) COLUMNÐMEDIAL LEMNISCUS PATHWAY (Figure 8-1 and 8-2; see also Figure 9-1) A.FUNCTION. tile discrimination, vibration sensation, form recognition, and joint and muscle sensa- tion (conscious proprioception). B.RECEPTORS include Pacinian and MeissnerÕs tactile corpuscles, joint receptors, mus- cle spindles, and Golgi tendon organs. C.FIRST-ORDER NEURONS are located in the spinal (dorsal root) ganglia at all levels. They project axons to the spinal cord through the medial root entry zone. First-order neurons give rise to The gracile fasciculus from the lower extremity. The cuneate fasciculus from the upper extremity. The collaterals for spinal reßexes (e.g., myotatic reßex). D.SECOND-ORDER NEURONS are located in the gracile and cuneate nuclei of the cau- dal medulla. They give rise to axons and internal arcuate Þbers that decussate and form a compact Þber bundle (i.e., medial lemniscus). The medial lemniscus ascends through the contralateral brain stem and terminates in the ventral posterolateral (VPL) nucleus E.THIRD-ORDER NEURONS are located in the VPL nucleus of the thalamus. They pro- ject through the posterior limb of the internal capsule to the postcentral gyrus, which is the primary somatosensory cortex (BrodmannÕs areas 3, 1, and 2). The most important tracts of the spinal cord are corticospinal (pyramidal), posterior (dor- sal) columns, pain and temperature. Know them cold! F.TRANSECTION OF THE POSTERIOR (DORSAL) COLUMNÐMEDIAL LEMNISCUS 1.Above the sensory decussation, transection results in contralateral loss of the 2.In the spinal cord, transection results in ipsilateral loss of the posterior (dorsal) LATERAL SPINOTHALAMIC TRACT (Figure 8-1 and 8-3; see also Figure 9-1) A.FUNCTION. The lateral spinothalamic tract mediates pain and temperature sensation. B.RECEPTORS are free nerve endings. The lateral spinothalamic tract receives input from and C, respectively). C.FIRST-ORDER NEURONS are found in the spinal (dorsal root) ganglia at all levels. They project axons to the spinal cord through the dorsolateral tract of Lissauer (lateral root entry zone) to second-order neurons. D.SECOND-ORDER NEURONS are found in the dorsal horn. They give rise to axons ventral white commissure E.THIRD-ORDER NEURONS are found in the VPL nucleus of the thalamus. They pro- ject through the posterior limb of the internal capsule to the primary somatosensory cortex (BrodmannÕs areas 3, 1, and 2). F.TRANSECTION OF THE LATERAL SPINOTHALAMIC TRACT results in contralateral loss of pain and temperature below the lesion. Figure 8-1 The major ascending and descending pathways of the spinal cord. The ascending sensory tracts are shown and the descending motor tracts are shown on the right. LATERAL CORTICOSPINAL TRACT (Figure 8-1 and 8-4; see also Figure 9-1) A.FUNCTION. The lateral corticospinal tract mediates voluntary skilled motor activity, (BabinskiÕs sign). B.FIBER CALIBER. (Figure 8-5) A.ANATOMIC LOCATION. The hypothalamospinal tract projects without interruption from the hypothalamus to the ciliospinal center of the intermediolateral cell column at T-1 to T-2. It is found in the spinal cord at T-1 or above in the dorsolateral quadrant of TRACTS OF THE SPINAL CORD DISEASES OF THE MOTOR NEURONS AND CORTICOSPINAL TRACTS (Figures 9-1 and 9-2) A.UPPER MOTOR NEURON (UMN) LESIONS ARE CAUSED BY TRANSECTION OF THE CORTICOSPINAL TRACT OR DESTRUCTION OF THE CORTICAL CELLS OF ORIGIN. THEY RESULT IN SPASTIC PARESIS with pyramidal signs (BabinskiÕs sign). B.LOWER MOTOR NEURON (LMN) LESIONS ARE CAUSED BY DAMAGE TO THE MOTOR NEURONS. THEY RESULT IN FLACCID PARALYSIS, areßexia, atrophy, fas- Poliomyelitis or Werdnig-Hoffmann disease (Figure 9-2A) results from damage to the motor neurons. An example of a combined UMN and LMN disease is amyotrophic lateral sclerosis (ALS, or Lou GehrigÕs disease) (Figure 9-2D). ALS is caused by damage to the corti- toms. Patients with ALS have no sensory deÞcits. SENSORY PATHWAY LESIONS (Figure 9-2C). This disease is seen in patients with neurosyphilis. It is characterized by a loss of tactile discrimination and position and vibration sensation. Irritative involvement of the dorsal roots results in pain and paresthe- COMBINED MOTOR AND SENSORY LESIONS A.SPINAL CORD HEMISECTION (BROWN-SƒQUARD SYNDROME) (Figure 9-2E) caused by damage to the following structures: dorsal columns [gracile (leg) and cuneate (arm) fasciculi]. Damage results Study the eight classic national board lesions of the spinal cord. Four heavy hitters are Brown- Siquard syndrome, B amyotrophic lateral sclerosis (ALS, or Lou GehrigÕs disease). D.SYRINGOMYELIA (Figure 9-2H) is a central cavitation of the cervical cord of PERIPHERAL NERVOUS SYSTEM (PNS) LESIONS Guillain-BarrŽ syndrome It primarily affects the motor Þbers of the ventral roots and peripheral nerves, and it pro- duces LMN symptoms (i.e., muscle weakness, ascending ßaccid paralysis, and areßexia.) Guillain-BarrŽ syndrome has the following features: Upper cervical root (C4) involvement and respiratory paralysis are common. Caudal cranial nerve involvement with facial diplegia is present in 50% of cases. Elevated protein levels may cause papilledema. To a lesser degree, sensory Þbers are affected, resulting in paresthesias. The protein level in the cerebrospinal ßuid is elevated but without pleocytosis INTERVERTEBRAL DISK HERNIATION Intervertebral disk herniation consists of prolapse, or herniation, of the posus through the defective anulus Þbrosus and into the vertebral canal. impinges on the spinal roots, resulting in spinal root symptoms (i.e., paresthesias, pain, sensory loss, hyporeßexia, and muscle weakness). results usually from a nerve root tumor, an ependymoma, or a dermoid tumor, or from a lipoma of the terminal cord. It is characterized by Severe radicular unilateral pain. Sensory distribution in a unilateral area. CHAPTER 9 Unilateral muscle atrophy and absent quadriceps (L3) and ankle jerks (S1). Unremarkable incontinence and sexual functions. usually results from an intramedullary tumor (e.g., ependymoma). It is characterized by Pain, usually bilateral and not severe. Sensory distribution in a bilateral area. Unremarkable muscle changes; normal quadriceps and ankle reßexes. Severely impaired incontinence and sexual functions. LESIONS OF THE SPINAL CORD from the pyramidal decussation to the posterior commissure. The brain stem receives its blood supply from the vertebrobasilar system. It contains cranial nerves (CN) III to XII (except the spinal part of CN XI). Figures 10-1 and 10-2 show its surface anatomy. (Figure 10-3) A.MEDIAL STRUCTURES which contains crossed Þbers from the gracile and cuneate (corticospinal Þbers) B.LATERAL STRUCTURES inferior cerebellar peduncle, which contains the dorsal spinocerebellar, cuneocerebellar, and olivocerebellar tracts tract of trigeminal nerve (Figure 10-4). The pons has a dorsal A.MEDIAL STRUCTURES Genu (internal) of CN VII (underlies facial nerve) (facial colliculus) 1)Study the transverse sections of the brain stem and localize the cranial nerve nuclei. 