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Similar to Diabetis & brain
Diabetis & brain
- 1. Dr. T. C.R. Rama Krishnan
- 2. Case vignettes Discussion Pearls
- 3. A 50year old male who is a known diabetic came with acute onset of weakness of left sided limbs of 30 min duration O/E Left UMN facial palsy with Hemiplegia
- 5. Capillary blood sugar:40mg /dl
- 6. Serum glucose< 50 mg/dl < 30 mg Confusion < 10 mg Seizures Coma Medullary phase of Hypoglycemia. < 70 mg is the level at which counter regulatory hormones get activated
- 7. Glucose isthe exclusive fuel for the brain Brain stores only trivial amounts of glucose as glycogen unlike liver and skeletal muscle Hyperglycemia is better tolerated by the brain than hypoglycemia Glucose sensor in the brain- STN
- 8. After foodis ingested Blood glucose level increases Release of insulin from the pancreas
- 9. Insulin causessuppressing of glucose production in liver and storage of glucose as glycogen in the liver Normally the liver contains sufficient glycogen stores to maintain the blood glucose concentration at 80-90 mg/dl for 24-36 hours
- 10. After thatgluconeogenesis is the principal mechanism for maintaining glucose levels Initially most of the gluconeogenesis takes place in the liver and subsequently in the kidney 50% of the glucose thus produced is utilized by the brain
- 11. Glucose reservein the brain will sustain activity for about 30 min once blood glucose is no longer available. If blood sugar falls to < 10 mg / dl & persists for minutes , recovery is delayed for weeks & may be incomplete
- 12. Neuroglycopenia isthe term used to refer to symptomatic hypoglycemia Sweating, tremor and the sensation of warmth is due to ANS activation
- 13. Decreased caloricintake Liver disease Uremia Infection and shock Burns Pregnancy Neoplasia
- 14. Acute Sub acuteChronic Usually due to insulin or OHA MC form and occurs in fasting state Rare seen in obsessively controlled diabetics or due to insulin secreting tumor Begins with vague symptoms Symptoms seen in acute hypoglycemia are absent Always consider in dementia
- 15. acute Subacute Chronic Patientsmay recognize these symptoms Usually accompanied by hypothermia HbA1C levels are helpful in making the diagnosis Attacks may end spontaneously or proceed to Sz and coma Any unexplained hypothermia always check blood sugar They usually arrive in the ED with coma Always consider in stroke & seizures responds well to treatment Poor response to treatment
- 16. Symptoms ofhypoglycemia will not be there if the person is on beta blockers or if they have autonomic neuropathy. Use of Beta Blockers in patients on insulin or OHA is not advisable
- 17. Hypoglycemia isa medical emergency and should be considered in all patients with altered mental status of unknown origin Exogenous glucose is harmful to brain during hypoxia or ischemia and caution must be exercised in giving glucose to them
- 18. A 54yr old female not a known diabetic came with H/O involuntary movements involving Left sided limbs of 2 days duration
- 21. Diagnosis lefthemiballismus Her blood sugar : 640 Ketones : Negative Serum Osmolarity : 311 mosm
- 23. A 64years old Non – diabetic presented with visual disturbances - seeing continuous flashes of light in Left ½ of vision x 3d O/E Left homonymous hemianopia Confused No focal deficit
- 24. Blood sugar 465mg HbA1C 15 %
- 25. DIAGNOSIS Hyperglycemiainduced seizures He was treated with insulin , AED for short time MRI repeated after 3 weeks was Normal
- 27. A 45Year old diabetic presented with acute onset weakness of left sided limbs of 12 hrs duration His CT Brain, MRI Brain ( DWI ) didn`t show any abnormality
- 28. His bloodsugar was 472 mg/ dl and his HbA1C was 14% We treated him with antiplatelets and control of sugar He recovered completely in 4 days time Repeat MRI done after 4 days was also normal
- 29. Hyperglycemia couldbe either associated with acidosis (DKA) or non – Ketotic Hyperosmolar coma ( Hyperosmolar Hyperglycemic state HHS ) Non ketotic coma may present with unexplained coma or seizures without any past history
