Peripheral Neuropathies Flashcards
Define polyneuropathy
Symmetric distal sensory loss with burning or weakness
Etiologies of polyneuropathy
Adverse effect of medication
Manifestation of systemic disease
Pathogenesis of Guillain-Barre Syndrome
Acute immune-mediated group of polyneuropathies, usually provoked by preceding infection
Acute inflammatory demyelinating polyneuropathy (AIDP)
Types of infections which commonly bring on Guillain-Barre Syndrome
Campylobacter jejuni
Respiratory tract infection
CMV
EBV
Guillain-Barre antibodies to what
Gangliosides which cause axonal injury or immune response to myelin
Guillain-Barre Clinical Features
Ascending symmetric muscle weakness Severe respiratory muscle weakness (intubation) Paraesthesia's common Sensory abnormalities frequently mild Severe back pain Dysautonia
What is Dysautonia?
Tachycardia alternating with bradycardia, urinary retention, HTN alternating with hypotension, orthostatic hypotension, ileus, loss of sweating
Guillian Barre Syndrome Diagnostics
Lumbar puncture
Electromyography (EMG)
Nerve conduction studies
Glycolipid antibodies to gangliosides
Features that make Guillian-Barre Syndrome doubtful
Sensory level
Marked, persistent asymmetry of weakness
Severe/persistent bowel/bladder dysfunction
More than 50 WBC in the CSF
Define Bell’s Palsy
Acute peripheral facial palsy of unknown origin
Bell’s Palsy Anatomy
Fibers for motor output to facial muscles
Parasympathetic fibers to the lacrimal, submandibular, & sublingual salivary glands
Afferent fibers for taste from the anterior 2/3 of tongue
Somatic afferents for external auditory canal and pinna
Pathogenesis of Bell’s Palsy
Most common- herpes simplex
Other infectious causes: EBV, adenovirus, rubella, mumps, influenza B, herpes zoster, coxsackie virus
Ischemia
Clinical Presentation of Bell’s Palsy
Sudden onset Unilateral facial paralysis Eyebrow saggio Inability to close the eye Disappearance of the nasolabial fold Mouth drawn to the non affected side Decreased tearing
Physical Exam for Bell’s Palsy
Assess facial movement
General physical and neurologic exam
Attention to external ear for vesicles or scabbing
Attention to parotid for mass lesions
Bell’s Palsy Course
Onset over hours to 2 days
Progressive with maximal paralysis within 3 weeks of onset
Recovery of some degree of function by 6 months
Bell’s Palsy Management
Glucocorticoid therapy
Patient Information for Bell’s Palsy
Usually caused by a virus
As nerve cell swells, it becomes compressed & it’s protective covering breaks down
Takes time to recover
What is Myasthenia Gravis?
Autoimmune disorder characterized by weakness and fatiguability of skeletal muscle
Pathogenesis of Myasthenia Gravis
Autoantibodies against acetylcholine receptors (AChR-Ab)
Decrease # of acetylcholine receptors due to binding
Destruction of receptors by a compliment-mediated process
T cells bind to acetylcholine receptors and activate B cells
Most have thyme abnormalities
Bimodal distribution of Myasthenia Gravis
Female- 20-30s
Male- 60-80s
Key Symptoms of Myasthenia Gravis
Fluctuating skeletal muscle weakness
Worsened by contractile force
True muscle fatigue not tiredness
Ocular Symptoms of Myasthenia Gravis
Ptosis
EOM often involved leading to diplopia
Ptosis increases with sustained upward gaze or by holding up the opposite eyelid
Bulbar Symptoms of Myasthenia Gravis
Weakness with prolong chewing, jaw weakness
Dysarthria
Dysphagia
Nasal regurgitation of liquids