2)Study the ventral surface of the brain stem and identify the exiting and entering cranial nerves. 3)On the dorsal surface of the brain stem, identify the only exiting cranial nerve, the trochlear nerve. Vestibular nuclei of CN VIII (Figure 10-5). The mid- CHAPTER 10 Figure 10-3 Transverse section of the medulla at the midolivary level. The vagal nerve [cranial nerve ( sal nerve (CN XII), and vestibulocochlear nerve (CN VIII) are prominent in this section. The nucleus ambiguus gives rise to special visceral efferent Þbers to CN IX, X, and XI. Figure 10-4 Transverse section of the pons at the level of the abducent nucleus of cranial nerve ( Dentatothalamic tract (crossed) C.CRUS CEREBRI (basis pedunculi cerebri, or cerebral peduncle). The lies in the middle three-Þfths of the crus cerebri. CORTICONUCLEAR FIBERS project bilaterally to all motor cranial nerve nuclei except the facial nucleus. The division of the facial nerve nucleus that innervates the receives bilateral corticonuclear input sion of the facial nerve nucleus that innervates the lower face receives Figure 10-5 Transverse section of the midbrain at the level of the superior colliculus, oculomotor nucleus of cranial ) III, and red nucleus. THE OLFACTORY NERVE, the Þrst cranial nerve (Figure 11-1), mediates olfac- . It is the only sensory system that has no precortical relay in the thalamus. The olfactory nerve is a special visceral afferent (SVA) nerve; see Appendix I. It consists of unmyelinated axons of bipolar neurons that are located in the nasal mucosa, the olfactory epithelium. It enters the cranial cavity through the THE OPTIC NERVE (CN II) is a special somatic afferent nerve that subserves vision and pupillary light reßexes (afferent limb; see Chapter 15). It enters the cranial cav- ity through the optic canal of the sphenoid bone. It is not a trueperipheral nerve tract of the diencephalon. A transected optic nerve cannot regenerate. 1)This chapter is pivotal. It spawns more neuroanatomy examination questions than any other chapter. Carefully study all of the Þgures and legends. 2)The seventh cranial nerve deserves special consideration (see Figures 11-5 and 11-6). THE OCULOMOTOR NERVE (CN III) is a general somatic efferent (GSE), general vis- ceral efferent (GVE) nerve. A.GENERAL CHARACTERISTICS. The oculomotor nerve pupil,accommodates, It exits the brain stem from the interpeduncular fossa of the midbrain, passes through the cavernous sinus, and enters the orbit through the superior orbital Þssure. arises from the oculomotor nucleus of the rostral midbrain. It innervates four extraocular muscles and the levator palpebrae muscle. ( SIN:s uperior muscles are torters of the globe.) medial rectus muscle adducts the eye. With its opposite partner, it con- verges the eyes. superior rectus muscle elevates, intorts, and adducts the eye. inferior rectus muscle depresses, extorts, and adducts the eye. elevates, extorts, and abducts the eye. CRANIAL NERVES Figure 11-1 ). (Reprinted from RC Truex, CE Kellner. lateral rectus and superior oblique muscles. The superior oblique and lateral rectus muscles are innervated by CN IV and CN VI, respectively. Oculomotor palsy results in (double vision) when the patient looks in the direc- THE TROCHLEAR NERVE (CN IV) nerve. A.GENERAL CHARACTERISTICS. The trochlear nerve is a pure motor nerve that inner- vates the superior oblique muscle. This muscle depresses, intorts, and abducts the eye. (Figure 11-2.) arises from the contralateral trochlear nucleus of the caudal midbrain. brain stem on its dorsal surface, caudal to the inferior colliculus. encircles the midbrain within the subarachnoid space, passes through the cav- ernous sinus, and enters the orbit through the superior orbital Þssure. B.CLINICAL CORRELATION. Because of its course around the midbrain, the trochlear nerve is particularly vulnerable to head trauma. The trochlear decussation under- lies the superior medullary velum. Trauma at this site often results in bilateral fourth-nerve palsies. Pressure against the free border of the tentorium (herniation) may injure the nerve (Figure 11-2). results in the following condi- 1.Extorsion of the eye and weakness of downward gaze. 2.Vertical diplopia, which increases when looking down. 3.Head tilting THE TRIGEMINAL NERVE (CN V) is a special visceral efferent (SVE), general somatic afferent (GSA) nerve (Figure 11-3). A.GENERAL CHARACTERISTICS. The trigeminal nerve is the nerve of pharyngeal (branchial) arch 1 (mandibular). It has three divisions: ophthalmic (CN V-1), maxil- lary (CN V-2), and mandibular (CN V-3). arises from the motor nucleus of trigeminal nerve that is found innervates CHAPTER 11 THE ABDUCENT NERVE (CN VI) A.GENERAL CHARACTERISTICS. The abducent nerve is a pure GSE nerve vates the lateral rectus muscle, which abducts the eye. It arises from the abducent nucleus that is found in the dorsomedial tegmentum Exiting intraaxial Þbers pass through the corticospinal tract. A results in alternating abducent hemiparesis. It passes through the pontine cistern and cavernous sinus and enters the orbit through the superior orbital Þssure. B.CLINICAL CORRELATION. CN VI PARALYSIS results from the long peripheral course of the nerve. It is seen in patients with menin- gitis, subarachnoid hemorrhage, late-stage syphilis, and trauma. Abducent nerve paral- results in the 1.Convergent (medial) strabismus (esotropia) 2.Horizontal diplopia THE FACIAL NERVE (CN VII) A.GENERAL CHARACTERISTICS. The facial nerve is a general visceral afferent (GVA), SVA, GVE, nerve (Figures 11-5 and 11-6). It general sensation from the external ear. is the nerve of the pharyngeal (branchial) arch 2 (hyoid). It includes the facial nerve proper (motor division), which contains the SVE Þbers that innervate the muscles of CRANIAL NERVES Figure 11-5 THE VESTIBULOCOCHLEAR NERVE (CN VIII) is an SSA nerve. It has two func- tional divisions: the vestibular nerve, which cochlear nerve, which . It exits the brain stem at the