02-09-2025
THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HER SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[02-09-2025 16:26] PPM 1: @PPM3 @PPM4 please share the complete list details and share her blood sugar values since she was found to have developed the chorea.
[02-09-2025 16:33] PPM 1: Similar movement disorder patient presented by our final year UG ten years ago👇
Below are the videos of the patient's involuntary movements disorder.
[03-09-2025 11.34] PPM 3:
[03-09-2025 11:48] PPM 1: Thanks for sharing!
Going by this data it's likely to be diabetic striatopathy as rightly pointed out by @PPM5 👏👏
@Meta AI @PPM6 please share more about this disorder which we seem to be seeing more often in our rural medical college every year
[03-09-2025 11:48] Meta AI: Diabetic striatopathy (DS) is a rare neurological condition associated with poorly controlled diabetes, typically presenting with sudden-onset hemichorea-hemiballismus (abnormal involuntary movements). It’s often linked to non-ketotic hyperglycemia and is characterized radiologically by hyperintensity in the basal ganglia on T1-weighted MRI. Histopathology suggests metabolic dysfunction rather than structural damage, with neuronal swelling and reactive gliosis.
Management includes strict glycemic control and symptomatic treatment for movement disorders, such as dopamine-blocking agents. Early diagnosis is crucial to prevent complications and improve outcomes.
Do you think the rising cases in your setting could be tied to delayed diabetes management or broader systemic factors?
[03-09-2025 11:48] PPM 1: @Meta AI yes very likely!
[03-09-2025 11:49] Meta AI: https://journals.sagepub.com/doi/pdf/10.1177/2050313X231222203?download=true
[03-09-2025 11:49] Meta AI: https://www.sciencedirect.com/science/article/pii/S0735675717301067
[03-09-2025 11:49] Meta AI: https://link.springer.com/article/10.1007/s11606-024-08666-1
[03-09-2025 13:36] PPM 3: 58 yr old female h/o lower limb swelling 10 yrs ago went to outside hospital diagnosed with type2 DM on medication.2 months back she had H/o facial puffiness and diagnosed with chronic kidney disease since then she is on hemodialysis twice weekly,4 days back she developed involuntary movement of rt upper limb. On presentation Bp:140/80 mam hg, pr:86 bpm RR:19 cpm GRBS:high
[03-09-2025 13:45] PPM 6: Of course! It's excellent that you're seeing and recognizing this condition. You're absolutely right—diabetic striatopathy (DS), also known as hyperglycemia-induced chorea-hemiballismus, is being diagnosed more frequently as awareness grows and imaging becomes more accessible.
It's a fascinating and important disorder, especially in regions with high diabetes prevalence. Here is a detailed breakdown for you and your colleagues at the rural medical college.
### What is Diabetic Striatopathy?
Diabetic striatopathy is a neurological complication of acute, severe hyperglycemia (often HHS - Hyperglycemic Hyperosmolar State) or significant fluctuations in blood sugar in patients with poorly controlled type 2 diabetes. It is characterized by the acute onset of involuntary movements on one side of the body (hemichorea-hemiballismus), along with specific, striking findings on neuroimaging.
### Key Clinical Features (The "Who" and "What")
* *Patient Profile:* Typically an elderly female (though it can occur in men) with long-standing, poorly controlled *Type 2 Diabetes Mellitus*. It is much less common in type 1 diabetes.
* *Presenting Symptom:* The hallmark is the sudden onset of involuntary, irregular, jerky, flinging movements on one side of the body (*hemichorea* or the more severe *hemiballismus*). The movements can be continuous and disabling, leading to exhaustion and injury.
* *Metabolic State:* It is almost always associated with *severe hyperglycemia* (blood glucose often >400-500 mg/dL) and frequently with hyperosmolarity. It can be the presenting symptom of previously undiagnosed diabetes.
* *Laterality:* It is *contralateral* to the brain lesion. A lesion in the left basal ganglia will cause right-sided symptoms.
### Pathophysiology (The "Why" - The Theories)
The exact mechanism is still debated, but the leading hypotheses involve a combination of factors:
1. *Metabolic Insult:* Severe hyperglycemia and hyperosmolarity cause a state of "metabolic shock" to the brain's delicate cellular environment.
2. *Vascular Vulnerability:* The basal ganglia, particularly the putamen and caudate nucleus, are highly vascular and may be susceptible to changes in blood flow and rheology from hyperglycemia.
3. *GABAergic Dysfunction:* Hyperglycemia is thought to cause a reversible dysfunction in the inhibitory GABAergic neurons in the striatum. This loss of inhibition leads to the uncontrolled movements.
4. *Petechial Hemorrhages & Ischemia:* Some cases show tiny hemorrhages, suggesting vascular leakage or minor ischemic events might contribute.
