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Coma Eelco F M Wijdicks Neurology in Practice THE BARE ESSENTIALS Coma Eelco F M Wijdicks Correspondence to Comatose patients present to the neurologist in should be discouraged. It is better to note a set of Professor E F M Wijdicks, several ways, mostly first in the emergency room or key findings and make comparisons over time (eg, Consultant, Neurosciences Intensive Care Unit, St intensive care unit. Given the many causes of coma, “the patient has improved, is now able to track my Mary’s Hospital, Mayo Clinic, the central focus is a comprehensive evaluation that finger, but eyes open only to a loud voice, localise to 200 first Street SW, Rochester, starts with a detailed history, although this has to be pain, extubated and able to protect the airway”). MN 55905, USA; wijde@ mayo.edu an account—at least to begin with—from bystand- Comatose patients have several outcomes: they ers, paramedics or even the police. This is followed may lose all brain function (brain death), remain by a neurological and general examination, gath- unconscious (persistent vegetative state) or regain ering of key findings, localisation of the involved consciousness (minimally conscious, fully con- brain structure, neuroimaging and other laboratory scious but disabled, or good recovery) (figure 1). tests. Sorting out the cause of coma is what neu- Most emerge from coma in 1–2 weeks. Survivors rologists do best—compared with other specialists. with abnormal consciousness may remain in a Of course the relatively recent availability of MRI minimally conscious state (MCS) or in a persis- has helped tremendously in understanding some tent vegetative state (PVS). Empirically, there is cases of coma but brain imaging can be normal. overlap between these states, particularly in the Indeed, unravelling the cause of coma remains in first weeks to months after the acute brain injury. many circumstances a clinical judgement. Some patients may have only a fraction of aware- Once treated, comatose patients can recover ness—for example, brief fixation to objects that suddenly (eg, after quick correction of hypo- is only detected by close observation over time. glycaemia) but many patients have significant These conditions are not diagnosed on the spot. structural brain injury and take days to awaken. About 25% of patients stay in a prolonged state of Persistent vegetative state (PVS) is defined as: unconsciousness but even then slow awakening is ▶ No awareness of self or environment. to be expected; only a very small fraction survive ▶ No sustained reproducible, purposeful or vol- but never emerge from coma. untary behavioural response to visual, audi- tory, tactile or noxious stimuli. DEFINITIONS OF ALTERED STATES OF ▶ No language comprehension or expression. CONSCIOUSNESS ▶ Mostly intact cranial nerve reflexes. Impaired consciousness has been traditionally ▶ Roving nystagmoid eye movements. regarded as a problem with alertness, awareness ▶ Presence of sleep and wake cycles, often eyes of self, or both. open during the day. ▶ A disturbance of arousal—mainly a function ▶ Stable unsupported blood pressure and intact of the reticular formation in the brainstem— respiratory drive. leads to diminished alertness. ▶ Bowel and bladder incontinence. ▶ A disturbance involving content—a function Minimally conscious state (MCS) is defined as: of multiple cortical areas—leads to dimin- ished awareness, and failure to accurately ▶ Patients make eye contact or turn head when integrate what is perceived. being talked to. These two components are interrelated but ▶ An abulic emotionless state but with eye track- sometimes dissociated. One can be awake and ing movements. aware, awake but not aware and not awake and ▶ May mouth words, may fend off pain. not aware. ▶ Eyes following moving person. Coma is best defined as a completely unaware ▶ Some intelligible verbalisation. patient unresponsive to external stimuli with only ▶ May hold object or use object when asked. eye opening to pain with no eye tracking or fix- ation, and limb withdrawal to a noxious stimu- The frequency of these prolonged comatose lus at best (often with reflex motor movements). states is not known, nor is it clearly established Brainstem reflexes can be partly absent or absent. where the point of no return is. Patient registries The degree of coma is more difficult to define. may provide some insight into the frequency Terms such as stupor, drowsiness, obtundation, of coma after severe traumatic brain injury or somnolence, light or deep coma are all vague and stroke but there are definitional difficulties and 2010;10:51–60. doi:10.1136/jnnp.2009.200097 51 PN200097.indd 51 1/14/2010 5:46:33 PM Neurology in Practice confounding factors; for example, sedation in the the thalamus, and monoaminergic neurons first