Diagnostic approach to patients with signs of encephalopathy (Proceedings)


Diagnostic approach to patients with signs of encephalopathy (Proceedings)

Aug 01, 2008

The word encephalopathy literally means "disease or disorder" of the brain. One can see that this would be an extremely vast topic if all disorders were discussed. The word also does not denote an etiology, and therefore, from a clinical standpoint the important learning issues for the clinician are: 1) what are the clinical signs associated with encephalopathy 2) what is the clinical problem solving approach to these patients 3) what diagnostics are generally required and 4) are there any breed related disorders. These four points will be addressed in general and not with detailed specifics because this topic is too vast. The clinician should grasp the concept of how to develop a "problem solving approach" to this neurologic presentation and then later focus on the specific disorders that can result in an encephalopathic patient.

Clinical presentation for encephalopathy

One can imagine that the neurologic deficits can be quite broad and diverse when the entire brain is included in this discussion. Some historical information may be beneficial to establish a category of disease and for initial development of a differential diagnosis list.

Clinical signs can be present as a focal, diffuse or multifocal encephalopathy. Focal encephalopathy often will result in asymmetric abnormalities on neurologic examination. Diffuse encephalopathy will show symmetric or bilateral neurologic deficits often with more severe changes in mentation. Metabolic and toxic disorders commonly have signs of a diffuse encephalopathy. Multifocal encephalopathy consists of multiple lesions within the CNS. Inflammatory diseases have this type of lesion distribution.

Time of onset of clinical signs will assist with ascertaining differentials. Specific disorders are associated with acute progressive, acute non-progressive and chronic time courses. Toxic, metabolic, and inflammatory causes have acute progressive clinical presentations. Disorders with an acute non-progressive time course include vascular insults and trauma. Degenerative, anomalous, neoplastic, and nutritional disorders often have chronic presentations. Obtaining an accurate history from the pet-owner is crucial for establishing a clinical time course, but also for gathering indirect evidence of brain disease.

Table 1: Neurologic Signs of Forebrain Dysfunction
Differentiation between clinical signs that reflect forebrain and brainstem dysfunction aids with the neuroanatomic localization. The forebrain processes input associated with responses or reactions to an external stimulus and serves to initiate specific reactions (Table 1). Clinical signs of forebrain dysfunction include altered mentation (obtunded, stupor, or coma), behavioral changes, head-pressing, wide-circling, head turn toward the side of the lesion, visual field deficits, and hemi-neglect (aversive syndrome). Gait often is normal with forebrain dysfunction, but may be aimless and without purpose. Postural reaction deficits are contralateral to the side of the lesion. Seizures also are a sign of cerebral or diencephalic dysfunction.

Clinical signs for diencephalic disease are similar to cerebral disease buy may show clinical signs of diffuse forebrain dysfunction. Alterations in mentation are more severe because of its close association with the ascending reticular activating system (ARAS). The gait can be normal and not manifest signs of asymmetry such as circling. Cranial nerve evaluation often shows menace response deficits with abnormal pupillary light reflex reflective of a CN II lesion. This relates to proximity of the diencephalon to the optic chiasm. Hypothalamic signs include endocrine dysfunction, abnormal eating patterns (polyphagia or anorexia), and temperature dysautoregulation. It is not uncommon for clinical signs of diencephalic disease to be vague making the lesion localization difficult.

Table 2: Neurologic Signs of Brainstem Dysfunction
Clinical signs of brainstem dysfunction reflect lesions of the midbrain through the medulla (Table 2). Mentation is more severely affected often causing stupor or coma as a result of direct involvement to the ARAS. Ipsilateral postural reaction deficits, vestibular dysfunction, and multiple cranial nerve deficits are characteristic of brainstem dysfunction.

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