- 30. DKA Non ketotichyperosmolar coma Common in type I diabetics Feature of type II diabetes Precipitated by infection Seen in older people commonly as first manifestation Hyperventilation due to acidosis Evolves more slowly than DKA Ketone bodies are positive Clinical symptoms are due to hypertonicity, hypovolemia and cerebral dysfunction with seizures in some DKA people who die are more often due to neurogenic dysfunction than CVS cause Precipitated by infection, AGE, pancreatitis and treatment with steroids and phenytoin Insulin is the corner stone of treatment
- 31. Main focusof treatment is correction of dehydration & electrolyte disturbance Overly vigorous treatment with rapid correction of plasma osmolality can lead to the development of cerebral edema Consider ICP management in DKA patients who deteriorate
- 32. 56 yearold male known case of uncontrolled diabetes – Came with history of left side severe ear pain x 10 days O/E Left LMN facial palsy Swollen Left ear
- 37. He wasreferred to ENT surgeon He was treated with oral quinolones, strict sugar control Local debridement of the wound was done DIAGNOSIS Malignant Otitis Externa
- 38. 72 yearold male known diabetic came with deviation of angle of mouth towards right side of 2 days duration Headache of severe degree interfering with sleep and ADL present
- 39. Day 1 Day2 Day 3 Day 5 Day 7 Left LMN Facial Palsy Left LMN Facial Palsy Left LMN Facial Palsy Operated Left LMN Facial Palsy Proptosis Left abduction impaired Left Complete Ophthalmoplegia Right hemiplegia
- 42. DM WITHFUNGAL SINUSITIS He underwent surgery along with Amphoterecin treatment, antibiotics and supportive measures Unfortunately he succumbed to his illness
- 43. 50 yrold known diabetic presented with acute onset binocular horizontal diplopia on looking to the right O/E Right VI th nerve palsy
- 45. 6O yrold diabetic presented with acute onset diplopia with drooping of eyelid O/E right third nerve palsy
- 48. Treatment fordiabetic cranial mono neuropathy is strict sugar control and physiotherapy Most of them recover over a period of 6 – 12 weeks
- 49. A 50year old diabetic presented with severe pain along the costal margin radiating from back to anterior aspect of 3 months duration USG Abdomen CT Abdomen UGIE, Colonoscopy MRI Whole Spine all are normal
- 51. Can presentwith severe pain in a dermatomal pattern Common in thoracolumbar region in diabetics
- 52. A 40years old male known diabetic came to us with numbness in the right hand since 1 month Numbness occurred while mixing food and holding to objects Numbness was more during night along with radiating pain from wrist to arm
- 53. No focaldeficit Tinel`s sign is negative Phalen`s test positive
- 55. Blood sugar236 mg/dl HbA1C 8.2% TSH - 1.23 , Free T4 1.35 NCS report showed Bilateral Carpal Tunnel Syndrome
- 57. Carpal tunnelSyndrome Cock up splint at night CTS exercises Surgery for severe cases
- 58. Diabetic neuropathyis a length dependent process Usually presents with lower limb sensory symptoms Presentation with upper limb symptoms always consider Entrapment Neuropathy
- 59. A 54years old diabetic female came to us with severe left shoulder pain and inability to lift the left shoulder overhead of 6 months O/E Left shoulder abduction restricted Wasting of left arm muscles present Sensation impaired over Left Axillary nerve area
- 61. She was treatedwith pregabalin, physiotherapy
- 62. A 56year old male who is a known case of diabetic came to us with low back pain radiating to left lower limb Pain is severe in nature interfering with ADL Numbness and burning pain in feet present O/E Wasting of left thigh Left KJ absent, Left AJ + Sensory - Normal
- 63. He wastreated with IV Methyl Prednisolone for 3 days Pregabalin, Duloxetene and supportive measures
- 64. Consider hypoglycemiain any altered mental status in a diabetic HHS can present for the first time with seizures or focal deficit or with delirium Always rule out aneurysm in IIIrd nerve palsy Facial palsy is not always as simple as it looks
- 65. Shoulder painin a diabetic is not always periarthritis shoulder Sciatica if not responding to treatment consider Lumbosacral Plexopathy Diabetic neuropathy is more of a sensory neuropathy If patient present with predominant weakness or if NCS shows demyelinating pathology consider CIDP