Clinical Vignette
Fluffy, a 3-year-old DLH spayed female cat, is presented after being found lying on her side and totally unresponsive to handling. Attempts by the owner to arouse Fluffy were unsuccessful. Fluffy was outside the previous night, but was normal at 10 PM when the owner let Fluffy out of the house. Your physical examination is normal except that Fluffy is in lateral recumbency and cannot be aroused. She withdraws her feet when the digits are pinched with a hemostat and consciously responds to the noxious stimuli. The pupils are midrange in size, equal, and have good pupillary light reflex responses. The tendon reflexes are all present and the oculocephalic reflex (sometimes incorrectly referred to as the “doll’s eye reflex”) is present. What level of consciousness would you categorize for Fluffy? What categories of disease fit best with the history? How would you proceed with your diagnostic approach?
Problem Definition and Recognition
Altered states of consciousness vary, from obtunded (depression) to coma (Kline 2005). The following definitions are used in this chapter:
An obtunded/depressed mental state has many causes, including such causes as a systemic illness. On the other hand, confusion, stupor, coma, and the vegetative state are always signs of abnormal brain function and are either due to primary brain disease or other secondary effects on the brain such as hypoglycemia, liver disease, and hypothyroidism.
Pathophysiology
Consciousness is maintained by sensory stimuli acting through the reticular activating system (RAS). The reticular formation of the rostral brain stem receives input from most of the sensory systems of the body, including somatosensory (e.g., touch, temperature, and pain), visual, auditory, and olfactory pathways. Pathways from the reticular formation project diffusely to the cerebral cortex by way of the intralaminar nuclei of the thalamus, maintaining a background of activity mediated through cholinergic synapses on cortical neurons. A second pathway projects to the hypothalamus and basal forebrain (Saper 1984). Activity in the RAS is balanced by an adrenergic system from brain stem and diencephalic nuclei, which influence sleep. Any disorder that alters the activity of RAS or interferes with its connections to the cortex can cause a change in the level of consciousness.
Coma is usually the result of one of four major categories of abnormality: (1) diffuse, bilateral cerebral disease, (2) metabolic or toxic encephalopathies, (3) compression of the midbrain or pons, or (4) destructive lesions of the midbrain or pons (Lorenz and Kornegay 2004).
Diffuse, bilateral cerebral hemisphere disease usually causes signs of depression to stupor, and only rarely coma. The vegetative state is seen in animals with severe cerebral disease. The animal will arouse, vocalize, and have brain stem reflex activity, including paddling movements of the limbs. However, there are no purposeful actions indicating cortical function. This state is most common after severe hypoxic episodes, cortical trauma, or prolonged hypoglycemia. Metabolic disease, such as hepatic failure, may cause stupor or coma with preservation of brain stem function.
Lesions of the brain stem in the region of the midbrain or pons frequently cause coma. Head trauma often causes hemorrhage in these areas. Typically, the animal is unconscious from the time of the injury and never regains consciousness. Other signs of brain stem dysfunction are usually present, including abnormal pupillary light reflexes, abnormal eye movements, other cranial nerve deficits, and postural test reaction deficits. Brain stem function can also be compromised by compression, either directly from mass lesions or secondarily by tentorial herniation of the cerebrum. The brain is enclosed in an inelastic case, the skull. Any increase in brain volume within the skull must displace part of the contents. Increased pressure causes displacement of the cerebral hemisphere under the tentorium cerebelli, resulting in compression of the brain stem. Unilateral masses produce a herniation on the same side, whereas generalized pressure increases, such as in hydrocephalus or cerebral edema, cause a central or bilateral herniation (Kornegay et al. 1983).
Diagnostic Plan
Anatomic Diagnosis
Coma always indicates severe brain dysfunction. Structural damage to the brain stem is a grave prognostic sign, so the neurologic examination should be directed toward evaluating brain stem function. Motor function, pupil function, and eye movements are important parameters to assess. Table 45-1 outlines the findings in the most common syndromes. See Chapters 46–48 for details on assessing the pupils and eye movements.
Diffuse cerebral disease with a normal brain stem rarely causes coma. When it does, the animal is blind, but the pupils are either normal or constricted. Vestibular eye movements may be present. Extensor hypertonus is not present, as is commonly seen with brain stem disease. Walking or paddling movements are often present. When this syndrome persists, it is called the vegetative state, and is seen most often after severe hypoxia, although it may occur with other metabolic problems such as a prolonged hypoglycemia. Signs of diffuse cerebral disease are likely to be symmetric.
TABLE 45-1. Clinical signs in coma
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