cerebellopontine angle and enters the internal auditory meatus. It is conÞned to the temporal bone. A.VESTIBULAR NERVE (see Figure 14-1) 1.General characteristics It is associated functionally with the cerebellum (ßocculonodular lobe) and It regulates compensatory eye movements. Its Þrst-order sensory bipolar neurons are located in the vestibular ganglion in the fundus of the internal auditory meatus. It projects its peripheral processes to the hair cells of the cristae of the semi- circular ducts and the hair cells of the utricle and saccule. It projects its central processes to the four vestibular nuclei of the brain stem and the ßocculonodular lobe of the cerebellum. It conducts efferent Þbers to the hair cells from the brain stem. 2.Clinical correlation. result in B.COCHLEAR NERVE (see Figure 13-1) 1.General characteristics Its Þrst-order sensory bipolar neurons are located in the spiral (cochlear) gan- It projects its peripheral processes to the hair cells of the organ of Corti. It projects its central processes to the dorsal and ventral cochlear nuclei of the It conducts efferent Þbers to the hair cells from the brain stem. 2.Clinical correlation. acoustic neuroma (schwannoma) is a Schwann cell tumor of the cochlear nerve that causes THE GLOSSOPHARYNGEAL NERVE (CN IX) GVA SVA nerve (Figure 11-7). A.GENERAL CHARACTERISTICS. The glossopharyngeal nerve is primarily a sensory nerve. Along with CN X, CN XI, and CN XII, it from the carotid sinus, which contains barorecep- tors that monitor arterial blood pressure. It also from the carotid body, which contains chemoreceptors that monitor the CO 1.Anatomy. CN IX is the nerve of pharyngeal (branchial) arch 3. It exits the brain stem (medulla) from the postolivary sulcus with CN X and CN XI. It exits the skull through the jugular foramen with CN X and CN XI. innervates part of the external ear and the external auditory meatus through the auricular branch of the vagus nerve. It has cell bodies in the superior ganglion. It projects its central processes to the spinal tract and nucleus of trigeminal nerve. CHAPTER 11 innervates only the stylopharyngeus muscle. It arises from THE VAGAL NERVE (CN X) GSA, GVA, SVA, SVE, nerve (see Figure A.GENERAL CHARACTERISTICS. The vagal nerve tion from the ear. It innervates the viscera neck,thorax, 1.Anatomy. The vagal nerve is the nerve of pharyngeal (branchial) arches 4 and 6. Pharyngeal arch 5 is either absent or rudimentary. It exits the brain stem (medulla) from the postolivary sulcus. It exits the skull through the jugular foramen with innervates the infratentorial dura, external ear, external audi- ganglion, and it projects its central processes to the spinal tract and nucleus of trigeminal nerve. GVA component innervates the mucous membranes of the pharynx, larynx, esophagus, trachea, and thoracic and abdominal viscera (to the left colic ßexure). It has cell bodies in the inferior (nodose) ganglion. It projects its central processes SVA component innervates the taste buds in the epiglottic region. It has cell bodies in the inferior (nodose) ganglion. It projects its central processes to the solitary tract and nucleus. (For a discussion of the central pathway, see innervates the pharyngeal (brachial) arch muscles of the lar- uvula, and the levator veli palatini and palatoglossus muscles. It receives SVE input from the cranial division of the spinal accessory nerve (CN XI). It arises from the nucleus ambiguus in the lateral medulla. The SVE component provides the effer- ent limb of the gag reßex. innervates the viscera of the neck and the thoracic (heart) and abdominal cavities as far as the left colic ßexure. Preganglionic parasympa- CHAPTER 11 B.CLINICAL CORRELATION. reßexes 1.Ipsilateral paralysis of the soft palate, pharynx, and larynx that leads to dyspho- nia (hoarseness), dyspnea, dysarthria, and dysphagia. 2.Loss of the gag (palatal) reßex (efferent limb). 3.Anesthesia of the pharynx and larynx reßex. 4.Aortic aneurysms and tumors of the neck and thorax that frequently compress the vagal nerve and can lead to cough, dyspnea, dysphagia, hoarseness, and THE ACCESSORY NERVE (CN XI) spinal accessory nerve, nerve (Figure A.GENERAL CHARACTERISTICS. The accessory nerve innervates laryngeal muscles. CRANIAL NERVES CN IX lar forame cle i perior lary erve tylophary erve ferior lary erve Forame gnu ory Facial Figure 11-8 (CN) XI]. The cranial division hitch-hikes a ride with the accessory nerve, then joins the vagal nerve to become the inferior (recurrent) laryngeal nerve. The recurrent laryngeal nerve innervates the intrinsic muscles of the larynx, except for the cricothyroid muscle. The spinal division innervates the trapezoid and sternocleidomastoid muscles. Three nerves pass through the jugular foramen (glo- mus jugulare tumor). CRANIAL NERVES B.CLINICAL CORRELATION. Lesionscause the following conditions: 1.Paralysis of the sternocleidomastoid muscle that results in difÞculty in turning 2.Paralysis of the trapezius muscle that results in shoulder droop and inability to shrug the shoulder. 3.Paralysis and anesthesia of the larynx if the cranial root is involved. THE HYPOGLOSSAL NERVE (CN XII) nerve (Figure 11-9). A.GENERAL CHARACTERISTICS. The hypoglossal nerve It arises from the hypoglossal nucleus of the medulla and exits the medulla in the pre- olivary sulcus. It exits the skull through the hypoglossal canal, and it innervates Extrinsic muscles are the genioglossus, B.CLINICAL CORRELATION Transection results in hemiparalysis of the tongue. 2.Protrusion causes the tongue to point toward the lesioned (weak) side because of the unopposed action of the opposite genioglossus muscle (Figure 11-10). B C D E H G F Figure 11-10 The basis cerebri showing cranial nerves and the ßoor of the hypothalamus: olfactory tract ; trochlear nerve . (Reprinted from JD Fix, , 3rd ed. Baltimore: Williams & Wilkins, 1996:293, with permission.) Trigeminal System The trigeminal system provides sensory innervation to the face, oral cavity, andsupratentorial dura through general somatic afferent (GSA) Þbers. It also through special visceral efferent (SVE) Þbers. glion cells. It has three divisions: ophthalmic nerve [cranial nerve (CN) V-1] It enters the orbit through the superior orbital Þssure and innervates the forehead, dor- ophthalmic nerve mediates the afferent limb of the corneal reßex. maxillary nerve (CN V-2) lies in the wall of the cavernous sinus and innervates the upper lip and cheek, lower eyelid, anterior portion of the temple, oral mucosa of TRIGEMINOTHALAMIC PATHWAYS (Figure 12-2) mediates pain and temperature sensation from the face and oral cavity. 