The pharmacologic management of major motor status epilepticus is summarized. When general anesthesia is required, the electroencephalogram (EEG) is used for monitoring the adequacy of treatment. The EEG findings may also be important in recognizing status epilepticus and monitoring its response to treatment when this is clinically difficult, as when it occurs in comatose or pharmacologically paralyzed patients or in the context of severe brain damage. Finally, the EEG helps to clarify the nature of motor activities of uncertain basis in patients in the intensive care unit and has indicated that non-convulsive seizures or status are more common than clinically suspected in such patients.

We report on our experience with long-term monitoring of the EEG power spectrum and somatosensory evoked potentials (SSEPs) in 103 patients with severe closed head injury (Glasgow Coma Scale - GCS ≤ 8). Patients were monitored for an average of 5 days post injury and monitoring was terminated when they died, regained consciousness or their intracranial physiologic parameters (primarily intracranial pressure - ICP) were stable for 2-3 days. Patients were treated according to a standard protocol that included mechanical ventilation, sedation, and neuromuscular blockade. At 7 of 9 twelve hour time intervals post injury, SSEPs were significantly (p < .05) different between outcome groups using the Glasgow Outcome Score collapsed to 3 categories. The percent slow (delta) activity in the EEG was not significantly different between outcome groups at any time point, post injury. The total power in the EEG power spectrum differed only at the last time epoch post injury (108 hr.). Based on the superior prognostic capabilities of the SSEP, we routinely base critical management decisions on SSEP values. We have not been able to rely on EEG parameters for these same decisions due to the lack of clear distinction between good and poor prognosis groups based on common EEG parameters.

The electroencephalogram (EEG) is an important diagnostic tool in coma. Although comatose patients may be similar on neurological examination, the EEG reveals a wide range of abnormalities. For metabolic and septic encephalopathies, the “anesthesia model” is a useful analogy. The EEG is very sensitive to the depth or severity of brain dysfunction in coma as well as the direction of the process if serial tracings or continuous recordings are used. While the EEG is rarely specific for the etiology of coma, it may help determine the class or general category of disease process. In conditions capable of causing neuronal death, e.g., anoxia-ischemia, the EEG can be of prognostic value.

Respiratory electrophysiological studies are useful in the investigation and monitoring of respiratory failure. Phrenic nerve conduction studies and needle electromyography of the diaphragm are invaluable in establishing the diagnosis, determining the severity, and following the progression of peripheral respiratory muscle dysfunction. In addition to these established methods, repetitive phrenic nerve stimulation is of diagnostic value in patients with neuromuscular transmission defects and dyspnea. The diagnosis of impaired central respiratory drive can often be accomplished by the newly-developed techniques of transcortical magnetic stimulation of the motor cortex with recording of the diaphragm and phrenic nerve somatosensory evoked potentials. These studies are of particular value in critically ill patients where both the central and peripheral lesions may impair respiration.

The neuromuscular system may be affected by disorders of the central nervous system as well as other disorders affecting motoneurons, axons, neuromuscular transmission, the sarcolemmal membrane, the contractile elements and other components of the muscle fibers themselves. One or a combination of these possibilities can present in patients in the critical care unit. This paper reviews various qualitative and quantitative methods for assessing the various components of the peripheral contributions to the electrical and force output as well as the central motor drive to motoneurons. These methods all have their own strengths and weaknesses but many are complementary and together, can provide important diagnostic and prognostic information to guide management.

Polyneuropathies frequently contribute to ventilator dependency and prolonged stay in the intensive care unit. As clinical examination is often limited in critically ill patients, electrophysiological studies are invaluable in establishing the diagnosis of neuropathy, determining its pathophysiology, severity and in following the patients' progression. Guillain-Barré syndrome (GBS) developing before intensive care unit admission and critical illness polyneuropathy (CIP) developing as a complication of sepsis and multiorgan failure are the commonest causes of neuropathy. Electrophysiological findings in CIP are that of an axonal neuropathy whereas the findings in GBS are usually consistent with a demyelinating neuropathy. Axonal GBS can be distinguished from CIP by the preceding illnesses, slow nerve conduction velocity in some cases, lack of spontaneous activity on the initial needle electromyographic study and cerebrospinal fluid findings.

All disorders of neuromuscular transmission (NMT) may cause ventilatory failure, albeit rarely. Respiratory muscle weakness is occasionally the presenting feature of myasthenia gravis (MG), the Lambert-Eaton myasthenic syndrome (LEMS), hypermagnesemia and botulism. Chronic MG, congenital myasthenic syndromes and LEMS may be acutely exacerbated by various intercurrent conditions and by drugs which interfere with NMT. Finally, in the ICU, difficulty in weaning from the ventilator may be caused by prolonged use of neuromuscular blocking agents. Electrophysiological studies of NMT disorders in the intensive care unit have rarely been reported. Nevertheless, the available data indicates that the electrodiagnosis of severe NMT disorders can be misleading. With severe NMT defects, the electrophysiological distinction between post-synaptic and pre-synaptic disorders is blurred and the differential diagnosis with myopathies may be difficult. A clinically suspected NMT disorder should therefore not be ruled out when electrodiagnosis fails to demonstrate the expected abnormalities.

Myopathies that occur in the intensive care unit can be divided into preexisting myopathies or newly acquired myopathies that develop in the intensive care unit. Myotonic dystrophy is an example of a preexisting myopathy that may render patients susceptible to acute respiratory failure following surgical procedures and anaesthesia. A group of myopathies that develop within the intensive care unit have been labelled acute necrotizing myopathy of intensive care, thick filament myopathy and acute steroid myopathy. Corticosteroids and nondepolarizing muscle blocking agents may play a role in their development.

Dr. Michael Aminoff, guest of the Canadian Society of Clinical Neurophysiologists, discussed the Management of Status Epilepticus. The EEG is essential for the recognition of status epilepticus where there are minor or no motor manifestations, and also in clarifying the nature of certain motor and behavioural disturbances that do not relate to seizures. It also is important in evaluating the adequacy of treatment, such as the response to barbiturate or midazolam induced anaesthesia.