Brain and the Circuits- AI is here, and it is us.

“You have one question and one minute. General examination only”

Prof. Antony looked at me with an intimidating glare. He liked me. But that did not show. Did he want me to fail? That was possible. For this was a battle between titans, and I was a pawn. I looked at a middle-aged man sitting up on the trolley. He smiled. He was breathing- a trifle rapidly.

It was fun being a final year at the Medical School in Thrissur. There were no residents then. The Professors were aware that students and interns existed. Keenly- oh, so keenly. That made us good, and we wanted to be.  My incessant beavering in the medical wards had begun to pay off. I skipped theory classes often, but haunted the hospital like the ghost that was rumoured to infest the M1 wards. Medical Diagnosis was a passion then. Talk, look at, feel, tap, listen. The patient could tell you his diagnosis, though he knew it not. Her body would whisper what was wrong with it- if only you knew the language. The language of clinical examination. One acquired it through books, constant practice by examining people and by instruction and feedback from teachers.

My teachers from the first unit of Internal Medicine, Profs- Vidyadharan and Gopiraj, eyed me keenly (I told you- keen eying was the main thing back then), as I approached the patient. I was a perpetual Unit1 student. I had all my clinical postings there.  It was a hall, and all the students and interns posted in Medicine were looking on (Yeah- keenly, dammit). Prof Antony was chief of unit 4, and hence a rival king. The Kings battled it out by bringing challenging cases to the weekly clinical meetings and letting their minions prove themselves.

My voice trembled slightly as I asked the patient-

“Are you being treated for any disease?”

“Yes. Tuberculosis. But I did not take the medicines regularly. It has been two years.”

I had noted the intercostal muscles acting and the flared nostrils. He was breathless. Lungs partially destroyed by tuberculosis will lead to breathlessness due to the ventilation-perfusion mismatch. Obvious. Too obvious. It cannot be that. Prof Antony was notoriously shrewd. I could not do a detailed cardiac or respiratory examination- he had said- ‘general examination only.’ And I had only one minute. My brain whirred. A few neurotransmitters flowed furiously. Receptors in synaptic vesicles sputtered in a dangerous manner.

His ankles were swollen. There was mild pallor, but that was non-specific. His neck- Yes! The skin on the right side, above the collar bone, was dancing with veins pulsing from beneath. One, two, three- three pulses with each beat- the A, C and V waves. The familiar elevated Jugular Venous Pulse denoting cardiac failure. But what was that- an inward distortion of the V? The celebrated exaggerated ‘y’ descent! It was like the aurora borealis to a tropical man. We students knew it existed, but we never see one. It was an extremely rare diagnosis, even in the nineties. Risky, but what the heck. I braced myself.

“Constrictive Pericarditis- Probably tuberculous” I said, and looked at Prof Antony. He looked impressed. I looked at my bosses. They were smiling broadly.

I can still feel the pride in my chest. I know I am blowing my own twenty thousand horns, and the cacophony may annoy you. But two of the Professors are still alive. They would remember me. You can ask. Ha.

Thumping my puny chest was not the original intention of this story, though it felt good. I was musing on the passage of time and how we were veering away from clinical skills. Now- we simply do not need it. An ECG, and then an Echocardiography and Imaging would have made everything clear. But for several reasons, it is important to be trained clinically.

I was searching for a challenging question to throw at ChatGPT3.5, the free version, and I remembered this episode from my life. I asked it-

I am a doctor and I have a 50-year-old patient from India. He has some breathlessness, and swelling of both legs. He has a history of tuberculosis, inadequately treated. Examination shows a raised JVP with large v wave and an especially prominent y descent. There is pedal edema and basal crepitations. what is he likely to have?


Based on the symptoms and clinical findings you’ve described in your 50-year-old patient from India, several possibilities come to mind, particularly considering the patient’s history of inadequately treated tuberculosis and the specific clinical signs you’ve mentioned. One likely diagnosis that fits the clinical picture is constrictive pericarditis.

Constrictive pericarditis is a condition characterized by inflammation and scarring of the pericardium, the sac-like membrane surrounding the heart. This scarring causes the pericardium to become thickened and rigid, impairing the normal filling and emptying of the heart chambers. Here’s how the symptoms and clinical findings correspond to constrictive pericarditis:

  1. Breathlessness: This symptom is common in constrictive pericarditis due to the impaired filling of the heart chambers, leading to decreased cardiac output and pulmonary congestion.
  2. Swelling of Both Legs (Pedal Edema): Constrictive pericarditis can cause systemic venous congestion, leading to fluid accumulation in the legs and other dependent areas of the body.
  3. Raised JVP with Large V Wave and Prominent Y Descent: The raised jugular venous pressure (JVP) with a large V wave and prominent Y descent is characteristic of constrictive pericarditis. The V wave reflects the increased pressure in the right atrium during ventricular systole, while the prominent Y descent indicates rapid emptying of the right atrium during early diastole.
  4. Basal Crepitations: Basal crepitations may occur due to pulmonary congestion secondary to impaired cardiac function in constrictive pericarditis.

Given the patient’s history of inadequately treated tuberculosis, it’s important to consider the possibility of tuberculous pericarditis as a cause of the constrictive pericarditis. Tuberculous pericarditis can lead to pericardial inflammation and scarring, resulting in constriction of the heart.

Further evaluation with diagnostic tests such as echocardiography, cardiac MRI, and possibly pericardial biopsy may be necessary to confirm the diagnosis of constrictive pericarditis and determine the underlying etiology. Treatment typically involves medical management to alleviate symptoms and, in some cases, surgical intervention to relieve pericardial constriction. Early recognition and management are crucial to prevent complications and improve patient outcomes.

Please note that this is the free version. Not the actual GPT4. GPT5 is coming, and that is reported to be many times more intelligent.

I cannot but assume that we have cracked ‘thinking’. These Large Language Models that use neural networks are not ‘auto-completion bots’. They build on what billions of us humans have cumulatively achieved over millennia. They are us. But they might become much more than us.

The world was always interesting. It has suddenly got more interesting.

(Jimmy Mathew)

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Dr Jimmy

I am a Doctor, Writer and Science Communicator. I am a member of Info- Clinic, and have written a few books. This site features my blog posts and stories. Thank you for visiting. ഞാൻ എഴുതാൻ ഇഷ്ടമുള്ള ഉള്ള ഒരു ഡോക്ടർ ആണ് . നിങ്ങളുടെ താത്പര്യത്തിന് നന്ദി .