Endocrine neuropathies

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Endocrine neuropathies:

Endocrine neuropathies

Diabetic neuropathy:

Most common endocrine cause of peripheral neuropathy Risk of symptomatic neuropathy estimated at 4-10% at 5 years and 15% at 25 years Possible relation between IGT and peripheral neuropathy( Sumner et al) Duration of diabetes is the most important factor Diabetic neuropathy

Classification :

Symmetrical polyneuropathies Distal sensory or sensorimotor polyneuropathy Small fiber neuropathy Autonomic neuropathy Large fiber neuropathy Asymmetrical neuropathies Cranial neuropathy (single or multiple) Truncal neuropathy (thoracic radiculopathy ) Limb mononeuropathy (single or multiple) Lumbosacral radiculoplexopathy (asymmetrical proximal motor neuropathy) Entrapment neuropathy Combinations Diabetic neuropathic cachexia Symmetrical polyneuropathies Classification

Classification :

Subclinical neuropathy Abnormal electrodiagnostic tests (EDX) Decreased nerve conduction velocity Decreased amplitude of evoked muscle or nerve action potential Abnormal quantitative sensory testing (QST) Vibratory/tactile Thermal warming/cooling Other Abnormal autonomic function tests (AFT) Diminished sinus arrhythmia (beat-to-beat heart rate variation) Diminished sudomotor function Increased pupillary latency Classification Consensus Panel: Report and Recommendations of the San Antonio Conference on Diabetic Neuropathy. Diabetes 1988; 37:1000.

Classification :

Clinical Neuropathy Diffuse neuropathy Distal symmetric sensorimotor polyneuropathy Primarily small fiber neuropathy Primarily large fiber neuropathy Mixed Autonomic neuropathy Abnormal pupillary function Sudomotor dysfunction Genitourinary autonomic neuropathy Bladder dysfunction Sexual dysfunction C lassification

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Gastrointestinal autonomic neuropathy Gastric atony Gall bladder atony Diabetic diarrhea Hypoglycemic unawareness (adrenal medullary neuropathy) Cardiovascular autonomic neuropathy Hypoglycemic unawareness

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Focal neuropathy Mononeuropathy (upper or lower extremity) Mononeuropathy multiplex Plexopathy Polyradiculopathy (can occur with diffuse neuropathy) Cranial mononeuropathy

Pathology and pathophysiology:

Loss of myelinated nerve fibers Segmental remyelination and demyelination Basement membranes of intraneural capillaries are thickened and duplicated Areas of perivascular inflammation ( said,dyck et al) Biochemical mechanisms Pathology and pathophysiology

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Deficiency of aldose reductase and elevation of sorbitol R eduction in trophic factors within diabetic nerves ( NGF,VEGF,erythropoietin ) Hyperglycemia generates rheological changes that increase endoneurial vascular resistance and reduce nerve blood flow . Glucose auto-oxidation

Distal symmetric polyneuropathy:

Most common Sensory loss in glove and stocking pattern Most common complaint is of tingling, buzzing or prickling sensations affecting the feet The cardinal sign is absent ankle reflexes Muscle weakness is usually mild and confined to the feet, mainly in the distribution of the common peroneal nerve Distal symmetric polyneuropathy

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Two types "large fibre type" (predominant loss of vibration, light touch, and joint position senses) "small fibre type" (predominant loss of pain and temperature When there is prominent weakness, the possibility of a superimposed chronic inflammatory demyelinating polyneuropathy (CIDP) has to be considered Small fiber neuropathy often accompanied by autonomic involvement If predominantly autonomic consider amyloid

Hyperglycaemic neuropathy :

Tingling paraesthesia , pain or hyperaesthesia in the feet described in patients with newly diagnosed DM or those with very poor glycaemic control. The symptoms, and slowing of nerve conduction, are rapidly reversed by improving glucose control Hyperglycaemic neuropathy

Painful DSDP variants:

Treatment induced neuropathy(insulin neuritis) Seen in relation to tightening of glucose control. Trying to improve glucose control in a patient already on insulin or Patients being started on insulin for the first time. Similar to transient worsening or retinopathy on starting insulin (DCCT) Clinical signs are minimal or even absent. Nerve conduction studies may be normal. Over a period of up to 12 months, recovery is usual. Painful DSDP variants

Diabetic neuropathic cachexia:

Occurs predominantly in male patients with poorly controlled type 1 diabetes. The distal lower limb pain is severe, with burning and tightness of the feet. Pronounced weight loss is the key feature. It can take up to 12 months for improvement to occur with insulin and a further 1–2 years for recovery of body weight back to normal (Yuen et al. 2001) Diabetic neuropathic cachexia

Acute diabetic mononeuropathy:

