Đang tải... (xem toàn văn)
Part 2 book “King’s applied anatomy of the central nervous system of domestic mammals” has contents: Extrapyramidal feedback and upper motor neuron disorders, summary of the somatic motor systems, the cerebellum, autonomic components of the central nervous system, the cerebral cortex and thalamus, embryological and comparative neuroanatomy, clinical neurology, imaging techniques for study of the central nervous system general considerations,… and other contents.
14 Extrapyramidal Feedback and Upper Motor Neuron Disorders Feedback of the Extrapyramidal System 14.1 Neuronal Centres of the Feedback Circuits Three major centres are involved in extrapyramidal feedback, namely the olivary nucleus, the cerebellum and the thalamus 14.1.1 Olivary Nucleus The olivary nucleus is an intermediate station on the pathway from the higher extrapyramidal command centres to the cerebellum (Figure 14.1) It corresponds to the pontine nuclei in the pyramidal feedback circuit (Figure 12.2) The site of the olivary nucleus in the medulla oblongata is shown schematically in Figure 8.3 (see also Figure 22.7) Figure 14.1 Diagram of the feedback circuits of the extrapyramidal system The motor centres are numbered 1 to 9 The red and black projections are the feedback circuits: the red projections lead to the cerebellum, and the black lines return from the cerebellum The globus pallidus is the focal point of, and in this diagram represents, the basal nuclei The globus pallidus has a feedback circuit through the thalamus and cerebral cortex, which enables the basal nuclei to collaborate with the cerebral cortex n = nucleus; nn = nuclei; m.r.c = motor reticular centre; and r.f = reticular formation 14.1.2 Cerebellum Two components of the cerebellum, i.e the cerebellar cortex and the cerebellar nuclei (such as the dentate nucleus), are involved in extrapyramidal feedback circuits Note the similarity to the pyramidal feedback circuit (Figure 12.2) 14.1.3 Thalamus The thalamus is the intermediate station between the cerebellum and the cerebral cortex, in those feedback circuits which return to the forebrain The ventral group of thalamic nuclei controls all thalamic feedback circuits Strictly, it is the ventrolateral thalamic nucleus, as in the pyramidal feedback circuits (Figure 12.2) (see Section 18.17) 14.2 Feedback Circuits All of the nine motor ‘command centres’ of the extrapyramidal system together with the pyramidal system have feedback circuits through the cerebellum (see Section 12.2) The function of these extrapyramidal feedback pathways is to inform the cerebellum of the intended motor actions of the extrapyramidal motor centres and enable the cerebellum to regulate these actions as they progress (see Section 16.9) One of the major motor centres of the extrapyramidal system, the basal nuclei (basal ganglia), has a shorter feedback circuit directly through the thalamus to the cerebral cortex This feedback circuit enables the basal nuclei to carry out their main role, namely collaboration with the cerebral cortex via the thalamus (see Section 13.3) The cerebellar feedback circuits of the nine extrapyramidal motor command centres (Nos 1 to 9) are as follows: 14.2.1 Centres 1 and 2: The Cerebral Cortex and Globus Pallidus The feedback pathways to the command centres 1 and 2 are similar, projecting (in sequence) to the olivary nucleus, to the cerebellar cortex, to a cerebellar nucleus, to the thalamus, and finally back to the cerebral cortex (Figure 14.1) These pathways decussate (either before or after the olivary nucleus) on their way to the cerebellar cortex, and then decussate again on the way back The circuit for the globus pallidus is finally completed by projections from the cerebral cortex back to the globus pallidus (Figure 14.1) These pathways enter the cerebellum through the caudal cerebellar peduncle, and exit through the rostral peduncle (see Sections 16.3 and 16.5) The relay in the thalamus takes place in the ventral group of thalamic nuclei (in the ventrolateral nucleus, see Section 18.17) 14.2.2 Centres 3 and 4: The Midbrain Reticular Formation and Red Nucleus Again these feedback circuits project first to the olivary nucleus, then to the cerebellar cortex, onwards to a cerebellar nucleus, and finally back to the midbrain reticular formation and red nucleus (Figure 14.1) As before, they also decussate twice, i.e on the way in and the way out of the cerebellum Entrance to the cerebellum is gained through the caudal peduncle, and the outlet is via the rostral cerebellar peduncle, as for Centres 1 and 2 14.2.3 Centres 5 and 9: The Tectum and Vestibular Nuclei Centres 5 and 9 are the extrapyramidal motor centres that are associated with information from the special senses Their feedback pathways miss out the olivary nucleus, projecting via the caudal cerebellar peduncle directly to the cerebellar