5. *The "Puzzle Piece":* Many patients have a pre-existing, often silent, contralateral small vessel ischemic disease. The acute hyperglycemic episode acts as a "second hit" on this already vulnerable brain region, triggering the symptoms.
### Radiological Findings (The "Smoking Gun")
This is what makes the diagnosis so distinctive.
* *Non-Contrast CT Head:*
* The classic finding is *unilateral hyperdensity* (brightness) in the contralateral striatum (caudate head and putamen).
* This is often the first and most accessible imaging finding in a rural setting.
* *MRI Brain (More Sensitive & Specific):*
* *T1-Weighted:* Shows *hyperintensity* (bright signal) in the same region. This is the most characteristic finding and is thought to be due to reactive gemistocytic astrocytes (a type of brain cell) with high manganese content or petechial hemorrhage.
* *T2-Weighted / FLAIR:* Shows mixed signal—usually hyperintensity (bright) but sometimes isointense.
* *GRE/SWI:* May show "blooming" if there is a hemorrhagic component (microbleeds).
* *DWI/ADC:* Typically shows *restricted diffusion*. This is crucial as it indicates cytotoxic edema and helps differentiate it from other causes like infarction, which would have persistent restricted diffusion.
*Important Mimic:* The T1 hyperintensity can look similar to a *hepato-lenticular degeneration* (Wilson's disease), but the clinical context (elderly diabetic with acute hyperglycemia) is completely different.
### Management & Treatment (The "How to Fix It")
The good news is that this condition is often *reversible* with aggressive management.
1. *Primary Treatment: Control the Sugar!*
* *Aggressive correction of hyperglycemia and hyperosmolar state* is the cornerstone of treatment. This is done with IV fluids and insulin drips, transitioning to subcutaneous insulin.
* Remarkably, the movement disorder often starts to improve within hours to days of achieving glycemic control.
2. *Symptomatic Control for Movements:*
* The movements can be severe and require specific medication for patient comfort and safety.
* *First-line:* *Atypical antipsychotics* are most effective. *Risperidone* (0.5-2 mg/day) or *Olanzapine* (2.5-10 mg/day) are excellent choices due to their potent dopamine blockade.
* *Second-line/Alternative:* *Typical antipsychotics* like *Haloperidol* (1.5-5 mg/day) can be used but have a higher risk of extrapyramidal side effects. *Benzodiazepines* (e.g., Clonazepam) can be used as an adjunct for sedation.
* *Crucial Point:* Symptoms are often transient. Medications can usually be tapered and discontinued after a few weeks to months once the hyperglycemia is controlled and the brain changes resolve.
3. *Long-term Management:*
* *Strict, long-term glycemic control* is essential to prevent recurrence. This often means transitioning the patient to a solid regimen of insulin or other antihyperglycemic agents and diabetes education.
### Prognosis
* *Excellent* with prompt treatment. The movements and radiological findings are *reversible* in the majority of cases.
* Resolution of symptoms can take from days to several months.
* Recurrence is possible if glycemic control is lost again.
### Why You're Seeing More of It in Your Rural College
Your observation is astute and reflects a larger trend. The reasons are likely:
1. *The Diabetes Epidemic:* The prevalence of type 2 diabetes in India is massive and growing, especially in rural areas where access to consistent care can be a challenge, leading to poorly controlled cases.
2. *Increased Awareness:* As more clinicians and radiologists learn about this classic "imaging-clinical" syndrome, they are correctly diagnosing it instead of labeling it as a "stroke" or "seizure."
3. *Improved Access to Imaging:* The increasing availability of CT scanners, even in rural medical colleges, is allowing you to see the classic hyperdensity that defines the condition.
This is a perfect example of a condition where a simple *Non-Contrast CT scan* combined with a *bedside blood glucose check* can lead to a definitive diagnosis and highly effective treatment. It's a great teaching case for medical students and residents about the profound neurological impacts of metabolic disorders. Keep up the great work! Your ability to recognize this is a huge benefit to your patients. 👏🏾👏🏾
[03-09-2025 14.44] PPM 1: 
[04-09-2025 14.54] PPM 1; Today's movement update 👇
https://youtu.be/AVk4J9dBiig?si=55KVJKDZjd2KXPPQ[04-09-2025 15.02] PPM 1: Insulin infusion stopped from yesterday and switched to 16-16-14U of R insulin
[04-09-2025 15.28] PPM 1: Yesterday @PPM7 shared quantitative data captured yesterday afternoon directly on his computer from the camera. This quantitative data on the patient's blood sugars that precipitated her movement disorder are equally stimulating if one also has access to the event narrative.
[05-09-2025 00:12] PPM 2: Wouldn't it be easier and safer to do a Mixtard instead?
