Vegetative state longer than 1 month is classified as a persistent vegetative state

Minimally conscious state (MCS)

Occurs in the setting of catastrophic hemispheric brain injury, with intact brainstem function and preservation of some corticocortical and corticothalamic circuits

Global alteration of consciousness with elements of arousal.

Intermittent evidence of self or environmental awareness. Might sporadically follow commands, attend to recognizable objects or voices, initiate meaningful speech, or engage in purposeful movement

Intact

Long-term outcomes of patients in MCS have not been studied well

Akinetic mutism

Typically the result of injury to the bilateral frontal lobes

Profound deficiency in executive function

Unable to initiate speech

Does not exhibit any motor or verbal response to verbal or noxious stimulus

Unable to initiate movement

Seems on the verge of initiating activity, yet this is never accomplished

Neurologic recovery has been reported

Pharmacologically induced coma

Deliberate induction of a coma-like state with the use of sedative or anesthetic agents

Virtually any clinical evidence of brain or brainstem activity can be abolished

Virtually any clinical evidence of brain or brainstem activity can be abolished

Agents commonly used for pharmacologically induced coma include barbiturates, propofol, and midazolam.

Confounds the clinician’s ability to diagnose coma or even brain death

Locked-in syndrome (LIS)

Focal injury to the ventral pons

Preserved arousal and awareness

Anarthria

Preserved vertical eye movements and eye blinking

Alternative presentations may occur in patients with injury of the rostral pons and midbrain, in whom even eye movements are lost (‘‘total LIS’’)

Quadriplegia

In its classic presentation, patients with LIS can express themselves only by blinking and with vertical eye movements

States analogous to LIS:

• Guillain-Barré syndrome
  
• Neuromuscular-blocking drugs without appropriate sedation

Table 4.10. Differences between brain death, vegetative state, minimally conscious state (MCS), akinetic mutism, pharmacologically induced states of decreased arousal, and the locked-in syndrome (LIS).

Brainstem Reflexes

Easily examined brainstem reflexes are pupillary light reflexes, eye movements (spontaneous and elicited), corneal reflex, and respiratory pattern. If these brainstem activities are preserved, the lesion causing coma is probably due to bilateral hemispheric dysfunction. At the other end of the spectrum, the absence of these reflexes indicates a lesion primarily originating or externally affecting (e.g., transtentorial herniation) the brainstem.

Respiratory Patterns

In comparison to other brainstem signs, these are of less localizing value. See the table above for a summary of abnormal respiratory patterns. Aside from the abnormal respiratory patterns mentioned above, other cyclic breathing variations have been described but their importance is less significant.

Pupillary Signs

Pupil shape, size, symmetry and response to light provide valuable information about brainstem function. Pupillary reactions are examined with a bright, diffuse light (not an ophthalmoscope). Normal size, reactive and round pupils fundamentally exclude midbrain damage.

Table 4.11 summarizes the localization value of pupillary abnormalities in a comatose patient. As a general rule, the pupillary light reflex is resistant to metabolic disturbances. An exception to this rule is pharmacologic iridoplegia. Administration of 1% pilocarpine can be used to differentiate pharmacologic iridoplegia (failure to constrict) from anoxic pupillary dilatation (preserved response). The ciliospinal reflex, instead of pharmacological dilation, can be used as an alternative method to dilate the pupils. It is important to recognize the patient in a locked-in state due to a midbrain syndrome with abnormal pupillary abnormalities or due to profound peripheral neuropathy as occurs in a patient with severe Guillain-Barré syndrome.

Table 4.11. Localization value of pupillary abnormalities in a comatose patient.

Ocular Movements

Spontaneous Eye Movements

Elevate patient eyelids and note the resting position and spontaneous movements of the globes. Lid tone progressively decreases as coma deepens. Table 4.12 summarizes spontaneous eye movement abnormalities.

Table 4.12. Spontaneous eye movement abnormalities.

Brainstem reflex eye movements and the corneal reflexes

The physiological arch of the oculocephalic reflexes relays signals through the ocular motor nuclei and their midbrain, pons and medulla interconnections. During a normal response, the examiner observes evoked eye movements in the direction opposite to head movement (either vertical or horizontal head movement). These reflexes are normally inhibited or suppressed in the alert patient. Intact oculocephalic reflexes in a comatose patient indicate intact brainstem function and imply that the underling etiology of coma is cerebral bihemispheric dysfunction. The absence of these reflexes indicates brainstem damage in most cases. Overdoses of certain drugs can also result in absent oculocephalic reflexes. If the cause is due to a drug reaction, pupillary size and light reaction would be normal in most cases.

The vestibulo-ocular response (also called the oculovestibular response) tests the physiological integrity of similar brainstem tracts, but the initial stimulus is thermal and is therefore also referred to as “caloric” testing. Thermal stimulus is stronger than head movements. After documenting intact tympanic membranes, the auditory canal is instilled with 50 ml of cool water with the patient’s head angled 30 degrees to the horizontal plane. This stimulus induces convection currents in the labyrinths that travel through the vestibular nerve to the brainstem pathways that stimulate the brainstem oculomotor nuclei. The normal response is a brief latency, followed by ipsilateral horizontal tonic eye deviation and contralateral horizontal nystagmus to the side of cool-water irrigation (sensory nerve stimulation), respectively. One mnemonic medical students use to remember the response of nystagmus to thermal stimulation is COWS (Cold Opposite, Warm Same). A common error when interpreting clinical findings is to “reverse the concept” of the normal direction of the tonic and nystagmus response to cold water. Loss of tonic conjugate eye deviation indicates brainstem damage. The absence of nystagmus in spite of tonic conjugate eye deviation indicates that the cerebral hemispheres are dysfunctional or metabolically inhibited.

