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New Treatments for Head Trauma and Coma

Intractable seizures are the kids that have multiple seizure types. The kids that are wearing the football helmets. Atonic seizures, myoclonic seizures, atypical absence and generalized tonic-clonic seizures. They have psychomotor retardation and they have a slow spike and wave. The EEG of Lennox-Gastaut consists of slow spike and wave, multifocal, sort of high voltage spikes.

So, the goals of therapy: I would put to you that one of our biggest problems in therapy has been that we have become therapeutic nihilists. We say, "Hey, they have epilepsy. They are supposed to have seizures." That’s sort of like saying, "Hey, they have heart disease. They are supposed to have heart attacks."

Finally, we have a whole slew of new medications. None of our medications are ideal. They all have both dose-dependent and idiosyncratic side effects, and now we have a whole slew of them. Unfortunately this whole slew is not being used by us. Actually the data suggests that with all our new medications, they only have about 10% of the number of patients that they should, 10% of the market. The pharmaceutical houses are saying, "Hey, you guys are happy with your drugs. We are not going to make any new ones." They should have a 40 or 50%.

So some of our new medications; gabapentin, Neurontin. We don’t know how it works but it is a relatively benign drug from a side effects standpoint, and its efficacy is fair. Tiagabine, a GABA re-uptake inhibitor, a new medication that was just released. Vigabatrin, another GABA … these two are both GABA agents. Vigabatrin is a suicide medication that binds irreversibly with the breakdown product of GABA, GABA-T, and then takes it out of commission. The body has to remake that enzyme. So both of these increase GABA to synapse, increasing the inhibitory surround. Again, gabapentin, we are not exactly sure how it works.

Okay, comatose patient. So consciousness requires the interaction of the reticular activating system in the hemispheres, right? Arousal is the reticular activating system and content is the hemispheres. There is a differential diagnosis of the unresponsive patient, the patient who is locked in. So any patient who is comatose, the question you always have to ask is, "Look up and look down."

Psychogenic coma; not uncommon in the ER. So what you have to remember is that not everything unresponsive is actually in coma. Rarely, global aphasia. Ultimately coma, it has to again either knock out reticular activating system or knock out both cerebral hemispheres. So the causes, diffuse or metabolic. Very common. Supratentorial with herniation, less common. Subtentorial, uncommon. So coma is a pathological loss of consciousness.

Another thing that I’d just like to talk about, and we are going to hit it again and again, is this whole idea of NMDA activation. I would put to you that again, this is the decade of the brain. The traditional bitch about neurologists are what? Diagnose and adios. Right? We can tell you what it is but we can’t do anything about it.

So, coma: evidence of trauma, evidence of drug use, and the key is again, we want to prevent further damage in the central nervous system, so we’ve got to give it what it needs; adequate airway, proper ventilation, adequate perfusion and adequate substrate, glucose. For those in a lot of the city hospitals we also have to protect against Wernicke-Korsakoff so you are also giving thiamin and you are also giving Narcan as a first line. Then the key, I really believe the key to the whole thing of dealing with a comatose patient is knowing if they are going up or going down. I think that what we should do is, since we don't know what stupor means.

So the history: onset of recent health problems, medical problems, drug use, psychiatric illness. And here’s the Glasgow coma scale. This scale is awful for medical illness, frankly. This was devised for head trauma. But the paramedics know it, the ER nurses know it, and again if you have someone who was 14 and now is 12, you are going to say, "Now, hold on. Something is going on here that this is worsening."

Neurological exam: verbal response, eye opening, eye movements, coronary response, gag, motor response, respiratory pattern, motor tone and deep tendon reflexes. For the neurological residents a piece of cake. No history, quick brain stem exam, out of here. So what are the motor responsiveness? The best motor responsiveness if I’m doing a noxious stimuli is to grab my hand and say, "Stop that".

The respiratory patterns tell us something. We’ve all seen people with Cheyne-Stokes, if you walk around most nursing homes in the middle of the night the whole place is Cheyne-Stokes-ing. And what does that mean? That means that the cortex is knocked out, their cortex is dysfunctional. What’s happening now? Rather than having a normal O2 drive, they are driving on CO2. So all that represents is that we’ve lost our oxygen drive and now we are CO2.

Pupils: pupils tell us a lot. The person can be in the deepest coma that can be, if the pupils are still working they will do okay. It’s non-structural. The pearl with the pupils, if they still have pupillary function and they have nothing else, it’ probably going to be drug overdose or metabolic. So the pupils are important. And again, the most important pupil that we want to look at is the so-called uncal herniation, because this is a neurological emergency.

Increased intracranial pressure. The key is really identification of ICP and remember the old Cushing’s triad, hypertension. What this really is is increasing pulse pressure. What is the brain trying to do? It wants more blood. So what happens is you have a widening pulse pressure. Then you become bradycardic, irregular respirations and then pupillary dilation, poor response to light and then you start to get into the posturing; decerebrate, decorticate, and cranial nerve III or cranial nerve IV paresis.

The herniation syndromes: uncal herniation, cranial nerve III, singular gyros herniation and central transtentorial herniation. Here’s the normal representation of the supratentorial contents. Around the vertex a person starts to get sleepy and then yawning, then boom, they are out. They have no warning. They don’t blow a pupil as a warning. So central herniation, while uncal herniation where there is clear herniation of the uncus into the stem trapping the third nerve and then.

Cingulum or transtentorial herniation: this is the most common herniation that we see in cerebrovascular disease. What happens is that the guy has a big stroke, a big MCA stroke, and then they start to get sleepy. And the sleepiness is actually due to transtentorial herniation.

Types of coma. Supratentorial with herniation, subtentorial affecting the RAS directly, and the diffuse metabolic etiologies. The old cerebral hemorrhage, hypertensive cerebral hemorrhage, blowing into the ventricular system. This guy did not do well obviously. Again, big hypertensive hemorrhage that then caused herniation and brain death. Trauma: subdural, big enough to cross midline and cause herniation. Subdural occasionally, and a glioblastoma multiforme with herniation. Subarachnoid hemorrhage. How does that really cause coma? If it’s big enough there is a gross rise in ICP and will really decrease blood flow and cause coma secondary to that. You see the blood in the sylvian fissure, and sort of the haziness over the tenth.