1)Cranial nerve (CN) V-1 is the afferent limb of the corneal reßex. 2.Second-order neurons are located in the principal sensory nucleus of CN V. They project to the ipsilateral VPM nucleus of the thalamus. 3.Third-order neurons are located in the VPM nucleus of the thalamus. They pro- ject through the posterior limb of the internal capsule to the face area of the somatosensory cortex (BrodmannÕs areas 3, 1, and 2). A.INTRODUCTION (Table 12-1) corneal reßex is a consensual disynaptic reßex. jaw jerkreßex is a monosynaptic myotactic reßex (Figure 12-3). CHAPTER 12 Figure 12-2 The ventral (pain and temperature) and dorsal (discriminative touch) trigeminothalamic pathways. THE CAVERNOUS SINUS (Figure 12-4) contains the following structures: A.INTERNAL CAROTID ARTERY B.CN III, IV, V-1, V-2, CHAPTER 12 Figure 12-4 The contents of the cavernous sinus. The wall of the cavernous sinus contains the ophthalmic cranial ) V-1 and maxillary (CN V-2) divisions of the trigeminal nerve (CN V) and the trochlear (CN IV) and oculomotor (CN III) nerves. The siphon of the internal carotid artery and the abducent nerve (CN VI), along with postganglionic sym- The auditory system is an exteroceptive special somatic afferent sys- THE AUDITORY PATHWAY (Figure 13-1) consists of the following structures: are innervated by the peripheral processes of bipo- lar cells of the spiral ganglion. They are stimulated by vibrations of the basilar mem- 1.Inner hair cells (IHCs) are the chief sensory elements; they synapse with dendrites of myelinated neurons whose axons make up 90% of the cochlear nerve. 2.Outer hair cells (OHCs) synapse with dendrites of unmyelinated neurons whose axons make up 10% of the cochlear nerve. The OHCs reduce the threshold of the project peripherally to the hair cells of the organ of Corti. They project centrally as the cochlear nerve to the cochlear nuclei. cochlear nerve [cranial nerve (CN) VIII] extends from the spiral ganglion to the cerebellopontine angle, where it enters the brain stem. receive input from the cochlear nerve. They project contralater- ally to the superior olivary nucleus and lateral lemniscus. superior olivary nucleus, which plays a role in sound localization, receives bilat- eral input from the cochlear nuclei. It projects to the lateral lemniscus. is located in the pons. It contains decussating Þbers from the ven- 1)Figure 13-1 shows an important overview of the auditory pathway. 2)What are the causes of conduction and sensorineural deafness? 3)Describe the Weber and Rinne tuning fork tests. 4)Remember that the auditory nerve and the organ of Corti are derived from the otic placode. contain the primary auditory cortex (Brod- mannÕs areas 41 and 42). The gyri are located in the depths of the lateral sulcus. A.CONDUCTION DEAFNESS through the external or middle ear. It may be caused by sclerosis, and is often reversible. B.NERVE DEAFNESS perceptive, deafness) and is caused by disease of the cochlea, cochlear nerve (acoustic neuroma), or central presbycusis that results from degenera- AUDITORY TESTS A.TUNING FORK TESTS (Table 13-1) 1.WeberÕs test is performed by placing a vibrating tuning fork on the vertex of the skull. Normally, a patient hears equally on both sides. hears the vibration more loudly in the affected ear. unilateral partial nerve deafness hears the vibration more loudly in the normal ear. compares air and bone conduction. It is performed by placing a vibrating tuning fork on the mastoid process until the vibration is no longer heard; then the fork is held in front of the ear. Normally, a patient hears the vibration in sound conduction is normal [air conduction (AC) is greater than bone conduction (BC)], whereas a indicates conduction loss, with BC greater than AC (Table 13-1). unilateral partial nerve deafness AUDITORY SYSTEM Weber Test Rinne Test TUNING FORK TEST RESULTS TABLE Vestibular System Like the auditory system, the vestibular system is derived from the surface ectoderm. posture and coordinates THE VESTIBULAR PATHWAYS (Figures 14-1 and 14-2) consist of the following structures: A.HAIR CELLS OF THE SEMICIRCULAR DUCTS, SACCULE, AND UTRICLE are inner- vated by peripheral processes of is located in the fundus of the internal auditory meatus. Bipolar neurons project through their peripheral processes to the hair cells. 1)This chapter describes the two types of vestibular nystagmus: postrotational and caloric (COWS acronym). 2)Vestibuloocular reßexes in the unconscious patient are also discussed (see Figure 14-3). Bipolar neurons project their central processes as the vestibular nerve [cranial nerve (CN) VIII] to the vestibular nuclei and to the ßocculonodular lobe of the cerebellum. C.VESTIBULAR NUCLEI 1.These nuclei receive input from The semicircular ducts, saccule, and utricle. The ßocculonodular lobe of the cerebellum. 2.The nuclei project Þbers to The ßocculonodular lobe of the cerebellum. CN III, IV, and VI through the medial longitudinal fasciculus (MLF). The spinal cord through the lateral vestibulospinal tract. The ventral posteroinferior and posterolateral nuclei of the thalamus, both of which project to the postcentral gyrus. are mediated by the vestibular nuclei, MLF, ocular motor nuclei, and CN III, IV, and VI. A.VESTIBULAR (HORIZONTAL) NYSTAGMUS direction of rotation. opposite direction. B.POSTROTATORY (HORIZONTAL) NYSTAGMUS opposite direction of rotation. direction of rotation. The patient past-points and falls in the direction of previous rotation. C.CALORIC NYSTAGMUS (STIMULATION OF HORIZONTAL DUCTS) 1.Cold water irrigation of the external auditory meatus results in nystagmus to the 2.Warm water irrigation of the external auditory meatus results in nystagmus to 3.Remember the mnemonic COWS: Test results in (Figure 14-3) VESTIBULAR SYSTEM Normal conscious subjectBrain stem intactMLF (bilateral) lesionLow brain stem lesion Figure 14-3 Cold caloric responses in the unconscious patient. When the brain stem is intact, the eyes deviate toward side. Destruction of the caudal brain stem results in no deviation of the eyes. Visual System The visual system is served by the optic nerve, which is a special somatic afferent nerve. THE VISUAL PATHWAY (Figure 15-1) includes the following structures: 1)Know the lesions of the visual system. 2)How are quadrantanopias created? 