Directed Neurological Examination Overview

The examination of the patient with altered consciousness begins by ensuring that the patient's vital signs and basic biochemistry are adequate to support brain function. It is essential to ensure that blood pressure, respiration, and oxygen saturation are adequate and that the patient is not hypoglycemic or thiamine deficient before proceeding with the examination outlined later. In many situations (e.g., emergency departments), naloxone is also administered at this point to reverse any putative effects of opiates. The empirical use of flumazenil to antagonize potential benzodiazepine intoxication as a routine measure is controversial because of the risk of provoking seizures or status epilepticus, especially in patients with mixed benzodiazepine and cyclic antidepressant overdoses.

The initial goals of the examination of the patient with apparent altered consciousness are first to determine whether the patient is conscious and then, in patients with altered awareness, to determine whether or not the reticular system is functional. Because altered awareness requires either reticular system dysfunction or bilateral hemispheric dysfunction, testing the structures immediately adjacent to the reticular system provides the major clues regarding the etiology of altered consciousness and

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TABLE 1-

1 -- CLINICAL FINDINGS WITH DIFFERENT

r LEVELS OF CENTRAL NERVOUS SYSTEM DYSFUNCTION

Dysfunction

Response to Noxious Stimuli

Pupils

Eye Movements

Breathing

Both cortices

Withdrawal

Small, reactive

Spontaneous conjugate horizontal movements; if none, cervico-ocular or vestibulo-ocular reflexes can be elicited

Posthyperventilation apnea or Cheyne-Stokes respiration

Thalamus

Decorticate posturing

Same as above, unless the optic tracts are also damaged

Same as above

Same as above

Midbrain

Decorticate or decerebrate posturing

Midposition, fixed to light

Loss of ability to adduct. Both eyes may be deviated laterally (wall-eyed) (CN III damaged)

Usually same as above; potential for central reflex hyperpnea

Pons

Decerebrate posturing

Usually small; may exhibit bilateral pinpoint pupils (especially with midline pontine hemorrhage); Horner's syndrome with lateral lesions

Loss of conjugate horizontal movements with retained vertical movements and accommodation. Often eyes are deviated medially (CN VII damage)

May exhibit central reflex hyperpnea, cluster (Biot's) breathing, or apneustic breathing

Medulla

Weak leg flexion (or none)

Usually small; Horner's syndrome with lateral lesions

Usually no effect on spontaneous eye movements; may interfere with reflex responses; rarely, nystagmus

Rarely, ataxic respiration; apnea if respiratory centers involved

thereby determines the direction of subsequent investigations. The major findings on examination and their expected anatomical correlates are presented in Table 1:1

. These correlations are with the level of dysfunction, which may involve a substantially larger portion of the nervous system than the degree of actual damage.1^1

The findings on these examinations are often summarized by use of the Glasgow Coma Scale. y Because the verbal response of intubated patients is difficult to assess, one either ignores it (assigning it a value of T, for intubated) or imputes a score based on the examiner's estimate of what the patient could do. Although the results of this evaluation are frequently presented as the sum of the values, this practice is of limited utility. This procedure is of value in indicating the severity of head injury, in which a total score of 3 to 8 indicates severe trauma, 9 to 13 moderate trauma, and 14 to 15 mild trauma. However, the real utility of the score is to provide a simple way of detecting changes in the examination over time, with good inter-rater reliability, in circumstances of global cerebral dysfunction (e.g., trauma, intoxication). The score has limited utility in patients with focal neurological dysfunction.

At all times in the initial examination of the patient with suspected impaired awareness, the examiner must recall that the patient may in fact be capable of sensing and remembering. Although noxious stimuli may be required for an adequate examination, the minimum necessary stimulation should be employed, and the examiner should always be cognizant of the need for explanation of procedures, especially potentially painful ones. This caveat should carry over from the first encounter with the patient throughout the course of treatment. Attempts to communicate the level of sedation in patients is particularly problematic. For patients who are intoxicated or therapeutically sedated, the scale proposed by Ramsay and colleagues is commonly used (.TableJ-? ). y

ASSESSMENT OF AROUSAL

Observation of the Patient's Ambient State. A great deal can be learned by watching the patient before the formal examination. Is the patient lying still in bed when not stimulated (required for the diagnosis of coma), or does he or she exhibit spontaneous movements? Evaluation of the patient's spontaneous movements often yields information of localizing and lateralizing significance. An externally rotated leg in a comatose patient is frequently evidence of corticospinal tract dysfunction due to a contralateral hemispheric lesion. Do the eyes open spontaneously, and are there other facial movements? Minor facial or extremity twitching is frequently the only physical finding in patients suffering from nonconvulsive status epilepticus. Is there evidence of trauma to the head or the rest of the body?

The examiner next asks the patient to follow verbal commands. Early in the examination, ask the patient to open the eyes and look up; this will detect patients with pontine lesions that prevent all other somatic motor output (the locked-in syndrome; see later). Such patients may appear comatose but are not, and care must be taken to recall that they are alert and cognizant, and have intact auditory and somatosensory systems despite their brain stem disorder. y

Pupillary Responses to Light. The parasympathetic reflex arc begins in the retina, traverses the base of the brain, runs through the midbrain, and returns to the pupil

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