Diabetic Neuropathy-common Complication of DM

8/13/2019 Diabetic Neuropathy-common Complication of DM

1/42

Diabetic neuropathy-common complication of

DMClassification:Symmetrical polyneuropathies

Focal/multifocal polyneuropthiesAutonomic neuropathies


2/42

Symmetrical

polyneuropathies Sensory/sensorimotor

polyn.(allodynia)

Acute/subacute motor polyn.

Autonomic neuropathy


3/42

Focal/multifocalneuropathies :

Cranial neuropathies(BellsPalsy,Ophthal-moplegia,Trigeminal

neuralgia) Trunk & limb neuropathy(Carpal

tunnel syndromeCTS- , Tarsal

TS,Peroneal Palsy) Proximal motor neuropathy


4/42

Autonomic neuropathies:

Cardiovascular disturbances(posturalhypertension, cardiac denervation)

Thermoregulatory disorders(distalanhidrosis, gustatoory sweating, abnormalvasomotor response to change intemperature)

Alimentory tract disorders(GItract atony) Genitourinary disturbances(bladder

atony,impotence)

Disturbances of respiratory

control(cardiorespiratory arrest)


5/42

Neurogenic bladder

Failure to store urinedue to ahyperactive bladder (CNS, cortical,

subcortical disorders) Failure to evacuate urinedue to PNS

disorder (atonic bladder)


6/42

Guillain-Barre syndrome

Acute inflammatory demyelinatingpolyneuropathy(AIDP)

Immunologically mediated

An unclassical form of polyneuropathy

Cause undetermined, often precededby an infection, viruses, HIV, enteritis


7/42

Confirmatory tests

High cerebro-spinal fluid (CSF) protein,no pleocytosis (cells) = albumino

cytologic dissociation. Electromyography (EMG) and Nerve

conduction velocity (NCV) signs of

demyelination. Treatment plasma exchange, plasma

pheresis, Immunoglobulin I.V.


8/42

Radicular syndrome =

Radiculopathies Most common in cervical (neck) and

lumbar (LBP) regions, with

Radiating pain, weakness, loss oftendon reflexes, opisthotonus,Lasegue and Kernig signs.

Cervical root syndromes, C5-6 and C7-8 radiculopathies.

Lumbar root syndromes, L4-L5-S1


9/42

HNP (Hernia nucleus

pulposus) Most common cause: herniated

intervertebral disk/slipped disk, mass

lesions, structural abnormalities. Symptoms and severity depends on:

location and type of herniation (central diskherniationmay result in conus cauda

syndrome, lateral disk herniationmayresult in root syndromes)


10/42

Spinal cord


11/42

Spondylolisthesis

Slipping or gliding forward of thelumbar vertebra on the sacrum.

Spondylolysis = fusion or fixation ofvertebral column.


12/42

Brainstem lesions :

Mesencephalon, Pons, Medullaoblongatainfarct, due to ischemic

vascular occlusion of Circulus Williscranial arteries at the

base of the brain,

Causing dysfunctions of cranial nerves.


13/42


14/42


15/42

Horner syndrome:

Ptosis,miosis, anhidrosis,enophthamos

Due to disruption of sympathetic

pathway in cervical region Cause not always detectable, most

often due to vascular, infection,

tumours, trauma.


16/42

Hemiplegia alternans :

Lesions of the bulb (med.obl.) of thelast four cranial nerves IX,X,XI,XII,

also called Wallenbergs syndrome. Contralateral hemiplegia due to

crossing/decussation of lateral cortico-

spinal tract in lower medullaoblongata.


17/42

Complete spinal

transection = Total tranverse lesion of myelum - cord

spinal will cause disruption of motor,

somato-sensory and autonomic fibers. Clinical features will be of upper motor

neuron type.

Cause: trauma,tumor,vascular obstruction.

Brown-Sequard syndrome is a hemi -transverse lesion of the myelum.


18/42

Cranial arteritis/vasculitis

Inflammation of bloodvessels, primaryor systemic (rheumatologic disease or

malignancies). Classification is complex and

neurologic effects are protean.

Well known is Temporal arteritis orgiant cell arteritis.


19/42

Multiple sclerosis (MS),

optic neuromyelitis :Are demyelinating diseases ( white

matter consisting of myelin, neural

fibers and tracts). The course is relapsing, remitting,

chronic and progressive.

Etiopathogenesis remains an enigma,appear to be immune related.


20/42

Amyotrophic lateral

sclerosis (ALS) : Motor neuron disease, chronic,

progressive, degenerative disease of

unknown origin. Progressive loss of motor neurons in

spinal cord, brainstem and cortex.

Clinically LMN (atrophic) and UMN(spastic) involvement.


21/42

Syringomyelia :

A disease of spinal cord and brainstem ofunknown cause associated with gliosis and

cavitation of spinal cord and brainstem. Clinically muscular waisting and weakness,

loss of pain and temperature sense butpreservation of touch and pressure

(dissociate anesth) Due to pain-temp. fibers crossing in spinal

cord, dorsal column fibers crossing in M.Obl.


22/42


23/42

Headache disorders :

Extremely common, classification ofInternational Headache Society.