3)There are two major lesions of the optic chiasm. Know them! 4)What is MeyerÕs loop? VISUAL SYSTEM THE PUPILLARY LIGHT REFLEX PATHWAY (Figure 15-4) has an afferent limb (CN II) and an efferent limb (CN III). It includes the following structures: THE PUPILLARY DILATION PATHWAY (Figure 15-5) is mediated by the sympa- Flashlight swung from right eye to left eye Looking straight ahead Looking right Eyes of a comatose patient Looking right Looking straight ahead No reaction to light Looking up Eyes converged Looking left and down Looking straight ahead Eyes converged Eyes converged Figure 15-5 Ocular motor palsies and pupillary syndromes. Relative afferent (Marcus Gunn) pupil, left eye. HornerÕs syndrome, left eye. Internuclear ophthalmoplegia, right eye. Third-nerve palsy, left eye. Sixth-nerve palsy, right eye. Paralysis of upward gaze and convergence (ParinaudÕs syndrome). Fourth-nerve palsy, right eye. Destructive lesion of the right frontal eye Þeld. Third-nerve palsy with ptosis, right eye. Hypothalamic neurons of the paraventricular nucleus project directly to the ciliospinal center (T1ÐT2) of the intermediolateral cell column of the spinal cord. THE NEAR REFLEX AND ACCOMMODATION PATHWAY projects from the primary visual cortex (BrodmannÕs area 17) to the visual association cortex (BrodmannÕs area 19). visual association cortex (BrodmannÕs area 19) projects through the corticotectal CORTICAL AND SUBCORTICAL CENTERS FOR OCULAR MOTILITY frontal eye Þeld is located in the posterior part of the middle frontal gyrus (Brod- mannÕs area 8). It regulates voluntary (saccadic) eye movements. 1.Stimulation (e.g., from an irritative lesion) causes (i.e., away from the lesion). 2.Destruction toward the lesion). B.OCCIPITAL EYE FIELDS are located in BrodmannÕs areas 18 and 19 of the occipital lobes. These Þelds are cortical centers for involuntary (smooth) pursuit and tracking the pons (Figure 15-6). Some authorities place the ÒcenterÓ in the paramedian pontine CHAPTER 15 level of the posterior commissure. It is called the rostral interstitial nucleus ParinaudÕs syndrome (see Figures 15-5F and16-3A). CLINICAL CORRELATION MLF syndrome, internuclear ophthalmoplegia (see Figure 15-5), there is dam- VISUAL SYSTEM Bilateral MLF syndrome Patient with MLF syndrome cannot adduct the eye on attempted lateral conjugate gaze and hasnystagmus in abducting eye. The nystagmus is in the direction of the large arrow- head. Convergence remains intact. Convergence Figure 15-6 (Figure 16-1) A.MEDIAL MEDULLARY SYNDROME (ANTERIOR SPINAL ARTERY SYNDROME). Affected structures and resultant deÞcits include (medullary pyramid). Lesions result in contralateral spas- tic hemiparesis. Lesions result in contralateral loss of tactile and vibration sensation from the trunk and extremities. hypoglossal nucleus or intraaxial root Þbers [cranial nerve (CN) XII]. Lesions result in ipsilateral ßaccid hemiparalysis of the tongue. When protruded, the tongue points to the side of the lesion (i.e., the weak side). See Figure 11-9. B.LATERAL MEDULLARY [WALLENBERG; POSTERIOR INFERIOR CEREBELLAR ARTERY (PICA)] SYNDROME I.B.6Ð7). Affected structures and resultant deÞcits include Lesions result in nystagmus, nausea, vomiting, and vertigo. inferior cerebellar peduncle. Lesions result in ipsilateral cerebellar signs [e.g., 1)The three most important lesions of the brain stem are occlusion of the anterior spinal artery (Figure 16-1), occlusion of the posterior inferior cerebellar artery (Figure 16-1), and medial longitudinal fasciculus syndrome (Figure 16-2). 2)WeberÕs syndrome is the most common midbrain lesion (Figure 16-3). (Figure 16-2A) A.MEDIAL INFERIOR PONTINE SYNDROME results from occlusion of the paramedian branches of the basilar artery. Affected structures and resultant deÞcits include Lesions result in contralateral spastic hemiparesis. Lesions result in contralateral loss of tactile sensation from the trunk and extremities. abducent nerve roots. Lesions result in ipsilateral lateral rectus paralysis. B.LATERAL INFERIOR PONTINE SYNDROME (anterior inferior cerebellar artery syn- drome; Figure 16-2B). Affected structures and resultant deÞcits include facial nucleus and intraaxial nerve Þbers. Lesions result in Ipsilateral facial nerve paralysis. Ipsilateral loss of taste from the anterior two-thirds of the tongue. Ipsilateral loss of lacrimation and reduced salivation. Loss of corneal and stapedial reßexes (efferent limbs). cochlear nuclei and intraaxial nerve Þbers. Lesions result in unilateral cen- vestibular nuclei and intraaxial nerve Þbers. Lesions result in nystagmus, nausea, vomiting, and vertigo. spinal nucleus and tract of trigeminal nerve. Lesions result in ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia). middle and inferior cerebellar peduncles. Lesions result in ipsilateral limb Lesions result in contralateral loss of pain and temperature sensation from the trunk and extremities. CHAPTER 16 Figure 16-1 Vascular lesions of the medulla at the level of the hypoglossal nucleus of cranial nerve ( Medial medullary syndrome (anterior spinal artery). inferior cerebellar artery) syndrome. C.MEDIAL LONGITUDINAL FASCICULUS (MLF) SYNDROME (INTERNUCLEAR (Figure 16-2C) interrupts Þbers from the contralateral abdu- cent nucleus that project through the MLF to the ipsilateral medial rectus subnucleus medial rectus palsy in the abducting eye. Convergence remains intact. This syndrome is often seen multiple sclerosis. D.FACIAL COLLICULUS SYNDROME usually results from a pontine glioma or a vascu- internal genu facial nerve Ipsilateral loss of the corneal reßex. Lateral rectus paralysis. Medial (convergent) strabismus. (Figure 16-3) A.DORSAL MIDBRAIN (PARINAUDÕS) SYNDROME (see Figure 16-3A) is often the result of a pinealoma or germinoma of the pineal region. Affected structures and result- LESIONS OF THE BRAIN STEM Figure 16-2 Vascular lesions of the caudal pons at the level of the abducent nucleus of cranial nerve ( Medial inferior pontine syndrome. Lateral inferior pontine syndrome (anterior inferior cerebellar artery syndrome). ) syndrome. rectus (CN VI) and superior oblique (CN IV) muscles. Ptosis (paralysis of the lev- ACOUSTIC NEUROMA (SCHWANNOMA) (Figure 16-4) is a benign tumor of Schwann cells that affects the vestibulocochlear nerve (CN VIII). It accounts for 8% of all intracra- nial tumors. It is a posterior fossa tumor of the internal auditory meatus and cerebellopon- tine angle. The neuroma often compresses the facial nerve (CN VII), which accompanies CN VIII in the cerebellopontine angle and internal auditory meatus. It may impinge on the pons