All of the following statements about Guitlain-Barre syndrome are true, except-
Ans. is 'c' i.e., Descending o Guillain Barre Syndrome is typically an 'ascending' (not descending) neuropathy.o Guillain Barre Syndrome is typically an acute inflammatory demvelinating polyneuropathy. The usually pattern is an ascending paralysis and cranial nerve involvement is common.o The acute immune-mediated polyneuropathies are classified under the eponym Guillain-Barre syndrome (GBS).o GBS is an acute monophasic paralyzing illness, usually provoked by a preceding infection.o Guillain Barre syndrome is thought to result from an immune response to preceeding infection that cross reactss to peripheral nerve.o The triggerring events for GBS is# Campylobacter jejuni (most common)# Cytomegalovirus# Epstein Barr virus# HIVOt her trigering events: -# Immunisation# Surgery# Trauma# Bone marrow transplantationo Historically, the GuiUain-Barre syndrome (GBS) was considered a single disorder:o It now is recoginized as a heterogeneous syndrome with several variant forms.o The major forms are : -# Acute inflammatory demyelinating polyradiculoneuropathy (AIDP).# The Miller Fisher syndrome (MFS).# Acute motor axonal neuropathy (AMAN)# Acute sensorimotor axonal neuropathy (AMSAN),Each form of GBS has distinguishing clinical, pathophysiologic and pathologic feature.Pathogenesiso One proposed mechanism for Guillain-Barre syndrome (GBS) is that an antecedent infection evokes an immune response, which in turn cross-reacts with peripheral nerve components because of the sharing of cross-reactive epitopes "molecular mimicry "o The end result is an acute polyneuropathy.o This immune response is directed towards the mvelin or the axon ofperipheral nerve.o Immune reactions directed against epitopes in Schwann cell surface membrane or myelin cause acute inflammatory demyelinating neuropathy (AIDP).o The pathology is that of multifocal inflammatory demyelination starting at the level of the nerve roots.o The earliest changes are frequently seen at the nodes of Ranvier.o Both the cellular and humoral immune responses participate in the process.o Invasion by activated T-cell is followed by macrophage-mediated demyelination with evidence of complement and immunoglobulin deposition on myelin and Schwann cell.o No specific myelin antigen have been identified.Symptomso The major clinical manifestations are motor manifestations i.e., weakness that evolves more or less symmetrically over a period of several days.o Weakness usually begins in the lower extremities and progressively involves the trunk, the upper limbs and finally the bulbar muscles a pattern known as landry ascending paralysisQ,o Proximal and distal muscles are involved relatively symmetricallyQ but asymmetry is seen in 9% of patientso Deep tendon reflexes usually disappearQ.o The weakness progresses in about 5% of patient to total motor paralysisQ with respiratory failureQ within few days.o Cranial nerve involvement can occur0.# The most common cranial nerve to be involved is facial nerveQ. Sometimes B/L facial nerve involvement can also occur. Other cranial nerves can be involved later on.o Disturbance of autonomicfunctionQ# (Sinus tachycardia and less often bradycardia, facial flushing, fluctuating hypertens ion and hypotension, loss of sweating or episodic profuse diaphoresis).o Urinary retention occurs in about 15% of patientsQ.# Bladder dysfunction usually occurs in severe cases.o Sensory involvement in case of Guillain Bar re svndrome-# Cutaneous sensory deficits e.g loss of pain and temperature sensation are usually relatively mild but function subserved by large sensory fibres such as deep tendon reflexes and proprioception are maximmally affected.
Inflammatory'
Demyelinating
Descending
Cranial nerve involvement
Peripheral Nerve & Muscles