Some familiair forms are : migraine,cluster headache, tension headache,chronic paroxysmal hemicrania.

Treatment are psychologic, physicaland pharmacologic.


24/42

Migraine :

Unilateral, pulsating, moderate tosevere headache, often increasing

with physical activity and reduced bysleep.

Often accompanied by nausea or

vomiting, photophobia andphonophobia with or without auras.


25/42

Cluster headache :

Mostly in men, any age.

Periodicity is the main feature.

Each period lasts 2-3 months andrecurs every year or two.

Mostly nocturnal and characterized bya circadian regularity.

Often precipitated by alcohol.


26/42

Tension-type headaches :

Episodic or chronic.

Diffuse, bilateral, pressing or

tightening in quality, mild to moderatein severity.

Pain involves posterior aspects of headand neck.

Photophobia, phonophobia, nauseamay occur.


27/42

Nociceptive pain =

Somato-sensory system divided into : spino-thalamic tract system (pain, temperatureand viscero reception) and dorsal columnlemniscal system (mechanoreceptionproprioception).

Afferent impulses via 1)lateral thalamic tractto parietal cortex 2)medial thalamic tract tofrontal lobe.

Information coded by nociceptors via A-delta myelinated & C-unmyelinated fibers.


28/42

Physiologic pain

pathways Spino thalamic tract-via

Thalamic relay splits into

Somato-sensory cortex

Frontal cortex


29/42

Neuropathic pain =

Lesions of PNS/CNS pathways for paincan produce : 1)loss or impairment of

pain sense 2)neuropathic pain like inH.zoster, Diabetes M. allodynia.

This increased spontaneous activity is

due to an increased conc. of sodiumchannels and N-epinephrine.


30/42

Motor unit : motor cell radix axon motor

endplate/synapse


31/42

Spinal cord-Referred pain

Axons of afferent nociceptors to cornupost.-spinal cord go to:1)Parietal lobe

2)Spinal neurons + input from viscera,deep muscles, skin spinal segments.

This convergence often mislocalize the

place by the same spinal segment.


32/42

Sensitization by:

Repeated, intense, prolonged stimulican damage the threshold of

nociceptors. Inflammatory mediators like Substance

P, Bradykinin, Prostaglandin,

Leukotrienes, low pH - can causetenderness - hyperalgesia.


33/42

N.V=Trigeminal N.

divided into : Sensory (p.major) skin face + anterior of head.

Motor (p.minor) masseter + pterygoid muscles.

Clinically: no objective sensory loss on examination

(4.5 per 100.000 persons) sudden excruciatingbouts for wksmonths with spontaneousremission.

Cause: compression by a bloodvessel,

demyelination, brainstem lesions, neoplasm Therapy: carbamazepine, phenytoin, surgical.


34/42

Bells Palsy N.VII

Location in Pons, close to N.VIvia internalauditory meatusinner earthrough for.Stylomastoid, gl. Parotis to facial muscles.

Clinically: taste anterior 2/3 of tongue,hyperacusis (N.stapedius), deafness,tinnitus.

Examination: MRI, EMG.

Treatment: eye closing (tape,ointment),massage, prednison. Cause: vascular, infection, trauma, etc.


35/42

Myasthenia gravis

A disease affecting the neuromuscularjunction (neurotransmitter-NT-Acethyl-

cholin disorder). Characterized by fluctuating weakness,

consisting of 2 forms, congenital andacquired.The latter is more common

as the ocular and generalized form.An autoimmune disorder.


36/42


37/42


38/42

Myopathy - classification

Inflammatory (dermato-polymyositis)

Endocrine, Metabolic, Toxic,

Congenital, Muscular dystrophies (Duchenne type)

Myotonic disorders (Myotonia)

Periodic paralysis


39/42

Poly-& Dermato-myositis

Are inflammatory, sporadic myopathies

Clinically: symmetric, painless, progressive

with dominant proximal weakness of limbs,dysphagia or respiratory muscle weaknessmay occur, commonly with DM.

Spontaneous exacerbations and remissions.

50% of Pts respond to corticosteroids.


40/42

Muscular dystrophy

2 forms, both are sex-linked,Duchenne type: acute,

progressive,malignant. The benignBecker type is rarely progressive.

Main features: family history, infantile

& juvenile spinal muscular atrophywith slowly progressive proximalweakness to rapidly fatal disease.


41/42

Clinical features DMP

Weakness, fatigue, pelvic & shouldergirdle muscle atrophy, next to a

Focal facio-scapulo-humeral type. Confirmatory tests: history, laboratory

biochemical aspects, muscle biopsiesand electromyographic (EMG) exam.

Etiology: genetic, metabolic, toxic,traumatic, inflammatory factors.


42/42

Neurofibromatosis

Also called von Recklinghausensdisease is a neuroectodermal disorder

due to genetic abnormalities with Skin caf au lait spots > 6

Neurofibromas of peripheral nerves

Optic nerve or chiasmatic glioma Neurocutaneous syndromes produces

defects in multiple organ systems.

Diabetic Neuropathy-common Complication of DM

Documents