cortex They receive return pathways from a cerebellar nucleus (Figure 14.1) The projections of the vestibular nuclei to and from the cerebellum are ipsilateral, and this is unique among the feedback pathways of the extrapyramidal centres; i.e the left vestibular nuclei project to, and receive return projections from, the left side of the cerebellum Correlate this with the fact that the vestibulospinal tract does not decussate (see Section 9.3) The tectal pathways to and from the cerebellum pass through the rostral cerebellar peduncle; the afferent and efferent vestibular pathways use the caudal cerebellar peduncle (see Sections 16.3 and 16.5) 14.2.4 Centres 6, 7 and 8: The Pontine Motor Reticular Centres the Lateral Medullary Motor Reticular Centres and the Medial Medullary Motor Reticular Centres The command centres in the reticular formation of the hindbrain project to the contralateral cerebellar cortex and receive return pathways via a cerebellar nucleus (Figure 14.1) All of these pathways from the hindbrain command centres of the reticular formation to the cerebellum travel in the caudal cerebellar peduncle (see Section 16.3) 14.2.5 Feedback between Basal Nuclei and Cerebral Cortex This feedback circuit runs from the globus pallidus, to the ventral group of thalamic nuclei, to the cerebral cortex, and finally back to the globus pallidus (Figure 14.1) Of the ventral group of thalamic nuclei, the ventrolateral thalamic nucleus is mainly involved in this feedback circuit 14.3 Balance between Inhibitory and Facilitatory Centres As indicated at the beginning of Chapter 13, some of the motor centres of the extrapyramidal system are facilitatory and others are inhibitory The normal functioning of the system depends on a perfect balance between these two antagonistic components 14.3.1 Facilitatory Components These are shown in Figure 13.2 (red), the most important being: the cerebral cortex itself (relatively restricted parts of it); large areas of the basal nuclei, especially the globus pallidus; the red nucleus, tectum and the reticular formation of the midbrain; the pontine motor reticular centres; the lateral medullary motor reticular centres of the medulla, which are strictly inhibitory but produce facilitation by disinhibition of the medial medullary motor reticular centres (see Section 13.7); and the vestibular nuclei 14.3.2 Inhibitory Components The main inhibitory components of the extrapyramidal system are shown in Figure 13.2 (black projections): Generally, the influence of the cerebral cortex on the lower extrapyramidal centres appears to be inhibitory rather than facilitatory The substantia nigra is a dense area of grey matter in the cerebral peduncle of the midbrain (Figures 12.1 and 22.13) It receives projections from the cerebral cortex, and in turn projects inhibitory pathways to the basal nuclei (Figure 13.2) Thus, it normally damps down the activity of the basal nuclei This is an important function, controlling the strong facilitatory drive of the basal nuclei, via the globus pallidus, upon the lower motor centres of the brainstem, and also controlling the influence of the basal nuclei on the cerebral cortex (see Section 13.2) The medial medullary motor reticular centres exert a massive inhibitory drive upon the descending reticular formation of the spinal cord by means of the medullary reticulospinal tract (see Section 13.8) 14.4 Clinical Signs of Lesions in Extrapyramidal Motor Centres in Man 14.4.1 General Principles Lesions of the extrapyramidal motor centres, notably in the basal nuclei, tend mainly to knock out inhibitory components: too much facilitation results, causing increased muscle tone Much of this hypertonus seems to arise from the increased firing of gamma neurons, once the inhibitory control from above has been lifted There are postural and locomotory abnormalities, which typically include involuntary movements, the latter being known as hyperkinesia Usually spinal reflexes are exaggerated (hyperreflexia) When the lesions are unilateral, the signs tend to be contralateral, though they may sometimes be bilateral If the lesions happen to affect mainly excitatory components of the extrapyramidal motor centres then muscle tone will be reduced, and this does happen in some clinical cases 14.4.2 Lesions in the Basal Nuclei In man, the single most characteristic sign of lesions of the basal nuclei is the presence of hyperkinesia This consists of involuntary movements ranging from continuous tremor to sudden jerking movements, and may even extend to uncontrollable flailing movements of the arm and leg on the opposite side to the lesion (hemiballismus) Tremor is a particular feature of lesions of the substantia nigra (see below, Parkinson’s disease) The much more violent hyperkinesia of hemiballismus is usually associated with a vascular lesion of the contralateral subthalamic