The blink reflex is probably mediated by the superior colliculus. It is elicited by stimulating the eye with bright light. A tonically retracted eyelid suggests pontine damage (particularly infarction) as a result of failure to inhibit the levator palpebrae muscles. The normal response to stimulation of the cornea by gentle touch with a wisp of cotton is a brief bilateral lid closure. The corneal reflexes depend on the pathway integrity between the fifth (afferent) and both seventh (efferent) cranial nerves in the pons. In conjunction with reflex eye movements, the corneal reflex is useful in clinical tests to evaluate pontine function. CNS depressant drugs can diminish or eliminate the corneal responses quickly after reflex eye movements are affected but before the pupillary light reflex is dysfunctional.

Motor Activity of the Body and Limbs

The localizing value of clinical observation of limb movements, tone and reflexes is less clear than the other neurological examination findings mentioned above. Metabolic coma is the most common cause of bilateral decerebrate (extensor) and decorticate (flexor) posturing. Also, the value of other motor findings (e.g., hemiparesis due to hypoglycemia) can be misleading.

Motor response should be elicited by assessing first for spontaneous movements followed by the response to increasing degrees of stimulus (verbal, then non-painful sensory, then painful stimulus). The man-in-the-barrel syndrome (bilateral arm weakness with spared lower extremity strength) suggests an anoxic lesion affecting the watershed area of the anterior cerebral and middle cerebral artery. Decorticate rigidity (arm adduction, elbow flexion, pronation and flexion of the wrist, and hip and knee extension) suggest a contralateral diencephalic and cerebral hemispheric lesion. Decerebrate rigidity (elbow extension, wrist flexion and pronation, and extension of the hip, knee and feet plantar flexion) can be due to a severe metabolic disorder or a structural upper brainstem lesion (below red nucleus but with intact pontine reticular formation).

Opisthotonus (periodic hyperextension of the trunk and hyperpronation of the arms, usually in response to painful stimulus) suggests dysfunction of the corticoreticular fibers (between the upper and lower colliculus) and has been described in cases of traumatic brain injury and tetanus. In neonates, opisthotonus is most likely secondary to meningitis, kernicterus or tetanus. Lesions in the pontine tegmentum can cause abnormal extension of the arms usually associated with weak flexion of the lower extremities. A flaccid quadriplegia, particularly if associated with areflexia, can be due to poliomyelitis or poliomyelitis-like syndromes (e.g., West Nile virus [WNV]), critical illness neuropathy, critical illness myopathy, or due to an acute demyelinating or axonal neuropathy (e.g., Guillain-Barré syndrome).

4.5.2 Evaluating the Patient With Suspected Central Nervous System Infection

The approach to the patient with suspected CNS infection begins with an evaluation of the clinical features that provide critical information leading to etiologic diagnosis. Identifying infectious agents in CNS infection depends largely on cerebrospinal fluid (CSF) and blood culture analyses, but biopsy of brain, spinal cord, or meningeal tissue may occasionally be needed

Clinical Presentation

Table 4.13 summarizes the main CNS infectious syndromes that should be suspected in the critically ill neurological patient.

Table 4.13. Main CNS infectious syndromes that should be suspected in the critically ill neurological patient.

ADEM = acute disseminated encephalomyelitis; CMV = cytomegalovirus; HIV = human immunodeficiency virus; HSE = herpes simplex encephalitis; HSV = herpes simplex virus; ICP = increased intracranial pressure; VZV = varicella-zoster virus; WMV = West Nile virus.

4.5.3 Intracranial Hypertension and Herniation Syndromes

Clinical signs and symptoms suggesting increased intracranial pressure include headache, nausea and vomiting, and bradycardia with or without increases in arterial blood pressure. Brain herniation corresponds to a shift of the normal brain through or across regions to another site due to mass effect. It is usually the result of focal structural pathology (e.g., tumour, trauma, infection, etc.), but it can also be due to a diffuse, more physiological process (e.g., encephalitis). Four major categories of herniation syndromes are distinguished: transtentorial, subfalcine, foramen magnum, and alar or sphenoid herniation.

Brain imaging serves as an extension to the clinical examination in the evaluation of these syndromes. Either CT or MRI of the brain can reveal signs of impending herniation before patients start demonstrating clinical signs. Although the use of “screening brain imaging” for possible or probable brain herniation in high-risk patients has not been validated, it is done frequently as a matter of routine. An example of this situation is ordering a “follow-up CT head” in a patient admitted with putaminal hemorrhage who is otherwise clinically doing well. Tables 4.14-4.16 summarize the clinical and imaging findings, as well as the potential complications of the mayor types of herniation syndromes.

Table 4.14. Transtentorial herniation (central or uncal).

Table 4.15. Ascending cerebellar transtentorial herniation.

Clinical findings	Imaging findings	Complications
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