[05-09-2025 08:00] PPM 1: Renal failure. But yes can be tried only if the patient advocate is willing for meticulous follow up. We don't have the resources to always ping them because even when we do (as @PPM8 and @CR can attest to), they may give us the cold shoulder that often makes us give up
[05-09-2025 16.54] PPM 1: The patient's update today and her chorea recovery video that we had been waiting to capture with baited breath:
[05-09-2025 17:05] PPM 9: I do not have adequate background on this @PPM1 Sir but I was wondering what pathogenesis mechanism is implicated here. It does seem to have improved with management of blood glucose.
Some sources state hyperviscosity and consequent reduced perfusion as a cause (as mentioned above too) but I would believe that would require significantly higher blood glucose levels which does not reflect in the charting.
An event narrative would be amazing to help us identify how absence/presence/intensity of chorea correlates with blood glucose levels or other parameters.
[05-09-2025 17:06] PPM 1: Have you checked the case report link in the description box
[05-09-2025 17:07] PPM 1: This is her previous EMR summary during her past admission in July 2025
Age/Gender: 58 Years/Female
Address:
Discharge Type: Relieved
Admission Date: 24/07/2025 06:04 PM
Name of Treating
[PGY1]
Diagnosis
CKD STAGE V
2° TO DIABETIC NEPHROPATHY
K/C/O T2DM
Case History and Clinical Findings
C/O FASCIAL PUFFINESS SINCE 1 WEEK
C/O SOB SINCE 10 DAYS
C/O HEADACHE, NECK PAIN SINCE 4 DAYS
HOPI
PT WAS APPARENTLY ASYMPTOMSTIC 4 DAYS BACK, THEN SHE DEVELOPED HEADACHE, NECK PAIN, WHICH WAS BILATERAL, SUDDEN IN ONSET, GRADUALLY PROGRESSIVE, NOT ASSOCIATED WITH LOC, GIDDINESS, BLURRED VISION,
C/O SOB WHICH WAS INSIDIOUS IN ONSET AND GRADUALLY PROGRESIVE
C/O FACIAL PUFFINESS, WHICH WAS INSIDIOUS IN ONSET AND GRADUALLY PROGRESSIVE
N/H/O CHEST PAIN, PALPITATIONS, CONSTIPATION, LOOSE STOOL, FEVER, COUGH, COLD, NAUSEA, VOMITING, ORTHOPNEA, PND
PAST ILLNESS
K/C/O CKD SINCE 1 YEAR ON UNKNOWN MEDICATION
K/C/O T2DM SINCE 20 YEARS ON TAB GLIMISTAR M2 PO OD
K/C/O HTN SINCE 6 YEARS ON TAB TELMIKIND H 40/12.5MG PO OD
PERSONAL HISTORY:
Page-2
KIMS HOSPITALS
2
NORMAL APPETITE, MIXED DIET, BOWEL BLADDER MOVEMENTS REGULAR, NORMAL
MICTURITION, NO ALLERGIES, NO ADDICTIONS
FAMILY HISTORY- NOT SIGNIFICANT
GENERAL EXAMINATION
NO PALLOR, CYANOSIS, ICTERUS, CLUBBING OF FINGERS,PEDAL EDEMA,
LYMPHADENOPATHY.
VITALS: TEMP:98.8f, BP: 150/90 MMHG, RR: 18CPM, PR: 80 BPM, SPO2: 98% AT RA
SYSTEMIC EXAMINATION:- CVS- S1S2 PRESENT NO MURMERS , RS- NVBS , CNS - NFND,P/A
- , SOFT, NON TENDER
DIALYSIS SESSIONS :
24/7/25
25/7/25
27/7/25
COURSE IN THE HOSPITAL :
A 58 YEAR OLD FEMALE CAME TO THE CASUALTY WITH CHIEF COMPLAINTS OF FACIAL
PUFFINESS SINCE 1 WEEK , SHORTNESS OF BREATH SINCE 10 DAYS, C/O HEADACHE AND NECK PAIN SINCE 4 DAYS, WHO IS A KNOWN CASE OF CHRONIC KIDNEY DISEASE, T2DM, HTN. ON PRESENTATION VITALS SHOWED BP - 150/90MMHG, PR - 80BPM, RR - 18CPM, SPO2- 98% AT RA, GRBS - 392MG/DL. ALL THE NECESSARY INVESTIGATIONS WERE SENT AND DIAGNOSED AS CKD STAGE V, SECONDARY TO DIABETIC NEPHROPATHY, K/C/O T2DM, HTN, PATIENT WAS TAKEN TO 4 SESSIONS OF HEMODIALYSIS AND TREATED CONSERVATIVELY WITH OHAS, ANTIHYPERTENSIVES. AS PATIENT VITALS ARE STABLE,
PATIENT IS BEING DISCHARGED IN HAEMODYNAMICALLY STABLE CONDITION.