nucleus (see Section 22.23, Subthalamus) Hypertonus, hyperreflexia and hyperkinesia seem to be among the relatively simple expressions of lesions in the human‐basal nuclei Much more elaborate manifestations may reveal themselves For example, during walking, there may be gradual acceleration, so that what starts as a somewhat tottery gait turns into uncontrollable running and ends in crashing over Sometimes a patient appears to be brought to a total standstill when confronted by a doorway, or when half‐way up the stairs 14.4.3 Parkinson’s Disease This is a particularly well‐known example of extrapyramidal disease It occurs in man but has no close parallel in domestic animals The balance between facilitatory and inhibitory areas is disturbed, the facilitatory components dominating Increased fusimotor neuron activity, and hence increased muscle tone, sometimes amounting to rigidity, is consequently the main sign There is also a fine tremor of the hands, abolished by sleep Usually the lesion is mainly in the substantia nigra The mechanisms by which the substantia nigra controls motor functions are not known However, it has been established that the cells of the substantia nigra are dopaminergic, and that the signs of Parkinson’s disease can be relieved by L‐ dopa Although nigrostriatal projections appear to be the largest dopaminergic pathway in the central nervous system, there are others extending from the substantia nigra to the midbrain reticular formation, and these may account for some of the undesirable side‐effects of L‐dopa 14.5 Clinical Signs of Lesions in the Basal Nuclei in Domestic Animals It seems likely that the clinical signs arising from lesions in the basal nuclei in domestic animals would, in principle, resemble those of man, i.e hypertonus, hyperreflexia, locomotory and postural deficits, and hyperkinesia Experimental lesions do sometimes produce hyperkinesia However, there is not much firm information about the clinical effects of naturally occurring lesions in the domestic species Lesions in the basal nuclei are evidently common in the dog, but it seems very difficult if not impossible at present to relate them to specific neurological signs Attempts to produce specific signs in experimental animals have also been rather unsuccessful However, small unilateral lesions in the caudate nucleus in cats have been followed by continuous exaggerated movements of the limbs in the form of alternating flexion and extension of the paws of the forelimb (resembling the ‘knitting’ movements of affection); these movements disappeared with sleep and during locomotion Although the lesions were unilateral, the hyperkinesia affected both forelimbs, possibly because of the midline pathways of the reticular formation which descend from the basal nuclei The clinical signs of spastic paresis in the Friesian bull may be partly due to the lesions that are consistently scattered throughout the higher centres of the extrapyramidal system, including the basal nuclei and red nucleus (as well as being found in various other parts of the CNS) The characteristic clinical signs include rigidity, or hyperkinesia, the hindlimb being thrown backwards when movement is attempted The immediate cause is hypertonus of the gastrocnemius and superficial digital flexor muscles, and in some cases of the quadriceps femoris muscles The hyperkinesia, which characterizes stringhalt and shivering in horses, is suggestive of basal nuclei lesions Ingestion of plants of the genus Centaurea (a knapweed found in North America) by horses results in bilateral, sharply circumscribed, necrosis of the substantia nigra or globus pallidus, or both, with facial rigidity and rhythmic tongue and jaw movements but not much involvement of the limbs; the hypertonia of the facial muscles resembles that of Parkinson’s disease in man 14.6 Upper Motor Neuron Disorders The term upper motor neuron (UMN) is widely used in both human and veterinary clinical neurology It is sometimes confined to neurons of the pyramidal tract, but is often extended to include all the pyramidal and extrapyramidal pathways that control voluntary activity Thus, there are a great many possible ‘upper motor neurons’, and the term is so ill‐defined as to be a source of considerable confusion; indeed it has been suggested that it ‘might with advantage be avoided’ Nevertheless, the term is strongly entrenched in the clinical literature in the concept of ‘upper motor neuron disorder’ In veterinary neurology, lesions of the spinal cord, which typically involve many of the descending motor pathways, are considered to give classical signs of upper motor neuron disorder These are: paralysis, or in less severe cases paresis, on the side of the lesion, gait and posture being obviously or drastically affected; hypertonus of the affected limb(s), often severe enough to be termed