and affect the spinal trigeminal tract (CN V). women as in men. Affected structures and resultant deÞcits include cochlear nerve of CN VIII. Damage results in tinnitus and unilateral nerve deafness. vestibular nerve of CN VIII. Damage results in vertigo, nystagmus, nausea, vom- CHAPTER 16 Figure 16-3 Lesions of the rostral midbrain at the level of the superior colliculus and oculomotor nucleus of cranial Dorsal midbrain (ParinaudÕs) syndrome. Paramedian midbrain (BenediktÕs) syndrome. midbrain (WeberÕs) syndrome. facial nerve (CN VII). Damage results in facial weakness and loss of the corneal reßex (efferent limb). spinal tract of trigeminal nerve (CN V). Damage results in paresthesia, anesthe- sia of the ipsilateral face, and loss of the corneal reßex (afferent limb). E.NEUROFIBROMATOSIS TYPE 2. This disorderoften occurs with bilateral acoustic neuromas. usually results from a posterior fossa tumor (e.g., glomus jugulare tumor, the most common inner ear tumor) that compresses CN IX, X, and XI. Affected structures and resultant deÞcits include glossopharyngeal nerve (CN IX). Damage results in Ipsilateral loss of the gag reßex. Ipsilateral loss of pain, temperature, and taste in the tongue. vagal nerve (CN X). Damage results in Ipsilateral paralysis of the soft palate and larynx. Ipsilateral loss of the gag reßex. accessory nerve (CN XI). Damage results in Paralysis of the sternocleidomastoid muscle, which results in the inability to turn Paralysis of the trapezius muscle, which causes shoulder droop and inability to shrug the shoulder. LESIONS OF THE BRAIN STEM Figure 16-4 is a lesion of the base of the pons as the result of infarc- tion, trauma, tumor, or demyelination. The corticospinal and corticonuclear tracts are affected bilaterally. The oculomotor and trochlear nerves are not injured. Patients are con- scious and may communicate through vertical eye movements. CENTRAL PONTINE MYELINOLYSIS is a lesion of the base of the pons that affects the corticospinal and corticobulbar tracts. More than 75% of cases are associated with alco- holism or rapid correction of hyponatremia. Symptoms include spastic quadriparesis, pseudobulbar palsy, and mental changes. This condition may become the locked-in syn- drome. CHAPTER 16 Aorta Aorta PCA SCA AICA PICA ACA ACOM ACOM PCA SCA AICA PICA ACA Figure 16-5 Anatomy of the subclavian steal syndrome. Thrombosis of the proximal part of the subclavian artery (left) results from embolic occlusion of the rostral basilar artery. Neurologic signs include optic ataxia and psychic paralysis of Þxation of gaze (BalintÕs syndrome), ectopic pupils, somnolence, and cortical blindness, with or without (AntonÕs syndrome). SUBCLAVIAN STEAL SYNDROME (Figure 16-5) results from thrombosis of the left is the junction of the medulla, pons, and cere- bellum. CN VII and VIII are found there. Five brain tumors, including a cyst, are often located in the cerebellopontine angle cistern. Remember the acronym . The percentages refer to cerebellopontine angle tumors. LESIONS OF THE BRAIN STEM The thalamus is the largest division of the diencephalon. It plays an important role in the integration of the sensory and motor systems. (Figure 17-1) receives hypothalamic input from the mamillary nucleus through the mamillothalamic tract. It projects to the cingulate gyrus and is part of the Papez circuit of emotion of the limbic system. is reciprocally connected to the prefrontal cortex. It has abundant connections with the intralaminar nuclei. It receives input from the amygdale, substantia nigra, and temporal neocortex. When it is destroyed, memory loss occurs (Wernicke-Korsakoff syndrome). The mediodorsal nucleus plays a role in the expression of affect, emotion, and behavior (limbic centromedian nucleus is the largest intralaminar nucleus. It is reciprocally con- nected to the motor cortex (BrodmannÕs area 4). The centromedian nucleus receives input from the globus pallidus. It projects to the striatum (caudate nucleus and puta- men) and projects diffusely to the entire neocortex. is the largest thalamic nucleus. It has reciprocal connections with the 1)Key entry and exit points into and out of the thalamus (demonstrated by Figure 17-1). 2)Anatomy of the internal capsule. (It will be on the examination.) What is the blood supply of the internal capsule (stroke)? BLOOD SUPPLY The thalamus is irrigated by three arteries (see Figure 5-1): posterior communicating artery. posterior cerebral artery. anterior choroidal artery (Figure 17-2) is a layer of white matter (myelinated axons) that separates the caudate nucleus and the thalamus medially from the lentiform nucleus laterally. CHAPTER 17 Figure 17-2 Horizontal section of the right internal capsule showing the major Þber projections. Clinically important tracts lie in the genu and posterior limb. Lesions of the internal capsule cause contralateral hemiparesis and contralat- , ventral posterior. A.GENERAL STRUCTURE AND FUNCTION. that subserves three systems: the autonomic nervous system, the endocrine B.MAJOR HYPOTHALAMIC NUCLEI AND THEIR FUNCTIONS medial preoptic nucleus (Figure 18-1) regulates the release of gonadotropic hormones from the adenohypophysis. It contains the sexually dimorphic nucleus, the development of which depends on testosterone levels. 1)Figures 18-1 and 18-2 show that the paraventricular and supraoptic nuclei synthesize CLINICAL CORRELATION CHAPTER 18 The limbic system is considered the anatomic substrate that under- lies behavioral and emotional expression. It is expressed through the hypothalamus by way of the autonomic nervous system. orbitofrontal cortex mediates the conscious perception of smell. It has recip- rocal connections with the mediodorsal nucleus of the thalamus. It is intercon- nected through the medial forebrain bundle with the septal area and hypothalamic dorsomedialmediodorsal nucleus of the thalamus has reciprocal connections with the orbitofrontal and prefrontal cortices and the hypothalamus. It receives input from the amygdala and plays a role in affective behavior and memory. receives input from the mamillary nucleus through the mamillothalamic tract and fornix. It projects to the cingulate gyrus and is a major link in the Papez circuit. septal area is a telencephalic structure. It has reciprocal connections with the hip- pocampal formation through the fornix and with the hypothalamus through the medial forebrain bundle. It projects through the stria medullaris (thalami) to the habenular includes the subcallosal area, paraterminal gyrus, cingulate gyrus and 1)Bilateral lesions of the amygdala result in KlŸver-Bucy syndrome. Recall the triad hyper- phagia, hypersexuality, and psychic blindness. 