Patients State

Awake, anxious and agitated, or restless Awake, cooperative, oriented, and tranquil Awake but responds to commands only

Appears asleep (this is not true sleep) but responds briskly to a light glabellar tap or a loud auditory stimulus Appears asleep, and responds only sluggishly to a light glabellar tap or a loud auditory stimulus Appears asleep, with no response to stimuli

From Ramsay MA, Savage TM, Simpson BR, Goodwin R: Controlled sedation with alphaxalone-alphadolone. BMJ 1974:2:656-659.

(see Chapters.® and 9 ). Disorders altering pupillary constriction typically affect the midbrain or the third cranial nerve. Compression of the superior colliculus (e.g., by a pineal region mass) interferes with input to the pretectal nuclei, resulting in pupils that are large (because the sympathetic system is not affected), unreactive to light, and sometimes displaying hippus. Lesions affecting the area of the Edinger-Westphal nucleus and the origins of the third cranial nerves are the most important, because this area is adjacent to the superior pole of the midbrain reticular formation. Because the descending sympathetic efferent fibers also traverse this portion of the brain stem, dysfunction produces pupils that are midposition (4 to 6 mm in diameter), unreactive to light, and frequently slightly irregular. Such pupils are an ominous finding, usually indicating that coma is due to structural damage affecting the upper midbrain, and unless its etiology can be reversed quickly, the patient's coma is usually irreversible. Because the pupillary constrictor has a muscarinic, rather than a nicotinic, acetylcholine receptor, it is not affected by drugs given to block neuromuscular transmission. However, it is affected by systemic antimuscarinic drugs (e.g., atropine), so one must be cautious about interpreting the examination if such agents are being used.

Unilateral loss of pupillary constriction in the comatose patient may rarely indicate subarachnoid hemorrhage from an internal carotid aneurysm that compresses the third nerve at the origin of the posterior communicating artery. Much more commonly, such a finding indicates the presence of a mass lesion that has shifted the diencephalon laterally. Although older studies suggested that this finding arose from compression of the third cranial nerve by the herniating temporal lobe, the unilaterally dilated pupil appears to develop before actual movement of the medial temporal structures over the tentorial edge. Ropper's work demonstrates that unilateral pupillary dilation results from traction on the third nerve produced when the diencephalon, being pushed away from an expanding lateral mass, pulls the midbrain with it. Because the third cranial nerve is tethered anteriorly at the cavernous sinus, the nerve ipsilateral to the mass is subjected to stretching and the pupil dilates. Early in the course of this process, therapies that decrease the degree of shift (e.g., administration of mannitol) can reverse the pupillary dilation.

The sympathetic pathways begin in the hypothalamus, descend through the brain stem and spinal cord to the first thoracic level, and then exit the central nervous system to traverse the face and reach the pupil. Most sedative drugs produce bilateral small pupils by antagonizing sympathetic outflow at the hypothalamic level; other agents, such as opiates, appear to have an additional effect of stimulating the parasympathetic system, resulting in very small (pinpoint) pupils. Lesions affecting the sympathetic system below the midbrain do not directly affect consciousness.

Conjugate Eye Movements. The position and movements of the eyes are observed, and certain easy-to-administer procedures are undertaken to evaluate the integrity of the cerebral hemisphere and brain stem. The neural pathways for the control of horizontal conjugate eye movements are outlined in Figure 1-1 (Figure Not Available) . Cortical control originates in the frontal gaze centers (Brodmann's area 8), and descending fibers controlling horizontal conjugate gaze cross the midline in the lower midbrain region and descend to

Figure 1-1 (Figure Not Available) Conjugate vision pathways; nuclei and paths are shaded to include those important to left conjugate gaze: fibers from the right frontal cortex descend cross the midline, and synapse in the left paramedian pontine reticular formation (PPRF). Fibers then travel to the nearby left cranial nerve VI nucleus (to move the left eye laterally) and then cross the midline to rise in the medial longitudinal fasciculus (MLF) to the right cranial nerve III nucleus (to move the right eye medially). In addition to the cortical influence on the left PPRF, there is vestibular influence. With cold water placed in the left external ear canal, the crossed pathway from the right vestibular nucleus to the left PPRF predominates and drives the eyes conjugately to the left. This procedure tests the integrity of the brain stem circuit that includes the vestibular nucleus, the PPRF, and cranial nerves III and VI and the MLF. If the eyes move to the side of cold water infusion, the brain stem from medulla to midbrain must be functioning. (From Weiner WJ and Goetz CG [eds]. Neurology for the Non-Neurologist, 3rd ed. Philadelphia, J.B. Lippincott Company, 1994.)

the paramedian pontine reticular formation (PPRF) in the pons. The systems producing conjugate eye movements in the conscious and unconscious states vary slightly. Conscious horizontal conjugate eye movements depend on the PPRF for their coordination, whereas such movement in the unconscious patient appears to bypass this region and depend directly on the abducens nuclei for their coordination. Because these small structures are directly adjacent to each other and are caudal to the portion of the reticular formation necessary for consciousness, this distinction is not usually of consequence. The region of PPRF and adjacent neurons is thus the major area of confluence of pathways controlling horizontal eye movements. Neurons from the PPRF project to the nearby abducens nerve (cranial nerve VI) nucleus and thereby stimulate movements in the lateral rectus muscle of the eye ipsilateral to the PPRF and contralateral to the frontal gaze center. In addition, fibers from the abducens nerve nucleus cross the midline and ascend the median longitudinal fasciculus (MLF) to the medial rectus nucleus of the oculomotor nerve (cranial nerve III) in the midbrain. This activation stimulates adduction of the eye ipsilateral to the frontal gaze center, and conjugate gaze is thus completed. Because this system overlaps in space with the midbrain reticular formation, conjugate gaze examination is of vital importance in the comatose patient. In contrast to the pupillary constrictors, these muscles have nicotinic neuromuscular junctions and are therefore susceptible to neuromuscular junction blocking agents.