spasticity; hyperreflexia of the affected limbs(s); and some muscle wasting in long‐term cases (due to atrophy of disuse, such as occurs in a limb immobilised in a plaster cast) In contrast, the classical signs of lower motor neuron (LMN) disease are: paralysis; hypotonus, often amounting to flaccidity; hyporeflexia or areflexia; and severe and relatively rapid muscle wasting (see Section 10.12) Intervertebral disc protrusions in the thoracolumbar spine of the dog classically result in UMN signs in the hindlimbs (see Section 4.9) However, if the lesion is in the region of the lumbosacral intumescence, damage may occur to the ventral horn location of the motoneurons innervating hindlimb musculature and resulting in an LMN disorder Hypertonus is commonly encountered in upper motor neuron disorders Indeed, in long‐term, naturally occurring disorders of the higher motor centres, or their tracts, in both man and domestic mammals, any changes in tone are nearly always in the direction of hypertonus There are a few exceptions, an example being the hypotonus of spinal shock (see immediately below); however, this phenomenon is essentially transient even in man and is generally too short‐ lasting in domestic animals to be observed clinically The mechanism of hypertonus in upper motor neuron disorders is not entirely understood However, an essential general feature appears to be a release of fusimotor neurons from inhibition Thus the corticospinal, rubrospinal and reticulospinal tracts evidently include fibres that normally have a tonic inhibitory effect on fusimotor neurons When this descending inhibition is removed, fusimotor neurons become active and reflexively induce a continuous partial contraction of the extrafusal muscle fibres in, for example, the muscles of the limbs This is perceived by the clinician as an increased resistance to the manual movement of the joints, i.e as increased tone In severe lesions of the spinal cord, widespread destruction of the white matter of the lateral and ventral funiculi on one side of the cervical spinal cord causes total paralysis of the ipsilateral fore‐ and hindlimbs (hemiplegia) If both sides of the spinal cord are damaged, all four “limbs may be totally paralysed (tetraplegia) Comparable lesions caudal to the second thoracic segment of the spinal cord affect the hindlimbs only, and can give paralysis of one hindlimb (monoplegia), or both hindlimbs (paraplegia) Less severe lesions give rise to medulla oblongata midbrain pons spinal cord thalamic retina retrograde transport Rexed’s laminae rhinencephalon limbic components olfactory components rhombencephalon rhythm of breathing righting test rigidity roaring in horses rods and cones rolling over rostral cerebellar peduncle rostral colliculus rostral commissure rostral crus of internal capsule rostral horn of lateral ventricle rostral lobe of cerebellum rostral medullary velum rostral perforated substance rostrum of corpus callosum rotatory nystagmus rough endoplasmic reticulum Ruffini endings ruminoreticular centre s sacral autonomic lesions sacral vertebrae salivary reflex salivation saltatory conduction sarcolemma Schiff‐Sherrington phenomenon Schwann cell scrapie in sheep second motor area second somatic sensory area segmental arteries of spinal cord seizures sensory analyser system sensory felunculus sensory homunculus septal nuclei septum pellucidum serotonin serotoninergic neurons sexual behaviour sexual functions shivering in horses short‐term memory sigmoid sinus skeletomotor neuron slaughter sleep sleep centre sleepiness sliding‐filament mechanism of axonal transport slipped disc slowly adapting mechanoreceptors slowly adapting receptor slow transport slow‐wave sleep small dense‐cored vesicles sodium ion channel sodium ions sodium‐potassium pump somatic afferents somatic efferents somatic reflex arc somatotopic localization somites of head spasticity spastic paresis in Friesian spatial summation special senses special visceral efferent specific pathways specific receptors on axolemma spike potential spina bifida spinal autonomic lesions spinal cord arteries end of grey and white matter horns ischaemic necrosis laminae of grey matter lesions regions segments tracts and see under tracts spinal reflexes spinal shock spinocerebellar pathways functions projections to cerebral cortex species variations spinocerebellum spinocuneocerebellar pathway spinothalamic pathways in domestic mammals spinothalamic tract of man splenium spondylosis spongioblast spontaneous nystagmus statoconial membrane stellate nerve cells of cerebrum stem cell stereoscopic vision storage diseases strabismus straining during parturition stretch reflex stria habenularis thalami stria medullaris thalami stria terminalis striatum, definition stringhalt stroke stuporous subarachnoid haemorrhage subarachnoid space subcallosal area subdural space subliminal impulse