weeks after major brain injury (physician projecting from the upper brainstem to the induced coma) may impact on time to awakening. thalamus, hypothalamus, basal forebrain and Here are some sobering facts. cortex (figure 2). ▶ Stimulation of the posterior hypothalamus ▶ Withdrawal of support is a common cause of causes arousal. death in comatose patients. ▶ Lesions of the cuneus and precuneus associa- ▶ MCS is far more common than PVS within tion cortex may be involved in the MCS. 6 months from brain injury. ▶ Lesions of the anterior cingulate gyrus result ▶ The diagnosis of PVS may not have been made in marked abulia. by a neurologist—misjudgements are more common than appreciated. ▶ Patients in PVS may be kept alive for decades NEUROLOGICAL EXAMINATION OF THE but with no prospects for improvement. COMATOSE PATIENT Finding the cause of coma requires many steps ANATOMY AND NEUROPHYSIOLOGY OF COMA and it helps to know the major categories before starting (table 1). ▶ Coma is currently understood as being caused by interruption of the ascending reticular acti- ▶ Structural injury of the cerebral hemisphere(s). vating system in the midbrain and pons pro- ▶ Intrinsic brainstem injury, or compression jecting to the thalamus and cortex. from surrounding damaged tissue such as ▶ The thalamus through its intralaminar swollen infarcted cerebellum. nuclei plays an important role in maintaining ▶ Acute metabolic or endocrine derangement arousal. (eg, hypoglycaemia, hyponatraemia, acute ▶ The thalamus and ascending reticular acti- panhypopituitarism). vating system can be damaged from shift or ▶ Diffuse physiological brain dysfunction (eg, displacement of the brainstem, as well as by seizures, intoxication or poisoning, hypother- direct destruction. mia, smoke inhalation, near drowning, heat ▶ The ascending reticular activating sys- stroke, acute catatonia, malignant neuroleptic tem contains cholinergic neurons of the syndrome). medial pontine tegmentum projecting to Every physician should be familiar with two pitfalls. Figure 1 Categories ▶ The first is failure to recognise the locked-in of altered states of Coma syndrome which can mimic coma. (Some consciousness, from patients in this state have been inadvertently coma to its potential insufficiently sedated, intubated and phar- consequences. MCS, maceutically paralysed.) In a classic form of minimally conscious state; Brain death Conscious PVS, persistent vegetative locked-in syndrome, they have their eyes open state. and can only blink to commands or move Good PVS MCS their eyes vertically. Their motor tracts are de- recovery efferented by a lesion in the ventral pons spar- ing the ascending reticular activating system Disability and thus they can hear, see and feel pain. ▶ The second, psychogenic unresponsiveness, is often only considered after exclusion of other causes and requires some clinical experience to definitively demonstrate its presence and to think about it in the first place and before ordering a battery of tests, some of which may be risky. The hand drop test is a classic but not completely reliable test (one arm is lifted and held in front of the face and when let loose slides next to the patient’s face rather Figure 2 The main than on to it). Closed eyes which open with pathways connecting tickling the nose hairs is more characteristic. the ascending reticular Some patients may have forced upward or formation with the downward gaze that may suddenly change in thalamus and cortex. From The comatose patient, direction. Others have abnormal movements, Wijdicks EFM, used misinterpreted as seizures, but these generally with permission of Mayo look more like ‘fish out of water’ flopping. (To Foundation for Medical complicate matters, I have seen a psychogenic Education and Research. locked-in syndrome with blinking as the only 52 2010;10:51–60. doi:10.1136/jnnp.2009.200097 PN200097.indd 52 1/14/2010 5:46:36 PM Neurology in Practice Table 1 Classification and causes of coma form of communication in a nurse assistant for Structural brain injury a full 48 h after a marital spat.) Cerebral hemisphere Examination of the comatose patient follows Unilateral (with displacement) a set of clinical tests to locate the lesion. These Intraparenchymal haematoma findings are then integrated with neuroimaging Middle cerebral artery ischaemic stroke or electrophysiology test results. Many comatose Intracranial venous thrombosis patients do not, however, have specific findings Haemorrhagic contusion which can be problematic. Nonetheless, a routine Cerebral abscess set of clinical tests is necessary to assess the depth Brain tumour of coma, the location of the lesion and possibly Subdural or epidural haematoma the underlying cause. Bilateral Subarachnoid haemorrhage ▶ Initial neurological
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