2)Memory loss is associated with bilateral lesions of the hippocampus. 3)WernickeÕs encephalopathy results from a deÞciency of thiamine (vitamin B are found in the mamillary bodies, thalamus, and midbrain tegmentum (Figure 19-3). 4)Know the Papez circuit, a common board question. THE PAPEZ CIRCUIT (Figure 19-2) includes the following limbic structures: hippocampal formation, which projects through the fornix to the mamillary nucleus and septal area. mamillary nucleus (BrodmannÕs areas 23 and 24). entorhinal area (BrodmannÕs area 28). CLINICAL CORRELATION A.KL†VER-BUCY SYNDROME results from bilateral ablation of the anterior temporal hyperphagia, docility (placidity), and hypersexuality. B.AMNESTIC (CONFABULATORY) SYNDROME results from bilateral infarction of the hippocampal formation (i.e., hippocampal branches of the posterior cerebral arteries LIMBIC SYSTEM Figure 19-2 Major afferent and efferent limbic connections of the hippocampal formation. This formation has three components: the hippocampus (cornu Ammonis), subiculum, and dentate gyrus. The hippocampus projects to the sep- tal area, the subiculum projects to the mamillary nuclei, and the dentate gyrus does not project beyond the hippocam- pal formation. The circuit of Papez follows this route: hippocampal formation to mamillary nucleus to anterior thalamic The cerebellum has three primary functions: A.MAINTENANCE OF POSTURE AND BALANCE B.MAINTENANCE OF MUSCLE TONE C.COORDINATION OF VOLUNTARY MOTOR ACTIVITY ANATOMY A.CEREBELLAR PEDUNCLES superior cerebellar peduncle contains the major output from the cerebellum, thalamus. It has one major afferent pathway, the ventral spinocerebellar tract. middle cerebellar peduncle receives pontocerebellar Þbers, which project to the neocerebellum (pontocerebellum). inferior cerebellar peduncle has three major afferent tracts: the dorsal spin- ocerebellar tract, the cuneocerebellar tract, and the olivocerebellar tract from the B.CEREBELLAR CORTEX, NEURONS, AND FIBERS 1.The cerebellar cortex has three layers. 1)Figure 20-1 shows the most important cerebellar circuit. 2)The inhibitory -aminobutyric acid (GABA)-ergic cerebellar output is regulated by Purkinje. 3)Purkinje cells give rise to the cerebellodentatothalamic tract. 4)What are mossy and climbing Þbers? vestibular nuclei. These cells are excited by parallel and climbing Þbers and THE MAJOR CEREBELLAR PATHWAY (Figure 20-1) consists of the following structures. Purkinje cells of the cerebellar cortex project to the cerebellar nuclei (e.g., den- CEREBELLUM Figure 20-1 The principal cerebellar connections. The major efferent pathway is the dentatothalamocortical tract. The cerebellum receives input from the cerebral cortex through the corticopontocerebellar tract. is the major effector nucleus of the cerebellum. It gives rise to the dentatothalamic tract, which projects through the superior cerebellar peduncle to the cerebellar peduncle is in the caudal midbrain tegmentum. receives the dentatothalamic tract. It pro- jects to the primary motor cortex of the precentral gyrus (BrodmannÕs area 4). motor cortex (motor strip, or BrodmannÕs area 4) receives input from the ventral lat- eral nucleus of the thalamus. It projects as the corticopontine tract to the pontine nuclei. receive input from the motor cortex. Axons project as the ponto- cerebellar tract to the contralateral cerebellar cortex, where they terminate as mossy A.HYPOTONIA is loss of the resistance normally offered by muscles to palpation or pas- sive manipulation. It results in a ßoppy, loose-jointed, rag-doll appearance with pen- dular reßexes. The patient appears inebriated. B.DYSEQUILIBRIUM C.DYSSYNERGIA is loss of coordinated muscle activity. It includes (Figure 20-2) A.ANTERIOR VERMIS SYNDROME involves the leg region of the anterior lobe. It results from atrophy of the rostral vermis, most commonly caused by alcohol abuse. It causes B.POSTERIOR VERMIS SYNDROME result of brain tumors in children and is most commonly caused by medulloblastomas C.HEMISPHERIC SYNDROME usually involves one cerebellar hemisphere. It is often the result of a brain tumor (astrocytoma) or an abscess (secondary to otitis media or mastoiditis). It causes arm, leg, and gait dystaxia and ipsilateral cerebellar signs. D.CEREBELLAR TUMORS. In children, 70% of brain tumors are found in the posterior fossa. In adults, 70% of brain tumors are found in the supratentorial compartment. 1.Astrocytomas constitute 30% of all brain tumors in children. They are most often found in the cerebellar hemisphere. After surgical removal of an astrocytoma, it is common for the child to survive for many years. 2.Medulloblastomas are malignant and constitute 20% of all brain tumors in chil- dren. They are believed to originate from the superÞcial granule layer of the cere- bellar cortex. They usually obstruct the passage of cerebrospinal ßuid (CSF). As a result, hydrocephalus occurs. CHAPTER 20 Motor System (Figure 21-1) A.COMPONENTS 1.Caudate nucleus 2.Putamen 3.Globus pallidus B.GROUPING OF THE BASAL NUCLEI (GANGLIA) lentiform nucleus THE STRIATAL (EXTRAPYRAMIDAL) MOTOR SYSTEM (see Figure 21-1) plays a role in the initiation and execution of somatic motor activity, especially willed movement. It is also involved in automatic stereotyped postural and reßex motor activity (e.g., normal A.STRUCTURE. The striatal motor system includes the following structures: 1.Neocortex. 2.Striatum (caudatoputamen, 3.Globus pallidus. 4.Subthalamic nucleus. 5.Substantia nigra 1)Figure 21-6 shows the circuitry of the basal ganglia and their associated neurotransmitters. 2)ParkinsonÕs disease is associated with a depopulation of neurons in the substantia nigra. 3)HuntingtonÕs disease results in a loss of nerve cells in the caudate nucleus and putamen. 4)Hemiballism results from infarction of the contralateral subthalamic nucleus. Figure 21-5 shows the major afferent efferent connections C.NEUROTRANSMITTERS are seen in Figure 21-6. CLINICAL CORRELATION A.PARKINSONÕS DISEASE. that affects the substantia nigra and its projections to the striatum. 