By following the pathways outlined in the figure, the consequences of lesions at various levels of the neuraxis can be deduced. Stimulation of fibers from the frontal gaze center of one cerebral hemisphere results in horizontal, conjugate eye movements to the contralateral side. If one frontal gaze center or its descending fiber tract is damaged, the eyes drift toward the involved cerebral hemisphere due to unopposed action of the remaining frontal gaze center. For example, a destructive lesion in the right cerebral hemisphere, involving descending motor fibers and frontal gaze fibers, causes a left hemiplegia, with head and eyes deviated to the right. In other words, the eyes appear to look at a destructive hemispheric lesion and look away from the resulting hemiplegia.

By contrast, a destructive left pontine lesion, for example, damages the left PPRF and surrounding region. The eyes, therefore, cannot move to the left and tend to deviate to the right. Because descending pyramidal tract fibers cross the midline in the medulla, damage to the pyramidal tract fibers in the pons on the left results in a right hemiplegia. Thus, the eyes appear to look away from a destructive pontine lesion but look toward the hemiplegia.

If the abducens nerve or nucleus is destroyed, there is a loss of abduction of the ipsilateral eye (cranial nerve VI palsy). With destruction of the tract of the medial longitudinal fasciculus, disconjugate gaze results, with loss of adduction of the ipsilateral eye (same side as the tract of the MLF). Abduction of the contralateral eye is preserved, but there is nystagmus in the awake patient. This type of disconjugate gaze abnormality is also termed internuclear ophthalmoplegia. The pathways for vertical eye movements are less well understood. Lower centers likely exist in the midbrain (pretectal and tectal) regions.

If a patient cannot follow verbal commands, two useful tests are employed to determine brain stem integrity. They activate the PPRF and subsequent pathways, not by cortical stimulation but rather by vestibular alterations. An oculocephalic or cervico-ocular (or doll's eyes) reflex is performed by turning the patient's head rapidly in the horizontal or vertical planes and by noting the movements or position of the eyes relative to the orbits. This test obviously should not be performed if a cervical neck fracture is suspected. If the pontine (horizontal) or midbrain (vertical) gaze centers are intact, the eyes should move in the orbits in the direction opposite to the rotating head. An abnormal response (no eye movement on moving the head) implies pontine or midbrain dysfunction and is characterized by no movement of the eyes relative to the orbits, or an asymmetry of movements.

Horizontal oculocephalic maneuvers are a relatively weak stimulus for horizontal eye movements. If a doll's eyes reflex is present, it is not necessary to continue with oculovestibular testing. If, however, the doll's eyes reflex is lacking, ice water calorics should be performed, because ice water is a stronger stimulus than oculocephalic maneuvers.

Oculovestibular responses (ice water calorics) are reflex eye movements in response to irrigation of the external ear canals with cold water. The head is raised to 30 degrees relative to the horizontal place, and the external canals are inspected for the presence of cerumen or a perforated tympanic membrane. Fifty to one hundred milliliters of cold water is instilled into the canal (waiting 5 minutes between each ear), and the resulting eye movements are noted. Ice water produces a downward current in the horizontal semicircular canal and decreases tonic vestibular output to the contralateral PPRF. Simplistically, one can think of this as an indirect means of stimulating the ipsilateral PPRF. Hence, after cold water instillation, there should be a slow, tonic, conjugate deviation of the eyes toward the irrigated ear if the brain stem is intact. In a comatose patient, there is a loss of the past-phase nystagmus, and only tonic deviation of the eyes is seen if appropriate pontine-midbrain areas are intact. Thus, if nystagmus is noted in a seemingly unconscious patient, the patient is not truly comatose.

Thus, a lack of oculovestibular responses suggests pontine-midbrain dysfunction. Ice water calorics can help differentiate between the conjugate gaze weakness, or paralysis caused by either cortical (cerebral hemisphere) or brain stem (pontine) damage. Oculovestibular responses should not be altered in patients with only hemispheric pathology other than the loss of nystagmus.

Movement of the ipsilateral eye toward the irrigated ear but no movement of the contralateral eye suggests an abnormality of the contralateral MLF.

Although tradition dictates that the head be elevated 30 degrees (in order to place the horizontal semicircular canal in a vertical orientation, thereby maximizing the effect of gravity on endolymphatic movement), the superiority of this position over others has not been solidly demonstrated.

Breathing Patterns. Various respiratory patterns have localizing significance in the patient with altered consciousness. These patterns are recognizable by bedside observation. Before proceeding to detailed analysis of the respiratory pattern, the examiner should be certain that the upper airway is intact. If it is not, endotracheal intubation should be performed immediately unless the patient has an advance directive prohibiting this maneuver. The respiratory pattern can be easily assessed after intubation, recognizing the confounding effects of drugs given to facilitate the procedure and the increased work of breathing required by the smaller diameter of the new airway.

The respiratory pattern is determined by observation but should be interpreted in the light of arterial blood gas results. Tachypnea should be interpreted differently in patients who are hypoxic than in those who are normoxic. In the analysis of blood gas results, recall that the brain stem



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