The Brain

Abstract

The level of consciousness is the most important and sensitive clinical indicator of neurological function in a critically ill patient. Different levels of consciousness have been defined (Table 7.1). Coma arises from bilateral cortical or subcortical dysfunction and/or brainstem injury involving the ascending reticular activating system. Unilateral hemispheric lesions only cause coma if a contralateral hemispheric lesion pre-exists or transtentorial herniation with brainstem compression has occurred.

Clinical Practices

Box 1 Clinical Features of the Central Anticholinergic Syndrome

Although anticholinergic mechanisms have been implicated in the pathogenesis of delirium in the critically ill patient, the central anticholinergic syndrome refers to a specific syndrome which resembles delirium but shows a combination of the following clinical features:

• Altered mental state (mostly agitation, hallucinations)

• Tachycardia (with or without arrhythmia)

• Dry and red skin

• Dilated pupils with impaired/blurred vision

• Elevated body temperature (rarely >38.5 °C)

• Urinary retention, constipation

• Myoclonic jerks

• Seizures

Alternatively the following mnemonic summarizes the main clinical signs of the central anticholinergic syndrome: “red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare, and full as a flask”.

Of note, many central anticholinergic syndromes occur in postoperative patients and are therefore encountered in the recovery room. The classical clinical scenario is acute, unexplained (paranoid) agitation in an otherwise stable postoperative patient. Rapid (<5–10 min) termination of agitation and normalization of the mental state in response to intravenous administration of 2 mg physostigmine confirms the diagnosis.

Box 2 Differential Diagnoses in the Awake, But Unresponsive, Patient

• Locked-in syndrome

  Results from bilateral pontine lesions with destruction of pontine motor tracts (e.g. in basilar artery thrombosis or pontine haemorrhage, osmotic disequilibrium syndrome); patients are tetraparetic, are spontaneously breathing and may communicate only with upward eye movements and eye blinking.

• Unresponsive wakefulness syndrome (formerly referred to as vegetative state)

  Persistent (>1 month) or permanent (>3–12 months) lack of awareness despite possible wakefulness (eyes open) following a traumatic or non-traumatic brain injury.

• Isolated frontal lobe damage

  Apathy, abulia (loss of motivation) and a delayed response to external stimuli can result from damage to one or both frontal lobes (e.g. by trauma or stroke).

• Akinetic mutism

  A specific frontal lobe syndrome in which the patient does not communicate but only makes minimal movements to perform selected tasks (e.g. eating).

• Global aphasia

  Inability to understand and speak mostly due to large left hemispheric stroke or trauma; particularly if caused by a stroke, other symptoms (right-sided hemisyndrome) are usually present; isolated global aphasia is rare and can leave the patient alert and unable to communicate but able to perform meaningful tasks.

• Postictal state

  For a limited time after a seizure (minutes to a few hours), patients may appear alert but unresponsive; in some cases paresis of one or more body parts (Todd’s paresis) is present.

• Metabolic encephalopathy

  Few patients with metabolic encephalopathy (mostly of uraemic or hepatic origin) can have their eyes open but not respond.

• Psychogenic or dissociative unresponsiveness

  See Box 4.

• Preterminal or agonal state

  Greyish skin colour, eyes open, staring, minimal blinking, mouth open, bradypnoea/gasping.

In contrast, only very few patients are responsive but cannot open their eyes. One important cause in a critically ill patient is eyelid apraxia or “cerebral ptosis”. It is most commonly observed in patients with (right-sided) hemispheric strokes in whom bilateral eyelid apraxia can be a sign of impending transtentorial herniation. Another potential cause is cranial nerve (e.g. CN III) neuritis/neuropathy as seen in Guillain-Barré syndrome or cranial polyneuritis.

Box 3 Differentiation Between Peripheral and Central Vertigo

	Peripheral vertigo	Vertigo central vertigo
Example	Vestibular	Neuronitis brainstem/cerebellar stroke
Underlying condition	Benign	Life-threatening
Onset	Sudden	Sudden or gradual
Nystagmus	Fatigable	Non-fatigable
Direction of	Unidirectional	Multidirectional
Associated neurologicaldeficits	None	Present
Hearing impairment or tinnitus	May be present	None
Nausea, vomiting	Frequent	Rare

Box 4 Differentiation Between Psychogenic Unresponsiveness and Stupor/Coma

• A history of (a) previous stressful event(s) or known history of psychiatric disease increases the likelihood that the patient presents with psychogenic unresponsiveness but is, on its own, not specific enough to make the diagnosis.

• Resistance to passive opening of the eyelids is an insensitive but fairly specific indicator of psychogenic unresponsiveness.

• After passive eye opening, eyelids only gradually close in comatose patients but rapidly close in patients with psychogenic unresponsiveness.

• An arm held over the head does not fall on the face or head when released but behind the head or next to the body in patients with psychogenic unresponsiveness.

• In psychogenic unresponsiveness, the level of mental state depression (often Glasgow Coma Scale score of 3) does not correspond with the overall appearance of the patient who usually presents with a normal breathing pattern, adequate airway control and promptly reacting normal-sized pupils.

• The plantar response is normal (flexor)/Babinski’s sign is absent.

• Patients with psychogenic unresponsiveness are often surprisingly resistant to painful stimuli.

• A non-fixed conjugate upward gaze may often be seen in patients with psychogenic unresponsiveness but is not specific as it may be a sign of significant cortical injury, too.

• Most patients with psychogenic unresponsiveness cannot suppress involuntary eye movements when their eyelids are passively opened and a mirror is moved in front of their eyes (optokinetic nystagmus test).

• Intravenous administration of 20 mg of furosemide has uncovered occasional patients with psychogenic unresponsiveness (not generally recommended).

Box 5 Differential Diagnosis of Neck Stiffness in the Critically Ill Patient

Neck stiffness throughout the range of movement:

• Infectious (e.g. bacterial, viral) meningitis

• Subarachnoid haemorrhage

• Neoplastic meningitis

• Posterior fossa mass/tumour

• Acute/chronic cervical spondylitis

Limited neck range of movement:

• Chronic cervical spondylosis

• Nuchal rigidity in movement disorders, e.g. (atypical) Parkinson’s disease