1.RESULTS ofParkinsonÕs disease are a CHAPTER 21 Figure 21-1 Coronal section through the midthalamus at the level of the mamillary bodies. The basal nuclei (gan- glia) are all prominent at this level and include the striatum and lentiform nucleus. The subthalamic nucleus and sub- stantia nigra are important components of the striatal motor system. , centromedian nucleus; , ventral lateral nucleus. (ModiÞed from TA Woolsey, J Hanaway, MH Gado, the human central nervous system , 2nd ed. Hoboken: John Wiley & Sons, 2003:68, with permission.) The cerebral cortex, the thin, gray covering of both hemispheres of the brain, has two types: the neocortex (90%) and the allocortex (10%). Motor cortex is the thickest (4.5 mm); visual cortex is the thinnest (1.5 mm). THE SIX-LAYERED NEOCORTEX Layers II and IV of the neocortex are mainly affer- ent (i.e., receiving). Layers V and VI are mainly efferent (i.e., sending) (Figure 22-1). A.LAYER I layer. B.LAYER II external granular layer. C.LAYER III external pyramidal layer. It gives rise to association and commissural Þbers and is the major source of corticocortical Þbers. D.LAYER IV internal granular layer. It receives thalamocortical Þbers from the thala- mic nuclei of the ventral tier (i.e., ventral posterolateral and ventral posteromedial). In the visual cortex (BrodmannÕs area 17), layer IV receives input from the lateral geniculate body. E.LAYER V internal pyramidal layer. It gives rise to corticobulbar, corticospinal, (Figure 22-2) A.FRONTAL LOBE (BrodmannÕs area 4) and premotor cortex (BrodmannÕs area 6). These two cortices are somatotopically organized (Figure 22-3). Destruction 1)This chapter describes the cortical localization of functional areas of the brain. 2)How does the dominant hemisphere differ from the nondominant hemisphere? 3)Figure 22-5 shows the effects of various major hemispheric lesions. b.Esthesioneuroblastomas (olfactory neuroblastomas) arise from bipolar sen- sory cells of the olfactory mucosa; they can extend through the cribriform plate into the anterior cranial fossa. Presenting symptoms are similar to those of the Foster Kennedy syndrome. hippocampal cortex (archicortex) , bilateral lesions result in the inability to consolidate short-term memory into long-term memory. Earlier memories are Figure 22-6A shows the symptoms of lesions in the dominant hemisphere. Figure 22-6B shows the symptoms of lesions in the nondominant hemisphere. SPLIT-BRAIN SYNDROME (Figure 22-7). This syndrome is a disconnection syndrome that results from dominant hemisphere CHAPTER 22 CEREBRAL CORTEX Figure 22-7 Functions of the split brain after transection of the corpus callosum. Tactile and visual perception is pro- jected to the contralateral hemisphere, olfaction is perceived on the same side, and audition is perceived predominantly in the opposite hemisphere. The left ( ) hemisphere is dominant for language. The right ( ) hemisphere is dominant for spatial construction and nonverbal ideation. (Reprinted from CR Noback, RJ Demarest, The human nervous system. Malvern, PA: Lea & Febiger, 1991:416, with permission.) A.ANTERIOR CORPUS CALLOSUM LESION IMPORTANT TRANSMITTERS AND THEIR PATHWAYS 1)In this chapter, the pathways of the major neurotransmitters are shown in separate 2)Glutamate (GLU) is the major excitatory transmitter of the brain; GABA is the major inhibitory transmitter. Purkinje cells of the cerebellum are GABA-ergic. from the extracellular space by astrocytes. In HuntingtonÕs disease, GLU is bound to the NMDA receptor, resulting in an inßux of calcium ions and sub- sequent cell death. This cascade of events with neuronal death most likely occurs in cerebrovascular accidents (stroke). 3.Nitric oxide is a recently discovered gaseous neurotransmitter that is produced when nitric oxide-synthase converts arginine to citrulline. It is located in the olfactory system, striatum, neocortex, hippocampal forma- tion, supraoptic nucleus of the hypothalamus, and cerebellum. Nitric oxide is responsible for smooth-muscle relaxation of the corpus caver- nosum and thus penile erection. It is also believed to play a role in memory In addition, nitric oxide functions as a nitrovasodilator in the cardiovascular FUNCTIONAL AND CLINICAL CONSIDERATIONS A.PARKINSONÕS DISEASE results from degeneration of the dopaminergic neurons that are found in the pars compacta of the substantia nigra. It causes a reduction of B.HUNTINGTONÕS DISEASE (CHOREA) CHAPTER 23 Figure 23-7 Distribution of glutamate-containing neurons and their projections. Glutamate is the major excitatory transmitter of the central nervous system. Cortical glutamatergic neurons project to the striatum. Hippocampal and subicular glutamatergic neurons project through the fornix to the septal area and hypothalamus. The granule cells of the cerebellum are glutamatergic. is the inability to perform motor activities in the presence of intact motor and sensory systems and normal comprehension. is impaired or absent communication by speech, writing, or signs (i.e., loss of the capacity for spoken language). The lesions are located in the dominant hemisphere. Asso- ciate the following symptoms and lesion sites with the appropriate aphasia (Figure 24-1). A.BROCAÕS (MOTOR) APHASIA Lesion in frontal lobe, in the inferior frontal gyrus (BrodmannÕs areas 44 and 45) Good comprehension 1)Be able to differentiate BrocaÕs aphasia from WernickeÕs aphasia. 2)What is conduction aphasia? Good comprehension D.TRANSCORTICAL MOTOR APHASIA Poor comprehension is a nondominant hemispheric language deÞcit that serves propositional language. Emotionality, inßection, melody, emphasis, and gesturing are affected. A.EXPRESSIVE DYSPROSODY results from a lesion that corresponds to BrocaÕs area but is located in the nondominant hemisphere. Patients cannot express emotion or inßec- B.RECEPTIVE DYSPROSODY results from a lesion that corresponds to WernickeÕs area but is located in the nondominant hemisphere. Patients cannot comprehend the emo- tionality or inßection in the speech they hear. CHAPTER 24 Table of Cranial Nerves TypeOrigin IIÐOptic IIIÐOculomotor Table of Common Neurological Characteristics Derived from the Schwann cell sheath investing cranial nerve VIII; accounts for most tumors located in the cerebellopontine angle Disorder of skilled movement; not due to paresis Most common cause of dementia; anatomical pathology shows neuroÞbril- lary tangles and senile plaques microscopically; cortical atrophy of the Neural tube defect in which the cerebrum and cerebellum are malformed Inability to perform voluntary actions or to make decisions; seen in bilateral frontal Increase in thickness of the Abducent nerve, 79, 163 Accessory nerve. Spinal accessory nerve

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