Mastering canine and feline neuroanatomy is a formidable task. The complexity of the subject matter often discourages the veterinary student, as well as the clinician, from becoming proficient in clinical neurology. Although understanding clinical neurology depends upon a working knowledge of neuroanatomy, an intricate knowledge of neuroanatomy is not necessary. This chapter reviews the basic functional and dysfunctional neuroanatomy necessary to understand the neurologic examination (discussed in Chapter 2) and to interpret clinical signs of neurologic dysfunction. Normal functions of specific areas of the nervous system, as well as clinical signs of dysfunction, are described concurrently.
The brain includes the cerebrum, the brain stem, and the cerebellum (Fig. 3.1). The brain stem includes the diencephalon (thalamus, hypothalamus), the midbrain (mesencephalon), the pons (ventral metencephalon), and the medulla oblongata (myelencephalon). Although the diencephalon is technically the rostral-most aspect of the brain stem, it is functionally (and dysfunctionally) more similar to the cerebrum than the remainder of the brain stem (midbrain through medulla). In this text, the term “forebrain” will be used to describe the combination of cerebrum and diencephalon, which is also known as the prosencephalon or thalamocortex. The cerebellum (dorsal metencephalon) is the final brain subdivision and will be discussed in more detail in Chapter 12. The upper motor neurons originate from various regions of the brain. The term “upper motor neuron” (UMN) refers to the neurons of the brain that control motor activity of the body. The UMNs exert their effects by stimulating or inhibiting the neurons that directly innervate the muscles. The actual neurons that innervate the muscles are lower motor neurons (LMNs). In other words, the UMN “tells” the LMN what to do (Fig. 3.2). The UMN system is responsible for (1) initiation of voluntary movement, (2) maintenance of muscle tone for support against gravity, and (3) the regulation of posture. The UMN system is often divided into pyramidal (mainly located in the motor area of the cerebral cortex) and extrapyramidal (mainly located in the brain-stem nuclei) neurons. In primates, the pyramidal system plays a very important role in control over the LMN and thus voluntary motor activity, whereas the extrapyramidal system is the predominant UMN system in dogs and cats. Gait is generated in the brain stem of dogs and cats. The exact location of the brain-stem center for gait generation in dogs and cats is unknown, but the midbrain is thought to play a major role.
Cerebrum (Fig. 3.3; see Table 3.1 for clinical signs of forebrain dysfunction)2, 5, 6, 9, 16, 18, 26, 36 (Video 7)
Table 3.1 Neurologic signs of forebrain dysfunction.
Contralateral postural reaction deficits; +/– mild motor abilities contralateral hemiparesis
Present or absent, especially in the cervical spine
Usually normal; may see mild contralateral sensory loss
May show inappropriate urination
Source: J. Coates, University of Missouri, Columbia, MO, 2014. Reproduced with permission of J. Coates.
Functional regions of the cerebrum can be conceptually divided into lobes (Fig. 3.4). These include frontal lobe (motor area, origin of corticospinal and corticonuclear tracts), parietal lobe (somatosensory area or somesthetic area, receives afferent conscious proprioceptive and nociceptive information), temporal lobe (receives afferent input from both auditory and vestibular systems), occipital lobe (termination of optic tract fibers for visual interpretation), and pyriform lobe (termination of olfactory tract axons for perception of smell). This is an oversimplification (e.g. the motor area of the cerebral cortex is actually partially represented in the parietal lobe as well as the frontal lobe), but is often helpful in understanding cerebral function or dysfunction in the clinical patient. In addition to these general functions, the cerebrum is the seat of consciousness and is important for cognition, interpretation of afferent input, and memory.
The descending tracts to the limbs (corticospinal tracts) are mainly (about 75%) contralateral (Fig. 3.5), and are located primarily in the dorsolateral funiculus of the spinal cord (lateral corticospinal tract). Similarly, cerebral cortical influence over cranial nerve nuclei (corticonuclear or corticobulbar tracts) is predominantly contralateral. These cerebral cortical tracts are of minor importance in dogs and cats, in comparison with humans. However, damage to cerebral cortical neurons or their associated white matter tracts may result in subtle, contralateral hemiparesis.
