Diabetis & brain

Dr. T. C. R. Rama Krishnan

DIABETES AND BRAIN

Case vignettes

Discussion

Pearls

Scheme of things

A 50 year 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

CASE I

Capillary blood sugar: 40mg /dl

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

HYPOGLYCEMIA

Glucose is the 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

Basics

After food is ingested

Blood glucose level increases

Release of insulin from the pancreas

Glucose homeostasis

Insulin causes suppressing 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

After that gluconeogenesis 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

Glucose reserve in 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

Neuroglycopenia is the term used to refer to symptomatic hypoglycemia

Sweating, tremor and the sensation of warmth is due to ANS activation

Even though the majority of symptoms of hypoglycemia are related to CNS dysfunction they are extremely varied, non specific and not always present even when blood glucose levels are very low

Decreased caloric intake Liver disease Uremia Infection and shock Burns Pregnancy Neoplasia

Risk factors for hypoglycemia

Acute Sub acute Chronic

Usually due to insulin or OHA

MC form and occurs in fasting state

Rare seen inobsessively controlled diabetics or due to insulin secreting tumor

Begins with vague symptoms

Symptoms seen in acute hypoglycemia are absent

Always consider in dementia

Clinical features of hypoglycemia

acute Subacute Chronic

Patients may 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

Symptoms of hypoglycemia 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

Hypoglycemia Unawareness

Hypoglycemia is a 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

A 54 yr old female not a known diabetic came with H/O involuntary movements involving Left sided limbs of 2 days duration

CASE II

Diagnosis left hemiballismus

Her blood sugar : 640 Ketones : Negative Serum Osmolarity : 311 mosm

A 64 years 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

CASE III

Blood sugar 465 mg

HbA1C 15 %

DIAGNOSIS

Hyperglycemia induced seizures

He was treated with insulin , AED for short time

MRI repeated after 3 weeks was Normal

A 45 Year 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

CASE IV

His blood sugar 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

Hyperglycemia could be 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

Hyperglycemia

DKA Non ketotic hyperosmolar 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

Main focus of 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

56 year old 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

CASE V

MRI brain

He was referred to ENT surgeon

He was treated with oral quinolones, strict sugar control

Local debridement of the wound was done

DIAGNOSIS Malignant Otitis Externa

72 year old 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

CASE VI

Day 1 Day 2 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

DM WITH FUNGAL SINUSITIS

He underwent surgery along with Amphoterecin treatment, antibiotics and supportive measures

Unfortunately he succumbed to his illness

DIAGNOSIS

50 yr old known diabetic presented with acute onset binocular horizontal diplopia on looking to the right

O/E Right VI th nerve palsy

CASE VI

6O yr old diabetic presented with acute onset diplopia with drooping of eyelid

O/E right third nerve palsy

III rd NERVE PALSY

RT III rd NERVE PALSY

VII th NERVE PALSY

Treatment for diabetic cranial mono neuropathy is strict sugar control and physiotherapy

Most of them recover over a period of 6 – 12 weeks

A 50 year 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

Can present with severe pain in a dermatomal pattern

Common in thoracolumbar region in diabetics

Diagnosis

A 40 years 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

CASE VII

No focal deficit

Tinel`s sign is negative

Phalen`s test positive

O/E

Blood sugar 236 mg/dl HbA1C 8.2% TSH - 1.23 , Free T4 1.35 NCS report showed Bilateral Carpal Tunnel

Syndrome

Investigation

Carpal tunnel Syndrome

Cock up splint at night CTS exercises Surgery for severe cases

Diagnosis & Management

Diabetic neuropathy is a length dependent process

Usually presents with lower limb sensory symptoms

Presentation with upper limb symptoms always consider Entrapment Neuropathy

A 54 years 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

CASE VIII

She was treated with pregabalin, physiotherapy

Diagnosis

A 56 year 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

CASE IX

He was treated with

IV Methyl Prednisolone for 3 days

Pregabalin, Duloxetene and supportive measures

Diagnosis

Consider hypoglycemia in 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

Take home message

Shoulder pain in 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

Thank you