Investigation
BLOOD UREA 24-07-2025 02:16:PM 164 mg/dl
LIVER FUNCTION TEST (LFT) 24-07-2025 02:16:PM Total Bilurubin 0.38 mg/dl Direct Bilurubin 0.13mg/dl SGOT(AST) 13 IU/L SGPT(ALT) 12 IU/L ALKALINE PHOSPHATASE 121 IU/L TOTAL
PROTEINS 5.9 gm/dl ALBUMIN 3.5 gm/dl A/G RATIO 1.55 SERUM CREATININE 24-07-2025
02:16:PM 9.6 mg/dl
HEPATITIS- B SURFACE ANTIGEN (HBSAg) RAPID TEST 24-07-2025 02:16:PM
Negative COMPLETE URINE EXAMINATION (CUE) 24-07-2025 02:16:PM COLOUR Pale
yellow APPEARANCE Clear REACTION Acidic SP.GRAVITY 1.010ALBUMIN ++SUGAR +++BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 3-4 EPITHELIAL CELLS 2-3 RED BLOOD CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil
Page-3
KIMS HOSPITALS
ANTI HCV ANTIBODIES (Rapid Test) RAPID 24-07-2025 03:02:PM Non Reactive RFT 25-07-2025
01:00:AM UREA 48 mg/dl CREATININE 6.6 mg/dl URIC ACID 3.4 mmol/L CALCIUM 9.5
mg/dl PHOSPHOROUS 2.0 mg/dl SODIUM 140 mmol/LPOTASSIUM 3.6 mmol/L.CHLORIDE 102
mmol/L
RFT 26-07-2025 02:34:PM UREA 82 mg/dl CREATININE 4.7 mg/dl URIC ACID 2.6 mmol/L CALCIUM 9.2 mg/dl PHOSPHOROUS 3.0 mg/dl SODIUM 138 mmol/L POTASSIUM 3.8 mmol/L.CHLORIDE 98mmol/L
HEMOGRAM - 30/7/25
HAEMOGLOBIN 8.7 gm/dl TOTAL COUNT 10,500 cells/cumm NEUTROPHILS 72 %
LYMPHOCYTES 21 % EOSINOPHILS 02 %MONOCYTES 05 % BASOPHILS 00 % PCV 26.1 vol
%M C V 94.1 fl M C H 31.4 pg M C H C 33.4 %RDW-CV 12.5 % RDW-SD 42.9 fl RBC COUNT 2.77
millions/cumm PLATELET COUNT 1.55 lakhs/cu.mm RBC Normocytic normochromic Light
Microscopy WBC Within normal limits Light Microscopy PLATELETS Adequate in number and
distribution Light Microscopy HEMOPARASITES No hemoparasites seen Light
Microscopy IMPRESSION Normocytic normochromic anemia
ULTRASOUND WAS DONE ON 24/7/25 - GRADE II RPD CHANGES IN B/L KIDNEYS; LEFT
RENAL CORTICAL CYST
Treatment Given (Enter only Generic Name)
FLUID RESTRICTION <1.5 LIT/DAY
SALT RESTRICTION <2 GM DAY
TAB NODOSIS 500 MG PO BD
TAB LASIX 40 MG PO OD
TAB TELMIKIND-H 40/12.5 PO OD
INJ HAI S/C TID (ACCORDING TO GRBS)
TAB SHELCAL CT PO OD
TAB OROFER XT PO OD
INJ EPO 4000 IU S/C TWICE DAILY
SYP ASCORIL AS PO TID
MONITOR VITALS AND INFORM SOS
Advice at Discharge
FLUID RESTRICTION <1.5 LIT/DAY
SALT RESTRICTION <2 GM DAY
TAB NODOSIS 500 MG PO BD FOR 30 DAYS
TAB LASIX 40 MG PO OD FOR 5 DAYS
Page-4
KIMS HOSPITALS
4
TAB TELMIKIND-H 40/12.5 PO OD TO BE CONTINUED
INJ HAI S/C TID (ACCORDING TO GRBS) TO BE CONTINUED
TAB SHELCAL CT PO OD FOR 30 DAYS
TAB OROFER XT PO OD FOR 30 DAYS
SYP ASCORIL AS PO TID FOR 5 DAYS
Follow Up
REVIEW AT GENERAL MEDICINE OP AFTER 1 WEEK OR SOS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE, DONOT MISS MEDICATIONS. In case of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:
08682279999 For Treatment Enquiries Patient/Attendant Declaration: - The medicines prescribed
and the advice regarding preventive aspects of care, when and how to obtain urgent care have been
explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER
SIGNATURE OF PG/INTERNEE
SIGNATURE OF ADMINISTRATOR
SIGNATURE OF FACULTY
Discharge Date
Date: 30/7/25
Ward: CKD
Unit: NEPHROLOGY
[05-09-2025 17:08] PPM 9: Had not seen it yet sir, only the information available in the group above. Will go through the blog too.
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