Coma and other altered states of awareness

In this post, I thought i shall talk about coma and other altered states of awareness. What do we mean when we say a patient is in coma? Just what does coma mean?

Coma has been defined differently in different medical and neurology textbooks. In simple terms it means a patient who has decreased conciousness to the extent he is not aware of his surroundings and does not respond when stimulated by the external means even when the stimulus is noxious or painful like a pinch applied to the skin of the nipple. These patients are usually seriously ill and are in the intensive care unit of the hospital. As they are unaware of their external surroundings they need to be supported, meaning that their diet has to be maintained, their fluid status, making sure they are not constipated etc.

There can be numerous causes for coma. some of them are related to the brain itself and some of them are systemic, that is they affect the body.

1) Neurotrauma: head injuries frequently can lead to a coma with loss of consciousness sometimes for prolonged periods of time. Intracranial hemorrhage or bleeding into the brain is one cause of this. This bleeding raises the intracranial pressure and this compresses the brainstem and hence leads to coma.

2) Large stroke: a large stroke can lead to loss of consciousness and coma. Again a large stroke frequently leads to an increase in intracranial pressure and this leads to a depression in the state of awareness and coma.

3) Infections of the brain like meningitis and encephalitis may also lead to a state of coma.

4) Large tumors of the brain can also present with depression in sensorium (decreased consciousness) and coma.

5) Frequent seizures one after the other (this condition is referred to as status epilepticus): patients may be unresponsive even though they are not visibly  “shaking” (that is there are no convulsive movements but patients are unresponsive because their brain is still having seizures).

6) Anoxic hypoxic injuries to the brain: anoxia is lack of blood flow and oxygen to the brain. This kind of coma is frequently irreversible.

7) Systemic causes of coma: metabolic conditions like low sodium (hyponatremia), low blood glucose (hypoglycemia), metabolic acidosis ( as seen in diabetic ketoacidosis), liver dysfunction (cirrhosis), renal dysfunction and renal failure, congestive heart failure, hypercapnia (where there is too much carbon dioxide in the blood) all are common causes of coma.

8) Toxins: ingestion of toxins like drugs of abuse, heavy metals, insecticides, overdose of antidepressants, pain killers, sedatives can all lead to coma.


As the causes of coma are protean, when patients present to the hospital in a comatosed state, we do a rapid triage and try to localize the etiology of the coma. Blood is drawn to check for sodium, potassium, liver and renal functions and glucose. If there is some evidence that an infectious etiology is the cause of coma we may draw blood for culture and do a spinal tap to examine the spinal fluid to rule out meningitis. Depending upon the history and examination findings other investigations may be carried out like CT scan brain, MRI brain, Chest X-ray, EEG and so on.

The treatment of “coma” depends upon the cause of coma. Frequently as I stated above these patients need to be admitted to the intensive care unit and need respiratory and circulatory support. Depending upon the cause of the coma, they may or may not need neurosurgical intervention. If there is a big bleed in the brain and the intracranial pressure is too high, the blood may need to be removed (evacuated). These patients may need broad spectrum antibiotic coverage if they have an infection or an antiepileptic drug if they are having seizures. If toxin or drug ingestion is the cause, then we try to remove the toxin or drug from the blood stream with the aid of an antidote.

Nitin Sethi, MD

Normal pressure hydrocephalus (NPH)

Normal pressure hydrocephalus (NPH) is another potentially reversible cause of “dementia” or rather memory problems in the elderly. NPH is characterized by the triad of gait disturbance, urinary incontinence and memory problems. The dementia in NPH is of the subcortical type meaning that it is mostly characterized by psychomotor retardation (patients are slow to respond), unlike cortical dementias like Alzheimers disease they do not have language deficits (aphasia), inability to do learned things (apraxia) or agnosia.

The etiology of NPH is still not fully elucidated but it is thought to involve some obstruction to the normal flow of the cerebrospinal fluid (CSF). This obstruction may be due to previous history of meningitis or CNS trauma. When you image these patients with either a CT scan or a MRI scan, one finds the ventricles are dilated (large enlarged ventricles) but there is not much corresponding cortical (brain0 atrophy. This is against what is found in cortical dementias like Alzheimers disease where apart from the ventricles been dilated and enlarged, the brain also is shrunken (atrophy).

So in which patients should the diagnosis of NPH be entertained? Mostly these are patients who are elderly and who have had a subacute onset of memory problems accompanied by difficulty in walking (patients who have NPH have a characteristic gait (they walk slowly and stiffly, we call their gait as magnetic gait). They may or may not have urinary incontinence (the entire triad may not be present in all the patients). Neurologists entertain the diagnosis of NPH if they see a patient with the above symptoms and if the imaging is characteristic.

To confirm the diagnosis though requires further testing. Normally what we do is a therapeutic as well as diagnostic spinal tap. What does that mean you may ask?

Well we bring the patient into the hospital and do a spinal tap. Before the tap is done the patient is examined to determine the memory deficits. A timed walking test is carried out ( we make the patient walk a fixed distance and measure the time taken to do so ). Then a good amount of spinal fluid is removed about 20-30 cc. The pressure of the spinal fluid is measured at that time and in a typical patient of NPH it should be normal (hence the name normal pressure hydrocephalus). Once the spinal fluid has been removed the patient is again tested. Has the memory improved. We make the patient walk the same distance as before. If now the walk is much faster and steadier, then we document a positive reponse to large volume CSF removal. Our diagnosis of NPH is now strengthened and there has also been a therapeutic response to the procedure ( remember I told you the test is both diagnostic and therapeutic).

Before I usually subject the patient to a surgical option for more definitive treatment, I usually like to repeat the above test at least two more times. If there is a consistent positive response to large volume CSF removal, then I feel confident in going ahead and asking the neurosurgeon to place a shunt.  What is a shunt? Well a shunt is a device which as the name suggests shunts the spinal fluid from the brain into the peritoneal cavitiy (the gut). It has a valve which can be set to open at a particular pressure. So whenever the CSF pressure rises above that pressure, the valve shall open and the extra spinal fluid shall be shunted from the brain into the gut.

Simple device but does have its own risk of complications. Shunts can get infected, they can get dislodged from the brain and start migrating, they may get obstructed and have to be replaced etc. Hence before I advise putting any sort of hardware into the brain, I try to be as sure as possible that my patient indeed does have NPH and not a cortical dementia like Alzheimers or Parkinsons disease (as these do not respond to shunt placement).

It is Friday the 20th, I am off home on my vacation but shall be keeping the blog active. Please do contact me if you have any questions or want me to discuss something particular.

Personal Regards,

Nitin Sethi, MD