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A Confused Patient

CNS dimensions to confusional state in malignant HTN

Douglas F Watt, Quincy Medical Center, Harvard Medical School, 17 Nov 2009 9:38 PM EST

Competing interests: None declared

This is a fine case review, but it leaves out the critical question "why does malignant HTN cause a confusional state?" This isn't an easy question because it still isn't clear. However, preliminary evidence suggests that the effects of this condition may be mediated by failure of the BBB, and subsequent 'forced' introduction of many proteins and cells that don't belong in the brain, subsequent up-regulation of pro- inflammatory cytokines, sustained inflammatory cascades, and subsequent disruption of synaptic function and global network dynamics.

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CONFUSED PATIENT

ANAND RV, 18 Nov 2009 1:29 AM EST

Competing interests: None declared

EXCELLENT ANALYSIS AND DISCUSSION

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Differential diagnosis

Newton Almeida, São Paulo, Brazil, 18 Nov 2009 1:21 PM EST

Competing interests: None declared

Could be considered as another differential diagnosis HUS?

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MALIGNANT HBP

JOE BARRY, PREVENTIVE MEDICINE ASSOCIATES,CAMILLUS ,NY, 18 Nov 2009 3:48 PM EST

Competing interests: None declared

Rolls Royce work up for this disease high lights that we do not see it hardly ever.There needs to be a discussion of the pathophysiology and more details on the dif diagnosis.We see patients who are asymptomatic with systolics of 240 frequently..Some causes off the top of my head are: base line hypertension complicated by salt binges plus or minus alcohol, severe tension, not taking BP meds, steroids, vasoconstrictor cold medicine, pseudo hypertension from non compressable brachial ateriey,and so on.

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CONFUSION,MALIGNANT HYPERTENSION

JAYARAJAN MENON, CALICUT, KERALA,INDIA, 18 Nov 2009 9:18 PM EST

Competing interests: None declared

All comprehensive appropriate differential diagnosis, and logical final diagnosis .Among the reported investigations an ECG was not seen !

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Confused Patient

DR.RABIA AKBAR VALI, CENTRAL PRIVATE HOSPITAL, 19 Nov 2009 8:03 AM EST

Competing interests: None declared

A GOOD LEARNING AND CLINICALLY APPLICABLE SUBJECT IN DAILY PRACTICE OF MEDICINE.

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Secondary causes of HTN

O Steichen, AP-HP, Tenon Hospital, Paris, 21 Nov 2009 5:51 AM EST

Competing interests: None declared

Despite high serum creatinin, serum potassium level is fairly low in this patient. I would certainly look for a secondary cause of HTN, including renal artery stenosis due to fibromuscular dysplasia, primary aldosteronism, and Cushing syndrome

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MALIG HYPERTENSION

JOE BARRY, Camillus ,ny, 19 Nov 2009 12:56 PM EST

Competing interests: None declared

Response to Douglas Watt from Harvard:.

Our knowledge about brain function is still in tne dark ages. I am finishing a 36 lecture series on"Understanding the Brain " by Dr.Jeannette Norden from Vandilt Univ. Like all the lectures from the Teaching Company ,this is excellent

The abnormal brain function of the patient with Malig Hypertension was associated with increased intracranial pressure seen on opthalmoscopy.

Assumed is that intense vasoconstriction in the major cerebral arteries causes hypoxic brain cell injury .The latter impacts the function of the intra cerebral fluid balance giving rise to cerebral edema.

Please run this by my all time hero ,Dr.Matin Samuels, chief of neurology at the Brigham.

I like this concept because it translates into treating hypoxic cerebral edema, which we can do.

A reflection of the lack of interest in Brain is that the entire 36 lectures cost $100. Considering that the Brain is the source of and or controls every human thought, action, pleasure, vision, memory, love, etc, the low price reflects the lack of interest in this 3 pound organ. Joe Barry, Camillus NY

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TTP versus hypertensive encephalopathy

Ragai Fouda, 24 Nov 2009 10:23 AM EST

Competing interests: None declared

Dear Sir,

I enjoyed reading the nicely presented case and the comprehensive discussion. I wanted to ask about the possibility of TTP (thrombotic thrombocytopenic purpura)..showing thrombocytopenia,microangiopathic haemolytic anaemia, renal impairment,and neurologic deficit) ..which isnt associated by severe hypertension but that might be secondary to the renalimpairment.

Wish to hear from you Sir

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follow-up comment to comment by Joe Barry

Douglas F. Watt, Cambridge City Hospital, Harvard Medical School, 25 Nov 2009 12:39 PM EST

Competing interests: None declared

dear Joe

Thanks for your comment. I suspect that we are describing different aspects of the elephant similar to the three blind men. No argument about how little attention is paid in modern medicine to mental status or the state of the brain. I think our two descriptions are probably complementary rather than competing. The effects of hypoperfusion/hypoxia probably synergize with the effects of upregulation of pro-inflammatory cytokines - and blood brain barrier dysfunction is common to both of these hypotheses (hypoxia/hypoperfusion versus a pro-inflammatory state in the brain). An interesting question, (perhaps you know the answer to but I don't) is whether someone has actually done intra-cerebral monitoring in an animal model of hypertension to prove Central hypoxia/hypoperfusion. Are you aware of any substantive research into this?

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hyperaldo

RJ Beneitone, 17 Dec 2009 9:24 PM EST

Competing interests: None declared

hypokalemia and raised SAC/PRA speak for Hyperaldo. Was this evaluated for?

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