Conscious proprioception (position sense), tactile sensation, and some nociception (deep pain perception; face) are represented in the contralateral cerebral hemisphere. Conscious proprioception refers to position sense as perceived at the cerebral level. The modality of conscious proprioception is conveyed to the cerebrum primarily via the dorsal column/medial lemniscus pathways (e.g. fasciculus cuneatus for thoracic limb, spinomedullary tract for pelvic limb; Fig. 3.6) and is best evaluated with the animal in a standing position (i.e. proprioceptive positioning; see Chapter 2). Note that some texts attribute the sense of pelvic limb conscious proprioception to the fasciculus gracilis and associated nucleus gracilis. There is evidence that the fasciculus gracilis conveys primarily discriminative touch perception, whereas the spinomedullary tract (whose afferent axons synapse on nucleus Z, rostromedial to the nucleus gracilis) is responsible for conveying the modality of conscious proprioception.
The combination of conscious proprioceptive deficits (usually contralateral to a cerebral lesion) with a normal or near-normal gait is a hallmark of cerebral dysfunction.
Lesions of the cerebrum often cause behavior change, altered mental status (e.g. obtundation), seizure activity, walking in circles (usually in the direction of the lesion), head pressing, and menace deficits. The deficits in the menace response are primarily contralateral. Contralateral deficits of facial sensation may also be appreciated.
Patients with structural disease (e.g. tumors) of the cerebrum, or any area of the brain, may exhibit neck pain (thalamic pain syndrome). This phenomenon is thought to be due to factors such as meningeal stretching and referred pain. It is important that the clinician realize that structural brain disease can cause neck pain, and that this clinical finding does not necessarily indicate multifocal or diffuse disease (i.e. another lesion in the cervical spinal cord area).
“Hemi-inattention syndrome,” or “hemineglect syndrome,” refers to a phenomenon in which a patient with a structural forebrain lesion ignores input from one-half of his or her environment. Since most sensory stimuli are interpreted primarily in the cerebral hemisphere contralateral to the stimulus side, the side that the patient ignores is contralateral to the side of the lesion. These patients may eat from only one-half of the food bowl, turn the opposite direction when called by name (i.e. when called from the ignored side), and ignore or have difficulty localizing nociceptive (e.g. skin pinch) stimuli when applied contralateral to the side of the brain lesion.
Signs of dysfunction are often similar to those associated with cerebral disease. In fact, all of the clinical signs of dysfunction listed for cerebral disease may be observed in patients with diencephalic disease (Table 3.1). One fairly consistent feature of patients with diencephalic disease is that they often will circle to either side. If a patient alternates which side he/she circles to, based either on hospital observation or owner-supplied history, this may point to a diencephalic lesion vs. a cerebral lesion.
Patients with diencephalic dysfunction may also exhibit evidence of endocrine dysfunction (e.g. PU/PD), abnormal eating patterns, and problems with temperature regulation. Uncommonly, animals with diencephalic disease act nonspecifically painful (thalamic syndrome). Absence of these signs does not rule out a diencephalic lesion, however.
The optic nerves or their relays with lateral geniculate nuclei may be affected, resulting in visual impairment and deficient menace responses.
Large lesions of the diencephalon may produce stupor and coma as the diencephalon is part of the ascending reticular activating system (ARAS) projecting to the cerebral cortex. The ARAS is responsible for maintaining the awake state in normal animals.
Although uncommon, peracute and acute diencephalon and midbrain lesions may cause a head tilt. (See Chapter 7.)
Midbrain (Fig. 3.9; see Table 3.2 for clinical signs of brain-stem [caudal to the diencephalon] dysfunc-tion)2, 5, 8, 10, 16, 18, 20, 28, 36, 42, 44, 45
Table 3.2 Neurologic signs of brain-stem dysfunction (midbrain through medulla).
Normal, obtunded, stupor, coma
Normal, head tilt (ipsilateral/contralateral), wide-base stance; recumbent patients may manifest decerebrate or decerebellate rigidity
Ipsilateral deficits; CN III–XII may be affected depending upon lesion extent (vestibular signs common); ipsilateral or bilateral Horner’s syndrome possible but uncommon
Mild–severe ipsilateral deficits
Intact; may have ipsilateral hyperreflexia
Present (inflammatory disorders) or absent
Usually intact; dependent upon mental status
Usually intact; severe lesions may manifest absent micturition reflex
Source: J. Coates, University of Missouri, Columbia, MO, 2014. Reproduced with permission of J. Coates.
