The evaluation of patients with acute disorders of consciousness is subdivided into three parts. First, it is necessary to determine the level of consciousness. For a preliminary assessment, the Glasgow Coma Scale (GCS) is appropriate in most cases (Table 4.2). This, however, does not release from the obligation to careful detailed psychopathologic examination at a later time. Second, the so-called vital signs must be checked, and appropriate measurements must be done. Third, a careful physical examination and a particularly detailed neurological examination must be conducted concerning presence or absence of focality of disorder, particularly, specific involvement of cortical or brainstem structures on the one hand and the level of dysfunction within the rostrocaudal neuraxis on the other hand, with the latter being particularly concerned with life-threatening brainstem herniation.

Subsequent to the initial assessment of consciousness and vital emergency care, a detailed examination of brain functions should be conducted. It starts out with observation and specific psychopathologic interview. The extent of the latter depends on the patient’s communicative ability and relates primarily to noopsychic functions. The interview begins with the assessment of psychomotorics, in other words the overall dynamic impression. After that, the noopsychic functions must be described in detail concerning the level and content of consciousness, orientation, attention, short- and long-term memory, process as well as content of thinking and, not least, perception disorders like hallucinations.

Subsequently, a detailed neurological examination focusing on pupillary and optomotor responses, general motor and autonomic functions is mandatory.

The specific observation of spontaneous posture and motor function, mainly in response to painful stimulation, is key to the assessment of the consciousness disturbance. Spontaneous-sustained fumbling fingers and wiping hand movements are typically observed in cases of delirious states. Gradually decreasing level of consciousness is paralleled by increasingly slowed and undirected movements both spontaneously and in reaction to pain. Some postures are typical of increasing intracerebral pressure and descending brain herniation. It starts with progressing plantar flexion of feet with increasing extensor tone in both lower extremities. Following increasing flexor tone occurs in the upper extremities which results in the so-called decorticate posturing. In chronological sequence, the flexor tone in the upper extremities changes to an extensor tone resulting in so-called decerebrate posture. Concurrently to these changes in tone and posture motion sequences change towards posture enforcing increasing mass – and synergistic spontaneous and pain-induced movements. A different posture occurs in the rare case of ascending herniation with extensor posture of the upper extremities and flaccid paralysis of the legs. It is necessary to be aware of the fact that assessment of cortical functions, and particularly of focal signs, gets lost in parallel to the previously mentioned progress with increasing disinhibition of autonomic brainstem functions. This characteristic course of posture and tone can be seen also as a consequence of metabolic disorders if not necessarily in full manifestation, sometimes only adumbrated, lacking characteristic spastic rigidity with frequently proven focal signs.

The next step is the examination of the pupils and the oculomotor system including the so-called brain stem reflexes to receive information about the integrity of the centres inside the midbrain and the pons. Commonly, the examination starts with the evaluation of the position and tone of the eyelids. Decreasing consciousness and coma are accompanied by reduced muscle tone and lost spontaneous blinking. Two brain stem reflexes involve the eyelids: the blinking reflex in response to bright light and the corneal reflex. Eye position and eye movement come next. Drowsiness, as well impaired consciousness, is associated with slight exophoria in resting position because of failing fixation. However, there are several spontaneous conjugate and disconjugate movements sometimes distinctive of local structural lesions, sometimes unreliable for localization. Examples for spontaneous eye movements caused by local structural lesions are conjugate lateral deviation of the eyes, nonconjugate eye deviation, ocular bobbing, nystagmus and myoclonic jerks. Unreliable movements concerning localization and mostly as a consequence of metabolic or hypoxic injury are roving eye movements, ocular dipping and periodic alternating gaze deviation. Following the observation of spontaneous eye movements, two reflexes should be assessed: the oculocephalic reflex and the caloric vestibuloocular reflex [14]. Both reflexes give information regarding the function of pontine-vestibular connections. The former, also known as doll’s eye response, is suppressed by fixation. Therefore, the conjugate eye rotation opposite to passive head rotation will only occur in case of neutralised fixation or comatose patients. In cases of uncertain reaction, sometimes occurring in deep coma, the caloric vestibuloocular response is an alternative. For this, the instillation of cool (30 °C) or warm (44 °C) water inside of the external auditory canal is used. Usually, this leads to brisk ipsiversive (cold) or contraversive (warm) eye deviation, occasionally also nausea and vomiting.

It is important to examine the pupils because size and light reaction are the most important physical signs to distinguish metabolic from structural reasons of disturbed consciousness [1].

Leaving aside the consequences of focal lesion, the size and light response of pupils can give a hint to the level of brain lesions causing impaired consciousness and coma. Small but reactive pupils are observed in case of metabolic encephalopathies but also in diencephalic lesions. Pretectal lesions cause large and fixed pupils. Lesions at the midbrain level lead to midposition of fixed pupils, whilst pontine lesions are associated with the pupil’s pinpoint size. The ciliospinal reflex, assessed by pinching the skin of neck or face, can also be used as a spinobulbar response.

The bedside evaluation of patients with subacute or chronic alterations of consciousness consists also of careful neuropsychiatric examination supplemented with special neuropsychologic test attempting to find out behavioural changes indicative of improving consciousness which can be used for further specific treatment measures. Alterations of consciousness appear in the context of extensive cerebral functional disturbances affecting both arousal system and sensory–motor pathways as set out above. To recognise the presence of consciousness poses a great challenge considering severe concomitant motor constraints impeding behaviour necessary for interpersonal exchange. First, stirrings of relapsing of consciousness functions are reactions to so-called visual and auditive autoreferential stimuli. Sustained visual tracking is one of the main clinical signs of responsiveness recovery. Many of the below-mentioned behavioural scales established the capability of visual fixation as a criterion for distinguishing VS from MCS. Its assessment is difficult because of fluctuations of patient responsiveness and different assessment tools. The various scales use different stimuli which range from baby photos (SMART) to different objects (DOCS), persons (WHIM) and light flashes (CNC), or confine themselves to observation of spontaneous eye movements (WNSSP) [15]. Use of mirrors shows a higher frequency of fixation compared to other stimuli and constitutes a very sensitive test [16, 17]. This has been confirmed by eye-tracking recordings [18]. Thereto, similarly autoreferential is the sound localization reflex. The most potent stimulus regarding this is one’s own name [19]. The own name is a signal of more significant information content shown in a range of studies. Babies are already automatically responsive to their names demonstrating strong degree of attention [20–22]. Even awaking from general anaesthesia, one’s own name creates reactions before pain reactions emerge [23].