Get access to all handy features included in the IVIS website
- Get unlimited access to books, proceedings and journals.
- Get access to a global catalogue of meetings, on-site and online courses, webinars and educational videos.
- Bookmark your favorite articles in My Library for future reading.
- Save future meetings and courses in My Calendar and My e-Learning.
- Ask authors questions and read what others have to say.
Clinical Recognition of Some Confusing Neurologic Syndromes
Get access to all handy features included in the IVIS website
- Get unlimited access to books, proceedings and journals.
- Get access to a global catalogue of meetings, on-site and online courses, webinars and educational videos.
- Bookmark your favorite articles in My Library for future reading.
- Save future meetings and courses in My Calendar and My e-Learning.
- Ask authors questions and read what others have to say.
Read
Modern equine veterinarians, armed only with patience, knowledge, a penlight, and a hemostat, should be able to locate a lesion and ultimately make a specific diagnosis.
1. Introduction
Ambulatory equine veterinarians cannot carry sophisticated electrodiagnostic or cross-sectional imaging equipment with them, and their clients often could not afford these diagnostics even if they could.1,2 Fortunately, armed with a penlight, a hemostat, some patience, and a little knowledge, modern equine clinicians should be able to work logically toward determining where the lesion(s) causing the clinical syndrome is located. The author tried to select a few syndromes that seem to commonly create confusion among veterinarians as they go about this process. Hopefully, working once again through selected clinical syndromes will help reinforce long-ago-learned principles of neurologic examination and neuroanatomic localization.
2. Syndrome 1: Mentation—Level of Consciousness and Behavior
Level of consciousness and behavior are two distinct components that should not be confused; veterinarians, however, frequently conflate the former, i.e., how alert an animal is, with the latter, i.e., how appropriately the animal interacts with the animate and inanimate environment. Although there are several overlaps between these two modalities of mentation, they are generated at separate sites: consciousness in the brainstem and behavior in the cerebrum (with assistance from the thalamus).
Alertness: Consciousness “originates” in the reticular formation, a loose network of neurons that extend longitudinally deep within the brainstem and continuously from the diencephalon to the medulla oblongata (Fig. 1). The reticular formation controls or modulates many basic life-sustaining processes such as heart rate and vascular tone, breathing and swallowing, maintenance of body tone, balance and posture, habituation to repetitive stimuli, and modulation of pain. Among the more than 100 networks that make up the reticular formation is the ascending reticular activating system (ARAS), which gathers and integrates stimulatory and inhibitory information from the internal and external environments and converts all of this information into waves of signals that are projected rostrally via thalamic connections to the cerebral cortex to keep the horse awake, i.e., conscious. The sources of stimulatory input are illustrated in Fig. 1. Most “alertness” signals projected to the forebrain from the ARAS are carried by monoamine neurotransmitters such as norepinephrine, serotonin, and dopamine.
Lesion localization: As described in Dr. Monica Aleman’s lecture, during the first hour of this session, level of consciousness or alertness is evaluated on a continuous scale from normal (i.e., bright and alert) to comatose. As shown in Fig. 1, the ARAS is most active in the midbrain and progressively less so in more rostral and caudal sections. This knowledge can be used to predict the effect of a model injury at different levels of the brainstem. For example, a moderate bleed in the midbrain produces the most profound obtundation (coma for a serious injury); the same injury to the rostral medulla may only cause lethargy, and there may be no effect on consciousness if the injury were caudally in the medulla near the foramen magnum. The effect cerebral lesions has on consciousness is often very little unless there is a severe multifocal or diffuse involvement of the forebrain. In other words, it is possible for a horse to have a large mass lesion on one side of its cerebrum (e.g., cholesterol granuloma, Streptococcus equi abscess) and be fully alert. More diffuse processes, especially metabolic encephalopathies such as those of hepatoencephalopathy or hypo-osmolality, are accompanied by more profound obtundation, although there is likely also an effect on the brainstem.
Behavior: Abnormalities of behavior may be termed dementia. Typical abnormal behaviors that result from central nervous system (CNS) disease include self-mutilation, seizures, head-pressing, compulsive walking (often in a circle), yawning, aggression (including unprovoked biting or kicking), timidity, loss of affinity of a foal for its dam, and loss of learned behaviors and skills. The inability or refusal of a trained horse to follow when being led is a form of dementia that may be obvious during a neurologic examination.
Lesion localization: It must be kept in mind that bizarre behavior may be seen in horses without organic CNS disease. For example, such behavior is an appropriate response to an extreme stimulus (e.g., stinging nettle reaction), and stereotypical or otherwise destructive patterns of behavior such as self-mutilation syndrome can be extremely abnormal and difficult to differentiate from true CNS disease syndromes. However, for those disturbances of behavior that are caused by brain disease, the forebrain is almost exclusively the location. Focal, asymmetric lesions usually manifest with asymmetric abnormal signs. For example, the horse may turn its head (usually, but not always, toward the side of the lesion) and walk compulsively in circles, often around the inside of an enclosure. Such lesions also may cause partial (focal) seizures that at least initially affect one side of the body. Although anatomic mapping of dementia syndromes has not been carried out in detail in horses, involvement of the various components of the nuclei of the extrapyramidal system in the forebrain (and possibly midbrain) likely explains compulsive, repetitive, or bizarre motor activities such as fluphenazine reaction, compulsive circling, and the orofacial dystonia of nigropallidal encephalomalacia. The frontal and temporal cortices are involved with learned behavior, and the limbic system is involved with inherent behavior.
3. Syndrome 2: Menace Deficit—Where Is the Neurologic Lesion?
Almost all neurologic lesions of the visual pathways can be localized by carefully evaluating menace responses and direct and indirect pupillary light reflexes (PLRs). Additional information on vision is provided by obstacle tests. Accurate neuroanatomic localization then is used to generate likely differential diagnoses and diagnostic plans. The basics of this approach are summarized in Table 1 and Fig. 2, which together illustrate the effects of 6 model lesions on left pupil size in ambient light; menace responses, vision, and direct PLRs, all performed on the left eye; and indirect PLRs performed on both eyes. [...]
Get access to all handy features included in the IVIS website
- Get unlimited access to books, proceedings and journals.
- Get access to a global catalogue of meetings, on-site and online courses, webinars and educational videos.
- Bookmark your favorite articles in My Library for future reading.
- Save future meetings and courses in My Calendar and My e-Learning.
- Ask authors questions and read what others have to say.
Comments (0)
Ask the author
0 comments