subliminal stimulus substantia chromatophilica substantia gelatinosa substantia nigra subthalamic nucleus subthalamus succinylcholine sulci, cerebral summation superficial arcuate fibres superficial pain superior longitudinal fasciculus supplementary motor area lesions supraoptic nucleus supraspinous ligament surgical replacement of joints in man sway test synapse synaptic bulb general structure recycling of membranes transmitter synthesis vesicle transport synaptic cleft synaptic delay synaptic end bulb synaptic knob synaptic vesicles recycling of membrane transport synthesis of neuronal membranes syringohydromyelia syringomyelia t tabes dorsalis tachycardia tactile placing response tail biting taste buds taste pathways tectum of midbrain tegmentum of midbrain tegmentum of pons telencephalic vesicles telencephalon temperature regulation temporal horn of lateral ventricle temporal lobe lesions temporal summation tentorium cerebelli terminal button termino‐terminal bulb tetanus tetanus toxin tetraparesis tetraplegia thalamus functions lesions in domestic mammals lesions in man thermoregulation thiamine deficiency third ventricle thirst thoracic vertebrae threshold thrombi thymus tilting of head tongue, muscles paralysis tonic neck and eye responses tract(s) corticopontine cranial spinocerebellar cuneocerebellar direct spinocerebellar dorsal corticospinal dorsal spinocerebellar indirect spinocerebellar lateral corticospinal lateral olfactory lateral spinothalamic lateral vestibulospinal Lissauer’s mammillothalamic tract medial olfactory medial vestibulospinal medullary reticulospinal mesencephalic of trigeminal nerve paraventriculohypophyseal pontine reticulospinal propriospinal pyramidal raphe spinal reticulospinal rubrospinal solitary spinal of trigeminal nerve spino cervical spinocervicothalamic spino‐olivary spinoreticular spinotectal spinothalamic supraopticohypophyseal tectospinal ventral corticospinal ventral spinocerebellar vestibulospinal transducer mechanisms of receptors transmitter substances transverse atlantal ligament transverse cerebral fissure transverse fibres of pons trapezoid body tremor triceps tendon reflex trigeminal neuralgia trigger region true pain fibre types pathways tuber cinereum tubulin tunnel vision twitch u unmasking upper motor neuron lesions uvulonodular fissure v vagina, sensory pathway valves of, veins of brain venous sinuses vascularity of neúraxis vascular zones of spinal cord vasodilation vasomotor depressor centre vasomotor pressor centre vein(s) angularis oculi azygos of brain cerebral deep cerebral dorsal cerebral emissary external ophthalmic facial great cerebral internal jugular intervertebral maxillary occipital retinal superficial cerebral ventral cerebral ventral spinal vertebral venous occlusion in brain venous sinus or sinuses cavernous connecting system cranial system dorsal group dorsal petrosal dorsal sagittal dorsal system drainage into systemic circulation emissary veins internal vertebral plexus longitudinal spinal petrosal sigmoid spinal system straight temporal territory drained transverse valves ventral system vertebral ventral arcuate fibres ventral funiculus ventral grey commissure ventral horn ventral longitudinal ligament ventral median fissure ventral tegmental decussation ventriculography VEP see visual evoked potential (VEP) vermis vertebrae mal articulation malformation vertebral‐occipital anastomosis vertical nystagmus vertigo vestibular disease vestibular nuclei vestibulocerebellar projections vestibulocerebellum viciousness visceral afferent non‐pain pathways visceral efferents visceral pain afferents of head visceral pain pathways visual area visual defects visual evoked potential (VEP) visual pathways constricting the pupil decussation eyeball movements one‐to‐one turning head and neck visual placing response vomiting w waking centre walking reflexes Wallerian degeneration warming of skin water closets wheelbarrow test white commissure white matter of spinal cord withdrawal reflex wobbler syndrome dog horse lesions WILEY END USER LICENSE AGREEMENT Go to www.wiley.com/go/eula to access Wiley’s ebook EULA ... engineering parlance, it is the control box in the feedback circuitry of the somatic motor nervous system The cerebellum is not a part of the pyramidal or the extrapyramidal systems, but is superimposed on both of these two systems... through the well‐defined pyramid on the ventral aspect of the medulla oblongata (Figure 22 .2) In fact, the ‘pyramidal’ pathways to the striated muscle of the head (corticonuclear pathways) leave the system before it reaches the pyramid... to the pontine nuclei in the pyramidal feedback circuit (Figure 12. 2) The site of the olivary nucleus in the medulla oblongata is shown schematically in Figure 8.3 (see also Figure 22 .7) Figure 14.1 Diagram of the feedback circuits of the extrapyramidal system