Cranial neuropathies Painful 3 rd nerve palsy with pupilary sparing 6th and 7 th also commonly affected Limb mononeuropathies carpal tunnel syndrome, ulnar neuropathy or common peroneal neuropathy Acute diabetic mononeuropathy

Diabetic pseudotabes:

severe lancinating pains , loss of joint sensation, and diabetic pupillary abnormalities (pseudo-Argyll Robertson pupils ) and neuropathic arthropathy Unlike syphilis diabetic neuroapthic arthropathy involves small joints of feet Diabetic pseudotabes

Diabetic lumbosacral radiculoplexus neuropathy (Bruns-Garland syndrome):

Clinical features Males more frequently affected than females Pain : Severe, affecting lower back, buttocks or anterior thighs, burning and aching in quality; worse at night Weakness : Follows pain within a matter of a few days to several weeks and usually unilateral at onset. Later may be bilateral but asymmetric. Mainly proximal, but not uncommon for distal muscles to be involved May slowly progress over several weeks Weight loss : May be dramatic (>10–20 kg) Diabetic lumbosacral radiculoplexus neuropathy ( Bruns -Garland syndrome)

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Investigations EMG/NCS : Denervation changes in paraspinal , proximal and distal leg muscles There is often an associated DSDP Lower limb f wave latencies may be more prolonged than usually seen in DSDP CSF examination Protein value often raised.Only helps if the clinical picture is unusual Nerve biopsy Microvasculitis and endoneurial mononuclear cell infiltration . arely helps management

Truncal Neuropathy:

Involving the T4-T12 roots Pain over a focal area on the chest and/or abdomen. Usually unilateral, the pain often burning in quality, and in a variety of distributions reflecting nerve root or intercostal nerve trunk involvement Focal contact hyperesthaesiae in the same area as the pain Truncal Neuropathy

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Focal anterior abdominal wall weakness may be evident Associated weight loss in some cases may be profound Good prognosis with spontaneous recovery over several months

Approach :


Diagnosis :

History- standardised scores Clinical examination Vibration perception Monofilament test Lab methods EDX QAFT QST Diagnosis

Michigan neuropathy screening score:

Michigan neuropathy screening score Feldman, EL, Stevens, MJ, Thomas, PK, et al. Diabetes Care 1994; 17:1281

Tuning fork test:

A 128 Hz tuning fork is placed on the interphalangeal joint of the right hallux The score is 2 points, if the patient feels no vibration The score is 1 point, if the vibration feels stronger at the wrist. The score is 0 points, if the vibration feels no different at the wrist. Tuning fork test Meijer J W et alBack to basics in diagnosing diabetic polyneuropathy with the tuning fork! Diabetes Care 2005 Sep;28(9):2201-5.

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Small epidermal nerve fibers stain positive for the neuronal antigen protein gene product 9.5 (PGP 9.5).

Treatment :

Strict glucose control from the time of diagnosis of DM is the most important aspect of treatment. This has been clearly demonstrated in type I DM where tight glycaemic control reduces the risk of developing DSDP by 69% at five years Once established, DSDP is irreversible and slowly progressive. At this stage, strict glucose control provides no clinically significant improvement from the patient’s perspective, despite modest improvement in vibration threshold and nerve conduction studies Treatment


Myoinositol Alpha lipoeic acid Aldose reductase inhibitors Nerve growth factor C peptide and VEGF tried in animal experients ruboxistaurin (a protein kinase C- β inhibitor) Others…

Adjunctive therapy:

Patient education Ulcer prevention Daily inspection of feet Emollient creams Adjunctive therapy

Hypothyroid neuropathy:

Carpal tunnel syndrome MC 1/3 rd of patients have clinical polyneuropathy with predominant sensory symptoms NCS- decreased SNAPs and slow motor conduction velocities Sural nerve biopsy- demyelination,remyelination and increased glycogen and lysosomes in axonal and schwann cell cytoplasm Hypothyroid neuropathy

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Hormone replacement improves the symptoms TFT to be checked in all patients with sensory polyneuropathy and carpal tunnel syndrome

Acromegaly :

Carpal tunnel syndrome One half of patients have distal paresthesias,sensory loss in a stocking-glove distribution,diminished muscle stretch reflexes, and distal muscle weakness . NCS-SNAPs diminished and motor NCVs - slightly to moderately reduced Acromegaly

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Nerve biopsy-reduced number of myelinated and unmyelinated fibers and enlargement of nerve fascicles d/t increase in endoneurial and subperineurial tissue .

Hypoglycemic Amyotrophy:

Slowly progressive distal muscle atrophy and weakness Painful paresthesias are common but no objective signs of sensory loss Amyotrophy may precede the onset of hypoglycemic illness Nerve biopsy shows e/o demyelination and remyelination Hypoglycemic Amyotrophy

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