It might seem as if it came straight out of a movie: a comatose patient suddenly moves his hand in a purposeful manner, trying to grab the bed rail or even your hand. There are times when a neurologist may be called to evaluate such a patient with limb movements that may seem rhythmic, chaotic, sudden, or purposeful, or even eyes that may be moving from side to side as if scanning the surroundings. For some, this concept may seem enigmatic or even raise doubts that the patient is in a coma. Although the novice may find such a consultation intellectually perplexing, the experienced neurologist encounters this routinely. Typically, the neurologist is asked to investigate because of clinical concerns of a seizure. While evaluating these patients, the clinician also must be able to distinguish between the different states of consciousness that may mimic coma, such as akinetic mutism, locked-in state, coma vigil, vegetative state, and even psychogenic unresponsiveness. This chapter will provide a review of different types of nonepileptic movements in coma patients.
There is a strong correlation between etiology, neuroanatomy, pathophysiology, and phenomenology in the production of nonepileptic movements in coma. It is because of this complexity that this chapter is outlined in two different forms. The initial part of the chapter follows the phenomenological view, and the latter part follows an etiologic approach.
To fully appreciate the variety of movements associated with the comatose state, an understanding of the anatomical basis of consciousness is necessary. The interactions between the ascending reticular activating system (ARAS) and the cerebral cortex enable consciousness. In 1949, Moruzzi described a distinct lesion to the ARAS that could induce a state of coma with persistent sleep patterns on electroencephalographic (EEG) studies, despite application of a noxious stimulus.1The ARAS projects from the paramedian tegmental rostral half of the pons up through the midbrain, to the dorsal hypothalamus, and into the thalamic reticular formation.2 The thalamus is rich in cholinergic, noradrenergic, and serotoninergic neurotransmitters, which play an important functional role within the reticular system and therefore with coma.3 When bilateral thalami are lesioned, their delicate neurochemical homeostasis is perturbed, resulting in neuronal dysfunction and a comatose state.4 Direct damage to these structures, or inhibition of their cortical inputs, results in impaired consciousness. The source of damage and inhibition is generally divided into two categories: metabolic and structural.
The metabolic comas are considered to be encephalopathic in nature. Abnormal movements such as tremor, asterixis, and myoclonus are commonly associated with metabolic encephalopathies.2 Primary encephalopathies are intrinsic disorders affecting glial or neuronal metabolism. Secondary encephalopathies are extrinsic to the metabolism of the central nervous system (CNS) and result from impaired metabolism and intoxication of other systemic organ systems. Ischemic encephalopathy is characterized by severe changes in cerebral blood flow. During sleep ...