Lesions from the midbrain through the medulla are more likely to produce severe disturbances of consciousness (stupor, coma) due to impairment of the ARAS.
Lesions from the midbrain through the medulla typically cause obvious gait abnormalities (UMN paresis or plegia). These can be unilateral or bilateral, depending on the size and rate of development of the lesion. On each side of the midbrain, ventrolateral to the mesencephalic aqueduct, is a collection of neurons called the red nucleus. Each red nucleus gives rise to axons that cross the midline and become the rubrospinal tract (Fig. 3.10). The rubrospinal tracts are thought to be important in gait generation in dogs and cats. If the midbrain lesion is focal enough (unlikely, due to the small size of the midbrain), an ipsilateral (caudal midbrain) or contralateral (rostral midbrain) hemiparesis with postural reaction deficits may predominate. The anatomic landmark for focal lesions that will produce ipsilateral gait and postural reaction deficits appears to be in the vicinity of the caudal midbrain and rostral pons. Lesions rostral to the midbrain cause contralateral postural reaction deficits and mild or inapparent contralateral paresis. Midbrain lesions seen in clinical practice are often large enough that the signs are bilateral and severe (e.g. decerebrate rigidity in brain-stem herniation).
The oculomotor nuclei (motor to extraocular muscles and parasympathetic to pupil) and trochlear nuclei are located in the midbrain. Axons from these nuclei comprise cranial nerves (CN) III and IV, respectively. CN III and IV indent and traverse across the cavernous sinus at the base of the brain. Other cranial nerves that traverse through the connective tissue overlying this sinus include the ophthalmic and maxillary branches of CN V (from the pons) and CN VI (from the medulla). Cavernous sinus syndrome refers to dysfunction of more than one of these aforementioned cranial nerves. In addition to these cranial nerves, the sympathetic pathway to the eye courses in the vicinity of the cavernous sinus for a short distance, before exiting through the orbital fissure with the ophthalmic branch of CN V. Therefore, Horner’s syndrome may also occur with lesions in the region of the cavernous sinus.
The origin of the tectotegmentospinal tract (sympathetic innervation of the eye) is in the midbrain (tectum refers to the dorsal aspect or roof of the midbrain; tegmentum refers to the body of the midbrain). The diencephalon has influence over this part of the midbrain.
The motor nucleus of CN V (trigeminal nerve) is located here. The sensory nuclei and tract of CN V are located from the midbrain to the cranial cervical spinal cord.
Lesions of the pons typically cause severe disturbances of consciousness and UMN paresis/plegia. Axons from the reticular formation of the pons give rise to the pontine reticulospinal tracts (Fig. 3.12).
The major respiratory centers are located in the pons and medulla (mainly), so abnormal respiratory activity may be apparent with damage to the pons.
The nuclei of CN V (trigeminal, sensory portion only), VI (abducent nerve), VII (facial nerve), IX (glossopharyngeal nerve), X (vagus nerve), XI (accessory nerve), and XII (hypoglossal nerve) are located in the medulla, so dysfunction of one or more of these cranial nerves (discussed in Chapter 2) may be evident.
This is also the location of the vestibular nuclei (rostral, medial, caudal, lateral). The functional neuroanatomy associated with the vestibular system is discussed in more detail in Chapter 11.
Clinically the medulla can be divided into rostral and caudal medulla. Lesions in the rostral medulla will frequently cause central vestibular signs, with or without facial nerve deficits. Lesions in caudal medulla will cause dysphonia, dysphagia, and occasionally tongue paresis.
Lesions of the medulla can cause alterations of consciousness, respiratory disturbance, and autonomic dysfunction (heart rate and blood pressure).
Axons from the medullary reticular formation give rise to the medullary reticulospinal tracts (Fig. 3.12). Damage to the medulla often results in UMN paresis/plegia from interference with these and other UMN tracts from the brain stem.
Abnormal respiration is possible, since the major respiratory centers are located in the medulla. The neurons of the medullary respiratory centers can be thought of as the UMNs of respiration, which send axons to the LMNs. The LMNs for respiration are located in the gray matter of the caudal cervical (C5–C7, phrenic nerve) and thoracic (intercostal nerves) spinal cord segments.